Hypothesis: Intra-abdominal hypertension exerts an effect on renal function independent of other confounding variables. Design: A prospective study of all patients admitted to an intensive care unit following abdominal surgery was undertaken between September 1, 1994, and July 31, 1997, in a single university hospital. Main Outcome Measures: Intra-abdominal pressure (IAP) was measured every 8 hours (normal IAP, 0-17 mm Hg); 18 mm Hg or higher was considered increased. Forward stepwise logistic regression determined whether intra-abdominal hypertension is an independent cause of renal impairment. Results: A total of 263 patients (174 after emergency surgery), whose mean ± SD age was 61.0 ± 18.7 years and Acute Physiology and Chronic Health Evaluation II score was 14.6 ± 7.7, were studied. Intra-abdominal pressure was increased in 107 (40.7%) of the 263 patients. Renal impairment occurred in 35 (32.7%) of the 107 patients with intra-abdominal hypertension and in 22 (14.1%) of the 156 with a normal IAP (odds ratio, 1.62-5.42). Using the Wald maximizing model, renal impairment was independently associated with 4 antecedent factors: hypotension (P = .09), sepsis (P = .006), age older than 60 years (P = .03), and increased IAP (P = .004). Conclusions: To our knowledge, for the first time in a large clinical study, IAP has been shown to be an independent cause of renal impairment, and it ranks in importance after hypotension, sepsis, and age older than 60 years. Surgeons need to be aware of the importance of intra-abdominal hypertension in patients postoperatively.

This study was designed to establish if clinical examination can accurately predict intraabdominal pressure (IAP). Between August 1998 and March 2000 a prospective blinded observational study of postoperative intensive care unit patients was undertaken at a major trauma center. IAP was measured using an intravesicular technique and compared with clinical evaluation. An IAP of at least 18 mmHg was considered elevated. The sensitivity, specificity, positive predicative value (ppv), negative predictive value (npv), kappa score, and reliability analysis were calculated. A total of 110 patients provided 150 estimates of IAP, which was elevated in 21%. The kappa score was 0.37; sensitivity, 60.9%; specificity, 80.5%; ppv, 45.2%; npv, 88.6%. The mean difference in IAP values between intravesicular readings and clinical estimates was -1.0 +/- 4.1. Prediction of IAP using clinical examination is not accurate enough to replace intravesicular IAP measurements.

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This study evaluated the potential association between increased intraabdominal pressure (IAP) and abnormally low gastric intramucosal pH (pHi) (/= 20 mmHg and a pHi of

This study prospectively analyzed outcomes in 49 consecutive patients undergoing temporary abdominal closure (TAC) between 1993 and 1996 at a single university hospital. There were 37 males and 12 females, mean age was 57 years (range, 25-79 years), mean Acute Physiology and Chronic Health Evaluation score was 27 (+7.8 SD), and mean Simplified Acute Physiology II score was 53.0 (+/-15.4). The reason for TAC was decompression in 22 patients, inability to close the abdomen in 10 patients, to facilitate reexploration for sepsis in 8 patients, and multifactorial in 9 patients. After TAC, there was a significant reduction in intra-abdominal pressure from 24.2+/-9.3 to 14.1+/-5.5 mm Hg and improvement in lung dynamic compliance from 24.1+/-7.9 to 27.6+/-9.4 mL/cm H2O (p < 0.05). Although 10 patients experienced brisk diuresis, there was no significant improvement in renal function; in fact, serum creatinine increased. The median length of stay was 35 days (range, 1-232 days). The mean number of abdominal operations after mesh insertion was 2.6+/-2.4. There were 21 deaths, for a standardized mortality rate of 0.80. Although it achieved significant reductions in abdominal pressures and improved lung dynamic compliance, TAC did not result in improved renal function or patient oxygenation.

Two patients with presumed impending cortical necrosis, after haemolytic uraemic syndrome in one and after Guy's Hospital, London SEI 9RT F E JONES, MRCP, DCH, senior house officer (paediatrics)

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