Dr M A Maleque Molla,

FRCP, FRCPCH

Conultant Pediatric Intensivist

February 23, 20201

Introduction

“Poisoning” refers to an injury that results from being

exposed to an exogenous substance that causes cellular

injury or death.

I z 3 4

Poisons can be inhaled, ingested, injected or absorbed.

Severity of poisoning and its outcome depends on;

types & formulation of poison

poison type

dose

dose
route of exposure route

age of the child presenceofother

presence of other poisons child age

state of nutrition of the child nutrition

WHO 2


Poisoning & Children

Infants are at increased risk of poisoning:

The infant’s desire to put any objects in the mouth.

Toxic chemicals stay in bodies for prolonged periods

of time.

Slower digestion and increased stomach emptying,

which promotes absorption.

me

Kidneys and livers have lower functioning capacity

than adults.

easily

Infant’s readily absorbs chemicals from the skin due

to lack of keratin,.

Infants have higher respiratory rates making more

vulnerable to poisoning by inhalation.

Epiodemiology

Global rate of poisoning 282.4 / 100,000 population

WHO

The global death rate from poisonings 1.8/ 100,000

population

*Estimated annual incidence in Qassim region, KSA

10.7/ 100 000 population (in 2003)

Non-fatal poisoning, more common among children

aged 1 to 4 years

Highest rates of afatal poisoning occurs among Children

under the age of one year.

Boys have higher rates of poisoning than girls.

Most poisoning occurs at home

Common rout of poisoning is oral

*M. Moazzam et all; Pattern of acute poisoning in Al-Qassim region: a

surveillance report from Saudi Arabia, 1999–2003

Common agents involved in poisoning

firstmostcommon

Household products: Bleach, disinfectants, detergents,

64 cleaning agents, cosmetics, vinegar.

cough/cold remedies, vitamins and iron tablets,

antihistamines and anti-inflammatory drugs.

Prescription medications: Antidepressants, narcotics,

analgesics and illicit drugs.

Paraffin/Kerosene.

Pesticides: insecticides (Organophosphorus compound).

Poisonous plants. 76years

Animal or insect bites: Scorpion sting, snake bite, Dog.

World report on child injury prevention, WHO 2004

mum

Evaluation of poisoned patient

A. Priority: Stabilization of the Airway, Breathing,&

Circulation
ABC

B. Diagnosis

History

Physical examination

Investigations

Note: concomitant trauma or illness must be

mmmm
recognized and addressed prior to initiation of

mm

decontamination

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

Following things should be enquire to evaluate a

suspected case of poisoning:

What poison has been taken?

How much has been taken?

When the poison has been taken?

What are the adverse effect of the poison?

Reliability- Whether any poison has been taken?

History (cont..)

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.

History (cont..)

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, hospital pharmacy

Poison Information centers:

Tel no. Riyadh # 011 4355555/1999,2003, Jeddah #

021 6720711, Makkah # 021 5575065, Madinah#

041 8462564

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History(cont..)

Whether any poison have been ingested?

If any doubt, take that the child has ingested the

poison.

esp psychiatric
A history of medication used by the family members.

2 drug

Poisoning should be considered for any child, who

present with acute onset of;

Altered mental status.

Multi organ 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 from head to toe

Evaluation of mental status and vital signs, should be repeated

frequently.

The diagnosis may be assisted by;

Alteration of vital signs- Temperature, BP, heart rate &

Respiration

Pupillary findings e.g. pin point pupil in insecticide

poisoning.

Skin findings

Neuromuscular abnormalities hypotonia seizure

Mental status alterations conscious

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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Substances causing specific odor

Substance Odor

Ethanol, isopropyl alcohol,

Acetone

chloroform, salicylates

Cyanide Bitter almonds

Organophosphates,

Garlic

phosphorus
o

Phosgene gas Freshly mown hay

Hydrogen sulfide joRotten eggs

13


Toxidromes

Toxidromes are combinations of specific signs and

symptoms that associated with a class of poisons.

The most common toxidromes are

Anticholinergics,

Cholinergics,

Sympathomimetics,

Opioids,

Serotonin syndrome

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Anticholinergic toxidromes
drying

Substances: Atropine, scopolamine, TCA’s, phenothiazines,

antihistamines, antipsychotic medications, mushrooms

Signs & Symptomes:

admit 2uh

CV: tachycardia, hypotension, hypertension, arrhythmia

GI/GU: Decreased bowel sounds, urinary retention.

CNS: agitation, hallucinations, coma, extrapyramidal

movements,

EYE: dilated pupils (mydriasis).

Skin: Fever, flushed, dry skin.

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Cholinergic Toxidromes

Substances: Organophosphates and carbamates

Signs & Symptoms:

Muscarinic effects Nicotinic effect

‘DUMBELS’ Muscle fasciculation

Cramping

Diaphoresis/diarrhea

Urination Weakness (extreme is

diaphragmatic failure)

Miosis

Autonomic

Brdycardia/bronchospasm hypertension,

Emesis tachycardia,

pupillary dilation,

Lacrimation excess

Salivation excess and pallor

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Sympathomimetic toxidrome
diapherosis

Substances: Salbutamol, Amphetamine, Cocain,

Ephedrine.

Signs & Symptoms:

Anxiety, Delusion, Diaphoresis, hyperreflexia,

mydriasis, seizure

Tachycardia, hypertension, mydriasis, agitation,

seizures, diaphoresis, psychosis, hyperthermia

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Opioid toxidrome

Substances; Morphine, hydrocodone, methadone

Signs & Symptomes:

Seizure, Coma

Sedation, t

Hypoventilation, b

Bradycardia , Hypotension, b

Miosis,

Hypothermia,
t

Ileus.

distension

18


Sedative Toxidromes

Sedatives/hypnotics: Benzodiazepines,

barbiturates

Signs & Symptoms:

Resp: respiratory depression

mm

CV: tachycardia, hypotension

CNS: Altered consciousness, coma, seizures,

mum

hypothermia

19


Serotonin syndrome

Substances: MAOIs, tricyclic antidepressants,

amphetamines, and fentanyl

Signs & Symptoms:

altered mental status,

Hypertension and tachycardia,

myoclonus,

hyperreflexia,

hyperthermia,

increase in muscle rigidity.

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Investigations

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

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Investigations

Further investigations indicated;

ECG for the patient who ingested cardiotoxic

medications

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 in case of

heavy metals poisoning (iron, arsenic, mercury,

thallium, and lead)

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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.

Remember the mainstay of therapy is supportive

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Management

A. General Management

1. ABC-Stabilization of the Airway, Breathing,&

Circulation

2. Decontamination: Techniques used to prevent the

absorption of the toxic substance

3. 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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2. Decontamination

Surface decontamination e.g. Organophosphate poisoning;

Removal of the cloths and wash with soap & water

Irrigation of eyes with saline if eyes are affected

GI Decontamination:

Gastric lavage: Should not used routinely

Activated charcoal in selected poisons.

Whole bowel irrigation

Endoscopy/surgery- when a life-threatening toxin has been

ingested and cannot be effectively removed by whole bowel

irrigation e.g. heavy metals

2 Purgation using cathartics- should avoid in children

Decontamination is not always warranted and may be

contraindicated.

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Activated charcoal(AC)

It is an insoluble, non absorbable, highly adsorbent fine

carbon powder
Maximum benefit while toxin remains in the stomach &
usually within 1 hour of ingestion.
Dose: 0.5- 1 g/kg (maximum 50 to 60 gm), can be repeated
0.5 g/kg Q4-6 hour
Multiple-doses : when life-threatening amount of
Carbamazepine, Dapsone, Phenoberbital, Quinine,
Theophyline, Acetylsalicylic acid, Phenytoin
Care must be taken to protect the airway, assess for the
presence of bowel sounds.

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 Activated charcoal(cont..)
Contraindication:
Absolute contraindication: Bowel obstruction or perforation
Depressed level of consciousness
Late presentation (ie, no toxin is likely to remain in the
stomach)
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 e.g. Iron, lead,
arsenic. mm

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Agents for which activated charcoal is not recommended
Heavy metals Corrosives
Arsenic Acids
Lead Alkali
Mercury Hydrocarbons
Iron Alkanes
Zinc
Alkenes
Cadmium
Alkyl halides
Inorganic ions
Aromatic hydrocarbons
Lithium
Alcohols
Sodium
Calcium Acetone
Potassium Ethanol
Magnesium Ethylene glycol
Fluoride Isopropanol
Iodide Methanol
Boric acid Essential oils
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 Whole bowel irrigation (WBI)
bowel wash

It refers to the administration of

esp heavy metals PEG-ES (GoLYTELY)

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Whole bowel irrigation (WBI)
Indication: Ingestion of large amounts of poisons
that are not well bound to AC, sustained-release
medications.
Contraindications: Intestinal obstruction,
perforation, ileus, or significant GI bleeding ,
Persistent vomiting
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.

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 D
dei Purgation- Use of Cathartics
Cathartics accelerate the evacuation by ↑ fluid load in the
intestine and stimulating bowel motility.
They should never be used as the sole method of GI
mm
decontamination.
Recommended agent:
Sorbitol: 0.5 g/kg (1 to 2 mL/kg) of 7% Sorbitol (0.9 g/mL)
Magnesium citrate: 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 mm

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3. Enhance elimination of Poisons
Urinary alkalinization :
Urinary excretion of some drugs can be enhanced
by altering the urine pH e.g. salicylates, tricyclic
antidepressants, phenobarbital, chlorpropamide
i
It is done by administering an IV bolus of 1-2
mm
mEq/kg of 8.4% percent sodium bicarbonate,
followed by continuous infusion of sodium
bicarbonate.
Goal is to achieve a urine pH of 7.5 or higher while
maintaining a serum pH 7.55 to 7.60

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3. Enhance elimination of Poisons
Hemodialysis: significant ingestion of alcohols,
theophylline, Lithium, Salicylates.
Hemoperfusion: Theophylline, Carbamazepine,
valproic acid, procainamide.
Exchange transfusion: arsine or sodium chlorate
poisoning
Hemofiltration- aminoglycosides, vancomycin

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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
Anticholinergics Physiostigmine
Beta Blockers Glucagon, Cateholamines
Carbon Monoxide Oxygen
Cyanide Amyl nitrate, Sodium Nitrate, Sodium Thiosulfate
Ethylene Glycol Dialysis, Fomepizole, Ethanol
Iron Desferrioxamine
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
Disposition of the patient depends upon the observed and
predicted severity of toxicity.
Patients with mild toxicity and who have only a low predicted
severity can be observed 4-6 hour until they are asymptomatic.
Always need hospital admission if:
Patient is Symptomatic.
ADIT
Ingestion of iron, tricyclic antidepressant, digoxin and
aspirin.
Ingestion of sustained release preparations, or multiple agents
Patient with decrease level of consciousness should be
admitted in pediatric intensive care unit.
Patients with intentional overdose require psychiatric assessment
prior to discharge.
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 Prevention of poisoning
All the parents should advice regarding prevention of
poisoning:
Keep all chemicals, medicines 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” or chocolate.
Read the label on all products including warnings and caution.
Never use medicine from a container, which is unlabeled.
Visitor’s bags may contain medicines & should be kept well out
of reach of children
Take extra care when measuring and giving medicines.
Keep the phone number of your doctor, Poison center, Hospital,
Police dept. and fire department or emergency rescue squad.

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SPECIFIC POISONING

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 Paracetamol
Most common ingestion in toddlers, preschoolers and
adolescents therapeutic dose to 15mg1kg
Toxic dose: > 150 mg/kg
Serum level to be checked 4 hours after ingestion.
Plot the result on the nomogram (Rumack-Matthew
nomogram) mum

4 hour toxic blood level >150µg/ml.

39
Rumack-Matthew nomogram for single acute paracetamol ingestions
40
 Paracetamol Poisoning
Signs & Symptoms:
Stage I(1/2 - 24 hours) I
Malaise, nausea, vomiting, pallor, diaphoresis
Stage II (24 - 72 hours) I 3 days
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
41
 Management
Patient need active management;
Acute ingestion of > 150mg/kg.
me
Ingestion of unknown quantity.
ummm
Repeated supratherapeutic ingestion of >
100mg/kg/day, thfever
given every 2h

42
 Management
Sample of blood for plasma paracetamol level at 4 hours
and plot on nomogram below this discharge
Activated charcoal 1 gm/kg
Start antidote -N-Acetylcysteine(NAC),
If serum level above the "treatment" line of the nomogram
for paracetamol poisoning.
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)
Patients with delayed presentation and laboratory evidence
of hepatotoxicity and a history of excessive paracetamol
ingestion.

43
 NAC therapy
Is most effective when initiated within 8 hr of ingestion,
N-Acetylcysteine(NAC), orally:
Dose : Loading Dose: 140mg/kg.
Maintenance Dose: 70mg/kg, 4 hourly for 17 doses
IV NAC : Indicated if:
patient is unable to take orally and present within 8-16 hours
mum
of ingestion
Hepatic failure
mm
Patients refusal of oral administration
Dose IV NAC:
Loading dose 150 mg/kg over 1hour, followed by 50 mg/kg
over 4 hr, followed by 100 mg/kg over 16 hr

44
 Iron
Common available preparations:
Ferrous gluconate- 12% elemental iron
Ferrous sulfate - 20% elemental iron
Ferrous fumarate - 33% elemental iron
Toxic Dose of elemental Iron
<20 mg/kg – sub toxic dose
20-60 mg/kg – mild to moderate toxicity
me
>60 mg/kg – potentially life threatening

45
 Clinical features
5 Phases
Phase 1 (Gastrointestinal): 30 min – 6 hours;
Nausea, Vomiting, Diarrhea; abdominal pain
GI haemorrhage – bloody diarrhea, hematemesis
mm
Severe hypotension & shock, if significant blood
volume is lost

46
 Clinical features
Phase 2 (Latent): 6-24 hours post ingestion
Clinically Patient appears better – apparent
improvement
In this stage, iron accumulates in mitochondria and
various organs
The vital signs worsen (eg, progressive
tachycardia, developing hypotension.
Progressive metabolic acidosis & end-organ
dysfunction (ie, elevation of transaminase levels).
In severe poising, this stage may be absent.

47
 Clinical features(cont..)
Phase 3 (Shock): 6-72 hours post ingestion;
It may occur within a few hours after a massive ingestion
of iron.
Consists of marked systemic toxicity due to
mitochondrial damage and hepatocellular injury.
Hypovolemic shock and acidosis due to GI fluid & blood
losses
Decrease cardiac output due to a decrease in myocardial
contractility.
Hypoglycemia, anion gap metabolic acidosis, Circulatory
Failure-Shock & coagulopathy
48
 Clinical features(cont..)
Phase 4 (Hepatotoxicity): 12-96 hours 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

49
 Clinical features(cont..)
Phase 5(Bowel obstruction): 2-8 weeks after ingestion
Signs of intestinal obstruction due to scarring of the
GI tract and leads to pyloric stenosis

50
 Investigations
Serum iron & Total iron-binding capacity (TIBC).
Clinical severity according to serum Iron level 2-6 hours post
ingestion: run
Mild - Less than 350 µg/dL
Moderate - 350-500 µg/dL
Severe - >500 µg/dL
Life thretening->1000 mcg/dL
Blood glucose, CBC, U&Es, LFT,
Plain x-ray abdomen if tablet ingested.
ABG/VBG
Coagulation profile

51
 Management
ABCD
Correct dehydration
Removal of Iron
Gastric lavage & activated charcoal are not benefited.
Whole bowel irrigation –if large number of tablets are
ingested.
Repeat x-ray abdomen after decontamination. If clumps of
tablets is seen in x-ray, surgical removal is indicated in rare
cases.

52
 Management
Definitive treatment: Desferrioxamine intravenous
infusion.
Indications:
Serum Iron at 4-8 hours >500µg/dl regardless of
symptoms or Mr
Serum Iron >350µg/dl + moderate to severe
symptom
Moderate to severe symptom regardless of serum
iron
Anion gap metabolic acidosis
Significant number of pills on abdominal x-Ray
53
 Management
Dose of Desferrioxamine :
By IV infusion 15 mg/kg/hour maximum 6 g/24
hours
By intramuscular 90mg/kg/dose 8 hourly
maximum 6g/24 hours
Duration: duration of desferrioxamine therapy
until resolution of clinical symptoms, usually 24
hour
g
Caution: Desferrioxamine should not be given orally

54
 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.

55
 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 - 4 to 6 in an infant, or 24 hours in an
adolescent or adult
Dehydration 5-10%
Worsening acidosis
Hypokalemia; hyperglycemia/hypoglycemia
Pulmonary edema, pulmonary hemorrhage
Cerebral edema
56
 Investigations
Plasma Salicylate level – no sooner than 6 hours
Urine pH hourly
Blood gas
Glucose, serum urea electrolytes and creatinine –
6 hourly
PT
LFT.

57
 Plasma Salicylate level
The usual therapeutic range is 10 to 30 mg/dL.
Most patients show signs of intoxication when the
plasma concentration exceeds 30 to 50 mg/dL .
Plasma salicylate concentrations >100 mg/dL in acute
& >60 mg/dL in chronic intoxication potentially life
threatening are indications for hemodialysis.

58
 Management
Plasma salicylate levels 45-65 mg/dl (moderate
poisoning), admit the patient.
Plasma salicylate level >65 mg/dl (severe poisoning),
treat and admit in the ICU
Decontamination:
Activated charcoal 1 gm/kg. Multiple dose of AC may be
needed in severe poisoning
Volume resuscitation:
Rehydrate the child and correct electrolyte specially
potassium;
Enhance elimination
Urine alkalinization by IV bicarbonate. The goal is to
achieve a urine pH >7.5 while maintaining a serum pH
7.55.
Hemodialysis
59
 Organophosphate poisoning
Agents: Malathion, Parathion, Diazenon, Chlorothion
Clinical features
1. Mascarinic effect 2. Nicotinic effect
Diaphoresis/diarrhea Muscle fasciculation
Urination Cramping
Miosis Weakness (extreme is
Brdycardia/bronchospasm diaphragmatic failure)
Emesis Autonomic : hypertension,
Lacrimation excess tachycardia, pupillary dilation,
Salivation excess and pallor
3. CNS manifestations:
Anxiety, restlessness, tremor,
confusion, coma, convulsion
60
 Management
ABC
Personal protective measure should be taken.
Decontamination:
Remove all cloths and wash the skin with soap and water
Activated charcoal if ingested <1 hour.
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)
mm
Regenerates acetylcholinesterase
20 - 50 mg/kg/dose (IM or IV)
Repeat in 1-2 hour if muscle weakness does not relieve
61
 Take home messages
Childhood poisoning is common and can be life threatening.
Household products are common poisons involved, followed
by over the counter preparation medications.
Most common age <6 yrs. Boys are more prone.
High suspicion is needed for the diagnosis when history is not
clear.
Few poisons have antidotes so mainstay of management is
supportive.
Take the help of poison center early.
All the parents should advice regarding prevention of
poisoning before discharge from the hospital.

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Thanks for attention
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