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Poisoning
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- 2. INTRODUCTION • A Poisonis 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. DEFINITION Poisoning represents theharmful effects on the human body of accidental or intentional exposure to toxic amounts of any substance.
- 4. EPIDEMIOLOGY 1. According toWHO data, in 2012 an estimated 193,460 people died worldwide from unintentional poisoning. Of these deaths, 84% occurred in low- and middle- income countries. 2. 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).
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- 6. The effect ofpoisoning may be :- Local Systemic Or both It may occur immediately or several hours or even days after the exposure.
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- 8. 1. Swallowed poisonsmay be corrosive. 2. Corrosive poisons include alkaline and acid agents that can cause tissue destruction after coming in contact with mucus membranes.
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- 12. • 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
- 14. SYMPTOMS OF POISONING 1.Vomiting 2. Diarrhoea 3. Upper abdominal pain 4. Jaundice 5. Difficulty breathing 6. Palpitations 7. Skin rashes 8. Scanty urine
- 15. SIGNS OF POISONING Fever Vomiting Diarrhoea Dehydration Jaundice Tonguediscolouration 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
- 16. DANGER SIGNS OFPOISONING 1. No breathing ,Wheezy or noisy breathing 2. Pulse below 50, or above110 beats per minute, irregular, or very weak · 3. Non-reacting pupils · 4. Loss of consciousness · 5. Continuous seizures · 6. Temperature > 39°C (mouth or rectum) or 38°C (armpit) · 7. Severe abdominal tenderness · 8. Anuria ·. 9. Asterixis
- 17. INVESTIGATIONS Toxicological analysis of identified substance Liver function tests· Fasting blood glucose BUN and creatinine Electrolyte levels TLC Tissue samples (e.g. gastric aspirate)
- 18. TREATMENT OBJECTIVES Tomaintain 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
- 19. Non Pharmacological Management Ensureairways 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
- 20. 1. Carry outgastric lavage or aspiration within the first 1 hour after the event or later if it involves slow release or highly toxic substances · 2. Detain the patient in the clinic or hospital for close and continuous observation, re-evaluation, and supportive and symptomatic treatment . 3. Maintain and continuously monitor vital signs
- 21. Pharmacological Management 1. InitialManagement For hypoglycaemia Glucose, IV,25-50 ml of 50% over 1-3 minutes 2. 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 3. Then, Naloxone, SC or IM, only if IV route is not feasible
- 22. MANAGEMENT Check and maintain ABC Take ECG Assess neurologic status Givewater to drink for dilution of strong acid and alkaline poison.
- 23. GASTRIC EMPTYING PROCEDURE 1.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 · 2. Detain the patient in the clinic or hospital for close and continuous observation, re-evaluation, and supportive and symptomatic treatment 3. Maintain and continuously monitor vital signs
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- 26. DEFINITION Food – poisoningis an acute gastro- enteritis caused by the ingestion of the food or drink contaminated with either living bacteria or their toxins or inorganic chemical substances and poison delivered from the plant and animals. It may be caused by:- - Bacteria or their toxins -Chemicals including metals -Plants or fish viruses -Mycotoxins
- 29. CARBON MONOXIDE POISONING Carbonmonoxide poisoning may occur as a result of industrial or household incidents or attempted suicide. Carbon monoxide bound Hb called Carboxyhemoglobin, does not transport O2.
- 33. A deep red,flushed skin color (cherry red) is the one telltale indicator of carbon monoxide poisoning. It comes from high levels of carboxyhemoglobin in the blood. Unfortunately, it is often a postmortem examination that reveals such a bright red coloring
- 35. CLINICAL MANIFESTATION 1. Headache 2.Muscular weakness 3. Palpitation 4. Dizziness 5. Confusion progress towards coma 6. Cyanosis 7. False reading of pulse oximetry
- 36. MANAGEMENT GOAL- To reversecerebral and myocardial hypoxia 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.
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- 38. DEFINITION 1. Organophosphate poisonsare the group of potent nerve agents, functioning by inhibiting the enzyme choline esterase. 2. Organophosphate Poisoning occurs after dermal, respiratory, or oral exposure to either organophosphate pesticides (e.g., chlorpyrifos, dimethoate, malathion, parathion) or nerve agents (e.g., tabun, sarin), causing inhibition of acetyl cholinesterase at nerve synapses.
- 40. CLININCAL MANIFESTATION Can bedivided into 3 broad categories, including: MUSCARINIC EFFECTS CNS EFFECTS. NICOTINIC EFFECTS
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- 48. 1. Check airway,breathing, and circulation. 2. Place patient in the left lateral position, preferably with head lower than the feet, to reduce risk of aspiration of stomach contents. Provide high flow oxygen, if available. 3. Intubate the patient if their airway or breathing is compromised. 4. Obtain I/V access and give 1–3 mg of atropine as a bolus, depending on severity. 5. Set up an infusion of 0·9% normal saline; aim to keep the systolic blood pressure above 80 mm Hg and urine output above 0·5 mL/kg/h. Side by side insert foley’s catheter.
- 49. 1. Record pulserate, blood pressure, pupil size, presence of sweat, and auscultatory findings at time of first atropine dose. 2. Give pralidoxime chloride 2 g (or obidoxime 250 mg) intravenously over 20–30 min into a second cannula. 3. Follow with an infusion of pralidoxime 0·5–1 g/h (or obidoxime 30 mg/hr) in 0·9% normal saline. 4. Insert NG tube ……Start Gastric lavage as advised by Doctor with activated charcoal dissolving NS.
- 50. Give atropine bolusesuntil the heart rate is more than 80 beats per minute, the systolic blood pressure is more than 80 mm Hg, and the chest is clear (appreciating that atropine will not clear focal areas of aspiration). Sweating stops in most cases.
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- 57. Stop digoxin anddiuretics GIT decontamination Decreasing absorption Estimate serum potassium Bradycardia: Mild toxicity : Potassium salts: 5-7.5g of KCl Serious arrhythmias: 40mEq of KCl in 500mlof 5% glucose IV OVER 2-4 hrs .
- 58. 1. Supraventricular tachyarrhythmias: 2. Propranolol : oral dose of 10-40mg every 6hrs /IV .5-1- 1mg. 3. Ventricular tachycardia : Lignocaine:1-2mg /kg IV repeat in 20-30mins. 4. Phenytoin: IV:250mg well diluted over 3-5min.
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