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
Autopsies were performed on four patients who had been treated with high-dose BCNU therapy for visceral, cutaneous, or lymphoid malignancies. Three had developed an encephalopathy or encephalomyelopathy within five weeks before death. In all four patients distinctive lesions were found within the central nervous system that were either (1) discrete foci of swollen axis cylinders and myelin vacuolization or (2) larger, symmetric areas of edema with white and gray matter necrosis. Fibrinoid necrosis and fibrin microthrombi were much more prominent in the latter. The small discrete foci of axonal and myelin alterations are similar, if not identical, to lesions previously associated with cranial radiation or combined cranial radiotherapy and chemotherapy. The larger lesions share features with "methotrexate encephalopathy" and delayed radionecrosis. The presence of these lesions in these patients, who had not received cranial radiation, suggests that high-dose BCNU therapy alone is associated with, and may produce, certain distinctive structural changes in the central nervous system. The presence of fibrinoid necrosis and fibrin microthrombi suggests that this possible pathologic effect of BCNU could be mediated by the drug's effect on the cerebrospinal vasculature.
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