Hospital Based Practice – Limb pain.

Orthopaedic history.
• What specific problem has caused patient to attend?
• Duration of problem
• Changes in symptoms
• Exacerbating and alleviating factors?
• Limitations of Activities of Daily Living.
• Previous treatments tried.
• Impact of previous treatments.

Trauma history.
• Need for pain relief now?
o Allergies
o History of.
 Peptic ulcers
 Asthma
 Opiate abuse.
o Beware of opiates causing drowsiness and limiting ability to report history.
• Cause of injury.
o Drop – attacks leading to fractures may suggest an underlying cardiac pathology.
o High – velocity car crashes need screening for injuries of.
 Head
 Chest
 Abdomen
• Direction of any falls.
• Any neurological signs

Investigations
• Plain X – rays.
o Always obtain at least 2 views at right angles to each other.
 AP view
 Lateral view
o Also view joint above and below.
 Exclude dislocation
• Bloods.
o Baseline.
 FBC
 U&E
o Other investigations as required.
 LFTs
 Clotting studies
 CRP/ESR
 G&S
 Crossmatch
o Blood cultures should be taken if osteomyelitis is suspected.
• Fluoroscopy.
o Real time X – rays to view bones and fractures.
o Allows manipulation to be watched on a monitor.
o Often used in theatre to check alignment when fixating fractures.
• CT and MRI.
 o Used with increasing frequency in diagnosis and monitoring.
o CT very good for looking at bone.
o MRI normally better for looking at soft tissues.
• Ultrasound.
o Shows joint effusions well.
o Gives some indication about articular surfaces.
o Can demonstrate free fluid in the pelvis.
 Suggests pelvic fracture.
• Joint aspiration.
o Establishes cause of swollen joint.
o Identifies pathogen in septic arthritis.
o Examine fluid for crystals in crystal arthropathies.
• Arthroscopy ± washout.
o Often undertaken in day – case.
o Allows direct visualisation of inside of joint to help confirm diagnosis.
 Commonly.
• Knee
• Ankle
• Wrist.
o Allows washing out of effusion and loose bodies.
o Many knee procedures now undertaken by arthroscopy alone.
 Cruciate ligament repair
 Meniscal surgery.
• DXA/DEXA scan.
o Dual energy X – ray absorptiometry.
o Used to assess bone mineral density.
 Deteriorates with age and osteoporosis.
• Other investigations.
o Depend on clinical need.
o Include.
 Microbiological cultures.
 Histological examination of biopsy and excision tissue.
 Electrophysiological studies of
• Nerve transmission
• Muscle response
 Radio – isotope uptake studies.

The pelvic radiograph.

• Confirm patient details and date of film.
• Does the film include a good view of both hips joints.
• Check to identify cortical break.
o Inner bony ring
o Obturator foramina
• Is symphysis pubis.
o Abnormally wide
o Asymmetrical
• Are sacro – iliac joints equal and visable.
• Contours of acetabulum.
o Smooth?
o Equal on both sides.
• Follow outline of both femurs.
 o Checking for breaks in the cortex.
• Check remaining bones individually for breaks in cortex.
o Ilium
o Ischium
o Pubis.

Hip fractures.
• Presenting symptoms.
o Pain
o Decreased range of movements.
o Limitation of activities of daily living.
 Walking
 Rising from seated position.
• Past medical & drug history.
o Previous episodes or surgery.
o Arthritis
o Trauma/ infections of the joint
o Problems as a child
o Steroid therapy
o Medical reasons for falls.
• Examination.
o Inspection.
 Leg shortening
 Deformity at rest.
• Internal rotation of hip
o Hip dislocation
• External rotation of hip.
o Fractured neck of femur
 Examine skin over joint.
• Surgical scars
• Sinuses
• Cellulitis
• Bruising.
o Palpation.
 Feel for bony landmarks.
• Greater trochanter
• Anterior iliac crest.
 Are bony landmarks at same height on both sides.
 Palpate joint during movement.
• Crepitus
• “Clicks”
o Supine.
 Allow patients to demonstrate active range of movements.
 Passively move joint.
 Check for fixed flexion deformity.
• Place hand in lumbar lordosis.
• Extend hip so popliteal fossa touches couch.
o Trendelenberg gait.
o Use of stick on side opposite to diseased hip.
• Common pathologies in children.
o Congenital dislocation.
 1% incidence
 Can be normal at birth.
o Tubercular arthritis.
 Two peaks in incidence.
• 2 – 5 year olds.
• Elderly
 Common in developing world.
o Perthe’s disease.
 Osteochondritis of femoral head.
 Commonly 4 – 7 years.
o Slipped femoral epiphysis.
 Usually 10 – 16 years old
 Often obese children.

• Common pathologies in adults.

o Osteoarthritis.
 Often degenerative disease.
 Can be precipitated by trauma and inflammation.
 Results predominantly in.
• Pain
• Limitation of function.
 Joint replacement commonly undertaken.
• Lasts up to 20 years before needing replacement.
o Fractured neck of femur.
 Common fracture in the elderly following a simple fall.
 Classically causes leg that is:
• Shortened.
• Externally rotated.
 Confirmed by AP and lateral hip X – rays.
 Often treated by.
• Hemi – arthroplasty.
o Replacement of femoral head and neck.
o Leaves original socket.
• Dynamic hip screw.
o Intertrochanteric fractures
o Sub – trochanteric fractures
o Risk of explosion if cremated.
o Usually used for Type I and Type II fractures.
 Garden’s classification.
 • Type I Best outcome.
Impacted into each other.
Facilitates vascular regrowth.
• Type II Minimal displacement from anatomical
position.
Bones unimpacted, and so less stable.
Good outcome.
• Type III Complete fracture.
Only partial displacement.
• Type IV Complete fracture.
Total displacement of bone ends with
complete separation.
 Surgery can be performed under spinal anaesthetic, so suitable for frail patients.
 Prognosis without surgery is poor.
o Intracapsular fractures.
 Occur just below femoral head.
 Often causes.
• External rotation
• Leg adduction
 Injuring force may be trivial
 Patient may be able to walk, with difficulty.
 As medial femoral circumflex artery supplies head via femoral neck, ischaemic
necrosis of the head may occur.
• Particulalry if there is much displacement.
 Femur fractures occupy 20% of UK orthopaedic beds, and numbers are rising.
• 1:100/year in females aged 75 – 84.
 Mortality is about 50%

 Treatment
• Assess vital signs
• Treat shock with Haemaccel.
o Beware incipient heart failure.
o If present, monitor CVP.
• Relieve pain.
o Morphine 0.2 mg/kg IM
o Prochlorperazide 12.5 mg IM
• Imaging.
o Good quality lateral film is essential for diagnosis if there is
impaction or minimal displacement.
o 5% are missed unless CT is used.
• Prepare for theatre.
o FBC
o U&E
o CXR
o Crossmatch 2 units
o Consent
• If displacement is minimal.
o Multiple screw fixation in situ.
• If displaced fracture.
o `Excise head
o Insert prosthesis.
o Intertrochantic – extracapsular fractures.
 Occurs between greater and lesser trochanters.
 Occur in younger age group.
 Blood supply is adequate, so non – union is rare.
 Treatment.
• Dynamic hip screw fixation
• Principle of DHS is to fix the fracture, but allow compression by
sliding.
• Surgery associated with decreased length of hospital stage and
improved rehab.

o Femoral shaft fracture.

 Risk of femoral artery also being torn.
• Swelling.
• Loss of distal pulses.
 Sciatic nerve injury may also occur.
 The proximal bone fragment is.
• Flexed by iliopsoas
• Abducted by gluteus medius
• Laterally rotated by gleuteus maximus.
 Distal bone fragment.
• Pulled superior by hamstrings
• Adducted and laterally rotated by adductors.

 Treatment.
• Normally with a locked intramedullary nail.
• Introduced proximally over a guide wire.
o Manipulated across fracture under fluoroscopic control.
• This management allows early mobilisation.

• Alternatively, manipulation under anaesthesia.

o Exact reduction is not needed.
• Followed up with traction.
o Fixed traction with Thomas knee splint
o Skeletal traction
o Sliding traction with thigh supported on a frame or cast brace
with hinge at knee.
• Also can weight bear early.
 Union takes 3 – 4 months.
o Condylar or tibial plateau fractures
 As these are intra – articular, they require accurate joint reconstruction to
minimise later osteoarthritis.
o Posterior
o Hip dislocation.
 Commoner in patients with prosthetic hips.
  Can occur in non – prosthetic hips when large force applied through knee
through flexed hip.
• Front seat passengers who’s knees hit the dashboard in high speed
crashes.
 Feel for femoral head in buttock.
 Leg is.
• Flexed
• Adducted
• Shortened
 Sciatic nerve may be damaged due to.
• Alceration
• Stretching
• Compression
 Early MRI diagnosis may prevent later equines foot deformity.
 Treatment.
• Reduction under GA by lifting head back into the joint.
• Traction for 3 weeks promotes join capsule healing.
o Referred pain.
 Common between hip and knee.
 Important to examine both during consultation.
• Emergency management of open fractures: The 6 As
o Assessment.
 Neurovascular status
 Soft tissue status
 Photograph wound.
• Reduces number of wound inspections.
o Antisepsis.
 Cover wound with large antiseptic – soaked dressing.
o Alignment.
 Align fracture and splint.
 Also provides analgesia by reducing fracture site movement.
o Anti – tetanus.
 Check status and immunize appropriately.
o Antibiotics.
 IV 3rd generation cephalosporin.
 Plus metronidazole if wound grossly contaminated.
o Analgesia.
 IV opiates titrated to effect.

• Gustilo classification of open fractures.

o Type I: Low – energy wounds < 1 cm long.
Eg. caused by bone piercing skin.
o Type II: Low – energy wounds > 1 cm causing moderate soft tissue damage.
o Type III: All high energy injuries, irrespective of wound size.
 Type IIIA: Adequate local soft – tissue coverage.
 Type IIIB: Inadequate soft – tissue coverage.
 Type IIIC: Secondary arterial injury needing repair.

• Preventing hip fractures.

o Prevent falls.
 Good lighting.
  Less sedation
 Keep fit training.
• Improves balance
• Reduces fear of falling.
• Halves rate of multiple falls.
o Prevent osteoporosis.
 Exercise
 Bisphosphonates.
o Ensure good vitamin D & calcium intake.
 Ensure plasma levels of vitamin D > 30 nmol/L
• Especially in northern countries.
 Low vitamin D and calcium levels are associated with hip fractures, even in
absence of osteoporosis.

• Preventing complications after hip injuries.

o Early mobilization.
 Prevents thromboembolism & stiffness
o Co – ordinated multidisciplinary inpatient rehabilitation.
o Good nutrition.
 Meta – analysis doesn’t support specific multi – nutritional commercial food
supplements.

The limping child.

• Common causes.
o Transient synovitis
o Septic arthritis
o Perthe’s disease
o Slipper Upper Femoral Epiphysis
o Inflammatory arthritis
o Apophyseal avulsion.

• Investigations.
o Ultrasound & Arthrocentesis.
 Based on clinical examination.
 Kocher’s critera.
• Non – weight bearing on affected side.
• ESR > 40 mm/hr
• Fever
• WCC > 12 x 109/L

• 4/4 criteria gives 99% probability of septic arthritis.

• 3/4 criteria gives 93% probability of septic arthritis.
• 2/4 criteria gives 40% probability of septic arthritis.
• 1/4 criteria gives 3% probability of septic arthritis.

 No point in simple US to detect fluid.

 Hip aspiration is diagnostic procedure of choice.
o Bone scintigraphy.
 Highly sensitive for bone disease.
  Very poor specificity
 No good for distinguishing between aetiologies.
 Mildly elevated uptake.
• May demonstrate transient decrease of technetium 99 phosphate.
o Isotope Bone scan.
 Diffusely increased activity in synovitis.
 Perthe’s disease
• Decreased activity in capital femoral epiphysis.

Irritable hip (transient synovitis)

• Most common cause of painful hip in children.
• Average of onset is 5 – 6 years.
• Suspected causes.
o Viral infection
o Trauma
o Allergy
• Child rarely appears ill
• Irritability subsides quickly.
• Resent history of respiratory infection in 50%
• Viral antibody titres raised in 84%
• X – rays are normal
o 58% show Waldenstrom’s sign.
 Lateral displacement of femoral epiphyses
 Surface flatterning.
• Need to exclude infection.
o WCC
o CRP
o ESR
• Examination.
o Movement is possible
o Rotation restricted.
• Management.
o Bed rest for 7 – 10 days.
o Until limp and pain have resolved.
 Don’t weight bear
 Avoid full unrestrictive activities.
o Repeat radiograph in 6 months.
 Exclude LCP disease.

Septic arthritis
• Children are acutely ill
• Patient presents with.
o Generalised symptoms of acute systemic infection.
 Fever
 Chills
 Malaise.
o Child resists all attempts to move the hip.
o Investigations.
 ESR > 20 mm/hr & fever > 37.5 oC.
• 97% sensitive for septic hip.
 MRI.
 • Signal intensity alteration in bone marrow.
• Can be differentiated from irritable hip.
o Treatment.
 Surgical emergency.
• Risk of hip being destroyed.
 Requires urgent irrigation and debridement.
 No place for medical management.
• Concomitant use of IV antibiotics.
 Monitor ESR.

Perthe’s disease
• Idiopathic infarction of bony epiphysis of femoral head.
• Cause remains unknown.
o Possibly a sequence of.
 Venous thrombosis
 Increased intraosseous venous pressure
 Reduced arterial flow
 Hypoxia
• Linked to.
o Thrombophilia
o Maternal smoking
o Deprevation.
• Investigations.
o Plain X – ray.
 Main modality for evaluation.
 Crescent sign in head of femur is seen.
 Early signs.
• Widened joint space
• Subchondral linear lucency
 Late findings.
• Fragmentation of femoral epiphysis
 • Increased sclerosis
• Loss of height.
o Scintigraphy.
 Useful in early disease when X – rays may still be normal.
• Catterall staging.
o Stage I Histological and clinical diagnosis.
No radiological changes
o Stage II Sclerosis.
With or without cystic changes.
Preservation of the contour and surface of femoral head.
o Stage III Loss of structural integrity of femoral head.
o Stage IV Loss of structural integrity of acetabulum.
• Treatment.
o Basic idea is to contain femoral head in acetabulum.
o Mild cases.
 No treatment needed.
 Self healing
o Severe cases.
 Need surgery to keep head in acetabulum.
 In the past.
• Cast
• Brace legs widely apart.
 Now.
• Intertrochanteric osteotomy of femur.
• Rotational osteotomy of acetabulum.
 Bisphosphonates
 Range of Movement exercises.

Slipped upper femoral epiphysis.

• Most common adolescent disorder of the hip.
• Suggested by unilateral waddling gait in male teenager.
• Consider SUFE in adolescent presenting with knee pain.
• Pathogenesis.
o Unknown
o Associated with several endocrine disorders.
 Although rare, consider hypothyroidism in patients with SUFE.
• Associated with.
o Short stature
o Obesity
o Delay in skeletal maturity.
• Investigations.
o Frog leg lateral gives better visualisation than AP X – ray films.
o Trethowan’s sign.
 Epiphysis moved posterior – inferiorly.
 Straight line down to greater trochanter.
• Normal femur will overlap line at some point.
 o Unstable slip.
 Sudden onset severe pain
 Walking not possible, even with crutches.
 Duration of preceding symptoms doesn’t determine stability.
o Stable slips have much better prognosis than unstable slips.
 Prognosis improved by early recognition of unstable slip.
• Treatment.
o Pinning
o Aims to prevent further slipping.
o Minimizes risk of later OA of the hip.

Secondary degeneration of hip joint.

• Management.
o Arthrosesis
o Cemented THR
o Uncemented THR – S – ROM
o Hip resurfacing.

Back pain.
• About 5% of all consultations in the UK are for back and neck pain.
• In the majority, there is no definite anatomical abnormalities.
o Non – specific back pain.
• It is important not to miss sinister causes of back pain.

• Causes.
o Mechanical back pain.
 Spondylolisthesis
 Spondylosis
 Intervertebral disc prolapse
 Spinal stenosis.
• Caludication type pain
 Apophyseal joint disease.
• Exacerbated by.
o Lumbar extension
 o Thoracic rotation
o Cervical rotation.
 Non – specific back pain.
 Trauma.
o Inflammatory back pain.
 Rheumatoid arthritis
 Seronegative spondyloarthritidies.
• Psoriatic
• Ankylosing Spondylitis
• Rewiter’s
• Enteropathic
• Behçet’s
o Serious causes.
 Infection.
• Discitis
• Epidural abscess
 Malignancy
 Myeloma
 Osteoporotic crush fractures
 Paget’s disease.
o Referred pain.
 Aortic aneurysm
 Pyelonephritis
 Renal stones
 Pancreatitis.

• History.
o First consideration is whether pain is likely to be mechanical, inflammatory or sinister in
origin.
 Mechanical back pain.
• Exacerbated by prolonged sitting or standing.
• Relieved by movement.
• Can be precipitated by trauma.
 Inflammatory back pain.
• Prolonged early morning stiffness.
• Allieviated by exercise.
 Sinister back pain.
• Pain at night
• Local bony tenderness
 • Accompanied by systemic symptoms.
o Sensory or motor symptoms.
o Changes in urinary or bowel function.

• Examination.
o General examination for evidence of malignancy.
o Palpate spine and para – spinal regions for tenderness.
o Check shape of spine.
o Look for muscle spasm.
o Cervical spine.
 Flexion
 Extension
 Lateral flexion
 Rotation
o Thoracic spine.
 Rotation
o Lumbar spine.
 Flexion
 Extension
 Lateral flexion
o Palpate sacroiliac joints.
o Neurological exam.
 Absent ankle jerks suggest slipped disc.
 Central disc prolapse in the lumbar region can cause S1 signs.
• Weak hip extension
o Push heel into couch with flexed knee.
• Weak knee flexion.
o PR exam
o Check perineal sensation.

• Tumour is suggested by.

o Acute onset back pain.
o Signs of L1 – L4 lesions
o Weak thighs
o Absent knee jerks.

• Age can suggest the most likely causes..

o 15 – 30 years
 Prolapsed disc
 Trauma
 Fractures
 Ankylosins spondylitis
 Spondylolisthesis.
• Forward shifting of one vertebrae over another.
• Can be congenital or due to trauma.
 Pregnancy.
 o 30 – 50 years.
 Degenerative spinal disease
 Prolapsed disc.
 Malignancy.
• Primary
• Lung
• Breast
• Prostate
• Thyroid
• Kidney
o > 50 years.
 Degrenerative
 Osteoporotic vertebral collapse
 Paget’s
 Malignancy
 Myeloma
 Spinal stenosis

• Investigations.
o Patient requiring investigation are those with.
 Pain at night
 Neurological signs.
o X – rays.
 Spine
 CXR
o Bloods.
 FBC
 ESR
 Calicum
 Phosphate
 LFTs.
• Particularly alkaline phosphatase.
 PSA
o Urine protein electrophoresis.
o Bence – Jones protien
o Myeloma markers.
 Immunoglobulins
 Protien electophoresis
o Acid phosphate.

o Further investigations.
 CT screen
 MRI scan.
• Better than CT for imaging spinal cord and roots.
 Technetium bone scan.
• Hot spots identify neoplastic or inflammatory lesions.
 Myelography
  Radiculography.
• Cord compression
• Root compression.

• Management.
o Analgesia
 NSAIDS
o Bed rest until acute pain settles.
o Physiotherapy and mobilization.
 May be managed at home
 Review with GP or specialist in 2 – 3 weeks.
o Appropriate referral to specialist
 If X – ray reveals fracture refer to orthopaedics
 If severe pain from inflammatory arthritidies, refer to rheumatologists.
o Most patients respond to conservative management.

• Red Flag symptoms.

o Age < 20 or > 55
o Acute onset in elderly patient
o Constant or progressive pain
o Nocturnal pain
o Increased pain on lying down
o Morning stiffness
o Systemic symptoms.
 Fever
 Night Sweats
 Weight loss
o History of malignancy
o Thoracic back pain
o Bilateral or alternating symptoms
o Neurological disturbances
o Sphincter disturbances
o Leg cluadication.
 Spinal stenosis
o Current or recent infection
o Immunosuppression.
 Steroids
 HIV
o Abdominal mass

• Yellow flag symptoms.

o Belief that pain and activity is harmful.
o Sickness behaviour, such as extended rest.
o Social withdrawl
 o Emotional problems.
 Low or negative mood
 Depression
 Anxiety
 Stress
o Problems/ dissatisfaction or time off work
o Problems with claims or compensation.
o Overprotective family or lack of support.
o Inappropriate expectations of treatment.
 Low active participation in treatment.

Disc prolapse.
• Acute postero – lateral herniation of lumbar disc.
o Usually
 L4 – L5
• Weakness of
o Extensor hallus longus.
o Dorsiflexion
o Ankle eversion
• Altered sensation
o Lateral aspect of calf
o Dorsum of foot
 L5 – S1.
• Weakness of.
o Plantarflexion
o Ankle eversion
• Reduced ankle jerk
• Altered sensation.
o Big toe
o Sole of foot
o Posterior calf.
• Common cause of incapacitating lower back pain.
• Often a clear precipitating event.
o Eg. lifting
• Pain may radiate in L5 or S1 distribution.

• Patients should be carefully examined for.

o Paraspinal muscle spasm
o Reduced straight leg raising on affected side.
o Nerve root signs.
o Sacral sensation
o Perineal sensation.
• Prolapse at L2 – L3 can cause
o Bilateral multiple root lesions
o Altered bladder and bowel function
 Cauda equine syndrome
o Neurosurgical emergency that requires immediate investigation and management for.
 Acute cauda equina compression
 Acute cord compression.
• Acute cauda equine compression
o Alternating or bilateral root pain in legs.
o Saddle anaesthesia
o Loss of anal tone on PR.
o Urinary and/or faecal incontinence.

• Causes
o Tumours
 Primary.
• Intradural + extramedullary.
o Schwannoma
o Meningioma
• Intradural + intrameduallary
o Astrocytoma
o Ependymoma
 Metastatic.
• Usually extradural
• Most common cause of cord compression.
• Look for missing pedicles on X – ray.
• Breast
• Prostate
• Lung
• Thyroid
• GI tract
• Lymphoma
• Meyloma
o Large disc protrusion
o Infection
 TB
 Staphylococcal abscess
 Infected dermoid.
o Cyst.
 Arachnoid
 Syringomyelia
o Haemorrhage
o Skeletal deformity.
 Kyphscoliosis
 Achodroplasia
 Spondylothiasis
Acute cord compression.
• Presentation.
o Back pain.
 Usually first symptom.
 Often starts several weeks before other symptoms
 Become progressively unremitting and keeping patient awake at night.
 Can also radiate to chest and abdomen.
o Sensory symptoms.
 Often next problem to follow back pain.
 Parasthesia
 Limb heaviness
 Limb “pulling”

 Sensory loss may be present at sensory level at testing.

• The height of sensory loss denotes the lowest possible level fo the
lesion, the lesion could actually be higher than this.
• Check for both.
o Pink prick sensation (spinothalamic tracts)
o Proprioception/ vibration (dorsal columns)
• Anterior or posterior aspects of the cord may be selectively
compressed.
 Sacral sparing is when sensation is preserved in the S3 – S5 dermetones.
• Relatively reliable sign of an intramedullary lesion
• Due to initial sparing of lateral spinothalamic tract fibres which serve
sacral sensation.
o Weakness.
 Often initially reported as “clumsiness”.
 Soon progresses to clear loss of power.
o Autonomic dysfunction.
 Occurs if sympathetic fibres are involved.
 Occurs especially in high thoracic and cervical lesions.
• Hypotension
• Bradycardia
• Cardiac arrest.
 Symptoms may be triggered by Noxious stimuli
• Pain
• UTI
• Abdominal distension,
o Constipation
o Bladder outflow obstruction
o Sphincter dysfunction.
 Starts as hesitance or urgency of micturation.
 May progress to painless urinary retention with overflow.
 Can also cause constipation.
o Fever.
 Should alert one to the possibility of an infectious cause.
o Respiratory failure.
 Occurs with high cervical cord lesions.
  Can present as acute neuromuscular respiratory paralysis.

o Conus medullaris lesions.

 Compresses sacral segments of cord.
 Leads to relatively early
• Disturbancees of micturation
• Constipation
• Impotence
• Reduced perianal sensation
• Reduced anal reflex
 Rectal and genital pain are later signs.
 Plantar response are extensor.
o Cauda equine lesions.
 Can be caused by lesions at or below L1.
 Leads to paraparesis that is:
• Flaccid
• Areflexic
• Often asymmetric.
 Lubosacral pain is an early sign.
 Bladder and bowel dysfunction are late signs.
 Sensory disturbances can stretch to L1 level.
o Combined Conus medullaris and caude equine lesions.
 Can show signs of bothe LMN an d UMN lesions.

• Severity is assessed on degree of:

o Weakness
o Sensory loss
o Sphincter dysfunction.

Management.
• Depends on diagnosis and condition of patient.
• If diagnosis unknown, make the diagnosis quickly and discuss case with regional neurosurgical
centre.
• If diagnosis not apparent, and immediate neurosurgical action not indicated.
o Discuss CT – guided biopsy with radiology.
• If the patient is known to have neoplastic disease and malignant compression is likely.
o Urgent radiotherapy is first line treatment.
o Not always appropriate to make interventions apart from giving analgesia.
o Always discuss with a senior oncologist.

• Obtain urgent spine X – rays.

o May show.
 Vertebral collapse
 Lytic lesions
 Sclerosis
• Perform CXR to look for malignancy.
 • MRI or CT is next line of investigation
o Arrange urgently
o If facilities not available, discuss with regional neurosurgical centre
• Use of high – dose steroids is controversial
o No definite evidence of benefit in malignancy
o May trigger fatal tumour lysis syndrome in some high – grade lymphomas
o Discuss with senior collegues.
• If cause of compression appears to be infective take blood and urine cultures
o Fever
o Raised WCC
o Raised CRP
• Monitor haemodynamic status and watch for autonomic dysfunction.
• Catheterise if there is bladder dysfunction.
• If immobile, give prophylactic SC heparin.
o 5000 units TDS
• If compression is high, or there appears to be respiratory dysfunction.
o Check Force vital capacity.
 FVC < 30 ml/kg implies reduced ability to clear secretions.
 FVC < 15 ml/kg is indication for immediate intubation and ventilation,
regardless of other respiratory parameters.
o Monitor ABGs

Hand and wrist fractures.

• Classification of fractures.
o Open/ closed.
 Skin broken/ skin intact
o Intra – articular/ Extra – articular
 Involving articulating surface of bone/ Not involving articulating surface
o Displaced/ undisplaced.
 Any movement of bone fragments.
• Impaction
• Angulation
o Direction of tilt of distal fragment in degrees.
• Opposition
• Rotation
• Subluxation.
o With reference to distal fragment.
o Site.
 Described as.
• Proximal third
• Medial third
• Distal third.

• Patterns of fractures.
.

Normal Transverse Oblique Spiral Comminuted

Segmental Avulsed Impacted Torus Greenstick

Distal radial/ ulnar fractures.

• Mechanism normally by fall onto outstretched hand.
• Tends to occur in two peak ages.
o 5 – 14 years
o 60 – 70 years
• Paediatric distal arm fractures.
o Plastic deformation.
 Commonly ulnar
o Torus fracture.
 Diaphysis causes metaphysic to buckle under compression forces.
o Greenstick fractures.
 Tension on side of bone that cracks.
o Complete.
 Propegates through entire bone.
 Oblique
 Transverse
 Spiral
o Epiphyseal fractures.
 Distal radial physis is most frequently injured.

• Older patients tend to fracture their wrist in a Colles’ or Smith’s fracture.

o Colles’ fracture.
 Most common extension fracture.
 Fracture through distal metaphysic.
• Approximately 4 cm proximal to articular surface of
 Fracture fragments are displaced dorsally.
• Causing “dinner fork” deformity.
 Ulnar styloid fractures also occur in 60% of cases
 Needs reduction if significant displacement.
• Especially backwards and proximal shifting of distal fragment.
 Classified according to the Association of Osteosynthesis or Frykman
classifications.
 • Type A: Extra – articular
• Type B: Partial articular
• Type C: Complete articular.
1. Simple articular and metaphyseal fracture.
2. Simple articular and complex metaphyseal fracture.
3. Complex articular and metaphyseal fracture.

 Treatment.
• Operate under a Bier’s block.
o Place a loose torniquet around the upper arm.
o Empty blood from the arm by elevating it above the heart for 1
minute, or by squeezing with a esmarch bandage.
o Inflate cuff to 100 mmHg above SBP
o Inject 30 – 40 ml 0.5% prilocaine into a dorsal hand vein.
 Never use bupivacaine for a Beir’s block due to risk
of cardiotoxicity if cuff accidentally released.
o Allow anaesthesia to develop over 20 – 30 minutes and
manipulate the fracture.
o Release cuff 30 minutes after injection
 Sudden early release of prilocaine into the circulation
can cause fits .

o Bruner’s 9Ps for minimising ischemic limb changes.

 sPan of tourniquet
• 10 cm for arm
• 15 cm for leg.
 Position
• Apply to upper arm or mid/upper thigh
 Padding.
• Use > 2 layers of orthopaedic wool beneath
cuff.
• Make sure it doesn’t get wet with skin prep.
• Use aqueous based skin prep so, if the wool
does get wet, it won’t cause burns.
 Pressure.
• Arm: 50 – 100 mmHg above SBP
• Leg: Double SBP
  Period of time
• Deflate within 2 hours.
 temPerature.
• Keep limb as cool as possible.
 Perfusion.
• Be cautious if limb is unhealthy.
• Allow time for adequate perfusion and
recovery before reapplying if needed.
 aPparatus.
• Calibrate weekly
• Maintain well
 Pen.
• Document duration and pressure of
tourniquet.

• Other methods, such as haeamatoma blocks, are less effective.

• Alternative is general anaesthesia.

• Manipulation.
o Prepare plaster back slab up to the knuckles.
o Ask an assistant to hold the elbow.
o Apply traction to
 Disimpact the fragment
 Push it forwards
 Push it to the ulnar side.
o Maintaining traction, apply back slab with wrist slightly flexed
and in ulnar deviation.
o Support in a sling once X – ray has shown good position.
o Re X – ray in 5 days, when swelling has reduced.
o If no problems, complete the plaster.
 Complications.
• Median nerve symptoms.
o Should resolve with good reduction.
• Ruptured tendons.
• Malunion
• Sudeck’s atrophy.
o AKA.
 Algodystrophy.
 Osteodystrophy
 Reflex sympathetic dystrophy
 Sympathetically maintained pain syndrome
 Post – traumatic sympathetic atrophy
 Shoulder – hand syndrome
 Minor causalgia.
• Causalgia is “burning pain”
  Post – traumatic painful osteoporosis
 Complex regional pain syndrome, Type I
o Complex disorder of.
 Pain
 Sensory abnormalities
 Abnormal blood flow
 Sweating
 Trophic changes in superficial or deep tissues.
o Central event is lack of vascular tone or supersensitivity to
sympathetic neurotransmitters.

o Diagnostic criteria were defined in 1994, but of unclear

validity.
 At least one symptoms from each of the following
categories
 At least one sign from at least 2 of the following
categories.
• Sensory
• Vasomotor
• Sudomotor/ oedema
• Motor/ trophic

o Presentation.
 May be weeks – months after an insult.
• Minor trauma
• Fracture
• Herpes zoster
• MI
 May occur in neighbouring areas to original insult,
rather than are of insult.
 Lancinating pain, which may have a trigger point,
accompanies vasomotor dysfunction.
 Limb may be.
• Cold and cyanosed
• Hot and sweating
 Temperature sensitivity may be heightened.
 Skin of affected limb may become oedematous.
• Later can become atrophic and shiny.
 Motor signs may occur.
• Hypereflexia
• Dystonic movements
• Contractures.
 No systemic signs.
 Timid, neurotic personalitiers are particularly
affected.
 • May be due to poor mobilization following
original insult.
o Tests.
 Patchy osteoporesis on X – ray.
• No joint space narrowing
o This would suggest thinning of
cartilage
 Bone scintigraphy shows characteristic uniform
uptake.
o Treatment.
 Refer to pain clinic.
 Standard pain killers often have limited effect.
 Consider.
• Physiotherapy
• NSAIDs
 Calcitonin and postganglionic sympathetic blockade
has been suggested.
• Guanethidine
• Bretylium
 Condition is ultimately self limiting.
• Right Colles’ plaster is unlikely to affect driving.

o Smith’s Fracture.
 Flexion fracture
 Much less common than Colles’ fracture.
 Full thickness fracture of distal radius.
• 1 – 2 cm proximal to wrist
• Volvar displacement of distal fragments.
 Classification is by the Thomas system.
• Type I:
o Most stable
o Extra – articular
o Transverse distal radial fracture.
o Palmar and proximal displacement.
• Type II.
o Barton, palmar – lip fracture of distal radius.
o Displacement of the carpus.
• Type III.
o Unstable
o Oblique juxta – articular fracture of distal radius
o Fragments tilted palmar.
 Manipulate with forearm in full supination
  Fixation often required.

o Bennett’s fracture.
 Carpometacarpal fracture/ dislocation of the thumb.
 Management.
• Percutaneous wire fixation.
• Exact reduction reduces risk of secondary OA.

o Carpal fractures.
 Scaphoid.
• Most frequently injured carpal bone.
• Due to hyperextension of the wrist.
• 25% occur at the waist of the scaphoid
• Can be easily missed on X – ray.
o Ask for special scaphoid view if fracture is suspected.
o If X – ray negative, and fracture likely, ask for long – axis CT.
 Also shows unstable fractures.
o If imaging unavailable, put in plaster and image in 2 weeks.
 Fracture more likely to be visible by this point.
• Diagnosis is mainly clinical.
o Tenderness in anatomical snuffbox is suggestive.
• Treatment.
o Non – displaced fractures involving the wrist or proximal pole

 Long – arm thumb – spica cast for several weeks.

 Follow with short – arm thumb – spica cast until
untion.
 Percutaneous Acutrak screw fixation allows faster
return to work, but have no impact on long – term
outcome.
• As nutrient artery enters distally, main complication is avascular
necrosis of proximal fragment.
o Leads to late wrist degeneration.

 Other carpal fractures.

Bone Incidence Mode Diagnsois Complications
Lunate Relatively Hyperextension of Clinically.
common wrist. Weakness of wrist
Impact of heel of with pain,
hand on hard aggrevated by
surface. pressure on 3rd
digidal tay
Trapezium Relatively Hyperextension Avulsion fracture
common and ulnar deviation of trapezium on X
of the wrist – ray
Capitate Relatively Forced Clinical suspicion. AVN
common dorsiflexion with Visable fracture on
radiat deviation of X – ray normally
the wrist. transversely
Crush injuries. orientated.
• Wrist dislocations.
o Eg. scapho – lunate or luno – triquetral.
o May be anterior or posterior.
o Require
 Manipulation and reduction.
• Often open.
 Plaster immobilization for about 6 weeks.
o Median nerve compression may occur.

• Radiological studies.
o Get 3 views.
 PS
 Lateral
 Oblique
o Can visualise soft tissue and bones.
o Check anatomical alignments.
 Radial width on PA view > 10 mm
 Ulnar angle on PA view between 15 – 30 degrees.
 Palmar angulation on lateral view between 10 – 25 degrees
o Check for invovlvement of.
 Radiocarpal joint.
 Distal radio – ulnar joint.
 Ulnar bone.
o Scaphoid views should be taken if scaphoid fracture suspected.
o Carpal view should be taken if suspected fracture of:
 Hamate
 Trapezium
o Further imaging may be required.
 CT
 MRI

• Management.
o Resuscitate.
 Analgesia
 Attend to broken skin.
 Give prophylactic antibiotics if an open fracture.
o Reduce.
 If displaced.
 Open
• In theatre by opening jont.
 Closed.
• Without cutting into joint.
 Traction
o Immobilise
 o Rehabilitate
 Physiotherapy
 Occupational therapy
 Job retraining
 Social services.

• Complications.
o Early.
 Damage to blood vessels and bleeding.
 Damage to nerves.
• Eg. median nerve damage causing carpal tunnel syndrome
 Damage to ligaments and tendons.
o Intermediate.
 Infection of open fracture.
 Infection of surgical interventions.
 Nerve problems.
 AVN
o Late.
 Malunion
 Non – union
 Ostheoarthritis
 Deformity
 Limited movement.

• Follow up.
o Prognosis depends on.
 Complexity of the fracture.
 Restitution of fracture ligaments
 Complete immobilisation in early stages.
o Generally.
 Distal radiaul/ ulnar fractures are put in casts for 6 – 8 weeks after swelling
subsides.
 Carpal bone fractures require spica casts fro 10 – 12 weeks.
o Factors that affect bone healing include.
 Diabetes mellitus
 Osteoporosis
 Smoking
 Excessive alcohol
o Advise calcium and Vitamin D supplements.
o Rehabilitate aggressively.
o Prevent future fractures, eg. wearing protective gear when doing dangerous activities.

Fractures in the hand.

• Metacarpal fractures.
o Require manipula to do this is bytion if grossly displaced or angulated.
o 5th metacarpal is often involved.
 Often due to a pounching injury (Boxer’s fracture)
o Immobilization for 10 days in wool and crepe bandage may be all that is required.
 Encourage finger movement after 2 – 3 days.
o Closed reduction and cast immobilization is also used.
o Longer periods of immobilizing can cause the hand to stiffen up.
 o Refer any fractures which clinically have an obvious rotational deformity.
 These can be disabling if not set right.
 Recognisable as cause finger rotation when fingers flexed and looked at nail on.
 Usually require plate and screw fixing in theatre.
o Fractures of more than a single metacarpal also require fixing in theatre.
o Beware wounds overlying MCP joints.
 Often from the teeth of the punched victim, so require sepsis cover.
• Fractures of proximal phalanx.
o Spiral or oblique fractures at this site are likely associated with rotational deformity.
 This must be found and corrected.
o Often the best way to do this is by open reduction and fixation with a single compression
screw.
• Middle phalanx fractures.
o Manipulate.
o Splint in flexion over malleable metal splint to its neighbour (“buddy splinting”)
o Aim is to control rotation which would interfere with finger flexion later.
• Distal phalanx fractures.
o May be caused by crush injuries.
o Are often open.
o Symptoms may be relieved by trepanning the nail to reduce swelling.
o Split skin grafts from thenar eminence may be required for partial amputations of the
finger tip.
o If subluxation is a problem, joint stiffness may be reduced by open fixation.
• Mallet finger.
o Finger tip will droop due to avulsion of the extensor tendon attachment to the terminal
phalanx.
o If avulsed tendon also contains bone union is easier.
 Special splint with no extension
 Use splint for 6 weeks.
o Interphalangeal arthrodesis may be needed if active extension remains limited.
o Poor outcome associated with.
 Delay in splinting.
 Age > 50
• Gamekeeper’s thumb.
o Rupture of ulnar collateral ligament of metacarpophalangeal joint of thumb.
 Sustained during forced thumb abduction when wringing a pheasant’s neck.
o Also can occur in dry ski – slopers who fall and catch their thumb in the matting
(“Hill – end thumb”)
o Diagnosis can be difficult as thumb is so painful to examine.
 Missing this injury can condemn patient to weak pincer grip.
 Inject 1 – 2 mL 1% plain lignocaine around ligament to facilitate examination.
o Differentiation of complete vs. partial tears is crucial, as complete tears have to be treated
surgically.
o X – ray will detect any bony avulsion fragments.
o Partial tears or those associated with undisplaced avulsion fractures of proximal phalanx
can be treated using short – arm thumb – spica casting.
Pelvic fractures.
• Fracture of the pelvis can be serious as it can threaten the integrity of the organs that are contained
within it.
• Due to the ring structure, a single fracture is often stable and need only a few weeks rest.
• In contrast, if there is more than one fracture it can destablise the ring and is very serious.
 o Even more so if one is above and one is below the hip.
o Internal injuries in 25%
o Eg. Fractures of ileum and pubic ramus.
o Eg. Fractures through sacroiliac joint and pubic ramus.
• The force producing the fracture may be.
o Anteroposterior
o Lateral compression
o Veritcle shear
• Signs to look for that suggest pelvic fractures include.
o Bruising
o Perineal or scrotal haematoma
o Blood at the urethral meatus.

• Malgaigne’s fracture.
o 20% of all pelvic fractures.
o 60% of unstable fractures.
o Disruption of pelvis anterioposteriorly
o Displacement of fragment containing hip joint.
• Acetabular fractures.
o Common sites.
 Posterior lip
 Transverse
o Two 45o oblique X – rays are needed to define injuries exactly.
 Consider CT as well
 Single films easily miss fractures.
o Treatment.
 Open reduction and reconstruction fo articular surfaces.
 Delay the onset of secondary ostheoarthritis.

• Examining patients with suspected pelvic fractures.

o Diagnosis mainly made from serial pelvic X – rays
o Even gentle palpation can disturb retroperitoneal haematomas and exacerbate
haemorrhage.

• Complications.
o Haemorrhage.
 Eg. internal iliac artery
  Check and regularly monitor
• Foot pulses
• BP
• CVP
• Urine output
 Transfusion is often needed.
o Shock.
 Mortality of 14 – 55%
• Towards higher end if base excess > – 5
 Even more problematic if patient is pregnanct.
• Huge haemorrhage from increased pelvic blood flow.
 Resuscitate vigerously and meticulously.
 Ways to reduce blood loss.
• Avoid manipulation of pelvis
• Internally rotate both legs to close “open – book” fractures.
• Apply pelvic binder
• Suspend patient in pelvic sling.
o Patinet lies supine with pelvis over sling’s webbing.
o Exerts upwards and medial trqaction via weights and runners
suspended above the bed.
 Compresses haemorrhage.
o An alternative is an external fixation frame.
• Apply traction to legs.
•
 Surgical reconstruction can start after bleeding reduced.
 Look for associated abdominal and pelvic injury.
• Spleen 37%
• Diaphragm 21%
• Intestine 17%
• Kidney rupture 8%
 Diagnosis is sometimes hard.
• Prompt spiral CT identifies patients and lesions which may benefit
from specialist procedures, such as angiographic embolization.
 The order of intervention is important.
• Laprorotomy, if indicated, to perform open fixation.
• Follow ith angiographic ambolization.
 Inter – disciplinary co – operation is vital.
o Bladder rupture.
 Can be intra– or extraperitoneal.
o Urethral rupture.
 Often at junction of prostatic and membranous urethra in males.
 Appearance of blood at the end of urethra is suggestive.
 May be unable to pass urine.
• Avoid repeated attempts.
 On PR.
• Prostate may be elvated out of reach
 CT is imaging of choice in trauma patients with haematuria.
o Vaginal and rectal perforation may occur.
 Rare
 Look for bleeding.
 o Trapping of sciatic nerve causes perisistnat pain.
• Treatment.
o Relieve pain and replace blood.
o If urethral rupture is suspected.
 Check with urethrogram before catheterizing.
 Avoid urethral catheters as they may make a false passage.
 Suprapubic catheter may be needed.
 Get urological help.
o Small urine volume suggests bladder rupture.
 Cystogram or CT is needed.
o If no pelvic fluid seen on CT, bladder rupture is unlikely.
• Reassuring signs on pelvic X – ray.
o Symphysis pubis separation < 1 cm
o Integrity of superior and inferior rami
o Integrity of acetabula & femoral necks.
o Symmetry of illium and sacroiliac joints.
 Eg. evaluate the arcuate lines.
o No fracture of transverse process of L5.

Rheumatoid arthritis
• Chronic systemic inflammatory disease.
• Characterised by polyarthritis that is
o Symmetrical
o Deforming
o Peipheral
• Peak onset is in 30s and 40s
• Female: Male ratio is > 2:1
• Prevalence of 1%.
o Increased in smokers
o Increased and more severe in HLA DR4/DR1

• Presentation.
o Typically sympetrical, swollen, painful and stiff small joints of hands and feet.
o Worse in morning, ease with movement.
o Can fluctuate and large joints become involved.
o Less commonly presents as a sudden onset of widespread arthritis or.
 Recurrant mono/polyarthritis of various joints.
 Persistent monoarthritis.
• Often of one knee, shoulder or hip.
 Systemic illness with extra – articular symptoms.
• Fever
• Fatigue
• Weihgt loss
• Pericarditis
• Pleurisy

• Minimal joint problems at first.

• This form is commoner in males.
 Polymyalgic onset.
• Vague limb girdle aches.
• Signs.
o Early.
 Inflammation, but no joint damage.
 Joint swelling
 Especially.
• Symmetrical MCP
• PIP
• Wrist
• Metatarsal joints
 Look for.
• Tenosynovitis
• Bursitis
o Later.
 Joint damage and deformity.
 Ulnar deviation of fingers
 Dorsal wrist subluxation
 Boutonniere or swan – neck deformity of fingers
 Z – deformity of thumb.
 Rupture of hand or foot extensor tendon
 Larger joints may also be involved.
 Atlanto – axial joint subluxation may threaten the spinal cord.

• Extra – articular.
o Nodules.
 Elbow
 Lungs
o Lymphadenopathy
o Vasculitis
o Fibrosisng alveolitis
o Obliterative bronchiolitis
o Pleural & pericardial effusions.
o Raynaud’s disease
o Carpal tunnel syndrome
o Peipheral neuropathy
o Splenomegaly.
 In 5%
 1% have Felty syndrome.
• RA
• Splenomegaly
• Neutropaenia
o Episcleritis
o Scleritis
o Scleromania
o Keratoconjunctivitis
o Sicca
o Osteoporosis
o Amyloidosis
• Tests.
o Rheumatoid factor is positive in 70%
 High titre associated with.
• Severe disease
• Erosions
• Extra – articular disease.
o Citrullinated peptide antibodies (anti – CCP).
 Highly specific
 Not widely available.
o Often anaeamia of chronic disease
o Inflammation can cause.
 Increased platelets
 Increased ESR
 Increased CRP
o X – ray show.
 Soft tissue swelling
 Juxta – articular osteopaenia
 Reduced joint space
 Later there may be.
• Bony erosions
• Subluxation
• Carpal destruction.

• Diagnostic criteria.
o Only used in research.
o Include 4 out of 7.

o Morning stiffness
 > 1 hour
 > 6 weeks
o Arthritis of > 2 joints
o Arthritis of hand joints
o Symmetrical arthritis
o Rheumatoid nodules
o Positive rheumatoid factors
o Radiographic changes.
• Management.
o Refer early to a rheumatologist for specialist assessment.
o Early use of disease modifying drugs.
 Improves symptoms
 Improves long tem outcome.

 Chief biological event is inflammation.

• Monocytes traffic into joints.
• Cytokines are produced
o Erode cartilage and bone.
o Also produce systemic effects.
 Fatigue
 Accelerated atherosclerosis
 Accelerated bone turnover.
• Fibroblasts and endothelial cells are activated
• Tissue proliferates.
• Fluid is generated as effusions.
 DMARDs modulate the above reaction and slow or stop disease progression
• Early therapy associated with better long – term prognosis.
• Can take 6 – 12 weeks to get a sympathetic relief.
• First line therapies are typically.
o Methotrexate.
o Sulphasalazine
• Can be used together
• Regular blood test monitoring is required.

• Methotrexate.
o Given weekly.
o Avoid in.
 Liver disease
 Pregnancy
 High alcohol consumption
o Caution if Pre – existing lung disease.
o Side effects.
 Oral ulcers
 Nausea
 Lethargy.
 Myelosuppression
 Hepatotoxicity
 Pneumonitis
• Rare, but can be life threatening.
o Give Folic acid 5 mg 2/3 times a week.
  Reduces side effects.
• Sulphasalazine.
o Side effects.
 Myelosuppression
 Nausea
 Rash
 Oral ulcers
 Reduced sperm count

• Leflunomide.
o May be used as alternative to sulphasalazine
o Side effects.
 Rash
 Oral ulcers
 Diarrhoea
 Hypertension
 Myelosuppression
 Hepatotoxicity.
o Contraindicated in pregnancy.
• Gold.
o Used by IM injection.
o More toxic that methotrexate or sulphasalazine.
o Side effects.
 Myelosuppression
 Renal toxicity
 Rash
 Mouth ulcers
 Photosensitivity.
• Penicillamine.
o Side effects.
 Myelosuppression
 Renal toxicity
 Loss of taste
 Oral ulcers
 Myasthenia gravis – like symptoms.
• Hydroxychloroquine.
o Least toxic
o Least effective.
o Side effects.
 Rash
 Retinopathy.
• Check vision with Amsler chart every 12
months.
• Azathioprine.
o Side effects.
 Myelosuppression
 Nausea
 Raised LFTs
 o Prevented from being metabolised by xanthine oxidase
inhibitors.
 Can rise to toxic levels if given with allopurinol.
• Cyclosporin
o Side effects.
 Nausea
 Tremor
 Gum hypertrophy
 Hypertension
 Renal impairment
 Myelosuppression.

• Anti – cytokine therapy.

o Cytokines are over – produced in RA synovium.
 Tumour necrosis factor (TNF – α)
 Interleukin – 1 (IL – 1)
o TNF blockers include.
 Infliximab.
• Chimeric murine/ human anti – TNF
antibody.
• IV every 8 weeks.
 Etanercept
• TNF – α receptor/ IgFc fusion protien
• SC twice weekly
 Adalimumab.
• Fully human anti – TNF monoclonal
antibody.
• SC every 2 weeks.
 Anakinra.
• IL – 1 inhibitor
• Still being evaluated.

o These drugs are licensed by NICE for severe RA after failure

to respond to 2 DMARDs.
o Clinical response can be striking, with greatly improved
outcome shown.
o Contraindicated in.
 Pregnancy
 Breats feeding
 Active infection
 Severe heart failure
 Demyelinating disease
 Previous cancer
o Side effects are normally well tolerated, but include.
 Injection reaction
 Infections
 Reactivation of TB
 • Screen before starting therapy
• Consider prophylaxis.
 Worsening of heart failure
 ANA and reversible SLE – like illnesses may evolve.
o Long – term safety is unknown.
 No clear increased cancer risk.
o Neutralizing antibodies may decrease the efficacy of
infliximab.

o Steroids.
 Rapidly reduce inflammation and controls symptoms in the short term.
 Useful for treating acute exacerbations of disease.
• IM depot of methylprednisolone 80 – 120 mg.
 Intra – articular steroids have a rapid but short term effect.
 Oral steroids.
• Prednisolone 7.5 mg OD
• May control difficult symptoms
• Not routinely recommended for long term therapy due to side effects
profile.

o Analgesia.
 Most will require NSAID to cover symptoms.
• Paracetamol with weak opiate is rarely effective.
• NSAIDS contra – indicated if active peptic ulcer
• Give lansoprazole 30 mg PO as gastric protection if patient.
o > 65 years
o Previous history of peptic ulcers.
 Not possible to predict which patients will respond to which NSAID.
• Try a variety until you find one which works.
 NSAIDs don’t affect disease progression.
o Encourage regular exercise.
 Review with physiotherapy and occupational therapy for aids, splints etc.
o Surgery may be considered in the long term.
 Relieve pain
 Improve function
 Prevent complications.
 For example.
• Ulna stylectomy
• Joint replacement.
o Risk of cardiovascular and cerebrovascular disease is increased due to acceleration of
atherosclerosis in RA.
 Manage other risk factors.
 Stopping smoking will help CVD and RA.

Osteoarthritis.
• Commonest joint condition.
• Female: Male ratio is 3:1
• Usually affects >50 year olds
• Usually primary.
o Sometimes is secondary to joint disease or other conditions.
o Eg. Haemochromatosis.
• Signs & symptoms.
o In localised disease.
 Usually knee or hip.
 Pain on movement
 Crepitus
 Worse at end of day.
 Background pain at rest
 Joint gelling.
• Stiffness after rest up to 30 minutes.
 Joint instability.
o In generalised disease.
 Commonly affected joints.
• DIP joints
• Thumb carpo – metacarpal joints
• Knee

o May be.
 Joint tenderness
 Joint derangement
 Heberden’s nodes.
• Bony lumps at DIP joints
• Seen mainly in post – menopausal women
 Bouchard’s nodes.
• Affect PIP joints.
• “Squared thumb”
 Reduced range of movment
 Mild synovitis
• Tests.
o X – ray shows.
 Loss of joint space.
 Subchondral sclerosis
 Cysts
 Marginal osteophytes.
 Joint space
narrowing
Periarticular
erosion
Osteophytes

Subarticular
sclerosis

Bone cysts
Soft tissue
swelling
o CRP may be slightly elevated.

• Treatment.
o Exercises.
 Quadriceps exercises increase muscle power and so stabilise the joint in knee
OA.
o Regular codeine, with or without codeine for pain.
 Consider oral NSAIDs.
• Only prescribe NSAIDs after careful risk – benefit analysis
individualised for each patient.
o Consider.
 Indication
 Proposed dose
 Proposed duration of therapy.
 Co – morbidities.
• Main serious side effects are.
o GI bleeding
o Renal impairment

• Many patients prescribed NSAIDs don’t actually need them all the
time.
o Tell patient to take them only when they need them and not as
regular medication.
• Patients who know more about their drugs are less likely to suffer side
effects.
• Explain that.
o Drugs are for relief of symptoms, on good days they shouldn’t
need them.
o Abdominal pain may be a sign of impending gut problems.
 Stop the tablets
 Seek medical advice if symptoms don’t resolve.
o Ulcers may occur with no warning.
 Seek advice if stools turn black.
 o Don’t supplement prescribed NSAIDs with ones bought over
the counter.
 Eg. ibruprofen
 Mixing NSAIDs can increase risk of bleeds 20 fold.
o Smoking and alcohol increase NSAID risk.

• COX – 2 inhibitors should only be considered if NSAID is essential

and there is a history of peptic ulceration.
o Risk of bleeding reduced, but not eliminated.
o Bleeds that do occur may be very serious.
• Consider COX – 2 over normal NSAID if.
o NSAID + omeprazole is problematic.
o Over 65 years (and not on aspirin)
o Needing high dose NSAID over a long period.
• PPIs can also be given with COX – 2 inhibitors.
o Not known if this has any effect.
• Problems with COX – 2 inhibitors, and possibly NSAIDs, are increased
risk of.
o Heart failure
o MI
o CVA
• Avoid in.
o Vascular disease
o Renal failure.
• Insufficient evidence for newer COX -2 inhibitors to recommend them
as first line therapy.
o Etoricoxib
o Parecoxib
o Lumiracoxib.
 Topical NSAIDs and capsaicin may help.
o Reduce weight if BMI > 28.
o Walking aids.
o Role of Hyaluronic acid is unclear.
o Study in 2006 showed no improvement with.
 Glucosamine
 Chondroitin sulphate
o Intra – articular steroid injections.
 Temporarily relieve severe symptoms.
o Joint replacement.
 Only fully curative treatment for OA.

Osteoporosis.
• Defined as reduction in amount of bone mass, leading to fractures after minimal trauma.
o WHO define it as bone density > 2.5 standard deviations below mean for healthy 20 –
year old female.
o Measured with DXA scan.
o Occurs when osteoclast activity is more than osteoblast activity.

• Epidemiology.
o By the age of 90, a related fracture affects.
 50% of women
  15% of men
o Cost of fracture treatment alone costs NHS £1 billion per year.

• Osteoblast activity stimulated by.

o TGF
o IGF
o LRP5
• Osteoclast activity.
o Stimulated by.
 Age
 Oestrogen withdrawl
 Calcitonin
 IL1
 TNF
 RANK/ RANKL
o Inhibited by.
 Oestrogen
 Bisphosphonate
 Osteoprotegerin

• Classification.
o Primary.
o Secondary.
 Endocrine.
• Cushing’s
• Thyrotoxicosis
 Rheumatological
• Especially steroid treatment
 Gastroenterological.
• Malabsorption
 Neoplasia
 Genetic.
• Osteogenesis imperfecta.

• Risk factors.
o Elderly women.
 Late menarche
 Early menopause
 Long hisotyr of oligomenorrhoea
o Smoking
o Alcohol
 o Sedentary lifestyle
o Family history
o Lean body type.
o Steroids.
 Decreases calcium absorption through the kidney.
 Decreases oestrogen levels.
 Increased trabecular bone loss

• Clinical features.
o Low impact fractures.
 Colles’
 Femoral neck
 Wedge fractures of vertebrae.
• Thoracic region
• Loss of height
• Exaggerated kyphosis.
o Dowager’s hump
• Pain.

• Investigations.
o X – ray
o DEXA
o Calcium
o Serum CTX
o Alkaline phosphatase
o Hormones
 Estradiol
 Gonadrotrophins
 LH
 FSH
 SHGB
 PSA
o Serum EPP
o Endomysial Antibodies.

• DEXA scans.
o Dual energy X – ray absorptionmetry.
o Involves X – rays
o Measures bone density
  Measured in g/cm2.
 Z – score
• Number of standard deviations above or below the mean for the
patient’s age and sex
o Used in.
 Pre menopausal women
 Men < 50 years
 Children
 T – score.
• Number of standard deviations above or below the mean for a healthy
20 year old of the same sex as the patient.
o Used in.
 Post – menopausal women
 Men > 50 years.
o Better predictor of future fractures.
• Normal is < – 1
• Osteopaenia is defined as – 2.5 to – 1
• Osteoporosis is defined as < – 2.5

o Lasts 10 – 20 minutes.
o Central DEXA scans
 Large machines
 Measure bone density in centre of skeleton.
• Hip
• Spine
o Peripheral DEXA scans
 Small, mobile machines.
 Measure bone density in peripheries.
• Wrist
• Heel
• Finger

o Indicated for.
 All women > 65 years.
 Younger post – menopausal women with at least one risk factor.
 Post – menopausal women who present with fractures.
• Confirm diagnosis
• Determine disease severity.
 Oestrogen deficient women at clinical risk of osteoporosis.
 Individuals with vertebral abnormalities.
 Individuals on, or planning, steroid therapy.
 Patients with primary hyperparathyroidism.
 Individuals being monitored to assess response or efficacy of approved
osteoporesis drug therapy.

• Management.
o Prevention.
 Stop smoking
 Reduce alcohol
 Weight bearing exercises.
o Reduce rate of bone loss.
 Calcium
 Vitamin D
 Bisphosphonates
• Various drugs.
o Alendronate
o Etidronate
o Risedronate
• Recommended to be used in women who are.
o > 75, without need for DEXA scan.
o 65 – 74, if osteoporosis confirmed by DEXA scan.
o < 65, if T – score is in negatives, or if osteoporosis diagnosed
in presence of.
 BMI < 16
 Mother with hip fracture when < 75
 Early, untreated menopause
 Co – morbidity that increases risk of osteoporesis
 Immobile.
• Side effects.
o Abdominal pain
o Dyspepsia
o Diarrhoea
o Constipation.
o Oesophagitis.
 Must remain upright for 30 minutes after taking
tablet.
 HRT
o Prevention of fractures.
 Prevent falls
 Review need for hypotensive drugs.
 Give hip protectors.

o Other drugs.
 Strontium ranelate
 Recombinant PTH
 Calcitonin.
Peripheral artery disease.
• Presentation
o Can be asymptomatic
o Can give signs of transient ischemia, like claudication.
 Aching pain in the leg muscles
 Usually felt in the calf
 Precipitated by walking
 Relieved by rest.
o Can cause persistent ischemic limb.
 Pale
 Pulseless
 Painful
 Perishingly cold
 Paralysed
 Paresthetic

• Assess by feeling the 4 arteries in the lower limb.

o Femoral
o Popliteal
o Dorsalis pedia
o Posterior tibial

• The main sites of atherosclerosis are.

o Proximal coronary arteries
o Thoracic arteries
o Internal carotid arteries
o Abdominal aorta
o Illiac arteries
o Femoral arteries
o Popliteal arteries.
o Vertebrobasilar system.

• Investigations.
o Ankle – Brachial pressure index
o ECG
o Doppler ultrasound with ABPI
o FBC
o Glucose
o Lipids
o Angiography.

• Management.
o Conservative
o Surgery.
 Important to involve patient in decision
 Have to weight up risk – benefit analysis

 Balloon angioplasty
• Percutaneous transluminal angioplasty
 Bypass graft
 • Arterial reconstruction

• Complications.
o Atherosclerosis.
 IHD
 Gangrene and eventual amputation
 Erectile dysfucntion
o Surgical.
 General.
• Bleeding
• Infection
• Thromboembolism
 Specific.
• Allergic reaction to angiography dye
• Stoke
• MI
• Embolus
• Ischemia
 Claudication

Evidence of vascular
disease?

No Yes

Diagnosis is cauda Limb acutely

equina syndrome threatened?

No
Yes

Moderate symptoms Severe symptoms Angiography

Stop smoking

Angioplasty Stenting
Symptoms improve Symptoms deteriorate