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Complications of Fractures
(Broken Bones)
Compartmental
Syndrome
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.
Thromboembolism
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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