Cyanosis and dyspnea are so pronounced that clinical recognition of pulmonary fat embolism is usually prompt if any considerable part of the pulmonary capillaries is blocked by fat. The cerebral variety is not so easily distinguished, for a number of reasons. One is that symptoms identical with or much like those of uremia may develop from obstruction of intertubular and glomerular capillaries in the kidneys. In experimental fat embolism the nitrogen in the blood is increased and extensive necrosis of the bowel has also been observed,1 a condition which in human disease has long been associated with terminal stages of nephritis. Another obstacle is the toxemia from parenteral digestion of fat in the blood stream or in spots where it has lodged. Disorders of metabolism also develop from lodgment of the oil globules in other organs, such as the liver, spleen, bone marrow and suprarenal glands. To these there
CEREBRAL FAT EMBOLISM. JAMA. 1929;93(2):121–122. doi:10.1001/jama.1929.02710020037018
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