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various types of poisoning

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  1. 1. Prepared By- Ms. Anshu M.Sc Nursing KGMU Institute of Nursing
  2. 2.  A poison is any substance that, when ingested, inhaled, absorbed, applied to skin, or produced within the body in relatively small amounts, injures the body by its chemical action.  The branch of medicine that deals with the detection and treatment of poisons is known as toxicology.
  3. 3.  Poisoning represents the harmful effects on the human body of accidental or intentional exposure to toxic amounts of any substance.
  4. 4. According to WHO data, in 2012 an estimated 193,460 people died worldwide from unintentional poisoning. Of these deaths, 84% occurred in low- and middle- income countries.  In the same year, unintentional poisoning caused the loss of over 10.7 million population a year of healthy life (disability adjusted life years, DALYs).
  5. 5.  Acute pesticide poisoning is one of the most common causes of intentional deaths worldwide  IN INDIA  National crime bureau of India has reported in Accidental Deaths & Suicides in India 2015 that:- 26,173 died of poisoning in year 2015
  6. 6.  Ingestion  Inhalation  Injection  Absorption
  7. 7. The effect of poisoning may be :-  Local  systemic or  both It may occur immediately or several hours or even days after the exposure.
  8. 8.  · Chemicals  · Household e.g. bleach, kerosene  · Industrial e.g. methanol, ethylene glycol, cyanide, arsenic  · Pesticides e.g. organophosphates, organochlorines (e.g. DDT), rat poison  · Therapeutic drug overdose e.g. paracetamol, aspirin, iron tablets, nifedipine, phenobarbitone  · Toxic plants e.g. poisonous mushrooms, toxic herbal preparations  · Bites and stings of venomous animals e.g. snakes, scorpions, bees, spiders, aquatic animals
  9. 9.  · Vomiting  · Diarrhoea  · Upper abdominal pain  · Jaundice  · Difficulty breathing  · Palpitations  Skin rashes  Scanty urine
  10. 10.  · Fever  · Vomiting  · Diarrhoea  · Dehydration  · Jaundice  · Tongue discolouration  · Unusual fetor (smell on breath)  · Changes in breathing rate or regularity  · Changes in pulse rate or regularity  · Skin lesions  · Abdominal tenderness  · Changes in pupil size (small or enlarged)  · Seizures
  11. 11.  · No breathing  · Wheezy or noisy breathing  · Pulse below 50, or above110 beats per minute, irregular, or very weak  · Non-reacting pupils  · Loss of consciousness  · Continuous seizures  · Temperature > 39°C (mouth or rectum) or 38°C (armpit)  · Severe abdominal tenderness  · Anuria  ·. Asterixis
  12. 12.  · TLC  · BUN and creatinine  Electrolyte levels  · Liver function tests  · Fasting blood glucose  · Toxicological analysis of identified substance or tissue samples (e.g. gastric aspirate)
  13. 13. Treatment objectives  · To maintain normal vital signs  · To decontaminate the site of exposure  .To prevent and reduce absorption  · To enhance elimination  · To relieve symptoms  · To prevent further organ damage or impairment without delay
  14. 14.  · Ensure airways are patent  · Remove contaminated clothing, if necessary  Wash chemical away from the skin with soap and a lot of water  if necessary Perform nasogastric aspiration if airway is protected
  15. 15.  Carry out gastric lavage or aspiration within the first 1 hour after the event or later if it involves slow release or highly toxic substances  · Detain the patient in the clinic or hospital for close and continuous observation, re-evaluation, and supportive and symptomatic treatment Maintain and continuously monitor vital signs
  16. 16. Initial Management  For hypoglycaemia Glucose, IV,25-50 ml of 50% over 1-3 minutes  For opioid overdose Naloxone, IV,  Adult= 0.4-2 mg, repeat every 2-3 minutes (maximum of 10 mg)  Children= 10 micrograms/kg stat, subsequent dose of 100 microgram/kg if no response to initial dose Then,  Naloxone, SC or IM, only if IV route is not feasible
  17. 17.  Swallowed poisons may be corrosive.  Corrosive poisons include alkaline and acid agents that can cause tissue destruction after coming in contact with mucus membranes.
  18. 18. Alkaline products:-  Drain cleaners, toilet bowl cleaners, bleach, non phosphate detergents, oven cleaners, and button batteries Acid products:-  Toilet bowl cleaners, pool cleaners, metal cleaners, rust removers, and battery acid.
  19. 19.  Petroleum distillates/hydrocarbons  Kerosene  Turpentine  Drug overdose  Food poisoning
  20. 20.  Check and maintain ABC.  Take ECG.  Assess neurologic status  Give water and milk to drink for dilution of strong acid and alkaline poison.
  21. 21. Gastric emptying procedure:-  Syrup of Ipecac to induce vomiting in the alert patient ( never use with corrosive poison).  Gastric lavage for the obtunded patient, gastric aspirate is saved and sent to the laboratory for testing (toxicologic screens)  Activated charcoal administration (1g/Kg).  Cathartic, when appropriate Sorbitol (1-2 g/kg) Sodium sulfate Magnesium citrate.
  22. 22.  If there is specific antidote then administer it as early as possible.  If antidote is not available then remove the ingested material by adminitration of charcoal, diureis, dialysis or hemoperfusion. Hemoperfusion involves detoxification of the blood by processing it through an extra corporeal circuit and an adsorbent cartridge containig charcoal and resin, after which clean blood is returned to the patient.
  23. 23.  Carbon monoxide poisoning may occur as a result of industrial or household incidents or attempted suicide.  Carbon monoxide bound Hb called Carboxyhemoglobin, does not transport O2.
  24. 24. Carbon monoxide exerts its toxic effect by binding to circulating Hb and thereby reducing the O2 carrying capacity of the blood. Hb absorbs Carbon monoxide 200 times more rapidly than O2.
  25. 25.  Headache  Muscular weakness  Palpitation  Dizziness  Confusion progress towards coma  Skin color blue  False reading of pulseoximetry
  26. 26.  GOAL- To reverse cerebral and myocardial hypoxia
  27. 27.  Carry the patient to fresh air immediately, open all doors and windows  Loosen all tight clothing  Initiate CPR if required; administer 100% O2.  Prevent chilling; wrap the patient in blanket.  Keep the patient as quiet as possible.  Do not give alcohol in any form or permit the patient to smoke.
  28. 28.  Skin contamination injuries from exposure to chemicals are challenging because of the large number of possible offending agents with diverse actions and metabolic effects.  The severity of a chemical burn is determined by the mechanism of action, the penetrating strength and concentration, and the amount and duration of exposure of the skin to the chemical.
  29. 29.  GOAL- prevent skin from exposure.
  30. 30.  Wash the exposed skin thoroughly with water. NOTE- water should not be applied to burns from lye or white phosphorous because of the potential for an explosion or for deepening of the burn.  All evidence of these chemicals should be brushed off the patient before any flushing occurs.
  31. 31.  Start with standard burn treatment according to size and location of wound (antimicrobial treatment, debridement, tetanus prophylaxis, antidote administration as prescribed)  Plastic surgery may be required for further management of wound.
  32. 32.  Organophosphate (OP) compounds are a diverse group of chemicals used in both domestic and industrial settings. 38
  33. 33.  The primary mechanism of action of organophosphate pesticides is inhibition of acetylcholinesterase (AChE).  AChE is an enzyme that degrades the neurotransmitter acetylcholine (ACh) into choline and acetic acid.  ACh is found in the central and peripheral nervous system, neuromuscular junctions, and red blood cells (RBCs).  Organophosphates inactivate AChE by phosphorelation.
  34. 34.  Once AChE has been inactivated, ACh accumulates throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic receptors.  Clinical effects are manifested via activation of the autonomic and central nervous systems and at nicotinic receptors on skeletal muscle. 40
  35. 35.  Organophosphates can be absorbed cutaneously, ingested, inhaled, or injected.  Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure, and rate of metabolic degradation.
  36. 36. Can be divided into 3 broad categories, including:  (1) muscarinic effects,  (2) nicotinic effects, and  (3) CNS effects.
  37. 37. SLUDGE  Salivation  Lacrimation  Urination  Diarrhea  GI upset  Emesis
  38. 38. DUMBELS  Diaphoresis and diarrhea  Urination  Miosis  Bradycardia, bronchospasm  Emesis  Excess Lacrimation  Salivation
  39. 39.  muscle fasciculations  cramping, weakness  diaphragmatic failure. Autonomic nicotinic effects  include hypertension  Tachycardia  mydriasis  pallor.
  40. 40.  Anxiety  emotional lability  Restlessness  Confusion  ataxia  tremors  seizures  coma.
  41. 41.  Airway control and adequate oxygenation are paramount in organophosphate (OP) poisonings.  Intubation may be necessary in cases of respiratory distress due to laryngospasm, bronchospasm, bronchorrhea, or seizures.  Immediate aggressive use of atropine may eliminate the need for intubation.  Succinylcholine should be avoided because it is degraded by acetylcholinesterase (AChE) and may result in prolonged paralysis.
  42. 42.  The mainstays of medical therapy in organophosphate (OP) poisoning include ATROPINE, pralidoxime , and diazepam  Initial management must focus on adequate use of atropine. Optimizing oxygenation prior to the use of atropine is recommended to minimize the potential for dysrhythmias.
  43. 43.  Anticholinergic agents  These agents act as competitive antagonists at the muscarinic cholinergic receptors in both the central and the peripheral nervous system.  These agents do not affect nicotinic effects.
  44. 44.  Adult  1-2 mg IV bolus, repeat q1-5min prn for desire effects (drying of pulmonary secretions and adequate oxygenation) Strongly consider doubling each subsequent dose for rapid control of patients in severe respiratory distress  Pediatric  0.05 mg/kg IV, repeat q1-5min prn for control of airway secretions Strongly consider doubling each subsequent dose to rapidly stabilize patients with severe respiratory distress
  45. 45.  WORLDWIDE  While reliable data are hard to obtain, it has been estimated that about 5 million snake-bites occur each year, resulting in up to 2.5 million envenomings, at least 100,000 deaths and around three times as many amputations and other permanent disabilities.
  46. 46.  INDIA  The peak incidence of snakebite cases is reported during the paddy sowing and harvesting periods, June to November. The common krait, Bunganrs caeruleus, is regarded as the most dangerous species of venomous snake in the Indian subcontinent.
  47. 47.  National crime bureau of India has reported in Accidental Deaths & Suicides in India 2015 that:- 8,554 deaths occur because of snakebite in 2015 in India
  48. 48.  In India, poisonous snakes belong to three broad families: 1. Elapidae: Cobras, Kraits 2. Viperidae: Vipers Russell’s viper, saw scaled viper Pit viper 3. Hydrophidae: Sea Snakes  Poisonous snakes can be identified by their characteristic morphology.
  49. 49. Poisonous snakes belong to three Families on the basis of poison secreted :  1. Elapidae : Neurotoxic 2. Viperidae : Vasculotoxic 3. Hydrophidae : Myotoxic
  50. 50.  R. = Reassure the patient.  70% of all snakebites are from non- venomous species. Only 50% of bites by venomous species actually envenomate the patient  I = Immobilise in the same way as a fractured limb.  Use bandages or cloth to hold the splints, not to block the blood supply or apply pressure. Do not apply any compression in the form of tight ligatures, they don’t work and can be dangerous!  G. H. = Get to Hospital Immediately.  Traditional remedies have NO PROVEN benefit in treating snakebite.  T= Tell the doctor of any systemic symptoms  such as ptosis that manifest on the way to hospital.
  51. 51.  Patient Assessment Phase: On arrival.  Deal with any life threatening symptoms on presentation. i.e. Airway, Breathing and Circulation.  If there is evidence of a bite, where the skin has been broken, give Tetanus Toxoid  Routine use of anti-biotic is not necessary, although it should be considered if there is evidence of cellulitis or necrosis
  52. 52.  Polyvalent antivenin is available in a lyophilized form (as liquid antivenin is unstable at room temperature).  Active against the four common poisonous snakes in India – cobra, krait, Russel’s viper and saw scaled viper (Echis).
  53. 53. Average potency of the antiserum available is that 1 ml will neutralize  0.6mg cobra  0.45mg krait  0.6mg Russel’s viper  0.45mg saw scaled viper venom
  54. 54.  Reconstitution involves the addition of 10ml of distilled water to an ampoule and shaking till the solution is clear.  It should be administered intravenously as early as possible. It is essential to enquire about allergy (specially to horse serum). It is well to be prepared for an anaphylactic reaction during the antivenin administration
  55. 55.  Standard High Dose: loading dose of 100ml followed by 50ml every 6 hours till the clotting time became normal.  Low Dose:  The basis of low dose therapy is that the venom is absorbed only gradually into the systemic circulation and the low dose is sufficient to neutralize the absorbed quantity of venom.  The low dose is given over a longer period as absorption of venom continues into the systemic circulation.
  56. 56.  Analgesics for pain – Tab PCM  Antibiotics for infection. The choice should cover for anaerobic infection.  Anti-tetanus prophylaxis  Replacement of coagulation factors / platelets if there is active significant bleeding or bleeding into a vital organ
  57. 57.  Respiratory failure  Edrophonium / atropine 10mg / 0.6mg as a test  Neostigmine / atropine 0.5mg/0.6mg every 30 – 60 min  Mechanical ventilation  Shock Treat as appropriate  Renal Failure Dialysis
  58. 58. To be effective, these had to be applied around the upper part of the limb, so tightly that the peripheral pulse was occluded.  This method was extremely painful and very dangerous if the tourniquet was left on for too long (more than about 40 minutes), as the limb might be damaged by ischaemia- gangrenous limbs  Confining this toxin in a smaller area, by use of compression techniques creates a greater risk of serious local damage.
  59. 59.  When the tourniquet is removed there is the problem of the venom rapidly entering the system and causing respiratory failure in the case of neurotoxic bites  The Rusell Viper’s venom contains pro-coagulant enzymes which cause the blood to clot. In the small space below the tourniquet the venom has a greater chance of causing a clot. When the tourniquet is released the clot will rapidly enter the body and can cause embolism and death.(Kevin Loria 2014)  Lastly, there has been a great deal of research showing that tourniquets DO NOT stop venom from entering the body
  60. 60. ASSESSMENT-  Assess the condition of patient.  Assess the type of poisoning  Assess the more injured area. GOALS-  Early detection, early management and prevention of complications
  61. 61. 1. Ineffective breathing pattern related to the swelling of the nasal mucosa wall as evidenced by: shortness of breath, breath with the lips, there rhinitis. 2. Acute pain related to gastric irritation as evidenced by: abdominal pain, looked grimacing while holding stomach. 3. Impaired skin integrity related to changes in circulation as evidenced by: swelling and itching of the skin and the nose, there are hives, urticaria.
  62. 62. 1. Ineffective breathing pattern related to the swelling of the respiratory mucosa wall  Assess the respiratory rate & depth  Maintain patency of airway.  Do ET intubation in case of laryngeal edema.  Give comfortable position.  Remove the cause of allergy.  Give anti inflammatory drugs/antidote as prescribed by doctor.
  63. 63.  Assess characteristics of pain.  Stop patient from eating.  Keep patient on NPO.  Give IV fluids.  Give activated charchol and cathartics as told by doctor.
  64. 64. 3. Impaired skin integrity related to changes in circulation  Assess skin condition.  Prevent the patient from exposure.  Wash the exposed area thoroughly with water.  Do aseptic dressing .  Apply antibiotic ointment as told by doctor.
  65. 65.  Thousands of deaths takes place every year because of intentional poisoning among adults and unintentional among children in our state.  Many snake bites and even deaths from snakebite are not recorded.  One reason is that many snake bite victims are treated not in hospitals but by traditional healers.  Some people who are bitten by snakes or suspect or imagine that they have been bitten, may develop quite striking symptoms and signs, even when no venom has been injected. This results from an understandable fear of the consequences of a real venomous bite.
  66. 66.  Brunner & suddarth’s. Text book of medical surgical nursing. 12th edition. Vol2. lippincott. 2017-2019 