Principles of poison treatment

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Information about Principles of poison treatment
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Published on April 21, 2009

Author: yogendranayak

Source: authorstream.com

General Principle of Treatment of Poisoning : 21-Apr-09 General Principle of Treatment of Poisoning Y Nayak Dept of Pharmacology MCOPS Manipal Slide 2: 2 Drug poisoning : 3 Drug poisoning Poison : 4 Poison Substance which when introduced into body in relatively small amounts causes in structural damage or functional disturbances Reason for poisoning 1. Accidental 2. Incidental 3. Iatrogenic 4. Intentional 90% of all chemically-related deaths are due to: Barbiturates, salicylates, ethanol or CO Environmental pollutants : 5 Environmental pollutants Pesticides Insecticides Fungicides Rodenticides Herbicides Fumigants Industrial pollutants Automobile pollutants Drug poisoning : 6 Drug poisoning Opioids Sedatives Anxiolytics Digoxin Alcohol Caffeine dTc Cocaine NSAIDs Iron Signs and symptoms of poisoning : 7 Signs and symptoms of poisoning GI signs/symptoms (nausea, vomiting, diarrhea, pain) Altered LOC, seizures, unusual behavior Pupil changes, salivation, sweating, other signs/symptoms of disturbed autonomic nervous system function Respiratory depression Burns, blisters of lips, mucous membranes Unusual breath odors Causes of unconsciousness : 8 Causes of unconsciousness Cardiac arrest Head injury Stroke Alcohol intoxication Overdose Diabetes hypoglycaemia hyperglycaemia Sub-arachanoid haemorrhage Epilepsy Meningitis/ encephalitis Hypothermia Shock - hypovolaemic Syncope Psychogenic (hysteric) opisthotonos : 9 opisthotonos Poison management : 10 Poison management Support Vital Function Identify drug poisoning as the problem Reduce the amount of drug in the body Based on route of entry Ingested Absorbed Inhaled Injected 1. Support vital life functions (ABC’s) : 11 1. Support vital life functions (ABC’s) Airway – endotracheal tube if needed, watch for fluid accumulation in airway (i.e.. Aspiration of vomit) Breathing – Supplemental Oxygen, bag valve mask (BVM) and respirator Circulation – Monitor ECG, watch for arrhythmias, cardiac arrest and shock Vasogenic Shock – faulty vasomotor tone, increase capillary permeability Cardiogenic Shock – inadequate cardiac output can be due to cardiac dilation (barbituate, Ca channel blocker) 2. Identify the poison : 12 2. Identify the poison Patient history Laboratory testing Comparison of drugs or chemicals with known toxicology standards. Identify Poison- sampling types : 13 Identify Poison- sampling types Urine - 1st choice – easier to detect presence of the drug due to the accumulation of drug in the urine Blood/Serum – 2nd choice – get exact serum levels to better identify the health effects of the drug (coma/stimulant panels) Gastric Contents – 3rd choice –less helpful, but can tell if you should perform a gastric lavage. Identify Poison- Tests : 14 Urine tests Immunoassay (EMIT, ELISA) – semiquantitative tests usually with automated instrumentation. Can detect cannabinoids, amphetamines, cocaine, barbs etc Thin Layer Chromatography (TLC) – ToxiLab, 4 stage solvents, qualitative test Urine/Blood tests High Performance Liquid Chromatography (HPLC), gas chromatography and Gas Chromatography/Mass Spectroscopy (GCMS) are quantitative tests that can detect many compounds Coma and Stimulant panels Can be done in 2 hours Identify Poison- Tests To reduce the amount of drug in the body : 15 To reduce the amount of drug in the body Inactivate with charcoal Gastric lavage Emesis Cathartics Others Activated charcoal : 16 Activated charcoal Names SuperChar InstaChar Actidose Liqui-Char Form Premixed in water (slurry) Usually bottle containing 12.5 gms Dosage 1 gm/kg of patient body weight Usual adult dose: 25 to 50 gms Usual child dose: 12.5 to 25 gms Activated charcoal : 17 Activated charcoal Contraindications Altered mental status Inability to swallow Ingestion of acids or alkalis Does not bind Alcohol Petroleum products Metals (iron) Side Effects Nausea, vomiting Black stools Syrup of ipecac : 18 Syrup of ipecac Induces vomiting by irritating stomach and stimulating vomiting center in brainstem Seldom used anymore May be helpful if ingestion has occurred within last 30 minutes Dose Children = 15 cc orally Adults = 30 cc orally Repeat once after 20 minutes as needed Be sure patient has H20 in stomach Should not be given at same time as activated charcoal Contraindication for emesis : 19 Contraindication for emesis Petroleum hydrocarbon solvent – chemical pneumonitis Caustic acid or alkali agent Seizing Patient Comatose Patient Cathartics : 20 Cathartics Promotes rapid passage of poison through the GI tract Counteracts the constipative effects of AC I.E. sorbitol, Mg Citrate, Mg Sulfate Other ways of removal of drug from the body : 21 Other ways of removal of drug from the body Alteration of pH of urine – to enhance excretion of the drug, useful for salicylates, chlorpropamide, etc Diuresis – often used in conjunction with urine pH alteration Dilution with water – useful in the treatment of skin or eye exposure to harmful agents emulcents – soothes mucous membranes and coats the stomach, i.e. milk of magnesia Hemodialysis – blood transverses a semipermeable membrane that is bathed in dialysis solution or dialysate Drugs or toxins diffuse across this membrane Antidote treatment-1. Complexation : 22 Antidote treatment-1. Complexation A. Heavy Metals Chelators (BAL, EDTA) complexes with the metals making them inert B. Heparin Protamine (base) binds to acidic heparin to terminate its action and is excreted by glomerular filtration. C. Toxins- Botulinum Toxin ALD- < 0.5mcg LD50=10ng/kg Most potent poison known, rapidly absorbed and prevents ACH release from nerve terminals Tx: ABCs, lavage, emesis, charcoal, Trivalent anti-toxin Mortality of 70% to 10% with treatment 1. Complexation Contd… : 23 1. Complexation Contd… D. Organophosphates Pralidoxime is a nucleophillic reagent that ties up the organophosphates and permits its excretion E. Cyanide Binds to cytochrome oxidase, LD50= 2mg/kg Causes death in 1 to 15 minutes at high doses. Chelator is made in the body, methemoglobin (Fe3+) Give Amyl Nitrites and Na Nitrite with O2 and whole blood to convert hemoglobin to methemoglobin (LD50 increases 5 fold) Slide 24: 24 2. Enhancement of metabolic conversion to a safer form Example: Cyanide Poisoning and thiosulfate treatment (LD50 increases 3 fold) 3. Inhibition of metabolic conversion to toxic forms A. Ethylene glycol / Methanol – ethanol administration prevents Alcohol dehydrogenase (ADH) from converting these substances into toxic forms. (Km – Mechanism of Toxicity) Slide 25: 25 4. Accelerating rate of excretion Compete with reabsorption (Renal Tubules). i.e. For Sr2+ or Ra2+ radiation give Ca2+; For Br1- poisoning give Cl1- to aid in excretion 5. Competition for Essential receptors Carbon monoxide poisoning: Artificial Respiration with pure O2 to promote displacement of CO Turbocurare/ pancuronium: Choliesterase inhibitors Coumarins: Vit K is given Opiates Naloxone is given 6. Repair or by pass the effect of poison : 26 6. Repair or by pass the effect of poison A. Nitrites/sulfa drugs Converts hemoglobin into methemoglobin, which reduces the ability of the blood to carry O2. Methylene blue causes a direct reduction of methhemoglobin back to hemoglobin B. Digitalis Toxic effects include GI disturbances, neurologic, disorders and cardiac arrhythmias Give antidote of Digibind C. 5-Fluorouracil and 5-fluodeoxyuridine Antitumor agents used to decrease DNA synthesis Thymidine is a specific and effective antidote 7. Blockade of receptors responsible for Toxic Effects : 27 7. Blockade of receptors responsible for Toxic Effects The toxic action and the therapeutic action are mediate by different receptors. A. Anticholinesterases Found in pesticides and chemical warfare agents. increases level of acetylcholine resulting in Cholinomimetic effects Atropine blocks muscarinic receptors to block the effect of the AChE inhibitors. (anticholinesterases) Antidote chart : 28 Antidote chart

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