Specific Poisonings PDF

Specific Poisonings Dr. Sulaiman Nimer Ethyl Alcohol (Ethanol) Poisoning  Alcoholic beverages Ethyl alcohol, or ethanol, is the active constituent (drug) that is contained in alcoholic beverages. Ethanol concentration in beverages ― 4% to 5% in beers 7% to 12% in wines...

Specific Poisonings Dr. Sulaiman Nimer Ethyl Alcohol (Ethanol) Poisoning  Alcoholic beverages Ethyl alcohol, or ethanol, is the active constituent (drug) that is contained in alcoholic beverages. Ethanol concentration in beverages ― 4% to 5% in beers 7% to 12% in wines 20% to 40% in cordials 40% to 60% in most distilled beverages (whiskeys, vodkas, rums, etc.)  Chemical Properties of Ethanol A clear volatile liquid Burns easily Slight, characteristic odor Is very soluble in water – miscible in all proportions  Causes of poisoning or death Accident ― Direct effect on body tissues ― Inhalation of vomitus ― Ingestion of other poisons or drugs ― Associated pathology of some organs ― Drowning, burning, falling from height ― Road traffic accident Commiting a crime As a catalyst in the assaults and homicides  Fate of ethanol in the body When an alcoholic beverage is swallowed, it is diluted by stomach juices & quickly distributed throughout the body Ethanol does not require digestion before its absorption into the bloodstream – some diffuses into bloodstream directly through the stomach wall – remainder passes into the small intestine rapidly absorbed & circulated  Alcohol Absorption Alcohol is absorbed from all parts of the gastrointestinal tract largely by simple diffusion into the blood – Small intestine is the most efficient region for absorption because of its large surface area The rate of absorption varies according to the particular beverage & the state of the consumer’s stomach  Alcohol Absorption Fasting individual – 20-25% of a dose of alcohol is absorbed from the stomach – 75-80% is absorbed from the small intestine – peak blood alcohol concentrations occur in 0.5- 1.0 hrs  Alcohol Absorption Non-fasting individuals – presence of food in stomach (especially fatty foods) delays absorption peak alcohol concentrations 1.0-6.0 hrs Alcohol ingested with carbonated beverages – ordinarily absorbed more rapidly than straight alcohol  Alcohol Distribution Once alcohol is absorbed into the blood, it will be distributed to all parts of the body. Is diffused in the body in proportion to the water content of the various tissues & organs – greater concentration in blood & brain – lesser concentration in fat & muscle  Alcohol Metabolism & Elimination More than 90% of the alcohol is metabolized in the liver. – oxidation via acetaldehyde & acetic acid to carbon dioxide & water  ADH (alcohol dehydrogenase) converts the alcohol to acetaldehyde acetaldehyde is a highly toxic substance  Aldehyde dehydrogenase converts acetaldehyde to acetic acid  Acetic acid is ultimately oxidized to CO2  Alcohol Metabolism & Elimination A person’s rate of metabolism depends on their experience and frequency of alcohol use. Heavy drinkers will metabolize more rapidly than light or nondrinkers. About 5-10% of a dose of ethanol is excreted unchanged in the urine. Remainder of eliminated through excretion in breath, sweat, milk & saliva  Primary pharmacological effect of alcohol A central nervous system (CNS) depressant The degree to which the CNS function is impaired is directly proportional to the concentration of alcohol in the blood.  Signs and symptoms of the acute alcohol intoxication BAC(mg/100ml) Clinical manifestations 10-50 Slight physiological impairment 50-100 Reduced inhibitions, talkativeness, euphoria, slight sensory disturbance 100-150 Incoordination, Staggering gait, slurred speech 150-200 Obvious drunkenness, nausea and ataxia 200-300 Staggering, vomiting, stupor, possibly coma 300-400 Impaired consciousness, coma, possible death 400 and over Unconsciousness, or death  Causes of death Most deaths in acute alcohol intoxication occur at blood alcohol levels of over 300mg%. Death can be caused either by the direct depressive effects on the brain stem mediated via the respiratory centers or through secondary events: – The traffic accident – Falling from height – Drowning, inhalation of vomitus  Alcoholism Alcoholism is a disabling addictive disorder. It is characterized by compulsive and uncontrolled consumption of alcohol despite its negative effects on the drinker's health, relationships, and social standing.  Alcoholism Long-term alcohol abuse produces physiological changes in the brain such as tolerance and dependence. Alcoholism is the cyclic presence of tolerance, withdrawal, and excessive alcohol use. Alcohol damages almost every organ in the body. Alcohol detoxification is conducted to withdraw the alcoholic person from drinking alcohol, usually with cross-tolerance drugs, e.g. benzodiazepines to manage withdrawal symptoms.  Signs and symptoms of alcoholism Poor nutrition, weight loss, lack of appetite Liver damage with jaundice, ascites, cirrhosis Pancreatitis Peripheral neuritis, tremor Insomnia, loss of memory, potomania, impaired power of judgment, alcoholic dementia Loss of vitality, intermittent infection An increased risk of developing cardiovascular disease, malabsorption, alcoholic liver disease, and cancer. Liver Mallory bodies = Alcoholic hyaline(arrow) It is characteristic of alcoholic hepatitis. Shows portal fibrosis (f) as well as pericellular fibrosis Corrosive Agents poisoning  Types of corrosive agents Strong inorganic acids ―Sulfuric, hydrochloric, nitric acid. The organic acid: ―Phenol (carbolic acid), Lysol, and cresol. The strong alkalis: ―Sodium and potassium hydroxide, ammonia.  Action of corrosive agents Cause functional and histologic damage on contact with body surfaces. Alkaline agents- liquefactive necrosis (deeper injury) Acid agents- coagulative necrosis by dehydrating the tissues (generally superficial injury)  Symptoms of caustics Ingestion: immediate severe burning, intense dysphagia Associated airway edema may cause airway obstruction and asphyxia Alkali ingestions can result in esophageal perforation, mediastinitis and death Acid ingestions can effect esophagus, but gastric necrosis and perforation with peritonitis more common Carbon monoxide poisoning  Chemical Properties of CO A colorless, odorless, tasteless gas Its density is slightly lighter than air gas It is the product of incomplete combustion of organic compounds.  Major source of carbon monoxide Cigarette smoke Coal gas The exhaust gas of automobile Smoke from conflagrations Fumes from defective heating appliances (furnace, stove, or water heater). Toxic effects of carbon monoxide Effects due to hypoxia ―binds to hemoglobin more readily than oxygen (200-300x more) ―COHb is more stable than oxyhaemoglobin, it can’t carry oxygen. Those tissues with the greatest oxygen demand (heart & brain) would be the most susceptible to toxic effects of CO.  Disposition of CO CO is readily absorbed through the lungs. Its primary route of elimination is through the lungs. There is no metabolism of absorbed CO. After absorption, CO rapidly distributes into the blood, and binds to Hb. CO is not spontaneously displaced from Hb but is displaced by the mass action of oxygen. The half-life of CO is 5-6h at normal oxygen concentration (21%), 30-90 min at 100% oxygen, and 30 min under hyperbaric oxygen conditions.  Carbon monoxide-symptoms The symptoms of CO toxicity are dependent on the concentration of CO in ―The inspired air ―The state of activity of the exposed person ―The duration of exposure ―The rate of accumulation of COHb The percentage of COHb in the Hb (COHb saturation) is used as a measure of the degree of CO toxicity.  Carbon monoxide-symptoms mild intoxication ( 10-20% COHb): headache, mild dyspnea, visual changes moderate intoxication (20-30%): drowsiness, faintness, tachycardia, dulled sensation, decreased awareness, emotional instability. 30-40%- weakness, incoordination, nausea and vomiting, dizziness, confusion, tremor. 40-50%-severe ataxia, respiration depression, hallucinations, hypotension, hypothermia. >50%- coma, convulsions, cyanosis, loss of reflexes, respiratory paralysis, and death.  Treatment of CO poisoning The first step is removal from the environment. Decontamination, 100% oxygen is administered for at least 120 min. Hyperbaric oxygen may be effectively used in poisoned patients with acute neurotoxicity, metabolic acidosis, angina, or other cardiac abnormalities. Normal supportive measures should also be instituted.  Autopsy finding CO poisoning is the leading cause of both accidental and intentional poisoning deaths. Smoke inhalation is the most common source of CO exposure. The most significant postmortem characteristic in fatal CO intoxications is the presence of a bright cherry-red coloration of blood, fingernails, mucous membranes, visceral organs, and skin. Organophosphates poisoning  Classes of insecticides Insecticides are pesticides used to kill insects. Classes of insecticides: ―Organochlorine compounds ―Organophosphates ―Carbonates ―Synthetic Pyrethroids ―Biological insecticides  Organophosphate Insecticides Developed following World War II because of synthesis of organophosphate “nerve gases” sarin, soman, and tabun. Are widely used insecticides available today. Degrade relatively rapidly in the environment. Commonly used OPs have included parathion, malathion, methyl parathion, chlorpyrifos, diazinon, dichlorvos, phosmet, fenitrothion.  Mechanism of Action Ops are cholinesterase inhibitor. Ops irreversibly inactivate acetylcholinesterase and prolong the action of acetylcholine. The actions are both muscarinic and nicotinic. On the CNS, the action is depression. They are one of the most common causes of poisoning worldwide, and are frequently intentionally used in suicides in agricultural areas.  Fate of OPs OPs can be absorbed by all routes, including inhalation, ingestion, and dermal absorption. Metabolism tends to hydrolyze by action of esterases in the liver. A part of the parent and the metabolised products are excreted in urine.  Signs and Symptoms Bronchospasm and bronchorrhea, Tightness in the chest, wheezing, pulmonary edema. Loss of consciousness, incontinence, convulsions and respiratory depression. Tachycardia, hypertension. Sweating, lacrimation, rhinorrhea. Vomiting, abdominal cramps, diarrhea Miosis, anxiety, restlessness, muscle twitching, weakness, tremor. Confusion, coma, and respiratory failure. Death results from bradycardia, hypotension, and respiratory failure  OPIDN (Organophosphate-induced delayed neuropathy) OPIDN is a rare toxicity resulting from exposure to certain OPs. It is characterised by distal degeneration of some axons of both the peripheral and central nervous systems occurring 1-4 weeks after single or short-term exposures. Inhibition of “neuropathy target esterase” (NTE). Predominantly legs. Manifests as cramping muscle pain in the lower limbs, distal numbness and paraesthesia occur, followed by progressive weakness, depression of deep tendon reflexes in the lower limbs and, in severe cases, in the upper limbs.  Intermediate Syndrome (IMS) It arise in the interval between the end of the acute cholinergic crisis and the onset of OPIDN. It occurs 24-96 hours after exposure. IMS was characterized by weakness of proximal limb muscles, neck flexors, respiratory muscles, and motor cranial nerves, and was attributed to muscle fiber necrosis following acute cholinergic crisis. Compounds involved are methyl parathion, fenthion and dimethoate. The incidence of IMS has been reported to be as high as 80%. The pathophysiology that underlies IMS remains unclear.  Autopsy findings Externally: cyanosis, congested face, frothy discharge from the nose and mouth, kerosene-like smell. Internally: the mucosa of the stomach and intestine is congested; the stomach content may give a kerosene-like smell; gross congestion and edema of the lungs, congestion of other organs; edema of brain; froth in the respiratory tract. Cholinesterase level of red blood cells and plasma is low.