A 24-year-old white man with no past medical history is admitted after sustaining bilateral, closed femur fractures in a motor vehicle accident. Within hours of the trauma, he is taken to the operating room for open reduction and internal fixation. Of note, preoperatively, his hematocrit is 40%. After surgery, he is easily extubated and transferred to an unmonitored bed for further care. Approximately 30 hours after admission, he develops tachypnea with a respiratory rate of 35 breaths per minute and hypoxia with an oxygen saturation of 86% on room air. He is tachycardic (120 beats per minute) and febrile to 39.0oC. His blood pressure remains stable. He is somnolent, and when awake, he is confused. Notably, his hematocrit is now 22%. An electrocardiogram shows sinus tachycardia, an initial chest X-ray is normal, and a high-resolution CT scan is negative for a pulmonary embolism (PE).
Is this clinical picture consistent with fat embolism syndrome and, if so, how should he be managed?
“Fat embolism” refers to the presence of fat globules that obstruct the lung parenchyma and peripheral circulation. Fat embolism syndrome, on the other hand, is a more serious manifestation involving multiple organ systems. Specifically, it is a clinical diagnosis presenting with the classic triad of hypoxemia, neurologic abnormalities, and a petechial rash.
Fat embolism syndrome is usually associated with multiple traumas, including long-bone injuries and pelvic fractures. It is more frequently associated with closed fractures than open fractures, possibly due to the higher pressures associated with closed fractures. This syndrome has been less commonly associated with a variety of nontraumatic conditions (Table 1).
With an increased incidence of long-bone fractures in the younger demographic, fat embolism syndrome is most common in the second or third decade of life. While fat embolism occurs in up to 90% of patients with traumatic skeletal injuries, fat embolism syndrome occurs in 0.5% to 10% of patients following trauma, with a higher incidence in multiple fractures (5% to 10%) than in single long-bone fractures (0.5% to 2%).1-3
With the increasing role of hospitalists in assisting in the management of orthopedic patients, their knowledge of fat embolism syndrome is important so that it can be included in the differential diagnosis of acute respiratory failure in these orthopedic patients.
Review of the Data
Pathogenesis. Clinical manifestations of fat embolism syndrome have been acknowledged for more than 100 years. Since its first description in the 1860s, there has been speculation about the etiology of this condition. In the 1920s, two theories were proposed to explain the origin of the fat droplets: the mechanical and biochemical theories.2,4
Mechanical theory suggests that trauma to long bones disturbs fat cells within the bone marrow or adipose tissue, causing fat globules to mobilize.2,3 There is a rise in marrow pressure above venous pressure, which allows fat particles to enter the circulation through damaged venules surrounding the fracture site. Once lodged in the pulmonary microvasculature, embolized fat causes local ischemia and inflammation. Fat globules may pass into the arterial circulation either by paradoxical embolism through a patent foramen ovale, or by microemboli that pass through the lungs into the arterial circulation. This explains embolization to other organs, including the brain, retina, and skin.