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CBRN and the Trauma Victim
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
The signs and symptoms of the hypnotic (or sedative) toxidrome include CNS depression (including coma), bradycardia, hypothermia and hypotension, respiratory depression and apnoea. The pupils will react variably. This toxidrome is caused by toxicants with GABA-a effects such as benzodiazepines, alcohols and barbiturates.
Neurotoxicology
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Sean D. McCann, Trevonne M. Thompson
The physical examination of a poisoned patient is guided by toxidrome recognition. A toxidrome is a constellation of signs and symptoms that reliably present as the result of the pharmacologic actions of a specific toxicant or class of toxicants. Commonly seen examples include the anticholinergic, cholinergic, sympathomimetic, opiate, and sedative/hypnotic toxidromes; however, many toxins may have their own unique toxidrome or “calling card.” With this in mind, the physical examination of the poisoned patient should include all aspects of a thorough examination with particular attention to core temperature, pupil size and reactivity, nystagmus, heart rate, respiratory rate and depth, bowel sounds, bladder distension, skin moisture (most reliably tested in the axilla), and presence of neuromuscular rigidity or clonus/hyperreflexia.
Opioids and Related Agents
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
The clinical presentation of the opioid toxidrome (triad) is characterized by CNS depression (including coma), miosis, and respiratory depression. Miosis is generally an encouraging sign, since it suggests that the patient is still responsive. Respiratory depression is a result of depressed brain stem and medullary respiratory centers, responsible for maintenance of normal rhythm. μ-Receptor agonists depress respiration in a dose-dependent manner and can lead to respiratory arrest within minutes. Fifty percent of acute opioid overdose is accompanied by a frothy, noncardiogenic pulmonary edema, responsible for the majority of fatalities. The condition involves loss of consciousness and hypoventilation, probably resulting from hypoxic, stress-induced pulmonary capillary fluid leakage. Peripheral effects include bradycardia, hypotension, and decreased GI motility. Urine output also diminishes as a consequence of increased antidiuretic hormone (ADH) secretion.
ToxNet: an artificial intelligence designed for decision support for toxin prediction
Published in Clinical Toxicology, 2023
Tobias Zellner, Katrin Romanek, Christian Rabe, Sabrina Schmoll, Stefanie Geith, Eva-Carina Heier, Raphael Stich, Hendrik Burwinkel, Matthias Keicher, David Bani-Harouni, Nassir Navab, Seyed-Ahmad Ahmadi, Florian Eyer
Chary et al. created an AI predicting toxidromes based on clinical findings [10]. This approach has the advantage that the AIs reasoning is understandable for users, however, it only predicts toxidromes. With our approach, we wanted to be able to give an accurate diagnosis proposition, since toxidromes might be helpful, but are not specific to one toxic etiology [18]. We also based our AI on real PCC patient data and not artificial synthetic cases to get a representation of cases that is as realistic as possible. One of the main issues will probably be for MDs to use results created by an AI without knowing how the result was created [19]. One advantage of ToxNet is that it uses the GAT technology as well as the literature-based approach. Especially in the extended cohort, the GAT approach alone did not perform well, but the AI’s overall results were stabilized by the literature branch.
Plant poisonings in Australia: a retrospective series of calls to the Queensland Poisons Information Centre
Published in Clinical Toxicology, 2023
Tamim Islam, Robert Knoeckel, Carol Wylie, Katherine Isoardi
More severe toxicity was seen in recreational or intentional exposures, particularly of anticholinergic plants, often occurring in young male adults, which is consistent with previous studies on plant exposures [2,4,8]. Our study identified anticholinergic plants to include Brugmansia spp., Datura stramonium, and, uniquely, Duboisia myoporoides. This may be due to species of Duboisia myoporoides being native to Queensland, further supporting the geographical patterning of plant poisonings [16]. In these cases, symptoms predominantly aligned with an anticholinergic toxidrome, including tachycardia, mydriasis, and delirium. However, since even small exposures to toxic plants can result in severe symptoms, eight cases with moderate toxicity were identified from unintentional ingestions.
Factors associated with seizure in tramadol overdose: a 12-year retrospective study in Hong Kong
Published in Clinical Toxicology, 2022
Wendy Cheng, Rex Pui Kin Lam, Chi Keung Chan
In total, 420 cases were retrieved from PICMS during the study period, of which 78 duplicate cases and 249 cases with an overdose of other co-ingestants were excluded. The demographic and clinical characteristics of the 93 included patients are shown in Table 1. The majority were Chinese (n = 84, 90%). Suspected suicidal was the most common reason for exposure, followed by intentional misuse and therapeutic error. Tramadol exposure was laboratory-confirmed in 56 patients (60%). The median ingested dose of tramadol was 1,050 mg (IQR 500–2,000 mg), which did not differ significantly between women and men (1,000 mg vs 1,225 mg, p = 0.49). Opioid toxidrome and respiratory depression occurred in 15 and 11 patients, respectively. Serotonin syndrome was recognised in 3 patients and hypoglycaemia in 9 patients. In total, 23 cases developed seizures, 10 patients had major effects and 2 patients died.