Zentralblatt für Chirurgie
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Administration of hypertonic solutions is the method of choice for acute treatment of intracranial hypertension. Recording of the intracranial pressure during treatment facilitates adjustment of the dosis to the actual ICP-response, avoiding thereby administration of an excessive osmotic load as a basis to prolong therapeutical efficacy. The mechanisms underlying reduction of the intracranial pressure by hypertonic solutions are still controversially discussed. ⋯ No evidence has been obtained in a variety of experimental studies that hypertonic/hyperoncotic solutions have adverse effects on the brain in the presence of a cerebral lesion. To the contrary, the fluid mixture has been found to lower the increased intracranial pressure. Administration of hypertonic/hyperoncotic solutions appears therefore appropriate in acute cerebral insults from head injury and impending circulatory failure from shock in order to inhibit development of secondary brain damage.
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The clinical syndrome sepsis has been redefined recently, and the SIRS (systemic inflammatory response syndrome) concept has been developed. In the initial phase of sepsis, different mediator systems are activated finally resulting in a generalized endothelial inflammatory reaction. This reaction may lead to a vicious circle with subsequent multiple organ failure. ⋯ Replacement of antithrombin III, continuous venovenous hemofiltration, application of high doses of immunoglobulins and of low doses of hydrocortisone have been used. A monoclonal antibody against endotoxin (Centoxin) was taken from the German market in January 1993. Experimental aspects of treatment include the administration of C1 esterase inhibitor, pharmacological inhibition of nitric oxide (NO), plasmapheresis, the application of non-steroidal anti-inflammatory agents and of high-dose naloxone as well as manipulation of cytokines.
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The present investigation was initiated to quantify the effect of a CO2-peritoneum on CO2-absorption (VCO2res) and other respiratory variables during laparoscopic surgical procedures. ⋯ This increase in ventilation can easily be established in pulmonary uncompromised patients. Problems in adequately increasing minute volume are expected in chronic obstructive lung disease and with maximal VCO2res. Monitoring of at least petCO2 is strongly recommended since the individual course of VCO2res cannot be predicted.
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94 patients have been operated upon for haemorrhagic gastroduodenal ulcer disease in the Wenckebach-Krankenhaus during the years 1986-1990. In all but 6 patients the ulcer has been controlled by an emergency gastroscopy. 25 of these patients had to undergo emergency operation at once for persistent bleeding after gastroscopy. From the other patients, another 31 suffered rebleeding and had to be laparotomised in an emergency procedure, too. ⋯ There was no difference in mortality-rates between resective and non resective procedures. Our aim to operate upon the patients in an elective way could be achieved in about one third only. Many patients refused an operation after primary control of bleeding.
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Shock induced microcirculatory failure is proposed to be causative for the impairment of hepatic function, which contributes to the development of multiple organ failure. In order to quantify the interrelation between hepatic microcirculatory disturbances and organ dysfunction, we have analyzed hepatic microcirculation (in vivo microscopy), energy metabolism (ketone body ratio) and liver excretory function (bile flow) during hemorrhagic shock in rats. ⋯ Liver microcirculation in hemorrhagic shock is characterized by sinusoidal perfusion failure with a reduction of erythrocyte flux, leukocyte velocity and enhancement of leukocyte adherence to the microvascular endothelial lining. Correlation of the impairment of energy metabolism and liver dysfunction with these microcirculatory disturbances may indicate their crucial role in the development of shock-induced organ failure.