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Cyanide poisoning by heba
This document summarizes information about cyanide poisoning. It discusses that cyanide inhibits cellular respiration by binding to cytochrome oxidase, stopping ATP production and oxygen utilization. Symptoms occur rapidly and include headache, weakness, confusion and potentially seizures or death. Treatment involves giving methemoglobin generators like methylene blue or sodium nitrite to bind cyanide, followed by thiosulfate to convert it to non-toxic thiocyanate. Oxygen may help displace cyanide but is not a specific antidote. Prompt treatment is needed given cyanide's fast mechanism of toxicity.
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Cyanide is rare as a poison; commonly from fruit seeds and industrial exposure. It can be dangerously accessed through inhalation and skin absorption.
Cyanide has a distinctive bitter almond smell. Toxicity varies; ingestion of 50-75 mg leads to respiratory issues. It acts rapidly, with symptoms worsening over time.
Cyanide leads to hyperpnea followed by respiratory arrest. Symptoms range from mild (3-15% cyanide levels) to severe (50-70% causing coma) affecting CNS and cardiovascular systems.
Immediate treatment is crucial. Antidotes like methylene blue and nitrites produce methemoglobin, helping detoxify cyanide. Oxygen is supportive, but not a specific antidote.
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Cyanide poisoning by heba
- 2. Cyanide ( hydrocyanicacid, prussic acid) is NOT a common poison. Most cyanide ingestions occur from accidental exposure or intentional ingestion of a cyanide-containing compound.
- 3. Some fruit seeds containTOXIC LEVELS of cyanide. Amygdalin, which is hydrolyzed to hydrogen cyanide is present in the seeds of apple, peach, plum, apricot, cherry, and almond.
- 4. Usually exposure occursin industry. Hydrocyanide and its derivatives are used in electroplating, metallurgy, and extraction of gold and silver from ores, plastic manufacture, and many other industries. It’s very important to know that intoxication does not happen only through ingestion, it also happens from inhalation or absorption through the skin. In the presence of cyanide gas, a gas mask alone does not offer complete protection from intoxication.
- 6. Hydrogen cyanide is readilyvolatilized to hydrogen cyanide, with a characteristic odor of bitter almonds. Cyanide salts are the most frequently encountered of all cyanide-containing compounds. LD50 for these salts is 2 mg/kg, and the ingestion of 50-75 mg of these salts results in syncope and respiratory difficulty.
- 8. Cyanide produces histotoxiccellular hypoxia by binding to ferric ( Fe3+ ) ion in the electron transport system. Cyanide binds to the cytochrome oxidase system inhibiting electron transport , consequently no ATP can be generated, this results in reduced cellular utilization of oxygen. As a summary, cyanide has the same pathophysiologic effect as a complete lack of oxygen . As a result, aerobic respiration ceases resulting in a decrease in pyruvate conversion in the Krebs cycle , therefore lactate increases resulting in metabolic acidosis .
- 10. cyanide is extremelyrapid acting and capable of producing death within minutes. the classic odor of bitter almond is not detected by everyone (genetically determined) . Hydrogen cyanide vapors are the most rapidly acting. But when cyanide salts are ingested toxicity is delayed because they are slowly absorbed. The severity of acute poisoning is determined by the dose and time since exposure.
- 11. Cyanide stimulates chemoreceptorsin aortic and carotid bodies to signal respiratory center in the brain which results in increased respiration (hyperpnea, i.e. increased minute ventilation) As cyanide levels increase (severe poisoning) respiration rate slows and gasping occurs, but still, with no or minimal cyanosis. Severe CNS oxygen deprivation may cause hypoxic convulsions and death due to respiratory arrest.
- 12. Cardiovascular and centralnervous system most affected body systems Exposure is rapidly fatal unless antidote quickly administered Depend on CN Levels in the body which are measured by the methemoglobin level: Normally <1% of our Hb is methemoglobin Pts remain Asx to a lvl up to 20% ,showing only skin discoloration Sx start to appear at lvls >20% ,and manifest mainly as neurological toxicity ,tachypnea & tachycarida
- 13. 1-3% - asymptomatic 3-15% - slight grayish-blue skin discoloration 15-20% - asymptomatic, but cyanotic So 25-50% headache, dyspnea, confusion, wea kness, chest pain 50-70% - altered mental status, delirium
- 14. Weakness Dizziness Headache Nausea and vomiting Tachycardia Flushing Those occur rapidly and non-specific .
- 15. Stuporous but responsiveto stimuli Tachycardia Tachypnea
- 16. Comatose Unresponsive Hypotension Bradypnea & gasping Dilated pupils Cyanosis ( at high levels) Death unless treated immediately
- 17. The aim isto decrease the amount of cyanide available for cellular binding, and decrease its binding to cytochrome oxidase. Treatment must be initiated immediately to be effective. But because it acts so rapidly, intentional ingestion (suicide) almost always leads to death. In addition, diagnosis can be delayed, which also may result in death. Luckily, specific antidotes are available.
- 18. Resuscitation :ABC 2. Decontamination: If due to Inhalation :(remove clothes ,flush with water ,removal of the individual from the source) If due to Ingestion : (Administer activated Charcoal /gastric lavage) 3. Cyanide Antidote Package 4. Other CN Antidote kits :4methylaminophenol ,Hyperbaric oxygen 1.
- 19. Cyanide (even attoxic concentrations) can dissociate from ferric ion binding sites and be converted to thiocyanate in the presence of thiosulfate and sulfur transferase. Thiocyanate is relatively nontoxic and is rapidly excreted by the kidneys. BUT, when this endogenous detoxification system becomes saturated, toxicity occurs, unless specific treat is initiated.
- 20. The main principleof treatment is to produce methemoglobin because it contains ferric (Fe3+ ) ion, and thus competes with cytochrome oxidase for binding cyanide. Cyanide + methemoglobin cyanomethemoglobin Methemoglobin has a greater affinity for cyanide than does cytochrome oxidase. Therefore, methemoglobin can bind to free cyanide and also cause dissociation of the cyanide-cytochrome oxidase complex, thus reactivating it. In summary, to treat cyanide poisoning we have to produce methemoglobin in the blood!!!
- 21. How to producemethemoglobin? 1. Methylene blue (in large doses) 2. Amyl nitrite (inhalation) produces only 5% 3. Sodium nitrite (IV) Hemoglobin(Fe+2 ) + amyl nitrite &/or sodium nitrite methemoglobin (Fe+3 ) The desired percentage of methemoglobin is around 40%.
- 23. BUT, all theabove reactions are REVERSIBLE and may shift in the opposite direction. This is the reason that there is a 2nd phase of treatment. The 2nd phase involves the binding of cyanomethemoglobin with thiosulfate in the presence of sulfur transferase to produce thiocyanate (which is excreted by the kidneys). Cyanomethemoglobin + thiosulfate thiocyanate + sulfite + methemoglobin
- 24. BE CAREFUL, becausetoo much methemoglobin can shift the oxygen dissociation curve to the left, thus decreasing the amount of oxygen available for the tissues. And because the tissue ability to utilize oxygen is already diminished by the presence of cyanide, too much methemoglobin can worsen tissue hypoxia. However, this doesn’t happen unless methemoglobin concentration reaches 40-50%. ALSO, nitrites can produce profound hypotension and cardiovascular collapse thus rendering the treatment completely ineffective.
- 25. Oxygen is NOTa specific antidote for cyanide poisoning. BUT, it is a necessary adjunct. Mechanisms: 1. Displace cyanide from cytochrome oxidase 2. Nonenzymatically convert reduced cytochrome to oxidized cytochrome enabling the electron transport system to function again Unlike treating CO poisoning, oxygen administration does not produce significant benefits.