Hemodynamically unstable: accidental atenolol toxicity?

Antihypertensive medications, including β-blockers, are widely used in patients with chronic kidney disease. Unlike most β-blockers, atenolol is excreted primarily by the kidney, and its clearance by peritoneal dialysis is poor. These pharmacokinetic factors may predispose patients to gradual accumulation of the drug over time.

To review the management of a diagnostic dilemma, the role of glucagon therapy, and the clinical implications of atenolol clearance.

A young woman with end-stage renal disease requiring peritoneal dialysis presented with sudden onset of abdominal pain and hemodynamic instability with hypotension and relative bradycardia. The patient reported that she took her regular four antihypertensive agents, including atenolol, with no excess ingestion or recent dose changes. After resuscitation and consideration of a broad differential diagnosis, the most likely cause of the patient's illness was determined to be unintentional atenolol toxicity, with secondary mesenteric ischemia due to a low-flow state that caused her abdominal pain. Glucagon therapy led to rapid correction of the patient's hemodynamic instability and pain.

The unique pharmacokinetics of long-term medications must be considered in patients with impaired clearance, such as this patient with end-stage renal disease treated by peritoneal dialysis. Medications may gradually accumulate to supratherapeutic levels, which over time may lead to symptoms of significant toxicity.