Table of Contents Author Guidelines Submit a Manuscript
Case Reports in Anesthesiology
Volume 2018, Article ID 1852016, 4 pages
Case Report

Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us?

Department of Anaesthesia and Intensive Care Medicine, Tallaght University Hospital (Adelaide and Meath Incorporating National Children’s Hospital), Ireland

Correspondence should be addressed to Ahmed Abdelaal Ahmed Mahmoud; moc.liamg@duomhamlaaledbademha.rd

Received 29 January 2018; Revised 1 June 2018; Accepted 19 June 2018; Published 9 July 2018

Academic Editor: Stefano Faenza

Copyright © 2018 Ahmed Abdelaal Ahmed Mahmoud et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The current case report represents a warning against serious hyperkalaemia and acidosis induced by ACE-I during surgical stress while normal renal function could deceive the attending anaesthetist. Arterial gas analysis for follow-up of haemoglobin loss accidentally discovered hyperkalaemia and acidosis. Glucose-insulin and furosemide successfully corrected hyperkalaemia after 25 minutes and acidosis after 3 hours. These complications could be explained by a deficient steroid stress response to surgery secondary to suppression by ACE-I. Event analysis and database search found that ACE-I induced aldosterone deficiency aggravated by surgical stress response with an inadequate increase in aldosterone secretion due to angiotensin II deficiency as a sequel of ACE-I leading to defective secretion of H+ and K+. Furosemide is recommended to secrete H+ and K+ compensating for aldosterone deficiency in addition to other antihyperkalaemia measures. Anaesthetising an ACE-I treated patient requires considering ACE-I as a potential cause of hyperkalaemia and acidosis.