In-hospital observation with repeated clinical examinations is commonly used in patients with an equivocal diagnosis of appendicitis. It is not known if repeated measurements of temperature and laboratory examinations have any diagnostic importance in this situation. The importance of repeated measurements of the body temperature, white blood cell (WBC) and differential cell counts, C-reactive protein concentration (CRP) and of the surgeon's repeated assessments was prospectively analyzed in 420 patients with an equivocal diagnosis of appendicitis at admission who were reexamined after a median of 6 hours of observation. The final diagnosis was appendicitis in 137 patients. After observation the inflammatory response was increasing among patients with appendicitis and decreasing among patients without appendicitis. The variables discriminating power for appendicitis consequently increased, from an area under the receiver operating characteristic (ROC) curve of 0.56 to 0.77 at admission, to 0.75 to 0.85 after observation. The ROC area of the surgeons' clinical assessment increased from 0.69 to 0.89. The WBC and differential cell counts were the best discriminators at the repeat examination. The change in the variables between the observations had weak discriminating power and had no additional importance in addition to the actual level at the repeat examination. To conclude, the diagnostic information of the temperature and laboratory examinations increased after observation. Repeated controls of the body temperature and laboratory examinations are therefore useful in the management of patients with equivocal signs of appendicitis, but the result of the examinations must be integrated with the clinical assessment.

Background/Purpose Continuous inflow vascular occlusion during liver resections causes less severe ischemia and reperfusion injury (IRI) if it is preceded by ischemic preconditioning (IP) or if intermittent inflow occlusion is used during the resection. No previous clinical trial has studied the effects of adding IP to intermittent inflow occlusion. Methods Consecutive patients (n = 32) with suspicion of malignant liver disease had liver resections (minimum 2 segments) performed with inflow occlusion (intermittent clamping in a manner of 15 min of ischemia and 5 min of reperfusion repetitively; 15/5). Half of the patients were randomized to receive IP (10 min of ischemia and 10 min of reperfusion before parenchymal transection; 10/10). The patients were stratified according to volume of resection and none had chronic liver disease. The patients were followed for 5 days with microdialysis (μD). Results All patients completed the study and there were no deaths. No differences were seen between the groups regarding demographics or perioperative parameters (bleeding, duration of ischemia, resection volume, complications, and serum laboratory tests). There were no differences in alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin, or prothrombin time (PT)‐INR levels, but μD revealed lower levels of lactate, pyruvate, and glucose in the IP group having major liver resections (analysis of variance; ANOVA). Nitrite and nitrate levels in μD decreased postoperatively, but no differences were seen between the groups. In one patient an elevated μD–glycerol curve was seen before the diagnosis of a stroke was made. Conclusions IP before intermittent vascular occlusion does not reduce the serum parameters used to assess IRI. IP seems to improve aerobic glucose metabolism, as the levels of glucose, pyruvate, and lactate locally in the liver were reduced, compared to controls, in patients having >3 segments resected. μD may be used to monitor metabolism locally.

Intraabdominal postoperative or posttraumatic infections remain a major threat to life in spite of generation after generation of increasingly effective antimicrobial drugs indicating the importance of immunological host defense failure following major trauma or surgical complications. The spectrum of infectious postoperative or posttraumatic complications can, in part, be explained by pathogenic factors inherent to the methodology of modern surgical intensive care and techniques. This report presents a survey of the historical background as well as current concepts of the multiple systems organ failure syndrome as related to postoperative or posttraumatic intraabdominal infectious complications. The pathophysiology of nosocomial infectious complications in the intensive care unit setting is analyzed. The concept of "gut origin sepsis" is presented and possible preventive and therapeutic actions discussed. A judicious use of antimicrobial drugs on strict indications is emphasized as is the importance of increased knowledge of the interactions between the gut flora, antibiotics, and absence of enteral nutrition.

Sepsis with subsequent multiple organ failure is the commonest complication seen in the surgical intensive care unit today. A gut mucosal barrier dysfunction is assuming an increasingly important role as one possible explanation for the initiation of the septic process. It is known that the gut bacteria and endotoxins can, in the presence of a seemingly intact epithelium, translocate to extraintestinal sites, but the exact mechanism behind this process is not understood. In the present study we have approached this problem by testing the gut permeability to two macromolecules, bovine serum albumin (BSA) and fluorescein isothiocyanate (FITC)-dextran, after 7 days of enteral or parenteral nutrition in the rat. The plasma values of FITC-dextran after 4 h of marker feeding showed a significant increase in gut permeability after parenteral but not after enteral nutrition as compared with the controls. The plasma values of BSA, however, did not show any significant change in any of the groups. Thus, parenteral nutrition, with the changes occurring in the gut mucosa, may be one of the etiologic co-factors behind a gut mucosal barrier dysfunction, eventually leading to absorption of noxious agents into the systemic circulation with subsequent multiple organ failure.

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