Compartmental, or closed-space, syndrome is the most frequent limb-threatening complication associated with extremity trauma. Swelling of injured muscle within a compartment surrounded by an unyielding envelope, such as fascia or a cast, leads to elevated tissue pressures that block normal perfusion. The resulting ischemia leads to further muscle injury and swelling and higher tissue pressures. The only solution to this ever-intensifying cycle is to remove all confining envelopes around the swollen muscular compartment. Thus, whenever patients complain of increasing pain or distal numbness in an immobilized, injured extremity, their casts, splints, and dressings must be thoroughly loosened immediately. If the muscle swelling has increased to the point that the surrounding fascia has become a constricting envelope, an emergency fasciotomy must be performed. Even a few hours of muscle ischemia can lead to irreversible injury and necrosis.
The most reliable clinical signs of impending compartmental syndrome are progressively increasing pain in an immobilized extremity, pain with passive flexion or extension of the toes or fingers, and numbness in a specific peripheral nerve distribution. The presence of distal pulses in a limb does not exclude compartmental syndrome; muscle necrosis and irreversible nerve damage occur at tissue pressures much lower than those required to obliterate arterial inflow. A definitive diagnosis of compartmental syndrome can be made using a device that percutaneously measures intramuscular pressures.
Pulmonary embolism is the most frequent fatal complication following leg trauma. Autopsies have shown that 38% of patients who die after hip fracture die of pulmonary embolism. Among patients with hip fractures who are not given anticoagulant therapy, about 50% develop deep venous thrombosis; about 10%, pulmonary emboli; and about 2%, fatal pulmonary emboli. The major predisposing factors for deep venous thrombosis are advanced age, leg trauma or surgery, history of deep venous thrombosis, immobilization, malignancy, and obesity. The associated clinical findings–pain, swelling, tenderness, Homans’ sign (pain on forced dorsiflexion of the foot), fever, and leukocytosis–are unreliable criteria for making a diagnosis. Venography remains the standard test, while ultrasonography has become the most effective noninvasive study for detecting deep venous thrombosis.
Ideally, patients with a femoral or pelvic fracture should begin prophylactic anticoagulant therapy for thromboembolic disease on admission and continue therapy until they are ambulatory. For orthopedic patients at high risk for deep venous thrombosis (eg, those with hip fractures), warfarin and dextran have traditionally been considered the most effective prophylactic agents. Neither aspirin, low-dose heparin, nor external pneumatic boot compression provides as much protection. If warfarin is used, the initial dose should be between 2.5 and 10 mg, depending on the patient’s age and weight. Subsequent daily doses are given to maintain prothrombin time at about 1.2 to 1.4 times control. A history of recent gastrointestinal bleeding, malignancy, bleeding tendencies, or stroke is a relative contraindication to anticoagulation. Newer agents such as low-molecular-weight heparin and heparinoids may be as effective as warfarin with a lower incidence of bleeding.
Fat Embolism Syndrome
Although microscopic fat emboli accompany most femoral fractures, overt symptoms and signs develop in only about 2%. Usually occurring 2 to 3 days after fracture, fat embolism syndrome includes at least one of these major signs: respiratory insufficiency, drowsiness and confusion, petechial rash. Minor signs include pyrexia, tachycardia, retinal changes, jaundice, renal changes, thrombocytopenia, and an elevated erythrocyte sedimentation rate. Chest x-ray shows variable streaks and infiltrates associated with overt pulmonary edema in 33% of patients. Prothrombin time and activated partial thromboplastin time are also mildly elevated. In some patients, adult respiratory distress syndrome with noncardiac pulmonary edema and clinically significant disseminated intravascular coagulation occur. A hyperacute syndrome may result in death secondary to emboli of the coronary arteries and brain.
Treatment of fat embolism syndrome is aimed at respiratory support. Corticosteroids are often used, although their efficacy is unproved. Fortunately, the mortality rate is only about 8%, compared with that of 50% for most other causes of adult respiratory distress syndrome.
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