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  1. Pharmacology. Naloxone is a synthetic N-allyl derivative with pure opioid antagonist activity that competitively blocks mu-, kappa-, and delta-opiate receptors within the CNS. It has no opioid agonist properties and can be given safely in large doses without producing respiratory or CNS depression. Take-home naloxone programs are being developed in which opiate users and their families are supplied naloxone for use on the scene in case of accidental overdose. The most common routes of administration for this purpose are intranasal and intramuscular or subcutaneous by autoinjector or syringe.

    1. Naloxone undergoes extensive first-pass metabolism and is not effective orally but may be given by intravenous, intramuscular, subcutaneous, nebulized, intranasal, and intraosseous routes. After intravenous administration, opioid antagonism occurs within 1–2 minutes and persists for approximately 30–120 minutes. The plasma half-life ranges from 30 to 81 minutes. Table III–11 is a comparison of the routes of administration for naloxone.

    2. Nalmefene is a pure opioid antagonist that has been used to treat acute opioid intoxication. It has a longer elimination half-life and duration of action than naloxone. However, its production was discontinued in 2008 and is no longer available in the United States.

    3. Naltrexone is another potent competitive opioid antagonist that is active orally and used to prevent recidivism in patients detoxified after opioid abuse. It has also been used to reduce craving for alcohol. It is not used for the acute reversal of opioid intoxication.

  2. Indications

    1. Reversal of acute opioid intoxication manifested by coma, respiratory depression, or hypotension.

    2. Empiric therapy for stupor or coma suspected to be caused by opioid overdose.

    3. Anecdotal reports suggest that high-dose naloxone may partially reverse the CNS and respiratory depression associated with clonidine, ethanol, benzodiazepine, or valproic acid overdoses, although these effects are inconsistent.

  3. Contraindications. Do not use in patients with a known hypersensitivity to naloxone or nalmefene (may have cross-sensitivity).

  4. Adverse effects. Human studies have documented an excellent safety record for naloxone.

    1. Use in opiate-dependent patients may precipitate acute withdrawal syndrome. Neonates of addicted mothers may have more severe withdrawal symptoms, including seizures. Aggressive use of opiate antagonists in so-called rapid opioid detoxification (ROD) and ultra-rapid opioid detoxification (UROD) has been associated with marked increases in plasma corticotropin, cortisol, and catecholamine levels and in sympathetic activity; pulmonary edema; acute renal failure; ventricular bigeminy; psychosis; delirium; and death.

    2. Pulmonary edema or ventricular fibrillation occasionally has occurred shortly after naloxone administration in opioid-intoxicated patients. Pulmonary edema has also been associated with postanesthetic use of naloxone, especially when catecholamines and large fluid volumes have been administered.

    3. Reversing the sedative effects of an opioid may amplify the toxic effects of other drugs. For example, agitation, hypertension, and ventricular irritability have occurred after naloxone administration to persons high on a "speedball" (heroin plus cocaine or methamphetamine).

    4. There has been one case report of hypertension after naloxone administration in a patient with clonidine overdose. Hypertension has been associated with postoperative use of naloxone. Use caution in patients with cardiovascular risk ...

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