Fat Emboli In Brain

Fat Embolism

Pathogenesis. As a consequence of bone fracture or crush injury to fat tissue in the pulmonary circulation a massive invasion of fat droplets can occur, increase the vascular resistance and lead to subsequent right ventricular failure. If this condition is survived, after an interval of 18 h to 4 days the patient is at risk of a cerebral fat embolism, which can ultimately lead to death or contribute to the fatal event. If fat em-boli pass through a patent foramen ovale of the heart or pulmonary arteriovenous shunts, the fat droplets

Brain Fat Embolism Histology

Fig. 9.29a-d. Fat embolism as demonstrated (a) macroscopi- cularly (b) and are characterized by phagocytosing macrophages cally (purpura cerebri) as well as histologically (b, c) by means of (c); paraffin-embedded tissue demonstrates spheric hemorrhag-oil red O stain and (d) by H&E stain. Fat droplets are seen intravas- es associated with edema (magnification, b, c X500; d X100)

Fig. 9.29a-d. Fat embolism as demonstrated (a) macroscopi- cularly (b) and are characterized by phagocytosing macrophages cally (purpura cerebri) as well as histologically (b, c) by means of (c); paraffin-embedded tissue demonstrates spheric hemorrhag-oil red O stain and (d) by H&E stain. Fat droplets are seen intravas- es associated with edema (magnification, b, c X500; d X100)

can be transported to the systemic circulation (cf. Mellor and Soni 2001).

Clinical Features. Cerebral fat embolism gives rise to uncharacteristic cerebral symptoms which are reminiscent of a differential diagnosis of brain edema. If there is an initial loss of consciousness, intervening neurologic signs cannot be detected, thus masking the cerebral fat embolism. Psychopathological changes such as an acute-onset confusional state, clouding of the sensorium, and cerebral convulsions are just as much symptoms of a fat embolism as are symptoms of generalized embolism, such as petechial bleeding in the skin of the trunk. Because the mortality associated with cerebral fat embolism is very high, the appearance of its symptoms must be regarded as predictive of a poor prognosis (Henn 1989).

Neuropathology. Macroscopically (Fig. 9.29), brain slices exhibit numerous punctiform hemorrhages located mainly in the white matter of the cerebrum and typically described as purpura cerebri. In the cerebellum, the cortex and white matter are equally affected. Most cases also exhibit signs of a brain edema. Microscopically, annular or ball-shaped hemorrhages are seen and the central vascular lumen is occluded by fat droplets. If the embolism is survived for days, fat- or siderin-containing macrophages appear perivascularis After survival of several months, circumscribed perivascular glioses appear, with my-elophthisis and expansion of the interior CSF spaces (internal hydrocephalus). This must be interpreted as the result of edema and hemorrhage-induced de-myelination. An intermittent clinical course can occur (Henn 1989), exhibiting various time-dependent reactive changes.

Differential Diagnosis. A few cases of cerebral purpura without fat embolism have been reported. They featured either a disseminated intravascular coagulopathy (DIC) with vessel thrombosis, a release of tissue thrombokinase from the injured organs, or a trauma-induced spasm of the small vessels (see above). The differential diagnosis in cases of purpura must include mercury poisoning with subsequent endothelial injury (arsphenamine or Salvarsan therapy) as well as hypothermic purpura cerebri.

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