- Overview of Cyanide Poisoning
- Case report of suicide by inhalation of nitrogen gas.
- Plant growth promotion
- Gram-Positive Bacteria | Microbiology
Acetaminophen Anacin-3, Liquiprin, Panadol, Paracetamol, Tempra, Tylenol, and many other brands is a widely used drug found in many over-the-counter and prescription analgesics and cold remedies. When it is combined with another drug, such as diphenhydramine, codeine, hydrocodone, oxycodone, dextromethorphan, or propoxyphene, the more dramatic acute symptoms caused by the other drug may mask the mild and nonspecific symptoms of early acetaminophen toxicity, resulting in a missed diagnosis or delayed antidotal treatment. Mechanism of toxicity.
Overview of Cyanide Poisoning
Hepatic injury. One of the products of normal metabolism of acetaminophen by cytochrome P CYP mixed-function oxidase enzymes is highly toxic; normally this reactive metabolite NAPQI is detoxified rapidly by glutathione in liver cells. However, in an overdose, production of NAPQI exceeds glutathione capacity and the metabolite reacts directly with hepatic macromolecules, causing liver injury. Renal damage may occur by the same mechanism, owing to renal CYP metabolism.
Overdose during pregnancy has been associated with fetal death and spontaneous abortion. Very high levels of acetaminophen can cause lactic acidosis and altered mental status by uncertain mechanisms, probably involving mitochondrial dysfunction. Acetaminophen is rapidly absorbed, with peak levels usually reached within 30— minutes.
Note: Absorption may be delayed after ingestion of sustained-release products [Tylenol Extended Release, Tylenol Arthritis] or with co-ingestion of opioids or anticholinergics. Volume of distribution Vd is 0. The elimination half-life is 1—3 hours after a therapeutic dose but may be greater than 12 hours after an overdose see also Table II— Children younger than 10—12 years appear to be less susceptible to hepatotoxicity because of the smaller contribution of CYP to acetaminophen metabolism.
In contrast, the margin of safety may be lower in patients with induced CYP microsomal enzymes because more of the toxic metabolite may be produced.
High-risk patients include alcoholics and patients taking inducers of CYP2E1, such as isoniazid. Fasting and malnutrition may also increase the risk for hepatotoxicity, presumably by lowering cellular glutathione stores. Chronic toxicity has been reported after daily consumption of supratherapeutic doses. Forgot Password? What is MyAccess?
Case report of suicide by inhalation of nitrogen gas.
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Plant growth promotion
AccessEmergency Medicine. Case Files Collection. Chronic, low-level cyanogenic glycoside exposure notably from Sorghum spp has been associated with musculoskeletal teratogenesis ankyloses or arthrogryposes and abortion. Excitement can be displayed initially, accompanied by rapid respiration rate. Dyspnea follows shortly, with tachycardia.
The classic "bitter almond" breath smell may be present; however, the ability to detect this smell is genetically determined in people, and anosmic people a significant proportion of the population cannot detect it. Salivation, excess lacrimation, and voiding of urine and feces may occur. Vomiting may occur, especially in pigs. Muscle fasciculation is common and progresses to generalized spasms and coma before death. Animals may stagger and struggle before collapse. In other cases, sudden unexpected death may ensue. Mucous membranes are bright red but may become cyanotic terminally.
Venous blood is classically described as "cherry red" because of the presence of high venous blood pO 2 ; however, this color rapidly changes after death. Serum ammonia and neutral and aromatic amino acids are typically increased. Cardiac arrhythmias are common due to myocardial histotoxic hypoxia. Death occurs during severe asphyxial convulsions.
Chronic cyanide poisoning: Chronic cyanogenic glycoside hypothyroidism will present as hypothyroidism with or without goiter. Cystitis ataxia toxidromes are typically associated with posterior ataxia or incoordination that may progress to irreversible flaccid paralysis, cystitis secondary to urinary incontinence, and hindlimb urine scalding and alopecia. Death, although uncommon, is often associated with pyelonephritis. Late-term abortion and musculoskeletal teratogenesis may also occur. Acute cyanide poisoning: Necropsy personnel may require appropriate personal protective equipment, including respirators with suitable cartridges.
Venous blood is classically described as being "bright cherry red"; however, this color rapidly fades after death or if the blood is exposed to the atmosphere.
Whole blood clotting may be slow or not occur. Mucous membranes may also be pink initially, then become cyanotic after respiration ceases. Rumen contents may provide a positive sodium picrate paper test or positive results on other rapid cyanide test strip systems. Rumen gases may provide positive results in cyanide Draeger tube rapid test systems. Agonal hemorrhages of the heart may be seen. Liver, serosal surfaces, tracheal mucosa, and lungs may be congested or hemorrhagic; some froth may be seen in respiratory passages.
Gram-Positive Bacteria | Microbiology
Neither gross nor histologic lesions are consistently seen. Multiple foci of degeneration or necrosis may be seen in the CNS of dogs chronically exposed to sublethal amounts of cyanide. These lesions have not been reported in livestock. Chronic cyanide poisoning: Goiter may be present. Cystitis ataxia toxidromes are characterized by opportunistic bacterial cystitis with or without pyelonephritis and diffuse nerve fiber degeneration in the lateral and ventral funiculi of the spinal cord and brain stem.
Hindlimb urine scalding and alopecia may be present. Appropriate history, clinical signs, postmortem findings, and demonstration of HCN in rumen stomach contents or other diagnostic specimens support a diagnosis of cyanide poisoning. Veterinarians should be aware of the possible need to use appropriate personal protective equipment, including a respirator, when collecting samples that may liberate cyanide gas eg, rumen contents and rumen gas cap. A rapid qualitative and presumptive diagnosis can be made by testing representative plant samples or stomach contents using the picric acid paper test or by collecting rumen gas cap samples by trocarization and testing with a Draeger cyanide gas detection tube or other cyanide gas detection system.
Negative results with such rapid presumptive tests do not completely exclude the possibility of cyanide poisoning. Antemortem whole blood is preferred; other specimens should be collected as soon as possible after death, preferably within 4 hr. Specimens should be sealed in an airtight container, refrigerated or frozen, and submitted to the laboratory without delay.
The rationale for using skeletal muscle is that cyanide will bind to the iron moiety in myoglobin. Where available, measurement of the urinary metabolite of cyanide, thiocyanate, may reveal increased concentrations after cyanide poisoning. Cyanide concentrations in muscle are similar to those in blood, but concentrations in liver are generally lower than those in blood. In dogs, whole blood cyanide concentrations may be 4—5 times greater than serum concentrations because of binding to ferric ions and sequestration in RBCs.
Differential diagnoses include poisonings by nitrate or nitrite, urea, organophosphate, carbamate, chlorinated hydrocarbon pesticides, and toxic gases carbon monoxide and hydrogen sulfide , as well as infectious or noninfectious diseases and other toxidromes that cause sudden death. Immediate treatment is necessary. The goal of treatment is to break the cyanide-cytochrome c oxidase bond and reestablish the mitochondrial electron transport chain.
Classically, various nitrites have been used for this purpose; eg, inhaled amyl nitrite followed by IV injection of a nitrite salt typically sodium nitrite has been used to rapidly induce methemoglobinemia. Cyanide bound to methemoglobin can then be detoxified by rhodanese to thiocyanate. Because the rhodanese-mediated detoxification of cyanide to thiocyanate is usually capacity and rate limited by the availability of sulfur donors, treatment with nitrites is usually followed up by injection of sodium thiosulfate. If possible, the contents of one 0. Thiosulfate is generally well tolerated; however, vomiting and hypotension can occur.
The thiosulfate injection can be repeated if necessary. Ideally, decisions regarding repeated treatment with nitrites should consider the degree of methemoglobinemia present. Notably, thiosulfate treatment alone has been successful in some cases. However, thiosulfate treatment should ideally be preceded by nitrite induction of methemoglobinemia in cases of confirmed cyanide poisoning.
However, because thiosulfate is generally well tolerated, it is often administered alone in situations when cyanide exposure is likely but unconfirmed eg, smoke inhalation or exposure to fires. Hydroxocobalamin vitamin B 12a is also used as a cyanide antidote. Hydroxocobalamin detoxifies cyanide by binding to it and forming cyanocobalamin ie, another decoy receptor approach , which is then excreted in urine.
It has the advantages that it is relatively well tolerated, does not compromise blood oxygen-carrying capacity, and does not produce hypotension. Hydroxocobalamin does produce chromaturia which may result in false urinalysis results , as well as infusion site reactions, GI upset, pruritus, and dysphagia. Sulfanegen as the sodium or triethanolamine salt has been developed for treatment of cyanide mass poisoning incidents.
This approach has the advantage that sulfanegen is water soluble and can be administered IM. Sulfanegen is a prodrug that generates 3-mercaptopyruvic acid 3-MP , an intermediate in cysteine metabolism, which again acts as a decoy receptor for cyanide. By itself, the half-life of 3-MP is too short to be effective against cyanide poisoning. For this reason, prodrugs such as sulfanegen have been developed to increase the duration of action of 3-MP in vivo.