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 Ingestion of toxin substances is a common problem in
the pediatric age group.
 Common causes are household products including
kerosene oil, drugs (barbiturates), chemicals (corrosives)
and pesticides (organophasphate compound.
 Majority of poison are ingested by children at home,
include products that are familiar and visual appealing
due to glossy packing.
 The inherent curiosity and tendency for exploration in
children contributes the high incidence of accidental
poisoning below 5 years of age.
 Usually classified as accidental, homicidal or suicidal,
whereas in a majority of cases are accidental.
In toddlers the risk is high due to their spontaneous
activity, curiosity, mouthing of the objects &
imitation of the adults.
Pharmaceutical toxicity is most common due to self
administration by the parents for the minor ailments.
 In developing countries the incidence is high due to
change in living habits and decreased awareness
about the industrial chemicals etc.
 Poisoning should be suspected in case of any unusual
drowsiness, odour, convulsions, respiratory distress
& circulatory failure.
 All children < 6 yrs with poisoning should be
hospitalised for at least 24 hrs for observation.
Common poisons
Hydrocarbon – Kerosene oil, solvents
Insecticides- DDT, glyphosate, malathion
Medicines – aspirin, iron, paracetamol etc.
Polish varnish
Detergents
Diagnosis:
Depend upon the type of poison and its severity.
Latter depends on the amount of substance
ingested.
Age of the patient.
Examination:
Vital parameters; Respiration, BP, Pulse,
temperature
Level of consciousness
Examination particularly observing pupillary size,
oral cavity, breath odor, skin color, sweating.
Any mark of injury, pigmentation, secretions from
oral and nasal orifices.
 Abdominal examination for peristaltic activity and
urinary retention.
Some clues of the poison by urine color
Orange/Red- Rifampicin
Grey/Black- Phenols/cresols
Blue/green-Methylene blue
General Principles of Management
First Aid:
 Decontamination:
 Remove from the source of poison
 Remove the clothing's
 Irrigate the skin and eyes with normal saline or
lukewarm soap water
 Treatment:
 Patients should be transported nearest medical care
facility.
 Initial treatment consist of managing the airway,
breathing and circulation.
 Take care of airway by inserting an appropriate size
endotrachial tube.
 Identification of poison& assess the type & amount of
the poison.
 Maintain IV line.
 In comatose patients a bolus of 2ml/kg of 25% Dextrose
may be given.
 In adolescent & malnourished children Inj. Thiamine 50 –
100 mg iv/im to avoid precipitating acute wernicke’s
encephalopathy.
 In comatose patient if respiration is shallow parental
naloxone in dose of 0.2 to 0.45ug/ kg is given.
 Removal of the unabsorbed poison.
 Gastrointestinal tract
 Emesis can be induced by Sy. ipecac which induced
vomiting in 80% within 20 minutes is given 30 minutes of
ingestion.
 Contra indicated in children below 6 month, corrosive or
caustic ingestion and those who are comatose.
Gastric Lavage:
 Gastric lavage can be used in place of emesis
 Done in left lateral position with head end low with
15 ml/kg NS ( max 400/clycle).
 CI in hydrocarbons & corrosive & paralytic ileus,
heart disease
 In comatose child only after cuffed endotracheal
intubation.
 Prevention of GI absorption.
Activated charcoal-1 to 2 g/kg/dose(1 g in 8 ml of
water through NG tube after Gastric lavage every 4
hourly.
Avoid in acids, alkalies, iron poisonings.
Cathartics :Na & Mg sulphate 25 mg/kg/dose
Promotion of excretion:
 Maintenance IV line
Diuresis:
Frusemide-2 to 4 mg/kg/day
Mannitol- .5 to 1 g/kg over 30 min
Forced alkaline diuresis in Salicylate & barbiturate
Specific antidotes:
 Depending upon the type of poison ingested
 Some clues of the poison by urine colour
Blue/green- Methylene blue
Orange/Red- Rifampicin
Grey/Black- Phenols/cresols
Lab. Investigation : Estimation of blood level for
glucose, urea, Serum creatinine, serum electrolytes,
ABG, ECG, X ray etc.
Laboratory findings indicating the poison:
 Hyperkalaemia- Beta blockers, digoxin
 Hypokalaemia- Theophylline, diuretics
 Hypoglycemia- Oral hypoglycemic agents, ethanol,
salicylates, quinine.
Hyperglycemia-Acetone, theophylline, calcium channel
blockers.
 Hypocalcemia- Ethylene glycol, oxalate.
 Hyperglycemia with ketoacidosis– Salicylate,
theophylline,
Increased anion gap- Methanol, ethanol, ethylene,
glycol, salicylates, ionized, iron.
Decresed anion gap- Lithium, bromide.
Pulmonary edema- Carbon monoxide, cyanide, irritant
gas.
Kerosene & Other Hydrocarbon Poisoning
 High volatile: Kerosene, Petroleum, Ether, Paint,
thinner
Low volatile: Furniture polish, Lubricating oils, Paraffin
wax.
Accidental ingestion of kerosene, petrol, diesel is
common.
Stored in unmarked container.
Taste prevent large amount to be consumed.
Systemic manifestations are due to absorption through
the lungs following aspiration;
Exceptions are non petroleum distillate hydrocarbons
(benzene, carbon tetrachloride, chloroform etc) which
are absorbed from GIT.
Clinical Features :
Topical effects :
 Irritation of oral, esophageal & gastric mucosa.
Pulmonary effects :
Fever, tachycardia, tachypnoea, cough, cyanosis and
rarely pulmonary edema.
CNS effects:
Euphoria, headache, restlessness, muscle twitching,
in coordination , confusion, lethargy ,stupor, coma &
convulsions.
Other features:
 Liver damage, renal tubular, bone marrow depression
& myocardial toxicity.
Management Protocol:
 Asymptomatic for a period of six hours- observe at
home
Symptomatic-
 Oxygen inhalation
 If required IPPV
 Emesis is contra indicated
 Maintain iv fluids
 Antibiotics are required in the presence of pre-existing
respiratory illness.
Chest X ray if normal, observe for 6 hrs & may be dis
charged and if shows lesions observe for 24 hrs & if no
symptoms may be discharged.
Organophosphate Poisoning
 Mostly used as insecticides & pesticides viz Malathion,
Parathion, carbamates, Fenthion, TEPP
 Cause an irreversible inhibition of cholinesterase
resulting in excessive accumulation of ach at receptor
sites leading to excessive cholinergic manifestations
Clinical features.-
 Muscarinic effects :
 Lacrimation
 Excessive salivation
 Urination
Diarrhea
 Nausea
 Vomiting
 Bradycardia
 Pin pointed pupil
 Pain abdomen
 Tightness of chest
 Wheezing
Nicotinic effects:
Weakness
 Muscle cramps
 Fasciculation
 HTN
 Respiratory paralysis
Central effects:
 Anxiety
 Headache
Confusion
 Restlessness
 Seizures
Slurred speech & coma
Diagnosis:
Based on history and clinical features.
RBC, cholinesterase level is less then 50% in case where only
exposure and less then 20% in symptomatic patients.
Management :
Cloth should be removed & skin washed with soap and
water.
Gastric decontamination done by lavage or emesis
Children older then 12 years Atropine 1.0–2.0 mg iv every
10–30 minutes until cholinergic sign are reversed. Younger
children 0.02-0.05 mg/kg every 10-30 min till signs of
atropinisation including warm, Dry skin, dry mouth,
tachycardia and pupillary dilatation.
Pralidoxime is the specific antidote for organ phosphorus
compound but muscarinic or central action are not
significantly reversed. Drug used in dose of 25-50 mg/kg
older then 12years over a period 15–30 minutes & repeated
after 1-2 hours.
Corrosive poisonings:
 Include washing soda, acids, alkalies, bleaching
powder, toilet & drain cleaners, strong detergent
granules.
Acids produce coagulative necrosis, which cause
superficial damage while alkali cause a deep
penetrating liquefaction necrosis.
 Acid ingestion cause gastric perforation & peritonitis
while alkali commonly cause damage in esophagus &
in severe case pneumonia.
Clinical features:
 Vomiting
 Dysphagia
 Drooling
 Abdominal pain
 Involvement of glottis leads to stridor & shock.
 Oral cavity shows edema, ulceration & pseudo
membrane over the palate, uvula and pharynx.
 Absence of oral burns& lack of symptoms do not rule
out the involvement of esophagus.
 Esophageal & gastric perforation leads to peritonitis.
 If required upper intestinal tract endoscopy with
fibrotic endoscope should be performed within 24-48
hours & after 2-3 weeks by an experienced person to
determine the extent of the injury.
Management Protocol
 Vomiting should not be induced.
 Small amount of water or milk to wash away any
residual caustic from the oral mucosa.
 Detailed history about the type & amount of the
corrosive.
 Ingestion with concentrated solutions of acid and
alkalis need hospitalization.
 Such children kept nil orally.
 Gastric lavage contraindicated.
 Neutralization by acid/alkali is also not recommended
 Milk of magnesia & antacids may be used to neutralize
strong acids.
 Irrigation of skin & eyes if involved
 H2 blockers - Ranitidine 2-4 mg/kg/day 12 hrly orally
for 6-8 wks or 1-2 mg/kg/d IV 12 hrly.
Use of corticosteroids is controversial.
As long as the child is able to swallow, liquids are
offered by mouth coz drinking is a self-dilatation & may
decrease the likely hood of esophageal stricture
formation.
Antibiotics if infection suspected
Drooling & dysphasia beyond 12-24 hrs have been
reported to be a good predictor of scar formation &
should prompt upper GI endoscopy.
Placement of a rubber tube in the esophagus allows it to
scar down in a functional position leaving a lumen.
Prognosis:
Mild cases have full recovery of corrosive injuries.
Moderate and severe cases will result in stricture
formation requiring regular dilatation and possible
surgery.
Avoid keeping poisonous plant in or around
house.
Take care while eating products such as berries,
roots or mushrooms.
Keep all potentially p oisonous substance out of
children reach.
Label the poisons in your home.
Store medicines, cleaning detergents, mosquito
repellants and paints carefully.

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Poisoning in Children.pptx

  • 1.
  • 2.  Ingestion of toxin substances is a common problem in the pediatric age group.  Common causes are household products including kerosene oil, drugs (barbiturates), chemicals (corrosives) and pesticides (organophasphate compound.  Majority of poison are ingested by children at home, include products that are familiar and visual appealing due to glossy packing.  The inherent curiosity and tendency for exploration in children contributes the high incidence of accidental poisoning below 5 years of age.  Usually classified as accidental, homicidal or suicidal, whereas in a majority of cases are accidental.
  • 3. In toddlers the risk is high due to their spontaneous activity, curiosity, mouthing of the objects & imitation of the adults. Pharmaceutical toxicity is most common due to self administration by the parents for the minor ailments.  In developing countries the incidence is high due to change in living habits and decreased awareness about the industrial chemicals etc.  Poisoning should be suspected in case of any unusual drowsiness, odour, convulsions, respiratory distress & circulatory failure.  All children < 6 yrs with poisoning should be hospitalised for at least 24 hrs for observation.
  • 4. Common poisons Hydrocarbon – Kerosene oil, solvents Insecticides- DDT, glyphosate, malathion Medicines – aspirin, iron, paracetamol etc. Polish varnish Detergents Diagnosis: Depend upon the type of poison and its severity. Latter depends on the amount of substance ingested. Age of the patient.
  • 5. Examination: Vital parameters; Respiration, BP, Pulse, temperature Level of consciousness Examination particularly observing pupillary size, oral cavity, breath odor, skin color, sweating. Any mark of injury, pigmentation, secretions from oral and nasal orifices.  Abdominal examination for peristaltic activity and urinary retention. Some clues of the poison by urine color Orange/Red- Rifampicin Grey/Black- Phenols/cresols Blue/green-Methylene blue
  • 6. General Principles of Management First Aid:  Decontamination:  Remove from the source of poison  Remove the clothing's  Irrigate the skin and eyes with normal saline or lukewarm soap water  Treatment:  Patients should be transported nearest medical care facility.  Initial treatment consist of managing the airway, breathing and circulation.  Take care of airway by inserting an appropriate size endotrachial tube.  Identification of poison& assess the type & amount of the poison.
  • 7.  Maintain IV line.  In comatose patients a bolus of 2ml/kg of 25% Dextrose may be given.  In adolescent & malnourished children Inj. Thiamine 50 – 100 mg iv/im to avoid precipitating acute wernicke’s encephalopathy.  In comatose patient if respiration is shallow parental naloxone in dose of 0.2 to 0.45ug/ kg is given.  Removal of the unabsorbed poison.  Gastrointestinal tract  Emesis can be induced by Sy. ipecac which induced vomiting in 80% within 20 minutes is given 30 minutes of ingestion.  Contra indicated in children below 6 month, corrosive or caustic ingestion and those who are comatose.
  • 8. Gastric Lavage:  Gastric lavage can be used in place of emesis  Done in left lateral position with head end low with 15 ml/kg NS ( max 400/clycle).  CI in hydrocarbons & corrosive & paralytic ileus, heart disease  In comatose child only after cuffed endotracheal intubation.  Prevention of GI absorption. Activated charcoal-1 to 2 g/kg/dose(1 g in 8 ml of water through NG tube after Gastric lavage every 4 hourly. Avoid in acids, alkalies, iron poisonings. Cathartics :Na & Mg sulphate 25 mg/kg/dose
  • 9. Promotion of excretion:  Maintenance IV line Diuresis: Frusemide-2 to 4 mg/kg/day Mannitol- .5 to 1 g/kg over 30 min Forced alkaline diuresis in Salicylate & barbiturate Specific antidotes:  Depending upon the type of poison ingested  Some clues of the poison by urine colour Blue/green- Methylene blue Orange/Red- Rifampicin Grey/Black- Phenols/cresols Lab. Investigation : Estimation of blood level for glucose, urea, Serum creatinine, serum electrolytes, ABG, ECG, X ray etc.
  • 10. Laboratory findings indicating the poison:  Hyperkalaemia- Beta blockers, digoxin  Hypokalaemia- Theophylline, diuretics  Hypoglycemia- Oral hypoglycemic agents, ethanol, salicylates, quinine. Hyperglycemia-Acetone, theophylline, calcium channel blockers.  Hypocalcemia- Ethylene glycol, oxalate.  Hyperglycemia with ketoacidosis– Salicylate, theophylline, Increased anion gap- Methanol, ethanol, ethylene, glycol, salicylates, ionized, iron. Decresed anion gap- Lithium, bromide. Pulmonary edema- Carbon monoxide, cyanide, irritant gas.
  • 11. Kerosene & Other Hydrocarbon Poisoning  High volatile: Kerosene, Petroleum, Ether, Paint, thinner Low volatile: Furniture polish, Lubricating oils, Paraffin wax. Accidental ingestion of kerosene, petrol, diesel is common. Stored in unmarked container. Taste prevent large amount to be consumed. Systemic manifestations are due to absorption through the lungs following aspiration; Exceptions are non petroleum distillate hydrocarbons (benzene, carbon tetrachloride, chloroform etc) which are absorbed from GIT.
  • 12. Clinical Features : Topical effects :  Irritation of oral, esophageal & gastric mucosa. Pulmonary effects : Fever, tachycardia, tachypnoea, cough, cyanosis and rarely pulmonary edema. CNS effects: Euphoria, headache, restlessness, muscle twitching, in coordination , confusion, lethargy ,stupor, coma & convulsions. Other features:  Liver damage, renal tubular, bone marrow depression & myocardial toxicity.
  • 13. Management Protocol:  Asymptomatic for a period of six hours- observe at home Symptomatic-  Oxygen inhalation  If required IPPV  Emesis is contra indicated  Maintain iv fluids  Antibiotics are required in the presence of pre-existing respiratory illness. Chest X ray if normal, observe for 6 hrs & may be dis charged and if shows lesions observe for 24 hrs & if no symptoms may be discharged.
  • 14. Organophosphate Poisoning  Mostly used as insecticides & pesticides viz Malathion, Parathion, carbamates, Fenthion, TEPP  Cause an irreversible inhibition of cholinesterase resulting in excessive accumulation of ach at receptor sites leading to excessive cholinergic manifestations Clinical features.-  Muscarinic effects :  Lacrimation  Excessive salivation  Urination Diarrhea  Nausea  Vomiting  Bradycardia  Pin pointed pupil
  • 15.  Pain abdomen  Tightness of chest  Wheezing Nicotinic effects: Weakness  Muscle cramps  Fasciculation  HTN  Respiratory paralysis Central effects:  Anxiety  Headache Confusion  Restlessness  Seizures Slurred speech & coma
  • 16. Diagnosis: Based on history and clinical features. RBC, cholinesterase level is less then 50% in case where only exposure and less then 20% in symptomatic patients. Management : Cloth should be removed & skin washed with soap and water. Gastric decontamination done by lavage or emesis Children older then 12 years Atropine 1.0–2.0 mg iv every 10–30 minutes until cholinergic sign are reversed. Younger children 0.02-0.05 mg/kg every 10-30 min till signs of atropinisation including warm, Dry skin, dry mouth, tachycardia and pupillary dilatation. Pralidoxime is the specific antidote for organ phosphorus compound but muscarinic or central action are not significantly reversed. Drug used in dose of 25-50 mg/kg older then 12years over a period 15–30 minutes & repeated after 1-2 hours.
  • 17. Corrosive poisonings:  Include washing soda, acids, alkalies, bleaching powder, toilet & drain cleaners, strong detergent granules. Acids produce coagulative necrosis, which cause superficial damage while alkali cause a deep penetrating liquefaction necrosis.  Acid ingestion cause gastric perforation & peritonitis while alkali commonly cause damage in esophagus & in severe case pneumonia.
  • 18. Clinical features:  Vomiting  Dysphagia  Drooling  Abdominal pain  Involvement of glottis leads to stridor & shock.  Oral cavity shows edema, ulceration & pseudo membrane over the palate, uvula and pharynx.  Absence of oral burns& lack of symptoms do not rule out the involvement of esophagus.  Esophageal & gastric perforation leads to peritonitis.  If required upper intestinal tract endoscopy with fibrotic endoscope should be performed within 24-48 hours & after 2-3 weeks by an experienced person to determine the extent of the injury.
  • 19. Management Protocol  Vomiting should not be induced.  Small amount of water or milk to wash away any residual caustic from the oral mucosa.  Detailed history about the type & amount of the corrosive.  Ingestion with concentrated solutions of acid and alkalis need hospitalization.  Such children kept nil orally.  Gastric lavage contraindicated.  Neutralization by acid/alkali is also not recommended  Milk of magnesia & antacids may be used to neutralize strong acids.  Irrigation of skin & eyes if involved  H2 blockers - Ranitidine 2-4 mg/kg/day 12 hrly orally for 6-8 wks or 1-2 mg/kg/d IV 12 hrly.
  • 20. Use of corticosteroids is controversial. As long as the child is able to swallow, liquids are offered by mouth coz drinking is a self-dilatation & may decrease the likely hood of esophageal stricture formation. Antibiotics if infection suspected Drooling & dysphasia beyond 12-24 hrs have been reported to be a good predictor of scar formation & should prompt upper GI endoscopy. Placement of a rubber tube in the esophagus allows it to scar down in a functional position leaving a lumen. Prognosis: Mild cases have full recovery of corrosive injuries. Moderate and severe cases will result in stricture formation requiring regular dilatation and possible surgery.
  • 21. Avoid keeping poisonous plant in or around house. Take care while eating products such as berries, roots or mushrooms. Keep all potentially p oisonous substance out of children reach. Label the poisons in your home. Store medicines, cleaning detergents, mosquito repellants and paints carefully.