POISONING IN CHILDREN

Prepared by,
Gayathri R
2nd yr MSc
(N)
INTRODUCTION
Poison was discovered in ancient times, and was used by ancient tribes
and civilizations as a hunting tool to quicken and ensure the death of
their prey or enemies. This use of poison grew more advanced, and
many of these ancient peoples began forging weapons designed
specifically for poison enhancement. Later in history, particularly at the
time of the Roman Empire, one of the more prevalent uses was
assassination. Poisoning occurs when people drink, eat, breathe, inject,
or touch enough of a hazardous substance (poison) to cause illness or
death.
DEFINITION
Toxicology
• Toxicology is the branch of medical science which deals with the sources,
pharmacokinetics and pharmacodynamics of poisons, the clinical
manifestation produced by them, their lethal dose and the therapeutic
measures to be employed to counter them.
Poison
• A poison has been defined as a substance which when introduced into or
absorbed by living organisms, causes injury or death.
Poisoning
• Taking a substance that is injurious to health or can cause death.
• An illness caused by eating, drinking, or breathing a dangerous substance .
CAUSES OF CHILDHOOD POISONING
• Kerosene and other • Eucalyptus oil
hydrocarbons. • Camphor
• House hold products • Naphthalene
• Insecticides • Neem oil
• Phenol • Alcohol
• Alkalis (Caustic soda, Slaked • Copper sulphate etc.
lime)
• Acids
• Turpentine
• Pharmaceutical products • Aspirin
• Phenothiazine • Piperazine
• Opiates • Antiseptic
• Tincture opii • Analgesic
• Diphenoxylate • Anticonvulsants
• Iron salts • Antihypertensive etc.
• Barbiturates
• Plants and plant product • Food poisoning
• Dhatura • Environmental poisoning
• Yellow oleander • Snake bite
• White oleander • Scorpion sting
• Castor seed • Insect bite
• Chandra jyothi seed
EPIDEMIOLOGY

Data available from the National Poison Information

Centre, New Delhi suggests a high incidence of
poisoning in children (36.5%). Accidental mode
(79.7%) as well as intentional attempts (20.2%) were
reported.
PHASES OF POISONING 

• Preclinical phase-some signs and symptoms may not be evident during this
phase; the priority is decontamination

• Toxic phase-signs and symptoms and lab changes are evident during this
phase and guide treatment; the emphasis is on shortening the duration of
poisoning and lessening the severity of toxicity

• Resolution phase-this phase encompasses peak toxicity to recovery; the goal

is to shorten the duration of toxicity.
GENERAL SIGNS AND SYMPTOMS OF POISONING

Eyes Face and scalp

• Miosis • Alopecia
• Mydriasis • Facial twitching
• Partial or total blindness • Dull and mask like expression
• Blurring of vision
• Purple yellow vision (Digitalis)
Skin and mucus membrane
• Deep brown (Bromide)
• Pallor
• Grey (Mercuric chloride)
• Cyanosis
• White (Phenol Derivative)
• Ashy coloration (Ergot, Lead)
Gastrointestinal tract
• Yellow color (Chlorinated
compound, arsenic, heavy • Nausea
metal) • Vomiting
• Sweating • Diarrhoea
• Dry, hot skin (Dhatura, • Dehydration
botulinum toxin) • Abdominal pain
• Brown black (Iodine)
Nervous system
Cardiovascular symptoms
• Headache
• Convulsions • Bradycardia, AV block
• Delirium
• Ventricular tachyarrhythmia’s
• Coma
Respiratory symptoms • Cardiomyopathy
• Tachypnea, cough, hoarseness,
stridor, dyspnoea, retraction, • Endocarditis
wheezing, chest pain
• Pulmonary edema
CORROSIVE POISONS
Corrosives are widely used for industrial, scientific and domestic
purposes. Ingestion by older children and adults is usually made with
suicidal intent poisoning with corrosive is more common among the
toddlers. The incidence all over India as computed varies from 4 to 6%.
Corrosives are divided into;
• Mineral acids (sulphuric acid, nitric acid, hydrochloric acid)
• Organic acids (oxalic acid, carbolic acid, acetic acid, salicylic acid)
• Vegetable acid (hydrocyanic acid)
• Alkalis (sodium hydroxide, potassium hydroxide, ammonium
hydroxide)
Sites likely to be affected by local effect;
• Skin of exposed parts of body and face
• Mouth and throat
• Upper GI tract
• Respiratory tract
 
Effects of corrosive
Delayed effects
Early effects
• Burning pain, tingling sensation
• Laryngeal stricture
• Vomiting often blood stained
• Oesophageal stricture
• Dysphonia due to laryngeal
edema • Pyloric fibrosis
Late effects • Pulmonary fibrosis
• Perforation of stomach and
oesophagus
• Pulmonary edema or
bronchopneumonia
Clinical picture
• Severe pain in the mouth and • Metabolic acidosis
pharynx • Liver and renal failure
• Chest and abdominal pain • Oesophageal and gastric
• Hematemesis and bloody perforation
diarrhoea • Respiratory distress due to
• Laryngitis glottis edema
• Bronchiolitis • Signs of shock
• Pulmonary edema • Vomiting and dysphagia
• Teeth loss • Drooling
• Burns • Stridor
Diagnosis
• History of ingestion
• Assessing the clinical features
• Assessing the breath odour
• Analysis of vomitus or stool
• Radiological – Lateral X rays of the soft tissue of neck to evaluate
upper airways compromise and chest and abdominal x rays should be
done to look for signs of oesophageal or gastric perforation in severe
cases.
• Endoscopy – Esophagoscopy and gastroscopy are diagnostic
procedures of choice in all documented or suspected cases of
corrosive ingestion to assess the extent and severity of injury.
• Urine routine and blood routine.
Treatment
• Detailed history and physical examination
• Gut decontamination procedures are contraindicated
• Milk of magnesia and antacids are used to neutralize strong acids
• To prevent secondary injury from reflux of gastric acid into the oesophagus,
proton pump inhibitors, H2 blockers or therapeutic doses of antacids
should be given.
• Use of steroids for prevention of oesophageal stricture formation is
controversial.
• Antibiotic is used if infection is suspected.
• Drooling and dysphagia persisting beyond 12-24 hours have been reported
to be good predictors of scar formation and should prompt upper GI scopy.
• To prevent oesophageal stricture, include beta aminoproprionitrite and
pencillamine.
KEROSENE AND OTHER
HYDROCARBONS
Petroleum distillate and hydrocarbon present in many household
products. These products may divided into two groups based on their
volatility, viscosity, surface tension and their respiratory manifestation.
• High volatility: Kerosene, petroleum, ether, gasoline and paint thinner.
• Low volatility: Furniture polish, lubricating oil, paraffin wax, mineral
and sea oil.
Toxicology
Petroleum distillate hydrocarbons are not absorbed from GI tract. The
systemic toxicity generally results from absorption through the lungs
following aspiration; important exceptions are the non-petroleum
distillate hydrocarbon which are absorbed from the GI tract. Due to its
low surface tension, kerosene tends to get aspirated into the lungs
during ingestion, vomiting and inhalation of vapours.
• Fatal dose is 30ml.
Route of exposure

• Accidental exposure among children

• Transdermal absorption through skin of neonate
• IV kerosene injection among IV drug abusers
Clinical features
• Topical effects: Irritation of oral, oesophageal and gastric mucosa.
• Pulmonary effects: Fever, tachycardia, tachypnea, cough, cyanosis and rarely
pulmonary edema.
• Chemical pneumonitis result from aspiration and may develop over 1-24 hours
after aspiration of high and low volatility substances.
• Children who are asymptomatic for 6 hours are unlikely to develop pneumonia
later.
• Pleural effusion, pneumatocele, pneumothorax, pneumomediastinum and
subcutaneous emphysema are found infrequently.
• CNS effects: Euphoria, headache, restlessness, weakness, muscle twitching,
incoordination, confusion, lethargy, stupor, coma and convulsion may occur.
• Hypoxia and acidosis
• Other features: Liver damage, renal tubular damage, bone marrow suppression
and myocardial toxicity.
Diagnosis

• History of ingestion.

• Assess the clinical features: cough, tachypnea, chest pain, cyanosis,

wheeze and characteristic breath odour, arrhythmias, tender
abdomen with hyperactive bowel sound, seizure and coma.

• Radiological: chest x ray shows fine punctate mottled densities in

perihilar areas/ pneumonitis of the lower lobe.
Management
• Evacuation of the stomach is contraindicated because it increases the risk
of aspiration.
• Dilution with oil or milk, commonly used as house hold remedy for
hydrocarbon exposure.
• If hydrocarbon are mixed with pesticides, metals or other toxic substances,
then gastric lavage or emptying is indicated.
• In unconscious patient gastric lavage after intubation is with a cuffed
endotracheal tube is the method of choice.
• Supportive treatment include correction of hypoxia by oxygen
administration.
• For wheezing selective beta 2 agonist are preferred over epinephrine as
latter may cause arrhythmias.
• Antibiotics, if secondary bacterial infection suspect.
• Observation for at least 24 hours.
ORGANOPHOSPHATE POISONING

Organophosphate compounds are commonly used as insecticides in

house hold and agriculture. The compounds used in house hold are less
toxic. The solvents used for these products are hydrocarbons. The
commonly used compounds are methyl parathion (Agrolex), dichlorovos
(Agrovan, Vapox), fenthion (Bytex, Fenthiosul), Malathion (Finit), diazinon
(Agrozinon), fenitrothion (Tik 20), and tetra ethyl pyrophosphate etc.
Toxicology

The toxicity occurs due to accidental or following absorption through

skin. They also cause excessive accumulation of acetyl choline at
receptor sites.
Clinical features
Muscarinic
• Salivation, lacrimation, urination, defecation or diarrhoea, broncho
constriction wheezing, increased pulmonary secretion, bradycardia,
nausea, emesis, abdominal cramps, intestinal hyper motility, excessive
sweating and constriction of pupil.
Central nervous system
• Anxiety, restlessness, confusion, headache, emotional liability, slurred
speech, ataxia, generalized seizures, hypotension, cheyn stokes
respiration, central respiratory paralysis, depression of cardiovascular
centre and trauma, delayed peripheral neuropathy.
Nicotinic

• Muscle fatigue, twitching, fasciculation, paralysis of respiratory

muscles with diminished respiratory effort, tachycardia, hypertension,
pallor, hyperglycemia.
Diagnosis
• History collection and physical examination.
• Assessing the clinical features.
• Symptoms relieved by atropine administration.
• The diagnosis confirmed by estimating RBC choline esterase activity.
• Estimation of urinary P- nitro phenol radical (PNP) is useful for the
diagnosis of parathion, methyl parathion and chlorothion which
contain this radicals.
• Electromyographic pattern consistent with detrimental conduction
with repetitive nerve stimulation and acute cholinergic illness.
Diagnosis

• Ancillary investigations;
• Increased leukocyte count- stress leucocytosis.
• high haematocrit
• Anion gap – poor tissue perfusion.
• Increased glucose and decreased potassium and magnesium-
catecholamine excess.
• Blood urea nitrogen, creatinine and urine specific gravity- patients’
hydration status.
Management

• Removal from the source of poison.

• Wash the skin.
• Gastric lavage with potassium permanganate.
• Cathartics
• Atropine: 0.05mg/kg IV repeated every 5-15 minutes until all secretions
become dry.
• Pralidoxime: 25-50mg/kg IV as a 5% solution.
• Symptomatic and supportive treatment including mechanical ventilation if
required.
• Management of airways
Management
• Artificial ventilation in case of diaphragmatic paralysis or respiratory
failure
Management of seizure;
• Oxygenation and large doses of benzodiazepines along with antidote
therapy.
• Rarely patient may require Phenobarbitone. Phenytoin is
contraindicated because of its membrane stabilizing and autonomic
effects. It also suppress cardiac activity and physiologic response.
• Ventricular premature contractions due to organophosphate
poisoning can be successfully terminated with IV magnesium
sulphate.
• Obidoxime chloride may be administered in a dose of 4-8mg/kg/dose,
as an alternative for children with organophosphate poisoning.
CARBOMATE POISONING

Carbomate is an insecticide are reversible cholinesterase inhibitors. The

signs of intoxication are of shorter duration and they do not penetrate
CNS; therefore no neurological manifestations are seen. They are more
readily absorbed from skin and GI tract. The common carbomate
compounds are propoxur, carboryl, methomyl, carbofuran etc.
Treatment

• Treatment is same as that of organophosphate poisoning, but the use

of cholinesterase reactivator, pralidoxime is contraindicated as
inhibition with cholinesterase is transitory and reversal occurs rapidly.

• IV atropine also used.

ORGANOCHLORINE INSECTICIDE
POISONING

These are lipid soluble low molecular weight compounds with a wide
range of toxicity. The commonly available compounds are DDT, gamma
benzene hexachloride etc.
DDT POISONING
DDT is a white crystalline powder, insoluble in water, moderately
soluble in mineral and vegetable oils and parasiticidal. In low
concentration, it is lethal to mosquitoes, house flies and lice and too
many arthropods. Accidental poisoning due to ingestion, transdermal
absorption or inhalations common in adolescent.
• Death usually takes place in 1-2 hours and rarely after 1-2 days.
• Lethal dose is approximately 150mg/kg body weight of pure DDT.
Clinical feature

• Excessive salivation • Cough

• Nausea • Pulmonary edema
• Vomiting • Head ache, fatigue, irritability
• Abdominal pain and mental apathy
• Dermatitis • Hyper excitability of CNS
(twitching of eye lid, muscular
• Dilated pupils tremor, fibrillation, convulsions,
• Blurring of vision CNS depression, paralysis of limb
muscles, cyanosis, laboured
respiration and coma)
Treatment
• Gastric lavage
• Change the clothing to prevent skin irritation and further absorption.
• Airway should be maintained and oxygen should be administered in the presence
of cyanosis.
• The signs of hyper excitability of CNS should be treated with either parenteral
barbiturates or diazepam.
• Adrenaline and other sympathomimetic should be avoided as they induce
ventricular fibrillation.
• If there is liver and renal damage, low fat, high carbohydrate and protein diet
should be given together with appropriate conservative management.
• Phenobarbitone 4-6mg/kg/ day in two divided doses may be given for tremor and
convulsions.
• Antibiotics are indicated in the presence of infection.
PARACETAMOL POISONING

Paracetamol is a safe analgesic antipyretic agent in therapeutic doses.

Hepatic damage after paracetamol poisoning occurs due to increased
formation of highly reactive intermediate (N acetyl p-
benzoquinonimine) which is produced by its metabolism.
Hepatotoxicity occurs may occur when a dose of more than 150 mg/kg
is ingested.
Clinical manifestation
• Stage 1 (6-24hrs): Anorexia, nausea, vomiting, pallor and excessive sweating
with cold skin.
• Stage 2 (24-48hrs): The clinical evidence of hepatic dysfunction supervene.
There is jaundice, enlarged tender liver and deranged liver functions with
elevated liver enzymes and prolonged prothrombine time. Renal dysfunction
is manifest by oliguria and elevation of blood urea and creatinine.
• Stage 3 (48-96hrs): The symptoms of stage 1 reappear and hepatic coma
supervenes with gross evidence of hepatic dysfunction.
• Stage 4 (4days-2weeks): After optimal supportive and specific therapy
recovery may occur gradually during 1-2 weeks period. It may take 3mth for
liver histology to return back to normal.
Management
• The blood level of paracetamol should be monitored after 4 hrs of ingestion and
serially thereafter.
• If serum paracetamol is >200mg/ml at 4hrs, >100mg/ml at 8hrs and >50mg/ml at
16 hrs. There is high risk of hepatotoxicity.
• Supportive management include induction of emesis or gastric lavage followed by
activated charcoal to adsorb unabsorbed paracetamol.
• Treatment for correction of hypoglycaemia, maintenance of hydration, electrolyte
balance, treatment of coagulopathy hemodialysis for acute renal failure and also
management of fulminant hepatic failure.
• N -acetyl cysteine is a specific antidote started with in 8 hrs. But preferably with
in 16 hrs. Of ingestion.
• Frequent monitoring of the LFT are needed.
• An alternative drug through less effective is oral methionine 2.5gm stat followed
by 2.5gm Q4H upto a total of 10gm over 12 hours.
PHENOTHIAZINE INTOXICATION

Phenothiazines are commonly used drugs for a variety of clinical

problems. The onset of toxic manifestations may be delayed for 6-24
hrs. After the ingestion and may be intermittent in nature.
Clinical features
Cardiovascular Central nervous system
• Tachycardia • Indifference to environmental
• Hypotension stimuli
• Ventricular arrhythmia • Lethargy
• Complete heart block • Coma
• Convulsions
• Hypothermia or hyperthermia
with rhabdomyolysis
Clinical features
Extra pyramidal symptom Autonomic nervous system
• Acute dystonic reactions • Tachycardia
• Akasthesia • Hypotension
• Pseudo parkinsonism • Diaphoresis
• Tardive dyskinesia • Dyspnoea
• Choreform movements of trunk • Incontinence
and limbs
• Neuroleptic malignant syndrome
Clinical features
Pulmonary • Miosis
• Tachypnea • Eye pigmentation
• Rarely respiratory depression Skin
Gastrointestinal • Dry and pigmented
• Nausea • Dermatitis
• Vomiting Allergic and idiosyncratic
• Decreased bowel sound
• Jaundice leukopenia
Eye
• Agranulocytosis
• Blurred vision
Treatment
• Assessing the clinical features.
• Monitor the ECG changes- flattening and inversion of T wave, prominent U
wave, ST depression, Prolonged PR, QRS and QT intervals.
• Plain X ray abdomen- radio opaque tablets.
• Urine analysis – phenistix strip test positive (when the strip is dipped into the
patient urine, deep purple shade of strip occur immediately in the presence of
phenothiazines. A false positive reaction occurs in case of salicylates or large
quantities of ketones.
• Estimation of blood level of the drug.
• Gastric lavage and emesis according to level of consciousness
• Activated charcoal through lavage tube
• Naloxone for comatose patient
Specific treatment
Hypotension
• IV normal saline or ringer lactate
• Trendelenberg position
• MAST pants if available
• Levarterenol, 0.1-0.2 mg/ kg/ min IV

Respiratory insufficiency
• Airway protection and ventilator assistance
Specific treatment

Arrhythmias
• Put the patient on cardiac monitor
• Sodium bicarbonate IV to normalize pH
• Lidocaine 1 mg/ kg IV in bolus followed by 0.03mg /kg/ min drip
• Phenytoin 1mg/ kg over a period of 5 min to a maximum of 10 mg/ kg
• Physostigmine 0.5mg slow IV
• Cardiac pacemaker for complete heart block
Specific treatment
Seizures
• Diazepam 0.2mg / kg slow IV
• Phenobarbitone loading dose 5mg/ kg IV slowly may be repeated in
20 min
Temperature control
• Extra pyramidal side effects
• Diphenhydramine 1 mg/ kg IM or IV
IRON POISONING
Iron poisoning is one of the most potentially fatal intoxication in
children. Widespread availability of iron tablets is particularly during
pregnancy and post natal period and ignorance of general public about
its potential lethality contribute to the high incidence of iron poisoning.
Toxicology and clinical manifestation
Toxicity of iron is due to its direct effect on the gastrointestinal mucosa
and the presence of free iron in circulation.
Gastro intestinal toxicity
• This is primarily due to direct mucosal injury, especially on gastric and
small intestinal mucosa by producing coagulation necrosis and platelet
aggregation. This stage include vomiting, diarrhoea, colicky abdominal
pain, hematemesis and melena. This stage last for about 2 to 12 hrs.
Stage of relative stability
• This poorly described second stage of iron intoxication begins as early
as 3 to 4 hrs after ingestion and last as long as 48 hrs. During this
phase patient appears better, while absorbed iron accumulates in the
mitochondria and various body organs.
Stage of circulatory collapse
• Acute circulatory failure, acidosis, and hypoglycaemia characterize
this phase. The various contributory factors for shock include
hypovolemia due to external losses and third space loss due to
increased capillary permeablility, acidosis and decreased cardiac
output.
Stage of hepatic necrosis
• This is a rare clinical manifestation of iron intoxication. After apparent
recovery, 2-4 days after ingestion of iron, severe hepatic necrosis with
elevation of transaminase and bilirubin may occur.
Stage of gastric scarring

• Following an acute corrosive insult to the gastro intestinal tract, the

healing process may result in area of stenosis in both the stomach
outlet and small intestine. This late consequences of iron poisoning
may occur rarely and present as late as 2-6 wks after the initial event.
Lab investigations
• Serum iron estimation
• Estimation of total iron binding capacity ( iron values > 350mg/dl is
taken as risk and value >1000mg/dl associated with morbidity or
mortality)
• X ray abdomen may show radio opaque shadows giving rough
indication for amount ingested and need for their removal by
endoscopy.
• WBC and blood glucose determination.
• Serum calcium and coagulation studies
• Determination of serum electrolytes
• LFT may be abnormal after 24 hrs of ingestion.
Treatment
• Early gastric evacuation by emesis with syrup of ipecac or gastric lavage.
• Antacids may be useful for complexing iron in the stomach and
decreasing corrosive effect of acid upon denuded gastric mucosa.
• Chelation therapy with IV infusion of dexferoxamine. During infusion
carefully monitoring the blood pressure.
• The chelation therapy should be continued till serum iron level falls
below 300mg/dl.
• Supportive fluid management.
• In selected patients whole bowel irrigation may be helpful.
ISONIAZID POISONING
• The toxic dose varies between 5-10gm. The symptoms appear within 30-
60min of ingestion. Gastrointestinal irritation, CNS manifestations
(lethargy, confusion, seizures and coma) and respiratory depression may
occur. The blood INH level of >50mg/dl is toxic.
• Besides supportive measures (prompt gastric lavage, administration of
activated charcoal and correction of metabolic acidosis with sodium
bicarbonate).
• Pyridoxine is a specific antidote and is given intravenously in a dose of
1.0mg for every mg of INH ingested. When the amount of INH ingested is
unknown, administer 500mg of pyridoxine IV and repeat every 5-20min if
needed.
CARBON MONOXIDE POISONING
Carbon monoxide (CO) is an odourless gas, colourless, non-irritating gas
present in atmosphere in concentration of <0.001%. Excessive CO may
be produced due to incomplete combustion of carbon mining
substances. CO poisoning occurs following accidental fire in a close
area, and use of coal or kerosene stove for keeping rooms warm during
winter.
Clinical features
• <10%: Impaired judgement, retarded psychomotor activity.

• 10-20%: Mild head ache, dyspnoea, decreased visual acuity.

• 20-40%: Irritability, nausea, fatigue, dizziness, tachypnea and

tachycardia, blurring of vision.

• 40-60%: Confusion, hallucination, ataxia, convulsion, coma.

• 70-80%: Death results from cardiorespiratory depression.

Diagnosis

• History of carbon monoxide exposure.

• Assess the clinical features such as thrombing headache, dypnea,

cyanosis, tachycardia, confusion, convulsion and coma.

• Estimation of carboxyhemoglobin in blood.

• Chemical method

• Spectroscopy
Management
• Remove the patient from the source of exposure.

• Administration of 100% of oxygen (hyperbaric).

• Blood transfusion; preferably packed red cell.

• 20% mannitol and IV dexamethasone in presence of cerebral edema.

• Patient with hypercarbia and respiratory failure may require

ventillatory support.
ALUMINIUM PHOSPHIDE POISONING
Aluminium phosphide is a grain preservative. It’s available as tablets
(cephalos, alphos, quickphos, phosphotek and phostoxin). It releases
phosphine, carbon monoxide and ammonia gas. Toxic effects are
produced due to disturbance in activities of various body enzymes. In
adolescents it may be ingested with an intention to commit suicide.
Fatal dose for adult is 150- 500mg.
Clinical manifestation
• Gastro intestinal symptoms: Nausea, vomiting, burning epigastric
pain, diarrhea, excessive thirst.
• Cardio vascular system: Hypotension, cardiac arrhythmia, myocardial
ischemia, myocarditis, pericarditis and congestive cardiac failure.
• Respiratory manifestation: Cough, dypnea, adult respiratory distress
syndrome.
• Liver: Hepatomegaly, increased transaminase, jaundice.
• Anxious and restless.
• Convulsions and coma.
Diagnosis
• History collection

• Assessing the clinical features

• Assessing hypotension or arrhythmias

• Foul or decaying fish like smell and metabolic acidosis strongly

suggest its possibility.

• Confirmatory test include analysis of blood or gastric fluid for

phosphine gas.
Treatment
• Supportive therapy.
• No specific antidote is used.
• For decreasing absorption of poison gastric lavage with KMnO4 may
be carried out but at the same time other supportive care started
immediately.
• Activated charcoal is administered.
• Cathartics can be used for evacuation of gut.
• For deceasing toxicity intravenous administration of magnesium
sulphate has been advocated to adults.
• The dose is 1gm magnesium sulphate stat followed by 1gm over next
2 hrs. and finally 1.0 – 1.5gm every 4 – 6 hrs. for 3- 5 days. The role of
magnesium sulphate in children is not well established.
Prognosis

Mortality is very high and depends on dose of aluminium phosphide

consumed, and the lag period between ingestion and reporting to the
hospital. Most of the fatalities results within 1 – 90 hrs. of ingestion of
poison. Cause of death in most patients is peripheral circulatory failure
due to cardiac toxicity.
OPIOID POISONING
Clinical features
Central nervous system • Vomiting
• Depression of CNS • Miosis
• Analgesia • Hyperactive spinal cord reflex,
• Respiratory depression convulsion
• Suppression of cough reflex • Change in mood
• Sleep • Euphoria / dysphoria
• Excitation of CNS • Dependence
• Nausea
Clinical feature

Adulterants Smooth muscle of various system

• Peripheral neuropathy • GI system

• Ambylopia • Decreased peristalsis

• Myelopathy • Decreased segmentation

• Leukoencephalopathy • Constipation
Clinical feature
Biliary tract Cardiovascular
• Biliary colic • Orthostatic hypotention
• Increased intra biliary pressure • Bradycardia
Respiratory tract • Dilatation of arterioles and veins
• Bronchospasm due to histamine Miscellaneous
release • Sweating
Urinary tract • Piloerection
• Urinary retention • Decreased sex drive
• Prolonged labor
Treatment
General management
• Maintenance of airways and oxygen administration, if necessary positive
pressure ventillation.
• An intravenous line should be secured with normal saline.
• Obtain blood samples for estimation of blood glucose, electrolyte,
hematocrit and toxicological analysis.
• The blood pressure should be maintained with IV crystalloids and
vasopressor amines.
• Activated charcoal in a dose of 1- 2g/kg should be left in the stomach
after completion of lavage to prevent further absorption of drug.
Treatment
Specific management
• Antidote therapy with naloxone Ina dose of 0.01 mg/ kg IM or IV and
may be repeated in 3 – 10 minute, if no response occurs.
• It’s important to monitor the patient with heroin overdose atleast
24hrs.
• Other antidote are nalophine, lavallorphan and naltrexone.
• The convulsions and cardiac arrythmias should be managed with
appropriate anticonvulsants and antiarrythmic drugs respectively.
• Appropriate antibiotics are given if there is any evidence of infection.
Treatment
Management of opioid withdrawal
• Physical examination of the patient.
• Assessment of liver function, neurological and for local and systemic infection should be
done.
• Proper nutrition is given and rest is advised.
• Treatment of withdrawal requires re administration of sufficient opiate on day one to
decrease symptoms followed by a more gradual withdrawal of drug usually over 5 – 10
days.
• Methadone 1mg also given in two divided doses, and after several days of stabilization, the
original dose of methadone is tapered by 10 – 20 percent each day.
• Clonidine, an alpha 2 adrenergic agonist may be used in part to decrease sympathetic over
activity.
• Psychiatric and social support for the patient requiring a comprehensive program for
rehabilitation.
THEOPHYLLINE POISONING

Theophylline is a commonly used drug for asthma by oral or parentral

routes. Because of its narrow therapeutic window, toxicity may result
due to accidental ingestion or therapeutic mishap.
Clinical features
GI manifestation Central nervous system
• Nausea manifestation
• Vomiting • Anxiety
• Epigastric pain • Restlessness
• Hematemesis • Seizures
Cardiovascular manifestation • Hypokalemia
• Hypotension • Hypophosphatemia
• Arrythmias (premature • Leukocytosis
ventricular beats, bigemini, • Metabolic acidosis
ventricular tachycardia and
fibrillations).
Theophylline toxicity mnemonic
T Tremor
H Heart (arrythmia)
E Electrolyte imbalance
(Hypokalemia)
O Oxidase inhibition (CYP)
P Pain in abdomen
H Head (head ache, insomnia,
seizure) Cytochromes P450 (CYPs) are a superfamily of
enzymes containing heme as a cofactor that
function as monooxygenases. In mammals, these
proteins oxidize steroids, fatty acids, and
xenobiotics, and are important for the clearance
of various compounds, as well as for hormone
synthesis and breakdown.
Diagnosis
• History of theophylline ingestion.
• Clinical manifestations.
• Theophylline levels in blood- concentration greater than 50mcg/ ml in
acute overdose, greater than 40mcg/ml in patients younger than 6
months indicate toxicity.
• Electrolyte and glucose levels- hypokalemia, hyperglycemia, or
hypercalcemia.
• Serum creatinine kinase- for evidence of rhabdomyolysis.
• Arterial blood gases- to monitor for acid base disturbance.
• CT scan- if seizure occur.
• Electrocardiogram for arrhythmias
Treatment
• Stabilization of airways.
• Gastric lavage must be done with normal saline if patient report
within 4hrs of ingestions.
• At the end of the gastric lavage, administer activated charcoal every 2
hrs until the serum theophylline level has fallen to less than 20- 25
mcg/ml.
• Charcoal hemoperfusion is indicated in;
• Patients with intractable seizure with duration longer than 30 minutes
or seizures at intervals of less than 20 minutes.
• Patient with persistent hypotension unresponsive to treatment with
fluids and pressure support.
• Patient with uncontrollable arrhythmias.
DATURA POISONING
These include flushing of face, dry skin and mucus membrane, dilated
pupils, blurring of vision, fever and tachycardia. Initially the patient is
restless but soon goes into depression, shock and coma. Respiratory
collapse may occur. Retention of urine is also common. Many patient
develops abdominal retention.
Treatment
• Specific antidote is physostigmine, 0.5 to 2.0mg. It can be repeated
every half an hour if needed.
• Other measure include induction of vomiting or stomach wash,
control of fever by hydrotherapy and or antipyretics, sedation to calm
down the patient and catheterization in case of prolonged retention
of urine.
LEAD POISONING (PLUMBISM)

It usually occurs in children suffering from ingestion of lead paint flakes,

artiste’s paints etc. from inhalation of fumes or batteries and from
practice of employing kajal or suruma containing black oxide or lead in
eyes.
Clinical features

• Head ache
• Transient abdominal pain
• Personality changes
• Resistant anemia • Ataxia
• Loss of weight • Poor physical development
• Seizures
• Irritability • Raised intra cranial pressure
• Vomiting • Lead line in gums

• Constipation
Diagnosis
• Urine lead level of more than 80 mcg/dl/24 hours.
• Blood level in symptomatic cases usually 80 mcg/dl.
• Red cell amino-levulinic acid dehydrase level are also good screening
test.
• Peripheral blood smear examination shows normocytic hypochromic
anemia with reticulocytosis and basophilic stippling of RBC.
• X-rays must reveal opaque flakes in the GIT.
• CSF pressure, protein and cell count are moderately raised.
Management
• Induce vomiting by saline cathartics
• Dimercaprol (BAL), 4mg/kg/dose every 4 hours intramuscularly, and
calcium EDTA, 125mg/kg/dose every 4 hours intramuscularly or
intravenously. After two days therapy with this drugs, there is need to
stop them and give pencillamine 25mg/kg/day orally for 5 days.
• Chelating therapy contraindicated when lead level below 60mcg/dl
• In case of encephalopathy anticonvulsants, mannitol and steroids are
indicated.
• Do not use BAL in presence of hepatic encephalopathy.
• Avoid too high calcium and phosphorous containing food which may
cause depositing of lead in bones.
 
MERCURY POISONING

Mercury poisoning may be acute or chronic and reversible or

irreversible, depending on the compound and extent of exposure. It
may from excessive inhalation of the mercurous vapors, oral intake or
repeated contacts with mercury containing products like paints, wall
papers, diaper rinses etc.
Acute mercury poisoning
• It is characterized by predominantly gastrointestinal and renal
manifestations. In exposure to high concentration of mercury vapor,
and renal manifestations. In exposure to high concentration of high
mercury vapor, manifestation includes pulmonary irritation or
pneumonitis, nausea, vomiting, diarrhea, abdominal pain and
headache.
• An oral exposure to mercury, manifestations include stomatitis,
gingivitis, esophagitis, and gastroenteritis with considerable
salivation. Abdominal pain and bloody diarrhea. In case of renal
damage, albuminuria, and uremia may develop.
• CNS manifestations like ataxia, slurring of speech, visual and hearing
impartment, numbness of hand and feet and delirium may occur.
Management
It consist of removal of mercury in stomach by gastric lavage (first with
milk and then with sodium bicarbonate). Correction of fluid and
electrolyte imbalance, peritoneal or hemodialysis for acute renal
failure, and symptomatic measures for restlessness and tachycardia.
Specific antidote is dimercaprol or BAL. Alternatively pencillamine is
recommended in case of adverse reaction of BAL.
Chronic mercury poisoning:

It is characterized by predominantly CNS and skin manifestation. It is

rare in children. Acrodynia and Minamata diseases are two well
recognized forms of pediatric chronic mercury poisoning.
Management
• Treatment is difficult. Administration of BAL (British Anti lewisite),
steroids and sedation, anticonvulsants. If CNS damage occurs it is
irreversible, survivors need rehabilitation, re education and long term
care.
SNAKE BITE
• Today snake bite is a common emergency, particularly among children
living in slums, villages. Three types of poisonous snakes encountered
in India are:-
• Neurotoxic cobra which causes paralysis of muscles of eyes (ptosis in
particular), palate, jaws, tongue, larynx, neck & chest, eventually
leading to respiratory failure. Cardiotoxicity (hypertension,
tachycardia, ECG alterations) and hemolysis may also occur. Onset of
manifestations is rapid. It will be within half an hour.
• Hemorrhagic hemotoxic viper which causes tissue distruction,
hemorrhage and has relatively slow onset of symptoms.
• Neuro hemotoxic krait which contains both neuro & hemotoxins. It is
the most common & dangerous poisonous snake in India.
• Other types: Poisonous water snakes.
Signs & symptoms
• General: - All snake bites are of frightening and case if shock.

• Nausea, vomiting, pallor, cold extremities.

• Local: - Burning pain at the site of the bite.

• Fang marks at the site of bite.

• Specific symptoms: - In cobra bite: - headache, dizziness, myalgia,

dysphagia, respiratory failure.
In viper poisoning
• Severe and increasing local pain with swelling.
• Discoloration & serosanguinous oozing from the puncture site.
• Pain, swelling, redness & numbness at the site of bite are commonly seen.
• Constitutional symptoms: - Appear after about 15-30 minutes of bite and include.
• Headache, dizziness, vomiting, CNS stimulation.
• Convulsion followed by depression, respiratory difficulty and various paralysis.
• Haemorrhage from different sites & circulatory collapse may occur.
• Haemorrhage signs which includes bleeding from fang punctures, venepuncture
sites, ecchymosis, and epistaxis, bleeding from gums, sub conjunctival and intra
cranial bleeding.
• Intracranial bleed is the usual cause of death within 24-48 hours.
Investigations
• Haemoglobin, complete blood count, platelet count.

• Clotting, time, bleeding time, prothrombin time.

• Blood urea nitrogen, creatine.

• ECG.

• Immuno-diagnosis by ELISA is useful (if available) to detect specific

snake venom in wound aspirate, serum or other body fluids
Grading of Envenomation
Grade Signs and symptoms
   
Grade 0  Nil
   
Grade 1
   Minimal with local swelling & pain that does not
  progress.
   
Grade 2  Moderate with swelling, pain & ecchymosis.
   
 
Grade 3  Severe, with remarkable local response, severe
  systematic findings & significant alteration in
laboratory tests.
 
 
Treatment
Immediate measures
• Patient should be kept recumbent, quiet and reassured. Only 25%
snakes are considered poisonous.
• Wound should be cleaned with saline/water.
• During transplantation to the hospital to prevent absorption of the
toxin a tourniquet is applied proximal to the bite site about 5cms
above the upper limit of swelling which allows one finger beneath.
• It should be left if Antivenin Serum (AVS) is not given.
• The bitten part should be immobilized and placed in dependent
position.
 
Treatment
Specific measures
• Antivenin is the remedy of choice, 20-30 ml of poly valent serum is given,
intravenously after a test dose.
• Through subcutaneous or intra muscular injection of antivenin is not helpful
because of the slow action.
• Antitoxin with dextran slowly given by the IV route. The dose can be repeated
after an hour & repeated when necessary.
• Children require larger doses, because there is greater concentration of
venom/kg/body weight.
• It is given IV infusion with distilled water or normal saline and diluted with 3
volumes of glucose saline, beginning at the rate of 1 ml/minute and increased
slowly as tolerated (usually 20 ml /kg/hour).
• Concurrent administration of steroids and antihistamines reduces the risk of
anaphylaxis due to antivenin.
Definitive indications for AVS in snake bite

• Systematic envenomation: - Bleeding, DIC, shock, ARF, neurotoxicity.

• Swelling over snake bite site: - Progressively spreading or bleeding.

Treatment
Supportive measures
• Fear should be allayed by reassurance and sedation with Phenobarbitone. The
child should be kept rest and given warmth by covering the blankets.
• Oxygen administration or artificial respiration.
• Antibodies for prevention of infection, drug of choice is ampicillin (200
mg/kg/day orally).
• Tetanus toxoid booster, if child had previous immunization.
• Corticosteroids (hydrocortisone) 1-2gm, intravenously every 4-6 hours decrease
the hypersensitivity reaction.
• Every 4hour vital signs check-up.
• Suctioning of the respiratory tract.
• Every 2 hourly change the position of the child.
Complications
1. Compartment syndrome characterized by six Ps namely:
• Pain out of proportion to injury.
• Pressure symptoms in the form of swollen part.
• Paraesthesia.
• Pulse being absent.
• Pain with passive stretch.
• Paralysis/Paresis.
2. Tissue necrosis
3. Bleeding diathesis
SCORPION STING
The incidence of scorpion sting is high especially during the tropical and
subtropical regions. Two species of scorpion namely Mesobuthus
tumulus and Palamneus swammerdani are poisonous in India. The
children are often brought to the hospital for manifestation with
various symptoms.
• Peripheral circulatory failure, profuse setting, cold and clammy skin,
restlessness, hypotension, vomiting.
• Generalised convulsions and hyperpyrexia, neurotoxicity and
symptoms and signs of congestive heart failure, tachycardia and
hepatomegaly.
• Severe pain over the sting site by tapping is often seen.
DIAGNOSIS

• Sudden onset of crying with profuse sweating, restlessness and

peripheral circulatory failure.

• Physical examination.
Treatment
Emergency measures

• If the heart rate is so fast, Adrenaline subcutaneously at 15 minute

interval and watch kept for return of pulse in the wrist and body
warmth.

• Anti-venom therapy with calcium gluconate 10% 5-10ml

intravenously, repeated if necessary.

• It may be helpful in relieving muscular cramps.

Lytic cocktail

• A solution containing pethidine 100mg, chlorpromazine (Largactil,

50mg) and promethazine (Phenergan, 100mg) made up to 50ml with
5% glucose in distilled water is prepared and administer intravenously
0.3cc/kg every 20minutes.

• Where signs of congestive heart failure are present (myocarditis)

adequate of digitalis and steroids in infants and 100mg every six
hourly in order children.
General measures
• Pain can be relieved by NSAID. Local ice packs, 2% xylocaine or
dehydroemetine locally. Diazepam is useful to quieten the restless
child, allays anxiety.
• Encourage oral fluid intake and give IV fluids judiciously to avoid
hypovolemia as well as pulmonary edema.
• Oxygen administration when necessary.
• Check vital signs, every hourly.
• Watch for complication like pneumonia, pulmonary edema and
myocarditis
GENERAL APPROACH TO
MANAGEMENT
Emergency treatment is initiated with the following goals:

• To remove or inactivate the poison before it is absorbed

• To provide supportive care in maintaining vital organ systems

• To administer a specific antidote to neutralize a specific poison

• To implement treatment that hastens the elimination of the absorbed

poison
DIAGNOSIS
History
• Most important indicator of toxic ingestion. Careful history regarding
involved toxins, amount of drug and timing should be recorded.
• Information regarding prescription medication, over the counter drugs
and illicit substances of abuse should be obtained.
• Friends, relatives and other involved healthcare providers should be
questioned and medications identified.
• Medication found on or near the patient should be examined and
pharmacy on the medication label should be called to determine the
status of all prescription medication.
Physical Examination

• Evaluation of Airway patency, Respiration,

• Circulation.

• Rapid assessment of mental status, temperature, pupil size, muscle

tone, reflexes, skin and peristaltic activity.
Laboratory evaluation
Clinical laboratory data include assessment of the three gaps of toxicology9
1. The Anion gap
2. The osmolal gap
3. The arterial oxygen saturation gap.

• Unexplained widening of the difference between calculated and measured

determination of these values raises the suspicion of toxic ingestion.
Toxicological Screening

It provides direct evidence of ingestions, but it rarely impacts initial

management and initial supportive measures should never await
results of such analysis. It is used to provide ground for treatment with
specific antidote or method for enhancing drug elimination also
identifies drugs that should be quantified to guide subsequent
management. Also look for characteristic signs of various kinds of
poisoning while immediate treatment measures are being started.
MANAGEMENT
Ingested poison
• Wash the mouth thoroughly with water
• Do not induce vomiting unless in hospital
• Do not give salt water, raw eggs, mustard, vinegar etc. orally
• Withhold food and drink
Eye contact
• Irrigate eyes with tepid water for at least 15 minutes making sure that
the eye lids are open.
Inhalation damage
• Move the patient from exposure site to fresh air
• Wear protective equipment in case need to enter the area
• Ensure clear airway
Dermal contact
• Remove contaminated clothing
• Wash skin thoroughly with soap and water for at least 15min
• Do not apply any medication or ointments on the affected area unless
advised
PREVENTION OF FURTHER
ABSORPTION
Dilution
Simple dilution is indicated when the toxin exerts a local irritant or
caustic effect on oral, oesophageal or gastric mucosa. These substance
include acids, alkalis and house hold cleansing agent. Both water and
milk acceptable as diluting agent. If suspected poison is medicinal toxin,
simple dilution is contraindicated because it may increase dissolution
rate of tablet or capsule and promote rapid transit into the lower
intestinal tract. Administration of fluids during induction of emesis is
appropriate.
GI decontamination
According to recent recommendations there is no place for routine gastric
lavage, emesis or activated charcoal. Gastric evacuation may be value upto 24
hrs. post ingestion, but in most effective if done within 1 – 2 hrs.
• Emesis may occur spontaneously following ingestion of many substances.
The use of emetic including ipecac syrup has declined in the recent past. A
dose of 30ml for adult, 15ml for children and 10ml for infants under one year
of age. Other emetics include Apo morphine, zinc sulphate, table salt, copper
sulphate etc. Induction of emesis is contraindicated in cases of hydrocarbon
ingestion.
• Gastric lavage is a commonly used procedure for evacuation of stomach but
it is used in pediatric patient is controversial. It should be done using normal
saline 15ml/kg maximum of 200- 400ml through oro-gastic tube. This should
be done in comatose clients after intubation with cuffed endotracheal tube.
Binding agents
• Activated charcoal is a binding agent, it should be prepared by the
pyrolysis of organic material such as wood pulp. It is activated by an
oxidising gas flow at high temperature to produce a fine network of
pores. It adsorbs wide variety of organic material in the GI tract thus
minimizing the absorption of toxin.
• Other binders including clays such as attapulgite, bentonite, fullers
earth, kaolin and pectin have been studied bedside cholestyramine.
These are less effective than activated charcoal. Carbonized resins and
modified silica gel were found to be effective as activated charcoal in
adsorbing methanol, ethylene glycol, kerosene and turpentine in
vitro.
Whole bowel irrigation
• Whole bowel irrigation is a recent addition to the emergency
treatment of poisoning. It removes the unabsorbed drug from the
entire gut mucosa. It’s a useful procedure for decontamination of gut.
It’s contraindicated in case of intestinal obstruction due to mechanical
cause of ileus, intestinal perforation and haemorrhage.
• For bowel irrigation isotonic balanced electrolyte solution containing
propylene glycol is administered in doses of 30 ml/ kg/ hr. in children
by NG tube or through oral route.
Diuresis
• Diuresis may be useful in cases of poisoning with agents that are
excreted primarily through the renal route. The diuresis is induced
with 20% mannitol in initial dose of 0.5gm/kg and then repeated to
ensure a urinary output of 6-9ml/ kg/ hr.
• Urinary alkalization can be achieved by use of sodium bicarbonate (1-
2 mEq/kg), IV infusion over a period of 1-2 hrs.
• Acidification of urine is usually initiated with ammonium chloride in a
dose of 75mg/ kg/ dose orally or through nasogastric tube every 6
hours to keep the urine pH 5 or less.
Important prerequisites for initiating diuresis are listed below:
• The drug should be well excreted through the renal route.
• The systolic blood pressure should be more than 90mm of Hg.
• There is no evidence of cardiac failure or respiratory insufficiency.
• Renal functions are normal.
• Blood levels of drug, if available, are in potentially toxic range.
SPECIFIC ANTIDOTES
Poison Antidote
Acetaminophen (Paracetamol ) N acetyl cysteine 140mg/kg ;orally
Toxic dose: 150mg/kg
Amphetamines Chlorpromazine 1mg/kg ;IM/IV
Toxic dose: 50mg
Atropine Pilocarpine 2-4mg orally or 0.25-0.5mg IM

Belladonna Physostigmine 0.5- 2mg IM

Benzodiazipines Flumazenil IV
Carbon monoxide 100% oxygen inhalation or hyperbaric oxygen
therapy
Cyanide Amyl nitrate0.3ml inhalation.
Fatal dose : 200- 300mg Sodium nitrate 3% slow IV.
Sodium thiosulphate 1.65ml/kg 25% solu IV
SPECIFIC ANTIDOTES
Ethylene glycol Ethanol 10ml/kg 10% solution IV
Heavy metals  
Mercury British anti lewisite 12-24mg/kg/day IM
   
Arsenic EDTA 50-75mg/kg/day IM or IV
   
Lead D pencillamine 20-40mg/kg orally
 

Heparin Protamine sulphate 1.0mg IV

 
Iron Deferoxamine 15mg/kg/hr IV infusion
Toxic dose: 35mg/kg
Isoniacid Pyridoxine 1mg IV
 
Methemoglobinemia Methylene blue 1-2 mg/kg/hr IV
SPECIFIC ANTIDOTES
Methylalcohol Ethyl alcohol 0.75-1.0ml/kg IV
Morphine, other opiates, semi synthetic Naloxone 0.1mg/kg IV
narcotics (heroin), meperidine, lomotil
(Diphenoxylate hydrochloride) and pentazocin

Organo phosphorous poisoning Atropine 0.02-0.05mg/kg/dose IV

Pralidoxime 25-50mg/kg IM

Phenothiazine and Metoclorpromide Diphenhydramine 1-2mg/kg IV

Propranolol (beta bockers) Atropine 0.01-0.02mg/kg SC
Warfarin, Dicumarol Vitamin K 5-10mg IM or IV
NURSING MANAGEMENT

• Ensuring airway patency and assessing for the risk of aspiration, especially after
any gastric decontamination process (make sure adequate suctioning equipment
is readily available)
• Checking vital signs and monitoring for hypotension or hypertension
• Monitor ECG and neurologic status closely for changes.
• An indwelling urinary catheter is inserted to monitor renal function.
• Blood specimens are obtained to determine the concentration of drug or poison.
• Determine what substance was ingested; the amount; the time since ingestion;
signs and symptoms, such pain or burning sensations, any evidence of redness or
burn in the mouth or throat, pain on swallowing, vomiting or drooling; age and
weight of the patient and pertinent health history.
NURSING MANAGEMENT

• Ensuring telemetry monitoring is intact and active (check for ventricular tachycardia or
Brady arrhythmias with hypotension)
• Initiating seizures precautions if necessary.
• The patient who ingested a corrosive poison is given water or milk to drink for dilution.
• Dilution is not attempted if the patient has acute airway edema or obstruction or if
there is clinical evidence of oesophageal, gastric, or intestinal burn or perforation.
• Do gastric emptying procedures such as syrup of ipecac to induce vomiting (never use
with corrosive poisons); gastric lavage; activated charcoal administration; and
cathartic.
• The specific chemical or physiologic antagonist is administered as early as possible to
reverse or diminish the effect of toxin.
NURSING DIAGNOSIS
• Imbalance nutrition less than body requirement

• Impaired oral mucous membrane

• Impaired swallowing

• Risk for poisoning

• Acute pain

• Risk for injury

CONCLUSION
Every episode of poisoning should be probed in detail to identify the
circumstances that lead to the accident. The opportunity should be
taken to allay guilt feelings and impart proper advice to the parents to
avoid recurrence of misadventure. There is a need to create public
awareness and impart health education through mass media to prevent
accidental poisoning. The drugs should be kept in cupboards away from
the reach of inquisitive children. Unused medicines should be discarded
properly.
REFERENCE
• Meherban Singh, Medical emergency in children, 5th edn, CBS publishers.
• Beherman, Nelsons text book of pediatrics, 17th edn, Elsevier publishers.
• Arun Babu, Pediatrics for medical graduates, 1st edn, Elsevier publishers.
• Terrikyle, Essentials of pediatric nursing, 1st edn, Wolterkluer publishers.
• Krishna Handa, Pediatric nursing, 1st edn, Lotus publishers.
• Wong’s; Marilyn, Essentials of Pediatric Nursing, 8th edition, Elsevier Publication.
• Rimple Sharma, Essentials of Pediatric Nursing, 2th edition, Jaypee Brothers Medical
Publishers.
• Manoj Yadav, A Text Book of ChildhealthNursing, 2011 edition, Choice books & printers
(P) ltd.
• https://www.google.com/search?q=accidents+in+children
Thankyou