P1.028: Hypotension, Non-Steroidal Anti-Inflammatory Drugs, and Acute Kidney Injury: A Pediatric Case Report

Introduction: Treatment options for migraine headaches often include combinations of agents, commonly referred to as migraine cocktails. We describe the use of repeated doses of a migraine cocktail in an adolescent who developed hypotension and acute kidney injury (AKI).

Case Description: A 15-year-old female with no significant medical history was admitted to the pediatric ward with 6 days of headache, fever, abdominal pain, and large-volume non-bloody diarrhea. Serum inflammatory markers were moderately increased (C-reactive protein 188 mg/L, procalcitonin 1.13 ng/mL, ESR 129 mm/hr, ferritin 920 ng/mL) while a brain MRI and CSF profile were within normal limits. On admission, blood urea nitrogen (BUN) was 5 mg/dL and creatinine was 0.78 mg/dL. She was treated with five doses of a migraine cocktail (diphenhydramine, prochlorperazine, and ketorolac) and empiric antibiotics (including four doses of vancomycin) over the initial 24 hours of hospitalization.
On hospital day (HD) 2, she developed hypotension and AKI, characterized by oliguria (urine output of 0.26mL/kg/hr) and increased serum creatinine (3.32mg/dL). She was transferred to the PICU where she was treated with vasopressors, fluid resuscitation, and antibiotics, as well as methylprednisolone and intravenous immunoglobulin. Her fractional excretion of sodium (FeNa) at this time was 0.6%, suggesting decreased renal perfusion and pre-renal AKI. Cultures of blood and CSF remained negative. On HD 4, BUN and creatinine peaked at 31 mg/dL and 5.84 mg/dL. Following careful fluid management, treatment of systemic inflammation, and strict avoidance of nephrotoxic medications, AKI improved and she was discharged home on HD 12. Six weeks after discharge, BUN and creatinine were within normal limits (7 mg/dL and 0.67 mg/dL).

Discussion: Hypotension in our patient was associated with repeated doses of diphenhydramine and prochlorperazine, while repeated doses of ketorolac (a nonsteroidal anti-inflammatory drug; NSAID) likely contributed to AKI. NSAIDs may cause a transient block in the production of prostaglandins with subsequent failure of the afferent renal arterioles to vasodilate, leading to a fall in glomerular filtration and loss of the physiologic response to hypotension. Our patient received medications that resulted in decreased organ perfusion pressure in addition to directly nephrotoxic medications. The additive effect of these medications can lead to AKI and longer hospitalization.

Conclusion: The association of hypotension along with failure of renal afferent arteriolar vasodilation suggests the need for caution with repeated doses of this migraine cocktail. This case highlights the combined risk of prochlorperazine, diphenhydramine, and ketorolac, and the summative impact of nephrotoxic medications in a previously healthy patient.