While the traditional intravenous N-acetylcysteine (NAC) dosing regimen works well for the vast majority of acetaminophen overdoses, there may be cases of massive overdose where additional NAC may be ...necessary. Recent evidence suggests that patients with acetaminophen concentrations above the "300-line" develop hepatotoxicity at a higher rate than those below the 300-line, suggesting that an increase of dose may be beneficial at this cut-off. Additional clinical data suggest a further increase in doses at the 450-line and 600-lines. I propose a strategy for step-wise increases in NAC dosing in response to high acetaminophen concentrations at the 300-, 450-, and 600-lines after acute massive acetaminophen overdoses.
Acute cannabis toxicity Noble, Matthew J.; Hedberg, Katrina; Hendrickson, Robert G.
Clinical toxicology (Philadelphia, Pa.),
08/2019, Letnik:
57, Številka:
8
Journal Article
Recenzirano
Objective: We describe the clinical effects of, and products associated with, acute exposures to cannabis during the early legalization period of recreational cannabis in Oregon and Alaska.
Methods: ...This was an observational study of Oregon/Alaska Poison Center data between 4 December 2015 and 15 April 2017. A standardized data collection instrument was created for this study that captured information about cannabis product description, route of exposure, intentional vs unintentional exposure, product dose, product manufacture source, product ownership source, initial vital signs, clinical signs and symptoms, and subject disposition. Subjects were included if the Poison Center received a call about an acute exposure to cannabis from the subject, subject's family member or friend, or healthcare worker participating in the subject's care. Subjects were excluded if there was no evident exposure, the exposure was chronic, there were co-ingestants, or the subject was non-human (e.g. pet).
Results: Two hundred fifty three individuals were acutely exposed to cannabis (median age 20 years; range 8 months - 96 years; 54.2% males): 71 (28.1%) children (<12 years), 42 (16.6%) adolescents (12-17 years), and 140 (55.3%) adults (≥18 years).
Children were most likely to unintentionally (98.6%) ingest (97.2%) homemade (35.2%) edibles (64.8%) belonging to a family member (73.2%) and experience sedation (52.1%). Adults were most likely to intentionally (88.6%) ingest (66.4%) retail (40.0%) edibles (48.6%) and experience neuroexcitation (47.1%). Adolescents' exposures had similarities to both adult and children; they were most likely to intentionally (81.0%) ingest (50.0%) homemade (23.8%) edibles (45.2%) belonging to a friend (47.3%) and to experience either neuroexcitation (42.9%) or sedation (40.5%).
Among all ages, tachycardia and neuroexcitation were more likely following inhalation exposures compared to ingestions. Eight subjects were admitted to an intensive care unit, including three patients who were intubated; one subject died. Edibles were the most common products to cause symptoms in all age groups, while concentrated products were more likely to lead to intubation, especially when ingested. Children in particular had a higher likelihood of intensive care unit admission and intubation following exposure to concentrated products.
Conclusions: Neurotoxicity is common after acute cannabis exposures. Children experienced unintentional exposures, particularly within the home and occasionally with major adverse outcomes. Concentrated products such as resins and liquid concentrates were associated with greater toxicity than other cannabis products. These findings may help guide other states during the early retail cannabis legalization period.
Introduction: E-cigarettes are battery-powered electronic nicotine delivery systems that simulate smoking by vaporizing nicotine-containing solutions. Systematic published data on e-liquid toxicity ...and exposures are limited to case reports and retrospective studies. Prospectively-collected data on the type of exposure, symptomatology, duration of symptoms, and concentration/flavor of e-fluids has not been published.
Methods: This was a prospective observational study over a 42-month period (07/01/2014-12/31/2017). For all calls to a single poison center that involved e-cigarette devices or refill fluid, a data collection instrument was filled out by the specialist in poison information (SPI).
Results: Two hundred sixty-five total cases were identified, including 193 children and 72 adults. The majority of both pediatric (72%; 139/193) and adult (61%; n = 44/72) exposures involved e-liquid refill containers or fluid. Fifty-six percent (n = 108/193) of pediatric exposures involved ingestion of refill liquid. Though children who ingested e-liquid received only a small amount, initial symptoms were evident in 32% (n = 35/108) of cases. Children who did not ingest or inhale the products were less likely to develop toxicity. Only 2 children who were asymptomatic on initial call became symptomatic on follow-up. Most patients symptoms resolved within 4 hours. Seventy-one specific products/brands were identified with nicotine concentrations ranging from 0 mg/mL to 60 mg/mL with one product containing 3000 mg in a single bottle. A variety of flavors were identified, including several with names that may be attractive to toddlers or adolescents.
Discussion: E-cig exposures tend to produce irritant effects from topical exposures and nicotine toxicity from ingestions, as well as some dermal and "sucking" toddler exposures.
Conclusion: Exposure to e-cig fluid or device frequently causes mild symptoms and rarely may produce systemic nicotine toxicity.
The aim of this narrative review is to describe the toxicologic confounders of brain death currently reported in the literature to offer guidance for physicians assessing brain death after a toxic ...exposure. We established an a priori definition of a “brain death mimic” as an unresponsive, intubated patient missing some, but not all brainstem reflexes. We completed a review of the literature utilizing MEDLINE and EMBASE to find case reports of patients of all ages in English, French, and Spanish meeting the criteria and hand searched the references of the results. We recorded xenobiotic dose, duration of physical exam suggesting brain death, and how the cases failed to meet full brain death criteria, when available. Fifty-six cases representing 19 different substances met the a priori definition of brain death mimic. Xenobiotic toxicities included: snake envenomation (13), baclofen (11), tricyclic antidepressants (8), bupropion (7), alcohols (4), antiepileptic agents (3), barbiturates (2), antidysrhythmics (2), organophosphates (2), and one case each of magnesium, succinylcholine, tetrodotoxin, and zolpidem. All patients except one survived to discharge and the majority at their baseline physical health. The most common means by which the cases failed brain death examination prerequisites was via normal neuroimaging. The xenobiotics in this review should be considered in cases of poisoning resulting in loss of brainstem reflexes and addressed before brain death determination. Brain death diagnosis should not be pursued in the setting of normal cerebral imaging or incomplete evaluation of brain death prerequisites.
Poisoning may lead to respiratory failure, shock, cardiac arrest, or death. Extracorporeal membrane oxygenation (ECMO) may be used to provide circulatory support, termed venoarterial (VA) ECMO; or ...respiratory support termed venovenous (VV) ECMO. The clinical utility of ECMO in poisoned patients remains unclear and guidelines on its use in this setting are lacking.
To perform a literature search and narrative review on the use of ECMO in poisonings. Additionally, to provide recommendations on the use of ECMO in poisonings from physicians with expertise in ECMO, medical toxicology, critical care, and emergency medicine.
A literature search in Ovid MEDLINE from 1946 to October 14, 2020, was performed to identify relevant articles with a strategy utilizing both MeSH terms and adjacency searching that encompassed both extracorporeal life support/ECMO/Membrane Oxygenation concepts and chemically-induced disorders/toxicity/poisoning concepts, which identified 318 unique records. Twelve additional manuscripts were identified by the authors for a total of 330 articles for screening, of which 156 were included for this report.
The use of ECMO in poisoned patients is significantly increasing over time. Available retrospective data suggest that patients receiving VA ECMO for refractory shock or cardiac arrest due to poisoning have lower mortality as compared to those who receive VA ECMO for non-poisoning-related indications. Poisoned patients treated with ECMO have reduced mortality as compared to those treated without ECMO with similar severity of illness and after adjusted analyses, regardless of the type of ingestion. This is especially evident for poisoned patients with refractory cardiac arrest placed on VA ECMO (termed extracorporeal cardiopulmonary resuscitation ECPR).
We suggest VA ECMO be considered for poisoned patients with refractory cardiogenic shock (continued shock with myocardial dysfunction despite fluid resuscitation, vasoactive support, and indicated toxicologic therapies such as glucagon, intravenous lipid emulsion, hyperinsulinemia euglycemia therapy, or others), and strongly considered for patients with cardiac arrest in institutions which are structured to deliver effective ECPR. VV ECMO should be considered in poisoned patients with ARDS or severe respiratory failure according to traditional indications for ECMO in this setting.
Patients with pre-existing comorbidities with low expected survival or recovery. Relative contraindications vary based on each center's experience but often include: severe brain injury; advanced age; unrepaired aortic dissection or severe aortic regurgitation in VA ECMO; irreversible organ injury; contraindication to systemic anticoagulation, such as severe hemorrhage.
ECMO may provide hemodynamic or respiratory support to poisoned patients while they recover from the toxic exposure and metabolize or eliminate the toxic agent. Available literature suggests a potential benefit for ECMO use in selected poisoned patients with refractory shock, cardiac arrest, or respiratory failure. Future studies may help to further our understanding of the use and complications of ECMO in poisoned patients.
Background: Acetaminophen is a common pharmaceutical ingestion reported to US poison centers. In overdose, toxic metabolites are known to cause hepato- and nephrotoxicity. While G6PD deficiency may ...be a risk factor for methemoglobin production in the setting of acetaminophen overdose, it is rarely reported in patients who do not have this condition.
Methods: We present two cases of methemoglobinemia following massive acetaminophen ingestion with no known history of G6PD deficiency or other substances known to induce methemoglobinemia. The two cases had peak methemoglobin measurements of 32% and 12% respectively, and both were treated with methylene blue.
Discussion: A number of mechanisms may be involved in production of methemoglobin in the setting of massive acetaminophen ingestion including NAPQI-induced oxidation, depletion of glutathione stores, and production of oxidant-metabolites including paraaminophenol. While it is unlikely that the majority of acetaminophen overdoses result in any clinically significant methemoglobinemia, massive acetaminophen overdose may be complicated by development of methemoglobinemia.
Conclusion: Physicians should be aware of the possibility that massive acetaminophen ingestion may be complicated by methemoglobinemia in rare instances. Further studies should aim to characterize the metabolic pathways leading to possible methemoglobinemia in humans after large acetaminophen ingestions.
Serotonin toxicity is a common cause of drug-induced altered mental status. However, data on the causes of serotonin toxicity, symptomatology, complications, and rate of antidotal treatment are ...limited.
This study evaluated cases of serotonin toxicity in the ToxIC registry, an international database of prospectively collected cases seen by medical toxicologists. Serotonin toxicity was diagnosed by bedside evaluation of medical toxicology specialists and explicit criteria were not used. The database was searched for "serotonin syndrome" between January 1, 2010, and December 31, 2016.
There were 1010 cases included. Females made up 608 (60%) cases. Ages are as follows: younger than 2 years (3, 0.3%), 2 to 6 years (8, 0.8%), 7 to 12 years (9, 0.9%), 13 to 18 years (276, 27.3%), 19 to 65 years (675, 67%), older than 66 years (33, 3.4%), unknown (6, 0.6%). Reasons for encounter: intentional (768, 76%), adverse drug event/reaction (127, 12.6%), unintentional (66, 6%), and unknown (55, 5.4%). Signs/symptoms: hyperreflexia/clonus/myoclonus (601, 59.5%), agitation (337, 33.4%), tachycardia (256, 25.3%), rigidity (140, 13.9%), seizures (139, 13.7%), and hyperthermia (29, 2.9%).
rhabdomyolysis (97, 9.7%), dysrhythmias (8, 0.8%), and death (1, 0.1%).
benzodiazepines 67% (677/1010), cyproheptadine 15.1% (153/1010). There were 192 different xenobiotics reported with 2046 total exposures. Antidepressants were most common (915, 44.7%) with bupropion the most frequent overall (147, 7.2%). Common non-antidepressants were dextromethorphan (95, 6.9%), lamotrigine (64, 3.1%), and tramadol (60, 2.9%).
Serotonin toxicity most often occurred in adult patients with intentional overdose. Antidepressants were the most common agents of toxicity. Interestingly, bupropion, a norepinephrine/dopamine reuptake inhibitor, was the most frequently mentioned xenobiotic. Though often cited as a potential antidote, only 15% of patients received cyproheptadine. Severe toxicity was rare. A single death was reported.
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