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Objective
Approach to patient with drug
- poisoning 1
How to manage patient with- 2
drug poisoning
3- Common poisoning special
treatment
-Paracetamol poisoning
-Aspirin poisoning
-Iron poisoning

Approach to a patient with

suspected or witnessed
:poisoning
o Primary survey
o History
o Physical examination
o Investigation

Primary Survey
Stabilization and rapid
assessment of
Airway
Breathing
circulation
mental status

History
o Witnessed Poisoning (suicide attempts,
abuse or misuse).
o Unwitnessed Poisoning .

History of Presenting Symptoms

o Age ( toddlers or adolescent ).
o Onset of symptoms ( usually acute onset
of symptoms without prodrome with
sudden alteration of mental status ).
o Progression of the symptoms.

Description of the exposure:

o Place (where the child was found) in case
of unknown exposure to generate a list of
potential toxins.
o Product (name; brand, generic or
chemical, concentration)
o Duration + Amount of drug:
1- For ingested substances: Count the
remaining pills or measure the remaining
volume of liquid ingested.
2-For inhalational, ocular or dermal
exposure: ask about the concentration of
the agent and the length of contact time
with the material.

o Note: parents should be instructed to

bring the products, pills, and/or
containers with them to identify and
quantify the exposure.
o If the pills are unknown, make a list
of ALL medications in the child's
environment including medications of
grandparents and visitors

Past Medical History:

o Underlying illnesses (toxic dose of the
drug or drug-drug interaction).
o Psychiatric illness (patients more prone
to substance abuse, misuse, or
intentional ingestions).

Social History:
o New baby, parents illness or financial
stress can lead to serious neglect or
intentional abuse.

Physical Examination
Targeted physical exam is done to:
Identify the toxin.
Assess the severity of the exposure.

In poisoned patient, the KEY features of the

physical exam are:

Vital signs.
Mental status.
Pupils (size, reactivity, nystagmus).
Skin (diaphoretic, dry or normal)
Bowel sounds.
Odor of the patient (aceton, alcohol or garlic).

Laboratory
Investigation
o CBC.
o Serum electrolyte.
o Select intoxications (salicylates,
iron, theophylline, acetaminophen
and carbon monoxide).
o Urine analysis.
o Toxicology screen.
o LFT
o RFT

Additional tests:
ECG
Prolong PR interval (digoxin).
Prolong QRS interval (cocaine,
propranolol).
Chest X-ray
pulmonary edema[salicylate toxicity].
pneumonitis [hydrocarbon ingestion].
Abdominal X-ray.
Further investigation is based on the
DD and pattern of presentation

Mangm
ent

MDAC

ipec
ac

Gastri
c
lavag
e

cathar
tics

Suppo
rtive
care

Antid
ote

Elimin
ation

Decontami
nation

Urinar
y
alkaliz
ation
charc
oal

dialysi
s

WBI

Routs of poisoning in children:

oIngestion (the commonest).
oInhalation.
oDermal exposure.
oOcular exposure.
The goal of decontamination is to prevent
absorption of toxic substance

Decontamination

Before applying decontamination method, you

have to consider the
following:
oProperties of the toxin.
oRoute of exposure.
oTime since exposure (the efficacy of
decontamination method
decreases with
oincreasing time since exposure).
Risks vs. Benefits of the decontamination

Gastrointestinal (GI)
:decontamination
It is most likely to be effective in the first hour
after an acute ingestion.
Consider GI decontamination after 1 hour of
ingestion of toxic substance with one of the
following properties:

Ipecac syrup
Its an emetic drug . It's
contraindicated after the
ingestion of caustics (acids
and bases)

Gastric lavage
Place a tube into the stomach to
aspirate contents, and then flush
with normal saline.

Single-dose activated
charcoal

Charcoal is activated via heating to

extreme temperatures, providing a
very large adsorptive surface area.
Many toxins are adsorbed onto its
surface, thus preventing absorption
from
the
GI
tract.
Charcoal is most likely to be effective
when given within 1 hr of ingestion.
Approximately 20% of children vomit
after receiving a dose of charcoal, so
it's important to:
1. protect the airway to avoid
aspiration pneumonia.
2. ensure normal abdominal exam.

Substances POORLY adsorbed by

activated charcoal:
o Alcohols.
o Caustics (acid & alkaline).
o Cyanide.
o Heavy metals (lead & iron).
o Lithium.
Adverse effects:
Constipation (common).
Bowel perforation (rare).

Cathartics
Cathartics (sorbitol, magnesium
sulfate, magnesium citrate) have
been used in conjunction with
activated charcoal to prevent
constipation and accelerate
evacuation of the charcoal-toxin
complex. Cathartics should never
be used in multiple doses
because of the risk of
dehydration and electrolyte

Whole bowl irrigation (WBI)

1. WBI involves instilling large volumes
(35 mL/kg/hr in children or 1-2 L/hr in
adolescents) of a polyethylene glycol
electrolyte solution (e.g., GoLYTELY) to
cleanse the entire GI tract.
2. WBI can be combined with activated
charcoal or with substances are not
well adsorbed .

Multiple-dose activated
:charcoal (MDAC)
MDAC enhance elimination via two mechanisms:
Interruption of enterohepatic recirculation.
GI dialysis which uses the intestinal mucosa as
the dialysis membrane and pulls toxins from
the bloodstream back into the intraluminal
space, where they are adsorbed to the
charcoal.
Contraindications to use of MDAC include an
unprotected airway and a concerning
abdominal exam; thus the airway and
abdominal exam should be assessed before
each dose.

Urinary alkalization
1. elimination of some drugs that are
weak acids which is accomplished
with a continuous infusion of sodium
bicarbonatecontaining intravenous
fluids, with a goal urine pH of 7.5-8.
2. It is most useful in managing
salicylate, methotrexate and
phenobarbital toxicity.
3. Serum PH should be closely
monitored.

Dialysis
Toxins that are amenable to
dialysis have the following
properties:

Low volume of distribution (<1 L/kg).

Low molecular weight.
Low degree of protein binding.
High degree of water solubility.
Examples: methanol and ethylene glycol.

Supportive care
The goal is to support the vital
functions of the patient until the
patient can eliminate the toxin
from the system.

Supportive care includes:

o
o
o
o

Careful attention to airway support.

Ventilator management.
Blood pressure support.
Appropriate and timely management
of seizures, dysrhythmias,
conduction delays, and electrolyte
and metabolic derangements.

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Epidemiology
In the US there were 70,984
acetaminophen-related cases reported
to the American Association of Poison
Control Centers in 2006
There were 1045 cases of major
acetaminophen toxicity and 110 cases of
acetaminophen-related deaths
In most developing countries, the
incidence of acetaminophen poisoning
rarely approximates that of the US or UK

Pathophisology
Acetaminophen

Sulfate

Glucouronid

Saturated

Mainly by
cytochrom
p450

xidized by cytochrom p450

-acetyl p- benzoquinon eimin

Detoxified by glutathione
Cystein

mercopturic

Not detoxified by glutathione

. React with cellular membrane

Hepatocyte damage and death

Presentation

Stage4
Stage3
Stage2
Stage1

: Stage 1

Symptoms: anorexia . Nausea .

. Vomiting . Diaphoresis
Neurological . CVS. Resp rare
affected
Sign : pallor . diaphoresis .
Hydration
Lab : ALT . AST elevated

Stage 2
o After 24 hours lasted to 48 hours
o Symptoms: symptoms of stage 1
resolve or decrease . Pain .
Tenderness at Rt upper Quadrant
o Sign : hepatomegaly . Decrease urine
output .tachycardia . Hypotension
o Acute pancreatitis abdominal pain.
Increase lipase . Amylase
o Lab : ALT . AST elevated , PT
prolonged . Nephrotoxcity

Stage 3
From 3-5 day
o Symptoms: anorexia . Nausea.
Vomiting . Jaundice
o Signs: abdominal pain . Jaundice .
GI bleeding
Encephalopathy . Cerebral edema .
Cardiomyopathy
o Lab: PT prolong . ALT.AST elevated
> 10,000
Elevated total biliruibin >4 mg\dl .
Hyperammonemia

Stage 4
From 5-14 day lasted 21 day
A. recover: period for
normalization may take several
week
B. death

Investigation
1- history and physical

examination
2-Rumack-Matthew nomogram
LFT -3
radiological studies -4

Rumack-Matthew
nomogram

used to interpret
acetaminophen
values to assess
hepatotoxicity risk
.in patients
It was initially
, developed for single
acute ingestions of
acetaminophen
is based on
observational data from
patients who overdosed
and
who did not receive
antidote

Radiology
o - CT scan indicate for patient
who developed altered mental
status or encephalopathy
o - ultrasonoghraphy : to
defined either hepatic or renal
abnormality

Risk factors for chronic

acetaminophen toxicity include
o sustained administration of high
doses
o fever
o poor oral intake
o young age

Management
1- ABC
2- stander of care for
acetaminophen N-actyl cystin
antidote to patient who
present within not more than 24
hours
3- GI decontaminated : with active
charchol and gastric lavage
4- surgical liver transplant

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EPIDEMIOLOGY
The number of pediatric exposures
to salicylates reported has
.declined in the last two decades
Deaths from exploratory salicylate
.overdose in children are rare

PHARMACOKINETICS AND
TOXICOKINETICS
salicylate ingestion
absorbed from jejunum
bind with plasma protein
In therapeutic dose,
overdose,
80% of salicylate
saturation of
is protein-bound.
protein- binding sites

In
over

In Fatal salicylate intoxication

can occur after the ingestion
of 3 g by children
3 g = 36 tablets of baby aspirin(81
mg)

MECHANISM OF ACTION

Activation of the
respiratory
center
increased RR, increase
the elimination of CO2,
respiratory alkalosis

increased renal elimination of H

to compensate

Stimulation of the
chemoreceptor trigger zo
Nausea
Vomiting
K depletion

Inhibition of
cyclooxygenase
(decreased synthesis
of prostaglandins,
and thromboxanes)

bruising or bleeding

Interference
with cellular
metabolism
metabolic
acidosis
Hyperpyrexia
hypoglycemia

CLINICAL MANIFESTATIONS OF
SALICYLATE OVERDOSE
(salicylism)
o Hypoxia
o increased RR, temperature, and
HR.
o Seizures
o Tinnitus
o Nausea and vomiting : loss of
potassium

o Pulmonary edema

o bruising or bleeding
o metabolic acidosis
o respiratory alkalosis: loss of HCO3- due to
compensation

o Glucose:
in early stage, there will be hyperglycemia from
glycogenolysis. And after a period of time, as glucose
.stores are depleted, hypoglycemia may started

INVESTIGATIONS
o plasma salicylate concentration:
if you suspect any one with salicylate
.intoxication, you must do this test

o ABG
o CBC and PT
o Electrolytes and glucose
o Plasma creatinine
o Urinalysis
o Chest radiograph
o Electrocardiogram

DIFFERENTIAL
DIAGNOSIS
oDiabetic ketoacidosis:
Polyphagia, polydipsia, polyuria

oSepsis:
Fever, signs of septic shock

o Iron intoxication:
By plasma iron concentration

MANAGEMNT
o Airway
o Breathing
o Circulation
o Supplemental glucose
o Potassium repletion
o Gastrointestional
decontamination:
o Urine alkalinization

Clinical and laboratory features

Common: tachypnea, tinnitus, nausea, vomiting, acid-base abnormalities
Severe cases: hyperthermia, altered mental status, pulmonary edema

Diagnostic evaluation
Plasma salicylate concentration, arterial blood gas (ABG), basic
electrolytes, BUN and creatinine, chest radiograph
Repeat salicylate concentration every two hours until it is declining
Repeat ABG every two hours until acid-base status stable or improving

Treatment
Avoid intubation if at all possible
Administer supplemental oxygen as needed
Volume resuscitate unless cerebral or pulmonary edema is present
Administer multiple doses of activated charcoal (first dose: 1 g/kg orally up to 50 g)
Administer supplemental glucose in patients with altered mental status, even if serum glucose
concentration is normal: IV dextrose 50 g as 100 mL of 50 percent dextrose
Alkalinize with sodium bicarbonate
Bolus therapy: sodium bicarbonate, 1 to 2 mEq/kg (maximum 100 mEq) IV push over 3 to 5 minutes
Maintenance therapy: 100 to 150 mEq sodium bicarbonate in 1 L of D5W, run at 250 mL/hour in adults OR run at 1.5 to
2 times maintenance in children
Correct hypokalemia, hypocalcemia and other electrolyte abnormalities. IV sodium bicarbonate is NOT compatible
with calcium salts.
Alkalemia (arterial pH up to 7.55) is NOT a contraindication to sodium bicarbonate therapy
DO NOT USE ACETAZOLAMIDE TO ALKALINIZE THE URINE

Alert nephrology team early in the patient's clinical course; indications for hemodialysis include:
Profoundly altered mental status
Pulmonary or cerebral edema
Renal insufficiency that interferes with salicylate excretion
Fluid overload that prevents the administration of sodium bicarbonate
A plasma salicylate concentration >100 mg/dL (7.2 mmol/L) in acute ingestion OR >60 mg/dL (4.3 mmol/L) in chronic
ingestion

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EPIDEMIOLOGY
o Almost 16,000 iron exposures annually are
reported in children less than six years of
age in the United States.
o The number of major effects and death in
children are improved when compared to
the period from 1990 to 2000.

Etiology
Ingestion of:
oPure iron preparations containing(ferrous
sulfate tablets),(more elemental iron per
tablet (60 to 65 mg) than other iron
preparations).

Why !!!
They are often:
o Brightly colored
o Sugar-coated
o Have the appearance of candy

Pathophysiology & clinical

manifestation
Pathophysiology & clinical
manifestation :
o To show signs of toxicity : 10-20
mg/kg of elemental iron.
o Serious toxicity : more than 60 mg/kg
o Iron Toxicity Manifestations =
Metabolic Acidosis

1. Initial phase (up to 6 hours post ingestion ):

Large dose of elemental iron ---->GI
mucosal irritation ---->vomiting and
diarrhea (may be bloody), Abdominal
pain..

2. Latent Period (after 6 Hours):

hypovolemia ----> Shock
---->drowsiness,coma and METABOLIC
ACIDOSIS ----> liver failure,
hypoglycemia and convulsions ..

?!!How to diagnose
History :
o
o
o
o

HPI
Does anybody at home Use Iron Tablets ?! (Who & from where &
when)
How many Tablets has been ingested &the formulation of iron in
the supplement ?! (How did you know)
Is it the first time ?!

Examination :
o
o
o

Abdominal tenderness
Signs of dehydration and Shock
Signs of systemic acidosis

Investigations :
o
o
o
o
o
o

CBC
Serum Iron level
Blood Gases
Chemistry (electrolytes & enzymes)
RBG
Abdominal X-ray

D/D
D/D :
o Gastroenteritis
o DKA
o Sepsis
o Myocarditis

Rx
Rx:
o Intravenous Desferrioxamine (both
bowel decontamination with whole
bowel irrigation and chelation)
o Gastric lavage in severe cases (only if
< 1 hour after ingestion)

Tricycle antidepressants
poisoning

epidemiology
among 12,234 tricyclic antidepressant
exposures reported by poison centers
in United States in 2004
in children < 6 years old 9%

Possible risk
factors
* Munchausen syndrome by proxy
form of abuse in which caregiver
causes injury to a victim
that leads to( usually a child )
unnecessary and harmful or potentially
.harmful medical care
child abuse*
homicidal intent*

Symptoms and sings

CAs have several important cellular effects, including

1-Inhibition of presynaptic neurotransmitter
reuptake (norepinephrine and serotonin)
reuptake
1 of
inhibitor
. alpha-1-2
Antagonism
peripheral
adrenergic receptors
alpha-1 adrenergic receptors action is to
reduceof
nor
adrenaline
and adrenaline
Blockade
cardiac
fast sodium
-3
channels
Antagonism of central and peripheral-4

muscarinic acetylcholine receptors

atropine like effect
ntagonism of histamine (H1) receptors
6-Antagonism of CNS gammaaminobutyric acid (GABA) A
receptors

1-Inhibition of presynaptic
neurotransmitter reuptake
(norepinephrine and serotonin)
reuptake
inhibitor: .
reuptake 11inhibitor
NET (norepinephrine
transporter) is also commonly
called uptake 1 or reuptake 1.
NET can be inhibited by
cocaine and tricyclic
antidepressant drugs,
resulting in an increase of
transmitter activity in the
synaptic cleft.

Antagonism of peripheral alpha-1-2

adrenergic receptors
alpha-1 adrenergic receptors action
is to reduce nor adrenaline and
So as a net result of those 2*
adrenaline
actions the body is loaded with
epinephrine and nor
epinephrine with high
concentration and freely
Agitation, confusion, Respiratory
..acting
depression , Hypotension
*Sinus tachycardia

3-Blockade of cardiac fast sodium channels:

The NA ions is substantial to myocardium action
potential; Therefore
The cardiac conduction system needs abet longer time
to complete action potential .
This delayed is obvious in QRS complex
QRS complex delayed = QT interval prolonged =
ventricular tachycardia

QRS > 0.1 second(>2.5 small

boxes) in lead II

Antagonism of central and-4

peripheral muscarinic
acetylcholine receptors atropine
like
effect
traditionally
characterized as
"blind as a bat, mad as a hatter,
red as a beet, hot as a hare,
"dry as a bone
blurred vision ,warm, fever, dry
skin ,dry mouth and
urinary retention

5-Antagonism of histamine
(H1) receptors
6-Antagonism of CNS gammaaminobutyric acid (GABA) A receptors:
*So if the main inhibitory mechanism get
lost may lead to abnormal electrical
activity appears with motor, sensory or
psychomotor experiences That whats
called seizure.

History and
Physical exam
Chief concern (CC):
Cardio vascular system
tachycardia
central nervous system effects
Drowsiness ,confusion,
delirium,coma,respiratory
depression,seizures
other anticholinergic effects
blurred vision warm, dry skin
,fever ,dry mouth ,urinary retention

History of present illness

: (HPI)
onset of effect usually within 2
hours after tricyclic
antidepressant ingestion but
may be up to 5 hours
thorough history for patient with
acute altered mental status
may require
interview with family and
friendsPast medical history
(PMH):
interview with emergency
medical services personnelask about depression,
attempted suicide
inspection of medication
packaging if availableSocial history (SH):
ask about history of
ask about
substance abuse
identity of medication
*time ingestion occurred
known or estimated amount
ingested

General physical:
assess airway, breathing, and circulation
common features on presentation after tricyclic
antidepressant overdose
hypotension
tachycardia
urinary incontinence
coma
HEENT:
dilated pupils
external ophthalmoplegia (divergent squint) in
comatose patients
Neuro:
myoclonus, tremors
confusion, delirium, agitation
seizure
assess level of consciousness with formal coma scale
such as Glasgow Coma Scale

Investigations

Electrocardiography (ECG)
: Blood tests
blood gas analysis
assess blood pH for acidosis on initial
evaluation and monitor during alkalinization
treatment
venous sample acceptable alternative to
sample
unless suspect hypoxia or
:arterial
toxicology
screen
hypoventilation
quantitative
general toxicology screen
usually not useful for management of
acute toxicity
qualitative toxicology urine screens may
be useful either
if abuse suspected in pediatric cases
for legal, forensic, or social service

Treatme
nt
Activated charcoal if within 1 hour
Cardiac monitoring
Treat arrhythmias conservatively
with sodium bicarbonate
Correct metabolic acidosis
Treat convulsions with diazepam

Prevention
Prevention strategies for
poisonings
1- primary (pre-event)
2-secondary (event)
3-tertiary (post-event)

Primary prevention
Primary prevention encompasses
all of the activities that prevent
a poisoning event from
occurring. Activities such as
o legislation
o product engineering
o educational efforts
o Anticipatory guidance

1-Legislation
legislation and regulatory means
were implemented to protect
children, adolescents, and adults
from toxic exposures
2- Product engineering :
oStorage and locking devices
oThe addition of bittering agents to make
dangerous substances unpalatable
oThe use of poison warning labels or stickers
that may alert adults and older children to the
toxic hazard

3- Education :
Primary prevention also includes
educational efforts targeted toward
avoidance of poisoning exposure

4- Anticipatory guidance :
Periodic anticipatory guidance for
poisoning prevention is recommended by
the American Academy of Pediatrics (AAP)

Secondary prevention
Secondary prevention involves
interventions that prevent injury
or illness once a poisoning
exposure has occurred
Poison centers
Education
Decontamination

Poison centers
o Poison information: telephone
management, advice, and consultation
about toxic exposures
o Hazard surveillance to achieve hazard
elimination
o Professional and public education in poison
prevention, diagnosis, and treatment

Education
Decontamination
Decontamination is another method of
modulating poisoning injury after poisoning
exposure has occurred

Tertiary prevention
o involves interventions that minimize injury
or toxic effects once symptoms have
appeared
o administration of antidotes, vary depending
upon the particular exposure (eg, Nacetylcysteine for acetaminophen exposure)

Reference
nelson textbook
Pediaitric uptodate
Illustrated pediatric 3rd edition
Medscap

Done by
Noor Marwas
Najlaa baddour
Rand Melibari
Israa Mahmoud Sader
Fatimah Hamza

Monitor
Rafat Mosalli MD,FRCPC,FAAP,UTP (McMaster Univ.)
Assistant professor of pediatrics