Symptoms And Diagnosis

The triad of coma, pinpoint pupils, and depressed respiration strongly suggests opioid poisoning. A patient who has taken an overdose of an opioid usually is stuporous or, if a large overdose has been taken, may be in a coma. The respiratory rate will be very low, or the patient may be apneic and cyanotic. As the respiratory exchange decreases, blood pressure, at first likely to be near normal, will fall progressively. If oxygenation is restored early, the blood pressure will improve; if hypoxia persists untreated, there may be capillary damage, and measures to combat shock may be required. The pupils will be symmetrical and pinpoint in size; if hypoxia is severe, they may be dilated. Urine formation is depressed, body temperature falls, and the skin becomes cold and clammy. The skeletal muscles are flaccid, the jaw is relaxed, and the tongue may obstruct the airway. Frank convulsions occasionally occur in infants and children. When death ensues, it is nearly always from respiratory failure. Even if respiration is restored, death still may occur as a result of complications that develop during the period of coma, such as pneumonia or shock. Noncardiogenic pulmonary edema is seen commonly with opioid poisoning.

TREATMENT Establish a patent airway and ventilate the patient. Opioid antagonists (see below) can produce dramatic reversal of the severe respiratory depression; naloxone is the treatment of choice. The safest approach is to dilute the standard naloxone dose (0.4 mg) and slowly administer it intravenously, monitoring arousal and respiratory function. With care, it usually is possible to reverse the respiratory depression without precipitating a major withdrawal syndrome. If no response is seen with the first dose, additional doses can be given. Patients should be observed for rebound increases in sympathetic nervous system activity, which may result in cardiac arrhythmias and pulmonary edema. For reversing opioid poisoning in children, the initial dose of naloxone is 0.01 mg/kg. If no effect is seen after a total dose of 10 mg, one can reasonably question the accuracy of the diagnosis. Pulmonary edema sometimes associated with opioid overdosage may be countered by positive-pressure respiration. Tonic-clonic seizures, occasionally seen as part of the toxic syndrome with meperidine and propoxyphene, are ameliorated by treatment with naloxone.


Drugs such as nalbuphine and butorphanol are competitive ^-receptor antagonists that exert analgesic actions by acting as agonists at k receptors. Pentazocine qualitatively resembles these drugs, but it may be a weaker ^-receptor antagonist or partial agonist while retaining its k-agonist activity. Buprenorphine, in contrast, is a partial agonist at m receptors. The clinical use of these drugs is limited by undesirable side effects and limited analgesic effects.


The CNS effects produced by pentazocine generally are similar to those of the morphine-like opi-oids, including analgesia, sedation, and respiratory depression. The analgesic effects of penta-zocine are due to agonistic actions at k opioid receptors. Higher doses of pentazocine (60—90 mg) elicit dysphoric and psychotomimetic effects; these effects may involve activation of supraspinal k receptors and sometimes are reversed by naloxone.

The cardiovascular responses to pentazocine differ from those seen with typical jl-receptor agonists, in that high doses cause an increase in blood pressure and heart rate. Pentazocine acts as a weak antagonist or partial agonist at j-opioid receptors. Pentazocine does not antagonize the respiratory depression produced by morphine. However, when given to patients dependent on morphine or other j-receptor agonists, pentazocine may precipitate withdrawal. Ceiling effects for analgesia and respiratory depression are observed above 50—100 mg pentazocine.

Tablets for oral use now contain pentazocine hydrochloride (equivalent to 50 mg of the base) and naloxone hydrochloride (equivalent to 0.5 mg of the base; talwin nx), which reduces the potential use of tablets as a source of injectable pentazocine. After oral ingestion, naloxone is destroyed rapidly by the liver; however, if the material is dissolved and injected, the naloxone produces aversive effects in subjects dependent on opioids. An oral dose of ~50 mg pentazocine results in analgesia equivalent to that produced by 60 mg codeine orally.


Nalbuphine is an agonist-antagonist opioid with a spectrum of effects that qualitatively resembles that of pentazocine; however, nalbuphine is a more potent antagonist at j receptors and is less likely to produce dysphoria.

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