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Marine Drugs Jan 2022Tetrodotoxin (TTX) is a crystalline, weakly basic, colorless organic substance and is one of the most potent marine toxins known. Although TTX was first isolated from... (Review)
Review
Tetrodotoxin (TTX) is a crystalline, weakly basic, colorless organic substance and is one of the most potent marine toxins known. Although TTX was first isolated from pufferfish, it has been found in numerous other marine organisms and a few terrestrial species. Moreover, tetrodotoxication is still an important health problem today, as TTX has no known antidote. TTX poisonings were most commonly reported from Japan, Thailand, and China, but today the risk of TTX poisoning is spreading around the world. Recent studies have shown that TTX-containing fish are being found in other regions of the Pacific and in the Indian Ocean, as well as the Mediterranean Sea. This review aims to summarize pertinent information available to date on the structure, origin, distribution, mechanism of action of TTX and analytical methods used for the detection of TTX, as well as on TTX-containing organisms, symptoms of TTX poisoning, and incidence worldwide.
Topics: Animals; China; Ciguatera Poisoning; Humans; Incidence; Indian Ocean; Japan; Mediterranean Sea; Tetraodontiformes; Tetrodotoxin; Thailand
PubMed: 35049902
DOI: 10.3390/md20010047 -
Clinical Journal of the American... Sep 2019Extracorporeal therapies have been used to remove toxins from the body for over 50 years and have a greater role than ever before in the treatment of poisonings.... (Review)
Review
Extracorporeal therapies have been used to remove toxins from the body for over 50 years and have a greater role than ever before in the treatment of poisonings. Improvements in technology have resulted in increased efficacy of removing drugs and other toxins with hemodialysis, and newer extracorporeal therapy modalities have expanded the role of extracorporeal supportive care of poisoned patients. However, despite these changes, for at least the past three decades the most frequently dialyzed poisons remain salicylates, toxic alcohols, and lithium; in addition, the extracorporeal treatment of choice for therapeutic removal of nearly all poisonings remains intermittent hemodialysis. For the clinician, consideration of extracorporeal therapy in the treatment of a poisoning depends upon the characteristics of toxins amenable to extracorporeal removal (, molecular mass, volume of distribution, protein binding), choice of extracorporeal treatment modality for a given poisoning, and when the benefit of the procedure justifies additive risk. Given the relative rarity of poisonings treated with extracorporeal therapies, the level of evidence for extracorporeal treatment of poisoning is not robust; however, extracorporeal treatment of a number of individual toxins have been systematically reviewed within the current decade by the Extracorporeal Treatment in Poisoning workgroup, which has published treatment recommendations with an improved evidence base. Some of these recommendations are discussed, as well as management of a small number of relevant poisonings where extracorporeal therapy use may be considered.
Topics: Humans; Poisoning; Renal Dialysis
PubMed: 31439539
DOI: 10.2215/CJN.02560319 -
Deutsches Arzteblatt International Oct 2020Poisonous mushrooms are eaten by mushroom hunters out of ignorance, after misidentification as edible mushrooms, or as a psychoactive drug. Mushroom poisoning commonly... (Review)
Review
BACKGROUND
Poisonous mushrooms are eaten by mushroom hunters out of ignorance, after misidentification as edible mushrooms, or as a psychoactive drug. Mushroom poisoning commonly leads to consultation with a poison information center and to hospitalization.
METHODS
This review is based on pertinent publications about the syndromes, toxins, and diagnostic modalities that are presented here, which were retrieved by a selective search in PubMed. It is additionally based on the authors' longstanding experience in the diagnosis and treatment of mushroom intoxication, expert consultation in suspected cases, macroscopic identification of wild mushrooms, and analytic techniques.
RESULTS
A distinction is usually drawn between mushroom poisoning with a short latency of less than six hours, presenting with a gastrointestinal syndrome whose course is usually relatively harmless, and cases with a longer latency of six to 24 hours or more, whose course can be life-threatening (e.g., phalloides, gyromitra, orellanus, and rhabdomyolysis syndrome). The DRG diagnosis data for Germany over the period 2000-2018 include a total of 4412 hospitalizations and 22 deaths due to the toxic effects of mushroom consumption. 90% of the fatalities were due to the death cap mushroom (amatoxins). Gastrointestinal syndromes due to mushroom consumption can be caused not only by poisonous mushrooms, but also by the eating of microbially spoiled, raw, or inadequately cooked mushrooms, or by excessively copious or frequent mushroom consumption.
CONCLUSION
There are few analytic techniques available other than the qualitative demonstration of amatoxins. Thus, the diagnosis is generally made on the basis of the clinical manifestations and their latency, along with meticulous history-taking, assisted by a mushroom expert, about the type(s) of mushroom that were consumed and the manner of their preparation.
Topics: Amanita; Germany; Hospitalization; Humans; Mushroom Poisoning; Syndrome
PubMed: 33559585
DOI: 10.3238/arztebl.2020.0701 -
British Journal of Anaesthesia Oct 2019Organophosphorus (OP) nerve agent poisoning made the headlines in 2018 with the nerve agent 'Novichok' poisonings in Salisbury, England. This event highlighted a gap in... (Review)
Review
Organophosphorus (OP) nerve agent poisoning made the headlines in 2018 with the nerve agent 'Novichok' poisonings in Salisbury, England. This event highlighted a gap in the knowledge of most clinicians in the UK. In response, this special article aims to enlighten and signpost anaesthetists and intensivists towards the general management of OP nerve agent poisoned patients. Drawing on a broad range of sources, we will discuss what OP nerve agents are, how they work, and how to recognise and treat OP nerve agent poisoning. OP nerve agents primarily act by inhibiting the enzyme acetylcholinesterase, causing an acute cholinergic crisis; death usually occurs through respiratory failure. The antimuscarinic agent atropine, oximes (to reactivate acetylcholinesterase), neuroprotective drugs, and critical care remain the mainstays of treatment. The risk to medical staff from OP poisoned patients appears low, especially if there is a thorough decontamination of the poisoned patient and staff wear appropriate personal protective equipment. The events in Salisbury in the past year were shocking, and the staff at Salisbury District General Hospital performed admirably in treating those affected by Novichok nerve agent poisoning. We eagerly anticipate their future clinical publications so that the medical community might learn from their valuable experiences.
Topics: Chemical Warfare Agents; Decontamination; Humans; Nerve Agents; Organophosphate Poisoning; Sarin
PubMed: 31248646
DOI: 10.1016/j.bja.2019.04.061 -
Toxicology Sep 2018The term organophosphate (OP) refers to a diverse group of chemicals that are found in hundreds of products worldwide. As pesticides, their most common use, OPs are... (Review)
Review
The term organophosphate (OP) refers to a diverse group of chemicals that are found in hundreds of products worldwide. As pesticides, their most common use, OPs are clearly beneficial for agricultural productivity and the control of deadly vector-borne illnesses. However, as a consequence of their widespread use, OPs are now among the most common synthetic chemicals detected in the environment as well as in animal and human tissues. This is an increasing environmental concern because many OPs are highly toxic and both accidental and intentional exposures to OPs resulting in deleterious health effects have been documented for decades. Some of these deleterious health effects include a variety of long-term neurological and psychiatric disturbances including impairments in attention, memory, and other domains of cognition. Moreover, some chronic illnesses that manifest these symptoms such as Gulf War Illness and Aerotoxic Syndrome have (at least in part) been attributed to OP exposure. In addition to acute acetylcholinesterase inhibition, OPs may affect a number of additional targets that lead to oxidative stress, axonal transport deficits, neuroinflammation, and autoimmunity. Some of these targets could be exploited for therapeutic purposes. The purpose of this review is thus to: 1) describe the important uses of organophosphate (OP)-based compounds worldwide, 2) provide an overview of the various risks and toxicology associated with OP exposure, particularly long-term neurologic and psychiatric symptoms, 3) discuss mechanisms of OP toxicity beyond cholinesterase inhibition, 4) review potential therapeutic strategies to reverse the acute toxicity and long term deleterious effects of OPs.
Topics: Agricultural Workers' Diseases; Animals; Antidotes; Chemical Terrorism; Chemical Warfare Agents; Cholinesterase Inhibitors; Dose-Response Relationship, Drug; Humans; Nervous System; Neurotoxicity Syndromes; Occupational Exposure; Organophosphate Poisoning; Organophosphates; Persian Gulf Syndrome; Pesticides; Prognosis; Risk Assessment; Risk Factors; Time Factors
PubMed: 30144465
DOI: 10.1016/j.tox.2018.08.011 -
JAMA Network Open Aug 2023The US and Canada currently have no formal published nationwide guidelines for specialists in poison information or emergency departments for the management of...
IMPORTANCE
The US and Canada currently have no formal published nationwide guidelines for specialists in poison information or emergency departments for the management of acetaminophen poisoning, resulting in significant variability in management.
OBJECTIVE
To develop consensus guidelines for the management of acetaminophen poisoning in the US and Canada.
EVIDENCE REVIEW
Four clinical toxicology societies (America's Poison Centers, American Academy of Clinical Toxicology, American College of Medical Toxicology, and Canadian Association of Poison Control Centers) selected participants (n = 21). Led by a nonvoting chairperson using a modified Delphi method, the panel created a decision framework and determined the appropriate clinical management of a patient with acetaminophen poisoning. Unique to this effort was the collection of guidelines from most poison centers in addition to systematic collection and review of the medical literature. Comments from review by external organizations were incorporated before the guideline was finalized. The project began in March 2021 and ended in March 2023.
FINDINGS
The search retrieved 84 guidelines and 278 publications. The panel developed guidelines for emergency department management of single or repeated ingestion of acetaminophen. In addition, the panel addressed extended-release formulation, high-risk ingestion, coingestion of anticholinergics or opioids, age younger than 6 years, pregnancy, weight greater than 100 kg, and intravenous acetaminophen use. Differences from current US practice include defining acute ingestion as an ingestion presentation from 4 to 24 hours after overdose was initiated. A revised form of the Rumack-Matthew nomogram was developed. The term massive ingestion was replaced with the term high-risk ingestion and denoted by a specific nomogram line. Other recommendations include specific criteria for emergency department triage, laboratory evaluation and monitoring parameters, defining the role of gastrointestinal decontamination, detailed management of acetylcysteine treatment, associated adverse effects, and stopping criteria for acetylcysteine treatment, as well as criteria for consultation with a clinical toxicologist. Finally, specific treatment considerations, including acetylcysteine dosing, fomepizole administration, and considerations for extracorporeal elimination and transplant evaluation, were addressed.
CONCLUSIONS AND RELEVANCE
This qualitative study provides a consensus statement on consistent evidence-based recommendations for medical, pharmacy, and nursing education and practice to optimize care of patients with acetaminophen poisoning.
Topics: Humans; Child; Acetaminophen; Acetylcysteine; Ambulatory Care; Evidence-Based Medicine; Canada; Drug-Related Side Effects and Adverse Reactions; Poisons
PubMed: 37552484
DOI: 10.1001/jamanetworkopen.2023.27739 -
Deutsches Arzteblatt International May 2019In 2016, according to the German Federal Statistical Office, 178 425 cases of intoxication (poisoning) were treated in German hospitals. The poison control centers in... (Review)
Review
BACKGROUND
In 2016, according to the German Federal Statistical Office, 178 425 cases of intoxication (poisoning) were treated in German hospitals. The poison control centers in the German-speaking countries gave advice in a total of 268 787 instances of poisoning in that year, and use of activated charcoal was recommended in 4.37% of cases. The application of activated charcoal plays a major role in both primary and secondary detoxification. This article serves as an overview of the mechanism of action, indications, contraindications, modes of application, and dosing of activated charcoal.
METHODS
This review is based on pertinent publications retrieved by a selective search in PubMed. The opinions of experts from the poison control centers in the German-speaking countries were considered in the interpretation of the data.
RESULTS
The administration of activated charcoal is indicated to treat moderately severe to life-threatening intoxication. It should be carried out as soon as possible, within the first hour of the ingestion; timed-release preparations can be given up to 6 hours after the ingestion. An important contraindication is impaired consciousness with the danger of aspiration in a patient whose air- way has not yet been secured. Activated charcoal is ineffective or inadequately effective in cases of poisoning with acids or bases, alcohols, organic solvents, inorganic salts, or metals. The proper dosage consists of an amount that is 10 to 40 times as much as that of the intoxicating substance, or else 0.5-1 g/kg body weight in children or 50 g in adults. Repeated application is indicated for intoxications with agents that persist for a longer time in the stomach and for intoxications with timed-release drugs or drugs with a marked enterohepatic or entero-enteric circulation. The routine combination of activated charcoal with a laxative is not recommended.
CONCLUSION
Even though intoxications are common, there is still no internationally valid guideline concerning the administration of activated charcoal. A precise analysis of the risks and benefits is needed for each administration, and a poison control center should be consulted for this purpose.
Topics: Adolescent; Adult; Ambulatory Care; Charcoal; Child; Humans; Poison Control Centers; Poisoning; Young Adult
PubMed: 31219028
DOI: 10.3238/arztebl.2019.0311 -
Cell Reports Jun 2022Nausea is a discomforting sensation of gut malaise that remains a major clinical challenge. Several visceral poisons induce nausea through the area postrema, a sensory...
Nausea is a discomforting sensation of gut malaise that remains a major clinical challenge. Several visceral poisons induce nausea through the area postrema, a sensory circumventricular organ that detects bloodborne factors. Here, we use genetic approaches based on an area postrema cell atlas to reveal inhibitory neurons that counteract nausea-associated poison responses. The gut hormone glucose insulinotropic peptide (GIP) activates area postrema inhibitory neurons that project locally and elicit inhibitory currents in nausea-promoting excitatory neurons through γ-aminobutyric acid (GABA) receptors. Moreover, GIP blocks behavioral responses to poisons in wild-type mice, with protection eliminated by targeted area postrema neuron ablation. These findings provide insights into the basic organization of nausea-associated brainstem circuits and reveal that area postrema inhibitory neurons are an effective pharmacological target for nausea intervention.
Topics: Animals; Area Postrema; Brain Stem; Mice; Nausea; Neurons; Poisons
PubMed: 35705049
DOI: 10.1016/j.celrep.2022.110953 -
Soins; La Revue de Reference Infirmiere Sep 2020
Topics: Data Collection; Humans; Poisons
PubMed: 33160583
DOI: 10.1016/S0038-0814(20)30173-0 -
Journal of Medical Toxicology :... Oct 2022All around the world, there are species of birds that have developed the ability to acquire toxic chemicals in their bodies making them less palatable or even lethal... (Review)
Review
All around the world, there are species of birds that have developed the ability to acquire toxic chemicals in their bodies making them less palatable or even lethal when consumed or contacted. Exposure to poisonous bird species is rare among humans, yet their poisons can produce serious clinical outcomes. In this study, we conducted a literature search focusing on seven avian species: the pitohuis (Pitohui spp.), blue-capped ifrita (Ifrita kowaldi), European quail (Cortunix corturnix coturnix), spur or spoor-winged goose (Plectropterus gambensis), North American ruffed grouse (Bonasa umbellus), Brush bronzewings (Phaps elegans), and European hoopoes and woodhoopoes (Upupa epops and Phoeniculus purpureus, respectively). We present the geographic distribution of each poisonous bird, toxin physiology and origin, clinical signs and symptoms of poisoning, cases of human toxicity if available and discuss the birds' ability to prevent self-intoxication. Our results suggest that most cases of contact with toxic birds produce mild symptoms as most of these birds apart from the European quail (C. c. corturnix) and North American ruffed grouse (B. umbellus) are not commonly consumed by humans. Furthermore, we discuss several methods of toxin acquisition in these bird species, which are mostly diet acquired apart from the hoopoes and woodhoopoes (Upupa and Phoeniculus spp.) who have a symbiotic relationship with chemical-producing bacteria in their uropygial glands. In summary, our study provides a comprehensive review of the toxic physiology, clinical manifestations, and evolutionary insight to avian toxins.
Topics: Animals; Coturnix; Humans; Poisons
PubMed: 35474563
DOI: 10.1007/s13181-022-00891-6