Reproduction studies with pralidoxime have not been conducted, and the human pregnancy experience is limited to two cases. No other reports describing the use of this drug in human pregnancy have been located. Although the risk this agent represents in pregnancy cannot be assessed, the maternal benefit clearly outweighs any concern regarding embryo or fetal toxicity. Therefore, pralidoxime should not be withheld because of pregnancy.
No reports describing the use of pralidoxime during human lactation have been located. Pralidoxime chloride is a quaternary ammonium compound, but the molecular weight of the free base (about 173) is low enough for excretion into breast milk. The rapid elimination of the drug should mitigate this transfer into milk. Moreover, the emergency nature of its use suggests that nursing is unlikely when it has been used. In any event, the maternal benefit is clear, and breastfeeding should be held for at least 6-7 hours (about five half-lives) after a dose is given.
Pralidoxime
Pregnancy Recommendation:CompatibleMaternal Benefit Embryo-Fetal Risk
Breastfeeding Recommendation:Hold Breastfeeding
Pralidoxime (2-PAM) reactivates cholinesterase (mainly outside of the CNS) that has been inactivated by phosphorylation due to an organophosphate pesticide or related compound. Its most critical effect is relieving the paralysis of the muscles of respiration. Pralidoxime is short-acting (apparent half-life 74-77 minutes) and is not bound to plasma proteins. Pralidoxime is available in an autoinjector that can be used rapidly in cases of exposure to nerve agents possessing anticholinesterase activity (organophosphate poisoning) (1).
Animal Data: Animal reproduction studies have not been conducted with pralidoxime, nor have studies for carcinogenesis, mutagenesis, or impairment of fertility (1).
Placental Transfer: It is not known if pralidoxime crosses the human placenta to the embryo or fetus. The molecular weight of the free base (about 173) is low enough for passage across the placenta. The rapid elimination of the drug should mitigate this transfer.
Human Data: A 1988 report described the pregnancy outcomes of two women who were treated with pralidoxime for self-induced organophosphorus insecticide poisoning (2). In the first case, a 22-year-old primigravida at 36 weeks was admitted to the hospital 3 hours after ingesting methamidophos. She was treated with pralidoxime and atropine and eventually recovered. Forty-four days after poisoning, she delivered a healthy 2.85-kg male infant with an Apgar score of 8 at 1 minute. The second case involved a 25-year-old woman at 16 weeks who ingested fenthion. She also was treated with pralidoxime and atropine and made a full recovery. She delivered a healthy 3.83-kg infant (Apgar 10 at 1 minute) 24 weeks after intoxication (2).
A 2005 case report described a 42-year-old female who was seen in the emergency room at 26 weeks after diazinon (organophosphate) inhalation exposure. The patient had a past medical history that included protein C deficiency, hypothyroidism, and diabetes mellitus type 2. Her maintenance medications included levothyroxine, nadroparin, and aspirin. She was diagnosed with organophosphate poisoning, and was treated for 40 hours with atropine 2 mg IV every 15 minutes (240 mg total) and pralidoxime 1 g IV over 30 minutes followed by an infusion of 500 mg/h (21 g total). The patient developed atropine toxicity. At 38 weeks, a healthy infant was delivered. The infant weighed 2944 g and had Apgar scores of 9 and 10. No other information was provided (3).