.jpg "Emily Jandasek, CCRN, CPNP, DNP photo")
Arya Payan, DO
Pediatric Critical Care Fellow
Helen DeVos Childrens Hospital, United States
Disclosure information not submitted.
Arianna Davis, ARNP
Nurse Practitioner
Helen DeVos Children's Hospital, United States
Disclosure information not submitted.
Elizabeth Prentice, DO
Pediatric Critical Care Intensivist
Helen DeVos Childrens Hospital, United States
Disclosure information not submitted.
Title: Amlodipine Overdose Leading to Severe ARDS and Fluid Refractory Shock Requiring V-V ECMO
Introduction: Amlodipine ingestions account for approximately 30% of cardiac pharmaceutical fatalities. Overdose of dihydropyridines have been known to cause arterial vasodilation leading to hypotension, reflex tachycardia, non-cardiogenic pulmonary edema, and cardiovascular collapse. Although it is known that an amlodipine overdose can cause these symptoms, this case is one of the first successful pediatric cases of V-V ECMO for a calcium channel blocker (CCB) overdose.
Description: A 12-year old female with shortness of breath and a non-productive cough was admitted with tachycardia and hypoxia. Workup was remarkable for leukocytosis and bilateral infiltrates on chest x-ray. Chest CTA was negative for pulmonary emboli. Despite non-invasive positive pressure ventilation, she was hypoxemic and hypercapnic (ABG pH 7.19, PaCO2 53, PaO2 68, HCO3 17) requiring intubation. Intubation was notable for copious frothy sputum. The patient was in fluid refractory shock of unclear etiology necessitating norepinephrine (0.25 mcg/kg/min) and epinephrine (0.2 mcg/kg/min) infusions. An echocardiogram demonstrated good left ventricular systolic function and mild right ventricular strain. Within 3 hours of admission, she required maximal ventilatory support (PRVC SIMV rate 28, TV 500, PEEP 22, PS 20) with inhaled nitric oxide. She had worsening lactic acidosis (4 to 6 mmol/L) and persistent hypoxemia and hypercarbia (ABG pH 7.23, PaCO2 50, PaO2 58, HCO3 21 and PaO2/FiO2 ratio of 57.7). V-V ECMO was initiated. She had improved clinical stability after cannulation. Urine toxicology was positive for amlodipine with a serum level of 34 ng/mL. She was decannulated from V-V ECMO on day 5 from admission. Hospital admission was complicated by a pleural and pericardial effusion requiring drain placements. She extubated after 9 days of mechanical ventilation and after 21 days was medically cleared for discharge with inpatient psychiatric evaluation.
Discussion: ARDS from a CCB ingestion is multifactorial, including pre-capillary vasodilation causing pulmonary capillary transudation and fluid resuscitation in the setting of shock. There are limited case reports in the pediatric literature. Many of these cases required V-A ECMO. This case is one of the first successful uses of V-V ECMO to treat complications of an amlodipine overdose.