Faculty Bibliography

Fluoroquinolones are commonly used antimicrobials with multiple known adverse effects, yet overdose events are rarely reported. Here, we report a case of a previously healthy middle-aged woman who unintentionally ingested 7 g of levofloxacin in one dose. Thereafter, she presented to the emergency department with hemiparesis concerning for ischaemic stroke and was administered tissue plasminogen activator. Her brain imaging showed no ischaemic injury and her symptoms resolved within 24 hours; this is consistent with a transient ischaemic attack. Our case highlights potential adverse effects of an acute overdose of levofloxacin that has not previously been well described.

BACKGROUND:Stroke mimics are non-vascular conditions that present with acute focal neurological deficits, simulating an acute ischemic stroke. Susumber berry (SB) toxicity is a rare cause of stroke mimic with limited case reports available in the literature. OBJECTIVES/OBJECTIVE:We report four new cases of SB toxicity presenting as stroke mimic, and we performed a systematic review. METHODS:MEDLINE/EMBASE/WoS were searched for "susumber berries," "susumber," or "solanum torvum." RESULTS:531 abstracts were screened after removal of duplicates; 5 articles and 2 conference abstracts were selected describing 13 patients. A total of 17 patients who ingested SB and became ill were identified, including our 4 patients. All but one presented with acute neurologic manifestation; 16 (94%) presented with dysarthria, 16 (94%) with unstable gait, 8 (47%) with nystagmus/gaze deviation, 10 (59%) with blurry vision, and 5 (29%) with autonomic symptoms. Six (35%) required ICU admission, and 3 (18%) were intubated. Fourteen (82%) had a rapid complete recovery, and 3 were hospitalized up to 1 month. CONCLUSIONS:SB toxicity can cause neurological symptoms that mimic an acute stroke typically with a posterior circulation symptom complex. Altered SB toxins (from post-harvest stressors or temperature changes) might stimulate muscarinic/nicotinic cholinergic receptors or inhibit acetylcholinesterase, causing gastrointestinal, neurological, and autonomic symptoms. In cases of multiple patients presenting simultaneously to the ED with stroke-like symptoms or when stroke-like symptoms fail to localize, a toxicological etiology (such as SB toxicity) should be considered.

INTRODUCTION/BACKGROUND:Clozapine is an atypical antipsychotic used to treat refractory schizophrenia; in both therapeutic use and overdose, it can cause significant toxicity. We report two young siblings who developed altered mental status after ingesting clozapine due to a pharmacy dispensing error. CASE REPORT/METHODS:A 5-year-old girl and her 19-month-old sister presented to the emergency department (ED) with altered mental status after they took their first dose of what was believed to be cimetidine, prescribed to treat molluscum contagiosum. Both children were discharged after a brief period of observation in the ED. Two days later, when the older child continued to be symptomatic, their mother used a web-based pill identifier and discovered that the pills dispensed by the pharmacy were 200 mg clozapine tablets, not the cimetidine that had been prescribed. Ingestion was confirmed with an elevated serum clozapine concentration in the older child of 17 mcg/L at 85 hours post-ingestion (adult therapeutic range: 350-600 mcg/L). Both children had complete resolution of their symptoms 4 days following the ingestion with supportive care alone. DISCUSSION/CONCLUSIONS:We report two cases of pediatric clozapine toxicity due to a pharmacy dispensing error. The error was due, in part, to similarly named medications being stored adjacent to each other on a shelf. Dispensing errors are not rare occurrences and their root causes are multi-factorial. This case demonstrates the importance of reducing such errors, particularly for medications with potential for severe toxicity.

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.