Poisoning 5z2o1

POISONING Dr. M.L.Siddaraju

History • Egyptians are said to have studied many poisons as early • • • • •

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 •

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 istration of

overdosage of drugs by the parents or by the medical staff is also frequent.

• Acute exposure is a single that

•

lasts for seconds, minutes or hours, or several exposures over about a day or less. Chronic exposure is 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 (pesticides), or injection (bites and stings, drug injection

• Accidental poisoning in children is a

•

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 issions in pediatric wards in India and s 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

•

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 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, • •

• •

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 • • • • •

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 • •

•

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 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 ing 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 • • • • • • •

& emergency medical system near the phone. Removal of the patient from the site of poisoning. Initial resuscitation and stabilization. Symptomatic and ive 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 istration 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 & ive Management • Hemodynamic - elevation of foot • •

end of the bed, oxygen istration, 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

•

blanket, thermo neutral environment maintenance, pre warmed IV fluids and inspired gases. Management of pulmonary edemaister 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, istration 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 istration; 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) istration 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 ed 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 istration • 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 istration of activated charcoal via an orogastric or nasogastric tube within 1-2 hours of ingestion. Dose of activated charcoal istered 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 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 istered 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.

ive 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 •

• •

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 • • • •

Epidemiology Clinical features Investigation Treatment

Epidemiology • Accidental – 33 to 60% in India & other •

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

0

1

0

SEVERE MALNUTRITION RESP. DISTRESS

0

1

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 •

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 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 istered. 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 ing 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

•

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 istering

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

• •

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 istered 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 istered 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, ister 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 ed pharmacists to prepare, mix or dispense any medicine on prescription of a medical practitioner.

The Drugs and Magic remedies Act1954. To ban ments procuring abortion/increase of sexual potency/treatment of veneral diseases/correction of menstrual disorders.