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Poisoning
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Activated charcoal can be given orally or via a nasogastric tube to those who present within an hour of a potentially toxic ingestion. The large surface area and high adsorptive capacity of activated charcoal enable it to bind to and reduce gastrointestinal absorption of most toxins. Due to the risk of serious complications, gastric lavage is no longer routinely recommended. Whole bowel irrigation is given for slow-release preparations and for body packers; its use should be guided by a clinical toxicologist.
Nutritional and Dietary Supplementation during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
From a practical standpoint, it has no clear indications for use during pregnancy; neither does this agent offer any advantage over simethicone. However, activated charcoal should be used without hesitation when it is needed in the treatment of acute poisoning.
Intrahepatic Cholestasis of Pregnancy
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Activated charcoal. Activated charcoal is a highly porous carbon compound. It is widely used to treat acute poisoning following oral ingestion, where it binds to the toxin and prevents its absorption from the stomach and intestine. It can effectively adsorb bile salts in vitro. Safety: FDA class C. Compared to no treatment, the reduction in bile salts was greater with charcoal, but there was no difference in pruritus or fetal/neonatal outcomes in a very small RCT [22].
Toxicoepidemiology and predictors of death in 2,4-dinitrophenol (DNP) toxicity
Published in Clinical Toxicology, 2021
A. J. Potts, N. J. Bowman, D. L. Seger, S. H. L. Thomas
There is no specific antidote for DNP poisoning [9,10] and no specific evidence to demonstrate the effectiveness of different approaches, so the management of DNP poisoning remains largely supportive. In the absence of contraindications, the use of oral activated charcoal should be considered if the patient presents soon after ingestion. Use of sedation (e.g., benzodiazepines) for aggressive control of agitation is rational as muscular activity increases heat generation. Cooling measures should be instituted early in those developing pyrexia, starting with simple non-invasive methods such as mist and fan techniques, external ice packs or other external cooling devices, progressing to invasive methods such as cold fluid lavage or intravascular cooling methods if temperature continues to increase. There is no rigorous evidence of efficacy for dantrolene in DNP poisoning and its role in management has been contested, [7] although successful use in those with extreme pyrexia has been reported [11]. Fluid loss may occur due to gastrointestinal disturbances or pyrexia and adequate replacement is important. This also requires careful monitoring of electrolytes to decrease the risk of hyperkalaemia. Intubation may be difficult in critically ill patients with advanced DNP toxicity as muscular spasms and jaw clenching can occur; early intubation and ventilation is therefore appropriate for the deteriorating patient with DNP toxicity.
Stoned on spices: a mini-review of three commonly abused household spices
Published in Clinical Toxicology, 2021
Kelly Johnson-Arbor, Susan Smolinske
The diagnosis of nutmeg intoxication is clinical; laboratory assays for nutmeg or its constituents are not readily available. Symptomatic and supportive care is sufficient for a majority of nutmeg exposures; patients with dehydration, prolonged hallucinations, or altered mentation may require hospitalization and pharmacologic treatment with anxiolytics and intravenous fluids. Gastrointestinal decontamination with activated charcoal may be beneficial for hospitalized patients who present soon after ingestion and who are at low risk for aspiration [17]. Two fatalities related to nutmeg exposure have been reported. In the first, an 8-year-old boy died 20 h after the ingestion of 2 nutmeg seeds [4]. The details surrounding this fatality are unclear as the report included very limited clinical information; it is unknown whether this outcome was affected by additional ingestions or underlying medical conditions. The second case involved a 55-year-old woman who died under unclear circumstances; postmortem toxicological examination revealed the presence of elevated concentrations of flunitrazepam and myristicin, and her stomach contents had an odor consistent with nutmeg [18].
Use of sorbitol as pharmaceutical excipient in the present day formulations – issues and challenges for drug absorption and bioavailability
Published in Drug Development and Industrial Pharmacy, 2019
Ranjeet Prasad Dash, Nuggehally R. Srinivas, R. Jayachandra Babu
Phenobarbital (BCS class I drug) is a nonselective central nervous system depressant. It promotes binding to inhibitory γ-aminobutyric acid subtype receptors, and modulates chloride currents through receptor channels and also inhibits glutamate induced depolarization [36]. Berg et al. (1987) demonstrated the impact of charcoal and sorbitol + charcoal on the disposition of phenobarbital dosed as an infusion for 1 h in a randomized crossover study in six healthy male subjects [28]. Activated charcoal is associated with constipation [37]. Clinical studies have shown that sorbitol-flavored charcoal decreased the half-life of phenobarbital and other drugs [38]. In the study by Berg et al. [28], although no effect on the Cmax of phenobarbital was observed in the presence and absence of charcoal or sorbitol + charcoal, a significant difference in the AUC0-t was observed where charcoal reduced the AUC of phenobarbital by 37% and a combination of sorbitol and charcoal reduced the AUC by 58% (Table 2), thus suggesting sorbitol has significant impact on reducing the exposure of phenobarbital although, the exclusive effect of sorbitol has not been elucidated in this study [28]. The half-life of phenobarbital decreased from 72 h to 36 h in the presence of charcoal and further reduced to 30 h by charcoal + sorbitol [28].