Opioid poisoning with

Abdominal examination may reveal ileus, which is typical of poisoning with antimuscarinic, opioid, and sedative drugs. Hyperactive bowel sounds, abdominal cramping, and diarrhea are common in poisoning with organophosphates, iron, arsenic, theophylline, A phalloides, and A muscaria. 

Acute opioid poisoning involves marked CNS depression, with drowsiness, loss of consciousness, and coma. Other prominent features are a reduced respiratory rate, hypotension, and sjmmetrical pinpoint pupils (unless the patient has been hjrpoxic for some time, in which case the pupils can be dilated). Reduced urine output, hypothermia, flaccid skeletal muscles, and pulmonary edema can also be present. Convulsions have occurred in children. 

Diphenoxylate is a narcotic-like substance that slows gastrointestinal motility and depresses the central nervous system producing coma and respiratory depression. Anticholinergic effects (secondary to the presence of atropine as an abuse deterrent) can be seen early after exposure with opioid effects occurring later. There is no correlation between the dose ingested and the severity of effects in children. Severe poisonings with coma and respiratory depression have been reported in children with small ingestions. 

Action on receptors provides numerous examples. Beneficial interactions are sought in overdose, as with the use of naloxone for morphine overdose (opioid receptor), of atropine for anticholinesterase, i.e. insecticide poisoning (acetylcholine receptor), of isoproterelol (isoprenaline) for overdose with a P-adrenoceptor blocker (p-adrenoceptor), of phentolamine for the monoamine oxidase inhibitor-sympathomimetic interaction (a-adrenoceptor). 

In one instance keratoconjunctivitis occurred in a patient taking co-phenotrope, confirmed by rechallenge but not with diphenoxylate alone (SEDA-16, 425). Adverse effects are rare during ordinary use in adults, but children can be particularly sensitive to the adverse effects of both components, and in cases of poisoning complex and prompt measures may be needed, particularly since respiratory depression can be delayed until a day after ingestion and can recur even after a good response to opioid antagonists. 

In addition to general supportive measures directed to the airway, breathing and circulation, the clinician may consider measures to decrease absorption in the alert patient they suspect has been exposed to a life-threatening dose of diphenoxylate. Charcoal may decrease absorption. Charcoal administration should be cautiously used in a patient with altered mental status to avoid charcoal aspiration pneumonitis. It is important to recognize the potential for delayed toxicity and monitor diphenoxylate poisoned patients for a minimum of 24 h. Transient recovery may be observed before this time. Repeat boluses or continuous infusion of naloxone may be necessary to reverse opioid sedating effects. 

IV. Diagnosis. Poisoning should be suspected in patients with pinpoint pupils, respiratory depression, hypotension, and bradycardia. Although clonidine overdose may mimic an opioid overdose, it does not usually respond to administration of... 

The term mental dependence is based on the euphoric effect of opioids. The loss of euphoria, concurrent with the appearance of physical withdrawal symptoms, makes it even more difficult for patients to overcome their addiction. For the therapeutic treatment of addiction, as well as for acute opiate poisoning, opiate antagonists (e.g. Naloxone) have been developed. 

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