Naloxone as an antidote for angiotensin converting enzyme inhibitor poisoning: a case report
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Naloxone as an antidote for angiotensin converting enzyme inhibitor poisoning: a case report Vatsal Trivedi, MD, FRCPC . Bryan A. Glezerson, MD, FRCPC . Dipayan Chaudhuri, MD, FRCPC . Morgan Davidson, MSc, RN . Ghislaine Doufle´, MD
Received: 4 March 2020 / Revised: 18 April 2020 / Accepted: 19 April 2020 Ó Canadian Anesthesiologists’ Society 2020
To the Editor, A 48-yr-old female (102 kg) with hypertension presented to a community hospital with intentional ingestion of amlodipine (252 mg) and perindopril (180 mg). She received 4 L intravenous crystalloid and
V. Trivedi, MD, FRCPC (&) Interdepartment Division of Critical Care Medicine, Toronto General Hospital, University of Toronto, Toronto, ON, Canada e-mail: [email protected] B. A. Glezerson, MD, FRCPC Department of Anesthesiology and Pain Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA D. Chaudhuri, MD, FRCPC Department of Medicine, McMaster University, Hamilton, ON, Canada M. Davidson, MSc, RN Medical-Surgical Intensive Care, University Health Network, Toronto, ON, Canada Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, ON, Canada G. Doufle´, MD Interdepartment Division of Critical Care Medicine, Toronto General Hospital, University of Toronto, Toronto, ON, Canada Medical-Surgical Intensive Care, University Health Network, Toronto, ON, Canada Department of Anesthesia and Pain Management, Toronto, General Hospital, University Health Network, Toronto, ON, Canada
norepinephrine to maintain a mean arterial pressure [ 65 mmHg. She received activated charcoal with subsequent aspiration. Her evolving vasoplegia required norepinephrine 1 lgkg-1min-1, vasopressin 8 Uhr-1, epinephrine 0.55 lgkg-1min-1, and high-dose insulin euglycemia therapy (HIET) with 10 Ukg-1hr-1 HumulinÒ (Eli Lilly & Company, Indianapolis, IN, USA). A transthoracic echocardiogram revealed normal biventricular function. Her hypoxemia necessitated transfer to a quaternary care centre, where she received lung protective ventilation, deep sedation (midazolam and fentanyl), paralysis (cisatracurium), prone positioning, and inhaled nitric oxide. This management was continued for the first 72 hr of admission, following which her hypoxemia improved. Her sedation was de-escalated to propofol only. Over the subsequent 24 hr (four days postadmission), the HIET was weaned rapidly as insulin sensitivity improved, a marker of recovery from calcium channel blocker poisoning. At this point, based on toxicologic pharmacokinetics and discussion with the Regional Poison Centre, there was concern for ongoing perindopril overdose causing vasoplegia. Given this, the patient was treated with intravenous naloxone in attempt to treat vasoplegia secondary to angiotensin converting enzyme (ACE) inhibitor. She received 200 lg aliquots of intravenous naloxone every three to five minutes to a to
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