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Seminar on poisoning

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Seminar on poisoning

  1. 1. SEMINAR ON POISONING By :MERON GIRMA ENGIDAW AMBELU MODERATOR: DR.GETA
  2. 2. OUTLINES: • DEFINITION, TYPE AND EPIDEMIOLOGY • HISTORY AND PHYSICAL EXAMINATION • CLINICAL DIAGNOSIS • PRINCIPLE OF MANAGEMENT • COMMON SELECTED POISONINGS
  3. 3. Definition Poison: “Poison is a substance ( solid/ liquid or gaseous ),that produce ill health or death, by its constitutional or local effects or both, by altering cell structure or functions.” The branch of medicine that deals with the detection and treatment of poisons is known as toxicology.
  4. 4. Poisoning: “The development of dose related adverse effects following exposure to chemicals, drugs or other xenobiotics.” It occurs when any substance interferes with normal body functions after it is Swallowed; ingested poisons => 78% Inhaled; breathed in poisons => 5.4% injected ;IV, IM, SQ or Intra Dermal => 0.3% Absorbed; poisons taken in through unbroken skin =>6.8% Enter through Opthalmic; => 5.9%
  5. 5. Types: Deliberate (intentional) Suicide & homicide  Accidental (unintentional) Dosage error Recreational use Environmental: • Plants • Food Venomous stings/bites Industrial exposures
  6. 6. • Epidemiology • Each day a child is exposed to potential toxin • Age • most common in<5yrs(50-60%) • Cause • most(93-99%) are accidental
  7. 7. Hx content of poisoned patient Identification of the patient and toxic agent. What? Description of the toxin. Product names (brand, generic, chemical) and ingredients, along with their concentrations Bring container to hospital with patient.
  8. 8. How much? Magnitude of the exposure. determine as accurately as possible how much of the substance has been consumed by counting the remaining tablets or measuring the remaining volume of liquid or gas after we ask the previous amount. It is better to overestimate than to underestimate
  9. 9. When ?Time of exposure. Knowing the time lapse between exposure and the onset of symptoms and/or medical evaluation w influence decisions of diagnostic testing as well as therapeutic intervention. Period of exposure • First time use or chronic user • If unknown—estimate the shortest and longest possible time.
  10. 10. Progression of symptoms. Knowing the nature and progression of symptoms is very helpful for assessing the need for immediate life support, the prognosis, and the type of intervention needed What interventions have been done? – Traditional home remedies may be harmful
  11. 11. Medical history Underlying diseases Concurrent drug therapy
  12. 12. The effects of poisoning maybe None, Mild or Severe depending on: • The amount of poison ingested. • The nature of the substance. • The age of the child. • The nutritional status of the child. • The state of the stomach-whether empty or full of food.
  13. 13. PHYSICAL EXAMINATION ODOR • Bitter- almonds Cyanide • Acetone -Isopropyl alcohol, Methanol, Paraldehyde, Salicylates • Alcohol-Ethanol • Wintergreen -Methyl Salicylate • Garlic -Arsenic, Thallium, Organophosphates OCULAR SIGNS • Miosis -Narcotics (except meperidine),Organophosphates, muscarinic,mushrooms,phenoth iazine's,barbiturates (late), PCP • Mydriasis -Atropine, alcohol, cocaine,CO • Lacrimation- Organophosphates, irritant gas or vapors • Poor vision- Methanol, botulism, CO
  14. 14. CUTANEOUS SIGNS • Dry, hot skin -Anticholinergic agents, botulism • Diaphoresis- Organophosphates, nitrates, muscarinic mushrooms, aspirin, cocaine • Erythema- Boric acid, mercury, cyanide, anticholinergics ORAL SIGNS • Salivation -Organophosphates, salicylates, corrosives, strychnine • Dry mouth- Amphetamines, anticholinergics, antihistamine • Burns- Corrosives, oxalate- containing plants • Gum lines- Lead, mercury, arsenic • Dysphagia -Corrosives, botulism
  15. 15. INTESTINAL SIGNS • Cramps -Arsenic, lead, thallium, Organophosphates • Diarrhea -Antimicrobials, arsenic, iron, boric acid • Constipation -Lead, narcotics, botulism • Hematemesis -Aminophylline, corrosives, iron, salicylates CARDIAC SIGNS • Tachycardia Atropine, aspirin, amphetamines, cocaine, cyclic antidepressants, theophylline • Bradycardia -Digitalis, narcotics, mushrooms, clonidine, Organophosphates, β blockers,CCB • Hypertension- Amphetamines, LSD, cocaine, PCP • Hypotension Phenothiazines, barbiturates, cyclic antidepressants, Fe, β blockers, CCB
  16. 16. RESPIRATORY SIGNS • Depressed respiration Alcohol, narcotics, barbiturates • Increased respiration - Amphetamines, aspirin, ethylene glycol, CO, cyanide • Pulmonary edema Hydrocarbons, heroin, Organophosphates, aspirin CNS SIGNS • Ataxia -Alcohol, antidepressants, barbiturates, anticholinergics, phenytoin, narcotics • Coma -Sedatives, narcotics, barbiturates, PCP,CO Organophosphates,lead • Hyperpyrexia Anticholinergics, cocaine
  17. 17. CNS sign… • Muscle fasciculation - Organophosphates, theophylline • Muscle rigidity- Cyclic antidepressants, PCP, phenothiazines, haloperidol • Paresthesia- Cocaine, camphor, PCP, MSG • Altered behavior- LSD, PCP, amphetamines, cocaine, alcohol, anticholinergics, camphor • Peripheral neuropathy- Lead, arsenic, mercury, organophosphates
  18. 18. Clinical Diagnosis • CBC • serum electrolyte • LFT, RFT • screening • RBS • SO2
  19. 19. Principle of Management 1. Initial resuscitation and stabilization 2. Removal of toxin from the body 3. Prevention of further poison absorption 4. Enhancement of poison elimination 5. Administration of antidote 6. Supportive treatment 7. Prevention of re - exposure
  20. 20. The management principle is applied based on triage • Triage is the process of rapidly examining all sick children when they first arrive in hospital in order to place them in one of three categories. E Emergency P Priority Q Queue (non-urgent) Categories after Triage Action required EMERGENCY CASES Need immediate emergency treatment PRIORITY CASES Need assessment and rapid attention
  21. 21. Emergency Management of Triaged Children If any sign positive: give treatment(s) for ABCDO Emergency Signs A: Airway problem B: Breathing problem C: Circulation or shock Cm: Coma or Unconscious Cn: Convulsion D: Dehydration, Severe Ds: Disability O: Bleeding child, poisoning (immediate), open fracture
  22. 22. SELECTED POISONS • Drugs Acetaminophen Phenobarbitone Salicylate Iron Digoxin • Insecticides (pesticides) Organophosphate Carbamates • Hydrocarbons • Venomous stings/bites Snake bite
  23. 23. • Toxic substances have seven common major pathophysiologic mechanisms that may produce symptom 1. Interfere with the transport or tissue utilization of O2 e.g. CO 2. Depress or stimulate CNS e.g. MDMA 3. Affect autonomic nervous system e.g. Organophosphate
  24. 24. 4.Affect the lungs by aspiration e.g. Hydrocarbon 5.Affect the heart and vasculature myocardial dysfunction e.g.Antidepressant 6.Produce local damage e.g. Corrosive 7.Effect on the liver e.g. Acetaminophen
  25. 25. Organophosphate poisoning • Less common (< 1%) in children • Mostly accidental and unintentional • More common in lower socioeconomic class • Used in agriculture(crop sprays) and home as insecticides & pesticides e.g. Insecticides – malathion(MLT), parathion, ethion, diazinon Nerve gases - sarin, tabun ophthalmic agents - echothiophate, isoflurophate Herbicides - tributes [DEF], merphos
  26. 26. Pathophysiology:cholinesterase inhibitor bind to the enzyme preventing degradation of Ach accumulation of Ach at nerve synapses affecting: • CNS • Neuromuscular junctions • Sympathetic & Parasympathetic NS
  27. 27. NORMAL PHYSIOLOGY
  28. 28. Clinical Manifestations: • Muscarinic s/Sx (Parasympathetic NS) Diaphoresis, emesis, Incontinence (urine, fecal), Tearing, bronchorrhea & bronchospasm Meiosis, hypotension, bradycardia MUSCARINIC SIGNS SLUDGE/BBB DUMBELS S=Salivation D=Diarrhea & diaphoresis L=Lacrimation U=Urination U=Urination M=Miosis D=Defecation B=Bronchocorrhe a,bronchospasm, bradycardia G=GI symptoms E=Emesis E=Emesis L=Lacrimation B=Bronchorrhea S=Salivation B=Bronchospasm B=Bradycardia
  29. 29. • Nicotinic S/S(Sympathetic NS) Muscle weakness, tremors, fasciculation, Hypoventilation, HTN, tachycardia, dysarhythmias • CNS effects confusion, delirium, coma, Seizure, anxiety, restlessness, Emotional lability, Confusion, Ataxia, Tremors,impaired memory, lethargy, psychosis
  30. 30. the balance between stimulation of muscarinic and nicotinic receptor depend on the - Type of organophosphate - Dose - Route and rate of absorption - Individual factor
  31. 31. Management: Supportive GID Antidotes (atropine)
  32. 32. Hydrocarbon Poisoning • Most commonly ingested hydrocarbons - gasoline, lubricating oil, motor oil, mineral spirits, lighter fluid/naphtha, lamp oil,and kerosene. • Other common sources of hydrocarbons -dry cleaning solutions, paint, spot remover, rubber cement, and solvents
  33. 33. • Type of toxic response depends on: • amount of ingestion • volatility(viscosity)
  34. 34. • Pathophysiology o Cause toxicity in 2 ways : a. Aspiration (most common) results in → Spasm, edema, inflammatory rxn, and necrosis of the respiratory passages & alveoli. → Vascular thrombosis & hemorrhage with chemical pneumonitis, atelectasis, & emphysema.
  35. 35. b. Systemic effects • volatile or low viscosity → degenerative changes in various organs (mostly CNS) Clinical Manifestations:mainly respiratory Choking, Coughing
  36. 36. vomiting & diarrhea, which may be bloody  dyspnea and cyanosis mild tracheobronchitis, severe necrotizing bronchopneumonia & pul.hemmorrhage atelectasis , pneumatocele, bacterial infection (secondary), pneumomediastinum  mild to moderate fever within 48hrs CNS -tremors, irritability, confusion, drowsiness, sz,& coma
  37. 37. management Correction of hypoxia & acidosis  NO emesis  NO lavage  NO prophylactic Antibiotic  NO STEROIDS
  38. 38. Paracetamol (Acetaminophen) Poisoning • mostly used & available at home • analgesic and antipyretic • overdose cause fatal and nonfatal hepatic necrosis with certain risk factors ,but is nearly always good if the antidote, N-acetylcysteine (NAC), is administered within 8 to 10 hours of ingestion
  39. 39. Patterns of exposure could be: 1) Intentional: more common in older children and adolescents with a single event and high dose. 2) Unintentional: common among younger children. occur through "exploratory" behavior or inappropriate dosing
  40. 40. Pathophysiology: due to toxic metabolite N-acetyl-P-benzoquinonemine (NAPQI), produced by P450 enzyme. Paracetamol → conjugation (sulfate,Glucuronide) Reactive Metabolite → Gluthatione → NAC (NAPQI) Binding to Hepatic macromolecules → Necrosis
  41. 41. Risk factors in children — Liver damage caused by excess N- acetyl-p-benzoquinoneimine (NAPQI) can occur in four circumstances : • Excessive intake of acetaminophen • Decreased capacity for glucuronidation or sulfation • Increased cytochrome P450 (CYP2E1) activity • Depletion of glutathione stores
  42. 42. Clinical Manifestations: if untreated, poisoned patient passes through 4 stages; • Stage I (up to 24 hrs) – Asymptomatic, but less commonly: nausea, vomiting, and, in large doses, lethargy and malaise • Stage II (24 to 72 hours after overdose) – RUQ pain, elevation in liver enzymes, prothrombin time (PT) and, in severe cases, evidence of nephrotoxicity (elevated blood urea nitrogen, creatinine, oliguria) and/or pancreatitis (elevated serum amylase, lipase)
  43. 43. • Stage III (72 to 96 hrs) – Evidence of liver failure and, in severe cases, renal failure and multi-organ failure; death most commonly occurs in this stage • Stage IV (4 to 14 days) – Recovery
  44. 44. Management: - Supportive -Emesis/lavage -NAC/Mucomyst
  45. 45. PHENOBARBITONE POISONING • Pathphysiology • 50% of phenobabitone is non-protein-bound, available to equilibrate with tissues. • ability to cross cell memrane(BBB) is inversely correlated with its degree of ionization. • cause depression of the brainstem RAS with resultant generalised depression of the CNS
  46. 46. •May result in : mild sedation, sleep or high doses—coma,& respiratory arrest  Absorbed from oral ingestion  onset of effects in 20-60min.  Slowly metabolized by liver microsomal enzymes & are eliminated –half-lives of 2-6days
  47. 47. Clinical Manifestations:  Early Euphoria Disinhibition Ataxia Dysarthric Nystagmus slow respiration but adequate superficial reflexes disappear corneal reflexes present pupils react briskly to light
  48. 48. Late limbs become flaccid DTR disappear pupils become constricted Sometimesbullous eruptions Terminal phase shallow & periodic respiration decreased BP-Shock
  49. 49. Management Supportive GID AC Saline catharsis Diuresis Alkalinization Dialysis
  50. 50. Snake Bite • Majority of the bites being on the lower extremities. • Males:Female: 2:1 • 50% of bites by venomous snakes are dry bites that result in negligible envenomation. • In the world 3000 species, 500 poisonous
  51. 51. Early Signs and Symptoms of Venomation • Increasing local pain (burning, bursting,throbbing) at the site of the bite • Local swelling that gradually extends proximally up the bitten limb and tender • painful enlargement of the Regional Lymph nodes. However, bites by kraits and sea snakes may be virtually painless.
  52. 52. Local Symptoms and Signs • Local pain • Local bleeding • Bruising • Lymphangitis • LN Enlargement • Blistering • Local infection&Abscess formation • Necrosis
  53. 53. Systemic Symptoms General • Nausea • Vomiting • Malaise • Abdominal pain • Weakness • Drowsiness • Prostration
  54. 54. Cardiovascular(vipridae) • Visual disturbances • Dizziness • Faintness • Collapse • Shock, Hypotension • Cardiac arrhythmias • Pulmonary oedema • Conjunctival oedema Bleeding and clotting disorders ( vipridae) • Bleeding from recent wounds (including fang marks, venepunctures etc) and from old partlyhealed wounds • Spontaneous systemic bleeding
  55. 55. Neurological (Elapidae,Russell’s viper) • Drowsiness • Paraesthesiae • Abnormal taste and smell • “Heavy” eyelids,Ptosis,Ext. ophthalmoplegia • Facial paralysis • Aphonia • Difficulty in swallowing secretion • Respiratory and generalised flaccid paralysis
  56. 56. Rhabdomyolisis • Generalised pain, stiffness and tenderness of muscles, trismus, myoglobinuria, hyperkalemia, cardiac arrest, acute renal failure • Occur with sea snakes, Russell’s viper
  57. 57. Renal (Viperidae, Sea snakes) • Loin (lower back) pain • Haematuria • Haemoglobinuria • Myoglobinuria • Oliguria / Anuria • Symptoms and signs of Uraemia
  58. 58. Endocrine • Acute pituitary/adrenal insuff. • with Russell’s viper • Acute phase: Shock, Hypoglycaemia • Chronic phase (mnths to yrs after): Weakness, • Loss of 2ry sexual hair, Amenorrhoea, • Testicular atrophy, Hypothyroidism etc
  59. 59. Management of Snake Bite • First aid treatment • Transport to hospital • Rapid clinical assessment and resuscitation • Detailed clinical assessment and species diagnosis • Investigations/laboratory tests • Antivenom treatment • Observation of the response to antivenom: • decision about the need for further dose(s) of antivenom • Supportive/ancillary treatment • Treatment of the bitten part • Rehabilitation • Treatment of chronic complications
  60. 60. • Antivenom is immunoglobulin (usually the enzyme refined F(ab)2 fragment of IgG) purified from the serum or plasma of a horse or sheep that has been immunised with the venoms of one or more species of snake.

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