Download Common poisoning in childhood

Common poisoning in childhood
1-Acetamiophen.
2-Salicylate .
3-Caustic ingestion .
4-Hydrocarbons .
5-Choline esterase inhibitor(insecticide).
Acetaminophen
 1) the most widely used analgesic and antipyretic in
paediatrics (due to relationship between Reyes syndrome and
salicylate).
 2) available in multiple formulations and different strengths,
is commonly in the home where it can be unintentionally
ingested by young children (good taste,chewable tables) or
taken in an intentional over dose by adolescent and adult
 3) acetaminophen intoxication is a common cause of acute
liver failure in adolescent and adult .
PathophysiologY
-Acetaminophen toxicity result from formation of N_ACETYLPENZOQUINONEIMINE(NAPQI) .
-When therapeutic dose are administered small amount (4%) of dose is
metabolized by hepatic cytochrome P450 to NAPQI ,Which is
conjugate with glutathione to form harmless mercapturic acid
conjugate.
-when hepatic store of glutathione are depleted to <70% of normal , the
NAPQI can combined to the hepatic macromolecules to produce
hepatocellular damage.
- The acute toxic dose of acetaminophen is >200mg/kg
- -single injection of 7.5mg is considered a minimal toxic dose for
adolescent and adult.
- -repeated administration of >60mg/kg /day for consecutive days may
lead to hepatic injury or failure in some children .
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Clinical and laboratory manifestation
 It consist of 4 stage :
 1) stage one : (30min to 24h): anorexia ,nausea ,vomiting
pallor, malaise and diaphoresis.
 2) stage two:(24h-48h): resolution of GIT symptoms ,right
upper quadrant abdominal pain and tenderness ,elevated
bilirubin , PT, hepatic enzymes , oligurea .
 3) stage three: (72h-96h) :peak liver function abnormalities
,anorexia, nausea ,vomiting and malaise.
 4)stage 4(4d-2w): resolution of hepatic dysfunction or
complete liver failure.
 - if a toxic ingestion is suspected the plasma acetaminophen
concentration should be measured 4h or more .
 Measurement earlier than 4h after ingestion maybe useful to
determine if ingestion has occurred, but it cant be used to
determine the severity of an overdose. The plasma
acetaminophen should be plotted on rumack-matthew
nomogram to determine whether antidotal treatment is
indicated or not.
INVESTIGATION
 LIVER FUNCTION TEST .
 HEPATIC ENZEMES .
 BILIRUBIN .
 ACETAMINOPHEN CONCENTRATION .
TREATMINT
 After a large acute oral overdose and when the need for antidotal
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treatment is determined , treatment should be started as soon as
possible within 1-2h of ingestion .
The antidote for acetaminophen is N-ACETYL CYSTIEN (NAC)
which serve as a precursor for hepatic glutathione synthesis
,replenishing glutathione stores and prevent NAPQI REACTION
with hepatocyte .
NAC is effective when administered early in the courseof
intoxication (8h),but may have value even if started 24-36h after
ingestion in sever cases .
NAC DOSE= 140mg/kg(loading dose)
70mg/kg/4h (maintenancedose)(total 17 dose )
Salycylate
-INCIDENCE : salicylate poisoning is low,
particularly in young children , because the use
of an alternative antipyretics has increased in
an effort to avoid Reyes syndrome .
-the common use of baby aspirin for
cardiovascular prophylaxis places the drug in
many home environment and thus make it
available for accidental poisoning .
 Pathophysiology:
 1-uncoupling oxidative phosphorylation .
 2-inhibit kerbs' cycle enzymes .
 3- inhibit amino acid synthesis .
 4-decrease platelet adhesiveness .
 5- increased pulmonary capillary permeability.
 The acute toxic dose of salicylate toxicity is generally
considered > 150mg/kg for mild symptoms and >
300mg/kg for moderate to sever symptoms .
Clinical and laboratory manifestations
 Chronic toxicity result in a symptoms and sign that are easily
attributed to other causes, such as flu or other febrile illness.
 Young children are more susceptible to toxic effect because they are
less able to buffer the acid load produced by salicylate.
 After acute salicylate ingestion ,nausea and vomiting occur due to
gastric irritation .
 Salicylate directly stimulate the respiratory system leading to
hyperventilation and hyperpnoea. An increased respiratory rate result
in respiratory alkalosis with compensatory alkalurea, both potassium
and sodium bicarbonate are excreted in the urine however soon after
the exposure the serum potassium concentration maybe in the normal
range . When sufficient potassium has been lost through the kidneys
,an exchange of potassium for hydrogen ion occur and the urine
becomes relatively acidic.
 This paradoxical acidurea occur in the presence of continued
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respiratory alkalosis.
Dehydration and progressive metabolic acidosis, caused by
the accumulation of lactic acid and other metabolic acids,
eventually develop .
Seriously poisoned patients are >5-10% dehydrated .
Patients with chronic salicylate poisoning usually present
with metabolic acidosis.
Important signs of serious toxicity are CNS changes .
Agitation, restlessness, and confusion are common in
children.
Coma may develop as a result of cerebral edema.
Pulmonary edema or haemorrhage may develop in sever
cases.
 Hyperglycemia in acute toxicity or hypoglycedmia in chronic
toxicity , particularly in infants has also been observed.
 Hepatotoxicity occur after chronic exposure or with very
large acute ingestions.
 Causes of death : pulmonary edema and respiratory failure,
cerebral edema, haemorrhage, sever electrolyte imbalance,
cardiovascular collapse .
Investigations
 Serial salicylate concentrations initially at 4hr post ingestion and
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then every 3-4hr ,should be monitored to evaluate for either
continued absorption or impairment excretion.
After acute ingestion, patients with serum salicylate concentration
of >20mg/dl should undergo continued observations and
monitoring.
Acute serum concentration of >70-100mg/dl may produce lifethreatening effects.
Urine PH and volume should be measured hourly in all seriosly
poisonied children .
Plasma PH ,glucose ,potassium and other electrolytes should be
monitored at regular intervals .
Clotting studies and liver function test should also be closely
monitored in all severely poisoned patients .
Treatment
 Gastric decontamination preferably with activated charcoal if
the patients presents soon after an acute ingestion.
 gastric decontamination is typically not useful after chronic
exposure .
 Intial therapy focuses on aggressive rehydration and
correction of electrolyte abnormalities.
 Large quantities of potassium and bicarbonate may be needed
if symptoms have been present for sometime after an acute
ingestion or in case of chronic salicylate poisoning because
body stores of these electrolytes maybe severely depleted.
 Urinary excretion of un-metabolized salicylate become an
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important route in elimination in over dose.
Urinary clearance is affected by urine PH.
Urinary salicylate elimination can be increased using ion-traping
by increasing urinary PH to convert salicylate into the ionized
form which is excreted in urine, and thus decrease CNS
penetration because un ionized drugs cross the BBB.
Each one unit increase in urine PH increase urinary salicylate
clearance 4 fold .
Urine PH should increase to 7-7.5 using IV BICARBONATE .
In sever cases DIALYSIS to remove salicylate and to correct
electrolyte abnormalities (change in neurological status, salicylate
concentration >90mg/dl, cardiovascular instability, refractory
metabolic acidosis, sever hypokalemia, renal failure ).
Caustic ingestion
 Caustic include acids and alkalis.
 Acid coagulate protein causing local tissue necrosis which
limits its tissue penetration.
 Alkalis digest and dissolve protein producing transmural
liquefaction necrosis with risk of perforation .
 The severity of chemical burn produced depend on PH ,
CONCENTRATION OF AGENT, LENGTH ON
CONTACT TIME .
 Agent with PH <2 >12 are most likely to produce significant
injury .
Clinical manifestation
 Oral burn ,redness area or whitish plaque .
 Pain, drooling, vomiting and difficult swallowing or refusal to
eat.
 Circumferential burn of the oesophagus are likely to cause
stricture on healing which may require repeated dilation or
surgical correction.
 Strong acid may produce scarring around the pylorus leading
to gastric obstruction.
 Caustic on the skin or the eyes can cause significant tissue
damage .
Treatment
 Removal of the product from the skin or eyes by flushing .
 Contaminated clothes should also be removed .
 Ingested agent should be rinsed from the oral cavity .
 Emesis and lavage are contraindicated.
 Activated charcoal should not be used( may lead to vomiting
and possible aspiration).
 Endoscopy should be performed in symptomatic or those
whom injury is suspected on the basis of the history.
 The use of CORTICOSTEROID is controversial.
 Prophylactic antibiotic don't improve the outcomes.
Hydrocarbons
 Include a wide array of chemical substance found in thousands of
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chemical product.
The most important adverse effect of hydrocarbons is aspiration
pneumonitis .
Aspiration usually occur at the time of ingestion when coughing
and gagging are common ,but can also be secondary to vomiting .
The propensity of hydrocarbons to cause aspiration pneumponitis
is inversally proportional to its viscosity .
Compound with low viscosity such as miniral spirit, kerosine,
gasoline, lamp oil spread rapidly a cross surface and cover large
area of the lung when aspirated .
 Only a small quantities <1ml of low viscosity hydrocarbons
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need be aspirated to produce significant injury .
Pneumonitis doesn't result from dermal absorption of
hydrocarbons or from ingestion in absence of aspiration.
Most of hydrocarbons have anaesthetic properties and can
cause transient CNS depression (halogen compound ).
Chlorinated solvent (carbon tetrachloride) can produce
hepatic toxicity .
Benzene is known to cause cancer in human (AML) and bone
marrow suppression .
Clinical and laboratory manifestation
 Transient mild CNS depression is a common after
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hydrocarbons ingestion .
Aspiration is characterized by coughing which usually the
first clinical finding (cough usually begins immediately or
within 5 minute of aspiration and persist).
Respiratory symptoms may remain mild or may progress
rapidly to respiratory failure .
CXR maybe normal for 8-12hr after aspiration but more
often will be posetive after 6hr of exposure .
Fever occur and may persist for 10 days with leukocytosis
(maybe misleading because no bacteria present in the lung).
 CXR may remain abnormal for long time and they shouldn't
be used to guide acute treatment.
 Pneumatocele may appear on CXR 2-3week after exposure.
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Treatment
 Emesis is contraindicated .
 Gastric lavage is contraindicated (if gastric lavage had been
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performed the patient should be intubated with cuffed tube
to protect the airways from further aspiration).
Activated charcoal also is not useful.
If the patient develop pneumonitis the treatment is
supportive .
Corticosteroid should be avoided ( increase risk of infection).
Prophylactic antibiotic shouldn't be given because bacterial
pneumonia occur in a small percentage of cases.
Choline esterase inhibitor
(insecticide)
 The most commonly used insecticide are organo-phosphate
and carbamates.
 Both are inhibitors of cholinesterase enzymes.
 Nerve agent used in war fare are usually organophosphate.
 Most pediatrics poisoning occur as the result of accidental
exposure to insecticide in or around the home or farm.
pathophysiology
 Both organophosphate and carbamate bind to cholinesterase
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enzymes preventing the degradation of acetylcholine resulting in
its accumulation at nerve synapses .
Enzymes affected include acetylcholine esterase in RBCs,
PLASMA and nervous system.
Organophosphate form permanent bond to these enzymes,
inactivating them (this process is called aging, which may occur as
soon as 18hr -3d after exposure).
A Period of weeks to months is required to regenerate the
inactivated enzymes .
Carbamates form temporally bond to the enzymes allowing
regeneration of the enzymes over several hours .
Clinical manifestations
(DUMB BELS)
 Muscarinic symptoms and sign include: diaphoesis, emesis,
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urinary and faecal incontinence, tearing, drooling, bronchorrhea
and bronchospasm, miosis, hypotension and bradycardia .
Nicotinic symptoms and sign include: muscle weakness,
fassiculation, tremors, hypertension, tachycardia and dysrhythmia.
CNS symptoms include : malaise, confusion, delirium, seizures
and coma.
DUMBBELS which is stand for diarrhea, urination, miosis,
bronchrrhea,bronchospasm,bradycardia, emesis,lacremation and
salivation .
Sever manifestation include : coma, seizures, shock, arrhythmia
and respiratory failure.
Investigation
 Red blood cells cholinesterase is abetter reflection of
enzymes activity in the nervous system and used mainly to
document the exposure.
 Significant symptoms don't occur until measured enzymes
concentration fall to< 25% of normal level .
Treatment
 Basic decontamination (washing all exposed skin with swap and
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water and immediate removal of exposed clothing).
Activated charcoal can be used for gastric decontamination .
Fluid, electrolyte replacement and intubation if necessary.
2 antidote are useful (ATROPINE and pralidoxime).
Atropine (antagonizes the muscarinic effect, is useful for both
organophosphate and carbamate intoxication ).
Large dose of ATROPINE must be given by intermittent bolus or
continuous infusion .
Pralidoxime break the bond between organophosphate and the
enzymes (only effective if used before the bond ages become
permenant).
For significant poisoning both antidotes are used and a large dose
of atropine is necessary .
Signs of atropinization
 1- flushing .
 2- mydriasis .
 3- tachycardia.
 4- dry mouth and nose .
Common antidotes for poisoning
ACETAMINPHEN
N-ACETYL CYSTEIN
ORGANOPHOSPHATE and CARBMATES
ATROPINE
DIGOXIN
FAB-AB (DIGIBIND)
IRON
DEFEROXAMINE
METANOL
ETHANOL
BENZODIAZEPENES
FLUMAZENIL
MET-HEMOGLOBINEMIA
METHYLENE BLUE
NARCOTICS
NALOXONE
CO
O2
COUMARINE
VITK
 IPECAC INDUCED EMESIS IS CONTRAINDICATED
AFTER THE INGESTION OF CAUSTICS,
HYDROCARBONS, AGENTS LIKELY TO CAUSE RAPID
ONSET OF CNS OR CVS SYMPTOMS.
 ACTIVATED CHARCOAL ARE NOT USEFUL IN HEAVY
METAL , IRON, LITHIUM, HYDROCARBONS, CYANIDE
AND ALCOHOL INTOXICATION.
THANK YOU
DR.MURAD ALBATAINEH