Faculty Bibliography

BACKGROUND:Zinc phosphide is a highly toxic rodenticide that reacts with hydrochloric acid in the stomach to form phosphine gas. Ingestion of zinc phosphide can result in consequential toxicity even when ingested in small quantities. Clear guidelines are lacking on appropriate personal protective equipment for providers to avoid additional exposure. CASE PRESENTATION/METHODS:We present the case of a four-year-old boy who suffered mild gastrointestinal symptoms after an unintentional ingestion of zinc phosphide. After discussion with the regional Poison Control Center, providers wore powered air-purifying respirators in a negative pressure room and experienced no symptoms of phosphine exposure. The patient was discharged the next day after a complete recovery. CONCLUSIONS:Clinicians should be aware of the potential clinical ramifications to patients who ingest zinc phosphide and the potential risks of caring for such patients. To prevent additional exposure, providers should don appropriate personal protective equipment and contact HAZMAT (or local health department) to safely remove additional zinc phosphide.

We report 2 pediatric patients who had acute overdoses of the direct oral anticoagulants medications. Both patients were managed conservatively; neither required reversal agents or blood products nor had any major or minor bleeding events. With therapeutic usage of direct oral anticoagulants, routine coagulation studies typically are considered insufficient measures of anticoagulation and the preferred chromogenic anti-Factor Xa assay is recommended but not widely available. Using a routine hybrid heparin anti-Factor Xa assay, 1 patient demonstrated a strong linear correlation up to a serum rivaroxaban concentration of 940 ng/mL.

BACKGROUND/UNASSIGNED:Severe acetaminophen (APAP) poisoning can result in fulminant hepatic failure and abnormal tests of coagulation. Although the international normalized ratio (INR) may be elevated, the actual hemostatic status of patients with APAP-induced hepatotoxicity is unknown. Few studies exist investigating the clinical use of thromboelastography (TEG) to evaluate the hemostatic status in the setting of APAP-induced hepatotoxicity. METHODS/UNASSIGNED:We performed a retrospective review of patients who were admitted for APAP toxicity and received TEG testing at a single transplant center. RESULTS/UNASSIGNED:Nine patients had detectable APAP concentrations and exhibited elevated aspartate and alanine aminotransferase activities. Seven had thrombocytopenia. TEG revealed a decreased median alpha angle and maximum amplitude but other values were within the normal reference range. DISCUSSION/UNASSIGNED:Based on our study of APAP-induced hepatotoxicity, TEG showed a decreased rate of fibrin formation and cross-linking, as well as reduced clot strength. These findings suggest that patients with APAP-induced hepatotoxicity and thrombocytopenia have a theoretically increased bleeding risk as demonstrated by both elevated INR and abnormal TEG values. However, these TEG findings are more likely related to thrombocytopenia rather than directly to APAP-induced hepatotoxicity. Further studies should be performed to elucidate the potential role of TEG in various stages of APAP-induced hepatotoxicity.