The workup of a patient with acute onset of shortness of breath after an orthopedic operative procedure should include consideration of pulmonary thromboembolism and fat embolism as possible causes. Fat embolus is a common occurrence in many orthopedic procedures. Although it has been described extensively in the setting of long-bone fractures and multiple trauma, fat embolism syndrome has not been widely reported as a complication of total hip arthroplasty.
In the patient described above, the diagnosis of fat embolism syndrome was entertained after the possibility of pulmonary thromboembolism was ruled out. The fat embolism syndrome was first described clinically by Von Bergmann,who cared for a man with a broken femur and symptoms of the syndrome in 1873. The prevalence of fat embolism syndrome among all fracture patients is reported to be between 0.25% and 1.25%. Among patients with multiple bone fractures, the prevalence can reach 5% to 10%.
The pathophysiology of fat embolism syndrome has not yet been definitively characterized. A mechanical theory holds that the embolization event results from a transient rise in pressure in a fat-containing cavity in association with torn blood vessels, allowing escape of marrow or adipose fat cells into the circulation.Two alternative biochemical theories posit explanations for fat embolism syndrome, both of which could account for the observation of the syndrome in nontraumatic settings. In one, fat droplets already in the circulation are broken down at distal sites to free fatty acids, which then exert a local toxic effect on the tissues. This theory explains the appearance of petechiae and the histologic changes in pneumocytes in association with fat-embolism-induced acute respiratory distress syndrome (ARDS).The obstructive explanation for fat embolism syndrome proposes that free fatty acids are mobilized by circulating catecholamines. Fat droplets in the circulation eventually coalesce and embolize, causing destructive effects.
Fat embolism syndrome can occur in immediate conjunction with a precipitating factor or it can be delayed for up to 3 days, although 85% of cases are apparent within 48 hours. The diagnostic workup of a patient suspected of having fat embolism syndrome should include serial arterial blood gas measurements, as hypoxemia is one of the cardinal features. Serial chest radiographs can be used to observe the progression of ARDS infiltrates in the lungs, although it should be noted that chest radiographic changes are often not apparent in the initial stages of the syndrome. An ECG might show a new right bundle-branch block or nonspecific T-wave changes. A late laboratory marker of fat embolism syndrome is serum lipase, which becomes elevated 3 to 5 days after embolization and peaks at 5 to 8 days.
Gurd and Wilson proposed the most widely accepted guidelines for the diagnosis of fat embolism syndrome, which require at least one sign from the major and at least four signs from the minor criteria ( Table 1). An alternative set of standards was later proposed by Lindeque et al, who believed that the criteria of Gurd and Wilson were too restrictive. The criteria of Lindeque et al are seldom used among clinicians, in part because of they are unable to distinguish fat embolism syndrome from other causes of respiratory distress.
The histologic diagnosis of fat embolism syndrome relies on observing fat globules in vascular spaces. This finding is most reliably obtained by a biopsy of superficial cutaneous petechial lesions. Fat globules can also be found in sputum and urine, although this evidence is made more elusive by the fact that fat must be actively circulating at the time the sample is collected.
The treatment of fat embolism syndrome is primarily supportive. As with other causes of ARDS, maintaining adequate tissue oxygenation and an arterial oxygen saturation of more than 90% should be the clinician's goal. The patient's lung disease might necessitate the use of positive airway pressure or even mechanical ventilation. Because many patients suffer fat embolism syndrome in conjunction with multiple trauma, general supportive measures, including hemodynamic stabilization, maintenance of normal electrolyte values, and prompt attention to orthopedic and soft-tissue injury should be maintained.
The effects of steroids on patients with fat embolism syndrome have long been debated in the literature. The theoretical basis for using corticosteroids is sound; they are thought to stabilize granulocyte membranes, reduce catecholamine levels, retard platelet aggregation, inhibit the activation of complement system, and protect the capillary endothelium. Corticosteroids have been shown to reduce the incidence of fat embolism syndrome when given prophylactically in the emergency department, although data showing a therapeutic role for them once clinically apparent fat embolism syndrome has developed have remained elusive.
Orthopedic surgeons might be able to reduce their patients' risk of fat embolism syndrome. Early fracture fixation has decreased the incidence of pulmonary complications and fat embolism syndrome related to long-bone trauma. Using a distal drain hole or a proximal and distal vacuum during the cementing stage of total hip arthroplasty has been associated with markedly reduced embolization. Recent studies using ultrasound have detected embolic events in routine total hip replacement operations in 94% and 100% of patients studied. No patients in either group, however, showed clinically observable symptoms, underscoring the complexity of the factors that contribute to the genesis of the fat embolism syndrome.
It is thought that the technique used to cement the intramedullary component of the prosthesis causes embolic events during total hip arthroplasty. In the traditional method, the femoral canal is first reamed out. Next, glue is inserted into the intramedullary canal, then the stem of the prosthesis. This technique generates tremendous pressures in the canal, which might cause the extravasation of marrow or cement into the vasculature. Use of a distal drain hole or vacuum greatly reduces the intermedullary pressures during total hip arthroplasty. Although such new approaches seem to reduce a patient's risk of fat embolism syndrome, surgeons caution that operative techniques which use a distal port might be associated with increased incidence of cement failure and femoral shaft fracture.
Table 1. Criteria for Fat Embolism Syndrome by Gurd and Wilson
Major Criteria Minor Criteria
Petechiae in a vest distribution Tachycardia (heart rate > 110 beats per minute)
Hypoxemia with PaO2 <> 38.5°C)
FI02 < /= 0.4
Central nervous system depression Emboli visible in retina
disproportionate to hypoxemia
Pulmonary edema Fat in urine
Fat in sputum
Unexplained drop in hematocrit or platelet count
Increasing erythrocyte sedimentation rate
PaO
2
- arterial oxygen pressure, FIO
2
- forced inspiratory oxygen.
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