Transcript Poisoning in children - Wikispaces

Dr M A Maleque Molla,
FRCP, FRCPCH
Conultant Pediatric Intensivist
October 15, 2014
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“All things are poison and nothing is
without poison, only the dose permits
something not to be poisonous.”
‘Paracelsus’
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Introduction
 “Poisoning” refers to an injury that results from being
exposed to an exogenous substance that causes cellular
injury or death.
 Poisons can be inhaled, ingested, injected or absorbed.
 Severity of poisoning and its outcome depends on;
 type of poison
 dose
 formulation
 route of exposure
 age of the child
 presence of other poisons
 state of nutrition of the child
WHO
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Epidemiology
 Global rate of poisoning 282.4 / 100000 population
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WHO
The global death rate from poisonings 1.8/ 100,000
population
Non-fatal poisoning, more common among
children aged 1 to 4 years
highest rates of fatal poisoning occurs among
Children under the age of one year.
Most poisoning occurs at home and common rout
of poisoning is oral
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Most common agents involved
 Over-the-counter preparations: paracetamol,
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cough/cold remedies, vitamins and iron tablets,
antihistamines and anti-inflammatory drugs.
Prescription medications: Antidepressants,
narcotics, analgesics and illicit drugs.
Household products: Bleach, disinfectants,
detergents, cleaning agents, cosmetics, vinegar.
Paraffin/Kerosene.
Pesticides e.g. insecticides.
Poisonous plants.
Animal or insect bites e.g Scorpion, snake.
World report on child injury prevention, WHO 2004
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Evaluation of poisoned patient
A. Priority: Stabilization of the Airway, Breathing,&
Circulation
B. Diagnosis
 History
 Patient age and sex, wt
 The type of substance involved,
 Method of exposure (i.e., skin contact, inhalation, or
ingestion).
 Assessment of the severity of the exposure
 Physical examination
 Investigations
Note: concomitant trauma or illness must be recognized and
addressed prior to initiation of decontamination
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History
 What?
 How much?
 When?
 Reliability- Whether any poison has
been taken?
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History
What poison has been taken ?: can be identified from;
 Container
 Illustrated chart
How much poison has been taken ?
 Calculating the missing amount from the container.
 In doubt, always calculate maximum amount of poison that has
been consumed.
When the poison has been taken?:
 Approximate time elapsed since ingestion or exposure.
What are the adverse effects of the poison? Information can get
from;
 From books, internet, pharmacy
 Poison Information center:
Tel no. Riyadh # 011 4355555/1999,2003, Jeddah # 021 6720711,
Makkah # 021 5575065, Madinah# 041 8462564
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History
Whether any poison have been ingested?
 Any doubt, take that the child has ingested the poison.
 A history of medication used by the family members.
 Poisoning should be considered for children who
present with acute onset of;
 Altered mental status.
 Multiorgan system dysfunction of unexplained
cause.
 Respiratory or cardiac compromise.
 Unexplained metabolic acidosis.
 Seizures, or a puzzling clinical picture.
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Physical examination
 Thorough physical examination
 Evaluation of mental status and vital signs, should be
repeated frequently
 The diagnosis may be assisted by
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Temperature alterations
Blood pressure and heart rate alterations
Respiratory disturbances
Pupillary findings
Skin findings
Neuromuscular abnormalities
Mental status alterations
Characteristic odors e.g. acetone, bitter almond, Garlic
 In case of unknown poison ingestion, physical findings
should be sought to define a particular toxic syndrome
(toxidrome).
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Toxidromes
 Anticholinergics: Atropine, scopolamine, TCA’s,
phenothiazines, antihistamines, antipsychotic
mushrooms,
 “Hot as a hare, Blind as bat, dry as a bone, red as a
beet, mad as a hatter”
 CV: tachycardia, hypotension, hypertension,
arrhythmia
 GI/GU: decreased bowel sounds, urinary retention
 Neuro: agitation, hallucinations, coma,
extrapyramidal movements, mydriasis, hyperthermia
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Toxidromes
Cholinergics: Organophosphates and carbamates
Mascarinic effect
Nicotinic effect
 Diaphoresis/diarrhea
 Muscle fasciculation
 Urination
 Cramping
 Miosis
 Weakness (extreme is
 Brdycardia/bronchospasm
diaphragmatic failure)
 Autonomic
 Emesis
 Lacrimation excess
 hypertension,
 Salivation excess
 tachycardia,
 pupillary dilation,
 and pallor
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Toxidromes
Sympathomimetic: Salbutamol, Amphetamine, Cocain,
Ephedrine.
 Anxiety, Delusion, Diaphoresis, hyperreflexia,
mydriasis, paranoia, seizure
 Tachycardia, hypertension, mydriasis, agitation,
seizures, diaphoresis, psychosis, hyperthermia
OPIOID; morphine, hydrocodone, methadone
 Hypoventilation, Hypotension, Miosis, Sedation,
Hypothermia, Ileus.
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Investigation
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Blood glucose, urea & Electrolytes
Blood gas & Acid base status
Serum osmolality & osmolal gap, anion gap
Quantitative serum concentration of drugs- paracetamol
salicylate, Iron
Urine analysis; Rabdomyolysis
Electrocardiogram.
Toxicology screens : indicated in children in whom the
diagnosis of poisoning is uncertain.
Samples of blood, first voided urine , vomitus, and gastric
contents should be save for subsequent analysis.
Plain radiographs of the chest & abdomen.
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Management
 Management of the poisoned child depends upon
Specific poison(s) involved,
Presenting and severity of illness,
Elapsed time between exposure and presentation.
 Mainstay of therapy is supportive
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Management
A. General Management
 ABCD
 Decontamination: Techniques used to prevent
the absorption of the toxic substance
 Enhanced elimination: techniques which
accelerate removal of a toxins from the body
B. Specific Management
 Antidote: a substance which can counteract a form
of poisoning
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Decontamination
 Surface decontamination e.g. Organophosphate
poisoning;
 Removal of the cloths and wash with soap & water
 Irrigation of eyes if affected
 GI Decontamination:
 Gastric lavage: Not used routinely, use only selected
cases
 Activated charcoal
 Whole bowel irrigation
 Purgation using cathartics
 Decontamination is not always warranted and may be
contraindicated.
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Activated charcoal(AC)
 It is an insoluble, non absorbable, fine carbon powder
 Maximum benefit, if administered within 1 hour of
ingestion
 Dose: 1 g/kg (maximum 50 to 60 gm), can be repeated
at 0.5 g/kg Q4-6 hour
 Multiple-dose: in case of ingested life-threatening
amounts of;
 Carbamazepine, Dapsone, Phenoberbital, Quinine,
Theophyline
 Care must be taken to protect the airway, assess for the
presence of bowel sounds.
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Activated charcoal(AC)
Contraindication:
 Absolutely contraindication: Bowel obstruction or
perforation
 Depressed level of consciousness
 Ingested non absorbable acidic or alkaline corrosives e.g.
sodium or potassium hydroxide, or hydrochloric or
sulfuric acid.
 Ingestion of hydrocarbons e.g., gasoline, kerosene,
liquid furniture polish
 The poisons which are not bound by AC.
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Agents for which activated charcoal is not recommended
Heavy metals
Arsenic
Lead
Mercury
Iron
Zinc
Cadmium
Inorganic ions
Lithium
Sodium
Calcium
Potassium
Magnesium
Fluoride
Iodide
Boric acid
Corrosives
Acids
Alkali
Hydrocarbons
Alkanes
Alkenes
Alkyl halides
Aromatic hydrocarbons
Alcohols
Acetone
Ethanol
Ethylene glycol
Isopropanol
Methanol
Essential oils
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Whole bowel irrigation (WBI)
 Controlled human studies have shown that WBI
significantly decreased absorption of
 Ampicillin by 67%,
 Enteric-coated aspirin by 73%
 Lithium by 67%
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Tenenbein M et all; Whole bowel irrigation as a decontamination procedure after acute drug
overdose. Arch Intern Med. 1987
Smith SW et all; Whole-bowel irrigation as a treatment for acute lithium overdose. Ann Emerg
Med. 1991;20(5):536.
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Whole bowel irrigation (WBI)
 Indication: Ingestion of large amounts of poisons
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that are not well bound to AC, sustained-release
medications.
Contraindications: Intestinal obstruction,
perforation, ileus, or significant gastrointestinal
bleeding
Technique: Administration ‘polyethylene glycol
electrolyte solution’ (PEG-ES) via nasogastric tube
Dose: 20 to 40 mL/kg per hour until the rectal
effluent is clear, which takes 4-6 hours.
The maximum recommended doses
PEG-ES (GoLYTELY)
 9 months to 6 years – 500 mL/hour
 6 to 12 years – 1000 mL/hour
 Older than 12 years – 1500 to 2000 mL/hour
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Use of Cathartics
 Cathartics accelerate the evacuation by ↑ fluid load in the intestine
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and stimulating bowel motility.
They should never be used as the sole method of GI
decontamination.
Recommended agent:
 0.5 g/kg (1 to 2 mL/kg) of 7 percent Sorbitol (0.9 g/mL)
 4 mL/kg or 250 mL of Magnesium citrate in a 6 percent
suspension
Sorbitol is not recommended for use in children younger than one
year of age
If a cathartic is used, it should be limited to a single dose in order to
minimize adverse effects
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Enhance elimination of Poisons
 Urinary alkalinization and forced diuresis: eg,
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salicylates and Phenobarbital.
Hemodialysis: significant ingestion of alcohols,
theophylline, Lithium, Salicylates.
Hemoperfusion: Theophylline, Carbamazepine,
valproic acid, procainamide.
Exchange transfusion: arsine or sodium chlorate
poisoning
Peritoneal dialysis,
Hemofiltration
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Specific treatment
 Antidotes
 Very few poisons have antidotes.
 Information can be found in books or from Poison
Information Center
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Table. Antidotes for some common toxicant
POISON
ANTIDOTE
Paracetamol
N-Acetylcysteine
Anticholinergics
Physiostigmine
Lead/Heavy Metals
BAL in oil (dimercaprol)
Anticholinergics
Physiostigmine
Beta Blockers
Glucagon, Cateholamines
Carbon Monoxide
Oxygen
Cyanide
Amyl nitrate, Sodium Nitrate, Sodium Thiosulfate
Ethylene Glycol
Dialysis, Fomepizole, Ethanol
Iron
Desferoxamine
Isonazid
Pyridoxine
Lead/Heavy Metals
DMSA, BAL, EDTA
Methemoglobin Producing agents
Methylene blue
Narcotics
Narcan
Organophosphates
Atropine, Pralodixime
Phenothiazines
Benadryl
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Disposition
 Patient can send home after 4-6 hour of observation if
poison is less toxic.
 Always admit if
 Symptomatic.
 Ingestion of iron, tricyclic antidepressant, digoxin and
aspirin.
 Unconscious child should be admitted in pediatric
intensive care unit.
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Prevention
All the parents of child with poisoning should advice regarding
prevention:
 Keep the poison out of reach and sight of the child under lock
and key.
 Never store food and cleaning product together.
 Avoid taking medicine in presence of child.
 Never suggest that the medicine is “candy”
 Read the label on all products including warnings and caution.
 Never use medicine from a container, which is unlabeled.
 Know what your child can do physically.
 Keep the phone number of your doctor, Poison center, Hospital,
Police and fire department or emergency rescue squad.
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Conclusion
 Poisoning should be considered in the differential diagnosis of
children who present with
 acute onset of multiorgan system dysfunction,
 altered mental status,
 respiratory or cardiac compromise,
 unexplained metabolic acidosis,
 seizures,
 puzzling clinical picture.
 High index of suspicion, if the child is in the "at risk" age group
(1-4 yrs) and/or has a previous history of poisoning
 Management begins with stabilization of Airway, Breathing,
Circulation, and evaluation and treatment of Disability
 Supportive care is the most important aspect of treatment and,
when coupled with decontamination, is usually sufficient for
complete recovery
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SPECIFIC POISONING
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Paracetamol
 Most widely used pediatric analgesic on the market
 Most common ingestion in toddlers, preschoolers
and adolescents
 Normal cytochrome P-450 metabolism yields small
amounts of free oxidants that are hepatotoxic
 Glutathione depletion
 Toxic dose: 150 mg/kg
 Kinetics dictate that a serum level to be checked
4 hours after ingestion
 4 hour toxic blood level 150mg/dl
 Apply the level to the management nomogram
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Rumack-Matthew nomogram for single acute paracetamol ingestions
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Paracetamol Poisoning
 Stage I(1/2 - 24 hours)
 Malaise, nausea, vomiting, pallor, diaphoresis
 Stage II (24 - 72 hours)
 Asymptomatic, right upper quadrant pain,
increasing LFTs, PT, PTT & INR
 Stage III (72 - 96 hours)
 Liver failure, in severe cases renal failure & multi
organ failure
 Stage IV (4 - 14 days)
 Resolution of liver injury & Recovery
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Management
 Activated charcoal 1 gm/kg
 Plasma paracetamol level at 4 hours and plot on nomogram
 N-Acetylcysteine(NAC), Orally:
 If serum level above the line of possible hepatotoxicity
 Ingested > 150 mg/kg & no facilities to do serum level of
paracetamol,
 Patients with an unknown time of ingestion beyond 24 hours and a
serum concentration >10 mg/L (66 µmol/L)
 Dose of NAC: Loading Dose: 140mg/kg. Maintenance Dose:
70mg/kg, 4 hourly for 17 doses
 IV : indicated if patient is unable to take orally and present
within 8-16 hours of ingestion
 Dose: (Acetadote) 150 mg/kg over 1hr, followed by 50 mg/kg
over 4 hr, followed by 100 mg/kg over 16 hr
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NAC therapy
 Is most effective when initiated within 8 hr of
ingestion,
 it has been shown to have benefit even in patients who
present in fulminant hepatic failure, likely due to its
antioxidant properties.
 There is no demonstrated benefit to giving NAC before
the 4 hr post ingestion mark.
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Iron
Toxic Dose: Elemental Iron
 <20 mg/kg – sub toxic dose
 20-60 mg – mild to moderate toxicity
 >60 mg/kg – potentially life threatening
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Clinical features
5 stages
Stage I: 30 min – 2 hours
 Nausea, Vomiting – correlate with high toxicity,
Diarrhea; abdominal pain
 GI haemorrhage – bloody diarrhea, hematemesis
 Severe hypotension
Stage II: 2-6 hours post ingestion
 Patient appears better – apparent improvement
 In severe poising, this stage may be absent.
 In this stage, iron accumulates in mitochondria and
various organs
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Clinical features(cont..)
5 stages
Stage III: About 12 hours post ingestion (stage of shock)
 Hypoglycemia, Metabolic acidosis, Circulatory FailureShock
Stage IV: 2-4 days post ingestion
 Signs of hepatic necrosis – raised AST, ALT and direct
bilirubin, prolonged PT
 Renal Failure, Metabolic Acidosis, Bleeding diathesis,
Adult Respiratory Distress Syndrome
 Coma  Death
Stage V: 2-4 weeks after ingestion
 Signs of intestinal obstruction due to scarring and pyloric
stenosis
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Investigation
 Serum Iron 2-6 hours post ingestion, TIBC
 Serum Iron >350µgm/dl - mild to moderate toxicity
 Serum Iron >500µgm/dl - severe toxicity needs
urgent intervention
 Blood glucose; Blood glucose >150 mg/dl moderate to
severe toxicity
 CBC, U&Es LFT,
 WBC > 1500 /cmm- associated with moderate to severe
toxicity
 Plain x-ray abdomen
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Management
Supportive care
 ABCD
 Correct dehydration
Removal of Iron
 Whole bowel irrigation – with colonic solution (colyte,
golytely) if large number of tablets are ingested.
 No activated charcoal to be given because it does not
bind iron.
 Repeat x-ray on abdomen after decontamination.
 If clumps of tablets can be seen in x-ray and fail to remove
with usual procedures, surgical removal is indicated in
rare cases.
 Desferoxamine orally – promote iron absorption, so
should not be given orally
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Management
Definitive treatment: Desferoxamine intravenous infusion.
Indications:
 Serum Iron at 4-8 hours >500µg/dl regardless of symptoms
or
 Serum Iron >350µg/dl + moderate to severe symptom
 Moderate to severe symptom regardless of serum iron
 Dose:
 By infusion 15mg/kg/hour maximum 6g/24 hours
 By intramuscular 90mg/kg/dose 8 hourly maximum
6g/24 hours
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Organophosphate poisoning
Agents: Malathion, Parathion, Diazenon, Chlorothion
Clinical features
1. Mascarinic effect
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Diaphoresis/diarrhea
Urination
Miosis
Brdycardia/bronchospasm
Emesis
Lacrimation excess
Salivation excess
2. Nicotinic effect
 Muscle fasciculation
 Cramping
 Weakness (extreme is
diaphragmatic failure)
 Autonomic : hypertension,
tachycardia, pupillary dilation,
and pallor
3. CNS manifestations:
Anxiety, restlessness, tremor,
confusion, coma, convulsion
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Management
 ABC
 Remove cloths and wash the skin with soap and water
 Atropine (vagal block)
 IV 0.02-0.05 mg/kg every 15 minute until complete
atropinization ( dilated pupil, dry mouth tachycardia, fever)
then 1-4 hourly for 24 hour
 Pralidoxime (Protopam, 2-PAM)
 Regenerates acetylcholinesterase
 20 - 50 mg/kg/dose (IM or IV)
 Repeat in 1-2 hour if muscle weakness does not relieve
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SALICYLATE POISONING
 Toxic Dose: >150 mg/kg
 Clinical Manifestation:
 Early: nausea vomiting tachypnea, deep
sighing respiration, tinnitus, high
temperature, lethargy, and dehydration.
 Late: Bleeding tendency, coma.
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Clinical features
Important signs and laboratory findings:
 Phase I: First 12 hours
 Tachypnea
 Alkalosis
 Phase II - 12-24 hours
 Tachypnea persist
 Hypokalemia
 Paradoxical aciduria
 Phase III - > 24 hours
 Dehydration 5-10%
 Pulmonary edema, pulmonary haemorrhage
 Hypokalemia; hyperglycemia/hypoglycemia
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Investigations
 Plasma Salicylate level – no sooner than 6 hours and
plot on the nomogram
 Urine pH hourly
 Blood gas
 Glucose, serum urea electrolytes and creatinine – 6
hourly
 PT
 LFT.
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Management
 Plasma salicylate levels 45-65 mg/dl (moderate poisoning), treat
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and admit the patient.
Plasma salicylate level >65 mg/dl (severe poisoning), treat and
admit in the ICU
Activated charcoal 1 gm/kg.
Multiple dose of AC
Rehydrate the child and correct electrolyte specially potassium;
Urine alkalinization
 The goal is to achieve a urine pH >7.5 while maintaining a serum pH
7.55.
 Hemodialysis
 A salicylate level and blood gas should be drawn every two hours
until both the plasma salicylate level is falling and the acid-base
status is stable or improving for at least two consecutive readings.
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