Clinical Pearls & Morning Reports
Fat embolism syndrome is most often observed after a traumatic injury, typically a long-bone fracture of the leg. Patients with fat embolism syndrome typically present with multiorgan dysfunction within 12 to 72 hours after the initial insult. The classic triad of manifestations is hypoxemia, neurologic abnormalities, and petechiae. Read the NEJM Case Records of the Massachusetts General Hospital here.
Q: Name some of the nonorthopedic causes of fat embolism syndrome.
A: Nonorthopedic causes of fat embolism syndrome are exceedingly rare and include pancreatitis, sickle cell disease, alcoholic liver disease, bone marrow harvest or transplantation, and liposuction. Liposuction is an increasingly common cosmetic surgery, with 305,856 procedures performed in 2015. During liposuction, rupture of small blood vessels may allow lipid microfragments to reach the venous circulation and in some cases the arterial circulation, resulting in end-organ injury.
Q: What are some of the signs and symptoms of fat embolism syndrome?
A: Pulmonary symptoms may progress from dyspnea and tachypnea to respiratory failure. Neurologic manifestations include focal deficits, confusion, lethargy, and ultimately coma. Hematologic findings include petechiae, thrombocytopenia, anemia, and disseminated intravascular coagulation. Patients with fulminant cases of fat embolism syndrome may present with right ventricular or biventricular failure, acute respiratory distress syndrome, or shock, or the illness may lead to death. Coronary occlusion caused by fat embolism after liposuction has been reported. The diagnosis of fat embolism syndrome is most often made clinically, on the basis of recognition of an appropriate predisposing insult, compatible symptoms and physical findings, and supportive imaging and laboratory studies.
A: The mainstay of treatment for fat embolism syndrome is supportive care. There are no evidence-based specific therapies for the management of cerebral fat embolism. Patients with cerebral fat embolism undergo intensive neurologic monitoring to assess for neurologic decline and the need for neurologic interventions. Although seizures and status epilepticus may occur, there is no role for prophylactic antiepileptic medications. There is insufficient evidence to support the use of glucocorticoid therapy in the treatment of cerebral fat embolism, although a meta-analysis reported its potential effectiveness in preventing fat embolism syndrome and hypoxia in patients with long-bone fractures.
A: Although initial neurologic symptoms — including coma, seizures, status epilepticus, elevated intracranial pressure, and progressive brain injury — can be grave, 72 to 90% of patients may regain functional independence, especially those with a milder burden of disease. In addition, 58% of patients in a coma and those with motor posturing may recover favorably. Residual impairments may include minor motor deficits; mild cognitive impairment, especially weaknesses in frontal function and verbal memory; and dysarthria. Neurologic improvement can occur over the course of several months. It is important to note that cerebral fat embolism does not necessarily imply irreversible structural brain damage, and establishment of a dire neurologic prognosis early in the course of the disease should be avoided.