Poisoning in Children by Dr Shamavu Gabriel .pptx

POISONING
In children
DR SHAMAVU GABRIEL
Department of Paediatrics
KIU-Teaching Hospital
Mentorship :
Professor Yamile Arias Ortiz
Mars 2022

outline
▷Definitions
▷Classsification (aetiology)
▷Clinical diagnosis
▷Toxidromes
▷Laboratory evaluation
▷Management
▷Common poisonong

Definitions
POISON :
• Any substance that is harmful to the body. It can be swallowed, inhaled, injected
or absorbed trough the skin.
• Any substance that can cause severe organ damage or death if ingested, breathed
in, injected to the body or absorbed through the skin.
POISONING :
• Harmful effect that occurs when too much of that substance has been taken (n
ot to be confused with enevnomation)
• Exposure to a chemical or other agent that adversely affects functioning of an org
anism.
• when cells are injured or destroyed by the inhalation, ingestion or absorption of a
toxic substance.(WHO)
ANTIDOTE : a remedy to counteract the effects of poison

Definitions
ANTIDOTE :
• Is a remedy to counteract the effects of poison
• Antidotal therapy is a vital component of management, as it may prove
useful in initiating therapy and in definitively identifying a particular toxin.
• Antidotes are agents that negate the effect of a poison or toxin.
• Antidotes mediate its effect either by preventing the absorption of the to
xin, by binding and neutralizing the poison, antagonizing its end-organ ef
fect, or by inhibition of conversion of the toxin to more toxic metabolites.

Classifications (aetiology)
 Classification According to the site and mode of action
 Classification of Poison according to motive or nature of use
 Classification of Poison according to modifications in vitals induced
 Classification of Poison according toxidromes

According to the site and mode of action
Local Action
Corrosive : Strong Acid; Strong alkali; Metallic salts…
Irritant
• Agricultural
• Inorganic (Non metallic: P, Iodine, Cl, bromine; Metallic: Arsenic, Anti
mony, Pb, Cu, Zinc; Mechanical: Glass, Diamond dust, Hair)
Organic
Animal: Snakes, insects Cantharides
Vegetable: Abrus, Castor, Croton, Calotropis

Systemic Action
Cerebral
• Somniferous: opium and its alkaloids, Barbiturates.
• Inebriant (Intoxicant): Alcohol, ether, Chloroform.
• Psychotropic: AD: TCAD, Amphetamines, Caffeine, MAOI
Neuroleptics: Phenothiazines, thioxanthenes
Hallucinogens: LSD, Phencyclidine, psilocybe
Deliriant: Dhatura, Belladona, Hyocyamus, cannabia Indica.
Hallucinogens
2) Spinal
-Strychnos Nux Vomica
- Gelsemium
3) Peripheral Nerves
-Local Anaesthetics: Cocaine, Procaine.
-Relaxants (curare).

- CNS DEPRESSANTS
1) Alcohols
2) General anaesthetics
3) Opioid analgesics
4) Sedative hypnotics
- Sedatives are those drugs that decrease activity, moderate ex
citement and exert a calming effect
- Hypnotics produce drowsiness and facilitate a state of sleep,
resembling natural sleep.
1) Barbiturates 2) Benzodiazepines
3) Non barbiturates 4) Alcohols
5) Propanediols 6) Glutethimide
7) quinazolines: methaqualone

Systemic Action
• Cardiac Poisons: KCN, NaCN, Digitals, Aconite, Nicotine, Quinine
, Oleander
• Asphyxiants: Carbon Dioxide, CO, hydrogen sulphide
• Miscellaneous: Food Poisons.

Classification of Poison according to motive or nature of use:
• Homicidal: Arsenic, Aconite, Digitalis, Abrus Precatorius, Strychnos nux vomica.
• Suicidal: Opium, Barbiturate, Organophosphorus,
• carbolic acid, copper sulphate.
• Accidental: Aspirin, Organophosphorus, copper sulphate, snakes bite, Ergot, CO, CO
2, H2S.
• Abortifacient: Ergot, Quinine, Calotropis, Plumbago.
• Stupefying agent: Dhatura, cannabis, chloral hybrate.
• Agents used to cause bodily injury: Corrosive acids and alkalies.
• Cattle Poison: Abrus precatorius, Calotropis, plumbago.
• Used for malingering: semicarpus anacardium
• Arrow Poison: Abrus precatorius, Calotropis, Aconite, Strychnos nux vomica.
• Aphrodisiacs : Cantharides, Cannabis, Cocaine, arsenic, opium

Classification of Poison according to modifications in vitals induced:
• Drug- and toxin-inducing changes in blood pressure and pulse,
• Drugs and toxins associated with respiratory dysfunction,
• Drug- and toxin-induced temperature abnormalities.

Classification of Poison according toxidromes
(see major toxidromes)

Clinical diagnosis
HYSTORY
Exposure history
• Obtain history from witnesses and/or close contacts.
• Route, timing, and number of exposures (acute, chronic, or repeated i
ngestion), prior treatments or decontamination efforts
Substance identification
• Attempt to identify exact name of substance ingested and constituents
, including product name, active ingredients, possible contaminants, ex
piration date, concentration, and dose.
• Consult local poison control for pill identification:

Clinical diagnosis
HYSTORY
Quantity of substance ingested
• Attempt to estimate a missing volume of liquid or the number of missing
pills from a container.
Environmental information
• Accessible items in the house or garage; open containers; spilled tablets;
household members taking medications, herbs, or other complementary
medicines.

Clinical diagnosis
Circumstances
• Intentional poisoning (suicid, parasuicid, criminal, Munchhausen
syndom)
• Food poisoning
• Accidental domestic poisoning
• Accidental occupational poisoning
• Therapeutic accidental poisoning
• Acute poisoning or overdose in a drug addicted
• Environmmental acute poisoning

Clinical diagnosis
PHYSICAL EXAMMINATION
GENERAL
Vital signs
Recognize lifethreatening compromise (initial evaluation ABC).
Recognize Toxidromes :
The classic toxidromes may be grouped into four categories:
 sympathomimetic/adrenergic,
 cholinergic,
 anticholinergic,
 and opiate-sedative-ethanol syndromes.

Clinical diagnosis
Cardiopulmonary
As noted in the primary survey, the priority is to recognize lifethreatening
compromise of ABC.
Toxins may cause an array of aberrations of the cardiovascular system, includin
g hypertension/hypotension due to direct action of the toxin on vascular smo
oth muscle, neurogenic effects on autonomic nervous centers, and direct cardi
ogenic or renal effects.

Clinical diagnosis
Neurologic
• The neurologic examination is especially important, as many toxins can be
expected to depress the level of consciousness by directly interfering with r
espiratory drive or hypoxia from loss of protective airway reflexes.
• Neurologic deterioration can be catastrophic; therefore, the patient should
be examined frequently.
• One must anticipate the potential for seizures. The pupillary exam is an ext
remely useful neurologic finding.
• Various toxins interfere with the autonomic innervation of the pupil and m
ay manifest as miosis or mydriasis.

Clinical diagnosis
Dermatologic Manifestations and Telltale Odors
Dermatologic examination may yield the identification of varied toxins.
Inhalant abuse may lead to skin rashes around the nose and the mouth.
Needle tracks or characteristic tattooing are suggestive of IV drug use.

Clinical diagnostic aids
Clinical Sign Intoxicant

Clinical Sign Intoxicant
salicylates, strychnine, theophylline

Epidemiology
• In 2004, acute poisoning caused more than 45000 death in children and youth under 20y
earsof age, and count for 13% of all fatal accidental poisonings worldwide.
• According to WHO data of 2012, estimated 193,460 people died worldwide from unintenti
onal poisoning, 10,7 million of unintentional poisoning and 84% occurred in low-and mid
dle income countries.
• More than 2 million childhood poisonings are reported yearly in the United States and m
ost cause minimal harm.
• Poisoning in children <5 years of age is usually accidental and accounts for ~85%–90%
of pediatric cases.
• Poisoning in a child >5 years is often intentional.
• Ssemugabo and Al. In 2017 a study on prevalence, circumstances, and Management of ac
ute pesticide poisoning in Hospitals in Kampala city, found in record from five hospitals 7
39 poisoning patients, and pesticides are responsible of 1,4/100000 case fatality rate.

Epidemiology
Epidemiology in Uganda
WHO has estimated that there were 11.4 deaths per 100,000 people due to
unintentional poisoning in 2004. In 1969, Bwibo described cases of accidenta
l poisoning in children based on data from a children’s ward of New Mulago
Hospital for the period of January 1963 to December 1968, inclusive. From t
he study, a total of 130 children were admitted with accidental poisoning of
which seven died (case fatality rate: 5.4%).

Epidemiology
The admission rate for the study period was 0.65%. Household chemicals which
included kerosene, pesticides, and other poisons used in homes and gardens ac
counted for the largest proportion of admitted cases (43.1%). For the househol
d chemicals, kerosene was the leading cause of accidental poisoning. With resp
ect to patient demographics, almost all the cases occurred in children under 5 y
ears old (93.1%), with more males (58%) than females. Of the seven deaths, 5 o
ccurred in boys.
All the deaths but one were as a result of medicaments.

Toxic syndrom / toxidrome
• In 1974, Mofensen an Greesher introduced the concept of « Toxidrome »:
consteellation of symptoms and signs which, when present, point the clin
ician towards a particular class of toxic.
• Althrough the clinical picture is somtimes less characteristic, especiallyin
cases of mixed poisoning, knoledge of toxic syndromes is particularly
useful for patients in whom a adequate clincal history cannot be
obtained.
• However, the clinical exaamination should never be limited to the search
for these toxidromes, but must be complete and systematic
Toxidromes

Toxidromes
1. Anticholinergic syndrom
2. Cholinergic syndrom
3. Extrapyramidal Syndrom
4. Serotoninergic syndrom
5. Sympathomimetic syndrom
6. Hallucinogen
7. Opiod syndrom
8. Swallowing solvent
9. Sedative syndrom

Toxidromes
ANTICHOLINERGIC SYNDROM
• "Red as a beet“ (cutaneous vasodilation)
• "Dry as a bone" (anhidrosis)
• "Hot as a hare" (anhydrotic hyperthermia)
• "Blind as a bat" (nonreactive mydriasis)
• "Mad as a hatter“
• "Full as a flask"

Toxidromes
• "Red as a beet“ (cutaneous vasodilation): occurs as a means to dissipate heat by
shunting blood to the skin, in order to compensate for the loss of sweat production.
• "Dry as a bone" (anhidrosis) : Sweat glands are innervated by muscarinic receptors
, so anticholinergic medications produce dry skin.
• "Hot as a hare" (anhydrotic hyperthermia) : Interference with normal heat dissipat
ion mechanisms (ie, sweating) frequently leads to hyperthermia.
• "Blind as a bat" (nonreactive mydriasis) : Muscarinic input contributes to both pu
pillary constriction and effective accommodation. Anticholinergic medications gener
ally produce pupillary dilation and ineffective accommodation that frequently manif
ests as blurry vision.

Toxidromes
• "Mad as a hatter" (delirium; hallucinations) – Blockade of muscarinic receptors in
the central nervous system (CNS) accounts for these findings. Manifestations may in
clude: anxiety, agitation, dysarthria, confusion, disorientation, visual hallucinatio
ns, bizarre behavior, delirium, psychosis (usually paranoia), coma, and seizures.
Hallucinations are often described as "Alice in Wonderland-like" or "Lilliputian t
ype," where people appear to become larger and smaller. (altered mental status)
• "Full as a flask" – The detrusor muscle of the bladder and the urethral sphincter ar
e both under muscarinic control; anticholinergic substances reduce detrusor contrac
tion (thereby reducing or eliminating the desire to urinate) and prevent normal ope
ning of the urethral sphincter (contributing to urinary retention).

Medications and other substances with anticholinergic properties that may
be involved in acute poisoning

Common causes of delirium and confusional states
Differential diagnosis of anticholinergic toxidrome

Laboratory evaluation
The following laboratory tests should be obtained:
Rapid determination of blood glucose
Acid base status
Electrolytes
Blood urea nitrogen and creatinine
Serum osmolality (suspected ingestion of toxic alcohols or presence of anion g
ap acidosis)
Aspartate aminotransferase (AST) and Alanine aminotransferase (if acetaminop
hen ingestion suspected)
Quantitative acetaminophen serum concentration (suicidal intent or if suspecte
d based on history)
Quantitative salicylate serum concentration (patients with respiratory alkalosis o
r metabolic acidosis)
Urine dipstick test
Urine pregnancy test (postmenarchal females

Laboratory evaluation
Electrolytes, blood urea nitrogen (BUN), and creatinine levels assess anio
n-gap acidosis,.
anion-gap calculation(3-16mEq/L)
Na (mEq/L) – [Cl (mEq/L) + HCO3 (mEq/L)]
The osmolal gap is evaluated(–3 to +6 mOsm/kg H2O.)
2 × Na (mEq/L) + BUN (g/L)/2.8 + glucose (mg/dL)/18
Electrocardiogram.
Other specific drug levels as indicated
A negative toxicology screen does not exclude a toxic exposure.

MANAGEMENT
OF POISONING
In children

outline
MANAGEMENT OF POISONING
In children
▷Rapid First Look (toxidome-oriented)
▷Systemic evaluation
ABCDEE approach
& Criteria of endotracheal intubation
▷Explosure & Elimination

PETAT ASSESSMENT
MANAGEMENT OF POISONING In children
Rapid evaluation of :
The initial approach to the patient with a witnessed or suspected poisoning s
hould be no different than that in any other sick child, starting with stabilizat
ion and rapid assessment of the general status, mental state, including Glasg
ow Coma Scale score and laryngeal reflexes, presence of visible trauma or sei
zures.
PAT Assessment.
mental status
Assess by using APVU scale/ GCS
vital signs,
Pulse, respiratory rate, blood pressure
and temperature, SPO2
 pupils reaction

Rapid First Look (toxidome-oriented)

Rapid First Look (toxidome-oriented)
Connect to cardiac monitor and oxygen
Secure an IV line ASAP
The possibility of concomitant trauma or illness must be recognize
d and addressed: C-Spine Injury (C. Spine immobilization.)
This quick initiation phase helps to direct initial stabilization efforts a
nd provides a clue to the etiologic agent or the cause of the toxidro
mic syndromes if present.

A
B
C
D
AIRWAY
BREATHING
CIRCULATION
DISABILITY
E
+ EXPOSURE
& ELIMINATION
SYSTEMATIC EVALUATION

Systematic evaluation: ABCDE approach.
Adapted basic ABC (airway, breathing, circulation) approach us
ed in cardiac and trauma resuscitation for the initial managem
ent of the critically ill is used.
The steps are organized according to the issues that pose the
most immediate life threats; problems are managed immediate
ly in the order encountered.

“A”: Airway stabilization
The patency of the airway and gag reflex should be evaluated.
• Suction if there any secretions like vomitus content.
The position of the head should be optimized to maintain airw
ay patency.
• head tilt chin left/ sniffing position
• Cervical spine stabilization must be maintained if trauma is susp
ected.
• semi-prone position of the patient if actively vomiting,
• Endotracheal intubation should be performed in all patients
in whom the airway is threatened.

Criteria of endotracheal intubation:
• Patients who cannot protect their airway,
• Patients with a caustic ingestion who manifest stridor and drooling
• Patients with profound tissue hypoxia from toxins which cause cellul
ar hypoxia, despite normal oxygen saturation readings,
• Patients with severe metabolic acidosis due to poisoning are at risk o
f decompensating rapidly from respiratory failure. Such patients shou
ld be intubated for any sign of respiratory failure, either clinically or
on blood gas testing
• One exception is when the clinical scenario suggests opioids overdos
e.
• Severe hypoglycemia should also be ruled out as a cause of depress
ed mental status prior to intubation.
• The hyperventilation seen initially in Patients with Aspirin poisoning
is beneficial and intubation should be avoided.

Breathing
Poisoned patients may develop respiratory failure for many reas
ons.
Supplemental oxygenation should be provided to maintain oxyg
en saturation >95 percent ( high flow 100% O2)
Intubation and ventilation are required in patients who cannot s
ustain adequate oxygenation or ventilation or who have severe
acid-base disturbances.

“C”: Circulation
Hypotension is treated with a rapid intravenous (IV)
infusion of 20 ML/KG of isotonic crystalloid, followed by a nore
pinephrine drip in many cases, pending more specific informatio
n to guide therapy,
Circulatory assist devices and extracorporeal life support may b
e needed in refractory shock
Antiarrhytthmias,…

“D”: Disability and neurological stabilization
• Once the airway, breathing, and circulation are secured, attention
is next directed towards neurologic stabilization.
• Hypoglycemia can present as any alteration of mental status,
including confusion, seizures, focal deficits, and coma. Treat these
symptoms with Glucose only when there is evidence of hypoglyce
mia.
• Seizures due to poisoning or withdrawal are best treated with esc
alating doses of benzodiazepines (e.g. Diazepam 5 mg IV, repeate
d and doubled every 5 to 10 minutes as necessary for refractory
seizures.
• Propofol has superseded the barbiturates and inhalational anesth
etics as second-line therapy for benzodiazepine-resistant seizures.

“D”: Disability and neurological stabilization
REMEMBER
Hypoxemia and hypoglycemia are two common causes of altere
d mental status in the poisoned patient that should be promptly
evaluated and addressed during initial stabilization.
Hypoglycemia :
- 2.5 mL/kg of 10 percent dextrose solution.
Seizures :
-Diazepam IV 0.3mg/kg, rectal 0.5mg/kg

Exposure and elimination
External decontamination:
Dermal decontamination
• remove clothing and other external contaminants,
• Flushing of the affected area with tepid water or normal sal
ine (NS).
• Treating clinicians should wear proper protective gear when
performing irrigation
• measure core temperature and treat hypothermia or hyper
thermia as necessary,
• After an inhalational exposure, decontamination involves m
oving the patient to fresh air and administering supplemen
tal oxygen if indicated.

Exposure and elimination
External decontamination:
Ocular exposure
Irrigation should begin immediately at the exposure site.
Visual acuity testing should be deferred until after irrigation is c
omplete.
Solid or particulate matter that can cause persistent injury and c
orneal abrasion can be detected by eversion of the eyelids and
gently removed with a cotton-tipped swab

Gastrointestinal decontamination
• The decision to perform GI decontamination is based upon t
he specific poison(s) ingested, the time from ingestion to pre
sentation, presenting symptoms, and the predicted severity of
poisoning.
• GI decontamination is most likely to benefit patients who: Pr
esent for care soon after ingestion (usually within one to two
hours)
• Have ingested a poison and amount suspected to cause toxic
ity,
• Do not have clinical factors (e.g. somnolence) that make deco
ntamination dangerous.

Gastric lavage
Technique:
• Gastric lavage involves placing a large tube orally into the sto
mach to aspirate contents, followed by flushing with aliquots
of fluid, usually water or NS.
Gastric lavage involves placing a large tube orally into the stom
ach to aspirate contents, followed by flushing with aliquots of fl
uid, usually water or NS with 10 mL/kg (up to 200 to 300 mL) al
iquots until the effluent is clear.

Gastric lavage
Indications
• there are rare cases (e.g. recent and potentially lethal ingestion) wher
e the procedure may be considered after carefully weighing the well-
documented risks against the unclear benefits.
• Only useful if done within 2 hours of poisoning (except with salicylat
es or anticholinergics when it may be of use within 4 to 6 hours).
Contraindications
• Unprotected airway,
• Caustic ingestion (due to risk of exacerbating any oesophageal or ga
stric injury)
• Hydrocarbon ingestion (due to high aspiration risk)
• Patients at risk of GI haemorrhage or perforation (recent surgery, un
derlying anatomic abnormality or pathology, coagulopathy).

Gastrointestinal dialysis
Mechanism of action
Gastrointestinal dialysis represent a relative non invasive metho
d that may benefit certain intoxicated patients even after syste
mic absorption has occurred.

Charcoal
Activated charcoal (AC) is a highly adsorbent powder preventin
g gastrointestinal absorption and subsequent toxicity.
Indications:
It is more effective the sooner(1h) it is given but may still work
up to 2 hours after poisoning (longer with modified-release pr
oducts and anticholinergics)
Dose: 1g/kg q4h. in 8–10 volumes of water, e.g. 5 g in 40
ml of water. Can be made more palatable by mixing with ic
e-cream.

Charcoal
Contraindications:
– Patients with altered conscious states.
– Ingestion of the following agents:
• Acids/alkalis
• Alcohols
• Metals and ionic compounds (iron, potassium, lithi
um)
• Hydrocarbons
• These are not adsorbed by activated charcoal.

Cathartics
• Cathartics (sorbitol, magnesium sulfate, magnesium citrate) h
ave been used in conjunction with activated charcoal to prev
ent constipation and accelerate evacuation of the charcoal-to
xin complex.
• There are no data demonstrating their value and numerous r
eports of adverse effects from cathartics, such as dehydration
and electrolyte imbalance.

Cathartics
Adverse effects associated with cathartic use include increase
d abdominal pain, nausea, vomiting, excessive diarrhoea, dehyd
ration, and electrolyte abnormalities.
Others
Syrup of Ipecac: Syrup of Ipecac (SoI)-facilitated gastric empt
ying is no longer recommended by the AACT, EAPCCT and AAP.
Dilution: Dilution was historically recommended following th
e ingestion of acidic or alkaline corrosives to decrease the conc
entration and, thus, the tissue damage from the ingestion
Endoscopy/surgery

Whole bowel irrigation
Whole bowel irrigation (WBI) refers to the administration of
osmotically balanced polyethylene glycol electrolyte solution (
PEG-ES) to induce liquid stool and mechanically flush pills, ta
blets, or drug packets from the GI tract.
Whole-bowel irrigation (WBI) involves instilling large volum
es (35 mL/kg/hr in children or 1-2 L/hr in adolescents) of a p
olyethylene glycol electrolyte solution (e.g., GoLYTELY) to “wa
sh out” the entire GI tract.

Whole bowel irrigation
Indications:
Potentially toxic ingestions of sustained-release or enteric coate
d pill formulations
Significant ingestions of toxins not adsorbed by activated charc
oal (e.g. iron tablets, lead containing foreign bodies),
Ingestion of illicit drug packets
Contraindications:
Ileus, bowel obstruction, or intestinal perforation,
Clinically significant GI haemorrhage,
Hemodynamic instability (concern for sequestration of bowel an
d worsening of shock),

Kidney poison elimination
• Forced diuresis
• Alkalinics diuresis
Elimination of some drugs (salicylates, Phenobarbital, chlorpr
opamide, and the chlorophenoxy herbicides) may be facilitat
ed by ensuring adequate urine output and using intravenous
sodium bicarbonate to alter the urinary pH and prevent reab
sorption across the renal tubular epithelium.
• Hemodialysis may be indicated to remove a drug/toxin
regardless of renal function or in cases of renal impairmen
t.

MOST COMMON
POISONING
In children

outline
MOST COMMON POISONING
In children
▷Organophosphates & carbamates
▷Acetaminophen
▷Paraffin / Kerosene
▷Iron
▷Corrosive
▷Carbon monoxide
▷Antiepileptics (phenobarbital, carbamazepine, …)
▷Opioids
▷Digitalis

ORGANOPHOSPHATES & CARBAMATES
POISONING in children and adolescents
1
CLINICAL SIGNS
The dominant clinical features of acute cholinergic toxicity include:
bradycardia, miosis, lacrimation, salivation, bronchorrhea, bronchospas
m, urination, emesis, and diarrhea
The muscarinic signs can be remembered by use of one of two
mnemonics:
- SLUDGE/BBB
- DUMBELS
The nicotinic effects include fasciculations, muscle weakness, and paralysi
s via acetylcholine stimulation of receptors at the neuromuscular junction.
Cardiac arrhythmias, including heart block and QTc prolongation may occa
sionally be observed.

1
The muscarinic signs can be remembered by use of one of two
mnemonics:
SLUDGE/BBB
S alivation,
L acrimation,
U rination,
D efecation,
G astric
E mesis,
B ronchorrhea,
B ronchospasm,
B radycardia
DUMBELS
D efecation,
U rination,
M iosis,
B ronchorrhea/Bronchospasm/Bradycardia
E mesis,
L acrimation
S alivation

1
TREATEMENT:
Patients with markedly depressed mental status require 100 percent oxyge
n and immediate endotracheal intubation,
Adequate volume resuscitation with isotonic crystalloid,
Atropine and oxime therapy (typically Pralidoxime).
For moderate to severe cholinergic toxicity, Atropine at a dose of 0.05 mg
/kg IV for children.
In patients with severe poisoning, HUNDREDS of milligrams of atropine b
y bolus and continuous infusion may be required over the course of sever
al days.

1
TREATEMENT:
Clinicians should avoid the use of succinylcholine when performing rapid s
equence intubation (RSI) in patients with organophosphate (OP) poisoning
.
Adequate volume resuscitation with isotonic crystalloid
Decontamination: if ingestion within 1 hour give single dose activated ch
arcoal, adult 50 g (1 g/kg in children) unless airway not protected or other
contraindication. Aggressive dermal and ocular irrigation as needed. Bag/
discard clothing.

1
TREATEMENT:
• Pralidoxime 25 to 50 mg/kg for children, based upon the severity of sy
mptoms.
• Pralidoxime should be administered slowly over 30 minutes, since rapid
administration has occasionally been associated with cardiac arrest, and
slow administration prevents the muscle weakness that results from the
transient inhibition of acetylcholinesterase as Pralidoxime binds to the e
nzyme

ACETAMINOPHEN (PARACETAMOL) POISONING
in children and adolescents
EPIDEMIOLOGY
ACETAMINOPPHEN remains a major cause of overdose in children throughout the wo
rld. In the United States, pediatric acetaminophen exposures account for approximatel
y 30,000 reports to the National Poison Data System annually. The outcome of aceta
minophen poisoning in children and adolescents is nearly always good if the antidote
, N-acetylcysteine (NAC), is administered within 8 to 10 hours of ingestion. Mortality i
s rare in children and adolescents.
2

Acetaminophen (paracetamol) poisoning
Patterns of exposure
Intentional
Unintentional
 Exploratory ingestions
 Inappropriate dosing
Acute ingestion
overdoses
Chronic ingestion
overdoses

Acetaminophen metabolism
Mecanism of liver damage
Depletion
of glutathione stores
Excessive intake
acetaminophen
Decreased capacity
for glucuronidation
or sulfation
Increased cytochrome
P450 (CYP2E1) activity

RISK FACTORS IN CHILDREN
• Age
• Pattern of ingestion,
• Nutritional status
• concomitant use of CYP2E1-inducing drugs
• comorbid illnesses
• Genetic background

10 to 15 mg/kg per dose
Every four to six hours
Not to exceed five doses per 24-hrs period (max daily dose 75 mg/kg)
325 to 1000 mg per dose every 4 to 6hrs (maximum daily dose 4 g)
from 10 to 20 mcg/mL
(66 to 132 micromol/L).
for children 12 years and older and adults
Therapeutic serum concentrations range
for children younger than 12 yrs
THE THERAPEUTIC DOSE OF ACETAMINOPHEN

TOXIC DOSE in acute ingestion
Minimal toxic dose for an acute ingestion
150 mg/kg for a child
or 7.5 to 10 g for an adult
Toxicity is likely to occur with single ingestions
greater than 250 mg/kg
or greater than 12 g in a 24-hour period
Virtually all patients who ingest doses in excess of 350 mg/kg develop
severe liver toxicity (defined as peak aspartate aminotransferase AST
or ALT levels greater than 1000 IU/L) unless treated

TOXIC DOSE in chronic ingestion
The minimum toxic threshold for children:
150 to 175 mg/kg over two to four days,
particularly in the setting of a febrile illness
and decreased oral intake

CLINICAL MANIFESTATIONS Acute exposures
• Stage I (up to 24 hours after overdose) – Asymptomatic
but less commonly: nausea, vomiting, and, in patients with very large
doses, lethargy and malaise
• Stage II (24 to 72 hours after overdose) – Right upper quadrant
pain, elevation in liver enzymes, prothrombin time (PT) and internation
al normalized ratio of PT, and, in severe cases, evidence of nephrotoxi
city (elevated blood urea nitrogen, creatinine, oliguria) and/or pancrea
titis (elevated serum amylase, lipase)
• Stage III (72 to 96 hours) – Evidence of liver failure and, in severe ca
ses, renal failure and multi-organ failure; death most commonly occur
s in this stage
• Stage IV (4 to 14 days) – Recovery

CLINICAL MANIFESTATIONS Chronic exposures
• Diagnosis of chronic acetaminophen intoxication (repeated excessive
dosing) is often difficult and requires the combination of astute history-
taking and recognition of typical clinical and laboratory abnormalities.
• Clinicians must specifically ask about acetaminophen ingestion (includin
g dose and frequency of administration) because patients and caregiver
s may not include it when asked about potentially toxic drugs. Signs an
d symptoms are insidious in onset, often nonspecific, and easily confus
ed with alternative diagnoses (eg, viral syndrome). Serum concentration
s of acetaminophen in this setting do not correlate with toxicity

Management
• Management focuses on ABC,
• decontamination with activated charcoal (AC) and administration of the ac
etaminophen antidote, N-acetylcysteine (NAC).
• Children who present soon after a potentially toxic ingestion of acetaminop
hen (single dose ≥150 mg/kg or 7.5 g) are likely to benefit from gastrointes
tinal decontamination.
• Activated charcoal (AC), 1 g/kg (maximum dose 50 g) by mouth in all patie
nts who present within four hours.
• AC should be withheld in patients who are sedated and may not be able to
protect their airway, unless endotracheal intubation is performed first.

Management acute poisoning
• Management focuses on ABC
• Administering activated charcoal within 4hrs of exposure
• Obtain a plotting timed serum acetaminophen level in 4hrs after in
gestion
• Administering the antidote, N-acetylcysteine to those children with a
n acetaminophen level that indicates possible toxicity.

Indications for NAC therapy in children and adolescents include
Serum acetaminophen concentration above the "treatment" line,
A suspected single ingestion of greater than 150 mg/kg (7.5 g total dose re
gardless of weight) in a patient for whom the serum acetaminophen conce
ntration will not be available until more than eight hours,
Patients with an unknown time of ingestion beyond 24 hours and a seru
m acetaminophen concentration >10 mg/L (66 µmol/L),

NAC therapy in children and adolescents
• Patients with delayed presentation (>24 hours after ingestion) consisting
of laboratory evidence of hepatotoxicity, and a history of excessive aceta
minophen ingestion,
• If it is not possible to estimate a time of ingestion (due to lack of informa
tion or multiple ingestions), there is no universally accepted approach to r
isk stratification.
• Our approach is to start treatment with acetylcysteine for any patient with
a detectable serum acetaminophen concentration

We then stop acetylcysteine if the patient fulfils all three of the foll
owing conditions:
Asymptomatic (e.g. no right upper quadrant pain),
Acetaminophen concentration is non-detectable,
The serum transaminase activity is decreasing significantly (has d
ecreased to the normal range or to <50 percent of the peak value)
.

Oral: It consists of a 72-hour oral course given as a 140 mg/kg loading do
se followed by 17 doses of 70 mg/kg every four hours (total dose 1330 mg/k
g).
Intravenous: The 21 hour intravenous (IV) protocol for acetylcysteine treat
ment state for a total dose of 300 mg/kg of NAC is given intravenously over
21 hours. IV NAC is compatible with 5 percent dextrose, 0.45 percent normal
saline (i.e., half normal saline), and water for injection.

NAC should be administered intravenously to children with any of the follow
ing:
 Intractable vomiting,
 Contraindications to oral administration (e.g, aspiration risk due to altered
mental status, pancreatitis, bowel Ileus or obstruction, or bowel injury),
 Hepatic failure,
 Patients who refuse oral administration,
 Pregnant adolescent females.

MANAGEMENT OF CHRONIC POISONING
There is no consensus regarding the management of these children.
One approach is to classify children with repeated overdose into one of thre
e treatment groups based upon the results of the initial evaluation (includin
g serum acetaminophen concentration and aminotransferases, which should
be monitored for 36 hours after the last ingested dose):
No hepatic injury and no unmetabolized acetaminophen: These children
may be discharged home.
No liver injury but with unmetabolized acetaminophen– Children without
liver injury, but with unmetabolized acetaminophen. These patients warrant
monitoring of serum alanine aminotransferases, prothrombin time, and supp
ortive care in the hospital.

Liver injury (with or without unmetabolized acetaminophen Children with
a history of multiple supratherapeutic doses of acetaminophen that is associ
ated with hepatic injury with or without unmetabolized acetaminophen sho
uld receive NAC and supportive care in the hospital.
Those patients with moderate to severe hepatotoxicity at initial evaluation w
arrant transfer to a liver transplant center,

After an acetaminophen overdose, otherwise healthy children and adolescen
ts may safely resume acetaminophen therapy if the following conditions are
met:
No clinical symptoms,
Serum acetaminophen level <10 mg/L (66 µmol/L),
Normal serum alanine aminotransferases,
Normal prothrombin time.

PARAFFIN / KEROSENE
3
CLASSES OF HYDROCARBONS
The four structural classes of hydrocarbons are:
• Aromatic hydrocarbons
• Aliphatic hydrocarbons
• Halogenated hydrocarbons
• Terpene hydrocarbons

PARAFFIN / KEROSENE
3
HYDROCARBON TOXICITY
Hydrocarbons also can be classified according to their potential for toxicity:
• Low toxicity (unless complicated by gross aspiration) , asphalt, tars, mi
neral oil, petroleum jelly, motor oil, and axle grease.
• Aspiration hazard (gasoline, kerosene,) , Clinical effects are typically limit
ed to direct pulmonary damage and subsequent inflammation
• Systemic toxicity (Halogenated and aromatic hydrocarbons ) Systemic eff
ects include cardiac arrhythmias secondary to myocardial sensitization and
central nervous system (CNS) depression.

PARAFFIN / KEROSENE
3
CLINICAL MANIFESTATIONS
Most patients who ingest aliphatic hydrocarbons are initially asymptomatic,
Those patients with symptoms (e.g, respiratory distress, hypoxemia) soon aft
er ingestion typically progress rapidly to respiratory failure,
characteristic odors can help identify the presence and type of hydrocarbons
ingested:
-Petroleum distillate odor - Kerosene and other aliphatic hydrocarbons ,
-Pine scent - Pine oil,
-Sweet solvent odor- Halogenated hydrocarbons.

PARAFFIN / KEROSENE
3
-Vital sign (fever, decreased oxygen saturation.)
-Respiratory (coughing, choking, gagging, and vomiting, tachypnea, dyspnea
, cyanosis, wheezing, diminished resonance on percussion, suppressed or tub
ular breath sounds, rales, nasal flaring, and/or grunting respirations.
-Central nervous system: direct central nervous system (CNS) effects by inh
alation, or secondary to hypoxia.
-Cardiovascular: Cardiac dysrhythmias and myocardial dysfunction may occu
r after hydrocarbon ingestion or inhalation.
-Gastrointestinal : local irritation to the pharynx, esophagus, stomach, and s
mall intestine, with edema and mucosal ulceration,
-Hematologic: Leucocytosis early, and hemolysis, hemoglobinuria, and cons
umptive coagulopathy rarely.
Physical findings after hydrocarbon exposure

PARAFFIN / KEROSENE
3
MANAGEMENT
Stabilization
• The initial treatment depends upon the degree of immediate toxicity,
including the presence of respiratory distress and altered mental stat
us
• Patients with severe respiratory distress, unresponsive to oxygen and
beta-2 bronchodilators or significant altered mental status (lethargy,
coma) shortly after hydrocarbon ingestion should undergo endotrach
eal intubation.
• Patients with seizures: iv lorazepam 0.1 mg/kg in addition to support
of airway and breathing.
• Patients with mild to moderate respiratory symptoms on presentatio
n: remain NPO during the initial observation period and receive main
tenance intravenous fluids.

PARAFFIN / KEROSENE
3
MANAGEMENT
Stabilization
Patients who are asymptomatic at presentation warrant serial examinations
with monitoring of pulse oximetry.
Activated charcoal (AC) should NOT be administered to patients with a singl
e agent ingestion of a hydrocarbon without systemic toxicity for the followin
g reasons:
• AC administration increases the risk of spontaneous vomiting and ad
ditional pulmonary aspiration,
• AC does not bind well to hydrocarbons,
• In this instance, toxicity arises from pulmonary aspiration rather than
systemic toxin absorption.

PARAFFIN / KEROSENE
3
MANAGEMENT
Stabilization
For patients who have ingested large quantities of hydrocarbons with significant
potential for systemic toxicity and who present for care within 60 minutes of ing
estion, we suggest gastric emptying using nasogastric lavage. These agents can
be remembered by using the mnemonic "CHAMP“:
• C: Camphor
• H: Halogenated hydrocarbons (eg, trichloroethane, trichloroethylene)
• A: Aromatic hydrocarbons (eg, benzene, toluene, xylene)
• M: Metal additives (eg, arsenic, mercury) in hydrocarbon base
• P: Pesticide additives (eg, organophosphates) in hydrocarbon base

PARAFFIN / KEROSENE
3
MANAGEMENT
Stabilization
Pulmonary management
• The treatment of hydrocarbon Pneumonitis is supportive and includes oxy
gen and close monitoring of respiratory status,
• Bronchospasm should be treated with selective beta-2 agonists,
• Endotracheal intubation and conventional mechanical ventilation if respira
tory failure or unable to maintain airway,
• Extracorporeal membrane oxygenation (ECMO) and high frequency ventil
ation.

PARAFFIN / KEROSENE
3
MANAGEMENT
Stabilization
Pneumonitis caused by hydrocarbon aspiration should not be treated routin
ely with antibiotics unless signs of secondary infection, including the followi
ng, are present:
• Recurrence of fever after the first 48 hours,
• Increasing infiltrate in chest radiograph,
• Leucocytosis after the first 48 hours,

SALICYLATES POISONING
4
As a general rule, ingestions of less than 300 mg/kg are associated with mil
d symptoms, ingestions of 300 to 500 mg/kg are associated with moderate
toxicity, and ingestions of >500 mg/kg are associated with death.
Salicylate poisoning leads to a variety of clinical features: increased respirat
ory rate, temperature, and heart rate, Tinnitus, Nausea and vomiting , Pul
monary edema , agitation, confusion, restlessness, seizures, and rarely, com
a, respiratory alkalosis.
Hypovolemia, leucocytosis, inhibition of platelet function, and disturbances i
n vitamin K-dependent and vitamin K-independent clotting factors.

4
MANAGEMENT
Supportive care — Key aspects of supporting the child or adolescent with
salicylate poisoning include maintaining oxygenation, ensuring adequate mi
nute ventilation, providing intravenous glucose, and repletion of fluid and p
otassium losses.
Therapy includes activated charcoal to prevent absorption and alkalinizati
on of the urine to enhance elimination. Hemodialysis is recommended for
extreme salicylate levels (>100 mg/dL), renal insufficiency, significant volum
e overload, pulmonary edema, or severe electrolyte aberrations.
Gastrointestinal Decontamination
AC, 1 g/kg; maximum single dose: 50 g

4
MANAGEMENT alkalinization of the urine
• Alkalinize with sodium bicarbonate
• Bolus therapy: sodium bicarbonate, 1 to 2 mEq/kg (maximum 100 mEq) IV push over 3 to 5 minu
tes
• Maintenance therapy: 100 to 150 mEq sodium bicarbonate in 1 L of D5W, run at 250 mL/hour in a
dults 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; i
ndications 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
• Clinical deterioration despite aggressive and appropriate supportive care

IRON POISONING in children and adolescents
5

5
Common in children, due to the candy-like aspect of iron tablets. Ingestion of a quantity 60 mg/kg
can cause serious toxicity.
Management :
Gastric lavage if ingestion within 1 hour from arrival or pills visible in the stomach at X-ray.
NB: charcoal is NOT EFFECTIVE f Patients who are asymptomatic after 6 hours from ingestion most l
ikely do not need specific treatment.
Monitor for at least 12 hours and give IV fluids to manage shock and hypovolaemia
Indication for use of antidote: – Severe symptoms – Metabolic acidosis f Desferroxamine continuous
infusion 15 mg/kg/ hour in normal saline or glucose 5% – Do not use for more than 24 hours – Inc
rease IV fluids if BP drops – Continue until metabolic acidosis clears or clinical condition improves –
Contraindication: renal failure/anuria

5
Indication for use of antidote: –
Severe symptoms –
Metabolic acidosis
Deferoxamine chelation is indicated for serum iron levels >500 mcg/dL or hem
odynamic collapse.
Desferroxamine continuous infusion 15 mg/kg/ hour in normal saline or glucos
e 5%
– Do not use for more than 24 hours
– Increase IV fluids if BP drops
– Continue until metabolic acidosis clears or clinical condition improves
– Contraindication: renal failure/anuria

CORROSIVE POISONING
6
Alkaline ingestion causes deep tissue injury, usually with liquefaction necros
is, in the oropharynx and proximal esophagus. Perforation occurs in severe
exposure. Automatic 147 dishwasher detergents have extremely high alkalin
ity.
Acid ingestion causes a superficial coagulation necrosis, with heat producti
on and eschar formation.Absorption may result in metabolic acidosis, hemo
lysis, and renal failure.

CORROSIVE POISONING
6
Management involves aggressive decontamination, with washing and dilutin
g of dermal or ocular exposures, fresh air and oxygen for inhalational injury,
and removal of any oral matter if ingested. Eye exposure requires urgent op
hthalmologic consult.
Neutralization is contraindicated, as an exothermic reaction can yield more
extensive tissue destruction. Ipecac, gastric lavage, and activated charcoal ar
e not indicated. Endoscopy is recommended within the first 24 hours. The us
e of steroids is controversial.

CARBON OXIDE POISONING
7
CO binds to haemoglobin with much greater affinity than oxygen, forming carb
oxyhemoglobin (COHb) and resulting in impaired oxygen transport and utilizati
on. CO can also precipitate an inflammatory cascade that results in CNS lipid p
eroxidation and delayed neurologic sequelae.
In young children, signs of carbon monoxide poisoning may be more subtle an
d nonspecific(fussiness and feeding difficulty ) than those in adults and older
children (headache, malaise, nausea, and dizziness and symptoms ranging f
rom mild confusion to coma).

7
Infants and toddlers may present with complaints such as fussiness and feedin
g difficulty as the sole manifestation of carbon monoxide poisoning
Because of their higher oxygen utilization and higher minute ventilation, young
children may develop signs and symptoms of carbon monoxide poisoning befo
re older children and adults who experience the same exposure

7
Management
• removal from the source of CO,
• High-flow oxygen provided via a nonrebreathing mask,
• Intubated comatose patients, or severely impaired mental status, and ventil
ated using 100 percent oxygen,
• For patients suffering from CO poisoning after smoke inhalation, it is import
ant to consider concomitant cyanide toxicity,
• IV fluids for hypotension.
• Diazepam for seizures

7
Treatment with hyperbaric oxygen (HBO) in the following circumstances:
CO level >25%
CO level >20% in pregnant patient
Loss of consciousness
Severe metabolic acidosis (pH <7.1)
Evidence of end-organ ischemia (e.g, ECG changes, chest pain, or altered ment
al status)

ANTIEPILEPTICS POISONING
8
Barbiturate Poisoning
Clinical features:
• Confusion, irritability, combativeness
• Drowsiness, lethargy
• Hypotension, bradycardia or tachycardia, until shock
• Respiratory depression, until coma

8

8
PHENYTOIN poisoning
The earliest signs of phenytoin toxicity are typically horizontal nystagmus and
unsteady gait.
More severe toxicity results in slurred speech, along with a gradually worsenin
g mental status typified by lethargy, confusion, or coma. Hyperreflexia is occa
sionally seen.
hypotension and bradyarrhythmias

8
PHENYTOIN poisoning
Treatment
Administer activated charcoal (1 g/kg up to 50 g) for symptomatic acute ingestio
ns, unless airway is not protected or other contraindications exist
Administer activated charcoal (1 g/kg up to 50 g) for asymptomatic patients who
report significant ingestions if less than 1 to 2 hours after ingestion
Provide supportive care as needed

8
Carbamazabin
• Carbamazepine toxicity frequently presents with neurologic, cardiovascular,
and anticholinergic symptoms.
• Patients with mild carbamazepine toxicity or those presenting shortly after
the ingestion when absorption remains incomplete may demonstrate sign
s, such as drowsiness, nystagmus, and tachycardia
• More severe intoxication may manifest as lethargy, seizure, coma, hypoten
sion, or arrhythmia

8
Carbamazabin
Clinical findings
• Tachycardia
• Hypotension
• Mental status changes
• Seiures
• Ocular examination frequently reveals nystagmus and mydriasis, and occas
ionally ophthalmoplegia

8
Carbamazabin
MANAGEMENT
Airway, breathing and circulation — Patients with significant CNS depressi
on may lose protective airway reflexes and should be intubated, particularly i
n light of their lower seizure threshold.
Gastrointestinal decontamination
Activated charcoal — Activated charcoal (AC) remains the most common
method of gastrointestinal (GI) decontamination for acute carbamazepine poi
soning

OPIOIDS POISONING
9
Clinical features:
• Respiratory depression
• Hypotension, hypothermia
• Pinpoint pupils
• Decreased mental status until coma

DIGITALIS POISONING
10
Digoxin toxicity produces increased sympathetic tone and cardiac automaticity.
Manifestations include:
nausea, vomiting, altered sensorium, and dysrhythmias.
The most typical dysrhythmias are bidirectional ventricular tachycardia and atrial
tachycardia with AV block. Serum drug levels are available. Heart block or sinus
bradycardia may be managed with atropine

DIGITALIS POISONING
10
MANAGEMENT
Basic measures and arrhythmias — When digitalis toxicity is suspected, th
e following measures should be performed:
Assess airway, breathing, and circulation; stabilize as necessary
Place the patient on continuous cardiac and pulse oximetry monitors
Establish intravenous (IV) access
Obtain an electrocardiogram (ECG)
Obtain a fingerstick glucose measurement if there is any alteration in mental
status

DIGITALIS POISONING
10
For serious dysrhythmias, therapy is digoxin-specific Fab fragments (Di
gibind, DigiFab)
If a patient with digitalis poisoning is hypokalemic, potassium should be
administered since hypokalemia exacerbates digitalis toxicity
Intracellular calcium is increased, so additional calcium should be avoide
Cardiac pacing may be used to treat heart block or other life-threatening
bradydysrhythmias.
Amiodarone, magnesium sulfate, and phenytoin have been used for recu
rrent life-threatening tachydysrhythmias

DIGITALIS POISONING
10
We suggest Fab fragments be given to patients with digitalis toxicity an
d any of the following:
Life-threatening arrhythmia (eg, ventricular tachycardia; ventricular fibrillation
; asystole; complete heart block; Mobitz II heart block; symptomatic bradyca
rdia)
Evidence of end-organ dysfunction (eg, renal failure, altered mental status)
Hyperkalemia (serum potassium >5 to 5.5 meq/L [>5 to 5.5 mmol/L])

REFERENCES
▷ Up-to-date 2018
▷ Children and poisoning- World Health Organization. http://www.who.int>poison_englis
h
▷ Poison statistics National data 2017 Poison control: http//www.poison.org>poison stat
istics.
▷ Wold report on child injury prevention: WHO
▷ Environ Health Insights. 2017; 11
▷ THE HARRIET LANE HANDBOOK TWENTY-FIRST EDITION, 2018
▷ ROGERS’ HANDBOOK OF PEDIATRIC INTENSIVE CARE FIFTH EDITION 2017
▷ Up To Date 2018
▷ UGANDA national guidelines and treatment 2016

Thank you
Dr Gabriel Shamavu
gabrielshamavu@gmail.com

Poisoning in Children by Dr Shamavu Gabriel .pptx

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