Pediatrics drug poisoning

P E D I A T R I C P O I S O N I N G S Dina F. El Wahaidi Supervised by: Dr. Mostafa El KahLout .

POISONING IN CHILDREN
Definition of Poisoning:
Exposure to a chemical or other agent that adversely affects functioning of an organism.
Circumstances of Exposure can be intentional, accidental, environmental, medicinal or recreational.
Routes of exposure can be ingestion, injection, inhalation or cutaneous exposure.
“ All substances are poisons...the right dose separates poison from a remedy.” Parcelsus

EPIDEMIOLOGY
US Poison Centers receive 1.5 million calls a year regarding pediatric ingestions.
79% of these calls involve children younger than age six.
56% of pediatric exposures are from products around the house including medicines, cleaning agents, pesticides, plants and cosmetics.

EPIDEMIOLOGY
99% of ingestions by children under 6 are unintentional.
Approximately 40% of ingestions reported to the poison center by adolescents are intentional.
Approximately 56% of adolescent ingestions are by females.

EPIDEMIOLOGY

Major four toxidromes are:
Anticholinergic
Sympathomimetic
Opiates/Sedatives- Hypnotics/ Alcohol
Cholinergic

IMPORTANT HISTORY POINTS
What toxic agent/medications were found near the patient?
What medications are in the home?
What approximate amount of the “toxic” agent was ingested?
How much was available before the ingestion?
How much remained after the ingestion?
When did the ingestion occur ?
Were there any characteristic odors at the scene of the ingestion?
Was the patient alert on discovery?
Has the patient remained alert since the ingestion?
How has the patient behaved since the ingestion?
Does the patient have a history of substance abuse?

ABC’S OF TOXICOLOGY:
A irway
B reathing
C irculation
D rugs:
Resuscitation medications if needed
Universal antidotes
D raw blood:
chemistry, coagulation, blood gases, drug levels
D econtaminate
E xpose / Examine
F ull vitals / Foley / Monitoring
G ive specific antidotes / treatment

Decontamination:
Ocular:
Flush eyes with saline
Dermal:
Remove contaminated clothing
Brush off
Irrigate skin
Gastro-intestinal:
Activated charcoal:
May Prevent /delay absorption of some drugs/toxins
Almost always indicated Only in the 1 st hour !!!!
Naso/oro-gastric Lavage
Bowel Irrigation:
Recent ingestions
Awake alert patient
500 cc NS Children / 2000cc adults
Orally / Nasogastric tube
Contraindications…?
ABC’S OF TOXICOLOGY:

in Children

IRON
The most common cause of death in toddlers.
Classically taught as having five clinical stages.

IRON
Toxic doses occur at 10-20mg/Kg of elemental iron.
Prenatal vitamins typically contain about 65 mg of elemental iron.
Children's vitamins contain about 10-18 mg of elemental iron.

THE FIVE STAGES :
Stage 1 ( first 6 hrs )
Nausea, vomiting, abdominal pain and diarrhea.
Stage 2 ( 6- 12 hrs )
This is the latent phase often between 4-12hours as the patient resolves GI symptoms.
Stage 3 ( 12 - 24 hrs )
Shock stage involving multiple organs including coagulopathy, poor cardiac output, Hypovolemia, lethargy and seizures.
Stage 4 (2-3 days)
Continuing of hepatic failure and ongoing oxidative damage by the iron in the reticuloendothelial system.
Stage 5 ( 2 -6 weeks )
Gastric outlet obstruction secondary to scarring & Liver Cirrhosis .

DIFFERENTIAL DIAGNOSES
Metabolic Acidosis
Other Problems to Be Considered
Gastroenteritis Hepatic failure

WORKUP LABORATORY STUDIES
It is a clinical diagnosis
Little is known about the absorption rate of iron in an overdose or the timing of peak serum iron level
Serum levels Of :
Mild - Less than 300 µg/dL
Moderate - 300-500 µg/dL
Severe - More than 500 µg/dL
TIBC has no utility in the acute
overdose setting.

MANAGEMENT
Detailed history and physical including
a rectal exam for frank blood.
Aggressive fluid resuscitation and intravenous access.
Whole bowel irrigation and KUB to
Look for pills.
Laboratory analysis for CBC,
chemistry, and iron levels (peak around 4 hours)
Will often require repeat levels with
a repeat chemistry

INDICATIONS FOR DEFEROXAMINE TREATMENT - shock, altered mental status, persistent GI symptoms, metabolic acidosis, pills visible on radiographs, serum iron level greater than 500 µg/dL, or estimated dose greater than 60 mg/kg of elemental iron - if a serum iron level is not available and symptoms are present

If the patient is in shock, remember to at least type and screen (if not cross match) for blood.
Deferoxamine was derived from streptomyces pilosus.
Ferrioxamin :This complex imparts a reddish, vin rosé, color to the urine
Hypotension and allergic reactions are seen.
ARDS is a known complication and usually limit its use to 24 hours or less.

COMPLICATIONS
Infectious - Yersinia enterocolitica septicemia
Pulmonary - Acute respiratory distress syndrome (ARDS)
Gastrointestinal - Fulminant hepatic failure, hepatic cirrhosis, pyloric or duodenal stenosis

ACETAMINOPHEN
Acetaminophen is the most widely used analgesic-antipyretic medication taken by people in the United States and the world.
or paracetamol, is also known by its chemical name, N -acetyl- p -aminophenol (APAP)

In Great Britain, acetaminophen toxicity is cited as the most common etiology of hepatic failure requiring liver transplantation

CLINICAL
History :
Patients with acetaminophen-induced hepatotoxicity present in 4 clinical stages :

Stage I 0-24 hrs
Early symptoms
Mild
Neurologic, respiratory, and cardiac symptoms are rare in stage 1. If CNS involvement and/or severe metabolic acidosis (elevated anion gap) are present, consider co-ingestants
Nausea, vomiting, malaise and diaphoresis.
Normal bilirubin Transaminases and PT but may elevate after 12 hrs Post Ingestion

Stage 2 (24-72 h )
Stage 1 symptoms become less evident or resolve.
pain and tenderness in the right upper quadrant. (hepatomegaly) can be present. Some patients may report (oliguria).
Serum studies reveal elevated ALT and AST levels, (PT), and bilirubin values.
RF may also be present and indicate nephrotoxicity

Stage 3 (72-120 h)
Stage 3 develops 3-5 days after ingestion
Severe toxicity is evident on sera laboratory studies. Lactic acidosis, prolonged PT or (INR), markedly elevated ALT and AST ( > 10,000 IU/L )
Death is most common during stage 3, with multiorgan failure as the primary cause

Stage 4 (5-14 d)
This stage can last as long as 21 days.
Patients either have a complete recovery or they die.
the period to normalization may take several weeks. Hepatic histiologic can take as long as 3 months to resolve.
DOES NOT cause chronic hepatic dysfunction

PHYSICAL EXAM
Stage 1 : non specific (Pallor, diaphoresis, & dehydration )
Stage 2 : RUQ Tenderness, tachycardia & hypotension
Stage 3 : hepatic injury (abdominal pain, jaundice, and GI bleeding ) Encephalopathy and cerebral edema& MOF
Stage 4 : resolve or death occurs.

Remember the Dose
Aceta = 4 gday for adults
= 80mgKgday for #
Aceta =352-650mg every 4-6hrs for adults
=10-15mgKg every 4-6 hrs for #
For #
Not more than 5 doses
Not more than 2.6g Per Day
# = Children < 12 Years Or < 50 Kg

DIFFERENTIAL DIAGNOSIS
Pancreatitis
Gastroenteritis
Peptic ulcer
Infections
CMV Infection Hepatitis A , B Or C
EBV or Varicella
Amatoxin
Wilson dis.
Reye syndrome

WORKUP
Measurement of acetaminophen serum concentration
Any serum sample drawn 4 hours or longer after a single ingestion may be plotted on (Rumack-Matthew nomogram) to estimate the risk of hepatotoxicity
Measurement of hepatic (ALT) and (AST) hepatic injury is defined by elevation of the plasma transaminases more than 1000 IU/L
Others

TREATMENT
Medical Care
Consider decontamination with activated charcoal in any patient who presents within 4 hours of ingestion. Consider gastric lavage if ingestion occurred within 1 hour of evaluation
Oral N-acetylcysteine (Mucomys)
Intravenous (IV) NAC (Acetadote)
INDICATIONs : altered mental status, GI bleeding and/or obstruction or a history of caustic ingestion, potential fetal toxicity from maternal toxicity, or an inability to tolerate oral
SE : flushing, pruritus, and a rash (15%)
Bronchospasm and hypotension (<2% of patients)

Probable toxicity should be treated with:
N-acetylcysteine bolus 140 mg/kg
Then 70 mg/kg Q 4 hrs for 17 doses.
Assess hepatic function:
On presentation
Daily
Continue other support

SALICYLATES

One teaspoon of 98% methyl salicylate contains 7000 mg of salicylate, the equivalent of nearly 90 baby aspirin and more than 4 times the potentially toxic dose for a child who weighs 10 kg !
consider salicylate poisoning when topical herbal medicinal oil is involved

PATHOPHYSIOLOGY
acetylsalicylic acid is rapidly converted to salicylic acid, its active moiety
salicylic acid is metabolized by the liver and eliminated in 2-3 hours
Salicylate poisoning is manifested clinically by disturbances of several organ systems
Salicylates directly or indirectly affect most organ systems in the body by uncoupling oxidative phosphorylation, inhibiting Krebs cycle enzymes, and inhibiting amino acid synthesis but lipid metabolism is stimulated

GI tract & Hepatic effects : Nausea and vomiting . Hepatitis at or above 30.9 mg/d & Rey syndrome
CNS effects : tinnitus , hearing loss at serum levels of 30-45 mg/dl, seizures, cerebral edema, hyperthermia, coma, cardiorespiratory depression
Acid-base status : normal anion-gap acidosis does not exclude salicylate.
Respiratory system effects 35 mg/dL
Glucose metabolism
Fluid and electrolyte effects : 5-10 %dehydration, Hypokalemia and hypocalcemia ( due to Resp. Alka. )
Hematologic effects Hypoprothrombinemia and platelet dysfunction
Musculoskeletal effects Rhabdomyolysis

Reye syndrome is characterized by acute noninflammatory encephalopathy and hepatic failure of unknown etiology , typically occurs after a viral illness, partic. an (URTI), influenza, Varicella or GE & it is associated with the use of aspirin during the illness .
Diagnostic criteria from the (CDC) :
1) Acute noninflammatory encephalopathy with an altered level of consciousness
2) Hepatic dysfunction with a liver biopsy showing fatty metamorphosis or a more than 3-fold increase in (ALT), (AST), and/or ammonia levels
3) No other explanation for cerebral edema or hepatic abnormality
4) CSF with WBCs (usually lymphocytes) (8 X 10 9 /L or fewer)
5) Brain biopsy with cerebral edema without inflammation

CLINICAL AND LABORATORY MANIFESTATIONS
Phase 1 : hyperventilation respiratory alkalosis and compensatory alkaluria. Both K & NaHCO3 are excreted in the urine. may last as long as 12 hours
phase 2 : paradoxic aciduria occurs when sufficient potassium has been lost from the kidneys. may begin within hours & may last 12-24 hours
Phase 3 : includes dehydration, hypokalemia, and progressive metabolic acidosis. This phase may begin 4-6 hours after ingestion in a young infant or 24 hours or more after ingestion in an adolescent or adult.

HISTORY
When possible take :
Type of salicylate
Amount
Approximate time of ingestion
Possibility of long-term ingestion
Potential co-ingestants
Presence of other medical conditions (eg, cardiac, renal diseases)
The presence of tinnitus is a clue for salicylate ingestion. Tachypnea, tachycardia, and elevated temperature can be detected by evaluating vital sign

DIFFERENTIAL DIAGNOSES
DKA
SEPSIS
Meningitis
Encephalitis
Other TOx

WORKUP LABORATORY STUDIES
Bedside ferric chloride testing (No longer)
ABG: the most common abnormality is a mixed acid-base disturbance
Salicylate concentration: Therapeutic range of salicylate is 15-30 mg/Dl
the peak serum concentration may not occur for 4-6 hours . A 6-hour salicylate level higher than 100 mg/dL is considered potentially lethal and is an indication for hemodialysis
the Done nomogram is regarded as not very useful and is seldom used by clinicians
Others . Repeat every 2 hrs till stabilization !

POTENTIAL SEVERITY AND MORBIDITY OF AN ACUTE, SINGLE EVENT, NONENTERIC-COATED, SALICYLATE INGESTION:
less than 150 mg/kg - ranges from no toxicity to mild toxicity
From 150-300 mg/kg - Mild-to-moderate toxicity
From 301-500 mg/kg - Serious toxicity
Greater than 500 mg/kg - Potentially lethal toxicity

TREATMENT
G astric lavage and activated charcoal are useful for acute ingestions but not in chronic salicylism.
A BCs & lactated Ringer or isotonic Na Cl solution for volume expansion at 10-20 cc/kg/h until a 1-1.5-cc/kg/h urine flow is established
G I tract decontamination :initial dose of activated charcoal is 1 g/kg of body weight to a maximum of 50 g in children and 1-2 g/kg to a maximum of 100 g in adults . If enteric-coated aspirin has been ingested or salicylate levels do not decrease despite charcoal, WBI should probably be used in addition to charcoal
U rinary alkalization the U pH to 7.5-8 . Ion trapping : ions are poorly reabsorbed in the tubules and are excreted more readily. C orrect h ypokalemia and dehydration

HEMODIALYSIS INDICATIONS :
serum level greater than 120 mg/dL (acutely) or greater than 100 mg/dL (6 h postingestion)
refractory acidosis,
coma or seizures,
noncardiogenic pulmonary edema,
volume overload
renal failure.
In chronic overdose, for a symptomatic patient with a serum salicylate level greater than 60 mg/dL.
Peritoneal dialysis is only 10-25% as efficient as hemodialysis

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Pediatrics drug poisoning

by CarDioSurgeon Doc. on Nov 05, 2010

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Pediatrics drug poisoning — Presentation Transcript