Transcript POISONING - Netmedico | A medico hangout

POISONING
Dr. M.L.Siddaraju
History
• Egyptians are said to have studied many poisons as early
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as 3000BC.
Among vedas- Atharvana veda (1500BC) describes
poisons.
Susrutha (350BC) described as how poisons were mixed
with food and drink, medicines, snuff, etc..
Italians brought the art of poisoning to its zenith prior to
6th century AD.
Orfila-(1787-1853) was first to attempt a systemic
correlation between the chemical and biologic information
of the poisons known then.
Others who worked are Marsh, Magendie, Ambrose,
Scheelle, Robert Christison and Rudolf Kobert.
POISONING IN CHILDREN
• Poison is a substance that causes harm
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if it gets into the body.
The poisoning in children could occur
due to diverse causes and could be
classified as
– accidental,
– homicidal or
– suicidal.
• Erroneous administration of
overdosage of drugs by the parents or
by the medical staff is also frequent.
• Acute exposure is a single contact that
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lasts for seconds, minutes or hours, or
several exposures over about a day or less.
Chronic exposure is contact that lasts for
many days, months or years.
A poison may get into the body through
ingestion, inhalation (gas, vapors, dust,
fumes, smoke, spray), skin contact
(pesticides), or injection (bites and stings,
drug injection
• Accidental poisoning in children is a
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global problem. The relative importance
of poisoning as a cause of childhood
morbidity and mortality increases when
malnutrition and infections are brought
under control.
Accidental poisoning is the twelfth
leading cause of admissions in pediatric
wards in India and accounts for about
one percent of the hospitalized patients.
Most cases of accidental poisoning are
preventable. Continuing morbidity and
mortality due to accidental poisoning is
serious challenge to the pediatricians
and public health officials.
Pattern of poisoning
• Chemical products, most often swallowed
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by children include household cleaners
(bleach, detergents) fuel (kerosene,
paraffin), cosmetics, medicines, paints and
products for household repairs and
household pesticides.
Bites and stings of animals and insects,
and ingestion of poisonous plants and
seeds also considerably account for
outdoor poisoning in children.
• Carbon monoxide poisoning can
happen when fires, stoves, heaters or
ovens are used in rooms, huts which
do not have proper ventilation to let
the gas out.
Ecology of poisoning
• Interaction between the host and the
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environment (including easy access to the
poisonous substances) determines the magnitude
of the problem.
Age. About 40% of all cases of accidental
poisoning in children are reported in the second
year of life; about 12% of the cases occur in the
first and 20% in the third year. As the children
start crawling and walking around 1 year, they
become very active and try to explore unfamiliar
objects by putting these into their mouth and
testing these. Thus they expose themselves to
accidental poisoning. Hyperactive male children
are more prone to accidental poisoning.
• Large families:In large families mother
is often too occupied with household
chores, is easily fatigued and often
careless in storage of potentially
poisonous household substances.
• Small accommodation
• Environment: Lead poisoning is common in
children living in areas were there are
workshops for automobile, lead storage
batteries or for manufacture of lead typesets
for printing presses. Caustic soda poisoning
used to be observed frequently in children of
families, which prepared washing soap for
domestic or commercial purposes in their own
houses. Insecticides, medicines, naphthalene
balls and kerosene are common household
things which are potential hazards.
• Rural or Urban areas:
• The pattern of poisoning varies in rural and
urban areas due to exposures to different
types of potential poisons. Snakebites are
more common in those wandering in
fields.Also pesticides are more common in
rural set up. The poor are driven by starvation
to experiment on roots and fruits thus leading
to poisoning.
• Time relationship:
• . Accidental poisoning is likely when
normal routine in the house is
disturbed such as during periodic
house painting, packing and
unpacking at the time of change of
residence, going for vacation etc.
Classification of poisons
Based on the chief symptoms they produce
1. Corrosives- strong acids, strong alkalis,
metallic salts.
2. Irritants- organic, inorganic.
3. Systemic- cerebral, spinal, peripheral,
CVS, asphyxiants.
4. Miscellaneous- food poisoning &
botulism.
Non toxic common
household agents
• Shampoos, toothpaste, lipstick,
creams, shaving cream, toilet soaps,
cosmetics, hair dye/oil.
• Antacids, house lizards, non nitrate
fertilizers, newspaper, adhesives,
water colors, chalk, ink (ball point/
fountain pen), candles.
Important causes of child
poisoning in India
• Kerosene and other hydro carbons(8-55%)
• Household products-insecticides, rodenticides,
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phenol, alkalis, turpentine, camphor,
naphthalene, neem oil, alcohol(14-30%).
Drugs- iron salts, barbiturates, anticonvulsants,
antihypertensives, aspirin, antiseptics(16-30%).
Plant and plant products- Dhatura, castor
seeds(6-32%).
Food poisoning(7-15%).
Venomous bites & stings(7-11%).
History taking
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What poison was ingested.
Time since ingestion.
Total amount of poison ingested.
Route of exposure.
Progression of signs and symptoms since
ingestion.
• Family history of epilepsy, mental sub normality,
bleeding disorder.
• Whether the patient is receiving other
medications which may interact with the poison.
General signs and symptoms
• Symptoms-odor, sweating, fever,
delirium, convulsions, burns of
mouth, blindness, GI symptoms,
abnormal movements, coma.
• Signs- miosis, mydriasis, blindness,
facial twitching, dull & mask like
expression, pallor, cyanosis,
hypothermia, sweating, respiratory
symptoms, CVS symptoms, CNS
symptoms.
Poisoning severity Grades
• None(0)- no symptoms or
signs/vague symptoms judged
not to be related to poisoning.
• Minor(1)- Mild, transient &
spontaneously resolving
symptoms.
• Moderate(2)- pronounced or
prolonged symptoms.
• Severe(3)- severe or life
threatening symptoms.
Diagnosis of Poisoning
• Cardiac arrythmias. Tricyclic
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antidepressants, amphetamine, aluminium
phosphide, digitalis, theophylline, arsenic,
cyanide, chloroquin.
Metabolic acidosis. Isoniazid, methanol,
salicylates, phenformin, iron, cyanide.
GIT disturbances. Organophosphorus,
arsenic, iron, lithium, mercury.
Cyanosis. Nitrobenzene compounds,
aniline dyes, and dapsone.
Basic Management of a
poisoned patient
• Antidotes are available for very few
commonly encountered poisons, and
treatment is usually non-specific and
symptomatic. In such cases
management consists of emergency
first aid and stabilization measures,
appropriate treatment to reduce
absorption, measures to enhance life
support followed by psychiatric
counseling.
Identification of Poison
• Identify the poison by careful history
and helpful clues. Determine what,
when and how much of the poison
was ingested or inhaled. Find the
supporting evidence for your
diagnosis from the nature of the
symptoms and physical signs. Some
common toxidromes based on certain
signs and symptoms :
Pupils
Pinpoint
Resp
Consci Possible agent
ousne
ss
Other
associations
Coma Organophosphorus
insecticides,
carbamates
Cholinergic:
bradycardia,
wheeze,
salivation
Hypotension,
hypothermia
Cardiac
arrhythmia
Coma Opioids
Coma Phenothiazines
Dilated
Agitation,
hallucination
Atropine
Coma
Tricyclic
antidepressants
Coma
Sedatives,
barbiturates
Agitation,
hallucination
Theophylline,
amphetamines
Anticholinerg
ic; fever, dry
mucous
membranes,
flushing,
urinary
retention
Cardiac
arrhythmia,
seizure
,hypotension
Hypotension,
hypothermia,
hyporeflexia
Seizures,
tachcardia,
hypertension
, acidosis
Normal
Coma
Uremia
Acidosis,
hyperkalemia
Coma
Salicylates
Tinnitus,
agitation,
diaphoresis,
alkalosis
followed by
acidosis
Principles of Management
• Keep the phone numbers of your doctor, hospital
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& emergency medical system near the phone.
Removal of the patient from the site of poisoning.
Initial resuscitation and stabilization.
Symptomatic and supportive measures.
Removal of unabsorbed poisons- from GI tract or
from skin, eye.
Hastening the elimination of absorbed poisons.
Use of specific antidote if available
Disposition of the patient with advice for
prevention.
Emergency Stablization Measures
• The unconscious patient should be transported
in the headdown semiprone position to minimize
the risk of inhalation of gastric contents. A clear
airway is established and ventilation is
maintained. Potentially serious abnormalities
such as metabolic acidosis, hyperkalemia and
hypoglcymia may require correction as a matter
of urgency. Neurological assessment is made by
calculating the Glasgow Coma Score (GCS).
• Many drugs and poisons can cause grand mal
convulsions, which, if repeated, should be
controlled with intravenous diazepam.
Hypotension with peripheral circulatory failure is
treated first by correction of hypoxia and acidosis,
and by elevation of the foot end of the bed. If
adequate perfusion is not restored by these
measures, the circulating volume should be
increased by administration of a plasma expander
intravenously. Cardiac arrhythmias are often
improved or abolished by correction of hypoxia,
acidosis and electroyte imbalance
Initial resuscitation
stabilization
• Includes airway- proper positioning head tilt and
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chin lift, suction of secretions from oropharynx,
falling back of tongue is prevented by suitable
airway tube.
Breathing- oxygen via a mask, when gag/cough
reflects is absent- ET tube inserted. if necessary
positive pressure ventilation with ABG
monitoring, respiratory stimulants for severe
respiratory depression.
Circulation- proper IV access, maintenance of
fluid & electrolyte balance, IV drugs for
treatment.
Symptomatic & supportive
Management
• Hemodynamic support- elevation of foot
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end of the bed, oxygen administration, IV
fluids, blood products.
Cardiac dysrrhythmias- correction of
hypoxia, acidosis, hypokalemia, ECG,
treatment with antiarrhythmic drugs.
Convulsions- correction of
hypoglycemia/hypocalcemia/hypoxia/cere
bral edema and other metabolic defects,
anticonvulsant therapy.
Continued…
• Management of hypothermia- cover with a
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blanket, thermo neutral environment
maintenance, pre warmed IV fluids and
inspired gases.
Management of pulmonary edemaadminister 100% oxygen, intermittent
positive pressure ventilation, IV
aminophylline(5-8mg/kg), IV
frusemide(1-2 mg/kg).
Continued…
• Management of stress ulcers- NG
intubation, cold saline wash,
administration of antacids, H2receptor antagonists.
• Management of pain- analgesics
(preferably- narcotics).
Removal of Toxin
• The aim of decontamination procedures is
to reduce the absorption of poison. It can
be achieved by:
– Eye decontamination. Ocular exposure to
solvents, e.g., hydrocarbons, detergents, and
alcohol, or corrosive agents, e.g., acid or alkalis
require immediate local decontamination. This
is achieved by copious irrigation with
neutralizing solution (e.g., normal saline or
water) for at least 30 minutes. Do not use acid
or alkaline irrigating solution.
– Dermal decontamination. Absorption of
organophosphorus and related
compounds through cutaneous route
can prove to be a fatal as oral route
absorption. Cutaneous absorption
depends on several factors such as lipid
solubility, skin condition, location,
caustic effect, physical conditions
• Remove all contaminated clothes and irrigate the
whole body including nail, groin, skinfolds with
water or saline as soon as possible after exposure
and continue irrigating for at least 15 minutes.
Water should not be used to decontaminate skin
in exposures to sodium and phosphorus. In
certain cases, specific agents may be indicated for
skin decontamination (e.g., mineral oil for
elemental sodium, Neosporin for super glue and
calcium gluconate for hydrofluoric acid).
• Gut decontamination. This includes (i) gastric
evacuation; (ii) adsorbent administration; and
(iii) catharsis. Emesis is the preferred method of
emptying the stomach in conscious children.
Vomiting can be induced by (a) tickling the fauces
with a finger, feather or a leafy twig of a tree; (b)
administration of copious draughts of warm
water; (c) gurgling with non-detergent soap; or
(d) saline emetics in warm water. To prevent
aspiration in small children, the head should be
kept low.
• Syrup of ipecac may be used for inducing
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emesis in children older than 6 months in a
single dose of 10 mL for 6-12 months age,
and 15 mL for children above 1 year of
age. The dose may be repeated in 20
minutes for those more than 1 year of age.
Induction of vomiting is contraindicatied
in corrosive or kerosene poisoning and in
comatose patients or those with absent
gag reflex.
• Gastric Lavage. If the vomiting
does not occur quickly, gastric
lavage should be done promptly to
remove the poison. In a
symptomatic but alert patient with
minor ingestion, activated charcoal
alone by mouth is sufficient for
gastrointestinal decontamination
• The child is kept in the left lateral position
with the head hanging over edge of the
table and the face down. A large single
lumen tube with multiple distal ports is
necessary. A restraint is required for most
children and mouth gag is placed in the
mouth before the procedure. The catheter
is passed gently and free end is dipped
under water to make sure that the
catheter is not in the airway.
• Generally tap water is used for lavage and
four or five washes are done. The volume
of each aliquot should be at least 10-15
mL/kg. After the fluid has been instilled, it
should be removed by gravity drainage or
tube suction. Catheter is pinched before it
is finally withdrawn or suction is
maintained during withdrawal to prevent
aspiration.
• Gastric lavage should not be
performed in children with poor gag
reflex or corrosive ingestion. In
kerosene poisoning, lavage may be
done very cautiously if the child has
consumed a large gulp of kerosene
and is brought quickly to the
hospital, otherwise it is better to
avoid stomach wash.
Adsorbent administration
• An agent capable of binding to a
toxic agent in the GIT is known as
adsorbent. Activated charcoal is the
most widely used adsorbent. It is
created by subjecting carbonaceous
material e.g., wood, coal etc. to
steam at 600-900 degree Celsius and
acid.
• For the comatosed patient (Grade 3 or 4)
with potentially serious overdose, gastric
lavage is followed by administration of
activated charcoal via an orogastric or
nasogastric tube within 1-2 hours of
ingestion. Dose of activated charcoal
administered should be atleast 10 times
the dose of ingested toxic material. In
asymptomatic patient presenting early or
without reliable history, 15-30 gram of
charcoal may be used.
Catharsis
• Laxative and purgatives may be given in
poisoning with substances which do not
cause corrosive action on gastrointestinal
mucosa. Increased motility of the gut may
reduce absorption. Commonly used
cathartics include sorbitol and mannitol (12 g/kg), and magnesium or sodium sulfate
(200-300 mg/kg). Do not give magnesium
salt cathartics in cases with renal failure.
Specific Antidotal Therapy
• The antidotes may be physiological, chemical or
physical. Chemical antidotes combine with the
poison and render it innocuous. Physiological
antidotes counteract the effects of the poison on
the metabolism and physiological functions of the
body and thus prevent its harmful effects.
Physical antidotes prevent the contact of the
poisonous substance with the target organ or
adsorb the toxic components, thus preventing
their toxicity.
• Specific antidotes may be life saving but
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unfortunately they are not often available
and are effective for less than 5% of
poisoning cases. When obtainable, they
must be given without delay for maximum
protective action.
Antidotes now considered obsolete include
universal antidote for ingested poisons,
acetazolamide for modification of urinary
pH, ascorbic acid for methemoglobinemia,
castor oil as cathartic, nalorphine for
opiates, sodium chloride for emesis and
tannins for alkaloids.
Promotion of Excretion of
Toxin
• The efficiency of regimens for
enhancement of drug elimination from
the body can be predicted to a large
extent if the physio-chemical properties,
disposition and pharmacokinetics of the
substance are known. The fluid intake is
increased to promote glomerular filtration
and excretion of poison through the
urine.
• Forced diuresis:Diuresis alone has relatively little
effect on drug elimination because at best the renal
clearance is only proportional to the urine flow rate.
In the case of drugs which are weak organic acids
and bases, a much greater effect on clearance can
be obtained by manipulation of the urine Ph. The
lipid solubility and hence tubular reabsorption of
such acidic and basic drugs is decreased in alkaline
and acid urine respectively. Theoretically for each
change of one unit in urine pH, the renal clearance
could change by a factor of 10. Urine pH is therefore
much more important than urine flow rate.
• In practices, forced alkaline diuresis is restricted
largely to poisoning with phenobarbitone and
salicylate, although much of the effect in lowering
plasma salicylate concentrations result from
haemodilution rather than increased urinary
excretion. Raise the urinary pH to 7.5 for weak
acids (e.g., barbiturates, salicylates) with 1.4
percent sodabicarb. Maintain urinary pH to 5.56.5 (forced acidic diuresis) in poisoning with
weak bases e.g., tricyclic antidepressant and
pheytoin, with ammonium chloride 4 g
administered every two hourly through Ryle’s
tube
• Any form of forced diuresis is potentially
dangerous. Forced diuresis is
contraindicated in patients with cardiac
and renal impairment; complications
include water intoxication, disturbances of
acid-base and electrolyte balance, left
ventricular failure with pulmonary oedema
and cerebral oedema.
• Hemodialysis, hemo-perfusion and
peritoneal dialysis. Drugs which can
be removed reasonably effectively by
hemoperfusion and haemodialysis
include barbiturates, carbamazepine,
salicylates, theophylline, dapsone,
most antibiotics, lithium, chloral
hydrate, methanol and ethylene
glycol.
• In general, hemoperfusion with
coated charcoal or exchange resins is
more preferred for simultaneous
correction of acid-base and
electrolyte balance (e.g., in salicylate
poisoning). Hemodialysis is also the
method of choice for removal of
methanol, ethylene glycol and
lithium.
• Peritoneal dialysis is much less effective and it is
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used rarely. It has the advantage that is does
not require special facilities but may be
complicated by fluid and electrolyte
abnormalities, perforations, peritonitis and
adhesions.
Dialysis is not useful in poisoning with digitalis,
antihistaminics, belladonna alkaloids, opiates,
etc.
Supportive Therapy
• Keep the airway open, give oxygen
for inhalation and be prepared for
intermittent positive pressure
respiration. Fluid and electrolyte
balance is maintained. Circulatory
failure should be managed to sustain
life. Anemia is treated with packed
cell transfusion.
• Severe convulsions and status
epilepticus are treated with
diazepam or midazolam. Renal failure
is managed as per standard protocol;
dialysis may be needed. Infections
are treated with antibiotics. Fever
and pain are relived with antipyretics
and analgesics.
Prevention of Poisoning
• Protection of the child from the
poisonous substances. The poisonous
substances should be kept in secure
places out of reach of the child. The
poisonous substances should be
replaced in their proper place. Potential
household poisons should not be
transferred to empty containers
otherwise used for innocuous food or
beverages.
• Drugs should be dispensed in the original
container. The word poison should be
exhibited prominently on the containers of
potential poisonous substances. Kerosene
oil and caustic soda should not be stored
in tumblers or beverage bottles. The
containers should not be left on the
ground. Kerosene bottles and stoves
should be kept out of reach of the children
in the kitchen.
• Education of parents about potential
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household poisons.
Need for parental supervision of toddler’s
behavior should be emphasized.
Safety regulations by the State should be
enforced.
Establishment of poison control centers to
collect, compile and disseminate
information on poisons and their
management. These should promote
research on prevention and treatment.
Some Specific Poisons
and Antidotes
KEROSENE POISONING
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Epidemiology
Clinical features
Investigation
Treatment
Epidemiology
• Accidental – 33 to 60% in India & other
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developing countries
Reasons for high incidence
1. Extensive use for cooking & lighting in
low socioeconomic status
2. Stored in soft drink bottles, beer
bottles within reach of children
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
Lab Investigations
• Blood – Leukocytosis
X – Ray changes
Changes appear within one hour
- commonly right basal infiltrates
- emphysema
- pleural effusion
- pneumatocoeles
Severity score
PARAMETERS
ABSENT
PRESENT
FEVER
SEVERE
MALNUTRITION
RESP. DISTRESS
0
0
1
1
0
0
0
2
4
CNS SYMPTOMS
0
2
4
• >4 – Significant
• <7 – Likely to survive
• >8 –– Risk of death is increased
OTHERS
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 G 50000/Kg/24 hrs
IV qid
• Kanamycin – 10-15mg/Kg/24 hrs - IM bd
• Steroids – Not helpful
Complications
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Pneumothorax
• Pneumatocoeles
• Pleural effusion
• Bronchopneumonia
• Coma
Organophosphorus
(insecticides and pesticides)
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, giddiness, 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
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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.
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
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.
Salicylate Poisoning
• Ingestion of 150 mg/kg of salicylates
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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
• 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
Acetaminophen
(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.
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
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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.
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.
Pyrethrin Poisoning
• Pyrethrin is an active ingredient of various
mosquito and fly repellant strips. These
insecticides quickly inactivate the insect.
Mammals are relatively resistant to these
agents and most cases of toxicity with
these agent occur because of allergic
reactions. Ingestion of these repellant
strips does not lead to significant
symptoms.
Lead Poisoning
• Exposure to lead occurs from old
lead based deteriorated house
paint (in old houses) and dust and
soil contaminated with lead such
as from leaded gasoline, lead
electrode plates from old
automobile batteries, adultered
food, folk remedies, broken lead
typesets scattered around old
printing establishments. Food may
be adulterated with colored
metallic salts or the black collyrium
used as surma may contain a
proportion of black oxide of lead.
Lead Poisoning
• Chronic lead intoxication occurs
usually in children who eat nonedible substances (pica) and
manifests as pain in abdomen and
resistant anemia. Lead is deposited
in the bones. Acute infections may
mobilize lead from storage areas in
bones and cause acute lead
poisoning leading to acute lead
encephalopathy.
• In these cases the child may be left with
neurological sequelae. Lead inhibits
sulfhydryl enzymes and formation of
heme. Heme precursors such as porphyrins
accumulate in the blood and are excreted
in the urine. Screening for lead
intoxication is done by measuring zinc
protoporphyrin or blood lead levels.
Treatment
• In symptomatic children, therapy is
usually started with dimercapol (BAL) (75
mg/m2 every 4 hourly IM). BAL may be
stopped after 48 hours, while calcium
disodium edetate is used for another 3
days but at a lower dosage of 50 mg/kg or
1000 mg/M2 per 24 hours by continuous
IV infusion.
• Maximum daily dose should not exceed
500 mg/kg. Stop BAL when blood lead
level falls below 60 microgram/dL. Give a
second course of edetate alone if blood
lead rebounds to 45-69 microgram/dL. A
second course of edetate in combination
with BAL is recommended for rebound
lead level of >70 microgram/dL. Wait for
5-7 days in between the two courses.
Barbiturate Poisoning
• Clinical features include hypoxia,
depression of respiration, pulmonary
complications and kidney failure.
Peripheral vascular bed is dilated;
shock which may sometimes be
delayed may occur
Treatment
• Hypoxia is managed by oxygen inhalation
•
and maintenance of open air way.
Circulatory collapse is treated with fluids
and plasma. Patients do not respond to
epinephrine.
Urine is alkalinized to facilitate excretion
of barbiturates. Mannitol is given. This
causes osmotic diuresis. In severe cases
peritoneal dialysis may be necessary to
remove barbiturates.
Alcohol Poisoning
• Ethyl alcohol 0.75-1 mL/kg is given
IV followed by 0.5 mL/kg every 4
hours. Three mL of 7.5% sodium
bicarbonate solution diluted 1 in 4 is
given IV. Dialysis should be done.
• Cyanide Poisoning
• Sodium nitrite 2.5 to 5 mL of 3.5
percent solution is given IV every
minute followed by sodium
thiosulfate 2.5 mL of 25 percent
solution every minute subject to a
maximum of 50 mL. Amylnitrite
capsules (10mg/kg) may be
inhaled.
• Opium (Morphine) Poisoning
• Respiratory depression occurs and pupils
are constricted; patients are excessively
drowsy.
• Treatment:-Stomach wash is done.
Specific antidote for opium poisoning is
naloxone given IV in a dose of 0.03
mg/kg/dose. If there is no response in 2
minutes the same dose may be repeated.
Naloxone can also be given by continuous
infusion (20-40 microgram/kg/h).
Analeptics may be used and oxygen is
administered by inhalation.
• Dhatura (Belladonna) Poisoning
• Accidental ingestion of dhatura
seeds causes delirium, confusion,
visual disturbances, photophobia,
dilated sluggishly reacting pupils,
dryness of skin and mouth, fever,
tachycardia and urinary retention.
• Treatment is by gastric lavage and
physostigmine in a dose 0.02
mg/kg (maximum 2 mg) IV slowly.
Dose may be increased and
repeated after 20 minutes.
• Isoniazid (INH) Intoxication
• Toxic effects of INH may be (i)
directly due to the drug i.e., jaundice,
SLE, arthralgias, altered sensorium,
hemolysis and hypersensitivity
reactions; or (ii) due to pyridoxine
depletion i.e., convulsions, peripheral
neuropathy, demyelination and
inhibition of phenytoin metabolism.
Lethal doses are>50 mg/kg.
• Gastric lavage is indicated. Patients are
given 1 g of pyridoxine (vit. B6) for each
gram of INH ingested. If amount of
ingested INH is not known, administer 70
mg/kg of pyridoxine intravenously. The
dose may be repeated if seizures recur.
Use diazepam or phenobarbitone to
control seizures. In severe cases with
seizures not responding to treatment
hemodialysis may be necessary to save
life.
Prevention
•
•
•
•
Parental education
Keep away from reach of children
Properly capped containers
Avoid storage in beverage bottles or colorful
containers which attract children
• Immediately seek medical care
Preventing childhood
poisoning
• 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.
• 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.
Laws on poison
The Drugs and Cosmetics act, 1940.
1. To control the quality, purity & strength of drugs.
2. Any patent/proprietary medicine should display on
the label or container & the list of ingredients
contained in it.
The Pharmacy Act-1948
The object of this act is to allow only the registered
pharmacists to prepare, mix or dispense any
medicine on prescription of a medical practitioner.
The Drugs and Magic remedies Act1954.
To ban advertisements procuring
abortion/increase of sexual
potency/treatment of veneral
diseases/correction of menstrual
disorders.