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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
Primary Survey
Stabilization and rapid
assessment of
Airway
Breathing
circulation
mental status
History
o Witnessed Poisoning (suicide attempts,
abuse or misuse).
o Unwitnessed Poisoning .
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.
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
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
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
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:
Supportive care
The goal is to support the vital
functions of the patient until the
patient can eliminate the toxin
from the system.
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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
mercopturic
Presentation
Stage4
Stage3
Stage2
Stage1
: Stage 1
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
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
MECHANISM OF ACTION
Activation of the
respiratory
center
increased RR, increase
the elimination of CO2,
respiratory alkalosis
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
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
?!!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*
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.
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
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