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INTRODUCTION:Colchicine is commonly used to treat diseases like acute gouty arthritis. However, colchicine has a very narrow therapeutic index, and ingestions of > 0.5mg/kg can be deadly. We report a fatal acute colchicine overdose in an adolescent. Blood and postmortem bile colchicine concentrations were obtained to better understand the degree of enterohepatic circulation of colchicine. CASE REPORT:A 13-year-old boy presented to the emergency department after acute colchicine poisoning. A single dose of activated charcoal was administered early but no other doses were attempted. Despite aggressive interventions such as exchange transfusion and veno-arterial extracorporeal membrane oxygenation (VA-ECMO), the patient died 8 days later. Postmortem histology was notable for centrilobular necrosis of the liver and a cardiac septal microinfarct. The patient's blood colchicine concentration on hospital days 1 (~30 hours post-ingestion), 5, and 7 was 12ng/mL, 11ng/mL, and 9.5ng/mL, respectively. A postmortem bile concentration obtained during autopsy was 27ng/mL. DISCUSSION:Humans produce approximately 600mL of bile daily. Assuming that activated charcoal would be able to adsorb 100% of biliary colchicine, using the bile concentration obtained above, only 0.0162mg of colchicine per day would be able to be adsorbed and eliminated by activated charcoal in this patient. CONCLUSION:Despite supportive care, activated charcoal, VA-ECMO, and exchange transfusion, modern medicine may not be enough to prevent death in severely poisoned colchicine patients. Although targeting enterohepatic circulation with activated charcoal to enhance elimination of colchicine sounds attractive, the patient's low postmortem bile concentration of colchicine suggests a limited role of activated charcoal in enhancing elimination of a consequential amount of colchicine.

Nitrous oxide is a commonly used inhaled anesthetic for medical procedures, as well as a drug of abuse throughout the world. Excessive nitrous oxide inhalation has been shown to cause a functional vitamin B12 deficiency and hyperhomocysteinemia, which can lead to peripheral neuropathy and hypercoagulability, respectively. While the development of neurologic toxicity from chronic nitrous oxide abuse (i.e., encephalopathy, myelopathy, and neuropathy) has been previously described, the thrombotic potential of chronic nitrous oxide abuse is less known. The authors report two cases of nitrous oxide abuse leading to both neurologic and thrombotic complications.
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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.

Allium tricoccum (commonly known as "ramps") is an edible plant known for its strong garlic-like odor and onion flavor. Unfortunately, A tricoccum mimics such as Lily of the Valley (Convallaria majalis) and False Hellebore (Veratrum viride) can lead to foraging errors and subsequent patient harm/toxicity. We describe 3 adults who foraged and ate what they believed were A tricoccum and then subsequently became symptomatic with detectable digoxin concentrations. A 41-y-old woman, 41-y-old man, and a 31-y-old man presented to the emergency department after ingesting an unknown plant that was believed to be A tricoccum. On arrival to the emergency department, the patients were hypotensive and bradycardic. They had detectable digoxin concentrations ranging from 0.08 ng·mL^-1 to 0.13 ng·mL^-1. One patient received 20 vials of digoxin antibody fragments. All 3 patients recovered without complication. Laboratory analysis of plant specimen was positive for cyclopamine, a teratogenic alkaloid found in Veratrum californicum. A tricoccum foraging errors can be a source of morbidity given their similarity in appearance to plants like C majalis and V viride. C majalis causes a detectable digoxin concentration via its cardiac steroid compound (convallatoxin) that is similar to digoxin. V viride contains alkaloid compounds (such as veratridine) that can cross react with digoxin assays and lead to a falsely elevated digoxin concentration. Clinicians should be prompted to think about ingestion of C majalis or Veratrum spp. when patients present with bradycardia, gastrointestinal symptoms, and detectable digoxin concentrations after plant ingestion and/or foraging for A tricoccum.

CASE REPORT/UNASSIGNED:A 12-month-old (former 24 week gestational age), 8.7 kg male was hospitalized after an uneventful colostomy reversal. In the postoperative unit, the patient unintentionally received 1000 mg IV (114.9 mg/kg) acetaminophen instead of the intended 100 mg IV. Serial acetaminophen concentrations were drawn. The patient received IV Nacetylcysteine and ultimately had no adverse outcomes. DISCUSSION/UNASSIGNED:This case report adds to the existing literature regarding toxicokinetics of IV APAP in infants. Our patient had a calculated ke of 0.263 h-1, correlating with a half-life of 2.63 hours. Based on current available data, the half-life of IV APAP in infants varies (2.6 to 4.9 hours). The reason for this variation is unknown and further research is needed in this area.