Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/40046
Title: Intrathecal Clonidine Pump Failure Causing Acute Withdrawal Syndrome With 'Stress-Induced' Cardiomyopathy.
Authors: Ruggoo V.;Graudins A. ;Lee H.M.D.
Institution: (Lee, Ruggoo, Graudins) Monash Health Clinical Toxicology and Addiction Medicine Service, Monash, Health, Dandenong Hospital, David Street, Dandenong, VIC 3175, Australia (Lee, Ruggoo, Graudins) Monash Emergency Program, Monash Health, Dandenong Hospital, David Street, Dandenong, VIC 3175, Australia (Lee, Graudins) School of Clinical Sciences at Monash Health, Nursing and Health Sciences, Monash Medical Centre, Monash University, Clayton, VIC 3168, Australia (Lee) Department of Emergency Medicine, Dandenong Hospital, 135 David Street, Dandenong, VIC, Australia
Issue Date: 19-Sep-2015
Copyright year: 2016
Publisher: Springer New York LLC (E-mail: barbara.b.bertram@gsk.com)
Place of publication: United States
Publication information: Journal of Medical Toxicology. 12 (1) (pp 134-138), 2016. Date of Publication: 01 Mar 2016.
Journal: Journal of Medical Toxicology
Abstract: Clonidine is a central alpha(2)-agonist antihypertensive used widely for opioid/alcohol withdrawal, attention deficit hyperactivity disorder and chronic pain management. We describe a case of clonidine withdrawal causing life-threatening hypertensive crisis and stress-induced cardiomyopathy. A 47-year-old man with chronic back pain, treated with clonidine for many years via intrathecal pump (550 mcg/24 h), presented following a collapse and complaining of sudden worsening of back pain, severe headache, diaphoresis, nausea and vomiting. A few hours prior to presentation, his subcutaneous pump malfunctioned. On presentation, vital signs included pulse 100 bpm, BP 176/103 mmHg, temperature 37.8 degreeC and O2 saturation 100 % (room air). Acute clonidine withdrawal with hypertensive crisis was suspected. Intravenous clonidine loading dose and a 50 mcg/h infusion were commenced. Five hours later, severe chest pain, dyspnoea, tachycardia, hypoxia, with BP 180/120 mmHg and pulmonary edema ensued. ECG showed sinus tachycardia with no ST elevation. Repeated intravenous clonidine doses were given (25 mcg every 5-10 min), with ongoing clonidine infusion to control blood pressure. Glyceryl trinitrate infusion, positive pressure ventilation and intravenous benzodiazepines were added. Bedside echocardiogram showed stress-induced cardiomyopathy pattern. Serum troponin-I was markedly elevated. His coronary angiography showed minor irregularities in the major vessels. Over the next 3 days in the ICU, drug infusions were weaned. Discharge was 12 days later on oral clonidine, metoprolol, perindopril, aspirin and oxycodone-SR. Two months later, his echocardiogram was normal. The intrathecal pump was removed. We report a case of stress-induced cardiomyopathy resulting from the sudden cessation of long-term intrathecal clonidine. This was managed by re-institution of clonidine and targeted organ-specific therapies.Copyright © 2015, American College of Medical Toxicology.
DOI: http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1007/s13181-015-0505-9
ISSN: 1556-9039
URI: https://repository.monashhealth.org/monashhealthjspui/handle/1/40046
Type: Article
Type of Clinical Study or Trial: Case series or case report
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