Ventricular tachycardia following naloxone administration in an illicit drug misuse

Ventricular tachycardia following naloxone administration in an illicit drug misuse

J O U R N A L O F CLINICAL FORENSIC MEDICINE Journal of Clinical Forensic Medicine 12 (2005) 218–219 www.elsevier.com/locate/jcfm Learning point V...

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J O U R N A L

O F

CLINICAL FORENSIC MEDICINE Journal of Clinical Forensic Medicine 12 (2005) 218–219 www.elsevier.com/locate/jcfm

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Ventricular tachycardia following naloxone administration in an illicit drug misuse R. Hunter Department of Emergency Medicine, Royal Liverpool University Hospital, Liverpool L7 8XP, UK Available online 29 April 2005

Abstract A case of ventricular tachycardia in a 37-year-old man after ingestion of heroin and cocaine, treated with naloxone is described. The arrhythmia is attributed to unopposed sympathomemetic effects of cocaine following administration of naloxone. The prorhythmogenic effects of naloxone may have contributed to the arrhythmia. He was initially treated sequentially with intravenous magnesium sulphate, calcium gluconate, sodium bicarbonate and lignocaine infusion, with no resolution of the ventricular tachycardia. He was admitted to the coronary care unit and was given an amiodarone infusion which converted the rhythm to sinus rhythm. Forensic physicians administering naloxone to poly-drug abuser in a custodial setting should be aware of potentially fatal consequences which they will be unable to detect. It is recommended that all such patients should be transferred to hospital for observation and investigation.  2005 Elsevier Ltd and AFP. All rights reserved. Keywords: Naloxone; Arrhythmia; Poly-drug misuse

1. Case history A 37-year-old male was admitted to the resuscitation area of the Emergency Department with respiratory depression and hypoventilation. Friends had discovered him in his room comatose with a syringe and needle in his hand. The friends had told paramedic staff that the man had injected a ‘‘speedball’’ (a mixture of heroin and cocaine). On arrival in the emergency department the man had a Glasgow Coma Scale of 10/15, pin-point pupils, a respiratory rate of 4 breaths per minute and a tidal volume of 100–150 mls. Pulse was recorded as 110 beats per minute and appeared as a sinus tachycardia on heart monitoring. Blood pressure was 143/85 mmHg. He was given 800 lg of naloxone intramuscularly, and was bag valve mask ventilated on 100% oxygen. Concomitant blood gas analysis was reported as pH

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7.292, pCO2 6.93 kPa, pO2 44.78 kPa, Standard Bicarbonate 22.5 mmol/L and Base Excess as 2.5 mmol/L. Within a few minutes his coma scale increased to 14/ 15 and his respiratory rate and tidal volume increased to 13 breaths per minute and 400 mls. Shortly after this, frequent episodes of ventricular tachycardia were noted on the heart monitor, (Fig. 1). He remained conscious and normotensive. Blood results were as follows: Hb 11.5 g/dL, WCC 8.2 · 109/L, platelets-aggregated. Sodium – 142 mmol/ L, potassium 4.6 mmol/L, Urea 2.7 mmol/L, Creatinine 90 lmol/L, Chloride 108 mol/L, Magnesium 0.82 mmol/ L, adjusted Calcium 2.09 mmol/L, and phosphate 1.8 mmol/L. He was sequentially treated with intravenous magnesium sulphate, calcium gluconate, sodium bicarbonate and then lidocaine infusion. None of these interventions resolved the episodes of ventricular tachycardia, which were increasing in frequency and duration. He was admitted to the hospital coronary care unit as was treated with an infusion of amiodarone, which

1353-1131/$ - see front matter  2005 Elsevier Ltd and AFP. All rights reserved. doi:10.1016/j.jcfm.2005.01.011

R. Hunter / Journal of Clinical Forensic Medicine 12 (2005) 218–219

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Fig. 1. Run of ventricular tachycardia.

converted the rhythm to sinus rhythm. An echocardiograph of the heart was normal, 12 lead electrocardiograph demonstrated a left bundle branch block pattern with multiple ventricular ectopics. A 24-h cardiac tape demonstrated further brief episodes of ventricular tachycardia. He was commenced on oral amiodarone and with no further episodes was discharged eight days after admission on oral amiodarone. At three month follow up, he had stopped the amiodarone himself, did not complain of any specific symptoms and admitted to still taking cocaine and heroin. He failed to attend for further appointments.

2. Discussion Naloxone is an effective and potentially life saving opiate antidote, however it is not without side effects.1 In a poly drug user the administration of naloxone may be harmful for two reasons. First, in a patient with combined opiate and sympathomimetic ingestion, the administration of naloxone may provoke potentially life threatening sympathomimetic toxicity by removing the CNS depressant effects of the opiate.2 Second, the arrhythmogenic effects of naloxone which are well documented in the literature,3,4 may act synergistically with cocaine.5 In this reported case treatment of the arrhythmia proved refractory and it is assumed that this was due either to acute myocardial toxicity or to poisoning of the conducting tissue. Respiratory depression or arrest is encountered from time to time in a custodial setting due to the ingestion of secreted drugs by the detained person in the cell. Of the seventy deaths in police custody in England and Wales during the period 1999–2000, 30 deaths (43%) involved people who were intoxicated by alcohol and/ or drugs.6 Customs officers may have similar experiences in detention centres where a body packer suffers

toxicity from a leaking ingested wrap. Furthermore in the authorÕs professional experience a significant proportion of heroin user currently also use crack cocaine or cocaine, and often present with a mixed clinical picture, which can at times complicate diagnostic and treatment decisions. Naloxone is readily available in police custody suites and is often carried personally by Forensic Physicians. Due to the potential life saving benefit of naloxone Forensic Physicians should not withhold its administration unnecessarily, however they should be aware of the possibility of serious cardiac dysrrhythmias, which without cardiac monitoring they will be unable to detect until the patient has a catastrophic cardiovascular collapse or cardiac arrest. It is therefore submitted that it should not be assumed that respiratory depression treated with naloxone in a custodial setting has occurred in a person using only opiates. The patient should be considered a poly drug user and the potential for serious occult cardiac arrhythmias should be appreciated. All detained persons being treated with naloxone should be referred to hospital for further assessment and cardiovascular monitoring as a matter of urgency.

References 1. British National Formulary; March 2004. 2. Hung O. In: Viccelio P, editor. Emergency toxicology. 2nd ed. Lippincott-Raven; 1998. p. 859. 3. Cuss FM, Colaco CB, Baron JH. Cardiac arrest after reversal of opiates with naloxone. BMJ (Clin Res Ed) 1984;288:363–4. 4. Merrigan KJ. Cocaine-induced ventricular arrhythmias and rapid atrial fibrillation related to naloxone administration [letter]. Am J Em Med 1993;11:96–7. 5. Byck R, Ruskis A, Ungerer J, et al.. Naloxone potentiates cocaine effect in man. Psychopharmacol Bull 1982;18(4):214–5. 6. Deaths in Police Custody. Statistics for England and Wales April 1999–March 2000. Home Office, Police Leadership and Powers Unit.