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POISONING
-AY
INTRODUCTION
• 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.
DEFINITION
Poisoning represents the harmful effects on
the human body of accidental or intentional
exposure to toxic amounts of any substance.
EPIDEMIOLOGY
1. 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.
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).
TYPES OF POISONING
Ingestion
Inhalation
Injection
Absorption
The effect of poisoning may be :-
Local
Systemic
Or both It may occur immediately or several
hours or even days after the exposure.
TYPES OF
POISONING
1. Swallowed poisons may be corrosive.
2. Corrosive poisons include alkaline and
acid agents that can cause tissue
destruction after coming in contact with
mucus membranes.
CAUSES OF POISONING
• 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
SYMPTOMS OF POISONING
1. Vomiting
2. Diarrhoea
3. Upper abdominal pain
4. Jaundice
5. Difficulty breathing
6. Palpitations
7. Skin rashes
8. Scanty urine
SIGNS OF POISONING
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
DANGER SIGNS OF POISONING
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
INVESTIGATIONS
Toxicological
analysis of
identified
substance
Liver function
tests ·
Fasting
blood
glucose
BUN and
creatinine
Electrolyte
levels
TLC
Tissue
samples
(e.g. gastric
aspirate)
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
Non Pharmacological Management
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
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
Pharmacological Management
1. Initial Management 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
MANAGEMENT
Check and
maintain
ABC
Take ECG
Assess
neurologic
status
Give water
to drink for
dilution of
strong acid
and alkaline
poison.
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
FOOD
POISONING
DEFINITION
Food – poisoning is 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
CARBON MONOXIDE POISONING
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.
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
CLINICAL MANIFESTATION
1. Headache
2. Muscular weakness
3. Palpitation
4. Dizziness
5. Confusion progress towards coma
6. Cyanosis
7. False reading of pulse oximetry
MANAGEMENT
GOAL- To reverse cerebral 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.
ORGANOPHOSPHATE
POISONING
DEFINITION
1. Organophosphate poisons are 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.
CLININCAL MANIFESTATION
Can be divided into 3 broad categories, including:
MUSCARINIC
EFFECTS
CNS
EFFECTS.
NICOTINIC
EFFECTS
PATHOPHYSIOLOGY
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.
1. Record pulse rate, 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.
Give atropine boluses until 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.
DIGOXIN
TOXICITY
TREATMENT OF
TOXICITY
Stop digoxin and diuretics
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 .
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.
Thankyou!

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Poisoning

  • 2. INTRODUCTION • 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. DEFINITION Poisoning represents the harmful effects on the human body of accidental or intentional exposure to toxic amounts of any substance.
  • 4. EPIDEMIOLOGY 1. 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. 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).
  • 6. The effect of poisoning may be :- Local Systemic Or both It may occur immediately or several hours or even days after the exposure.
  • 8. 1. Swallowed poisons may be corrosive. 2. Corrosive poisons include alkaline and acid agents that can cause tissue destruction after coming in contact with mucus membranes.
  • 9.
  • 10.
  • 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
  • 13.
  • 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 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
  • 16. DANGER SIGNS OF POISONING 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  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
  • 19. Non Pharmacological Management 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
  • 20. 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
  • 21. Pharmacological Management 1. Initial Management 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 Give water 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
  • 24.
  • 26. DEFINITION Food – poisoning is 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
  • 27.
  • 28.
  • 29. CARBON MONOXIDE POISONING 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.
  • 30.
  • 31.
  • 32.
  • 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
  • 34.
  • 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 reverse cerebral 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.
  • 38. DEFINITION 1. Organophosphate poisons are 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.
  • 39.
  • 40. CLININCAL MANIFESTATION Can be divided into 3 broad categories, including: MUSCARINIC EFFECTS CNS EFFECTS. NICOTINIC EFFECTS
  • 41.
  • 42.
  • 44.
  • 45.
  • 46.
  • 47.
  • 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 pulse rate, 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 boluses until 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.
  • 51.
  • 53.
  • 54.
  • 55.
  • 57. Stop digoxin and diuretics 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.
  • 59.