UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2016 UpToDate®

Opioid withdrawal in the emergency setting

Authors
Andrew Stolbach, MD
Robert S Hoffman, MD
Section Editor
Stephen J Traub, MD
Deputy Editor
Jonathan Grayzel, MD, FAAEM

INTRODUCTION

Opiates, extracted from the poppy plant (Papaver somniferum), have been used recreationally and medicinally for millennia. Opiates belong to the larger class of drugs, the opioids, which include synthetic and semi-synthetic drugs, as well.

The Drug Abuse Warning Network in the United States estimates there were 162,137 heroin-related emergency department visits and 37,007 unspecified opiate-related emergency department visits in 2004 [1]. In addition to opioid overdose, a significant number of these visits related to opioid withdrawal.

This topic review will discuss the clinical features and management of opioid withdrawal in the emergency setting. A summary table to facilitate emergency management is provided (table 1). Discussions of opioid withdrawal during detoxification treatment, opioid intoxication, opioid withdrawal in neonates, and general management of the poisoned patient are found elsewhere. (See "Medically supervised opioid withdrawal during treatment for addiction" and "Acute opioid intoxication in adults" and "Neonatal abstinence syndrome" and "General approach to drug poisoning in adults".)

PHARMACOLOGY AND CELLULAR TOXICOLOGY

Repeated, regular use of opioids produces tolerance that predisposes an individual toward withdrawal. Chronic opioid exposure causes adaptations that increase excitability in neurons in the locus ceruleus, the major noradrenergic center in the brain. The presence of opioids brings these neurons toward their normal firing rates [2].

KINETICS

The vast number of opioids precludes presenting pharmacokinetic data for each one here. A few clinically important generalizations can be made. The majority of opioids have volumes of distribution of 1 to 10 L/kg, which makes removal of a significant quantity of drug by hemodialysis impossible. They have variable protein binding (from 89 percent for methadone to 7.1 percent for hydrocodone) and are renally eliminated. Many opioids are metabolized to active metabolites. Examples include hydrocodone (metabolized to hydromorphone by Cytochrome [CY] P2D6) and morphine (metabolized to morphine-6-glucuronide). Cytochrome P polymorphisms cause variations in clinical effect.

                  

Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Nov 2016. | This topic last updated: Wed Oct 19 00:00:00 GMT+00:00 2016.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2016 UpToDate, Inc.
References
Top
  1. United States Substance Abuse and Mental Health Services Administration. Emergency Department Data. http://www.samhsa.gov/data/emergency-department-data-dawn/reports. (Accessed on October 10, 2016).
  2. Nestler EJ. Under siege: The brain on opiates. Neuron 1996; 16:897.
  3. Wesson DR, Ling W. The Clinical Opiate Withdrawal Scale (COWS). J Psychoactive Drugs 2003; 35:253.
  4. Tompkins DA, Bigelow GE, Harrison JA, et al. Concurrent validation of the Clinical Opiate Withdrawal Scale (COWS) and single-item indices against the Clinical Institute Narcotic Assessment (CINA) opioid withdrawal instrument. Drug Alcohol Depend 2009; 105:154.
  5. Dahan A, Yassen A, Romberg R, et al. Buprenorphine induces ceiling in respiratory depression but not in analgesia. Br J Anaesth 2006; 96:627.
  6. Boas RA, Villiger JW. Clinical actions of fentanyl and buprenorphine. The significance of receptor binding. Br J Anaesth 1985; 57:192.
  7. Aghajanian GK, Wang YY. Common alpha 2- and opiate effector mechanisms in the locus coeruleus: intracellular studies in brain slices. Neuropharmacology 1987; 26:793.
  8. Elman I, D'Ambra MN, Krause S, et al. Ultrarapid opioid detoxification: effects on cardiopulmonary physiology, stress hormones and clinical outcomes. Drug Alcohol Depend 2001; 61:163.
  9. Suzuki T, Tsuda M, Narita M, et al. Diazepam pretreatment suppresses morphine withdrawal signs in the mouse. Life Sci 1996; 58:349.
  10. Streel E, Verbanck P. Ultra-rapid opiate detoxification: from clinical applications to basic science. Addict Biol 2003; 8:141.
  11. Johnson K, Gerada C, Greenough A. Treatment of neonatal abstinence syndrome. Arch Dis Child Fetal Neonatal Ed 2003; 88:F2.
  12. Beauman SS. Identification and management of neonatal abstinence syndrome. J Infus Nurs 2005; 28:159.