Sudden hypoxia during knee surgery

TESTS THAT AID THE CLINICAL DIAGNOSIS

Although no single laboratory test is pathognomonic for fat embolism syndrome, several tests may help raise suspicion of it, especially in the setting of fracture or an orthopedic surgical procedure.

Arterial blood gases must be measured. A Pao₂ of less than 60 mm Hg with no other obvious lung pathology in an orthopedic surgery patient is highly suspicious.¹² An alveolar-arterial gradient of greater than 100 mm Hg may further increase suspicion.

Tests for fat. The blood and urine may be examined for fat, although positive findings are not specific for fat embolism syndrome.³³ Fat in the urine indicates the occurrence of massive fat embolism, but this is not always accompanied by the syndrome.³⁴ Gurd and Wilson¹³ found fat globules larger than 8 μm circulating in the serum in all documented cases. They stated that, even though the relationship of large fat globules to the pathogenesis of the clinical picture remains obscure, the demonstration of their presence can be helpful in the diagnosis.¹³

Also, samples obtained with bronchoalveolar lavage may be examined for fat. The macrophages may be stained for fat using the oil red O stain. Again, this is a nonspecific marker, as fat-stained macrophages are seen in trauma patients,³⁵ but the finding has a very high negative predictive value.³⁶ Anemia, thrombocytopenia, hypofibrinogenemia, an elevated lipase level, and a high erythrocyte sedimentation rate may be found in fat embolism syndrome.¹³

Chest radiography may show bilateral infiltrates, as in ARDS, but this is not diagnostic for fat embolism syndrome.

Electrocardiography may show changes in ST and T waves and signs of right heart strain.

Transesophageal echocardiography may show increased right heart and pulmonary artery pressures.

Computed tomography is often negative,^37,38 but T2-weighted MRI is useful in the diagnosis of cerebral fat embolism syndrome, as it can show intracerebral microinfarcts as early as 4 hours after the onset of neurologic symptoms, and these findings correlate well with the clinical severity of brain injury.

Diffusion-weighted MRI may enhance the sensitivity and specificity of the neuroradiologic diagnosis. Diffusion-weighted MRI typically shows multiple nonconfluent areas of high-intensity signals or bright spots on a dark background, known as a “starfield pattern.” This pattern has been suggested to be pathognomonic of acute cerebral microinfarction. The abnormalities presumably reflect foci of cytotoxic edema that develops immediately, unlike vasogenic edema, seen in T2-weighted images, which may take up to several days to develop. Although these images are not necessarily specific for fat emboli, they are useful in helping make the diagnosis. Thus, diffusionweighted MRI should be done if fat embolism syndrome is suspected.^38,39

CASE CONCLUDED

The patient’s course in the intensive care unit was further complicated by gastrointestinal bleeding and renal failure. His neurologic status did not improve. Repeated MRI of the brain showed evolving bilateral watershed infarction throughout the cortices. The neurologic consult service diagnosed the patient as having severe encephalopathy with a very poor prognosis. The decision was made to withdraw care. He was placed under palliative care and died on postoperative day 22.

DRUG TREATMENT OF FAT EMBOLISM SYNDROME

5. Which of the following drugs has been proven to be effective in treating fat embolism syndrome?

• Intravenous ethanol
• Steroids
• Heparin
• Dextran
• Aspirin
• None of the above

None of the above has been proven to be effective in treating this disorder. The management is largely supportive. Thus, prevention, early diagnosis, and symptom management are vital.

Pulmonary and hemodynamic support are the cornerstones of successful treatment. Aggressive respiratory support is often needed. Management of acute lung injury and ARDS focuses on achieving acceptable gas exchange while preventing ventilator-associated lung injury. Intravascular volume must be supported. Inotropes and pulmonary vasodilators may be required to maintain hemodynamics. Exacerbation of central nervous system ischemia from hypotension or hypoxia should be avoided.

If the thrombocytopenia leads to clinical bleeding, platelet transfusions may be warranted.

Supportive care should include prophylaxis of deep venous thrombosis and of gastrointestinal bleeding, and maintenance of nutrition.⁴⁰ Patients who receive supportive care generally have a favorable outcome, with a mortality rate of less than 10%.²⁸

Drug studies have been inconclusive

Drugs suggested in the treatment of fat embolism syndrome include heparin, aspirin, dextran, hypertonic glucose, and alcohol, but the results have been inconclusive.^{3,11,23,40–43}

Heparin stimulates lipase activity, consequently decreasing the concentration of circulating fat globules. However, the increase in levels of free fatty acids may actually worsen the clinical picture. For this reason, and because of anticoagulation concerns and evidence of increased mortality rates, heparin is now contraindicated in the treatment of fat embolism syndrome.^2,41,43

Alcohol. Patients with a higher blood alcohol level at the time of injury have been reported to have a lower incidence of fat embolism syndrome. Alcohol inhibits lipase, suppressing the rise of free fatty acids. In experimental studies, the incidence of fat embolism syndrome was lower when the blood alcohol level was maintained at 20 mg/dL. However, no prospective randomized trial has been done to determine the clinical efficacy of ethanol as a treatment for this condition.^5,42

Dextran has been advocated, owing to its ability to improve small-vessel perfusion, but bleeding risk and acute renal failure associated with this drug have limited its use.⁵

N-acetylcysteine has been shown to attenuate fat-induced lung injury in a study of rats with induced fat embolism syndrome.⁴⁴

Corticosteroid treatment for this condition is controversial. Studies in patients with femoral and tibial fractures show that steroids reduce the incidence of fat embolism syndrome when given prophylactically, and those treated with steroids had a higher Pao₂ than controls. Doses of methylprednisolone in these studies ranged between 9 mg/kg to 90 mg/kg. A drawback of these studies is their small number of patients.^12,32,45,46

A meta-analysis⁴⁷ of randomized trials of corticosteroids to prevent fat embolism syndrome in patients with long-bone fractures identified 104 such studies. Only 7 of the 104 were considered adequate. In 389 patients with long-bone fractures, prophylactic corticosteroids reduced the risk of fat embolism syndrome by 78% (95% confidence interval 43%–92%) and corticosteroids also significantly reduced the risk of hypoxia with no difference in rates of infection or death. However, the overall quality of the trials was poor, and the authors of the meta-analysis concluded that more study is needed before corticosteroids could be formally recommended.⁴⁷

There is no evidence that steroids improve the overall clinical course of already established fat embolism syndrome.^12,32,45 The dosing and optimal timing of administration have also not been established. High doses pose a risk of septic complications, which may be devastating for the posttrauma or postoperative patient.