Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us?
Ahmed Abdelaal Ahmed Mahmoud M AlkhatipMark CampbellMargarita BlajevaPublished in: Case reports in anesthesiology (2018)
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.
Keyphrases
- angiotensin ii
- angiotensin converting enzyme
- vascular smooth muscle cells
- case report
- type diabetes
- risk factors
- emergency department
- coronary artery disease
- insulin resistance
- stress induced
- adipose tissue
- replacement therapy
- climate change
- acute coronary syndrome
- atrial fibrillation
- tertiary care
- skeletal muscle
- room temperature
- drug induced
- newly diagnosed