POISONING

1. POISONING Dr. M.L.Siddaraju

2. History • Egyptians are said to have studied many poisons as early as 3000BC. • Among vedas- Atharvana veda (1500BC) describes poisons. • Susrutha (350BC) described as how poisons were mixed with food and drink, medicines, snuff, etc.. • Italians brought the art of poisoning to its zenith prior to 6th century AD. • Orfila-(1787-1853) was first to attempt a systemic correlation between the chemical and biologic information of the poisons known then. • Others who worked are Marsh, Magendie, Ambrose, Scheelle, Robert Christison and Rudolf Kobert.

3. POISONING IN CHILDREN • Poison is a substance that causes harm if it gets into the body. • The poisoning in children could occur due to diverse causes and could be classified as • accidental, • homicidal or • suicidal. • Erroneous administration of overdosage of drugs by the parents or by the medical staff is also frequent.

4. Acute exposure is a single contact that lasts for seconds, minutes or hours, or several exposures over about a day or less. Chronic exposure is contact that lasts for many days, months or years. • A poison may get into the body through ingestion, inhalation (gas, vapors, dust, fumes, smoke, spray), skin contact (pesticides), or injection (bites and stings, drug injection

5. Accidental poisoning in children is a global problem. The relative importance of poisoning as a cause of childhood morbidity and mortality increases when malnutrition and infections are brought under control. • Accidental poisoning is the twelfth leading cause of admissions in pediatric wards in India and accounts for about one percent of the hospitalized patients. Most cases of accidental poisoning are preventable. Continuing morbidity and mortality due to accidental poisoning is serious challenge to the pediatricians and public health officials.

6. Pattern of poisoning • Chemical products, most often swallowed by children include household cleaners (bleach, detergents) fuel (kerosene, paraffin), cosmetics, medicines, paints and products for household repairs and household pesticides. • Bites and stings of animals and insects, and ingestion of poisonous plants and seeds also considerably account for outdoor poisoning in children.

7. Carbon monoxide poisoning can happen when fires, stoves, heaters or ovens are used in rooms, huts which do not have proper ventilation to let the gas out.

8. Ecology of poisoning • Interaction between the host and the environment (including easy access to the poisonous substances) determines the magnitude of the problem. • Age. About 40% of all cases of accidental poisoning in children are reported in the second year of life; about 12% of the cases occur in the first and 20% in the third year. As the children start crawling and walking around 1 year, they become very active and try to explore unfamiliar objects by putting these into their mouth and testing these. Thus they expose themselves to accidental poisoning. Hyperactive male children are more prone to accidental poisoning.

9. Large families:In large families mother is often too occupied with household chores, is easily fatigued and often careless in storage of potentially poisonous household substances. • Small accommodation

10. Environment: Lead poisoning is common in children living in areas were there are workshops for automobile, lead storage batteries or for manufacture of lead typesets for printing presses. Caustic soda poisoning used to be observed frequently in children of families, which prepared washing soap for domestic or commercial purposes in their own houses. Insecticides, medicines, naphthalene balls and kerosene are common household things which are potential hazards. • Rural or Urban areas: • The pattern of poisoning varies in rural and urban areas due to exposures to different types of potential poisons. Snakebites are more common in those wandering in fields.Also pesticides are more common in rural set up. The poor are driven by starvation to experiment on roots and fruits thus leading to poisoning.

11. Time relationship: • . Accidental poisoning is likely when normal routine in the house is disturbed such as during periodic house painting, packing and unpacking at the time of change of residence, going for vacation etc.

12. Classification of poisons Based on the chief symptoms they produce • Corrosives- strong acids, strong alkalis, metallic salts. • Irritants- organic, inorganic. • Systemic- cerebral, spinal, peripheral, CVS, asphyxiants. • Miscellaneous- food poisoning & botulism.

13. Non toxic common household agents • Shampoos, toothpaste, lipstick, creams, shaving cream, toilet soaps, cosmetics, hair dye/oil. • Antacids, house lizards, non nitrate fertilizers, newspaper, adhesives, water colors, chalk, ink (ball point/ fountain pen), candles.

14. Important causes of child poisoning in India • Kerosene and other hydro carbons(8-55%) • Household products-insecticides, rodenticides, phenol, alkalis, turpentine, camphor, naphthalene, neem oil, alcohol(14-30%). • Drugs- iron salts, barbiturates, anticonvulsants, antihypertensives, aspirin, antiseptics(16-30%). • Plant and plant products- Dhatura, castor seeds(6-32%). • Food poisoning(7-15%). • Venomous bites & stings(7-11%).

15. History taking • What poison was ingested. • Time since ingestion. • Total amount of poison ingested. • Route of exposure. • Progression of signs and symptoms since ingestion. • Family history of epilepsy, mental sub normality, bleeding disorder. • Whether the patient is receiving other medications which may interact with the poison.

16. General signs and symptoms • Symptoms-odor, sweating, fever, delirium, convulsions, burns of mouth, blindness, GI symptoms, abnormal movements, coma. • Signs- miosis, mydriasis, blindness, facial twitching, dull & mask like expression, pallor, cyanosis, hypothermia, sweating, respiratory symptoms, CVS symptoms, CNS symptoms.

17. Poisoning severity Grades • None(0)- no symptoms or signs/vague symptoms judged not to be related to poisoning. • Minor(1)- Mild, transient & spontaneously resolving symptoms.

18. Moderate(2)- pronounced or prolonged symptoms. • Severe(3)- severe or life threatening symptoms.

19. Diagnosis of Poisoning • Cardiac arrythmias. Tricyclic antidepressants, amphetamine, aluminium phosphide, digitalis, theophylline, arsenic, cyanide, chloroquin. • Metabolic acidosis. Isoniazid, methanol, salicylates, phenformin, iron, cyanide. • GIT disturbances. Organophosphorus, arsenic, iron, lithium, mercury. • Cyanosis. Nitrobenzene compounds, aniline dyes, and dapsone.

20. Basic Management of a poisoned patient • Antidotes are available for very few commonly encountered poisons, and treatment is usually non-specific and symptomatic. In such cases management consists of emergency first aid and stabilization measures, appropriate treatment to reduce absorption, measures to enhance life support followed by psychiatric counseling.

21. Identification of Poison • Identify the poison by careful history and helpful clues. Determine what, when and how much of the poison was ingested or inhaled. Find the supporting evidence for your diagnosis from the nature of the symptoms and physical signs. Some common toxidromes based on certain signs and symptoms :

25. Principles of Management • Keep the phone numbers of your doctor, hospital & emergency medical system near the phone. • Removal of the patient from the site of poisoning. • Initial resuscitation and stabilization. • Symptomatic and supportive measures. • Removal of unabsorbed poisons- from GI tract or from skin, eye. • Hastening the elimination of absorbed poisons. • Use of specific antidote if available • Disposition of the patient with advice for prevention.

26. Emergency Stablization Measures • The unconscious patient should be transported in the headdown semiprone position to minimize the risk of inhalation of gastric contents. A clear airway is established and ventilation is maintained. Potentially serious abnormalities such as metabolic acidosis, hyperkalemia and hypoglcymia may require correction as a matter of urgency. Neurological assessment is made by calculating the Glasgow Coma Score (GCS).

27. Many drugs and poisons can cause grand mal convulsions, which, if repeated, should be controlled with intravenous diazepam. Hypotension with peripheral circulatory failure is treated first by correction of hypoxia and acidosis, and by elevation of the foot end of the bed. If adequate perfusion is not restored by these measures, the circulating volume should be increased by administration of a plasma expander intravenously. Cardiac arrhythmias are often improved or abolished by correction of hypoxia, acidosis and electroyte imbalance

28. Initial resuscitation stabilization • Includes airway- proper positioning head tilt and chin lift, suction of secretions from oropharynx, falling back of tongue is prevented by suitable airway tube. • Breathing- oxygen via a mask, when gag/cough reflects is absent- ET tube inserted. if necessary positive pressure ventilation with ABG monitoring, respiratory stimulants for severe respiratory depression. • Circulation- proper IV access, maintenance of fluid & electrolyte balance, IV drugs for treatment.

29. Symptomatic & supportive Management • Hemodynamic support- elevation of foot end of the bed, oxygen administration, IV fluids, blood products. • Cardiac dysrrhythmias- correction of hypoxia, acidosis, hypokalemia, ECG, treatment with antiarrhythmic drugs. • Convulsions- correction of hypoglycemia/hypocalcemia/hypoxia/cerebral edema and other metabolic defects, anticonvulsant therapy.

30. Continued… • Management of hypothermia- cover with a blanket, thermo neutral environment maintenance, pre warmed IV fluids and inspired gases. • Management of pulmonary edema- administer 100% oxygen, intermittent positive pressure ventilation, IV aminophylline(5-8mg/kg), IV frusemide(1-2 mg/kg).

31. Continued… • Management of stress ulcers- NG intubation, cold saline wash, administration of antacids, H2- receptor antagonists. • Management of pain- analgesics (preferably- narcotics).

32. Removal of Toxin • The aim of decontamination procedures is to reduce the absorption of poison. It can be achieved by: • Eye decontamination. Ocular exposure to solvents, e.g., hydrocarbons, detergents, and alcohol, or corrosive agents, e.g., acid or alkalis require immediate local decontamination. This is achieved by copious irrigation with neutralizing solution (e.g., normal saline or water) for at least 30 minutes. Do not use acid or alkaline irrigating solution.

33. Dermal decontamination. Absorption of organophosphorus and related compounds through cutaneous route can prove to be a fatal as oral route absorption. Cutaneous absorption depends on several factors such as lipid solubility, skin condition, location, caustic effect, physical conditions

34. Remove all contaminated clothes and irrigate the whole body including nail, groin, skinfolds with water or saline as soon as possible after exposure and continue irrigating for at least 15 minutes. Water should not be used to decontaminate skin in exposures to sodium and phosphorus. In certain cases, specific agents may be indicated for skin decontamination (e.g., mineral oil for elemental sodium, Neosporin for super glue and calcium gluconate for hydrofluoric acid).

35. Gut decontamination. This includes (i) gastric evacuation; (ii) adsorbent administration; and (iii) catharsis. Emesis is the preferred method of emptying the stomach in conscious children. Vomiting can be induced by (a) tickling the fauces with a finger, feather or a leafy twig of a tree; (b) administration of copious draughts of warm water; (c) gurgling with non-detergent soap; or (d) saline emetics in warm water. To prevent aspiration in small children, the head should be kept low.

36. Syrup of ipecac may be used for inducing emesis in children older than 6 months in a single dose of 10 mL for 6-12 months age, and 15 mL for children above 1 year of age. The dose may be repeated in 20 minutes for those more than 1 year of age. • Induction of vomiting is contraindicatied in corrosive or kerosene poisoning and in comatose patients or those with absent gag reflex.

37. Gastric Lavage. If the vomiting does not occur quickly, gastric lavage should be done promptly to remove the poison. In a symptomatic but alert patient with minor ingestion, activated charcoal alone by mouth is sufficient for gastrointestinal decontamination

38. The child is kept in the left lateral position with the head hanging over edge of the table and the face down. A large single lumen tube with multiple distal ports is necessary. A restraint is required for most children and mouth gag is placed in the mouth before the procedure. The catheter is passed gently and free end is dipped under water to make sure that the catheter is not in the airway.

39. Generally tap water is used for lavage and four or five washes are done. The volume of each aliquot should be at least 10-15 mL/kg. After the fluid has been instilled, it should be removed by gravity drainage or tube suction. Catheter is pinched before it is finally withdrawn or suction is maintained during withdrawal to prevent aspiration.

40. Gastric lavage should not be performed in children with poor gag reflex or corrosive ingestion. In kerosene poisoning, lavage may be done very cautiously if the child has consumed a large gulp of kerosene and is brought quickly to the hospital, otherwise it is better to avoid stomach wash.

41. Adsorbent administration • An agent capable of binding to a toxic agent in the GIT is known as adsorbent. Activated charcoal is the most widely used adsorbent. It is created by subjecting carbonaceous material e.g., wood, coal etc. to steam at 600-900 degree Celsius and acid.

42. For the comatosed patient (Grade 3 or 4) with potentially serious overdose, gastric lavage is followed by administration of activated charcoal via an orogastric or nasogastric tube within 1-2 hours of ingestion. Dose of activated charcoal administered should be atleast 10 times the dose of ingested toxic material. In asymptomatic patient presenting early or without reliable history, 15-30 gram of charcoal may be used.

43. Catharsis • Laxative and purgatives may be given in poisoning with substances which do not cause corrosive action on gastrointestinal mucosa. Increased motility of the gut may reduce absorption. Commonly used cathartics include sorbitol and mannitol (1-2 g/kg), and magnesium or sodium sulfate (200-300 mg/kg). Do not give magnesium salt cathartics in cases with renal failure.

44. Specific Antidotal Therapy • The antidotes may be physiological, chemical or physical. Chemical antidotes combine with the poison and render it innocuous. Physiological antidotes counteract the effects of the poison on the metabolism and physiological functions of the body and thus prevent its harmful effects. Physical antidotes prevent the contact of the poisonous substance with the target organ or adsorb the toxic components, thus preventing their toxicity.

45. Specific antidotes may be life saving but unfortunately they are not often available and are effective for less than 5% of poisoning cases. When obtainable, they must be given without delay for maximum protective action. • Antidotes now considered obsolete include universal antidote for ingested poisons, acetazolamide for modification of urinary pH, ascorbic acid for methemoglobinemia, castor oil as cathartic, nalorphine for opiates, sodium chloride for emesis and tannins for alkaloids.

46. Promotion of Excretion of Toxin • The efficiency of regimens for enhancement of drug elimination from the body can be predicted to a large extent if the physio-chemical properties, disposition and pharmacokinetics of the substance are known. The fluid intake is increased to promote glomerular filtration and excretion of poison through the urine.

47. Forced diuresis:Diuresis alone has relatively little effect on drug elimination because at best the renal clearance is only proportional to the urine flow rate. In the case of drugs which are weak organic acids and bases, a much greater effect on clearance can be obtained by manipulation of the urine Ph. The lipid solubility and hence tubular reabsorption of such acidic and basic drugs is decreased in alkaline and acid urine respectively. Theoretically for each change of one unit in urine pH, the renal clearance could change by a factor of 10. Urine pH is therefore much more important than urine flow rate.

48. In practices, forced alkaline diuresis is restricted largely to poisoning with phenobarbitone and salicylate, although much of the effect in lowering plasma salicylate concentrations result from haemodilution rather than increased urinary excretion. Raise the urinary pH to 7.5 for weak acids (e.g., barbiturates, salicylates) with 1.4 percent sodabicarb. Maintain urinary pH to 5.5-6.5 (forced acidic diuresis) in poisoning with weak bases e.g., tricyclic antidepressant and pheytoin, with ammonium chloride 4 g administered every two hourly through Ryle’s tube

49. Any form of forced diuresis is potentially dangerous. Forced diuresis is contraindicated in patients with cardiac and renal impairment; complications include water intoxication, disturbances of acid-base and electrolyte balance, left ventricular failure with pulmonary oedema and cerebral oedema.

50. Hemodialysis, hemo-perfusion and peritoneal dialysis. Drugs which can be removed reasonably effectively by hemoperfusion and haemodialysis include barbiturates, carbamazepine, salicylates, theophylline, dapsone, most antibiotics, lithium, chloral hydrate, methanol and ethylene glycol.