DEPARTEMEN ORTHOPEDI

FAKULTAS KEDOKTERAN April 2017

UNIVERSITAS MUSLIM INDONESIA Case Report

Fracture Tibia Plateau

Hernawati Bagenda
111 2015 2190
Supervisor : dr. M. Alihasti, Sp.OT
Advisor : dr. Michael B.W

DIBAWAKAN DALAM RANGKA TUGAS KEPANITRAAN KLINIK

DEPARTEMEN ORTHOPEDI
FAKULTAS KEDOKTERAN
UNIVERSITAS MUSLIM INDONESIA
PARE-PARE
2017
 LEMBAR PENGESAHAN

Yang tersebut namanya dibawah ini:

Nama : Hernawati Bagenda

Stambuk : 111 2015 2190

Adalah benar menyelesaikan laporan kasus yang berjudul FRACTURE TIBIA

PLATEAU dalam rangka tugas kepaniteraan klinik disiplin Ilmu Orthopedi.

Pare-pare, April 2017

Mengetahui,
Pembimbing

dr. M. Alihasti, Sp.OT

 TOPIC I

CASE REPORT

I. IDENTITY

Name : Ms. SU

Age : 21 years

Sex : Female

Religion : Muslim

Address : Sidrap

Marriage status : Married

RM : 127097

Admission date : April 4th 2017

II. ANAMNESIS

Chief complaint: Pain at left knee

Patients came to the emergency room of Andi Makkasau hospital with

complaint of pain in the left knee since 2 hours ago, After traffic accident. Patient

fell down from her motorcycle and then hit the asphalt. History of syncope (-),

vomiting (-).

Past History: Hypertension and Diabetes Mellitus was denied

Social economic history : BPJS

III. PRIMARY SURVEY

- Airway and C-spine control : Patent

- Breathing and Ventilation : RR = 20 x/minute, reguler, spontaneous,

thoracoabdominal type, symmetric

- Circulation and Hemorrhagic Control : BP = 130/80 mmHg, HR = 90

x/minute, reguler, strong pulse, CRT <2second

- Disability and Neurology Evaluation : GCS 15 (E4M6V5), pupil isochor,

2.5 mm/2.5 mm, light reflex +/+

- Exposure and Environment Control : Axilla temperature= 36.8oC

IV. SECONDARY SURVEY

Regio Left Cruris

- Look : Vulnus excoriasi (+), Deformity (+), Swelling (+), Hematoma

(+)

- Feel : Tenderness (+)

- Move : Active and passive movement of left knee joint was limited due

to pain

- NVD : Sensibility is good, CRT < 2 seconds, pulsation of posterior

tibial artery and dorsalis pedis artery is palpable

CLINICAL PICTURE
V. LABORATORY

Items Result Unit N Value

Hematology:
WBC 13.2 103/ul 4-12
Eosinofil .213 % 2-4
Basofil .093 % 0-1
Netrofil 3.56 71.5 % 50-70
Limfosit 1.48 23.9 % 25-50
Monosit .457 3.16 % 1-6
RBC 3.97 106/ul 3,8-5,2
Hemoglobin 11.3 g/dl 12,8-16,8
Hematokrit 33.8 % 35-47
MCV 85.2 Fl 80-100
MCH 28.5 Pg 26-34
MCHC 33.5 g/dl 32-36
PLT 151. 103/ul 150-450

Items Result Unit N Value

Imuno-Serologi: Negative
HBsAg Negatif
(Kualitatif)
Minutes
Hemostasis: minutes < 1500
CT 1000 100 300
BT 130
VI. RADIOGRAPHY

X-Ray Left Cruris AP on April 4th 2017

VII. RESUME

Patient, female, 21 years old was admitted to hospital on April 4th 2017 with

complaint of pain in the left knee since 2 hours ago, after traffic accident.

Patient fell down from her motorcycle and then hit the asphalt.

In physical examination of left knee joint there are vulnus excoriasi (+),

deformity(+), swelling(+), hematom(+), Tenderness (+). Range of motion;

active and passive movement of left knee joint was limited due to pain,

Sensibility is good, CRT < 2 seconds, pulsation of anterior tibial artery and

dorsalis pedis artery is palpable.

Radiologic examination of left genu AP show complete fracture in metafisis

left sinistra.
VIII. DIAGNOSE

Closed Fracture Left Tibia Plateau

IX. MANAGING

A. Medikamentosa

- IVFD Ringer Lactate

- Sanmol 1gr/ 12h/ iv

- Antibiotik profilaxis

B. Operatif

- Closed reduction Percutaneus Pinning (K wire fixation)

- Knee hemarthrosis aspiration

 TOPIC II

Literature Review

I. Anatomy Of Tibia Plateau

- The tibial plateau is composed of the articular surfaces of the medial and lateral

tibial plateaus, on which are the cartilaginous menisci. The medial plateau is

larger and is concave in both the sagittal and coronal axes. The lateral plateau

extends higher and is convex in both sagittal and coronal planes.

- The normal tibial plateau has a 10-degree posteroinferior slope.

- The two plateaus are separated from one another by the intercondylar eminence,

which is nonarticular and serves as the tibial attachment of the cruciate

ligaments. Three bony prominences exist 2 to 3 cm distal to the tibial plateau.

Anteriorly is the tibial tubercle on which the patellar ligament inserts. Medially,

the pes anserinus serves as attachment for the medial hamstrings. Laterally, the

Gerdy tubercle is the insertion site of the iliotibial band.

- The medial articular surface and its supporting medial condyle are stronger than

their lateral counterparts. As a result, fractures of the lateral plateau are more

common.

- Medial plateau fractures are associated with higher energy injury and more

commonly have associated soft tissue injuries, such as disruptions of the lateral

collateral ligament complex, lesions of the peroneal nerve, and damage to the

popliteal vessels.

-
II. EPIDEMIOLOGY

- Tibial plateau fractures constitute 1% of all fractures and 8% of fractures in the

elderly.

- Isolated injuries to the lateral plateau account for 55% to 70% of tibial plateau

fractures, as compared with 10% to 25% isolated medial plateau fractures and

10% to 30% bicondylar lesions.

 - From 1% to 3% of these fractures are open injuries.

III. MECHANISM OF INJURY

- Fractures of the tibial plateau occur in the setting of varus or valgus forces

coupled with axial loading. Motor vehicle accidents account for the majority of

these fractures in younger individuals, but elderly patients with osteopenic bone

may experience these after a simple fall.

- The direction and magnitude of the generated force, age of the patient, bone

quality, and amount of knee flexion at the moment of impact determine fracture

fragment size, location, and displacement.

i. Young adults with strong, rigid bone typically develop split fractures and

have a higher rate of associated ligamentous disruption.

ii. Older adults with decreased bone strength and rigidity sustain depression

and split-depression fractures and have a lower rate of ligamentous injury.

iii. A bicondylar split fracture results from a combination of forces.

IV. CLINICAL EVALUATION

- Neurovascular examination is essential, especially with high-energy trauma.

The trifurcation of the popliteal artery is tethered posteriorly between the

adductor hiatus proximally and the soleus complex distally. The peroneal nerve

is tethered laterally as it courses around the fibular neck.

 - Hemarthrosis frequently occurs in the setting of a markedly swollen, painful

knee on which the patient is unable to bear weight. Knee aspiration may reveal

marrow fat.

- Direct trauma is usually evident on examination of the overlying soft tissues,

and open injuries must be ruled out. Intra-articular instillation of more than 120

cc of saline may be necessary to evaluate possible communication with

overlying lacerations.

- Compartment syndrome must be ruled out, particularly with higher energy

injuries and/or fracturedislocations.

- Assessment for ligament injury is essential.

V. CLASSIFICATION

Schatzker Classification

Type I: Lateral plateau, split fracture

Type II: Lateral plateau, split depression fracture (most common)

Type III: Lateral plateau, depression fracture

Type IV: Medial plateau fracture

Type V: Bicondylar plateau fracture

Type VI: Plateau fracture with separation of the metaphysis from the diaphysis
VI. TREATMENT

Nonoperative

- This is indicated for nondisplaced or minimally displaced fractures and in

patients with advanced osteoporosis.

- Protected weight bearing and early range of knee motion in a hinged fracture

brace are recommended.

- Isometric quadriceps exercises and progressive passive, active-assisted, and

active range-of-knee motion exercises are indicated.

- Partial weight bearing (30 to 50 lb) for 8 to 12 weeks is allowed, with

progression to full weight bearing.

Operative

Surgical indications

- The reported range of articular depression that can be accepted varies from >2

mm to 1 cm.

- Instability >10 degrees of the nearly extended knee compared to the

contralateral side is an accepted surgical indication. Split fractures are more

likely to be unstable than pure depression fractures in which the rim is intact.

- Open fractures

- Associated compartment syndrome

- Associated vascular injury

Operative treatment principles

- Reconstruction of the articular surface, followed by reestablishment of tibial

alignment, is the goal.

 - Treatment involves reducing and buttressing of elevated articular segments

with bone graft or bone graft substitute.

- Fracture fixation can involve use of plates and screws, screws alone, or external

fixation.

- The choice of implant is related to the fracture patterns, the degree of

displacement, and familiarity of the surgeon with the procedure.

- Adequate soft tissue reconstruction including preservation and/or repair of the

meniscus as well as intra-articular and extra-articular ligamentous structures

should be addressed.

VII. COMPLICATIONS

- Arthrofibrosis: This is common. It is related to trauma from injury and surgical

dissection, extensor retinacular injury, scarring, and postoperative immobility.

It is more common in higher energy injuries.

- Infection: This is often related to ill-timed incisions through compromised soft

tissues with extensive dissection for implant placement.

- Compartment syndrome: This uncommon but devastating complication

involves the tight fascial compartments of the leg. It emphasizes the need for

high clinical suspicion, serial neurovascular examinations, particularly in the

unconscious or obtunded patient, aggressive evaluation, including

 compartment pressure measuring if necessary, and expedient treatment

consisting of emergency fasciotomies of all compartments of the leg.

- Malunion or nonunion: This is most common in Schatzker VI fractures at the

metaphyseal diaphyseal junction, related to comminution, unstable fixation,

implant failure, or infection.

- Posttraumatic osteoarthritis: This may result from residual articular

incongruity, chondral damage at the time of injury, or malalignment of the

mechanical axis.

- Peroneal nerve injury: This is most common with trauma to the lateral aspect

of the leg where the peroneal nerve courses in proximity to the fibular head and

lateral tibial plateau. It can be iatrogenic.

- Popliteal artery injury: This is rare.

- Avascular necrosis of small articular fragments: This may result in loose

bodies within the knee.

VIII. Healing Bone

It is commonly supposed that, in order to unite, a fracture must be immobilized.

This cannot be so since, with few exceptions, fractures unite whether they are splinted

or not; indeed, without a built-in mechanism for bone union, land animals could

scarcely have evolved. It is, however, naive to suppose that union would occur if a

fracture were kept moving indefinitely; the bone ends must, at some stage, be brought
to rest relative to one another. But it is not mandatory for the surgeon to impose this

immobility artificially nature can do it with callus, and callus forms in response to

movement, not to splintage. Most fractures are splinted, not to ensure union but to: (1)

alleviate pain; (2) ensure that union takes place in good position and (3) permit early

movement of the limb and a return of function. The process of fracture repair varies

according to the type of bone involved and the amount of movement at the fracture site.

a. Healing by callus

This is the natural form of healing in tubular bones; in the absence of rigid

fixation, it proceeds in five stages:

1. Tissue destruction and haematoma formation

Vessels are torn and a haematoma forms around and within the fracture. Bone at

the fracture surfaces, deprived of a blood supply, dies back for a millimetre or two.

2. Inflammation and cellular proliferation

Within 8 hours of the fracture there is an acute inflammatory reaction with

migration of inflammatory cells and the initiation of proliferation and

differentiation of mesenchymal stem cells from the periosteum, the breached

medullary canal and the surrounding muscle. The fragment ends are surrounded

by cellular tissue, which creates a scaffold across the fracture site. A vast array of

inflammatory mediators (cytokines and various growth factors) is involved. The

clotted haematoma is slowly absorbed and fine new capillaries grow into the area.

3. Callus formation

The differentiating stem cells provide chrondrogenic and osteogenic cell

populations; given the right conditions and this is usually the local biological

and biomechanical environment they will start forming bone and, in some cases,

also cartilage. The cell population now also includes osteoclasts (probably derived

from the new blood vessels), which begin to mop up dead bone. The thick cellular

mass, with its islands of immature bone and cartilage, forms the callus or splint on

the periosteal and endosteal surfaces. At the immature fibre bone (or woven

bone) becomes more densely mineralized, movement at the fracture site decreases

progressively and at about 4 weeks after injury the fracture unites.

4. Consolidation

With continuing osteoclastic and osteoblastic activity the woven bone is

transformed into lamellar bone. The system is now rigid enough to allow

osteoclasts to burrow through the debris at the fracture line, and close behind them.

Osteoblasts fill in the remaining gaps between the fragments with new bone. This

is a slow process and it may be several months before the bone is strong enough

to carry normal loads.

 5. Remodelling

The fracture has been bridged by a cuff of solid bone. Over a period of months, or

even years, this crude weld is reshaped by a continuous process of alternating

bone resorption and formation. Thicker lamellae are laid down where the stresses

are high, unwanted buttresses are carved away and the medullary cavity is

reformed. Eventually, and especially in children, the bone

reassumes something like its normal shape.

b. Healing by direct union

Clinical and experimental studies have shown that callus is the response to

movement at the fracture site (McKibbin, 1978). It serves to stabilize the fragments as

rapidly as possible a necessary precondition for bridging by bone. If the fracture site

is absolutely immobile for example, an impacted fracture in cancellous bone, or a

fracture rigidly immobilized by a metal plate there is no stimulus for callus

(Sarmiento et al., 1980). Instead, osteoblastic new bone formation occurs directly
between the fragments. Gaps between the fracture surfaces are invaded by new

capillaries and osteoprogenitor cells growing in from the edges, and new bone is laid

down on the exposed surface(gap healing). Where the crevices are very narrow (less

than 200 m), osteogenesis produces lamellar bone; wider gaps are filled first by woven

bone, which is then remodelled to lamellar bone. By 34 weeks the fracture is solid

enough to allow penetration and bridging of the area by bone remodelling units, i.e.

osteoclastic cutting cones followed by osteoblasts. Where the exposed fracture

surfaces are in intimate contact and held rigidly from the outset, internal bridging may

occasionally occur without any intermediate stages (contact healing).

Healing by callus, though less direct (the term indirect could be used) has

distinct advantages: it ensures mechanical strength while the bone ends heal, and with

increasing stress the callus grows stronger and stronger (an example of Wolffs law).

With rigid metal fixation, on the other hand, the absence of callus means that there is a

long period during which the bone depends entirely upon the metal implant for its

integrity. Moreover, the implant diverts stress away from the bone, which may become

osteoporotic and not recover fully until the metal is removed.

c. Union, consolidation, and non union

Repair of a fracture is a continuous process: any stages into which it is divided

are necessarily arbitrary. In this book the terms union and consolidation are used,

and they are defined as follows:

- Union Union is incomplete repair; the ensheathing callus is calcified.

Clinically the fracture site is still a little tender and, though the bone moves in

one piece (and in that sense is united), attempted angulation is painful. X-Rays

show the fracture line still clearly visible, with fluffy callus around it. Repair is

incomplete and it is not safe to subject the unprotected bone to stress.

- Consolidation Consolidation is complete repair; the calcified callus is

ossified. Clinically the fracture site is not tender, no movement can be obtained

and attempted angulation is painless. X-rays show the fracture line to be almost

obliterated and crossed by bone trabeculae, with well-defined callus around it.

Repair is complete and further protection is unnecessary.

- Timetable How long does a fracture take to unite and to consolidate? No

precise answer is possible because age, constitution, blood supply, type of

fracture and other factors all influence the time taken. Approximate prediction

is possible and Perkins timetable is delightfully simple. A spiral fracture in the

upper limb unites in 3 weeks; for consolidation multiply by 2; for the lower

limb multiply by 2 again; for transverse fractures multiply again by 2. A more

sophisticated formula is as follows. A spiral fracture in the upper limb takes 6

8 weeks to consolidate; the lower limb needs twice as long. Add 25% if the

fracture is not spiral or if it involves the femur. Childrens fractures, of course,

join more quickly. These figures are only a rough guide; there must be clinical
 and radiological evidence of consolidation before full stress is permitted

without splintage.

- Non-union Sometimes the normal process of fracture repair is thwarted and

the bone fails to unite. Causes of non-union are: (1) distraction and separation

of the fragments, sometimes the result of interposition of soft tissues between

the fragments; (2) excessive movement at the fracture line; (3) a severe injury

that renders the local tissues nonviable or nearly so; (4) a poor local blood

supply and (5) infection.

 REFERENCE

1. Thompson, John C. Leg and Knee in: Netter's Concise Orthopaedic Anatomy. 2th

Edition..Philadelphia: Saunders Elsevier. 2010.p. 288, 321-2.

2. Kenneth, A Egol. et all. Tibial plateau in Handbook of Fractures. 5th edition. 2015