Download Poisoning in Children

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Transtheoretical model wikipedia , lookup

Transcript
Poisoning in Children
Poisoning in Childhood
• 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.
Poisoning in Children
• Ingestion of a harmful substance is
among the most common causes of
injury
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
– How has the patient behaved since the ingestion?
• Does the patient have a history of substance abuse?
Management
General measures:
• Quick assessment & triage
• Limit absorption:
– Vomiting
– Lavage
– Activated charcoal instillation
Specific:
ABC’s of Toxicology:
• Airway
• Breathing
• Circulation
• Drugs:
• Resuscitation medications if needed
• Universal antidotes
• Draw blood:
•
•
•
•
• chemistry, coagulation, blood gases, drug levels
Decontaminate
Expose / Examine
Full vitals / Monitoring
Give specific antidotes / treatment
• Decontamination:
1.Ocular:
– Flush eyes with saline
2.Dermal:
– Remove contaminated clothing
– Brush off
– Irrigate skin
3.Gastro-intestinal:
– Activated charcoal:
– May Prevent /delay absorption of some drugs/toxins
– Almost always indicated
– Naso/oro-gastric Lavage
– Bowel Irrigation:
– Recent ingestions 4-6 hrs
– 500 cc NS Children / 2000cc adults
– Orally / Nasogastric tube
poising Treatment
– Do not induce vomiting
– Do not attempt gastric lavage
– Risk of aspiration outweighs any benefit from
removal of substance
– CXR around 2-4 hrs “not before 2hrs”
– Observe in ER for 6-8 hrs
Preventing
• Education is the major component of
any poison prevention programme.
• Keep medicines, insecticides, etc…
out of the reach and sight of your
children.
• Never store food & cleaning products
together. Store medicine and
chemicals in original containers.
Hydrocarbon Poisoning
• These may be divided into aliphatic
or aromatic compounds. Aliphatic
hydrocarbons include kerosene,
turpentine, lubricating oils, tar and
have greatest risk of aspiration and
pulmonary symptoms. Aromatic
compounds have mainly neurological
and hepatic toxicity and include
benzene compounds.
• Type of toxicity with a hydrocarbon
depends on its volatility, viscosity or
surface tension. The lower is
viscosity, more is the risk of
pulmonary aspiration. Mineral spirit,
kerosene and furniture polish have
both low volatility and viscosity and
thus carry a higher risk of aspiration
pneumonia.
• Benzene derivates, toluene and xylene are
components of various solvents and
degreasers. These are highly volatile but
have low viscosity. Inhalation is the
primary route of toxicity which manifests
with CNS symptoms. Gasoline and naphtha
are constituents of lighter fuel and lacquer
diluent and primarily cause depression of
the central nervous system (CNS).
• Turpentine oil is highly volatile but has low
viscosity also. Toxicity results from inhalation and
gastrointestinal absorption. They can also cause
CNS toxicity.
• Halogenated hydrocarbons are used as solvents
and spot removers. Freon is used as a refrigerant.
• Toxic exposure to hydrocarbons may result in
cardia, gastrointestinal, neurological, pulmonary,
renal, hepatic, metabolic and hematological
manifestations.
• Induced emesis or gastric lavage is
contraindicated for kerosene oil
poisoning. It is done only when large
quantities of turpentine have been
ingested or the hydrocarbons product
contains benzene, toluene,
halogenated hydrocarbons, heavy
metals, pesticides or aniline dyes.
Other specific modalities including
steroids and antibiotics are not
efficacious.
KEROSENE POISONING
•
•
•
•
Epidemiology
Clinical features
Investigation
Treatment
Clinical features
• Age – 1 to 3 years
more than 70% symptomatic within
10 hours
SYMPTOMS
RS – breathlessness, cough
CNS – convulsions, coma
GPE – fever, restlessness, cyanosis
GI – vomiting, diarrhea
Kerosene poising
• Kerosene ingestion:
– Risk of aspiration
– GIT & Respiratory effects.
– Burning sensation, nausea and diarrhea
– Cough, chocking, gagging and grunting.
– CXR 2-8 hrs later: Pulmonary infiltrates or
perihilar densities.
– pneumatoceles, pleural effusion or
pneumothorax and bacterial superinfection
– Resolution 2-7 days.
Lab Investigations
• Blood – Leukocytosis
X – Ray changes
Changes appear within one hour
- commonly right basal infiltrates
- emphysema
- pleural effusion
- pneumatocoeles
Management
• Avoid emetics
• Avoid gastric lavage – In case of massive
•
•
•
•
•
•
amount use a cuffed endotracheal tube
After lavage leave magnesium or sodium
sulphate in the stomach
Oxygen may be useful
Assisted Ventilation
Antibiotics - Penicillin
Kanamycin
Steroids – Not helpful
Complications
•
Pneumothorax
• Pneumatocoeles
• Pleural effusion
• Bronchopneumonia
• Coma
Organophosphorus Poisoning
• Organic phosphate insecticides cause
irreversible inhibition of the enzyme
cholinesterase. As result
acetylcholine accumulates in various
tissues. Excessive parasympathetic
activity occurs. These agents are
absorbed by all routes including skin
and mucosa.
• Symptoms manifest quickly usually within
a few hours and include weakness, blurred
vision, headache, nausea, and pain in
chest. These patients have excessive
secretion in the lungs and they sweat
profusely. Salivation is marked. Pupils are
constricted and papilledema may occur.
Muscle twitching, convulsions and coma
occur in severe cases. Reflexes are absent
and sphincter control is lost.
Treatment
• If the insecticide was in contact with skin
•
or eyes, these are thoroughly washed.
Stomach wash is done.
Atropine sulphate: 0.03 to 0.04 mg/kg IV
(atropine sulphate is usually available in
ampules 1 in 1,000 or 1 mg/mL). Other
strengths may also be available. Repeat
half the dose in 15 minutes and if
necessary every hour (until signs of
toxicity appear), subject to a maximum of
1 mg/kg in 24 hours.
• Pralidoxime (PAM) is given in dose of 25-
50 mg/kg IM or IV over 30 min infusion.
The dose may be repeated in 1-2 hours,
then at 6-12 hour intervals as needed.
Monitor for hypertension. Never inject
morphine, theophylline, aminophylline or
chlorpromazine. Intravenous fluids should
only be given with caution. No oral
tranquilizers are administered. Artificial
respiration may be necessary to sustain
life.
• Metabolic acidosis supervenes
quickly due to disturbances of
oxidative phosphorylation and
reduction of hepatic glycogen with
resultant ketonemia. The patients are
treated with adequate replacement
of fluids to restore renal function.
• Urine is alkalinized by administering
1-2 mEq/kg of sodium bicarbonate at
half hourly intervals for 4 hours to
promote excretion of urine, because
in alkaline urine, salicylates do not
diffuse back into the tubular cells
from the lumen. Potassium salts
should be given (3-5 mEq/kg/day) to
replace the potassium losses
paracetamol
• It is safe in pharmacological doses.
Overdosage may cause hepatic
damage. Acetaminophen overdosage
is treated with acetylcysteine to be
used orally within 16 hours after
ingestion in a loading dosage of 140
mg/kg diluted to 5 percent solution
orally followed by 70 mg/kg q 4h for
another 16 doses.
Carbon Monoxide Poisoning
• Carbon monoxide poisoning results from
inhalation of fire smoke, automobile
exhaust, fumes from faulty gas stoves and
ingestion of paint and varnish removers.
Clinical manifestations include headache,
cyanosis, convulsions, and coma. Patients
are administered 100 percent oxygen and
if carboxyhemoglobin levels are above 40
percent, hyperbaric oxygen therapy is
considered.
• The label should be read before using the
•
drug. No drug should be given or taken in
the dark. Drugs after their expiry date
should be disposed in a safe manner.
Avoid taking medicine in your child’s
presence. Never suggest that medicine is
candy.
Children should be taught not to eat plants
or berries.
Iron Intoxication
• Ingestion of a number of tablets of ferrous
sulphate may cause acute poisoning.
Lethal dose is 300 mg/kg of iron. Severe
vomiting and diarrhea occur. These may
contain blood due to extensive
gastrointestinal bleeding. The child may go
into severe shock, hepatic and renal failure
within a few hours or after a latent period
of 1 to 2 days
Iron Poisoning
• Five Stages but variable
– Stage 1
•Gastro-intestinal stage: within several
hrs of ingestion:
–abdominal pain
–Severe: fluid loss, bleeding,
shock(acidosis, tachycardia +/hypotension)
–Fever. Lethargy. Coma
Iron Poisoning
• Stage 2
–Quiescent stage: 4-48hrs
•Clinical improvement
•Subtle hemodynamic changes:
–Tachycardia
Iron Poisoning
• Stage 3:
–Circulatory collapse : 48-96 hrs
•Metabolic acidosis, hypotension, low
Cardiac output.
•Coagulopathy
•Multiorgan system failure
Iron Poisoning
• Stage 4:
–Hepatic failure: 96 hrs
•Increased mortality
•Rarely fulminant hepatic failure
•Hepatic necrosis
–Liver transplant can save lives
Iron Poisoning
• STAGE 5:
–Bowel obstruction 2-6 wks
–Due to scarring
•Gastric outlet obstruction
•Small intestinal obstruction
–May not pass through stage 4
Treatment
• Vomiting should be induced and stomach
should be washed with sodium
bicarbonate solution. Shock is corrected by
infusion of fluids parenterally. Three mL of
7.5 percent sodium bicarbonate solution
per kg of body weight are diluted with 3
times its volume of 5 percent glucose
solution and injected intravenously for
treatment of acidosis. This dose may be
repeated after an hour if acidosis is
persisting.
• Iron salts are chelated with
desferrioxamine IV at 15mg/kg/hour until
the serum iron is <300 mg/dL or till 24
hours after the child has stopped passing
the characteristic ‘vin rose’ colored urine.
Presence of ‘vin rose’ color to urine
indicates significant poisoning.
Iron Poisoning
Management:
1. Gastric decontamination:
• Forced emesis
• Gastric lavage with 5% NaHCO3
• No activated charcoal
2. Secure good IV
3. Get initial the 4hrs levels and TBC
4. Chelate with Deferoxamine if levels>
300mg/dL
Iron Poisoning
• Chelate with Deferoxamine:
– Stable pts : levels< 500 mg/dL 40mg/kg
IM/IV
– Unstable: bleeding/ level > 500
• Give 20cc/kg NS/RL
• Deferoxamine at 15 mg/kg IV over 1hr
• Continuous drip at 15mg/kg/hr
• Continue till “vin rose” urine color
disappears.
Iron Poisoning
• Observe for:
– Systemic BP
– ECG
• Signs of hepatic failure:
– Bleeding
– Glucose intolerance
– Hyperammonemia
– Encepalopathy
SALICYLATES
• Oral ingestion commonest
• Transdermal less
• Peak levels at 12 hrs
– Early : hyperpnea  respiratory alkalosis
– Then metabolic acidosis
– Severe cases: Cerebral edema and increased
ICP
Salicylate Poisoning
• Ingestion of 150 mg/kg of salicylates
•
causes intoxication. Salicylate level of 5080 mg/dL causes moderate symptoms.
Severe symptoms are associated with
blood levels above 80 mg/dL.
Initially, there is a respiratory alkalosis,
because of hyperventilation induced by
sensitization of the respiratory center by
salicylates. Kidneys compensate for this
alkalsis by increasing the excretion of
sodium and potassium bicarbonate
SALICYLATES
• MANAGEMENT
– Treat electrolyte imbalance
– IV hydration
– Hemodialysis
– Diuretics