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 acid...
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2018-01-01
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Series: | Case Reports in Anesthesiology |
Online Access: | http://dx.doi.org/10.1155/2018/1852016 |
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doaj-4c030361ac7947ab98736a876fc104782020-11-24T20:45:57ZengHindawi LimitedCase Reports in Anesthesiology2090-63822090-63902018-01-01201810.1155/2018/18520161852016Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us?Ahmed Abdelaal Ahmed Mahmoud0Mark Campbell1Margarita Blajeva2Department of Anaesthesia and Intensive Care Medicine, Tallaght University Hospital (Adelaide and Meath Incorporating National Children’s Hospital), IrelandDepartment of Anaesthesia and Intensive Care Medicine, Tallaght University Hospital (Adelaide and Meath Incorporating National Children’s Hospital), IrelandDepartment of Anaesthesia and Intensive Care Medicine, Tallaght University Hospital (Adelaide and Meath Incorporating National Children’s Hospital), IrelandThe 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.http://dx.doi.org/10.1155/2018/1852016 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ahmed Abdelaal Ahmed Mahmoud Mark Campbell Margarita Blajeva |
spellingShingle |
Ahmed Abdelaal Ahmed Mahmoud Mark Campbell Margarita Blajeva Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us? Case Reports in Anesthesiology |
author_facet |
Ahmed Abdelaal Ahmed Mahmoud Mark Campbell Margarita Blajeva |
author_sort |
Ahmed Abdelaal Ahmed Mahmoud |
title |
Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us? |
title_short |
Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us? |
title_full |
Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us? |
title_fullStr |
Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us? |
title_full_unstemmed |
Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us? |
title_sort |
can ace-i be a silent killer while normal renal functions falsely secure us? |
publisher |
Hindawi Limited |
series |
Case Reports in Anesthesiology |
issn |
2090-6382 2090-6390 |
publishDate |
2018-01-01 |
description |
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. |
url |
http://dx.doi.org/10.1155/2018/1852016 |
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