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Coagulation, fibrinolytic, kallikrein, and complement systems were studied in 20 patients with multiple trauma. Three of four patients with a trauma score less than 10 on hospital arrival died, compared to one of 16 with a score over 10. Five patients developed disseminated intravascular coagulation. Signs of activated cascade systems were evident in most patients on hospital arrival. Changes were not related to trauma score, but patients with an arterial pressure below 110 mm Hg had significantly lower levels of antithrombin III and alpha 2-antiplasmin than those with higher BP. This study confirms that the cascade systems are activated very soon after multiple trauma.

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The pressure in the proximal axillary vein (AVP) was compared with central venous pressure (CVP) in eight patients during and after elective abdominal surgery. Both pressures were recorded from soft, elastic, polyurethane catheters inserted in the basilic or cephalic veins ("half-way" catheters), punctured at the fossa cubiti (AVP), and via the right jugular vein (CVP). The AVP and CVP were recorded simultaneously using hydrostatic, conventional disposable venous pressure measurement sets. The measurements were performed during intermittent positive pressure ventilation with positive end-expiratory pressure from 0 to 7.5 cmH2O (0-0.74 kPa), as well as during spontaneous breathing. During both controlled and spontaneous respiration, small mean differences (0.2-1.0 cmH2O) (0.02-0.1 kPa), and a highly significant (P less than 0.001) positive correlation between CVP- and AVP-values were found. An increase of 1 cmH2O (0.10 kPa) in the CVP was associated with an increment of practically identical order (0.99-1.04 cmH2O) (0.10-0.11 kPa) in the AVP. The results suggest that monitoring of the AVP by a basilic "half-way" catheter produces diagnostic information similar to that from the measurement of the CVP from subclavian, external or internal jugular, as well as "long-way" brachial catheter, with no risk of the major mechanical complications which accompany the use of the latter catheters.

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A special program for management of massive gastrointestinal bleeding was 1976 introduced in the surgical service of Sahlgren's Hospital in Göteborg. The main points in this program were: careful observation in an intensive care unit, standardized treatment, early diagnostic gastroduodenoscopy, strict indications for emergency operation and recommendation of type operation. This paper deals with 55 patients subjected to emergency operations in 1976 with the diagnosis erosive gastritis, gastric ulcer or duodenal ulcer. The results are compared to an earlier study in 1962-71 in the same hospital. It was found that the mortality was unchanged during the two periods, 25% during 1962-71 and 24% during 1976. At a first glance the new program might seem ineffective. However, the part of elderly patients was much higher during 1976 than during 1962-71. Thus, the patients during 1976 must be considered much more of a surgical challenge. As old patients often have coexisting severe diseases they are surgically most unfit. Probably a more conservative attitude is justified in this particular group of patients.

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During laparoscopy the carbon dioxide used to achieve a pneumoperitoneum is absorbed from the peritoneal cavity into the blood. The object of the present study was to clarify certain aspects concerned with anesthetic and ventilatory techniques, mostly in connection with the comparison between the effects of insufflation of either carbon dioxide or nitrous oxide. Anesthesia included ventilation with a volume controlled ventilator in curarised patients. Respiratory volumes were calculated according to the patient's body area. The results show a sharp rise in PaCO2 and a fall in pH after intraperitoneal insufflation with carbon dioxide, while no changes were observed when nitrous oxide was used. The clinical consequences of these findings are discussed.

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The refinement of techniques for extremity surgery makes it urgent to get more information at cell level of the effects of tourniquet times exceeding the usually accepted 90--120 min. Therefore, in the present experiments, the cellular metabolic and functional restitution of canine skeletal muscle after 3 h of complete tourniquet ischemia was studied. During the ischemia and after recirculation, repeated skeletal muscle samples were taken for ATP, CP and lactate analyses. At the same time periods, blood from a regional vein and vena cava was drawn for pH, pyruvate and lactate analyses. Cellular function was evaluated from repeated measurements of transmembrane potentials. The tourniquet ischemia resulted in a rapid decrease of CP to 40% of the initial level within 1 h and a continuous decrease of ATP. The lactate levels increased continuously. The transmembrane potentials decreased from an initial level of --90 to --54 mV. The release of the tourniquet resulted in a hyperemic reaction and a rapid regain of tissue CP and ATP levels within 5 min of recirculation. There was a continuous washout of lactate up to about 1 h after the release and the transmembrane potentials were normalized after about the same time period. The latter parameters indicate that areas of no-reflow persisted for up to 1 h after restored circulation. The results indicate that after a 3-hour tourniquet ischema, the cellular energy metabolism as well as the membrane function are completely normalized after about 1 h of recirculation.

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The relevance of two direct techniques for monitoring of cellular function during tissue hypoxia has been evaluated. Tissue pH and cellular transmembrane potentials were registered in canine skeletal muscle during intestinal exteriorization shock and during prolonged local tourniquet ischemia. The obtained pH and transmembrane potential changes were correlated to simultaneous changes in high-energy phosphagen (ATP + CP) and lactate levels in skeletal muscle. In control dogs no significant changes in either of the studied variables occurred. Intestinal exteriorization shock as well as local tourniquet ischemia resulted in a gradual increase in tissue lactate and a concomitant decrease in tissue pH and transmembrane potentials. In both experimental situations there was a close correlation between the transmembrane potential reduction and the tissue lactate increase. Tissue pH registrations, on the other hand, did not similarly reveal the full extent of the tissue lactate increase under the two experimental conditions. Possible reasons for this discrepancy are discussed. On the basis of the present results it may therefore be concluded that the transmembrane potential seems to be a better variable for revealing the full extent of cellular metabolic deterioration during various situations with tissue hypoxia.

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