Naloxone hydrochloride (Narcan) is a pure narcotic antagonist that is the drug of choice in the treatment of central nervous system and cardiores-piratory depression due to narcotic agonist drugs. It has virtually no agonist activity and therefore produces no narcotic effect even when administered in greater than recommended doses, in contrast to nalorphine hydrochloride and levallorphan tartrate, which have mixed agonist-antagonist activity.
In 1975 the FDA approved a dosage form of naloxone in a concentration of 0.02 mg/ml that was specifically designed for use in newborns whose mothers receive narcotic analgesics during labor and who are born with narcotic-induced respiratory depression; this drug was marketed for general prescription use. Three years after its introduction, the role of naloxone in the management of the depressed newborn merits clarification. In addition, recent information regarding opiate receptors and endogenous opioids raises questions concerning the long-term safety of naloxone in neonates. A review of available published and unpublished data pertaning to naloxone use in the newborn infant by the Committee on Drugs forms the basis for the following commentary and recommendations.
EFFICACY
The potent narcotic antagonist activity of naloxone is well documented in infants and children as well as in adults. Naloxone has been effectively used postoperatively to reverse respiratory depression in infants and children who received narcotics for analgesia.1,2 Additional cases have been reported in which naloxone was successfully and safely used to treat children who were poisoned with narcotic agonists such as diphenoxylate hydrochloride (Lomotil),3,4 methadone hydrochloride, 57 and propoxyphene hydrochloride (Darvon).8
Most of the controlled clinical trials to study the safety and efficacy of naloxone in treating respiratory depression in the narcotic-exposed newborn have been carried out on full-term, healthy infants whose mothers received morphine or meperidine hydrochloride during labor, but who showed no overt clinical evidence of respiratory or CNS depression at birth.
Intermittent hypercapnic hypoxia induces respiratory hypersensitivity to fentanyl accompanied by tonic respiratory depression by endogenous opioids