!

!
COMPLETE
ORTHOPEDICS
! ! With!reference!from:!
1) Y&Z!Orthopedics!
2) Jo!&!Li!(edited!by!Wai!Wai)!
3) Orthopedia!

! 1!
Contents!Page!

General!Orthopedics!

• Physical!Examination!
• History!Taking!
• Principles!of!Fractures!and!Dislocations!
• Polytrauma!
• Open!Fractures!!
• Limb!threatening!conditions!

Regional!Orthopedics!

• Shoulder!
• Humerus!
• Elbow!and!Forearm!
• Wrist!and!Hand!!
• Pelvis!
• Hip!and!femur!
• Knee!
• Tibia!and!Fibula!
• Foot!and!Ankle!!
• Spine!

Orthopedic!Conditions!

• Osteoarthritis!!
• Rheumatic!Diseases!!
• Crystal!deposition!diseases!!
• Metabolic!Diseases!
• Genetic!Disorders!
• Osteochondritis!
• Bone!Tumours!!
• Diabetic!Foot!
• Paediatric!
• Conditions!
• Trauma!
• Bone!and!Joint!Infections!
!

! !

! 2!
Chapter!1:!Orthopedics!Physical!Examination!
BASIC OF CLINICAL EXAMINATION

LOOK
• Skin: scar, colour changes, abnormal creases, swelling!(soft!tissue!or!bony),!sinuses,!discoloration
• Muscle:!wasting,!fixed!deformities!
• Bone:!deformity,!alignment,!swelling

FEEL
• Skin: Temperature
• Bone/ joints: outlines normal/ synovium thickened/ excessive fluid in joint
• Tenderness : distribution (Ligaments,!tendons,!muscles,!Bony!landmarks)
• Wasting!(with!measurement)

MOVE
• Active: to test power
• Passive: to test ROM, painful, crepitus
• Abnormal movement: unstable joint

SPECIAL TESTS

NEUROVASCULAR EXAMINATION: motor, sensation, reflexes

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Chapter!2:!History!Taking!for!Orthopaedic!Conditions!
Biodata: Name, Age, Race, Gender, Occupation Deformities
PRESENTING COMPLAINTS & ASSOCIATED SYMPTOMS • Normal variation
o Associated symptoms • Pathological
! General o Bow legs- genu varum/ varus (part distal to joint displaced
• Swelling –esp in hip, knee, ankles towards the midline)
o Permanent or acute(after injury) o Knock-knees- genu vagum/ vagus (part distal to jt away
• Suspect spine pathology: back/neck pain, from midline)
paresthesia/numbess o Kyphosis/ lordosis
! Shoulder: weakness, cervical spine o Scoliosis
! Hand: crepitus, cervical spine o Bony lumps
! Hip: lumbar spine o Fixed deformity- particular movement cannot be completed
! Knee: giving way, locking, crepitus, lumbar spine ! In spine: structural deformity (others: postural
! Foot: giving way, lumbar spine deformity)
! Other medical illness: RA, AS, Down’s syndrome • 6 causes of bone deformity
o Congenital
Pain (SOCRATES) o Rickets/ osteomalasia
o Bone dysplasia
• Site: location and referred location – back pain only? Or radiation
o Physeal injury
to thigh and feet (ask specific sites" dermatomal/peripheral
o Fracture malunion
nerve distribution)
o Paget’s dx
• Character: shooting (nerve), cramping
• 6 causes of joint deformity
• Timing:
o Skin contracture- burn
o Early morning pain- inflammation
o Fascial contracture- Dupuytren;s
o Relieved at night- mechanical in nature
o Muscle contracture – Volkmann;s
o Night pain- implies severity, malignancy, infx
o Muscle imbalance
• Relieving factor:
o Joint instability
o Medications (include analgesics and TCM), posture
o Joint destruction
• Aggravating factor Weakness
o History of trauma
• Ddxneuro causes
o RTA
! If fell: able to get up? How did you come to Change in sensibility
hospital • Establish the exact distribution → identify the faulty source
! Motorcyclist: able to get up aft injury • Tingling / numbness →
! car: seat belt was on? o Pressure from neighbouring structure- prolapsed disc
• Duration o Local ischemia
o How long each time, when the pain appears o Peripheral neuropathy
o Similar previous episode or pain? Specific to region
• Previous treatment done (ask from the least invasive • HIP
o Medication : glucosamine, NSAID, TCM, acupuncture, o Whether pt can take care of their feet/ pedicure
hyaluronic acid, analgesic • KNEE
o Others : osteotomy, TKR , other sx o Locking: implies mechanical block/ meniscus tear
o Previous x ray ! Any pain on walking down stairs ?
• Severity: o Giving way/ jumps out- ligamentous deficiency, recurrent
o How far can you walk before resting subluxation,patellofemoral problem)
o When rest how long is needed before walking o Pain at one point at the joint (meniscus tear) or pain along
o Any pain at rest? joint line (OA)
Swelling o Problem climbing stairs (patellofemoral joint) or pain on
• From ST/joint/ bone?Appear immediately after injury- hematoma standing (patellotibial joint)
• Appear slowly- inflammation, joint effusion o Stiffness
• Painful – inflammation/ infection/ CA ! Morning (OA) relieved during the day
Stiffness ! Inflammatory arthritis: constant pain
o Swollen now? Before this?
• By features o Any noise along the joint ?crepitus
o Generalised – RA/AS or localised o Can walk? Climb stairs? Squat down?
o Early morning + involve many joints – RA
• LUMBAR SPINE
o Transient (esp after activity) + involve a few joints- OA
in sciatica –compression / injury to sciatic nerve→ pain, altered
• By grades of joint stiffness
sensation (along L4/L5,S1,2,3), loss ankle jerk, if severe muscle
o All movements absent:
! surgical fusion (anthrodesis) power loss along distrubtion of nerve
! pathological fusion(ankylosis) o Pain: Radiation (look for dermatomal distribution)
• Acute suppurative arthritis- bony ankylosis o History of injury
• Tuberculous arthritis- fibrous ankylosis o Ask features of neurogenic claudication (spinal stenosis)
o All movements limited ! Sleep at night?
! Non infective arthritis- usually due to synovial o Weakness in muscle innervated by sciatic nerve
swelling/ capsular fibrosis ankle flexion, extension, inversion and eversion, great
o One or two movements limited toe extension
! Mechanical or joint contracture o Radiation (dermatomal distribution) and neuro deficit)
Lax joints ! Neurological symptoms (numbness/ paresthesia)
• Generalised hypermobility- in 5% of population; Marfan’s & distribution
syndrome, osteogensisimperfecta (brittle bone disease with blue o Relate to hx: Common due to herniated IVD (young ) or
scelra) spinal canal/ root canal stenosis (elderly)

! 4!
 o Cauda equina: sphincter disturbance (bladder and bowel
symptoms, saddle anaesthesia, lower limb weakness)
o Red flags:
! Suggestive of infection/ cancer
• Non-mechanical pain: Night pain (wakes
one up, cannot sleep), rest pain, night
sweats
• Constitutional symptoms: Fever,
unexplained LOW (>10kg in 6 months),
LOA
• Medical history: Cancer, recent bacterial
infection
• Age of onset: <20years, >55years
• Obvious deformities
• Hx of TB
! Suggestive of spinal fracture: Trauma,
osteoporosis, obvious deformities
! Suggestive of serious injuries
• Cauda equina: saddle anaesthesia,
bladder or bowel incontinence, disturbed
gait
• Neurological deficits
• Pain for >4-6weeks
• Failure to improve with therapy
! Suggestive of high risk of permanent damage to
nerve
• Significant muscle wasting/weakness
• Loss of tendon reflexes
• Positive Babinski reflex
! Progressive
! Thoracic back pain
! Hairy patch/ café-au-lait spots (esp in kids)
o Scoliosis
! When was the deformity first noted
! Manner it was noted- health screening, family,
doctor?
! Perinatal history
! Development milestones
! Family history of scoliosis and dx that may aff M/S
system
! Women with scoliosis has 1% higher risk of giving
birth to child with scoliosis, hence scree n kid
• FEET
o Referred pain: back pain
o Pins and needle ( lumbar spine patho/ nerve entrapment/
peripheral neuropathy)
o Footwear
Constitutional symptoms: Fever, night sweats, LOW, LOA
FUNCTION
Loss of function
• LL
o How does it affect function: walking distance, use of stairs
o Factor affecting living: lift landing, walking aid
• UL
o How does it affect function: washing, dressing, combing,
feeding, writing, use of chopsticks (fine motor skill)
o Factor affecting living: hand dominance
• ADL dependence vs pre-morbid status
o DEATHS: dressing, eating, ambulating, toileting, hygiene,
swallowing
Lower limb • Walking distance
• Going to shops
• Use of stairs
• Use of walking aids (community ambulance)
• Hip: ability to put on socks/ clip toenails
Upper limb • Hand dominance
• Washing, dressing (hook bra), combing, feeding,
writing
• Fine motor skills: chopsticks, reading newspapers,
driving, using handphones
FAMILY HISTORY
PAST MEDICAL HISTORY
• Medical history
• Past treatment
o Analgesic
o Warfarin, aspirin, blood thinner → assess fitness for
operation
o TCM and acupuncture
o glucosamine, NSAID, TCM, acupuncture, hyaluronic acid
o surgery done: osteotomy, TKR , other sx
• Personal- comorbidities (fitness for op/ RF), medication history
(current medication, previous medication, TCM, drug allergies),
previous surgery/ admissions/ illness/accidents
• Family- musculoskeletal disorders within fx
SOCIAL HISTORY (ASSTOSsED)
• Alcohol, smoking, support, travel, occupation/past jobs, similar
symptoms, exercise, diet
• Functional Asessemnt of disability
o Walking aids? Ambulant? ADLS, how far can she walk?
o Work, travek, recreation, home, level of support from fx and
friends
o Previous status and current disability
• Caregiver after surgery!

SYSTEMIC REVIEW
• Usual systemic review
• Recent history of trauma/ falls
• Rule out extra-articular manifestations of certain diseases (eg RA)
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! 5!
Chapter 3: Principles of Fractures o angulation, rotation & axial compression #: consist of an
oblique component caused by compression and a
GENERAL PRINCIPLES transverse component caused by angulation " oblique #
History Metaphysial vs Diaphyseal Fractures
Causes • Metaphyseal
o Healing: not by callus, but by ingrowth (as little
Mechanism movement)
Assessing injury o Movement: Little because usually compaction fracture
Fracture Emergencies (stable) as lots of cancellous bone in metaphyses
Metaphyseal vs Diaphyseal Fractures o Rapid repair: Consolidate within 3 weeks
Joint Injuries o Management
! Minimal displacement, extra-articular: Simply cast
Imaging and allow healing by ingrowth
Radiographic Description of fractures ! Displacement, intra-articular: Once reduced will
Stability of Fractures become unstable, hence must stabilize; might
Healing even need to fill with bone graft to fill gaps from
disimpaction (put in cast)
ASSESSING COMPLICATIONS OF FRACTURE • Diaphyseal
MANAGEMENT o Healing: by callus
Initial management o Movement: Lots of motion
Definitive management Fracture Emergencies
PRINCIPLES OF MX OF DISLOCATIONS • Open fractures
• Compartment syndrome (tibia, forearm, femur, foot, hand –
TABLE SUMMARY OF #S AND DISLOCATIONS
areas with myocutaneous or myofascial compartments)
GENERAL PRINCIPLES • Neurovascular compromise
History • Very bad fractures with haemodynamic instability: Unstable
• Clinical Features pelvic fractures - Openbook pelvic fractures
o Pain and tenderness • Spine
o Deformity & abnormal resting position • Multiply injured
o Swelling • Fracture-dislocations – skin or soft tissue compromise (closed
o Loss of function: inability to weight bear, abnormal FD can become open if not reduced)
mobility and crepitus (avoid) Joint Injuries
o Neurovascular compromise (impt to document)
• Ligament Injuries
! Concomitant injuries
o Types
• High vs Low velocity
! Sprain: Painful twisting without actual tearing of
o Indication of injury severity (concomitant injuries) ligaments or capsule
o Pathological fractures ! Strain: May involve tearing of some fibers
• Mechanism of injury ! Tear/Ruptured ligament: Partial/ complete rupture
Causes o Management
• Trauma: direct and indirect trauma ! Conservative: Splint " Physiotherapy " Replace
• Stress Fractures (repetitive mechanical loading): Normal bone; splint with functional brace
abnormal stress ! Surgical reconstruction: Symptomatic instability or
o Common sites avulsion of large enough bone fragment
! Metatarsal (esp 2nd) • Articular Injuries
! Femoral Neck o Types
! Tibia ! Dislocation: Complete loss of articulation at joint
! Others: Shaft of humerus, Pars interarticularis of 5th • Associated with
lumbar vertebra, pubic rami, femoral shaft, patella, o Shaft #s often require open reduction
calcaneum, navicular, fibula o Peri-articular fracture may increase
• Pathological Fractures: (OMIT) Abnormal bone; normal stress instability (eg. Hill-sachs lesion)
o Osteopenia/osteoporosis • Anatomy
o Metabolic bone disease (hyperPTH, hyperthyroidism, • Ligamentous laxity (especially for
osteoporosis, osteogenesis imperfect, rickets) recurrent dislocations)
o Infection
• Common: Shoulder (commonest), knee
o Tumour
(2nd commonest) – stability of knee
• Periprosthetic
depends on ligaments, hip, elbow
Mechanism ! Subluxation: Partial loss of articulation at joint
• Direct trauma o Management
o Tapping fracture; occur when a force is applied over small ! Reduction as soon as possible (usually with
area, usually transverse fracture line (eg nightstick fracture) anesthesia and muscle relaxant)
o crush fracture: with extensive soft tissue damage, Imaging
extensive comminution • X-ray: rule of 2s
o penetrating fracture: produced by projectiles, gunshot o 2 views (orthogonal views; AP and lateral)
• Indirect trauma o 2 joints (above and below site of injury)
o avulsion or tension #: # line is perpendicular to line of force; o 2 sides (for paediatric cases)
happen to the patella or olecranon when the knee or elbow o 2 times (before and after reduction)
is forcibly flexed while extensor muscles are contracting o 2 opinions
o angulation #: transverse #, may form butterfly fragment • MRI: Soft tissue injury, Occult fractures
o rotation fracture ; when a piece of chalk is twisted until it
• CT: Image bone surface (often for complicated fractures)
breaks, a characteristic spiral fracture line is produced
• Bone scan (radioisotope scanning): only +ve abt a week after #
o compression fracture ; T- or Y-shaped fracture (e.g. at the
o Stress fractures
lower end of the humerus or femur)
o Undisplaced fractures
! 6!
Description (on Xray) (ACS MAAD) Stability of Fractures
• Identify view + date + patient identification (“This is an AP X-ray • Stable: When upon reduction, it remains reduced with simple
view of the knee joint taken on 1/12/10 for Mdm Gee”) splintage and normal movement
• Anatomy o Inferred by x-rays and clinical examination (eg. can move
o What – Which bone >50% of normal range)
o Where – Diaphysis / Metaphysis / Epiphysis • Types of fractures
! If diaphyseal, describe by thirds (prox/ middle/ distal) o Oblique/spiral – Unstable
• Complete vs Incomplete ! Translational/rotational displacement hence need
• Simple vs Comminuted complex splint to reduce and hold
• Fracture Morphology o Avulsion – Unstable
! Muscle pull keeps fragments apart
o Complete transverse translation – Unstable
! Periosteal stripping circumferentially
o Intra-articular
• Acceptable displacement – if deemed acceptable, can just
immobilize in that position
o Bone union requires >50% of bone contact
o Angulation can accept up to 20 deg for long bones (in
children) – but in adults may accept lower because of
poorer remodeling capacity

Healing
• Purpose of splinting
o Alleviate pain
o Ensure union takes place in good position
o Permit early movement and return to function
• General stages in normal healing process
o 0h: Haematoma formation
o Transverse # o Within 8h: Inflammation and cellular proliferation under
! Mechanism: 3 point bend; direct force, high energy periosteum and within the medullary cana
! Stability: ! Macrophages, undifferentiated stem cells and
• Usually remain in place after reduction platelets surround fracture site
• But may be unstable in upper limb (due to ! Granulation tissue
lateral motion as opposed to lower limb where ! Involve osteoclasts hence fracture gap accentuated
axial loading stabilizes #) within first few weeks
o Oblique # o 3-12 weeks: callus proliferation (formation & calcification)
! Mechanism: unequal force distribution of 3 point ! 3-6 weeks: osteoclasts remove sharp edges (thus #
bend; angular and rotational force more visible on radiographs); fibrocartilage callus
! Stability: Tendency to slip/displace forms within hematoma
o Spiral # (# line > 2x bone width) • Soft callus - cartilage
! Mechanism: Torsion; rotational force, low energy ! 6-12 weeks: bone forms within the callus
! Stability: Tendency to slip/displace (endochondral calcification of cartilage), bridging
o Comminuted # (>2 pieces) vs Simple # fragments; forming woven bone
! Mechanism: Often complicated; direct force, high • Hard callus – calcified cartilage: # union
energy o 6-12 months: Consolidation
! Stability: Often unstable ! Woven bone replaced by lamellar bone
o Butterfly # (2 lines break out obliquely from point of contact o 1-2 years: normal architecture achieved thru remodeling
of blow, producing a free-floating butterfly fragment) ! Takes years
! Mechanism: low velocity injuries due to 3 point bend • 2 main ways
o Avulsion #: strong muscle inserting into small bone
o Callus formation
! Eg. quads to patella, triceps to olecranon, peroneus
! In response to movement
tertius to 5th MT head
! Main advantage: Stronger
o Compression #
o Gap healing: In response to absolute immobilization
• Intra vs Extra Articular
• Shape of fracture affects rate of healing
o Extra-articular: diaphysis or metaphysis
o Spiral heal faster than transverse fracture due to larger
o Intra-articular: salter-harris classification (for children)
area of contact
• Associated structures (aka soft tissue):
• XR evaluation of healing: trabeculae cross # site, visible callus
o Calcification, gas, foreign bodies
bridging site
• Displacement (Type and plane): only comment w 2 views!
• Union vs Consolidation
o Translation/ apposition (% displacement)
Union Consolidation
! Shifting of fragments (sideways, forwards,
Fracture line Fracture line visible Fracture line almost
backwards etc) resulting in loss of contact between
obliterated and crossed
fragments " any shortening? (ie. Bayonet #)
by bone trabeculae
o Angulation/deformity
! With respect to apex (eg. volar apex angulation – State of callus Ensheathing callus Calcified callus ossified
apex of angulation pointing volar) calcified
! Angle Tenderness Fracture site tender Fracture site non-tender
o Rotation: Rotation on its longitudinal axis to palpation or
o Altered length angulation stress
! Fragment distraction and separation Completion Incomplete repair: Complete repair
! Fragment overlap Unsafe to subject bone
• Open vs Closed to stress
• State of bone (any underlying pathology?)
! 7!
ASSESSING COMPLICATIONS OF FRACTURES
Local Early Soft Tissue Injury 1. Nerve injury: neuropraxia, axonometsis, neurotmesis (REFER to hand injuries)
2. Vascular Injury
3. Visceral Injury
4. Fracture blisters (refer to Cx of open #)
Swelling related 1. Compartment syndrome (refer to Cx of open #)
2. Haemarthrosis
Infection Gas gangrene, osteomyelitis
Late Union-related • Delayed union
(refer to Cx of open #) • Non-union: atrophic, hypertrophic, infected
• Malunion
Avascular necrosis • Common sites: Head of femur, proximal scaphoid, lunate, neck of talus
(refer to Cx of open #)
Growth disturbance
Joint related • Joint instability
• Osteoarthritis
• Joint stiffness
Complex regional pain • Chronic progressive disease characterized by severe pain, swelling, skin changes due to
syndrome dysregulation of ANS post trauma
Soft tissue related • Heterotrophic ossification
• Muscle contracture
• Tendon rupture
• Nerve compression or entrapment
Systemic • Fat embolism syndrome (long bones) " refer to Cx of open #
• Hemorrhagic shock
• ARDS, MODS
• DVT/PE
• Sepsis
MANAGEMENT
Principles of management FRIAR: First aid " Reduction " Immobilisation " Active Rehabilitation
Initial management: refer to “open fractures - emergency care”
o General Mx of #
! ABCDE
• Assess neurovascular status, beware of compartment syndrome
• If hypovolemic " IV fluids, packed cells, whole blood
! Analgesics
! Preliminary skin traction " relieve pain, minimize further displacement
! How to determine if # is displaced or not: compare continuity of trabeculae lines
Definitive Management – Steps: 1) reduce 2) stabilize 3) rehabilitate
o Concepts:
! Operative vs Non-Operative
• Non-operative: Analgesia, splint/protect, restore function
• Operative: Reduction, fixation, others (arthroplasty, amputation)
o Contraindications: severe osteoporosis, active infection or osteomyelitis, severe comminution that cannot be
reduced, severe soft injury, poor general condition, nondisplaced fracture
! Broad principles:
• Reduce: Restore articular surface and normal alignment
• Stabilise: Allow healing and minimize pain
o Indications for # fixation
! To save life or limb
! To reconstruct displaced articular fractures
! To prevent deformity
! To promote union when it is delayed
! Improved function following early motion
• Rehab: Restore function
! Objectives: Restore function, Prevent OA
o Reduction
! Objective: adequate (not perfect) apposition and normal alignment (except for intra-articular #s where anatomic reduction is
mandatory to restore joint congruency with absolute stability as irregularity will predispose to OA)
• Imperfect apposition may be acceptable while imperfect alignment is rarely acceptable
• Attempt closed reduction as much as possible
o If successful: then stabilize
o If unsuccessful: open reduction, then stabilize (usually internal fixation)
! Contraindications
• Little or no displacement (i.e reduce when amt of displacement is unacceptable)
• When displacement does not matter – eg. clavicle, fibula
• When reduction unlikely to succeed – eg. compression # of vertebrae
! 3 Methods: 1) Manipulation 2) Mechanical Traction 3) Open Reduction
• Closed Reduction
o Principles:
! 8!
 ! Minimse damage to BS
! Rely on soft tissue attachments
! Rarely adequate for intra-articular #
! Difficult in babies whose bones cannot be seen in XR
o Manipulation
! Indications
• Minimally displaced #
• Most fractures in children
• Initial management for unstable fractures (prior to definitive mechanical fixation)
! Method
• Distal part of limb pulled in line of the bone
• Repositioning of disengaged fragments
• Alignment adjusted in each plane
o Mechanical Traction: Indications: When manipulation difficult due to powerful muscle pull
• Open Reduction (Operation)
o Indications: NO CAST
! N – Non-union
! O – Open fracture
! C – neurovascular Compromise (associated injuries)
! A – intra- Articular fractures (where there is large articular fragment that needs accurate positioning; require
anatomic reduction)
! S – Salter-Harris 3, 4, 5 and/or special situations depending on Site
• Cannot cast or apply traction due to site (eg. hip fracture)
! T – polyTrauma
! Others:
• Failure of closed reduction (soft tissue interposition/difficulty controlling fragments)
• Avulsion fractures (fragments held apart by muscle pull)
• Pathological fractures
• When internal fixation needed (unstable fractures like fracture dislocations)
• Fracture in paraplegics for nursing access
• Potential for improved function w ORIF
• Infection
• New fracture thru screw holes
• Implant failure
• Stabilisation
o Principle: Stabilize the fracture site but do not completely immobilize the limb if possible; maintain till united; jt above & below for shaft #
o Principles of # fixation: Translational stability (3 point contact) + Rotational stability (engaging e metaphysis) + Axial stability
(quality/strength of implant)
External stabilization
1. splints/tape Non-rigid fixation – risk of loss of reduction
2. casts but stimulate rapid callus formation
3. traction
4. external fixator
Internal fixation Rigid fixation – immediate
1. percutaneous pinning (Kirschner or K-wires) loading but does not
2. extramedullary fixation (screws, plates, wires) stimulate callus formation
3. intramedullary fixation (rods) - biomechanically advantageous
o Sustained traction
! Principles
• Line of pull in alignment with long axis of bone
• Continuous traction maintained
• No interruption with line of pull
• Adequate counter traction
! Mechanism: Traction can be skin or skeletal
• Gravity
• Skin: Works by friction
• Skeletal: Works by tension
o Skeletal traction can be with Thomas’s splint or pulley frame or both
o Sites of Steinmenn pin insertion: tibia, distal femur, skull – as deep as inner table, calcaneum
! Types: Fixed, Balanced, Combined
! Complications:
• Circulatory embarrassment
• Nerve injury (Common peroneal palsy " weakness of dorsi flexion " foot drop)
• Skin: Pin-site infection, blisters, ulcers, pressure sores (Buttocks, Tendo Achilles, under heel)
• Problems with immobilization: DVT, pneumonia, bed sores, UTI
• Loosening of Steinmann pin
• Ring pressure (Thomas’s splint)
! Traction care
! Specific Examples (refer to traction slides)
• Straight leg traction (Buck’s traction): 10% of body weight
• Hamilton Russell: Vertical and horizontal line of pull to create a diagonal vector pull that is in line with the femur
! 9!
 o Usually for proximal femur fractures
• Thomas Splint with Traction: Subtrochanteric/Femoral shaft fractures
• Bryant’s traction: position BrYant’s traction: Bent Y
o Patient’s body is the stem of the Y lying on the bed, and legs are the ends of the Y up in the air
• Pearson knee piece: Distal femur or femoral shaft fractures where gastrocnemius needs to be relaxed
o Cast splintage – Need to cover joint above and below
! Principles
• One joint above and below the #
• Cast is well molded with no pressure points
• Padding at bony prominences
• Backslab instead of full cast in acute setting as swelling likely to occur
• Always place a backslab/ U slab even if patient if just admitted for pain control
• Elevation to prevent swelling
• All hand fractures have a standard functional hand position cast
! Indications
• Fractures that can be reduced and stably maintained
• No major soft tissue injury
• No suspicion of compartment syndrome
• No vascular compromise
! Complications
• Immobility: Stiffness
• Pressure
o Vascular compression (tight cast): Compartment syndrome
o Pressure sores – if cast not applied smoothly
o Skin abrasion or laceration (during removing plaster)
• Looseness: Delayed union (fracture not held due to loose cast)
! Types of plaster casting
• Forearm U slab: forearm #
• Shoulder U and O slab: proximal an midshaft humeral #
• Intrinsic plus hand slab: hand # Figure'1:'Air'Cast'
• Above knee cylinder slab: knee injuries
• Above knee slab: tibia/fibular #
• Below knee slab: ankle #
• Air cast - Advantages: can remove (more hygienic), can weight bear
o Functional bracing
! Mechanism: Segments of a cast are applied only over the shafts of the bones leaving the joints free; cast segments connected
by hinges allowing movements in one plane
! Use
• Usually used after 3-6 weeks of traction or conventional plaster
• Commonly used for humerus and tibia
o Internal fixation
! Indications
• Fractures that cannot be reduced except by operation
• Inherently unstable #s – eg. dislocation fracture
• #s that unite poorly (NOF fracture)
• Pathological #s – where bone disease may prevent healing
• Multiple #s
• #s in patients with severe nursing difficulties
! Types
• Screws (have screw head and screw tract)
o Reducing single fragments onto main shaft of tubular bone
o Fitting together fragments of metaphyseal fracture
• Wires (Kirschner wires) – Used when fracture healing is predictably quick
o Children fractures
o Distal radius fractures
o Tension band wiring for patellar fracutres
• Plates and Screws
o Metaphyseal fractures of long bones
o Diaphyseal fractures of radius and ulna
o Intra-articular
• Intramedullary nail
o Used for long bones: Femur, tibia, humerus
o Have holes for interlocking screws
! Complications of Internal Fixation / Prosthesis
• Immediate
o Surgery Related: Blood loss, Infection, Neurovascular compromise
o GA Related: Cardiovascular, allergy, paralysis, AMI, stroke
o Prosthesis related: Peri-prosthetic fracture
• Late
o Systemic: DVT – for lower limb (thus importance of early mobilization!!!! " fixation construct is stable enough
to allow postopersative functional care)
! 10!
 o Local
! Peri-prosthetic fracture
! Implant failure – wear and tear
! Non-union
! Re-fracture
o External fixation: Bone is transfixed above and below the fracture with screws or pins or tensioned wires and then connected to each
other by rigid bars
! Rationale: Achieve immediate stability without traumatizing periosteum and endosteum further
! Role: Usually used as a temporary measure when difficult for definitive fixation initially; often replaced by other forms of fixation
as soon as soft tissue lesions have healed
! Indications
• Fractures with severe soft tissue damage (where wound indicated to be left open for inspection) or swelling – need to
wait for swelling to subside for definitive management
• Severely comminuted and unstable fractures
• Unstable joints
• Haemodynamically unstable patients
• Fractures of pelvis (which cannot be controlled by other method)
• Infected fractures – Internal fixation not suitable (external fixator can be easily removed in event when biofilm is formed)
• Severe multiple injuries/Poly trauma – Early stabilization reduces risk of serious complications
! Parts of external fixator: Schanz pins + Trans-fixation bar + Pin bar clamp
! Methods to increase stability of external fixator
• Multifixator: Fix in multiple planes
• More bars and more pins
• Position: 2 outer (as far apart) and 2 inner (as close as possible)
! Advantages and disadvantages
• Advantages
o No foreign material in wound
o Minimal further soft tissue damage
o Provides easy access to wound
o Can be removed easily (if infected or need further debridement)
• Disadvantages
o Potential for pins to injure neurovascular structures
o Pin loosening
o Pin-track infections
• Rehabilitation
o Prevention of edema: Elevation
o Exercise: Active exercise + Assisted movement " avoid joint stiffness + regain strength and function
! Isometric exercises to avoid muscle atrophy
! ROM for adjacent joints
! Continuous passive motion (CPM) following rigid fixation of fracture allows joint motion to prevent stiffness for intra-articular
fractures
! After cast/splint removed and # healed " resistive muscle strengthening
! Evaluate bone healing (clinical + XR)
o Functional activity
• Alternative management: Arthroplasty, Amputation

Principles of management of dislocations

• 5 main clinical presentations:
o Pain + swelling + change of normal contour of joint (eg. flattening of deltoid in shoulder D/L) + loss of motion + postural change
• Always closed reduction is possible under general or local anesthesia / sedation
o Indications for open reduction
! failed closed reduction due to interposition of soft tissue or bone fragment
! redislocation after closed reduction or impossible to maintain the
! reduction state
! neurologic deficit after closed reduction
! no improvement of circulation after closed reduction
• Emergently try to reduce as soon as possible
• Immobilization (cast, splint, traction)
• Associated injury of neurovascular structure (more often affected than in fractures)
o Sciatic nerve injury in posterior D/L of of hip
o Common peroneal nerve in medial D/L of knee
o Axillary nerve or brachial plexus in shoulder D/L
o Popliteal artery injury in knee dislocation
• Rehabilitation (early mobilization!)
o starts A.S.A.P.
o keep non-immobilised joints mobile
o avoid muscle wasting
o physiotherapy

! 11!
 Table summary of fracture and dislocations
Radial head trauma: MUA (supination, direct Monteggia #, PI Nerve
Upper limb fractures dislocations by Lee Yizhi dislocation pressure), cast 6/52 inj
Fracture Method Remarks
Clavicle Sling 3/52 Malunion in adults
Physio Excellent remodeling
in children Pulled elbow Sling 3/7 or Pain, lateral
Scapula body: Sling & physio Associated with 1)rib # Supinate + flex elbow tenderness, refusal to
Scapula neck: ORIF if # dislocatn 2)lung contusion move arm
3)hemo/pneumothorax 9m-6yrs
Body # by crushing No X-ray findings
force Radial head slips out
AC subluxatn: Sling ~1/52 & physio Partial dislocatn: AC of annular lig
AC dislocatn: young and active : Arthrodesis, ligaments torn Radius and ulnar Compartment sx, PIN/
3/52 rest, physio Complete dislocation: in adults: ORIF (plates/screws/rods) AIN inj,
Inactive: Sling & physio CC ligaments torn in children: Long arm cast 6/52, check x-ray at delayed/non/mal-
Late OA: excision outer 1/3 clavicle (conoid & trapezoid) 2/52 union, PIN
Tenting of skin may
cause necrosis Single forearm ORIF or long arm cast 12/52 Non-union!
Sternoclavicular Anterior: conservative Post dislocatn: bone Cross-union
dislocatn Posterior: ORIF Tracheal and vascular Monteggia’s: ORIF (ulnar plating, reduce radial Radial/ PIN palsy
compressn head), long arm cast 90o flexion, (Mont), ECU & EDM
Anterior dislocatn: Reduction under GA X-ray to exclude # partial supinatn inj (Gal) myositis
Hippocrates/Kocher’s Axillary n often Galeazzi’s: ORIF (radial plating, reduce ulnar Ossificans, non-union,
Sling 3/52 damaged head), long arm cast in supination missed dislocation
Physio 95% of shoulder 6-8/52
# prox humerus: ORIF dislocatns Both in children: Reduction under GA, immobilisatn
Recurrent: Surgery 6/52
Posterior GA Reductn Commonly missed! Colles’ Undisplaced: Splintage in plaster EPL rupture, malunion,
dislocatn: Same as ant dislocatn 4% of shoulder slab median n
dislocatns Displaced: MUA (Bier’s/ hematoma compression,
Prox humerus: Neers 1: Sling 6/52 Usually seen in block), below elbow backslab 6/52 Sudeck’s atrophy,
Neers 2: Collar cuff 6/52 osteoporotic pple >50y in neutral or slight flexion, xray @ DRUJ subluxatn, hand
Neers 3: ORIF/HemiA Try to conserve head 2/52 shoulder stiffness
Neers 4: HemiA in young pts even with Smith’s (reverse As for Colles’ but with wrist
All followed by physio Neers 3/4 Colles’) extension
Shaft of humerus U-slab 3-6/52 + sling Suspect mets in Barton’s ORIF with buttress plate
If very unstable, plate/nail elderly! Radial styloid/ Percut K-wire/ lag screw A/w lunate dislocatn
Chauffeur’s
Supracondylar Closed reductn ASAP Cx: Shortening,
Undisplaced Below elbow cast (exclude PIPJ) AVN, non-union,
C&C 3/52 then sling 3/52 angular deformity
scaphoid 10/52 scaphoid collapse, OA
ORIF (dbl plating) in adult for early (gunstock), ↓ROM
f(x) Acute: Brachial A inj, Displaced ORIF, cast 3/52
GENTLE physio compartment sx, scaphoid
volkmann’s ischaemia Trans-scaphoid Chronic carpal
Myositis ossificans perilunate instability
Lateral condyle Undisplaced: C&C 3/52 Cubitus valgus, tardy dislocation
Displaced: ORIF (Kwire) ulnar palsy: corrective
osteotomy Peri-lunate Closed reduction, cast 6/52 Median n compression
Proximal radius Mason 1: C&C 3/52, gentle physio dislocation If irreducible, OR with IF of Lunate AVN leading to
in adults: Mason 2: ORIF plate & screw scaphoid # if present, CTR and OA
Mason 3: Excision in 48hrs ligamental + capsular repair
Mason 3 with Essex L: Prosthesis, Metacarpal Undisplaced: Crepe bandage 3/52 Rotational malunion,
splint 2/52, physio and finger exercises stiffness
<20o: C&C 2/52 Displaced: Closed reduction,
>20o: MUA, if fail OR. If unstable, IF plaster slab 3/52, finger exercises
In children: (K-wire) Displaced + unstable: ORIF with K-
Olecranon Stable & undisplaced (<2mm + no wire
change in flexion + extend against Bennet’s (intra- CRIF with precut kwires
grav): C&C 3/52 art # dislocation
Displaced: tension band wiring @ base of CMCJ
Displaced + comminuted: plate & of thumb)
screw Phalangeal Undisplaced: buddy splintage 3/52 Treat open wounds
Elbow dislocation MUA (tractn, flexion, push Posterolateral most Displaced: MUA, plasterslab 3/52 first!!
olecranon) then C&C 3/52 or above common or IF with Kwires
elbow backslab Cx= brachial A, Mallet finger Splinting in extension 6/52
median (AIN)/ulnar,
Game-keeper’s Partial tear: short arm cast w thumb
stiffness, myositis
thumb spica
ossificans, associated
Gross instability: ligamental repair
#s

! 12!
Impt Hip & Lower Limb #s and Ds (plus impt tendon ruptures)
Type
Acetabulum, #
Hip, post. D
-- Hip is flexed, add & int rot
Hip, ant. D
-- Hip is abd, ext rot
Fem epiphysis, slipped
-- fem shaft move up & ext rot on epiphysis
Neck of Fem (intracap) #
-- shortened, ext rot
-- 1. subcapital, 2. transcervical
-- osteoporosis impt factor
Garden Classification
o Typ 1: incomplete #, trabeculae angulated
o Typ 2: complete #, trabeculae disrupted
but NOT angulated
o Typ 3: complete #, fem head rotated,
trabeculae disturbed, displc
o Typ 4: complete #, totally displc
Neck of fem, basal (extracap) #
-- shortened, ext rot
Intertroch #
-- shortened, ext rot
Types:
1) # line thru mass of Great Troch,
2) (1) + separation of Less Troch,
3) separation of Great & Less Troch,
4) 4. w a spiral # down prox fem shaft
Fem shaft #
-- leg is shortened, ext rot, abd " due to pull
of quds & hams
Fem Supra, Uni, T & Y condylar #
! 13!
Treatment Remarks & specific Cxs
o minimal displc/ highly frag " Traction, Hamilton-Russell Cxs
o main part intact, fem head displc " ORIF w cancellous o Hemorrhage > 5L
screws & plates o Ruptured urethra, bladder
o Bowel injury
o Muscle relaxant + Reduce, flex knee, hip 900, correct add Cxs
& int rot, lift fem head into acetabulum o Irreducible due to in-turned labrum
o OR if irreducible or bony frags in acetabulum
o ORIF if a/w #s elsewhere o # (fem head, NOF, patellar, fem
shaft)
o Sciatic nerve palsy
o Muscle relaxant + Reduce, flex knee, hip 900, correct abd o AVN due to tearing of capsule
& ext rot, push down, convert to post. D, lift fem head into o 20 OA
acetabulum o Recurrent D
o Myositis Ossifcans (post
exploration or D a/w head injury)
o IF w screws + Manipulate if slip > 30% + epiphyseal
o AVN
closure
o Involvement of Other Hip
o Subtroch Osteotomy if epiphysis closed (chronic)
Tx principles
o Young (< 50 y.o.) ! CRIF
o Undisplc --> CRIF
o Elderly --> arthroplasty
o Displc --> Arthroplasty
o unfit for multiple Sx or badly displc, typ 4, avn & non-union
likely --> Hemiarthroplasty/ Total hip replacement w/o Cxs
tryring CRIF o AVN " disruption of arterial ring
@ base of neck
o Non-union " typ 3 & 4, bone
graft (young), arthroplasty (elderly)
o Displc/ Undisplc --> ORIF w DHS or Gamma Nail, fixation Cxs
not removed unless pat < 45 y.o or pain o AVN & non-union NOT common
o Stable, little frag " DHS w long plate
o Unstable " DHS w long plate or Gamma Nail, then non- Cxs
weight bear crutches after 48 hrs to 16 weeks o Failure of fixation (cutting out of
o Alt -->Traction +/- Thomas’s splint fixation device) " coxa vara*
*if early, bedrest & skeletal traction
o Traction to overcome pull of quads & hams
o Intramed Nail
o Alt --> Traction, EF (Ilizarov), Plating
Cxs
o Fem & Tib # " Cx rate high, early mobilisation by o Hypovolemic shock
Intramed Nail o Fat embolism
o Metastatic # " Intramed Nail + packed cement to o Delayed Union, Non-union "
relieve pain & give support esp. conservative
o Fem shaft # w nerve palsy " exploration w repair + IF o Mal-union "lat. Angulation " Tx
o Fem neck & prox shaft # "DHS + long Plate = osteotomy
o Fem shaft & patellar # " close nailing for both, mobilise o Limb Shortening
knee early o Knee stiffness " due to quads
o Open # "deribement + IF tethering, knee jt invovlement or
o Open #, IIIB,C "conservative or EF prolonged immobilisation
o Child supracondylar " plaster o Infection
o Others " IF for good reduction & permit early
mobilisation
o If displc, grossly comminuted " conservative w traction
Patellar D
Patellar #
Tibial tubercle, avulsion
Quads tendon, rupture
Patellar ligament, rupture
Tibial plateau, #
o all involve articular surface
o key is to get knee f(x) vs pretty x-ray
o knee exercises ASAP
o “bumper #”
o commonly lat. tibial condyle
Tibia & Fibula, #
o Usu. # both, esp. adult
o commonly open
o usu. spiral #
Ankle, ligament injury
o partial/ complete tear of lateral
ligament
o bruising, swelling, tenderness
o painful passive inversion
o complete tear --> excessive
movement
Ankle #
o normally talus seated in mortise
o one or both mall can be #
o eversion + ext rot = oblique # of lat
mall (pushed off), transverse # of
med mall (pulled off); vice-versa for
inversion
Distal tibial & fibular epiphyses, #-
separation
o physeal injury
Calcaneum #
o fall from height
o calcaneum driven up against talus
o flattened Bohler’s angle
o check hip, pelvis, spine for #
o extra-art --> involve posterior part,
calcaneal processes
o intra-art --> oblique # line, run to
superior articular surface
! 14!
o CR, plaster backslab x 3/52, knee exercise Remarks
o vertical # --> cylinder cast 6/52 w crutches during first Injuries to patellar & extensor apparatus of
2/52, physio after cast removal knee
o horizontal, undisplc # --> as of above (patellar #, rupture of quads tendon, rupture
o horizontal, displc # --> 1. sight communition: ORIF, 2. of patellar ligament, avulsion of tibial
limited damage to patellar: partial patellectomy, 3. tubercle) due to:
major damage: patellectomy, repair quads insertion &
1) direct force on knee
lateral expansions
2) violent contraction of quads
Every knee injury, exclude:
o CRIF (w screw)
o ORIF (risk of premature epiphyseal fusion in child) o damage to extensor apparatus
o lateral D of patellar w spontaneous
o Tendon reattachment, plaster cast, quads exercises at reduction
2nd week, weight bear at 4th week, felxion at 6th week o torn ligaments
o As of above o torn mensici
o minimally displc --> aspirate hemarthrosis, compression
bandage, CPM & active exercise, weight bear after 6/52 Cxs
o comminuted--> aspirate, compression bandage, sk o Compartment syndrome
traction, CPM & exercise crutches after 6/52 o Valgus deformity
o depressed # --> CR or ORIF, active exercises ASAP, o Joint stiffness
cast-brace after 2/52
o closed, minimally displc --> full cast x 12/52 (upper thigh Cxs
to MT necks, knee slight flexion, ankle at 900), exercise
foot, ankle, knee ASAP o Infection
o closed, displc --> MUA (IF when CR fails), full cast x o Vascular injury (prox # damage pop
artery)
12/52, exercise ASAP
o comminuted --> EF x 6/52 + partial weight-bear, then o Compartment Syndrome
f(x)al brace o Delayed, Non-union --> Intramed Nail +
o open --> Ab ASAP, debride, clean, leave open (above bone graft indicated
grd II), EF to stabilise, WI, suture or graft when granulate o Malunion --> angulated --> osteotomy
o partial --> crepe bandage, activity ASAP
o complete --> plaster immobilisation or operative repair
Cxs
o Adhesions
o Recurrent subluxation
o 1 mall # --> reduce, cast x 6/52 (below knee), IF with Tx principles
screw if frag large o reduce to restore shape of mortise
o 2 mall #, below tibiofibular jt --> CR, +/- IF ,cast o plaster x 8/52
o 2 mall #, above tibiofibular jt --> unstable, IF with screw
for frag & plate for fibula, +/- transverse screws between Cxs
tibia & fibula
o Joint stiffness
o OA (not common)
o Salter-Harris 1,2 --> MUA, full cast x 3/52, below knee Cxs
cast x next 3/52
o Mal-union (valgus)
o Salter-Harris 3,4 (undisplc) --> as above, re x-ray 5d
o Asymmetrical growth (# thru epiphysis
after to ensure good reduction
may cause fusion of physis)
o Salter-Harris 3,4 (displc) --> ORIF, below knee cast x
o Shortening of leg
6/52
o undisplc --> exercise ASAP, bandage after swell Tx principles
subside, nwb crutches x 6/52 o elevate leg + ice packs --> decrease
o displc, avulsed tuberosity --> CRIF, immobilise in swelling
equinus (relieve tension of tendon Ach), wb after 6/52 o x-rays, CT scans (better views)
o displc, intra-art --> ORIF + bone grafts, splint & elevate,
exercises ASAP, nwb crutches after 3/52, wb after 12/52 Cxs
o Broadening of foot
o Talocalcaneal stiffness --> subtalar
arthrodesis or triple arthrodesis
Chapter 4: Polytrauma
KEY CONCEPTS
Definition, death, types
LIFE THREATENING CONDITIONS
PRINCIPLES OF MANAGEMENT
SCORING SYSTEMS
LATE COMPLICATIONS
PHYSIOLOGIC RESPONSE TO POLYTRAUMA

Key concepts
Definition of polytrauma
• ????presence of 2 long bones# plus 1 visceral injury OR 2
visceral injuries OR ≥ 3 #
• Injury to >1 physical regions or organ systems where at least 1
injury or a combi of several injuries is life threatening
o In polytrauma patients, limb injuries are the commonest and
this can take the form of long bone # or soft tissue injuries.
However it is the head and visceral injuries that are most lethal.
• Different from multipled injuries – not life threatening – or a severe life-threatening single injury (barytrauma)
Death
• Trimodal pattern
o 1st hr: Cerebral, cardiovascular injury, airway obstruction, external bleeding " most patients die
o 1-4 hs after injury (golden hour – deaths avertable): Hypoxia, hypovoemic shock (uncompensated blood loss)
o Days or weeks after (ICU): Complications of trauma and multiple organ failure " attributed to initial Mx of injury
Types of trauma
• Examples: deceleration trauma, being run over, crush trauma, avulsion trauma, penetrating injury, explosion injury, thermal injury, chemical
injury, radiation injury

Life threatening conditions

Airway
• Facial fractures
o Major fractures of maxilla and mandible
o Nasal intubation not recommended
• Larynx injuries
o Presents with stridor, hoarseness, crepitus in the neck and rapid respiratory obstruction
o Do tracheostomy to secure airway
Breathing
• Spinal injury
o Always assume cervical injury until proven otherwise
o High cervical cord transection paralyses intercostal muscles and diaphragm, resulting in apnoea in minutes to hours.
o Steroids useful if administered within first 8 hrs
• Chest injuries
o Rib fracture: presents with tenderness and crepitus
o Tension pneumothorax: accumulation of air under pressure in the pleural space. This dvlps when the injured tissue forms a one way
valve, allowing air to enter the pleural space and preventing the air from escaping naturally
! Air trapped pushes heart and mediastinal structures to the contralateral side, impinging on the contralateral lung
! Hypoxia decreases venous return and cardiac output, causing hypotension
! Haemodynamic collapse leads to death
o Haemothorax
o Pulmonary contusion: parenchymal damage leads to impaired gaseous exchange.
o Flail chest: paradoxical movement of a segment of chest wall, usually caused by fracture of 3 or more ribs, resulting in injury to heart
and lungs, leading to pulmonary contusion, VQ mismatch and respiratory distress.
! 15!
• Fat embolism
o Results when embolic marrow fat macroglobules damage small vessel perfusion leading to endothelial damage in pulmonary capillary
beds
o Risk factors:
! Long bone #: note that the risk is esp high w femoral shaft # and concomitant head injury
! Risk if higher w non-operative therapy but is also higher w overzealous reaming of femoral canal
! Multiple trauma w major visceral injuries and blood loss (incidence may be as high as 5-10%)
o CAUSE OF DEATH ON 3RD DAY AFTER PELVIC # IS DUE TO FAT EMBOLISM
o NOTE: Cx of skeletal traction does not include fat embolism
o Clinical manifestations:
! Symptoms usually begin 24-48 hrs after injury
! Gurd’s DIAGNOSTIC CRITERIA: 1 MAJOR + 4 MINOR CRITERIA + FAT MICROGLOBULINEMIA must be present to formally
diagnose fat embolism syndrome
1. Axillary or subconjunctival petechiae
2. Hypoxaemia (PaO2 < 60 mmHg; FiO2 = 0.4)
Major criteria
3. CNS depression/ AMS disproportionate to hypoxaemia
4. Pulmonary edema
1. Tachycardia (> 110 bpm)
2. Tachypnea
3. Hypotension
4. Renal dysfunction
5. Jaundice
Minor criteria 6. Pyrexia (> 38.5°C)
7. Emboli present in the retina on fundoscopy
8. Fat present in urine
9. A sudden unexplainable drop in haematocrit or platelet values
10. Increasing ESR
11. Fat globules present in sputum
o Treat the hypoxaemia!!
Circulation
• Posterior dislocation of sternoclavicular joint
• Abdominal injuries: liver injuries and splenic rupture
• Pelvic ring fracture
• Hip injuries: may sustain internal bleeding and neuropathies as well. Usually caused by dislocations and fractures.
• Femoral shaft fractures: femoral artery involved

Principles of management
General principles in management of orthopaedic injuries in polytrauma
• Management: Primary survey + Secondary survey
• 4 different periods in orthopaedic management of trauma injuries
o Acute or resuscitation period (1-3 hrs after trauma)
! Decompression of organ cavities (tension pnemothorax, cardiac tamponade)
! Haemorrhage control
! If pelvis is fractured, early stabilisation with pelvic clamp is crucial
o Primary or stabilization (of #) period (<24hrs)
! Decision on temporary and definitive fixation of fractures
! Limb salvage v.s. amputation (many scoring systems i.e. mangled extremity scores/Hannover fracture scale)
! Optimal timing of long bone # stabilization in trauma patients in the primary period - Divided into 3 groups of patients:
• 1. Polytrauma without brain and chest injury
o Early stabilization (within 48hrs) does not improve survival but it will benefit some patients (eg. reduces no. of
days of mechanical ventilation etc.) " ?improves morbidity
o Thus it is preferable to perform long bone stabilisation in polytrauma patients
• 2. Brain injury 3. Chest injury
o No evidence that early long bone stabilisation (within 48hrs) improves survival/ morbidity or decreases Cx
compared to late stabilisation
! All polytrauma patients should preferably undergo early long bone stabilisation (Class II evidence) in the primary period
o Secondary or regeneration period (3-8 days)
! Continued haemodynamic and resp stability
! Debridement of soft tissue necrosis
! Eliminate septic foci
! Wound closure
! Joint reconstruction
! In definitive treatment of #, in order to preserve normal function, there should be
• articular congruity
• stable fixation
• axial alignment with the rest of the extremity
• restoration of full range of motion
o Tertiary or rehabilitation period (>8 days)
! Patient weaned off intensive care
! Physiotherapy initiated
! If patient has developed multiple organ failure, no further operative procedures can be considered at this stage.
! 16!
• Special considerations
o Pelvic #
! Ensure that there’s no need for general surgical intervention e.g. intra-abdominal or retroperitoneal haemorrhage
! Haemorrhage control with pelvic packing and temporary stabilisation with ext fixators and pelvic-clamps
o Spine #
! Urgent spinal stabilisation is required (urgent = within 24 hrs of the injury)
o Long bones #
! Pts with # shaft of femur can lose up to 1 l of blood. Femoral shaft fractures should undergo immediate stabilization of the
fracture within 24 hours of injury
! Immediate stabilization of long bone fractures has many advantages in the multiply injured patient, such as improved long-term
function, prevention of DVT and decubitus ulcer, decreased need for analgesia, and reduction in the incidence of adult
respiratory distress syndrome and fat emboli
! Recommendations for staged treatment of femoral shaft fractures!

Management at Scene of Accident

• Access: Free head and trunk by moving covering objects if patient trapped
• (Airway, Breathing) Establish airway (but protect cervical spine) and ensure ventilation
o Immobilise neck as may have cervical spine injury
o Jaw thrust
o Use finger to check airway if difficulty breathing
o If difficulty breathing still persists, may have pneumothorax, haemothorax, flail chest or sucking wound of chest wall
o If equipment available, can intubate, chest drain and administer oxygen
• Arrest haemorrhage and combat shock
o Apply pressure on site of bleed
o Give IV fluids if facilities available but do not give food or fluids by mouth
• Cursory examination:
o Feel pulse
o Observe respiratory rate and capillary return
o Palpate head, chest, abdomen, limbs
• Analgesia
• Extricate: Clear obstructions
• Splint fracture: to reduce pain, blood loss, ischemic necrosis of tented skin and
injury to nerves and blood vessels
• Transport
o Move patient onto stretcher with at least 4 ppl (move patient in 1 piece)
o Repeatedly check ABC (before and during transport)
Management in Hospital
• Triage – Sort patients according to severity / immediacy for help
• Ample (allergies, medication, past med hist, last meal, events) History
• Primary Survey (ABCDE) and Resuscitation
o Airway (and cervical spine control)
! Establish airway without compromising C-spine (cervical collar)
! Chin lift – jaw trust – finger sweep – suction – oropharyngeal tube –
orotracheal tube – if necessary, surgical cricothyroidotomy
o Breathing
! Inspection: respiratory rate, open injuries, equilateral chest
movements, bruising, tracheal deviation, cyanosis
! Percussion: dullness, hyperresonance
! Auscultation: Normal / abnormal or absent breath sounds
! Life threatening pathologies: Tension pneumothorax, sucking chest wound, haemothorax, flail chest
! Management: Cannula, chest tube, artificial ventilation
! Blood sample to measure PCO2 and PO2
o Circulation (and control breathing)
! Control external hemorrhage by direct pressure
! Inspection: Pale, sweaty, external bleeding, jugular venous distension
! Palpation: Coolness of extremities, capillary return, pulse rate
! Measure: BP
! 2 large (14g) bore cannulas " Blood sent to lab for cross matching
! Volume replenishment (if necessary):
• Warmed crystalloid (2L for initial bolus)
• Blood transfusion if failure to respond to crystalloid
! 17!
 ! Cardiac tamponade:
• Signs: Significant chest injury, penetrating wound, BP cannot be maintained by infusions, distended neck veins,
paradoxical pulse
• Management: Immediate decompression with needle or atheter inserted below xiphisternum
o Disability
! Brief neurological examination (AVPU): Alert, Voice, Pain, Unresponsive
! Assess pupil size and limbs for equality of movement
! Factors affecting consciousness
• Injury related: Hypoxia, hypovolemia, head injury
• Exogenous: Alcohol, drugs
o Exposure (and avoidance of hypothermia)
! Exposure for complete examination
! Covered after examination to prevent hypothermia
• Ad-juncts
o Exclude life threatening injuries
o Urethral catheter: Unless uretheral injury then suprapubic catheter (don’t catheterize via urethra if cannot feel prostate during PR exam;
indicate that prostate pulled up by trauma)
o Nasogastric tube: Reduce risk of gastric dilatation and aspiration of fluid (aspiration pneumonia) – pass by mouth if basal skull fracture
suspected (suggested by blood in aspirate)
o ECG monitoring
o Other indicators: BP, ABG, oxygen saturation, expired CO2 concentration, CVP
• Constant Re-Evaluation: Assess response to resuscitation and detect deterioration
• Secondary Survey (after resuscitation):
o Head to toe examination including 4 limbs, pelvic compression, log roll
! Tubes and fingers in every orifice
! Spine: Tenderness, bruising, step deformities
o Complete neurological examination:
! Record Glasgow Coma Scale (GCS)
• Important to break the figure down into its components, such as
E3V3M5 = GCS 11
• >/=13: mild brain injury
• 9 – 12: moderate injury
• </=8: severe brain injury
! ASIA (American Spinal Injury Association Score)
o X-rays:
! AP chest
! AP pelvis
! AP abdomen: GI bleed, perforated gut
! Lateral C-spine or spiral CT
o Remaining diagnostics, imaging, special studies
• Definitive care
o Based on findings of primary and secondary survey
o Transfer when stable AIS Score Injury
1 Minor
Other Relevant Scoring / Staging Systems
2 Moderate
• Abbreviated Injury Scale
o An anatomical scoring system. 3 Serious
o Injuries are ranked on a scale of 1 to 6, with 1 being minor, 5 severe and 6 an unsurvivable injury 4 Severe
• Injury Severity Score
5 Critical
o Each injury is assigned an AIS score and is allocated to one of six body regions (Head, Face, Chest,
Abdomen, Extremities (including Pelvis), External). Only the highest AIS score in each body region is 6 Unsurvivable
used. The 3 most severely injured body regions have their score squared and added together to produce
the ISS score.
o The ISS score takes values from 0 to 75. If an injury is assigned an AIS of 6 (unsurvivable injury), the ISS score is automatically
assigned to 75.
o The only anatomical scoring system in use and correlates linearly w mortality, morbidity, hospital stay and other measures of severity
o Weaknesses
! any error in AIS scoring increases the ISS error,
! many different injury patterns can yield the same ISS score and injuries to different body regions are not weighted.
! the ISS (along with other anatomical scoring systems) is not useful as a triage tool.
Region Injury Description AIS SquareTop 3
Chest Cerebral Contusion 3 9
Head & Neck No Injury 0
Face Flail Chest 4 16
Abdomen Minor Contusion of Liver 2 25
Complex Rupture Spleen 5
Extremity Fractured femur 3
External No Injury 0
Injury severity 50

! 18!
• Tscherne classification for closed fractures and soft tissue injury
o Grade C0: Little or no soft-tissue injury.
o Grade CI: Superficial abrasion (shaded area) and mild to moderately severe fracture configuration.
o Grade CII: Deep, contaminated abrasion with local contusional damage to skin or muscle (shaded area) and moderately severe
fracture configuration.
o Grade CIII: Extensive skin contusion or crushing or muscle destruction (shaded area) and severe fracture.

• Gustilo-Anderson for Open Fractures (Refer to open fracture notes)

• Mangled Extremity Severity Score
o High energy transfer or crush resulting in some combination of injuries to arteries, bones, tendons, nerves and/or soft tissue
o Acutely differentiates salvageable and unsalvageable limbs

Complications / Subsequent Issues

• Compartment syndrome
• Crush syndrome (traumatic rhabdomyolysis) " Myoglobinuria may lead to acute renal failure
• Thromboembolism
o Develops 5 days later, worried about pulmonary embolism
o Prevention of DVT can be carried out by: Early stabilization + Early mobilization + Clinical signs monitoring everyday after trauma +
Anticoagulant if necessary
• Tetanus
o Develops 7 days later
o Administer tetanus toxoid as prophylaxis, especially with lacerations, abrasions, dirty wounds and open fractures.
• Fat embolism syndrome (lung, brain, skin): refer to “life threatening conditions”
• Systemic inflammatory response syndrome (Temp, HR, RR, TWC)
• Disseminated intravascular coagulation (DIC)
• Hypothermia
• 2nd Hit Phenomenon: Exaggerated inflammatory response when surgery undertaken leading to:
o Acute respiratory distress
o Multi organ dysfunction syndrome

Physiologic response to Polytrauma

• Mediated mainly by: Tissue damage, Hypovolaemia
• Manifested by
o Changes in cardiovascular system
o Inflammatory reaction → SIRS → ARDS → MOF → ?immune suppresion
o Changes in metabolic status: Closely interlinked by the neuroendocrine system.
• Hypovolaemia
o Systemic compensation by sympathetic activation + RAA activation + ADH secretion
! 19!
 ! Reduced right heart filling pressure → reduced oxygen uptake
! Reduced left heart filling pressure 2° reduced pulmonary venous return → reduced cardiac output
! Less inhibitory stimulation of baroceptors in aortic arch & carotid sinus → reflex inhibition of vagal activity + ↑sympathetic
stimulation to heart & vessels → ↑ CO & SVR
• Cerebral & myocardial vessels not involved; peripheral vasoconstriction in cutaneous, skeletal & visceral tissue, preserving
circulation to important organs (brain, heart & kidneys)
! Further intravascular loss → distortion of incompletely filled chambers stimulates cardiac C fibres → reflex vagal slowing of
heart rate + vasodilation → circulatory collapse
! Chemoceptors of carotid sinus & aortic arch becomes more sensitive to ↓PaO2 at ↑PaCO2 (↓pH) → tachypnea, vagal slowing
of HR, sympathetic vasoconstriction in skeletal muscles
! High sympathetic drive causes catecholamine release from adrenals → activation of RAAS → further release of corticosteriod,
ADH, glucagon, insulin & human growth hormone → Na & water retention to incr circulating blood volume & maintain BP
o Cellular compensation by anaerobic respiration " lactic acidosis
o Classification of shock
(% of blood loss) Class I Class II Class III Class IV
<15% 15-30% 30-40% >40%
Pulse pressure ↑ ↓ ↓ (SPB↓) ↓
Resp Rate 14-20 20-30 30-35 >35
Urine outpt >30 20-30 5-15 Neg
Mental status - Mild anxiety Confused Lethargic/ obtunded
• Inflammatory response
o Any tissue injury generates a local inflammatory response (with/without pre-existing infection) " directed at elimination of dead tissue,
foreign invaders & healing
o Greater trauma causes more inflammatory reaction
o Mechanisms:
! Cellular mediators: PMNs, macrophages & fibroblasts
! Cytokines: esp IL-1 & TNF-α
! Complement system: esp C3 (anaphylactoid reaction) & C5 (PMN stimulator)
! Prostaglandins: thromboxane, prostacyclins etc
! Acute-phase reactants: Liver synthesis of acute phase reactants such as opsonins (CRP), protease inhibitor, haemostatic agents
(fibrinogen) & transporters (transferin)
! Stress hormones: adrenaline, cortisol release, Insulin secretion suppressed, glucagon enhances glycogenolysis → overall
hyperglycaemia
• Overwhelming inflammatory response
o Both pro-inflammatory + anti-inflammatory cytokines are generated in an inflammatory response
o Major trauma causes systemic release of inflammatory agents
o Spill over of such inflammatory agents systemically can occur with major trauma " SIRS " ARDS /MOF
! In severe states, SIRS can evolve into ARDS or MOF
• SIRS can occur in a non-septic state
• ARDS or lung failure is usually the first to occur followed by other organ systems damage with hypoxia (MOF).
• MOF can occur without SIRS
• SIRS can be ppted by a 2nd time injurious event (eg: Sx or secondary infx) after e initial trauma → “2-hit” theory of SIRS
o Clinical manifestation of SIRS
! Defined as presence of >/= 2 of the following signs of systemic inflammation:
• Hyperthermia >38C or hypothermia <36C
• Tachycardia >90bpm
• Tachypnea >20breaths/min or PaCO2<32mmHg
• Elevated/ depressed white cell count (>12000/uL or <4000/uL) or 10% immature band forms
• Initial hypermetabolism
o Early hyperglycaemia
! Plasma cortisol increases in proportion to injury with corresponding sympatho-adrenal response (until adrenal perfusion fails)
! Early hyperglycaemia occurs with increased sympatho-adrenal activity
! Peripheral insulin resistance & depressed insulin secretion with high circulating catecholamines & glucagon release
! Skeletal glycogenolysis
! Liver → Glycogenolysis & gluconeogenesis
! Anaerobic metabolism → lactic acidosis
o Skeletal muscle catabolism (-ve nitrogen balance) substrate for liver gluconeogenesis (negative nitrogen balance)
o Lipolysis → release of FFA & glycerol (↑TG & LDL)
o High resting energy expenditure - General catabolic state
o ↑ body temperature
• Convalescent state
o Insulin secretion resumes, insulin resistance decreases; Aerobic respiration reestablished

! 20!
Chapter 5: Open Fractures " EMERGENCY!
DEFINITION: A fracture or its haematoma that communicates with the environment (may not be obvious! Eg. communication w bladder cavity)
Diagnosis
• See bone
• Marrow bleed – fat globules
• When apply pressure
o Skin or subcutaneous bleed will stop for awhile
o Bone bleed will not stop
CLASSIFICATION: Gustilo Anderson (for prognostication and management)
Types Features
Type I Size: Small (<1cm)
Soft tissue injury: Minimal damage, no crush
Contamination: Mild (will not be the case if environment of injury dirty – eg football field); clean puncture (compound from within)
Usually low impact: simple fracture " transverse, short oblique, little comminution
Risk of amputation: 5%
Type II Size: Medium (1-10cm)
Soft tissue injury: Moderate crushing, no flap/avulsion
Contamination: Moderate
Usually low impact: Moderate comminution (eg. butterfly fragment)
Risk of amputation: 10%
Type III Size: >10cm
Soft tissue injury: extensive damage to skin, muscle and neurovasculature
Contamination: Significant
Usually high impact: extensive comminution and instability
IIIA: Adequate soft tissue coverage of bone (muscular coverage adequate; NOT SKIN) despite extensive lacerations/ flaps
Segmental # (# at 2 levels)
Eg. Farm injuries / any injury occurring in a highly-contaminated environment, GSW
Risk of amputation: 20%
IIIB: 1) Inadequate soft tissue coverage 2) Periosteal stripping and exposure of bone 3) Severe comminution
Risk of amputation: 30%
IIIC: Arterial injury which needs repair (major artery) regardless of wound size/soft tissue injury
Prophylactic fasciotomy always done to prevent post-op compartment syndrome
Risk of amputation: >40%
*Note: can only differentiate Grade 3 into a, b and c after formal debridement has been done
EMERGENCY CARE
Approx 30% of patients w open # are polytrauma patients who have suffered damage to 2 or more systems. Manage according to ATLS. Only
manage the # when the patient is stable (In red: for open #s)
1. Primary Survey
a. Stabilise Patient: ABCDE
b. Assess neurovascular status of the limbs (above and below)
i. Control any hemorrhage w direct pressure. Set IV line and start IV fluids
ii. Don’t reduce any # unless there is an apparent neurovascular compromise from the position of #
iii. Dressings and splints that might have been put on at the accident site shld be removed partialy to assess soft tissue conditions
and neuromuscular function. All sterile wound dressings shld be left in place because redressing wounds in the emergency
room increases the infection rate
c. Rule out any other fractures (esp joint above and below) and injuries (visceral, c-spine etc) – remove gross debris (ie. Turf, rocks)
d. Rule out open fracture
i. Closed Fractures: Reduce + Stabilise + Exercise
2. Early Management (Make patient comfortable)
a. Analgesia: 75mg I/M pethidine
b. Splint fracture (one joint above and one joint below): to decrease pain, progression of soft tissue injury, blood loss
3. Proceed with finding out more: Take an AMPLE history + Imaging (XR) + Take photograph (for documentation)
4. Prepare for EOT
a. Start IV Abx (after wound c/s samples are taken) in all open # during the first 3-5 days (empirical NOT prophylactic!)
i. Use broad spectrum Abx: usually Benzylpenicillin + flucloxacillin or 1st gen Cephalosporin
ii. If wound heavily infected (esp GA type 3), add gentamycin +/- metronidazole (flagyl) to cover gram negative and anaerobes,
and monitor for toxicity
b. Tetanus toxoid booster (TTB): 0.5ml
Human anti-tetanus immunoglobulin (HATI): 250 units
Simple wound Tetanus-prone wound
Full course + booster within 10yrs - TTB
Full course + booster 10yrs ago TTB TTB + HATI
Non-immunised / unknown TTB TTB + HATI
c. NBM
d. Must get into OT within 6hrs (golden hrs) since risk of infx increases after this time " done under LA/GA
e. Sterile scrub: use scrubbing brush and scrub the site to debride all necrotic tissues (dead muscle/ fat/ other tissues)
4Cs Dead muscle Live muscle
Consistency Mushy Turgid
Colour Pale pink/ purple Pink/bright red
Contraction when stimulated (most impt) Absent Present
Capillary No bleed when cut Bleeding

! 21!
 IRRIGATION AND DEBRIDEMENT (most important steps in treatment of open #)
• Principles of Treatment
o Only now are all the splints and bandages removed " reexamine thoroughly for neurovascular function.
o Wound Debridement (under regional or GA): Remove foreign material and dead tissue, leaving a good blood supply (within
golden period of 6 hours, otherwise the wound is considered infected)
! Wound margin excision: Just enough to leave healthy skin edges
! Wound extension: Ensure adequate exposure (including the joint) for inspection of wound site and thorough cleansing (but
must take into account possible need for skin flap)
! Removal of devitalized tissue: Devitalised tissue provides a nutrient medium for bacteria
• All non-viable, mutilated or macerated skin removed: no bleed when cut, dusky colour
• Fascia is expendable so it can be safely removed without fear of functional deficit.
• Free fragments of bone removed; #ed bone ends must be exposed so they can be cleaned w brushes or removed
! Nerves and tendons: Leave cut nerves and tendons alone unless wound is clean + no dissection required and necessary
expertise available
• Exposed tendon will not survive for long: early skin coverage, skin grafting or a muscle/skin flap may be necessary to
preserve its viability
o Wound cleansing: Irrigation with saline and removal of foreign material, blood clots and tissue debris
! Fluids delivered under pressure and under a pulsed system " Repeat irrigation at regular intervals as there is a higher
chance of removing contaminated material
! Dilute bacterial contamination
o Take wound cultures

f. Repair vascular injury if present (ie. Re-anastomose the vessels)

g. For crushed injuries involving both vascular and nerve injury " AMPUTATE
h. Remove comminuted fragments (anything that is dead and without soft tissue attachments " DISCARD)
i. Wash w 10L of saline (to dilute bacterial load)
j. Take wound cultures at the end of procedure
k. Then REDUCE
l. Then MAINTAIN
STABILISATION OF FRACTURE
• Importance: crucial for the healing of soft tissue and bone
o Prevents further injury to the surrounding soft tissue + limits inflammatory response + reduces infx spread + facilitates tissue
perfusion + encourages early wound repair
o Allows early mobilisation
• Broad principles
o Should still provide free wound access for repeated debridement and placement of local or distant flaps and bone grafts.
o Shldnt interfere with BS of # segments and should be sufficiently rigid to allow early jt motion and at least partial weight bearing
• Factors governing choice of management: Degree of contamination + Length of time fr injury to Sx + Soft tissue damage
o Slings, splints, casts and traction may be used as definite care of simple grade I and grade II injuries and as temporary methods
for more complex fractures.
! Slings: # of humeral shaft or to provide additional support for internally or externally stabilized forearm lesions.
! Splints: initial stabilization of fractures below the elbow and knee.
! Circular casts have no place in early management because they cannot accommodate swelling.
• May prevent detection of further soft tissue damage, circulatory impairment &/or increase in compartment pressures.
! Casts can be used as subsequent care of stable grade 1 and 2 tibial # after the wound is closed & swelling subsided.
• Can also be used as a secondary method of immobilization after removal of an external fixator.
! Traction may be indicated for pelvic #, acetabular lesions and femoral fractures. But rarely used in the upper extremity.
o Internal fixation (treatment as closed injuries): Minimal contamination, time lapse <8hours
! Good stabilization, allows early ROM and facilitates # consolidation while preventing malalignment " superior
healing compared to external fixation
• Disadvantage: must strip soft tissue thus avoided for grade 2 and above + additional exposure can cause partial loss
of periosteal, cortical or intramedullary blood supply " increases risk of infection.
o External fixation: More severe injuries with significant contamination and soft tissue injury
! External fixation preferred: can be temporary (for 2/52 until youre sure there’s no infx at site, then internal fixation) or
permanent (for 3-6 months until # unites)
! Reduced likelihood of further infection + Allow easy reassessment / additional debridement
! External fixation is indicated for most contaminated grade 3b and c fractures.
! Advantages: 1) No foreign material in the wound. 2) Applied without any additional soft tissue dissection, which would have
added on more trauma which we want to avoid 3) Provides easy access to the wound 4) Easily dismantled if further
debridement needed 5) Don’t want to close the wound too early before we make sure it is clean.
! Disadvantages: 1) Potential for pins to injure neurovascular structures and tie down muscle-tendon units " interfere w
joint motion and rehabilitation. 2) Possible interference of the pins in reconstructive procedures as well 3) Pin loosening –
not as ideal as internal fixator for proper fixation of the # 4) Secondary infection (pin-track infection)
! Usually removed or replaced by casts, braces or internal fixation as soon as soft tissue lesions have healed (or enough soft
tissue coverage by planning either a flap or graft) and wound clean.
o Screws: usually used with a plate or external fixator for intra-articular and peri-articular #.
o Plates: less severe diaphyseal, periarticular & intraarticular # of the UL & around joints in LL (but must be covered well)
o Intramedullary nails: femoral # or as a secondary method after external fixation
! May spread infx, thus contraindicated if there is a history of local or pin track infection.
m. Wound usually left open to drain

! 22!
 5. 48hr later
a. “Relook operation”: see if repeat I&D necessary
b. Ensure soft tissue coverage over exposed area by 48th hr – exposed tendon will not survive for long…NEED FLAP!!
WOUND COVERAGE
• Primary closure w immediate suturing: Small, uncontaminated type I wound that is free from contusion
• Leave open for 2 days until dangers of tension & infection have passed (for all other open #) – ideally wound cover w/i 3-5 days
o Principles:
! Keep moist meanwhile
! Once wound is clean and tissues are viable, delayed primary closure or skin grafts can be done.
! Aims of covering wound: 1) Achieve a safe early closure 2) Avoid nosocomial infx 3) Obliterate dead space 4) Facilitate
future reconstruction
o Suture
o Skin graft (no BS): has to achieve a new BS within 2-3 days to ensure viability (graft requires the bed to have good BS)
! Often used as in intermediary measure before a flap
! 2 types:
• Split thickness skin graft
o Features
! Consists of epidermis and part of dermis
! Taken from inner thigh or lateral buttocks
o Advantages
! Good for large defects
! Can tolerate less ideal conditions and less vascularity than full thickness skin graft
! Multiple grafts may be obtained from same site
o Disadvantages
! Grafts contract
! Have poor growth in children
! Abnormal pigmentation
• Full thickness skin graft
o Features
! Composed of full thickness of skin
! Acquired from groin, postauricular, supraclavicular areas
o Advantages: for fresh, small, uncontaminated wounds
o Flap (has own blood supply)
! Principles:
• Choice of flap coverage must take into account age and needs of patient, location, size and condition of the defect,
likelihood of subsequent reconstructive surgery and associated zone of injury, tissues available for the flap
! Advantage: Can be used to reconstruct skin and soft tissue defects regardless of their vascularity (but delayed bone or
soft tissue reconstruction is proposed, especially if bone graft or tendon transfer are being planned)
o Eg. Tibia (Common site for open fractures, and has a poor vascular bed)
! Prox tibia: Gastrocnemius flap
! Middle tibia: Soleus flap
! Distal tibia: Free flap, soleus flap
! 4 types: skin, fasciocutaneous, muscle, musculocutaneous
• 2 kinds of skin grafts:
o Free: tissue with blood supply detached from original location
! Free microvascular flap is used for large defect.
• Helps prevent multiple reoperations. Provide durable coverage of the # site, diminishes the
infection rate and shortens the healing time. Eg. latissimus dorsi and vertical rectus abdominis.
o Pedicled/ local: tissue left attached to donor site & transposed to new location keeping pedicle intact as a
conduit for blood supply
! Eg. 1 of the 2 heads of the gastocnemius is used and there must be a functional soleus for lesions
around the knee and proximal third of the tibia
! Distant vs Regional
• Vacuum Assisted Closure (VAC) Dressing / Negative pressure wound therapy
o Mechanisms
! Stimulate angiogenesis by stimulating granulation tissue
! Reduce edema and fluid – expedite healing
! Reduce size of wound
! Reduce bacterial count (remove some bacteria, reduce oxygen levels)
o Indications: Diabetic foot, open fractures (act as sterile dressing) large wounds)

! 23!
 6. 4-6weeks later: bone graft/ transport
MANAGEMENT OF BONE LOSS
• Bone Loss
o Mechanism: Either from initial direct injury or from subsequent repeated debridements
o Any bone replacement methods should only be done after adequate soft tissue coverage and revascularization
o Bone graft
! Mechanisms
• Osteoinduction (most impt): Undeveloped tissue transformed to bone by inducing agent
• Osteoconduction: Transferred bone acts as scaffold for new bone to grow (+ neovascularization)
• Osteogenesis: New bone formed from live osteoblasts in transplanted autograft
! Principles
• Cancellous grafts incorporated more quickly and more completely than cortical grafts
• Vascularised grafts are ideal (but technique consuming and requires microsurgery) – lower rate of necrosis
• Autografts > allografts > xenografts
• Reduction of antigenicity in allografts: Freezing, freeze drying, ionizing radiation, demineralization, impregnation of
graft with host marrow
! Applications
• Vascularised grafts: Exceptional circumstances such as congenital pseudoarthrosis of tibia, non-union of NOF #
• Cortical graft (can fill large gaps): Bone loss due to trauma or tumour
• Cancellous grafts (wide variety of uses): filling cavities, filling spaces due to fracture etc (MANY MANY USES)
o Bone transport: Used for large gaps
! Ilizarov’s principle of distraction osteogenesis: Controlled gradual distraction gives rise to neovascularisation and new
bone formation between bone surfaces
• Callostasis: Corticotomy or osteotomy to create segment of bone in one of the fracture fragments; fragment moved
gradually (1mm a day) by wires and new bone forms in the gap
o Free composite tissue transfer
! Example: fibula, which is mainly a cortical bone that provides excellent strength and length for large segmental bony
defects. It is used together with muscle and skin with its pedicle.
!
7. Then SKIN GRAFT: after swelling subsides; if not, compartment syndrome may occur after grafting

COMPLICATIONS OF OPEN FRACTURES

• Bone: osteomyelitis, arthritis, malunion, delayed union, non-union, avascular necrosis
o Osteomyelitis
o Arthritis
o Mal-union: fragments join in an unsatisfactory position (angulation, rotation, shortening)
! Causes: failure to reduce # adequately, failure to hold reduction while healing proceeds, gradual collapse of comminuted or
osteoporotic bone
o Delayed union
! Delayed union is when healing has not advanced at the average rate for the location and type of fracture. Ie. reconstitution of
mechanical stability but over a prolonged period of time and with associated morbidity.
! Causes:
• Biological: poor BS, severe soft tissue damage, infection
• Biomechanical: periosteal stripping, imperfect splintage, over-rigid fixation
! Rx: adequate immobilization, internal fixation or even bone grafting.
o Non-union:
! Evidence, clinically or radiologically, that healing has ceased (both pieces not united by 6 months). Ie. failure of reconstitution
of mechanical stability after appropriate time intervals
! Common sites: tibia (commonest of all is junction of distal 1/3 and proximal 2/3 of tibia; due to poor muscle coverage),
scaphoid, lateral condylar fracture, NOF (due to poor BS), distal ulna, midshaft humerus
! Causes: SPLINTS
• Soft tissue interposition: Distraction & separation of fragments (may be due to interposition of soft tissues btw fragments)
• P osition of reduction (excessive traction, immobilization, or movement at fracture line)
• L ocation (eg. lower third of tibia is slow to heal)
• I nfection
• N utritional (damaged vessels thus poor local BS, diseased bone)
• T umour (pathologic fracture)
• S everity of injury: Severe injury that render local tissues non-viable
! Risk factors: Smoking, NSAIDs, Diabetes, Infection, Anemia, Old age
! Types:
• Hypervascular/ hypertrophic
o Cause: insecure fixation/ premature weight bearing " insufficient stability
o Types:
! A1: elephant foot – rich in callus (Florid streams of callus ard # gap)
! B1: horse hoof, poor in callus
! C1: oligotrophic pattern
o Management: Just stabilize as blood supply still good (?stable internal
fixation)
• Avascular/atrophic
o Cause: poor BS, ends osteoporotic (eg. in DM, vasculopathy, infx, significant tissue damage) " impaired repair
process (fibrosis instead of repair may result in pseudoarthrosis)

! 24!
 ! Infection resulting in infected non-union
• Infected pseudoarthrosis
• Infx especially likely with tissue necrosis (vascular compromise) which acts as a nidus for infection
o Types:
! A2: torsion wedge, intermediate fragment
! B2: comminuted, necrotic intermediate fragment
! C2: defect, loss of fragment of the diaphysis
! D: atrophic pattern, scar tissue with no osteogenic potential
is replacing the missing fragment)
• Appearance: Penciling of ends, round edges
o Management: Bone graft, open decortications, bone transport or
free composite tissue transfer.
o AVASCULAR NECROSIS *** (refer to “hip”)
• Regional: neurovascular injury, soft tissue blisters, CRPS, heterotrophic ossification, joint stiffness, compartment syndrome
o Neurovascular injury
o Fracture blisters (Soft tissue blisters):
! Types: hemorrhagic and non-hemorrhagic
• Usually hemorrhagic – indicate deep soft tissue damage
! Mechanisms of injury: shearing of skin (may become infected if operated on), delamination due to ischemia (can be due to
compartment syndrome)
• Blisters commonly appear in compartment syndrome (but often serous instead of hemorrhagic)
o Complex regional pain syndrome:
! A chronic pain state induced by
• Soft tissue/ bone injury: CRPS 1 aka reflex sympathetic dystrophy aka Sudeck’s dystrophy
• Nerve injury: CRPS 2 aka causalgia
! Pathophys: pain is a/w autonomic changes (eg. sweating or vasomotor abnormalities), and/or trophic changes (eg. skin/bone
atrophy, skin loss, joint contractures)
! Aetiology unknown
! Rx: no cure; pain relief only
o Heterotrophic ossification
o Joint stiffness
o COMPARTMENT SYNDROME ************ (Orthopaedic emergency!!)
! Pathology: Increased intracompartmental (muscle and tissue bounded by fascia and bone with little room for expansion like in
forearm, calf) pressure sufficient to occlude microvascular circulation causing ischemia and tissue necrosis
subsequently (most commonly deep posterior)
! Pathophysiology " decreased blood inflow + outflow
• Tissue injury results in bleeding and edema
• Increased intracompartmental pressure disrupts Starling’s forces
• Compromised perfusion results in further tissue damage
• Further edema and perfusion compromise
• Order of collapse: capillaries " venules " arterioles (last to
collapse because have muscles)
! Significance:
• Muscle will die within 4-6 hours of ischemia
• May lead to rhabdomyolysis and kidney failure if untreated
• Nerve then undergoes necrosis later
! Complications
• Volksmann ischemic contracture
• Permanent functional impairment
• Renal failure from release of myoglobin from muscle necrosis
• Death
! Common Sites: Leg (proximal third of tibia), forearm flexor compartment, hand, foot, elbow
! Etiology: external restriction of compartment or internal increase in compartment volume
• Trauma – Crush injury, fracture, dislocation, soft tissue damage and muscle swelling " edema and hemorrhage
• Vascular: arterial compromise (post ischemic swelling), muscle anoxia, venous obstruction, increased venous pressure
• Iatrogenic: Tight cast, constrictive dressing, splint
! Diagnosis
• Clinical (5Ps)
o Lack of oxygenated blood and lack of waste product removal results in pain and decreased peripheral sensation
secondary to nerve irritation
o Early: Pain, Paresthesias, Pallor, Palpable tense swollen compartment, blistering
! Most important feature is PAIN out of proportion to injury (Other signs are ‘late signs’)
• Not relieved by analgesics
• Increase w passive stretch (stretching of muscles traversing compartment): dorsiflexion of toe for leg
o Late signs: Pulselessness (pulses are usually still present; CRT normal), Paralysis
Anterior leg Volar forearm
Fracture Type Tibial fracture Supracondylar (humerus)
Weakness Toe, foot extension Finger, wrist flexion
Pain Toe, foot flexion Finger, wrist extension
Sensory 1st dorsal web space Volar aspect of fingers

! 25!
 • Investigation
o Split Catheter (Compartment pressure monitor): perfusion pressure (difference between diastolic pressure and
intracompartmental pressure) <30mmHg or absolute pressure of >30mmHg
! Role: Unresponsive patients
! Normal tissue pressure is abt 0 mmHg
! Management
• Remove: Cast, constrictive dressings
• Place limb at level of heart
• Bivalve casts down to skin and spread open
• Fasciotomy – Open all 4 compartments with medial and lateral incisions in leg
o Usually indicated when the perfusion pressure falls to <30mmHg (inadequate perfusion and/or ischemia begins) in
a patient who has any signs or symptoms of a compartment syndrome - even if distal pulses still present
o Or indicated if unable to monitor and there is no improvement in clinical signs after 2hrs of splitting the dressings
(examine at 15mins interval)
• Systemic:
o Hypovolemic shock
o Fat embolism
! Pulmonary: SOB, hypoxemia
! Neurological: Agitation, delirium, coma
! Dermatological: Petechial rash (esp chest)
! Haematological: Anaemia, low platelets
o Venous thromboembolism (DVT/PE) from immobility
o MODS
o ARDS (esp in polytrauma patients)
• Classification by early and late Cx

Early Late
Local Neurovascular injury Malunion
Swelling Nonunion
Compartment syndrome AVN
Infx Post-traumatic arthritis
Implant failure Osteomyelitis
Soft tissue blisters (" infx) Heterotrophic ossification
Growth disturbance in children
Joint instability
Joint stiffness
Nerve compression/ entrapment
Reflex sympathetic dystrophy (RSD)
Systemic Hemorrhagic shock MODS
Sepsis Renal failure
Fat embolism Shocked lung
DVT/PE PTSD, depression
ARDS

! 26!
Chapter 6: Limb threatening conditions
• Vascular Impairment
o Haemorrhage: visible or occult
o Ischaemia: acute interruption of BF to a limb/organ " anaerobic respiration predominates " leading to lactic acidosis and
eventually cell death
o Causes: Dislocations or fractures
o Arteries involved: Axillary, brachial, femoral, popliteal
• Mangled Extremity (refer to “Polytrauma)
• Acute Compartment Syndrome (refer to “Complications of Open fractures)
• Necrotizing Fasciitis
o Insidious soft tissue infection characterized by tissue necrosis
o Organisms spread from subcutaneous tissue along superficial and deep tissue planes, of which the latter causes vascular occlusion,
ischaemia and tissue necrosis.
o Less seen in multiple trauma
o 3 types of NF: Type 1 – Polymicrobial NF
Type 2 – Grp A Strep NF (Flesh-eating bacterial infection)
Type 3 – Gas gangrene
o Presents with fever, chills, erythema and painless bullae formation
o Treatment: antibiotics and surgical debridement
• Gas Gangrene
o Onset: 12-24hrs after injury
o Commonly Clostridial infection, but may be caused by other organisms
o Decreased oxidation reduction potential promotes advance of a highly lethal condition
o Less seen in multiple trauma
o S/S:
! Present with intense pain and swelling around the wound
! Associated with a brownish discharge and bronze discolouration of wound
! Gas (with a musty odour) formation usually not marked
o Important to distinguish from anaerobic cellulitis, which presents with abundant gas formation that is foul smelling in nature
! Distinction between the two can be made by doing a Gram stain of the exudate
o Management: fluid & electrolyte replacement, antibiotics, multiple incisions & fasciotomy, hyperbaric oxygen
• Osteomyelitis (refer to “Bone and Joint Infections”)
o Infection of bone and bone marrow
o Difficult to treat, can be life threatening as well due to septicaemia
o Routes of spread: haematogenous, contiguous from a focus of infection
o Bacteria can be inoculated at the time of trauma
o Present with fever, headache, vomiting, severe bone pain
o Treatment: antibiotics and extensive debridement of necrotic tissue

! 27!
Shoulder!

Atraumatic! Traumatic!

Impingement' Instability'&'Dislocations'
syndrome' • Glenohumeral'(ant,'post,'inf)'
• Tendinitis' • Acromioclavicular'
• Tear' • Sternoclavicular!

Fractures!
• Clavicle!
Frozen'Shoulder' • Scapula!

Biceps'
• Tendinitis'
• Tendon'rupture'

Shoulder!Joint!
• TB!
• OA!
• RA!
• Milwaukee!Shoulder!

Scapula'
• Congenital'Elevation'
• Klippel2Feil'Syndrome'
• Winged'Scapula'

! 28!
Examination of the Shoulder
The preliminaries: Introduce yourself to patient, ask for permission to
examine. Ensure adequate exposure (remove shirt; expose shoulders
up to and including scapula) but consider patient modesty also.
Ensure good lighting, and good positioning of bed.
4 main parts of shoulder girdle: sternoclavicular joint,
acromioclavicular jt, glenohumeral jt, scapulothoracic articulation
LOOK—Front, Side, Back X2
1. General appearance and vitals – pallor, BP, and HR.
2. Scars/ sinuses: shoulder, in axilla- ask patient to lift arms
3. Swelling
- Bump(s) over sternoclavicular jt, clavicle,
acromioclavicular jt
- Effusion points in the axilla – remember to look
4. Deformity – asymmetry between two shoulders
- Foreshortening of the shoulder joint indicates previous
clavicular fracture, acromioclavicular joint problem
5. Discolouration – redness, bruising, etc
6. Muscle wasting – squaring of shoulders (deltoids);
hollowing of supra- or infraspinous fossa; trapezius
FEEL
1. Warmth
2. Tenderness and deformities—Palpate in a U-shape
- Start fr SC jt, ballot SC jt, go along clavicle to AC joint,
then ballot AC joint
- Follow back to spine of scapula, and palpate in
supraspinous and infraspinous fossae for tenderness
- Locate coracoid process anteriorly, palpate that (short
head of biceps, coracobrachialis)
- Head of humerus
- Greater tuberosity (particularly supra/infra-spinatus
insertion)
- Bicipital groove (gently rotate forearm & feel for cord-like
structure)– tendon of long head of biceps
MOVE
1. Range of movements:
- Active first; if restriction in ROM, assess passive range –
differentiates between pain, joint stiffness or muscle
weakness.
In supraspinatus impingement or tear, passive range is greater
than active range as active range is limited by pain and/or
weakness; limitation is usually only in one movement e.g.
abduction.
In frozen shoulder, passive and active ROM are equally restricted,
and usually in more than one type of movement.
NOTE: for abduction and flexion, important to fix the scapula. note
the glenohumeral joint mvment; scapulothoracic mvment
compensate for decreased mobility at the glenohumeral joint.
a. Abduction (normal passive: 0-180) (raise both arms to
meet above the head) – also assess “painful arc” of 60 to
120 degrees for supraspinatus impingement.
b. Adduction (normal P: 0-45) (cross-shoulder – get patient to
touch other shoulder with hand, observe how far the hand
can reach).
c. Flexion (normal P: 0-180) and extension (normal: 0-?).
d. Internal rotation (normal P: thumb at T4) (place hands
behind back and see how which level the patient’s
extended thumb can reach e.g. inf angle of scapula – T7).
e. External rotation (normal P: 0-45) (with elbows tucked
close to sides and flexed 90 degrees, rotate outwards).
! 29!
2. Power of rotator cuff muscles (0-5):
- Abduction (supraspinatus): lift up arms 90deg in abduction,
forward 30deg in plane of scapula, internal rotate (completely
pronate) both arms, resist downward movement
- Internal rotation (subscapularis) – Gerber’s lift-off test: get
patient to place hands behind back, then examiner presses the
hand against the patient’s back while patient attempts to lift his
hand off. If patient is unable to place hands behind back due to
restricted ROM, perform the belly press test, Pt presses palms
against abdomen and keep elbows forward (if there is any
weakness if the subscapularis, the elbow will fall backwards),
examiner attempts to pull the hand off the abdomen.
- External rotation (infraspinatus and teres minor) arms tucked at
the side, actively external rotate arms, push out against
resistance
***Release suddenly to check for counter action (test for muscle tear)
SPECIAL TESTS
Supraspinatus impingment tests:
1. Neer’s Test: stabilise the scapula/shoulder, pronate/internally
rotate arm and passively flex the arm 90deg (holding the
forearm distal to elbow) and look for expression of pain
2. Painful arc (between 60 to 120 degrees of passive abduction
classically, greater tuberosity hits acromion & the
supraspinatus is caught in btwn).
3. Hawkin’s test – passively flex shoulder and elbow to 90
degrees then internally rotate the arm; look for expression of
pain
Supraspinatus tendonitis:
1. Jobe’s test (or beer can test) – with arm abducted 90 degrees
and in neutral rotation, internally rotate the arm, like inverting
a beer can held in the hand.
Supraspinatus tear:
1. Abduction paradox & Drop-off sign – unable to initiate
abduction but passively abducted to more than 90 degrees,
abduction proceeds by deltoid action. Less than 90 degrees
of abduction, arm will fall to pt’s side, unable to maintain
abduction.
2. Rotator cuff tear: complete and large tear, patient cannot
actively abduct shoulder but may be able to do so passively
w positive drop arm sign when allowed to return to neutral
position
Biceps tendinitis (tendon of long head of biceps)
1. Speed’s test – with elbow fully extended and forearm
supinated, the patient flexes his shoulder against resistance
on the arm; test is positive when there is pain localised to the
bicipital groove.
2. Yegarson’s test – with elbow flexed to 90 degrees and
forearm pronated, patient attempts to supinate forearm
against resistance; test is positive when there is pain
localised to the bicipital groove
3. Popeye’s sign (degenerative rupture of long head of biceps):
actively flex elbow to 90deg and resist flexion; look at
prominent muscle belly of biceps muscle.
Stability (glenohumeral joint)
1. Anterior apprehension test (anterior dislocation; done for
suspected cases of shoulder instability) patient seated, stand
behind patient and passively abduct shoulder to 90deg and
external rotate the arm, thumb apply pressure anteriorly
against humerus head and look at patient’s face for
apprehension or guarding.
Laxity
1. Sulcus Sign (inferior glenohumeral instability) patient
standing, grasp arm and pull downwards, depression
between acromion and humeral head.
Labrum Tear (not necessary)
1. O’Brien’s Test with thumbs down, flex shoulder to 90°, adduct
to 20°. Press and resist should be painful. Thumbs up is
relieving.
FINISH with assessment of neurovascular status of the upper
limb, and examine the cervical spine.
IMPORTANT HISTORY TO TAKE FOR SHOULDER PAIN Important features to look out for on shoulder X-ray:
- Duration (time course of frozen shoulder – pain and stiffness for - Narrowing of subacromial space
first 6 months, less pain but persistent stiffness for next 6 to 12 - Bony spur on inferior aspect of acromion or acromioclavicular joint
months, and recovery of joint mobility 18 months after start of - Calcification of supraspinatus tendon (acute calcific tendinitis)
symptoms). - Narrowing of joint spaces esp. glenohumeral joint
- Any preceding trauma (frozen shoulder and rotator cuff tear often - Osseous lesion(s) if any
follow minor precending injury). - Subluxation/dislocation
- Neck vs shoulder pain – shoulder pain may be due to cervical - Bone erosions
pathology; shoulder pain is typically located over the deltoid
insertion and tip of shoulder, not along the trapezius or neck. CAUSES OF SHOULDER PAIN
o Pain on top of shoulder suggests AC or C-spine pathology
- Shooting pains travelling down arm, numbness and/or weakness Tendon (rotator Tendinitis
of hand – indicative of cervical spine pathology or nerve problem. cuff disorders) Rupture
- Pain on lying on shoulder while sleeping. Frozen shoulder
- Function of shoulder (see below). Joint disorders Glenohumeral arthritis
- Diabetes (very important as diabetes is a cause of idiopathic Acromioclavicular arthritis
frozen shoulder). Other structures in jt:
- Heart disease – may result in referred pain to shoulder. subacromial bursitis etc
- Red flags – night pain, worsening pain, constitutional symptoms Referred pain Cervical spondylosis
Cardiac ischaemia
FUNCTIONAL ASSESSMENT IN SHOULDER PROBLEMS Mediastinal pathology
- Ability to reach for objects placed in overhead positions Instability Dislocation
- Ability to comb hair Instability
- Ability to touch opposite shoulder and back (for personal hygiene) Bone lesions Infection
- Ability to wear top e.g. shirt, T-shirt, blouse Neoplasm
Nerve lesions Suprascapular nerve
INVESTIGATIONS: entrapment
- No blood investigations are required usually
- Shoulder X-ray is the most useful invx: need >/= 2 views Think 4 Ss for Shoulder:
o AP, axillary (w arm abducted to see relation of humeral Stiffness: Frozen Shoulder, Post-traumatic/post-surgical stiff shoulder.
head to glenoid) Strength: Rotator cuff tear
- Other Ix: double contrast arthrography, U/S, CT/MRI Stability: TUBS vs AMBRII
Smoothness: Subacromial abrasion Primary degenerative joint
disease, AVNs, Recurrent dislocations, post-surgery arthritis, RA.

1. Rotator Cuff Impingement***

GENERAL INFORMATION
• About the rotator cuff
o Subscapularis (front), supraspinatus (above), infraspinatus (back), teres minor (back)
o Innervation
! Suprascapular n: Infraspinatus, supraspinatus
! N. to subscap: Subscapularis
! Axillary n: Teres minor
o All but subscapularis (lesser tuberosity) insert into greater tuberosity
o Role:
! Pull it firmly into glenoid (stabilize)
! Depress humerus (hence damage narrows sub-acromial space)
o Supraspinatus crosses beneath coracoacromial arch formed by acromion (post-sup),
coracoacromial lig, coracoid process (ant)
o Subacromial bursa separate tendon from arch, allowing sliding
o Coracoacromial arch: roof formed by the coracoacromial ligament running between the
coracoid tubercle anteriorly to the anterior third of the acromion posteriorly
• Aetiology of rotator cuff impingement
o Impingement: attrition of cuff due to repeated rubbing of the rotator cuff tendons under the
coracoacromial arch greatest in the “impingement position” during abduction, slight
flexion, internal rotation
! Contributing factors to impingement: structural fx (bone, tendon, bursa) +
functional fx (muscles)
• Bone: osteoarthritic thickening of AC joint, osteophytes along
anterior edge of acromion (subacromial spur), hooked acromion
(Neer’s classification)
• Tendon: rotator cuff swelling (in inflammatory disorders such as
rheumatoid arthritis and gout)
• Bursa: subacromial bursitis (in inflammatory disorders like RA/gout)
• Functional factors: weak rotator cuffs (decreased depression of
humerus)
o Site of impingement is usually the “critical area” of decreased vascularity in the supraspinatus tendon 1cm proximal to its insertion into
the greater tuberosity
o Vascular reaction occurs in an attempt to repair a torn tendon or to revascularize a degenerate area. New blood vessels grow in and
calcium deposits are resorbed. This vascular reaction causes congestion and pain. Pain is caused by wear, tear and repair of the
tendons! All 3 happen in varying levels across the ages.
• Pathophysiology of rotator cuff impingement
! 30!
 o Structural and functional predispositions " impingement syndrome " tendinitis or tear (often co-exist)
o Pathological processes can be summed up into “wear, tear and repair”
! Friction leads to localised oedema and swelling (tendinitis) – “wear”
! Tendinitis is usually self-limiting but with prolonged or repetitive impingement minute tears can occur, especially in elderly – “tear”
• Tears can be complicated by scarring, fibrocartilaginous metaplasia or calcification in the tendon (esp near
supraspinatus insertion as relatively avascular)
! Healing is accompanied by a vascular rxn and local congestion which is painful, and this may contribute to further impingement
• Healing more rapid and complete but more painful in young " acute calcific tendinitis
• Healing less vigorous and less painful in elderly " chronic tendinitis (that doesn’t heal completely)
• Investigations
o X-ray
! Usually normal in early impingement
! May be erosion, sclerosis or cyst formation at the greater tuberosity (insertion of the supraspinatus tendon) in chronic tendinitis
! May see calcification of the supraspinatus tendon (just above greater tuberosity) " incidental and not the cause of pain
! May see narrowing of the space between the acromioclavicular joint and the humeral head
! May see signs of AC and glenohumeral joint wear – osteophytes
! Acromial spur
o Arthrography (X-rays after injection of contrast)
! Full thickness tear: medium escapes from joint into subacromial space
! Not in partial/ intra-tendinous tear
o US: may detect large tears, but operator dependent
o MRI: accurate delineation of anatomy; can help determine site and size of a tear if present
o Arthroscopy

ACUTE CALCIFIC TENDINITIS

• Pathology: Deposition of calcium hydroxyapatite crystals in supraspinatus tendon (in critical zone just medial to insertion) associated with
pain secondary to vascular reaction (and swelling and tension); calcific material resorbed and soften within weeks " intensely painful
but rapidly better
o NOTE: chronic calcification is common and usually asymptomatic; incidental finding
• Risk Factors: Yong Adult (<40yo)
• Symptoms
o Acute intense pain (especially with overuse/unaccustomed activity)
! Character: Aching
! Time Course: pain of increasing severity, reaching a climax after a few days, and then subsiding
! Joint usually too tender to allow movement or palpation
• SIGNS OF SUPRASPINATUS TENDINITIS
o Pain at the point of insertion of the supraspinatus along the anterior border of the acromion, best felt
with the arm held in extension; tenderness may disappear on flexion
o Painful arc: Pain on active abduction between 60 and 120 degrees of motion, with disruption of
scapulohumeral rhythm (abduction pain relieved by ext rotation)
o Impingement sign (Neer’s sign, Hawkin’s test): Pain elicited when affected arm is passively flexed,
abducted and internally rotated (the greater tuberosity is brought under the coracoacromial arch impinging the supraspinatus)
o Impingement test: Pain on doing the above procedure is reduced after injection of lignocaine into the subacromial space
• Management
o Mild: conservative
! Rest in sling
! Lifestyle: eliminate aggravating activity, and avoid “impingement position”
! Physiotherapy
! Short courses of analgesia e.g. NSAIDs
o Moderate: Subacromial (1-2cm lateral to acromial edge) hydrocortisone & lignocaine (H&L) / triamcinolone & xylocaine injections for
pain relief (LA takes effect immediately and lasts 1 day; corticosteroid takes effect 3-5 days later)
o Severe: Surgical removal of calcific material considered if symptoms recur and above Rx ineffective

CHRONIC TENDINITIS
• Pathology: Chronic vascular response in tendon in response to 1) overuse 2) minor tears 3) impingement (factors above)
• Risk Factors: Adult (40-60)
• Symptoms
o Pain
! Site: In shoulder and over deltoid
! Exacerbating: Certain movements/ demanding activities
! Relieving: NSAIDs and rest
! Time course: characteristically worse at night; cannot lie on affected side
! May have Hx of recurrent attacks of subacute tendinitis
! Pain and stiffness may restrict daily activities
• Signs
o As above in acute tendinitis
o In long standing: Muscle wasting, power loss, restricted movement
• Complications
o Chronic cuff pathology " Subluxation of humeral head upwards " joint incongruity " Osteoarthritis " decreased ROM
o Rotator cuff tears
• Management

! 31!
 o Conservative: refer to Mx of acute tendinitis
o Surgical (usually arthroscopic acromioplasty)
! Subacromial decompression: Excision of coracoacromial ligament and antero-inferior part of acromion
! Osteotomy of subacromial osteophytes

ROTATOR CUFF TEAR

• Pathology: partial (continuity allows repair and vascular ingrowth) or complete tear (little or no rxn and no repair; proximal fibres may retract
and become stuck down) with progressive fibrosis and disruption of rotator cuff
o Subscapularis usually torn last in degenerative tears
• Risk Factors
o Adult (45-75)
o Background of rotator cuff tendinitis, fibrosis
o Precipitated by trauma: weight lifting, protecting oneself from falling, sprain, jerking injury of shoulder
• Symptoms: Refractory shoulder pain (including night pain) w increasing stiffness and weakness (impaired abduction)
o In acute complete tears, patient complains of acute pain and inability to abduct arm; painless soon after injury but injury never mends
• Signs
o Tenderness (diffused or localized to tip of acromion)
o Supraspinatus weakness on Jobe’s test
o Neer’s Test: Injecting H&L to differentiate between partial and complete tears (able to abduct after administration indicates partial tear)
o Partial tear: painful arc, crepitus or clicking, may have normal ROM (only pain limits movement)
o Complete tear
! Abduction paradox (supraspinatus tear): unable to initiate abduction but can abduct (by deltoid) after raising above right angle
! Drop arm sign: Arm suddenly drops past certain angle on lowering
o Wasting:
! Commonest cause of Isolated supraspinatus (or supra+infra-spinatus) wasting: rotator cuff tear esp in elderly (normally involves
supraspinatus first), suprascapular nerve palsy in younger patients (eg. neuritis)
! Infraspinatus tear almost never occurs isolated; thus wasting is most likely due to nerve entrapment; most commonly due to
ganglion cyst
• Management
o Acute Phase – Conservative: Heat therapy, PhysioRx to improve strength, local anesthetic
o Later – Surgical (indicated by pain and weakness after failure of conservative treatment; esp for young active individual)
! Complete tears repaired unless 1) long standing and painless with acceptable function 2) old and sedentary
• If amenable to repair, open or arthroscopic cuff repair followed by subacromial decompression
• If not amenable to repair, open or arthroscopic debridement of degenerate cuff tissue and subacromial decompression
! Partial tears do not require surgery unless persistent pain or considerable instability

On inspection, I (note / do not note) any (scars / swelling / skin changes) over the (left / right) shoulder.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also (note / do not note) any bony deformity of the clavicle or shoulder joint.

On palpation the clavicle is (non-tender / tender) and there (is / is no) step deformity noted.
The acromioclavicular joint is (non-tender / tender) , the area just anterior to the acromion is also (non-tender / tender) . There is no tenderness
over the bicipital groove.

Active ROM for shoulder flexion is ___ degrees, shoulder extension is ___ degrees.
Patient is unable to initiate abduction of the shoulder but was able to __________________. OR
Patient is able to abduct shoulder from ___ to ___ degrees but this was subsequently limited by pain.
External rotation was ___ degress and patient is able to reach up to T__ with his thumb.
(when testing passive abduction, push on shoulder to prevent scapula from rotating)

I would like to move on to assess the power of the rotator cuff muscle.
There (is / is no) weakness of the (supraspinatus / infraspinatus / teres minor or subscapularis) .

Impingement tests namely Neers and Hawkins tests are (negative / positive) .

My diagnosis is (left / right) (supraspinatus tendonitis / OA of AC joint / partial rotator cuff tear) .

2. Frozen Shoulder (adhesive capsulitis)

• Pathology: Chronic tendinitis involving entire cuff and joint capsule characterized by progressive pain and stiffness which resolves
spontaneously after 18 months
• PRIMARY ADHESIVE CAPSULITIS
o Idiopathic in cause
o Associated with DM (esp type 1), Dupuytren’s contracture, hyperlipidaemia, hyperthyroidism, cardiac disease
o Global contracture of the shoulder joint, but maximally in the rotator interval area and around the coracohumeral ligament
• SECONDARY ADHESIVE CAPSULITIS
o Intrinsic causes
! Chronic rotator cuff injuries
! Post-traumatic scarring following injuries at the shoulder e.g. fracture of the surgical neck, greater tuberosity.
o Extrinsic causes
! Painful disorders resulting in decreased movements of the shoulder: referred pain from cervical radiculopathy, post-hand, wrist or
elbow surgery, post-MI

! 32!
• Clinical features
o Patient aged 40-60 years
o Symptoms
! Aching in the arms and shoulder after trauma, often trivial
! Pain gradually increases in severity and prevents sleeping on the affected side
! Subsides after several months with increasing stiffness that continues for 6-12 months
! Movement is regained gradually but may not return to normal
o Signs: Shoulder appears normal w no/slight wasting; most marked feature is decreased active & passive movement in all directions
Stage 1 (freezing) Pain # with movement, worse at night
2 – 9 months Surgical release contraindicated in this stage – will get recurrence from ongoing inflammation
Stage 2 (frozen) Pain $, with ROM $ 50% less (stiffness)
4 – 12 months Surgical release indicated (MUA not recommended, may cause # or labral & cuff tears)
Stage 3 (thawing) Resolution
12 – 18 months
• Differentials (for shoulder stiffness)
o Post traumatic stiffness (stiffness max at start then lessen; without much pain)
o Disuse stiffness
o Regional pain syndrome aka reflex sympathetic dystrophy. Either post acute trauma, MI or stroke.
o Infection
• Investigations
o X-ray:
! Usually normal (may have decreased bone density in humerus)
! Useful in excluding ddx of painful shoulder, such as glenohumeral arthritis, infection, post-traumatic stiffness, diffuse stiffness
(eg. due to overly cautious nursing) and reflex sympathetic dystrophy (pain pattern is different anyway)
o Arthrography: contracted joint
• Management
o Conservative: Analgesia (NSAIDs), corticosteroid injections, local heat, exercise
! Aim of conservative treatment is to relieve pain and prevent further stiffening while waiting for recovery (since natural course is
recovery in 12-18 months)
! Physiotherapy:
• Repeated circular movement of shoulder
• Assisted abduction – use towel or rope, loop it over an overhead bar like a pulley system, and hold on to each end with
one hand. Patient uses downward pull of normal arm to passively abduct painful arm overhead.
• Assisted internal rotation – both hands gripping either end of a towel slung across the patient’s back diagonally; the hand
on the painful side holds the lower end while the hand on the normal side holds the end above the shoulder. Patient uses
hand on normal side to pull upwards on towel, passively internally rotating the painful shoulder.
• Wall-crawling – patient uses fingers to “crawl” up a wall slowly, increasing flexion movement.
o Surgical:
! Poorly defined role, only for patients who fail conservative management (no progress for 12 weeks)
! Manipulation under anesthesia (MUA; gold standard – but not for diabetics, osteoporotics)
• Passive stretching of e capsule while patient is under anaesthesia, but be careful of causing #s especially in the elderly
• Followed immediately by active exercises
! Arthrosopic capsular release: division of interval between supraspinatus and infraspinatus
• May dramatically improve ROM; must be followed by aggressive physiotherapy post-op
! Distend the joint by injecting a large volume of sterile saline under pressure
• Prognosis:
o Better in younger patients with post-traumatic frozen shoulder
o Idiopathic frozen shoulders that occur in diabetics tend to recur and not improve.

On inspection, I (note / do not note) any (scars / swelling / skin changes) over the (left / right) shoulder.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also (note / do not note) any bony deformity of the clavicle or shoulder joint.

On palpation the clavicle is (non-tender / tender) and there (is / is no) step deformity noted.
The acromioclavicular joint is (non-tender / tender) , the area anterior to the acromion is also (non-tender / tender) . There is no tenderness over
the bicipital groove.

Active ROM for shoulder flexion is ___ degrees, shoulder extension is ___ degrees.
Rom for abduction is ___ and adduction is ___. (limited by pain)
External rotation was ___ degrees and paitnet is able to reach up to T__ with his thumb.
(ER and IR limited in frozen shoulder)
(when testing passive abduction, push on shoulder to prevent scapula from rotating –movment at scapulo thoracic joint vs glenohumeral joint)
Passive ROM was also limited for the above actions.

My diagnosis is frozen shoulder.

Differentials include: post-traumatic stiffness / disuse stiffness / regional pain syndrome
I would like to complete the rest of the shoulder examination.

! 33!
3. Biceps
BICIPITAL TENDINITIS
• Pathology: Inflammation of biceps tendon secondary to rotator cuff impingement due to its proximity to rotator cuffs
o Rarely, presents as an isolated problem in young individuals after a shoulder strain
• Risk Factors
o Young: unaccustomed shoulder strain
o But still commoner in elderly
• Symptoms: Pain and tenderness sharply localized to bicipital groove
• Signs: Speed’s/Yergason’s" pain in bicipital groove
• Management
o Conservative: Rest, heat treatment
o H&L injection if healing is delayed
o Surgery for refractory case or if a/w cuff lesions: anterior acromioplasty

TORN LONG HEAD OF BICEPS

• Background of Paul’s biceps
o Origin: long head from the supraglenoid tubercle and lies in the bicipital groove, short head is from
the tip of the coracoid process of the scapula
o Insertion: posterior part of the tuberosity of the radius and deep fascia on medial aspect of forearm
via bicipital aponeurosis
o Action- supinator of the forearm, flexor of the elbow jt and weak flexor of the shoulder jt
• Pathology: Degeneration and disruption of tendon; can be part of rotator cuff lesion
• Risk Factors
o Adult (usually >50yo)
o Precipitated by heavy lifting
o Rotator cuff pathology
• Symptoms
o Snapping sensation felt in shoulder during tear
o Pain in upper arm + Bruising in front of arm
! Pain soon subsides and function returns
• Signs: Popeye’s sign (lump over lower pt of arm in elbow flexion) " detached belly of long head of biceps
• Management
o Function minimally impaired hence usually not treated in elderly if isolated lesion
o Surgery for young or if a/w cuff lesions: anterior acromioplasty w reattachment of tendon (splint arm w elbow flexed for 4wks) or biceps
tenodesis (attachment of tendon to bicipital groove)

On general inspection, I note a ___ by ___ cm hemispherical swelling over the (left / right) arm. There is no overlying scar or skin changes.
I would like to move on to palpate the lump. (ask pt for any pain first)
The surface of the swelling is smooth, the edges are well defined and it is firm in consistency. It is non-tender and not warm. The overlying skin is
freely mobile.
(attempt resisted biceps flexion)
The lump becomes more prominent with resisted elbow flexion " popeye bulge
Slip sign is negative.

Differentials include: ruptured biceps tendon / skin lesions (e.g. lipoma)

SUPERIOR LABRUM ANTERIOR POSTERIOR (SLAP) LESIONS

• Pathology: A tear of the superior labrum anterior and posterior to attachment point of biceps tendon
(biceps tendon can be involved as well)
• Mechanism of Injury: Acute trauma or repetitive shoulder action (typically compressive loading of shoulder
in flexed abducted position – eg. FOOSH); age associated degeneration can also contributed to tears in
older patients
• Symptoms
o Painful ‘click’ on lifting arm above shoulder height
o Loss of power when using arm in that position
• Signs: Symptoms reproduced by abducting and externally rotating arm
• Management
o Conservative
o Surgical: Arthroscopy – SLAP repair

4. Shoulder Instability / Dislocation***

GENERAL INFORMATION
• Articulation: occurs btw the rounded head of the humerus and the shallow pear-shaped glenoid
fossa of the scapula
• Relations:
Ant- subscapularis, axillary vessels, brachial vessels
Post: infraspinatus, teres minor
Sup: supraspinatus, subacromial bursa, coracoacromial lig, deltoid
Inf: long head of the triceps, axillary nerve, posterior circumflex humeral vessels

! 34!
• Joint stability
o Rotator cuffs (mainly)
o Glenoid labrum: deepens socket
o Ligaments (weak)
! Glenohumeral ligaments – inferior, middle, superior (*note that the inferior ligament prevents anterior dislocation of humerus)
! Transverse humeral ligament, coracohumeral ligament
o Capsule
o " Least supported part of the jt lies in the inferior location where it is unprotected by the muscles
• NOTE: Shoulder laxity is not equivalent to instability!!!
• Recurrent shoulder instability classification
o TUBS: Traumatic, Unilateral (& directional), Bankart lesion (tear in glenoid labrum), Sx
! Less trauma associated w higher likelihood fo recurrence
o AMBRII: Atraumatic, Multidirectional, Bilateral, Rehabilitation, Inferior capsular shift, Interval closure
! Patients have excessive shoulder laxity (capsular & ligamentous) bilaterally (thus instability usually responds to a rehab program)
" often able to voluntarily dislocate and relocate joint (habitual dislocation) + sulcus sign
! Surgery: rarely indicated; but if necessary it involves tightening of inferior capsule (via inferior capsular shift or interval closure)
• X-Ray views

ANTERIOR (INFERIOR) DISLOCATION (most common)

• Mechanism of Injury
o Fall on backward stretching arm, driving humerus head forward, tearing capsule or
avulsing glenoid labrum, and usually ends up just below coracoid process (fixed coz
spasm of pec major pulls it medially)
o Arm forced into abduction, external rotation, extension
• Symptoms: severe pain
• Signs: shoulder deformity
o Lateral outline of shoulder flattened (prominent acromion)
o Small bulge seen and felt just below clavicle
• Complications Anterior'dislocation'
o Early
! Rotator cuff tear: occurs usu in older people, difficulty in abducting the arm after reduction " KIV repair
! Nerve injury: Axillary nerve, radial nerve, median nerve, musculocutaneous nerve, ulnar nerve, posterior cord
• Axillary nerve injury: patient unable to contract the deltoid (can inititate abduction but difficulty in abduction beyond a
certain angle) and small patch of anaesthesia over the muscle (regimental badge area); usu a neuropraxia (thus
spontaneous recovery after few weeks)
o Course of the axillary n.: arises from posterior cord of the brachial plexus (C5, 6) in the axilla, passes through
quadrangular space then comes into close relationship with the inf aspect of the capsule of the shoulder jt and
medial side of the surgical neck of the humerus
! Axillary artery injury: examine for ischaemia before and after reduction
! Fracture-dislocation: associated fracture of the proximal humerus (eg. Greater tuberosity, neck)
o Late
! Shoulder stiffness
! Unreduced dislocation: closed reduction can be attempted up to 6wks after injury
! Anterior instability: common if the glenoid labrum is detached/damaged or the
capsule is stripped off the front of the neck of the glenoid or if repair doesn’t occur;
more common in younger patients – 90%, 50% in older patients
• Investigations
o X-Ray
! AP View: Overlapping shadows of humeral head and glenoid fossa with head lying
below and medial to socket
! Y Scapular View: Humeral head deviated from center of Y (Y formed by coracoid
process, acromion, body of scapula)
! Axillary (Best View)
• Management
o Manipulation and reduction w sedation or sometimes GA to minimize risk of further
damage (after neurovascular exam) Normal'Shoulder'
! Hippocratic method: pull arm in slight abduction w body stabilized in counter traction (eg.
use a towel slung around the chest under the axilla)
! Stimson’s technique: lie prone with arm hanging over side of bed (15-20min)
• Used esp if anesthesia CI

! 35!
 ! Kocher’s method: elbow flexed 90deg ad close to body " arm slowly rotated 75deg laterally " elbow lifted forwards and
adducted " rotate arm medially
• Not recommended due to risk of nerve, vessel and bone injury
o X-ray post-reduction to confirm reduction and exclude fracture
o Check muscle + neurovascular status: Test abduction to rule out axillary nerve injury (deltoid) or rotator cuff tear. Also rule out median,
radial, ulnar and musculocutaneous nerve injuries.
o Arm rested in sling for 1-2 weeks (shorter period for >30yo due to risk of stiffness)
o Abduction and lateral rotation avoided for 3 weeks

ANTERIOR INSTABILITY
• Pathology: Recurrent dislocations or subluxations post acute anterior dislocation w detached/stretched labrum or capsule (50% of patients
<25yo have recurrent dislocation following acute anterior dislocation)
o Most common type of instability (95%)
• Symptoms
o Recurrent dislocations during relatively trivial actions (w increasing ease) esp over arm movements (abduction, extension, external
rotation) such as swimming, dressing, reaching back or upwards " can often reduce the dislocation himself
o Recurrent subluxation: ‘Catching’ sensation followed by numbness or weakness (dead arm syndrome) when attempting to throw a
ball
o ROM full btw episodes of dislocation
• Signs
o Check for generalised ligamentous laxity (treat more aggressively): sulcus sign
o Anterior apprehension sign: examiner lifts the arm into abduction, external rotation and
extension, patient’s body tautens in apprehension when he senses that the humeral head is abt
to slip anteriorly. Repeat test by applying pressure to the front of the shoulder at the same time,
patient will feel more secure now
o Drawer test: scapula is stabilised with one hand while examiner grasps the upper arm with the
other hand to manipulate the head of the humerus forwards and backwards with the patient
supine
o Fulcrum test: patient lies supine and examiner places one hand behind the patient’s shoulder to
lever the humeral head forward by extending and laterally rotating the arm, patient becomes
apprehensive
• Investigations HillJSachs'Lesion'
o X-Ray: AP, lateral, axillary views
! Hill-Sachs lesion: Depression in posterosuperolateral part of humeral head due to
repeated impact with anterior rim of glenoid (impaction fracture) " May destabilize joint and predispose to further dislocation
• Best seen in AP (w arm internal rotated)
! Axillary view: subluxation of humeral head toward anterior lip of glenoid
o MR Arthrogram (galodinium dye injected into joint to detect fine cuts)
! Bankart lesion: Avulsion of anteroinferior glenoid labrum at its attachment to inferior glenohumeral ligament complex
• Management
o Surgery
! Indications:
• Frequent dislocations (esp if painful)
• Fear of dislocation/subluxation that prevents participation in daily
activity
! Types:
• Bankart (gold standard) – Repair/ re-attachment of glenoid labrum
• Putti-platt: shorten and tighten anterior capsule and muscles
• Bristow – Reinforcement of anterior-inferior capsule using adjacent
muscles

On inspection, I (note / do not note) any (scars / swelling / skin changes) over the (left
/ right) shoulder.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also (note / do not note) any bony deformity of the clavicle or shoulder joint.

PROCEED WITH STABILITY TEST Position'of'Bankart'lesion'

Sulcus sign is positive (inferior glenohumeral instability)
Apprehension test is positive (anterior dislocation)

PROCEED TO TEST INTEGRITY OF AXILLARY NERVE

Power for abduction of the (left / right) shoulder is ______.
Patient does not have numbness over the regimental badge area.

This patient has (left / right) shoulder instability that is not complicated by axillary nerve palsy.
I would like to complete the rest of the shoulder examination.

POSTERIOR DISLOCATION (rare; <2% of shoulder dislocations)

• Mechanism of Injury:
o Direction of force: Indirect force producing internal rotation and adduction
o Commonly during an epileptic fit or electric shock

! 36!
 o Trauma: direct blow to front of shoulder, fall on flexed and adducted arm, fall on outstretched hand
o Typically a fracture-subluxation instead of a complete dislocation
• Signs
o Arm locked in medial rotation
o Front of shoulder flat; prominent coracoid
• Complications
o Recurrent dislocations (posterior instability)
o Unreduced dislocations: OR in injuries up to 8week old in young
• Investigations
o Xray
! Axillary view (BEST): can also best see reverse hill sach and posterior labrum tear
! AP view
• NOTE: may miss dislocation coz humeral head may seem in contact w glenoid
• Possible empty glenoid sign: humeral head appear “away” from glenoid fossa
• Classic electric light bulb appearance (medially rotated humeral head looks
globular/symmetrically bulbous)
! Lateral view
• Shows posterior subluxation
• Sometimes shows indentation on anterior humeral head
• May have accompanying #s of humeral neck, posterior glenoid rim or lesser
tuberosity
• Management
o Manipulation and reduction: Arm pulled and laterally rotated while head of humerus pushed
forward
o Rest of management as for anterior dislocation Light'bulb'sign'

POSTERIOR INSTABILITY (much less common than anterior)

• Pathology: almost always a recurrent posterior subluxation (humeral head riding back on posterior lip of glenoid) instead of complete
dislocation when arm is in flexion and internal rotation " may be sequelae of acute posterior dislocation
• Signs:
o Posterior drawer test: humeral head pushed backwards while the scapular spine and coracoid process are held by the other hand
o Posterior apprehension test: forward flexion and internal rotation of the shoulder with a posterior force on the elbow
• Management
o Conservative: Strengthening exercises
o Surgery (up to 50% recurrence:
! Indications: Marked disability without gross laxity
! Procedure: Soft tissue reconstruction with posterior bone block to block abnormal posterior movement
! Then spica for 6 weeks (arm abducted & ext rotated)

INFERIOR DISLOCATION
• Mechanism of Injury: Humeral head is levered out of its socket (when arm is hyperabducted) and pokes into axilla
• Symptoms: Arm locked in abduction
• Signs: Humeral head may be felt in or below axilla
• Complications
o Severe soft tissue injury
o Avulsion of capsule and surrounding tendons
o Muscle rupture
o Fracture of glenoid or proximal humerus
o Neurovascular injury: Brachial plexus or axillary artery
• Investigations: X-ray " humeral shaft points upwards w head sitting below glenoid
• Management:
o M&R: pull upwards in the line of the abducted arm w counter-traction
downwards over the top of the shoulder
! Examine for neurovascular damage post-reduction
! Rest arm in sling for 3 weeks
o Open reduction if above doesn’t work

5. Acromioclavicular Dislocation/Instability
• General Information
o ACJ is the only point of ligamentous attachment to the clavicle and thorax
o Scapula is fixed to clavicle by ACJ and coracoclavicular ligaments
• Mechanism of Injury
o Fall on shoulder " tear ligaments " upward subluxation of clavicle
o Tear of acromioclavicular ligaments (subluxation)
o Accompanying tear of coracoclavicular ligaments (complete
dislocation)
• Symptoms: Pain
• Signs
o Tenderness isolated to site

! 37!
 o Prominent ‘step’ deformity (indicative of complete dislocation; absent in subluxation)
– AC ballotment
o Scarf test: Place hand over opposite shoulder and move up; pain localized over AC
joint
• Classification (Rockwood): 5 types depending on ligament, capsule and fracture
involvement
• Complications
o AC Instability: Discomfort and weakness (if unreduced) esp with strenuous
overhead activity
o Rotator cuff tendinitis!
o Secondary OA (due to subluxation)
• Investigations
o X-Ray
! AP, axillary, cephalic tilt views
! Stress view (stand + hold 5kg weight in each hand): Diff subluxation from dislocation
• Management
o Subluxation: Armsling till pain subsides" shoulder exercises
o Dislocation (in young with a)prominent clavicle, b)inferior or posterior clavicular dislocation)
! ORIF + repair torn ligaments (screw inserted downward from clavicle into coracoid process and left for 8 weeks)

On inspection, I (note / do not note) any (scars / swelling / skin changes) over the (left / right) shoulder.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also note a step deformity at the AC joint.

On palpation the clavicle is (non-tender / tender) and there (is / is no) step deformity noted.
The acromioclavicular joint is slightly tender with a palpable step deformity, the area just anterior to the acromion is also (tender / non-tender) to
palpation.
There is no tenderness over the bicipital groove.

Diagnosis is that of AC joint dislocation, I would like to complete the rest of the shoulder examination:

Active ROM for shoulder flexion is ___ degrees, shoulder extension is ___ degrees.
Patient is unable to initiate abduction of the shoulder but was able to __________________. OR
Patient is able to abduct shoulder from ___ to ___ degrees but this was subsequently limited by pain.
External rotation was ___ degress and patient is able to reach up to T__ with his thumb.
(when testing passive abduction, push on shoulder to prevent scapula from rotating)

I would like to move on to assess the power of the rotator cuff muscle.
There (is / is no) weakness of the (supraspinatus / infraspinatus / teres minor or subscapularis) .

Impingement tests namely Neers and Hawkins tests are (negative / positive) .

AC JOINT OSTEOARTHRITIS
• Risk factors:
o Middle aged/ elderly
o Trauma or occupational stress
• Symptoms: pain
• Signs
o Tenderness at ACJ
o Pain at extremes of abduction and flexion (shoulder movements unaffected unless shoulder involved)
• Management
o Conservative
o Surgery: excision of lateral end of clavicle

6. Scapula and Clavicle Fractures (content from lecture only)

SCAPULA FRACTURES
• Mechanism of injury: Neck (blow/fall on shoulder), Acromion (direct force), Glenoid (shoulder dislocation), Corocoid, Body
• Associated injuries: rib # (significant trauma: may have pneumothorax, flail chest, lung injuries), clavicle #, cervical spine injuries, brachial
plexus injuries, AC injuries
• Usually not significantly displaced (unless significant trauma)
• Possible rotator cuff dysfunction
o Due to some degree of luxation of shoulder joint during injury
• Management:
o Benign neglect (non surgical with sling)
o Ability to compensate due to universal motion (scapulothoracic and glenohumeral)
o Surgery mainly for displaced glenoid #, >40deg angulation
• Scapulothoracic dissociations
o Mechanism of injury: Violent traction force to upper limb" scapula and arm wrenched from chest
o X-ray: Medial border of scapula more laterally displaced
o Examination: patient frequently obtunded (high mortality), haematoma
o Limb-threatening injury (often ruptured subclavian vessels and brachial plexus)

! 38!
CLAVICLE FRACTURES
• Generally heal with minimal treatment; but recent studies show up to 15% don’t heal well
• Site: Usually at junction between middle and lateral third
o Bone transits from tube to flat area
o Lack of muscle attachment (medial has SCM, lateral has deltoid)
o Little cancellous bone
• Surgery is indicated if
o Neurovascular compromise
! Subclavian artery
! Brachial plexus
o Open fractures
o Risk of open fractures (eg tented skin –impending perforation of soft tissue)
o Multiple fractures/injuries
! Easier for nursing and rehab (eg femur fracture hard to use crutches if clavicle fracture)
o Polytrauma
o Failure of conservative management
o Mal/nonunion
o Floating shoulder (unhingement of shoulder from axial skeleton)
! Scapula fracture + clavicle fracture
o Significant displacement/shortening/ angulation > 20 degrees
o Lateral third fractures (weight of arm + possible tears of coracoclavicular ligaments cause certain degree of displacement " affect
function)
• Management
o Conservative: Arm sling, clavicle brace
o Surgery (internal fixation)
! May damage supraclavicular nerve (numbness or neuromas) in openly invasive techniques
! Hook plate (for distal third #): Hook placed under acromion to hold fragment down " must eventually remove due to
impingement
• Complications
o Early (rare)
! Damage to vital structures – pneumothorax, subclavian arteries, brachial plexus
o Late
! Non-union (often in displaced lateral 3rd fractures)
! Malunion (lump often disappears with time)
! Shoulder stiffness

STERNOCLAVICULAR DISLOCATIONS
• High risk injury because (IMPINGEMENT ON MEDIASTINAL FRACTURES)
o Trachea, Esophagus, aorta
• Side impact (because of obliquity of joint)
• Management
o Push shoulders out (reduction) OR
o Clamp clavicle and pull it out
!
ACROMIOCLAVICULAR BURSA
!
On inspection, I note a ___ by ___ cm hemispherical swelling over the (left / right) shoulder.
There is no overlying scar or skin changes.
There (is / is no) wasting of the (supraspinatus / deltoid) muscle.
I also (note / do not note) any bony deformity of the clavicle or shoulder joint.

I would like to move on to palpate the lump. (ask pt for any pain first)
(determine if mass is arising from AC joint with palpation)
The mass seems to be arising from the AC joint. The surface of the swelling is smooth, the edges are well defined and it is tense. It is non-
tender and not warm. The overlying skin is freely mobile and it is superficial to the muscle.
The swelling (is / is not) transilluminable and it is slightly compressible and fluctuant. There is no punctum seen.

Differentials include: acromioclavicular bursa / PVNS / skin lesions (e.g. lipoma)

Mx: aspirate and excise if it recurs
!

! 39!
Humerus!

Fractures!

Proximal'Humerus'

Shaft'of'Humerus'

Distal'Humerus'in'
Children'
•  Supracondylar'
•  Lateral'Condylar'
•  Medial'Condylar'

Distal'Humerus'in'
Adults'
•  Supracondylar'
•  Condylar'
•  Capitulum'
!

! 40!
1. Proximal Humerus***
• MOI: FOOSH resulting in fracture of surgical neck +/- one or both tuberosities
o Usually occurs after middle age: most common in osteoporotic post-
menopausal women
! In elderly:
• Transverse fracture extend across surgical neck often with
greater tuberosity involvement
• Shaft usually impacted into head in abducted position
! In young: FOOSH usually causes dislocation in younger patients
but proximal end may be broken into several pieces
o Proximal humerus fractures in children
! In children, the physis can separate or there can be metaphyseal
fractures, considerable displacement and angulation is acceptable
! Fractures may be pathological as proximal humerus is a common
site of bone cysts and tumors in children
• Fractures due to bone cyst: rest the arm in a sling for 4-6 wks
• Risk Factors: Adult (after middle age), Osteoporosis
• Symptoms: Pain (may not be severe as fracture firmly impacted), Large bruise in upper arm
• Complications
o Immediate:
! Neurovascular injury:
• Axillary nerve (most common)– Test regimental badge area as testing deltoids might be painful
• Bachial plexus injury
• Brachial artery injury
! Shoulder dislocation
o Late: Stiffness, AVN of humeral head associated with anatomical neck fractures (10% of 3-part #; 20% of 4-part #), Malunion w loss
of rotation
• Investigations: X-rays
o AP: Single impacted fracture extending across surgical neck in elderly, fragments more clearly separated in younger patients
o Obtain axillary and Y-scapular lateral views to exclude shoulder dislocation
o Inf subluxation of the femoral head as fracture heals
• Management
o GENERALLY DON’T NEED OPERATION
! Reasons: Extra-articular + Healing good at humerus as in plane of movement
! Recommended management (conservative)
• Send patient home with collar and cuff (not arm sling) and analgesia
• Allow gravity to assist reduction of fragments (will gradually occur as patient relaxes fr initial holding of arm close to body)
! M&R often don’t work well as patient holds arm close to body
o Based on Neer’s classification (distinguishes btw no of displaced fragments which is defined as >45deg angulation or 1cm separation)
*Note: Number of parts refer to number of significant parts (i.e shaft, head, lesser and greater tub) and not gross number of parts

One part No matter how many fracture
lines there are, as long as they
are undisplaced or firmly
impacted, considered as 1 part
Two part 1 fragment displaced (surgical
neck/greater
tuberosity/anatomical neck)
Three part 2 fragments are displaced, usu
head (# along surgical neck) and
greater tuberosity
Four part All the major parts are displaced
(surgical neck + both
tuberosities)
Fracture- 2-part, 3-part or 4-part fracture-
dislocation dislocation
Rest with arm in collar and cuff (6 weeks)
Active exercises once fracture unites (usu aft 6wks)
Cause few problems
- Closed reduction, collar and cuff for 4wks
- IF if reduction fails or fracture unstable after reduction
- Anatomical neck: in young patients, M&R with screw fixation; in older patients,
hemiarthroplasty due to risk of AVN of humeral head (rare)
- Surgical neck or greater tuberosity fractures: M&R " arm bandaged to chest (3-4
weeks) " active exercises
- For 2-part fracture dislocations, closed reduction usu possible
- Fracture of the greater tuberosity may be a/w ant dislocation of shoulder while
fracture of the lesser tuberosity a/w post dislocation
- Young: ORIF with plates and screws
- Elderly (with osteoporosis): M&R " physiotherapy
- 3 part fracture dislocation requires ORIF, at risk of brachial plexus injury
- A/w poor outcome, high risk of vascular injury, brachial plexus damage, injuries of
chest wall
- Usu needs Prosthetic replacement (reserved for elderly) - Hemiarthroplasty (esp
in elderly) due to risks of incomplete reduction, non-union, AVN of humeral head
Treat as above according to number of parts

! 41!
2. Shaft of Humerus***
• Mechanism of Injury
o FOOSH twisting humerus causing spiral fracture
o RTA: Fall on elbow with arm abducted, hinging the bone " oblique or transverse fracture
o Direct blow to arm causing transverse or comminuted fracture
o NOTE: in elderly, fracture may be due to mets
• Symptoms: Pain, Bruise, Swelling
• Signs: Displacement of fragments depends on relation of site of fracture to insertion of deltoid
o If # line proximal to deltoid insertion, prox fragment adducted by pec major, lats dorsi, teres major while distal fragment abducted by
deltoids
o If # line distal to deltoid insertion, prox fragment abducted by deltoid and distal fragment pulled proximally by biceps and triceps
• Complications
o Immediate:
! Brachial artery injury (dx w arteriography)
! Radial nerve injury in spiral groove on posterior surface of humerus under the cover of the
triceps (nerve seldom divided in closed injuries hence to rush to operate; usually heals in 3mths)
• Patient presents with wrist drop and paralysis of the MCP extensors; common with oblique
fractures at the junction of the middle and distal 1/3 of bones
o Common in Holstein Lewis fracture (oblique) where nerve may become
entrapped in fracture site if attempt to reduce (hence must do open reduction) –
lateral sided spike; lower third #
• Function can be restored by tendon transfer in neurotmesis
• Test nerve before and after treatment: MCPJ extension, wrist extension (ECRL may be
supplied by branch prox to fracture)
o Late:
! Delayed/Non/Mal-union: common in conservatively managed patients
! Joint stiffness
• Investigations: XR to look for tumours in elderly as fractures may be pathological
• Management: Usually conservative Holstein'Lewis'Fracture'
o Conservative normally: U-slab (over tip of shoulder) or functional brace + collar and cuff + exercises
(but avoid abduction until fracture heals)
! Most heal readily; weight of arm with external cast enough to pull fragments together. Hanging cast is applied from shoulder to
wrist with elbow flexed and forearm is suspended by a sling ard patient’s neck
! Spiral fractures unite in abt 6wks while other fractures take 4-6wks longer
o ORIF with plate and screws or intramedullary nail with locking screws
! Indications: Pathological #s, open #, polytrauma, segmental #, floating elbow (radius and ulnar + humerus fractures), vascular
injuries, radial nerve palsy after M&R, non-union, displaced intra-articular extension
! Cx rate after IF of humerus high (compression plate, screws, intramedullary nail, external fixation)
o External fixation for open fractures

3. Distal Humerus Fractures in Children

GENERAL INFORMATION
• Mechanism of fractures close to elbow
o Fall on elbow
o FOOSH with elbow forced into valgus or varus
• Ossification Centers appearance (epiphyseal displacement not apparent on X-ray before these ages)
o Capitulum – 1yr
o Radial head – 3yr
o Internal epicondyle – 5yr
o Trochlea – 7yr
o Olecrenon – 9yr
o External epicondyle – 11yr
• Elbow is slight valgus when elbow extended (~15deg)

LATERAL CONDYLAR FRACTURE *** (usually Salter Harris IV)

• Mechanism of Injury:
o FOOSH with elbow extended " Elbow forced into varus " Fragment
of lateral condyles avulsed by attached wrist extensors
o Fracture line usually runs from metaphysis" along physis to enter joint
through the trochlea or capitulatrochlear groove (results in unstable
fracture which may dislocate)
o May damage growth plate and always involves joint
• Symptoms: Swollen, deformed elbow
• Signs
o Tenderness over lateral condyle
o Passive flexion of wrist (pulling on the extensors) may be painful
• Complications
o NON-UNION and malunion (bathed in synovial fluid + BS compromised
+ pull of extensors): Cubitus valgus deformity as disruption of lateral
area of growth plate results in medial side of humerus being longer "
instability if untreated
! 42!
 ! Tardy ulnar nerve palsy: Ulnar nerve gradually stretched with progressive cubitus valgus
• Causes of TUNP: medial/lateral condylar #, Monteggia #
o Recurrent posterolateral dislocation of elbow
• Investigations
o X-ray: oblique view
! Extent of injury often not appreciated as capitellar epiphysis largely cartilaginous & only ossification center in fragment is visible
on XR
! Two types of fractures
• # thru lateral condyle to trochlea (SH type 4): Humero-ulnar joint not involved hence stable
• # through middle of trochlea (SH type 2)
o More common
o Elbow unstable and may dislocate
o Fragment often grossly displaced and capsized
• Management
o Undisplaced #: Splint elbow (backslab with elbow flexed and wrist extended: relaxes extensor mechanism) for 2/52 " Exercise "
Check for displacement with Xray
! Even if undisplaced, need close surveillance to intervene if there is any further displacement (by muscles)
o Moderately displaced #: M&R
o Severely displaced # (gap >2mm): ORIF with screw or K wires " immobilize arm in a cast for 3-4/52

SUPRACONDYLAR FRACTURE **
• Fractures in distal 1/3 of humerus proximal to trochlea and capitulum
• Background:
o “In Singapore, the typical child who has a supracondylar # is a 7yo falling
off a monkey bar with his non-dominant hand”
o One of the commonest # in children; Most common # in KKH requiring Sx
o Mechanism of Injury
! Hyperextension injury due to FOOSH: Posterior displacement and
inward twist of distal fragment as forearm usually in pronation
(most common) " proximal fragment can poke into the soft tissue
anteriorly, injuring the brachial artery or median nerve
! Ant displacement of dist fragment (rare): Due to over-reduction of
post displacement or due to direct trauma w joint in flexion
! Weakest point in olecranon fossa
• Symptoms: Pain over elbow
• Signs: Elbow swelling, S-deformity of elbow (in posterior displacement)
o Assess neurovascular status
• DDx: elbow dislocation (equilateral triangle by epicondyles and olecranon is disrupted)
• Complications
o Early
! Median nerve injury, esp anterior interosseous branch (loss of function usually temporary; recovery expected in 6-8/52)
! Arterial obstruction: Brachial artery injury/ kinking by proximal fragment % compartment syndrome, Volkmann’s ischemic
contracture (irreversible contracture of flexor muscles of the hand due to ischemic processes in the forearm)
• Symptoms 5Ps: pain, pallor, paresthesia, paralysis, perishingly cold, swelling, bruising
! Compartment syndrome: pain + 1 positive sign [pain on passive extension of the fingers, tense and tender forearn,
pulselessness, blunted sensation, increased capillary refill time], KIV angiography, vessel graft, forearm fasciotomy
! Ulnar nerve: damaged by careless pinning
o Late
! Malunion: uncorrected angulation and internal rotation of distal
fragment may lead to cubitus varus deformity (gunstock deformity;
may cause ulnar tunnel syndrome); rarely valgus (may cause late ulnar
n. palsy)
• Disability is slight: increased extension but reduced flexion
• Conservative Rx OR supracondylar corrective osteotomy for jt
malalignment
! Stiffness of elbow joint
! Myositis ossificans
• Investigations
o X-ray: AP + lat (# best seen on lateral view)
! # line across distal humerus, posterior tilt/displacement of distal
fragment +/- medial or lateral displacement
! Fat pad sign in undisplaced fracture: elevated anterior lucency/ visible posterior Fat'Pad'Sign'

lucency due to fat pad being pushed forward by a hematoma

! Baumann’s angle: assess degree of medial angulation " Angle
subtended by longitudinal axis of humeral shaft and line through
coronal axis of capitellar physis
• Normally less than 80deg (if distal fragment tilted in varus
increased angle readily detected)
• Measures degree of sideways tilt
• Increase in Baumann’s angle occur in residual varus and internal
rotation deformities
! 43!
• Classification and management
o Wilkins or Gartlands classification (for extension type; flexion type is always a grade 3)
o Observation: overnight, esp for Cx of vascular compromise
Type Description
1 • Undisplaced fracture
• X Ray: Fat pad sign
2 Angulated fracture with posterior
cortex still in continuity
• IIA: less severe and merely
angulated; Baumann angle =
75deg, anterior humeral line
bisects capitulum
• IIB: Angulated + Malrotated /
Posteriorly displaced "
increased risk of
neurovascular injury or
circulatory compromise due
to swelling
Management Details of Mx
Immobilize in 90o, Splint or cast w sling x 3wks Indications for reduction:
Check x-ray 5-7days later to ensure no displacement - Arterial obstruction
- # displacement &/or angulation
- <50% bony contact
- Backward tilt >/=15%
- Medial or lateral tilting of
>/=10% (may cause tardy ulnar
nerve palsy)
- Severe torsional deformity
• Type IIa:
o M&R under GA:
! Disimpaction: traction applied at
20deg flexion w countertraction
applied to arm
! Reduce post-tilt/ displacement:
flex elbow to 80deg while
maintaining traction
! Correct lateral displacement/
torsional deformity: manipulate
epiphyseal complex
! Check pulse
o + Collar and cuff x3wks
• Types IIb and III: Traction and CRPP

3 Completely displaced w no cortical
contact " increased risk of
neurovascular injury or circulatory
compromise due to swelling
• Brachial artery (pulseless
hand) and median nerve
may kink (NOT rupture)
• Presents as a pulseless
hand
• Ulnar n usually not affected
(if affected, usually
iatrogenic)
Closed reduction and percutaneous pinning (CRPP): Fixation:
M&R under GA + held by percutaneous K wires - Fix w elbow at greatest angle of
Indications for open reduction: flexion possible w/o
(i) closed reduction fails compromising circulation
(ii) open fracture (check radial pulse)
(iii) vascular damage present - Never apply a complete plaster
OR due to risk of swelling
Continuous traction through a screw in the olecranon Remanipulation if reduction is poor
or skin traction with the elbow almost straight and - No more than 2
the arm in a small Thomas splint (Dunlop traction) remanipulations due to risk of
• Indications for continuous traction swelling. Employ continuous
o Fracture severely displaced and cannot traction instead
be reduced by manipulation - K-wires and plaster backslab
o Severe injuries / multiple injuries may be used for unstable #s
o With elbow flexed at 100deg pulse
obliterated
+
Support: collar and cuff for 3weeks + sling for
another 3 wks to avoid extension, but flexion allowed

SEPARATION OF MEDIAL EPICONDYLAR APOPHYSIS / MEDIAL CONDYLAR INJURY

• Mechanism of Injury: Between age 5-16 when medial epicondylar apophysis ossifies and has yet to fuse to the shaft, FOOSH with wrist and
elbow extended & elbow forced into valgus or FFH w direct blow to elbow " may cause avulsion of medial fragment of apophysis by
wrist flexor muscles or medial collateral ligament of elbow; possible lateral dislocation in severe injury
• Symptoms: Pain, swelling and bruising on medial side of elbow
• X-Ray: INTRA-ARTICULAR #
o AP View: Medial epicondylar epiphysis tilted or shifted downwards
o Lateral View: Epicondyle looks like a loose body in joint
o NOTE: in younger children, much of the medial condylar epiphysis is cartilaginous and may not be visible on x-ray, an arthrogram may
be useful in some cases
• Complications:
o Early: tardy ulnar nerve palsy, trapping of medial epicondyle in the elbow joint
o Late: Stiffness of elbow, late ulnar n palsy due to friction in roughened bony groove
• Management
o Minor displacement: splint and repeat XR
o Epicondyle trapped in joint: Must be freed by manipulation or surgery (ORIF)
o Displaced fractures (Without trapped fragment): Manipulation but don’t need surgery (CRPP)

FRACTURE SEPARATION OF DISTAL HUMERAL PHYSIS

• Mechanism of Injury
o Up to 7 years of age the distal humeral epiphysis is a solid cartilaginous segment with maturing centers of ossification
o With severe injury (eg.birth injuries, child abuse) it may separate en bloc
! 44!
• X-ray:
o Younger child: Displacement of capitellar ossification center or proximal radius and ulna
o Older child: Obvious deformity
• Management: Treated like supracondylar fracture

4. Distal Humerus Fractures in Adults

OVERVIEW

Type A Type B Type C

Extra-articular Intra-articular bicondylar# with varying degrees of
Intra-articular unicondylar #
supracondylar # comminution
- rare in adults - high energy # with soft tissue damage
- usu displaced and - examine for vascular or nerve injury
unstable

Rx Undisplaced #
ORIF Posterior slab with elbow flexed almost 90 deg
Check x-rays 1/52 after injury
Displaced#
ORIF, elbow held at 90 deg with arm in a sling, healing occurs by 12wks
Skeletal traction may be considered for severely comminuted #
Elbow replacement in the elderly
Complications
Early-1.Vascular injury
2.Median n. or ulnar n. damage
Late- 1. Elbow stiffness
2. Heterotopic ossification

SUPRACONDYLAR FRACTURES (EXTRA-ARTICULAR)

• Rare in adults (refer to above for supracondylar fractures in children)
o Fractures are more proximal in adults, commonly w comminution, spiraling and angulation
• When occur, usually displaced or unstable
• Management: ORIF

CONDYLAR FRACTURES (INTRA-ARTICULAR)

• Mechanism of Injury: High energy injury driving olecrenon process upwards, splitting condyles apart
• Types: T shaped, Y shaped, Comminution
• X-ray: Fracture extends from lower humerus into elbow jt
• Complications
o Early
! Vascular injury
! Nerve injury: Ulnar or median nerve
o Late
! Stiffness
! Heterotopic ossification (due to severe soft
tissue damage)
• Management – Early movement prime objective (prolonged immobilization results in stiffness)
o Undisplaced Fractures: Posterior slab with elbow flexed at 90 deg
o Displaced: ORIF via intra-articular olecrenon osteotomy
! Unicondylar w/o comminution: Fixed with screws (add contoured plate if fragment large)
! Bicondylar with comminution: Double plate and screw fixation + bone grafts in gaps

CAPITULUM FRACTURES (INTRA-ARTICULAR)

• Mechanism of Injury: FOOSH with elbow straight resulting in anterior part of capitulum shearing off and displacing
• Signs:
o Fullness in front of elbow
o Lateral side of elbow tender
o Flexion grossly restricted
• X-ray (lateral view):
o Capitulum seen in front of lower humerus
o Radial head not opposed to capitulum
• Management:
o Undisplaced Fractures: Rest in sling for 4-5 days
o Displaced Fractures: ORIF
! 45!
Elbow!and!Forearm
Atraumatic! Traumatic!
' Dislocations'
• Tennis'elbow' • Elbow''
• Golfer's'elbow' • Isolated!dislocation!of!radial!head!
• Cubitus'varus' • Pulled!elbow!
• Cubitus'valgus'
• Olecranon'bursitis'

Fractures'(Proximal)'
• Radial'head'/'neck'
• Olecranon!Process!
• Radius'and'Ulna'
• Radius!OR!ulna!
• Monteggia'fracture'
• Galeazzi'fracture'

Fractures'(Distal)'
• Colles''fracture'
• Smith's'fracture'
• Radial!styloid!process!
• Barton's'fracture'
• Comminuted!intraWarticular!fractures!in!
young!adutls!
• Distal!forearm!fractures!in!children!

! !

! 46!
Examination of the elbow Ligaments:
The preliminaries: Introduce yourself to patient, ask for permission to Lateral collateral lig attached by apex to the lateral epicondyle and
examine. Ensure adequate exposure of entire UL, remove all base to annular lig of radius
accessories. Medial collateral lig attached to medial epicondyle to medial margins of
LOOK: olecranon and coronoid process
1. Ask patient to flex shoulders and extend elbows to look for obvious
deformities: eg. cubitus varus/valgus; comment on carrying angle if no Nerve supply: branch from median, ulnar, musculocutaneous, radial n.
deformity
2. Ask patient to flex elbows to look at region of olecranon: obvious Movements:
deformities, lumps & bumps Flexion"brachialis, biceps brachii, brachioradialis, pronator teres; in
PALPATION: flexion, the bony points form the boundaries of an equilateral triangle
1. Feel for lateral epicondyle and palpate for tenderness (MUST do for Extension" triceps, anconeus; in extension, the med and lat
tennis elbow) epicodyles and top of the olecranon are in a straight line
2. Feel for radial head (can be located by gently supinating and
pronating the forearm as it moves under the palpating fingers) Relations:
3. Feel for medial epicondyle and along cubital tunnel (where ulnar Ant" brachialis, biceps tendon, median n., brachial artery
nerve is) Post" triceps, small bursa
4. Feel olecranon for any obvious swelling, bursa, gouty tophi Med"ulnar n. passes behind the med epicondyle and crosses medial
ligament of the jt
MOVE: move both arms tgt to allow comparison Lat" common extensor tendon, supinator
1. Flexion & Extension
2. Supination Forearm normally slightly in valgus in relation to the upper arm,
3. Pronation average carrying angle in children being abt 15 degrees.
In children, the secondary ossific centres can be seen on x-rays. The
SPECIAL TESTS average ages at which the ossific centres appear are ‘CRITOE’
1. Provocative tests for lateral epicondylitis: fully extend elbow, C apitulum-2yrs
pronate forearm and actively extend wrist against resistance " pain R adial head- 4yrs
at lateral epicondyle shld be increased I nternal(medial) epicondyle-6yrs
2. Provocative tests for medial epicondylitis: fully extend elbow, Trochlea-8yrs
supinate forearm and actively flex wrist against resistance " pain at O lecranon-10yrs
medial epicondyle shld be increased E xternal(lateral) epicondyle-12yrs

Complete examination by assessing the neurovascular status of

the upper limb, especially the peripheral nerves.
!
Background:
ANATOMY OF THE ELBOW JOINT
Type of jt: Hinge jt, Stability due to the shape and fit of the bones that
make up the jt and the capsular and collateral ligaments
Articulation: Btw the trochlea and capitulum of the humerus and the
trochlea notch of the ulna and head of the radius

! 47!
1. Atraumatic
TENNIS ELBOW (LATERAL EPICONDYLITIS/ GOLFER’S ELBOW (MEDIAL EPICONDYLITIS)
• Pathology:
o Tennis elbow: minor trauma or repetitive strain on common tendon of origin of wrist extensors attached to lateral humeral epicondyle/
chronic tendinitis and fibrosis of origin of ECRB
o Golfer’s elbow: minor trauma or repetitive strain on common tendon of origin of wrist flexors attached to medial humeral epicondyle
• Risk Factors: Occupational stress/ unaccustomed activity (painter, carpenter, cook etc)
• Symptoms
o Pain
! Site: latera/medial epicondylar pain (radiates widely in severe cases)
! Aggravated by shaking hands, pouring tea, opening doors
! Pain on active wrist extension w a straight elbow (tennis elbow)
o NORMAL ROM
• Signs
o Elbow looks normal, full and painless flexion and extension
o Tenderness
! Tennis elbow
• Just below lateral epicondyle
• Pain reproduced by
o Actively extending wrist against resistance
o Passively flexing wrist (stretch common extensor tendon)
! Golfer’s elbow
• Just below medial epicondyle
• Pain reproduced by passive extension of wrist
• Management
o Mild: rest, exercise (straighten elbow and flex wrist), lifestyle modification
o Moderate: Corticosteroid and local anaesthetic (H&L)
o Severe (symptoms recur): Surgery to detach common tendon on lateral side of elbow from origin at humeral epicondyle, lengthen
tendon (ECRB), excision of fibrous mass, extra-corporal shockwave

CUBITUS VARUS (GUNSTALK DEFORMITY)

• Cause: Malunion of supracondylar #
• This is usually a cosmetic deformity, no real functional problem.
o Cx: median nerve palsy
• Rx: wedge osteotomy of lower humerus. Surgery is only for cosmesis.

CUBITUS VALGUS
• Cause: non-union of # lateral condyle (a/w bony knob on medial elbow)
o Results ∵ medial condyle grows more than lateral condyle
• Mx:
o Undisplaced – backslab
o Moderate displacement – closed reduction and backslab
o Unstable – K-wire and cast
o Rotated – Open reduction and K-wire
o X-ray weekly to detect slipping
• Treat early if getting more and more valgus. If the child is asymptomatic, elbow not worse, monitor and watch.
• Cx: Tardy ulnar nerve palsy – manage by transposing ulnar nerve anterior to elbow (so that no longer tented up) or osteotomy

OLECRANON BURSITIS
• Causes: pressure, friction, infxn, gout (a/w tophi), RA (a/w polyarthritis & SQ nodules over the olecranon)
Olecranon bursa
There is a __ x __ cm hemispherical mass over the olecranon. The overlying skin is thickened, shiny, white and cracked (from repeated rubbing).
There are no signs of erythema or any scars noted.

I would like to move on to palpate the mass. (ask pt for any pain first)
The mass is smooth, with an indistinct edge and a soft and spongy consistency. It is neither warm nor tender.
It is fluctuant and transilluminates (may not if wall of bursa is thick or there is small amt of fluid).
It is immobile and fixed to the underlying structure + / - fixed to the overlying skin.

There may be underlying skeletal abnormality (e.g. exostosis, deformed joint), thus bursa develop to ease movement of skin over the skeletal
abnormality. I would like to complete the examination by examining the contralateral limb for symmetrical lesions, the joint for joint disease and
skeletal abnormalities.
DDx: olecranon bursa / synovitis / RA nodule / gout
Cx: bursitis (inflamed from repeated trauma / RA / gout / haematogenous infection)

! 48!
2. Dislocations
ELBOW DISLOCATION (commoner in adults)
• Mechanism of Injury:
o (90%) FOOSH w elbow in extension " forearm bones dislocated posteriorly or posteolaterally (lateral shift may occur)
o (10%) Side swipe injury (driver w elbow out of the window) causes forward dislocation usu a/w # and severe soft tissue damage
• Symptoms: Pain and swelling (marked if very severe)
• Signs
o Deformity; displacement of bony landmarks
o Patient supports forearm with elbow in slight flexion
• Complications
o Early: considerable soft tissue disruption and possible neurovascular injury
! Vascular injury: brachial artery (emergency)
! Nerve injury: median, ulnar nerves (spontaneous recovery in 6-8weeks usually)
o Late
! Recurrent dislocation if there is a large coronoid #, radial head # or olecranon process #
• Reduction usually stable and recurrent dislocation unlikely if there are no associated #
! Elbow stiffness
! Unreduced dislocation: can attempt M&R till 3weeks after injury
! Heterotopic ossification, myositis ossificans (soft tissue ossification)
• Associated with forceful reduction and excess passive movement of elbow
• Signs: excessive pain, tenderness, tardy recovery of active movements
• Management: splint until pain subsides, then resume movements; NSAIDs; excise bone once it is mature if bone mass
markedly restricts movement
! Secondary osteoarthritis
• Investigations: X-Ray to confirm dislocation and exclude fracture (esp medial epicondyle, lat condyle, coronoid, radial head and neck,
olecranon process in rare ant dislocations)
• Management
o For uncomplicated dislocation: M&R under anaesthesia
! Administer anaesthesia" slightly flex elbow and apply traction on forearm to correct lateral displacement" further flex elbow
and push olecranon forward " check neurovascular status " check XR
! Week 0: Arm rested in light cast with elbow flexed just above 90deg and wrist supported in collar and cuff
Week 1: Cast is removed, gentle exercises
Week 3: collar and cuff removed
o For fracture dislocation
! Internal fixation
! Side swipe injuries: repair vascular damage, skeletal stabilisation
! Hinged external fixator used if elbow remains unstable after anatomical restoration to maintain mobility while tissues heal

RADIAL HEAD DISLOCATION

• Isolated dislocation rare
o usu a/w ulna # (Monteggia injury)
• Common in children; rule out NAI
o Another MOI: parents pulling kids by the hand (yanking)
• Impt to identify ulnar # in children as if a minor deformity allowed to persist, may prevent full reduction of
dislocation
• Look for posterior interosseous nerve injury
• XR: line drawn down the long axis of the radius does not intersect the capitulum, indicating radial head
dislocation
• Treatment: MUA (supination, direct pressure), cast 6/52

PULLED ELBOW
• MOI: pull on the arm with forearm pronated, causing subluxation of annular ligament over head of radius into radiocapitella joint.
o Usually affects a child btw 2-3yrs
• No x-ray findings
• Treatment: Supinate then flex the elbow, ligament pops back in place

3. Fractures of the forearm (proximal)

GENERAL NOTES
• Commonly both forearm bones are fractured
• If only 1 bone is fractured, check for dislocation of the other
• Displaced fractures of forearm usually treated by ORIF as non-surgical means limit pronation/ supination

OLECRANON FRACTURE
• Mechanism of Injury:
o Direct blow or fall on elbow " comminuted fracture
o Avulsion by contraction of triceps when patient falls on hand " clean transverse fracture
• Signs and symptoms
o Comminuted fracture: graze, bruise
o Transverse fracture: palpable gap, inability to extend elbow against gravity

! 49!
 • Investigations: X-ray (lateral view) " check position of radial head as it may be dislocated
• Management
o For comminuted fracture (commonly in elderly): treat as bruise and rest in sling for 1/52 as immobilization can lead to
stiffness in elderly; review XR
o For undisplaced transverse fracture: immobilize at 60deg in cast for 2-3/52
o For displaced transverse fracture: ORIF w cancellous screw fixation/ tension band wiring
• Complications
o Early: transient ulnar nerve palsy
o Late:
! Joint stiffness, secondary OA
! Non-union (treat via internal fixation and bone graft)

FRACTURE OF RADIAL HEAD/ NECK

• Mechanism of Injury
o FOOSH with elbow extended and forearm pronated / direct violence" elbow forced into valgus and radial head impacted against
capitulum " articular cartilage of the capitulum may be bruised or chipped
o In adults: usually fracture radial head
o In children: usually fracture radial neck (as head is largely cartilaginous)
o NOTE: terrible triad – Radial head # + coronoid process # + MCL injury
• Symptoms
o Elbow pain: Aggravated by pronation and supination
o Swelling, bruising, tenderness over radial head
• Signs
o Tenderness posterolaterally over proximal end of radius
o Restricted elbow extension
o Pain on supination and pronation
• Complications
o Late
! Joint stiffness of elbow and RUJ
! Heterotopic ossification
! Myositis ossificans
! Recurrent instability of elbow (if MCL was injured and radial head excised)
! OA of radiocapitellar joint (for radial head fracture)
• Investigations
o X-Ray (AP projections in mid-prone and full pronation to assess type of #)
! Wrist should be x-rayed to exclude concomitant injury of the distal RUJ (ie damage to the interosseous membrane)
! Adults: 3 types
• Type I: vertical split through radial head
• Type II: marginal fragment (fragment of lat portion broken off & distally displaced)
• Type III: comminuted head
• Exclude subluxation of distal end of ulna (damage to interosseous membrane)
! Children: fracture through neck
• May have SH type 2 injury: proximal fragment tilted distally, forwards and outwards
• Management
o Adults (radial head fracture): Mason classification

Fracture Management
Undisplaced (hairline/ marginal): vertical split in -Support elbow in collar and cuff or light compression bandage and
the radial head sling (+ backslab if pain severe) for 3 weeks
-Encourage active movements
-LA injection and aspiration of hematoma

Displaced (marginal): single fragment of lateral -ORIF with small screws

portion of head broken off and usu displaced distally -Review in 3 months
-Late excision of radial head if movements are severely restricted

Comminuted -Reconstruction of radial head if there are forearm injuries, disruption

of the DRUJ which increases risk of proximal migration of the radius
and instability
-(if above fails) Radial head excision (w/I 48hrs) +/- metal or silicone
prosthetic replacement " splint for 3 weeks

Fracture dislocation Reduction and fixation; need to restore radial pillar " then treat
according to Type II or Type III

! 50!
 o Children (radial neck fracture)
Fracture Management
Radial head tilt of <30deg and up to 3mm -Rest in collar and cuff
transverse displacement -Exercises after 1 week

Radial head displacement >30deg -M&R + K-wire if unstable: Extend elbow and apply traction and varus
(>20deg in adults) force (or pronate and supinate and apply pressure when prominent part of
radial head presents) " push radial fragment into position
-(if above fails) Open reduction (no int fixation) then splint in 90deg flexion
for 1-2 weeks" then encourage movements
***NOTE: never excise radial head in children, will interfere with
synchronous growth of radius and ulna
Seen 1 week after injury -Untreated/ only with light splintage

FRACTURE OF RADIUS AND ULNA

• Background of forearm fracture-dislocations
o More commonly fracture of both bones of the forearm, usually displaced
o If only one bone fractured, look for dislocation of the other " Monteggia and Galeazzi
o Displaced fractures of the forearm usually trated by ORIF as non-Sx means often result in limitation of pronation/supination
• Mechanism of Injury
o Twisting force (fall on hand) produces spiral fractures with bones broken at different levels
o Direct blow/ angulating force causes transverse fractures of both bones at same level
o High tendency for bone fragments displacement by contraction of strong muscles attached to radius
• Complications
o Early
! Nerve injury (usually from SURGERY): exposure of prox 1/3 of radius risk damage to PIN where it’s covered by supf part of
supinator muscle
! Vascular injury to radial or ulnar arteries seldom problematic (good collateral circulation)
! Compartment syndrome (high risk areas: elbow, forearm, prox tibia)
o Late
! Delayed union and non-union: High energy and open fractures at risk of non-union" will require bone-grafting and IF
! Malunion: Include angulation, rotational deformity, cross-union of fractures (radius malunites w ulna), shortening, disruption of
distal RUJ" may improve mobility with correctional osteotomy
! Complications from plate removal (neurovascular, infection, fractures)
! Decreaed ROM: Loss of pronation/supination, loss of elbow extension
! Frozen shoulder (shoulder to hand syndrome)
• Investigations
o X-Ray
! Adults: fractures easy to see
! Children: fractures often incomplete (greenstick fractures)
• Management
o Children
! Closed reduction + full length cast from axilla to metacarpal shafts (control rotation)
• Elbow at 90deg
• For upper 3rd radial fracture prox to pronator teres, forearm is supinated
• For middle 3rd radial fracture distal to pronator teres, forearm held in neutral
• For lower 3rd radial fracture, forearm is pronated
! X-ray after 1 week
! Remove splintage when both fractures united (6-8weeks)
! Encourage hand and shoulder exercises throughout
o Adults
! ORIF w plates & screws" deep fascia left open to prevent compartment syndrome (only skin & subcutaneous tissues sutured)
! Keep arm elevated after operation until swelling subsides, and start early ROM exercises but avoid stress
! Takes 8-12weeks for bones to unite

MONTEGGIA FRACTURE (ULNAR #)

• Acronyms
o #ed bone: MUGR – Monteggia = ulna, Galeazzi = Radius
o MUF: Montaggia ulnar fracture; GUD: galeazzi ulnar dislocation
• MOI: Direct violence on forearm or forced pronation (eg. FOOSH w trunk rotation) "
fracture of prox 3rd of ulna (shortening and angulation)+ dislocation of radial head
• Signs: ulnar or radial head deformities; tenderness on lat side of elbow
Ulnar shaft fracture Radial head displacement
Apex anterior (commonest) Anterior
Apex posterior Posterior
Lateral Lateral

! 51!
• Complications: below Cx + common Cx above
o Neurovascular injuries: Radial nerve, median nerve, tardy ulnar nerve palsy (Rx: transposition of ulnar nerve), brachial artery
o Unreduced dislocation (diagnosis missed or dislocation imperfectly reduced)
! Radial head remains dislocated, limiting elbow flexion
! Children: no treatment until end of growth
! Adults: operative reduction, or radial head excision
• Investigations: X-Ray (lateral)
o Fractured prox 3rd of ulna
o Radial head lies in a plane anterior to capitulum (normally radial head points directly to capitulum)
• Management (principle: restore length of fractured bone then reduce dislocation)
o Children: M&R + plaster cast (good remodeling potential)
o Adults/ children with displaced fractures:
! Try M&R (reduce ulnar # by pulling along longitudinal axis of forearm and pushing radial head back into joint and fixed w plate
and screws)" radial head usually reduces after ulna is fixed" open reduction if radial head doesn’t reduce, or unstable.
! Plaster cast in 90deg flexion and supination
! If elbow is stable, mobilize in 10days; if unsure, immobilize arm in plaster with elbow flexed for 6 weeks
o Malunion and non-union

GALEAZZI FRACTURE (RADIAL FRACTURE; COMMONER THAN MONTEGGIA #-Dx)

• Mechanism of Injury: Fracture of distal 3rd of radius + dislocation/subluxation of DRUJ w ulnar displacement
• Signs
o Prominence or tenderness over lower end of ulna
o Piano-key sign
• Complications: below Cx + common Cx above
o Nerve injury: ulnar nerve lesion
o Unreduced dislocation (diagnosis missed or dislocation imperfectly reduced)
! Prominent ulna and chronic wrist pain (treat by excision of distal ulna)
! Torn ligaments" DRUJ instability (treat by casting arm in supination or K-wires)
• Investigations: X-Ray
• Management (principle: restore length of fractured bone then reduce dislocation)
o Children: M&R + plaster cast
o Adults: M&R" then ORIF with compression plating of radius
o X-ray to ensure distal RUJ is reduced and stable
! If yes: encourage active movements
! If reduced but unstable, fix RUJ with K wire and splint in an above-elbow cast for 6 wks
! If a large ulnar styloid fragment present, reduce and fix

4. Fractures of the forearm (distal)

COLLES’ FRACTURE
• Mechanism of Injury: FOOSH (low impact injury) resulting in transverse fracture of
radius just above the wrist + dorsal displacement of distal fragment
o " fracture of radius within 2.5cm of wrist – extra-articular!
• Risk Factors: Elderly lady (postmenopausal osteoporosis)
• Symptoms and signs
o Undisplaced fractures: wrist pain, tenderness over distal radius, swelling with little
deformity
o Displaced fractures: dinner fork deformity (dorsal tilt just above the wrist)
! Palmar and ulnar angulation (AUA), dorsal and radial displacement (DRD) of
distal fragment, torsional deformity, DRUJ disruption (ulnar styloid avulsion or tearing of
fibrocartilage)
• Investigations
o X-ray
! Transverse radial fracture at corticocancellous junction 2cm from wrist +/- ulnar styloid #
! Distal fragment is dorsally displaced w dorsal comminution, dorsally tilted fragment w
apex of # volar, supinated, radially deviated and shortened
! Volar apex angulation of fracture apex
! Loss of radial inclination (i.e more tilted towards radial side)
! Rule of 11s (Normal measurements)
• Radial height from scaphoid (fr head of ulna to tip of radial styloid): 11cm (<11mm
in #s)
• Radial inclination: 22 degrees (<20deg in fractures)
• Volar tilt of radius (lateral view): 11 degrees (<11deg in fractures)
• Management
o Undisplaced fractures: non-surgical
! Dorsal splint for 1-2 days until swelling resolves" cast until # stable (~4wks)"
mobilization
o Displaced fractures: M&R under anaesthesia
1. Types of local anaesthesia
• Haematoma block: inject 5–10 ml of 2% lidocaine directly into the fracture
haematoma (intraosseous)

! 52!
 • Bier’s block: exsanguination" pneumatic tourniquets to retain agent" inject IV lignocaine " tourniquet is
depressurized to restore circulation
o Need to have: monitoring equipment for lignocaine toxicity, assistant, and cast trolley with cast prepared
• Axillary block: inject local anaesthesia in close proximity to brachial plexus
• Or GA
2. Manipulation and reduction
• Indications: displaced, deformity or angulation present, joint line in lateral XR
tilted >/=10deg posteriorly
• Method:
o Exaggerate deformity (disimpact and address dorsal translation):
apply traction in line of forearm w countertractiion applied by assistant to
flexed elbow
o Traction (address shortening): maintain traction w elbow extended
o Volar tilt (address dorsal angulation)
o Ulnar tilt (address radial deviation)
• Post-manipulation:
o X-ray to check position
o Check circulation and assess swelling " complete plaster if swelling is
minimal
3. Dorsal plaster slab from just below elbow to metacarpal necks, 2/3 around
circumference of wrist" held by crepe bandage: Wrist in pronation, slight ulnar
deviation, slight palmar flexion " final moulding w pressure over posteriorlat
aspect of distal fragment
4. Post reduction:
• Elevate arm for 1-2days and start shoulder, elbow and finger exercises asap
• X-ray 10days later to check reduction
• Remove back-slab after 5 weeks and begin exercises
o Comminuted and unstable Colles’ fracture
! Same as above but with percutaneous K-wire fixation" remove plaster and wires after 5 weeks and begin exercises
! For very unstable fractures: external fixation (prox pins through radius, distal pins through shaft of 2nd metacarpal)
• Complications
o Early
! Circulatory impairment
! Carpal tunnel syndrome from swelling in carpal tunnel: most common Cx
! TFCC injury from RUJ subluxation
! Associated scaphoid #
! Comminution of radial fragment
o Late
! Malunion (treatment not necessary but can be corrected by osteotomy): radial drift of distal fragment
! Ligament injuries around wrist: pain and weakness persist even after fracture healed
! Tendon injury: frayed EPL may rupture weeks after (require tendon transfer with an extensor tendon of index finger)
! Joint stiffness: shoulders and fingers
! Complex regional pain syndrome: Pain, tenderness, trophic skin changes, vasomotor instability & osteoporosis of finger joints
if exercises are neglected, due to sympathetic overactivity - swelling, erythema, warmth, changing to cyanosis with blotchy, cold
& sweaty skin, stiff hand
• Mx: physioRx, rest & splintage for pain, chemical sympathetic blockade if severe

SMITH’S FRACTURE (REVERSED COLLES’)

• Mechanism of injury: fall on back of the
hand resulting in transverse fracture of
radius just above the wrist + volar
displacement and posterior
angulation of distal fragment
• Mx: Manipulation by traction and Type!a!
extension of wrist " splintage w wrist Type!b! Type!c!
extended " forearm immobilized in
above-elbow cast for 6 wks

BARTON’S FRACTURE (SUBLUXATION OF WRIST)

• NOTE: Barton’s fracture = Smith’s fracture that enters radiocarpal
joint resulting in anterior subluxation of distal fragment
carrying the carpus w it
• Mechanism of injury: Oblique fracture of radius from volar
surface of distal radius into wrist joints + anterior
displacement of fragment carrying carpus with it (fracture-
dislocation/subluxation)
• Management: ORIF with anterior buttress plate (# is unstable)

! 53!
DISTAL FOREARM FRACTURES IN CHILDREN (JUVENILE COLLE’S #)
• Mechanism of injury: FOOSH with wrist in extension, resulting in distal radial physis fracture or metaphyseal greenstick/buckle fracture +
dorsal displacement of distal fragment
• Symptoms: Pain and swelling around wrist
• Signs: Dinner fork deformity
• Complications
o Early
! Compartment syndrome: hence avoid over-forceful or repeated manipulations, split plaster, elevate arm for 1-2days, encourage
exercise
o Late
! Malunion: uncommon in children <10yrs old; deformity up to 30deg will straighten with remodeling over next 5 yrs
! Radioulnar discrepancy: premature fusion of radial epiphysis" bone length discrepancy
• Investigations
o X-ray
! Physeal injuries: Salter-Harris 1 or 2 with dorsal and radial displacement and angulation of epiphysis
! Metaphyseal injuries: 3 types
1. Buckling of cortex
2. Greenstick fractures with angulation
3. Complete fractures with displacement and shortening
! NOTE: ulnar may be bent though not fractured if only radius is fractured
• Management
Fracture Management
Physeal -M&R under anaesthesia
-Immobilize with full length cast with wrist slightly flexed and ulnar deviated
and elbow at 90deg for 4 weeks

Buckle -Cast for 2 weeks

-very stable -Then restrict activity for another 2 weeks
Greenstick -If deformity unaccepted, M&R by thumb pressure
-Accept angulation of up to 30deg in -Immobilize in full-length cast with wrist and forearm in neutral and elbow
children <10yrs; up to 15deg in children flexed 90deg
>10yrs -X-ray in 1 week
-Remove cast after 6 weeks
Complete -M&R in same way as Colles’ fracture
-X-ray
-Immobilize with full-length cast with wrist in neutral and forearm supinated
-X-ray 10days later
-Remove cast after 6 weeks
-If fracture slips, stabilize with percutaneous K-wire

NIGHTSTICK INJURY
• Isolated fracture of the ulnar with minimal displacement.
• MOI: Holding up arm to protect face from blow
• Rule out fracture clinically and radiographically
• Rx: Below elbow cast for 6 wks for distal one-third #. If angulation of proximal two-thirds severe, consider ORIF.

!
!
!
!
!
!
! 54!
Wrist!&!Hand!
Atraumatic! Traumatic!

Nerve' Fractures'
• Median' • Scaphoid'
• Ulnar' • Ulnar!side!wrist!injuries!
• Radial' • Metacarpals!
• Bennett's!fractureWsubluxation!
• Phalanges!

Lumps'&'Bumps' Dislocation'
• Ganglion' • Lunate'and'perilunate'
• Pigmented'Vilo'Nodular' • Scapholunate!Dissociation!
Synovitis' • Carpometacarpal!
• Lipoma' • Metacarpophalangeal!
• Implantation'Dermoid' • Interphalangeal!

Deformities' Joint'Disorders'
• RA! • Chronic'carpal'instability'
• OA! • Kienbock's'Disease'
• Dupuytren's'Contracture' • Tears'of'triangular'
Vibrocartilage'complex'(TFCC)'
• Torn!collateral!ligament!of!thumb!
MPCJ!

Tendon'Sheath'
InVlammation'
• Tenosynovitis'
• De'Quervain's'Disease'
• Trigger'Finger'
Tendon!Rupture!
• Mallet!Finger!
• Boutonniere!Deformity!

Acute'Infection'

! 55!
APPROACH TO THE HAND EXAMINATION: LOOK (forearm, wrist, hand)
Start off with a quick screen – expose both hands up to elbow, look at Observe hands palmar & dorsal surfaces
the plantar aspect with hands open, then ask patient to close hand, 1. Scars
then look at the dorsal aspect 2. Swellings: Lumps and bumps on the hand
- Tenderness (infx/inflamm; neuromas may feel
uncomfortable)
By this time you should have ascertained the problem:
- Site, size, shape, borders, surface
1. A lump - Overlying skin changes (eg. red & indurated in inflamm,
2. Deformity – arthritis hyperpigmentation may be due to previous therapeutic
3. Nerve palsy procedures like steroid injection)
- Consistency: 3 types
Approach to nerve palsies: • Soft may indicate soft tissue origin like lipoma or
1. Which nerve is involved? nerve tumours
2. What level is the nerve involved? • Firm may indicate cystic or fluid filled lump
3. What is the cause? which has undergone solidification
• Hard may indicate chronic inflamm like
Ulnar nerve dequervian tenosynovitis where tendon sheath
Look: Claw hand underwent changes or origin from bone)
Wasting of the first dorsal interosseous, guttering - Fluctuance (fluid filled lumps; test by holding lump w thumb
Test: Abduction of index finger (first dorsal interosseous) and index finger and use other finger to press lump
perpendicularly; positive if examining thumb and index
Adduction (cross the first two fingers)
fingers are displaced outwards)
FDP of the little finger - Slip sign (to test if lump is isolated and mobile)
Froment’s sign - Compressability (for soft or firm lumps; lump flattens and is
Sensation to little finger, hypothenar eminence restored upon release of pressure)
Site of lesion: FDP and sensation to hypothenar lost in elbow - Blanching of hyperpigmented area on compression and
lesion, preserved in lesion at wrist refilling when pressure is released indicates that swelling is
Cause: Carrying angle of elbow vascular in origin
- Transilluminability (requires torch to be in contact w the
Lacerations over medial aspect of elbow
lump; fluid or other light-porous contents; negative despite
Thickened ulnar nerve initial suspicion if content replaced by hematoma, bleeding
Ulnar nerve subluxation into ganglion cyst or other non light porous contents)
- Mobility (if lump is attached to tendon, moves along tendon
Median nerve course in active movement and can move perpendicular to
Look: Wasting of thenar eminence the course passively)
Test: FPB (abducting thumb) - Increase (superficial to muscle) or decrease (intramuscular
lump) in size with flexion (muscle contraction)
FDP and FPL (making OK sign)
- Attachment to overlying skin and surrounding structures
FDS (flexion of PIPJ) - Tinnels sign elicted from lump (neuromas; sensation of
Sensation to index finger, thenar eminence tingling distal to lump and in the area of distribution of the
Site of lesion: Carpal tunnel spares thenar sensation, FDP, FPL, sensory nerve)
FDS but affects FPB; AIN lesion hits FDP, FPL; - Common DDx of any lump: ganglion (most common lump of
high lesion loses all hand/wrist), PVNS (2nd most common), implantation dermoid,
pyogenic granuloma
Cause: Tinel’s and Phalen’s at carpal tunnel
- Common sites for ganglions: dorsal radial wrist, dorsal distal
IP jt, volar radial wrist, volar distal thumb (A1 pulleys of
Radial nerve fingers)
Look: Finger drop with or without wrist drop - Common sites for PVNS: synovial line tissues (over finger jts,
Test: EPL (retropulsion of thumb) hand tendons)
Extension of fingers (ED) 3. Sinuses
Extension of wrist (ECR, ECU) 4. Deformity (elbow, wrist, fingers, distal radioulnar jt)
Loss of hand cascade (little finger is most flexed, index finger
Extension of elbow (triceps brachii)
least flexed, in resting position of hand)
Sensation over first web space
- Joint contractures if any
Site of lesion: PIN lesion will cause finger drop but not wrist drop
- Dinner fork deformity
and no sensory loss; spiral groove injury will cause - Rheumatoid features:
wrist drop and sensory loss • Elbow: swelling, deformity, subluxation of radius
Cause: Humeral neck fracture most common • Wrist: synovial/bony swelling, prominenece of
ulnar head, volar subluxation of carpus,
Examination of the Hand radial/ulnar deviation of wrist " Any deformity
at wrist must be tested to see if reducible
The preliminaries: Introduce yourself to patient, ask for permission to
! Caput ulnar syndrome has prominent
examine. Ensure adequate exposure beyond elbows, remove all ulnar head: piano key sign done by
accessories. Ensure good lighting, and good positioning by placing supporting distal radius and using
patient’s hands on a pillow. thumb to depress ulnar head " +ve
The focus of hand examination is the 5 different tissues in the when ulnar head reduced on
pressure and returns to a dorsally
hand – (1) Skin and subcutaneous tissue; (2) Muscle and
subluxed position when pressure
tendon; (3) Blood vessels; (4) Nerves; and (5) Bones and joints. released
Note which tissue(s) the pathology lies in. • MPJs: MP jt ulnar deviation, synovial/bony
swelling, MP volar subluxation/dislocation
(proximal phalanx volar to MP heads) " ulnar
! 56!
 deviation may be chronic and must test if
reduction can be achieved
• Fingers: boutonneire or swan-neck deformity
• Thumb: carpometacarpal jt swelling or
subluxation, Z deformity (boutonneire or swan-
neck type)
• Movement: full flexion of fingers (decreased
ROM, subluxation of extensor tendons where
tendons appear on ulnar aspect of MP jt), pinch
fingertips, extend fingers (extension lag may be
due to loss of tendon function like rupture of
extensor tendon, contracture of MP jt,
subluxation/ dislocation of MP jt)
• Synovitis common on wrist which appears as
soft to firm lump that is not well defined
• Offer to examine rest of MSK, including
shoulder, hip & knees esp C-spine (esp impt if
planning for sx)
• Look for assoc nerve pathology: wasting of
muscles due to nerve pathologies (w typical
pattern of deficits) or due to disuse atrophy
- OA features (elbow, wrist, MP jts usually not significantly
involved):
• PIP jts: radial/ulnar deviation, bouchard nodes
• DIP jts: Heberdens nodes, mallet deformities
(due to laxity of extensor tendons), radial/ulnar
deviation
• Thumb: swelling and subluxation of
carpometacarpal jts (do standard PE for every
swelling found), laxity of carpometacarpal jt,
grinding test (may elicit pain)
• Movement: Fully extend and flex fingers
(decreased ROM with or without pain in
extremes of motion)
- Tendinopathy:
• Trigger digits
• DeQuervain tenosynovitis: Tenderness and hard
swelling over first dorsal compartment of wrist
5. Discolouration, skin changes
6. Muscle wasting
- Forearm
- Thenar eminence, hypothenar eminence
- Wasting of the interossei " guttering
FEEL
1. Temperature
2. Tenderness over:
- Anatomical snuffbox – base (scaphoid); borders (EPL, APL,
EPB)
- Distal radio-ulnar joint – check for subluxation (piano-key
sign)
- Lister’s tubercle on dorsum of distal radius - scapholunate
junction is just distal to this landmark
- Radial and ulnar styloids
3. Feel joints of hands for:
- Tenderness
- Nodules
- Joint line irregularity
- Subluxation
MOVEMENTS
1. Quick screening tests
- With forearm supinated (palms face-up), get patient to fully
flex fingers and extend – tests patency of flexor tendons
and nerves. " median nerve (eg. Benediction sign), trigger
fingers, jt pathology that prevents full ROM etc
- With forearm pronated (dorsum face-up) and wrist
extended, observe for any wrist and/or finger drop, then get
patient to fully flex fingers and extend – tests patency of
ECRB, ECRL and ECU for wrist, EDC for the MCP joints,
intrinsics for the PIP and DIP joints. " radial nerve
- With elbows tucked in close to patient’s sides, get patient
to pronate and supinate forearm to check range of movement
! 57!
– assesses proximal and distal radioulnar joint, and biceps
action. Flex elbows to look at elbow and dorsum of forearm.
2. Quick Nerve Screening
- Median: Oppose thumb to little finger
- Ulnar: Cross index & middle finger
- Radial: Thumbs up sign
3. Assessment of active and passive range of movements
- If active range of movements < passive range of movements,
there is muscle weakness (nerve palsy), tendon rupture, or
tendon adhesion to surrounding tissue.
- If passive range of movement is restricted, there is joint
contracture.
- Symmetry of movements is a useful guide to whether there is
abnormality.
NERVE TESTING: median + ulnar + radial
3 impt functions: SENSORY, MOTOR, and AUTONOMIC
- Sensory: pinprick sensation over area supplied by nerve; most
sensitive testing is using 2 point discrimination.
- Motor: Power of muscle(s) supplied by nerve.
- Autonomic: Skin warmth, dryness. Use a plastic pen and rub over
finger supplied by that nerve; normally there should be feeling of
friction, but if autonomic supply is lost the pen will slide smoothly
over the skin.
VASCULAR EXAMINATION
- Colour of the skin (pink, or dusky, or pale)
- Pulses
- Capillary refill (should be <2 seconds)
- Temperature
- Tissue turgor
- Allen’s test (hand; test patency of palmar arch which is the
communication btw radial and ulnar artery): Get patient to clench
fist tightly, place fingers of each hand on radial and ulnar arteries
respectively, then get patient to squeeze hand 5-6 times to drain
venous blood, then get patient to open hand and examiner
releases one hand, noting the time that is required for the hand to
turn pink. Then release the other side to allow hand to reperfuse,
and repeat for the other artery.
- Allen’s test (finger): Bend finger tightly. Same concept.
OTHER TESTS (consider wrist examination steps)
Finklestein’s test – for DeQuervain’s tenosynovitis
- Pt closes fist with thumb tucked into clenched fingers.
- Holding arm outstretched with forearm in neutral rotation i.e. thumb
facing upwards, patient is told to ulnar deviate the wrist.
- Positive test is when there is pain localised to the radial styloid
region (1st dorsal compartment)
- Finklestein’s is a very sensitive test for DeQuervain’s.
- Tinel’s test: tap on radial nerve along its course (anterior forearm
up to spiral groove) " +ve when there are shooting pains along
course of radial nerve (up to the sensory ss of the hand)
FINISH with examination of the cervical spine.
General Information
• 6 Tissues of Hand: Skin, Joints, Bone, Nerve, Vessel, Muscle/Tendon
Lumps ! Ganglion ! Haemangiomas
! Pigmented villonodular synovitis (PVNS) ! Pseudoaneurysms
! Implantation dermoid cyst ! SCC
! OA – Heberden’s & Bouchard’s nodes ! Glomus tumours
Joint ! RA hands ! OA hands
Vascular ! Hemangiomas
Nerve ! Ulnar n palsy ! Radiculopathies
! Median n palsy ! Erb’s palsy (C5-6)
! Radial n palsy ! Klumpke palsy (C8-T1)
! Carpal tunnel syndrome
Muscle / ! de Quervain’s dz ! Trigger finger
tendon ! Tenosynovitis ! Dupuytren’s contracture
! RA – Swan neck & Boutonniere deformities, tendon rupture ! Mallet finger
Bones ! Colles’ # ! Boxer’s #
! Smith’s # ! Scaphoid dislocation
! Scarphoid # ! Lunate dislocation
! Bennett’s # ! Gamekeeper’s thumb
Painful Wrist Painful Hand
Referred Cervical spondylosis Neck
Shoulder
Mediastinum
Joint RA RA
OA OA
Infection
Periarticular De Quervain Carpal tunnel
Tenosynovitis Tenosynovitis
Instability Infection
• Pathology: Trauma, Infection, Inflammation, Degeneration, Tumour
• Anatomy of Finger Tip
o Nail bed + Nail plate
! Sterile matrix (pink part)
! Germinal matrix (small white area): where nail growth primarily takes place
o Terminology
! Eponychium – proximal fold
! Paronychium – lateral nail fold (border tissue around nail)
! Hyponychium – epithelium beneath nail btwn free edge of skin nail and skin
! Lunula – white semicircle
• Dorsal vs Palmar skin
o Palmar:
! No pilosebaceous system
! Exocrine sweat glands
! Thick dermis
! Tough and resistant to pressure
! Anchored to fascia by fibrous tracts
o Dorsal:
! Pilosebaceous system
! Thin epidermis, dermis
! Loose connection with deeper planes: supple, mobile, stretchable
! Hence all swellings shows up on dorsal hand 1st (even if problem on volar side)
• Flexor tendon sheath
o 5 annular pulleys
o 3 cruciate pulleys
o Palmar aponeurosis
o Thumb = 2A + oblique pulley
o A2 and 4 most important
o A1 in trigger finger
• X-ray
o AP View: alignment of carpal bones in Gilula lines (carpal arc)
! Some lovers try positions that they cannot handle: (lateral to medial)
scaphoid lunate triquetrium pisiform trapezium trapezoid capitate hamate
o Lateral view: Radius, lunate, capitate, 3rd metacarpal in one straight line
• Other Imaging Modalities
o CT: Articular and carpal bone #s, Tumours
o MRI: Soft tissue injury, Kienbocks’ disease, scaphoid #, tumours
o Arthroscopy: Wrist (carpal instability, TFCC tears)
• Position for Immobilisation: Intrinsic plus position (MCPJ in flexion & PIPJ in extension)
o Stretch collateral ligaments for MCPJ
o Stretch fibrous part of volar plate of IPJ
• Congenital Deficiency: Too little (absence and hypoplasia), Too many (duplications), Undifferentiated (syndactyly)

! 58!
 • H&L (hydrocortisone and lignocaine) injections:
o Common hand indications (ReaCTeD): RA, CTS, Trigger finger, De Quervain’s tenosynovitis
o Up to 2 injections on the same digit (interval of >/= 3 months)
o General notes on H&L:
! Can H&L everything except plantar fascitis and archilles tendonitis
! SEs of H&L include:
• Hypopigmentation of the skin } particularly if too much steroid
• Depression in the skin due to lipoatrophy } injected into space and spills over
• Infx: generally takes quite long for the onset (at least a few weeks compared to after other procedures) because steroid
is anti-inflammatory and hence body takes very long to mount a response against the infx. One common cause of infx is
from introduction of skin micro-organisms and hence good skin preparation is required.
• Tendon rupture: steroids can weaken the tendon. This SE is not so common
except if the doctor moves in and out of the tendon too much and damage the
tendon. This is also a SE only related more commonly to multiple injections.
• Can hit the nerve: in the case of De Quervain’s disease, can get neuroma. This
is because the radial nerve here is purely sensory and no motor components
and hence no radial nerve palsy will be seen. The neuroma is painful and feels
like a electric shock when touched.
• Zones of the hand:
o Zone 2 is no man’s land
o Return of function is difficult in Zone 1 due to short stump of FDP
• Wallerian degeneration: degeneration of axons distal to site of transection (resorbed by phagocytes)
• Seddon’s classification
o Neuropraxia (mildest form of nerve injury)
! Mechanism: Mechanical pressure causing segmental demyelination (interruption in
conduction of impulse down nerve fiber w axonal continuity conserved) "
likely a biochemical lesion caused by concussion/ shock-like injuries to e
fibres
! Effect:
• Recovery takes place w/o Wallerian degeneration
• Temporary loss of function reversible within hrs to mths of the injury
(mean is 6-8wks; not the 1mm/day rule)
• Often greater involvement of motor than sensory w autonomic fx retained
! Recovery: Within few days or weeks
! Example: Saturday night palsy
o Axonotmesis
! Mechanism: loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue
framework of the nerve " usually the result of a more severe crush or contusion than neuropraxia
! Effect:
• Loss in both motor and sensory
fx is more complete than in
neuropraxia
• Small extent of wallerian degen
! Recovery:
• Axonal regeneration begins
within hours of nerve damage
• Eventually axonal processes join
to end organs in weeks,
resuming function
! Example: Nerve injury after closed #s
or dislocations
o Neurotmesis
! Mechanism: Destruction of endoneural
tubes with subsequent scarring
impairing regenerating axons from
entering distal segment to reach target
organs " occurs on severe
contusions, stretch, lacerations
! Recovery:
• Regenerating fibers mingle with proliferating Schwann cells and fibroblasts to form a neuroma at site of injury
• New axons fail to reach target audience or fail to become myelinated, hence function impaired
• Surgical repair essential and quality of recovery always imperfect.
! For neurotmesis is better to use a new, more complete Sunderland system
• Sunderland system
o First-degree: "Seddon’s neuropraxia"
o Second-degree: "Seddon’s axonotmesis"
o Third-degree: endoneurium disruptured, epineurium & perineurium intact
! Thus, when the axons regenerate, they may enter an incorrect nerve sheath, resulting in abnormal regeneration.
! Accompanying e loss of e nerve sheath is intraneural scarring, which further obstructs axonal regrowth thru the site of injury.
! Recovery may range from poor to complete and depends on degree of intrafascicular fibrosis;
o Fourth-degree: interruption of all neural and supporting elements; epineurium intact; the nerve is usually enlarged.
o Fifth-degree: complete transection with loss of continuity. Grade V corresponds to Seddon's classification of a neurotmesis lesion
! 59!
1. Nerve
GENERAL INFORMATION
• Assess the following components • Extrinsic: ganglion
o Neurological: Sensory, Motor, Autonomic o Metabolic: Diabetes – peripheral neuropathy
o Muscle wasting o Degenerative: OA around elbow (cubital tunnel
o Deformities impingement)
o Special Tests • Investigations
• Quick screen o Nerve conduction study
o Sensory o EMG (electromyography) – inclusive of neuromuscular
! Radial – Over dorsum of first web space junction
! Ulnar – Over tip of little finger o X-ray (previous injuries may lead to nerve lesions)
! Median – Over tip of thumb
o Motor
! Radial – Thumbs up
! Ulnar – Criss cross fingers
! Median – Abduction of thumb
! AIN – O sign
• After determining neurological problem, move on to make
pathological diagnosis:
o Inspect: Scars, injuries, deformities (valgus)
o Palpate along course of nerve Nerve Site of entrapment Provocative test
! Thickened nerve Brachial Supra/infra- Arm elevation
! Lump plexus clavicular Pressure btw scalene muscles
o Move Radial Distal forearm Forearm pronation + wrist ulnar
! Range of motion: may be affected in OA nerve deviation
! Eg. Look for subluxation of ulnar nerve during Pressure over tendinous junction of
movement ECT and brachioradialis
o Provocative Tests: Eg. Phalen’s Ulnar Cubital tunnel Elbow flexion + pressure on cubital
• Causes of nerve lesions nerve tunnel region
o Trauma Guyon canal Pressure at guyons canal
! Acute – fracture, dislocation Median Proximal forearm Forearm supination + pressure on
! Chronic – Tardy ulnar nerve (cubitus valgus) nerve pronator teres
o Infection – leprosy (thickening of nerves) Carpal tunnel Wrist flexion and/or extension w
o Compression pressure proximal to carpal tunnel
! Tumour
• Intrinsic: neurileimoma (schwanomma)

MEDIAN NERVE
• Sensory supply:
o Palmar surface of radial 3½ digits and corresponding area
of palm, over thenar eminence
o Palmar cutaneous branch to thenar eminence is given off
before carpal tunnel, thus no loss of sensation over the
thenar eminence. Unless high median nerve palsy.
o Test tip of index and middle fingers and thumb, and thenar
eminence
• Motor supply:
o AIN (2 ½): FPL, PQ, radial ½ of FDP
o Median nerve proper (5 ½): FDS, PT, FCR, PL, L1, L2
o Recurrent motor branch (3): thenar muscles (APB, OP,
FPB)
o General steps: clench fist & test power of FPL (benediction
sign) " Test FDS " Test radial 3 FDP " OK
o Intrinsics –Test abductor pollicis brevis (APB) by fixing 4
digits to the table and getting patient to abduct thumb (in a
plane perpendicular to the plane of the palm) against
resistance " elicit abduction and look for belly of APB.
The APB is the thenar muscle that is solely supplied by the
median n. 99% of the time; the other two muscles may
receive cross-supply from the ulnar n.
o Anterior interosseous nerve supplies FPL, pronator
quadratus and radial half of FDP
! Testing FDP: Fix middle phalanx of index finger and
get patient to flex the DIPJ
! Testing FPL: Flexion of the IP joint of the thumb
while fixing the proximal phalanx
! OK sign: Ask patient to make an “OK” sign by
forming a circle with the thumb and index finger; this
action involves flexion of DIPJ of index finger and IPJ
of thumb, so if there is anterior interosseous nerve
palsy these two joints are extended (like holding a

! 60!
 needle) and the OK sign cannot be made properly. The FDS is still intact, however, since the patient is able to flex his PIPJ of
the index finger.
o Testing the FDS and its tendons (supplied by median nerve proper): Fix the distal phalanges of the fingers adjacent to the finger
being tested, and get patient to flex the PIP joint of the finger being tested.
• Others
o Tinel’s sign: tap over proximal edge of the palm (carpal tunnel). Positive sign is when there is shooting pain and numbness radiating
towards the radial 3.5 digits.
o Compression test: apply direct pressure over carpel tunnel w thumb up to 1 min (numbness can be elicited after 30s in severe
cases). +ve when numbness over radial 3.5 digits is reproduced by this test.
o Phalen’s test: examiner’s thumb is placed over the carpal tunnel and patient’s wrist is flexed for up to 1 min (numbness can be
elicited after 30s in severe cases) or ask patient to put dorsal surfaces of hands together and fully flex wrist. Positive when numbness
over radial 3.5 digits is reproduced by this test.
• High lesion (pronator tunnel syndrome, forearm fractures, elbow dislocation, elbow – ligament of Struthers)
o Carpal tunnel (carpal tunnel syndrome, #, dislocations abt the wrist)
o Deformity/ sign: Benediction sign (or median claw) on flexion; *note: middle finger can still flex slightly despite lack of median
innervation because small, ring and middle finger share a common FDP body
o Posture: Loss of thumb abduction
o Wasting of flexor pronator mass, thenar eminence
o Motor:
! Long Flexors: Paralysis of long flexors to thumb, index, middle finger (both FDS and FDP knocked out)
! Intrinsics: Loss of opposition and abduction of thumb
o Sensory: lateral 3.5 fingers, over thenar eminence
• Anterior interosseous nerve lesion (trauma at elbow or forearm, usually at origin of deep head of pronator teres)
o Motor: flexor pollicis longus, pronator quadratus, radial half of FDP
o Deformity/sign:
! Benediction Sign: Usually partial (some flexion of index; but still absence of flexion at thumb IPJ)
! Inability to produce O sign (inability to flex DIPJ of index and IPJ of thumb)
• NOTE: In median high lesions, failure of producing O sign is even greater due to loss of thumb abd (not affected in AIN)
o Sensory loss: none (AIN has no cutaneous innervation but has articular proprioception)
• Low Lesions (Carpal tunnel syndrome, cut at wrist, carpal dislocations)
o Wasting of thenar eminence (Opponens pollicis, abductor pollicis brevis, flexor pollicis brevis)
o Posture: Loss of thumb abduction
o Motor: lack of ability to abduct and oppose thumb
o Sensory loss: lateral 3.5 fingers on volar aspect up till nail bed (skin over thenar eminence not affected as palmar cutaneous
branch spared)
o Special tests:
! Tinel’s test
! Compression test
! Phalen’s test
! Strength testing of abductor pollicis brevis (palmar abduction)
• Muscles supplied by median nerve (flexors of forearm less FCU and ulnar 2 FDP + LOAF): pronator teres, flexor carpi radialis, palmaris
longus, FDS, lateral 2 FDP, flexor pollicis longus, pronator quadratus, thenar muscles, 1st and 2nd lumbricals

CARPAL TUNNEL SYNDROME

• Anatomy
o Anatomical boundaries
! Radial side: scaphoid + trapezium
! Ulnar side: pisiform + hook of hamate
! Volar: transverse carpal ligament (flexor retinaculum)
o Contents: Flexor digitorum profundus (4), Flexor digitorum superficialis (4), Flexor pollicis longus
• Background:
o Definition: compression ischemia of median nerve
o Pathophysiology:
! Pressure on nerve " BF obstruction in vasa nervorum " venous congestion and edema
! With time, fibroblast proliferation occurs in the nerve " inefficiency of cell transport mechanisms and the sodium pump "
nerve conduction impairment
• Epidemiology
o Women 40-50yo
o Causes: (any condition that reduces space within carpal tunnel)
! Mostly idiopathic
! Anatomical abnormalities:
• Bone: previous wrist #s (eg. Colles #), acromegaly
• Soft tissues: lipomas, ganglia
! Physiological abnormalities:
• Fluid imbalances: Pregnancy, menopause, cardiac/renal failure, obesity, hypothyroid, amyloidosis
• Inflammatory: RA, GA
• Trauma: Previous wrist fracture
• Metabolic: Gout
• Neuropathic: DM, Alcoholism
• Endocrine: Hypothyroidism (cause myxedema), acromegaly

! 61!
 • History
o Presentation
! Sensory
• Burning pain & Parasthesia over lateral 3.5 fingers (often on flexion): GRASPING ACTIVITY like reading newspaper,
driving, on phone
• Usually night pain that wakes patient from sleep and relieved by hanging arm over side of bed or shaking arm
! Motor: Weakness: Incoordination of finger movement, poor grip
o Associated Conditions
o Ruling out differentials: Neck pain
• Physical Examination: Refer above for signs
o Look: Thenar wasting, Loss of abduction posture of thumb (autonomic innervations by median nerve)
o Feel: Dryness region of supply, sensory test
o Move: Test thumb abduction (APB), FDS and FDP (working), wrist extension (rule out C6)
o Special tests: Phalen’s, Compression/Durkan’s test (more specific but less sensitive), Tinel’s test
• Investigation: Nerve conduction studies (TRO other differentials), EMG
• Differentials
o Cervical nerve root lesion (neck pain, other suggestive neurological deficits; cervical spondylosis of C6-7 lvls or secondary to cervical
disc herniation)
o Thoracic outlet syndrome
! Background:
• Lower trunk of brachial plexus n subclavian artery pass btw the ant n middle scalene muscles and over the 1st rib.
• Compression maybe due to cervical rib (rare), fibrous bands or abnormalities of scalene attachments, pancoast tumour
! S/S
• Typically woman in her 30s complains of pain n paresthesia extending down from her shoulder down the ulnar aspect of
her arm to the medial two fingers
• Worse at night, agg by bracing shoulders or raising arms above shoulder height
• Symptoms increase with increasing age as shoulders sag
o AIN syndrome: entrapment usually at the origin of the deep head of pronator teres; ss FPL, pronator quadratus and radial side of
FDP " inability to make OK sign but sensory INTACT
o Pronator syndrome: compression of median n by ligament of Struthers (fibrous band arising from medial epicondyle of humerus,
attaches to supratrochlear spur on the lower anterior humerus), pronator teres muscle or proximal arch of FDS
• Management
o Conservative
! Lifestyle modification: Reduce repetitive activity
! Occupational therapy: Splint wrist in neutral position (esp at night; help with night pain or pregnancy related symptoms)
! Supplements: Vitamin B complex
! Pharmacological: NSAIDs
o H&L injection just proximal to carpal tunnel
o Surgery (Carpal Tunnel Release) – Division of transverse carpal ligament
! Open/ Endoscopic
! Complications
• Scar –hypertrophic/ keloid, scar tenderness
• Failure of relief – Incomplete division of flexor retinaculum
• Nerve injury – palmar cut branch of median n (lies supf to flexor retinaculum) and motor branch of thenar (usually leaves
the radial side of median n towards distal extent of the standard incision) " risk of nerve injury can be decreased by
making the skin incision on the ulnar side of the palmar crease

Patient is a (age) (gentleman / lady) . Sensation was intact over the radial side of the left palm but decreased
On inspection, both hands are in the normal resting position with the over the radial 3 ½ digits.
forearm supinated and the wrist extended. The MCP and IP joints are
flexed, more pronounced in the little finger and less in the index finger. Tinel’s was positive over the ventral aspect of the proximal wrist.

I note wasting of the thenar eminence of the left hand, in addition there My diagnosis will be a severe left median nerve palsy secondary to
is a ___ cm scar over the transverse carpal ligament of the right hand carpal tunnel syndrome. I would like to complete the examination by
signifying possible previous carpal tunnel release of the right hand. doing a neck examination to rule out cervical spondylosis which could
have resulted in radiculopathy that may mimic the symptoms of CTS.
Abduction of the left thumb was weak (power: ___) but power of the
long flexors of the thumb and index finger was full on testing of flexion
of the DIP joint of the index finger.

! 62!
ULNAR NERVE
• Sensory supply
o Dorsal and palmar surfaces of ulnar 1½ fingers and
corresponding areas of palm and dorsum of hand
o Cutaneous branch to the dorsum of the hand is given
off before the wrist, so there is sparing of sensation
over that area in an ulnar nerve lesion at the wrist.
o Test the little finger, over the hypothenar eminence,
and over medial side of the dorsum.
• Motor supply
o Ulnar nerve proper (1 ½): FDP, FCU
! Loss leads to wasting on medial side
o Deep motor branch (15 ½): hypothenar muscles
(AbDM, FDMB, ODM), interossei, 2 medial lumbricals,
adductor pollicis, deep head of FPB
! 1st sign of loss in hand is usually wasting of the
1st dorsal interossesous muscle (hollowing of 1st
web space)
o Intrinsics
! Test palmar interossei – cross index & middle
! Test dorsal interosseous – abduction of the
index finger against resistance. (Not necessary)
! Test Abductor Digiti Minimi (ADM) – Abduct
fingers and push both little fingers to each other
! Froment’s sign – get pt to hold a piece of paper
between thumb and radial border of the hand.
This tests action of adductor pollicis. Pt with
paralysis of this muscle the will compensate by
flexing the thumb (FPL median n). Compare to
normal side.
! Wartenburg sign – ask patient to hold fingers
adducted & extended; the little finger will
become abducted as the adduction ability of the
intrinsics is lost, and the extension action of the
extensor digiti minimi (EDM) pulls the little finger
into abduction.
o FDP of the ring and little finger: hold middle phalanx of
finger and get patient to flex the DIP joint of the finger.
• Other tests:
o Tinel’s sign: tap along the course of the ulnar nerve as
it runs behind medial epicondyle; if patient has had
operation to anteriorly transpose ulnar nerve, then tap anterior to the medial epicondyle. Positive when there are shooting pains
along the course of the ulnar nerve.
o Ulnar nerve subluxation: place a finger on the ulnar nerve and slowly passively flex patient’s elbow, feeling for anterior subluxation
of the ulnar nerve; may fully flex elbow and leave finger on ulnar nerve for 30-60s to test if there is an increase in numbness
• High lesion – Majority
o Common sites of lesion: Cubital tunnel, elbow #s, ulnar subluxation, medial epicondyle (ulnar neuritis from local friction, pressure
or stretching (eg. cubitus valgus), distal to elbow (compression as it passes btw 2 heads of FCU), brachial plexus (trauma, tumour)
o Ulnar tunnel syndrome (ganglion, hook of hamate fracture)
o Wasting: guttering btwn metacarpals, 1st dorsal interossei wasting, hypothenar eminence, adductor pollicis
! & hypothenar + 1st dorsal interosseous wasting + guttering btw MP & valgus/varus deformity of elbow
o Motor: poor finger abduction, inability to cross fingers (Earle and Vlastou’s), weak FDP of little and ring finger
o Sensory loss: volar and dorsal aspect of medial 1.5 fingers
o Tinel’s + posterior to medial epicondyle
o Deformity/Sign:
! Minimal clawing: Less clawing as medial half of FDP no longer working to facilitate clawing
! Wartenberg sign: Ulnar deviation of little finger in extension due to unopposed action of extensor digiti minimi which insertion
is slightly medial(only in extension; must ask patient to keep fingers together)
! Radial deviation of wrist on flexion (Unopposed FCR)
o Management
! Anterotransposition
! Cubital tunnel release (if compression at cubital tunnel)
o History: Repetitive activity (gym), osteoarthritis, history of #
• Low lesion
o Common site of lesion: Wrist (lacerations, occupational trauma, guyon’s canal, pressure from deep ganglion)
o Wasting: intrinsic muscle wasting (as above)
o Motor: Medial FDP function normal, but poor finger abduction and poor thumb adduction (difficult to pinch)
o Sensory loss: volar 1.5 fingers (@ level 5cm prox to guyon’s canal, dorsal branch of ulnar nerve)
o Deformity:
! Clawing (hyperextension of MCP of little and ring fingers, flexion of IPJ of little and ring fingers)
• Unopposed FDS and FDP (flexion of MCP)
• Loss of 3rd and 4th lumbrical + interossei function which normally flex MCP and extend IPJs

! 63!
 • Middle and index finger not flexed because lateral lumbricals supplied by median nerve
! Wartenburg sign: Ulnar deviation of little finger
o Special Tests
! Froment’s sign: Must keep palms together
o History: Trauma (ulnar hammer), fractures, tumour, ulnar artery thrombosis
• Muscles
o In forearm: flexor carpi ulnaris, medial half of FDP
o In hand (all except LOAF): hypothenar (opponens digiti minimi, abductor digiti minimi, flexor digiti minimi), 3rd and 4th lumbricals,
dorsal and palmar interossei, adductor pollicis

Patient is a (age) (gentleman / lady) .
On inspection, I note the presence of clawing of the left hand with
hyperextension of the 4th and 5th MCP joints and flexion of the proximal
(and distal in low lesion) IP joints of the ring and little finger.
There is also wasting of the hypothenar eminence of the left hand and
the dorsal interossei muscle signified by hollowing of the first web
space. There are no scars noted over the wrist, forearm or medial
epicondyle.
Froment’s test was also positive with flexion of the IP joint of the thumb
signifying weakness of the adductor polliciis.
There was also weakness of the long flexors of the ring finger (FDP).
Sensation was decreased over the ulnar 1 ½ fingers and the dorsum
and palmar aspect of the ulnar side of the hand.
Further examination of the upper limb revealed cubitus valgus
deformity of the left elbow.
Tinel’s was negative over the medial epicondyle and the left forearm.

On examination, finger abduction of the left hand was weak (power: _). My diagnosis will be a high ulnar nerve lesion secondary to a malunion
of left supracondylar #.

ULNAR TUNNEL SYNDROME

• Compression of ulnar n as it passes thru Guyon’s canal (btwn pisiform & hook of hamate)
• Clinical features: Small muscle wasting, weakness of hand, sensory disturbance on volar aspect of little finger.
• Causes: ganglions, trauma, ulnar artery disease, old carpal or metacarpal #s
• DDx: Cubital tunnel syndrome, cervical spondylosis

CUBITAL TUNNEL SYNDROME

• Male> Female
• Compressive ulnar neuropathy at the elbow, in the retrocondylar groove or as ulnar nerve passes between the 2 heads of the FCU
o Caused by constriction of fascial bands, subluxation of ulnar nerve over medial epicondyle, cubitus valgus, bony spurs, tumours,
ganglions, repetitive elbow flexion & extension
• Presentation:
o Paraesthesia along ulnar 1.5 fingers
o Weak grip strength, esp when patient rest upon or flexes the elbow
o +/- nocturnal symptoms
o Loss of fine dexterity
o Rarely, wasting of intrinsic muscles and clawing/abduction of little finger
• DDx: cervical spondylosis, ulnar tunnel syndrome (compression at canal of Guyon at the wrist) – preserved strength of wrist and 4th & 5th
digit flexors
• McGowan Grading system
o 1) Parasthesia in distribution, clumsiness in hand
o 2) weak interossei and muscle wasting
o 3) paralysis of interossei, marked weakness.
• Rx: Simple decompression, medial epicondylectomy if a/w non-union of epicondyle #, anterior transposition of ulnar nerve, injection of
steroids in the cubital tunnel

! 64!
RADIAL NERVE
• Sensory supply:
o Numbness classically over dorsal surface of radial 3½ digits
and corresponding area of dorsum of hand (esp base of
thumb extending to first web space; anatomical snuff box)
o Test the dorsal aspect of the first web space.
• Motor supply:
o Posterior interosseous nerve (9): ECRB, supinator, EDC,
EDM, extensor indicis, ECU, APB, EPL, EPB
o Radial nerve proper (4): triceps, brachialis, brachioradialis,
ECRL
o General steps: pronate " clench fist " extend wrists (high
radial nerve)" wrist to neutral position " claw hand
(extend MP and flex IPs; lower radial nerve) " put palms
flat against table & extend thumb
o The most distal extensor muscle supplied by the posterior
interosseous nerve is the extensor indicis propius (EIP) but
this cannot be tested accurately due to the tendon slip from
EDC to the index finger.
o Instead, the next most distal muscle, the extensor policis
longus (EPL), is tested instead – place the hand flat on a
table and get the patient to lift his thumb off the table
(tendons are well demarcated showing retropulsion of the
thumb). If EPL function is intact all other muscles supplied
by radial nerve should be intact.
o Extensor Digitorum (Communis) ED(C) testing – get
patient to extend MCP joints and flex the PIP and DIP joints
(like making a claw) to isolate action of the ED(C). Or simply
test finger extension against resistance " posterior
interosseus nerve
o Higher lesions e.g. shaft of humerus fracture result in
paralysis of the wrist extensors (ECRL, ECRB, ECU) and
wrist-drop results i.e. low lesions of radial nerve do not
result in wrist-drop, so be careful.
o Elbow extension. Triceps function is usually preserved
unless lesion is very high up; shaft of humerus # usually
does not result in triceps paralysis.
• Very high
o Common sites affected:
! Axilla: Saturday night palsy (back of a chair), crutch palsy
! Mid-humeral lvl (spiral groove during humerus shaft fracture, tourniquet palsy)
! At or below elbow (elbow dislocations, monteggia fractures, ganglions, surgical trauma)
o Motor: inability to extend 1)fingers, 2)thumb, 3)wrist (test with cogged wrist)
o Muscle wasting: forearm extensor compartment, triceps (only for very high injuries)
o Sensory loss: over anatomical snuffbox, base of thumb extending to first webspace, dorsum of lateral 3.5 fingers short of nail beds
o Deformity/sign: wrist drop + finger drop
• Radial tunnel syndrome (at level of epicondyles)
• Low lesion (fracture/dislocation at elbow injuring posterior interosseous nerve – around level of elbow; given out btwn 2 heads of
supinator)
o Motor: inability to extend MCP joints (NOT IPJ – Intrinsics) and extend thumb
o Deformity: Radial deviation (extensor carpi ulnaris knocked out), Finger drop
o Sensory loss: none (except for articular proprioception)
• Muscles
o Direct branches from radial n: triceps, anconeus, brachioradialis, extensor carpi radialis longus
o Deep branch of radial n: extensor carpi radialis brevis, supinator
o Posterior interosseous nerve: extensor digitorum, digiti minimi, carpi ulnaris, pollicis brevis, pollicis longus, indicis, abductor pollicis
longus

Patient is a (age) (gentleman / lady) .
On inspection, both hands are in the normal resting position with the
forearm supinated and the wrist extended.
The MCP and IP joints are flexed, more pronounced in the little finger
and less in the index finger.
I do not note any wasting of the thenar or hypothenar eminences or
intrinsic muscles of the hands.
There are no scars noted on the hands. Wrist drop and finger drop of
the left hand was noted.
On examination, power of left wrist extension was ___ and extension of
the left MCP joints was ___.
Power was full on extension of the left PIP joints. Power of elbow
extension is ___.
Sensation was decreased over the 1st dorsal web space of the hand
and the dorsum of the forearm.
Further examination of the upper limb revealed a ___ cm scar over the
arm.
My diagnosis will be a left radial nerve palsy at the level of the arm
possibly secondary to a previous # of mid shaft of humerus.

! 65!
OTHERS
• Complete claw / Simian hand (with thumb involvement – unable to oppose)
o T1 root, combined median and ulnar palsy
• Axillary nerve
o Motor: Deltoid
o Sensory: Lateral cutaneous nerve of arm
• Musculocutaneous nerve
o Motor: Flexors of arm
o Sensory: Lateral cutaneous nerve of forearm
• Spinal accessory nerve
o Motor: Trapezius
o Injury due to: Lymph node biopsy, stab injury
• Long thoracic nerve
o Motor: Serratus anterior (winging of scapula)
o Roots: C5-7

On inspection, I note there is asymmetry of the shoulder joints.

(ask pt to push against the wall) There is winging of the scapula.
(ask pt to abduct shoulder) I note there is difficulty in abducting the shoulder.
I would like to perform a neurological examination of the UL to determine the cause and exclude possible muscular dystrophy, and take a
history to find out if there was any trauma to the axilla or shoulder.
Determine level of lesion:
• Axilla (scars) " damage to long thoracic nerve (UL power preserved)
• Brachial plexus (look for Horner’s syndrome)
• Injury to C5, C6, C7 nerve roots " arm held to side + internally rotated & pronated ($ biceps reflex)
• Muscular dystrophy " fascioscapulohumeral dystrophy (sensation preserved)
• Trapezius palsy 2° injury to the spinal accessory nerve
• Post-glenohumeral fusion
• Abduction contracture of deltoid
Mx: disability usually slight and accepted, if function impaired " tendon transfer to stabilise scapula

• Brachial Plexus Lesions:

o Types
! Lesions in continuity – more than half of plexus injuries. Traction commonest
cause. Nerve roots affected postganglionic. Treatment is expectant.
! Lesions with ruptured nerve roots – only surgical intervention can offer any hope
of recovery
! Complete avulsion lesions – nerve avulsed from cord (both dorsal n ventral roots
ruptured) as opposed to brachial plexus injuries where dorsal roots are spared.
! Partial avulsion – dorsal roots spared thus muscle paralysis with preservation of
sensation
o Long standing plexus lesions
! Obstetric brachial plexus palsy
• Background
o Mostly neuropraxia; v few avulsions
o 80-90% of children w OBPP will attain normal/near normal function
! Preganglionic: worse prognosis (avulsion) + Horner’s syndrome
! Postganglionic: better prognosis (rupture in continuity)
o If by 3 months, elbow flexion and shoulder abduction okay = functional recovery
• Erbs’s palsy (C5, 6, sometimes C7) – overweight babies w shoulder dystocia at delivery (upper obstetrical palsy)
o Asymmetric Moro’s reflex, waiter’s tip deformity (shoulder internally rotated, elbow extended, wrist flexed n
pronated); N to rhomboids and long thoracic N spared.
• Klumpke’s palsy (C8, T1) – lower obstetrical palsy. intrinsic muscles wasted, clawhand, sensory loss on medial side of
forearm n wrist, commonly a/w horner’s syndrome bc T1 affected.
! T1 root only – wasted intrinsic muscles, sensory loss on medial side of hand, (incomplete lower obstretical palsy, cervical
spondylosis, neurofibromatosis, CA)
! Acute traumatic lesions – commonest mechanisms - depression of shoulder with lat flexion of the neck to opp side or traction
of arm" will find bruise on lateral jaw, inferior jaw and on shoulder.
• Might have subclavian artery trauma

! 66!
2. Lumps and Bumps
GENERAL INFORMATION
• 6 S: Site, Shape, Size, Surface, Skin, Slip sign
• 3 C: Consistency, Color, Compressibility
• 2 F: Fluctuance, Fixity (mobility)
• 3 T: Tenderness, Transillumination, Tinel’s
Based on consistency
• Cystic and soft: Ganglions, lipoma, vascular malformation
• Firm: PVNS< neuroma, fibroma
• Hard: Osteochondroma, bone tumours
Characteristics of a lump There is a ___ x ___ cm, (shape: hemispherical / elliptical / fusiform) swelling over the
(site: dorsum / volar / plantar aspect of the forefoot / midfoot / hindfoot / finger / palm /
S4 Size, shape, site, surface wrist) , with a ___________ surface, well-defined edge and is soft to firm in consistency.
E Edge It is non-tender and not warm to touch.

C2 Consistency, colour (& skin) The overlying skin is (normal / has a punctum / coloured) and the lump (is / is not)
T3 Tenderness, temperature, mobile from side to side, and (is / is not) attached to the skin or underlying structures
transilluminable such as (muscle / tendon / bone) . The lump moves upon flexion of the fingers
suggestive of tendon attachment / the lump deceases in size with elevation of the lump.
O Others:
Mobility, fluctuance, pulsatile The lump (is / is not) (fluctuant / compressible/ pulsatile / transilluminable) .
Slip sign is/ is not positive. Tinel’s (is / is not) positive.
R Relations / related signs

GANGLION***
• Definition: Mucinous cyst of unknown cause (possibly due to cystic degeneration in joint capsule or tendon sheath)
• Theories for pathogenesis
o Myxomatous cycstic degeneration
o One way check valve communication with synovial body (eg.
tendon sheath, synovial joint)
• Features
o Shape: Spherical; may be multi locular
o Sites (IMPORTANT DETERMINANT): fr most to least common
! Dorsal wrist (scapholunate junction)
! Volar wrist (radial aspect – scapholunate, scapho-trapezio-
trapezoid)
! Volar MCP joint
! Dorsum of DIPJ (digital mucus cyst) – OA due to
osteophyte
! Proximal digital crease (flexor sheath ganglion)
! NOTE: Big ganglion cyst in GH joint almost always a/w rotator cuff tear
o Well-defined, cystic, smooth, firm
o Tenderness: usually non-tender; may be so for flexor sheath ganglia
o Attachments:
! Attached to underlying fibrous tissue
! Usually not attached to skin
! If attached to joint capsule, tendon sheath, or IM spetum, ganglion becomes less mobiles when structures made tense
o Transilluminable – unless bleeding or infection (pus)
o Flunctuance: Positive
o Content: Glairy fluid (uncooked egg white colour and consistency)
• Types:
o Simple
o Compound: chronic inflammation distends tendon sheath above and below the flexor retinaculum (a/w TB, RA)
o Occult
o Interosseous
• Treatment
o Unnecessary –usually resolves spontaneously after some months
o Surgery (if compressing nerve etc)
! Aspiration: high recurrence in 6-12 months (10-15%)
! Excision if recurrence: cosmesis or if ganglion is causing pain (recurs in 20-30%)

PIGMENTED VILO NODULAR SYNOVITIS (AKA GIANT CELL TUMOUR OF TENDON SHEATH)***
• COMMONEST hand lump disorder esp in patients 20-50yo
• Definition: benign proliferative disorder of synovial lining of joint, bursa and tendon sheaths, producing localized/ diffuse inflammation and
nodular thickening of the synovial membrane
o PVNS is a histological diagnosis: Pigmented (haemosiderin) vilonodular (multilobulated) synovitis (affecting joints and tendon
sheath); multinucleate giant cells present
o 2 types (+ sites)
! Diffuse form – affects entire synovial lining of a joint, bursa or tendon sheath
• Affects large joints (knee > hip > ankle, shoulder)

! 67!
 ! Localized/nodular form – affects tendon sheaths around small jts of hands & feet (termed nodular tenosynovitis)
• Appears in the form of a localised nodule or mass in a synovium, and the surrounding synovium is generally normal
• Features:
o Insidious onset of a solitary, well circumscribed, multilobulated, tan coloured (sometimes has pale yellow regions of lipid
deposition) nodular/ diffuse joint swelling that is accompanied by a dull aching joint pain.
o Site: Most commonly on volar aspect near DIPJ (often index and middle digit)
o Consistency: Firm to soft rubbery
o Fixity: Attached to tendon sheath or IPJ
o Does not transilluminate
o Tenderness: Absent
o May have decreased ROM and locking of joint
• XR: joint swelling, periarticular erosions (saucerisations), joint space narrowing, sub chondral cyst, osteophytes formation (secondary OA
changes)
• Treatment: Synovectomy
o However, diffuse lesions have a high rate of recurrence (>50%) unless synovectomy complete
o If refractory to repeated Sx, may be managed with low-dose radiotherapy

LIPOMA
• Definition: Cluster of fat cells that have become over-active and distended with fat that they have become palpable lumps
• Features
o Surface: Lobulated (more prominent with firm pressure)
o Edges: Well circumscribed
o Consistency: soft
o Attachment to neighbouring structures: possible
o Slip sign: Not very useful diagnostic feature
o Fluctuance: Yield to pressure but do not fluctuate
o Non-tender
o Transillumination: Negative
• Treatment -- Surgical: marginal excision (pre-op staging and biopsy for liposarcoma if atypical)

IMPLANTATION DERMOID
• Definition: Cyst that develops as a result of implantation of epidermal fragment into dermis by a penetrating injury; epidermis continues to
grow and forms a cyst lined by stratified squamous epithelium and filled with keratin
• Features
o Site: Sites commonly subjected to injury (eg. volar surfaces of fingers and palms)
o Consistency: Hard and tense
o a/w trama to overlying skin: May have scar
• Most diagnostic feature is previous injury at site and presence of scar

NERVE SWELLINGS
• Neuroma: general term for tumor of any component of a nerve bundle
o Type: Usually neurilemmoma/schwanomma
! Benign nerve sheath tumour composed of Schwann cells
o Features:
! Along nerve route
! Positive Tinel’s sign
! Homogeneous texture
• Neurofibroma (benign neoplasms derived from the myelin sheath of peripheral nerves; schwannoma has mostly just schwann cells in it,
whereas a neurofibroma has a bunch of other cell types, like fibroblasts, endothelial cells, and mast cells)
o Localized to digit and part of hand
o 4-5cm, irregular and wrinkled skin, soft, mobile w skin, a/w café au lait spots

VASCULAR MALFORMATIONS
• Types: Usually venous, or AV malformations
• Features: Compressible, Posture dependent, Discoloration, may have thrills and bruits

OTHERS
• Gouty Tophi
o Relatively immobile, stuck to tendon/ joint, firm (can be soft), whitish, not transilluminant, tender in acute cases
o Site: ear, ankle, elbow, finger
o Cx: skin ulcerations
o DDx: PVNS
• Squamous cell CA
o Due to burns, sunburn, Arsenic
o Spread by lymphatics
• Glomus tumours (AKA glomangioma, or nonchromaffin paraganglioma)
o Rare benign neoplasm that is a specialized arteriovenous anastamosis and is usually found in the skin of the extremities
o It arises from the glomus body (Component of the dermis layer of skin, involved in body temperature regulation), which consists of an
AV shunt surrounded by a capsule of connective tissue
! Glomus bodies are most numerous in the fingers and toes

! 68!
 ! The role of the glomus body is to shunt blood away from the skin surface when exposed to cold temperature, thus preventing
heat loss, and allowing maximum heat flow to the skin in warm weather to allow heat to dissipate.
o Small, vascular & tender swelling, usually occurs at the region of the nail beds.
o Treatment: Radiotherapy and Surgery
• Pyogenic Granuloma
o Relatively common benign vascular lesion of skin and mucosa. Exact cause unknown
o Usually occurs in children and young adults as a solitary, glistening, friable, polypoid bright red papule or nodule. Prone to bleeding
and ulceration.
o Ranges from few mm to several cm in size.
o Regressing lesions: Appear as soft fibroma. Normally occurs at Head and Neck and distal extremities.
o Typically evolves rapidly over a period of a few weeks.
o Usually Hx of trauma preceding the onset of lesion may be elicited
o Untreated lesions eventually atrophy, fibrose and slowly regress.
• Enchondroma
o Commonest primary bone tumour of hand
o Hard, irregular, fixed swelling
• Malignant melanoma
• Giant cell tumour
• Osteochondroma

3. Deformities
DUPUTREN’S CONTRACTURE
• Epidemiology: Often in middle-aged, Caucasian male
• Definition: Nodular hypertrophy & contracture of palmar aponeurosis, resulting in tendons attached to finger not being able to move
properly
• Pathogenesis: Local microvessel ischemia " Increase xanthine oxidase activity " Superoxide free radical production " Stimulate
myofibroblast proliferation and type III collagen formation (specific platelet-derived and fibroblast GF also play a role in etiology)
o Allopurinol may help to reduce symptoms (XO inhibitor)
o The process of chronic inflammation is thought to be essential to the subsequent fibrosis
• Examination
o Look (usually ring and little finger affected) @ BOTH HANDS
! Scar from previous Sx
! Visible cords
! Pitting/tethering of skin on palmar aspect of hands
! Flexion deformities – MCPJ and PIPJ
! Garrod’s pads at dorsum of PiPJ (thickening of s/c tissue)
! Involvement of thumb and 1st web space is a sign of more aggressive disease
o Feel: swellings are fixated to skin
o Move
! Assess ROM (active and passive)
! Table top test
o Offer:
! Enquire abt causes and associations
! Assess function – writing, dressing, fine movement etc
! Look for other features of diffuse fibromatosis
• Differentials: Skin contracture (look for scar from previous wound), tendon contracture (thickened area or cord moves on passive flexion of
involved finger), congenital contracture of little finger (affects PIPJ), ulnar claw
• Associated Conditions (DEAFEST PAIL): DM, Epilepsy, Age, Family history (AD)/ fibromatoses, Epileptic medication (eg. phenobarbitone),
Smoking, Trauma & heavy manual labour, Peyronie’s disease (fibrosis of corpus cavernosum; seen in 3% of patients w Dupuytrens
contracture), AIDS, Idiopathic, Liver disease (secondary to alcohol)
• Sx Rx: indicated when deformity interferes with function or is rapidly progressive (ie. When MCPJ or PIPJ contracture >30deg)
o Fasciotomy: for prominent bands
o Partial fasciectomy (w Z-plasty) to length wound: in conjuction w post-op physioRx (early active flexion ROM exercses for grip strength)
and night-time splintage in extension
o Dermofasciectomy (w full-thickness skin grafting): a/w lowest risk of recurrence
o Arthrodesis/ amputation: for late presentations and repeated recurrences

SKIN CONTRACTURES
- Cuts and burns are liable to heal with contractures, causing puckering of the palm or fixed flexion deformities. Surgery incisions should never
cross flexor creases.
- Rx: Established contractures may require excision of the scar and Z–plasty of the overlying skin.

OTHERS
Ruptured extensor pollicis longus
• Injury to long thumb extensor after fraying
• Secondary to colle’s fracture, rheumatoid arthritis
• Treatment: Tendon transfer usually required
Dropped finger
• Rupture of extensor tendon
• Patient unable to hold finger at extension at MCP joint
• Treatment: (1) direct repair (2) distal portion of the tendon attached to adjacent finger extensor
! 69!
Boutonneire
• Flexion deformity of PIP joint due to interruption of central slip of extensor tendon
• Lateral slips separate and head of proximal phalanx pops up in between the lateral slips
• Treatment: post traumatic usually repairable. Chronic deformity (in RA) usually cannot be repaired
Swan neck deformity
• Reverse of Boutonniere – PIP hyperextended, DIP flexed
• Due to imbalance of extensor vs flexor action in finger (commonly in rheumatoid arthritis)
• Treatment: tendon rebalancing and joint stabilisation
Polydactyly: Post-Axial associated w renal failure

MUSCLE CONTRACTURE
Forearm ! Ischaemic contracture of forearm muscles, commonly caused by:
o Volkmann’s ischaemic contracture: # causing compartment syndrome resulting in muscle ischaemia & necrosis. Infracted
muscles replaced by fibrous tissues. Usually follows circulatory insufficiency due to injuries at or below the elbow.
o Tight plaster cast & limb swelling
! Shortening of long flexors causing flexion deformity of fingers which is only correctable on wrist flexion (tendodesis effect)
! May be a/w ulnar and/or median nerve palsies
! Treatment: If marked disability: muscle release, Excise dead muscle or tendon transfer
Intrinsic ! MCPJ flexion, IPJ extension & thumb adduction
muscles ! Causes: spasticity (eg CP), scarring (trauma and infection)
! Treatment: muscle release
! Aka intrinsic plus. Intinsic minus is used to describe Ulnar claw due to paralysis of the intrinsic muscles.

4. Tendon Sheath Inflammation

TENOSYNOVITIS/ TENOVAGINITIS
• Definition: Inflammation of tendon sheath surrounding tendon
• Pathology: synovial inflammation " secondary thickening of sheath and stenosis of compartment " further compresses the tendon " Rub
against restricted space " Worsen inflammation
• Etiology
o Unaccustomed movement
o Overuse
o Repetitive minor trauma
o May be spontaneous
• Common conditions
o Extensor Compartment: extensor retinaculum contains 6 cmpts which transmit tendons lined w synovium
Dorsal Tendons Tenderness
compartment
1st (common) Abductor pollicis longus, extensor pollicis brevis Tip of radial styloid
2nd (common) Extensor carpi radialis longus + brevis Just medial to anatomical snuffbox
3rd Extensor pollicis longus
4th Extensor digitorum comunis (4 tendons)+ extensor indicis
5th Extensor digiti minimi
6th Extensor carpi ulnaris Just distal to head of ulnar
o Flexor compartment: Trigger finger/thumb

DE QUERVAIN’S DISEASE/ STENOSING TENOSYNOVITIS ***

• Definition: entrapment tenovaginitis of first dorsal compartment affecting EPB and AbPL, causing pain w tendon movement
o Inflammation causes thickening and stenosis of synovial sheath
• Epidemiology
o Women aged 30-50yrs
o A/w clothes wringing, pruning roses, cutting with scissors
• Symptoms: Radial sided pain (tip of radial styloid most severe)
• Sign
o Swelling and palpable thickening of sheath over course of tendons
o Pain on extension of thumb
o Finkelstein’s test (pathognomonic; also +ve in CMC OA) – ulnar deviation of wrist
with thumb tucked in closed first causes pain over radial styloid; repeating with
thumb free relatively painless
• Ix: if diagnosis is still in doubt, obtain Robert’s view in order to profile CMC joint
• Management
o Conservative
! Lifestyle modification – rest, reduce painful movements
! Occupational therapy - thumb spica for 1mth (thumb in extension and wrist in neutral)
! Physiotherapy – ultrasound therapy
! Pharmacological – NSAIDs
o H&L injection in sheath
o Surgical
! Decompression of 1st compartment sheath (tendon sheath release)
• Determine if there is any instability of wrist joint and correct it if present

! 70!
 ! Complications
• Infection
• Radial nerve palsy – Superficial radial nerve
• Snapping of extensor tendon (due to extreme radial release of extensor retinaculum)
• APL and EPB adherence (will limit thumb movements)
• Differentials for radial sided wrist pain (proximal to distal)
o Intersection syndrome: Inflammation at intersection where 1st dorsal compartment (APL, EPB) muscle bellies cross over 2nd
compartment (ECRL, ECRB) muscle bellies
o De Quervain’s disease
o Wartenberg’s syndrome: Irritation/compression of superficial branch of radial nerve
o Scaphoid fracture: Pain over anatomical snuffbox
o Scapholunate instability
o 1st CMC joint OA
• Other sites of extensor tenosynovitis
o ECRB (most powerful extensor of the wrist; 2nd Compartment): Pain and point of tenderness just medial to anatomical snuff box
o Extensor Carpi Ulnaris (6th compartment): Pain and point of tenderness immediately distal to head of ulnar
o Treatment: Splintage and H&L injections usually effective.!

On inspection, both hands are in the normal resting position with the forearm supinated and the wrist extended. The MCP and IP joints are flexed,
more pronounced in the little finger and less in the index finger.

I do not note any obvious deformities. However, I note slight swelling over the radial side of the wrist.
The overlying skin is not erythematous. I do not note any scars in the surrounding skin.

I would like to proceed to palpate the patient’s wrist. (ask pt for any pain first)

The overlying skin of the wrist joint does not feel warm. I note tenderness at the tip of the radial styloid.
ROM of flexion and extension of bilateral wrist is full at 80 degrees.
Ulnar deviation of both wrist is 40 degrees. Radial deviation of both wrists is 15 degrees.
Supination and pronation of both wrists is full at 90 degrees.

Finkelstein’s test is positive.

My diagnosis is (left / right) De Quervain’s disease.

TRIGGER FINGER (STENOSING TENOVAGINITIS) ***

• Pathology: Disorder characterized by catching, snapping or locking of involved flexor tendon, due to a disparity in size between the flexor
tendon and surrounding retinacular pulley system (tendon normally glides under the A1 pulley in the region of the metacarpal head)
o Usually due to thickening of fibrous tendon sheath (or pulley ligament) and formation of nodule in FDS tendon, causing flexor
tendon to become temporarily trapped at entrance of tendon sheath, and on forced extension, pass the constriction with a snap
• Epidemiology
o 55-60 years old
o Women > Men
o Common in ring finger, middle finger and thumb of dominant hand
o Risk factors: overuse or local trauma, DM, RA, gout
• Classification (Green’s Classification)
Stage Features
I: Pre-triggering Tenderness of A1 pulley region; triggering not demonstrable on PE
II: Triggering Demonstrable catching but patient can actively extend digit
III: Triggering and Locking Demonstrable locking:
IIIA: Require passive extension
IIIB: Inability to actively flex (Require passive flexion)
IV: Contracture Fixed flexion contracture of PIP joint
• DDx: RA, septic arthritis, suppurative tenosynovitis, tumour of tendon sheath, dislocation, dupuytrens contracture
• Examination
o Look
! Visible nodules over A1 pulley region (distal transverse palmar crease)
! Fixed flexion deformity of affected fingers possible
o Feel
! Palpable (tender) nodule over A1 pulley region (usually approx. at lvl of proximal transverse palmar crease/ MCPJ)
! Tenderness at A1 pulley region
! (May have associated ganglion)
o Move
! Determine triggering (if pain present) on extension (snapping sensation)
! Check range of movement
• Management
o Conservative
! Lifestyle modification: Reduce trauma
! Occupational therapy: Splint PIPJ at 15 degrees " not very efficacious

! 71!
 o Injection
! H&L into tendon sheath – Triamcinolone and lignocaine: approx 70% success rate but not administered more than twice due to
lowered efficacy and risk of tendon rupture (other side effects: infection, hypopigmentation over area of injection, steroid flare, fat
necrosis, periarticular osteoporosis)
• Higher rate of success in female patients, with short duration of symptoms (<4months), for discrete palpale nodule, single
digit involvement, no associated conditions (eg. DM, RA)
o Surgery
! Procedure: Division of A1 pulley in the midline (tendon sheath), then ask patient to actively move digit to confirm full release
(motion encouraged immediately following the procedure)
! Indications: Stage 4 or failed injection therapy
! Complications: May cut on A2 pulley causing bowstringing

On inspection, I note an abnormal resting position of the (L / R) hand.
The (index / middle / ring / little) finger is flexed at the PIP joint.
Resting position of the (left / right) hand is normal.
I do not note any skin changes or scars on the hands. I also do not
note any wasting of the intrinsic muscles.
I would like to move on to palpate the hand. (ask pt for any pain first)
I feel a nodule in the palm just proximal to the (index / middle / ring /
little) finger at the level of the distal transverse palmar crease. The
surface is smooth, edges distinct and it feels firm. It is tender and not
warm to touch. The overlying skin is mobile.
He / she is able to actively extend his / her finger.
My diagnosis is grade (1 / 2 / 3 / 4) trigger finger of the (left / right)
(index / middle / ring / little) finger.

INFECTIOUS TENOSYNOVITIS OF FLEXOR TENDON SHEATH IN HAND

• Kanavel’s sign
o Slight flexed position of affected finger
o Fusiform swelling over affected tendon
o Tenderness on percussion along tendon sheath
o Tenderness on extension of affected finger
• Zones of Hand
o Zone 1: FDP
o Zone 2: FDP and FDS (‘No man’s land as healing is poor)
o Zone 3: Palm
o Zone 4: Carpal tunnel
o Zone 5: Forearm

5. Infections
BACKGROUND
• Most commonly due to implanted staph aureus
• Pathology: inflammation and suppuration in small closed compartments" increased pressures may
reach levels that threaten local blood supply" MAY LEAD TO tissue necrosis or a stiff and uselss
hand
• Clinical features:
o Usually a hx of trauma, may be unnoticed
o Local: pain (may become throbbing pain), swelling, tenderness, red and tense tissues with decreased ROM
o Systemic: fever
• Principles of treatment
o Antibiotics:
! Prophylactic: usually flucloxacillin; (in severe cases) fusidic acid or cephalosporin
! Altered when bacterial sensitivity known
o Rest and elevation: sling; roller towel
o Analgesics
o Drainage: drain pus when there’s signs of abscess (throbbing pain, marked tenderness, toxaemia)
! Tourniquet + GA/LA
! Incision never across a skin crease/ interdigital web as healing will result in soft-tissue contracture across crease
! Excise necrotic tissue + thoroughly cleanse area
! Either leave wound open/ suture" cover with non-stick dressings
! Send pus for microbiological investigation
o Splintage: In position of safe immobilization (wrist slightly extended, MCPJ flexed, IPJ extended, thumb abducted) as ligaments are at
greatest length" reduce likelihood of stiffness
o Physiotherapy
• Possible compartments:
o 1) nailfold (paronychia)
o 2) pulp space (whitlow, felon): usually prick or splinter of finger tip
o 3) subcutaneous tissues
o 4) tendon sheath (suppurative tenosynovitis)
! Uncommon but dangerous- risk of tendon necrosis and patient may end up
w useless hand
! Clinical features: Affected digit swollen, painful, held bent, tender, no active
/passive movement
! Treatment:
• IV antibiotics
• Surgical drainage if no improvement after 24hrs

! 72!
 o 2 incisions (proximal end + distal end of sheath)" irrigate sheath with saline or Ringer’s lactate solution using a
fine catheter" leave for postoperative irrigation for 2 days" dressing and splinting
o Tendon-sheath infection in thumb/ little finger may spread prox to synovial bursa" drain via incision above wrist
o 5) deep fascial spaces: Spread from infection of web space/ tendon sheath" palm is ballooned and normal concavity lost, w whole
hand held still" Rx is I&D
o 6) joint infx
! Clinically hard to distinguish from Acute Gout. So Aspirate joint
! Can be infected directly or indirectly.
! Rx: IV antibiotics and splint. If no improvement in 24 hrs " open drainage
o Others:
! Bites
• Animal bites pathogens: Staph and strep, (consider rabies)
• Human bites pathogens: Staph aureus, Strep A, Eikenlla corrodens, anaerobes
• XR done to exclude fracture or foreign body
• Mx:
o Fresh wound: Examined in OT. Swab for c/s. Explore for foreign bodies such as tooth. Splint elevate and start
prophylactic antibiotics
o Infected Bites: debridement and washout. Start IV antibiotics—Broad sprectrum penicillin and cephalosporin.
o Post op: Physiotherapy. Deal with tendon lacerations when tissues are completely healed

! Chronic
• TB: May present with compound palmar ganglion (above and below the carpal tunnel)
• Leprosy (Hansen’s Disease): Cause auto-resorption

TRAUMATIC HAND INJURIES

• Must consider 5 tissue components of hands (not just X-ray) " Mx is Total reconstruction (transplant, flap etc)
• Consider functional deficit: Tendon, nerve especially

6. Fractures
• NOTE 1: commonest Cx of hand # is tendon adhesion
• NOTE 2: Complications of wrist #
O Most common complications are poor grip strength, stiffness and radial shortening
O 80% have normal function in 6-12 months
O Early Cx:
! Difficult reduction +/- Loss of reduction
! Compartment syndrome
! EPL tendon rupture
! Acute carpal tunnel syndrome
! Finger swelling with venous or lymphatic block
O Late:
! Malunion, radial shortening
! Painful wrist sec to ulnar prominence
! Frozen shoulder (shoulder-hand syndrome; aetiology unknown)
! Post-traumatic arthritis
! Carpal Tunnel Syndrome
! Reflex sympathetic dystrophy
• NOTE 3: deformity in hand # is due to MALunion

SCAPHOID FRACTURE *** (most commonly fractured carpal bone – 75% of wrist #s)
• Mechanism of Injury: ALWAYS INTRA-ARTICULAR
o FOOSH with wrist extended
o Combination of dorsiflexion and radial deviation results in force passing between 2 rows of carpal bones, resulting in scaphoid
fracturing transversely across its waist (as it lies btwn both rows)
o May have accompanied disruption of scapholunate ligaments
• Risk Factors: Rare in children and elderly
• Symptoms
o Pain (over anatomical snuffbox)*** & over scaphoid tubercle (following course of FCR)
o Swelling (over anatomical snuffbox)
o Restriction of thumb movement (not so much of wrist movement)
• Signs: painful motion of wrist joint; distraction & axial loading of e 1st MC can increase the pain
• Classification
o # of scaphoid tubercle
o Undisplaced # of waist
o Displaced # of waist
• Investigations
o X-ray: often hard to see
! 5 Views: AP, lateral, SCAPHOID VIEW, 2 oblique (semi-pronated and semi-supinated)
! X-ray again in 2 weeks later if unsure as fracture may not be seen in first few days
! Usually # is thru narrowest part of the bone (waist); other potential # sites include tubercle and proximal pole
o MRI: useful in diagnosing occult scaphoid # and showing AVN of bone
o Not CT (for articular #s)
! 73!
• Management
o Initial (in the event that fracture not seen on x-ray):
! Scaphoid plaster & sling: hand pronated, wrist dorsiflexed & radial deviated & thumb forwards in ‘glass holding’ position
! Plaster to extend from below elbow to just below MCP and IPJ of thumb; incorporate proximal phalanx of thumb
o # of scaphoid tubercle: don’t need splintage; crepe bandage and movement encouraged (treated as sprain)
o Undisplaced # of waist
! No need reduction
! Scaphoid plaster for 6-12 weeks (union is slow): 90% should heal
! Internal fixation and bone graft if delayed/non-union signs at 12 weeks
o Displaced or unstable #, or delayed/non-union:
! ORIF with scaphoid compression screw
! Acute #: favours percutaneous fixation and arthroscopy assisted
! Non-union: favours open fixation w bone grafting
• Vascularized bone grafting when there is AVN
• Complications
o Avascular necrosis of proximal pole (blood supply diminishes proximally – supplied by dorsal and volar branches of radial artery)
! Can cause secondary radiocarpal OA (excise scaphoid and consider arthrodesis of proximal to distal row of carpal bones)
! Diagnosed by increased density of prox fragment on X-ray after 2-3 months
! Occurrence
• 1% of distal third fractures
• 20% of middle third
• 40% of proximal third
! Management
• Remove entire proximal row of carpal bones (carpectomy)
• Remove scaphoid and fuse the proximal to distal row (4 corner fusion: capitate-hamate-triquetrum-lunate)
o Non-Union v common (union may be slow <months> due to poor BS at prox part of scaphoid) " chronic pain on motion and loading
! Management: plaster fixation, internal fixation and Bone graft (or same as for AVN)
o Osteoarthritis
! Excision of radial styloid if arthritis confined to distal pole
! Salvage procedures: intercarpal and radiocarpal fusion

BOXER’S FRACTURE
• Transverse # of 5th metacarpal neck
• Dropped knuckle deformity permanent
• Indications for surgery: Usually severe angulation (>30degrees)

BENNETT’S FRACTURE-SUBLUXATION
• Fracture of 1st metacarpal base extending to CMCJ
• XR: small medial fragment of bone seen. Proximal and lateral subluxation of 1st MC present
• Management: M&R + 4 weeks in plaster cast

ROLANDO’S FRACTURE
• Comminuted fracture of 1st metacarpal base extending to CMCJ
• Management: Fixation (K-wires)

GAMEKEEPER’S THUMB/ SKIIER’S THUMB

• Torn ulnar collateral ligament of 1st MCPJ from hyperabduction of thumb (FOOSH)
• s/s: progressive MCPJ subluxation and impaired grasp results, w tenderness over medial side of MCPJ; may be a/w avulsion #
• Management
o Partial tears/ minimally displaced: scaphoid cast 6wks or splint 2-3weeks
o Complete tears: internal fixation & operative repair + thumb spica +/- MCPJ fusion depending on severity of displacement/tear

MALLET FINGER
• Rupture of extensor tendon of terminal phalanx as fingertip forcibly bent during active extension
• Loss of active extension of DIPJ, normal passive extension of DIPJ
• Rx:
o If soft tissue injury (muscle imbalance): treat conservatively w mallet splint for 8weeks if pure soft-tissue injury
! For cases with hyperextensible PIP, splint with DIPJ extension & PIPJ flexion, using a skintight cast.
o If avulsion #
! Extra-articular or involving <2/3 of joint: conservative Rx (splint for 6weeks if large flake of bone avulsed)
! Intra-articular or involving >/= 2/3 of joint: surgical reduction
RUGGER-JERSEY FINGER
• Opposite MOI from mallet finger: rupture of FDP as fingertip forcibly extended during active flexion (eg. player grasping jersey of
opponent during tackling)
o Tendon may rupture directly fr its insertion into the bone or it may avulse bone fragment from base of distal phalanx
o Commonly affects 4th finger (75%)
• Usually present late (pain, tenderness over volar distal finger, swelling, finger in slight extension relative to other fingers in resting
position, bruising absent, X-rays negative usually)
• Management: Repair" tendon grafting" arthrodesis of DIPJ

! 74!
METACARPAL SHAFT FRACTURE
• Mostly stable and undisplaced.
• If displaced, need ORIF with plates or K-wire. Make sure no rotational deformity. Otherwise will have scissoring of fingers on flexion.

7. Dislocations
LUNATE AND PERILUNATE DISLOCATIONS
• Mechanism of Injury: Fall w hand forced into dorsiflexion may tear ligaments that normally bind carpal
bones
o Types of injury:
! Lesser arc injury: lunate and periluante dx (no fracture)
• Perilunate dislocation (most common): Lunate remains attached to radius while
rest of carpus displaced backwards
• Lunate dislocation: Hand usually immediately snaps forwards again, but in the
process, lunate may be levered out of position to be displaced anteriorly
! Greater arc injury: trans-scapho perilunate # dislocation (w scaphoid #)
• Trans-scaphoid perilunate dislocation: Sometimes scaphoid remains attached to
radius and force of perilunar dislocation causes it to fracture through waist
• Symptoms
o Wrist is painful and swollen
o Wrist held immobile
o May have symptoms of carpal tunnel compression – parasthesia, blunting sensation over median
nerve territory + weakness of palmar abduction of thumb
• Complications
o Delay may result in difficulty in reduction and AVN and secondary OA" Partial arthrodesis Perilunate'Dislocation'
considered if symptomatic (stiff and painful)
o Carpal tunnel compression
o Improper reduction of perilunate dx may result in secondary lunate dx
o Sudeck’s atrophy
• Investigations
o X-ray
! Perilunate dislocation
• PA view: disruption of carpal anatomy (using Gilula lines)
o Carpus diminished in height
o Bone shadows overlap abnormally
o May have accompanying scaphoid fracture
• Lateral view: disruption of carpal anatomy (using multiple stack of C lines)
o Lunate not displaced forward
o Capitate displaced backwards
! Lunate dislocation:
• AP view: Lunate appears triangular instead of quadrilateral (crescent moon shape
of bone becomes obvious)
• Lateral view: Dislocated lunate tilted forwards and displaced in front of radius, while
capitate and metacarpal bones line in line with radius
• Management Lunate'Dislocation'
o Closed reduction
! Reduce: Pull hand with wrist in extension and apply thumb pressure to displaced bones
! Plaster slab applied holding wrist neutral
! Percutaneous K wires may be needed to reduction
o Open reduction
! If closed reduction fails
! Carpus exposed by anterior approach (concomitant decompression of carpal tunnel)
! Hand pulled and lunate levered into place
! Held in place by K wire

SCAPHOLUNATE DISSOCIATION
• Mechanism of Injury: Subluxation of scaphoid and disruption of ligaments between scaphoid and lunate
• X-ray:
o Foreshortening of scaphoid and appearance of large gap between scaphoid and lunate
o Ring sign: rotation of scaphoid cause it to be viewed end on in PA view

SCAPHOID DISLOCATION
• Displacement is usually anterior
• Rx: closed reduction + plaster fixation in stable position. If instability is present, fix with K-wires

! 75!
8. Joint Disorders
CHRONIC CARPAL INSTABILITY
• Causes: Injury, Arthritis, Kienböck’s disease (patchy lunate AVN after trauma)
• Features: Pain, Weakness, Clicking on movement
• Commonest type: Scapholunate dissociation – X-ray shows Terry Thomas sign (abnormal gap between scaphoid & lunate)
• Rx:
o Acute: reduction & fixation with plaster or K-wires
o Chronic: splintage, analgesics, H&L injections, arthrodesis

KIENBOCK’S DISEASE
• Patchy AVN secondary to post-stress/injury of the lunate.
• Predisposing factor: relative shortening of ulna " excessive stress on lunate
• Presentation: ache and stiffness, localised to centre of dorsal wrist. Possible limitation of wrist extension
• Imaging: Earliest signs of osteonecrosis only detected by MRI. XRay – increased density, later irregularity and flattening of bone. Eventually
OA features.
• Treatment:
o Osteotomy of distal end of radius (reduce pressure on lunate)
o Microrevascularisation of bone if expertise available
o Partial arthodesis in late cases.

TRIANGULAR FIBROCARTILAGE COMPLEX (TFCC) TEARS

• Anatomy: ligament fans out from base of ulnar styloid to medial edge of distal radius
• Symptoms
o Chronic pain and clicking esp on supination
o Loss of grip strength
• Signs
o Tenderness around ulnar styloid
o Piano-key sign (instability of DRUJ)
• Management: Arthroscopic (also diagnostic) repair and removal of fragments

! 76!
Pelvis!
Fractures!

General'
Principles'of'
Pelvic'Fractures'

Isolated'
Fractures'

Fractures'of'
Pelvic'Ring'

Fractures'of'
Acetabulum'

Injuries'of'
Sacrum'and'
Coccyx'
!

! 77!
1. General Principles of Pelvic Fractures
• Most common fracture involves pubic rami, followed by ilial, ischial, acetabular, coccygeal and sacral bones
• Tile’s Classification of pelvic fractures

Type!A! Type!B!
Type!C!

o Type A: stable, minimally displaced, includes avulsion fractures and fractures not involving pelvic ring, e.g. rami fracture
o Type B: partially unstable, rotationally unstable, but vertically stable, e.g. “open book” fracture from external rotational force to pelvis
o Type C: unstable, rotationally and vertically unstable, associated with rupture of ipsilateral ligaments, e.g. vertical shear fracture
• Diagnosis
o History of injury, high energy trauma
o Examination reveals local swelling, tenderness; if unstable, may have deformity of the hips and instability of pelvis with palpation
o MCQ " trendelenberg test is a test of stability of pelvis on femur
• General Treatment
o ABCs
o Assess genitourinary injury (rectal exam/vaginal exam mandatory)
o Type A - bedrest and mobilization with walking aids
o Type B/C - external or internal fixation
• General Complications
o Hemorrhage - life threatening
o Fat embolism
o Bladder/bowel injuries
o Neurological damage
o Obstetrical difficulties
o Persistent sacro-iliac (SI) joint pain
o Post-traumatic arthritis of the hip with acetabular fractures

2. Isolated Fractures
Avulsion Fractures
• Mechanism of Injury: Piece of bone pulled off by violent
muscle contraction (sportsmen)
• Examples
o Sartorius pull off ASIS
o Rectus femoris pull off AIIS
o Adductor longus pull off piece of pubis
o Hamstrings pull off part of ischium
• Management: Rest
Direct Fractures
• Mechanism of Injury: Direct blow to pelvis (usually fall from
height) may fracture ischium or iliac blade
Stress Fractures
• Often affects pubic rami in osteoporotic or osteomalacic
patients

3. Fractures of Pelvic Ring

• General Information
o Innominate bone and sacrum form a ring held together by weak symphyseal joint anteriorly and strong sacroiliac and iliolumbar
ligaments posteriorly
o Break at one point accompanied by disruption at second point (except for comminuted fractures due to direct blows or ring fractures
in children whose symphysis and SI joints are springy)
• Mechanism of Injury
o Anteroposterior compression
! Usually caused by frontal collision btwn pedestrian and car
! ‘Open book’ injury: Pubic rami fractured or innominate bones sprung apart and externally rotated w diastasis of symphysis
! May have torn SI ligaments or fracture of posterior part of ilium
! Stability:
• Stable: Separation of < 2cm
• Unstable: Greater separation or when CT scan shows displacement at SI joint
o Lateral compression
! Usually due to side on impact or fall from height
! Side to side compression causes pelvis ring to buckle and break
! Anteriorly: Pubic rami on one or both sides fractures
! Posteriorly: Severe SI strain or fracture of ilium or sacrum
! If SI injury much displaced pelvis is unstable
! 78!
 o Vertical sheer
! Usually when fall from height onto one leg
! Innominate bone on one side is displaced vertically fracturing pubic rami and disrupting SI region on same side
! Usually severe and unstable
! Associated with gross tearing of soft tissue and retroperitoneal hemorrhage
• Signs and Symptoms
o Stable injuries
! Pain on trying to walk
! Localised tenderness
o Unstable injuries
! Severely shocked
! Great pain
! Unable to stand
! Widespread tenderness and attempt to move ilium painful
! Risk of visceral damage
! Other possible signs/symptoms:
• Unable to pass urine
• Blood at external meatus – indicative of urethral damage, hence cannot catheterize via urethra
• Partially anaesthetic leg due to sciatic nerve injury
• Complications
o Urogenital damage (usually due to compression fractures)
o Nerve injury: Sciatic nerve or lumbosacral plexus
o Persistent SI pain: May necessitate arthrodesis of SI joint
o Massive bleeding
• Management
o Early
! Persistent bleeding:
• Pelvic binder, clamps, compression belt or external fixator; can bind feet too
• Investigate source of bleed with peritoneal aspiration / lavage / angiography
! Urological Injury:
• Occurs in 10% of pelvic ring fractures
• If unable to pass urine, cannot be catheterized
• Urethra rupture diagnosed with retrograde urethrography
• If urethra ruptured, urine drained by suprapubic cystotomy
o Treatment of Fracture
! Undisplaced Ring Fracture: 4 weeks rest in bed
! Anterior disruptions without SI displacement:
• Open book injuries with gap <2cm: 6 week bed rest + posterior sling/elastic girdle to ‘close the book’
• More severe: External fixation with pins in both iliac blades connected by anterior bar
• Pubic ramus #s (usually due to lateral compression): Sling inappropriate hence bed rest if displacement not severe
! Displaced fractures with SI disruption:
• Anterior external fixation and posterior stabilization using screws across SI joint OR
• Plating the symphysis anteriorly and screws across the SI joint posteriorly

4. Fractures of Acetabulum
• Mechanism of Injury
o Head of femur driven into pelvis
o Due to:
! Blow on side (fall from height)
! Blow on front of knee (dashboard injury)
o Usually due to severe injury, hence suspect other injuries/fractures
• Patterns of Fracture
o Acetabular wall
! Fractures of acetabular wall affect depth of socket
! May lead to hip instability (unless properly reduced and fixed)
o Anterior column
! # Separates a segment btwn AIIS and obturator foramen
! Uncommon
! Good prognosis (does not involve weight bearing area)
o Posterior column
! # runs upwards from obturator foramen into sciatic notch separating the
posterior ischiopubic column of bone and breaking the weight bearing part of
the acetabulum
! Associated with posterior dislocation of hip
! May injure sciatic nerve
! Usually treated urgently with internal fixation
o Floor of acetabulum (uncomminuted transverse #)
! # separates iliac portion above from pubic and ischial portions below
! Sometimes there is also a vertical split into obturator foramen (T-fracture)
! Easy to reduce and hold

! 79!
 o Complex fractures (combinations of above)
! Damage various portions of acetabulum
! Require ORIF
• Tile’s classification of acetabular fracture
o a,b: Simple fractures involving either anterior or
posterior wall or column
o c: Transverse fractures
o d: T-type fractures involving two columns
• X-rays (i.e. AP, inlet, and outlet views) judet view for
acetabular fractures
o 6 lines to look for in a pelvic X-ray specifically
looking for acetabular fracture
! Iliopectinael line – anterior column of pelvis
! Ilioischial line – posterior column
! Acetabular teardrop – should be in line w ilioischial line
! Dome – superior weight bearing area costing of both ant and post column
! Ant wall of acetabulum
! Post wall of acetabulum
• Complications
o Nerve injury: Sciatic nerve (posterior fractures) – but nerve usually not severed hence
good chance for recovery
o Avascular necrosis of femoral head
o Heterotopic bone formation (prevented with prophylactic indomethacin)
o Osteoarthritis (especially if weight bearing surface involved)
• Management
o Initial
! Manage shock
! Reduce dislocation
! Definitive fracture management delayed until patient fit (not >7 days)
o Conservative: For undisplaced fractures and simple fractures which do not involve
weight bearing portion – (roof)
! Maintain traction for 6-8 weeks
o Operative:
! Indications (in young as likelihood for OA is great hence ORIF is justified)
• Unstable fractures
• Fractures resulting in significant distortion of ball and socket congruence
• Associated fractures of femoral head
• Retained bone fragments in joint
! Aim: Perfect anatomical reduction

5. Injuries of Sacrum and Coccyx

• Mechanism of Injury: Blow from behind or fall onto coccyx may fracture sacrum / coccyx or sprain joint between them
• Management:
o Reduction of markedly displaced fracture: Lower fragment pushed backwards by finger in rectum
o Use of rubber-ring cushion when sitting until recovery
o Excision of coccyx if pain not relieved by cushion or injection of local anaesthetic into tender area

! 80!
Hip!and!femur!
Atraumatic! Traumatic!
Age'0'yrs' Dislocations'
• DDH/CDH' • Hip'dislocation'

Age'0J5yrs' Fractures'(prox'
• Transient' femur)'
synovitis'
• Femoral'neck'fractures'
• Septic'arthritis'
• Intertrochanteric'
fractures'
• Subtrochanteric'
Age'5J10yrs' fractures'
• Perthes''disease'
• Juvenile!chronic!
arthritis! Fractures'(shaft/'
distal'femur)'
• Femoral'shaft'fractures'
Age'10J20yrs' • Supracondylar'fractures'
• Slipped'upper' • Condylar'fractures'
femoral'epiphysis'

Adults' Labral!Tear!
• OA!
• Femoral!acetabular!
impingement!
• RA!
• AVN'

Others'
• Acetabular'dysplasia'and!
subluxation!of!hip!
• Protrusio!Acetabuli!
• Coxa!Vara!
• Femoral!anteversion!

!
!
! !

! 81!
Examination of the Hip
The preliminaries: Introduce yourself to patient, ask for permission to
examine. Ensure adequate exposure til underwear but consider patient
modesty also. Ensure good lighting, good positioning of bed.
With patient standing:
LOOK: front, side, back
1. Posture and Deformities
2. Swelling
3. Scars, Sinuses – in e gluteal folds, make sure to check
4. Discolouration – redness, bruising, etc
5. Muscle wasting – gluteal muscles
GAIT AND RELATED TESTS
1. Get patient to walk a distance – notice if there is any obvious
antalgic or Trendelenburg gait, of if one of e limbs appear shorter
than e other
2. Trendelenburg test: SSS (sound side sags)
- Get patient to stand in front of you and place both hands on top
of your own (palms down on your palms up)
- Then make patient stand on one foot at a time, lifting the other
hip off the floor
- If the side that the patient is supporting his weight on has a
pathology, there will be dipping of the contralateral hemipelvis
and his hand will press harder on that side to lever himself
Causes of positive Trendelenburg test:
- Fulcrum problems e.g. hip OA, AVN
- Lever arm problems e.g. NOF#, coxa vara
- Effort problems e.g. weak abductors
- Nerve problems e.g. Superior Gluteal N or L5
- Others: legg perthes dz, DDH, slipped capital epiphysis
With patient lying supine, knees fully extended: observe attitude of hip,
knee and ankle jt when patient climbs up the bed
LOOK
1. Deformity of the hip – fixed adduction or abduction deformities;
asymmetry in attitude of the limb
2. Obvious swelling(s) -- Hernia can cause hip pain
FEEL
o Feel for temperature – any increased warmth
o Palpate bony landmarks of the hip and note any tenderness:
ASIS " down inguinal ligament " pubic tubercle " hip jt
(2cm below and lateral to midpoint of inguinal ligament) "
gluteus medius " greater trochanter
LIMB LENGTH MEASUREMENT
Relative/Apparent limb length (eg. scoliosis, contractures)
- For measurement of relative limb length just ask patient to adopt the
most comfortable position: “shoulders above hip above feet”; ensure
both limbs are parallel; pelvis needn’t be squared
- Locate xiphisternum and then measure from that point to the medial
malleolus on either side
Contractures and apparent length discrepancy
- Adduction deformity results in shortening of the abnormal side
- Abduction deformity results in lengthening of the abnormal
side
True length:
Square the pelvis for true length measurement; ensure axes of both
lower limbs are at right angles to the line joining the two ASIS (both ASIS
to be made level). If not possible to square pelvis due to contracture on
one side then arrange the other limb in the same position when measuring
true length for that limb.
- Locate ASIS by feeling laterally from the pubic tubercle; the ASIS is
the first bony prominence that the hand feels
- Measure from ASIS to medial malleolus (use the same relative point
on the malleolus on either side e.g. superior border, midpoint, etc)
- If one side has an abduction contracture, then place the other leg in
the same relative position when measuring true length; same for other
deformities
Galeazzi’s test (done when there is a true length discrepancy)
- Place the hips 45deg and knees 90deg and ensure both heels are
tgt with both malleoli touching. Look at knee from side to side. If
knee of affected side is proximal, then there is femoral shorterning
or hip dx. If knee of affected side is distal, then there is tibial
shortening.
- This screening test helps to assess the segment shortening the
affected limb (if the shortening is due to femur or tibia or both)
! 82!
Bryant’s triangle
- This is constructed with the patient supine as a rough means of
detecting disturbance of the normal anatomy of the femoral
head and neck. It is a right-angled triangle, with the following sides
(assuming patient is lying down):
- If shortening is in the femur, it is important to assess if the
shortening is above or below the greater trochanter
- Shortening of the horizontal line on one side as compared to the
other indicates shortening above the greater trochanter
- Bryant’s triangle is formed by a line joining the ASIS and the greater
trochanter, a line dropped vertically from the ASIS, and a line
running horizontally across from the greater trochanter
- The length of C is gauged on each side, and the sides compared.
Pathology of the femoral head or neck which displaces the greater
trochanter will tend to shorten this side of the triangle
MOVE
1. Thomas’ Test for fixed flexion deformity of the hip
- Place patient’s legs at 90 degree knee flexion
- Then place your hand under patient’s lumbar region
- Get patient to flex one leg at the hip until the lumbar lordosis is
obliterated (back pressing your hand to the bed) and then ask
patient to hold on to the flexed leg at the knee
- Ask patient to fully extend the other leg to see if there is any
fixed flexion of the hip " measure w goniometer if there is fixed
flexion
- Repeat with the other side
- Be consistent in performing the test – amount of pressure of
lumbar region on the hand should be equal when testing either
side
NOTE: if patient has a knee contracture, shift him such that
his knee joint lies over the edge of the bed, to accurately
assess for FFD of the hip
2. Range of movements:
- Hip movements are mostly assessed passively
- While during Thomas’ test, also assess degree of full hip flexion
on either side (normal is 140 degrees flexion)
- Abduction and adduction – place hand on the ASIS to assess
movement of the hip joint when the pelvis is not moving;
measure angle when the resting hand on ASIS detects
movement (normal range is 45 degrees abduction and 25-30
degrees adduction)
- External and internal rotation – flex hip and knee to 90 degrees
each, place left hand on knee pressing downwards to fix pelvis
(normal is 45 degrees external rotation, 45 degrees internal
rotation; if hip is extended flat on bed, measure angle by
drawing imaginary axis thru patella and compare it to the 90deg
sagittal plane)
NOTE: If patient cannot flex hip due to pain, internal and
external rotation of the hip can be assess with patient in
prone position and the knee flexed
- Turn patient to the prone position to assess extension of the hip
FINISH with examination of the neurovascular status of the lower limb
(distal pulses, “tip-toe” and “stand on heel”, examination of the spine and
knee joints & SLR.
Approach to Hip Pain
• Causes of painful hip
Referred pain ! Discogenic dz ! True hip pain referred to knee: anterior obturator nerve
Joint disorders ! Infection ! Perthes’ dz ! Slipped capital femoral epiphysis
! OA ! RA ! Osteonecrosis
Periarticular disorders ! Hernia ! Tendinitis ! Bursitis / synovitis
• History and PE
o Site of pathology
! Hip pain (anterior) — usually at groin
! Pain at gluteal region (posterior) — usually lumbar pathology
• Most sensitive hip test which can be used for quick screening of hip: internal rotate (capsule in spiral fashion)
o Impingement test: Flexion, adduction, int rotation
• Caveat: acetabular pathology may present only as gluteal pain
• Other conditions presenting w “hip” pain: trochanteric bursitis, IT pathology (snapping, tendinitis), gluteal muscle strain,
referred pain from spine, SI pathology, non-ortho pathology (hernia, LN, pelvic inflammatory dz)
o Cause of pathology
! Vascular: Perthes’ disease, AVN
! Infection: OM, septic arthritis, TB, Transient synovitis
! Trauma: OA (degenerative), dislocation, fracture
! Autoimmune: RA
! Metabolic
! Iatrogenic
! Neoplastic
! Congenital: SCFE, DDH
o Look for predisposing factors e.g. Osteoporosis and fall risk
o Look for complications of pathology
o Assess premorbid status (goal for mgmt is to regain premorbid status)
o Assess carer support
• Special Ix: MR arthrogram (if other radiological modalities all negative)

Features of AP hip x-ray to note

• General Observations
o Shenton’s line: Inf border of superior pubic ramus and along inferomedial border of NOF
! Hip: DDH, hip dislocation (congenital, posterior, pathological), Tom-smith arthritis (septic arthritis of the hip in infnts which
destroys the whole head of femur), NOF fracture (except impacted ones)
! Pubis: pubic rami fracture
o Neck/shaft angle (normal 120-135deg; <120deg is coxa varus; >135deg is coxa valgum)
o Iliopectineal line
o Ant sacral foramina (at least 2 on each side should be visible)
• OA:
o Acetabular margin
o Joint space
o Femoral head
o Other OA features: LOSS
• Fractures
o Proximal Femur: NOF (subcapital, transcervical, basal), Intertrochanteric, Subtrochanteric
o Pelvic: Pubic symphysis (Open-book injury; anterior-posterior compression), Acetabular, SIJ, Pubis, Ischium
• Quality of bone: Bone texture; density of femoral head
• DDH:
o Perkin’s line (line drawn along lateralmost aspect of acetabular roof) and Hilgrenreihner’s line (line drawn horizontally thru superior
aspect of the triradiate cartilages) – both lines are perpendicular to one another. Femoral head shld be in the innder lower quadrant
of both these lines
o Acetabular index: Should be low (high means shallow acetabulum; acetabulum supposed to hug femoral head)
o Medial gap: Greater the gap, greater possibility of dislocation

Gait analysis
• Normal Gait
o Stance phase—heel strike + mid stance + push off
o Swing phase—Acceleration + initial swing + midswing + deceleration
Type of gait Notes Causes
Antalgic Short stance phase, increased swing phase Pain (infection, inflammation, transient synovitis)
Short limb Ipsilateral hip drops when weight on short leg Previous fracture
Congenital shortening
Hand-to-knee Patient places hand on thigh to keep knee Commonly due to diabetic neuropathy affecting femoral nerve
extended due to weak quadriceps
Trendelenburg Sound side sags" sideways lurch of trunk to Abductor weakness
bring patient’s body weight over affected limb 1) Bone (shortened contraction length causing
Gluteal/abductor Patient tilts toward side of problem to prevent weakness) –hip dislocation/ subluxation, short NOF,
lurch jamming of femur into acetebulum by gluteal coxa vara, flattened femoral head
muscle 2) Muscle –myositis
3) Neuro –poliomyelitis, L5, sup gluteal nerve
! 83!
 Hip pain –OA, AVN, Perthes disease
Adductor lurch Hip dysplasia
Cerebral palsy
Toe to heel Cerebral palsy
Club foot
Idiopathic
High stepping Foot lands flat or on ball Proprioception loss
Circumduction gait Foot drop (L5 injury/ common
Foot slap Due to partial paralysis of peroneal n Commonly due to peroneal nerve or sciatic nerve
(weakness) mononeuritis multiplex palsy)
Hip-hike gait Due to knee stiffness
Ataxic Broad based Cerebellar lesions
Parkinsonian/ Shuffling Parkinson’s disease
festinant
Scissoring (spastic) Jerky, feet in quinus, hips adducted UMN lesion (cord compression, multiple sclerosis, cerebral palsy)

FOOT DROP
1. Expose patient adequately, roll up pants
2. Observe face (eye / facial asymmetry / skin) + ULs
3. Observe LL for wasting / abnormal posture / skin lesions " note unilateral foot drop
4. Walk the patient " high stepping gait
5. Ask pt to stand on heels to confirm

Neurological Examination
6. Test for fasciculations
7. Tone (+ clonus)
8. Reflexes (brisk = cortical foot drop; absent = sciatic nerve lesion)
9. Power
• Hip internal rotation (normal " sciatic nerve lesion; weak " consider L5 root or lumbosacral trunk lesion)
• Knee flexion & extension
Common Peroneal Nerve:
• Ankle dorsiflexion (weak) and plantar flexion (weak if tibial nerve is involved) • Part of sciatic nerve (L4, L5, S1, S2)
• Eversion & inversion of foot (weak if tibial nerve is involved) • Supplies short head of biceps femoris
Common peroneal in thigh, crosses post to lat head of
Sciatic nerve L5 radiculopathy Cortical lesion
nerve gastrocnemius and becomes
Ankle dorsiflexion Weak Weak Weak Weak subcutaneous behind head of fibula
Ankle • Divides into superficial & deep
Strong Weak peroneal nerves
plantarflexion
• Gives off lateral sural cutaneous
Foot inversion Strong Weak Weak branch which joins with medial sural
Foot eversion Weak Weak Weak Weak cutaneous nerve " sural nerve
Hip internal
Strong Weak
rotation
Hip abduction Strong Weak
Ankle DTR Present Absent
10. Sensation
• Loss over L5 dermatome " L5 radiculopathy
• Numb over whole limb " sciatic nerve
• Glove & stocking distribution " peripheral neuropathy

CAUSES
Cortical foot drop Stroke, SOL
L5 PID, lumbar spondylosis
Sciatic Nerve Pelvic / hip #, hip posterior dislocation, nerve tumours
Common peroneal External pressure (casts)
nerve Trauma (tibia / fibula #, dislocation of knee, surgery)
Masses (ganglion, popliteal cysts, tumours)
Entrapment in fibular tunnel
DM, Leprosy
Bilateral foot drop Peripheral neuropathy
Bilateral L5 radiculopathy
Cauda equina syndrome
Motor neurone disease
Spastic paraplegia

MANAGEMENT
• Avoid further compression
• Identify & treat underlying cause
• Surgical exploration if progressive or no identifiable cause

! 84!
Approach to limping child
• Presentation: limping child/ delayed walking/ abnormal gait
• Things to consider: Site, Painful or painless, Age (rmber that regardless of age, must always include red flags (tumour, trauma & infx
<septic arthritis, OM, synovitis>) under painful cases)
Age Painful Painless
<3yo Most commonly due to infx Limb length discrepancies
Trauma (exclude NAI) - Bone: femur vs tibial shortening
- Toddler’s # (1-4yo): distal tibial # - Joint: commonly DDH
3yo to 7yo Transient synovitis (3-10yo; boys) - Generalized:
schoolgoing - Diagnosis of exclusion!!! o Muscle hypertrophy on one side
- COMMONEST cause of irritable hip ! Causes: nerve (NF), vessels (hemangiomas)
Inflammatory arthritis o Polio infx
Growing pain - Physiological:
- Diagnosis of exclusion!!! o Metatarsal adductors
- Usually btw 4-5yo and during puberty o Tibial torsion
- Bone growth rate faster than rate of increase in length o Femoral anteversion
of muscle and tendon o Flat foot
- Pain occurs usually at the end of the day, often Biggest concern: undiagnosed DDH
relieved w massage/ after a good night’s rest
Leukaemia (4-10yo)
7-10yo Perthe’s disease (4-8yo)
Transient synovitis
Adolescents SCFE (~15yo)
>10yo Growing pains

1. Age 0yrs
DEVELOPMENTAL DYSPLASIA OF THE HIP (DDH)/ CONGENITAL DISLOCATION OF THE HIP (CDH)
• Epidemiology
o Incidence
! 1 in 1000 live births; common enough for condition to be screened by neonatologists
! Girls > boys; Left hip > right hip (bilateral in 20%)
o Risk factors
! Family history: generalized joint laxity or shallow acetabulum
! Intrauterine malposition/ crowding: multiple pregnancies, oligohydramnios, fibroids, large baby, small mother, extended
breech delivery
! Postnatal posture: carrying babies with hips and knees fully extended
• Pathology
o Acetabulum unusually shallow and roof slopes upward too steeply; includes
! frank dislocation, subluxation or partial displacement of hip OR
! acetabular dysplasia without actual displacement
o Usually femoral head displaced posteriorly and superiorly
o Reduction impeded by joint capsule which folds inward and by fibrocartilaginous labrum
o Maturation of acetabulum and femoral epiphysis is retarded" femoral neck anteverted
o **Circular head needs to be in constant contact with acetabulum to ensure that
it remains spherical, concentric and well covered, ensuring proper Distribution
of body weight (prevent OA) + ROM
o Other contributing factors: tight iliopsoas, hypertrophic ligamentum teres,
hourglass capsule, fibrous tissue in acetabulum
• Diagnosis
o Newborn: Positive Barlows and Ortolani
o High risk cases (hip laxity or hip clicks): Ultrasound at 4-6 weeks
o Beyond 3 months (clinical signs) + X-ray
! Reduced hip abduction
! Assymetrical thigh skin creases
! Galleazi test – femur shortening
! Trendelenberg/waddling gait
• Symptoms
o Delayed walking, limping, hip clicks
o Unilateral dislocation: skin creases asymmetrical, hip abduction limited,
leg slightly short and internally rotated
o Bilateral dislocation: perineal gap abnormally wide, hip abduction limited,
waddling gait may be mistaken for normal toddling
• Signs
o Ortolani’s test (tests reducibility) - ABDUCT
! Passively flex hips to 90deg and abduct" on impeded hip abduction
apply pressure on greater trochanter" feel clunk as dislocation
reduces and hip abducts fully
! Normally smooth abduction to 90deg
o Barlow’s test (tests dislocatability) - ADDUCT
! Dislocate the hip by flexing the hip jt and adducting it followed by posterior force in the line of the shaft of femur
o Trendenlenburg’s test positive

! 85!
• Investigations
o NOTE: DX IS CLINICAL (US and XR are both not used to diagnose at birth)
! U/s not done at birth due to laxity of hip joint (due to maternal hormones; for baby to
come out of birth canal) and thus inaccuracy of reading " earliest u/s at 6 weeks
! X-ray has radiation + hip not ossified
o Ultrasonography (<3 months):
! Indications:
• Screen for high-risk cases (above RF, hip laxity, hip clicks): US at 6weeks to
look at acetabular alpha/beta angles
• To ensure concentric stable reduction after treatment
• Weekly after w splint to ensure reduction & correct application of splints
• Every 6 weeks after once hip reduced
• Most effective <3months old (3 months onwards: XR)
! Abnormal acetabular shape and femoral head position
! Big alpha angle means hip held well
o X-rays in older children (>3months old)
! Acetabulum: shallow + roof slopes upward too steeply
! Femoral head: small + ossific centre of femoral head underdeveloped +
displacement superiorly and posteriorly
! Shenton’s line: line fr inf border of femoral neck to inf border of pubic ramus broken
! Perkin’s line: vertical line drawn along lateral most aspect of acetabular roof " Normally epiphysis should lie medial
! Hilgenreiner’s line: horizontal line drawn thru superior aspect of triradiate cartilages " Normally epiphysis should lie below
! Acetabular roof angle (Acetabular index): Normally 30deg or less
! Von Rosen’s lines: hips abducted 45deg" femoral shafts should point toward acetabula.
! Medial gap: Greater the gap, greater possibility of dislocation

• Management:
o Goal of management is to achieve concentrically reduced and stable hips with good acetabular cover (to avoid early OA)
! NOTE: the earlier the treatment the likelier the child will develop a normal hip.
! If treatment started at 1yr, only <50% chance of absence of hip trouble in future
o 0-6 months (diagnosis at birth or from ultrasound followup)
! Wait and see: watch instead of intervening if unsure of diagnosis
• Just observe if: hip laxity ONLY or hip clicks
• Repeat US at 4-6 weeks:
o If hips reduced and stable " no further Rx
o Otherwise treat as DDH
! Reducible – Pavlik harness or abduction splint (old method) for 6wks – 3-4 months
• Details about abduction splint
o Double napkins/ abduction pillows for newborn
o Pavlik harness for larger infants
! Human position: Hips 100deg flexed and 50deg abducted; allow
some movement in splint
! AVOID: Frog position w hip abducted at 90deg- can cause AVN
(femoral head v sensitive to tension)
o U/S to ensure hip reduction before splinting " repeat US IN HARNESS after
1/52 to check position
• Repeat U/S OUT OF HARNESS after 6/52
o If stable on reexamination, observe for 6 mths (U/S every 6 weekly until 1st XR at 3months, then 6months)
o If unstable on reexamination, apply abduction splintage until hip is stable and acetabular roof developing
satisfactorily (usually 3-6months)
• OR wear for at least 3 mths till 1st XR: if XR shows concentric hips w good acetabular cover, then wean off splints
! Irreducible carry out: Adductor tenotomy; Closed reduction + hip spica (Change cast every 6 weeks)
o 6-18 months (persistent/ missed dislocation, failed pavlik, failed tenotomy, persistent irreducibility)
! Closed reduction can still be attempted but more difficult to achieve stability
• Blocks to reduction (hence hard to do adductor tenotomy)
o Extra-articular: adductors, iliopsoas
o Intra-articular: tight hour glass capsule, transverse ligament, pulvinar
• M&R under anaesthesia (gradually to prevent femoral head necrosis)
o Traction + gradual increase in abduction for 3 weeks
! Arthrography to check reduction (medial pool of dye = unreduced)
• If reduced, apply plaster spica at 60deg flexion, 40deg abduction, 20deg int rotation" after 6 wks replace w abduction
splint that prevents adduction but allows movement " regular XR (6monthly) " discard if XR show concentric femoral
head w normal acetabular roof
• If unreduced, perform open reduction (usualy involves femoral derotation and shortening)" apply plaster spica for
3mths
o Beyond 18 months: Salter osteotomy + open reduction
! Less potential for acetabular remodeling " both acetabular and proximal femoral Sx will be required
• Acetabular Sx (Salter osteotomy): Innominate osteotomy (bring acetabulum down to provide acetabular cover)
o Done at 2yo
o The entire acetabulum, tgt w the pubis and ischium, is rotated anteriorly and laterally as a unit, w the symphysis
pubis acting as a hinge. The osteotomy is held open anterolaterally by a wedge of full thickness bone graft, usually
taken from the anterior part of the iliac crest
! 86!
 o Osteotomy redirects the entire acetabulum so that its roof covers femoral head both anteriorly and superiorly
o In young children, the acetabular deficiency is usually anterior, and thus the
Salter Osteotomy is designed to provide coverage anteriorly at the expense
of posterior coverage
o Success of procedure depends to some extent on the flexibility of the
symphysis pubis (which decreases w age), thus the importance of
screening so as to intervene earlier
! Open reduction
o Chronic neglected dislocations (rare) usually not reduced if:
! >8 yrs for unilateral (no more remodeling past 8 yrs so reduction would cause OA)
! >5 years for bilateral
• Prognosis: *All will walk assuming muscles and nerves are functional
o Good results if treated <6yo if unilat
o Consequences of not reducing
! Partial dislocation (formation of false joint): progressive deformity, disability and
secondary hip OA
! Complete dislocation: Trendelenburg gait" scoliosis
! Bilat: waddling gait (hips dislocated behind so nothing to hold pelvis in btw)" lordosis

2. Age 0-5yrs
TRANSIENT SYNOVITIS
• Incidence
o Commonest cause of hip pain in children (3-10yrs old)
o Boys 2X more than girls
• Pathology: inflammation of the synovium of the hip joint, postulated due to URTI/ pharyngitis/ bronchitis/ otitis media or trauma (weak link)
" no definite cause known
• Diagnosis: of exclusion.
• Symptoms (last for 1-2weeks)
o Unilateral groin/ hip pain; inability to bear weight
o V young children may have no symptoms other than crying at night
o Recent Hx of above illnesses (in >50% of cases)
• Signs
o Log roll (most sensitive test): detect involuntary muscle guarding of one side
o Antalgic gait
o Tenderness on palpation even during passive movement
o Mild restriction of ROM (2/3 of patients)
• Investigations
o U/S: joint effusion
o X-ray: no changes
• Management (non-operative)
o Heat, massage, bed rest for 7-10days in a position of comfort
o Medications: NSAIDs (naproxen/ ibuprofen)
• Important to rule out RED FLAGS

SEPTIC ARTHRITIS (MEDICAL EMERGENCY)

• Pathology: Organism (usually staph aureus) reaches joint by haematogenous/ local spread from femoral OM" cartilaginous femoral head
liable to be destroyed by proteolytic enzymes of bacteria and pus
• Diagnosis: aspiration of pus from joint
• Incidence: Common in children <2yrs
• Symptoms
o Fever + signs of inflammation (absent in NEONATES- blood tests often normal)
o Pain (diffused)
o Pseudoparalysis of affected limb
• Signs: Tenderness maximal over hip
• Investigation
o U/S: joint effusion
o X-ray:
! Slight lateral displacement of femoral head (suggest effusion)
! Hyperdensity or fragmentation of femoral epiphysis (necrosis)
! In adults: rapid erosion of articular surfaces
o C/S + gram stain: Of joint aspirates (under GA) and blood " guides ABx choice
o Blood test: Raised ESR, WBC
• Complications if untreated
o Complete destruction of articular cartilage and underlying epiphysis
o Loss of adjacent growth plate
o Joint dislocation
• Management
o Medical
! IV Abs (penicillin for strep, cloxacillin for staph)
• Until ESR or CRP is normalized (CRP more sensitive than ESR)

! 87!
 • Oral Abs also acceptable: provided adequate blood lvls of Abx are demonstrated, parents are reliable, and Abx does not
cause GI disturbances that would interfere with absorption
• NOTE: Consider septic joint to be a closed abscess (don’t expect Abs alone to work " Sx!)
o Surgical
! Perform repeated percutaneous joint aspirations
• Only if easily accessible peripheral joint, clinical course <6days, no OM, no immune deficiency or chronic illness
! If condition fails to improve, perform open drainage in OT
• Indications:
o Hip and shoulder joints
o Peripheral joints that do not respond to percutaneous aspiration
o Patients who are systemically ill
o Suspected organism (S.aureus/gram-) produce cartilage-damaging enzymes
! Gonococaal arthritis less likely to rapidly damage a joint thus may be managed w repeated aspirations if
the joints involved are peripheral. Open drainage should stil be done for gonococcal arthritis of hip
! Apply traction on hip / splint in abduction until infection resolves; if instability is suspected (esp if Rx was delayed and
substantial capsular damage may have occurred), immobilize patient for a longer period
• Neglected septic hip with radiographic instability requires spica cast; Unstable shoulder requires a sling and swathe
o Follow up (at least up to 1yr after surgery)
! Assess joint function
! X-ray: ensure no radiographic evidence of loss of joint space, AVN of epiphysis, joint instability, damage to growth plate
3. 5-10yrs
PERTHES’ DISEASE (COXA PLANA)
• Epidemiology
o 1 in 10 000
o Children aged 4-8yrs old
o Boys 4X affected compared to girls
o R=L; Bilateral 10-15%
• Normal BS of femoral head:
o 0-4months: femoral head supplied by
! 1) Metaphyseal vessels,
! 2) Lateral epiphyseal vessels in retinacula (from medial &
lateral femoral circumflex from profunda femoris),
! 3) Scanty vessels in ligamentum teres (from obturator)
o By 4yrs: metaphyseal supply disappeared
o By 7yrs: vessels in ligamentum teres developed
o 4-7yrs: femoral head blood supply mostly fr lateral epiphyseal vessels
• Pathology
o Trauma/ non-specific synovitis results in effusion in hip joint" increased pressure on lateral epiphyseal vessels in retinacula
disturbs blood supply" avascular necrosis of femoral head " collapse & fragmentation, healing & remodeling " can cause
progressive deformity of hip jt & eventually early degenerative disease
• Pathological stages (similar to AVN)
Stage Process X-ray
1 Ischemia causing death of part of femoral head Normal (femoral head stops enlarging)
2 Revascularisation and repair - Epiphysis flat and sclerosed (new bone is laid; healing and
- If only part of epiphysis involved and repair process rapid reossification " small dense capital epiphysis)
- Bony architecture completely restored - Apparent widening of joint space
3 Distortion and remodeling - Epiphysis:
- If large part of epiphysis involved or repair process slow • Coxa plana (flattened)
- Epiphysis may collapse" subsequent distorted growth of • Coxa magna (enlarged)
head and neck • Fragmentation (collapse)
• Lateral displacement
- Metaphysis: Rarefaction, Broadened
- Femoral head incompletely covered by acetabulum
• DDx: non-specific transient synovitis
• Symptoms
o Hip pain and irritation; referred pain to knee
o Limp; Shortened leg
• Signs
o Early: all ROM limited and extremes painful
o Late: abduction and internal rotation often limited
• Investigations
o X-ray (described above)
o Radioisotope scanning: ischaemic area appears as a ‘void’ even before X-ray changes appear
• Prognostic grading (Catterall grading: according to degree of femoral head involvement)
Grade Severity Prognosis
1 Involves anterior portion of epiphysis only Revascularisation may be complete
No collapse or sequestrum w/o bone collapse
2 ≤50% epiphyseal involvement with a sequestrum Bony collapse inevitable
3 ~75% epiphyseal involvement with collapse and sequestrum Bony collapse inevitable
4 Whole epiphyseal involvement Poor prognosis

! 88!
 o Natural Hx: 75% have eventual healing and revascularization of the necrotic femoral head within 2-3 years
o Age: Younger better – as head can regrow
o ROM – less impaired better
o Disease severity/head involvement – the lesser the involvement the better
• Management: Aim for resolution of symptoms, and a spherical, well covered femoral head
1) Initially: skin traction on affected leg until pain subsides (~3 weeks)
2) Definitive: depending on prognosis Treatment
Favourable prognostic signs No active treatment
• Onset <6yo (Maintain/Improve ROM with activity modification)
• <50% femoral head involvement
• No stiffness or shortening on examination
• Absence of metaphyseal rarefraction
• Normal femoral head shape
Unfavourable prognostic signs Containment of femoral head (1 of 3 ways)
• Onset >6yo 1. Abduction splint (for a year, for bone changes to
• Involvement of >50% femoral head run their course)" unpopular
• Significant stiffness or shortening on examination 2. Varus osteotomy of femur
• Severe metaphyseal rarefraction 3. Innominate osteotomy of pelvis
• Lateral displacement of femoral head

4. 10-20yrs
SLIPPED CAPITAL FEMORAL EPIPHYSIS (EPIPHYSIOLYSIS)
• Commonest cause of hip pain in adolescence (11-15yo)
• Risk factors
o Associations: fat pubertal children, family Hx, precocious puberty, rickets, down’s
o Think of endocrinopathies in Bilateral SCFE: hypogonadism, hypothyroidism, hypopituitarism,
growth hormone deficiencies
o +/- history of trauma (30%)
o 2M: 1F
• Pathology: Insufficiency/stress fracture through hypertrophic zone of cartilaginous growth plate "
femoral neck glides upwards (head stays in place) " limb shortens and externally rotates (may
become fixed) " stiffness of hip " AVN " chrondrolysis (early onset OA)
o Excessive weight on predisposed hip
o Possibly due to imbalance btwn growth hormone (for bone growth) and gonadal hormone (physeal fusion)" immature physis too
weak to resist stress imposed by increased body weight
o Hence impt to rule out endocrine problems: pituitary, growth, thyroid, parathyroid, gonadal
• Symptoms
o Pain in groin +/- radiation to ant part of thigh or knee (referred pain; thus diagnosis delayed coz they
can present w knee pain)
! Painful = unstable (weight bearing not possible)
o Limp
o Bilateral SCFE in 1/3 of cases
• Signs
o Pain on movement (for acute slip)
o Coxa vara deformity
o Leg 1-2cm short; externally rotated and flexed
o Limited abduction and internal rotation
• Investigations
o X-ray
! AP view:
• Epiphyseal plate appears too wide and woolly
• Trethowan’s sign: Kline’s line drawn along
superior surface of neck remains superior to
head instead of passing through it (“ice cream
falling off cone”)
! Lateral view:
• Femoral epiphysis tilted backward
• Detect tilt by measuring angle btwn epiphyseal
base and middle of femoral neck
o If angle is <90deg, epiphysis has
slipped posteriorly
• Prognosis depends on severity and stability of slip
• Complications
o AVN (may also be seen after reduction or pinning of slip)
o Coxa vara deformity: If displacement not reduced and epiphysis fuses in deformed position" may need correction by osteotomy to
prevent secondary OA
o Secondary OA: In unreduced displacement and AVN
• Management: ONE GOOD SCREW (cannulated screw inserted percutaneously; always need Sx to stop progression)
NOTE: (manipulation is contraindicated)
o Displacement <1/3 epiphyseal width: Accept position, Epiphyseal fixation with pins

! 89!
 o Displacement of 1/3 – ½ epiphyseal width
! Epiphyseal fixation with pins +/- compensatory osteotomy (if residual deformity present even after remodeling)
o Displacement > ½ epiphyseal width
! Surgery (2 choices)
1) Epiphyseal replacement with piece of femoral neck + fixation with pins
2) Epiphyseal fixation with pins +/- compensatory osteotomy
o Femur divided just below greater trochanter" distal fragment repositioned in valgus, flexion and internal rotation

5. Avascular necrosis of the hip ***

• Susceptible areas: Occurs especially in those bones extensively covered in cartilage which rely on intra-osseous blood supply and distal to
proximal blood supply
o Femoral head (anterolateral), femoral condyles, humeral head, proximal tibia, vertebrae, small bones of hands and feet
[proximal pole of scaphoid, lunate, body of talus]
o NOTE: often no Rx needed for AVN of upper limb
• Risk factors/ causes
o Vacular/blood: hemoglobinopathies (eg. sickle cell anemia)
o Infective: septic arthritis
o Trauma: post-traumatic fracture/dislocation (esp. NOF fracture)
o Autoimmune: SLE, RA
o Metabolic: alcohol abuse (leading to hyperlipidemia), obesity, smoking, Caisson’s dz (deep sea diving/the bends), Gaucher disease
(hereditary, AR disease of glucocerebroside metabolism, results in accumulation of cerebroside-filled cells in bone marrow),
Cushing’s dz, Antiphospholipid antibodies
o Iatrogenic: steroid use – NOT dose related – idiosyncratic
! Glucocorticoids (inc. TCM) causes 2 things: 1) changes in circulating lipids" microemboli 2) changes in venous
endothelium"stasis"increased intraosseous pressure" necrosis
o Neoplastic: malignant infiltration
o Congenital: Perthes’ disease, SCFE, Clotting disorders (Inherited thrombophilia like Factor V Leiden)
o Idiopathic
o Other structural RFs: acetabular dysplasia, coxa vera, Paget’s
• Pathogenesis: multifactorial
o Metabolic factors
o Local factors affecting blood supply to bone
! Arterial supply interruption/ vascular damage
• Fracture, dislocation, infection
! Intravascular occlusion/venous stasis and retrograde arteriolar stoppage
• Sickle cell disease, vasculitis, Caisson disease
! Capillary compression (from marrow swelling)
• Steroids, alcohol, Gaucher’s disease
o Cycle: vascular stasis, hemorrhage or marrow swelling" capillary occlusion" ischemia" reactive edema/inflammation"
marrow swelling" increased intraosseous pressure" further ischemia
o Starts w BS interruption " hyperemia of surrounding area " demineralization, trabecular thinning " collapse of bone w mild stress
" Pathologic changes include resorption, subchondral fractures and loss of cartilage
• Diagnosis:
o Clinical, based on typical symptoms w compatible findings on imaging
o Rule out other causes of pain and bony abnormalities
• DDx: secondary OA due to trauma/RA, low grade septic arthritis, malignancy
• Presentation
o Pain is the usual complaint, felt near a joint and is accompanied by stiffness
! Pain often weight-bearing and motion-induced
• Rest pain in 2/3 patients, night pain in 1/3
o Nearby joint may be swollen
o Signs: ROM restricted + Local tenderness
o To differentiate AVN from OA, ask for the list of causes + OA tends to affect one joint whereas AVN causes usu systemic so tend to
affect both joints together (other than post-traumatic)
• Investigations (pictures at http://emedicine.medscape.com/article/386808-overview )
o Bloods: FBC (anemia, WBC tro infx), ESR/CRP (acute phase reactants), UECr and LFT (baseline), Rheumatoid factor & ANA, GXM
and PT/aPTT (for pre-op)
o X-ray: Hip XR weight bearing (AP/lat), pelvis XR AP
o MRI: only reliable method of picking up early signs of AVN (shows AVN up to 1 yr before XR; 98% sensitivity and specificity)
! Changes can be seen early in dz when other Ix are negative
! Earliest finding is a single low-density line on T1 weighted scan (separation btwn normal and ischemic bone)
! High-intensity line on T2 weighted scan represents hypervascular granulation tissue" pathognomonic double-line sign (low
density line + high density line)
o Radionuclide bone scan/ Radioscintigraphy
! Either diminished activity in avascular segment OR increased activity from vascular reaction in surrounding bone

! 90!
 • Ficat Arlet Staging + Management
o Extent of disease for stage 1,2,3 " A: <15%, B: 15-30%, C: >30%
Stage Processes & X-ray (Ficat-arlet staging) Radiographs Management (ELIMINATE
Clinical features CAUSE!!)
0: preclinical Hip at risk -Normal; may have signs of
" Preclinical phase previous trauma
of ischemia &
necrosis; no pain
1: pre- - Bone death -CT scan and X-ray normal Conservative: for early stage
radiographic (Marrow necrosis & (XR may be normal for disease or in medically unfit "
cell death within months after symptoms begin) ineffective at halting progression;
48hours) w/o -MRI: edema prevent bony collapse with
structural change -Bone scan: increased uptake - bed rest
" pain, typically in - weight relief (crutches)
groin - splintage
- NSAIDs/ other analgesics
- Bisphosphonates (slows resorption
of necrotic bone)
- PhysioRx
- Control RF
Coronal T1-weighted MRI in a patient with AVN
shows decreased signal within the femoral head Surgical: Core decompression +/-
(arrow), representing edema bone grafting
2: pre- - Repair and early X-ray • used if venous stasis or marrow
collapse structural failure - Earliest findings are mild edema
- Small # appear in density changes: Subarticular • Centre of head of femur
dead bone segment of increased bone excavated
- Days/weeks after density due to increased • Fibular/other graft to fill up cavity
infarction, new bone sclerosis/ cyst formation • Used in young active pts (best
laid down upon (reactive new bone formation chance of preserving femoral
dead trabeculae in the surrounding living tissue head)
which increases the total mass
" Pain & stiffness of calcified bone)
- Normal bone contour
- Osteopenia T2 weighted: AVN of bilateral femoral heads
- NO collapse -reparative border appear hypo/hyperintense
(double rim sign) on right side indicating granulation
MRI: geographic defect and sclerosis respectively.
Bone scan: increased uptake -Dark line bordering the AVN focus on left side
represents sclerosis.
-Normal cartilage and acetabulum
3: collapse - Major structural - Radiographic changes Surgical: (bone collapse alr
failure obvious occurred!!)
- Necrotic portion - Step-off in contour of - Femoral head resurfacing
crumbles subchondral bone - Hemiarthroplasty
- Bony outline - Pathognomonic crescent - Sugioka transtrochanteric rotational
distorted sign: subchondral lucency osteotomy
(evidence of subchondral - Realignment osteotomy: angular
" Painful & collapse; indicate early osteotomy
stiffness, limping flattening of femoral head) • redistributes weight-bearing
- Acetabulum intact forces to undamaged articular
cartilage supported by healthy
MRI: crescent sign and bone and may relieve pain and
cortical collapse prevent further bone distortion.
• also for late stage 2 disease with
cyst formation

-Frogleg lat view of the right hip in a patient w AVN

-Crescent sign, indicating subchondral fracture.
Frogleg lateral view > AP projection, because the
anterior and posterior margins of the acetabulum on
the AP projection are superimposed over the
superior portion of the femoral head, the usual
location of the sign.
4: - Articular - Signs of early OA Surgical: Rx for OA
osteoarthritis destruction, - Loss of sphericity, -Resurfacing arthroplasty
secondary OA subarticular fracturing, -Total hip replacement
- Cartilage collapse/flattening of • for stage 4 disease/ in older
breakdown though femoral head & Collapse of sedentary patients with not so
cartilage mainly articular surface severe disease
nourished by - Joint space narrowing
synovial fluid -Degenerative changes in
acetabulum
" Very painful, -Shortening of limb (lesser
stiffness, limping trochanter at different lvls/
migration of femoral head/
acetabular protrusion) -AP X-ray view of the pelvis
-Flattening of the outer portion of the right femoral
MRI: secondary degenerative head from AVN (arrow)
changes -Adjacent joint-space narrowing, juxta-articular
sclerosis, and osteophytes representing
degenerative joint disease
! 91!
Mr / Mdm XXX is a __ years old (race) gentleman / lady,
premorbid status: (ADL independent, community ambulant) ,
occupation: ____________________,
with a significant PMHx of: 1. Medical condition requiring long-term steroid use (RA / SLE / transplant)
2. Medical condition for which there is TCM use
3. Septic arthritis of the hip
4. Trauma to the hip
5. Left / right THR in XXXX year
presenting complaint: currently admitted for elective (left / right) total hip replacement.

He / she presents with a (duration) history of bilateral progressive groin pain (right > left / left > right) that has:
1. Failed to improve with conservative management
2. Gotten progressively disabling over the years
3. Resulting in marked loss of functioning
The pain is associated with:
1. Morning stiffness in the hip / stiffness after resting
2. Progressive shortening of 1 limb

The knee pain started (duration) years ago and has gotten progressively worst.
He / she describes the pain as (nature: sharp / dull / aching) . It is mechanical in nature, aggravated by movement when he / she does (type of
activity) and relieved by rest. It is also worst at the end of the day.
The pain is felt in the groin with radiation to the knee.
His / her current pain score is ___ and the pain (severity: affects sleep / requires frequent use of painkillers) .
In addition, he / she experiences stiffness in the hip after a period of rest.
Over the years, he / she noted that her (left / right) limb has shortened in length.

Functional Status
He / she suffers marked functional impairment from his / her condition. He / she walks with a limp. (if any)
His / her walking distance is limited to ______ from ______ previously, (with / without) a walking aid.
He / she (has / has no) difficulty putting on her socks & shoes and tying her shoelaces / wearing pants.
Currently, he / she is (able / unable) to climb the stairs, with (2 feet per stair / alternate foot per stair) .
He / she is (able to / not able to) sit cross legged.
He / she is (able to / unable to) squat / use a squatting toilet since (duration) years ago.

Systemic Review
There are no symptoms suggestive of referred pain such as back pain or neurological symptoms like weakness or numbness of the lower limbs.
Although pain radiated to the knee, it did not radiate to the calf or the foot.
He / she (has / does not have) any previous trauma or childhood injury to his / her hip. (+ details)
There is no involvement of other joints in the body. He / she also does not have a history of joint infection.
There is no fever, night pain or constitutional symptoms like loss of weight or loss of appetite.

Management so far (options tried)

He / she was treated conservatively with analgesia: (type) as well as non-pharmacological agents like advice on lifestyle modification,
physiotherapy and functional aids for the past ___ years. However, the above have not been able to control his / her symptoms. He / she is keen for
operation as his / her symptoms affect his / her functioning.

Past Medical History

Mr / Mdm XXX has a past medical history of _____________ for (duration) .
He / she has no history of SLE, rheumatoid arthritis, septic arthritis of the hip joint or any malignancies.
He / she also does not have a history of peptic ulcer disease / GI bleeding.
He / she had previous operations for ____________ / THR for the other knee.

Family History
There is no family history of blood disorders or similar joint problems (sickle cell disease or Gaucher’s disease).

Drug History
He / she has NKDA and is currently on: (esp. long-term steroid use) for her medical condition(s): ___________.
He / she has been taking TCM (details) for (medical condition) for (duration) .

Social History
He / she (does not smoke / smokes / is an ex-smoker and has quit XX years ago) , ( sticks/day x years).
He / she (has / does not have) a habit of regular intake of alcoholic drinks.
He / she has (good / poor) social support. He / she works as a ________.
He / she (has / has never) engaged in deep sea diving or worked in compressed air environment.
He / she lives with his / her _________. His / her main caregiver is his / her ______________.
He / she lives in a residential (with / without) lift landing. There (is / is no) squatting toilet in the house.
Currently, the family (does not have any financial issues / is receiving financial aid from ) .

In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with a significant past medical history of _______ on long term steroids and
________ / previously a heavy drinker, presenting with bilateral progressive groin pain for (duration) , worst on the (left / right) associated with
stiffness and progressive shortening of the limb that has failed conservative management and is currently admitted for hip replacement surgery.

My provisional diagnosis will be that of avascular necrosis of the (left /right) hip secondary to _________.
! 92!
PHYSICAL EXAMINATION

On physical examination, Mr / Mdm XXX is alert and comfortable at rest.

Appearance: I noted that he / she has cushingoid features such as moon face, truncal obesity, buffalo hump and
thin skin with purple striae over her abdomen.
Vitals: Her PR is _______, RR is _______ and BP is _______. (SpO2: ______; VAS: _____.)
Heart: S1S2 were heard on auscultation.
Lungs: Lungs are clear.
Abdo: Soft, non-tender

Examination of the upper limbs did not reveal any Herberden’s nodes or Bouchards nodes, gouty tophi or rheumatoid nodules.

Mr / Mdm XXX has an (antalgic gait / lateral thrust) on walking.

He / she (requires / does not require) the use of a walking frame / assistance in walking.
I also note that he / she has a shoe raise on the (left / right) leg.
His / her hip is held in an adducted position at rest. His / her pelvis is tilted to the (left / right) . There is increased lumbar lordosis / scoliosis of the
spine. There is wasting of the gluteal muscles.
There were no scars, sinuses, swelling or erythema over the anterior or posterior aspect of the joint.
Trendelenburg test was positive when he / she stood on her (left / right) leg. (cannot comment if pain on wt bearing)

Apparent limb length is ______ cm while true limb length is ______ cm.
There was no tenderness on palpation of the greater trochanter.
Thomas’ test for fixed flexion deformity was positive for the (left / right) limb.
Range of motion was severely limited over the (left / right) hip.
Internal rotation ___, external rotation ___, abduction ___, adduction ___. Flexion of the hip ranged from ____.
There is / is no fixed external rotation deformity or fixed flexion deformity of the hip.

Screening of the knee joint and the back did not reveal any abnormalities.
Popliteal, posterior tibial and dorsalis pedis pulses were well felt in both lower limbs.
Neurologically, power of bilateral lower limbs is full and sensation is intact bilaterally.

In summary, Mr / Mdm XXX has bilateral osteoarthritis of the hip likely secondary to avascular necrosis from (long term steroid use as evidenced
by the cushingoid features noted on general inspection / heavy alcohol consumption / SLE) . He / she has an (antalgic / Trendelenburg gait) and
the Trendelenburg test was also positive over the (left / right) . Marked gluteal wasting was noted, he / she also has a fixed flexion deformity of the
hip and apparent as well as true limb length shortening. Range of motion of the hip: (internal rotation / external rotation / abduction / adduction /
flexion / extension) were severely limited at ____ degrees.

! 93!
6. Hip dislocations
GENERAL PRINCIPLES
Cause X-ray Management
Septic arthritis Absent femoral head (surviving area too -Traction
- Partial/complete dissolution of femoral head osteoporotic to be seen) - (if above fails), open reduction with greater
trochanter in acetabulum + varus osteotomy of
femur
Muscle imbalance - Improper greater trochanter - As for DDH + muscle rebalancing operation
- Cerebral palsy, myelomeningocele, polio - Valgus femoral head
Trauma - Look for associated acetabular rim # - Reduction (ORIF if rim # is present)
After total hip arthroplasty (main cause)
- 1-4% in primary THA, 16% in revision cases
- 74% Posterior > 16% anterior > 8% central
- THA unstable in flexion & int rotation

POSTERIOR vs ANTERIOR vs CENTRAL DISLOCATIONS

Posterior dislocation (COMMONEST) Anterior dislocation Central dislocation
Incidence

Mechanism of - Dashboard injury" femur thrust upward and femoral head Fall on side/ blow
injury forced out of socket; often a piece of bone at back of over greater
acetabulum sheared off trochanter" femoral
Associated injuries head forced
1. PCL injury medially, fracturing
2. Posterior wall acetabulum # acetabulum
3. Femur # (distal, neck, head)
4. Sciatic nerve
Signs - Shortened limb - Abduction, external rotation
- Adduction, internal rotation - Slight flexion
- Slight flexion
Investigations AP film: (NOTE: AVN is a distinct possibility!) AP film:
(X-ray) - Femoral head above acetabulum - Occasionally head directly ant to
- Femoral head smaller, trochanter less prominent (due to normal position" confirm with lateral
adduction + int rotation) film
Multiple views (or CT):
- Exclude acetabular rim/ femoral neck fracture
Management M&R (Bigelow’s manoeuvre) M&R (Barlow’s equivalent)
- Relax muscles: conscious sedation (IV fentanyl)/ spinal/ GA - Muscle relaxation
- Assistant stabilizes pelvis - Assistant stabilizes pelvis
- Fully flex hip (by simply hooking leg and stand up over - Fully flex hip + adduct + int rotate
patient) & apply upward traction + abduct + ext rotate + downward pressure on femur
- X-ray
- Maintain via traction until pain free (~2 weeks)
- After 3 weeks walk with crutches
Complications Early:
• Fractures (femoral head, neck, shaft)
• Vascular injury: femoral vein" thrombosis & embolism
Late:
• Myositis ossificans
• Coxa magna (in up to 50% of children after hip dislocation)
• Recurrent dislocation
• Secondary OA (due to cartilage injury or intra-articular loose bodies)
Early: AVN of femoral head
• Nerve injury: Sciatic nerve (damaged in 10-20% but • If necrotic segment small, carry
usually recovers within months; occurs esp when rim # out realignment osteotomy
is present)" splint ankle (ankle foot orthosis) to • Younger patients:
overcome footdrop hemiarthroplasty of femoral
Late: head or hip arthrodesis
• AVN of femoral head: 10% occurrence; increases to • Patients >50yr: total hip
40% if reduction delayed by a few hours replacement
• Post-traumatic OA
o Due to 1) cartilage damage, 2) retained fragments
in joint (loose bodies), 3) femoral head ischemic
necrosis

! 94!
7. Fractures of proximal femur
GENERAL INFORMATION
• DDx of hip #: pubic ramus #, acetabular #, isolated # of greater trochanter, trochanteric bursitis/ contusion
• Female to male ratio is 2:1
• Type of fractures
Location Capsule Type Note Incidence
Neck of femur Intracapsular Subcapital -Tardy healing - Seen in same
Transcervical frequency
Extracapsular Basal -Treated like intertrochanteric #
Intertrochanteric Extracapsular -Unite very easily
Pertrochanteric (trochanter #ed) -Seldom cause AVN
Subtrochanteric Extracapsular -Blood loss greater than - Rarest
intertrochanteric/ NOF fractures
• Risk factors
Non- • Old age Modifiable Causes of increased risk of falls
Modifiable • Female sex • Poor vision, vestibular dysfunction
• Early menopause • Lower limb weakness
• Nulliparity • Co-morbidities (CCF, CVA)
• Family/ personal history of • Hazards at home
fractures Reduction of bone strength
• Caucasian • Osteoporosis, low Ca intake
• Steroids, alcohol, smoking, increased/decreased T4
• Physical immobility
• Pathological bone conditions
• Chronic liver and renal failure
• WHO fracture risk assessment tool (FRAX)
o Gives 10-year probability of hip # and 10yr probability of a major osteoporotic # (spine, forearm, hip, shoulder)
! For local chinese: use Hong Kong chinese
! For local Indians: use US (Asian)
o Disadvantges:
! Cannot calculate for patients <40yo
! Does not take into account type of #, number of #
! Does not tell u who to treat; still rely on clinical judgement
o Risk factors used: age, sex, weight, height, previous # (spontaneous or from low impact trauma), present fractured hip, current
smoking, steroids (>3 months of 5mg daily), RA, secondary osteoporosis (eg. type 1 DM, osteogenesis imperfecta, untreated long
standing hyperthyroidism, hypogonadism or premature menopause [<45yo]), chronic malnutrition, malabsorption and chronic liver
disease), alcohol >/=3 units a day, bone mineral density
• History
o Fall: how patient fell, pain/ tenderness/ deformity, can walk?
o What happened before fall: hazards at home, LOC?
o Predisposing fx to #: modifiable and non-modifiable
o Comorbidities
o Premorbid functional status
o Osteoporotic RF
• Symptoms
o Painful limited hip movements +/- Bruising (suggestive of extra-capsular fracture)
• Signs
o Shortened, externally rotated
o Fracture of proximal half: Flexed, abducted
o Bruising suggest extra capsular #
o Tenderness over femoral neck
o Painful limited hip movements
• Investigations: confirm Dx + determine severity + pre-op Ix
o Radiological
! AP pelvis (not hip)
! Lateral x-ray of affected hip
o Pre-op
! Haemotological: FBC, PT, aPTT, GXM (group and cross match)
! Renal panel: U/E/Cr, urinanalysis
! Liver panel
! Chest x-ray
! ECG
• Initial management
o Analgesia
o Antibiotics if infection suspected
o Pre-op traction for pain relief and to ensure union takes place in good position
o Thromboembolism prophylaxis (SC heparin 5000units BD)
• General principles of management
o Conservative: if undisplaced, clinically stable & ROM is full and painless
o THR indications: OA hips, Pathological #, Acetabular involvement, Revision hip

! 95!
 • After care:
o Weight bearing
o Physiotherapy (preserve joint movement, restore muscle power, access type of mobility aids needed)
o Treat osteoporosis and comorbidities
• Cx of femoral #s:
o Non-union in 30%; also delayed union and malunion (coxa vera) " OA
o Redisplacement
o Erosion of femoral head in unstable IT # causing coxa vera
o AVN in intracapsular NOF #, rarely in intertrochanteric

FEMORAL NECK FRACTURE (INTRA-ARTICULAR)

• Mechanism of injury: fall directly on greater trochanter
o More common in osteoporotic elderly (catching toe in carpet/ twisting hip in ext rotation)
o In young: fall from height/ road accident
• Garden’s classification
Fracture (X-ray) Innominate vs femoral trabecular lines (X-ray)
Type I Incomplete impacted fracture Not in line (head is valgus impacted)
Type II Complete fracture but no displacement Directly in line
Type III Complete fracture + moderate displacement Not in line (head is varus; head internally rotated and
• Prox fragment still connected by post retinacular abducted while distal fragment is externally rotated)
attachments
Type IV Complete fracture + severe displacement Parallel but displaced
• Prox fragment retains neutral position in acetabulum
• Pauwel’s classification
o Based on verticality of fracture line
o Higher Pauwel’s angle" greater vertical sheer forces" higher rates of non-union & failure in surgical fixation
Type I Type II Type III

<30deg from horizontal 30 - 70deg from horizontal >70deg from horizontal

• Investigations: X-ray (as above)
• Management (patient’s aims and premorbid ADL status, prob of successful op, risk of requiring 2nd op – these are governed by 1.
Physiological age 2. Premorbid medical status 3. Fracture configuration)
o Undisplaced fractures in CHILDREN: Plaster casting (hip spica) until fracture reunites
o Displaced or undisplaced fractures in young (generally <60 but consider physiological age) " PRESERVE HEAD
! 1) M&R
! 2) Secure Internal fixation: 3 cancellous screws/ a dynamic compression screw (w anti-rotational screw) attached to femoral shaft
o Undisplaced (Gardens 1, 2) fractures in old (>60 but consider physiological age):
! ~65yo (unless severely osteoporotic): cancellous screw
! ~90yo: hemiarthroplasty (uni/bipolar)
o Displaced (Gardens 3, 4) fractures in old: Hemiarthroplasty (unipolar/ bipolar), THR
! Role for THR: Borderline age groups with displaced #s (because last longer than hemiarthroplasty in such active adults)
! Fixation not indicated because of high risk of AVN and non-union (due to blood supply)
• Complications
o General complications in elderly: thromboembolism, pneumonia, bed sores, UTI (associated with prolonged bed rest)
o Prognosis;
! 25% mortality at 1 year
! 10% bedbound
! 33% wheelchair bound
! 33% ambulating +/- walking aid
o AVN of femoral head
! Risk is 10-30% in Stage I and II; 50-80% in Stages III and IV
! Pathogenesis
• Blood supply of femoral neck
a) Nutrient artery of femur (from profunda femoris)
b) Retinacular arteries in capsule (from medial and lateral circumflex arteries from profunda femoris)
c) 10% by ligamentum teres vessels (from obturator)
• Fracture and displacement of femoral neck severs (a) and if there is significant displacement (b) as well " (c) may be
insufficient" ischemic necrosis and collapse of femoral head.
• Fracture may still unite but femoral head distorted" joint irreversibly damaged
! Rx: THR
o Atrophic non-union
! Union normally takes about 3 months
! >1/3 of femoral neck fractures fail to unite; Stages III and IV at higher risk
! Causes; poor blood supply, imperfect reduction, inadequate fixation, tardy healing of intra-articular fractures
! Symptoms: pain, shortened limb, difficulty walking
! 96!
 ! Management
• Patients <50yo: bone-graft across fracture + re-insert fixation device
• Patients >50yo: hemiarthroplasty or total hip replacement
o Secondary OA: From subarticular bone necrosis or femoral head collapse

INTERTROCHANTERIC/ PERTROCHANTERIC FRACTURES + SUBTROCHANTERIC FRACTURES

Intertrochanteric fractures Subtrochanteric fractures
Notes " IT fractures have more bruising than NOF fractures as - Least common hip fracture, seen in younger population
they are extra-capsular with high energy injuries
Evans-Jensen classification - Highly unstable
I 2 fragments, undisplaced
II 2 fragments, displaced
III 3 fragments w/o posterolateral support
(greater troch #)
IV 3 fragments w/o medial support (less troch #)
V 4 fragments
R Reversed oblique # (prone to displacement)
Ix Diagonal fracture from greater to lesser trochanter (may - Fracture below lesser trochanter
(Xrays) hardly be visible; or comminuted and severely displaced) • Transverse, spiral or oblique
• frequently comminuted
- Flexed + abducted prox fragment (pull of iliopsoas on
lesser troch; gluteus medius & minimus on greater troch.)
Mx - M&R under x-ray - M&R under x-ray
- Internal fixation with DHS (nowadays increased use of - Internal fixation with PFNA (proximal femoral nail
cephalomedullary nail such as PFNA as DHS cannot antirotation; form of intramedullary nailing) OR fixation
handle some unstable fractures) with locking plate
- Resume walking with crutches when fracture unites (8- - Postoperative partial weight-bearing with crutches until
12weeks) union is secure

If patient unfit for surgery, then conservative:

-Wheelchair (with morphine)
-High mortality normally
-Used to do Hamilton Russell traction
-For reverse IT fractures: fix with PFNA
Cx -General
-Failure of fixation (screws may cut out of osteoporotic bone if reduction poor)
-Malunion: If treated conservatively, possible varus and ext rotation deformities but seldom interfere with function

8. Fractures of femoral shaft and distal femur

FEMORAL SHAFT FRACTURES
• Note: muscle pull severely displace fractures, hence reduction difficult
• Mechanism of injury: High-energy injury (MVA, FFH, GSW) fracture of young adults
o Diaphyseal fractures in elderly to be considered pathological until proven otherwise
o Children <4yo: tro NAI (spiral fractures from low-energy injury)
• Signs
o Leg shortened, externally rotated; unable to bear weight
o Proximal third/ midshaft fractures: prox fragment flexed, abducted, ext rotated (iliopsoas, gluteus medius), distal fragment adducted
o Distal third fractures: prox fragment adducted, distal fragment flexed (gastrocnemius)
• Investigations
o X-ray:
! Degree of comminution reflects amount of force involved (often comminuted w soft tissue trauma)
! Displacement in any direction
• Management
o Adults
! Immobilize leg with Thomas splint (or hydraulic traction) at scene of accident
! ABCDEs of trauma; RULE OUT OPEN # & SOFT TISSUE COMPROMISE; assess neurovascular status
! Analgesia
! M&R under conscious sedation
! Hold with traction with Thomas’ splint
! Intramedullary nail (method of choice) within 24hrs (high rate of surgical union after 6-12 weeks)
• Locking screws inserted transversely at prox and distal ends
• NOTE: external fixation indicated in
o severe open fractures (leave wound open after debridement)
o patient with multiple injuries to reduce operating time
o carrying out bone transport in cases of severe bone loss
o femoral fractures in adolescents
! Early mobilization of hip and knee
o Infants
! Gallow’s traction (1-2 weeks)
! Spica (another 3-4weeks)

! 97!
 o Children until 10yo
! Traction (3-4weeks)
• Gallow’s traction for children <12kg
• Thomas’ splint with pearson knee attachment for older children
! Spica (another 6weeks)
o Teenagers
! Longer time in traction and spica
! ORIF with plate and screws if reduction unsatisfactory
• Complications
o Prognosis: high morbidity/ mortality; often need blood replacement
! General Cx (from high-energy injuries): Haemorrhage, shock, fat embolism, ARDS, DIVC, MODS
o Early
! Vascular injury (to be repaired or grafted immediately) – Femoral artery
! Neurological: Sciatic nerve
o Late
! Thromboembolism
! Fat embolism
! Infection (from open injuries or internal fixation)
! Delayed union/ non-union: If #ed femur doesn’t unite in 100 +/- 20days, do exchange nailing w larger nail +/-bone-grafting
! Malunion: Esp fractures treated by traction and bracing
! Joint stiffness of knee: From joint injury at same time or due to soft-tissue adhesions during treatment

SUPRACONDYLAR FRACTURES OF FEMUR (intra/extra-articular)

• Mechanism of injury: Usually direct violence causing high-energy multiple trauma in young adults or in elderly, osteoporotic individuals
o Knee joint is severely disrupted w bicondylar #
• Symptoms: Pain (knee movement extremely painful)
• Signs
o Swelling, deformity of knee
o Palpate tibial pulses
• Investigations
o X-rays
! Fracture just above femoral condyles
! Transverse or comminuted (poor prognosis)
! Distal fragment tilted posteriorly due to pull of gastrocnemius
• Management
o For slightly displaced, extra-articular fractures that reduce easily with knee in flexion
! Non-operative:
• Skeletal traction through proximal tibia with limb cradled on Thomas’ splint with a knee flexion piece (pearson knee
piece which allows flexion, thus decreasing pull and preventing flexion deformity) + early ROM
• At 4-6weeks replace traction with cast-brace + partial weight-bearing with crutches + quad strengthening
! ORIF if closed reduction fails + early knee ROM & quad strengthening
• ORIF with angled compression plate or locked intramedullary nails
• Unprotected weight-bearing disallowed until fracture consolidated (~12weeks)
• Complications
o Joint stiffness in knee
o Non-union (esp with knee stiffness)
o Secondary OA (high incidence) esp in intra-articular fractures (reduce risk with anatomical reduction)

CONDYLAR FRACTURES (INTRA-ARTICULAR)

• Symptoms: Swelling
• Signs: Doughy feel of haemarthrosis
• Investigations
o X-ray
! 1 condyle fractured and shifted upward OR
! Condyles split apart
! Possible supracondylar fracture
• Management
o Aspirate haemarthrosis ASAP
o ORIF for anatomical reduction (fracture is intra-articular)
• Complications
o Knee stiffness
o Secondary OA as fracture is intra-articular

! 98!
9. Hip arthroplasty

Bipolar arthroplasty
Hemi-arthroplasty (only
femoral component)
Unipolar arthroplasty
Hip arthroplasty -Moore's &
Thompson
Total Hip Replacement (femoral +
acetabular components)

Thompson Austin Moore

• Has no holes, needs cement • Has 2 holes, doesn’t need cement

• Has neck (hence used for fractures near base of NOF) • No neck (used for subcapital and mid-neck fractures)
• Better for osteoporotics
• Material: ultra high molecular weight polyethylene and surgical grade stainless steel
• Lifespan: abt 10 years (must explain to patients before and after op that lifespan varies btw patients – if no symptoms past
10yrs, don’t need to replace it immediately)
• Note: Bipolar is better because of its modularity (more sizes) vs Moore’s which has only 2 sizes
• After-care
o Weight bearing:
! Implant: try and get patient to sit up by 24hr, walk by 72hr
! Internal fixation: sit up by 24hr; encourage mobility w non-weightbearing by 72hr (wheelchair); do not weight bear until healing
of # occurs else high risk of cutout
o PhysioRx:
! Preserve joint movement
! Restore muscle power
! Assess what type of mobility aids needed
o Treat osteoporosis and comorbidities
• Indications of THR: OA, pathological fracture, revision of implant!
o THR: cobalt chrome femoral head + acetabular plate + plastic cap on acetabulum
o Lifespan: 15-20yrs
• Complications of Total Hip Replacement
o Intraoperative:
! GA: AMI/ stroke/ death
! Infx, bleeding, nerve injury (sciatic, femoral; sciatic nerve palsy commoner in
post. surgical approach to the hip joint)
! Perforation fracture of acetabulum or femur
o Immediate (within 24hrs): Dislocation (due to incorrect placement of prosthetic components)
o Early (within 30days)
! Infection
! DVT (most common Cx)/ PE
• Pre-op: thromboembolic deterrent (TED) stockings
• Peri-op: TED stockings, minimize duration of surgery, compression boots & foot pumps
• Post-op: low dose LMW heparin, early mobilization with physiotherapy
! Fat embolism
o Late (after 30days) Dynamic hip screw
! Infection
! Heterotopic ossification Sliding
! Disuse osteoporosis screw
! Tissue atrophy
! Limb length discrepancy (TKR doesn’t have this Cx)
! Implant failure Barrel with
• Wearing of articular surfaces (esp acetabulum for unipolar’s) attached
• Loosening side plate
• Erosion, cut-out
• Peri-prosthetic fracture
Screws used to
anchor sideplate
onto proximal
femur

! 99!
Knee!
Atraumatic! Traumatic!

Deformities' Fractures'
• Genu'Valgus' • Tibial'Plateau'Fractures'
• Genu'Varum' • Patella'Fractures'

Dislocation'
• Patella'Dislocation'
Osteochondritis' • Knee'Dislocation'
Dissecans'

Tibiofemoral!Joint! Ligament'Injuries'
• OA! • Acute'Knee'Ligament'Injuries'
• RA!
• TB!

Knee'Joint'Swelling'
• Tibial'tubercle'
• Acute'swelling'of'entire'joint' Patellar/Quadriceps!
• Chronic'swelling'of'entire'jt' tendon!rupture!
• Swellings'in'front'of'joint'
• Swellings'at'back'of'knee'
• Swellings'at'side'of'joint'

Meniscal'Lesions'
Patellofemoral!Overload/!
Chondromalacia!Patellae/!
Patella!Pain!syndrome!
!
!

! 100!
 Examination of the Knee
The preliminaries: Intro urself to patient, ask permission to examine.
Ensure adequate exposure (underwear) but consider patient modesty
also (midthigh). Ensure good lighting, and good positioning of bed.
With pt standing. Ask pt to stand with feet side by side:
LOOK— Inspect knee and LL fr Front " Side " Back " Side
1. General appearance and vitals – pallor, BP, and HR.
2. Limb alignment & Deformity: varus (normal M 7° F 9°)/ valgus
- measure intercondylar distance (normal <5cm) and
intermalleolar distance (normal < 2cm)
- Fixed flexion deformity (fr side)
- Pelvic tilt (best fr back)
3. Scars over anterior and posterior aspect of knee
4. Swelling
- effusion w/ obliteratn of medial parapatellar fossa
- cyst e.g. Baker’s cyst over popliteal fossa
5. Sinuses
6. Discolouration – redness, bruising, etc
7. Muscle wasting – quadriceps
WALK +SQUAT: assess gait especially looking for antalgic gait
With patient lying supine, knees fully extended:
LOOK AND FEEL
1. Feel for temperature gradient over the knee joint (proximal to
distal), and any temp diff compared to the other knee
2. Effusion – obliteration of medial parapatellar fossa
- Fluid shift/ bulge test (10-20cc) (sensitive for small
amounts) – milk fluid from suprapatellar pouch, stroke
medial parapatellar fossa to empty it, then swipe the lateral
side and look for refilling of the medial fossa (bulge)
- Cross-fluctuance (30-50 cc): milk fluid from suprapatellar
pouch w L hand and apply pressure on medial aspect of
knee and feel for cross-fluctuance on lateral aspect of knee
- Patellar tap/ ballotment test (>60cc) – milk fluid from
suprapatellar pouch downwards w L hand, use index &
middle fingers of R hand to press down on patellar to feel
for ballotment; positive when patellar hits femur w a tap
3. Feel the articular surface of the patella for tenderness,
osteophytes.
4. Muscle wasting over quadriceps (esp vastus medialis) &
hamstring
- Measure circumference of quadriceps 10-15cm (or 4
fingerbreadths; 15cm safer to avoid the patella and
suprapatellar pouch) proximal to superior border of the
patella) – “objective assessment of wasting”; significant if
difference is >2 cm.
5. Other swellings eg. cysts arnd knee, osteophytes in OA knee
6. Feel medial & lateral patella facet: use fingers to gently
sublux patella medially/laterally to palpate the facets
7. Patella grinding test (damn pain): apply downward pressure
on patella and observe patient’s face for any pain " PFOA
8. Patellar apprehension test for recurrent patellar dislocation –
apply lateral force on patella and attempt to sublux the patella
laterally and look for apprehension on patients face or do it
while flexing and extending the knee joint; positive when
patient feels like patella is about to dislocate
With knee flexed to 90 degrees:
1. Palpate for tenderness with one thumb:
- Tibial tuberosity
- Patellar tendon
- Around either side of e patella (retropatellar tenderness)
- Quadriceps tendon arnd e superior border of the patella
- Medial and lateral joint lines, one at a time
- Femoral condyles
- Gerdy’s tubercle: insertion of IT band
- Lateral collateral ligament: start at prominence of head of
fibula and palpate upwards towards lateral epicondyle
- Medial collateral ligament: feel medial epicondyle and
palpate downwards
! 101!
MOVE
1. Active range of movements:
- Get pt to flex knee all the way and then extend, look for
any restriction of full flexion or extension (compare both
sides and measure difference if unequal)
- Fixed flexion deformity of the knee---Ask patient to push
down on examiner’s hand placed in the popliteal fossa to
see if patient is able to press hand against bed (or
obliteration of space under popliteal fossa). (N: 0-135°) "
if there is residual deformity, patient has some degree of
extensor lag " measure extent of deformity with
goniometer
2. Passive range of movements:
- Passive extension: Ask patient to relax and assess for
fixed flexion deformity by raising leg at the ankle "
measure angle if present
- Passive flexion: flex patient’s knee and ensure no pain,
then measure angle at maximal flexion
- If patient has restricted ROM, need to differentiate fixed
flexion deformity from extensor lag by assessing if there
is a joint contracture or muscle weakness
3. Crepitus: Feel with hand over patella during passive movement
SPECIAL TESTS
With legs placed in 90 deg flexion & aligned (heels in the same line):
1. Posterior sag sign (MAKE SURE DONE 1ST)
- Flex both knees to 90deg and view knees from side
looking for posterior sag of tibial tuberosity on the
femoral condyles " posterior cruciate injury
2. Posterior drawer test
3. Anterior drawer test " ensure not false +ve
- Sit on patient’s feet, use both hands to splint the
hamstrings (ensure they are relaxed), with thumbs on the
joint line, and pull towards you. Compare both knees
- In ACL tear, there will be no end-point on pulling forward
4. Lachman’s test
- With knee in 20-30 degrees flexion, place left hand on
thigh pressing downwards to stabilize femur, and right
hand under the proximal calf with thumb over the joint
line pulling the tibia towards you
- Also testing for ACL, but more sensitive test
5. Pivot shift for ACL
- Lift leg up and with lower limb adducted and knee
extended, patient is told to relax and the leg is internally
rotated with valgus force applied to the knee, and then
flexed; positive when tibia suddenly shifts forward on
femur with a click sound
6. Collateral ligaments (varus and valgus stress test)
- test in full extension (where capsular elements and
cruciates are also taut and restrict displacement) and in
30 degrees flexion (where only the MCL and LCL are
responsible for preventing displacement
7. Other special tests that can be done:
- Quadriceps active test for PCL – with patient’s knee
joint in 90 degree flexion and examiner sitting on
patient’s foot, get patient to contract quadriceps
muscle; positive when tibia shifts forward eliminating
the posterior sag appearance
- McMurray’s test (NOTE: test is painful, thus don’t do it
during exam): start pain=post horn; end pain= ant horn
• Insensitive test; better for big tears/ bucket handle
• Start with knee in full flexion, and place thumb and
fingers on jt line
• To test medial meniscus, externally rotate tibia w
your R hand at e ankle, and apply valgus force at
the knee with your left hand, then extend the knee
• To test lateral meniscus, internally rotate tibia and
apply varus force at the knee, then extend
• Repeat the test, looking out for palpable or audible
click in the knee during extension, or for pain
- Check Q-Angle of knee
FINISH with assessment of neurovascular status of the lower
limb (palpate distal pulses, “tip-toe” and “heel-step”, and
examine the back, hip and ankle joints for any pathology.
Approach to Knee Conditions
Symptoms o Non-Mechanical
• Pain ! Constitutional features
o Referred Pain: Always examine hip if knee is normal – ! Constant/ night pain
obturator nerve crosses both joints ! Morning stiffness (>1 hr for >/=6 weeks)
o Generalized: arthritis (OA, RA) ! Progressive deterioration
o Localized (mechanical disorders) ! Panarthritis
! PF disorders: patellar instability, PF overload, o Mechanical
PFOA, osteochondral injury, chondromalacia ! Local symptoms
patellae ! Progressive (very gradual)
! Jt disorder: osteochondritis dessicans, loose body, ! Specific mechanical correlation (arthritis of specific
synovial chondromatosis, ligament tears, meniscal area)
tears Examination & Ix
! Periarticular disorders: patellar tenditnitis, patellar • Suspect systemic
ligament strain, bursitis, OSD o General examination
• Swelling • Suspect local
o Anterior knee lump: OSD, housmaid’s knee, clergyman’s o Knee examination
knee ! Effusion
o Posterior: baker’s cyst, popliteal cyst, popliteal aneurysm • Very turbid – Gout, Infection (eg. TB)
o Lateral: meniscus cyst • Straw coloured - RA
o Traumatic knee swelling: • Clear – OA (Mechanical)
! Effusion, usually represents hemarthrosis (swelling • Purpose of arthroscopy:
instantly) o Establish or refine accurary of Dx
! Ligamentous injury w hemarthrosis o Help decide whether to operate; plan Sx approach w
! Meniscal injury (swelling after hrs) more precision
! Traumatic synovitis o Record progress of knee disorder
o Non-traumatic knee swelling o Perform Sx procedures
! Septic or crystal induced arthritis • XR:
! Seronegative arthritis (P-A-I-R: psoriatic, AS, IBD, o AP weight bearing, lateral
Reiter’s) o Skyline view (knee flexed and beam aimed from anterior
! Seropositive arthritis (RA, SLE) tibia to ant femur): PFJ
! Avascular necrosis (rare) o Tunnel view: knee bent, can see the hollow btw 2
! Sickle cell dsease articular surfaces
! Synovitis o Oblique: for intra-articular #
• Stiffness o Erect-leg full-length view:
o Early morning: inflammatory ! Radiograph from hip to foot w patient standing
o After periods of inactivity: OA ! Useful in evaluating limb length discrepencies and
• Weakness genu varus/valgus
• Locking – spontaneous block to full extension "torn meniscus, o Rosemberg view:
loose body (jammed btw articular surfaces) ! 30-40deg flexed weight bearing view w the XR
• Pseudo-locking: restricted ROM without mechanical block beam tilted caudal to profile the jt line
o Arthritis (effusion, pain), muscle spasm following injury ! Best view to visualize loss of medial jt space
• Instabilitity (giving out) • Other Ix: Aspiration (colour, uric acid crystals, c/s), MRI, bone
o Ligamentous instability: ACL, PCL, LCL, MCL scan, bloods (FBC, ESR, CRP, uric acid, RA profile….)
o Recurrent dislocation of patella/ patellar subluxation Problem Based Approach
o Torn meniscus, loose body • Serious
o OCD o Presentation usually non mechanical in nature
o RA o Diagnosis: Infection, Tumour, Inflammation
o Muscle weakness • Disabling
• Function impairment – Limping (could be due to pain, o Usually mechanical in nature
weakness, locking etc) o Diagnosis: Ligament injury, meniscal injury,
• Deformities: osteochondritis dissecans, osteoarthritis
o RA, TB, genu varum/valgum, charcot joint • Bothersome: causes concern and requires care/reassurance
Epidemiology but precise dx may not be necessary
• Age o Evaluation reveals it is not serious or disabling: tendinitis,
o Children – Often developmental Conditions OSD " explain, reassure, rehab
! DDH Pitfalls
! Discoid meniscus (prone to tear) • Malingering – Dangerous diagnosis to make
! Patellar dislocation (not developmental) o When evaluation exhausted, seek or ask patient to seek
o Adolescents/Adults – Trauma Conditions (meniscus, second opinion
ligament) ! Eg. Stress fractures may not appear on xrays;
o Elderly – Degenerative early infx like necrotizing fasciitis
• At all Ages • Major knee trauma
o Infection (eg. septic arthritis, TB) o Xray may look alright after reduction; but important to
o Inflammation assess neurovascular status; monitor and manage
! Young - Still’s Random
! Older - SLE, RA • 80% of haemarthrosis due to ACL Injury
o Tumour (osteogenic sarcoma) • Septic arthritis and gout have acute onset
History • White count raised in gout but not in RA
• Mechanical vs Non-Mechanical

! 102!
1. Lower limb malalignment (intoeing due to malalignment of hip, knee, ankle or foot)
General Information
• Deformity gauged by observation with patient standing and weight bearing
• Foot progression angle – angle that the axis of foot makes with midline
o Normal – 6-10 degrees external rotated
o Intoeing – negative 20-30 degrees
• Knee deformities:
o Genu varum: Measure distance between knees with legs straight and medial malleoli just touching (should be <6cm)
o Genu valgum: Measure distance between medial malleoli when knees held touching with patellae facing forwards (should be <8cm)
• Deformities common in children and most correct spontaneously by 10-12, hence no need to treat but just follow up every 6 months
• Physiologic evolution of leg alignment at various ages (2, 4, 6yo are milestones!)

Salenius curve of tibiofemoral angles

!
o 0-18months/2yrs: genu varus (tibial intortion)
o 2-6yo: genu valgus due to laxity of ligaments (valgus maximal at 4yo)
! Reassure parents; monitor child’s inter-malleolar distance every 6 mths to record progress
o 6-7yo: ligaments tighten and deformity starts to straighten out
! Operative correction shld be advised if a marked deformity persist past 10yo
o Normal adults/teens: slight valgus (5-7deg)
• Etiology of malalignments
o Trauma to growth plate " growth arrest
o Infection (neonatal period)
o Tumour (osteochondromas)
o Bone dysplasias: multiple epiphyseal dysplasia (Rx: hemiepiphysiodesis) etc
o Rickets
! Pathology: Failure of mineralization of physes or bone due to Vit D deficiency
! Causes: nutritional deficiency, GI absorption, renal tubular defects etc
! Investigations
• X-ray: Epiphysial flaring – prominent physes
• Bloods: Reduced calcium and phosphate, increased ALP
! Management: Correct cause + Correct deformity
o Blount’s disease (infantile)
! Pathology:
• Growth disorder: Idiopathic arrest of growth plate on medial side of tibia
• Progressive genu varum due to abnormal growth of posteromedial part of proximal tibia " varus angulation of
proximal tibia and medial rotation of tibia
• Often bilateral
• Rotational element often present
! Epidemiology:
• Overweight children
• Children who start walking early
• Female
! X-ray:
• Sloping of medial half of epiphysis
• Abnormal flattening
• Metaphyseal-diaphyseal angle: Abnormal if >11 degrees
! Management:
• </=3yo: circumferential brace/ AFO
• >3yo: high tibial osteotomy
• Mechanism of malalignment/ intoeing
Child HIP: medial femoral torsion (femoral anteversion; Twisted thighbone)
- Excessive internal rotation due to femoral anteversion
- Usually bilateral
- History of ‘W-sitting’
- Management
! Cross legged sitting
! Surgery only indicated if intoeing interferes with walking/running
! Derotational osteotomy

! 103!
 Toddler LEG: medial tibial torsion (Twisted shin)
- Commonest cause of bow-leggedness in 1yos
- Negative thigh foot angle (refer to photo) indicative of tibial torsion
- Thigh foot angle
! Normal: 15 deg!
! Negative angle

Infant FOOT: metatarsus adductus (curved foot)

- Usually improves over first 4-6 months of life
- Features:
! Metatarsus deviates medially
! Kidney shaped sole
! Splaying of 1st web space
! Inverted sole

• Management:
o Importance of aligning early
! Genu valgus:
• Accept valgus till about 5-7yo
• If valgus >7yo, mechanical axis will be lateral (ie. Pressure at lateral portion of growth plate) " inhibition of lateral growth
plate compared to medial " OA of lateral compartment (abt 30-40yo)
! Callosities may form in intoeing
o Surgery for knee deformities
! Indications: Marked deformity and instability
! Procedures
• Epiphyseodesis (in young): Stapling of one side of physis to slow growth on that side
• Osteotomy
o Valgus: Supracondylar femoral
o Varus: High tibial
• Joint reconstruction
• Adult onset knee deformities:
o Rheumatoid arthritis – Usually valgus
o Osteoarthritis – Usually varus

2. Osteochondritis Dissecans
• Pathology: Avascular necrosis of a fragment of subchondral bone predisposes overlying cartilage and subchondral bone itself to
fragmentation; osteochondral fragments (loose bodies) within joint space causes further pain and damage
o Usually affected lateral part of medial femoral condyle
o NOTE: unlike AVN of femur – dome of femoral condyle
• Risk Factors
o Male (15-20yo)
o Trauma:
! Single impact with edge of patella
! Repeated contact with adjacent tibia ridge
• Symptoms (bilateral in 25%)
o Intermittent ache or swelling
o Giving way
o Locking
• Signs
o Diagnostic Signs
! Tenderness localized to one femoral condyle
! Wilson’s sign
• Pain felt when knee flexed to 90 deg, rotated medially and gradually straightened
• Absence of pain when test repeated with lateral rotation
o Quadricep wasting, Joint effusion
• Investigations
o X-ray (intercondylar/tunnel view)
! Line of demarcation around lesion
! Empty hollow and possibly a loose body elsewhere (once fragment detaches)
o Radionuclide scans: Increased activity around lesion
o MRI: Area of low signal intensity in T1-weighted images
• Management
o Conservative – During early stage when cartilage intact and lesion is stable
! Lifestyle modification: Curtail activity for 6-12 months; small lesions often heal spontaneously
o Surgery – Unstable fragments (detachment)
! Small, ill-fitting fragment: Arthroscopic removal and the base drilled and eventually covered by fibrocartilage
! Large fragment >1cm diameter: In situ fixation with pins or Herbert screws
! Cartilage transplantation
! After Sx, knee casted for 6 weeks thereafter movement encouraged but weight bearing deferred until x-ray shows healing
! 104!
• NOTE: Other causes of loose body in knee
o Injury (chip of bone, cartilage, meniscus)
o OA (pieces of cartilage or osteophyte)
o Synovial chondromatosis: cartilage metaplasia in synovium " sometimes produce 100s of loose bodies
o Charcot’s joint (large osteochondral bodies separated by repeated trauma in insensate joint)
! Jt that has lost protective sensation thus progressively deforms as it suffers repeated trauma
! Causes: DM, peripheral neuropathy, tertiary syphilis, tabes dorsalis, syringomyelia, myeomeningocele, cauda equina
! S/S:
• Rapidly progressive OA
• Gross jt deformity but painless
• Unstable joint, effusion, no warmth
! Rx:
• Rest and immobilize
• Stabilize w cast/calipers
• Surgical arthrodesis
o S/S of LB: sudden locking (ranging positions of getting stuck), swollen jt (synovitis), palpable LB (sometimes like a joint mouse)
o Rx: if symptomatic, remove LB unless joint is severly osteoarthritic (?TKR)

3. Knee Joint Swelling

TIBIAL SWELLING
Osgood-Schlatter’s Disease
• Pathology: Traction injury to unfused apophysis into which part of the patellar ligament is inserted (traction apophysitis) " partial avulsion
of tibial tuberosity coz of unequal growth rate btw patellar ligament and bone " Traumatised apophysis becomes inflamed
o Overuse injury (strenuous sports) in adolescents
• S/S
o Typical profile: usually young adolescents engaged in strenuous sports
o Tender prominence of tibial tuberosity
o MOVE: Pain on active extension of knee (esp after activity)
o No effusion (extra-articular)
• Diagnosis: Primarily clinical diagnosis, X-ray knee (AP / Lat) tro tumour and infx
o Superficial ossicle in patellar tendon
o Irregular ossification of prox tibial tuberosity
o Calcification within patellar tendon
o Thickening of patellar tendon
o Soft tissue edema proximal to tibial tuberosity
o X-ray: Displacement or fragmentation of tibial apophysis
• DDX
o Young man + knee pain: Osteochondritis dessicans (degeneration / aseptic necrosis & recalcification of ossification centre)
o Young female + knee pain: CMP (softening and breakdown of the articular surface of patella)
• Management: spontaneous recovery
o Apply ice every 20min for 2-4 hours
o Analgesia (NSAIDs) for pain relief & to $ inflammation
o Rest; activity modification, restrict strenuous sports x 2-4/12
o Physiotherapy (quadricepts stretching exercise) to reduce tension on tibial tuberosity
o Orthotic devices (infrapatellar strap, knee brace)
• NOTE for MCQ: patient doesn’t present w loose bodies in knee joint coz its extra-articular!
Patient is a young (Chinese / Malay / Indian) (gentleman / lady) .
On inspection, I note the presence of bilateral ___ by ___ cm swellings over the tibial tuberosity on both lower limbs.
There are no overlying skin changes or scars noted.
Thre is no wasting of the quadriceps muscles.
No genu valgus or genu varus deformity is noted.

I would like to move on to palpate this swelling. (ask pt for any pain first)

The swelling has well defined edges and the surface is smooth. It is firm in consistency.
There is slight tenderness on palpation but it does not feel warm. It is not attached to the overlying skin.
The swelling is not transilluminable nor is it compressible. It is fluctuant in nature.

Given the above findings, my diagnosis is that of Osgood Schlatter Disease.

Differentials ill include bony lesions such as hereditary multiple exostosis and osteosarcoma (but lump not hard).

I will like to complete the examination by completing the rest of the knee examination.

! 105!
ACUTE SWELLING OF ENTIRE JOINT
• Haemarthrosis
o Post-traumatic
! Signs and Symptoms
• Immediate swelling after injury
• Painful, warm, tense
• Restricted movement
• Later may feel doughy
! Etiology
• Fracture (Patellar, femoral condyle)
• Ligament (ACL) tear
o Non-traumatic
! Pathology: Acute bleed into knee (most common site) in patients with clotting disorders
! Aspirate + splint + infuse CF
• Acute septic arthritis
o Signs and symptoms
! Signs of inflammation – tenderness, redness, warmth, swelling
! Investigations
• Raised white cell count and ESR
• Aspiration reveals pus in joint " c/s
! Common pathogens: Staph aureus, strep gonorrhea (in adults)
! Management: IV antibiotics, drainage of joint
• Synovitis
o Traumatic
! Pathology: Injury stimulates a reactive synovitis
! Signs and Symptoms
• Swelling appearing after some hours (unlike haemarthrosis) and subsides spontaneously over a few days
• Quadriceps wasting (due to inhibition of quadriceps action)
• Decreased ROM
! Management: Aspiration (if fluid amount considerable; hastns recovery)
o Aseptic non-traumatic
! Etiology: Gout or pseudogout
! Content: Turbid fluid
! Investigation: Microscopy reveals crystals
! Management: NSAIDs

CHRONIC SWELLING OF ENTIRE JOINT

• Arthritis: OA or RA
• Synovial disorders: Rule out TB

SWELLING IN FRONT OF JOINT

• Prepatellar bursitis (‘housemaid’s knee’)
o Pathology: Uninfected bursitis due to constant friction between skin and patella
o Risk factors: carpet layers, paving workers, floor cleaners, miners
o Signs and Symptoms: Fluctuant swelling confined to front of patella
o Management:
! Conservative: Firm bandaging, avoid kneeling
! IF chronic, aspiration or excision
• Infrapatellar bursitis (‘clergyman’s knee’): similar to prepatellar bursitis except for location (below patella and superficial to patellar ligament)

SWELLINGS AT BACK OF KNEE

Tissue type Pathology PE & comments

Skin and SQ Lipoma B Soft to firm; smooth/lobulated surface
tissues B If large and soft " elicit fluctuation
B Slip sign
B Elicit which layer lipoma is in (eg. SC or IM): in the latter the lipoma disappears on muscle
contraction
Sebaceous cyst B Soft to firm; smooth appearance
B Punctum in 50%
B Attached to the skin, hence does not move independently from the skin
Artery Popliteal artery aneurysm B 50% bilateral; expansile pulsation
B Comment on diameter (>/= 2cm diameter)
B Palpate all LL pulses (distal pulses may not be palpable if aneurysm is thrombosed
Vein Saphena varix @ Look for Cx of varicose veins (esp in Gaiters area)
saphenopopliteal junction B Venous eczema, lipodermatosclerosis, ulceration (active and healed; latter causes white patch
called atrophie balnche), peripheral edema
Look for varicosities along LSV
Tourniquet test, trendelenburg test, perthes test
DVT

! 106!
Nerve Neuroma Eg. tibial nerve
Enlarged B Above the joint line
bursae B Painless, slightly medial and most prominent w knee extended
B Lump fluctuant and transilluminates
B a/w semimembranosus and medial head of gastrocnemius medially and w poplitues and lateral
head of gastroc laterally
B spontaneously resolves even if aching
Cysts Baker’s cyst B Below jt line and deep to gastroc
B a/w degerneative changes in knee jt
Popliteal cyst B enlargement of popliteal bursa
B knee jt is normal
• Semimembranosus bursa
o Pathology: Enlargement of bursa between semimembranosus and medial head of gastrocnemius
o S/S: Painless, fluctuant and transilluminable swelling in medial part of popliteal fossa (most conspicuous with knee straight)
o Management: Waiting (as usually disappears); excision if symptomatic (pain)
• Baker’s cyst
o Pathology:
! Posterior herniation of knee jt capsule
! Leading to escape of synovial fluid into the posterior bursa, stiffness and knee swelling (fluid distension of the gastrocnemio-
semimembranosus bursa)
! Common in children, occurring more often in boys
! Often a/w OA, RA and Charcot’s joint
! Impt TRO DVT, but the 2 can co-exist
o Signs and Symptoms
! Swelling usually below the joint
• Fluctuant, may be transilluminable, non-tender, positive slip sign (it is a deep structure)
• Reducible only if connected to knee jts which not all baker’s cysts are (esp in children)
! If cyst ruptures & synovial contents spill into muscle planes, pain & swelling experienced in calf (may be mistaken for DVT)
o Cx:
! Due to their anatomic location, Baker’s cysts can increase risk of DVT
• Most commonly, the baker’s cyst is located btw tendons of the medial head of gastroc and the semimembranosus bursa
• BUT sometimes, the cyst can be found btw the heads fo the gastroc muscles " can result in a lateral deviation of the
popliteal vein " compression of the popliteal vein " predisposes to venous stasis and DVT
o Ix: U/S: fluid btw semimembranosus & medial gastroc tendons in communication with posterior knee cyst (100% accuracy)
o Management
! Children: Sx excision of cysts rarely indicated
• Usually spontaneous resolution of cysts in 10-20 months thus a prolonged period of observation is strongly recommended
before surgical excision is considered
• In protracted cases, cysts may respond to aspiration and steroid injection
o NOTE: unlike in adults, cysts in children may not be intra-articular and thus may respond to aspiration
! Adults: Excision not advised as recurrence likely unless underlying condition treated
• Popliteal cyst
o Pathology: cyst located on the medial side of popliteal fossa, just distal to flexion crease of the knee, under medial head of gastroc
o Epidemiology:
! Found n children and young adults
! 2x more common in boys
! Usually unilateral
o Signs:
! More prominent during knee extension and vice versa
! If cyst is not found in medial part of popliteal fossa or has a solid component (on US), rule out tumour with CT/MRI
o Rx: Conservative unless symptomatic; may spontaneously remit

On inspection, do not note any skin discolouration, scars, sinus or any obvious swellings anteriorly.
There is no muscle wasting, genu varum or genu valgum deformity.
There is no fixed flexion deformity of the knee.
Semimembranosus Bursa
There is a ___ x ___ cm hemispherical lump in the popliteal fossa, it
lies above the level of the joint line, slightly to the medial side of the
fossa. It appears well-defined. There are no overlying skin changes
or scars. There is no wasting of the quadriceps muscles.
I would like to move on to palpate the swelling.
(ask pt for any pain first)
(palpate with knee flexed – mass becomes soft, fluctuant & mobile)
Popliteal Cyst
There is a ___ x ___ cm hemispherical lump in the popliteal fossa, it
lies below the level of the joint line, deep to / bulging out between
the 2 heads of the gastrocnemius. It appears well-defined. There are
no overlying skin changes or scars. There is no wasting of the
quadriceps muscles.
I would like to move on to palpate the swelling.
(ask pt for any pain first)
(palpate with knee flexed – mass becomes soft, fluctuant & mobile)

The lump is non-tender and not warm. The surface is smooth, the The lump is non-tender and not warm. The surface is smooth, the
edge is regular and it is firm in consistency. It fluctuates, but is non edge is regular and it is firm in consistency. It fluctuates, but is non
pulsatile, not compressible and slip sign is negative. pulsatile, not compressible, and slip sign is negative.

I would like to move on to transilluminate the mass. I would like to move on to transilluminate the mass.
The mass transilluminates. The mass does not transilluminate (muscle covers it).

! 107!
Bend the knee to see if it empties into the knee joint (empties = popliteal cyst; does not empty = semimembranosus cyst).

Differentials include:
• Skin and subcutaneous tissue lumps (lipoma, sebaceous cyst)
• Artery (popliteal artery aneurysm)
• Vein (saphena varix, DVT)
• Nerve (neuromas)
• Bursa (semi-membranosus bursa – bursa between the SM and the medial head of the gastrocnemius)
• Cyst (popliteal cyst – bulging of the posterior capsule & synovial herniation, often 2° to OA / RA)

I would like to complete the examination by completing the rest of the knee examination. (for OA / RA / effusion)
I would like to perform a neurological and peripheral vascular examination, including feeling for peripheral pulses.
I would like to examine the hip and ankle as well.

SWELLINGS AT SIDE OF JOINT

• Meniscal Cyst
o Pathology: A cyst containing gelatinous fluid and surrounded by fibrous tissue, arising post
trauma due either to a small horizontal tear or repeated squashing of peripheral part of
meniscus " may have hx of jt injury
o Signs and Symptoms
! Small lump along the joint line that is tender and tense (esp when extended)
! Usually on lateral side of joint
o Management: Arthroscopic decompression or removal if symptomatic
• Calcification of Collateral Ligament (usually medial)
o Signs and symptoms: acute pain and tenderness " rubbery consistency
o Treatment: operative excision of deposit provides immediate relief
• Bony Swelling: Large non-discrete and painful swelling may suggest tumour (that arise in long bone metaphysis)

4. Patellofemoral Overload
Patellofemoral Overload / Patellar Pain Syndrome / Chondromalacia of Patella
• Pathology: Softening and fibrillation of articular surface of patella due to repetitive
mechanical overload of patellofemoral joint due to:
o Malcongruence of patellofemoral surfaces (because of abnormal shape of patella or
intercondylar groove) OR
o Malalignment of extensor mechanism or relative weakness of vastus medialis
which causes patella to tilt, subluxate or bear more heavily on one facet during
flexion and extension (PATELLA MALTRACKING)
• Risk factors for patella maltracking:
o Lateral patella tilt (due to malalignment of extensor mechanism or relative weakness
of vastus medialis)
o Tightness of lateral side
! Attachment to ITB
! Lateral retinaculum tighter than medial
o Weakness of VMO
o Large Q angle: ASIS " Center of patella " tibial tubercle
! Measure of how lateral the quadriceps pull is
! Q angle is the angle formed by a line drawn from the ASIS to the central patella and a
second line drawn from the central patella to the tibial tubercle.
! An increased Q angle is a risk factor for patellar subluxation.
! Normally Q angle is <18 deg for males and <22 deg for females with knee in full
extension; and <8 deg for males and <9 deg for females w knee in 90 deg extension.
! Biomechanics of PF joint are effected by patellar tendon length & the Q angle.
! Q angle is increased by:
• genu valgum
• Increased femoral anteversion
• External tibial torsion
• laterally positioned tibial tuberosity
• tight lateral retinaculum
• Larger pelvis (hence maltracking more common in females)
! Note: The Q angle may not be accurate in extension, since a laterally dislocated
patella may give the false impression that the Q angle is normal; In flexion, this is not a
problem since the patella is well seated in the trochlear groove
o Valgus knee
o Internal femoral torsion
o Abnormal patella: High or small
• Epidemiology: Teenage girls, Athletic young adults
• Symptoms: Anterior knee pain (beneath patella): Aggravated by activity (climbing stairs, standing after prolonged sitting)
• Signs
o LOOK: Quadriceps wasting, small effusion
o FEEL: retropatellar tenderness

! 108!
 o MOVE: Crepitus
o Patella grind test: Pain when pressing on patella against femur + contract quads (central + medial + lateral pressure)
• Cx: assoc w dvlpment of PFOA
• Investigations
o X-ray
! Skyline view: Show abnormal tilting or subluxation (LATERAL CONDYLE HIGHER)
! Lateral view (with knee partly flexed): See if patella is high or small
o CT/MRI – with knees in full extension and varying degrees of flexion
! Measure patellofemoral malposition most accurately
o Arthroscopy: Exclude other causes of knee pain
• Management
o Conservative " most patients recover
! Lifestyle modification
! Physiotherapy: Strengthen vastus medialis obliques to counterbalance tendency for lateral tilting or subluxation of patella
! Analgesics
o Surgery – If symptoms persist
! Arthroscopy lavage & shaving of fibrillated cartilage
! Lateral release +/- patellar realignment (if patella unstable)
! Drill exposed subchondral bone: revascularization may help repair w fibrocartilage
! Patellectomy
• Differentials (other causes for anterior knee pain)
o Patella tendinosis (Jumper’s knee): Pain at inferior pole of patella or along tendon due to overuse of extensor mechanism
o Patella subluxation
o Osgood Schlatters
o Plica syndrome: Plica (an extension of the protective synovial capsule of the knee) becomes irritated due to catching onto femur, or
pinching between femur and patella
o Hoffa syndrome: Impingement of fat pad between femoral condyle and patella

5. Fractures
TIBIAL PLATEAU FRACTURES
• Mechanism of Injury: Crushing or splitting of one or both tibial condyles by opposing
femoral condyle due to strong bending forces combined with axial loads (eg. car
striking pedestrian on side of knee - bumper fracture) or fall from a height in which
knee is forced into valgus or varus
o Lateral > medial
• Signs and Symptoms:
o Joint swelling (may have hemathrosis)
o Diffuse tenderness on side of fracture
o Tenderness on opposite side indicates ligament injury
• Associated injuries/ complications
o Compartment syndrome (esp Types 5 and 6)
o Popliteal artery injury
o Ligament/meniscal tear (esp contralateral side)
o Malunion
o Joint stiffness (minimize by early ROM)
o Secondary OA: esp with marked plateau depression, deformity (valgus or varus)
and ligamentous instability
• Classification (Schatzker’s Classification)
Type Description
1 Simple split of lateral condyle
2 Split of lateral condyle with more central area of depression (the force may have been greater or
underlying bone may be osteoporotic and unable to resist depression)
3 Depression of lateral condyle with intact rim
4 Fracture of medial condyle
5 Fractures of both condyles but central portion of metaphysis still connected to tibial shaft
6 Combined condylar and subcondylar fractures (split extends to metadiaphysis)
• Ix: XR multiple view and sometimes tomography to shoe the true extent of fracture
• Management by fracture type
Fracture Management
Lateral condylar #: Conservative
Undisplaced/minimally Aspirate haemarthrosis, compression bandage" hinged cast-brace + knee
displaced # movements when pain and swelling subsides" avoid weight bearing for 3wks
- Acute pain and swelling often subsides in 1 wk
Lateral condylar #: ORIF (lag screws and buttress plate)
Markedly displaced/
comminuted
Medial condylar # ORIF +/- lateral ligament repair
Bicondylar # ORIF
Osteoporotic condylar # ORIF or TKR (if # pattern permits)

! 109!
• Management by extent of depression
o Fracture displacement ranging from 4-10mm can be treated non-operatively
! If depression is <3mm: traction + mobilization (Sarmiento program of functional cast bracing + NWB for 2 months; # requires abt
2-3 months to heal)
! If depression >3mm, displaced or comminuted; or if there is doubt abt degree of displacement:
• ORIF +/- bone graft to elevate fragment
• Indications for Sx
o Absolute indications for Sx:
! Open plateau #
! # with an associated compartment syndrome
! # assoc w a vascular injury
o Relative indications for Sx:
! Most displaced bicondylar #
! Displaced medial condylar # (coz medial # are more complex)
! Lateral plateau # that result in joint instability
o Contraindications to Sx
! Presence of a compromised soft-tissue envelope (for immediate open reduction)
! # that do not result in joint instability or deformity and can therefore be treated w non-operative modalities

PATELLAR FRACTURES
• Mechanism of Injury
Type Mechanism
Undisplaced crack Direct blow
Comminuted/Stellate Fall or direct blow on front of knee
Transverse fracture with gap Indirect traction injury due to forced, passive flexion of the knee while the quads muscle is contracted
between fragments (entire extensor mechanism is torn across and active knee extension is impossible)
• Symptoms
o Pain
o Swelling (haemarthrosis)
o Inability to extend knee (esp in transverse #; affects treatment)
• Signs
o Bruising of knee jt w or w/o abrasions
o Patellar deformity; Gap may be felt
o Tenderness over patella
o Proximal displacement of patella (esp in transverse #)
• X-ray (AP, lateral, skyline)
o Note: Don’t confuse with congenital bipartite patella (common congenital
fragmentation of patella " Type I: inf pole of patella, Type II: lat. margin, Type
III: smooth line extends obliquely across superolateral angle of bone)
• Complications: PFOA
• Management (depends on state of extensor mechanism): all require PhysioRx after initial Rx
o General indications for Sx:
! Significant articular step-off >2mm
! Loss of extensor mechanism with displacement >3mm
! Open fracture
o Undisplaced or minimally displaced crack: CONSERVATIVE
! Aspirate haemarthrosis (if present)
! Protection with plaster cylinder holding knee straight (4-6/52) if extensor mechanism intact + early ROM to preserve mobility
o Comminuted (stellate) fracture:
! Acceptable displacement: Backslab + early ROM
! Severe displacement: complete or partial patellectomy (depending on severity of displacement) to avoid damage to
patellofemoral joint predisposed by irregular undersurface of patella
o Displaced transverse fracture:
! Internal fixation (tension band wiring + 2K-wires)
! Extensor expansions repaired if torn
! Plaster backslab worn until active extension of knee regained

6. Dislocation
PATELLAR DISLOCATION (FIRST TIME)
• Mechanism of Injury
o Normal anatomical predisposition: Knee angled in slight valgus hence tendency for patella to pull towards lateral side when quads
contract (medial retinacular fibers may be torn)
o Precipitation: Sudden contraction of quadriceps while knee is stretched in valgus and external rotation
• Symptoms
o Tearing sensation
o Feeling that knee has gone ‘out of joint’
o Often patella reduces spontaneously
o Joint may be swollen (blood stained effusion)
• Signs
o If patella does not reduce spontaneously, uncovered medial femoral condyle is prominent
(may be mistaken for patella)

! 110!
 o Tenderness on medial joint + swollen knee
o Active and passive movement not possible
• X-ray
o If unreduced, patella seen to be laterally displaced (and tilted or rotated)
o May have associated osteochondral fracture
• Management: Reduction + Backslab + PhysioRx
o Plaster cylinder/splint for 2-3/52 + walk w crutches
• Complications: Recurrent dislocation/subluxation (non-operative treatment for 1st time dislocation has 15-20% recurrence chance)

RECURRENT PATELLAR DISLOCATION

Patella Instability
Habitual / Congenital Acquired
• Dislocate in flexion 1. Traumatic (Mx: physiotherapy)
• Difficulty squatting, climbing stairs 2. Predisposed: Laxity (Marfan’s / Down’s) or # Q angle
• Mx: surgical realignment 3. Recurrent (Mx: surgical reconstruction of MPFL)
4. Chronic dislocated (Mx: surg realignment)
• Mechanism of Injury: Dislocation / subluxation after minimal stress (after a previous dislocation)
• Risk factors (if have the following may not have initial injury, and usually bilateral) " think of bone, joint, ligaments, muscles
o Generalised ligamentous laxity
o Underdevelopment of lateral femoral condyle
o Maldevelopment of patella (too high or small or lateral)
o Abnormalities of lateral femoral condyle (flattening of intercondylar groove)
o Genu valgus
o Tibial tubercle malalignment
o Primary muscle defect
o More common in girls
• Signs and Symptoms
o Episode characterized by acute pain with knee stuck in flexion and patella displaced laterally
o Apprehension test positive
• Ix:
o Skyline view: shows tilt/subluxation
o Lateral view: shows high or small patella
• Management
o Conservative
! Reduction and backslab
! Isometric quadriceps-strenghtening exercises (focus on vastus medialis to counterbalance lat tilt/subluxation)
! Conservative Rx may suffice if recurrences few as patellar mechanism tends to stabilize as child grows older
o Surgery
! Indications: frequent, repeated and distressing episodes of dislocation (Sx for ~15% of children w patellar instability)
! Procedures
• Repair/strengthen medial patellofemoral ligaments
• Re-align extensor mechanism to produce a mechanically more favourable angle of pull (transpose patellar ligament
medially)
• Lateral release if lateral retinaculum tight
• Complications
o Repeated dislocations damages the contiguous surfaces of patella and femoral condyle and may result in further flattening of condyle
" facilitate further dislocations " secondary PFOA

KNEE DISLOCATION
• Mechanism of Injury
o Significant trauma (eg. RTA) where cruciate ligaments and one/both collaterals are torn
o Can be anterior (most common), posterior, rotatory or lateral
• Symptoms: Bruising + Swelling + Gross deformity
• Complications
o Early
! Vascular injury (35-50%) and ischemia: Popliteal artery (tethered to knee joint: geniculate arteries and ant tibial artery goes
thru hiatus in interosseous membrane) – may have an intimal tear which may bleed insidiously or a disruption
• If merely kinked, pulse should return post reduction
• If tear:
o Full tear: Pulse wont return
o Intimal tear: Weak pulse returns
• If weak pulse/no pulse, investigate with arteriogram
! Nerve injury: Posterior tibial, common peroneal nerves
! Capsular/ ligament/ meniscal injuries
! Compartment syndrome
o Late
! Reperfusion injury
! Joint instability (AP glide, lateral wobble)
! Joint stiffness

! 111!
• Investigations
o X-ray: Rule out tibial spine fracture due to cruciate ligament avulsion
o Arteriogram/ doppler: If have doubts about circulation
• Management
o Reduction + Backslab in 15 deg flexion (dangerous to use cylinder plaster due to swelling)
! If unstable or if vascular repair – external fixator
! If open wound/ vascular damage (need to operate anyway), take opportunity to repair ligaments and capsule
o Above knee cast applied after swelling subsides (for 4-12 weeks)
o Quadriceps muscle exercises

7. Knee Ligament Injuries

GENERAL INFORMATION
• Stabilisers of knee
o Strong capsule
o Intraarticular ligaments (ACL, PCL)
o Extraarticular ligaments (MCL, LCL)
o Muscles (quadriceps)
• Consider functional (directional instability) and anatomical (which ligaments injured) aspects
• Unhappy triad (O'Donoghue's triad): ACL + MCL + Medial meniscus
• Common Signs and Symptoms
o Concomitant immediate swelling indicates haemarthrosis
o Partial vs Complete tear
! Partial: No abnormal movement permitted; but (severe) pain on attempted abnormal movement
! Complete: Abnormal movement permitted; may have little/no pain
! Grade 1 Sprains. The ligament is mildly damaged in a Grade 1 Sprain. It has been slightly stretched, but is still able to help
keep the knee joint stable (PCL: step-off present, 0-5 mm)
! Grade 2 Sprains. A Grade 2 Sprain stretches the ligament to the point where it becomes loose. This is often referred to as a
partial tear of the ligament (PCL: 5-10mm of posterior translation)
! Grade 3 Sprains. This type of sprain is most commonly referred to as a complete tear of the ligament. The ligament has been
split into two, and knee is unstable (PCL: > 10mm posterior translation)
o Note: Angulation in full extension: Rupture of capsule + Cruciate ligaments + Collateral ligament
• Investigation
o Examination under anaesthesia when in doubt
o XR:
! Stress XR: assess instability
! Plain XR: to identify avulsion fractures
• MCL – from femur
• LCL – from fibula
• ACL – from tibial spine
• PCL – from back of upper tibia
o MRI: Definitive diagnosis
• Management (management depends largely on activities of patient)
o Conservative
! Procedure
• Aspirate haemarthrosis
• Apply icepacks to relieve pain
• Knee protected in functional brace or heavily padded bandage (weight bearing permitted but protection from rotation
or angulation)
• Muscle-strengthening (hamstring & quads) after symptoms subside – muscle strength can compensate for stability loss
• Assessment to identify need for ligament reconstruction
! Indications
• Sprains and partial tears: Intact fibers splint torn ones and spontaneous healing occurs
• Isolated MCL, LCL and PCL tears
• Isolated ACL in non-sportsman
o Immobilisation in plaster cylinder for 6 weeks
! Indications: Avulsion fracture where fragment can be manipulated back into position and allow full extension of knee
o ORIF + Immobilisation in plaster cylinder
! Indications: Avulsion fracture where fragment cannot be reduced or if there is block to full extension
o Joint Bracing + Physiotherapy + ACL reconstruction (not repair)
! Indications: ACL with collateral ligament injury or PCL with collat lig injury
! Stabilization/reconstruction procedure (3Rs)
• Grafts: Hamstrings (semitendinosis), gracilis or patella tendon bone (may be autograft or allograft)
• Reattachment: tightening of loose ligament/capsule
• Reinforcement: diversion of healthy muscles or tendons to strengthen weak structures; using hamstrings, patellar, quads
• Replacement: rerouting living structures or inserting synthetic material
• Complications
o Adhesions
o Chronic instability (sense of jt wanting to or actually giving way; w or w/o pain and recurrent swelling) " Predispose to OA

! 112!
ACL INJURY (more common than PCL injury)
• Attachments
o Medial aspect of lateral femoral condyle
o Intercondyloid eminence of tibia
• Function
o Prevent anterior translation
o Prevent internal rotation of tibia
• Components
o Anteromedial – taut in flexion
o Posterolateral – taut in extension
• Mechanism of Injury
o Internal rotation on hyperextended knee
o Indirect varus blow to knee
o " patients w greater Q-angle got greater chance of ACL tear
• Hx:
o Audible pop
o Giving way " knee instability " inability to continue activity
o Immediate swelling if hemarthrosis
• Signs
o Anterior drawer + Lachman’s + Pivot shift + Apleys distraction test
o Note false +ve in PCL tears
• ACL does not have ability to heal:
o Synovial fluid keeps 2 ends apart
o Synovial fluid produces proteolytic enzymes which exacerbates damage
o Synovial fluid prevents formation of a fibrin platelet clot at wound site
• Blood supply: Medial geniculate artery (ruptured in ACL tear)

Inspect for skin changes / scars / wasting / deformities / swelling (if present " do effusion test)
If no specific instructions: “At this point of time, I would like to proceed to test the ligaments first”
Flex knee to look for posterior sag Flex knee to look for posterior sag
" There is no posterior sag of the knee " There is posterior sag of the knee
(Warn patient about sitting on feet) (Warn patient about sitting on feet)
(Compare both sides when examining the ligaments) (Compare both sides when examining the ligaments)
Posterior drawer " Posterior drawer is negative Posterior drawer " Posterior drawer is positive
Anterior drawer " Anterior drawer is positive Anterior drawer " Anterior drawer is negative
Lachman test " Lachman test is positive (false positive anterior drawer / Lachman test)

My diagnosis is a (left / right) ACL tear. My diagnosis is a (left / right) PCL tear.
I would like to test for the integrity of the collateral ligaments.
Varus & valgus stress test at 30 degrees and knee in full extension " The collateral ligamants are intact.
I would like to look for associated meniscal injuries by palpating the joint line.

PCL INJURY
• Mechanism of Injury
o Dashboard injury (hit ant tibia on dashboard and tibia forced backwards)
o Hyperflexion or hyperextension w anterior tibial force
o Fall onto flexed knee w plantarflexed foot
• Attachments: Medial condyle of femur, Posterior intercondylar area of tibia
• Signs: Posterior sag + Posterior drawer + Reversed pivot shift + apleys distraction test

MCL & LCL INJURY

• Mechanism of Injury: Varus (LCL) and valgus (MCL) force
• Signs
o Swelling + tenderness above and below joint line
o Valgus and varus stress test: Assess joint space opening with valgus/varus force
! Laxity with end point – partial tear
! Laxity with no end point – complete tear
! Pain
o Impt TRO ACL and medial meniscus tears
o Impt TRO common peroneal nerve injury in LCL tear (difficult dorsiflexion and decreased sensation at foot dorsum)
• Management
o Minor/ moderate: Can be treated with functional brace (hole in front of functional brace reduces patellofemoral pain and provides gift for
patellofemoral slide) to immobilize + early ROM + strengthening
! NOTE: ligaments take 3/52 to heal
o Severe or combined: Sx repair of associated injuries
! Sx repair of isolated MCL/LCL tear is controversial

! 113!
8. Meniscus Tears
• Role of menisci
o Increase stability of knee (screw home mechanism)
o Control complex rolling and gliding actions of joint
o Distribute load during movement
• Mechanism of Injury: Meniscus split in its length by force grinding it between femur and tibia
o In young: Weight taken on flexed knee with twisting strain " usually during sports (esp football)
o Older (>40): Relatively little force needed as fibrosis restricts mobility of meniscus
! May not have a notable initial injury and main compliant is of recurrent giving away or locking
• Anatomy
o Semilunar shaped fibrocartilaginous wedges
o Medial: larger, kidney shaped
o Vasculature: Periphery supplied by radial branches of geniculate arteries while majority is avascular and obtain nutrition from
synovial diffusion
• Pathology
o Medial meniscus affected more because:
! Attachment to medial collateral ligament make it less mobile
! Absence of popliteus muscle insertions which can pull meniscus into more favorable position during sudden movements (as
with lateral meniscus)
o Types of Tears
! Bucket handle tears
• Split is vertical but runs along part of circumference of meniscus creating a loose sliver still attached anteriorly and
posteriorly
• Loose sliver may displace toward center of joint and jam between femur and tibia causing locking (block to extension)
! Horizontal tears
• Usually degenerative or due to repeated minor trauma
• Some are associated w meniscal cysts
o Most of meniscus is avascular and does not repair (except outer third which is vascularised from capsule)
o Loose tag " mechanical irritant " synovial effusion " secondary OA
• Symptoms
o Severe pain (over joint line) post trauma (hence further activity avoided)
o Knee may be locked in partial flexion (torn part jammed btw tibia and femur, blocking extension)
! Locking suggestive of bucket handle tear
! Patients may learn to ‘unlock’ knee by bending it fully or by twisting it from side to side
o Swelling (hours later or next day; unlike in ligament tear)
o Initial symptoms subside with rest but recur with trivial twists and strains or even give way spontaneously (followed by pain and
swelling)
• Cx: recurrent synovial effusion and articular cartilage damage due to loose meniscal tag " swelling, secondary OA
• Signs
o Tenderness localized to joint line (usually medial)
o McMurray’s test
o Apley’s grinding test
o Joint may be held slightly flexed; may have limited extension
o Effusion
o Quadriceps wasting (in late presentation)
• Investigations
o MRI
o Arthroscopy: If lesion identified can be treated at same time
• Management: Meniscus preservation if possible
o Arthroscopic surgery (subtotal or total menisectomy)
! Outer 1/3: good vascular ss (fr capsule), good healing " attempt repair
! Mid 1/3: intermediate vascular ss and healing
! Inner 1/3: avascular and poor healing " total or subtotal (displaced portion) excision
o Postoperative physiotherapy

9. Patellar/ Quadriceps tendon rupture

• Mechanism of injury
o Low energy injury, sudden forceful contraction during attempt to stop fall
o Partial or complete rupture
• RF: more common in patients w DM, SLE, RA, steroid use
• History: Fall onto flexed knee then inability to extend knee
• Signs:
o Palpable gap btw patella and quadriceps
o May have hemarthrosis/effusion of knee
• Ix:
o Knee XR TRO patellar #
o Joint aspirate may show hemarthrosis
• Rx: surgical repair of tendon

! 114!
Tibia!and!Fibula!Fractures!

Fractures!

Tibia'and'
Fibula'
Fractures'

Tibial'
Diaphysis'
Fracture'

Tibial!plateau!
fractures!(refer!
to!knee)!

Pilon!fracture!
of!Distal!Tibia!
(refer!to!ankle)!

! 115!
1. Tibia and Fibula Fractures
• Mechanism of Injury:
o Forces
! Twisting force: Spiral fracture of both leg bones at different levels
! Angulatory force: Short oblique fractures; usually with separate triangular butterfly fragment
o Subcutaneous position predisposes to open fractures
! Direct injury (eg. motorcycle accident): May crush or split overlying skin (out " in)
! Indirect injury (spiral or oblique): Bone fragment pierces skin from within (in " out)
• Management
o Objectives
! Limit soft tissue damage and preserve skin cover
! Obtain and hold fracture alignment
! Recognise compartment syndrome
! Start early weight bearing (loading promotes healing)
! Start joint movements ASAP
o Low Energy Fractures
! Undisplaced # (or minimally displaced): Cast from thigh to metatarsal neck
! Displaced #: Reduction under GA + Cast application
! Skeletal Fixation (can be done where appropriate skills and facilities available)
• Locked intramedullary nailing (diaphyseal fractures)
• Plate fixation: Metaphyseal fractures
• External fixation: Metaphyseal and shaft fractures
o High Energy Fractures
! External fixation: Inflicts little damage to badly injured limb
o Open Fractures
! Antibiotics
• Gustilo I-IIIA: Broad spectrum cephalosporin
• Gustillo IIIB-C: Additional Aminoglycoside (gentamicin) + Metronidazole (soil contamination)
! Debridement
! Stabilisation: External fixation favoured for more severe injuries
! Soft tissue cover
! Rehabilitation
• Complications
o Vascular injuries: Popliteal artery
o Compartment syndrome
o Infection
o Malunion " Predispose to early OA
o Delayed-union/Non-union: Due to poor muscle cover hence poor blood supply
o Joint stiffness
o Algodystrophy (complex regional pain syndrome)

2. Tibial diaphysis fractures

• Mechanism of Injury:
o High intensity injury: associated w crush injuries and MVAs
o Most common long bone fracture
o Commonly open #
• Asssociated injury:
o Soft tissue, nerve and vessel injury common " assess neurovascular status!!
• Management:
o General principles:
! ATLS principles first!!
! Displacement is difficult to control
! Good reduction is required to ensure minimal shortening and angulation
! Healing time: 16 weeks on average
o Conservative management: closed injuries = closed reduction
! Long leg cast for 4-6/52
! Followed by below-knee cast until healed
o Surgical management:
! Indications:
• Definitive Indications: associated intra-articular and shaft #, open #, major bone loss, neurovascular injury, limb
reimplantation, compartment syndrome, floating knee
• Relative indications: associated intra-articular and shaft #, unstable #, inability to maintain reduction, relative
shortening of segmental #, tibial # with an intact fibula, transition zone #, polytrauma
• Delayed indications: failure to maintain reduction, unacceptable reduction, complications
! Open #: ORIF w external fixator
• Wounds on anterior surface heal poorly and may necrose
! Unstable injuries or failed closed reduction: IM nail
! Patients w high risk of compartment syndrome:
• Closed reduction and cast
• Admit and observe for compartment syndrome
• Prophylactic fasciotomy if operating on tibia fracture

! 116!
Foot!and!ankle!

Atraumatic! Traumatic!

Deformities' Ankle'injuries'
• Congenital'clubJfoot' • Ligament'injuries''
• Flat'foot' • Fracture'
• Pes'cavus'
• Hallux'Valgus'
• Hallus'Rigidus'
• Deformities'of'lesser'toes'

Generalised'diseases' Hindfoot'injuries'(talus!&!
• RA! calcaneum)'
• OA! • Fractures'of'talus'
• Gout! • Fractures'of'calcaneum'

Others' Midfoot'injuries'(navicular,!
• Disorders'of'tendo'achillis' cuboid!&!3!cuneiforms)'
• Diabetic!foot! • MidJtarsal'injuries'
• Tarsometatarsal'injuries'

Pain' Forefoot'injuries'
• Painful'ankle' (metartarsals!&!phalanges)'
• Painful'foot' • Metartarsal'fractures'
• Toenail'disorders' • Fracture'toes'
• Fractured'sesamoids'

!
! !

! 117!
 Examination of the Foot and Ankle • Isolate and test ROM of Subtalar jt: maximal dorsiflexion to lock
The preliminaries: Introduce yourself to patient, ask for permission to talus in ankle mortis (isolate talus and cup heel) and isolates
examine. Ensure adequate exposure (midthigh downwards w shoes inversion and eversion; compare both sides.
removed) but consider patient modesty also. Ensure good lighting & good • Isolate and test ROM of Midfoot jt: neutral flexion, immobilise
hindfoot w opposite hand (isolate with thumb on talar neck) and
positioning of bed.
test isolated movement of midfoot
SPECIAL TESTS
With patient standing: Ankle instability
LOOK – Front, Medial Back, Lateral With ankle in 10° plantarflexion
1. General appearance and vitals – any pallor, BP, HR etc. 1. Valgus and varus test
2. Posture: Knee and Foot alignment 2. Anterior Drawer test for insufficiency/ laxity of anterior
3. Foot and soles: Scars, Sinuses, Swelling, Lumps, Hair Loss, talofibular ligament (ATFL) – stabilise/immobilise tibia with L
Trophic changes, ulcerations, callosities hand, cup heel with R, keep ankle in abt 10deg plantar flexion
4. Forefoot: and apply anteriorly directed force on heel; compare amt of
& Toe defotmities, splaying laxity w other side
& Halux Valgus 3. Talar tilt – inversion and eversion force
& Crossed toes ** look out for generalised ligament laxity
& Hammer toes
Simmond’s test: for integrity of tendo archilles: prone position, foot
& Claw toes
5. Mid foot: overhanging the bed so that it is free to move; cup and squeeze calf
& Pes Planus or Pes Cavus muscles and observe for plantarflexion; likely that tendo archilles is torn if
6. Hind foot: plantarflexion doesn’t occur
& Achilles Tendon (swellings?) Coleman Block Test
& Heel alignment - Used to evaluates hindfoot flexibility and pronation of forefoot;
& Hindfoot Valgus/varus - initial deformity is in the forefoot followed by subsequent
& Hindfoot swelling changes in the hindfoot;
& Too many toes sign - test is performed by placing the patient's foot on wood block,
7. Clues 2.5 to 4 cm thick, with the heel and lateral border of foot on the
& Walking aid, shoes (patterns of abnormal/ block and bearing full weight while the first, second, & 3rd
asymmetric wear in the soles), orthosis. metatarsals are allowed to hang freely into plantar flexion and
8. Ask patient to tip-toe: pronation;
& Look at heel alignment: Valgus vs Varus - Interpretation:
(protection vs predisposition to sprains) o test is based on premise that there is fixed flexion of
i. Neurological cause—CP, SB, SCI 1st metatarsal;
ii. Muscular—Disuse, CMT, MD o this test negates effect that forefoot (first metatarsal
iii. Tendinous-- PTTD in plantar flexion) may have on the hindfoot in
& Look at calf contraction stance;
9. Quick inspection of knee (gross abnormalities) o if heel varus corrects while the patient is standing on
10. Squat the block, hindfoot is considered flexible;
11. Gait: Foot drop, stiff ankle, fixed equinus o if subtalar joint is supple & correct w/ block test,
then surgical procedures may be directed
With patient sitting down or lying supine to correcting forefoot pronation, which is usually due
LOOK to plantar flexion of 1st metatarsal;
1. Deformities of the Sole—Corns, callousities, Ulcers o if hindfoot is rigid, then surgical correction of both
2. Restng position of the foot: normally equinovarus forefoot & hindfoot are required;
FEEL Specific Conditions
ASK FOR PAIN 1. Posterior Tibial Tendon Dysfunction
1. General palpation: begin post to med malleolus (post tibial Inflammation of the posterior tibial tendon – acquired flat foot
tendon), over bony medial malleolus, along medial jt line, along (most common cause in adults). Progressive flattening of arch
ant jt line, over lateral jt line, bony lateral malleolus, post to a/w pain. May lead to OA
lateral malleolus (peroneal tendons), archilles tendon ! Examine tibial posterior (tenderness)
(tenderness or gaps in tendon) ! Perform Jack’s test
- Bone: metatarsal head, sesamoid bones ! Check Tendo Achilles tightness
- Tendon: extensor digitorium brevis (top of foot), 2. Hallux Valgus
tibialis posterior (posterior to medial malleolus), ! MTPJ dorsal osteophyte, pain with extension
peroneals (lateral malleolus), ATFL (lateral ! Test PROM, sesamoiditis, 1st TMTJ laxity
malleolus), plantar fascia 3. Pes Cavus (think Charcot Marie Tooth)
- Ankle joint line ! Claw toes
2. Increased warmth: suggestive of inflammation – RA/Gout ! Test tibialis anterior & peroneii
3. Tenderness: ! Test sensation & deep tendon reflexes
- Along the bone " Osteomyelitis (missing/decreased in CMT)
- Along joint lines " Septic Arthritis ! Champagne bottle legs
4. Joint Effusion ! Intrinsic Muscle wasting
5. Lumps: document in detail with layer of attachment ! Hand involvement
6. Jack’s test/Hubscher manoeuvre: in pes planus – extension ! Marionette Gait
of the big toe with weight bearing FINISH with examination of neurovascular status of foot and ankle.
- Arch formation (+ve): flexible flat foot Esp polio (sensory is normal) or CMT/ Pes cavus. Offer to examine the
- No arch (-ve): rigid flat foot knee.
MOVE
1. Peripheral pulses, Capillary Refill
Active ROM (combined movements), then Passive ROM (isolate and test 2. 5 Nerves that ss foot and ankle:
ROM of subtalar jt and midfoot jt) - Superficial peroneal nerve over dorsum of foot
• Active Dorsiflexion & Plantarflexion –observe from side and - Deep peroneal nerve in first web space
compare both sides - Saphenous nerve on medial border foot
• Active pronation and supination - Sural nerve on lateral border of foot
- Tibial nerve in sole

! 118!
General information
• Foot has a transverse arch and 2 longitudinal arches
o Medial arch: calcaneum, talus (apex), navicular, 3 cuneiforms, 3 medial metatarsals
o Lateral arch: calcaneum, cuboid, lateral 2 metatarsals
• Arches are maintained by
o Ligaments
! Spring ligament- from sustentaculum tali of calcaneum to navicular tuberosity
! Short plantar ligament- from calcaneum to cuboid
! Long plantar ligament- from calcaneum to 2/3/4 metatarsals
o Muscle tendons
! Medial arch by: tibialis posterior, tibialis anterior
! Lateral arch by: peroneus longus
• Movements
o Plantarflexion and dorsiflexion at ankle joint
o Pronation and supination at intertarsal and tarsometatarsal joints
! around axis through 2nd metatarsal
! pronation – sole turns laterally; supination –sole turns medially
o Abduction and adduction by rotation of leg below the knee
! toes turn toward or away from midline
! forced abduction or adduction may disrupt mortise by
1. diastasis of tibiofibular joint
2. tearing of collateral ligaments
3. fracturing of malleoli
o Inversion = plantarflexion + adduction + supination
Eversion = dorsiflexion + abduction + pronation
• Positions
o Equinus: downward pointing foot
o Calcaneus: upward pointing foot
o Plantaris: only forefoot pointing downward
o Pes valgus: pronation with abduction
o Pes varus: supination with adduction

Evaluation of foot complaints

• History: pain, swelling, loss of function, sensory changes, deformity, mechanism of injury, activity level of patient
• Physical
o Inspection, palpation, active and passive ROM, weight bearing status
o Neurovascular status
• X-rays: AP, lateral, oblique (as a minimum)

! 119!
1. Deformities
IDIOPATHIC CLUB FOOT (CONGENITAL TALIPES EQUINOVARUS)
• Incidence:
o 1 or 2 per 1000births: screened at birth by neonatologists
o Boys affected 2X of girls!
o Bilateral in 1/3 of cases
o Also seen in neurological conditions (myelomeningocele, arthrogryposis)
! Arthrogryposis: non-progressive condition characterized by multiple
joint contractures found throughout the body at birth
• Note difference between flexible/positional VS structural
o Flexible/positional –
! Able to dorsiflex foot; foot can be passively externally rotated
and has a full ROM
! Due to position in womb
! Rx: easily correctable PhysioRx and stretching
o Structural " requires intervention
! Idiopathic (mainly)
! Neuromuscular/paralytic (eg. hemiplegia CP, spina bifida;
peroneals <S1> not working, resulting in muscle imbalance)
! Syndromic (eg. distal type arthrogryphosis)
• Typical Signs: CAVE
o Midfoot Cavus
o Forefoot adducted (metatarsus) and supinated
o Hindfoot in varus
o Heel in equinus
• Clinical features
o Heel unusually small and high
o Normally foot can be dorsiflexed and everted until toes almost touch front of leg; in club-foot,
manoeuvre meets varying degrees of resistance
o Signs of severity:
! Deep creases appear posteriorly and medially
! Atrophic calf muscles
• Complications if untreated
o Secondary growth changes in bone (as skin and soft tissues of calf and medial side of foot are short and underdeveloped)
• Management: Painless, plantigrade, function (note: foot will always remain small due to tight ligaments)
o Principles: Correct early, fully and maintain correction
o Rule out associated disorders (DDH, spina bifida)
o Conservative (w/i 1 or 2 days of birth): manipulation & serial casting (up to 4wks) THEN Abduction orthoses
! Repeated manipulation: 4-6 manipulations wkly to fortnightly until external rotation of 60 degrees achieved
• Ponsetti Casting: Toe to groin casting with Plaster of Paris
• Order of manipulation (Distal to proximal – CAVE)
o Cavus – Dorsiflex first ray to correct cavus
o Metatarsus adductus – Reduce talus with counter pressure on medial distal tibia
o Hindfoot varus: Forefoot abducted in supination
o Equinus: not manipulated (forced dorsiflexion will cause vertical talus and rocker bottom foot)
" if equinus persists after forefoot correction, treat w surgical release of achilles tendon by percutaneous
tenotomy
! Foot abduction orthosis: maintenance of correction & prevent relapses!
• Dennis Browne boots: for infants
o 23 hrs/day for 3 months, then wean till child begin to cruise
o Then night and nap until 4 years old
• Moulded ankle-foot orthoses (for older children)
o Operative (for resistant cases) – SELDOM DONE
1. a)release capsular and ligamentous contractures and fibrotic bands
2. b)lengthen tendons to reposition foot
3. Hold with cast +/- K wires for 6-8 weeks
4. Maintain using Dennis Browne boots or customized orthosis for older
children
o For late or relapsed club foot:
! Revision of soft-tissue releases +/- shortening of lateral side of foot by calcaneocuboid fusion or
cuboid enucleation
! OR Gradual correction by circular external fixator (Ilizarov method)
o In adolescence: corrective osteotomies and fusions

! 120!
FLAT FLOOT (PES PLANUS)
• Definition: condition whereby arch of foot collapses w the entire sole of the foot coming into
complete/ near complete contact w the ground
• Examination
o Look
! In weight bearing position:
• Hindfoot: ankle neutral, subtalar joint in valgus
• Midfoot: planus
• Forefoot: pronation
• Foot: abduction
! Too many toes sign (in normal foot, only 5th and part of 4th toe seen; in flat foot more than Rocker'bottom'deformity'
that are visible)
o Move
! Tip toe/ dorsiflex – does medial longitudinal arch re-form (if re-forms, indicative of
flexible flatfoot)
! Jack’s test – great toe passive extension
o Special: Ligament laxity (if score 4 or more, indicative of ligament laxity)
• General principles of Rx:
o Indications for Rx:
! Rigit flatfeet
! Associated foot or lower leg pain
! Condition affects knees or lower back
o Use of orthotics: arch support (to be used for the rest of patient’s life) + exercises
recommended by podiatrist
o Sx as last resort: usually time-consuing and costly
• Infantile flat-foot (congenital vertical talus)
o Incidence: rare; usually bilateral
o Signs
! Midfoot: Rocker-bottom foot (medial arch not only flat but curves opp way from normal)
! Foot: valgus
o Investigations
! X-ray:
• Calcaneum in equinus
• Talus points into sole of foot
• Navicular dislocated dorsally onto neck of talus
o Management
! Operation ideally before 2 years (no passive correction as tendons and
ligaments on dorsolateral side of foot usually shortened)
• Flat-foot in children and adolescence
o Note: 90% of children less than 2 have flat foot
o Signs: when weight bearing, foot pronated, medial border of foot in contact
with ground, heel becomes valgus
1. Flexible flat foot (dynamic)
! Causes: rmber to check for laxity and tight TA
• Generalized ligamentous laxity
o All children have ligament laxity till abt 7
o Normal dvlpmental stage in toddlers " usually
disappears in a few yrs
• Tight tendoachilles: growth spurts creates muscle tightness
esp TA due to imbalance of muscle and bone growth
o Patient accommodates by everting foot causing arch to eventually 'Beighton'score'for'ligamentous'laxity'
collapse
• Collagen tissue disorders: eg. Marfans Talocalcaneal!bar!(coalition)!
! Symptoms: NIL
! Signs:
• Jack’s Test: Great-toe extension test (arch restored by dorsiflexing
great toe as plantar fascia tightens)
• Tip toe: heels invert and arch forms in flexible flat foot
! Management: If TA tight, stretching, good shoes, medial arch support
! Investigations unnecessary
2. Rigid flat foot/ spasmodic flatfoot (fixed)
! Cannot be corrected passively
! Causes (bone, ligament, muscular):
• Tarsal coalition (abnormal bar of bone connecting calcaneum to
talus/navicular) w or w/o peroneal spasm (Peroneal and extensor tendons
appear to be in spasm)
o Calcaneo navicular (9-12yo): do an oblique XR
o Talo-calcaneum (12-15yo): 50% bilateral; do CT
• Inflammatory joint condition
• Neuromuscular disorder – cerebral palsy
• Ligament – Marfan’s, Ehler Danlos

! 121!
 • Idiopathic
! Symptoms: pain
! Investigations:
• X-ray (AP, lateral, oblique): identify underlying disorders
• CT to demonstrate tarsal coalitions
! Management
• If due to underlying disorder (polio): splintage or operation + muscle rebalancing
• Spasmodic flatfoot: treat underlying problem; usually needs Sx
o Rest in cast or splint; remove bony irregularity; triple arthrodesis if pain intolerable
o Treat tarsal coalition if <30% involved, w soft tissue interposition (fat and EDB)
• Flat foot in adults
o Possible causes
! Constitutional flat-feet (asymptomatic for many years) causing pain after change in daily activities
! Recent onset:
• Underlying disorder (RA, general muscular weakness)
• Tibialis posterior tendon dysfunction (tendon inflamed or torn): Tibialis post. synovitis or rupture (esp unilateral
flatfoot) – may be due to trauma or repetitive impact (sports)
o Management
! For painful rigid flatfeet: footwear and arch supports
! For underlying disorder: treat disorder
! For tibialis post rupture: operative repair/ tendon replacement
o Signs
! Forefoot: pronated
! Midfoot: medial arches dropped, tuberosity of navicular prominent
! Hindfoot: heels in valgus, too many toes sign
o Investigations: X-ray
! Talometartarsal angle (line bisecting talus vs line through shaft of metatarsal
on lateral view: normal is 0)

This is a young boy with bilateral pes planus of the feet as evidenced
by a loss of medial arch of the foot. The foot also appears to be
pronated and the heels are in valgus with toes visible lateral to the
outer edge of the heel. (too many toes sign)
(ask pt to go on tip toes)
The pes planus is flexible as evidenced by inversion of the heels on tip
toeing and restoration of the arch on dorsiflexion fo the big toe. OR The
pes planus is rigid as evidenced by failure of the heels to invert on tip
toeing.
There are no other deformities of the foot noted.
The extensor and peroneal tendons (appear / did not appear) to be
in spasm.
There (is / is no) wasting of the muscles in the foot.
There are no scars / swelling / erythema of the overlying skin.
There (is / is no) tenderness of the foot over the ___________ on
palpation.
ROM was ___ for ankle dorsiflexion, ___ for ankle plantarflexion. OR
Ankle dorsiflexion was limited to ___ due to a tight Achilles tendon
(compensatory flat foot) while ankle plantarflexion was ___.
Inversion was ___ and eversion was ___ at the subtalar joint.
Rotation at midtarsal joint was ___.
There are no signs of joint hypermobility at the __________ joints.
There are also no signs of neuromuscular abnormalities.
I would like to end my examination by screening the spine, hip and
knees for any abnormalities.

PES CAVUS/ CLAW TOES

• Etiology
o CAUSES OF CLAW TOES
! Imbalance between intrinsic (lumbricals and interossei) and extrinsic (long flexors and extensors) muscles of the lesser toes
! More common in females / elderly / RA
! Can be 2° to neurological disorders • CHARCOT MARIE TOOTH DISEASE
• peripheral neuropathy – DM / CMT o Peroneal muscle atrophy
• LMN disease – polio o Pes cavus + claw toes
• UMN disease – CP / MS / stroke o Distal muscle atrophy (inverted champagne bottle legs)
• CMT: peroneal muscle atrophy presents in early adult o Bilateral foot drop / high stepping gait / weak ankle
life or puberty " progressive weakness of peroneal dorsiflexion
muscles, dorsiflexors, plantar flexors and intrinsic o Absent reflexes
muscles of the foot " claw toes + varus + caval o Slight / no sensory loss in the limbs
deformities of the forefoot and hind foot o Thickened nerves (type 3 CMT inheritance)
o CAUSES OF PES CAVUS o Optic atrophy
! Imbalance between the agonist and antagonist muscles in
the foot
! Neuromuscular disorders (intrinsic muscles weak):
• CP / FA / spinal cord tumours / syringomyelia
• Polio / CMT / polyneuritis / muscular dystrophy/ ?spina bifida
! Others: burns / compartment syndrome / malunion of calcaneal or talar #
• Signs
o Forefoot: clawed toes, callosities under metatarsal heads
o Midfoot: highly arched
o Hindfoot: heel often in varus; soft tissues in sole are tight
o Coleman’s block test
• Symptoms: Pain under metatarsal heads or toes (shoe pressure most marked)
! 122!
• Management
o Rule out spinal disorders and neuromuscular abnormalities –If deformity still mobile (as in early stages)
! Conservative: custom-made shoes with moulded supports
! Surgical: tendon rebalancing operation (long toe flexors released"
transplanted to extensor expansions to pull toes straight)
o Fixed deformities (as in later stages)
! Surgical: soft-tissue releases + transfers + arthrodesis of IP joints +/-
arthrodesis of hindfoot
• Investigations: X-ray " Talometartarsal angle (line bisecting talus vs line through shaft
of metatarsal on lateral view: normal is 0)

Thi is a patient with bilateral pes cavus deformity of the feet / pes cavus
deformity of the (left / right) foot as evidenced by an accentuated
longitudinal arch of the (feet / left foot / right foot) .
I also note that the (left / right) heel is inverted.
There is associated clawing of the _____ toes of the (left / right) foot
with flexion of the POP joints and DIP joints and hyperextension of the
MTP joints. The MTP joints are (subluxed / dislocated) .
I also note the presence of callosities / ulcers on the dorsal aspect of
the POP joints of the toes as well as on the plantar surface of the foot
over the heads of the metatarsal bones which are the pressure points.
In addition, I note that there is wasting of the intrinsic muscles of the
feet and the _____ muscles of the ______.
Otherwise, there is no other skin changes / swelling / scars noted.
There is tenderness over the IP joints of the clawed toes as well as the
metatarsal heads of the foot.
The claw toe deformity is (mobile / fixed) as the patient is (able /
unable) to straighten the toes on both active and passive movement of
the IP joints.
I would like to move on to do a neuro exam of the foot to look for
peripheral neuropathy which can present with pes cavus.
I would like to complete the examination by:
• Walking the patient to look for antalgic gait / foot drop / varus
deformity
• Examining the shoes for signs of abnormal wear
• Enquiring about the effect of the condition on his / her life

HALLUX VALGUS
• Incidence: commonest foot deformity
o Usually bilateral
• Risk factors: Idiopathic, hereditary, loss of muscle tone, RA, wearing enclosed footwear (narrow toe box with heels)
• Associated deformities: inflamed bunion, hammer toe, metatarsalgia, secondary OA of 1st MTPJ, callosities, pes planus
• Signs
o Lateral deviation and rotation of hallux
o a/w Bunion from hypertrophy of medial part of metatarsal head and
overlying bursa
• Symptoms
o +/- pain from
! Shoe pressure on inflamed bunion
! splaying of forefoot and muscle strain (metatarsalgia)
! associated lesser toe deformities
! secondary OA of 1st MTP joint
• Investigations: weight-bearing X-ray to assess
o Degree of metatarsal and hallux angulation
o Presence of OA of 1st MTPJ
• Management
o Adolescents
1. Conservative: footwear modifications (deep toe-boxes, soft uppers and low heels), physiotherapy
2. Operative (~30% recurrence in adolescents): corrective osteotomy of 1st metatarsal + soft tissue rebalancing around MTPJ
o Adults
! Operative: Indications – Pain, function, cosmesis
• Bunionectomy
• 1st metatarsal realignment osteotomy + soft-tissue rebalancing
• Keller’s procedure/ excision arthroplasty (removal of medial eminence + resection of base of prox phalanx)
• Arthrodesis if MTPJ very osteoarthritic
o Contraindications to surgery: Diabetes, PVD

1. Comment on hallux valgus (note angle) This is a patient with bilateral hallux valgus deformity of ___ degrees on
2. Comment on overriding toe if any the right foot and ___ degrees on the left foot. OR This is a patient with
3. Comment on bunion + overlying skin a hallux valgus deformity of ___ degrees noted on the (left / right) foot.
4. Look for callosities over the dorsal PIP joint of 2nd toe / plantar It (is / is not) associated with an overriding second toe.
surface I note that the big toe is rotated with the nail facing medially. / There is
5. Proceed to touch bunion no associated rotation of the big toe.
6. Move 1st MTP joint (comment on hypermobility + ROM)
7. Ask patient to stand " look for pes planus (if so, differentiate In addition, there is a bunion present on the (left / right) foot (with / with
flexible or rigid) no) erythema of the overlying skin suggestive of inflammation of the
8. Ask to look at hands + walk the patient bursa. (if transilluminable ! more likely a ganglion)
9. Request to look at shoes There are also callosities noted over the plantar surface of the (left /
right) foot / dorsal aspect of the PIP joint of the 2nd toe.
The bunion is (tender / non-tender) and (felt / did not feel) warm
on palpation.
! 123!
Tenderness (was / was not)) present on palpation of the first
metatarsophalangeal joint.
There (is / is no) hypermobility of the metatarsophalangeal joint
indicative of instability.
ROM was ___ for plantarflexion, ___ for dorsiflexion, ___ for abduction
and ___ for adduction.
Patient (has / does not have) pes planus which can be associated
with hallux valgus secondary to ligamentous laxity. This is evidenced by
a loss of medial arch of the foot. The foot also appears to be pronated
and the heels are in valgus with toes visible lateral to the outer edge of
the heel (too many toes sign). The pes planus is (flexible – normal
arch regained on tip-toe / rigid – failure of heels to invert on tip toeing) .
(ask to look at pt’s hands) I note there are no deformities of the small
joints of the hands or other deformities of the toes in the feet which may
suggest presence of RA.
(ask pt to walk) I note that patient has an antalgic gait, but no other
deformities of the heel and ankle. OR
Patient does not have an antalgic gait or any other deformities of the
heel and ankle.
I would like to complete my examination by:
• Assessing the ROM of the other toe joints
• Examining the shoes to look for abnormalities of weight bearing
• Enquire about the functional impairment caused by this condition

Bunions:
• Definition: localized painful swelling at the base of the big toe
o Joint is enlarged, toe is often malaligned
o Frequently assoc w inflammation
o Can be a/w degenerative joint dz (OA) or bursitis
• Epidemiology: 10x more common in women
• 2 primary causes: hereditary, shoewear
• Diagnosis and pathogenesis: a/w hallux valgus deformity
o Valgus alignment of MTPJ is aggravated by eccentric pull of EHL and intrinsics
o Secondary exostosis forms with bursa and thick skin creating the bunion
• Rx: for cosmesis or pain w shoes
o Conservative: properly fitted shoes and toe spacer
o Sx: removal of bunion w realignment of 1st MTPJ

HALLUX RIGIDUS (1ST MTPJ)

• Incidence: 2nd commonest deformity of 1st MTPJ
• Pathophysiology: primary OA of MTPJ of great toe
• Risk factors:
o Young adolescents and adults: trauma, OCD of 1st metatarsal head
o Old: gout, pseudogout, OA
• Clinical diagnosis:
o Symptoms
! Pain on top of great toe: Esp on walking esp on slopes or rough ground (big toe cannot dorsiflex
at MTPJ" push-off at end of stance phase painful)
! +/- diffuse lateral forefoot pain (due to increased weight-bearing on lateral foot to offload hallux)
o Signs
! Slightly antalgic gait
! Hallux is straight, MTPJ feels knobbly
! Tender dorsal bunion (osteophyte) at 1st MTPJ (usually confirms diagnosis)
! Limited ROM: Dorsiflexion restricted and painful (esp at end of ROM); plantarflexion less limited
• Investigations: X-ray " OA changes
• Management
o Lifestyle modifications:
! Rocker-soled shoe to allow foot to roll w/o dorsiflexion of MTPJ or in-sole orthotics
! Avoid toe dorsiflexion (squatting or kneeling)
o Pharmacological: paracetamol, NSAIDs
o Operative:
! Young:
• Extension osteotomy of prox phalanx (mimics dorsiflexion at IPJ)
• MT osteotomy: based on premise that metatarsus elevates or a long 1st MT are e underlying causes of hallux rigidus
! Old:
• Cheilectomy (remove osteophytes at dorsal edge of metatarsal head) to restore dorsiflexion
• Keller’s procedure/ joint arthroplasty (excision of base of prox phalanx): indicated in moderate to severe cases in
individuals w low functional dds who desire the maintenance of jt motion
o Cx are common: hallux weakness, elevation, floppiness, short hallux, dvlpment of transfer lesions under 2nd MTPJ
! Badly arthritic joint: arthrodesis of MTPJ
• Salvage procedure shld other Sx interventions fail and hallux rigidus is severe enough

! 124!
LESSER TOE DEFORMITIES

Hammer toe Mallet toe Claw toe Overlapping toes

Epidemiology Females, elderly, with RA

Pathophys -Imbalance btwn intrinsic (lumbricals & interossei) and extrinsic (long flexors & extensors) muscles of -Valgus big toe " 2nd
lesser toes toe ride on top of hallux
-For claw toes: -Congenital overlapping
• secondary to neuro disorders like peripheral neuropathy (CMT disease, DM), LMN disease 5th toe
(polio), UMN disease (CP, stroke, multiple sclerosis)
• pes cavus
LOOK Affects lesser toes (most commonly 2nd toe) Usually all lesser toes affected, Usually 2nd or 5th toe
may be bilateral
• Flexion deformity at PIPJ • Flexion deformity at DIPJ Flexion deformity at PIPJ & DIPJ
• +/- DIPJ extension • No PIPJ or MTPJ + hyperextension of MTPJ
• +/- MTPJ extension involvement
Corns on dorsally projecting Corns in forefoot and callosities
PIPJ and callosities under under metatarsal heads
metatarsal heads
FEEL Any tenderness? • 2nd toe: correct hallux
MOVE Is the deformity fixed or mobile? valgus
Mobile deformity Mobile deformity Mobile deformity • 5th toe: dorsal V/Y
Flexor-to-extensor tendon FDL tenotomy Flexor-to-extensor tendon transfer plasty + flexor-to-
transfer extensor tendon
Fixed deformity Fixed deformity Fixed deformity
transfer" hold with
• Resection of prox • Resection of middle • Resection of prox phalangeal
tape or Kwire for 6
phalangeal head & neck phalangeal head & neck head & neck +/- flexor and
+/- flexor and extensor +/- flexor tenotomy extensor release weeks
release • DIPJ arthrodesis • IPJ arthrodesis + tendon
• Fix toe in straight position • Amputation of distal ½ of transfers
with Kwire distal phalanx (to include • Extensor tenotomy for MTPJ
• Proximal phalangectomy nail and matrix) contractures
• PIPJ arthrodesis • Resection of metarsal heads of
Painful callosities the lesser toes
• Terminal phlangectomy
OFFER Watch patient walk + examine patient’s shoes + ask qns to assess effect of condition on his/her life
Management Footwear modification (Note: usually unhelpful for mallet toe)
Surgery options (details above): Tenotomy, Tendon transfer, Resection, Arthrodesis

2. Others
DISORDERS OF TENDO ARCHILLES
• Peritendinitis
o Pathophysiology: local irritation of paratenon around tendoachilles
o Symptoms: pain and swelling around tendoachilles
o Risk factors: athletes, joggers, hikers
o Management:
! Conservative: rest, ultrasound, heel raise
! Operative; excision of inflamed and degenerate tissue
• Archilles tendonitis
o Chronic inflammation from running and shoe-wear (high heels)
o May dvlp heel bumps (Haglund’s deformity: prominence of the posterior superior calcaneus where the archiles tendon laterally inserts
into calcaneus)
o Diagnosis:
! Pain, aggravated by passive stretching
! Tenderness, swelling
! Crepitus on plantar flexion
o Rx:
! Rest, gentle stretching, NSAIDs
! Proper footwear +/- orthotics
! Don’t inject steroids!!! (prone to rupture!)
• Rupture
o Pathophysiology: when pushing off (jump, run), calf muscle contracts but contraction resisted by body weight (usually involves
eccentric loading on a dorsiflexed ankle w knee extended; soleus and gastroc on maximal stretch) " rupture of degenerate tendon
! Rupture at musculous tendinous junction occurs most often in young ppl, but ruptures near the calcaneus also occur
! 125!
 o Risk factors
! Age >40yrs
! Long term steroid use
o Symptoms: feeling of having been struck just above the heel, inability to tip-toe
o Signs
1. Get pt to kneel on the chair This patient likely has a ruptured (left / right) Achilles tendon as I notice that there
2. Comment on step in the tendon is a step in the tendon. I would like to proceed to confirm my diagnosis.
(Gap seen and felt 5cm above insertion of
tendon (musculotendinous junction)) There is a palpable gap in the tendon just 5cm above the point of insertion of the
tendon. Plantarflexion on the (left / right) is weak, and not a/w tautening of
3. Ask patient for any pain tendon, consistent with the diagnosis.
4. Palpate tendon
5. Weak plantarflexion without tautening of Simmond’s test is positive on the (left / right) . Hence the diagnosis is a ruptured
tendon (pt in kneeling position, ask pt to push (left / right) Achilles tendon.
sole against your hand)
6. Perform Simmond’s test
(lack of plantarflexion on squeezing calf)
o Management
! Conservative (re-rupture rate 10%) in acute cases: 8weeks of casting heel in equinus to approximate tendon ends " 6weeks
of shoes with raised heel
! Operative (more reliable): Operative repair to equinus + the above OR a lockable brace (allows early ankle movement but
blocks tension on repaired tendon)
PAINFUL ANKLE
• Footballer’s ankle/ anterior ankle impingement syndrome
o Definition: painful mechanical limitation of full ankle ROM secondary to an osseous or soft-tissue abnormality
o Pathophys: repeated forced dorsiflexion " tearing of anterior capsule of ankle joint " subsequent bone spur formation (osteophytes)
aka anterior exostoses of the tibia " subsequent pain + limited ROM
o Rx:
! Acute phase:
• Conservative: NSAIDs, physioRx, orthotics, bracing
• Sx: arthroscopic excision and debridement
! Recovery phase:
• Posterior splinting for 1/52 w supportive brace and compression stocking
• physioRx for 2/52 for strengthening, ROM, proprioception and sports-specific rehabilitation
• Tenosynovitis
o often tibialis posterior or peroneal tendons
o Signs: tenderness and swelling localised to affected tendon
o Symptoms: pain aggravated by active movement against resistance
o Management: local injection of corticosteroids
• Rupture of tibialis posterior tendon
o Symptoms: pain (arises suddenly), may have felt the tendon snap
o Signs:
! Hindfoot: heel in valgus during weight bearing
! Midfoot: pes planus
! Tenderness around medial malleolus
! Active inversion of ankle painful and weak
o Management
! Physically active patients: operative repair or tendon transfer using FDL
! Poorly mobile patients: splintage
• Osteochondritis dissecans of talus
o Symptoms: pain, slight limitation of movement in ankle esp in young patients
o Investigations:
! X-ray: small osteochondral fracture of dome of talus
! MRI, Arthroscopy
o Management
! Articular surface in tact: restrict activities
! Separated fragment: operative removal
• Avascular necrosis of talus
• Chronic ligamentous instability

PAINFUL HEEL
Posterior heel pain
• Traction apophysitis (pulling osteochondritis)
o Mechanism: mild traction injury
o Suspect in: young boys
o Symptoms and signs:
! Pain and tenderness localized to tendoarchillis insertion
o Investigations: X-ray
! Increased density or irregularity of apophysis (but painless heel often
look similar)
o Management: raise heel of shoe, restrict strenuous activities for a few weeks
! 126!
• Retrocalcaneal bursitis
o Suspect in: older girls and young women
o Symptoms: painful bumps on back of their heels
o Signs: prominent posterolateral portion of calcaneum" shoe friction causes bursitis
o Ix:
! X-ray: look for Haglund deformity (# prominence of the posterosuperior aspect of the calcaneus)
! U/S
o Management:
! Conservative: Physiotherapy, Change footwear (use open back shoes to relieve pressure on the affected region, avoid shoes
with lace, pad heels by inserting heel cup in the shoe to help raise the inflamed region slightly above the shoe’s restricting heel
counter), NO STEROID INJX
! Operative: removal of calcaneal prominence (Haglund deformity)
• If fail conservative therapy & symptoms persist

On inspection, I note the presence of a ___ by ___ cm

hemispherical swelling over the Achilles tendon of the (left / right) Differentials include:
foot. There are no overlying skin changes or scars noted. • Retrocalcaneal bursitis
• Achilles tendon synovitis
I would like to move on to palpate the swelling. (ask pt for any pain • Gouty tophi (look for more tophi at pinna, MTP joint, elbow,
first) hands)
The surface is smooth, edges are well defined, and the swelling is • Exostosis (usually around the knee – distal femur, proximal
firm. It is lsightly tender and does not feel warm. It is not attached to tibia)
the overlying skin but it is fixed to the tendon. The swelling (is / is
not) fluctuant and not compressible.

Inferior heel pain

• Plantar fasciitis (COMMONEST CAUSE OF HEEL PAIN)
o Pathogenesis: chronic inflammation from repetitive strain injury & microtears of plantar fascia (run from medial calcaneal
tuberosity to heads of metatarsal bones)
o Risk factors:
! Men aged 30-60yrs
! Runners, jumpers, ballet dancers, obese individuals
! Association with systemic diseases (DM, enthesopathies like seronegative and seropositive arthritis)
o Symptoms:
! Intense pain on waking or after rest
! Subsides on walking
o Signs:
! Swelling and tenderness along plantar fascia: Mostly at medial calcaneal tubercle
! Pain with toe dorsiflexion (stretches plantar fascia)
o Ix: Lateral XR may show heel spur at insertion of fascia into medial calcaneal tubercle (NOTE: spur is reactive, not e cause of pain)
o Management:
! Conservative (90% resolve)
• Rest and NSAIDs (4-6months)
• Stretching exercises (loosen plantar fascia or tight tendoachilles); roll golf/tennis ball on heel
• Supportive shoes with heel cup
• Ice cubes
• U/S therapy to stimulate healing
• Corticosteroid injections
! Surgical in refractory cases (rule out nerve entrapment as cause of pain first!)
• Plantar fascia release (50% effectiveness at pain relief)
• Spur removal not required
• Calcaneal bone lesions: Infection, tumors (osteoid osteoma), Pagets disease, stress fracture

PAIN OVER MIDFOOT

• Crushing osteochondritis of navicular (Kohler’s disease)
o Suspect in: children <5yrs
o Symptoms: pain in midtarsal region
o Investigations: X-ray shows flattened navicular with increased density
o Management: no (resolves spontaneously)
• Overbone
o Ridge of bone on adjacent dorsal surfaces of medial cuneiform and 1st metatarsal
o Suspect in: adults with pes cavus
o Symptoms: pain over bump by shoe pressure
o Management: shoe adjustment" remove lump

! 127!
PAIN OVER FOREFOOT
Generalised pain
• Metatarsalgia (commonest expression of foot strain)
o Conditions that give rise to faulty weight distribution (forefoot deformities, prolonged walking or standing etc)" mismatch btwn
loads applied to foot, structure on which loads are acting, muscular effort to maintain structure.
• RA: Starts off at MTPJ" symmetrical and bilateral swelling and tenderness
Localised pain
• Sesamoiditis
o Inflammation of peritendinous tissues around sesamoids (esp medial)
o Causes:
! Acute: trauma, unaccustomed stress
! Chronic: sesamoid displacement, local infection, AVN
o Signs: pain and tenderness directly under 1st metatarsal head, aggravated by walking or passive dorsiflexion of great toe
o Management: conservative" injection " operative removal of sesamoid
• Freiberg’s disease (crushing osteochondritis of 2nd metartarsal head)
o Suspect in: young adults esp women
o Signs
! Tender bony lump of enlarged 2nd metatarsal head
! Painful movement of MTPJ
o Investigations: X-ray shows 2nd metatarsal head wide and flat
o Management
! Conservative: footwear modifications (moulded insoles)
! Surgical: operative synovectomy, debridement and trimming of metatarsal head
• Stress fracture (2nd and 3rd metatarsal bones)
o Suspect in: young adults after unaccustomed activity, old osteoporotic patients
! Other common sites of stress # (MCQ): head of femur, distal end of femur, tibia
o Signs: Affected metatarsal shaft feels thick and tender
o Investigations: X-ray
! Early: normal
! Later: fusiform callus around a fine transverse fracture
o Management: Rest
• Morton’s metatarsalgia
o Interdigital nerve compression" secondary thickening of nerve
o Suspect in: women aged ~50yrs
o Symptoms: pain in forefoot radiating to toes, aggravated by tight-fitting shoes
o Signs:
! tenderness over one of the intermetatarsal spaces (usually 3rd)
! pressure just prox to interdigital web may elicit pain and tingling distally
! Mulder’s click: painful click on squeezing metatarsal heads together
! ‘Blocking test’: pain relieved on injecting local anaesthesia beneath transverse intermetatarsal ligament
o Management
! Conservative: footwear modifications (protective padding and wider shoes)
! Operative:
• Nerve compression release by dividing tight transverse intermetatarsal ligament.
• Intractable cases: excision of ‘neuroma’

TOENAIL DISORDERS
• Ingrown toenail
o Nail burrows into nail groove" ulcerates and wall grows over nail
o Management;
! Conservative: cut the nail square, insert pledgets of wool into nail groove, keep feet clean and dry
! Operative excision or chemical ablation with phenol of affected portion of germinal matrix
! Rare: remove entire nail or ablate nail bed
• Overgrown toenail (onychogryposis)
o Nail becomes hard, thick and curved
o Management: chiropodist or complete excision
• Subungual bone growth
o Nail lifted from bed by exostosis growing on dorsum of terminal phalanx
o Investigations: X-ray shows exostosis
o Management: remove exostosis

3. Ankle injuries
GENERAL INFORMATION (EVALUATION OF ANKLE COMPLAINTS)
• History: pain, swelling, mechanism of injury, effect on standing/walking
• PE
o Neurovascular status
o Look, feel, move (dorsiflexion, plantarflexion)
o Also assess tenderness at knee (Maisonneuve), lateral and medial malleoli
o Special tests: anterior drawer (for ankle), talar tilt, squeeze test, simmond’s test, Thompson test
• X-ray
o Views: AP, lateral, mortise (30deg internal rotation to give true view of talus in tibiotalar joint)
! 128!
 ! Medial & lateral jt spaces should be symmetric and <4mm w no talar tilt" disrupted space signifies ligamentous or bony injury
! Signs of ligamentous injury:
• Widening of tibiofibular space, asymmetry of talotibial space, widening of medial joint space, tilting of talus
o When to x-ray (Ottawa ankle rules)
! Pain in malleolar zone, AND
! Bony tenderness over posterior aspect of distal 6cm of medial or lateral malleolus OR
! Inability to weight bear both immediately and in the A&E for 4 steps
o Foot x-ray series only required w (Ottawa foot rules):
! Pain in midfoot zone AND
! bony tenderness over navicular or base of 5th metatarsal OR
inability to weight bear both immediately and at A&E for 4 steps
• Ring Principle of the Ankle
o The ankle can be thought of as a ring comprising:
! a: lateral malleolus
! b: medial malleolus
! c: posterior medial malleolus
! d: deltoid ligament
! e: syndesmotic ligament (syndesmosis)
! f: calcaneofibular ligament

ANKLE LIGAMENT INJURIES

• Lateral ligament complex
o Responsible for lateral stability
o Comprises: ant talofibular, post talofibular, calcaneofibular
o Incidence: involved in >90% of ankle ligament injuries
! Freq of injury: ATFL > CFL > PTFL
o Mechanism of injury: inversion while ankle in plantarflexion
o Symptoms: Pain, tenderness, swelling and bruising anterior to lateral malleolus,
giving way
o Signs (ATFL injury):
! Tenderness max just distal and anterior to lateral malleolus
! Pain on passive inversion of ankle
! Anterior drawer test for grade III ATFL injury
! Carry out talar tilt test to test integrity of other ligaments
o Investigations (ATFL injury)
! X-ray views: AP, lateral, mortise, stress x-rays to demonstrate instability
only if operative repair in considered
! Localised soft tissue swelling +/- small avulsion of tip of lateral malleolus
or anterolateral surface of talus
• Recurrent lateral instability
o Symptoms: recurrent giving way or feeling of instability when walking on uneven surfaces
o Signs:
! Talar tilt test: ankle in neutral" stabilize tibia with one hand and force the heel into maximum
inversion" compare ROM with normal ankle
! Anterior drawer test: ankle in 10deg plantarflexion" pull heel forward
o Investigations: X-ray
! Talar tilt test: (stress X-ray in mortise view), 15deg of talar tilt, or 5deg more than normal
ankle " injury to CFL + ATFL
! Anterior drawer test: (lateral view), anterior displacement of 10mm, or 5mm more than
normal side" abnormal laxity of ATFL
• Medial ligament complex (deltoid ligament)
o Comprises: ant tibiotalar, post tibiotalar, tibionavicular, tibiocalcaneal
o Responsible for medial stability
o Investigations: X-ray
! (mortise view) widened medial joint space, diastasis of
tibiofibular joint, +/-talar tilt
o A/w fracture of lateral malleolus or tearing of distal tibiofibular
ligaments
• Recurrent ankle subluxation
o Aetiology: ligamentous laxity
o Joint (loss of normal proprioception)
! Internal derangement of anatomy
! Intra-articular loose body
o Treatment depends on cause
o Strengthening and balance training for neuropathic joint
! Ligament reconstruction for lateral laxity and talar tilt
! Arthroscopy / arthrotomy for internal derangement
• Grading and Rx of ankle ligamentous injuries
o Goal of therapy: decrease pain, restore ROM & regain strength
o Focus of rehabilitation (Note: allow sufficient healing of ligament first = 3wks)
! Restore full ROM at the knee
! Controlled strengthening: often in the knee, the functional strength of the quads, esp the VMO, is weak and atrophied

! 129!
 ! Sport-specific or function-based trng: upon achieving full strength and pain-free ROM in the lower extremity, the athlete can be
cleared to return to sport, most often without any brace or external support
Grade Pathology Signs Treatment
I Microscopic tear -Minimal tenderness and swelling; Non-operative
of collagen fibres pain but no gift -RICE (rest, ice, compression, elevation)
II Macroscopic tear -Moderate tenderness and swelling -Treat with activity: apply bandage/ brace (usualy in
of some collagen (not as painful as grade 1; pain on dorsiflexion and eversion; individualized to patient’s
fibres motion); solid end point to gift (opens discomfort; remove when swelling disappears)" begin
up and stops); physioRx exercise immediately" protective weight
-Some instability bearing instituted w crutches and stopped as soon as
patient can walk (usually few days) " usually return to
play within 2-3wks
III Complete tear of -Significant tenderness and swelling Non-operative
collagen fibres (?little or no pain) -RICE
-Significant instability (no end point -Brace w a hinged knee orthosis and crutches for 1-2wks
to ligament laxity) (in past: BK cast immobilization for 6 weeks: from knee
-Talar tilt (apparent on mortise view) to toes with foot plantigrade)" physiotherapy "
Usually return to play after >/=6wks

Consider operative repair in athletes

ANKLE DISLOCATIONS
• Commonly at the subtalar joint rather than tibiotalar joint (tibiotalar joint dislocation only in fracture dislocations as mortise holds joint strongly)
• Management
o Reduction done before X-ray: Ulceration may occur if delay

PERONEAL TENDON SUBLUXATION

Recurrent subluxation of peroneal tendon over the lateral malleolus due to
rupture of superior peroneal retinaculum

Look
• Painful snapping sensation over lateral ankle • Ankle deformity
• (+/- weakness, pain) • Swelling / bruising
• Chronic lateral ankle instability • Prominence of tendon with dorsiflexion / internal
MANAGEMENT rotation
• Surgical anatomical repair of the Bankart-type lesion of the superior Feel: Tenderness posterior to lateral malleolus, Clicking
peroneal retinaculum Move
• + below-knee plaster cast with foot in equinus x 6/52 • Flex knee and ask pt to dorsi- & plantarflex
• + physiotherapy • Inversion / eversion

4. Ankle fractures
• Fractures of the ankle involve
o ipsilateral ligamentous tears or bony avulsion
o contralateral shear fractures
• Pattern of fracture
o Determined by mechanism of injury
o Avulsion fractures are transverse
o Shear fractures are oblique if pure inversion / eversion
o Shear fractures are spiral if rotational force
MALLEOLI FRACTURES
• Mechanism of injury:
o (COMMONEST) abduction and/or lateral rotation of ankle "
! lateral malleolus sheers off at oblique angle
! medial side: strain may rupture deltoid ligament or produce transverse avulsion fracture of medial malleolus
o sudden adduction of ankle "
! medial malleolus sheers off
! lateral side: strain injury or fibular fracture
o forward lunge of tibia " posterior edge of tibia fractures against the dome of talus
o axial compression of ankle (fall from height)" shatters articular plafond of tibia
• Symptoms: Intense pain and inability to stand on leg, Swelling, deformity
• Signs: Tenderness over medial and lateral sides" suspect double injury

! 130!
• Classifications:
o Lauge-Hansen classification (based on adduced mechanism of injury" reduce displaced fragments by reversing injurious forces
during manipulation of ankle): 1st word refers to position of foot & 2nd word refers to direction of movement of the talus in relation to leg
o Danis Weber classification (based on level of fibular fracture relative to syndesmosis)
!
Danis Weber classification
Type A (Infra-syndesmotic):
• Transverse fibular fracture below tibiofibular
syndesmosis
• Avulsion of lateral malleolus below plafond
or torn calcaneofibular ligament
• +/- oblique or vertical fracture of medial
malleolus
Type B (Trans-syndesmotic)
• Oblique fibular fracture at syndesmosis
• +/- avulsion of medial malleolus or
rupture of deltoid ligament
• +/- fracture of posterior malleolus
• +/- disruption of anterior fibres of
tibiofibular ligament
Type C (Supra-syndesmotic)
• Fibular fracture above syndesmosis
• Fracture of medial malleolus OR disruption
of deltoid ligament
• Frequently tears syndesmosis
• +/- Maisonneuve fracture if at proximal
fibula
• Torn tibiofibular ligament OR ligament
avulses small piece of tibia
! 131!
Lauge-Hansen classification Prognosis (risk of
syndesmotic injury)
Supination-Adduction (Supination = inversion) Low risk of
• Sequence of injury syndesmotic injury
o Supination force may rupture portions of lateral collateral and ankle instability
ligaments or may avulse distal fibula, resulting in transverse
fracture below the level of intact syndesmosis;
o Adduction forces talus against the medial side of the joint,
resulting in vertical fracture of the medial malleolus
Supination-External rotation 50% risk of
• Most common (45-65%) syndesmotic injury and
• Supination and external rotation, resulting in oblique fracture at ankle instability
the level of the sydesmosis
Pronation-abduction (pronation = eversion)
• Sequence of injury
o Avulsion fracture of medial malleolus or rupture of deltoid
ligament;
o Abduction force then either ruptures the syndesmosis or ~100% risk of
avulses its bony attachment sites; syndesmotic injury and
o Lateral force from talus impacts and fractures fibula at or
ankle instability
above level of syndesmosis and ruptures interosseous
membrane
Pronation-external rotation
• Sequence of injury
o Transverse # of the medial malleolus or disruption of deltoid
ligament;
o External rotation then results in rupture of the anterior
tibiofibular ligament or its bony insertion;
o Oblique or spiral fracture of fibula above the level of the jt;
o Posterior injury with tibiofibular ligament rupture or avulsion
of posterior malleolus
• Fibular fracture may be proximal (i.e., Maisonneuve #, which is
a spiral # of the proximal third of the fibula a/w a tear of the
distal tibiofibular syndesmsis and the interosseous membrane)
*Note: Syndesmotic injury managed with a syndesmotic screw
• Management
o Reduce swelling (elevate leg +/-foot pump; may need to wait days)
o Reduction
! Undisplaced fractures: NWB BK cast
• Type A: stable hence minimal splintage with bandage or plaster slab
• Type B: if stable, apply below-knee cast with ankle in neutral" remove in 6-8weeks" physiotherapy
• Type C: fix
! Displaced fractures: reduce ASAP
• Type A: closed reduction + IF with screws " cast 6-8weeks
• Type B: closed reduction + IF " cast 6-8weeks
• Type C: ORIF " cast 6-8weeks
• NOTE: fix fibula with plates and screws; medial malleolus with screws
o Indications for ORIF
! fracture-dislocations
! type C fractures
! trimalleolar (lateral, medial, posterior) fractures
! talar shift or tilt
! failure to achieve or maintain closed reduction
• Complications
o Early
! Vascular injury in severe fracture-subluxation
! Wound breakdown and infection (esp diabetics)
o Late
! Incomplete reduction (common)" secondary OA
! Non-union of medial malleolus due to flap of periosteum" prevent with ORIF
! Joint stiffness" prevent with mobility
! Reflex sympathetic dystrophy (swelling and diffuse tenderness, trophic changes and osteoporosis)
! High incidence of posttraumatic OA from malunion / incomplete reduction
o Prognosis dependent upon anatomic reduction

POSTERIOR MARGINAL FRACTURE OF TIBIA

• Mechanism of injury: forward thrust of leg, resulting in fracture of posterior margin of tibial articular surface +/-malleolar fracture
• Investigations
o Lateral X-ray: check size and displacement of fragment
• Management
o Small posterior fragment: ignore
o Large/ displaced posterior fragment: ORIF with screw or buttress plate
• Complications: OA if incomplete reduction

PILON FRACTURE OF DISTAL TIBIA (COMMINUTED FRACTURES OF TIBIAL PLAFOND

• Mechanism of injury: severe axial compression of ankle joint (FFH) drives talus into tibial plafond,
leading to comminution of tibial plafond (cortical bone shatters and softer metaphyseal bone can also
be affected)
o Combination of talar # and distal tibial metaphyseal #, usually w intra-articular (damage to
articular cartilage) +/- comminution may extend up shaft of tibia
o 20-25% will be open #
• Types
o Type I: undisplaced
o Type II: minimally displaced
o Type III: markedly displaced

• Associated injuries/complications
o 30% will have ipsilateral injuries and 5-10% will have bilateral injuries
! Compartment syndrome
! Compression # of vertebral column, esp L1
! Contralateral # of: os calcis, tibial plateau, pelvis, acetabulum (vertical shear injuries)
! Vascular injuries
! 132!
 • Signs: severe swelling, fracture blisters
• Investigations:
o X-ray; CT in severe injuries
o Comminuted fracture of distal end of tibia, extending into ankle joint
• Management
o Conservative
! Pain relief + Abx prophylaxis (open #/ internal fixations) + Elevation (control soft tissue swelling) + splint (cast
immobilization if # is undisplaced)
o Surgical:
! Primary stabilization: calcaneal traction or external fixator (due to high risk of infection) for 2-3wks +/- fibular # fixation
! Definitive surgery after condition of soft tissues is optimized (blisters have epithelized, skin is wrinkled)
• Types: ORIF, external fixation, limited internal fixation w external fixation, percutaneous pinning
! Indications for surgery
• Open fracture
• Displaced fracture
o Articular fragments with gap of >2mm or step of >1mm
o Rotational malalignment
• Vascular compromise
• Compartment syndrome
o Post-op: elevation, post-op physiotherapy, partial weight bearing after 6 weeks
• Complications
o Secondary OA from cartilage injury

ANKLE FRACTURES IN CHILDREN

• Mechanism of injury: with foot fixed, leg is twisted to one side" tibial or fibular physis wrenched apart (usually Salter-Harris type 1 or 2)
• Incidence: 1/3 of physeal injuries
• Symptoms: pain, swelling, bruising
• Signs: Acute tenderness
• Investigations: X-ray
o undisplaced physeal fractures easily missed" repeat x-ray in 1wk with any hint of physeal widening
• Management
o Salter-harris 1 and 2 (extra-articular): treated conservatively
! With displacement: closed reduction under GA
• 3 weeks in full-length cast" 3weeks in below-knee walking cast
• Surgery to extract periosteal flap if required
o Salter-harris 3 and 4 (intra-articular)
! Undisplaced: treat in same way
! Displaced: ORIF with interfragmentary screws inserted parallel to physis" 6 weeks in below-knee cast
• Complications
o Malunion if reduction imperfect (usually valgus deformity)
! Children <10yrs: accommodated by growth and modeling
! Children >10yrs: osteotomy
o Asymmetrical growth
! Fusion of physis (usually medial half)" lateral half growth" distal tibia veers into varus
! If bridge is small, excise and replace with pad of fat
! If >1/2 physis involved/ child near end of growth period, perform supramalleolar osteotomy
o Limb shortening
! Early physeal closure in 20% of children
! Treatment: proximal tibial epiphysiodesis in opposite limb if child is young

5. Hind foot injuries

FRACTURE OF TALUS (RARE)
• Mechanism of injury: considerable violence (FFH, MVA) " axial loading or hyper-plantar flexion " talar neck drive into tibial margin
o Includes fractures of the head, neck, body, bony processes; dislocations, osteochondral fractures of superior articular surface, avulsion.
o Impt TRO potential associated injuries: spinal injuries, femoral neck #, tibial plateau #
• Symptoms
o pain, swelling of foot and ankle
o (if fracture displaced) deformity, tenting or split of skin" skin may slough and get infected
• Investigations: X-ray (AP or lateral) +/- CT
• Management: aim is revascularisation and fracture healing
o For trivial displacements: split plaster (BK cast), NWB " complete plaster when swelling subsides, in plantigrade position for 6-8wks
o For displaced fractures/ fracture dislocations: closed reduction" fixation with 1 or 2 lag screws" below knee plaster for 6-8weeks
o ORIF if above fails: to reduce displacement and prevent AVN or non-union
• Complications
o AVN
! Fractures of neck of talus has high risk of AVN of body (posterior fragment)
• Undisplaced: 0-10% risk of AVN
• Displaced: 100% risk of AVN
! 60% of talus covered by articular surface (7 articular facets!) thus decreased surface area for vascular perforation
! Blood supply of talus from distal to proximal
! Fracture fails to unite" posterior half of bone collapses" may need arthrodesis
! 133!
FRACTURES OF CALCANEUM
• Mechanism of injury: FFH onto heels" axial loading " calcaneum crushed or split against talus
• NOTE: >20% suffer associated injuries of spine, pelvis, hip (femoral neck) (as well as tibial plateau #, knee ligamentous injuries)
• Type of fracture
o Goals of Mx: prevent widened heel and maintain subtalar joint congruency
Description Management
Extra- • 25% of calcaneal injuries *Elevate and treat with ice
articular • involve anterior process, calcaneal Non-operative:
body, calcaneal tuberosity, Bandage" exercise (NWB for 4 wks, then partial for another 4 wks; early ROM)
sustentaculum tali, posterior part of
body Displaced avulsion of tuberosity need reduction + screw fixation " immobilise in
slight equinus (relieve tension on tendoachilles)
Intra- • oblique fracture that splits *Elevate and treat with ice
articular talocalcaneal articular facet +/- • Undisplaced: treat same as above
comminution • Displaced: ORIF with interfragmentary screws once swelling subsides"
splint and elevate" partial weight bearing when fracture heals (~8months)"
full weight bearing (restoration takes 6-12months)
o ORIF if depressed centrally or tongue-type #
o Closed vs open Rx is controversial: open has potential vascular Cx
" primary arthrodesis if severe
• Symptoms: Pain, swelling, bruising on soles
• Signs
o LOOK:
! Heel (viewed from behind): broader, shorter, flatter, varus tilt
! Obliteration of normal concavity below lateral malleolus
o FEEL: Tissues thick and tender
o MOVE: Subtalar joint can’t be moved; ankle movements possible
o Exclude compartment syndrome of foot (intense pain, extensive bruising,
decreased sensibility)
• Investigations
o X-rays
! Lateral, Broden’s view (oblique view of subtalar joint), axial views
! Bohler’s angle: measured at intersection of a line drawn btwn post. sup.
aspect of calcaneal tuberosity to highest point of post. articular facet and
another line drawn to ant. process of calcaneum
• normally 25-40deg
• decreased/ flattened in intra-articular fractures
! X-ray knees, spine, pelvis in severe injuries
o CT for definition of intra-articular fractures
• Complications
o Early
! Swelling and blistering " may jeopardise operative treatment
! Compartment syndrome (10%)
o Late
! Malunion (in closed reduction or injudicious weight-bearing)" calcaneal widening " increased shoe size and valgus foot
! Peroneal tendon impingement
• Lateral displacement of calcaneal body" compress peroneal tendons against lateral malleolus" operative paring down
of protuberant bone on lateral wall of calcaneum
! Insufficiency of tendoachilles due to loss of heel height
! Talocalcaneal stiffness and subtalar OA in displaced intra-articular fractures
! Chronic heel pad pain

6. Midfoot injuries
MID-TARSAL INJURIES
NOTE: Assume fractures in this region to be combination fractures or fracture-subluxations
• Symptoms
o Bruising, swelling of foot
• Signs
o Diffused tenderness across midfoot
o Deformities (medial mid-tarsal dislocation looks like ‘acute club foot’; lateral dislocation has valgus deformity, longitudinal stress
injuries have no obvious deformity)
o Exclude compartment syndrome
• Investigations
o Multiple X-ray views: ensure that all tarsal bones are clearly shown
o CT
• Management
o Ligamentous strains: Bandage until pain subsides" mobilise
o Undisplaced fractures: Elevate foot" below-knee cast" limited weight bearing on crutches" remove in 4-6weeks
o Fracture-dislocations
! Closed reduction under GA +/- K-wires" below knee cast for 6-8weeks (restoration in 6-8months)

! 134!
TARSOMETATARSAL INJURIES
NOTE: Sprains are common; dislocations are rare. Suspect fracture-dislocation in pain, swelling and bruising after an accident even with no
obvious deformity.
• Investigations
o Multiple X-ray views +/- CT for full extent of injury
! Medial edge of 2nd metatarsal should be in line with medial edge of 2nd cuneiform
! Medial edge of 4th metatarsal should be in line with medial side of cuboid
• Management
o Undisplaced sprains: cast for 4-6weeks
o Subluxation or dislocation: M&R under GA" fix with Kwires or
screws + cast
• Lisfranc Injury
o Mechanism: Twisting force; fall onto plantarflexed foot or direct
crush injury
o Injury
! Term used in general to describe a 2nd tarso-metatarsal
displacement injury
! Can be used specifically for injury to the Lisfranc
ligament (between medial cuneiform and base of 2nd
metatarsal)
! May be merely a ligament tear, dislocation
(tarsometatarsal joint) or fracture dislocation (speck
signl; shortened forefoot prominent base " ORIF)

7. Forefoot injuries
METATARSAL FRACTURES
• Anat: as with hand, 1st, 4th, 5th MT are relatively mobile while 2nd and 3rd are fixed
• Mechanism of injury: direct blow, twisting injury, avulsion fracture, repetitive stress (march fracture)
• Symptoms: pain and swelling
• Types
Fracture Mechanism Clinical Features Treatment
Avulsion of base of 5th MT Sudden inversion followed by • Oblique fracture ORIF if displaced
contraction of peroneus brevis • Tenderness at base of 5th MT
Jones Fracture (Midshaft 5 MT) Stress injury
th • Tenderness along shaft of 5th MT Non-weight bearing below
• Tends to displace due to knee (NWB BK) cast x 6/52
peroneus brevis and tilting ORIF if athlete
• Transverse fracture
• Prone to non-union as injury at
watershed area of BS
March # (below): shaft 2nd 3rd MT Stress injury
1st MT Fracture Trauma Painful 1st MT ORIF if displaced
If not: NWB BK cast x3ks then
walking cast x2wks
• Stress injury (march fracture)
o Risk factors: young adult (recruit or nurse), osteoporotics after operations that shorten big toe hence
extra stress on adjacent metatarsals
o Signs: tender shaft of 2nd/ 3rd MT & tender lump just distal to mid-shaft of metatarsal bone (usually
the 2nd)
o Investigations: X-ray normal at first" hairline crack" mass of callus or periosteal new bone
o Management: NO reduction nor splintage (support forefoot with Elastoplast and encourage walking)

FRACTURED TOES
• Management:
o Disregard fracture" encourage walking in suitably adapted boot
o If pain is marked, buddy splint for 2-3weeks

FRACTURED SESAMOIDS
• Mechanism of injury: direct injury (landing on ball of foot), sudden traction, repetitive stress (dancers
and runners)
• Symptoms: Pain directly over sesamoid
• Signs
o Tenderness over sesamoid
o Pain exacerbated by passive hyperextension of big toe
• Management
o Often unnecessary
o Local injection of lignocaine for pain
o Immobilise in short-leg walking cast for 2-3 weeks
o Excision of offending ossicle

! 135!
Spine!
Atraumatic! Traumatic!

Important'Concepts'
• Anatomy'
• Approach'
• Flexion'vs'Extension'
Neurological'Pattern'
• Radiculopathy'
• Myelopathy'
• Spinal'Stenosis'
• Cauda'Equina'Syndrome'
Cervical'Spine'
• C1'Fracture'
• Fracture'of'C2'Pedicle'
• Fracture'of'Odontoid'Process'
• Wedge'Compression'Fracture'
• Burst'Fracture'
• Flexion'Rotation'Injuries'
• Avulsion'of'C7'Spinous'
Process'
• Sprained'Neck'
• Cervical'subluxation'

Causes'of'Neurological'
Presentation'
• PID' Thoracic'Spine'
• Sondylosis'
• Spondylolisthesis'

Thoracolumbar'and'
Deformity' Lumbar'Spine'
• Scoliosis'
• Wedge'Compression'Fracture'
• Kyphosis'
• Burst'Fracture'
• FlexionJDistraction'
• Fracture'Dislocation'

Tuberculosis!(refer!to!
"infx")! Traumatic'Paraplegia'

! 136!
Examination of the Cervical Spine
The preliminaries: Introduce yourself to patient, ask for permission to
examine. Ensure adequate exposure (remove shirt) but consider
patient modesty also. Ensure good lighting, good positioning of bed.
LOOK (patient sitting upright, shirt off): back, side, front
1. Gait: myelopathic gait, high stepping gait
2. General appearance and vitals – any pallor, BP, and HR.
3. Posture: erect, splinting, tilting & cervical lordosis & symmetry
4. Deformity – namely tilting of the head (‘wry neck’)
- Normally, head is balanced over the shoulders
- Causes: torticollis (congenital), PID, inflamed neck glands,
cerebellar dysfunction, ophthalmologic disorders, congenital
scoliosis, atlanto-axial rotatory dislocation, etc
5. (Scars, sinuses, swellings) E.g. cervical lymph nodes
6. Tandem gait, rombergs etc
FEEL
Bony Landmarks:
(A) Thyroid cartilage: C4 superiorly, C5 inferiorly
(B) Hyoid Bone: C3
(C) Cricoid Bone: C6
1. Palpate for tenderness along spinous processes and
interspinous ligaments (from midline of the occiput downwards):
use either the tip of the thumb or tips of the index & middle
fingers for palpation of midline and paraspinal structures
- palpate for any step deformity (high-grade listhesis), and
ligamentous gap (more applicable for trauma).
2. Move hands along shoulder: feel for tenderness and warmth
3. ‘Trigger points’: Points that are extremely tender with radiation;
reproduces patient’s usual pain symptoms (myofascial pain
syndrome?).
4. Palpate paravertebral muscles for spasm
5. Sternocleidomastoid for swelling/tenderness
6. Lymph Nodes
MOVE
1. Flexion-extension:
- 50% at atlanto-occipital junction.
- Flexion: chin touch chest
- Extension: occipitomental line (chin to occipital
protuberance) at least 45° to the horizontal (usually more
than 60° in young patients)
2. Lateral flexion:
- Check symmetry of movements
- 45° both sides
3. Rotation
- 50% at the atlanto-axial joint (odontoid)
- check for symmetry of movements on both sides
- 80° both sides
SPECIAL TESTS
o For cervical spondylosis:
1. Spurling’s and Davidson’s tests (provocative test to elicit
pain along nerve root for patients w pain due to
compression of nerve roots or radiculopathy)
- Spurling’s: Active extension, lateral flexion and rotation
of patient’s neck to affected side with axial pressure "
radicular symptoms reproduced
- Davidson’s: Subsequent abduction of the arm on the
affected side " relief.
2. Cervical compression and distraction
- Axial loading of the cervical spine results in radicular
symptoms
- Distraction of the neck (pull the head superiorly)
relieves the symptoms.
o For cervical myelopathy:
- Lhermitte’s sign: neck flexion " electric shock-like
sensations (centre of back to all 4 limbs).
- Ulnar drift: flex shoulder w elbows extended and palms down
" ulnar deviation of little finger away from fingers
! 137!
o For thoracic outlet syndrome:
- Adson’s manoeuvre: palpate radial pulse, extend neck
actively and rotate it towards the side being tested and take
a deep breath. Positive is diminished pulse. (interscalene
compression of the subclavian neurovascular bundle)
- Wright’s Test: palpate radial pulse, passively abduct
shoulder. Feel for diminished pulse.
NEUROLOGICAL EXAMINATION (esp. if susp myelopathy)
UPPER LIMB:
1. Tone, clonus, muscle wasting
2. Power (0-5): C5-T1
3. Reflexes (0-3+) – biceps, triceps, brachioradialis
- C5/C6: ‘inverted supinator reflex’ (spastic finger flexors)
↓elbow flexion ↑finger flexion on tapping the brachioradialis
tendon; associated with hyper-reflexic triceps jerk.
- above C5: Shimizu’s sign (scapulo-humeral reflex) tap
spine of scapula, hyperactive when the scapula elevates or
the humerus becomes abducted.
4. Sensory function (0-3+)– compare with chin and not chest
pathology is in the cervical region and the chest belongs to
thoracic dermatomes
5. Proprioception – thumb
6. Cerebellar function – dysmetria, dysdiadochokinesia
7. Myelopathic hand:
(ii) Thenar atrophy
(iii) Hoffmann’s sign
- Hold patient’s right hand with examiner’s left hand, and
ensure wrist, MP and IP jts are extended " index
finger of examiner on volar surface of patient’s middle
finger and middle finger over dorsal surface and flicks
the patient’s distal phalanx downwards with thumb.
- Positive: flexion of the thumb and index finger
(iv) Grip and release test
- 20 cycles of open-close fist in 10 seconds.
- In cervical myelopathy the movement is slow, difficult
and incomplete.
(v) Finger escape sign
- When patient is asked to keep fingers adducted and
extended, the ulnar two fingers drift into flexion and
abduction within 30 seconds.
LOWER LIMB
1. Tone, clonus (usually increased tone in LL)
2. Power (usually decreased)
3. Reflexes – Knee, ankle, plantar reflexes (usually hyper-reflexic)
4. Sensation (usually decreased)
5. Proprioception and cerebellar function
- Gait is usually broad-based and clumsy, check Romberg’s.
DRE: For saddle anaesthesia, anal wink reflex, anal tone.
Examination of the Thoracolumbosacral Spine
The preliminaries: Introduce yourself to patient, ask for permission to
examine. Ensure adequate exposure (in underwear) but consider patient
modesty also. Ensure good lighting, good positioning of bed.
LOOK (patient standing, back and legs exposed)
1. General appearance and vitals – any pallor, the BP, and HR.
2. Front: scars
3. Side:
• Deformity
o Loss or exaggeraton of thoracic kyphosis/ lumbar lordosis
o Hyperkyphosis (protruded abdomen) – Scheuermann’s
disease (adolescents) or multiple osteoporotic compression
fractures in old ladies
o Gibbus deformity (angular kyphosis) – in infections like TB
• Skin changes
4. Back:
• Postural: Sciatic listing (relieve impingement)
• Deformity
o Scoliosis (postural/fixed) " Adam’s fwd bend test
! Imbalance in heights of shoulders (R usually higher
than L in idiopathic scoliosis), asymmetrical limb
waist distance, prominence of hips (R typically
more prominent), truncal shift (plumline from C7
spinous process should be in line with natal cleft;
measure amt of shift of plumline w ruler)
! Measure rib hump and lumbar hump w
scoliometer: measure w patient bent forwards
o Tilting of the shoulder (one of the shoulders/scapula
may be higher in thoracic scoliosis), pelvis (one of the
hip or iliac crest may be prominent in lumbar or
thoracolumbar scoliosis), limb shortening
• Skin changes: Birthmarks, hemangioma, neuro-fibromata, cafe
au lait spots, hariy patches/midline dimples
5. Gait: walk tendem gait (myelopathy), then toes only, then heels only
• Recognise antalgic gait, broad based gait, high step gait etc
FEEL
1. Palpate for
- Tenderness along spinous processes
- step deformity (high-grade listhesis)
- ligamentous gap (more applicable for trauma)
- Palpate from C7 (most prominent spinous process)
downwards " L4 (at level of imaginary line drawn btw iliac
crest) " sacrum: use either tip of the thumb or tips of index
& middle fingers for palpation of midline and paraspinal
structures
2. Palpate paravertebral muscles for spasm/ tenderness
3. Palpate area of sacroiliac joint: PIIS
4. Percuss for tenderness
- Pain on percussion " pathology in the antr vert body
(infection or tumour)
- Do a renal punch to exclude renal pathology
MOVE (mostly passive)
NOTE: There are no “normal” range of movements in the spine, but
assessment of ROM helps establish a baseline range that is useful for
future monitoring of disease progress or efficacy of Rx
1. Flexion-extension:
- Flexion: Schoeber’s test (“bend forward to touch your toes”)
– mark the level of the PSIS (1st bony prominence while
palpating the iliac crest posteriorly) and a point 10 cm above
it and another pt 5cm below it– increase in distance when
bending forwards should be >5cm.
- Extension: normally about 30° (support the pelvis)
2. Lateral flexion:
- “Slide your hand down side of ur leg as far as u can go”
- Touching knees should be normal
3. Rotation
! 138!
- Make patient sit down to fix pelvis OR stabilise iliac crest,
then cross arms over chest then rotate
- Angle between line joining shoulders and line joining ASIS is
the extent of rotation
NERVE ROOT TENSION SIGNS
1. Straight leg raising test (SLR)
- Knee extended, raise the leg being tested, checking
patient’s face to assess pain
- Stop when patient complains of pain & ask what kind of
pain: +ve SLR when there’s pain radiating into e lower limb
(radicular pain)
- note angle at which pain occurs
- Also assess cross-SLR – patient complains of radicular
pain in the affected side when the normal lower limb is being
raised
2. Lasegue test/ SNST (not commonly done, beware of
variations)
- With knee and hip flexed to 90 degrees each, slowly extend
knee and look out for radicular pain
- OR after measuring angle of SLR, lower LL by 5deg (or till
no pain) & dorsiflex ankle" +ve if radicular pain reproduced
- More specific than a simple SLR, because positive SLR can
be due to other causes e.g. hamstring tightness
3. Bowstringing test
- Hip flexed ~100°, knee flexed 80-90°: press biceps femoris
tendon (lat side of popliteal fossa) – should be no pain.
- Press medial to the tendon (common peroneal nerve)
- Positive test: pain radiates proximally and/or distally from the
point of pressure.
- Most useful confirmatory test of nerve root tension
Femoral Stretch Test: patient lies prone, hip extended and knee
flexed to 90deg. Cup hand on knee and support thigh, and leg
supported by forearm. L hand supported on hip and gently extend hip
to 15-20deg " +ve if patient complains of anterior thigh pain.
(test femoral root compression: L2, L3, L4)
Pump handle test: flex hip and knee of involved side and bring knee
across to opp shoulder
Positive if this increases pain in region of sacroiliac jt
Gaenslen’s Test (test femoral root: L2,L3,L4): lie supine w legs
hanging freely; flex both hips, then extend hip on involved side "
+ve if extension causes increase in pain in sacroiliac region
Patrick/Faber Test
- for sacroilitis – in young male, may indicate ankylosing spondylitis
- Flex, ABduct and Externally Rotate the hip (“4”) " L hand placed
on opposite ASIS and R hand placed on apex of “4” (knee)
- Positive if pain elicited in sacroiliac jt region on exerting downward
force on apex
NEUROVASCULAR EXAMINATION
1. Tone: ankle clonus
2. Reflexes (0-3+): DTR + Babinski reflex (+ve if big toe moves
up and small toes fan out)
3. Sensation by dermatome (0-3+): light touch + pain
4. Power (0-5): Particularly knee extension for L4; ankle and big
toe dorsiflexion for L5; ankle and big toe plantarflexion for S1
5. Pulses
6. PR
- Saddle anaesthesia (S3, 4, 5)
- Inspect anal orifice for tone (“crow’s feet”)
- Anal wink reflex – scratch perianal skin and watch for anal
wink
- Put finger in rectum to assess anal tone
FINISH by offering to examine the hip joint.
1.!Important!concepts
Anatomy!

!
!
History o Positive Babinski reflex
• Pain: Mechanical vs Pathological (inflammatory, infective, • Other medical illness: RA, AS, Down’s syndrome
tumour) Investigations
• Stiffness • Imaging
• Deformity o X-ray: bony alignment
• Neurological symptoms (radiculopathy vs myelopathy vs o MRI: nerve, soft tissue
specific cord syndrome) o CT: Bony details
• Systemic Review: Note that visceral pathologies can lead to o Bone scan: Screening metastasis
spine pain as well – eg. AAA • Blood Tests
Red flags of spinal conditions o FBC (infection, tumour)
• Suggestive of infection/ cancer o Renal panel
o Non-mechanical pain: Night pain (wake up, cannot o ESR (infection, tumour, spondyloarthropathies)
sleep), pain at rest, night sweats • Infection (nerve root/facet blocks)
o Constitutional symptoms: Fever, unexplained LOW Flexion vs Extension
(>10kg in 6 months), LOA • Mechanical Pain (as above)
o Medical history: Cancer, recent bacterial infection • Neurological Deficit / Pain
o Age of onset: <20years, >55years o Flexion: Worsens PID
o Obvious deformities o Extension: Worsens neurogenic claudication (spinal
o Thoracic back pain (metastasis) stenosis)
• Suggestive of spinal fracture: Trauma, osteoporosis, obvious Sites of Pathology
deformities • Vertebrae: Fracture, Tumour, Infection
• Suggestive of serious injuries • Disc: Discogenic degeneration, PID, Infection
o Cauda equina: saddle anaesthesia, bladder or bowel • Facet Joint: Degeneration, Instability
incontinence, disturbed gait • Nerve Root: Radiculopathy
o Neurological deficits • Spinal Cord: Myelopathy
o Pain for >4-6weeks • Ligaments: Stretched, torn
o Failure to improve with therapy Spine X-ray
o Bilateral leg pain • AP View
• Suggestive of high risk of permanent damage to nerve o Opening: Which level of spine (which levels shown)
o Significant muscle wasting/weakness o General comments
o Loss of tendon reflexes ! Posture: Scoliosis
! 139!
 ! Alignment: whether vertebral bodies are sit ! Prevertebral space –normally
squarely above each other • <6mm at C2 (above trachea)
! Osteopenic • <22mm or 1 vertebral body at C6 (below
o Pathology trachea)
! Parts ! Trauma
• Pedicles: ‘Owl winking’ sign • Fracture line
• Spinous processes: centered? • Displacement
! Vertebral body ! OA: LLOSS
• Vertebral body shape: Squaring? • Oblique view: defect in the pars inter-articularis (spondylolysis)
• Vertebral height " scotty dog sign
! Disc space
• Lateral View
o Opening
o General comments
! Posture: lordosis, kyphosis
! Alignment:
! Lines: Anterior vertebral, posterior vertebral,
spinolaminar, posterior spinous
! Osteopenic?
o Pathology
! Vertebral (loss of height, fragmentation,
displacement)
! Disc space (increasingly larger down the levels)

2. Neurological Deficit (NOTE: various patterns can co-exist)

RADICULOPATHY

• Pathology: Nerve root lesion resulting in neurological deficits of affected dermatomes and myotomes
• Causes
o PID
o Spondylosis – narrowing of neural foramen, facet joint hypertrophy, bony spurs
o Spondylolisthesis
o Other causes: CIN DVT M
• Presentation:
o Neurological defects
! Sensory: Pain, parasthesia, sensory loss
! Motor: Weakness, loss of reflexes
o Pattern
! Shooting pain down e leg according to compressed n. root (radicular pain)
! Isolation to specific dermatomes / myotomes
o PE: any test that triggers compression of nerve root will be positive (eg. SLR)
• Management
o ACDF (Anterior cervical discectomy and fusion), ACCF (Anterior cervical corpectomy and fusion)
o Anterior discectomy without fusion (artificial disc replacement)
! 140!
 • Dermatomes and Myotomes, Reflexes (Babinski’s Reflex: L5, S1, S2)
Level Motor Sensory Reflex
C4 Spontaneous respiration (diaphragm) Clavicles
Shoulder abduction
Regimental Biceps jerk/
C5 Elbow flexion (biceps, brachialis,
badge Supinator
brachiobrachialis)
jerk
C6 (radial nerve) Wrist extension (ECRL, ECRB) Thumb
C7 (median n.) Elbow extension (triceps), wrist flexion Middle finger
Triceps Jerk
C8 (ulnar nerve) Finger grip (FDP) Little finger
T1 Finger abduction/ adduction (interossei) Medial forearm
T2 Medial arm
T3 Armpit
Lvl Motor Sensory Reflex
L1 Underwear
L2 Hip flexion (iliopsoas; femoral nerve) Lateral quads
Knee extension (quads; femoral nerve)
L3 Lat & above knee Knee
Hip adduction (obturator nerve)
jerk
Ankle dorsiflexion (prominent TA tendon; deep peroneal n);
L4 Medial aspect of leg
hip abduction (superior gluteal nerve)
Big toe dorsiflexion (EHL)
L5 1st web space
Toes dorsiflexion (EDL)
Big toe plantarflexion (FHL)
Ankle plantarflexion (gastrocsoleus; tibial nerve) Sole of foot, lateral Ankle
S1
Knee flexion (sciatic n) heel jerk
Hip extension (inferior gluteal n)
S2 Posterior thigh

• DDx (rmber that conditions can co-exist!):

o Thoracic outlet syndrome: look for signs of limb ischemia
! Do Roos test and Adson’s manouvre
! a/w ulnar nerve palsy
o Carpal tunnel syndrome or ulnar nerve entrapment: s/s worse at night and may be postural
! Nerve conduction studies, electromyography
o Rotator cuff lesions: abnormal shoulder movements, no neurological signs
o Cervical tumour: symptoms are constant

Mr / Mdm XXX is a __ years old (race) gentleman / lady, Past Medical History
premorbid status: (ADL independent, community ambulant – w / wo aid) , Mr / Mdm XXX has a past medical history of ___________ for (duration) .
occupation: ____________________, (note any DM & peripheral neuropathy)
with a significant PMHx of , He / she also does not have a history of peptic ulcer disease / GI bleeding.
presenting complaint: currently presents with a (duration) history of neck He / she had previous operations for ____________.
pain associated w (duration) of (numbness / weakness) in e (left / right) UL. He / she has NKDA and is currently on ___________ for her medical conditions.

The neck pain started (duration) ago and has gotten progressively worst.
He / she describes the pain as (nature) .
It is mechanical in nature, aggravated by movement such as (type of activity)
and relieved by rest.
The pain is localised at the (site) of the neck (and shoots down to the lateral
aspect of the arm / forearm / thumb / fingers / with no radiation) .
Current pain score is ___ & the pain (affects / does not affect) his / her sleep.
There is no hx of any specific activity that precipitated e onset of e pain initially.
There (is / is no) associated stiffness in the back especially in the morning
that does not last more than 30 mins.
In addition, he / she experiences (numbness / weakness) over the (site) of
his / her upper limb that has gotten progressively worst over the last (duration)
. There are no associated neurological symptoms such as weakness or
numbness in the lower limb. He / she also does not complain of clumsiness or
unsteady gait.
Functional Status
Currently, his / her symptoms have limited his / her function such as (carrying
heavy objects / ability to work / drive) .
Family History
He / she (has / has no) family history of cancer or similar back pathologies.
Social History
He / she (does not smoke / smokes / is an ex-smoker and has quit XX years
ago) , ( sticks/day x years).
He / she (has / does not have) a habit of regular intake of alcoholic drinks.
He / she has (good / poor) social support. He / she works as a _________
and his / her condition affects her job. He / she lives with his / her ________. His
/ her main caregiver is his / her ______________.
He / she lives in a residential (with / without) lift landing. There (is / is no)
squatting toilet in the house.
Currently, the family (does not have any financial issues / is receiving financial
aid from ) .
In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with co-
morbidities of ________________, currently presenting with chronic neck pain
for (duration) associated with progressive (numbness / weakness) of the
(left / right) upper limb which has failed to improve with conservative
management and has affected his / her daily functioning.

Systemic Review My provisional diagnosis will be that of possible ___ cervical radiculopathy
He / she does not have any red flag symptoms like changes in bowel or urinary secondary to cervical spondylosis / PID.
habits, fever, or constitutional symptoms like loss of weight or loss of appetite.
There (is / is no) history of previous trauma to the neck. PHYSICAL EXAMINATION
On physical examination, Mr / Mdm XXX is alert and comfortable at rest.
Management so far (options tried) Vitals: Her PR is _______, RR is _______ and BP is _______. (SpO2:
He / she was treated conservatively with __________ for the past (duration) . ______; VAS: _____.)
However, the above have not been able to control his / her symptoms. He / she Heart: S1S2 were heard on auscultation.
is keen for operation as his / her symptoms affect his / her functioning. Lungs: Lungs are clear.
Abdo: Soft, non-tender

! 141!
 Power was:
He / she (does / does not) have wrying of the neck or other abnormal posture. ___ for shoulder abduction,
There (is / is no) wasting of the trapezius muscles noted. ___ for elbow flexion,
There (is / is no) (skin changes / previous scars / swelling) arnd e neck region. ___ for elbow extension,
___ for wrist extension,
Palpation (revealed / did not reveal) tenderness over the cervical vertebrae or ___ for finger flexion and
paravertebral muscle spasm. ___ for finger abduction
Creptius was felt on flexion of the neck. (on the left / right arm) and full in the (left / right) arm.
Flexion of the neck was ____.
Extension of the neck was ____. Sensation was decreased over e (C5 / C6 / C7 / C8 / T1) dermatome in e
Lateral flexion was ____ bilaterally and lateral rotation was ____ bilaterally. (left / right) arm and normal in all dermatomes in e (left / right) arm.

Lhermitte’s test was negative. Neurological examination of the lower limb was normal.
Spurling’s test was positive.
I would like to complete the examination with a digital rectal examination to rule
There is marked wasting of the (biceps / triceps / intrinsic muscles of the hand) out cauda equina syndrome.
noted.
Pronator drift was negative, no finger escape sign noted. In summary, Mr / Mdm XXX has signs consistent with that of a _____
Tone in the upper limbs was normal. radiculopathy in the (left / right) arm as evidenced by a decreased (biceps /
(Biceps / triceps / supinator) reflexes were (normal / absent) over the (left / triceps / supinator) jerk, loss of power in ________ and loss of sensation over
right) arm. the (C5 / C6 / C7 / C8 / T1) dermatome. Spurling’s test was positive when the
Hoffman’s reflex was negative bilaterally. neck was flexed to the (left / right) . No other abnormalities were noted on
inspection and palpation of the neck. ROM of e neck was limited to _____ / full.

MYELOPATHY
• Pathology: Compression of spinal cord (cervical or thoracic)
o C5-6 > C4-5 > C3-4 > C6-7
• Causes:
o Common: Cervical spondylosis (bony spurs and thickened ligament), PID
o Others: infection, trauma, tumours, demyelinating disorders, vascular disease
o Anatomically (applies for spinal stenosis?)
! Anterior: protruding disc, posterior syndesmophyte, ossification of posterior longitudinal ligament (OPLL)
! Anterolateral: jts of Luschka (uncovertebral jt)
! Lateral: cervical facets (thickening, bony spurs)
! Posterior: ligamentum flavum
• Presentation: think of dorsal cord vs ventral cord vs lateral cord vs total cord vs pure motor vs central cord vs CES
o Clumsiness in hands and legs (first symptom):
! Gait disturbance (ataxic, broadbased, clumsy) – damage to ascending proprioception fibers
! Loss of dexterity (clumsiness of fine actions) – fewer nerves supplying muscles has decreased capacity for modulation;
strength is usually normal because muscle can hypertrophy to compensate
o Neurological
! Sensory:
• Parasthesia but usually not significant pain
• Numbness (depends on part compressed –spinothalamic/ DCML)
• Tightness, hot or cold sensations in the trunk
• Tingling in the legs
! Autonomic: Bladder and bowel symptoms (severe cases)
o TRO malignancy: LOW, LOA, malaise…
• Signs
o Clinical picture: LMN signs at level of lesion and UMN below level of lesion
o Upper Extremity
! Finger escape sign: patient hold out hand w fingers extended and the medial fingers drift into flexion
! Hoffman’s
! Lhermitte’s sign: Parasthesia down limbs on neck flexion
! Grip and release: Less than 20 in 10s
! Inverted brachioradialis reflex
! Jaw jerk
! Scapulohumeral reflex
o Lower Extremity: Hypertonia (Babinski’s sign, clonus, may have involuntary spasms in legs), hyperreflexia, Oppenheim’s sign
(dorsiflexion of big toe elicited by downward irritation of medial side of tibia)
• Investigations: EXCLUDE TUMOUR
o Plain X Ray
o CT – bony spurs and ligament ossification
o MRI – disc prolapse and cord compression
o Special tests/criterion
! Pavlov’s ratio: Ratio of canal diameter to AP width of vertebral body (normal:
≥ 1; abnormal ≤ 0.85)
! Sagittal diameter of midcervical canal (post surface of vert body to base of
spinous process) <11mm
• Management
o Conservative
! Analgesics, collar, isometric exercises, gait training
! Avoid manipulation and traction

! 142!
 o Canal widening procedure (almost always requires Sx; else will worsen)
! Anterior approach: Anterior cervical discetomy and fusion (ACDF) or anterior cervical corpectomy and fusion (ACCF)
! Posterior approach: Laminoplasty or Laminectomy & fusion
Mr / Mdm XXX is a __ years old (race) gentleman / lady,
premorbid status: (ADL independent, community ambulant – w / wo aid) ,
occupation: ____________________,
with a significant PMHx of ,
presenting complaint: 1. (duration) hx of neck / subscapular / shoulder pain
2. (duration) of numbness / weakness in the right /
left upper / lower limbs
3. (duration) of unsteady gait
The neck pain started (duration) ago and has gotten progressively worst.
He / she describes the pain as (nature) . It is mechanical in nature, aggravated
by movement such as (type of activity) and relieved by rest. The pain is
localised at the (site) of the neck and (radiates into the arms bilaterally / has
no radiation) . Current pain score is ___ and the pain (affects / does not affect)
his / her sleep. There is no history of any specific activity that precipitated the
onset of the pain initially.
There (is / is no) associated stiffness in the back especially in the morning
that does not last more than 30 mins.
In addition he / she experiences (progressive / non-progressive) (numbness
/ weakness) over the (site) of her bilateral (upper / lower) limb for the last
(duration) . He / she also complains of an increasingly unsteady gait with
(weakness / stiffness of the LL) and weakness & clumsiness of the hands for
the last (duration) .
Functional Status
Currently, his / her symptoms have limited his / her function such as (loss of
fine motor control in the hands secondary to sensory deficits: using chopsticks,
difficulty holding a pen to write) .
Systemic Review
He / she does not have any red flag symptoms like changes in bowel or urinary
habits, fever, or constitutional symptoms like loss of weight or loss of appetite.
There (is / is no) history of previous trauma to the neck.
Management so far (options tried)
He / she was treated conservatively with __________ for the past (duration) .
However, the above have not been able to control his / her symptoms. He / she
is keen for operation as his / her symptoms affect his / her functioning.
Past Medical History
Mr / Mdm XXX has a past medical history of ___________ for (duration) .
(note any DM & peripheral neuropathy)
He / she also does not have a history of peptic ulcer disease / GI bleeding.
He / she had previous operations for ____________.
He / she has NKDA and is currently on ___________ for her medical conditions.
Family History
He / she (has / has no) family history of cancer or similar back pathologies.
Social History
He / she (does not smoke / smokes / is an ex-smoker and has quit XX years
ago) , ( sticks/day x years).
He / she (has / does not have) a habit of regular intake of alcoholic drinks.
He / she has (good / poor) social support. He / she works as a _________
and his / her condition affects her job. He / she lives with his / her ________. His
/ her main caregiver is his / her ______________.
He / she lives in a residential (with / without) lift landing. There (is / is no)
squatting toilet in the house.
Currently, the family (does not have any financial issues / is receiving financial
aid from ) .
In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with co-
morbidities of ________________, currently presenting with chronic neck pain
for (duration) associated with progressive (numbness / weakness) of the
(left / right) (upper / lower) limbs and unsteadiness in gait which has failed to
improve with conservative management and has affected his / her daily
functioning.
! 143!
My provisional diagnosis will be that of possible cervical myelopathy secondary
to cervical spondylosis / PID.
PHYSICAL EXAMINATION
On physical examination, Mr / Mdm XXX is alert and comfortable at rest.
Vitals: Her PR is _______, RR is _______ and BP is _______. (SpO2:
______; VAS: _____.)
Heart: S1S2 were heard on auscultation.
Lungs: Lungs are clear.
Abdo: Soft, non-tender
He / she (does / does not) have wrying of the neck or other abnormal posture.
There (is / is no) wasting of the trapezius muscles noted.
There (is / is no) (skin changes / previous scars / swelling) around the neck
region.
Palpation (revealed / did not reveal) tenderness over the cervical vertebrae or
paravertebral muscle spasm.
Creptius was felt on flexion of the neck.
Flexion of the neck was ____.
Extension of the neck was ____.
Lateral flexion was ____ bilaterally and lateral rotation was ____ bilaterally.
Lhermitte’s test was positive.
Spurling’s test was negative.
There is marked wasting of e (biceps/ triceps/ intrinsic muscles of e hand) noted.
Pronator drift was negative, with finger escape sign noted.
Tone in e (upper / lower) limbs was normal. Clonus was elicited in e lower limbs.
(Biceps / triceps / supinator) reflexes were (normal / absent) over e (L/ R) arm.
He / she was hyperreflexic in the lower limbs.
Hoffman’s reflex was positive bilaterally.
Power was:
___ for shoulder abduction,
___ for elbow flexion,
___ for elbow extension,
___ for wrist extension,
___ for finger flexion and
___ for finger abduction
(equal bilaterally / the left / right arm) .
Power was ___ for hip flexion, ___ for knee extension, ___ for knee flexion, ___
for ankle dorsiflexion, ___ for ankle plantar flexion bilaterally.
Pin prick sensation was decreased over the (C5 / C6 / C7 / C8 / T1)
dermatome in the upper limb / (L2 / L3 / L4 / L5 / S1) dermatome in the lower
limb. Proprioception and vibratory sensation was (lost / present) in the LL.
Mr / Mdm XXX has a (broad based / spastic) gait on walking.
Rhomberg’s test is (positive / negative) .
He / she (is / is unable) to perform tandem gait.
I would like to complete the examination with a digital rectal examination to rule
out cauda equina syndrome.
In summary, Mr / Mdm XXX has signs consistent with that of a _____
myelopathy as evidenced by a positive Lhermitte’s test, spastic broad based
gait, inability to perform tandem gait and signs consistent with a UMN lesion as
evidenced by presence of clonus, hyperreflexia, generalised weakness in the
lower limbs and presence of finger escape sign, positive Hoffman’s reflex,
hyperreflexia of the triceps & biceps jerk and weakness in the upper limbs. In
addition, he / she has loss of pin prick sensation, proprioception and vibratory
sensation in the lower limbs and loss of pin prick sensation over the (C5 / C6 /
C7 / C8 / T1) dermatomes in the upper limbs. Examination of the neck also
revealed creptius with restriction of lateral flexion and rotation.
SPINAL STENOSIS
• Pathology: Narrowing of spinal canal resulting in compression of spinal cord (if cervical) or cauda equina (because spinal cord ends at
L1/2 and spinal stenosis often at L4,5, S1 level)
• Causes
o Spondylosis leading to bony spurs and hypertrophy of facet joint
o Spondylolisthesis (usually degenerative; spondylolytic too)
o PID
• Presentation: root canal vs central canal stenosis (signs are variable depending on site & severity of stenosis)
o Neurogenic claudication – during walking, nerves require greater blood supply; hence demand outstrips supply; also due to epidural
venous congestion
! Posterior thigh, calf or buttocks cramping pain (travel down leg), weakness, numbness or parasthesia after standing
upright/walking (note: leg pain >>>>> back pain, unless back pain due to underlying pathology)
! Relieved by flexion (decrease stenosis) – pain worse when extends " patient often stands in slight flexion
! Segmental sensory deficits, decrease power, decrease reflexes
o NOTE: diagnosis mainly made w Hx; PE usually unremarkable

Neurogenic Claudication Vascular Claudication

Claudication distance Variable – position dependent Consistent
Less pain Walking uphill – due to spine flexion Walking downhill – less effort
Relief ‘Park bench to park bench pain’ – pain only relieved on sitting ‘Shop window to shop window pain’ – pain relieved by
(where spine is flexed); pain even on standing resting (even if standing)
Night pain Absent – patient sleeps in lateral decubitus fetal position Present
***Also ask for PMHx of PVD, hx of smoking etc…always check UL for polyneuropathy and LL for signs of PVD
• Imaging
o Lateral view Xrays – show degenerative spondylolisthesis, disc degen, OA, measure spinal canal
o MRI for surgical planning
o CT myelogram (waisting of dye column, posterior indentation, extent of narrowing)
• Management
o Conservative: education on spine posture
o Surgical
! Wide laminectomy – decompression for nerve root compression (will not improve backache)
• May have Cx of spinal instability " instrumentation and fusion
! +/- Segmental fusion – for spinal instability

Mr / Mdm XXX is a __ years old (race) gentleman / lady,
premorbid status: (ADL independent, community ambulant – w / wo aid) ,
occupation: ____________________,
with a significant PMHx of ___________________,
presenting complaint: currently presents with a (duration) history of low
back pain associated with (duration) history of (bilateral / left / right) leg
pain on walking.
The low back pain is (nature) , with a pain score of ___, shooting down the
(anterior / lateral / posterior) aspect of the thigh(s) and the (anterior / lateral /
posterior) side of the leg(s) to the (dorsum / sole) of the feet bilaterally (right
> left / left > right) upon walking (distance) or even when he / she is
standing.
The leg pain is aggravated by standing upright and walking up slope, but
persists even when he / she stops walking. It is only relieved by (flexion of the
back / sitting down / walking down slope) . There is no associated rest pain in
the lower limbs.
In addition, he / she experiences (progressive / non-progressive) weakness of
the (left / right) lower limb and associated numbness over the (site) of her
(L/ R) LL for the past (duration) , usually after standing upright or walking.
There (is / is no) associated stiffness in the back especially in the morning
that does not last more than 30 mins.
Functional Status
Currently, his / her symptoms have limited his / her daily function.
His / her walking distance is limited to ______ from ______ previously, (with /
without) a walking aid.
He / she also does not have a history of peptic ulcer disease / GI bleeding.
He / she had previous operations for ______________.
He / she has NKDA and is currently on __________ for her medical conditions.
Family History
He / she (has / has no) family history of cancer or similar back pathologies.
Social History
He / she (does not smoke / smokes / is an ex-smoker and has quit XX years
ago) , ( sticks/day x years).
He / she (has / does not have) a habit of regular intake of alcoholic drinks.
He / she has (good / poor) social support. He / she works as a _________
and his / her condition affects her job.
He / she lives with his / her ________. His / her main caregiver is his / her
______________.
He / she lives in a residential (with / without) lift landing. There (is / is no)
squatting toilet in the house.
Currently, the family (does not have any financial issues / is receiving financial
aid from ) .
In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with co-
morbidities of ________________, currently presenting with symptoms
suggestive of mechanical axial back pain and neurogenic claudication,
associated with a ______ radicular pain, evidenced by a low back pain that
shoots down the ______ that is associated with weakness of the lower limb and
numbness over the ____ dermatome.
My provisional diagnosis will be that of spinal stenosis.
PHYSICAL EXAMINATION

Systemic Review On physical examination, Mr / Mdm XXX is alert and comfortable at rest.
He / she does not have any red flag symptoms such as changes in bowel or Vitals: Her PR is _______, RR is _______ and BP is _______. (SpO2:
urinary habits, history of night pain, fever or constitutional symptoms like loss of ______; VAS: _____.)
weight or loss of appetite. There is also no hx of previous trauma to the back. Heart: S1S2 were heard on auscultation.
Lungs: Lungs are clear.
Management so far (options tried) Abdo: Soft, non-tender
His / her symptoms have failed to improve with conservative management such
as _________ for the past (duration) . Mr / Mdm XXX gait is ____________________.
He / she stands in slight forward flexion, has a list to the (left / right) and there
Past Medical History is reduced lumbar lordosis on inspection. There were no other deformities of the
Mr / Mdm XXX has a past medical history of _____________ for (duration) .

! 144!
spine. There are no scars, no sinuses, no swelling and no other skin changes
over the spine.
There is tenderness on palpation over the lumbar vertebrae. Paravertebral
muscle spasm was noted over the (left / right) side of the lumbar spine. There
is no step deformity noted.
Lumbar excursion is _____ cm. (Schober’s test)
Extension of the spine is _____.
His / her fingers are able to reach ______ bilaterally on lateral flexion of e spine.
Lateral rotation of the spine was ________ bilaterally.
___ for plantar flexion.
Sensation was decreased over the ____ dermatome in the (left / right) leg and
normal in all dermatomes in the other leg as well as both upper limbs.
Pulses in the lower limb were well felt.
I would like to complete the examination with an abdominal examination to
check for a palpable bladder, to rule out retroperitoneal pathology and perform a
digital rectal examination to check for saddle anaesthesia and the anal tone to
rule out cauda equina syndrome.

Straight leg raise was ____ degrees on the right and ____ degrees on the left In summary, Mr / Mdm XXX has signs consistent with that of a _____
lower limb, associated with a positive Bowstring test / Lasegue sign. FABERE’s radiculopathy in the (left / right) lower limb, likely secondary to a ______
test was negative bilaterally. lateral recess stensosis, as evidenced by a decreased (knee / ankle) jerk
reflex, loss of power in _________, loss of sensation over the ____ dermatome,
Neurological examination of the LL did not reveal any wasting or deformities. as well as a positive straight leg raise in the (left /right) lower limb to _____
Tone in the lower limbs was normal. degrees with a positive Bowstring and Lasegue test. I also note a slight forward
(Knee / ankle) reflex was absent over the (left / right) leg, reflexes over the flexion and sciatic list on inspection associated with paravertebral spasm on the
other leg was normal. OR (left / right) side of the lumbar spine, reduced lumbar lordosis and tenderness
(Knee / ankle) reflex was absent bilaterally. on palpation of the lumbar vertebrae. Excursion of spine was severely limited
Plantar reflexes were down going bilaterally. due to pain.
Power:
___ for hip flexion, In summary, Mr / Mdm XXX has signs suggestive of a central canal stenosis as
___ for knee flexion, evidenced by bilateral lower limb involvement, with no distinct signs of a
___ for knee extension, particular nerve root involvement suggestive of a lateral recess stenosis.
___ for ankle dorsiflexion and

CAUDA EQUINA SYNDROME – SURGICAL EMERGENCY!!!!!

• Pathology: Compression of cauda equina (L2 and below) resulting in acute loss of lumbar plexus function
• Occurs in 1-2% of PID
• Causes
o Commonly central PID (lumbar disc herniation)
o Infection – abscess
o Neoplasm – tumour, lymphoma
o Vascular – spinal epidural hematoma, spinal anaesthesia, IVC thrombosis
o Trauma
o Others – late stage ankylosing spondylitis, spondylosis, spondylolisthesis
• Presentation
o Saddle anesthesia – can ask if toilet paper feels different when wiping
o Bowel and/or bladder dysfunction: initial presentation may be of difficulty starting or stopping a stream of urine that may be
followed by frank overflow incontinence first of urine then of stools
! Early signs: Increased urinary frequency, waking up at night to pass urine, poor stream, hesitancy
o Lower limb weakness (affects both legs) +/- wasting (if chronic)
o Radiating pain (affects both legs; acute or chonic)
o Low back pain and tenderness
o Lower extremity/perineal area sensory loss
• Other problems to be considered: conus medullaris syndrome, spinal cord compression, lumbosacral plexopathy, peripheral n. disorder
o Signs of cord/ UMN involvement rules out CES: eg. hyperactive reflexes, babinski
• Ix:
o Imaging:
! Plain radiography: unlikely to be helpful in CES but may be done in cases of traumatic injury or in search of destructive
changes, disk-space narrowing, or spondylolysis
! CT w or w/o contrast: lumbar myelogram followed by CT
! Consult senior for use of MRI or CT
! U/S can be used to estimate or measure post-void residual volume
o Other tests: catheterization for residual urine volume may reveal urinary retention suggesting a neurogenic bladder
! A significant volume w little or no urge to void, or as a post-void residual, may indicate bladder dysfunction
! Bedside ultrasonography may also be used to estimate or measure post-void residual bladder volume
• Management:
o Pre-hospital care shld focus on associated symptoms related to pain (ie. What besides the pain is different)
! Stabilize acute life-threatening conditions
! Immobilize spine if traumatic
o ED care:
! No proven medical Rx exists and therapy is generally directed at the underlying cause of CES
! For mechanical compression of the cauda equina due to disk herniation, surgical intervention may be indicated
o Admit patients to appropritate service (usually neurology, neurosurgery or orthopedic Sx) w frequent neurological checks
o Surgical decompression within 48 HOURS
• Potential Cx if Rx delayed: residual weakness, permanent urinary/ bowel incontinence, impotence, and/or sensory abnormalities

! 145!
3. Causes of Neurological Deficit
PROLAPSED INTERVERTEBRAL DISC
• Pathology: ACUTE posterior or postero-lateral herniation of nucleus pulposus through annulus fibrosis;
nucleus pulposus (accompanied by local edema due to inflammation) then compresses on neural structures
o Extents of herniation: Sequestration (separation of herniated segment from rest of nucleus pulposus),
Protrusion (nucleus pulposus herniates through large tear), Extrusion (nucleus pulposus herniates
through small tear), Bulge
• Background:
o Commonly in adults 25-40yrs
o Causes: precipitating event of a local strain or injury (weight lifting, stooping) – usually predisposing
defect present (degenerate disc)
o Common levels affected:
! Cervical: immediately above/below C6 vert, hence nerve root of C6/7 affected
! Lumbar: L4/5 commonest then L5/S1
o Postero-lateral vs Central disc prolapse
! Central disc prolapse
• May only present with back pain
• Often no leg pain (especially if lower level as other lumbar nerve roots supplying leg
sensation have exited)
• May present w bilateral radiculopathy if prolapse is significant
! Postero-lateral prolapse: Usually compresses traversing nerve (radicular symptoms)
o Cervical (exit canal) vs Lumbar (root canal) PID (refer to diagram on the right)
! For usual posterior/postero-lateral herniation: Exiting cervical nerve root while traversing lumbar nerve root affected
! But for both, it is always the lower level affected (btwn C1 and C2 its C2, and between L1 and L2 is L2 affected)
! Occurs as such because of course of the nerve: At cervical level the nerve travels horizontally to exit out (no concept of
traversing nerve) while at lumbar level, exiting nerve exits early at the neural foramen while the traversing nerve travels down
across the level of compression
• Presentation
o Neurological Conditions
! Radiculopathy (posterolateral compression of nerve root when exiting) % radicular pain
! Myelopathy (posterior compression of spinal cord – if spinal cord present at level)
! Spinal stenosis (posterior compression of cauda equina or cervical cord)
! Cauda equina syndrome (severe spinal stenosis)
o Pain
! Pressure on post. intervertebral ligament – pain & stiffness fr back of neck to scapula & occiput
! Pressure on dural envelope of nerve root – radicular pain
! Pressure on nerve – numbness, parasthesia, muscle weakness
o Signs
! LOOK: Listing (to relieve pain from nerve root compression), Paravertebral muscle spasm,
Protective scoliosis, loss of lumbar lordosis, may have acute torticollis
! Feel: Midline tenderness
! Move: Pain (& listing) worse on flexion, increase intra-abd pressure (coughing, straining,
lifting, laughing), decreased ROM due to pain
! SLR test positive (if nerve root compression present); cross SLR positive if large central disc herniation (prodrome of CES)
• Bowstringing, Laseague’s, femoral stretch test (L4)
! Restricted ROM
! Segmental myotomal / dermatomal deficits (corresponding to level of lesion; sensory, power, reflexes)
• DDx: pain Hx and imaging tro DDx!
o Soft tissue sprain – neurological SnS absent.
o Neurological amyotrophy (acute brachial neuritis) – sudden, sever pain @ shoulder, back or shoulder. Multiple neurological sites
affected n might have winging of scapula. Pain followed by flaccid paralysis a few days later.
o Cervical spine infx (inc TB spine) – unrelenting n local spasm with severe pain. X-ray: erosion of bone
o Vertebral/nerve tumors – neurological signs progressive. X-ray/MRI shows bone destructn. Primary tumors rare, secondary more
common. Of primary, sarcoma n multiple myeloma most common
o Others: AS
• Investigations
o Xray (AP, lateral, oblique): decreased jt space; exclude bone disease
o MRI: for surgical planning and for cauda equina syndrome
• Management – Rest, Reduce, Remove, Rehab
o Conservative: Rest + Reduce " symptoms in 75% of patients will resolve
! Rest: continuous bed rest (spinal corset/ collar to prevent unguarded movement), physiotherapy (& heat) and analgesia/anti-
inflammatory (NSAID; can consider epidural steroid + LA injection)
! Reduce: traction can reduce herniation (intermittent traction applied to pelvis w hip & knees slightly flexed; 30mins @ a time up
to 8kg) + back care education
! " Continuous bed rest & traction for 2wks decreases herniation in >90% of cases
o Surgical: Removal + Rehab
! Indications
• Cauda equina syndrome
• Failure of conservative Rx (after 3mths) – persistent pain and neurological deterioration with frequently recurring attacks
! 146!
 ! Procedure: Fenestration & discectomy OR microdiscectomy
• May fuse affected areas or maintain height using bone graft
• Alleviate symptoms of radiculopathy but not lower back pain
! Rehabilitation (post-op); Light work after 1 month & heavy work after 3 months
Mr / Mdm XXX is a __ years old (race) gentleman / lady,
premorbid status: (ADL independent, community ambulant – w / wo aid) ,
occupation: ____________________,
with a significant PMHx of ____________________,
presenting complaint: currently presents with a (duration) history of acute
low back pain.
Regarding the low back pain, it is constantly present.
The pain shoots down the (anterior / lateral / posterior) aspect of the thigh and
the (anterior / lateral / posterior) side of the leg to the (dorsum / sole) of the
foot, in a radicular pattern in the (L4 / L5 / S1) nerve root / dermatome.
He / she describes the pain as (nature: sharp, shooting, tingling) .
It occurred suddenly after (activity: carrying heavy objects / bending forward /
precipitated by sitting for long periods) and is aggravated with coughing and
straining, and relieved with lying down.
The current pain score is ____ and the pain can be so severe that he / she
cannot straighten his / her back.
There (is / is no) associated stiffness in the back especially in the morning
that does not last more than 30 mins.
In addition, he / she experiences weakness of the (left / right) lower limb and
associated numbness over the (site) of his / her (left / right) lower limb
corresponding to (dermatome) for the past (duration) . His / her neurological
symptoms are non-progressive.
Functional Status
Currently, her symptoms have limited her daily function such as: ___________.
Systemic Review
He / she does not have any red flag symptoms such as changes in bowel or
urinary habits, history of night pain, fever or constitutional symptoms like loss of
weight or loss of appetite.
There is also no history of previous trauma to the back.
Management so far (options tried)
He / she was treated conservatively with ___________ for the past (duration) .
Past Medical History
Mr / Mdm XXX has a past medical history of _____________ for (duration) .
He / she also does not have a history of peptic ulcer disease / GI bleeding.
He / she had previous operations for ____________.
He / she has NKDA and is currently on ___________ for her medical conditions.
Family History
He / she (has / has no) family history of cancer or similar back pathologies.
Social History
He / she (does not smoke / smokes / is an ex-smoker and has quit XX years
ago) , ( sticks/day x years).
He / she (has / does not have) a habit of regular intake of alcoholic drinks.
He / she has (good / poor) social support. He / she works as a ___________
and his / her condition affects her job. He / she lives with his / her ________. His
/ her main caregiver is his / her ______________.
He / she lives in a residential (with / without) lift landing. There (is / is no)
squatting toilet in the house.
Currently, the family (does not have any financial issues / is receiving financial
aid from ) .
In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady with co-
morbidities of ____________________, currently presenting with symptoms
suggestive of a _____ radicular pain as evidenced by a low back pain that
! 147!
shoots down the (left / right) that is associated with weakness of the lower limb
and numbness over the _____.
My provisional diagnosis will be that of a ____ prolapsed intervertebral disc.
PHYSICAL EXAMINATION
On physical examination, Mr / Mdm XXX is alert and comfortable at rest.
Vitals: Her PR is _______, RR is _______ and BP is _______. (SpO2:
______; VAS: _____.)
Heart: S1S2 were heard on auscultation.
Lungs: Lungs are clear.
Abdo: Soft, non-tender
Mr / Mdm XXX gait is _____________.
He / she has a list to the (left / right) and reduced lumbar lordosis on
inspection. There were no other deformities of the spine. There are no scars, no
sinuses, no swelling and no other skin changes over the spine.
There is tenderness on palpation over the lumbar vertebrae. Paravertebral
muscle spasm was noted over the (left / right) side of the lumbar spine. There
is no step deformity noted.
Lumbar excursion is _____ cm. (Schober’s test)
Extension of the spine is _____.
His / her fingers are able to reach _________ bilaterally on lateral flexion of the
spine.
Lateral rotation of the spine was ________ bilaterally.
Straight leg raise was _____ degrees on the right and _____ degrees on the left
lower limb, associated with a positive Bowstring test / Lasegue sign. FABERE’s
test was negative bilaterally.
Neurological examination of the lower limb did not reveal any wasting or
deformities.
Tone in the lower limbs was normal.
(Knee / ankle) reflex was absent over the (left / right) leg, reflexes over the
other leg was normal.
Plantar reflexes were down going bilaterally.
Power:
___ for hip flexion,
___ for knee flexion,
___ for knee extension,
___ for ankle dorsiflexion and
___ for plantar flexion.
Sensation was decreased over the ____ dermatome in the (left / right) leg and
normal in all dermatomes in the other leg as well as both upper limbs.
Pulses in the lower limb were well felt.
I would like to complete the examination with an abdominal examination to
check for a palpable bladder, to rule out retroperitoneal pathology and perform a
digital rectal examination to check for saddle anaesthesia and the anal tone to
rule out cauda equina syndrome.
In summary, Mr / Mdm XXX has signs consistent with that of a ____
radiculopathy in the (left / right) lower limb, likely secondary to a _____
prolapsed intervertebral disc, as evidenced by a decreased (knee / ankle) jerk
reflex, loss of power in _________, loss of sensation over the ____ dermatome,
as well as a positive straight leg raise in the (left /right) lower limb to _____
degrees with a positive Bowstring and Lasegue test. I also note a sciatic list on
inspection associated with paravertebral spasm on the (left / right) side of the
lumbar spine, reduced lumbar lordosis and tenderness on palpation of the
lumbar vertebrae. Excursion of spine was severely limited due to pain.
SPONDYLOLISTHESIS (LUMBOSACRAL)
• Pathology: Vertebral displacement (forward translation of upper over lower vertebral body) usually at L4/5 (more common) or L5/S1 level
due to failure of normal laminae-facet locking mechanism
• Causes: SPOTED
o Spondylolytic/ Isthmic (50%; most common) – break in pars interarticularis
! Epidemiology: Often young patients
! Presentation
• Intermittent back pain (worsened on movement)
• Buttocks look flat
• Step deformity felt on spine palpation
! Effect on spinal canal size
• Initially: Unlikely to lead to spinal stenosis as only anterior portion of vertebrae translates forward (due to break)
• Late: Potential spinal stenosis if fibrosis is marked (attempted healing)
o Pathological (neoplasm) & other Destructive conditions like infx (TB)
o Operative – due to laminectomy for decompression
o Trauma
o Elderly (degenerative; 25%) – OA degeneration of facet joints (usually L4/5)
! Mechanism:
• Degeneration of intervertebral disc (lose height, bulge)
• Arthritis of facet joints " weakening of joint and ligaments " allow sliding of one vertebrae over the other
• May have an unnoticed break in pars during adolescence, predisposing to spondylolisthesis in adulthood
! Occurs in women >40 with facet joint arthritis
! May cause spinal stenosis as whole vertebrae translates forward, leading to narrowing of spinal canal
o Dysplasia (20%): congenital lumbosacral facet joint dysplasia
! Seen in children
! May be a/w unduly protruding abdomen and associated scoliosis; usually no pain
• Presentation
o Back pain: intermittent, worse on some form of movement (due to sliding), esp w exercise or straining
o Bending backward in stepwise movements
o Step deformity of spine
o Back stiffness: for degenerative type
! ROM usually normal in younger patients
o LOOK: buttocks flat, short lumbar spine, long sacrum, transverse loin creases
o Neurological symptoms:
! Radiculopathy – Often both traversing and exiting root affected
! Spinal stenosis
• Imaging
o X-ray (lateral, oblique): Forward shift of upper spinal column
o Elongation of arches / defective facets
o Gap in pars interarticularis on oblique view (Scotty dog sign) – for spondylolytic cause
o Flexion and extension views to assess stability
• Meyerding Classification

• Management
o Conservative: Bed rest and supporting corset
! Old patient, non-disabling symptoms
o Operative: Spinal fusion (Transforaminal Lumbar Interbody Fusion – TLIF)
! Disabling symptoms, young adult, neurological compression

SPONDYLOSIS (DEGENERATION)
• Epidemiology: >40yo, M>F, usually C5/6
o RF: smoking, drinking, excessive driving (for cervical spondylosis)
• Pathology:
o Disc Degeneration
! Loss of proteoglycan and hence water content (reduction in shock absorptive ability)
! Collapse, flattening and loss of disc space height
! Disc bulging or herniation
o Facet Joint Arthritis
! Experience increased pressure due to disc degeneration
! Wearing away of cartilage lining facet joints
! Rubbing of bone: Hypertrophy of facet joint + syndesmophyte formation on anterior and posterior margins of vertebral
bodies (response to abnormal stress to compensate loss of ligamentous and articular stability)
• NOTE: vertebral spurs are v common in elderly but may not be cause of S/S, thus need to exclude DDx
o Thickening of ligamentum flavum: ligamentum flavum calcification and buckling

! 148!
 o Degenerative kyphoscoliosis
! Uneven shoulders and hip asymmetry
! Flat back (loss of lumbar lordosis)
! Knee and hip pain because patient has to flex knee and extend hip to look straight
• Presentation
o Chronic neck or back pain (and stiffness; decreased ROM throughout w pain): gradual progression, worse in morning
! Discogenic pain – Due to disc degeneration (annulus becomes stressed on loading as disc loses elasticity with age; mechanical
receptors on outer 1/3 of annulus stimulated causing back pain)
• Pain on loading of the disc: Worse on flexion, sitting/standing for too long, carrying weights in front, coughing/sneezing
• Extent of pain: Back and buttocks
! Facet joint pain – Due to facet joint arthritis
• Pain on loading of facet joint: Extension, rotation, pressing on joint, getting up from chair, turning in bed
• Extent of pain: Can radiate down back of upper leg (rarely radiate below knee) for lumbosacral joints; Can radiate from
posterior neck down shoulders & upper back or up to occiput (“headache”) for cervical joints
! " symptoms relieved by lying down
o Neurological deficits
! Radiculopathy: Due to 1) Loss of disc height 2) syndesmophyte (posterior spurs may encroach upon the IV foramina
compressing nerve roots) 3) Facet joint hypertrophy
! Spinal stenosis: Due to 1) Facet hypertrophy 2) Thickening/infolding of ligamentum flavum 3) Bulging of degenerate
disc 4) Spur formation 5) Listhesis (joint instability)
• Imaging (X-ray)
o AP view: vertebral tilting/ asymmetry of disc space or facet joints
o Lateral view
! Disc space narrowing/ vacuum sign (abnormal lucency in disc space)
! Anterior traction spurs (syndesmophyte)
! Localised sclerosis of vertebral body adjacent to disc space
! Spondylolisthesis/retrolisthesis
! Osteoarthritic changes in unco-vertebral joint
o Oblique view: encroachment of IV foramina
o Flexion/extension view: assess spine stability
• Management
o Conservative: mainstay of Rx; try as long as possible as disability is rarely severe and may decrease as spine stabilizes
! Activity modification: weight loss, stop bending, lifting, climbing
! Physiotherapy: Exercises, gentle passive manipulation, heat treatment
! Intermittent traction
! Occupational therapy: Restraining collar, corset
! Analgesics
o Surgery
! Indications: progressive neurological deficits, multiple levels of cord compression, severe symptoms that are only relieved by
uncomfortable support
! Anterior disc removal with fusion of most painful level
• Discectomy ± anterior fusion
• Corpectomy
• Laminoplasty
• Laminectomy ± foraminectomy

4. Deformity (*Note: Corrected by 3 point fixation with bracing)

SCOLIOSIS
• Definition: Abnormal lateral curvature of the spine
• Classification
o Postural Scoliosis: Secondary / compensatory tilt to a condition outside the spine (eg. short leg, pelvic tilt due to hip contracture,
muscle spasm due to lumbar PID ie sciatic scoliosis) " curve
disappears when patient sits (cancels leg asymmetry)
! Usually disappears when patient sits
o Structural Scoliosis: Always accompanied by bony abnormality
or vertebral rotation
! Fixed deformity that does not disappear w postural changes
! Secondary curves may dvlp to counterbalance pri deformity
! Once established, deformity liable to increase throughout
growth period
! Types
• Adolescent (>/=10yo onset) idiopathic scoliosis (most
common; 80%)
• Infantile (<4) idiopathic scoliosis (may resolve or
progress)
• Osteopathic scoliosis: Due to congenital vertebral
anomalies (hemivertebrae, wedge vertebra, block
vertebrae) " rare
• Neuropathic scoliosis: Due to asymmetrical muscle
weakness (polio, cerebral palsy, myelomeningocele)
• Myopathic scoliosis: Seen in rare muscular

! 149!
 dystrophies, spinal muscular atrophy (SMA)
• Syndromic: Ehler-danlos, marfan’s, NF, VACTERL
! 5 patterns of idiopathic scoliosis:
• Infantile thoracic: 60%M, 90% convex L, a/w ipsilateral plagiocephaly, progressive type becomes severe
• Adolescent thoracic: 90%F, 90%R convex, rib rotation exaggerates scoliosis, 50% dvlps >70deg
• Thoracolumbar: abit F>M, convex abit R>L
• Lumbar: F>M, 80%L, 1 hip prominent but no ribs to accentuate deformity, not noticed early, backache till adult life
• Combined: 2 primary curves (1 in each direction), clinical deformity rather slight coz always well balanced though may be
radiologically severe
• Complications
o Pulmonary: Decrease total lung capacity and fixed vital capacity due to thoracic lordosis (Cobb angle >70deg)
! Usually only affects early onset scoliosis as it affects pulmonary alveoli dvlpment
o Cardiac: Right heart disease due to pulmonary hypertension (Cobb angle >80deg)
o Early OA of the back
o Radiculopathies
o Backache
• Physical examination:
o General assessment (listing, gait, limb length discrepancy) + height
o Back examination:
! Adam’s forward bend test: Brings apex of kyphosis into view from lateral
position (seen as thoracic hump; ddx postural and structural) !
! Scoliometer
! Spinal balance – plumbline
o Neurological examination: esp LL neuro exam, abdominal reflexes, back sensation esp
L thoracic curves
• Important points in Hx for idiopathic scoliosis: Chronological age, menarche, family Hx, time of
Dx, severity of first XR, any previous Rx, associated symptoms (back pain, neurological
symptoms inc. clumsiness/weakness and bladder/bowel function)
• Red flags of atypical scoliosis (scolisis that is NOT idiopathic)
o Hx
! Back pain that is well localized, constant and progressive
! Weakness or clumsiness
! Bladder and bowel incontinence; Ejaculation problems
o PE:
! Foot deformity, esp unilateral
! Abnormal curve pattern: not R thoracic and/or L lumber (rule out syringomyelia)
! Hyperkyphosis
! A lack of rotational deformity on Adam’s forward bending test
! Tight hamstrings (popliteal angle >50-60deg)
! Unequal or abnormal reflexes
o XR:
! Widened pedicles
! Kyphosis
! Atypical curve pattern
! Lack of vertebral rotation
! Rapid curve progression (>1deg/month)
! Absent pedicles (“winking owl”)
! Limb length discrepancy
o MRI:
! When to order
• Neurologic abnormalities on PE (rmber the feet)
• Structural (congenital) abnormalities on plain film
• Excessive kyphosis
• Apex L thoracic or thoracolumbar curves
• Early onset scoliosis
• Syndromic features present
! What to look for: syringomyelia, chiari malformations, tethered cord, diastematomyelia
• Adolescent Idiopathic Scoliosis (more females)
o Epidemiology: Usually present between 10-15 (usually present before puberty, greatest progression during pubertal growth spurt,
minimal progress post-puberty)
o Pathology
! Postulated that localized extension (straightening out) of normal dorsal kyphosis would inevitably force spine to swivel round thus
producing appearance of a lateral curvature
! Thoracic or lumbar spine
! Vertebrae involved are rotated arnd vertical axis so the bodies point to convexity and the spinous process point to concavity
! In thoracic curves, ribs on convex side are carried around posteriorly and stand out as a prominent hump
! Mobile secondary curves may dvlp above and/or below primary curve to maintain normal head and pelvic position
o Symptoms
! Deformity
• >pronounced on flexion (vs postural curve which disappears on flexion)
• Shoulder elevated on side of convexity & hip sticks out on side of concavity
• For thoracic scoliosis: Breasts asymmetrical + rib angles protrude
! 150!
 o X-ray: Full length AP spine + lateral flexion XR + pelvis
! Cobb’s angle measured: Lines projected from uppermost and lowermost
vertebral bodies in the curve
! Risser’s sign: Extent of ossification and fusion of iliac apophysis of pelvis;
measures progressive ossification from anterolaterally to posteromedially
(suggests skeletal maturity and provides indication for curve progression)
• Grade I: 25% ossification action of iliac apophysis
• Grade II: 50%
• Grade III: 75%
o Patient has passed peak of growth spurt, a period of rapid spinal
growth during which scoliosis curvatures can increase rapidly
• Grade IV: 100%
• Grade V: Iliac apophysis fused to iliac crest after 100% ossification
o Management
Cobb’s angle Grade 0/ premenarchal Grade 1 or 2 (pubertal) Grade 3, 4 or 5 (post-pubertal)
<20 Observation: 4 monthly f/u and full length spine XR to check for progression of scoliosis
20-40 Brace therapy (begin when Brace therapy Observation
curve is >25deg)
>40 Surgery + supports post-op to prevent recurrence Surgery (when curve >50deg): Sx indicated
coz progression is expected to be 1-2deg/year
although there is no longer growth
! Conservative
• Exercise: Alone has no effect on curve
o Indications: approaching skeletal maturity, deformity <30deg
• Bracing
o Indications
! Progressive curves between 20 and 40 deg (when iliac apophysis not fully ossified and fused –
usually Risser 0,1,2)
! Apex lower than T7
! Well balanced double curves
! Stabiliser for younger children who need surgery (await fusion)
! Prevent recurrence after spinal fusion
o Types: Boston brace (curves below T9), Milwaukee brace (1hr break in 24hrs)
o Prevents progression, doesn’t improve deformity
! Surgery
• Indication: Curves > 40deg for pre-pubertal/ pubertal and >50deg for post-pubertal
• Method
o Expose entire length of curve
o Apply a distraction rod to concave side of curve to ‘jack’ curved segment out as straight as possible
! A more robust instrumentation will have a higher risk of neurological Cx
o Entire length of curve then prepared for bone-grafting in the hope that it will fuse when back is ‘immobilised’ in
plaster jacket
• 50% correction regarded as satisfactory

KYPHOSIS
• Pathology: Excessive dorsal curvature of spine
• Classification
o Postural kyphosis: Associated with postural defects such as flat feet
o Structural kyphosis: Fixed and associated with changes in shape of vertebrae
! Common causes: Elderly –Degenerative, Adults –AS, trauma, TB spondylitis, Adolescents -Scheurmann’s disease
• Kyphos/Gibbus: Sharp posterior angulation due to localized collapse or wedging of one or more vertebrae (due to congenital defect, fracture,
spinal TB)
• Scheuermann’s Disease (Adolescent Kyphosis) –affects boys>girls
o Pathology:
! Developmental disorder of growing spine in which there is irregular ossification and possibly some fragmentation of vertebral
body epiphyses
! Resulting in irregularity of mature vertebral endplates and small central herniations of disc material into vertebral body
(Schmorl’s nodes)
! Increasing growth and muscular activity in thoracic spine may cause vertebrae to give way slightly and become wedged,
exaggerating the normal kyphosis
o Types
! Thoracic Scheuermann’s Disease (more common)
• Epidemiology
o Starts shortly after puberty
o More common in boys than girls
• Symptoms
o Round shouldered
o Backache
o Fatigue
• Signs: Smooth but well-marked thoracic kyphosis
• X-ray (lateral view)

! 151!
 o Patchiness or irregularity of vertebral end plates
o Schmorl’s nodes
o Wedging of vertebral bodies (later on)
• Management
o Conservative: Extension brace (curves <40deg)
o Surgery: Operative correction with fusion
! Thoracolumbar Scheuermann’s Disease
• Epidemiology
o Less common than thoracic Scheuermann’s
o Occur in adolescence or early adulthood
• Symptoms
o Usually no local deformity
o Low back pain
• X-ray (lateral view): Similar to thoracic variant but no vertebral wedging
• Management:
o Conservative: Back strengthening
o Surgery: Indicated only if there is discogenic disease

5. Injuries of Spine and Thorax

GENERAL INFORMATION
• Degree of canal compromise: incomplete vs complete cord
compression/ lesion
o Central cord, anterior cord, posterior cord, brown
sequard, conus medullary, cauda equina etcetc
• Non-union very rare, malunion common
• Stability
o Injuries
! Stable Injury: Vertebral components will not
displace with normal movement
! Unstable Injury: Vertebral components have
significant risk of displacement and hence
damage to neural tissues
o Components involved in stability
! Integrity of vertebral bodies
! Ligaments that link adjacent vertebrae
! Posterior arches
• Denis 3 Column Theory
o 1 column involved: Stable
o 2 columns involved: Might be unstable
o 3 columns involved: Unstable Posterior ligaments: supra & infra-spinous lig, ligamentum flavum
• Basic types of spine # and their mechanism: defined in terms of
the degr of involvement of each of the three columns. Each type is defined also in terms of its pathomechanics, roentgenograms, and
computerized axial tomograms, as well as in terms of its particular stability.
o The compression fracture is basically stress failure of the anterior column with an intact middle column and posterior.
! Mechanism: anterior flexion (anterior #), lateral flexion (lateral #)
! XR: decrease in height in anterior 50% for anterior #
! Causes: pathological (infx, tumour, osteoporotic)
o The burst fracture indicates failure under compression of both the anterior and middle columns.
! Mechanism: axial load +/- flexion/ rotation
! XR: decrease in height throughout
! Causes: trauma
o The seat-belt-type/ flexion-distraction/ chance # is the result of failure of the posterior and middle columns under tension with an
intact anterior hinge.
! Causes: common in lap-belted motor vehicle collisions
o In # -dislocations (more severe), the structure of all three columns fails fr forces acting to various deg fr one or another direction
! Mechanism: flexion-rotation, shear, flexion distraction
• Mechanisms of Injury
o Traction: Avulsion of transverse process (L vert) or spinous process (C7 vert)
o Direct: Penetrating injuries
o Indirect:
! Fall from height: Spinal column collapses in its vertical axis
! Violent free movements of neck or trunk
! Variety of forces: Axial compression, flexion, lateral compression, flexion rotation, shear, flexion distraction, extension
• Grading of Spinal Cord Injury
o Frankel Scale

! 152!
 o Complete vs Incomplete
! Complete: No function below level of injury
! Incomplete: Some degree of function retained " sacral sparing (perianal sensation, sphincter tone, big toe flexion)
• Treatment of SCI
o Attributed to contusion and/or compression " microvascular disruption
o Rx: methylprednisolone: bolus 30mg/kg followed by 5.4mg/kg/hr over 23 hrs. patients treated within 8hrs respond best

CERVICAL SPINE INJURIES

• General Information
o Notable features: Mechanism of injury, Stability, Neurological involvement, Management
! Mechanism of Injury: Fall from height, diving accident, vehicle accident in which neck is forcibly moved
o Suggestive signs and symptoms of cervical spine fracture / spinal cord injury
! Unconscious from head injury
! Abnormal position of neck
! Tenderness on palpation
! Pain or parasthesia in limbs (spinal cord or nerve root injury)
o General Management Principles
! Stabilise
! Spinal precaution (sandbag on either side to prevent head tilting or rolling)
! Primary survey: Rule out other injuries/open fractures etc
! Investigations (to determine if C spine injury)
• Neurological assessment (ASIA, baseline neurological scoring)
• X-ray; CT if necessary
! Immediate treatment
• Steroids – prevents metabolic trauma
• Oxygen
• Fluid hydration
! Pre-op preparation: Bloods, NBM
! Skull traction principles
• Start with 5 kg
• Progressively increase by 5kg until reach maximum weight (5 + 5xlevel of Cspine)
• If dislocation/fracture reduces, half the weight to maintain position
! Management after radiological Ix:
• If films negative remove collar and complete exam.
o Palpation- one person supports the head with axial traction while the other palpates from occiput to T1. Check for
tenderness, swelling, stepoff. Cannot rely on clinical exam if decreased mental status or distracting injury.
! If symptomatic replace collar.
! If negative then proceed to ROM.
o Active ROM only. Should be full and pain free.
! If exam completely -ve and films negative at this point may remove collar. Write order that C-spine is clear
! If unable to perform ROM but the rest of exam is -ve: replace collar and have patient return in 10-14 days
for flexion and extension views. If done acutely muscle spasm or guarding may hide a ligamentous injury.
• Obtunded patient with normal films - Leave the collar on. Dynamic Fluoroscopy. MRI
o Hangman’s Fracture of C2
o Flexion Tear drop fracture of ant-inf part of vertebral body. Unstable fracture.
o Treatment – gardner-wells tractn tongs, halo device
o Imaging: AP, lateral, open mouth odontoid (C1, C2)
! AP View
• Lateral outlines should be intact
• Spinous processes and tracheal shadow in midline: spinous processes shld line up and have equal gaps
• Sagittal plane fractures
• Lateral mass fractures
• Facet fractures/ dislocations
! Open-mouth view (odontoid view): Show C1 and C2 for odontoid and lateral mass fractures + C1/2 alignment

! 153!
 ! Lateral view
• Must include all 7 cervical vertebrae and upper half of T1 (cover for cervicothoracic junction injury); swimmers view or
CT if unable to see T1
• Specific things to look out for:
o Anatomic lines: 4 parallel curves (look for deviation)
! Down e front of vertebral bodies (ant vertebral line)
! Down the back of the bodies (post vert line)
! Through posterior borders of lateral masses
(spinolaminar line)
! Along bases of spinous processes (post spinous line)
o Soft tissue outlines:
! Look for soft tissue swelling or hematoma in
retropharyngal space: Prevertebral soft-tissue
shadow (fat stripe) should be <5-6mm in width above
trachea (@ C2) and < 1 vertebral body’s width/
<2mm below that (@ C6)
o Step deformity of >3.5mm anywhere
! Anterior subluxation of 1 vertebra on another
indicates facet dislocation
• <50% of the width of a vertebral body implies
unifacet dislocation
• >50% implies bilateral facet dislocation
! This is usually accompanied by widening of the
interspinous and interlaminar spaces
o Atlantodens interval (ADI): distance btw odontoid process &
post. border of arch anterior of atlas – atlantoaxial instability (AAI) present if >3mm in adults & >5mm in children
o Uniformity of shape and height (disc herniation) of IV disc (all the same except C1 & 2)
! Fracture types: wedge compression, burst (refer below)
o Angulation 11deg greater than contiguous segments (disruption of the PLL, subluxation of C3 on C4)
o Anterior occipitoatlantal dislocation (Powers ratio)
! SCIWORA (SCI without radiological abnormality): Normal radiographs do not exclude possibility of SCI (esp in children)
• Cervical subluxation
o Pure dislocation of the spine is commonest in the cervical region
o Mechanism of injury: Flexion injury (esp lower ½ of spine)
o Bones intact but posterior ligaments torn
o Vertebra above tilts forward on the one below, opening up interspinous space
o X-ray: Flexion extension x-rays – gap btwn spines unusually wide
o Management
! Stable: Splintage for 6 weeks
! Unstable: posterior spinal fusion
• Wedge Compression Fracture: anterior wedging of vertebral body or teardrop #s of antero-inferior portion of body
o Mechanism of Injury: Pure flexion injury causes compression of ant. pt of vertebral body (usually in mid and lower cervical segments)
o Stable injury
o Management: Collar for 6-8weeks
• Burst Fracture: anterior compression of >40% of normal vertebral body height (w retropulsion of fragments of the vertebral body into the
spinal canal)
o Mechanism of Injury: Axial compression of C-spine (usually in diving or athletic accidents) " Affect anterior and middle column
o Neurological involvement: Common
o Imaging
! X-ray
• Comminuted fracture of vertebral body
• Middle column damage and posterior displacement of body fragment
! CT/MRI: Look for retropulsion of large fragments into spinal canal
o Management
! No neurological deficit: Halo-vest immobilisation
! Neurological deficit: Anterior decompression + halo vest immobilisation
• Flexion Rotation Injuries
o Unilateral facet dislocation
! Mechanism of Injury: Flexion rotation injury resulting in dislocation of one facet join
! X-ray:
• Lateral: Vertebral body appears partially displaced (<25% its width) " stable
• AP: Alignment of spinous process disrupted
• Oblique: expected tilting of the laminae is disrupted, and the dislocated superior articulating facet of the lower vertebra
can be seen projecting within the neural foramina
! Neurological involvement rare
! Usually stable
! Management
• Closed reduction: Skull traction + gentle extension and rotation maneuver
• Open reduction: Only if closed reduction fails
o Bilateral facet dislocation or Fracture dislocation
! Mechanism of Injury:
• Severe flexion and rotation resulting in articular facets riding forwards over facets below
! 154!
 • May have facet fracture or pure dislocation
• Posterior ligaments ruptured
! Unstable
! Cord damage common
! X-ray: Forwards displacement (>1.5x its width) of vertebra on one below
! Management
• Closed reduction: Skull traction + collar / posterior fusion
• C1 ring fracture classification: Posterior arch (28%), Jefferson burst #, anterior arch “blow out”, lateral mass #, transverse process #
o Burst fracture of C1 (Jefferson’s Fracture)
! Mechanism of Injury: Sudden severe load on head may fracture ring of atlas
! X-ray (open mouth view): Lateral masses spread away from odontoid peg
• >6.9mm = transverse ligament avulsion
! Neurological involvement: Usually no neurological damage (no encroachment on neural canal)
! Management
• Undisplaced (stable; intact transverse ligament): Rigid collar or halo vest
for 10-12 weeks
• Sideways spreading of lateral masses (unstable): Skull traction
reduction or halo-body orthosis for 6 weeks + 6 weeks of semi-rigid collar
• Late instability: C1/2 fusion
! Associated w other C-spine injury in 50% of cases (rule out odontoid and
hangman’s #)
• Fracture of Pedicle(s) of C2 (Hangman’s Fracture)
o Mechanism of Injury:
! Commonly in RTA when forehead strikes dashboard
! Combination of extension, compression and flexion
o Neurological damage unusual because # of posterior arch tends to decompress spinal cord
o Management
! Undisplaced: Collar or halo vest
! Displaced: Reduction (but not via traction as mechanism of injury often involves distraction) + halo vest
• Fracture of Odontoid Process (C2)
o Mechanism of Injury:
! Flexion injury in young adults due to high velocity accidents or severe falls OR
! Low energy trauma in osteoporotic patients where neck is forced into hyperextension
o Neurological Involvement: ¼ of cases
o Classification (Anderson and D’Alonzo)
! Type 1 (Avulsion of tip): Immobilisation + Rigid collar
! Type 2 (Fracture through the junction of the odontoid peg and body of C2)
• Unstable and prone to non-union + easily missed " WORST type
o 10% SCI due to translation
o Poor prognosis
o Associated # in 20-30%
• Undisplaced: Halo-vest
• Displaced: Traction + Screw fixation or Halo-vest
! Type 3 (Fracture through body of C2 only): Treatment as for Type 2
• Good prognosis; heals easily
• Avulsion Injury of C7 Spinous Process
o Mechanism of Injury: Severe voluntary contraction of muscles at the back of neck
o Painful but harmless
• Sprained Neck (Whiplash injury)
o Mechanism of Injury: Hyperflexion or hyperextension of neck " soft tissue sprain of neck (acceleration-decceleration often
associated with car accidents)
o Symptoms: Pain and stiffness usually appear 12-48 hours after injury
o X-ray: Normal
o Management: Pain relief initially, then physiotherapy for return of neck movement

THORACIC SPINE INJURIES

• Mechanism of Injury: Usually due to hyperflexion
• Types of Injury
o Wedge compression in osteoporotic (usually mechanically stable but may lead to progressive kyphosis)
o Severe injuries in younger people (esp at T11 and T12 which are not splinted by rib cage) have high risk of cord damage
• Imaging
o X-ray: Shows lower thoracic clearly
o CT/MRI
! Determine fragmentation or displacement of posterior part of vertebral body (risk to spinal cord)
! Interpret upper thoracic spine where scapula and shoulders in the way
• Management
o Stable fracture with <30 deg kyphosis and no neurological involvement: Managed symptomatically
o Angulation marked: Bracing or posterior fusion (avoid increasing kyphosis)
o Severe bony injury: Internal fixation

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THORACOLUMBAR AND LUMBAR INJURIES
• General Information
o Thoracolumbar junction particularly prone to injury because of transition btwn relatively fixed thoracic spine and relatively mobile
lumbar spine
o Minor Injuries: Fracture of vertebral processes and pars interarticularis
o Major Injuries: Compression, burst, fracture-dislocation, jack-knife injuries
• Wedge / Compression Injury
o Mechanism of Injury: Spinal flexion with posterior ligaments in tact (minimal trauma needed for osteoporotic patients) resulting in
failure of anterior column
o Usually stable
o Neurological involvement rare
o Management
! Minimal wedging: Bed rest until pain subsides + Strengthening exercise
! Marked wedging (anterior vertebral height reduced by 25-50%):
Thoracolumbar brace
! Even more severe (usually indicative of damage to posterior ligaments):
Posterior spinal fusion
• Burst
o Mechanism of Injury: Failure of both anterior and middle columns (posterior
usually spared) where posterior part of vertebral body is shattered and fragments
of bone and disc may be displaced into spinal canal
! Usually due to axial compression
! Most common at thoracolumbar junction – T spine rigid while L spine
mobile
o Usually unstable
o May have neurological involvement
o Imaging
! X-ray: Spreading of vertebral body with an increase of interpedicular distance
! CT: Check for posterior displacement of bone into spinal canal
o Management:
! Minimal retropulsion of bone, no neurological damage, minimal anterior wedging: Patient kept in bed and mobilized in
thoracolumbar brace
! Neurological symptoms present (tingling, weakness, alteration of bladder or bowel function): Anterior decompression and
stabilisation
• Flexion-Distraction / Jack-knife injury / Chance
o Mechanism of Injury:
! Combined hyperflexion and distraction causes mid-lumbar spine to ‘jack knife’ around an axis that is placed anterior to the
vertebral column (commonly lap belt injuries)
! Posterior and middle columns fail in distraction (unstable in flexion)
! Compressive failure of anterior column
o Chance Fracture (ideal example of tensile failure)
! Split runs through spinous process, transverse process, pedicles, vertebral body
! All 3 columns affected
! Heals rapidly: Requires 3 months in plaster jacket / brace
! Usually T12-L2
! Types
• Bony Chance – Can heal with immobilization
• Ligamentous Chance – Need surgery
o Neurological damage uncommon
o Unstable
o X-ray: (CT scan can assist w diagnosis)
! Horizontal fractures in pedicles or transverse processes
! Increased apparent height of vertebral body (AP view)
! Opening up of disc space posteriorly (lateral view)
! Gap between spinous process increased
• Fracture dislocation
o Mechanism of Injury:
! Combination of flexion, compression, rotation and shear forces may result in segmental displacement (usually high energy
injuries)
! All 3 columns disrupted and spine unstable
! Commonly at thoracolumbar region
o Neurological involvement common: Lowermost part of cord or cauda equina
o Imaging
! X-ray:
• Fractures through vertebral body, pedicles, articular processes, laminae, transverse process, ribs
• Subluxation or dislocation
• Total dissociation between one part to another part of spinal column (both AP and lateral views look bad)
! CT: Determine degree of spinal canal occlusion
o Management: Surgery

! 156!
TRAUMATIC PARAPLEGIA
• General Information
o Burst fractures and fracture dislocations most likely to have neurological involvement
o Complete vs Incomplete Transection
! Complete: Spinal shock " Neural deficit persists after spinal shock ends
• Spinal shock: state of complete spinal areflexia
o Physiological dysfunction of spinal cord (complete paralysis and anaesthesia, with loss of anal reflex) – loss of
basal excitatory stimulus from brain to neurons
o Bulbocavenosus reflex signifies end of spinal shock (can last up to 3 days)
• Neural deficits: paraplegia (thoracic and lumbar lesions) or quadriplegia (cervical lesions)
! Incomplete: Persistence of sensation distal to injury suggests incomplete lesion
• Neural deficits: partial sensory and motor loss below level of lesion
• Types: Central cord syndrome, anterior cord syndrome, posterior cord syndrome, Brown-Sequard
o Type of Neural Injuries
! Neurapraxia: Neurological deficits recover within mins or hours (occurs in patients whose spinal canal have small AP diameter)
! Cord Transection: Spinal shock " Followed by UMN signs
! Root Transection: Neurological deficit in distribution of damaged roots (may recover and residual motor paralysis remains
flaccid)
• Management
o Incomplete transection: surgical decompression + stabilization of spine
Complete transection: overall management
o Skin: Prevent pressure sores with meticulous nursing
! Wash, dry and powder patient’s back
! Patient taught to relieve pressure intermittently during prolonged sitting
o Bladder and bowel:
! Bladder: Catheterise to prevent overflow incontinence which can predispose to infections + Bladder training subsequently
! Bowel: Trained with help of enemas, aperients and abdominal exercises
o Muscles and joints: Prevention of contractures
! Preventing contractures: Passive exercises, standing, walking
! Reversing contractures: Tenotomies

SPASTIC PARAPARESIS

1. Expose pt’s lower limbs

2. Inspect, look at face (eyes / facial asymmetry)
3. Look at UL and LL for abnormal posture, wasting of muscles, skin lesions
4. Look for fasciculations
5. Tone + clonus " spastic (beware Gegenhalten)
6. Reflexes " hyperreflexia
7. Power " weak
8. Sensation
• Pin prick level found " transverse myelopathy (cord compression / cord infarction / myelitis)
• Dorsal column loss " subacute combined degeneration of spinal cord, taboparesis (check gait / Romberg / Argyll Robertson pupils /
pallor)
• Dissociated sensory loss " syringomyelia
9. Test for cerebellar signs (+ in MS, FA, brainstem lesion – strokes)
10. Offer:
• Check spine for scars, tenderness, deformity
• PR for anal tone
• Sacral sensation (S2/3/4) sparing for intrinsic cord compression
• Examine UL:
o UMN " bilateral stroke / high cervical myelopathy
o Inverted supinator " C5/6 lesion
o Wasted hands " syringomyelia / cervical myelopathy / MND
• Test cranial nerves (bulbar / pseudobulbar palsy)
11. Ddx: spastic diplegic CP / parasagittal cranial tumour / hereditary spastic paraparesis (UL milder than LL)

! 157!
1. Osteoarthritis
DEFINITION
Degenerative disorder of synovial joints primarily affecting cartilage and subchondral bone.
Progressive softening & disintegration of articular cartilage + new growth of cartilage & bone at joint margins (osteophytes) + capsular fibrosis
BACKGROUND
Epidemiology • Secondary
• Frequency of OA: o Vascular
o Asians: knees > hips o Infective: Syphillis
o Caucasians: hip > knees o Site with history of Trauma (injury to articular surface):
• OA of hands and knes: F > M eg. scaphoid fracture, Kienbock’s disease
• OA of hip: M > F ! Loose bodies
Morphological Changes o Autoimmune: RA
1. Cartilage degeneration o Metabolic: HyperPTH, crystal deposition dz
o Cartilage breakdown usually starts in area of excessive o Inflammatory, Iatrogenic
loading (eg. changes most marked in medial o Neoplastic
compartment in varus deformity) o Congenital
o Fissuring o Degenerative
o Pitting Types
o Eburnation as joint motion polishes surface 1. Polyarticular OA (usually primary OA): Common joints affected:
2. Bone hypertrophy " osteophyte formation 1) DIPJ of hands most common (Heberden’s nodes) 2) PIPJ of
3. Mild synovitis hands (Bouchard’s nodes) 3) 1st CMCJ, 4) 1st MTPJ, 5) knees,
4. Capsular fibrosis 6) hip 7) cervical and lumbar facet joints
X-ray Presentation (LLOSS) 2. Monoarticular OA: In weight bearing areas
1. Loss of joint space (usually only in 1 compartment; unlike 3. OA in unusual sites: If OA appears in shoulder, elbow, wrist,
panarthritis in inflammatory conditions) ankle, suspect a previous abnormality or generalized disease.
2. Loose body Grading of chondral damage (Outerbridge classification)
3. Osteophytes at margins of joint • Grade 0: Normal cartilage
4. Subchondral cyst • Grade 1: Cartilage softening and swelling due to
5. Subchondral sclerosis degeneration
6. Others: bone irregularity, signs of old injuries o water content increases from 80% to 90%
Causes • Grade II: Partial thickness defect with fissures on surface that
• Primary do not reach subchondral bone or exceed 1.5cm in diameter
o Idiopathic o Collagen fibres exposed
o Senile (degenerative) • Grade III: Fissuring to level of subchondral bone in an area
o Post-menopausal with diameter more than 1.5cm
o Joints: DIPJ and carpometacarpal joint in thumb • Grade IV: Exposed subchondral bone
o Polyarticular presentation o Cartilage completely worn off (including basal layer)

SIGNS/ SYMPTOMS & HISTORY

Presentations' Loss!of!Function'
• Mechanical!Pain! • Job!
• Stiffness!(w!crepitus)! • Recreation! Poor'Quality'of'life'
• Swelling! • Compare!with!premorbid!
• Deformity!(usually!varus)!

Important aspects of history o High dose or multiple NSAIDs

• NO systemic involvement o Concomitant use of corticosteroids and/or warfarin
• Joint pain o Age >60 yrs
o The usual 6 points about pain Pathophysiology of s/s
o Which joints? • Causes of mechanical pain
o Insidious onset o *Mechanical pain characterized by: exacerbation on
o Morning stiffness not prominent (<30mins) movement, relief with rest, minimal night pain,
o Worsened by activity morning stiffness < 30min
o Alleviated by rest o Vascular congestion of subarticular bone (pain due
• ASK ABOUT BACK/ HIP PAIN WHICH CAN BE to bone pressure)
REFERRED TO THE KNEE o Capsular fibrosis (pain on stretching the shrunken
• Precipitating causes capsule)
o Trauma o Muscular fatigue
o History of contact sports / occupation o NOTE: OA itself does not cause pain; cartilage and
o Associated conditions – RA, syphilis synovium have no nerve supply
o BMI of patient • Causes of stiffness: Capsular fibrosis
• Functional Loss • Causes of swelling
o Job scope o Intermittent: effusion
o Recreational activity restriction o Continuous: capsular thickening or large
o Premorbid status: function & mobility osteophytes
• Social hx – ask about housing (floor, lift landing) • Causes of joint instability in late stages
• Treatments tried (TCM?) o Loss of cartilage and bone
• GI bleed risk o Asymmetrical capsular contracture
o History of ulcer disease and/or GI bleeding o Muscle weakness
! 158!
DIFFERENTIAL DIAGNOSIS (FOR HIP AND KNEE PAIN)
1. Referred pain from hip or back d. X-ray:
2. Vascular – AVN i. Uniformity in joint space narrowing
a. Articular cartilage preserved despite progressive bone ii. Absence of hypertrophic bone changes
collapse and deformity, unlike in OA (osteophytes, sclerosis)
Ischaemic pain Neuropathic pain iii. Presence of erosive bone changes (juxta-articular
! Fixed claudication distance ! Variable claudication erosions)
! Better walking downslope distance 4. Trauma
! Recovers quickly with rest ! Better walking upslope 5. Autoimmune: PMHx (refer point 3)
! Pain present at night ! Recovers slowly with rest 6. Metabolic – Gout, pseudogout
! Pt usu sleep in kyphosed 7. Infective – TB, other forms of septic arthritis
position with no pain a. Warmth, fever, tenderness, swelling, trauma,
3. Inflammatory – RA, AS, Reiter’s disease inoculation (eg. intraarticular injection)
a. Short history 8. Neoplastic: other bone pain, LOW, LOA, SOB, goiter,
b. Signs of inflammation (systemic manifestations) urinary, GIT
c. Sites: RA usually more proximal (MCPJ, wrist) unlike
OA (DIPJ, PIPJ) and has severe morning stiffness

INVESTIGATIONS: 1) to confirm Dx & exclude DDx 2) to look for causes 3) to look for Cx (2 & 3 usually not applicable)
• Haematological o Culture
o FBC: raised total white for infection, Hg and platelet o Gram stain, AFB smear
for operation suitability o Crystal tests – for gout
o ESR/CRP: Inflammation o Cytology
• Biochemical • Radiological
o Renal and Liver panel: baseline renal and liver • Others (pre-op)
function, particularly if long term NSAIDs considered o Chest X-ray
• Microscopy o ECG
MANAGEMENT
• Conservative (non-surgical) • Surgical
o Non-pharmacological o General Indications
! Lifestyle modification: weight loss, exercise, avoid ! Significantly symptomatic (instability, pain, deformity,
kneeling and squatting disability)
! Physiotherapy: strengthen muscles, preserve and ! Failure of conservative management
improve joint mobility, improve symptoms ! Of adequate health status to tolerate surgery and
• Knee extension or leg lifting exercises, utilize prosthesis
stationary cycling, hydrotherapy o Types of surgery
• ?Application of warmth: eg. radiant heat, ! Arthroscopic debridement and washout
shock wave diathermy ! Realignment osteotomy (in younger patients)
! Occupational therapy: load reduction with walking ! Arthrodesis: done only if strong contraindication to
aids, soft soled shoes arthroplasty / as a salvage procedure
o Pharmacological ! Arthroplasty: Last approx 15 years
! Analgesia: o Post-Sx: physioRx + CPM (continuous passive movment)
• Acetaminophen (paracetamol): shld be 1st line to maintain joint ROM and muscle power
drug; effective in some o Complications:
• NSAIDs (aspirin, ibuprofen, naproxen) ! Intraoperative
o Must be used with special care in: • Fracture: Tibia/femur for TKR and
>60y, previous history of GI bleed, acetabulum/femur for hip replacement (HR)
concurrent warfarin/ steroid • Neurovascular injuries – peroneal nerve in
medications, renal dysfunction TKR and sciatic nerve in HR
o Prescribe with PPI/H2RA in patients • GA complications
with increased likelihood of GI bleeding • Blood loss
• COX-2 inhibitors (celecoxib, etoricoxib): Vioxx ! Early
a/w increased risk of stroke & cardiac events • Infection
• Tramadol: consider if highly resistant pain • Fat embolism syndrome
! Glucosamine (anti-inf) with chondroitin (inhibits • DVT and pulmonary embolism
cartilage breakdown and stimulate cartilage repair): o DVT prevention:
at least as effective as NSAIDS, with the added o 1) pre-operative: thromboembolic
advantage of fewer side effects deterrent (TED) stockings
! Intra-articular injections: relieve pain, increase ROM o 2) peri-operative: TED stockings,
• H&L (triamcinolone + lignocaine): Consider in compression boots and foot pumps
patients with highly resistant pain. It is (eg. pneumatic intermittent
recommended that no more than 4 compression devices), minimize
glucocorticoid injections be administered to a length of surgery
single joint per year because of the concerns o 3) post-operative: low dose LMW
with long-term damage to cartilage heparin, early mobilization (physio)
• VIscosupplementation with hyaluronic acids • Late
(Synvisc): Marketed as ‘joint replacement’ o Heterotopic ossification
substances; expensive, no evidence to o Periprosthetic fractures
support its efficacy o Loosening of joint (septic or aseptic)
o Disruption of extensor mechanism

! 159!
OSTEOARTHTITIS OF THE KNEES
• Risk factors ! May be accompanied by cartilage regeneration
o >50yr old procedures
o Overweight • Chondrocyte transplant: Harvest condrocytes
o Hereditary from non weight-bearing sites, e.g.
o Competitive contact sports (also contributed by previous patellofemoral surface, culture, reimplant
injuries like torn meniscus etc) • Microfracture of subchondral bone:
o Deformities (eg. genu valgus/varum) Subchondral penetration of bone, inducing
o Secondary OA (injury to articular surface, torn meniscus, regrowth of fibrocartilage
ligamentous instability) • Mosaicplasty: Cylindrical cartilage taken from
o NOTE: recreational running is NOT a RF non-weight bearing areas, implanted on knee
• Symptoms joint surface to form a new layer of cartilage,
o NOTE: TFOA often more significant in 1 cmpt of joint consisting of the intact original cartilage and
o Pain in knee joint the transplanted grafts
! Medial tibiofemoral compartment OA: on walking o Realignment osteotomy:
! Patellofemoral OA: on walking up and down stairs, ! Only in certain cases (eg. unicompartmental
squatting involvement)
o Stiffness ! Typically an high tibial valgus osteotomy done in
! After inactivity (but jts feel stiff after rest and knee younger patients with medial TF compartment OA
hurts to get going after sitting for awhile) • Redistributes weight to lateral side
! Morning stiffness <30min • Often successful in relieving symptoms,
o Swelling (mild) staving off the need for TKR
o Deformity ! Contraindications:
! Genu varum • Inflammatory arthritis
o Locking and pseudo-locking • Severe flexion deformity >15deg
! Locking • Varus/valgus > 15deg
! Pseudo-locking (reaction to pain) • >5mm loss of subchondral bone
o Instability/ giving way
• Lateral trust while walking
• Look
! Mechanical axis vs Anatomical axis
o Surgical scars
• Mechanical: centre of hip to centre of ankle
o Alignment: genu varum usually (genu varum/valgus
• Anatomical: line of femur to line of tibia
predisposes to OA); externally rotated
(normally 4-6deg valgus)
o Muscle wasting of quadriceps (usually medial side)
o Arthrodesis: done only if strong contraindication against
o Gait: antalgic
arthroplasty / as a salvage procedure
o Squat: painful, cannot squat full or get up
o Arthroplasty (unicompartmental or total knee)
o Impt –ves: rheumatoid nodules, tophi, rashes, Sjogren’s
! Indications: when symptoms are severe
• Feel
• Try to avoid doing in patients <60 as TKRs
o Joint line tenderness (for tibiofemoral OA)
usu last only 10-15y
o Patella medial or lateral facet tenderness (in PFOA)
! Types
o Joint effusion (usually mild)
o Impt -ves: no warmth or synovial membrane thickening • Unicompartmental
• Move • Total +/- preservation of PCL; PCL
o Decreased ROM (extension lag due to quads wasting, preservation preserves proprioception function
fixed flexion deformity) but ↑ wear of prosthesis
o Crepitus (PF or TF?) ! Complications
• Special tests • Intraop – GA, # of tibia or femur
o Patella grinding test (for PFOA) • Immediate – vascular injury to superficial
o Signs of ligamentous/ meniscal injuries which can initiate or femoral, popliteal and genicular vessel
accelerate OA • Early – DVT/PE, fat embolism, infx, peroneal
• Request: nerve palsy (1%)
o Examine other joints esp hip and back (exclude hip and • Infection: Management: 2 stages
back causes of knee pain " Referred pain) o Removal of implant, plus 6 weeks IV
o Neuro exam SMART: sensory, motor, autonomic, reflexes, antibiotics
trophic changes o Reimplantation after Abx completed
• Radiological (for knee): 4 views to view 3 compartments • Late – loosening, patellar instability, #,
o Weight bearing AP view: so that even small degrees of disruptn of extensor mechanism,
articular cartilage thinning can be seen periprosthetic #, Wear of polythene surfaces
o Skyline (tangential) view o For rare cases where OA confined to patellofemoral joint
! Different patterns of PFOA: lateral, medial, global ! Arthroscopy to confirm diagnosis
! NOTE: lateral condyle is higher ! Types of Sx:
o Lateral • Realignment procedures
o Long film (to see degree of varus/valgus) • Patellectomy: problems a/w it include loss of
* For knee important to view all 3 compartments: medial, lateral, normal knee power and function, quads
patellofemoral compartment weakness, and failure to resolve anterior knee
* Peripheral osteophyte formation is most specific sign pain " may eventually require TKR for knee
• Surgical Management: arthritis
o Arthroscopic debridement and washout: • Patellofemoral arthroplasty
! For early OA or as a temporizing procedure to delay • Total knee arthroplasty
arthroplasty (up to 5 yrs) or if CI to osteotomy/ TKR • Cartilage transplantation (under research)
! Degenerate meniscal tears, loose bodies and
osteophytes can be trimmed

! 160!
Mr / Mdm XXX is a __ years old (race) gentleman / lady,
premorbid status: (ADL indep, community ambulant – w/wo aid),
occupation: ____________________,
with a significant PMHx of (left / right TKR in XXXX year) ,
presenting complaint: currently admitted for elective (left / right)
total knee replacement.
He / she presents with a (duration) history of bilateral progressive
knee pain (right > left / left > right) that has:
1. Failed to improve with conservative management
2. Gotten progressively disabling over the years
3. Resulted in marked loss of functioning
The knee pain is associated with:
1. Recurrent swelling
2. Morning stiffness / stiffness after resting
3. Progressive deformity
The knee pain started (duration) years ago and has gotten
progressively worst.
He / she describes the pain as (sharp / ) in nature. It is mechanical in
nature, aggravated by movement when he / she does (type of
activity) and relieved by rest. It is also worst at the end of the day.
The pain is felt in the (site: anterior / medial) aspect of both knees
with no radiation.
His / her current pain score is ___ and the pain (severity: affects
sleep / requires frequent use of painkillers) .
In addition, he / she experiences morning stiffness in both knees
that do not last more than 30 minutes.
He / she also has recurrent swelling of the knees that recurred after
aspiration.
Over the years, he / she noted that her knees have become
progressively deformed.
He / she also experiences instability of the knees characterised by a
feeling of his / her knee giving way when he / she walks at times. He /
she does not have any symptoms of locking (exclude meniscal
injury).
Functional Status
Currently, he / she is (able / unable) to climb stairs, with (2 feet
per stair / alternate foot per stair) .
He / she is also unable to squat since (duration) years ago, and is
unable to (kneel down to pray etc.) .
His / her walking distance is limited to ______ from ______
previously, (with / without) a walking aid.
Systemic Review
He / she has no hip pain, back pain or neurological symptoms like
weakness or numbness of the lower limbs.
He / she does not have any previous trauma to his / her knees and
there is no involvement of other joints in the body. He / she also does
not have a history of joint infection.
There is no fever or constitutional symptoms like loss of weight or
loss of appetite
Systemic review is unremarkable – no SOB / CP / change in bowel
habits / urinary symptoms.
Management so far (options tried)
He / she was treated conservatively with analgesia: (type) , intra-
articular injection of _____________, as well as non-pharmacological
agents like advice on lifestyle modification, weight loss, physiotherapy
and knee braces for the past ____ years. However, the above have
not been able to control his / her symptoms. He / she is keen for
operation as his / her symptoms affect his / her functioning.
Past Medical History
Mr / Mdm XXX has a past medical history of _____________ for
(duration) .
He / she has no history of gout, rheumatoid arthritis or septic arthritis
of the knee joint.
He / she also does not have a history of peptic ulcer disease / GI
! 161!
bleeding.
He / she had previous operations for ____________ / TKR for the
other knee.
He / she has NKDA and is currently on ___________ for her medical
conditions.
Social History
He / she (does not smoke / smokes / is an ex-smoker and has quit
XX years ago) , ( sticks/day x years).
He / she (has / does not have) a habit of regular intake of alcoholic
drinks.
He / she has (good / poor) social support. He / she works as a
_________ and his / her condition affects her job. He /she lives with
his / her ________. His / her main caregiver is his / her
______________.
He / she lives in a residential (with / without) lift landing. There (is
/ is no) squatting toilet in the house.
Currently, the family (does not have any financial issues / is
receiving financial aid from ) .
In summary, Mr / Mdm XXX is a __ years old (race) gentleman /
lady with co-morbidities of ________________, currently presenting
with bilateral mechanical knee pain for (duration) , worst on the
(left / right) associated with recurrent swelling, stiffness and
progressive deformity that has severely affected her daily functioning.
She has failed conservative management and is currently admitted
for elective (left / right) total knee replacement.
PHYSICAL EXAMINATION
On physical examination, Mr / Mdm XXX is alert and comfortable at
rest.
Appearance: He / she appears overweight, with a BMI of
_______.
Vitals: Her PR is _______, RR is _______ and BP is
_______. (SpO2: ______; VAS: _____.)
Heart: S1S2 were heard on auscultation.
Lungs: Lungs are clear.
Abdo: Soft, non-tender
Examination of the upper limbs did not reveal any Herberden’s nodes
or Bouchards nodes, gouty tophi or rheumatoid nodules.
Mr / Mdm XXX has an (antalgic gait / lateral thrust) on walking. He /
she (requires / does not require) the use of a walking frame /
assistance in walking. There is a genu varus and fixed flexion
deformity of ____ degrees of his / her knees. There is also wasting of
the quadriceps muscles, with thigh circumference of ____ cm and
____cm on the right and left lower limb respectively.
There (were no scars and sinuses / was a longitudinal well-healed
midline scar across the (left / right) knee joint) , and no erythema
of the skin around the knee joint. There were no distinct swellings
around the knee joint.
There was fullness noted in the parapatellar fossa of the knee joint
and the (bulge test / patellar tap / cross fluctuance) was positive,
indicating (size: small / moderate / large) effusion.
The knee did not feel warm.
There was no retropatellar tenderness, patellar grind was negative
Tenderness was noted on palpation of the medial / lateral joint line.
Flexion of the knee joint is limited to _____ degrees and creptius was
felt on movement.
The anterior and posterior cruciate ligaments are intact – the anterior
and posterior drawers as well as Lachman tests were negative. There
(is / is no) laxity of the medial / lateral collateral ligaments when
tested at 30 degrees of flexion of the knees.
Screening of the hip joint and the back did not reveal any
abnormalities.
The popliteal, posterior tibial and dorsalis pedis pulses were well felt
in both lower limbs.
Neurologically, power of bilateral lower limbs is full and sensation is
intact bilaterally.

In summary, Mr / Mdm XXX is likely to have bilateral osteoarthritis of

the knees as evidenced by genu varum and fixed flexion deformity of
____ degrees of the (left / right) knee. He / she also has quadriceps
wasting of the (left / right) knees and an antalgic gait / lateral thrusting
on walking. There is _____ knee effusion with ______ test positive. I
also note tha there is retropatellar tenderness / positive patellar grind
and tenderness along the ______. Flexion of the knees are limited to
_____. Collateral and cruciate ligaments are intact. Neurovascular
status of the lower limbs are intact.

OSTEOARTHTITIS OF THE HIP

• Causes: o Leg usually in external rotation and adduction
o Young adults: congenital subluxation, Perthes’ disease, (appears shortened)
SCFE (" coxa vara), acetabular deformities/injuries • Move
(eg. acetabular dysplasia**) o Decreased ROM (esp int rotation, abduction and
o Older adults: RA, AVN***, Paget’s disease, primary OA extension)
• Symptoms o Thomas’ test: may have slight fixed flexion
o Pain in groin" may radiate to knee o Trendelenberg’s test may be positive
o Joint stiffness • Special tests
! Unable to put on socks and shoes, tie shoelaces, o Referred pain: exclude back causes of hip pain (SLR,
clip toenails Faber’s)
! Unable to use squatting toilets • Investigations: Superolateral joint space narrowing, “elephant
o Deformity trunk osteophytes”
! Externally rotated and adducted leg • Surgical Management
! Leg feels shorter o Intertrochanteric realignment osteotomy (in younger
o Limping patients)
• Look o Total hip arthroplasty (in older patients)
o Gait: trendelenburg, antalgic o Arthrodesis (in young adults with marked destruction or
if arthroplasty contraindicated)

OSTEOARTHTITIS OF THE HANDS

• Risk factors o Tenderness (tenderness localized to 1cm distal to radial
o Post menopausal women styloid in CMCJ OA)
o Primary OA: polyarticular and bilateral disease o Swelling at base of thumb
o Secondary OA: CINDVTM (scaphoid fracture, o Nodes
kienbock’s disease) • Move
• Symptoms o Decreased ROM
o Pain, stiffness, swelling of finger joints o Crepitus
! DIPJ > PIPJ > 1st CMCJ o Laxity of 1st CMCJ
! Usually starts w 1 or 2 fingers which spreads to o Grind test positive- sharp pain on compressing and
all fingers and both hands rotating metacarpal longitudinally against trapezium
o Deformity due to bony thickening (Herbeden’s nodes, • Investigations
Bouchard’s nodes) o Often a clinical diagnosis
• Look • Management: Conservative and Arthrodesis
o Deformity: o Rest, Splint
! Herbeden’s nodes (DIPJ) o CMCJ of thumb: Can treat conservatively (& w H&L inj)
! Bouchard’s nodes (PIPJ) + ulnar deviation of or excision arthroplasty or replacement arthroplasty
fingers o DIPJ: Can treat by arthrodesis
! CMCJ (trapezio-metacarpal joint) of thumb: Bony o Operative (only if very painful or unstable)
thickening, adduction (late) hence squaring, ! Arthroplasty
metacarpal subluxation (late), +ve grind test ! Excision of trapezium (for 1st CMC joint)
! Mallet deformity (DIPJ) ! Arthrodesis
• Feel
!
This is an elderly (Chinese / Malay / Indian) lady.
On inspection, I note the presence of Heberden’s nodes over the DIP joint(s) of the (left / right) (index / middle / ring / little) finger(s), and
Bouchard’s nodes over the PIP joint(s) of the (left / right) (index / middle / ring / little) finger(s), characteristic of OA of the hand. There (are /
are no) associated swellings of the hand joints.
I do not note any scars or skin changes over the hand.
I would like to move on to palpate the joints of the hands. (ask pt for any pain 1st)
The swellings are bony hard with smooth surfaces. They are non-tender, and the joints do not feel warm.
I would like to proceed to test for the range of motion. (test finger flexion & extension)
The ROM of the finger joints (are / are not) limited.
I would want to perform a functional assessment by asking the patient to pick up coins & hold a cup. I would also want to examine the other joints
(e.g. knee joint) for arthritis.!
!

! 162!
2. Rheumatoid Conditions
RHEUMATOID ARTHRITIS
Definition: Systemic chronic inflammatory disease of unknown cause that affects the peripheral joints in a symmetrical fashion
Epidemiology
• Prevalence: 0.8% of adult population
• Risk factors
o Women (3W:1M) aged 40-50yrs old
o Genetic susceptibility
• Morbidity:
o High lvl of functional impairment
o If untreated, 20-30% will become permanently work disabled within 3yrs
• Mortality: related mainly to extra-articular manifestations
Pathophysiology
• Genetic susceptibility (HLA-DR4, HLA-DR1) " immune reaction on synovial tissue" inflammatory reaction in joints and tendon
sheaths" anti-IgG autoantibodies (rheumatoid factors) in blood and synovium " chronic synovitis and articular cartilage
destruction
o Cause unknown; postulated to be response of genetically susceptible host to an infectious agent
! Persistent infx of articular structures/retention of microbial products in synovial tissues
! Alterations of joint components by microorganisms/ response to microorganism
! Molecular mimicry
Stage Pathology Signs X-Ray
Stage 1: • Synovitis of proximal joints and tendon • Pain (acute), chronic fusiform swelling (thickened • Soft tissue
Synovitis sheaths synovium), wasting, effusion, stiffness in MCPJ, swelling and
o Inflammation and thickening of PIPJ, wrists and tendon sheaths around the joints. osteoporosis
synovial membrane (Synovial cell • Gradually affects other joints: around joints
hyperplasia and proliferation) " wrists > feet > knees > shoulders
cell-rich effusion (Neutrophils and • Extensor tenosynovitis (thickening, tenderness and
aggregates of organizing fibrin) into crepitation over back of wrist or palm on passive
joints (synovial surface) and tendon movement)
sheaths • In larger joints: warmth, synovial hypertrophy,
o Increased vascularity (angiogenesis) intraarticular effusion
• Joints and tendons painful and
swollen but still intact
• Potentially reversible
Stage 2: • Joint (cartilage, subarticular bone, jt • Pain (constant ache) • Narrowing of
Destructive capsule), tendons, ligaments • Joint instability, ligamentous laxity joint spaces
destroyed • Tendon ruptures • Small
• Erosion of articular cartilage & • Restricted ROM periarticular
subarticular bone • Muscle wasting erosions
o Invasion by pannus
o Proteolytic enzymes (secreted by
neutrophils)
o Osteoclastic resorption
• Tendon sheaths: tenosynovitis,
invasion of collagen bundles " partial
or complete tendon ruptures
Stage 3: • Articular destruction (cartilage and • Pain, deformity, instability, decreased ROM, • Marked
Deformity subarticular bone), capsular stretch, disability articular
(often ligament damage & tendon rupture " o Loss of function destruction
results in progressive deformity and instability of ! Class 1: normal functional activity • Joint deformity
loss of joints " loss of function ! 2: normal functional ability despite discomfort and dislocation
function) o Fibrosis/ calcification of pannus ! 3: can only perform a few tasks of work/ self care
o Fibrous/ bony ankylosis ! 4: almost/complete incapacity
• Thumb: Z-deformity
• Fingers: ulnar deviation, subluxation or dislocation of
MCPJ, swan-neck/boutonniere deformities
• Wrist: radial and volar displacement
• Elbows: limited extension
• Shoulders: limited abduction
• Knees: swollen, held in flexion and valgus
• Toes: clawed

Diagnosis criteria: mostly clinical

• 1) bilateral, symmetrical polyarthritis
• 2) involving proximal joints of hands or feet
• 3) present for at least 6 weeks
• 4) confirmed with subcutaneous nodules or periarticular erosions on x-ray
• 2010 ACR / EULAR Rheumatoid Arthritis Classification Criteria
o American College of Rheumatology / European League Against Rheumatism

! 163!
 o Those with a 6points or higher is classified as an RA patient, provided he has synovitis in at least one joint and given that there is
no other diagnosis better explaining the synovitis.
1) Joint involvement 1 large joint: 0 point
- Small joints: MCPJ, PIPJ, IPJ, MTPJ, wrist 2-10 larger joint: 1 point
- Large joints: shoulder, elbow, hip, knee, ankle 1-3 small joints: 2 points
4-10 small joints: 3 points
More than 10 joints (with at least 1 small joint): 5 points
2) Serological parameters Negative RF and negative ACPA: 0 points
Low positive RF or low positive ACPA: 2 points
High positive RF or high positive ACPA: 3 points
3) Acute phase reactants Elevated ESR or CRP: 1 point
4) Duration of arthritis Symptoms lasting at least 6 weeks: 1 point

Rheumatoid arthritis: features RHEUMATOID:

Ragocytes/ Rheumatoid factor (anti-IgG), HLA-DR4/ HLA-Dw4, ESR increase/ Extra-articular features (restrictive lung disease, subcutaneous
nodules), Ulnar deviation, Morning stiffness/ MCP joint, Ankylosis/ Atlantoaxial joint subluxation/ Autoimmune/ ANA, T-cells (CD4)/ TNF,
Osteopenia, Inflammatory synovial tissue/ Idiopathic/ IL-1, Deformities (swan-neck, boutonniere)

Differential diagnoses
• Seronegative inflammatory polyarthritis: psoriatic arthritis, Juvenile chronic arthritis (still’s disease), SLE
• Ankylosing spondylitis: Primarily affect SIJ and intervertebral joints but may involve peripheral joints
• Reiter’s disease
o Primarily affects larger joints and lumbosacral joints
o + urethritis, colitis, conjunctivitis
• Polyarticular gout
o X-ray: erosions different from RA
o Nodules tend to be asymmetrical
• Pseudogout
• Polyarticular OA
• Polymyalgia rheumatica
o Giant-cell arteritis (vasculitis) that carries risk of temporal arteritis resulting in blindness
o Common in middle-aged or elderly women
o Signs and symptoms
! Pain and post-inactivity stiffness around shoulders and hips
! Muscular weakness
! Muscles are tender, not joints
o Investigations: ESR remarkably high
o Management: corticosteroids provide rapid and dramatic relief of all symptoms (response used as diagnostic test)
Symptoms (periods of relative quiescence + periods of flare)
• Usual pattern is insidious onset (but usually more rapid onset than OA) of symmetrical polyarthritis affecting mainly hands and feet +
early morning stiffness + constitutional symptoms; sometimes may start in other joints as a chronic monoarticular synovitis
• Joints: typically PIP, MCP, wrist, elbow, shoulders, knees, ankles, feet
o Pain (insidious onset)
o Stiffness – early morning stiffness >1hour
o Swelling – symmetrical, red, warm
o Progressive deformity
! Z-collapse (if 1 of 2 adjacent joints changes direction, then overlying long tendons will pull other joint in opposite direction)
o Decreased ROM
• Constitutional symptoms – fever, fatigue, malaise, LOW
• Associations
o Sjogren’s syndrome: dry eyes, dry mouth, recurrent chest infx
o Felty’s syndrome: splenomegaly, leg ulcers, recurrent infx, LN, weight loss
• Extraarticular manifestations: refer below
Other aspects of Hx:
• Previous Rx history
o Medications: NSAID, steroids (assess for adverse SEs)
o Intra-articular injections
o Previous operations
• Family Hx
• Social Hx: occupation, family setup, caregiver
Deformities of the hand
• Thumb:
o Z thumb deformity (flexion of IPJ and hyperextension
of MCPJ), carpometacarpal instability, ulnar collateral
instability, CMCJ swelling
• MCPJ:
o Volar subluxation or dislocation of MCPJ most
commonly over index and middle fingers – Prominent
metacarpal heads: chronic synovitis" failure of
palmar plate and collateral ligaments" flexors drag
prox phalanx palmarward" subluxation of joint
o Ulnar subluxation of extensor tendons
! 164!
 • Fingers:
o Ulnar drift/deviation of fingers, involving the more lateral digits in the more advanced cases:
palmar grip and thumb pressure naturally tend to push fingers ulnarwards" weakening of
collateral ligaments reduce normal resistance to this force
o Boutonniere (hyperextension of DIPJ, flexion of PIPJ): rupture of central slip" lateral slips
separate and head of prox phalanx thrusts through gap of extensor tendon
o Swan-neck (flexion of DIPJ, hyperextension of PIPJ)!
1. Failure of palmar plate of PIPJ
2. Rupture of FDS
3. Dislocation/subluxation of MCPJ and tightening of intrinsic muscles
o Swelling of PIPJ
• Rheumatoid nodules: Subcutaneous, rubbery lumps (usually at pressure areas like olecranon, pulp
of fingers and radial side of index finger; also on tendons (cause triggering or rupture), viscera, eye)
o Palpate the elbows for rheumatoid nodules (present in 25% of patients): Small granulomatous
lesion consisting of central necrotic zone surrounded by histiocytes and inflammatory
granulation tissue
• Carpus: Radial tilt of and volar subluxation of carpus
• Wrist:
o Deformity
1. Prominence of DRUJ (caput ulnar syndrome): Piano key sign positive (subluxation of DRUJ causing head of ulna to pop
up on dorsum of wrist where it can be jogged up and down)
2. Radial deviation of wrist
3. Volar subluxation
4. Subluxation of extensor tendon
o Tenosynovitis related
1. Carpal tunnel compression from flexor tenosynovitis (early)
2. Swelling of tendon sheath: Dorsum of wrist on ulnar side (ECU), Volar aspect (proximal phalanges)
• Tenosynovitis (treatment to include flexor synovectomy)
o Can affect flexor and extensor tendons
o Complications
1. Joint stiffness
2. Carpal tunnel syndrome
3. Triggering
4. Tendon rupture
5. Deformity (eg. FDS synovitis contributes to swan neck)
• Tendons
o Extensor tenosynovitis and rupture
o Flexor tenosynovitis
o 2nd problems: carpal tunnel syndrome, trigger finger, tendon ruptures
Other aspects of PE:
• Look: above deformities, palmar erythema, wasting of interossei (best seen in 1st dorsal web space)
• Feel: Palpate over swollen joints to detect warmth and tenderness of acutely inflamed joints
• Move:
o Functional assessment: unbutton shirt, write w pen
! Function
• Diminished grip strength – muscular weakness, pain, tendon malalignment / rupture, joint stiffness, nerve compression
• Loss of extension
o Joint problem – subluxation / dislocation
o Tendon – subluxation, rupture
o Hand examination: median nerve for any carpal tunnel syndrome ****
• Offer:
o Examine other joints in the body that are affected by RA
o Examine the rest of the patient for extra-articular manifestations of RA
! Extra-articular manifestations (occurs later in course of disease)
• Opthalmic – scleritis, episcleritis, keroconjunctivitis sicca
• Pulmonary – effusion, fibrosis
• Cardiac – pericarditis
• Vacular – vasculitis (predisposes to poor healing ulcers/wounds)
• Reticuloendothelial – lymphadenopathy, splenomegaly, Felty’s syndrome
• Neurological – carpal tunnel syndrome, multifocal neuropathies, ant subluxation of C1 on C2
o Ask patient how the condition affects his/her life
Investigations
• Haemotological
o FBC –Normocytic hypochromic anaemia (abnormal erythropoiesis from chronic inflammation), thrombocytosis, WBC & D/C:
eosinophilia " exclude infx
o Inflammatory markers: raised ESR, present CRP, high mucoprotein levels
! Indicates active disease; used for disease progression monitoring, treatment response
o RF (anti-IgG autoAb) positive (in 80%)
! Not specific (present in healthy ppl, SBE, TB, viral infx)
! Not required for RA diagnosis
! Prognostic: persistently high titres herald more serious disease and poorer prognosis
o ANA present (in 30%): positive in autoimmune disease: Not specific (also in SLE, scleroderma, Sjogren’s disease, Raynaud’s dz)
! 165!
 o ACPA –anticitrullinated protein antibodies (in 67%)
! Higher specificity (rarely positive if RA not present)
o UECr + LFT: assess renal and liver function before starting treatment
• Joint aspiration
o Analysis of synovial fluid: straw coloured, cloudy, flecks of fibrin, large numbers of WBCs esp neutrophils
o Biopsy: histological features non-specific and not diagnostic
• Imaging: X-ray " disease monitoring, treatment response
o Early (stage 1): soft tissue swelling, periarticular osteopenia
o Later (stage 2): juxta-articular erosions, narrowing of joint space (but lack of osteophytes c.f OA)
o Advanced (stage 3): articular destruction and joint deformity
o C-spine: atlanto-axial subluxation
Management
• Goals:
o Control dz activity
o Prevent/control joint damage
o Prevent loss of function
o Control pain
o Maximize QOL
• Treatment modalities
o Non-pharmacological: rest, patient education, PT, OT, splint (decrease synovitis, increase stability)
o Pharmacological: (early aggressive treatment, Esp those w poor prognostic factors)
! NSAIDs: Indomethacin, Diclofenac, Naproxen
• Symptomatic treatment: anti-inflammatory, analgesia
• Does not alter disease progression
• ADRs: PUD
• Contraindication: Renal impairment
! Steroids: Prednisolone
• Symptomatic treatment: anti-inflammatory
• May help slow disease progression/joint damage
! Disease modifying anti-rheumatic drugs (DMARDs): Methotrexate, Gold, Hydroxychloroquine (See Table)
• Slow down disease progression of bone & cartilage destruction
• Take 1-6 months to be effective
• Monotherapy/Combination
! Anti-TNF α: Etanercept, Abcliximab, Infliximab
o SURGICAL MANAGEMENT
! Surgical Release for nerve entrapment syndromes (eg. Trigger finger, CTS, De Quervain’s)
! Synovectomy
• For persistent synovitis > 6 mths
• Symptomatic relief of pain and swelling
• Restore ROM
! Arthroplasty
• Mainly for knees, can also be done for hip, shoulder, elbow
• Total joint replacement advised when bone destruction is present and joint unstable
• Pain relief, correction of deformity, Stability and alignment, Preserve ROM
! Others:
• Tendon repair
• Osteotomy (femoral or tibial osteotomy " improves function and relieves pain): genu valgum
• Arthrodesis (mainly triple arthodesis of ankle): surgical fusion of jt to give stability, pain relief, deformity correction
• Treatment by symptoms
o Synovitis: local corticosteroid injections, surgical synovectomy, splinting
o Tendon ruptures: repair, bypass by tendon transfers
o Joint instability: arthroplasty, arthrodesis
o Deformities: reconstructive surgery, splintage (eg. ulnar drift)

Onset of disease Conservative: physiotherapy, activity modifications (maintain muscle tone and joint mobility)
Pharmacological: NSAIDs (analgesics)
Early phase Conservative: physiotherapy, rest
(6-12 months) Pharmacological: NSAIDs, corticosteroids (5-7.5mg prednisolone) for up to 2 years (intra-articular
Control synovitis injections?), +/- 2nd line drugs (gold or penicillamine)
Progressive erosive Conservative: preventive splintage, orthotic devices
arthritis (1-5years) Pharmacological: already on 2nd line drugs (methotrexate, gold, penicillamine)
Operative:
• Soft tissue: synovectomy, tendon repair/replacement, joint stabilization, nerve entrapment
release (carpal tunnel, trigger finger, De Quervain’s)
• Bone: osteotomy
Late rheumatoid Occupational therapy for function
disease (5-20years) Operative:
• Indications: severe joint destruction, fixed deformity, loss of function
• Arthrodesis, osteotomy, arthroplasty

! 166!
 DMARDs Pharmacology Toxicity Investigations
Methotrexate - Recommended as initial DMARD - N+V - Baseline FBCs, U/E/Cr
- Rapid onset of action (1-2mths) - Mucosal ulcers - LFTs, Hep B/C status
- Retards progression of radiological erosions - Liver cirrhosis, ↑ LFTs - CXR
- Interstitial pneumonitis
- Severe BM suppression
- Teratogenic
Hydroxy- - Rash - Eye examination (6-12 mthly)
chloroquine - Abdominal cramps
- Diarrhoea
- Retinal pigmentation
Sulfasalazine - Faster onset (1-3 mths) - N+V - FBC, LFTs
- Retard Radiographic progression - Headache
- Rash
- BM suppression
- Teratogenic
Gold - Oral: Slow onset (6mths) - Rash - FBC
- IM: Faster onset (weekly injection of 22 wks) - Ulceration, mucositis - UFEME, U/E/Cr (at every
- Nephrotic syndrome injection)
- Panctyopenia
Leflunomide - Alternative to MTX - Diarrhoea - FBC, U/E/Cr
- Slows radiographic progression - Alopecia - LFTs, Hep B/C status
- Headache
- Immunosuppression
- ↑ LFTs
- Teratogenic!

Complications
• Fixed deformities
• Muscle weakness –prevent with physiotherapy and analgesia
• Tendon rupture from nodular infiltration (mostly at wrist)
• Joint lining rupture " synovial contents spill into soft tissues
o Manage underlying synovitis: splintage and injection; synovectomy
• Infection (septic arthritis; esp those on corticosteroid therapy)
o Signs: sudden clinical deterioration, increased pain in single joint
o Management: joint aspiration
• Secondary OA due to articular damage
• RARE
o Spinal cord compression (rare complication of cervical spine instability)
o Systemic vasculitis
o Amyloidosis

This is an elderly (Chinese / Malay / Indian) lady. On inspection, I
note that she has a pair of rheumatoid hands as evidenced by the
presence of bilateral symmetrical deforming polyarthropathy of the
small joints of the hands, namely the MCP joints and the PIP joints,
with sparing of the DIP joints. (I also note that she is Cushingoid in
appearance.)
There is radial deviation of the wrist accompanied by dorsal subluxation
of the distal radioulnar joint with prominence of the radial styloid
process. Piano key sign (is / is not) present.
There is also wasting of the intrinsic muscles of the hands.
In addition, there is volar subluxation of the MCP joints and ulnar
deviation of the fingers.
I note the presence of Z thumb deformity of the (left / right) thumb
and swan neck deformities over the (index / middle / ring / little)
finger(s) as well as Boutonniere’s deformities over the (index / middle /
ring / little) finger(s).
The joints are not swollen, not warm and not tender, hence disease is
in the quiescent stage.
(move joints – fingers + wrist, Tinel’s test, pronation & supination of
forearm)
She is unable to make a fist and there is severe limitation of movement
at the wrist joint.
ROM of wrist flexion and extension is ____.
Ulnar deviation is ____ and radial deviation is ____.
Supination is ____ and pronation is ____.
There are no trigger fingers or dropped fingers suggestive of tendon
rupture or any CTS release / tendon release scars.
I would like to proceed to look for rheumatoid nodules at the elbow.
I did not find rheumatoid nodules over the extensor surfaces of the UL
or over the olecranon process.

There (are / are no) swelling over the small joints of the hands. I do
not see any overlying skin changes or erythema.
There (are / are no) scars seen over ___________ suggestive of
previous tendon repair or arthrodesis.
I would like to proceed to palpate the joints. (ask pt for any pain first)
I would like to test for functional impairment by asking the patient to
pick up coins & to hold a cup.
Her hand function is (grossly impaired / relatively preserved) . She is
able to hold a cup with both hands. She is unable to (button her shirt /
uncap a pen to write) .

! 167!
 SERONEGATIVE SPONDARTHRITIS
• PAIRS –psoriatic arthritis, ankylosing spondylitis, IBD, reiter’s disease, still’s disease
• Characteristic spondylitis and sacroilitis
o Grades of sacroilitis
o Sacroiliitis: causes PUB CAR: (seronegative arthropathies + Bechet’s) Psoriasis, Ulcerative colitis, Behcet's disease, Crohn's
disease, Ankylosing spondylitis, Reiter's disease
• Associated w HLA B27
• Familial aggregation
• Overlap within families

ANKYLOSING SPONDYLITIS
• Risk factors
o 4M:1F, onset at 15-25years
o Genetics: HLA-B27
! First degree relatives at risk of psoriatic arthritis, IBD and Reiter’s syndrome
• Pathology
o Definition: chronic multi-systemic inflammatory disorder of the SIJ and axial skeleton,
w effects mainly in spine and SIJ, leading to progressive stiffening and fusion of axial skeleton
I Widening of joint Rome criteria NY criteria
II Joint erosioni Bilateral sacrolitis > grade I + any of the following: Bilat Sacroilitis > grade I OR unilat Sacroilitis > grade
III Sclerosis on both sides • LBP + stiffness > 3 mths not relieved by rest 2 AND any of the following:
IV Ankylosis • Thoracic pain or stiffness • LBP of inflammatory nature
o Pathophysiology: • ↓ lumbar spine ROM • ↓ lumbar spine movt in sagittal & frontal planes
! 1) Synovitis of • ↓ chest expansion • ↓ chest expansion
diarthrodial joints: SIJ • Hx of uveitis
and vertebral facet
joints
! 2) Inflammation of fibro-osseous junctions
• intervertebral discs, sacroiliac ligaments, symphysis pubis, manubrium sterni, bony insertions of large tendons
• 3 stages of Enthesitis: 1)inflammation with subchondral granulation tissue formation and erosion of adjacent bone,
2)fibrosis of granulation tissue " fibrocartilage, 3)ossification of fibrous tissue leading to ankylosis of joint (occurs in
ligamentous capsule attachment sites to bone)
o In the spine, this occurs in the junction btw vertebral bodies and annulus fibrosus of IV discs. Outer fibres of the
discs eventually undergo ossification " syndesmophyte formed " progresses to the characteristic bamboo spine
• DIAGNOSTIC CRITERIA (NEW YORK CRITERIA): (AS = radiological criterion + 1 clinical criterion)
o Low back pain > 3/12 (improved by exercise, not relieved by rest)
o Limitation of lumbar spine motion in both sagittal & frontal planes
o Limitation of chest expansion relative to normal values (< 5cm at 4th IC space)
o Radiological features of sacroilitis
• Symptoms
o Recurrent backache and stiffness
! Worse in early morning and after inactivity; relieved w exercise
! Insidious onset, >3months, Dull character
! Often begins unilaterally and intermittently (recurring at intervals over number of years) " as disease persists, it becomes more
persistent (gradually becomes continuous) and bilateral and progresses more proximally
! MAY start with symptoms in peripheral joints" eventually backache will predominate
o Radicular pain from referred pain in buttocks and thighs
o Later symptoms: pain and swelling of joints, tenderness at tendoachillis insertion,
intercostal pain and tenderness, difficulty breathing/ chest tightness from costovertebral and
costotransverse joint involvement, jaw pain/decreased ROM from TMJ involvement
o Extraskeletal manifestations
! Systemic: Fatigue, amyloidosis, osteoporosis
! Ophthalmo: iritis, acute anterior uveitis " glaucoma
! Cardio: Aortic valve disease (esp AR), carditis, cardiac conduction defects (arrhythmia)
! Respi: apical pulmonary fibrosis
! Archilles tendonitis, plantar fasciitis
• Signs
o Documentation of progression
! Loss of horizontal gaze (not quantitative)
! Finger floor distance
! Schober’s test
! Occipital-wall distance
! Chest expansion (costovertebral joints)
o Early:
! Slight flattening of lower back
! Tenderness over spine and SIJ
! Limited extension in lumbar spine
! Peripheral joints: occasionally swelling and tenderness of single large joint
o Late:
! Loss of lumbar lordosis, increased thoracic kyphosis and forward thrust of neck (loss
of cervical extension)

! 168!
 ! Upright posture maintained by flexed hips and knees
! Limited ROM in all directions but loss of extension earliest and most severe
• Wall test: heels, buttocks, scapulae and occiput unable to touch wall simultaneously
• Decreased chest expansion (should be >7cm in young men): <5cm at 4th IC space
! Peripheral joints (shoulders, hips, knees): inflammatory arthritis (tenderness, swelling, loss of ROM, tenderness of tendon
insertions)
! Most advanced stages: severe deformities (eg. Hyperkyphosis)
• Complications
o Spinal fractures as spine is rigid and osteoporotic
o Myelopathy (uncommon): Due to atlanto-axial subluxation or ossification of PLL
o Lumbosacral nerve root compression " may lead to cauda equina syndrome
• DDx: primary OA, causes of LBP (esp OM, TB, mets)
• Investigations
o Bloods: Raised ESR, HLA-B27 (can be –ve in 10% of cases), Rh -ve, normochromic normocytic
anemia, MCHC from NSAIDs use
o ECG: conduction defects
o Synovial fluid complement: not depressed, decreased viscosity, leukocytosis
o X-ray
! SIJ: Erosion and fuzziness of SIJ " may have periarticular sclerosis esp on iliac side "
ankylosis
• Whiskering: calcification of tendons attached to ischial tuberosity
! Vertebrae: AP, lateral spine XR; AP, lateral, open mouth C-spine
1. Flattening of normal concavity (squaring) of vertebral body: (erosions at the
vertebrae occur 1st at e anterosuperior anteroinferior corners)
2. Erosion of anterior corners of vertebrae
3. Sclerosis of edges (shiny corner sign/ Romanus lesion)
4. Ossifications of ligaments around IV discs producing syndesmophytes btwn adjacent vertebrae
5. Facet joint fusion + vertebral fusion
6. Bridging at several levels + syndesmophyte formation gives
appearance of bamboo spine
7. Costovertebral joint involvement
8. Atlantoaxial dislocation
• Osteoporosis common in long-standing cases" hyperkyphosis of
thoracic spine from wedging of vertebral bodies
! Peripheral joints: erosive arthritis or progressive bony ankylosis
o Bone scan: sacroilitis & spinal involvement
• Management
o Aims:
! Relieve pain and stiffness Romanus'lesion'
! Maximize skeletal mobility
! Avoid dvlpment of deformities
o Conservative
! Education: genetic counseling (50% chance of passing to children), chronic disease, fall prevention (osteoporosis)
! Lifestyle mod: PhysioRx (spinal extension exercises, postural trng, breathing exercises), exercise (swimming, dancing,
gymnastics), Avoid rest (increases stiffness)
! Phamacological:
• NSAIDs (usually indomethacin): ask abt renal function, hx of GIB, coagulant Rx
• Sulphasalazine: for persistent peripheral arthritis. Not useful for axial disease
! Radiotherapy: if drug therapy is ineffective
! Local corticosteroid injection: for plantar fasciitis and enthesopathy
! Systemic steroids: for acute iritis
! Anti-TNFα!(Infliximab)
o Surgical
! Peripheral joints: THA/ TKA + post-op indomethacin/ RT to decrease heterotrophic bone formation
! Spine flexion deformity: lumbar or cervical osteotomy (rare)
• Anesthesia related problems (difficult to give anesthesia in AS patients):
o Stiff neck hence hard to intibuate
o Breathing problems
He / she describes the pain as (nature) and it radiates to the buttocks
Mr / Mdm XXX is a __ years old (race) gentleman / lady, and thighs. The current pain score is ___. The symptoms of pain and
premorbid status: (ADL indep, community ambulant – w/ wo aid), stiffness are worse in the mornings, lasting more than 30 min and after
occupation: ____________________, periods of inactivity. It is not aggravated by movement of the patient.
with a significant PMHx of (ankylosing spondylitis if patient offers) ,
presenting complaint: currently admitted for (THR / corrective There (is / is no) associated hip pain / knee pain for (duration) .
surgery for the spinal deformity) . There (is / is no) associated neck pain / neck stiffness for (duration)
. (from atlantoaxial subluxation)
He / she presents with a (duration) history of (progressive / non-
progressive) low back pain and back stiffness associated with an He / she also complains of pain over:
increasing inability to (extend / flex) his / her (back / neck) over 1) Sole of his / her (left / right) foot ! plantar fasciitis
(duration) . 2) Posterior aspect of his / her (left / right) leg over the area of the
Archilles tendon ! Archilles tendonitis

! 169!
3) Peripheral joints ! similar changes in RA, peripheral arthropathy, Social History
pauciarticular juvenile idiopathic arthritis He / she (does not smoke / smokes / is an ex-smoker and has quit XX
4) Bony prominences ! iliac crest / ischial tuberosity / greater years ago) , ( sticks/day x years).
trochanter involvement He / she (has /doesnt have) a habit of regular intake of alcoholic drinks.
OR He / she has (good / poor) social support. He / she works as a
He / she has no complaints suggestive of peripheral joint involvement _________ and his / her condition affects her job. He / she lives with
or enthesopathies. his / her ________. His / her main caregiver is his / her ___________.
He / she lives in a residential (with / without) lift landing. There (is /
Functional Status is no) squatting toilet in the house.
Currently, his / her symptoms have limited his / her daily function, such Currently, the family (does not have any financial issues / is receiving
as (sitting / squatting / climbing up & down stairs / using the toilet – financial aid from ) .
having to stand to defaecate / lying down flat) .
His / her walking distance is limited to ______ from ______ previously, In summary, Mr / Mdm XXX is a __ years old (race) gentleman / lady
(with / without) a walking aid. with co-morbidities of ________________, currently presenting with
Systemic Review
He / she does not have any weakness or numbness of his / her lower PHYSICAL EXAMINATION
limbs or any red flag symptoms such as changes in bowel or urinary 1. Look:
habits, night pain, fever or constitutional symptoms like loss of weight • Loss of lumbar lordosis + fixed kyphosis
or loss of appetite. There is also no hx of previous trauma to the back. • Stooped “question-mark” posture
In addition, he / she has systemic complaints of: • Extension of C- spine to maintain horizontal visual gaze
1) Chest pain on breathing / SOB / palpitations ! AR / cardiac • Protuberant abdomen
conduction defects / apical pulm fibrosis o Restricted chest expansion from a fixed spine
2) Colicky abdominal pain / bloody diarrhoea ! Crohn’s disease / results in predominant diaphragmatic breathing
Ulcerative Colitis 2. Feel: tenderness
3) Blurring of vision / eye pain ! acute anterior uveitis / iritis 3. Move:
4) Rash ! psoriaform rashes • Examine pt’s gait
Management so far (options tried) • Limitation in range of motion
His / her symptoms have failed to improve with conservative o Lumbar flexion + Schober’s test
management such as __________________ for the past (duration) . o Lumbar extension
Past Medical History o Lumbar lateral flexion
Mr / Mdm XXX has a past medical history of _____________ for o Lumbar rotation
(duration) . (note any previous fractures) o Neck rotation
He / she also does not have a history of peptic ulcer disease / GI o Touch chest with chin
bleeding. • “Heels, hips & occiput” test to measure occiput-to-wall
He / she had previous operations for ____________. distance
He / she has NKDA & is currently on _____ for her medical conditions.
• FABERE test (SI joint involvement)
Family History
• Tests for Achilles tendonitis and plantar fasciitis
He / she (has / has no) family history of cancer or similar back
4. Complete the examination by:
pathologies.
• Shoulder and knee involvement
• Look for extra-articular involvement / complications
• Abdominal examination to look for signs of inflammatory
bowel disease

PSORIATIC ARTHRITIS
• Epidemiology: Affects men and women equally
• Signs/ distinguishing features
1. Assymetrical polyarthritis
2. Affects mainly IPJ of fingers and toes (may become completely flail and deformed (arthritis mutilans))
3. ¼ have sacroilitis and spondylitis like ankylosing spondylitis
4. Absence of rheumatoid nodules
5. Psoriasis of skin or nails usually precedes arthritis (hidden lesions in natal cleft or umbilicus
overlooked)
REITER’S DISEASE AND REACTIVE ARTHRITIS
• Pathology: aseptic inflammatory arthritis triggered by non-specific urogenital or bowel infection
o Shigella, Campylobacter, Yersinia, lymphogranuloma venereum, chlamydia trachomatis
• Epidemiology: Affects men more than women (10:1)
• Signs
o Clinical triad: polyarthritis, conjunctivitis, non-specific urethritis (+/- colitis)
o Mainly affects large joints like knee and ankle
JUVENILE CHRONIC ARTHRITIS (STILL’S DISEASE)
• Pathology: non-infective inflammatory joint disease for more than 3 months in children under 16years
• Epidemiology: 1 per 1000children; Affects boys and girls equally
• Types
o Pauciarticular JCA (commonest): pain and swelling of medium-sized joints –knees, ankles, elbows, wrists
o Polyarticular seropositive JCA: multiple small-joint involvement
! Positive for RF
! Juvenile RA
o Seronegative spondarthritis: sacroiliitis and spondylitis
! Juvenile AS
o Systemic JCA (classic Still’s disease): fever, rashes, malaise, lymphadenopathy, splenomegaly, hepatomegaly, joint swelling
• Prognosis: most children recover from arthritis; left with only moderate deformity and limitation of function

! 170!
SYSTEMIC CONNECTIVE TISSUE DISEASE
SLE
• Symptoms
o Systemic symptoms: malaise, anorexia, weight loss, fever
o Butterfly rashes, Raynaud’s phenomenon, peripheral vasculitis, splenomegaly, disorders of kidney, heart, lung, eye and CNS
o Joint pain (often overshadowed by above)
• Investigations
o Haematology: anaemia, leucopenia, elevation of ESR
o Anti-nuclear factor always positive
• Complications: AVN of femoral head (predisposed by disease and steroid medication)

3. Crystal Deposition Disease

GOUT
• Background:
o Pathology
! Definition: inflammatory arthritis caused by cellular rxn to uric acid crystal deposition (monosodium urate)
! Nucleic acid and purine metabolism" hypoxanthine and xanthine " catalyzed by xanthine oxidase into uric acid" excreted
mainly by kidneys, partly in gut
• Monosodium urate: 70% from endogenous purine metab, 30% from purine-rich foods
• Urate poorly soluble (plasma saturation of 7mg/dl or 0.42mmol/l)
! Urate crystals deposited in CT and cartilage (commonly in small joints of hands and feet) where they remain inert " perhaps
due to local trauma, crystal dispersed into joint and surrounding tissues" acute inflammatory reaction
o Risk factors
! Men (90%) >30yrs old
! Women seldom affected until after menopause
! Family history
! Dietary excess (esp sardines, kidney, liver, meat extracts)
! Secondary gout: ruddy complexion, obesity, hypertension, alcohol, diuretics, aspirin, lead poisoning
o Classification
! Primary (95%): absence of cause
! Secondary (5%): prolonged hyperuricaemia due to acquired disorders (myeloproliferative diseases, diuretics, renal failure)
o NOTE: most individuals w hyperuricemia do not have gout, but if high uric acid are not treated, 90% dvlp gout in 30 years; only 90% of
individuals w gout have hyperuricemia
• Signs and symptoms
o Acute attack: due to acute changes in the lvl of uric acid
! Sudden severe joint pain for 1-2 weeks (typically most intense in first 24 hrs)
• Usually spontaneous but may be precipitated by trauma, operation, illness,
unaccustomed exercise, alcohol
• Usually monoarticular and common sites are MTPJ of big toes (podagra), ankle
and finger joints, tendoachilles, olecranon bursae, pinnae of ears, lesser toes
o Monoarthritis differential GHOST: Gout, Haemarthrosis, Osteoarthritis,
Sepsis, Trauma
! LOOK: Skin red, shiny, swelled (asymmetrical involvement)
! FEEL: Joint feels hot and tender
! MOVE: decreased ROM
! Others: fever, chills, carpal tunnel syndrome
o Chronic gout
! Chronic pain, stiffness, deformity from joint erosion
! Gouty Tophi (may ulcerate through skin and discharge chalky material)
• Firm tumourous growth over joints and tendons
• Destruction of joint and deformities
• Ask for history of gout
• Typically multiple joints: MPJ, IPJ, fingertips, Wrist, olecranon, pinna of ears, 1st MTPJ, ankle, achilles tendon
• Differentials
o Infection (cellulitis, septic bursitis, infected bunion, septic arthritis)" exclude by joint aspiration
o Reiter’s disease –history more protracted, response to NSAIDs less dramatic
o Pseudogout
! Tends to affect large joints rather than small
! Commoner in women than men
! Articular calcification
o RA (esp if polyarticular gout)
o Hemarthrosis
• Investigations
o Bloods
! FBC: leukocytosis (w L shift) in acute attacks (no signs of infx infection: to exclude septic arthritis)
! Increased ESR
! Hyperuricemia in 95% but not diagnostic
! 24hour urine uric acid level after control of acute gout (to choose medications to control associated hyperuricemia)
o X-rays
! Acute attack: soft-tissue swelling

! 171!
 ! Chronic gout:
• Tophi: excavations at joint/ rat bitten lytic areas/ punched-out ‘cysts’ or deep erosions (occupied by crystalline tophi) in
para-articular bone ends (larger than rheumatoid erosions) w overhanging edges " usually only found after 1 yr of dz
• Erosion w joint space preservation is typical
• But may have secondary OA (thus joint space narrowing)
o Joint aspiration & Polarizing microscopy (diagnostic)
! Turbid fluid
! Needle-shaped strongly negatively birefringent
urate cyrstals in synovial fluid (vs rhomboid
shaped crystals in pseudogout)
! Crystals appear bright on dark background
! If compensator added, background appears
purple, birefringent crystals yellow or blue
depending on spatial orientation a)urate!crystals!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!b)!pyrophosphate!crystals!
! Synovial fluid WBC count usually elevated
• Management: to relieve pain, prevent dz progression and prevent tissue deposition of uric acid
o NOTE: avoid aspirin (increases urate absorption)
o During acute attack
! Rest and protect foot
! Phamacological: NSAIDs +/- colchicine
• NSAID (e.g. naproxen 500mg twice daily or indomethacin 50mg three times daily) at full dosage (2-5 days), reduce to1/2
or 1/4 once attack controlled
• Low dose NSAIDs for the 1st 6-18 mnts Mx of underlying hyperuricemia - ppt gouts in up to 50% of patients
• Oral colchicine (anti-inflammatory) frequently causes unpleasant side-effects
! For tense joint effusion: aspiration and local injection of hydrocortisone
o Between attacks: Treatment of underlying hyperuricemia – most untreated pts with gout will experience a recurrent episode in 2 yrs
! Lifestyle modifications: weight loss, stop alcohol and diuretics, dietary modifications
• Dietary: caloric restriction (↑ protein – low fat dairy not meat/fish, replace refined with complex carbos, ↓saturated fat)
! Pharmacological (AVOID during acute attack, cover by NSAIDs or colchicine)
• Xanthine oxidase inhibitor: allopurinol
o Allopurinol (antihyperuricaemic) – once daily
! Frequent and disabling attacks,Signs of chronic gouty joint disease, Tophi, Renal insufficiency, Recurrent
nephrolithiasis, or Urinary uric acid excretion > 1100 mg/day
• Uricosuric drugs: probenecid, sulfinpyrazone
o Probenicid, Sulphinpyrazone (urocosuric) – multiple times daily
! Initial therapy < 60 who excrete <800 mg of uricacid perday, no renal insufficiency, hx of urolithiasis or tophi
• Colchicine: Low dose prophylaxis during the initiation of anti hyperuricemic therapy. NSAIDs if cannot tolerate colchicine
• **Normalising uric acid level (<0.4mmol/l)" tophi may dissolve " ulcerating tophi that fail to heal evacuated by curettage
! Surgical: treat complications (infection, nerve compression, joint deformities, intractable pain, cosmesis)

This is an elderly (Chinese / Malay / Indian) gentleman. On Some of the swellings have ulcerated and are extruding a chalky white
inspection, there are multiple swellings located at the extensor surface substance onto the surface of the skin.
of the hands involving the _____________ joints. These swellings
range from ___ cm to ___ cm. I would like to move on to palpate the swellings. (ask patient for any
There are no overlying skin changes or erythema or scars noted. pain first)
OR
! 172!
The swelling is firm, non-tender and not warm. The overlying skin is not
attached to the swelling but it is attached to the underlying structure.
The joints are non tender and not warm to touch.
The above findings are consistent with that of gouty tophi, my
differentials will be:
• Multiple exostosis (if at knee)
• Pigmented villionodular synovitis (PVNS)
• Ganglion
• Bony lesion like enchondroma
I would like to test the ROM of the joints. There is limitation of the
________________.
I would like to look for gouty tophi over the pinna, olecranon bursa,
prepatellar bursa and Achilles tendon.
I would like to complete my examination by performing a functional
assessment (ask pt to hold a cup and to pick up coins).

CALCIUM PYROPHOSPHATE DIHYDRATE DEPOSITION

• Risk factors: women >60yrs old
• Comprises
1) Chondrocalcinosis –calcific material in articular cartilage and menisci
2) Pseudogout (acute synovitis) –crystal induced synovitis
3) Chronic pyrophosphate arthropathy –degenerative joint disease
• Pathology
o Abnormal cartilage generates pyrophosphate by enzyme activity" combines with calcium ions in matrix" crystal nucleation in
cartilage matrix
o Most pronounced in fibrocartilaginous structures (menisci, TFCC, pubic symphysis, intervertebral discs); also in hyaline cartilage,
tendons and periarticular soft tissues
o Occasionally CPPD crystals extrude into joints" inflammatory reaction
• Investigations
o X-ray
! Chondrocalcinosis
• Often bilateral and symmetrical
• At sites mentioned above
• Articular cartilage: appears as thin line parallel to joint
• Fibrocartilaginous menisci and discs: appears as cloudy irregular opacities)
! Chronic pyrophosphate arthropathy (degenerative changes)
• Similar to OA but usually in non-weightbearing joints (patellofemoral compartment, talonavicular joint)
o Aspirate " pathology " Polarizing microscopy
! Weakly positively birefringent rhomboid shaped crystals in synovial fluid
• Signs
o Pseudogout (acute synovitis)
! Acute pain and swelling in larger joints (usually knee; not as acute as gout)
! Often precipitated by minor illness or operation
! If untreated, lasts for few weeks and subsides spontaneously
o Chronic pyrophosphate arthropathy
! Polyarticular OA affecting larger joints (hips, knees) and unusual joints (ankles, shoulders, elbows, wrists)
! Pain, stiffness, swelling, joint crepitus, decreased ROM
• Differentials
o During acute attack
! Acute gout –typically in men, smaller joints, differentiate with polarized microscopy
! Post-traumatic haemarthrosis –aspiration of blood-stained fluid
! Septic arthritis –systemic features, blood tests, joint aspiration
! Reiter’s disease –conjunctivitis, urethritis, colitis
o Chronic CPPD arthropathy
! OA –doesn’t usually affect unusual joints like elbow, wrists, ankle
! Inflammatory polyarthritis –systemic features
! Metabolic disorders
• Haemochromatosis: chronic iron overload
o Liver cirrhosis, diabetes, bronze pigmentation of skin
o Joint symptoms in hands, fingers, back
o Investigations
-X-ray: chondrocalcinosis and destructive arthropathy typically in MCPJ
-Raised plasma iron and iron-binding capacity
• Alkaptouria
o Pathology: congenital absence of homogentistic acid oxidase in liver & kidney"accumulation of homogentistic acid
o Signs: Homogentistic acid in urine; dark pigmentation of CT (ochronosis), calcification of hyaline and fibrocartilage
o Symptoms: At 30-40yrs old: present with pain and stiffness of spine and larger joints
o X-ray: calcification of intervertebral discs and spinal osteoporosis; chondrocalcinosis and OA of peripheral joints
• Hyperparathryoidism: hypercalcemia
• Management
o Pseudogout
! Rest
! Phamacological for younger patients: NSAIDs
! For elderly patients: joint aspiration and local injection of hydrocortisone (NSAIDs side effects)
o Chronic pyrophosphate arthropathy: treatment as per OA

! 173!
CALCIUM HYDROXYAPATITE DEPOSITION DISORDERS
• Risk factors: Local tissue damage: torn ligaments, tendon attrition, cartilage damage or degeneration
• Pathology
o HA crystals deposited around chondrocytes in cartilage and damaged parts of tendons and ligaments (esp shoulder and knee)"
crystal accretion
o Crystals may be inert; in symptomatic cases surrounded by acute vascular reaction and inflammation
o Crystals shedding into joints can cause synovitis
• Signs and symptoms
o Acute or subacute periarthritis
! Pain close to larger joints (shoulder or knee)
! Swelling, warm, tenderness of tissues around joint (tendon or ligament rather than the joint)
! Symptoms may subside after weeks or months or require removal or decompression
o Chronic destructive arthritis
! Rapidly destructive OA of joint
• Investigations
o X-ray
! Periarthritis: calcification in tendons or ligaments close to joint esp rotator cuff
! Destructive arthritis: loss of joint space, no sclerosis, no ostepophytes
• Management
o Periarthritis:
! Rest
! Pharmacological: NSAIDs
! Local injection of steroids for resistant cases
! Operative: removal of calcific deposit or decompression of affected tendon or ligament
o Erosive arthritis
! Treatment as for OA
• Shoulder: synovectomy and soft tissue repair
• Hip: THA

4.!Metabolic!Conditions!
1. General Information
• Bone Types
o Woven – immature bone where collagen fibers are arranged haphazardly
o Lamellar – mature bone where collagen fibers arranged parallel to each other
! Compact (Cortical): Found where support matters most: outer walls of all bones (esp shaft of tubular bones), subchondral
plates supporting articular cartilage
! Cancellous (Trabecular): Interior meshwork of all bones and ends of tubular bones and vertebral bodies
• Role of Vitamin D and Parathyroid hormone
o Vitamin D
! Sources
• Diet
• Action of UV light on 7-dihydrocholesterol in skin " 25 hydroxylation in liver " 1 hydroyxlation in kidney
! Action
• Small Intestine: Increase absorption of calcium and phosphate
• Bone: Promote osteoclastic resorption (release calcium and phosphate into blood)
o Parathyroid hormone
! Kidney:
• Increase phosphate excretion (restrict absorption) and conserve calcium (increase reabsorption)
• Controls 1 hydroxylation of vit D metabolite
! Bone: Promote osteoclastic resorption (release calcium and phosphate into blood)
! Small Intestine: Indirect effect via vit D (refer to 2nd point of ‘kidney’)

2. Osteoporosis
Background
• Definition:
o Normal mineralization (qualitatively normal)
o Decrease bone mass per unit volume (quantitatively deficient)
o Weakening of microarchitectural structure of bone
o WHO Definition (1994): Bone mineral density > 2.5 SD below the mean seen in peak bone mass of young (25-30) normal subjects
(T-score ≤ -2.5SD)
• Pathogenesis of osteoporosis
o Loss of balance between bone resorption and bone formation
! Bone matrix manufactured by osteoblasts. Bone resorption by osteoclasts.
o Each cyle of remodelling takes abt 4-6 mnths. Annual rate of turnover is abt 4% for cortical and 25% for trabecular bone.
! Bone loss occurs within 2weeks; bone formation takes 3 months

! 174!
 o Normal physiology:
! Between puberty and 30 years: Bone density increases (haversian canals and intertrabecular spaces filled in and cortices
increase in overall thickness) at about 3% per year
and peaks during 3rd decade
! From 30 years onwards: Slow loss (haversian spaces
enlarge, trabeculae thin, endosteal surface resorbed,
medullary space expands
• 0.3% per year in men
• 0.5% per year in women till menopause
o From onset of menopause (and for next
10 years): bone loss of 3%/yr due to
decrease is oestrogen.
! Age 65-70: Rate of bone loss tails off to approx 0.5%
per year
! Wolff’s law - Bone is deposited and resorbed in
accordance with the stresses placed upon it.
o Estimated that half of all women and 1/3 of men will sustain
a fragility fracture in their lifetimes
• Scoring
o BMD T Score
! Number of sds below means of peak bone mass of young healthy adults (based on BMD of 25yo Caucasian females)
• Normal: > -1
• Osteopenia: between -1 and -2.5
• Osteoporosis: <-2.5
• Severe osteoporosis: <-2.5 + fragility #
o Z Score: Number of standard deviations below average person of the same age
o Normal Z score, abnormal T score " Primary osteoporosis
o Abnormal Z and T scores " Secondary osteoporosis
• Classification
o Site: Generalised vs Localised
o Pathology: Primary vs Secondary
o Congenital
! Osteogenesis imperfecta
! Neuromuscular diseases and dystrophies Osteoporosis!
! Gonadal dysgenesis
! Trisomy 18, 13-15
! Ehlers Danlos Syndrome
! Inborn errors of metabolism
o Acquired Primary! Secondary!
! Endocrine
• Hypogonadism
• Adrenal cortical (Adrenal cortical
hyperplasia or neoplasm, Addison’s
dz) Postmenopausal! Senile! Congenital! Acquired!
• Pituitary (Cushing’s syndrome,
acromegaly)
• Thyroid (hyperthyroidism)
• Hyperparathyroidism
! Pancreatic (Diabetes mellitus)
! Disuse atrophy
! Nutritional deficiency (Vit C, protein, calcium deficiency, malnutrition)
! Liver disease
! Iatrogenic (Steroid therapy, heparin)
• Risk Factors
o Non-modifiable
! Race: Caucasoid / Asiatic
! Family history of osteoporosis/ fragility fracture
! History of anorexia nervosa and amenorrhea
! Low peak bone mass in early adulthood
! Estrogen exposure related
• Early onset of menopause (<45yo)
• Early oophorectomy
! Previous adult # history
o Modifiable
! Dietary insufficiency
! Alcohol abuse and Cigarette smoking: both assoc w nutritional deficits
! Chronic lack of exercise/ immobilisation
! Drugs: Corticosteroids, thyroxine, anticonvulsants
! Lifelong low calcium intake (<500mg/day)
! Comorbidities: hyperthyroidism, hyperPTHism, cushings syndrome, liver disease, COPD, CRF, RA, organ transplant etc
! Weight: lean ppl predisposed to osteoporosis

! 175!
 • Clinical Features
o Mostly asymptomatic
o Fragility fractures:
! Vertebral compression #
• Compression # of vertebrae
• Back pain
• Increased thoracolumbar kyphosis (Dowager hump)
• Diminished height
! Hip #: Neck, intertrochanteric, subtrochanteric #s
! Forearm # (esp distal radius -Colles)
! Pubic rami
! Humeral head
• Screening
o Indications
! Individuals with prior fragility fractures during adulthood
! Radiological evidence of osteopenia or vertebral deformity
! Patients w strong RF
! High risk postmenopausal women as categorized by OSTA
! Women who are considering prevention therapy for osteoporosis
! Monitoring of Rx
o US National Osteoporosis Foundation (NOF) guidelines (Uses age as the criterion)
! Recommends BMD testing in all women over the age of 65 years
! Recommends BMD testing in postmenopausal women under 65 yrs of age with risk factors for hip fracture:
• History of previous fractures as an adult
• Family history of fragility fracture
• Body weight < 57kg
• Cigarette smoking
o Osteoporosis Self Assessment Tool for Asians (OSTA):
! Use weight and age to stratify risk: age – weight = x
• If x>20: measure BMD
• If x 0-20, measure if other RF present
• If x<-20: low risk, don’t need to measure unless +ve hx of fragility fracture
o Frequency of screening
! Women with osteoporosis: Yearly (monitor
progression or treatment outcome)
! Women with osteopenia: Every 2 years
! Normal BMD: Every 2-5 years (for peri/post
menopausal women)
o Method: Dual Energy X-ray Absorptiometry
o Criteria
• Investigations
o BMD
! Indications
! Methods
• Dual Energy X-ray Absorptiometry; DEXA (Gold standard)
o Rationale for dual energy: to take XR of soft tissues and of bone at different penetrance lvls
o DEXA of hip for diagnosis, spine for monitoring of treatment
! DEXA of lumbar spine preferred site for monitoring therapeutic response as largest chances in BMD with
treatment occur at this site
• Other rarely done investigations: quantitative U/S heel/ tibia, quantitative CT scan, Single-energy x-ray absorptiometry
! Criteria
o X-rays
! Picture frame vertebrae–accentuation of cortical outline
! Increased concavity of endplates
! Vertical trabeculae bears the most weight of stress hence disappears last
• Osteoporosis got prominent vertical trabeculae but no horizontal.
! Codfish appearnace of vertebrae due to concave end-plates
! Pathological fractures – vertebral compression fracture (ant height of
vertebrae is 80% or less of the posterior height)
• If multiple of spine -> Dowager’s hump
! Singh’s index for trabeculae at hip jnt/ femoral neck fractures: radiographic
measurement of osteoposis (grade I only one present to grade VI all
present)
• Grade 1: principal compressive trabeculae are markedly reduced in
number and are no longer prominent
• Grade 2: only principal compressive trabeculae stand out
prominently, remaining trabeculae have been absorbed
• Grade 3: a break in the continuity of the principal tensile trabeculae opp e greater trochanter " definite osteoporosis
• Grade 4: principal tensile trabeculae are markedly $ but can still be traced from lat cortex to upp pt of the femoral neck
• Grade 5: principal tensile & principal compressive trabeculae is accentuated
• Grade 6: all normal trabecular groups are visible, upper end of femur completely occupied by cancellous bone

! 176!
 o Bloods:
! Calcium and phosphate levels NORMAL in osteoporosis, low in osteomalacia
! FBC, ESR, UECr, VitD
! Others if susepect underlying assoc disease: TFT; LFT; Tumor markers and myeloma screen (FBC, ESR, bone marrow
aspiration, urine electrophoresis, skull X-ray)
• Management

Management!

Underlying!Cause:!
Osteoporosis! For!Secondary! Fractures!
Osteoporosis!

NonW
Pharmacological! pharmacological!
BMD T-score Action
>+1 Re-BMD in 5y
1 to -1 Re-BMD in 2y
-1 to -2.5 Medical prevention, F/U BMD @ >1yr
Prophylactic! Definitive! < -2.5 + fragility fracture Medical treatment, F/U BMD @ >1yr

o Lifestype measures to be encouraged in everyone

Nutrition Age Calcium Vitamin D
11-18 1000mg 400IU
18-65 800mg 400IU
>65 800mg 800IU
Exercise Weight bearing exercises (3x30min/wk)
Smoking, alcohol cessation
Fall prevention Remove hazards (+ install bars, anti-slippery mats etc)
Treat comorbidities predisposing to fall e.g. cataracts
Correct postural hypotension
o Pharmacological
! Prophylactic
• Calcium supplements
o Calcium intake should >1200mg/day
o Side effects: Renal calculi, constipation
• Vit D supplements
o Vit D intake should >700-800IU/day
o Mechanism: 1) Increase calcium and phosphate absorption by small intestine 2) Promote osteoclastic resorption
of bone and enhance calcium transport across cell membrane and assist with osteoid mineralisation
! Definitive
• Bisphosphonates
o Examples: Alendronate (Fosamax), Residronate
o Mechanism: Potent inhibitors of osteoclasts (similar in structure to pyrophosphate, thus osteoclasts undergo
apoptosis when they ingest it)
o Adverse effects: GIT (gastritis, ulceration, stricture, diarrhea, vomiting), esophageal rxn (eg. heartburn)
osteonecrosis of jaw (rare), dizziness, hypersensitivity
! Take medication sitting up, keep upright for 30min after swallowing, weekly dosing
! Overuse will result in SSBT (severe suppression of bone turnover): bone would hence be brittle
• Hormone replacement therapy
o NOT used if osteoporosis is the only problem!
! Used only if other indications (eg. unbearable hot flushes)
! Switch to other Rx when symptoms ablate
! Administer adjuvant progestogens to protect against endometrial cancer
o Mechanism: Estrogen acts to decrease bone resportion in post-menopausal women
o Side effects: Thromboembolic events, stroke, invasive breast cancer
• Calcitonin (nasal spray)
o Mechanism: slows down osteoclasts
• Strontium ranelate
o Mechanism: Decreases bone resorption and stimulates bone formation
o Side effects: Venous thromboembolism, contraindicated in patients with severe renal impairment
• Intermittent Parathyroid hormone
o Mechanism: Increase rate of new bone formation by preferentially stimulating osteoblastic formation over
osteoclastic resorption
o Side effects: Osteosarcoma
! 177!
 o EXPENSIVE
• SERM – Selective Estrogen Receptor Modulator (eg. raloxifene/EVista)
o Mechanism: Decrease rate of bone resportion and induces osteoclast apoptosis (agonist in bone; antagonist in
breast and uterine cells)
o SE: Hot flushes, sweating, leg cramps, Increased risk of clots (e.g. DVT, PE), Teratogenic
o Has also been shown to be protective against breast ca
• Synthetic steroid: tibolone (livial)
o Has progestogenic and some androgenic properties as well as oestrogenic effects
o Also has value in controlling hot flushes
• Cyclical etidronate

PRIMARY OSTEOPOROSIS
Post-Menopausal
• Pathology:
o Increased bone resorption due to withdrawal of estrogen which restricts osteoclastic activity
o Accelerated rate of bone loss (about 3% per year) compared to 0.3% during preceding decade
• Distinctive Clinical Features
o Only affects women
o Onset around menopause
Senile Osteoporosis
• Pathology: Gradual slowdown in osteoblastic activity
• Increased risk factors:
o For osteoporosis: Dietary insufficiency, lack of sunlight exposure, muscular atrophy
o For fractures: Preceding post-menopausal osteoporosis, predisposition to falls, concomitant osteomalacia
SECONDARY OSTEOPOROSIS
Hypercotisonism
• Pathology: Endogenous Cushing’s disease or glucocorticoid overload
• Mechanism: Suppress osteoblast function, reduce calcium absorption, increase calcium excretion
Gonadal Hormone Insufficiency
• Conditions: Oophrectomy, Turner’s syndrome, ovarian agenesis, amenorroeic femal athletes, anorexia nervosa
• Mechanism: Decreased estrogen to limit osteoclast activity
Hyperthyroidism" Mechanism: Increase rate of formation and resorption; but extent of resorption increase greater
Multiple myeloma and carcinomatosis " Mechanism: Overproduction of local osteoclast-activating factors
Alcohol abuse " Mechanism: Decreased calcium absorption, liver failure, toxic effect on osteoblast function

3. Osteomalacia and Rickets

Definition
• Inadequate mineralization of bone – incompletely calcified hence softened
Etiology
• Calcium deficiency
• Hypophosphatemia
• Defect along Vit D metabolism pathway (nutritional lack, lack of sunlight, intestinal malabsorption)
Clinical Features
Osteomalacia: features "Vit-D deficiency in ADULT":
Acetabuli protrusio, Decresed bone density, Under mineralization of osteoid, Looser's zone (pseudofracture), Triradiate pelvis (females)
• Children
o Tetany or convulsions
o Bone deformity (skull) and thickening (knees, ankles, wrist)
o Bow legs or knock knees
o Joint swelling
o Delayed growth
o Disturbed gait
• Adults (insidious)
o Back pain, ache
o Muscle weakness
o Vertebral collapse (loss of height, kyphosis)
X-Ray
• Rickets
o Thickening and widening of growth plate
o Cupping of metaphysis
o Bowing of diaphysis
• Osteomalacia
o Looser’s zone: Thin transverse band of rarefaction in otherwise normal-looking bone (incomplete stress fractures which heal
with callus lacking calcium)
o Lateral indentation of acetabula (trefoil pelvis)
o Biconcave vertebra (codfish vertebrae)
o Spontaneous fractures
Biochemistry
• Diminished serum calcium and phosphate
• Increased alkaline phosphatase
• Decreased urinary excretion of calcium

! 178!
Clinical Varieties
• Vitamin D Deficiency
o Dietary lack
o Under-exposure to sunlight
o Malabsorption
• Vitamin D Metabolites Deficiency
o Reduced conversion to active metabolite (liver and kidney disease)
o Increased breakdown of active metabolite
• Hypophosphataemic Rickets and Osteomalacia (impaired renal tubular reabsorption of phosphate where calcium levels normal but
bone mineralization defective) – managed with phosphate and vit D
o Familial Hypophosphatemic Rickets / Vit D Resistant Rickets
! Excessive urinary excretion of phosphate
! Postulated mutation that results in failure to inactivate normally synthesized phosphatonin which then exerts
unrestrained action on kidney tubules " excessive phosphate loss
! Symptoms: Growth lag, knee deformities
o Adult-onset Hypophosphatemia
! Cause of unexplained bone loss in adults
o Osteogenic Osteomalacia
! Induced by tumours: Vascular tumours, fibrohistiocytic lesions (GCT, PVNS)

4. Hyperparathyroidism
Pathology
• Biochemical Changes
o Hypercalcemia: Increased tubular absorption, intestinal absorption, bone resorption
o Hypercalciuria: Increased glomerular filtration (despite increased tubular reabsorption)
o Hyperphosphaturia: Suppressed tubular reabsorption
• Clinical features:
o Kidney: Calcinosis, stone formation, recurrent infection, impaired function
o Soft tissue: Calcification
o Bone
! Osteoporosis
! Osteitis fibrosa cystica: Replacement of marrow spaces by vascular granulations and fibrous tissue
! Brown tumour:
• Arises due to excessive osteoclast activity
• Contents: Fibrous tissue, woven bone, supporting vasculature
Primary Hyperparathyroidism
• Cause: Solitary adenoma
• Clinical features
o Hypercalcemia: Anorexia, nausea, abdominal pain, fatigue, muscle weakness, polyuria, kidney stones, nephrocalcinosis
o Joint symptoms: Chondrocalcinosis
o Bone: Minority; and even so it is usually osteoporosis ONLY
• X-ray
o Pathognomonic feature: Subperiosteal cortical resorption of middle phalanges
o Osteoporosis (may have vertebral collapse and cortical erosion)
o Brown tumours
• Biochemical
o Hypercalcaemia
o Hypophosphatemia
o Raised PTH (other causes of hypercalcemia like multiple myeloma, metastasis usually have lowered PTH)
• Management
o Conservative (Usual): Hydration, decreased calcium intake
o Surgery: Parathyroidectomy
Secondary Hyperparathyroidism
• Cause: Parathyroid oversecretion in response to chronic hypocalcemia
• Etiology
o Kidney failure
o Calcium deficiency
o Impaired phosphate breakdown
o Vit D disorders
• Biochemical
o Phosphate
! High – Kidney failure
! Low – Absorption problems
Tertiary Hyperparathyroidism
• Cause: Secondary hyperplasia leading to autonomous activity

! 179!
5. Renal Osteodystrophy
• Pathology: Combination of rickets/osteomalacia, secondary hyperparathyroidism, osteoporosis
• Mechanism (due to renal failure)
o Phosphate retention: Phosphate complexes with calcium to form insoluble calcium phosphate, reducing calcium levels
o Decreased 1 hydroxylation of Vit D: Decreased vit D activity
• X-ray
o Widened, irregular or even displaced epiphyseal plates
o Osteosclerosis (mainly in axial skeleton) – may produce ‘rugger jersey’ appearance of alternating bands of increased and
decreased bone density
• Biochemical
o Low serum calcium
o High serum phosphate
o High alkaline phosphatase
o Decreased urinary calcium and phosphate

6. Paget’s Disease (Osteitis Deformans)

Pathology
• Increased osteoblastic and osteoclastic activity resulting in enlargement and thickening of bone but abnormal and brittle internal
architecture
Clinical Features
• Usually above 50 years old
• Affected bones: pelvis and tibia commonest
• Signs and symptoms
o Dull pain
o Bone
! Tibia bow anteriorly
! Femur bow anterolaterally
! Enlarged and flattened (platybasia) skull
! Kyphosis
! Otosclerosis: Deafness
o Neurological
! Cranial nerve compression: Impaired vision, facial palsy, deafness etc
! Spinal cord / nerve root compression: Due to vertebral thickening
o Steal syndromes: Cerebral impairment and spinal ischemia
X-ray
• Early
o Flame-shaped lesions along shaft of long bone
o Osteoporosis circumscripta: Circumscribed patch of osteoporosis in skull
• Late
o Sclerosis and thickening of bone
o Pathological fractures
Biochemistry
• Calcium and phosphate normal
• Raised serum alkaline phosphatase – osteoblastic activity
• Increased hydroxyproline urine excretion – osteoclastic activity
Complications
• Fractures
• Osteoarthritis
• Nerve and spinal stenosis
• Bone sarcoma
• High output cardiac failure
• Hypercalcemia
Management
• Drugs that suppress bone turnover: Calcitonin and Bisphosphonates
• Surgery: Fixation of pathological fracture with concomitant straightening of bone if deformity present

5. Genetic Disorders
1. General Information
• Classification
o Disorders of cartilage and bone growth
! Physeal and Metaphyseal: Hereditary multiple exostosis, Dyschondroplasia
! Epiphyseal
! Metaphyseal and diaphyseal
! Mixed
o Connective tissue disorders
! Marfan’s
! Ehlers-Danlos Syndrome
! Osteogenesis Imperfecta
o Storage disorders and other metabolic defects
o Chromosome Disorders

! 180!
2. Hereditary Multiple Exostosis (Diaphyseal Aclasis/ Osteochondromatosis) – refer to bone tumour
3. Dyschondroplasia (Enchondromatosis/Ollier’s Disease)
• Pathology
o Defective transformation of physeal cartilage columns into bone
o Embryonal disorder ( not inherited)
• Clinical features
o Usually unilateral
o Signs and Symptoms
! Deformities (Bone grows bent): femur or tibia bowing, valgus/varus knee or ankle etc
! Multiple enchondromata at fingers or toes – may undergo malignant change
• X-Ray
o Radiolucent streaking extending from physis into metaphysis
o Multiple enchondromata at fingers or toes
• Maffucci’s Syndrome: Multiple enchondromas + haemangiomas of skin and viscera
o Associated with higher risk of malignant change
4. Marfan’s Syndrome
• Pathology
o Generalised disorder affecting skeleton, ligaments, eyes, CVS structures
o Due to cross linkage defect in collagen and elastin
o Autosomal dominant inheritance
• Clinical Features
o Appearance: Tall, disproportionately long legs and arms, pectus excavatum, arachnodactyly
o Spine: Scoliosis, spondylolisthesis
o Joint laxity: flat feet, dislocation of patella or shoulder
o Eyes: Lens dislocation, retinal detachment
o CVS: Aortic aneurysm, mitral or aortic incompetence
o Others: SCFE, High arched palate, hernias
5. Ehlers Danlos Syndrome
• Pathology
o Abnormality of elastin and collagen formation
o Manifestation: Skin laxity, joint hypermobility, vascular fragility
• Clinical Features
o Hypotonia
o Joint laxity: Recurrent dislocation
o Skin: Soft, hyperextensible and easily damaged
o Vascular fragility: Spontaneous bruising
o Scoliosis
6. Osteogenesis Imperfecta (Brittle bones)
• Pathology
o Heritable connective tissue disorder (Abnormal synthesis and structural defects of type I collagen)
o 2-3 new cases per yr in Sg (25% sporadic mutations, 75% inherited)
o Affects: Bones, teeth, ligaments, sclera, skin
• Clinical Features
o Bone fragility, osteopenia, recurrent #s
! Fractures heal with florid callus producing lumps and deformities
o Ligament laxity
o Dentinogenesis imperfecta (crumbling teeth)
Type I Most common, mildest (structure of collagen normal, but low quantity)
Little or no bone deformity, but fragile (prone to #s, cracked teeth / cavities)
Blue sclera
Type II Most severe (collagen structure defect)
Bones break while fetus is in the womb " many infants don’t survive
Type III Improperly formed collagen
Infant often born with #s
+ / - Blue sclera
Shorter than average
Spinal deformities, respi complications, brittle teeth
Type IV Moderately severe, improperly formed collagen
No blue sclera
Bone deformities mild to moderate
• X-Ray
o Generalised osteopenia: Thinning of long bones, fractures in various stages of healing, vertebral compression, spinal deformity
7. Neurofibromatosis
• NF1 (aka Recklinghausen’s Disease)
o Inheritance: Autosomal dominant – NF1 genes on Ch17 and 22
o Clinical Features:
! Neurofibromata (Schwann cell tumours)
! Café-au-lait spots

! 181!
 ! Single large plexiform neurofibroma
! Spine
• Scoliosis – very sharp, short curve
• Localised vertebral abnormalities: Scalloping of posterior aspects of vertebral bodies, erosion of pedicles, intervertebral
foraminal enlargment
• Dystrophic spinal deformities: Deformities of cervical spine
• Dumbell lesions of spine
! Eye: Lisch nodules (pigmented spots on iris)
! Tibia: Dysplasia and pseudoarthrosis
! Malignant change
• NF2: Associated with intracranial lesions like acoustic neuromas and meningiomas

6. Osteochondritis
Definition: Group of conditions in which there is compression, fragmentation or separation of small segment of articular cartilage and bone
Features
• Pathology
o Ischemic necrosis
o Reactive vascularity
o Osteogenesis in surrounding bone
• Symptoms
o Pain
o Limit ROM
o Swelling
o Joint locking (esp for splitting osteochondritis)
Note: No signs of inflammation
Risk Factors
• Adolescents and young adults
• Trauma: Physical activity, repetitive stress
• Vascular coagulopathy
Types
• Crushing: Impact injuries cause bleeding/edema in subarticular bone, resulting in capillary compression, thrombosis and localized ischemia
o Freiberg’s disease (metatarsal)
o Kohler’s disease (navicular)
o Kienbock’s disease (lunate)
o Panner’s disease (capitulum)
o Scheuermann’s disease (vertebra)
• Splitting (Osteochondritis dissecans): Osteoarticular fractures can cause severance of local blood supply and separation of a necrotic
osteochondral fragment
o Lateral surface of medial femoral condyle in knee
o Anteromedial corner of talus in ankle
o Superomedial part of femoral head
o Capitulum
o First metatarsal head
• Pulling (Traction apophysistis): Traction injuries may damage blood supply to apophysis
o Osgood Schlatter’s disease (tibial tuberosity)
o Sever’s disease (calcaneal apophysis) !

! 182!
7.!Bone!Tumours!

Cell type Benign Malignant

Bone ! Osteoid osteoma ! Osteosarcoma
Cartilage ! Enchondroma ! Chondrosarcoma
! Osteochondroma
Fibrous tissue ! Fibroma ! Fibrosarcoma
Marrow ! Eosinophilic ! Ewing’s sarcoma
granuloma ! Myeloma
Vascular ! Haemangioma ! Angiosarcoma
Uncertain ! Giant-cell tumour ! Malignant giant-
cell tumour

FACTORS IN ASSESSMENT
1. Age of patient – Young (<30) vs Old (>30)
a. Malignancy commoner in adults (except osteosarcoma
and Ewing’s sarcoma in young)
b. ***NOTE: Osteosarcoma has bimodal distribution; occurs in elderly because of Paget’s disease
c. NOTE MCQ: child w cystic lesion at epiphysis of long bone, most likely diagnosis is osteoblastoma
2. Location in long bones
a. Epiphysis
i. Young: Chondroblastoma, infection
ii. Over 20: GCT
iii. Older: Geode
b. Metaphysis: Osteosarcoma (esp knee and proximal humerus), non-ossifying fibroma (cortex), SBC, ABC, GCT (proximal tibia, distal
radius, distal femur), osteochondroma, chondromyxoid fibroma, chondrosarcoma, infections
c. Diaphysis: Ewing’s sarcoma, fibrous dysplasia, osteoblastoma
d. Non-specific: enchondroma, osteoid osteoma, metastatic
3. Location of lesion in skeleton
a. Finger: Enchondroma
b. Calcaneum: GCT
c. Spine: ABC, GCT, Multiple myeloma, mets (note that disc space not eroded in spinal mets)
d. Pelvis: Mets
e. Flat bones: Chondrosarcoma, Ewing’s sarcoma
f. Skull: Multiple myeloma
g. Red marrow populated areas: multiple myeloma, metastatic
h. Cartilage cap of osteochondroma OR central medullary: chondrosarcoma
4. Morphology – Malignant looking vs Benign looking
a. Transition zone: Applies only to osteolytic lesions
i. Narrow zone: Benign
ii. Broad zone: Malignant
b. Periosteal reaction: Left to right " Solid, lamellated, spiculated (sunburst), Codman’s

! 183!
 c. Soft tissue mass
d. Cortical destruction
5. Single vs Multiple
a. Commonly mutiple: Metastasis, multiple myeloma, osteochondromatosis (multiple exostosis), enchondromas (Maffucci syndrome)

" NOTE DDx for tumours

• Chronic osteomyelitis
o Systemic features may have been suppressed by Abx
o Submit tissue for histological and bacteriological examination
o Ewings and osteomyelitis can be confused due to: swelling, diaphyseal location, periosteal bone formation, exploration reveals
liquefied material like pus
• Stress # (young adult w localized pain near a large jt)

DIAGNOSIS OF MSK TUMOURS

• Imaging
o Plain XR
! Description:
1. Type of X-ray
2. Age (skeletally immature vs mature)
3. Solitary or multiple
4. LUCENCY (lytic) vs DENSITY (blastic)
5. Site (bone and area – metaphysis, diaphysis, epiphysis)
6. Features
a. Zone of transition: Well definted or ill-defined (ie. Narrow or widened zone of transition)
b. Periosteal reaction: Any periosteal new bone formation & extension of tumour into soft tissues (malignant!)
i. Note that periosteal hypertrophy may also mean infx, stress #, soft tissue bruising
c. Any cortical destruction or cortical thickening
7. NOTE: stipled calcification inside a vacant area is characteristic of cartilage tumours
o CT & MRI
! Useful to assess the true extent of tumour and its relationship to surrounding structures
! Assuming that there are no mets, e local extent of e tumour is e most impt factor in deciding how much tissue to remove
o Radionuclide scanning w technetium
! Shows non-specific reactive changes in the bone
! Useful to reveal site of small tumour (eg. osteoid osteoma) or the presence of skip lesions/ silent secondary deposits
• Biopsy: essential for diagnosis and planning of Rx
o Open Bx more reliable
o Site is selected so that it can be included in any subsequent ablative operation
o As little as possible of the tumour is exposed; block of tissue is removed (ideally in the boundary zone), so as to include normal
tissue, pseudocapsule and abnormal tissue
o Frozen section examined; several samples taken if necessary
o If bone removed, the raw area is covered w bone wax or methlmethacrylate cement
o Drains shld be avoided to minimize risk of tumour seeding
o For tumours that are almost certainly benign: excisional biopsy can be done (remove entire lesion)
o For cysts: careful curettage to remove representative tissue

CLASSIFICATION
Epiphysis Metaphysis Diaphysis
Young Benign Malignant Benign Malignant Benign Malignant
(<20) Chondroblastoma SBC (simple bone cyst) Osteosarcoma Osteoid osteoma Ewing’s
Infection Non-ossifying fibroma sarcoma
Enchondroma (arise at puberty,
presents ~30yo)
Osteochondroma
Osteoid osteoma
Adult (20- Benign Malignant Benign Malignant Benign Malignant
40) GCT ABC (aneurysmal bone cyst) Osteoid osteoma
GCT (to epiphysis)
Enchondroma
Osteoid osteoma (<30)
Middle/ Benign Malignant Benign Malignant Benign Malignant
elderly Geode Osteosarcoma (~50yo)
(>40) (degen cyst) Chondrosarcoma
Multiple myeloma (solitary
type/non-specific)
NOTE: consider 1)infections, 2)metastasis from primary sites esp in older age groups
• Head and neck: thyroid, NPC
• Thorax: breast, lung
• Abdomen: kidneys, GIT (except rectum), prostate, testes
*Midline & paired structures
*Most are osteolytic except prostatic CA (blastic) & breast (blastic & lytic
Malignant bone tumours by frequency: 1) metastatic 2) multiple myeloma 3) osteosarcoma 4) chondrosarcoma 5) ewing’s sarcoma

! 184!
TREATMENT

Intra-compartmental Extra-compartmental
Low grade Wide excision (w/o exposing tumour) Radical incision +/- bone graft or prosthetic replacement
High grade Radical incision and prosthetic replacement or
amputation +/- chemo to reduce risk of mets
1. Osteosarcoma: neoadjuvant chemotherapy given before surgical resection
2. Mets (ELDERLY)
a. Wheelchair and admit patient (avoid weight bearing) – even if not yet fractured; fracture risk
b. Possible differential infection

STAGING FOR MALIGNANT BONE TUMOUR

1. MSTS Staging
a. Stage IA: Low grade, intracompartmental
b. Stage IB: Low grade, extracompartmental
c. IIA: High grade, intracompartmental
d. IIB: High grade extracompartmental
e. III: Any grade, metastasis

DETAILS ON SOME TUMOURS

Multiple Myeloma
• Pathology
o Malignant B-cell lymphoproliferative disorder of marrow, with plasma cells predominating
o Effects on bone due to marrow cell proliferation and increased osteoclastic activity
• Clinical features
o Osteoporosis and discrete lytic lesions throughout skeleton
! Pain: Bone pain, back ache
! Pathological fracture
o Plasmacytoma: large colony of plasma cells forming solitary tumour
o Blood: Plasma protein abnormalities, Anemia, Increased blood viscosity
o Hypercalcemia: Due to bone resorption
o Renal Dysfunction
o Spinal cord/root compression: Due to vertebral collapse
• X-Ray
o Generalised osteoporosis
o Classic lesion of punched out defects with soft margins in skull, pelvis, proximal femur
o Crushed vertebra
o Solitary lytic tumour in large bone metaphysis
• Biochemistry
o Mild anemia
o High ESR
o Raised creatinine
o Hypercalcemia
o Bence-Jones protein in urine
o Plasmacytosis with typical myeloma cells
• Prognosis: Poor (median survival of 2-3 years)

Fibrous Dysplasia
• Pathology
o Developmental disorder in which trabecular bone is replaced by fibrous tissue containing flecks of osteoid and woven bone
• Clinical Features (mono or polyostotic)
o Pathological Fractures
o Deformities
o Albright’s syndrome: Café-au-lait spots, precocious sexual development in girls
o Malignant transformation: 5-10% in patients with polyostotic lesions
• X-Ray
o ‘Ground glass’ cystic lesions in metaphysis or shaft
o Shepherd’s crook deformity of proximal femur

Osteosarcoma risk factors PRIMARY: Paget's, Radiation, Infaction of bone, Male, Alcohol, poor diet, sedentary lifestyle [adults only]
Retinoblastoma, Li-Fraumeni syndrome, Young [10-20 yrs].
Osteosarcoma is the most common primary malignant tumor of bone.

Osteosarcoma: features PEARL HARBOR:

Paget's disease (10-20%)*, Early age (10-20 yrs), Around knee, Raised periosteum by expanding tumor: "sunburst pattern", Lace-like
architecture, Hyaline arteoriosclerosis, Alkaline phosphatase increased, Retinoblastoma*, Boys predominantly, Osteomyelitis DDx, Radiation*
· Sunburst pattern was Japanese Navy emblem during WWII.
*: Predisposing factors.

! 185!
Osteochondroma
Pathophysiology
• Lump that sticks out of bone, mainly cancellous bone with a covering of cortical bone and a cartilaginous cap
• Derived from small pieces of metaphyseal cartilage which were not remodelled during growth of bone and have become separated from the
main cartilaginous epiphyseal plate
• Continue to grow and ossify and produce a bony knob just above the epiphyseal line, sometimes have an adventitious bursa over their cap
• Usually single, may be congenital and multiple

On inspection, I note a ___ by ___ cm spherical lump over the medial aspect of the (left / right) knee. There are no overlying skin changes or
scars noted in the surrounding skin. The surface is smooth, edges are distinct and the lump feels bony hard (can be masked by soft, fluctuant bursa
overlying cap). It is non-tender and not warmth to touch. The overlying skin is not attached to the lump; it is attached to the deep structures and is
not freely mobile. (move joint and feel)

ROM of the knee joint (is / is not) limited by the lump

My diagnosis will be an exostosis.
I would like to ask the patient for the presence of similar lumps over other sites of the body.
Differentials: gouty tophi / enchondroma

Hereditary Multiple Exostosis (Diaphyseal Aclasis/ Osteochondromatosis)

• Pathology
o Unrestrained transverse growth of cartilaginous physis
o Only affects endochondral bones
o Autosomal dominant inheritance
• Clinical Features
o Hard lumps at end of long bones (ulna, fibula) and along apophyseal borders of scapula and pelvis
o Deformities: Ulnar deviation of wrist, bowing of radius, subluxation of radial head, valgus kness, valgus ankles, large lumps often
around knee
o Neurovascular compromised by pressure
o Malignant change: Cartilage cap of exostoses transform to chondrosarcoma (a sign is continued growth after normal growth period
of bone)
• X-Ray
o Broad and poorly modeled long bone metaphyses
o Pedunculated or sessile exostoses arising from cortices

SOLITARY EXOSTOSIS / OSTEOCHONDROMA MULTIPLE EXOSTOSES

• Present when large enough to cause symptoms "
teenage & early adult life
• p/w lump, disfiguring, interference with movement of joint +
tendons (limited ROM a/w clicks or jumps as tendons slip
over lump), overlying bursa can become enlarged and
History
• Hereditary condition (AD) – family hx
• Widespread generalised abn of bone remodelling at
epiphyseal line (failure of growth plate remodelling)
• All bones that ossify in cartilage can be affected with
exception of spine & skull

inflamed • Sites: end of long bones, apophyseal borders of scapula

• Continues enlarging till end of normal growth period,
subsequently, consider malignant change
• Site: usually adjacent to epiphyseal line of bone, just on
diaphyseal side, majority at lower end of femur and upper
end of tibia (fast growing ends of long bone + crest of ilium)
• X-ray: well defined bony protuberance emerging from
metaphysis, smaller (cartilage don’t show up) / surrounded
by blotches of calcified material (if cartilage gets calcified)
Investigation
• Long bones may be shorter than normal (slightly short child
with bowing of forearms & valgus knees)
• Occasionally lumps become tender / cause trouble with
pressure on a tendon
• Grows only when child grows (subsequent enlargement:
malignant change to chondrosarcoma)
• X-ray: broadening & lumpiness of metaphyses

• Excise if symptomatic, recent # in size + pain (malignant • Remove if troublesome + start to grow after parent bone
change) stops growing
Management

• Risk of malignant change: esp with pelvic exostoses (may • Risk of malignant change: 6% for multiple lesions
go unnoticed for long periods even with enlargement); 1%
for solitary lesions

! 186!
!! 187!
!! 188!
8.!Diabetic!Foot!
Epidemiology
• Prevalence of 12% (no sex prevalence; malays>Indians>chinese)
• 5% develop foot ulcers
o Mortality: 10% at amputation, 30% within 1 year, 70% within 5 years
Pathogenesis
• Neuropathy (20-40% of all diabetics)
o Sensory: Glove and stocking sensory distribution (hands and feet)
o Motor – Clawing of toes
o Autonomic – Dryness of skin
• Vasculopathy
o Macrovascular (Peripheral Vascular Disease)
! Atherosclerosis: Involve large/medium sized arteries (eg. dorsalis pedis,
posterior tibial)
o Microvascular (Microangiopathy)
! Thickening of basement membrane of terminal arteriole endothelium
! Pulses can be normal but gangrene taking place because of microangiopathy
• Immunopathy
o Susceptibility to infection due to defective leukocyte function and renal failure
o Exact mechanism unknown but postulated decrease in leukocyte phagocytosis and chemotaxis
o Pathogens involved (commonest 2 are staph aureus and pseudomonas aeruginosa)
! Predominantly GPC: Staph aureus, Group A strep pyogenes, Group B strep agalactiae, MRSA, coagulase –ve staph like
epidermidis, enterococci, corynebacterium
• Staph a/w increased risk of mortality!
! Followed by gram negative rods and anaerobes
• GNR: Pseudomonas aeruginosa, E. coli, Proteus vulagris
• Anaerobes: Bacteroides fragilis, peptostreptococcus
! " prior use of ABx predisposes to MRSA and Pseudomonas
o Mild (monomicrobial) infections and severe (polymicrobial; a/w osteomyelitis) infections dominated by gram positive cocci
o Diabetics covered with Augmentin (amoxicillin + clavulanate)
Presentations of Diabetic Foot
• Ulcer (neuropathic, vascular, decubitus –pressure ulcer): commonest complaint
• Cellulitis: IMPT TO DIFFERENTIATE FROM NECROTISING FASCIITIS
• Gangrene: Dry, Wet
• Infection
o Osteomyelitis: Metatarsals, Phalanges
o Septic Arthritis: MTPJ, PIPJ
o Abscess: supf or deep
• Charcot Joint Disease
o Pathology: Degeneration of foot joints due to damage sustained from loss of proprioception
o Increased size of foot
o Rocker bottom deformity (severe)
o Often unilateral but can be bilateral
• Necrotising Fasciitis
History
• Biodata
o Age: Mainly in 5th to 6th decades of life
o Race: Malays and Indians have higher incidence than Chinese
o Socio-economic status: DM foot affects lower socioeconomic group (Malays, education up to secondary school, average monthly
household income <2000SGD)
o Occupation: high risk jobs like housewife, taxi driver, manual labourer, factory workers wearing safety boots
• Presenting complaint: ulcer/ abscess/ gangrene, pain/ swollen/ infection
o General questions about CPC
! Lesion: when, how, what he was doing
! Precipitating injuries: trauma (when, how, what you were doing), foreign body penetration (eg. rusty nails), pressure
! Discovery of lesion: when and how
• If not discovered at point of injury, why? Numbness (check for neuropathic conditions if no pain), weakness?
! Type of wound: open/closed, bleeding
! Progression of injury: grew bigger, more painful, discharge, gangrene
! 1st episode? Any previous injuries of similar nature? Ask for poor wound healing
! Footwear (ill-fitting shoes, slippers, barefeet)
! Functional impairment
o Ulcer
! Site
• Ischemic: Dorsum foot, 1st web space, heel, toes
• Neuropathic: Sole of foot, pulp of toe
• Decubitus: Heel, lateral aspect base of 5th metatarsal
! Size
! Pain
• Painful: Infective, Ischemic
• No pain: Neuropathic
! 189!
 ! Presence of Pus (Note colour and odour)
! Differentiating between vascular and
neurogenic Organism Colour Smell Abx
• Vascular: Punched out, Gangrene, Staph aureus Brownish Little smell Cloxacillin
Ischemic limb symptoms Bacteroides fragilis Feacal smell
• Neurogenic: Painless, Deformed joints, P. aeruginosa Greenish Rotten fruit smell Ciprofloxacin
Loss of sensation (vibration, proprioception)
o Gangrene
! Site: Toes, forefoot, heel
! Type: dry or wet
! Other symptoms of ischemia: claudication, rest pain, cold extremities, discolouration
o Swelling
! Abscess: Acute onset, painful, red, warm
! Septic arthritis: must rule out deep osteomyelitis!
• Joints: MTP, PIP
• Symptoms of inflamm (red, hot, swollen, pain, loss of function) + Severe limitation in joint ROM
• Difficulty in walking
! Associated fever, chills, rigors (absent in 80% of elderly; and likely to be immunopathic too)
o Charcot’s arthropathy: Weakness, difficulty walking, deformity
o Pain: SOCRATES
! Infection
! Ischemia – In gangrene, pain felt at junction of living and dead tissue
• Vascular claudication
o Pain in calf (usu described as a cramp)
o Brought on by exercising (claudication distance) and relieved by rest – especially rest while standing because
column of blood above site of compromised supply exerts pressure and facilitates perfusion
o Not common in diabetic foot
• Rest pain
o Continuous severe aching pain due to severe ischemia
o Usually at most distal part of limb (toes and forefoot)
o Difficulty in walking
o Night pain affecting sleep " Hangs leg over side of bed (below level of heart); Prefer to sleep in sitting position
o Begs for amputation
• Medical History
o Medication/Treatment
! Self Treatment: Cutting callosity (w unsterile scissors, rusty blades), digging of nails
! TCM: Malays – Coffee powder, Indians – Turmeric, Chinese – Sinseh powder (skin burns " ulceration " sepsis)
! Foot reflexology, massage chairs
o Medical Conditions
! Type II DM > Type 1
• Diagnosis: when, how, how long
• Treatment: diet, OHGA, insulin, combinations + dosage/med changes
• Control:
o Follow-ups, past hospitalisations for DM, any Sx done (DKA, HHNK, abscess, ulcer, gangrene etc?
o Medicine compliance
o Symptoms of poor control: Polyuria, Polydypsia, Polyphagia
o Monitoring of DM: Hypocount, HbA1C usual values? How often f/u? doctor say good control?
• Complications (usually approx 20 years): Ask for symptoms and screening, and duration of Cx
o Macrovascular
! Coronary artery disease: IHD (chest pain, SOB), AMI, cardiomyopathy
! Cerebrovascular accident: Transient ischemia attack, stroke
! PVD: parasthesia, intermitten claudication, pallor, poor wound healing
o Microvascular
! Retinopathy: blurring, cataract, previous laser PRP
! Nephropathy " Chronic renal failure (bubbly urine, sallow appearance), 24hr urine test CCT, UTP
! Neuropathy – Glove and stocking disturbance (numbeness, parasthesia, loss of proprioception), motor
(weakness), autonomic (postural hypotension, gastroparesis, diarrhea, impotence)
*Note: CRF + DM: Worst combination
! Other Co-Morbidities: Hypertension (worsen atherosclerosis; increased risk of major amputation), Hyperlipidemia, IHD, CVA
• Family History: DM in parents/siblings as well as their life span
• Social History
o Footwear
! 70% wear slippers or sandals for outdoor use
! Appropriate footwear must cover all toes, foot and heel
o Smoking
o Functional status (ADL): important for prognosis
! Walking ability: Community walker, Housebound, Unable to walk
! Able to do household chores (esp cooking)
! How does the current orthopedic problem affect the patient’s function in general?
! Occupation: High risk jobs: Cook, housewife, taxi driver, factory worker wearing safety boots
o Care-giver Profile: Spouse, sibling, domestic help

! 190!
Examination of the Diabetic Foot
The preliminaries: Introduce yourself to patient, ask for permission to examine. Ensure adequate exposure (at least til mid thigh) but consider
patient modesty also. Ensure good lighting, and good positioning of bed.
The examination of a diabetic patient is to elicit signs in the following 4 aspects: 1) Neuropathy 2) Vasculopathy 3) Immunopathy 4) Dermopathy

GENERAL EXAMINATION -- Start with GE before moving to local examination of the foot:
General Inspection
- Well or toxic looking (RR, comfortable?), Kussmaul breathing (ketoacidosis)?
- Mental state – alert, oriented or drowsy (hypoglycemia)
- Dehydration – furrowed tongue, dry mucosa, sunken eyes
- Skin: scars, sinuses, healed wounds, sallow (RF)
- Eyes: conjunctival pallor, cataract, sunken (dehydration), Fundoscopy for diabetic retinopathy
Volunteer to check vitals
- Temperature – fever suggests sepsis
- BP – both sides, postural hypotension
- Hypocount
- PR
- RR
Quick general examination
- Locate apex beat (exclude cardiomegaly, which may point to CVS problem for the feet)
- CVS, respiratory (infx), abdomen (hepatic abscess, AAA) screen

LOCAL EXAMINATION
General examination
- Generally: scars, sinus, healed wounds, muscle wasting (motor neuropathy)
- Deformity:
& Charcot’s joint – other causes include leprosy, syphilis:
! Enlargement of the affected joint (usually unilat)
! Hypermobility of the joint
! Warm and swollen initially, followed by crepitus in the later stages
! Mid-tarsal joints are the most commonly affected followed by the metatarsophalangeal and ankle joint
! Can have rocker-bottom deformity from collapse of the midfoot
& Mallet toes – can occur in RA as well:
! Flexion deformity at the DIPJ of involved toes, usually the 2nd toe with no PIPJ or MTPJ involvement; caused by imbalance
btw intrinsic (lumbricals and interossei) and extrinsic (long flexors and extensors) muscles
& Claw toes – other causes include RA, polio, stroke:
! Flexion deformity at the PIPJ and DIPJ which usually affect the lesser toes; due to imbalance btw intrinsic and extrinsic
muscles
& Others: High arch foot, Hammer toe, hallux valgus, jt subluxations
- Ulcer – must describe:
& 5Ss – Site (interdigital web space, dorsum, sole, heel), Size, Shape, Surrounding tissue condition (erythematous, gangrenous, necrotic,
warm, tender), Smell
& Inside the ulcer – Depth, Edge (vascular is punched out; irregular? Everted? Gangrenous?), Floor (pus, exudate, slough, necrotic tissue,
granulation tissue, exposed bone/ joint capsule/ tendons), foreign body
& Palpation – Tenderness, Discharge (squeeze surrounding skin and note qty, colour and odor of dc), Bogginess around ulcer
& Ask for PAIN! Painless ulcers/sores=> neuropathy
- Trophic changes (dermopathy, signs of ischemia & signs of neuropathy)
& Signs of PVD: Shiny, loss of hair, dusky discolouration/pale, trophic nail changes, hyperpigmentation, NO varicose veins
& Signs of autonomic neuropathy: dry skin/ scaling, fissuring, callosity (tips of toes, sole)
- Swelling – cellulitis, abscess " note site and size/extent
- Gangrene – wet vs dry; dusky looking? " note site and extent
- Any amputations – eg AKA, BKA

Assess for immunopathy – to exclude abscess, septic arthritis, osteomyelitis, necrotizing fasciitis
- Ulcers + discharge
- Warmth – Compare with other foot
- Tenderness – palpate foot ray by ray for osteomyelitis (MT, phalanx) from tip of toe over MT, tip of toe to Ankle joint, one Ray at a time "
dorsal surface + deep palpation of sole (pus tends to be dependent)
o Probe test: If a sterile metal probe or the gloved finger on palpation reaches bone = Osteomyelitis of Bone is present
- Move all joints – PIPJ, DIPJ, MTPJ for septic arthritis
- Look for cellulitis and document extent: impt to differentiate from necrotising fasciitis; wrinkle sign indicates subsiding cellulitis
- Gas Gangrene – Crepitus under skin
- Common DM foot infections

Assess for vasculopathy:

- 5 Ps of chronic ischemia – Pain, Parasthsia, Pulselessness, Perishing cold, Paralysis
- Venous vs Arterial Ulcers
& Venous: Oedema, loss of hair, warm/cold, pain, parasthesia
& Arterial: Cold, Pale, Loss of hair, Not oedematous
- 1. Colour of skin – pink or pale (ischemia)
- 2. Temperature of skin – warm (normal), hot (infected) or cold (ischemia)
- 3. Pulp capillary refill – > 2s (ischemia) & >15-30 secs = severe ischaemia

! 191!
- 4. Palpate all pulses: (report as palpaple/not palpable)
& Carotids –feel for thrill and listen for bruit
& Upper limb – axillary, brachial, radial, ulnar
& LL – dorsalis pedis (absent in 10% of population " try anterior tibial), posterior tibial, popliteal, femoral

Note: Pulses can be preserved till late in the disease due to calcification of the walls.
Vasculopathy assessment (prognostic significance for distal amputation)
- 2 pulses palpable: v good chance (80-90%) of success
- 1 pulse: fairly good (60-70%)
- 0 pulse: POOR chance ! do BKA

- 5. Buerger’s test – conduct if 1 or more pulse not palpable: 2 components

& Pt supine, raise LL, look for pallor of sole and toes, record vascular angle
o Normal: 90deg pink
o Ischaemia: 15-30deg pallor
o Critical Ischemia: <20deg
& Sit patient up and hang foot over bed – reactive hyperemia (turns from white to pink/red)
o Normal: remain pink
o Ischaemia: white to pink

Assess for neuropathy: all 5 modalities done w eyes closed!

- Pin-prick testing (hyperesthesia, hypoesthesia, anaesthesia)– map out distribution. Usually follows glove and stocking distribution and bilateral
- Proprioception – Hold the sides of the big toe
- Tendon reflex – ankle jerk (Motor: usually not needed)
- Protective sensation w Monofilament testing (Volunteer): Semmes-Weinstein
monofilament (5.07 gauge applies 10g of force – test 9 points on sole and 1
point in 1st web space – if pt cannot feel means loss of protective sensation
& Patient should feel by the time filament bends - </= 7 out of 10 sites
(loss of protective sensation)
& 3 most impt points: weight bearing tripod (1st MT head, 5th MT head,
calcaneum)
& +ve SWMT is more accurate than pinprick + proprioception +
vibration to detect sensory neuropathy
- Vibration sense (Volunteer; over malleoli and tibial crest): Tuning Fork,
Bioesthesiometer
- Note: test UL for glove and stocking too! (10% have hands affected)

Other things you would like to check:

- Systemic review:
! Heart: cardiomegaly (apex beat)
! Lungs: pneumonia
! Abdomen: AAA, hepatic abscess
- Other limbs for similar pathologies
- Complications of DM: Retinopathy, Nephropathy, Stroke/AMI
- Vascular assessment:
o Ankle Brachial Index (ABI)
! Ankle systolic pressure measured using a cuff and a handheld continous wave Doppler ultra sound probe placed over pedal
vessels (dosalis paedis or tibialis posterior = whichever is higher)
! Doppler ultrasound probe used to measure Ankle systolic pressure / Brachial systolic pressure (should have 3 waveforms –
systolic, diastolic, recoil. If only 2 means already partial obstruction.)
! Measure of perfusion at ankle level
! ABI:
• Calcification of artery: >1.3 (hence a limitation of the ABI)
• Normal: 1-1.2
• Ischaemia: <0.8
• Min to mod dz: 0.5 – 0.9
• Severe dz: <0.5
• Critical ischemia: <0.3
! Advantages: Non-invasive, relatively cheap
! Disadvantages: Can be misleading as operator dependent and affected by calcification of artery
o Toe Brachial Index (TBI): (more accurate than ABI as distal vessels don’t get calcified)
! Photoplethysmography (PPG) used to measure digital blood flow using infra red light
• Normal: >0.7
• Ischemia: 0.4-0.6
• Critical Ischemia: ≤ 0.3
! Measure perfusion at toe level
! No calcification of artery at this level
o Arterial duplex scan of lower limb (expensive)
o Angiogram, femoral (if vascular reconstruction needed): localize areas of occlusion amenable to bypass Sx or angioplasty

! 192!
Investigations
• Biochemical
o Markers of Infection
! FBC: TWC w differential count for infx (Leukocytosis, Increase in polymorphic neutrophils), Anemia
! Acute phase reactants: ESR, CRP
o Renal panel: Assess renal function
o HbA1C (Glycosylated haemoglobin)
! Normal: 4-7%
! Indicator of diabetes control over last 3 months
o Hypocount monitoring 4 times daily: normal 4-8mmol/l
o Urinanalysis: Glycosuria, ketonuria (DKA), proteinuria (nephropathy)
o Hb: nutritional status (affects ulcer healing)
o For medical case: include urine dipstix, lipid profile
• Culture (blood/ ulcer swab): blood culture done for all cases even w/o fever (often no systemic response due to immopathy or old age)
o Taken before starting antibiotics
o Take pus and swab from deepest portion of ulcer to increase yield
o Gram stain + c/s (aerobic and anaerobic organisms)
• Imaging
o ECG, CXR (anaesthesia fitness)
o X-ray of foot / ankle
! AP, lateral views
! Osteomyelitis –osteopaenic/ rarefaction, erosions, periosteal reaction(early), cortical sclerosis(chronic)
! Septic arthritis –widened joint space, perarticular osteoporosis(early), joint space narrowing +/- erosions (late)
! Gas gangrene (clostridium, strep. microaerophiles) –exclude necrotizing fasciitis if gas present
! Bony destruction (Charcot’s foot) and other neuropathic changes
! Calcification of vessels
! Foreign body
!
Management
• Classifications
o Wagner classification of DM foot ulcers: determines Mx " generally lower grades respond to Abx + debridement while higher grades
(2-5) require amputation
King’s College Classification Wagner’s classification
Stage Features Grade Description Treatment
Stage 1: Normal No risk factors present: 0 No ulcer in a high risk Conservative:
Foot foot education, footwear,
• Neuropathy
regular clinical and
• Ischemia
podiatry exams
• Deformity (eg. dystrophic nails)
1 Superficial ulcer Conservative:
• Callus
involving the full skin Total contact cast for
• Swelling thickness but not offloading, walking
Stage 2: High Risk One or more of 5 aforementioned risk factors present underlying tissues; no brace, special
Foot infection) footwear
Stage 3: Ulcerated • Skin breakdown and ulceration 2 Deep ulcer, penetrating Surgical debridement
Foot • Infective, ischemic or neuropathic down to ligaments and Wound care
Stage 4: Cellulitic muscle, but no bone Offloading
Foot involvement or abscess Culture specific Abx
formation
3 Deep ulcer with inf of Surgical debridement
deep tissue w pus; or partial amputation
cellulitis, deep abscess Offloading
tendinitis, osteomyelitis Culture specific Abx
Stage 5: Necrotic Gangrene (dry or wet)
Foot 4 Forefoot gangrene Lower extremity
amputation
Stage 6: Major Indications for Amputation
Vascular consultation
Amputation • Agonising pain
5 Whole foot gangrene Major extremity
• Overwhelming infection in foot
amputation
• Extensive necrosis in foot Vascular consultation
• General measures
o Hydration status:
! IV line at least 1.5L a day to prevent dehydration
! Intake/output charts –urine output monitoring
o Diabetic chart –hypocount TDS including 10pm (watch out for hypoglycemia)
o IV antibiotics: Broad spectrum Augmentin (GPC, GNR, anaerobes) OR Clindamycin (gram positive, anaerobes, esp for
necrotizing fasciitis) + Ciprofloxacin (gram negatives) " change to culture-specific antibiotics
o Topical antibiotics
! BNP (bacitracin, neomycin, polymycin) powder for pseudomonas
! Bactroban cream for MRSA
o Daily wound dressing –Chlorhexidine, flush with H2O2 and saline, then chlorhexidine dressing
o Elevate leg if swollen

! 193!
 • Surgery
o Abscess: I&D
o Ulcer: radical debridement
! All slough and exposed tendons excised else become necrotic (in heel whole part of tendoarchilles exposed excised)
! Heel ulcer/ gangrene unless successfully resurfaced" Below Knee Amputation
o If vascular cause, consider whether amenable to bypass or not
o Dry gangrene
! Pulses usually very bad
! Toe may auto-amputate
! Management: clean with ethanol, splint, dressing, prophylactic antibiotics (sides usu get infected), consider ray amputation
in young patient (better to leave it alone in older patients as it is quite easy to care for dry gangrene) +/- hyperbaric oxygen
therapy (HBOT)
o Wet gangrene " AMPUTATE
! Types of amputation
Amputation Site
Disarticulation at jt PIP, DIP
Ray (open or closed) Through metartarsal
Open ray: for adequate drainage of pus involving 1 ray, upon
healing w healthy granulation tissue, split skin graft is used
Closed ray: if after debridement all infectious tissue has been
removed, close wound by tagging
Forefoot
Lisfranc Tarsometatarsal
Chopart’s Mid-tarsal
Syme’s (rare) Through ankle (requires good post tibial pulse)
Below knee (requires 30% more energy to walk; bilateral BKA 40%; Able to
fit patella tendon bearing prosthesis)
Stokes-Gritti Through knee
Above knee (Requires 40% more energy to walk)
Hip disarticulation
Hindquarter Hemipelvectomy
• Multidisciplinary
o Case manager manages clinical pathway for DFP
! Surgeons: orthopaedic surgeon, vascular surgeon
! Medical: endocrinologist, Infectious diseases specialist
! Others: podiatrist, dietitian, physiotherapist, occupational therapists, MSW
! Nurses: diabetic nurses, wound-care nurses
! Amputation support group

Charcot Joints
• Pathology: Progressive degeneration of a weight bearing joint resulting in deformity
• Pathophysiology
o Neurovascular theory (German): Neuropathy " loss of autonomic tone " vasodilation " increased blood supply " increased
osteoclast load to site " brittling and osteopenia " collapse
o Neurotrauma theory (French): Sensory loss " abnormal movements" repetitive trauma " inflammatory resorption of traumatized
bone " further damage (vicious cycle) " collapse
• Clinical Features
o Inflammation: erythema, pain, warmth
o Loss of protective sensation
o Rocker bottom deformity
! Bone arches collapse + soft tissue contracture
! Complications: callosities" fissures" infection
• X-ray
o Atrophic: Osteolysis
o Hypertrophic (more common)
! Distended joint
! Density increase
! Debris
! Dislocation
! Disorganisation
! Destruction
• Classification
o Brodsky Classification
! Type 1: Tarsometatarsal and naviculocuneiform joints
! Type 2: Subtalar joint
! Type 3A: Ankle joint
! Type 3B: Posterior calcaneal tuberosity

! 194!
 o Eichenholtz Classification and management: classification, characteristics and Rx strategies for charcot foot
Grade
0 Clinical stage
1 Fragmentation stage
2 Coalescence stage
3 Reparative stage
Characteristics
Erythema, edema, increased
temperature to foot; but radiographs
negative
Periarticular #s, joint dislocation,
instability, deformed foot
Reabsorption of bone debris
Remodelling and reorganisation
Stable foot
Treatment*
Limited weight bearing (possibly TCC or PPWB; prefabricated
pneumatic walking brace), close observation, Pharmacological
(Bisphosphonate)
TCC (total contact cast), limited weight bearing
TCC followed by CROW (Charcot restraint orthotic walker)
Possible surgical intervention (osteotomy) for removal of bony
prominences associated with ulceration: esp if young

Charcot’s joint song
On inspection, I note the presence of a grossly deformed ankle joint
which (is / is not) swollen, associated with a rocker bottom foot.
There is a previous amputation of the _____________________.
The skin around the joint is not erythematous / there are skin changes
suggestive of diabetic dermopathy.
There are no scars noted. There is wasting of the intrinsic muscles of
the foot.
In addition, there is a ___ by ___ cm irregularly shaped ulcer located on
the sole. The ulcer has a regular edge, the floor consists of
_____________. The surrounding skin around the ulcer looks normal /
does not appear erythematous. There are callosities located over ____.
I would like to move on to palpate the joint. (ask pt for any pain first)
The joint is non tender and does not feel warm. There is creptius felt on
passive movement of the joint. The normal contours of the joint are lost
and the joint may be subluxed or dislocated.
The ulcer is non tender and the surrounding skin does not feel warm.
There is no discharge expressed from the ulcer.
(move the joint)
There is instability of the joint as evidenced by abnormal movements
and hypermobility.
The above findings are consistent with that of a Charcot’s joint which is
likely complicated by a neuropathic ulcer.
I would like to complete the examination by performing a neurological
examination of the affected limb to look for loss of sensation and joint
position sense.
I would also like to palpate the pulses in the LL to determine if there is
concurrent arterial insufficiency.
I would also like to perform a urine dipstick to look for glycosuria.

Mr / Mdm XXX is a __ years old (race) gentleman / lady, INFECTIVE

premorbid status: (ADL independent, community ambulant) ,
occupation: ____________________,
with a significant PMHx of (T2DM / HTN / "lipids etc.) ,
presenting complaint: currently admitted for _____ days/ weeks
history of
1. Ulcer
2. Gangrene
3. Calf pain/ foot pain
4. Cellulitis/ OM: swelling, erythema and pain over the _____
5. Deformity
ULCER
He / she first noticed the ulcer ____ days/ weeks ago over the (site) ,
after he noted (pain / bleeding / foul smelling purulent discharge)
from the ulcer.
There was associated (pain / bleeding / foul smelling purulent
discharge) of the ulcer.
It was progressively increasing in size and has previously healed and
broken down ____ times.
There was history of (trauma / ill-fitting shoes) prior to the development
of the ulcer. (+ details of trauma / footwear)
The patient (also has / does not have) a history of similar ulcers on
the sole of his feet previously.
PVD
He / she noted darkening of his (site) for the past (duration) , which
is (a/w foul smelling discharge / dry) .
Claudication: He c/o claudication pain for the past (duration) in
the (site) , which is cramping in nature,
precipitated by walking (distance) and relieved
by rest. Pain score is _____.
This is associated with numbness and
paraesthesia in the skin of the (site) .
The pain over his / her (site) started (duration) ago and became
progressively worst.
It was a/w redness of the overlying skin and swelling of e (site) .
There (was no / was) a prior history of trauma to the foot.
DEFORMITY
The above was associated with _________, swelling of the ankle joint,
and progressive instability on walking.
Functional Status
Due to his / her condition, he is limited functionally by _________ and
requires a walking aid for ambulation.
Systemic Review
He / she (does not have / has) fever for (duration) with a Tmax of
___°C, associated with chills & rigors.
There are no complaints of loss of weight or loss of appetite.
He / she (has no / has) urinary or bowel complaints.
He / she (has no / has) other systemic complaints (chest pain / SOB
/ swelling of LL / weakness / numbness / fainting / blurred vision) .
Management this Admission
During this admission, he / she was treated with IV antibiotics and daily
dressing / VAC dressing.
Possibility of a need for (amputation / wound debridement) has been
discussed with the patient if conservative management fails. OR He /
she has undergone (amputation / wound debridement) .
Diabetic History
He / she was diagnosed with diabetes ____ years ago, when he
presented with polyuria, polydipsia and polyphagia/ weight loss OR
during a health screening/ health check-up. His / her diabetes is
complicated by (retinopathy / nephropathy / neuropathy / peripheral
vascular disease / previous CVA / previous AMI).

Rest Pain: There is presence of rest pain for the past

1. Retinopathy He / she noted decrease in vision since
(duration) over the (site) which has gotten
(duration) ago and underwent ___ sessions
progressively worst. The pain is described as
of laser photocoagulation therapy. Currently
sharp, aggravated by (movement / pressure)
on yearly eye screen.
and relieved by hanging the foot over the side of
the bed at night. Pain score is _____. 2. Nephropathy He / she c/o (polyuria / frothy urine / PU
symptoms) .

! 195!
 Doctors have told him / her from blood tests The (femoral / popliteal / posterior tibial / dorsalis pedis) pulse(s) is /
that kidney function is poor. are well felt on the (left / right) limb.
His / her DM is complicated by ESRF, However the (left / right) (femoral / popliteal / posterior tibial /
currently on (haemodialysis / peritoneal dorsalis pedis) pulse(s) is / are diminished.
dialysis) .
There are no significant foot deformities or signs suggestive or previous
3. Neuropathy He / she c/o (weakness of his foot / difficulty amputations of toes OR
walking / decrease in sensation / frequent There is a BKA of the (left / right) leg and there is Charcot’s foot
falls / postural hypotension / bladder or bowel deformity over the (left / right) foot, as evidenced by joint swelling,
dysfunction) since (duration) ago. rocker bottom deformity and loss of plantar arch. There is also wasting
4. PVD He c/o (claudication pain / rest pain) . of intrinsic muscles over the dorsum of foot, clawing of the (left / right)
He has previous (amputations / surgeries) toe, and overriding of the ___ toe over the ___ toe.
done in __________________.
ULCER
5. Previous CVA/ AMI Mr / Mdm XXX has a ____ x ____ cm, (shape) ulcer over the (site:
medial malleolus / heel / underneath the metatarsal heads / webspace),
6. Previous DM-related hospital admissions (sepsis (DKA), AMS
with a clean, punched-out edge.
(HHNK), hypoglycaemia)
The floor of the ulcer is (clean / dirty) and has (slough / pink
granulation tissue / exposed tendon & bone) .
(Drug History & Diabetic Drug History) The ulcer is adherent or invading deep structures such as (tendon /
He / she has NKDA and is on (insulin / OHGA) for DM control (+ periosteum / bone) .
name of drug & frequency). A (quantity) of (odour: foul smelling) , (colour: serous /
Mr / Mdm XXX (is / is not) compliant with his / her medications and serosanguinous / purulent) discharge was noted.
has no SE of medications / complications of treatment such as
(hypoglycaemia / lipodystrophy / infection at injection site / weight gain) GANGRENE
. Mr / Mdm XXX has (dry / wet) gangrene noted over (site) .There is
There (has been no / has been) recent adjustment to his medication. a clear line of demarcation at the (site) .
He / she is also on (other drugs) for (other comorbidities) . It is a/w a (quantity) of (odour: foul smelling) , (colour: serous /
serosanguinous / purulent) discharge.
(Follow-up, Control and Lifestyle Management) There (is / is no) associated erythema and / or (generalised /
He / she is on regular ___-monthly follow-up at the (polyclinic / GP) discrete) swelling in the surrounding skin over the foot extending up to
and his recent HbA1c is _____. the _____________.
He / she was told by his / her doctor that his / her control is (sub- However / in addition, I note that there are scars suggesting the
optimal / good) . presence of previous ulcers.
He / she (does not perform / performs) self monitoring of blood The skin appears (pale / normal / dusky) and has signs of chronic
glucose levels at home. ischaemia such as (shininess of skin / loss of hair / trophic nail
He / she has adjusted his / her diet to ______, and he usually eats changes) . There (is no / are) signs of diabetic dermopathy as
(outside / hawker food / home-cooked food) . evidenced by the increased skin pigmentation as well as dry skin
He / she (is / is not) compliant to foot wear advice and visits the suggestive of autonomic neuropathy.
podiatrist (frequency) . There is presence of callosities over the (sole / tip of the toes / side of
the foot) .
Family History
He / she has a significant family history of Type 2 Diabetes Mellitus. PALPATION
His / her _____________ has DM diagnosed at (age) and has The foot is non-tender and does not feel warm. The capillary refill is less
passed away because of (cause of death) . than 2 seconds. OR
There is tenderness in his / her foot over the (site: 1st / 2nd / 3rd / 4th /
Social History 5th ray – distal phalanx / middle phalanx / proximal phalanx / metatarsal
He / she (does not smoke / smokes / is an ex-smoker and has quit XX bone / up to the ankle; between the rays) on superficial and deep
years ago) , ( sticks/day x years). palpation.
He / she (has / does not have) a habit of regular intake of alcoholic
drinks. MOVEMENT
He / she has (good / poor) social support. He / she works as a There is pain on movement of the (PIPj / DIPj / MTPj) .
_________ and lives with his / her ________. The ankle joint is subluxed / dislocated, with creptius (in Charcot’s foot).
His / her main caregiver is his / her ______________. There is hypermobility and instability noted on the (left / right) ankle.
He / she lives in a residential (with / without) lift landing.
Currently, the family (does not have any financial issues / is receiving NEUROLOGICAL EXAMINATION
financial aid from ) . There is glove & stocking sensory loss over the (left / right) foot. The
Semmes Weinsein Monofilament test revealed an inability to perceive
PHYSICAL EXAMINATION sensation over (1st toe / 3rd toe / 5th toe / forefoot below 1st toe /
forefoot below 3rd toe / forefoot below 5th toe / medial mid foot / lateral
On physical examination, Mr / Mdm XXX is alert n comfortable at rest. mid foot / heel / dorsum of foot between 1st & 2nd toe) , indicating loss
Appearance: He / she does not appear to be sallow, pale or of protective sensation with less than 7 sites felt by patient. There is
dehydrated. loss of vibration and proprioception over the (left / right) foot and the
Vitals: Her PR is _______, RR is _______ and BP is ankle jerk is absent.
_______. (SpO2: ______; VAS: _____.)
Heart: S1S2 were heard on auscultation. Buerger’s test is positive at ____ degrees.
Lungs: Lungs are clear. In summary, Mr / Mdm XXX has diabetic foot (ulcer) with / without signs
Abdo: (look for lipodystrophy at insulin injection sites & of infection such as erythema, warmth and tenderness on palpation and
comment on absence / presence) movement over ___________. There are also signs of vasculopathy as
evidenced by pallor, coldness, prolonged capillary refill time and
Pulses: diminished ____________ pulses, associated with a positive / negative
The axillary, brachial, radial and ulnar pulses are well felt bilaterally. Buerger’s test. In addition, he / she has peripheral neuropathy as

! 196!
evidenced by loss of pain, vibration and proprioception over _______,
with an inability to perceive ___ out of 10 pts in the monofilament test.

OR

In summary, Mr / Mdm XXX has wet / dry gangrene of the (site),

associated with other signs of vasculopathy such as pallor, coldness,
prolonged capillary refill time and diminished ___ pulses, associated
with a positive / negative Buerger’s test. There are also signs of
infection such as erythema, warmth and tenderness on palpation and
movement over _____. In addition, he / she has peripheral neuropathy
as evidenced by loss of pain, vibration and proprioception over ______,
with an inability to perceive ____ out of 10 points in the monofilament
test.

9. Paediatric Conditions

TORTICOLLIS aka WRY NECK

• Types:
o Congenital/Primary/Muscular/idiopathic (commonest: due to fibrosis and shortening of SCM)
! infants after difficult delivery - breech presentation (delivery buttocks first instead of heads first)
! Skeletal anomalies, Atlantoaxial instability
! Klippel Feil syndrome (bony fusion of C-spine)
o Acquired/Secondary: always exclude and treat this first since this is the underlying cause
! Acute: " C1/C2 rotatory subluxation
• Muscular damage caused by inflammatory diseases (eg. myositis, lymphadenitis, TB and other infx); from cervical spinal
injuries that produce scar tissue contracture; and, less commonly, from tumor or medication
! Spasmodic - organic central nervous system disorder, probably due to irritation of the nerve root by arthritis, osteomyelitis, PID
! Benign paroxysmal torticollis – might be migraine variant.
! Ocular torticollis - compensatory mechanism enacted by patients with trochlear nerve palsy or superior oblique muscle weakness
! Others: Hysterical, Hearing problem, Flat head/plagiocephaly
• Symptoms
o Child tilts or looks to the side opposite to the tight SCM
o Limited lateral flexion to opp side and rotation to same side
o Painless if long-standing
! Facial asymmetry on side of torticollis in congenital or long-standing torticollis: facial hemiatrophy, smaller eye – reduced
stimulus to affected side thus decrease growth
! SCM “tumour” may be present in 1st few weeks of life: subsequent deformity may be prevented by gentle daily neck manipulation
o Painful if acute torticollis
• X-ray (ACQUIRED)
o Loss of cervical lordosis
o Pretracheal inflammation (if infection in pretracheal region)
o C1-C2 subluxation
• Management (for congenital; for acquired treat underlying cause)
o Conservative (under 1YO): physioRx (heat, massage, stretching)
! Drug induced toriticollis: treat w diphenhydramine, benztropine, benzodiazepines, anti-cholinergics
o Surgery (above 1YO; don’t need to try conservative Rx): Surgical release of SCM (+/- reconstruction of sternal head) + traction +
custom made cervical collar for immediate post-op period + Post op aggressive physioRx

! 197!
TIBIAL BOWING (& PSEUDOARTHROSIS)
• Posteromedial bowing: physiological
o Clinical problem: limb-length discrepancy (treat if >/=5cm difference)
• Anteromedial bowing: deformity
o Missing cruciates
o Ankle valgus
o Tarsal coalition!
o Limb-length discrepancy
• Congenital pseudoarthrosis of tibia
o Associated w NF-1
o Crawford’s classification
! Type I – medullary canal is preserved, cortical thickening
! Type II – thinned medullary canal, cortical thickening
! Type III – cystic lesion, may be fractured
! Type IV – pseudoarthrosis (tibial & fibular non-union)
o Management: circumferential brace to protect leg from fracture
o Definitive Rx: excision and reconstruction (bone transplantation using fibular graft)

CEREBRAL PALSY
• Definition
o Non-progressive insult on a dvlping brain
o The brain lesion is permanent and non-progressive, but the natural history of CP is not static
o If non-progressive insult on a dvlped brain = stroke
• Aetiology:
o Abt 10-15% of patients documental perinatal hypoxia
o CP is not solely the result of prematurity coz 60-65% of afflicted children were born at full term
o Although only abt 10% of CP patients weigh <1500g at birth, in this low birth ewight grp, the risk of having CP is 90 per 1000, compared
w 3 per 1000 if weighing >2500g and appropriate for gestational age
o Low birth weight for gestational age and prematurity are commonly a/w dvlpment of spastic diplegia
• Types
o Neuropathic types:
! Spastic: overactive Golgi apparatus; the only one in which the ortho team can intervene
! Other types: ataxic, athetoid, hypotonic, mixed
o Anatomic patterns: hemiplegic, diplegic, quadriplegic, total body, triplegic, monoplegic
• Management: dependent on functional assessment of child
Type Functional aim
Hemiplegic Efficient walking: supple hamstrings & TA
UL is the best position for function
Diplegic Walker
- Efficient walking
! No crouch/ jump gait
! No tiptoeing
! Feet in neutral position
! No scissoring
- Consider need for assistance if power
and control poor
- Dietary control (optimal BMI: patient
cannot bear weight if too heavy)
- All should walk!!! (if not, could be due to
poor parental support, laziness; rehab
into society would be even more difficult)
Non-walker
- Investigate reason
- If reason for inability to walk is
neurological then aims same as
quadriplegic sitter
Quadriplegic - Painless seating: seating clinic
- Spine fairly straight and stable
- Hips painless and reduced
- No pelvic tilt
- Adequate abduction for hygiene care
- Adequate knee flexion
o Areas to address
! UL
! Spine: paralytic scoliosis
! Hip: paralytic subluxation/ dislocations
! Knee: contractures, gait problems
! Foot/ ankle: equinus, varus/valgus
o Methods
! Conservative:
• Early intervention for stimulation
• Seating for poor trunk control
! 198!
 • PhysioRx
• Orthotics
• Botulinum A toxin
o Intramuscular injection of neurotoxin produced by Clostridia bacteria
o MOA:
! Delivered into or near sites of nerve arborisation, and blocks the release of Ach from presynaptic vesicles at
myoneural junction
! Recovery of tone results form the sprouting of new nerve terminals, which peaks at abt 60days
o Technique:
! To reach muscles that are deep/difficult to localize,
electromyographic guidance & electrical stimulation
can be used
! BTX diffuses readily, so the injection shld be placed
in the muscle belly
! Surgical: Single event multi-level surgery
• Soft tissue Sx: Post-op casting required! --------------------------"
o Only done when deformity progresses to contracture and is
not dynamic (passive ROM still possible) anymore
o CI in joints w correctable deformity
o Purpose: Sx done w functional aim in view; cosmesis only
a consideration in UL
o Tendo-archilles lengthening (done percutaneously in v young): indicated when ankle cannot be dorsiflexed to
neutral in walker
o Hamstring release: In those w v severe crouch gait and popliteal angles usually >45deg
! Release of semitendinosus and fractional lengthening of semimembranosus and biceps femoris
o Adductor release:
! Done for significant scissoring in walker
! Uncorrectable tight adductor in non-walker such that perineal hygiene is compromised
! Painful subluxed hips
• Bony Sx: Usually in older children
o When soft tissue Sx has failed w recurrence of deformity (ie. once joints are stuck/immoible)
o In areas where soft tissue Sx alone is inadequate:
! Spine
• Paralytic scoliosis due to muscle imbalance
• Not treatable w bracing
• Seating is difficult for quadriplegics if uncorrected
! Unstable hips
• Hips need to be reduced due to 1) pain 2) severe pelvic tilt causing secondary scoliosis 3) pressure
sores due to unequal pressure when sitting
• Not the same as DDH!
• Usualy needs open reduction +/- femoral and/or acetabular osteotomy
! Feet: Severly deformed due to uncorrected muscle imbalance
• Usually done in the older age grp
• Many methods; principle is to correct the foot alignment
• Indicated in walkers w passively uncorrectable deformities
• Valgus feet: calcaneal shift, grice extra-articular fusion
• Tendon transfers: split posterior tibialis tendon transfer
• Bony fusion " Triple arthrodesis: salvage procedure

Paediatric Fractures
BASIC PRINCIPLES
• Presence of growth plate which gets injured before ligaments (" avulsion #s)
• Presence of secondary ossification centre – CRITOE
o Ossification starts at
! Capitalium (1yo)
! Internal/medial epicondyle (3yo)
! Trochlea (5yo)
! Olecranon (7yo)
! External/lateral epicondyle (9yo)
• Potential for remodeling in <10yo
o Remodelling occurs 75% at physis, 25% at fracture site
o Physeal remodeling
! Once physis is aligned, it resumes symmetrical growth
o Diaphyseal remodeling
! Follows Wolff’s law – “form follows function”
o The closer the fracture to an active physis, the greater the
remodeling potential
• Greenstick fractures
o Definition: Break at one cortex with bending at opposite cortex
(no disruption)
o For reduction, need to complete break of other cortex
! 199!
 • Buckle fractures: due to buckling of the periosteum
o Definition: Incomplete fracture resulting in
buckling/bulging of cortex
o Often due to axial compression
• Plastic deformation
• Pathological #s
• Non-accidental #s
o Specificity of skeletal trauma for abuse
! High specificity: classic metaphyseal lesions,
posterior rib #, scapular #, spinous process #,
sternal #
! Moderate specificity: multiple #s esp bilateral,
#s in various stages of healing, epiphyseal
separation, vertebral body # or subluxation,
digitial #, clavicular #, long-bone shaft #, linear
skull #
! Low specificity: complex skull #!

SALTER-HARRIS CLASSIFICATION
• Classification for physeal injuries: Salter Harris Classification uses visualizing long bone distal portion w diaphysis superiorly placed and
epiphysis inferiorly placed
• 5 Types (SALTR)
o Type 3-5 may result in growth disturbance due to involvement of reproductive layers of physis
o Type 2 most common
Type Description Example Basic Mx principles of physeal #s
I Straight across - Transverse # of cartilage in physis 11yo w ankle inversion injury Extra articular #s usually treated
(presents as widened epiphyseal plate) Distal fibula # w M&R; # crosses hypertrophic
II Above physis- Type 1 + triangular metaphyseal fragment Distal radius fracture zone thus wont affect growth
III Lower than physis in epiphysis - # splits through 13yo w ankle injury
epiphysis and veers off transversely to one side through Tillaux fracture Intra-articular extension
hypertrophic layer Requires anatomical reduction
IV Through metaphysis, physis and epiphysis - Type 3 + 5yo w elbow injury Usualy involves ORIF
metaphyseal involvement Lateral condylar # of humerus
V Rammed, as in a compression injury – physis crushed

PRINCIPLES OF MANAGEMENT
• All dislocation must be stably reduced ASAP
• Aim for acceptable alignment based on
o Age
o Potential for remodeling
o Plane of motion
o Fractured bone
o Fracture site: epiphysis, metaphysis, diaphysis
o Fracture personality: spiral, oblique, transverse, buckle, greenstick,
Bayonet and Salter Harris
• Reduction maintained w plaster as children less likely to get joint stiffness
• Rx usually non-surgical
o If Sx is required
! Minimal dissection to ensure no damage to growth plate
! Usually smooth pins used instead of plate & screws as smooth
pins produce minimal damage to growth plate & periosteum
! Usually combined w casting postoperatively for added stability
to fixation
! Pins inserted percutaneously where possible

COMMON FRACTURES IN CHILDREN

• Clavicle #s
o V common amonst the v young after falling off the sofa at home
o Also as a result of birth trauma
o Almost never treated w Sx " Arm sling will usually suffice
o ONLY # ACCEPTABLE AS NON-NAI IN THE V YOUNG
• Proximal humeral #s
o Has great potential remodeling due to fact that the shoulder is most mobile joint in body
o Usually treated w collar and cuff OR an O slab
• Supracondylar #s (refer to humerus fracture)
• Lateral condylar #s (refer to humerus fracture): Impt because it is a SH IV fracture w joint extension
• Radius/ulnar #s
o Unlike in adults radius/ulna, can usually be treated by M&R
! Immobilize w U slab of sugar tong slab
o Sx indicated if unable to achieve stable acceptable alignment, eg.
! In older children/teenagers
! 200!
 ! Excessive rotation
! Excessive angulations (>20deg)
o Sx if indicated done w minimal disturbance of growth plate and periosteum
o Also think of Monteggia/Galeazzi #s
o Radial neck MUST bisect the capitulum of humerus in all views
• Distal radius #s
o Can be different varieties
o Salter Harris 2 involving the distal radius epiphysis " below elbow cast after M&R
o Distal 1/3 # of the radius ulna which is the most unstable
! Above elbow cast after M&R
! Bayonet acceptable for those <10yo if delayed presentation
o Buckle Fracture: V stable " no M&R required & may treat w brace only
• Femur #s
o General concerns: adequate pain relief, ATLS for multiply injured
o Be aware of NAI: In those not ambulating, mentally retarded, not communicative yet
o Be aware of pathological #s
o Rx:
! Gallows traction for those <2yo or 20lbs
! Russell’s traction for others till next elective list
! Early 1 leg hip spica: allows for sitting " better accepted
• Tibial #s
o Most common type of #s in children
! # of distal 1/3 to distal ½ of tibia, is undisplaced an dhas a spiral pattern
! Occurs after a low energy trauma, sometimes w a rotational component
o Aim is to achieve acceptable alignment
! No varus or recurvatum
! Angulation <10deg
! No rotation
o Mx: above knee cast backslab, allow weight bearing
o Admit if
! Concerns of compartment syndrome
• FHL: pain on stretching of ischemic muscles " extend the child’s toe (small movement but great pain)
! Good alignment cannot be achieved
! Open #: tibia is superficial thus predisposes to osteomyelitis & non-union (a/w poor BS for tibia unlike femur thus vicious cycle)
o Beware of Toddler’s fracture (9months-3yo) refuses to walk, keeps on falling)

FRACTURES IN ADOLESCENTS
• Tibial spine #s
o In older children/adults, more likely ACL tear (ligament < bone); but since
ligament is stronger than bone, more likely avulsion # of tibial spine (site of
attachment still has cartilaginous contact, not bone)
o Classification: Meyers & McKeever
! Type I: minimal or no displacement
! Type II: angular elevation of anterior portion w intact posterior hinge
! Type III: complete displacement w or w/o rotation
• Tillaux #s
o Fracture of anterolateral distal tibial epiphysis
! Tibal fragment avulsed fr its epiphyseal attachment due to strong anterior
tibiofibular ligament (growth plate not completely closed yet & ligament >
bone) in an external rotation injury of the foot in relation to the leg
o More unfused physeal parts = more # parts (eg. triplane # in a 12yo): surgical Rx,
w partially threaded cancellous screws
! Multiplanar # (SH type 3 on AP, SH type 1 on lat), extends thru transverse (growth
plate), sagittal (epiphysis), and coronal (distal tibial metaphysis) anatomic planes
• Imbalance of muscle and bone growth cause tension in unfused apophysis " Tension can convert
to # during sporting activity esp in those who are heavy for their age
o Eg.
! Tibial tuberosity (OSD)
! Inferior pole of patella (Sindig Johanssen Larsen)
! Apophysis of calcaneum (Sever’s syndrome)
TRAUMATIC BIRTH INJURIES
• Osteogenesis imperfect: LIFE THREATENING CONDITION " refer early
• Humerus fracture: mechanism of injury ------------------------"
• Obstetric Brachial plexus injuries (REFER to hand injuries)
• Clavicle fracture
o No intervention
o Reassure family
o Ensure no pressure on # site!
o Exclude brachial plexus injury
o In the infant initially demonstrates discomfort w the fracture, the long arm sleeve of the infant’s shirt can be pinned to the shirt for 7-10
days to provide adequate immobilization
• Femur fracture: treat w pavlik harness!
! 201!
10.!Bone!and!Joint!Infections!
• Types:!
o Acute haematogenous osteomyelitis!
o Subacute haematogenous osteomyelitis!
o Post-traumatic/operative osteomyelitis!
o Chronic osteomyelitis!
o Acute suppurative arthritis!
o TB infxns of bone & joints!
• Waldvagel Classification!
o A – haematological spread!
o B – a/w wound!
o C – contiguous spread from local infection!
• 3 things to consider:!
o 1) type of organism!
o 2) site of infection!
o 3) host response (immunocompromised?)!
• Principles of Rx:!
o Rest affected part!
o Provide analgesia and general supportive measures!
o Initiate Abx Rx
o Surgical debridement (of pus and necrotic tissue)
• Osteomyelitis complications FIBRES: Fractures, Intraosseous (broidie) abscesses, Bacteremi/ Brodie abscess, Reactive amyloidosis,
Endocarditis, Sinus tracts/ Squamous cell CA

ACUTE HAEMATOGENOUS OSTEOMYELITIS

• Common organisms:!
o Children <4YO: H. influenza!
o <1YO: GBS, Staph A, E Coli!
o 1-16YO: Hib, Staph A, Strep, Enterobacter!
o Adults: Staph, Strep, Pseudomonas, E Coli !
o Hx of sickle cell anaemia: salmonella!
• Site: !
o Adults: anywhere, esp thoracolumbar spine. Adults are usu immunocompromised!
o Children: usu. metaphysis of growing long bone. Growth plate limits spread towards epiphysis.!
o Infants: risk of epiphyseal extension, jt involvement & growth disturbance.!
• Pathology!
o Infection spreads to form subperiosteal abscess!
o Bone dies, forming a sequestra encased by the involucrum (periosteal new bone)!
o Chronic osteomyelitis: pus discharges through cloacae (perforations) in the involucrum!
• Clinical features!
o Pain, malaise, fever, toxaemia!
o Cellulitis, swelling, oedema, erythema, warmth, tenderness, ↓ROM!
• Investigations!
o X-ray: normal in first 10 days. Later, rarefaction of metaphysis & periosteal new bone formation. Sclerosis when healing occurs!
o FBC: leukocytosis!
o ESR ↑!
o Blood C/S!
o Bone scan (usu. technetium or gallium radioisotopes used): turns + before x-ray changes appear. For doubtful cases.!
• Complications!
o Spread – septic arthritis, metastatic OM (i.e. to other bones)!
o Growth disturbance – shortening / deformity if physis is damaged!
o Chronic OM!
• Management!
o Empirical antibiotics first, changing when C/S returns!
! Adults/older children – flucloxacillin & fusidic acid (IV 3/7, PO 3-6/52)!
! Children <4YO or G negative organisms cultured – Cephalosporin!
o Analgesia!
o CRIB & splintage (+ traction in upper femur OM to prevent hip dislocation)!
o Drainage – for subperiosteal abscess or persistent pyrexia & local tenderness of > 24 hrs!

SUBACUTE HAEMATOGENOUS OSTEOMYELITIS

• Milder form of acute OM – less virulent organism or better patient resistance!
• Common sites: distal femur, prox & distal tibia!
• PT: child/adolescent!
• X-ray: Brodie’s abscess (small oval cavity surrounded by sclerotic bone) (DDx: osteoid osteoma)!
• Management: drainage & ABx cover!
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POST-TRAUMATIC / OPERATIVE OSTEOMYELITIS
• Risk factors: DM, old age, immunosuppressed, steroid Rx, chronic disease, obese, multiple ops at same site, difficult / long ops,
haematoma formation, tight dressings, wound tension!
• Organism: Staph. Aureus!
• Opley classification:!
A Early – 1 mth
B Intermediate – 1mth to 1 yr
C Late – >1 yr
• Management!
o Clean surgical technique!
o Thorough debridement !
o Drainage !
o Antibiotic cover!
o External fixation of unstable/unfixed #!
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CHRONIC OSTEOMYELITIS
• Sequelae of acute haematogenous, post-traumatic & post-op OM!
• Recurrent flares of acute infxns – pain, pyrexia, erythema, tenderness, discharging sinus, non- healing ulcer!
• Investigations:!
o X-ray: bone rarefaction surrounded by sclerosis ± sequestra!
o Bone scan: to reveal hidden foci of infx!
• Management:!
o Incise abscess, remove necrotic bone, fill with bone chips!
o ABx – fusidic acid or cephalosporins!
o Sequestrectomy!

ACUTE SUPPURATIVE ARTHRITIS

• Common organisms:!
o Adults: Staph. Aureus!
o Children <4YO: H. influenza!
• Clinical features!
o Acute monoarthropathy – usu. hip in children & knee in adults!
o Swelling, erythema, warmth, tenderness, fluctuation, ↓ROM, pain, spasm!
• Investigations!
o Blood C/S!
o Joint aspiration, pus microscopy & C/S!
o X-ray: widened joint space & soft tissue swelling; subarticular bone destruction if late stage!
o U/S: joint effusion!
• Complications:!
o Dislocation!
o Epiphyseal destruction & pseudoarthrosis!
o Growth disturbance – shortening or deformity if physis is damaged!
o Ankylosis – if articular cartilage is eroded!
o Sepsis – 25% if untreated!
• Management:!
o Joint aspiration!
o Systemic ABx!
o Splintage!
o Drainage and joint washout!
o Rehab: increasing movement when joint is not inflamed. If cartilage has been destroyed, keep immobile to allow ankylosis to occur!

TUBERCULOSIS (uncommon)
• Common sites (wt bearing joints): Spine (50%; usually settles in vertebral body adjacent to intervertebral disc), Hip, Knees
• Main TB entities in orthopaedics: TB spondylitis, TB osteomyelitis, TB arthritis, TB tenosynovitis, TB myositis!
• Pathology!
o Starts as osteitis, rarely diagnosed til arthritis supervenes!
o Spreads to skeleton by haematogenous seeding!
o May spread to articular surfaces causing jt destruction and fibrosing ankylosis!
o May spread to soft tissue to form subacute abscess, which may form a chronic discharging sinus!
• Clinical features!
o TB S/S: fever, wt loss, night sweats, enlarged lymph nodes etc!
o Joint symptoms: chronic course (months), constant pain & stiffness, swelling, wasting, synovial thickening, ↓ROM, deformity, diffuse
warmth and tenderness!
o Spine: !
! May have kyphos
! Long history of ill health and backache
! Local tenderness, restricted ROM
! Pott’s Paraplegia
• Pathology: Compression of spinal cord by soft inflammatory material (abscess, caseous mass, granulation tissue) or by
hard solid material (bony sequestrum, ridge of bone at kyphos); vertebrae may collapse causing a Pott’s gibbus (usu.
thoracic)

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 • S/S: Paraplegia (motor and sensory neurological signs) + aforementioned spine TB signs and symptoms
• Types
o Early onset paresis:
! Due to pressure by abscess or bony sequestrum
! Treatment: anterior decompression + debridement + spinal fusion
o Late onset paresis:
! Due to increasing deformity or reactivation of disease or vascular insufficiency of cord
! Treatment: Operative removal of necrotic tissue (if MRI shows block)
• Investigations:!
o X-ray:
! Early: soft tissue swelling, generalized rarefraction of bone, joint space narrowing & irregularities w bone erosion of jt surfaces
! Late stages: may have cystic destruction of the joint, periarticular osteoporosis
! Spine:
• Local osteoporosis of 2 adjacent vertebrae
• Narrowing of intervertebral space
• Fuzziness of end plates
• Collapse of adjacent vertebrae onto each other (produce angular deformity of spine)
• Paraspinal soft tissue shadows: edema, abscess
o Synovial biopsy
o Spine: Diagnosed with needle biopsy
o ESR ↑
o Mantoux test +
• Management:
o Anti-TB drugs – as for pulmonary TB (isoniazid, rifampicin, pyrazinamide - RHZ)
o Rest (rest the joint until acute symptoms settle), traction, splintage, operation
o If articular surfaces are destroyed – Immobilize joint
o Long term – Joint arthrodesis or replacement
! Indications: repeated flares, articular surfaces extensively destroyed
o Surgical indications for spinal TB
! Abscess formation – drainage
! Marked bone destruction and progressive deformity – spinal fusion
! Threatened paraplegia that does not respond to conservative treatment

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