In a standardized porcine model of acute, hyperdynamic endotoxemia the distribution of intraorgan blood flow within heart, kidney and brain was analyzed. Twelve pigs received either short-term (23 min) or long-term (205 min) continuous intravenous infusion of endotoxin (Salmonella abortus equi). A high cardiac output/low peripheral resistance state was maintained throughout the 3.5 h observation period. Total organ blood flow in heart, kidney and brain remained high; however, already small amounts of endotoxin provoked a significant redistribution of intraorgan blood flow within the left ventricle and the kidney. These characteristic alterations were absent in a control group of 5 animals subjected to the same protocol, but receiving 0.9% saline instead of endotoxin. Deterioration of respiratory function developed exclusively after continuous intravenous endotoxin infusion over 205 min, indicating incipient organ failure. Using electron microscopy, endothelial cell swelling and entrapment of blood cells in capillaries of the midmyocardium as well as severe ultrastructural damage in the kidney could be demonstrated already after 90 min of endotoxemia in two additional animals. It is concluded that already in the initial phase of acute endotoxemia, in presence of high cardiac output and high global organ blood flow microcirculatory deterioration and organ failure develops. As small amounts of endotoxin are capable of inducing these alterations, earliest possible diagnosis of endotoxemia should be achieved in critically ill patients.
In the University Hospital of Granada (Spain), 359 surgical trauma patients underwent intraoperative autotransfusion. The patients were divided into 2 groups, according to their blood loss: group I (blood loss less than or equal to 2000 ml) and group II (blood loss greater than 2000 ml). Patients from group I did not require homologous blood transfusion. So the high risk involved in this type of transfusion was avoided. Macroscopic haemoglobinuria was only found in those patients where the Solcotrans, Viavae type of autotransfusion system was used; with the Bentley ATS system, no macroscopic haemoglobinuria was registered. With patients from group II, however, that is, those with a blood loss of more than 2000 ml, we had to fall back on homologous transfusion in addition to retransfusing autologous blood. When the transfusion exceeds 4000 ml there is increasing bleeding, which requires treatment with fresh frozen plasma, platelets and/or fibrinogen. The mortality rate of patients in group II was very high but the patients died from the severity of their injuries or from postoperative complications which were not due to autotransfusion in itself with the exception of 3 patients who underwent massive autotransfusion (12,000 to 25,000 ml) and died from acute renal failure. The main indication for intraoperative autotransfusion is without doubt abdominal and thoracic trauma which lead to high blood loss.
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