Introduction We will investigate the medical necessity of pediatric emergency department presentations, specifically for emergency department poison cases where a poison control center was not contacted prior to presenting. Methods A retrospective analysis of 348 poison control center cases involving patients aged < six, originating from a healthcare facility were evaluated. Toxicologists were presented with case summaries and were asked: “would you send this patient to the emergency department?” Evaluators answered on a 4-point Likert scale from “definitely would not send” to “definitely would send.” Reviewers had the opportunity to write in additional information that would be beneficial to deciding their disposition. To simulate the need to make a yes or no decision on whether to send, Likert scores were manipulated into a binomial score of 0/1. Binomial regression analysis and qualitative thematic analysis were completed. Results Toxicologists found that 38% of patients definitely did not require emergency department evaluation, and 27% were unlikely to require it. The presence of clinical symptoms were significantly associated with increased concern by toxicologists. Qualitative analysis from reviewer free text case comments, demonstrated that understanding the situation surrounding the exposure (certainty, past medical history, etc. n = 26) and presence of specific symptoms in each case (fever, vomiting, etc. n = 25) were desired to better determine the need for an emergency department. Discussions About 65% of cases were evaluated as not requiring emergency department evaluation. The presence of clinical symptoms is a key factor related to clinician level of concern. Further work should include finding ways to prevent these emergency department presentations. Conclusions Many emergency department evaluations for poison exposure amongst children less than six years old are not medically required. Further work should focus on improving parental knowledge of poison centers and poison safety, while continuing to promote poison centers as accessible resources to the public.

Introduction The common krait (Bungarus caeruleus) is a leading cause of neuroparalytic snake envenomation in South Asia. Current guidelines recommend escalation from 10 to 20 vials of polyvalent antivenom if neurotoxicity persists, despite limited evidence supporting this strategy. Methods This open-label, randomized pilot study was conducted in North India, enrolling patients with krait envenomation who presented with neurotoxic paralysis but without respiratory failure. Patients were assigned to receive either 10 vials or 20 vials of polyvalent antivenom. The primary outcome was time to recovery from neurotoxic paralysis. Secondary outcomes included the need for invasive mechanical ventilation, time from enrolment to intubation, duration of mechanical ventilation, and in-hospital mortality. Results Of 97 patients screened, 53 underwent randomization (26 assigned to the 10-vial group and 27 to the 20-vial group). Baseline characteristics, severity of neurotoxic paralysis, laboratory parameters, and time from bite to enrolment (median 5 hours) were similar between groups. The median time to recovery from neurotoxic paralysis was 42.5 hours (IQR, 29.8–54.3) in the 10-vial group and 45.0 hours (IQR, 35.5–59.5) in the 20-vial group (median difference, −5.0 hours; 95% CI, −15.5 to 5.5; P = 0.24); Kaplan–Meier analysis showed no significant between-group difference (log-rank P = 0.38). Invasive mechanical ventilation was required in 34.6% of patients in the 10-vial group and 22.2% in the 20-vial group (risk ratio, 1.34; 95% CI, 0.77 to 2.31). Among ventilated patients, the median time to intubation and duration of mechanical ventilation were similar between groups. One death occurred in the 10-vial group. Discussion Routine escalation of antivenom dosing may not be necessary in krait neurotoxicity with close respiratory monitoring and supportive care. Conclusions Among patients with neuroparalytic krait envenomation who presented without respiratory failure, a 10-vial antivenom regimen was associated with clinical outcomes comparable to those with a 20-vial regimen.

Introduction Ethylene glycol intoxication can be life-threatening, but clinical signs lack sensitivity and specificity. Hence, the diagnosis relies on the detection of this compound in serum. Chromatographic methods are the gold standard, but they are hard to routinely apply. As a result, we implemented an enzymatic assay on automated analyzers. The aim of this study is to review the results of real samples and compare both methods over 10 years. Methods The enzymatic assay relies on oxidation of ethylene glycol to glycolaldehyde. All results were confirmed by gas chromatography coupled to mass spectrometry. Both methods share a lower limit of quantification of 50 mg/L. Results During the study period, 405 unique patient samples were analyzed: 305 samples tested negative by both methods (75.3% true negative) while 34 tested positive on both instruments (8.4% true positive). Only four samples tested negative by enzymatic assay were positive with chromatography (<1% false negative) and chromatography failed to confirm 62 samples that screened positive by enzymatic assay (15.3% false positive), yielding a sensitivity of 89% and a specificity of 83%. Discussion The sensitivity and specificity of the enzymatic assay are high. Most of the false positive samples were below a treatment threshold (200 mg/L). Some false positive results could be explained by high blood concentrations of lactate and/or high lactate dehydrogenase activity but a small proportion remained unexplained. The main advantage of the enzymatic reagent is a significant reduction of turnaround times compared to chromatography. Conclusions A rapid enzymatic assay for ethylene glycol allows for quick adjustments to patient care, avoiding unnecessary treatment or, conversely, insufficient treatment. However, any positive result should be confirmed by chromatography and interpreted in the context of the patient’s medical history and clinical findings.

Background Paracetamol poisoning and the associated liver damage can be effectively managed by the timely administration of acetylcysteine. Most treatment protocols depend on the line intersecting 150 mg/L (992 μmol/L) at 4 h on the Rumack–Matthew nomogram (150-treatment line), which requires accurate determination of ingestion time to assess risk. The paracetamol concentration aminotransferase activity multiplication product has emerged as a predictive measure for paracetamol-induced hepatotoxicity in patients receiving acetylcysteine, without necessitating the precise knowledge of ingestion time. This study aims to assess the diagnostic performance of the multiplication product in identifying cases with paracetamol concentrations surpassing the 150-treatment line and to establish an optimal cutoff value for this clinical tool. Methods A retrospective review of acute paracetamol overdoses admitted to Siriraj Hospital in Bangkok, Thailand, from January 2007 to December 2016 was conducted. The multiplication product was calculated by multiplying the serum paracetamol concentration (mg/L) by the higher activity of alanine aminotransferase or aspartate aminotransferase (U/L), both measured from simultaneous blood samples. The diagnostic accuracy of the multiplication product in predicting paracetamol concentrations above the 150-treatment line was evaluated through receiver operating characteristic curve analysis, sensitivity, and specificity. The optimal cutoff value was determined using the Youden index. Results Among the 934 patients included, 43.5% (406 cases) presented paracetamol concentrations above the 150-treatment line. The multiplication product had an area under the receiver operating characteristic curve of 0.874. An optimal cutoff of 1,501.6 mg * U/L2 yielded a sensitivity of 84.8% and a specificity of 79.8%. Discussion The 150-treatment line on the Rumack–Matthew nomogram demonstrated a sensitivity of 100.0% (95% CI: 93.7 − 100.0%) and a specificity of 60.2% (95% CI: 56.9 − 63.5%) for predicting hepatotoxicity. In comparison, the 1,500 mg * U/L2 cutoff of the paracetamol concentration aminotransferase activity multiplication product showed a sensitivity of 98.3% (95% CI: 90.6 − 100.0%) and a specificity of 50.7% (95% CI: 47.4 − 54.1%). Conclusions The paracetamol concentration aminotransferase activity multiplication product demonstrates predictive ability for serum paracetamol concentrations at or above the 150-treatment line on the Rumack–Matthew nomogram.

Introduction Antidysrhythmic medications are commonly prescribed, but there is little information on the incidence of adverse effects following an inadvertent extra dose of these medications. This poses a challenge to poison centers when trying to decide which patients need to be sent to a healthcare facility for monitoring. Methods A retrospective data review of cases reported to a regional poison center between January 1, 2012 and December 31, 2022 was performed. Cases were included if the exposure was a double dose or less of the patient’s own antidysrhythmic medication, the exposure was unintentional or a result of therapeutic error, and the antidysrhythmic(s) belonged to Vaughan Williams Class I or III. Cases were included even if other medications were included in the therapeutic error. Descriptive data were collected on cases meeting the inclusion criteria. Results One hundred and sixty-two exposures were included. Of these, only 49 were monitored in a healthcare facility for which coded outcomes were available. Of these, the majority had no or minor effects (83.7%). Two of the exposures developed hypotension, but both also involved either a beta-adrenoceptor blocking drug or a calcium-channel blocker. Of the 25 cases that only included an antidysrhythmic, adverse effects were even less common, with 92.0% having no or only minor effects. Discussion In this small cohort, adverse events were uncommon with inadvertent extra dose antidysrhythmic exposures. However, serious outcomes have been reported in other studies. It appears adverse events are less common if the extra dose exposure does not involve other cardioactive medications. Conclusions Extra-dose exposures of some antidysrhythmics belonging to Vaughan Williams Class I or III were generally well tolerated, but more data are needed to determine whether certain patients can be safely monitored at home. For example, only three cases involved Class IA drugs. Based on our findings, patients who reportedly ingest an extra dose of an antidysrhythmic plus another cardioactive medication should be evaluated at a healthcare facility.