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

Area of Science:

• Anesthesiology
• Nephrology
• Endocrinology

Background:

• Angiotensin-converting enzyme inhibitors (ACE-I) are commonly prescribed medications.
• Surgical stress can trigger physiological responses, including hormonal changes.
• Normal renal function may mask underlying metabolic disturbances in patients on ACE-I.

Observation:

• A case report highlights serious hyperkalemia and acidosis in a patient on ACE-I during surgical stress.
• Arterial blood gas analysis, initially for hemoglobin loss, unexpectedly revealed these metabolic abnormalities.
• The patient's normal renal function initially obscured the severity of the condition.

Findings:

• Hyperkalemia and acidosis were successfully treated with glucose-insulin and furosemide.
• These complications are attributed to a deficient steroid stress response secondary to ACE-I, leading to aldosterone deficiency.
• ACE-I-induced angiotensin II deficiency impairs the secretion of H+ and K+ during surgical stress.

Implications:

• Anesthetizing patients on ACE-I requires vigilance for potential hyperkalemia and acidosis.
• Furosemide can aid in secreting H+ and K+, compensating for aldosterone deficiency.
• This case underscores the importance of considering ACE-I as a potential cause of metabolic derangements in surgical patients.