Extreme Hyperkalaemia Caused by Concomitant use of a Nsaid and an Ace Inhibitor in an Elderly Patient

Abstract

Extreme hyperkalaemia is a life-threatening electrolyte disorder. It is relatively common in patients with severe renal insuffi ciency. This report describes a case of extreme hyperkalaemia caused by drugs in an 82-year-old female patient without severe renal insuffi ciency, who was successfully treated without haemodialysis. The patient had been treated for arterial hypertension and type 2 diabetes mellitus for 30 years. Over the last years she had been receiving enalapril and metformin. Three weeks before the admission to the hospital, she was receiving a non-steroidal anti-infl ammatory drug (NSAID) because of the back pain. She was admitted to hospital due to a collapse and weakness in the limbs. Laboratory tests showed extreme hyperkalaemia, high blood sugar, metabolic acidosis, elevated serum creatinine and blood urea nitrogen (BUN), and a slightly elevated serum sodium. On ECG, we noticed typical signs of hyperkalaemia. The patient was treated with a slow intravenous bolus of calcium gluconate and intravenous infusion of sodium chloride with insulin, glucose with insulin and sodium bicarbonte. After the treatment, all laboratory fi ndings normalised together and the patient felt better. This case shows that physicians should be very careful when prescribing NSAIDs to elderly patients treated with drugs that affect renal function.

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“…Combinations of two or more NSAIDs may increase the risk of stomach bleeding [19], the combination of diuretics with NSAIDs increases the risk of nephrotoxicity due to volume depletion, and NSAIDs combined with angiotensin-converting enzyme (ACE) inhibitors can cause or increase the risk of acute renal failure and hyperkalemia, especially in geriatrics and dehydrated patients [11,20,21]. ACE inhibitors decrease synthesis of angiotensin II, causing dilation of the efferent arteriole (blood vessels that exit from the glomerulus), thereby reducing the glomerular capillary hydrostatic pressure necessary to reduce glomerular ultrafiltration.…”