Poisonings (Contd…)

An analgesic and antipyretic

Oil of wintergreen
•Contains methyl salicylate
•very toxic yet is available over the counter for
oral and topical use
•Smells great and children may drink it
Don’t keep this drug around
Risk factors/ etiology
•Salicylates uncouple oxidative phophorylation
and increase the metabolic rate, resulting in
tachypnea, tachycardia, fever, hypoglycemia
•Krebs cycle inhibited causing a metabolic
acidosis
•Damage to hepatocytes occurs, causing liver
toxicity, prolonged PT, platelet inhibition and
prolonged BT
Presentation/ physical examination
Mild salicylate ingestion
•Vomiting, hyperpnea, fever, lethargy, mental
confusion

Severe salicylate ingestion

•Convulsions, coma, respiratory and
cardiovascular collapse

Chronic salicylate ingestion

•Hyperventilation, dehydration, bleeding
disorders, seizures, coma
Three phases of salicylate ingestion

Phase1

Respiratory alkalosis from direct stimulation of

the respiratory center
Potassium and sodium bicarbonate excreted in
the urine
Lasts 12 h in an adolescent , but may not be
evident in a small child
Phase 2

“Paradoxical aciduria” 12 – 34 h after salicylate

ingestion in the adolescent
Begins shortly after salicylate ingestion in the
young child

Aciduria may lead to hypovolemia

Phase 3

Metabolic acidosis, dehydration, hypokalemia

4 – 6 h after ingestion of salicylates in an infant
and ≥ 24 h after ingestion in an adolescent

Metabolic acidosis results from lactic acidosis

Hyperpnea is secondary to acidosis rather than

to stimulation of respiratory centers
•WBC, hematocrit, platelets increased

•BUN, creatinine also increased

•Na+, K+

•Blood glucose

•ABG show a metabolic acidosis with respiratory

compensation in children and a respiratory
alkalosis alone in adolescents; or mixed ABG
disorder
In acute overdose,
salicylate serum level is predictive of the clinical
course at 6 h after ingestion

Serum level should be plotted on the Done’s

nomogram
Done’s Nomogram
•If the serum salicylate level is < 35 mg/dl,
asymptomatic

•If at 6 h after ingestion, the salicylate level is

35 – 70 mg/dl, mild to moderate toxicity

•Salicylate level between 70 and 100 mg/dl ,

severe toxicity

•Salicylate level > 100 mg/dl, potentially fatal

Treatment
Gastric decontamination performed
Patient hydrated
To enhance the excretion of salicylate the
intravenous route should be used to administer
bicarbonate
Urine pH should be raised to a pH of 7.0 – 7.5
Hemodialysis required in severe cases of
salicylate toxicity (salicylate level > 100 mg/dl)
Complication/ follow-up

Causes of death from

•Respiratory failure
•Cerebral edema
•Hemorrhage
•Cardiovascular collapse
A colorless, odorless gas produced from the
combustion of carbon-containing fuel

Risk factors/ etiology

•Affinity of CO to hemoglobin is 250 times that of
oxygen
•Results in the formation of carboxyhemoglobin,
decreasing the oxygen carrying capacity of blood
Presentation/ physical examination
Symptoms depend on the carboxyhemogloin
levels

0-10%: None
11-20%: Mild headache
21-30%: Throbbing headache, irritability
31–40%: Severe headache, lethargy, nausea,
vomiting
41–50%: Confusion, syncope, tachycardia,
tachypnea
51-60%: Syncope, coma, seizures
Diagnostic tests
•Presence or absence of the classic cherry-red
skin color no diagnostic value
•Carboxyhemoblobin level and ABG analysis
should be obtained
•Urinalysis for myoglobin (Severe CO poisoning
may have muscle breakdown)
•CBC and electrolytes
Treatment
•Patient should be removed from the environment
•100% supplemental oxygen or hyperbaric
oxygen in severe cases, administered until the
carboxyhemoglobin level is ≤ 5%
•Urine output should be >1ml/kg/h

Complications/follow-up
Behavior changes, memory loss, blindness in
10-30% of cases, even after a single exposure
Acids: batteries, toilet bowel cleaners, metals etc.
Bases: dishwashing detergent, Liquid Plummer
etc.

Risk factors/ etiology

•Acids coagulate proteins, resulting in tissue
necrosis, and alkalis produce liquefaction
necrosis with the risk of perforation if the burn
located in the intestinal tract
•Serious injuries tend to occur with a pH <2 or
>12
Presentation/ physical examination
•Burns of mucous membranes may be
visualized
•Patient may drool and refuse to swallow
secondary to pain
•Esophageal strictures may be found
•Acids may be responsible for delayed gastric
emptying from pylorus scarring

Diagnostic tests
CBC, Abdominal radiograph
Treatment
•Caustic should be removed by flushing copiously
with water
•Emesis and gastric lavage contraindicated in
caustic patients
•Activated charcoal not used
•Endoscopy completed in the first 24 h if the
patient is symptomatic or the history is
suggestive of burns from caustic ingestion
•Use of steroid controversial and prophylactic
antibiotics do not seem to improve outcome
•An alkaloid extracted from Erythroxylon coca
•Supplied as a hydrochloride salt in crystalline form
•Absorbed from the nasal mucosa
•Detoxified in the liver and excreted in the urine
•Half-life approximately 1 h

Risk factors/ etiology

•All coacaine not “pure” as drugs such as PCP, heroin,
or amphetamines may be added or sbstituted for
cocaine
•May be snorted (nasal application), injected, or smoked
Presentation
•Euphoria
•CNS stimulation, ie, restlessness, excitement, agitation,
increased motor activity, increased respiratory rate, and
hypertension
Later,
•Hypotension with seizure, coma, and respiratory
depression
•Chest pain secondary to myocardial injury that ranges
from angina pectoris to myocardial infarction
•Nausea, insomnia, and emaciation in the chronic user
Physical examination
•There may be a perforated nasal septum from snorting

Diagnostic tests
•Urine drug screen
•If smuggling suspected, a flat-plate abdominal
radiograph will show opaque densities within the bowel
highlighted by a gas halo
Treatment
•Activated charcoal indicated only when “body packing”
suspected
•Intensive supportive therapy applied to the clinical
manifestations
•Half-life for cocaine is appox 1 h and prognosis is good
if adequate support

Complications/ follow-up
•Hypertension may lead to a CVA
•Chronic cocaine users may develop a cardiomyopathy
that leads to depressed cardiac function and death
Carbon compounds that become liquid at room
temperature

Risk factors/ etiology

•Found in fuels, solvents, household cleaners, and
polishes
•Aspiration of hydrocarbons may cause a chemical
pneumonitis
Presentation
•Cough, emesis, and fever
•Symptoms may be delayed for 6 h

Physical examination
•SOB, wheezing, rales, dullness to percussion and
respiratory difficulty

Diagnostic tests
•CXR may show and infiltrate
Treatment
Gastric lavage contraindicated, unless a risk of
severe poisoning, eg, CNS involvement
If gastric lavage is necessary, endotracheal
intubation

Patients who remain asymptomatic after 6 h and

have a negative CXR may be discharged

Antibiotics not indicated unless a secondary

bacterial infection
Corticosteroid not beneficial
Complication/ follow-up

Recovery in most cases, but course may include

•Lethargy, seizures, and coma

•Pneumothorax, pleural effusions, secondary
infections
•Respiratory failure and death
Acetylesterase inhibitors that may be ingested,
inhaled, or absorbed through the skin
Commonly found in insecticides

Used as nerve gases in chemical warfare

agents

Presentation/ physical examination

•Muscarinic, nicotnic, and CNS signs and
symptoms
Muscarinic symptoms: salivation, lacrimation,
urination, defecation, GI cramping, and emesis

Nicotinic symptoms: cramps, fasciculations,

twitching, weakness, and areflexia, and paralysis
of voluntary muscles, including respiration,
occurs after the muscarinic effects

Nicotinic symptoms not seen in mild poisoning

CNS symptoms: anxiety, ataxia, dizziness,
headache, convulsions, coma
Diagnostic tests:
•History of exposure and clinical presentation
•Odor of insecticide
•Decreased RBC cholinesterase
Treatment:
•ABC’s
•Gastric lavage and activated charcoal
•If exposure via skin, wash with soap and water and
contaminated clothing placed in a plastic bag
•Health-care workers should take precautions not to get
organophosphate on their skin
Atropine (for muscarinic symptoms)
Pralidoxime (for nicotinic symptoms)
•Most common cause of death form poisoning in
childhood

•Severity of the poisoning depends on the

amount of elemental iron ingested

•Adult preparations responsible for serious

poisonings
Presentation/ Physical examination
Iron poisoning occurs in four stages:
•Stage 1: occurs 30 min - 6 h after ingestion, nausea,
vomiting, diarrhea and abdominal pain; hemorrhagic
gastroenteritis in more serious iron ingestion
•Stage 2: occurs 6 – 12 h after ingestion, relative clinical
improvement mistaken for recovery (honeymoon phase)
•Stage 3: occurs 24- 48 h after ingestion, severe
poisoning, progressive circulatory collapse (shock),
hepatorenal failure, bleeding, metabolic acidosis, and
coma
•Stage 4: occurs 1-2 months after ingestion and causes
GI scarring and obstruction and pyloric stenosis
Diagnostic tests
•Based on history and development of symptoms
•Serum iron levels obtained
•Serum iron levels >500 ug/dl severe poisoning
•Iron is radiopaque and iron tablets may be seen
on plain abdominal films
•Children’s multivitamins may not be visualized
on X-ray because of their low iron concentration
Treatment
•Syrup of ipecac may be used to remove iron
tablets from stomach if there is no evidence of
gastroenteritis
•Whole bowel irrigation used to flush tablets from
the intestine
•If tablets continue to adhere to the gastric
mucosa, then they must be removed by
endoscopy or surgery
•Treatment is supportive and includes airway
and fluids if the patient is in shock
Antidote is deferoxamine (IV) administered
1)To symptomatic patients and those with
hypotension and lethargy regardless of the serum
iron level and total iron binding capacity (TIBC)
2)If the serum iron is greater than TIBC
3)If the serum iron level is >350 ug/dl

The urine turns “vin rose” when free iron binds

with deferoxamine
Treatment should continue until the patient is
symptom free
Complication/ follow- up
Iron is corrosive to the GI mucosa, and may
cause hypotension and metabolic acidosis and
coagulopathies
Drowsiness and coma
Toxic ingestions may result in death
A chronic disorder often seen in children who are
near environmental exposure risk, such as ingestion
of paint chips or plaster from old buildings

Presentation/ physical examination

•Depends on blood lead level and age of the child

•Most asymptomatic ; picked up on routine screen
•Anorexia, apathy, lethargy, anemia, decreased play
activity, aggressiveness, and poor coordination
Diagnostic tests
•Elevated blood lead levels
•increase in free erythrocyte protoporphyrin and
•increased lead excretion in the urine after
administration of a chelating agent such as Calcium
EDTA
•Minimal lead screening should be done for patients who
are 6 months – 6 years old age
•Blood lead levels of >10 ug/dl are abnormal

•Sideroblastic anemia
•X-ray shows lead lines at the metaphyses of the long
bones and radiopaque foreign material within the small
bowel
Treatment
The goal of management is to eliminate or
remove the child from the source of lead

*DMSA, Meso-2,3-
dimercaptosuccinic acid
**BAL, Dimercaprol

* **

Complications/ follow-up: Encephalopathy after 3-

6 weeks of actively ingesting lead (<3 years)
•Used as sedatives , for allergies, for antinausea, and for
motion sickness
•Found in some cold medication such as liquid cough
medication

Presentation/physical examination
•Drowsy or
•Insomnia, nervousness, restless
•Children may be hyperactive and hallucinations

•Tonic clonic seizures

•Anticholinergic effects such as flushed skin, fever,
tachycardia, fixed dilated pupils
Treatment

•Activated charcoal unless a sustained release

antihistamine, in which case, whole bowel
irrigation
•Seizures should be controlled
•Supportive therapy

Complication/ follow up:

•Death from uncontrolled seizures leading to
coma and cardiopulmonary arrest
•Mild to moderate toxicity mimics alcohol
intoxication
•Severe toxicity results in CNS problems
including lethargy and coma

Physical examination
•Constricted pupils, confusion, hypotension, poor
coordination, respiratory depression, coma
Treatment:
•ABC’s
•Gastric lavage
•Multiple doses of activated charcoal
•IV fluids and forced diuresis and alkalinization for
long-acting barbiturate intoxication
•In severe cases, hemodialysis

Complications/ follow- up
•Shock or cardiopulmonary arrest leading to early
deaths
•Aspiration pneumonia or pulmonary edema leading
to later deaths
Presentation/physical examination
•CNS and heart systems affected
•Drowsiness, delirium, hallucination,
disorientation, seizures, coma, hypertension,
later, hypotension, and arrhythmias

Diagnostic tests
•ECG to check for QRS widening and QT and
QTc prolongation
Treatment
•Supportive therapy
•Activated charcoal
•Sodium bicarbonate to treat and prevent dysrhythmias
(Lidocaine if not responding)
•Hypotension treated with fluids and NE
•Seizures resolves without treatment
•Symptomatic patients should be monitored in ICU
•Patients completely asymptomatic after 6 h of
observation may be discharged home

Complications/ follow-up
•Seizures and arrhythmias