Faculty Bibliography

INTRODUCTION/UNASSIGNED:Many hospitals are unable to determine toxic alcohol concentrations in a clinically meaningful time frame. Thus, clinicians use surrogate markers when evaluating potentially poisoned patients. INDEX CASE/UNASSIGNED:A patient presented after an intentional antifreeze (ethylene glycol) ingestion with an osmol gap of -10.6 that remained stable one hour later. Further investigation revealed that the serum osmolality was calculated and not measured. The true osmol gap was 16.4, which correlated to a measured ethylene glycol concentration of 808 mg/L (80.8 mg/dL, 13.0 mmol/L). SURVEY/UNASSIGNED:A telephone survey of hospital laboratories in our catchment area was performed to investigate the potential for similar events. RESULTS/UNASSIGNED:Thirty-eight (47 percent) hospitals responded. No laboratories were able to test for toxic alcohols. One hospital (2.6 percent) reported routinely calculating osmolality based on chemistries, while two hospitals (5.3 percent) reported scenarios in which this might occur. Thirty-five (92.1 percent) hospitals could directly measure osmolality. Two hospitals (5.3 percent) were reliant on outside laboratories for osmolality measurement. LIMITATIONS/UNASSIGNED:The 47 percent response rate and one geographic area are significant limitations. DISCUSSION/UNASSIGNED:Over 10 percent of hospitals that responded could have significant difficulty assessing patients with toxic alcohol ingestion. CONCLUSIONS/UNASSIGNED:Until the standard of rapidly obtaining toxic alcohol concentrations is broadly implemented, we recommend that policies and procedures be put in place to minimize errors associated with the determination of the osmol gap.

OBJECTIVE/UNASSIGNED:To highlight the similarity between madd fruit seeds and enteral drug concealment ("body packing") on computed tomography when evaluated by Hounsfield Units. CASE REPORT/UNASSIGNED:) seeds, which can cause bezoar formation and intestinal obstruction. CONCLUSION/UNASSIGNED:Madd fruit seeds may appear similar to drug packets on computed tomography with similar Hounsfield Unit characteristics. History and clinical context are paramount to avoid misdiagnosis.

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.

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.

Objectives/UNASSIGNED:Emergency medical services (EMS) clinicians are on the front lines of the opioid epidemic and are often the first health care personnel system to contact patients experiencing opioid toxicity. Although national educational guidelines include opioid toxicity, no specific standardized prehospital educational objectives or competencies exist. The goal of this project was to identify objectives for an EMS opioid toxicity curriculum that could be used for EMS training. Methods/UNASSIGNED:A list of preliminary educational objectives from U.S. EMS training programs was compiled and reviewed by a group of experts. The Delphi method was used to attain consensus on a final list of objectives for an EMS opioid curriculum. Results/UNASSIGNED:A total of 107 opioid-related preliminary objectives were identified and then narrowed down to 81 preliminary objectives after accounting for redundancy. After four successive rounds of evaluating/accepting/rejecting objectives, 18 final objectives were identified and unanimously approved by the expert panel. Conclusion/UNASSIGNED:We identified 18 objectives to serve as a framework for an opioid toxicity curriculum for EMS clinicians. These objectives can serve as a basis for creating a standardized didactic training program for EMS training programs nationwide. Further evaluation will be needed to explore the best means for educational program delivery.

CONTEXT/BACKGROUND:Anion gap metabolic acidosis (AGMA) is common in patients presenting for emergency care. While some disease processes and ingestions are easily excluded, diagnosing toxic alcohol (TA) ingestion can be challenging. This is especially true if drug concentrations are not readily available, which forces clinicians to rely on surrogate markers. Like TA ingestion, alcoholic ketoacidosis (AKA) produces an elevated osmol gap and an AGMA. The aim of this study was to identify risk factors suggestive of AKA when TA ingestion was the primary alternative differential diagnosis. We hypothesized that the odds of an AKA diagnosis would increase as ethanol concentration increased. METHODS:This was a retrospective analysis of data from 2000 through 2019 from a single US Poison Control Center. Records were reviewed to identify cases coded as "methanol" or "ethylene glycol"; or coded as "alcohol" or "ethanol with acidosis." The case definition for AKA required: (1) documented alcohol use disorder; (2) urine or serum ketones or elevated blood beta-hydroxybutyrate concentration; (3) anion gap ≥ 14 mmol/L. The inclusion criterion for TAs was a detectable methanol or ethylene glycol concentration. RESULTS: = .03). CONCLUSIONS:In this retrospective analysis, the odds of diagnosing AKA instead of TA ingestion increased as ethanol concentration increased. The limited ability of common clinical factors to differentiate these diagnoses highlights the need to obtain quantitative TA concentrations in real time. Until prospective validation, interpretation of ketone concentrations and toxic alcohol concentrations (when available) will continue to guide decision making.

OBJECTIVE:Although hemodialysis is recommended for patients with severe metformin-associated lactic acidosis (MALA), the amount of metformin removed by hemodialysis is poorly documented. We analyzed endogenous clearance and hemodialysis clearance in a patient with MALA. METHODS:A 62-year-old man with a history of type II diabetes mellitus presented after several days of vomiting and diarrhea and was found to have acute kidney injury (AKI) and severe acidemia. Initial serum metformin concentration was 315.34 μmol/L (40.73 μg/mL) (typical therapeutic concentrations 1-2 μg/mL). He underwent 6 h of hemodialysis. We collected hourly whole blood, serum, urine, and dialysate metformin concentrations. Blood, urine, and dialysate samples were analyzed, and clearances were determined using standard pharmacokinetic calculations. RESULTS:The total amount of metformin removed by 6 h of hemodialysis was 888 mg, approximately equivalent to one therapeutic dose. Approximately 142 mg of metformin was cleared in the urine during this time. His acid-base status and creatinine improved over the following days. No further hemodialysis was required. CONCLUSION/CONCLUSIONS:We report a case of MALA likely secondary to AKI and severe volume depletion. The patient improved with supportive care, sodium bicarbonate, and hemodialysis. Analysis of whole blood, serum, urine, and dialysate concentrations showed limited efficacy of hemodialysis in the removal of metformin from blood, contrary to previously published data. Despite evidence of acute kidney injury, a relatively large amount of metformin was eliminated in the urine while the patient was undergoing hemodialysis. These data suggest that clinical improvement is likely due to factors besides removal of metformin.