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

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.