Kidney Week

Abstract: PUB258

Respiratory Acidosis in Salicylate Toxicity: An Unusual Initial Presentation

Session Information

• Publication Only

Category: Fluid, Electrolytes, and Acid-Base Disorders

• 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

• Chang, Hoon, Renal, Electrolyte and Hypertension Division, University of Pennsylvania, Philadelphia, Pennsylvania, United States

Hoon Chang, MD

• Kwok, Jonas, Renal, Electrolyte and Hypertension Division, University of Pennsylvania, Philadelphia, Pennsylvania, United States

Jonas Kwok, MD

• Brotman, Christina HW, Renal, Electrolyte and Hypertension Division, University of Pennsylvania, Philadelphia, Pennsylvania, United States

Christina HW Brotman, MD, MSCE

Introduction

Salicylate toxicity is classically associated with mixed respiratory alkalosis and increased anion-gap metabolic acidosis. We present a case of primary respiratory acidosis in a patient with severe salicylate toxicity.

Case Description

A 59-year-old female with major depressive disorder on sertraline and quetiapine presented to the emergency room after being found unconscious next to an empty bottle of aspirin. Upon arrival, she was hypotensive with blood pressure of 83/71 mmHg and tachycardic with a heart rate of 115 bpm, and had a Glasgow Coma Score of 7. Initial laboratory data were notable for creatinine of 0.76 mg/dL, serum bicarbonate of 14 mmol/L, and phosphorus of 6.7 mg/dL. Venous blood gas showed a pH of 7.26 and pCO2 of 49 mmHg. Salicylate level was 115 mg/dL, with the urine toxicology screen otherwise negative. Due to a witnessed seizure, she was intubated for airway protection. Subsequent arterial blood gas revealed a pH of 7.15, pCO2 of 85 mmHg, bicarbonate of 21.4 mmol/L, and a lactic acid level of 1.7 mmol/L. She was initiated on a continuous bicarbonate infusion, underwent placement of a non-tunneled dialysis catheter, and started on intermittent hemodialysis. The repeat salicylate level was 38.1 mg/dL, and she was transitioned to continuous kidney replacement therapy due to worsening vasodilatory shock and concerns for early cerebral edema based on head imaging.

Discussion

The traditional acid-base disturbance associated with salicylate toxicity is the co-occurrence of metabolic acidosis from increased anaerobic metabolism and respiratory alkalosis from hyperventilation due to direct stimulation of the respiratory centers within the cerebral medulla. Respiratory acidosis is typically considered in cases of co-ingestion and is a rare presentation of isolated salicylate ingestion. However, it is important to recognize that hypoventilation is a late or severe manifestation of salicylate toxicity and is a harbinger of respiratory failure. In this case, the patient developed severe cardio-pulmonary collapse, acute kidney failure, and cerebral edema within the first 12 hours of presentation. This highlights the importance of early recognition and prompt management of primary respiratory acidosis in severe salicylate toxicity.