Acidosis, hypoxia, and generalized CNS depression predispose to the development of cardiac arrhythmias. Respiratory acidosis rapidly subsides as ventilation is restored and hypercapnea eliminated, but residual lactic acidosis may require i.v. bicarbonate for prompt correction. Electrocardiographic monitoring is essential. In addition to the use of a narcotic antagonist, the patient may require careful titration with an anticonvulsant to control seizures. Gastric lavage may be useful, and activated charcoal can adsorb a significant amount of ingested propoxyphene.
Dialysis is of little value in poisoning due to propoxyphene.
Efforts should be made to determine whether other agents, such as alcohol, barbiturates, tranquilizers, or other CNS depressants, were also ingested, since these increase CNS depression as well as cause specific toxic effects. Such symptoms include central nausea and vomiting, tinnitus and deafness, vertigo and headaches, mental dullness and confusion, diaphoresis, rapid pulse, and increased respiration and respiratory alkalosis. Treatment of acute salicylate intoxication includes minimizing drug absorption, promoting elimination through the kidneys, and correcting metabolic derangements affecting body temperature, hydration, acid-base balance, and electrolytic balance. The technique to be employed for eliminating salicylate from the bloodstream depends on the degree of drug intoxication. If the patient is seen within 4 hours of ingestion, the stomach should be emptied by inducing vomiting or by gastric lavage as soon as possible.