Because of the common, and particularly the illicit, use of opioids, poisoning is a frequent occurrence. This happens also as a result of ingestion or injection accidentally or with suicidal intent, errors in the calculation of dosage, the use of a substitute or contaminated street product, or unusual sensitivity. Children exhibit an increased susceptibility to opioids, so that relatively small doses may prove toxic. This is true also of adults with myxedema, Addison disease, chronic liver disease, and pneumonia. Acute poisoning may also occur in persons who are unaware that opioids available from illicit sources vary greatly in potency and that tolerance for opioids declines quickly after the withdrawal of the drug; upon resumption of the habit, a formerly well-tolerated dose can be fatal.
Unresponsiveness, shallow respirations, slow respiratory rate (e.g., 2 to 8 per min) or periodic breathing, pinpoint pupils, bradycardia, and hypothermia are the well-recognized clinical manifestations of acute opioid poisoning. In the most advanced stage, the pupils dilate, the skin and mucous membranes become cyanotic, and the circulation fails. Later in the course, pulmonary edema may arise, or aspiration pneumonia may become evident as summarized the review of opioid overdose by Boyer. The immediate cause of death is usually respiratory depression with consequent asphyxia. Patients who suffer a cardiorespiratory arrest are sometimes left with all the known residua of anoxic encephalopathy (see Chap. 39). Mild degrees of intoxication are reflected by anorexia, nausea, vomiting, constipation, and loss of sexual interest. Toxicology screens for opiates may be useful but action must be taken before the results of these tests are completed.
Treatment of Overdose
This consists of the support of ventilation and administration of naloxone (Narcan), or the longer-acting nalmefene, both specific antidotes to the opiates and also to the synthetic analgesics. The dose of naloxone in adults is usually 0.4 to 0.5 mg and repeated in larger increments (the second dose is typically 2 mg) every 2 min to a dose of 15 mg intravenously as outlined by Boyer. For children, a higher initial dose of 0.1 mg/kg is recommended. Intranansal preparations of 2 mg and 4 mg are available for emergency treatment but are less consistently effectively than the intravenous preparation. The improvements in circulation and respiration and reversal of miosis are usually dramatic. Failure of naloxone to produce such a response should cast doubt on the diagnosis of opioid intoxication. A narcotic withdrawal response may be seen and can be dramatic and resistant to treatment. If an adequate respiratory and pupillary response to naloxone is obtained, the patient should nonetheless be observed for up to 24 h and further doses of naloxone (50 percent higher than the ones previously found effective) can be given intramuscularly as often as necessary.
Naloxone has less direct effect on consciousness, however, and the patient may remain drowsy for many hours. This is not harmful provided respiration is well maintained. Although nalmefene has a plasma half-life of 11 h, compared to 60 to 90 min for naloxone, it has no clear advantage in emergency practice. Gastric lavage is a useful measure if the drug was taken orally. This procedure may be efficacious many hours after ingestion, as one of the toxic effects of opioids is ileus, which causes some of the drug to be retained in the stomach. Concerns of precipitating opioid withdrawal by giving naloxone are generally unfounded.