Severe Acute Pancreatitis In Patients Research Articles

The Panc 3 Score

The goal of our study was to develop a simple rule that could rapidly identify those at risk for severe acute pancreatitis (SAP) in the ER. We identified all published studies reporting risk factors for SAP. We identified 3 risk factors which had been shown to predict SAP. The risk factors we identified were a serum hematocrit greater than 44 mg/dL, a body mass index (BMI) greater than 30 mg/kg, and a chest x-ray which reveals a pleural effusion (Panc 3 criteria). We computed the test-operating characteristics and likelihood ratios for each risk factor using the patients originally sampled in each of the studies (n=393). For validation, we examined Panc 3's ability to predict SAP in patients seen at our medical center [University of North Carolina at Chapel Hill (UNC) hospitals n=238]. The likelihood ratios positive and negative for HCT, BMI>30 kg/M, and a chest x-ray with a pleural effusion were 14, 9.8, and 8.7, respectively, for the original data and 178, 2.4, and 1.3 for the UNC data. Sensitivity analysis revealed satisfaction of the HCT, BMI, and pleural effusion criteria had a posttest likelihood of disease 99% when the pretest probability of disease varied from 12-25%. These values were true for the original and UNC data. The Panc 3 score is easy to use and accurate for the prediction of SAP. The serum HCT was the strongest predictor of SAP. The combination of the Panc 3 variables was highly predictive of SAP.

Strategic management of severe acute pancreatitis in the Jehovah's witness

Haemorrhage can be a lethal complication of severe acute pancreatitis. Management includes identification and control of the source of bleeding and supportive therapy such as blood transfusion. Individuals who refuse transfusion on the grounds of religious belief can provide a further major challenge. The management in these individuals can be focused from the outset with a strategy that aims to avert anaemia and transfusion. This article reports a case of severe acute pancreatitis in a woman of the Jehovah's Witness faith. The episode was complicated by infected pancreatic necrosis requiring surgical intervention. Careful strategic planning is critical to the management of severe acute pancreatitis in patients of the Jehovah's Witness faith. In this case, acute pancreatitis complicated by infected necrosis was successfully managed by the use of preoperative erythropoietin, venesection using paediatric blood vials, meticulous intraoperative attention to haemostasis and the use of adjunctive intraoperative techniques such as argon diathermy.

Efficacy of continuous regional arterial infusion of a protease inhibitor and antibiotic for severe acute pancreatitis in patients admitted to an intensive care unit.

To investigate the efficacy of continuous regional arterial infusion (CRAI) of a protease inhibitor and antibiotic for severe acute pancreatitis (SAP) in patients admitted to an intensive care unit (ICU). A total of 51 patients with SAP requiring admission to an ICU were studied. The patients were divided into two groups: one received the protease inhibitor nafamostat mesylate and the antibiotic imipenem by continuous regional arterial infusion (CRAI group) and the other received protease inhibitors and antibiotics by intravenous infusion (non-CRAI group). To evaluate the therapeutic usefulness of CRAI of a protease inhibitor and antibiotic for SAP, the rate of surgery and the cumulative survival rate were compared between the non-CRAI group and the CRAI group. The rate of surgery was 32% in the non-CRAI group and 9% in the CRAI group (P = 0.08). Cumulative survival rates at 1, 6, and 12 months were 77.9%, 48.9%, and 48.9% in the non-CRAI group compared with 100.0%, 100.0%, and 87.1% in the CRAI group. Outcome was thus significantly better in the CRAI group than in the non-CRAI group (P = 0.002). CRAI of a protease inhibitor and antibiotic may decrease the need for surgical therapy and reduce mortality in patients with SAP.

Proteinuria y microglobulina β2 urinaria, como marcadores de lesión tubular renal, en la valoración de la gravedad de la pancreatitis aguda

Proteinuria is a common finding in acute pancreatitis (AP). Increased urinary beta 2-microglobulin can be explained by renal tubular malfunction induced by substances released from the pancreas. The degree of renal tubular malfunction may reflect the severity of AP. To assess proteinuria and urinary beta 2-microglobulin as prognostic factors in AP. We retrospectively studied patients with AP with symptom onset within 24 hours before admission. Random urine specimens were obtained on days 1, 2 and 3 after admission. In a subgroup of 25 patients, urine samples could be obtained within 24 hours of symptom onset on day 1. The severity of AP was established using the Atlanta criteria. Proteinuria and beta 2-microglobulin were determined and were adjusted by urinary creatinine concentrations. We studied 51 patients with AP (26 men and 25 women; age: 59.6 (+/-16.7 years). Fifteen cases of AP were severe and 36 were mild. The most frequent etiology was gallstones (60.1%). Levels of proteinuria were (median and interquartile range) in mg/g creatinine: day 1: 180.5 (84.0-250.9), day 2: 164.3 (16.7-421.7), and day 3: 136.7 (24.0-371.29). Differences between severe and mild AP were significant on day 2 of admission: 339.7 (191.7-471.8) versus 120,1 (11.0-382.6); p = 0.04. Levels of urinary beta 2-microglobulin in AP on days 1 to 3 postadmission were: 9.7 (1.1-93.3), 27.6 (4.7-421.4) and 88.3 (7.3-415.2) microg/mg of creatinine, respectively. When urinary beta 2-microglobulin was compared between severe and mild AP, no significant differences were found among days 1, 2 and 3. Selection of only the subgroup of patients whose urine samples were obtained within 24 h of symptom onset, did not improve the results of these urine markers for the group as a whole. 1) Proteinuria was slightly increased in severe AP and was able to discriminate between mild and severe episodes on day 2 of admission. 2) Urinary beta 2-microglobulin as a tubular malfunction marker did not discriminate between mild and severe AP in patients in our study.

Tissue kallikrein in severe acute pancreatitis in patients treated with high-dose intraperitoneal aprotinin.

The activation of the kallikrein-kinin system is thought to be one of the pathophysiologic mechanisms in acute pancreatitis. A radioimmunoassay for human urinary tissue kallikrein was developed and used to measure tissue kallikrein peritoneal exudate and plasma from 48 patients with severe acute pancreatitis. All patients were treated with intraperitoneal lavage. One group (n = 22) received high doses of the protease inhibitor aprotinin (aprotinin group), and the other group, saline (control group). Levels of kallistatin in peritoneal exudates and plasma were measured with an enzyme immunoassay. A large increase in tissue kallikrein was observed in the peritoneal exudate, which declined in both groups after multiple lavages. Complexing of liberated tissue kallikrein with kallistatin was evidenced by gel filtration in both peritoneal exudates and plasma in both groups. The decrease in kallistatin observed in both peritoneal exudate and plasma is therefore regarded as being due not only to repeated lavage, but also to true consumption of the binding protein. Some of the liberated tissue kallikrein in the peritoneal fluid and plasma was complexed to aprotinin. In the control group, six patients were operated on because of pancreatic necrosis, compared with none in the aprotinin group. The levels of tissue kallikrein in the lavage fluid were lower in the control group, but this was the result of the very low tissue kallikrein values in the six patients operated on for pancreatic necrosis. Levels of kallistatin in plasma and peritoneal exudate in these six patients were lower on the day of admission compared with the other patients, and the plasma levels continued to be lower during the first week. Large amounts of tissue kallikrein were found to be released into the peritoneal exudates in acute pancreatitis. Lavages effectively cleared the released tissue kallikrein. The tissue kallikrein was complexed to kallistatin, whereas in the aprotinin group, also to aprotinin both in plasma and in peritoneal fluid. The partitioning of kallikrein between the two inhibitors was the result of the interaction between enzyme and inhibitors and the turnover of the complexes formed. The low admission levels of kallistatin in the six patients operated on because of pancreatic necrosis suggest that kallistatin may act as an early marker of severity in acute pancreatitis.

Prevalence and predictors of severe acute pancreatitis in patients with acquired immune deficiency syndrome (AIDS).

Recent case control data suggested that a severe course of acute pancreatitis in HIV+ patients was 1) common (50% of cases), 2) poorly predicted by Ranson's criteria (sensitivity 41%), and 3) accurately predicted by a diagnosis of AIDS (positive predictive value 67%). However, the definition of severity included length of stay in hospital and excluded commonly accepted markers (local complications, systemic complications, and need for surgery). The aim of this study was to determine 1) the prevalence of severity and 2) the value of these predictors with regard to severity, as defined by commonly accepted standardized criteria in patients with AIDS and acute pancreatitis. A retrospective review identified 50 patients with AIDS exhibiting clinical, laboratory, and/or radiological features of acute pancreatitis. Only five patients followed a severe course as defined by accepted markers. Of these patients, 29 had values available for at least nine of 11 of Ranson's criteria (sensitivity 80%, specificity 54%). Points were awarded most commonly for decreased serum Ca2+ (n = 14) and elevated serum LDH (n = 7). In patients with AIDS and acute pancreatitis at our institutions, 1) the prevalence of severity and 2) the sensitivity of Ranson's criteria with regard to severity is comparable to that reported in large historical case series of immunocompetent patients. Pseudohypocalcemia and/or elevation in LDH are frequent, likely due to the catabolic infectious disease state.

Prevalence and predictors of severe acute pancreatitis in patients with acquired immune deficiency syndrome (AIDS)

OBJECTIVE: Recent case control data suggested that a severe course of acute pancreatitis in HIV+ patients was 1) common (50% of cases), 2) poorly predicted by Ranson’s criteria (sensitivity 41%), and 3) accurately predicted by a diagnosis of AIDS (positive predictive value 67%). However, the definition of severity included length of stay in hospital and excluded commonly accepted markers (local complications, systemic complications, and need for surgery). The aim of this study was to determine 1) the prevalence of severity and 2) the value of these predictors with regard to severity, as defined by commonly accepted standardized criteria in patients with AIDS and acute pancreatitis. METHODS: A retrospective review identified 50 patients with AIDS exhibiting clinical, laboratory, and/or radiological features of acute pancreatitis. RESULTS: Only five patients followed a severe course as defined by accepted markers. Of these patients, 29 had values available for at least nine of 11 of Ranson’s criteria (sensitivity 80%, specificity 54%). Points were awarded most commonly for decreased serum Ca 2+ (n = 14) and elevated serum LDH (n = 7). CONCLUSIONS: In patients with AIDS and acute pancreatitis at our institutions, 1) the prevalence of severity and 2) the sensitivity of Ranson’s criteria with regard to severity is comparable to that reported in large historical case series of immunocompetent patients. Pseudohypocalcemia and/or elevation in LDH are frequent, likely due to the catabolic infectious disease state.