Rodenticide Toxicity Treatment & Management

Points to remember in prehospital patient care for rodenticide poisoning include the following:

• As in most poisoning situations, it is best to "scoop and run”; very little can be done in the field
• Always look for a container, so that the specific product can be determined
• Decontamination may be necessary for situations in which patients and their garments are contaminated with the pesticide
• Administer benzodiazepines in patients with seizurelike activity
• Secure airway and place intravenous (IV) lines in hemodynamically unstable patients

Evidence-based guidelines on the management of long-acting anticoagulant rodenticide poisoning are available from the AAPCC.^[8]

Patients who present or develop renal failure may require hemodialysis. Patients with severe respiratory compromise from zinc phosphide, arsenic, or barium may require endotracheal intubation for ventilatory support.

Severe hemolysis from phosphine gas (released from zinc phosphide) may require exchange transfusion of RBCs.

GI evacuation is rarely useful; however, consider it for exceptional cases in which a huge overdose is suspected and in which the patient presents early to an emergency facility.

Give all patients with rodenticide overdose activated charcoal as soon as possible to prevent further absorption of ingested toxins. With anticoagulant overdoses, perform a careful physical examination to look for any sign of bleeding.

Other medical therapy depends on identification of specific substances involved. Examples are as follows:

• If a heavy metal is suspected, institute chelation therapy (see Arsenic Toxicity in Emergency Medicine and Thallium Toxicity)
• If an organophosphate is suspected, administer atropine for initial management and consider oxime use
• Monosodium fluoroacetate and zinc phosphide have no specific antidotal therapy that has been of any consistent advantage; only supportive care is available
• PNU induces an alloxan-like destruction of pancreatic beta cells, which may be prevented with nicotinamide

If no coagulopathy or active bleeding is found in the setting of an anticoagulant exposure, prophylactic treatment with vitamin K is absolutely contraindicated. This would potentially mask the onset and severity of an ingestion and would obfuscate the time required for clinical and/or laboratory monitoring.

If a coagulopathy is documented, institution of vitamin K therapy is suggested. If frank bleeding occurs, the administration of fresh frozen plasma and concentrated clotting factors may be warranted. (See Warfarin and Superwarfarin Toxicity for an extended discussion regarding treatment.) Since all of the vitamin K–dependent clotting factors may be affected, the hemolytic factors C and S may be affected early and may cause the presentation to be one of acute thrombosis rather than anticoagulation.^{[9, 10]}

For small, unintentional ingestions of an anticoagulant rodenticide, repeat PT measurements 24 and 48 hours postingestion to ensure that no effects on the coagulation pathway are present. This may be done on an outpatient basis if no other reason for inpatient hospitalization exists.

Intentional exposure to an anticoagulant rodenticide for suicidal or other reasons may require substantial treatment with vitamin K for a protracted period of time, particularly in the face of exposure to one of the superwarfarins. It may be wise to monitor brodifacoum levels to determine a treatment endpoint.^[7] The source of exposure to a superwarfarin should be disclosed to avoid recidivism.