{"title":"Abnormalities in brain magnetic resonance imaging associated with vigabatrin therapy in an infant with infantile epileptic spasms syndrome.","authors":"Maria Inês de Sá, Filipa Proença","doi":"10.1080/15563650.2024.2418979","DOIUrl":"https://doi.org/10.1080/15563650.2024.2418979","url":null,"abstract":"<p><strong>Introduction: </strong>Vigabatrin, an anticonvulsant drug used for refractory epilepsy and as first-line treatment for infantile epileptic spasms syndrome, can rarely cause brain abnormalities detectable on magnetic resonance imaging. These complications, potentially related to dose, young age, and concomitant high doses of adrenocorticotropic hormone and/or prednisolone, can lead to neurological symptoms. Upon withdrawal or dose reduction, symptoms and imaging changes tend to resolve.</p><p><strong>Case summary: </strong>A 7-month-old infant diagnosed with infantile epileptic spasms syndrome started treatment with vigabatrin and prednisolone. However, spasms recurred, prompting an increase in the dose of vigabatrin and the addition of adrenocorticotropic hormone, which reduced the frequency of spasms. The patient later developed encephalopathy and upper limb tremors.</p><p><strong>Images: </strong>Magnetic resonance imaging revealed symmetrical hyperintense lesions with concomitant restricted diffusion localized in the thalami, basal ganglia, brainstem, and cerebellar dentate nuclei.</p><p><strong>Conclusion: </strong>We report an infant with infantile epileptic spasms syndrome treated with vigabatrin who developed abnormalities on magnetic resonance imaging. There is currently no treatment other than drug withdrawal or reduction.</p>","PeriodicalId":10430,"journal":{"name":"Clinical Toxicology","volume":" ","pages":"1-2"},"PeriodicalIF":3.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chelsea V Hayman, Kyle D Pires, Emily T Cohen, Rana Biary, Mark K Su, Robert S Hoffman
{"title":"Authors reply to comment on Hayman et al. \"elevated osmol gaps in patients with alcoholic ketoacidosis\".","authors":"Chelsea V Hayman, Kyle D Pires, Emily T Cohen, Rana Biary, Mark K Su, Robert S Hoffman","doi":"10.1080/15563650.2024.2440551","DOIUrl":"https://doi.org/10.1080/15563650.2024.2440551","url":null,"abstract":"","PeriodicalId":10430,"journal":{"name":"Clinical Toxicology","volume":" ","pages":"1-2"},"PeriodicalIF":3.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Why so blue? A novel presentation of methaemoglobinaemia secondary to an inhaled occupational nitric acid exposure.","authors":"James M Colalillo, Kirsty Skinner","doi":"10.1080/15563650.2024.2440547","DOIUrl":"https://doi.org/10.1080/15563650.2024.2440547","url":null,"abstract":"<p><strong>Introduction: </strong>Nitric and hydrofluoric acids are commonly used in the commercial cleaning industry. We are unaware of reports of nitric acid inhalation forming methaemoglobin. Additionally, methaemoglobinaemia and treatment with methylthioninium chloride (methylene blue) may precipitate clinical uncertainty due to similar wavelengths of absorbance in pulse oximetry.</p><p><strong>Cases: </strong>We report two patients with respiratory distress from symptomatic methaemoglobinaemia following a prolonged, inhaled occupational exposure to nitric acid in the context of industrial cleaning. Their methaemoglobinaemia was successfully treated with methylthioninium chloride, per remote toxicology advice. However transient oxygen desaturation as reported by pulse oximetry resulted in concern from the treating team.</p><p><strong>Discussion: </strong>The liberation of oxides of nitrogen from nitric acid bypasses the upper airway without irritation and dissolves in the mucoid lower respiratory tract, oxidising haemoglobin to methaemoglobin. Prolonged undetected exposure with filter saturation, and impaired ventilation is the proposed cause of methaemoglobinaemia in the cases presented. Additionally, methylthioninium chloride absorbs light at the 660 nm wavelength interfering with pulse oximeter interpretation, precipitating the appearance of rapid, severe oxygen desaturation.</p><p><strong>Conclusion: </strong>Lack of upper airway irritation can lead to unrecognised prolonged nitric acid fume exposure causing methaemoglobinaemia. Remote toxicology advice should include pulse oximeter interference expectations in the presence of methaemoglobinaemia and when administering methylthioninium chloride.</p>","PeriodicalId":10430,"journal":{"name":"Clinical Toxicology","volume":" ","pages":"1-3"},"PeriodicalIF":3.0,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michael Keenan, Precious Alabi, Ahmed Alsakha, Jeanna Marraffa, Susan Wojcik, Sarah Burke
{"title":"Does the time between doses in an unintentional double dose bupropion exposure affect the incidence of adverse effects? A retrospective cohort study.","authors":"Michael Keenan, Precious Alabi, Ahmed Alsakha, Jeanna Marraffa, Susan Wojcik, Sarah Burke","doi":"10.1080/15563650.2024.2439019","DOIUrl":"https://doi.org/10.1080/15563650.2024.2439019","url":null,"abstract":"<p><strong>Introduction: </strong>Unintentional therapeutic errors with bupropion are common. The impact of the timing of the second dose in a double dose exposure on adverse effects is not well studied. This study aims to compare adverse effects between double doses separated by <720 min and ≥720 min.</p><p><strong>Methods: </strong>This was a retrospective cohort study of unintentional double dose bupropion ingestions in patients reported to a regional poison center between January 2018 and December 2022. Patients were included if the double dose was their own medication, unintentional, and a single substance exposure. Data collected included age, gender, bupropion formulation, prescribed home dose, dosing error details, time between doses, caller site, referral to the emergency department, patient observation at healthcare facilities, clinical effects, and outcome.</p><p><strong>Results: </strong>Among 663 cases screened, 294 met inclusion criteria. The majority involved extended-release preparations (69.0%). Seventy-four were observed in a healthcare facility and monitored for 24 h from initial dose. The incidence of seizures was 5.3%, including one case not observed for a full 24 h. There was no significant difference in the incidence of seizures (2.7% versus 7.7%), tachycardia (27.0% versus 30.8%), hypertension (18.9% versus 38.5%) other signs/symptoms (27.0% versus 23.1%), or any signs/symptoms (48.6% versus 61.5%) between double doses of extended release bupropion separated by <720 min and those separated by ≥720 min, respectively.</p><p><strong>Discussion: </strong>In patients with double dose exposures to extended-release bupropion, it does not appear that the timing of the second dose can be used to risk-stratify patients. Our data are limited by sample size.</p><p><strong>Conclusion: </strong>In this study, the time between double doses of bupropion did not affect the incidence of seizure, tachycardia, hypertension, other signs/symptoms, or any signs/symptoms. Larger, prospective studies investigating this difference would strengthen our understanding and management of these patients.</p>","PeriodicalId":10430,"journal":{"name":"Clinical Toxicology","volume":" ","pages":"1-6"},"PeriodicalIF":3.0,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142834342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Robert G Hendrickson, Amber L Lin, Courtney Temple
{"title":"Pediatric exposure to illicit fentanyl is associated with drug availability in the community.","authors":"Robert G Hendrickson, Amber L Lin, Courtney Temple","doi":"10.1080/15563650.2024.2438271","DOIUrl":"https://doi.org/10.1080/15563650.2024.2438271","url":null,"abstract":"<p><strong>Introduction: </strong>Fentanyl has replaced diacetylmorphine (heroin) as the primary illicit opioid in the United States. Over the last several years, exposures to illicit fentanyl in small children have increased nationally. We hypothesized that the increase in illicit fentanyl in the community, as measured by regional drug seizures, would be associated with the number of pediatric exposures to illicit fentanyl.</p><p><strong>Methods: </strong>To assess the number of pediatric illicit fentanyl exposures, we searched the regional poison center database for human exposures in children under 6 years old from January 1, 2019-December 31, 2023. We searched for all cases with fentanyl in the substance field and excluded cases that identified prescription fentanyl in the substance code, product code, or had an exposure reason not consistent with illicit fentanyl. We quantified illicit fentanyl drug seizures in our state by using the Drug Enforcement Administration data. We used Poisson regression to assess the association between drug availability in the community (drug seizures) and pediatric fentanyl exposures.</p><p><strong>Results: </strong>Between 2019 and 2023, there was an increase in both illicit fentanyl drug seizures (from 11.7 kg/year to 177 kg/year) and pediatric fentanyl exposures (from zero to 16), and there was a significant association (incident rate ratio 1.90; 95% CI: 1.50-2.53; <i>P</i> <0.001) between these rates.</p><p><strong>Discussion: </strong>We report a strong association between drug availability in the community and pediatric exposures, suggesting that drug seizure data may be a valuable tool for poison centers, medical toxicologists, and public health officials.</p><p><strong>Conclusions: </strong>Our data suggest that monitoring regional drug seizure data may be a tool to determine new trends in pediatric exposure, guide research in the area, and target outreach and education.</p>","PeriodicalId":10430,"journal":{"name":"Clinical Toxicology","volume":" ","pages":"1-3"},"PeriodicalIF":3.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katherine Z Isoardi, Angela L Chiew, Cuong Do, Michael Humphreys, Ahmead Mustafa, Michael S Roberts, Geoffrey K Isbister
{"title":"A prospective study of acute propranolol overdose defining dose thresholds of severe toxicity (ATOM - 9).","authors":"Katherine Z Isoardi, Angela L Chiew, Cuong Do, Michael Humphreys, Ahmead Mustafa, Michael S Roberts, Geoffrey K Isbister","doi":"10.1080/15563650.2024.2435397","DOIUrl":"https://doi.org/10.1080/15563650.2024.2435397","url":null,"abstract":"<p><strong>Introduction: </strong>Propranolol is a beta-adrenoceptor blocking drug with sodium channel-blocking properties that can cause life-threatening toxicity in overdose. Limited research defines dose thresholds of toxicity. We aimed to investigate propranolol overdose and dose thresholds for severe toxicity.</p><p><strong>Material and methods: </strong>This is a prospective series of patients with acute propranolol overdose ≥360 mg from August 2014 to December 2023 enrolled through the Australian TOxicology Monitoring (ATOM) collaboration. Severe toxicity was defined as seizure, coma, inotrope therapy, electrocardiographic evidence of sodium channel blockade, or cardiac arrest.</p><p><strong>Results: </strong>There were 209 presentations in 165 patients (median age 30 years [range 15-80 years]; 117 females, 71%). The median reported dose ingested was 1,000 mg (IQR: 600-2,000 mg; range 360-16,000 mg). Co-ingestion occurred in 155 (74%) patients, most commonly involving benzodiazepines (<i>n</i> = 52). Bradycardia (heart rate <50 beats/min) occurred in 41 (20%), and hypotension (systolic blood pressure <90 mmHg) in 88 (42%). Severe toxicity occurred in 51 patients (24%), with 17 (8%) having a seizure and 29 (14%) developing coma. Forty-one (20%) received inotropes, including 31(15%) who were given epinephrine and 20 (10%) high-dose insulin. Electrocardiographic evidence of sodium channel blockade occurred in 16 (8%). Seven (3%) had a cardiac arrest (reported dose range 2,400-16,000 mg), with two deaths following the ingestion of propranolol 4,000 mg and 16,000 mg. The median length of stay was 17 h (IQR: 11-32 h). In 79 patients who ingested only propranolol, the lowest reported propranolol dose for hypotension was 400 mg and for bradycardia, 800 mg. The lowest reported dose for severe toxicity was propranolol 2,000 mg. In those ingesting propranolol only, 17 of 32 (53%) patients who ingested ≥2,000 mg had severe toxicity.</p><p><strong>Discussion: </strong>Severe toxicity was common, occurring in a quarter of all propranolol overdoses and half of the isolated propranolol ingestions (≥2,000 mg). The outcome was usually favourable with good supportive care, even in severe toxicity.</p><p><strong>Conclusion: </strong>The dose threshold for severe toxicity in isolated propranolol overdose appeared to be 2,000 mg.</p>","PeriodicalId":10430,"journal":{"name":"Clinical Toxicology","volume":" ","pages":"1-9"},"PeriodicalIF":3.0,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jason Dietz, Samantha S Klein, Rana Biary, Stephen Blumberg, Suzanne Roberts, Asher Bercow, Bernard Goldwasser, Robert S Hoffman
{"title":"Pediatric opioid use-associated neurotoxicity with cerebellar edema (POUNCE) syndrome.","authors":"Jason Dietz, Samantha S Klein, Rana Biary, Stephen Blumberg, Suzanne Roberts, Asher Bercow, Bernard Goldwasser, Robert S Hoffman","doi":"10.1080/15563650.2024.2435396","DOIUrl":"https://doi.org/10.1080/15563650.2024.2435396","url":null,"abstract":"<p><strong>Introduction: </strong>Unfortunately, children are not spared from the devastating effects of the ongoing opioid epidemic. In rare cases, young children exposed to opioids present with unique neuroimaging findings affecting the white matter, reminiscent of what was once seen with diacetylmorphine (heroin)-associated leukoencephalopathy. This constellation of findings is termed the pediatric opioid use-associated neurotoxicity with cerebellar edema (POUNCE) syndrome.</p><p><strong>Case summary: </strong>A 31-month-old child was found floppy and unresponsive. Upon hospital arrival, there was right gaze deviation, shaking of the arms and legs, miosis, and bradypnea. Response to naloxone was incomplete, and methadone was confirmed in the child's urine.</p><p><strong>Images: </strong>Magnetic resonance imaging of the brain performed 24 h after admission showed abnormal T2/FLAIR hyperintensity with associated restricted diffusion symmetrically involving the cerebellar hemispheres.</p><p><strong>Conclusion: </strong>The imaging findings, although far from pathognomonic, should be recognizable by radiologists and toxicologists when considering possible opioid exposure in a young child.</p>","PeriodicalId":10430,"journal":{"name":"Clinical Toxicology","volume":" ","pages":"1-3"},"PeriodicalIF":3.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Electrocardiographic changes in severe quetiapine poisoning.","authors":"Fumiya Inoue, Yuji Okazaki, Toshihisa Ichiba, Takuyo Chiba, Akira Namera","doi":"10.1080/15563650.2024.2436618","DOIUrl":"https://doi.org/10.1080/15563650.2024.2436618","url":null,"abstract":"<p><strong>Introduction: </strong>Quetiapine shares sodium channel-blocking properties with tricyclic antidepressants. We present the electrographic findings in two patients with severe quetiapine poisoning.</p><p><strong>Case summaries: </strong>Two patients poisoned with quetiapine presented with impaired consciousness, requiring mechanical ventilation and vasopressor support, with one also experiencing status epilepticus. Their peak serum quetiapine concentrations were 4.52 mg/L and 25.6 mg/L.</p><p><strong>Images: </strong>On admission, electrocardiograms for both patients revealed a tall R wave in lead aVR, deep S wave in lead I, and QRS complex duration of 120 ms. These findings gradually resolved in parallel with the improvement in their symptoms.</p><p><strong>Conclusion: </strong>Severe quetiapine poisoning may cause electrographic changes. Further studies are needed to determine the utility of these electrocardiogram findings for predicting the severity of quetiapine poisoning.</p>","PeriodicalId":10430,"journal":{"name":"Clinical Toxicology","volume":" ","pages":"1-3"},"PeriodicalIF":3.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}