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TOKSIKOLOGI KLINIK Noor Wijayahadi
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Definitions Toxicology Ilmu  pelajari bahan toksik: detection, properties, effects and regulation of toxic substances, including poisons. Racun (Poison) Semua bahan yang menimbulkan efek merugikan (harmful effect)  digunakan sengaja ataupun tidak sengaja Poisoning is quantitative concept
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Dose Response Curve related to Toxicity
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Dose/Time Principle Toksisitas dipengaruhi oleh: Besar Dosis Lama Paparan
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Blood Plasma Level Toxicity
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Toxicological Terms 1. LD50 – dose at which 50% die Only animals TD50 – dose at which 50% have toxicity Measure of harmfulness 2. T.I. – Therapeutic Index TD50 / ED50 The larger the number, the safer the drug Measure of safety 3. Acute Toxicity Single dose within 24 hrs Defines intrinsic toxicity
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Toxicological Terms (con’t) 4. Chronic Toxicity Daily exposure for up to a lifetime 5. TLV – Threshold Limit Value Concentration below which there is no expected untoward effect over a period of 8hrs/day 5 days/week NOEL – no observable effect level ADI – allowable daily intake ADI = (NOEL) / x x is some safety factor (i.e., 100)
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Toxicological Terms (con’t) 6. STEL – Short term exposure level 4x a day, with the average being equal to the TLV 7. ALD – Average Lethal Dose Estimated from accidental deaths in humans 8. Toxicon Toxic principle of a given chemical entity Tylenol – quinone imine CCl4 – free radicals 9. Primary Determinant of Toxicology Dose, Dose and Dose
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Selective vs. Nonselective Toxicity Nonselective Nearly all chemical are nonselective in their actions Few chemicals are sufficiently selective to harm certain cells Selective One man’s poison is another man’s pill. What may be harmful to one specimen may be relatively harmless to another. Garden spray
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Kasus 1 Seorang wanita 29 tahun Diantar ke UGD Tidak sadar Riwayat: telah meminum sesuatu Tidak ditemukan pil atau botolnya di lokasi Tidak ada keluarga/relasi Apa yang harus kita lakukan? Apa yang sudah ditenggaknya?
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You can. . . Start with the basics Airway, Breathing, Circulation Get a better history Get EMS to get pill bottles, tell you what they do know (found outside, inside, garage…) Call friends, family, neighbors Call psych or primary MD to see what he is on regularly Get him to tell you Always remember that suicidal patients (just like everyone else) can lie so be skeptical of their history
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Or. . . Establish a pattern to his symptoms Toxic syndrome Also known as a: TOXIDROME
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Toxidromes Not every drug fits into a broad based category Lots of meds have unique effects not easily grouped 5 Basic Toxidromes Sympathomimetic Opiate Anticholinergic Cholinergic Seditive Hypnotic
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Common Causes of Death in the Acutely Poisoned Patient Comatose patient: Loss of protective reflexes Airway obstruction by flaccid tongue Aspiration of gastric contents into tracheobronchial tree Loss of respiratory drive Respiratory arrest Hypotension – due to depression of cardiac contractility
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Common Causes of Death in the Acutely Poisoned Patient Shock – due to hemorrhage or internal bleeding Hypovolemia – due to vomiting, diarrhea or vascular collapse Hypothermia – worsened by i.v. fluids administered rapidly at room temperature Cellular hypoxia – in spite of adequate ventilation and O2 admin. – due to CN, CO or H2S poisoning
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Common Causes of Death in the Acutely Poisoned Patient Seizures – may result in pulmonary aspiration;asphyxia Muscular hyperactivity resulting in hyperthermia, muscle breakdown, myoglobinemia, renal failure, lactic acidosis and hyperkalemia Behavioral effects –traumatic injury ferom fights, accidents, fall from high places. Suicides, etc
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Common Causes of Death in the Acutely Poisoned Patient Massive damage to a specific organ system: Liver (acetaminophen; amanita phylloides [poison mushroom] Lungs (paraquat) Brain (demoic acid) Kidney (ethylene glycol) Heart (cobalt salts) Note: death may occur in 48 – 72 hrs
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II. Management of a Poisoning Segera Lakukan: Support Vital Functions Identifikasi racun 3. Upaya pengeluaran racun dari tubuh
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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)
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General Treatment of a Comatose Patient
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Supportive Drug Therapy Treat all patients who come into the hospital in a coma with glucose, insulin and naloxone. Use drugs to treat emergent conditions, ie: Seizures – anticonvulsants (valium) Cardiac Dysrhythmias – anti-arrhythmias (lidocaine, digoxin) Severe Agitation – anxiolytics (benzo)
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Identifikasi Racun? 1. Patient history 2. Laboratory testing 3. Comparison of drugs or chemicals with known toxicology standards.
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Identification of the Poison (Sample 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.
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Identify Poison (Tests) 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
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Removal of the Drug (Emesis) Utilize syrup of Ipecac to Induce emesis to remove unabsorbed drug. Emesis inducers Mechanical Apomorphine Syrup of ipecac Contraindications?
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Contraindications of Emesis Emesis is contraindicated in cases of: Petroleum hydrocarbon solvent – chemical pneumonitis Caustic acid or alkali agent (rupture) Seizing Patient Comatose Patient
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Removal of the Drug (Gastric Lavage) Gastric Lavage – washing of the stomach. (early tx.) A tube is inserted through the nose or mouth, down the esophagus, and into the stomach. Sometimes a topical anesthetic may be applied to minimize irritation and gagging as the tube is being placed. Stomach contents can be removed using suction immediately or after irrigating w/ fluids through the tube.
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Activated Charcoal/Cathartics Activated Charcoal (AC) Used to bind compounds and to prevent absorption in the GI tracts. (many drugs) Contraindicated with caustic agents and petroleum distillates due to the lack of absorption of these agents by the charcoal and risk of vomiting associated with the charcoal Order of use of charcoal and ipecac Cathartics Promotes rapid passage of poison through the GI tract Counteracts the constipative effects of AC I.E. sorbitol, Mg Citrate, Mg Sulfate
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Removal of the Drug (Other) Alteration of pH of urine – to enhance excretion of the drug, useful for salicylates, chlorpropamide, etc (tx) Diuresis – often used in conjunction with urine pH alteration Dilution with water – useful in the treatment of skin or eye exposure to harmful agents. ( no neutralizers) Demulcents – 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. (protein binding)
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B. Antidotal Treatments (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
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Complexation (con’t) 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) .
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Antidotal Treatments (con’t) 2. Enhancement of metabolic conversion to a safer form Example: Cyanide Poisoning and thiosulfate treatment (LD50 increases 3 fold) CN- SCN Rhodanese Sulfur Treatment: Give Thiosulfate (Sulfur source)
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Antidotal Treatments (con’t) 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) 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.
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5. Competition for Essential receptors A. Carbon Monoxide CO is found in cigarette smoke (5%) and auto exhaust (9%). Not in natural gas itself. Commonly used as a means of suicide; over 5000 fatalities a year from CO poisoning. Carboxyhemoglobin is found in very small amounts in non-smokers ~2.5% of the body’s hemoglobin and 7-10% for smoker TLV – 35ppm STEL – 200ppm (15min) ALD - 0.1% CO has a 210x greater affinity for Hb than O2 does
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Carbon Monoxide Poisoning Treatment: Artificial Respiration with pure O2 to promote displacement of CO
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Competition for Essential receptors (con’t) B. Turbocurare/pancuronium Cause a competition between the poison and Ach at the skeletal muscle endplate. Treatment: Cholinesterase Inhibitors (i.e. Neostigmine and physostigmine) Administration of ACH alone ineffective C. Coumarin Anticoagulant that interferes with synthesis of coagulation factors II, VII, IX and X. Treatment: Vitamin K D. Opiates Competition at opiate receptors with antagonists like naloxone and naltrexone.
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6. Repair or Bypass 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.
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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)
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SPECIFIC ANTIDOTES Poison Acetaminophen Acetylcholinesterases, OP’s, physostigmine Iron salts Methanol, Ethylene glycol Mercury, lead Narcotic drugs Anti/muscarinics-cholinergics OP anticholinergics Antidote Acetylcysteine Atropine Deferoxime Ethanol Metal Chelators Naloxone Physostigmine Praladoxime (2-PAM)
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Toxidromes Toxidromes are clinical syndromes that are essential for the successful recognition of poisoning patterns  sindroma toksik. The most important toxidromes, clinically, are:
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Sympathomimetic Toxidrome
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Sedative/Hypnotic Toxidrome
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Opioid/Opiate
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Anticholinergic Toxidrome
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Cholinergic Toxidrome
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Tricyclic Antidepressant Toxidrome
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Salicylate Toxidrome
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2. Base Specific Poisons Frequently Encountered
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Differences between acids and Bases Acids 1. Immediate pain in buccal cavity and esophagus 2. Less often swallowed than bases No esophageal perforation Bases 1. Primary cause of chemical burns 2. Rapidly penetrating liquefactive necrosis. 3. Primary effects on esophagus and only 20% on stomach. 4. Esophageal damage severe including perforation.
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3. Opiates Specific Poisons Frequently Encountered
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4. Meperidine Specific Poisons Frequently Encountered
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5. Atropine Specific Poisons Frequently Encountered
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6. Barbiturates Specific Poisons Frequently Encountered
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7. Benzodiazepines Specific Poisons Frequently Encountered
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8. Ethanol Specific Poisons Frequently Encountered
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9. Neuroleptics Specific Poisons Frequently Encountered
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10. Kerosene Specific Poisons Frequently Encountered
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11. Parathion Specific Poisons Frequently Encountered
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12. Salicylates Specific Poisons Frequently Encountered
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13. Acetaminophen Specific Poisons Frequently Encountered
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Acetaminophen Blood level Effects Plasma levels of > 250mcg/ml at 3-5 hours post ingestion. Rumack Matthew nomogram – Probable toxicity Children (9-10yrs) are less susceptible to the toxic effect of acetaminophen.
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14. Cocaine Specific Poisons Frequently Encountered
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Forms of cocaine Crack (type of free base) Baking soda, hard rock, volatile Cocaine HCL (salt) Non-volatile, white crystalline powder
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15. Phencyclidine (PCP) Specific Poisons Frequently Encountered
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16. Tricyclic Antidepressants Specific Poisons Frequently Encountered
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17. Methaqualone Specific Poisons Frequently Encountered
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18. Digoxin Specific Poisons Frequently Encountered
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19. Phenytoin Specific Poisons Frequently Encountered
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20. Theophylline Specific Poisons Frequently Encountered
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21. Dioxin (2,3,7,8 TCDD)
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Dioxin Poisoning Viktor Yushchenko: Ukraine President