Cardiovascular changes after induction of anaesthesia.
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Biomedical subjects
Publications and source records attributed to J Harten.
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BACKGROUND: Emergency abdominal surgery carries considerable postoperative morbidity and mortality. Hypovolaemia is considered to be a cause of renal hypoperfusion, which is associated with a decreased clearance of serum urea and creatinine. This study examines whether the perioperative serum urea and creatinine concentrations are predictors of mortality in patients undergoing emergency abdominal surgery. METHODS: Consecutive patients (n=300) who underwent emergency abdominal surgery were studied. Age- and sex-specific reference intervals were used for the data analysis. Patients with incomplete biochemical (n=51) or mortality data (n=31) or with pre-existing renal failure (n=9) were excluded from the analysis. RESULTS: 209 patients were analysed, of whom 162 (78%) remained alive and 47 (22%) died following surgery. The non-survivors were older (P<0.05), had undergone more extensive surgery (P<0.001) and were more likely to have been admitted to the intensive care unit (P<0.001). The serum urea concentration was higher preoperatively (P<0.05) and on day one postoperatively (P<0.001) in the non-survivors. On multivariate logistic regression analysis, age (odds ratio [OR] 3.27, 95% confidence interval [CI] 1.43-7.47, P<0.005), severity of surgery (OR 2.21, 95% CI 1.14-4.29, P<0.019), admission to intensive care (OR 0.54, 95% CI 0.11-0.54, P<0.001), seniority of anaesthetist (OR 0.50, 95% CI 0.27-0.90, P<0.022) and day one urea (OR 3.33, 95% CI 1.39-7.99, P<0.007) were independently associated with 30-day mortality. CONCLUSIONS: These results indicate that an increased serum urea concentration, but not serum creatinine concentration, in the postoperative period is associated with an increase in 30-day mortality in patients undergoing emergency abdominal surgery.
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We have studied the intubating conditions in 60 ASA I or II patients, after induction of anaesthesia with propofol 2 mg kg-1, allocated to one of the following three groups: group 1, remifentanil 1 microgram kg-1; group 2, remifentanil 1 microgram kg-1 and lignocaine 1 mg kg-1; group 3, remifentanil 2 micrograms kg-1. No neuromuscular blocking agents were administered. Intubating conditions were assessed using a four-point scoring system based on ease of laryngoscopy, jaw relaxation, position of vocal cords, degree of coughing and limb movement. Overall intubating conditions were acceptable in 35% of patients in group 1, 100% of patients in group 2 and 85% of patients in group 3. There was a statistically significant drop in blood pressure after induction in groups 2 and 3, and two patients in each group required ephedrine 6 mg i.v. boluses, as dictated by the intervention criteria (mean arterial pressure fall > 25% from baseline). Similarly, there was a drop in heart rate in groups 2 and 3, but this did not reach statistical or clinical significance, and no patient required atropine.
A 51-year-old man, known to have chronic-aggressive hepatitis B, HIV infection and exertional dyspnoea, was hospitalized because of acute physical deterioration, cough with whitish exudate and dyspnoea at rest. Despite a CD4/CD8 ratio of 0.16 no prophylactic measures against Pneumocystis carinii had been taken. On examination the lungs were unremarkable, but the liver was enlarged and there were petechiae over all parts of the body. Laboratory tests showed impaired liver functions and a rise in lactate dehydrogenase activity (538 U/l). Chest radiogram demonstrated small to very small infiltrates in the lung. As Pneumocystis carinii pneumonia was suspected but bronchoscopy was too risky, he was at first treated with trimethoprim/sulphamethoxazole (four times 320/1600 mg/24 h intravenously). When this failed, he received pentamidine (4 mg/kg, after 4 days 2 mg/kg intravenously), and finally cefotiam (twice 2 g daily), tobramycin (three times 40 mg daily) and corticoids (100 mg). Despite this treatment he died after 10 days from respiratory failure. Autopsy revealed interstitial pneumonia throughout the lung as well as focal mucor infiltrations in the wall of middle-calibre lung veins. Mucor is a ubiquitous, facultatively pathogenic mold fungus.