Platelet abnormalities associated with massive autotransfusion.

Although hemostatic defects have been reported with large-volume autotransfusion, the effect on platelet function has not been well defined. Twenty adult mongrel dogs underwent controlled intraperitoneal hemorrhage with collection and reinfusion using the Sorenson System. Each animal was autotransfused twice its E.B.V. over a 4-hour period. A.C.D., delivered at the sucker tip, served as the only anticoagulant. Mean arterial pressure and cardiac output remained stable during the study period with the additional volume support of 50 cc/kg Ringer's lactate. A moderate consumptive coagulopathy ensued. The P.T., P.T.T., and T.C.T. were all significantly prolonged, with a decrease in fibrinogen at 4 hours compared to baseline. Platelet counts fell significantly to 71% of baseline. In addition, platelet aggregation response to A.D.P. and collagen was markedly depressed, with corresponding prolongation in bleeding times at 4 hours. Twenty-four hours following autotransfusion the P.T., P.T.T., T.C.T., and fibrinogen levels returned toward normal. In contrast, the platelet counts continued to fall and the aggregation response remained markedly impaired. Methylprednisolone (30 mg/kg), administered to 10 animals, had no statistically significant effect on the coagulation parameters.

Glutaric aciduria: biochemical and morphologic considerations.

Biochemical and morphologic studies on a patient with glutaric aciduria are presented. Generalized aminoaciduria, alpha-aminoadipic aciduria, and saccharopinuria were noted just prior to death, as well as glutaconic aciduria greater than beta-hydroxyglutaric aciduria. Mutant liver mitochondria did not oxidize glutaryl-CoA to glutaconyl-CoA, indicating deficiency of glytaryl-CoA dehydrogenase. Autopsy revealed cerebral edema, ischemic neuronal changes, and striatal degeneration in the brain with fatty changes in liver, kidney, and myocardium.