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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 administration of
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
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
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.
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
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.
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. 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:
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.
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.
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.
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
Resp
Other associations
Pinpoint
Dilated
Agitation, hallucination
Atropine
Coma
Coma
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
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 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.
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
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.
Continued
Management of hypothermia- cover with a
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
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).
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.
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.
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
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.
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.
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.
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.
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.
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 Ryles tube
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.
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.
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.
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.
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.
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.
household poisons. Need for parental supervision of toddlers 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.
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 FEVER SEVERE MALNUTRITION RESP. DISTRESS CNS SYMPTOMS ABSENT 0 0 0 0 PRESENT 1 1 2 2 OTHERS 0 0 4 4
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
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
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.
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.
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
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
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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
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 childs 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 Drugs and Magic remedies Act1954. To ban advertisements procuring abortion/increase of sexual potency/treatment of veneral diseases/correction of menstrual disorders.