The syndrome of fat embolism and its origin.

Szabo, G

doi:10.1136/jcp.s3-4.1.123

Cited by 15 publications

(9 citation statements)

References 11 publications

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“…Among the latter are increased venous pressure in the superior vena cava secondary to the pulmonary fat emboli,"' "• ™ coagulopathy," 174 hypotension," hypoxia, 2 ' '• " vasoconstriction, 72 and toxic metabolites of lipids. 7 ' These secondary factors have not been rigorously studied in the context of either human or experimental cerebral fat embolism, although some have been the subject of much interest with respect to the lung.…”

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confidence: 99%

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

Kamenar

Burger²

1980

Stroke

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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

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confidence: 99%

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

Kamenar

Burger²

1980

Stroke

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“…Although coma and myoclonic jerks could be attributed to FES, these could also have been due to cerebral anoxia, and the clinical signs and symptoms of the 2 have been described to be very similar. 16 Petechiae were not noted.…”

Section: Discussionmentioning

confidence: 92%

“…14 The biochemical theory is that free fatty acids are liberated when lipase produced by the lungs acts on embolic fat. 16 Free fatty acid is toxic to pulmonary endothelial cells and pneumocytes. 18 This leads to perivascular hemorrhage and alveolar edema that combine with the obstructive effects of the otherwise unimportant pulmonary fatty emboli leading to arterial hypoxemia.…”

Section: Discussionmentioning

confidence: 99%

Fat embolism syndrome after shoulder hemiarthroplasty

Paredes

Syquia

Chang

et al. 2011

Journal of Shoulder and Elbow Surgery

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“…It is known that unemulsified fat injected into the circulation of experimental animals can be recovered from the lungs (Brueke et al, 1971) after both intravenous and intra-arterial injection (Szabo, 1970). In man fat seems to disappear from the lungs with time because the amount of embolic fat detected histologically decreases as the time lapse between injury and examination increases (Szabo, 1970).These and similar observations at autopsy are necessarily static and so reflect only the presence of fat at a single moment. They do not provide information about the rate of fat accumulation in the lungs.…”

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confidence: 89%

“…It is a basic assumption that in order to produce the pathological features of fat embolism the fat must be unemulsified and not part of a lipoprotein complex, yet little is understood about the way in which unemulsified fat is handled in the body. It is known that unemulsified fat injected into the circulation of experimental animals can be recovered from the lungs (Brueke et al, 1971) after both intravenous and intra-arterial injection (Szabo, 1970). In man fat seems to disappear from the lungs with time because the amount of embolic fat detected histologically decreases as the time lapse between injury and examination increases (Szabo, 1970).…”

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confidence: 98%

Experimental fat embolism: A dynamic assessment of pulmonary fat-handling characteristics

Sikorski

Pardy

Dudley

1977

Journal of British Surgery

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Injection 125I-glyceryl trioleate (0-5 mg/kg) into the right atrium of anaesthetized greyhounds caused the following changes: sequestration of far in the right side of the heart; 95 per cent removal by the lungs in a single passage through the pulmonary circulation; subsequent release of fat into the systemic circulation; rapid overall turnover of fat trapped in the lungs and slow removal of recirculating fat by other tissues. We believe that if there is release of unemulsified fat into the circulation in traumatic fat embolism these findings are of significance in interpreting the subsequent pulmonary events.

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The syndrome of fat embolism and its origin.

Cited by 15 publications

References 11 publications

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

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

Fat embolism syndrome after shoulder hemiarthroplasty

Experimental fat embolism: A dynamic assessment of pulmonary fat-handling characteristics

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