From the diagnosis to the therapeutic management: cerebral fat embolism, a clinical challenge

Abstract

Cerebral fat embolism (CFE) is an uncommon incomplete type of fat embolism syndrome (FES), characterized by purely cerebral involvement. It usually occurs 12–72 hours after the initial trigger, mainly represented by closed, long-bone multiple fractures of the lower extremities. Neurological manifestations are mainly characterized by headache, confusion, seizures, focal deficit, and alteration of the consciousness state up to coma onset. It represents a diagnostic challenge, above all when secondary to uncommon nontraumatic causes, because neurological signs and symptoms are variable and nonspecific, not satisfying the Gurd and Wilson’s criteria, the diagnostic features most widely used today for FES diagnosis. Neuroimaging (mainly MRI, but in some cases, brain computed tomography too) can hasten the diagnosis, avoiding other unnecessary investigations and treatment. Usually self-limiting, CFE may sometimes be fatal. Treatment is to date mainly supportive and prophylactic strategies are considered an important tool to decrease the development of fat embolism and, consequently, the rate of CFE.

A traumatic traveler

“…FES is a rare complication associated with long bone fractures and orthopedic manipulation. 1,2 The exact mechanism of fat emboli production is unknown, but two theories prevail. The mechanical theory states that an outside mechanical source causes bone marrow contents or adipose tissue contents to be dislodged into the circulation where they travel through the venous circulation to become embedded in the lungs.…”

“…1,2 These fragments may also migrate to the arterial circulation, through a patent foramen ovale or intrapulmonary shunts, leading to end organ damage. 1,2 The biochemical theory suggests that fat emboli in the venous circulation precipitate an inflammatory and prothrombotic cascade that triggers fibrin production, platelet aggregation, and release of free fatty acids into the circulation, predisposing patients to develop multifocal systemic emboli. 1 Although the classic triad in FES includes respiratory symptoms, rash, and CNS symptoms, all three findings are only present in 1%-29% of cases.…”

“…1 Although the classic triad in FES includes respiratory symptoms, rash, and CNS symptoms, all three findings are only present in 1%-29% of cases. 1,2 Respiratory abnormalities, ranging from tachypnea and dyspnea to ARDS and hypoxic respiratory failure, occur in up to 75% of patients with FES. 1 Central nervous system (CNS) complications, including headache, confusion, coma, seizures, and death caused by cerebral ischemia, occur in up to 86% of patients.…”

“…1 Central nervous system (CNS) complications, including headache, confusion, coma, seizures, and death caused by cerebral ischemia, occur in up to 86% of patients. 1,2 Petechiae may occur in 20%-60% of patients and are usually located on nondependent regions of the body such as the head, neck, and chest.…”

“…Corticosteroids have been suggested to help prevent FES in patients with long bone fractures, but there is no evidence to suggest they are helpful once FES is diagnosed. 2 There is conflicting evidence for the efficacy of heparin or low-molecular-weight heparin as treatment in FES. 2,6 After discussions with consulting physician teams, the patient, and his family, enoxaparin and aspirin were started for this patient in light of his tenuous condition in order to decrease the risk of further embolic complications.…”