Your patient is at home, lying on the sofa in the front room with his leg elevated on a stack of pillows. He has a cast on his left leg. He tells you he fractured his tibia and fibula on a ski trip two days earlier. He is taking oxycodone, yet reports 10 out of 10 for pain. When you assess pulse, motor and sensory for the foot on the affected leg, there is no palpable pulse, numbness of the toes, or pain with passive manipulation. You suspect your patient is suffering from compartment syndrome. You place your patient supine on the stretcher with his leg at the level of his heart, cut the cast down both sides, loosen the padding and transport to the ER.
Compartment syndrome, first identified by Hippocrates in 400 BC, is a limb-threatening medical emergency that often results in significant disability when treatment is delayed.1,2 Compartments are areas of the body where muscles, blood vessels and nerves may be compressed. There are 36 compartments located in the extremities.3 When pressure builds up in a compartment, capillary perfusion decreases3,4 and blood flow to muscles and nerves is compromised.5 Compartment syndrome should always be considered after any limb injury,1 for any fracture or sprain, or after orthopedic surgery,3 where muscles exist in tight fascial compartments.5 Injury is often proximal to the compartment involved, with decreased blood flow to the distal area. Distention is limited within the compartment because bone and fascia lack expandability.3
Commonly seen in the calf or forearm, compartment syndrome can happen in the upper arm, thigh, buttock, foot or hand.1,3,6 Fractures are the most common cause of compartment syndrome in the arm, while femur fractures treated with skin traction and tibial fractures are primary precursors in the leg.3,7 An open fracture is just as likely to cause compartment syndrome as a closed fracture.7,8 Compartment syndrome of the thigh, lower leg and foot after blunt trauma without any fracture is rare.2,4
Acute compartment syndrome is the most severe time-sensitive diagnosis and surgical emergency because the immediate occurrence3 following fractures, soft tissue trauma and re-profusion injury4 poses a threat to both life and limb.9 Onset usually occurs within 6 to 8 hours after injury but can manifest as late as 48 hours after injury, and children are just as vulnerable as adults.3
Internal causes include fractures, contusions and abrasions, thrombosis, bleeding disorders, anticoagulation, bleeding secondary to thrombolytic therapy, vena-punctures in hemophiliac patients, burn eschar, vascular repair, exercise, inactivity following surgery, falls, overdose, venous obstruction, ischemia, an infiltrated IV site, misplaced intraosseous needles, pressurized IV infusions of hypertonic contrast, intravenous or intra-arterial injection, venous or arterial puncture in anti-coagulated patients, fasciitis, gas gangrene, rhabdomyolysis, prolonged limb compression, cellulitis, nephrotic syndrome, frostbite damage, and venomous bites.3,5,6,8,9
External causes include tight dressings or casts, braces, traction, closure of fascial openings, pneumatic anti-shock garments, positioning, automatic blood pressure cuffs, external fixation, high pressure injection injuries, industrial vacuum accidents, and prolonged pressures on the arm during sleep or unconsciousness. Additionally, tourniquets can cause compartment syndrome with excessive pressure and prolonged ischemic times.1,3–6
Fractures with soft tissue trauma produce most pediatric compartment syndromes, with boys outnumbering girls by 4 to 1 and forearm fractures most frequently occurring.6 High energy fractures are responsible for compartment syndromes of the forearm with men under 35.1,6 Comminuted fractures increase the risk for developing compartment syndrome.4 Femoral fractures do not always produce compartment syndrome because the fascial compartments are large and connect with muscles of the hip allowing for pressure release from extravasation.8 An open wound should not be expected to provide adequate decompression.7
Compartment syndrome of the foot is often the result of joint dislocations caused by high-energy deceleration trauma, falls greater than two meters and motor vehicle accidents.4 In the thigh, vascular injury may result in localized compartment syndrome without distal circulatory compromise. Injury to popliteal vessels with concomitant fracture is more likely to result in compartment syndrome.8
Drug addicts who inject heroin, morphine, LSD and methadone into an artery are at risk for compartment syndrome.8 Continued use of muscles involved in compartment syndrome further increases intra-compartmental pressure.8
Development of compartment syndrome requires the presence of a surrounding envelope with limited ability to expand, and a rise in pressure caused by an increase in content or decrease in space.4,7 When injury occurs, swelling within the space begins and intra-compartmental pressure increases. As compartment pressure approaches capillary pressure, perfusion ceases1,3 with compressive closure of the venules at the venous end of the capillary beds4,8 causing ischemia of muscles and nerves. Resulting tissue membrane damage causes fluid leakage from capillary and muscle membranes further increasing compartment pressure and continued obstruction of venous outflow.1 Resulting hypoxia causes colloid proteins to escape from the capillaries into the soft tissues, fluid shift, edema, and a further rise in compartment pressure.3,4,8 The time required from initial injury to possibly irreversible injury to nerves and muscle varies by location. Muscles will become functionally impaired after 2–4 hours of ischemia and functional loss begins after 4–12 hours.1,3–5 After several days, muscle tissue reacts to the ischemia with scar formation, myotendinous adhesions and contractures.4,6 Muscle contractures are evident with stiffness and deformity distal to the affected compartment.4 Rhabdomyolysis of necrotic muscle tissue causes myoglobinemia and renal dysfunction4,5 that may require dialysis or plasma exchange.8 Nerve tissue shows abnormal function after 30 minutes of ischemia with reversible loss after 12–24 hours.5
Early identification of the symptoms will prompt immediate treatment and prevent the loss of a limb.3 Diagnosis requires analysis of physical signs and patient symptoms that include pain out of proportion to the injury, pain on passive stretching, presence of a tense and swollen extremity, possible blister formation, weakness, and paresthesia.7 Palpable peripheral arterial pulses are not an exclusionary sign.7
The most significant symptom of acute compartment syndrome is severe pain over the affected compartment disproportionate to the apparent injury.1,3–5,8 Additionally, the extremity may be tense and swollen with pain on passive stretching of the muscle, and sensory loss.1,3,4,9 The patient may describe deep, unrelenting pain that is throbbing and localized3 with sensations of numbness and tingling in the affected extremity. Special attention should be given to a patient complaining of increased pain despite compliance with analgesic medication.3 The appearance of blisters indicate late stage compartment syndrome. In the forearm, pain is worsened by passive stretching of the fingers.5
During your assessment, note the time of occurrence and mechanism of injury with attention given to the position of the body and extremities during and after injury. Determine if there was a gradual increase in pain, if the pain is localized, throbbing, deep, unrelenting, and if the pain increased with passive motion and stretching. Check for paresthesia with loss of two-point discrimination. Inspect the skin for tightness, warmth or a shiny appearance. Check for a distal pulse and check capillary refill time. Evaluate your patient’s ability to move the affected limb. Pulselessness, decreased capillary refill, paralysis and motor deficit are all indications of advanced compartment syndromes.1,3–5,8 Diagnosis can be challenging in children and patients with neurological compromise or altered mental status,1 and elderly patients with pre-existing nerve damage or psycopathology may have an atypical presentation.9
Treatment is aimed at decreasing tissue pressure, restoring blood flow, and minimizing tissue damage and functional loss.1 The primary treatment for compartment syndrome is decompression by fasciotomy1,4,6,8 accomplished within the first four hours of ischemia,6 with potential nerve and tissue damage occurring if delayed.5 More than two-thirds of the patients experiencing compartment syndrome regain normal function when fasciotomy is performed within 12 hours after onset.5
In the prehospital environment, relief of external causes of compartment pressure will be a necessary part of pain management. Loosen or remove any external device(s),3 constricting bandages, occlusive dressings or any cast encircling the limb.1 Casts and dressings should be split completely with cast padding or circumferential dressings released around the entire circumference of the limb.4,6 The affected limb should be placed at the level of the heart.1,7 Placing the limb above the heart can further compromise perfusion due to decreased arterial blood flow, narrowed arterial venous pressure gradient and worsening ischemia.1,3,4,7,8 Hydration should be accomplished to maintain mean arterial pressure3 and prevent hypotension that would reduce perfusion pressure and cause further tissue damage.7 Rapid transport for eschar debriding and fasciotomy for internal swelling should be accomplished.4,6 Immobilization and casts will not reduce pain.4
Medical treatment includes mannitol, vasodilators, corticosteroids, antispasmodics6 and hyperbaric oxygen therapy.1,8 Mannitol reduces the incidence of compartment syndrome after revascularization by acting as a free-radical scavenger and edema reducer.1,8 Hyperbaric oxygen therapy shows promise as an adjunct to fasciotomy or when immediate surgical treatment is not possible.1,8
Remember, diagnosis is primarily based on the presentation of swelling, severe pain disproportionate to the apparent injury worsened by elevation of the limb and passive muscle stretching. Early identification, performance of measures to prevent further ischemia and damage, and transport for fasciotomy are necessary to prevent additional limb damage, possible amputation and death.1 And finally, the presence of a palpable peripheral pulse is not an exclusionary sign.
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Robert E. Sippel, Major, USAF (Ret.), MS, MAEd, NRP,FP-C is an assistant professor and clinical instructor in the Emergency Health Science Department at the University of Texas Health Science Center, San Antonio, TX and a civilian training officer with the San Antonio Fire Department’s EMS division.