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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
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
In 28 dogs with controlled ventilation and circulation, the passage of microspheres (MS) injected into the carotid in size ranges from 1\ g=m\ to 100\g=m\through the brain was observed. A cannula placed into a cortical vein provided recovery of MS from pure cortical venous blood and a semicontinuous outflow measurement. In control animals MS up to 7\g=m\passed freely through the brain; bigger MS were almost completely entrapped. In states of ischemic and hypoxemic hypoxia, as well as in prolonged reactive hyperperfusion caused by a previous hypoxic exposure, MS up to 76\g=m\passed through the brain within two minutes after injection. Hypercapnia did not change the filter capacity. The presence in the dog's brain of arteriovenous connections much larger than capillaries, but not larger than 76\g=m\,is postulated. These connections, closed in the normal brain, are opened by hypoxia. (26:479-488, 1972) tive hyperperfusion; hypercapnic and hypoxic cerebral blood flow regulation; regional cerebral outflow measurement. A) .LTHOUGH the presence of arterio¬ venous connections larger than capillaries (AV shunts) has been demonstrated in dif¬ ferent organs of the body (skin, muscle, heart, intestine, liver, spleen, lung, eye),14 the existence of cerebral AV anastomoses is still moot. Histological investigations have produced contradictory results. While some investigators5·6 specifically denied the exis¬ tence of anatomically verifiable AV shunts in the brain, others710 described pial and intracerebral shunts in cats, dogs, and humans. Hasegawa et al7 described two types of intracerebral AV connections bigger than cap-illaries: the "thoroughfare channel" of Zwei¬ fach,11 common in the angioarchitecture of many organs, with a diameter of 8µ to 24µ, and a rare straight and short AV shunt of 14/t to 25/x in the subcortical white matter.Rowbotham and Little8 described shunts up to µ, in the superficial pial vascular net¬ work. Further extracerebral intracranial AV shunts were found in the choroid plexus12 and in the "rete mirabile conjugatum"13 of rabbits, guinea pigs, and rats. Salamon and Raybaud14 demonstrated by means of a microradiographic technique AV shunts of 60µ to µ diameter in cerebral ischemie areas in humans, while they were not detectable in normal brain tissue. These findings appar¬ ently have not found general recognition and acceptance; at least they are not used in the discussion and interpretation of cerebral hemodynamic problems.Another approach to investigate the pres¬ ence of AV shunts in animals is the detec¬ tion of the passage of different sized parti¬ cles through the cerebral vascular system. Emboli of different materials (blood clots, fat, paraffin, metal powder, carbon, clay, glass beads, plastic, human albumin) and of different sizes, with and without radioactive labels, have been used, mainly to study the histopathology, size, and distribution of is¬ chemie lesions following intracarotid (IC) injections. Morphological alterations of the vessels occluded by the microemboli and the ultimate fate of...
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