Cerebral fat embolism: a neuropathological study of a microembolic state.

Abstract

SUMMARY Multiple cerebral petechlae associated with intravascular globules of neutral fat and localized primarily within the white matter are distinctive lesions which secure the pathologic diagnosis of cerebral fat embolism. The abundance of these lesions in an unknown, but presumably small, percentage of cases of fat embolism, along with the even more widespread distribution of embolic fat droplets throughout both white and gray matter, suggest that these lesions and emboli must hare a profound effect on neurologic function. Nevertheless, respiratory insufficiency is by far a more common clinical manifestation of the fat embolism syndrome and the neurologic involvement of such patients is often attributed to the secondary effects of generalized hypoxia. The following patient with orert respiratory and neurologic symptoms re-emphasizes the direct primary effect of fat emboli within the central nervous system as a cause of white matter hemorrhages and neurologic deterioration. Explanations for the selectivity of the lesions for the cerebral white matter are explored. Stroke, Vol 11, No 5, 1980FOR OVER A CENTURY, fat embolization has been recognized as a potentially serious, but poorly understood, sequela of skeletal trauma. Relative to the frequent subclinical embolization of fat droplets following fractures, 1 ' 2 the "fat embolism syndrome" is less common and is unpredictable in the severity with which it affects the major target organs, the lungs and the brain. Because of its greater incidence, the pulmonary, rather than the cerebral, component has received primary attention in clinical and experimental studies which attempt to define the relationship between embolic intravascular fat and clinical disease.3 In contrast to the lung, however, the brain may present more distinctive, if not diagnostic, pathologic lesions in this syndrome. With the aid of an illustrative patient, this discussion reviews cerebral fat embolism from the perspective of the pathologist and surveys our incomplete understanding of its pathogenesis. Patient PresentationThe patient was a 45-year-old man who sustained in an automobile accident multiple right-sided rib fractures and a comminuted fracture of the right femur. He did not lose consciousness. After initial treatment for shock at an outside hospital, he was transferred to Duke University Medical Center where his blood pressure on admission was 120/80 mm Hg, pulse 120/min, and respiratory rate 28/min. He was dyspneic, but neurologically intact except for anisocoria (right 4 mm, left 2 mm). Arterial blood gases revealed a Po 2 of 51 mm Hg, O 2 saturation of 83%, pH of 7.31, HCO, of 14 mEq/1, and a Pco 2 of 28 mm Hg. Bilateral pneumothoraces were noted; he was intubated and chest tubes were placed. Alveolar densities were also seen throughout both lung fields. His right leg was splinted in traction.Four hours after arrival (12 hours after the accident), he became lethargic and responded to pain

Dynamic MR Imaging Patterns of Cerebral Fat Embolism: A Systematic Review with Illustrative Cases

“…Clinically, despite the fact that fat emboli are small, the lesions tend to be distributed in white matter rather than gray matter. Sevitt 18 proposed that rich vascularity in the gray matter could have sufficient anastomotic potential to protect against the injury, and Kamenar and Burger 19 suggested that white matter lesions are indirectly produced by the cortical emboli through venous sludging and white matter edema. However, myelin has a high lipid content and a slow turnover; all the myelinated tracts are particularly vulnerable to the accumulation of lipophilic substances and to lipid peroxidation.…”

Magnetic Resonance Diffusion W Imaging in Cerebral Fat Embolism

“…1,2 It is often the sequelae of displaced long bone fractures of the lower extremities, and is a potentially lethal complication. 3 Neurologic involvement in FES has been termed cerebral fat embolism (CFE) and has traditionally presented a diagnostic challenge.…”

Cerebral fat embolism syndrome mimicking thrombotic thrombocytopenic purpura in a patient with hemoglobin SC disease

“…The presence of numerous hypointensities predominantly in the white matter on susceptibilityweighted or gradient echo (GRE) sequences is considered to be pathognomic for microhemorrhages, and can also be seen in 60-88% of the acute to late stages of cerebral FES [5,[10][11][12]. These correlate with the petechial cerebral hemorrhages observed on autopsy [13]. While occasional punctate foci of diffusion restriction may also be seen in TMAs, they are not as numerous as those seen in the starfield pattern of FES [14].…”