Elamin M, Bashir R, Kolbeck M
… +3 more, Calleo V, Meyer JA, Beutler T
J Med Toxicol
· 2026 May · PMID 42192053
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BACKGROUND: Botulism is a rare, life-threatening condition caused by potent neurotoxins that inhibit the release of acetylcholine into the neuromuscular junction, resulting in cranial nerve palsies, flaccid paralysis, an...BACKGROUND: Botulism is a rare, life-threatening condition caused by potent neurotoxins that inhibit the release of acetylcholine into the neuromuscular junction, resulting in cranial nerve palsies, flaccid paralysis, and respiratory compromise. Most cases are caused by type A and B toxins produced by Clostridium botulinum. CASE REPORT: Here, we describe a 41-year-old woman who presented with acute onset binocular diplopia, nausea/vomiting, slurred speech, and unsteady gait, symptoms that resemble a posterior fossa stroke. The patient was initially admitted to the stroke service; however, her symptoms quickly progressed to flaccid quadriparesis with generalized areflexia, fixed and dilated pupils, and respiratory failure requiring intubation, raising concerns for neuromuscular junction disorders. Stool and rectal swabs were sent for botulinum toxin screening. Repetitive nerve stimulation showed decremental compound muscle action potential (CMAP) response with 3 Hz stimulation, mild incremental response to exercise, and incremental response with 50 Hz stimulation, findings suggestive of presynaptic pathology. The CDC was contacted and the patient received botulinum antitoxin on the second day of hospitalization. Positive PCR testing on rectal swab was reported on day 4, and the patient was ultimately diagnosed with Type F botulism, an exceedingly rare variant of the disease typically associated with Clostridium baratii. The patient was extubated after two weeks. No source of the toxin was identified. DISCUSSION: This rare type of botulism Type F (less than 1% of all botulism cases) is characterized by a more rapid progression of symptoms compared to typical Type A/B botulism and might present clinically like a posterior circulation stroke. Therefore, maintaining high clinical suspicion for neuromuscular disorders (especially in patients presenting with stroke-like symptoms of the posterior fossa) and early administration of antitoxin are critical factors for mitigating disease severity and improving clinical outcomes.
INTRODUCTION: While use of factor Xa inhibitors has increased, there are relatively few cases of overdose reported. Clinically relevant bleeding is often absent, and the behavior of drug levels in overdose is not fully a...INTRODUCTION: While use of factor Xa inhibitors has increased, there are relatively few cases of overdose reported. Clinically relevant bleeding is often absent, and the behavior of drug levels in overdose is not fully agreed on. CASE REPORT: A 70-year-old male presented after a polysubstance overdose including at least 250 mg of apixaban with massive gastrointestinal (GI) hemorrhage and parafalcine and tentorial subdural hematoma. He was treated with 1 gram tranexamic acid (TXA), anti-inhibitor coagulant complex (FEIBA), and massive transfusion. No further episodes of bleeding were observed. Anti-Xa levels were trended until undetectable. DISCUSSION: Bleeding from an overdose of factor Xa inhibitors is a relatively rare occurrence; however, this case illustrates that life threatening hemorrhage can occur and may require aggressive supportive care. Anti-Xa levels demonstrated a first order pattern of elimination even at markedly supratherapeutic concentrations, consistent with several prior case reports.
INTRODUCTION: Hemodialysis is often used to enhance the clearance of dialyzable poisons, but intradialytic hypotension (IDH) can impede timely toxin removal and impact clinical outcomes. We summarize mechanisms and evide...INTRODUCTION: Hemodialysis is often used to enhance the clearance of dialyzable poisons, but intradialytic hypotension (IDH) can impede timely toxin removal and impact clinical outcomes. We summarize mechanisms and evidence-based strategies to prevent or treat IDH during toxicology-directed hemodialysis. METHODS: We searched PubMed (via MEDLINE), Embase and Web of Science from January 1980 to July 2025 for English language studies addressing IDH during hemodialysis, toxicology-related extracorporeal treatments, or pharmacologic adjuncts (“intradialytic hypotension,” “hemodialysis,” “hypertonic saline,” “albumin,” “vasopressin,” “methylene blue,” “carnitine,” “dialysate calcium,” “dialysate magnesium,” and “toxicology”). We performed snowballing of references from retrieved articles and included both randomized and observational studies without restriction. DISCUSSION: IDH results from the interaction of hypovolemia with inadequate plasma refilling, myocardial stunning, and vasoplegia due to blunted vasopressin release or nitric oxide-mediated vasodilation. Interventions with supportive evidence include albumin to augment oncotic pressure; hypertonic agents to preserve plasma osmolality; methylene blue to inhibit soluble guanylate cyclase; cooled dialysate to blunt vasodilation; optimization of dialysate calcium and magnesium to improve vascular tone and contractility; levocarnitine for myocardial metabolism; and vasopressors for persistent instability. When fluid removal is required, minimizing ultrafiltration or sequencing continuous therapies can improve hemodynamic tolerance. Extracorporeal membrane oxygenation permits simultaneous support and solute clearance in refractory shock. CONCLUSION: Selective use of hyperoncotic albumin or crystalloids, methylene blue, cooled dialysate, tailored dialysate composition, levocarnitine, delayed ultrafiltration, vasopressors/inotropes and extracorporeal membrane oxygenation offers an array of approaches to preserve perfusion, enable adequate toxin clearance, reduce interruptions to therapy, and improve clinical outcomes in poisoned patients requiring extracorporeal toxin clearance.
J Med Toxicol
· 2026 Mar · PMID 41904310
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INTRODUCTION: It is commonly taught that beta blocker toxicity is associated with development of hypoglycemia, however, empirical evidence is lacking. We aimed to evaluate the association of beta blocker toxicity with hy...INTRODUCTION: It is commonly taught that beta blocker toxicity is associated with development of hypoglycemia, however, empirical evidence is lacking. We aimed to evaluate the association of beta blocker toxicity with hypoglycemia. METHODS: We performed a retrospective cohort study of cases reported to a regional poison center from 1/1/2018 to 1/1/2025. Beta blocker toxicity was defined as cases coded as beta blocker exposure with documented bradycardia. Cases of acetaminophen or selective serotonin reuptake inhibitor (SSRI) overdose were selected as controls. Primary outcome was development of hypoglycemia defined as glucose concentration less than 70 mg/dL. A pre-planned subgroup analysis was performed for all groups, comprised of patients meeting the following criteria: single substance exposures, no documented diabetes, and no documented insulin administration. Descriptive statistics were performed, and relative risk for hypoglycemia was calculated between beta blocker and control groups. RESULTS: There were 225 cases that met inclusion criteria for beta blocker toxicity, with 1,586 acetaminophen cases, and 1,955 SSRI cases included as controls. The relative risk of hypoglycemia for beta blockers compared to acetaminophen at any time was 1.44 (95% CI: 0.74, 2.80; p = 0.38) and 1.74 (95% CI: 0.89, 3.38; p = 0.15) compared to SSRI. No differences were identified between groups when evaluating the initial presenting glucose or in the pre-planned subgroup analysis. CONCLUSIONS: There was no significantly increased risk of hypoglycemia in beta blocker poisoned patients compared to controls. This suggests that hypoglycemia would not be an expected finding in beta blocker toxicity.
Nohara R, Kuwahara H, Kawai H
… +4 more, Sano T, Ishikawa K, Kanda T, Nishida Y
J Med Toxicol
· 2026 Apr · PMID 41886018
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BACKGROUND: Habitual exposure to n-hexane can cause polyneuropathy through axonal degeneration and secondary demyelination. To our knowledge, n-hexane-toxic neuropathy presenting with a cauda equina-like syndrome has not...BACKGROUND: Habitual exposure to n-hexane can cause polyneuropathy through axonal degeneration and secondary demyelination. To our knowledge, n-hexane-toxic neuropathy presenting with a cauda equina-like syndrome has not previously been reported. CASE PRESENTATION: A 55-year-old man developed sensory and motor polyneuropathy over a 3-month period, with nerve conduction studies indicating demyelination. Initial treatment for suspected chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with steroids and plasma exchange was ineffective, leading to worsening symptoms. The patient and his colleagues were found to have been habitually exposed to n-hexane in their printing work, and a sural nerve biopsy revealed the pathological findings typical of n-hexane-toxic neuropathy. Notably, cauda equina inflammation was observed on MRI and in the cerebrospinal fluid. Following intravenous immunoglobulin therapy, both neurological symptoms and findings from nerve conduction studies, MRI, and cerebrospinal fluid analysis gradually improved, eventually leading the absence of impairment in activities of daily living. CONCLUSION: In cases of polyneuropathy accompanied by inflammation of the cauda equina, and if exposure to n-hexane cannot be ruled out, sural nerve biopsy could be considered to assess for n-hexane-toxic neuropathy.
Carpenter JE, Love J, Mazer-Amirshahi M
… +4 more, Falise A, Gonzales L, Aldy K, Abston S
J Med Toxicol
· 2026 Apr · PMID 41882449
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These are the selected abstracts for the 2026 American College of Medical Toxicology Annual Scientific Meeting, which will take place from March 20 to 22, 2026, in Boston, Massachusetts. This year the meeting received a...These are the selected abstracts for the 2026 American College of Medical Toxicology Annual Scientific Meeting, which will take place from March 20 to 22, 2026, in Boston, Massachusetts. This year the meeting received a record number of submissions, with 283 abstracts submitted for review. The abstracts accepted for presentation span original research studies, contributions from the Toxicology Investigators Consortium, and case-based work that offers practical clinical insights into uncommon exposures, diagnostic challenges, and management considerations. Together, these presentations demonstrate the expanding scope and scientific rigor of medical toxicology scholarship. They offer attendees timely perspectives on current clinical practice, evolving public health concerns, information technology, advances in toxicologic investigation, and ongoing efforts to improve patient care across diverse populations and practice settings.
Watson CJ, Simpson MD, Saraiya N
… +6 more, Wilkosz CA, Yu MB, Burns MM, Neavyn MJ, Simone KE, Strout TD
J Med Toxicol
· 2026 Apr · PMID 41857443
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INTRODUCTION: Toxicologists may use high dose n-acetylcysteine (HD-NAC) for early-treated high-risk acetaminophen ingestions (EHRAI) given concerns over standard NAC (S-NAC) dosing’s efficacy. We utilize the novel, clini...INTRODUCTION: Toxicologists may use high dose n-acetylcysteine (HD-NAC) for early-treated high-risk acetaminophen ingestions (EHRAI) given concerns over standard NAC (S-NAC) dosing’s efficacy. We utilize the novel, clinically relevant outcome of mean additional 16-hour NAC maintenance infusions (NMI) to evaluate differences in treatment duration for EHRAI patients treated with S-NAC versus HD-NAC. METHODS: Retrospective multistate poison center study from 1/1/2019-7/4/2024 of patients ≥ 13-years-old who were treated with S-NAC or HD-NAC within eight hours of a high-risk acetaminophen ingestion. The primary outcome was mean additional NMI. Secondary outcomes were NAC infusion duration, hepatotoxicity, coagulopathy, transplant, and death. Sensitivity analyses evaluated for robustness of findings. RESULTS: Of 127 included cases, 52.0% (66/127) received HD-NAC. 7.1% (9/127) had anti-peristaltic co-ingestions. HD-NAC cases received more fomepizole (23.1% versus 1.6%; difference 21.1%). Acetaminophen concentrations controlled for time since ingestion were similar (mean acetaminophen ratio for HD-NAC: 2.7, IQR: 2.3, 3.3 versus S-NAC: 2.4, IQR: 2.2, 2.7; difference − 0.3). 26.0% (33/127) received NMI solely for residual detectable serum acetaminophen. There was no difference in mean additional NMI (HD-NAC: 0.53 versus S-NAC: 0.38; p = 0.240). Median NAC infusion durations were equal across groups (21.0; IQR: 21.0, 37.0; difference 0.0) (p = 0.137). One patient per group developed hepatotoxicity; there were no transplants or deaths. Sensitivity analyses yielded similar results. CONCLUSIONS: We found no difference in mean NMI for EHRAI based on NAC dose. These findings support additional NMI as an objective, common, clinically relevant outcome for acetaminophen toxicity research.
Horowitz KM, Hoang D, Kazmierczak S
… +1 more, Castelli R
J Med Toxicol
· 2026 Apr · PMID 41817913
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INTRODUCTION: People have attempted to extract opiates from the surface of unwashed poppy seeds for recreational consumption. However, the opiate quantity within these homemade poppy seed teas is not well known, complica...INTRODUCTION: People have attempted to extract opiates from the surface of unwashed poppy seeds for recreational consumption. However, the opiate quantity within these homemade poppy seed teas is not well known, complicating risk assessment. Prior studies investigating this have used small volume samples made using laboratory-grade equipment, which may not accurately reflect opiate extractions attainable by laypersons. We quantified opiate extraction using recipes, ingredients, and equipment available to the public and at real-world volumes. METHODS: This is a two-part experiment. In the first part, we identified which of eight brewing techniques – collectively representing the possible combinations of variables we identified from our search of online forums – yielded the highest concentration of morphine and codeine. In the second part, the technique identified in the first part was applied to a composite recipe derived from recommendations found on publicly accessible online forums. Three replicates (A-C) of full volume recipes using each of three seed brands (1–3) were made using commonly available equipment. Morphine and codeine concentrations were measured using liquid chromatography/tandem-electrospray mass spectrometry. RESULTS: For part 1, all techniques yielded morphine (range: 138–2873 ng/mL) and codeine (range: 41–1083 ng/mL), but technique 2 produced the greatest yields. For part 2, technique 2 was applied to real-world equipment and ingredient ratios yielding samples with morphine concentrations of 1837–19,483 ng/mL and codeine concentrations of 296–20125 ng/mL. CONCLUSIONS: Brewing poppy seed tea using techniques and proportions replicating real-world extractions produce widely variable quantities of morphine and codeine, including some that may be clinically relevant.
Chandru P, Schriber K, Brasted HBF
… +2 more, Butler E, Gunja N
J Med Toxicol
· 2026 Apr · PMID 41792544
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BACKGROUND: Sedative overdoses, particularly involving opioids, γ-hydroxybutyrate (GHB), and benzodiazepines, are an increasing contributor to toxicology admissions and intensive care unit (ICU) utilisation in Australia....BACKGROUND: Sedative overdoses, particularly involving opioids, γ-hydroxybutyrate (GHB), and benzodiazepines, are an increasing contributor to toxicology admissions and intensive care unit (ICU) utilisation in Australia. While pharmacological mechanisms are well characterised, identifying which patients will deteriorate remains challenging. Existing risk stratification tools, such as the Glasgow Coma Scale (GCS), lack toxicology-specific nuance and may not adequately account for early physiological derangement, highlighting the need for improved, patient-centred risk assessment. AIMS: To evaluate clinical and exposure-related features associated with ICU admission, endotracheal intubation, and in-hospital complications following sedative overdose. METHODS: This retrospective cohort study included patients referred to a district toxicology service with suspected sedative overdose between November 2022 and November 2023. Data extracted from electronic medical records included demographics, ingestion characteristics, clinical course, and investigation results. Sedatives were defined by central nervous system depressant effects. Outcomes were ICU admission, endotracheal intubation, and in-hospital complications. Associations were examined using univariable analyses and multivariable logistic regression; venous pH was modelled separately using penalised logistic regression. RESULTS: A total of 374 patients were included. Common agents were benzodiazepines (32.1%), opioids (29.1%), and GHB (20.6%). In-hospital complications occurred in 35.8% of patients, ICU admission in 17.9%, and intubation in 13.6%. After adjustment, ICU admission was independently associated with lower venous pH and non-benzodiazepine GABA-ergic agent ingestion (e.g. pregabalin and Z-drugs) (adjusted OR 3.35, p = 0.04). Lower venous pH was consistently associated with all adverse outcomes. The model-estimated probability of intubation increased non-linearly with worsening acidaemia, rising from 8% at pH 7.35 to 66% at pH 7.20. In-hospital complications were independently associated with opioid ingestion (adjusted OR 3.81, p < 0.001) and lower GCS, while intubation was associated with lower GCS and lower venous pH. GHB ingestion was inversely associated with intubation. CONCLUSION: Lower GCS, reduced venous pH, and ingestion of high-risk sedative agents—particularly opioids and non-benzodiazepine GABA-ergic ingestion —were key features associated with clinical deterioration in sedative overdose. These findings support multifactorial, toxicology-specific risk stratification incorporating early physiological and pharmacological markers, with prospective validation required before clinical implementation.
Senthilkumar A, Hays HL, Kistamgari S
… +4 more, Rine NI, Rhodes AL, Gaw CE, Smith GA
J Med Toxicol
· 2026 Apr · PMID 41784916
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INTRODUCTION: As glucagon-like peptide-1 receptor agonist (GLP-1) use has increased among children, a better understanding of the related adverse effects in this population is needed. METHODS: National Poison Data System...INTRODUCTION: As glucagon-like peptide-1 receptor agonist (GLP-1) use has increased among children, a better understanding of the related adverse effects in this population is needed. METHODS: National Poison Data System data from 2017 to 2024 were analyzed to compare characteristics and trends of exposures involving GLP-1s reported to United States (US) poison centers (PCs) among children 6-17 years old with those of adults. RESULTS: There were 13,924 single-substance GLP-1 exposures reported to US PCs from 2017 to 2024. The rate of exposures per one million US population increased by 1,830.8% from 0.97 in 2017 to 18.79 in 2024, including a 4,805.0% increase among children 6-17 years old from 0.04 in 2017 to 1.97 in 2024, with the majority of the increase occurring after 2021. Most exposures (91.7%) were associated with no or mild effects, while moderate effects were observed in 8.0% and major effects occurred in 42 exposures; there were two deaths. Children 6-17 years old were more likely (RR: 2.66, 95% CI: 1.73-4.11) to be admitted than adults, and children 12-17 years old were more likely (RR: 1.68, 95% CI: 1.08-2.63) to experience a more serious medical outcome than adults. Children 6-17 years old with at least one clinical effect experienced vomiting (88.2%) more commonly than adults (61.3%) (RR: 1.44, 95% CI: 1.34-1.55). Additionally, exposures among children 6-17 years old were more likely to be attributable to intentional misuse (RR: 8.12, 95% CI: 6.47-10.17) than among adults. CONCLUSIONS: This study provides national-level, real-world findings that may help inform clinical practice.
Kent JT, Culbreth R, Lebin JA
… +14 more, Burkhart K, Hendrickson RG, Dezman ZDW, Aldy K, Brent J, Falise A, Campleman S, Logan BK, Levine M, Chary M, Krotulski A, Perrone J, Wax P, ToxIC DOTS Study Group
J Med Toxicol
· 2026 Apr · PMID 41781809
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BACKGROUND: Fentanyl concentrations are typically interpreted in forensic contexts using postmortem and driving under the influence data, both of which have important limitations. This study describes fentanyl and norfen...BACKGROUND: Fentanyl concentrations are typically interpreted in forensic contexts using postmortem and driving under the influence data, both of which have important limitations. This study describes fentanyl and norfentanyl concentrations measured in an acute, clinical setting among patients presenting to the emergency department with a suspected opioid overdose. METHODS: A prospective observational study was performed utilizing the Toxicology Investigators Consortium (ToxIC) Drug Overdose Toxico-Surveillance (DOTS) Reporting Program enrolling patients ≥ 13 years old from April 2023 to July 2024 following a life-threatening overdose treated at 17 EDs within the United States. Fentanyl and norfentanyl concentrations were determined by liquid chromatography tandem quadrupole mass spectrometry (lower limit of quantification (LLOQ) 1 ng/mL). Fentanyl and norfentanyl concentrations were summarized using descriptive statistics and stratified by time of ED presentation to blood collection. Fentanyl concentrations were also stratified by norfentanyl concentrations. RESULTS: Three hundred and thirty-one patients presented with a clinical presentation consistent with an opioid overdose and were included in the study. Of these, 248 (74.9%) had fentanyl concentrations above the LLOQ. The median concentration of fentanyl and norfentanyl was 4.5 ng/mL (IQR: 2.4, 8.8) and 2.7 ng/mL (IQR:1.6, 5.3), respectively. The median time to blood draw was 165 min. The median fentanyl/norfentanyl (F/NF) ratio was 0.5 (IQR: 0.4, 1.0). CONCLUSIONS: Quantitative fentanyl and norfentanyl concentrations in the acute emergency department setting among patients with a suspected opioid overdose were lower than those in the postmortem literature with significant toxicity observed at levels below the LLOQ. Use of an arbitrary F/NF ratio of 1 did not delineate acute exposure.