What Is the Best E&M of Fat Embolism Syndrome?

Alternatively, biochemical theory hypothesizes that fat embolism syndrome is contingent on the production of toxic intermediaries from the breakdown of embolized fat.^2,3 This theory suggests that the release of catecholamines after severe trauma can liberate free fatty acids from fat stores, or that acute-phase reactants at the trauma site affect fat solubility, causing agglutination and embolization. This theory helps to explain nontraumatic fat embolism syndrome, as well as the delay in development of the clinical syndrome after acute injury.

Clinical presentation. Most patients have a latent period after trauma of 12 to 72 hours before symptoms of fat embolism syndrome become apparent; however, clinical manifestations might occur immediately or up to one to two weeks following injury.^2,4 As previously mentioned, the classic triad of symptoms includes respiratory compromise, neurological impairment, and a petechial rash.

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Table 2. The different diagnostic criteria used for diagnosis of fat embolism syndrome

The most common and usually earliest manifestation is acute hypoxia, which must be distinguished from other treatable causes of hypoxia, including pneumothorax, hemothorax, PE, and pneumonia. Pulmonary changes might progress to respiratory failure similar to acute respiratory distress syndrome. Neurological manifestations are primarily nonspecific and include headache, irritability, delirium, seizures, and coma. Focal neurological deficits are rare but have been described.⁵ Almost all neurological symptoms are fully reversible. The petechial rash is distinctive and occurs on the chest, axilla, and subconjunctiva. Although the rash occurs in only 20% to 50% of patients and resolves fairly quickly, in the appropriate clinical setting, this rash is considered pathognomonic.^1,2,4

A variety of other nonspecific signs and symptoms might also occur: pyrexia, tachycardia, fat in the urine or sputum, retinal changes, renal insufficiency, myocardial dysfunction, and an otherwise unexplained drop in hematocrit or platelet count.

Diagnosis. Fat embolism syndrome is a clinical diagnosis and a diagnosis of exclusion. There are no specific confirmatory tests. An arterial blood gas will usually reveal a PaO2 of <60 mmHg.3 Laboratory evaluation might also show fat globules in the urine or sputum on Sudan or Oil Red O staining, but these findings are nonspecific.^3,4 Bronchoscopy with bronchial alveolar lavage (BAL) might similarly detect fat droplets in alveolar macrophages in the BAL fluid; however, the sensitivity and specificity for diagnosis of fat embolism syndrome are unknown.⁴ None of these tests can be used solely for the diagnosis of fat embolism syndrome.

Thrombocytopenia and anemia out of proportion to the expected drop from surgery are not uncommon in addition to other nonspecific laboratory findings, including hypocalcemia, elevated serum lipase level, and elevated erythrocyte sedimentation rate.⁴ Several radiological findings have been observed on lung and brain imaging, though the findings are nonspecific and none are diagnostic. A chest X-ray might be normal, but abnormalities are seen in 30% to 50% of cases.² Typically, when abnormal, the chest X-ray shows diffuse interstitial and alveolar densities, as well as patchy perihilar and basilar infiltrates resembling pulmonary edema. These X-ray findings might not be seen for up to 12 to 24 hours following the onset of clinical symptoms.

The most commonly used diagnostic criteria for the diagnosis of fat embolism syndrome are published by Gurd et al.⁶ At least two major criteria or one major criterion and four minor criteria are required for the diagnosis of fat embolism syndrome. The major criteria are based on the three classic signs and symptoms of fat embolism syndrome; the minor criteria include the finding of fat globules in the urine and sputum as well as some of the previously mentioned nonspecific clinical signs and laboratory tests.