9.2 Musculoskeletal Trauma: Fractures, Dislocations & Compartment Syndrome

Principles of Open Fracture Management: The Gustilo-Anderson Framework

An open (compound) fracture is defined by a direct communication between the fracture hematoma and the external environment through a disruption of the overlying skin and soft tissue envelope. The overriding surgical objectives in open fracture care are the prevention of chronic osteomyelitis, preservation of the surrounding soft-tissue envelope, restoration of skeletal stability, and salvage of functional extremity mechanics.

The Gustilo-Anderson Classification

The Gustilo-Anderson classification system remains the universally adopted standard for categorizing open fractures, predicting infection rates, and guiding the timing and extent of reconstructive surgery:

• Type I: Clean cutaneous puncture wound <= 1 cm in length, typically produced by an inside-to-outside piercing bone spike with minimal soft tissue contusion and a simple, non-comminuted fracture configuration (infection rate: 0–2%).
• Type II: Laceration > 1 cm but <= 10 cm in length without extensive soft tissue damage, periosteal stripping, or severe tissue avulsion; moderate comminution (infection rate: 2–7%).
• Type III: Extensive soft-tissue laceration > 10 cm, high-energy trauma mechanism (high-speed vehicular collision, blast injury, agricultural machinery), extensive muscle devitalization, periosteal stripping, severe skeletal comminution, and gross environmental contamination (overall infection rate: 10–50%). Type III is subdivided into three prognostic categories:
  • Type IIIa: Adequate soft-tissue coverage of the underlying bone remains possible despite extensive lacerations and high-energy comminution.
  • Type IIIb: Extensive soft-tissue loss with marked periosteal stripping and bone exposure; local tissue closure is impossible, mandating local rotational or free microvascular tissue transfer.
  • Type IIIc: Any open fracture accompanied by an arterial injury requiring direct surgical repair or revascularization to restore and maintain distal extremity viability, irrespective of soft-tissue wound dimensions.

The Emergency Management Bundle

The initial resuscitation of an open fracture follows Advanced Trauma Life Support (ATLS) priorities. Extremity care must adhere to a standardized, time-critical clinical bundle:

1. Wound Protection: In the emergency department, gross surface debris should be gently lifted, but the wound must never be probed, vigorously scrubbed, or extensively irrigated at the bedside. Probing drives superficial environmental pathogens into deep tissue planes and disrupts early clot organization. The open wound is immediately covered with a sterile, saline-moistened gauze dressing and left undisturbed until the patient reaches the operating theater.
2. Immediate Antimicrobial Prophylaxis: Intravenous broad-spectrum antibiotics must be administered as early as possible—ideally within 1 hour of injury; administration delayed beyond 3 hours is associated with a fourfold increase in deep surgical infection rates.
   • Gustilo Types I and II: First-generation cephalosporin (e.g., intravenous Cefazolin 2 g every 8 hours).
   • Gustilo Type III: First-generation cephalosporin combined with an aminoglycoside (e.g., Gentamicin 5 mg/kg once daily) to provide comprehensive Gram-negative coverage.
   • Contamination-Specific Cover: Farm/soil contamination warrants additional clostridial coverage, such as IV benzylpenicillin (3 to 4 million units every 4 hours). Saltwater contamination requires Vibrio coverage, such as doxycycline plus ceftazidime or a fluoroquinolone, according to local advice.
3. Tetanus Immunization: Tetanus toxoid (0.5 mL IM) and human tetanus immunoglobulin (250 to 500 units IM at a separate anatomical site) must be administered according to the patient's vaccination history and wound contamination grade.
4. Realignment and Splinting: Gross angular deformities are reduced with gentle axial manual traction, and the limb is immobilized in a rigid, padded splint to stabilize the fracture hematoma, reduce pain, and relieve neurovascular tension.
5. Urgent Formal Operative Debridement: Debride immediately for heavy agricultural, aquatic or sewage contamination, vascular ischemia or compartment syndrome. NICE/BOAST otherwise recommend within 12 hours for high-energy open fractures and within 24 hours for other open fractures.

Acute Compartment Syndrome: Pathophysiology & Operative Release

Acute compartment syndrome (ACS) is an orthopedic and surgical emergency resulting from elevated tissue pressure within an inelastic, closed osteofascial compartment, causing capillary perfusion to drop below the level required for tissue viability.

Microvascular Pathophysiology

The normal resting intracompartmental pressure (ICP) of resting skeletal muscle is between 0 and 8 mmHg. When an acute insult (fracture hematoma, post-ischemic reperfusion edema, crush injury, or tight circumferential constricting casts/dressings) elevates ICP, intracompartmental venules collapse. The resultant rise in venous pressure narrows the arteriovenous hydrostatic gradient. Rising ICP progressively reduces microvascular perfusion, especially when systemic blood pressure is low. Progressive tissue hypoxia triggers endothelial cell death, cellular membrane breakdown, and intracellular fluid extravasation, establishing an escalating vicious cycle. Irreversible muscle infarction and peripheral nerve necrosis supervene after 4 to 6 hours of sustained ischemia, culminating in Volkmann ischemic contracture, rhabdomyolysis, myoglobinuric acute tubular necrosis, or limb loss.

Clinical Presentation: The 6 Ps

Acute compartment syndrome is primarily a clinical diagnosis. The classical "6 Ps" include:

1. Pain Out of Proportion: Severe, deep, relentless, burning pain that is strikingly disproportionate to the apparent underlying skeletal injury and totally unresponsive to escalating parenteral opioid analgesia.
2. Pain on Passive Muscle Stretch: The earliest, most sensitive, and most reliable clinical sign of evolving compartment syndrome. Passive elongation of the muscle bellies traversing the affected compartment produces agonizing discomfort (e.g., passive extension of the toes in the deep posterior compartment of the leg, or passive finger extension in the volar forearm).
3. Pressure / Tense Compartment: The osteofascial boundaries feel hard, tense, non-compressible, and "wooden" on direct palpation.
4. Paresthesia: Decreased sensation or tingling along the sensory distribution of peripheral nerves traversing the compartment (e.g., deep peroneal nerve web-space numbness between the 1st and 2nd toes in the anterior leg compartment).
5. Pallor: Marked coolness and pale, mottled skin distal to the compartment.
6. Pulselessness: Absence of palpable distal arterial pulses.
7. Paralysis: Inability to actively contract muscles originating within the compartment.

Critical Clinical Caveat: Pallor, pulselessness and paralysis are ominous findings requiring urgent assessment; absent pulses also suggest associated arterial injury or systemic hypotension. Never wait for pulselessness to diagnose compartment syndrome: distal arterial pulses can remain palpable despite severe microvascular ischemia.

Objective Compartment Pressure Measurement

In unconscious, obtunded, head-injured, or pediatric patients where clinical assessment is unreliable, repeated or continuous intracompartmental manometry (using a handheld transducer or side-port catheter) assists diagnosis:

• Absolute Pressure: Interpret ICP alongside blood pressure, examination and trends. BOAST advises considering urgent decompression when ICP exceeds 40 mmHg; no single reading establishes every diagnosis.
• Delta Pressure (Perfusion Pressure) Rule: Because tissue perfusion depends upon the arteriovenous pressure gradient, the perfusion pressure or delta pressure is calculated as:

Delta Pressure = Diastolic Blood Pressure (DBP) - Intracompartmental Pressure (ICP)

A Delta Pressure <= 30 mmHg is concerning for compromised perfusion and warrants urgent orthopedic assessment, with repeated or continuous measurements when the diagnosis is uncertain. For example, DBP 50 and ICP 25 mmHg give a delta of 25 mmHg: a concerning gradient, not proof that flow has ceased. Once compartment syndrome is diagnosed, do not delay fasciotomy.

Emergency Management: The Decompression Pathway

The immediate initial bedside step is the complete removal of all external circumferential constrictions: split and bivalve all casts, cut padding, and release tight dressings completely down to bare skin. This single maneuver can reduce intracompartmental pressure by 50% to 70%. The limb must be positioned at the level of the heart; elevating the limb above heart level is strictly contraindicated because it reduces local arterial hydrostatic pressure and further compromises capillary perfusion.

Persistent concerning symptoms or pressure trends require immediate senior surgical assessment. Once acute compartment syndrome is diagnosed, proceed directly to emergency multi-compartment decompressive fasciotomy. In the leg, this requires a two-incision, four-compartment fasciotomy (an anterolateral incision releasing the anterior and lateral compartments, and a posteromedial incision releasing the superficial and deep posterior compartments). Fasciotomy wounds are left open and dressed with sterile negative pressure wound therapy (NPWT) for delayed primary closure or split-thickness skin grafting 48 to 72 hours later.

Major Joint Dislocations & Neurovascular Risks

Acute joint dislocations represent orthopedic emergencies because displaced articular surfaces compress adjacent neurovascular bundles and compromise articular cartilage nutrition.

Anterior vs. Posterior Shoulder Dislocation

• Anterior Shoulder Dislocation (95% of cases): Triggered by forceful abduction, external rotation, and extension of the humerus. On examination, the patient holds the injured arm in slight abduction and external rotation; there is a loss of the normal rounded lateral contour of the shoulder ("squared-off shoulder"), a prominent acromion process, and a hollow subacromial space with the humeral head palpable anteriorly in the subcoracoid region. The axillary nerve is at high risk of traction injury; axillary nerve integrity must be documented prior to reduction by testing sensation over the "regimental badge" area of the lateral deltoid muscle and assessing isometric deltoid contraction. Closed reduction is performed under procedural sedation using the Milch, Stimson (prone with hanging weights), or Kocher technique.
• Posterior Shoulder Dislocation (< 5% of cases): Classically precipitated by high-voltage electrical shocks, lightening strikes, or generalized grand mal epileptic seizures causing violent, unbalanced contraction of the internal rotators (latissimus dorsi, subscapularis, pectoralis major) overwhelming the external rotators. The arm is locked in adduction and internal rotation, with external rotation completely blocked. AP radiographs often display the subtle "lightbulb sign" (due to fixed internal rotation of the humeral head), mandating an axillary or scapular Y view for definitive confirmation.

Posterior Hip Dislocation

Posterior dislocations account for greater than 90% of traumatic hip dislocations, typically resulting from high-energy frontal motor vehicle collisions where the flexed knee strikes the dashboard ("dashboard injury"), driving the femoral head posteriorly out of the acetabulum.

• Clinical Presentation: The injured extremity is characteristically shortened, adducted, and internally rotated, with the knee resting on the opposite thigh.
• Neurovascular Vulnerability: The sciatic nerve (specifically its peroneal division) is stretched or compressed by the displaced femoral head in up to 15% to 20% of cases, manifesting as foot drop and sensory loss over the dorsum of the foot and first web space.
• Vascular Complication: The medial femoral circumflex artery supplies the bulk of the blood flow to the femoral head. Prolonged posterior displacement kinks and compresses these retinacular vessels; delays in reduction beyond 6 hours dramatically escalate the risk of irreversible femoral head avascular necrosis (osteonecrosis) and secondary post-traumatic osteoarthritis. Emergency closed reduction under deep sedation and muscle relaxation using the Allis or Captain Morgan technique is mandatory within the 6-hour window.

Pelvic Fractures, Massive Hemorrhage & Fat Embolism Syndrome

High-energy blunt pelvic ring disruptions (Young-Burgess classification: anteroposterior compression [APC], lateral compression [LC], and vertical shear [VS]) carry acute mortality rates exceeding 30% when accompanied by hemodynamic shock.

Source of Pelvic Bleeding & Emergent Tamponade

In pelvic fracture shock, 85% to 90% of hemorrhage arises from low-pressure presacral and perivesical venous plexuses alongside bleeding cancellous fracture bone surfaces; only 10% to 15% stems from arterial lacerations (most commonly branches of the internal iliac artery, such as the superior gluteal, internal pudendal, or obturator arteries). Disruption of the pelvic ring expands internal pelvic volume dramatically, preventing natural tissue tamponade.

Emergency stabilization dictates the immediate application of a commercial pelvic circumferential compression device (pelvic binder) or an improvised bedsheet. The binder must be centered precisely over the greater trochanters (not over the iliac crests), closing the open-book diastasis, re-approximating cancellous surfaces, and restoring pelvic retroperitoneal pressure to tamponade venous bleeding. If hemodynamic instability persists despite mechanical binder application and balanced blood resuscitation (1:1:1 packed red cells, fresh frozen plasma, and platelets), the patient requires emergency transcatheter pelvic angioembolization or surgical preperitoneal pelvic packing.

Fat Embolism Syndrome (FES)

Fat embolism syndrome is a life-threatening systemic manifestation arising 24 to 72 hours after fractures of marrow-rich long bones (femur, tibia) or unstable pelvic fractures. Disrupted marrow fat globules enter lacerated venous sinuses, traveling to the pulmonary capillary bed where mechanical obstruction is compounded by biochemical degradation of neutral triglycerides into toxic free fatty acids by pulmonary lipases, precipitating severe endothelial damage and ARDS.

Diagnosis rests on Gurd and Wilson criteria, centered on the classic clinical triad:

1. Acute Respiratory Insufficiency (95%): Severe dyspnea, tachypnea, refractory hypoxemia, and diffuse bilateral alveolar "snowstorm" infiltrates on chest radiography mimicking ARDS.
2. Neurological Dysfunction (80%): Acute confusion, unheralded delirium, agitation, or progressive coma unexplainable by traumatic brain injury.
3. Petechial Cutaneous Rash (20–50%): Pathognomonic non-palpable, pinhead-sized petechiae distributed across the chest wall, axillary folds, neck, and palpebral conjunctivae, caused by microvascular embolization and capillary fragility.

Management is predominantly supportive, including high-flow oxygen, early mechanical ventilation with positive end-expiratory pressure (PEEP), aggressive hemodynamic support, and early surgical stabilization of long-bone fractures, which reduces movement-related further embolization; timing and technique depend on physiological stability.