Objective: To determine the accuracy of BISAP score in comparison with Ranson’s score in detection of severe acute pancreatitis. Methods: This cross sectional study was performed in Emergency department and Surgery department of Dow university hospital from January 2015 to December 2015. A total of 206 patients were included. Those diagnosed with acute pancreatitis on the basis of epigastric pain, serum amylase levels more than 300 (more than 3 times normal) and meeting the inclusion criteria were subjected to investigations for Ranson’s and BISAP scoring. BISAP score was calculated at 24 hours and Ranson’s score both at 24 and 48 hours. A score of > 3 was used to label severe acute pancreatitis according to both scoring systems. Results: In our study accuracy to predict SAP by BISAP score was 76.2 % and Ranson’s score was 82.2%. On the basis of sensitivity, Ranson’s scores predicted SAP more accurately than BISAP scores (97.4% vs. 69.2%). Regarding specificity, both scores predicted SAP almost equally (78.4% vs. 77.8%). Conclusion: BISAP score is a valuable tool in predicting severe Acute Pancreatitis in early hours. doi: https://doi.org/10.12669/pjms.35.4.1286 How to cite this:Arif A, Jaleel F, Rashid K. Accuracy of BISAP score in prediction of severe acute pancreatitis. Pak J Med Sci. 2019;35(4):---------.  doi: https://doi.org/10.12669/pjms.35.4.1286 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This is the largest study to date comparing the effects of desflurane and isoflurane on patients undergoing craniotomy for supratentorial mass lesion with evidence of midline shift or edema. Neither desflurane nor isoflurane significantly altered lumbar cerebrospinal fluid pressure when moderate hypocapnia was maintained.

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The effects of Gö-6976, a Ca(2+)-dependent protein kinase C (PKC) isozyme inhibitor, and rottlerin, a PKC-delta isozyme/calmodulin (CaM)-dependent kinase III inhibitor, on responses to vasopressor agents were investigated in the feline pulmonary vascular bed. Injections of angiotensin II, norepinephrine (NE), serotonin, BAY K 8644, and U-46619 into the lobar arterial constant blood flow perfusion circuit caused increases in pressure. Gö-6976 reduced responses to angiotensin II; however, it did not alter responses to serotonin, NE, or U-46619, whereas Gö-6976 enhanced BAY K 8644 responses. Rottlerin reduced responses to angiotensin II and NE, did not alter responses to serotonin or U-46619, and enhanced responses to BAY K 8644. Immunohistochemistry of feline pulmonary arterial smooth muscle cells demonstrated localization of PKC-alpha and -delta isozymes in response to phorbol 12-myristate 13-acetate and angiotensin II. Localization of PKC-alpha and -delta isozymes decreased with administration of Gö-6976 and rottlerin, respectively. These data suggest that activation of Ca(2+)-dependent PKC isozymes and Ca(2+)-independent PKC-delta isozyme/CaM-dependent kinase III mediate angiotensin II responses. These data further suggest that Ca(2+)-independent PKC-delta isozyme/CaM-dependent kinase III mediate responses to NE. A rottlerin- or Gö-6976-sensitive mechanism is not involved in mediating responses to serotonin and U-46619, but these PKC isozyme inhibitors enhanced BAY K 8644 responses in the feline pulmonary vascular bed.