poisoning.ppt

8/11/2019 poisoning.ppt

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POISONING

Dr. M.L.Siddaraju


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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

6

th

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.


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Acute exposure is a single contact thatlasts for seconds, minutes or hours, orseveral exposures over about a day or less.Chronic exposure is contact that lasts formany days, months or years.

A poison may get into the body throughingestion, inhalation (gas, vapors, dust,fumes, smoke, spray), skin contact(pesticides), or injection (bites and stings,drug injection


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Accidental poisoning in children is a

global problem. The relative importanceof poisoning as a cause of childhoodmorbidity and mortality increases whenmalnutrition and infections are broughtunder control.

Accidental poisoning is the twelfthleading cause of admissions in pediatricwards in India and accounts for aboutone percent of the hospitalized patients.

Most cases of accidental poisoning arepreventable. Continuing morbidity andmortality due to accidental poisoning isserious challenge to the pediatriciansand public health officials.


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Pattern of poisoning

Chemical products, most often swallowedby children include household cleaners(bleach, detergents) fuel (kerosene,

paraffin), cosmetics, medicines, paints andproducts for household repairs andhousehold pesticides.

Bites and stings of animals and insects,

and ingestion of poisonous plants andseeds also considerably account foroutdoor poisoning in children.


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Carbon monoxide poisoning canhappen when fires, stoves, heaters or

ovens are used in rooms, huts whichdo not have proper ventilation to letthe gas out.


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Large families:In large families motheris often too occupied with household

chores, is easily fatigued and oftencareless in storage of potentiallypoisonous household substances.

Small accommodation


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Environment: Lead poisoning is common inchildren living in areas were there areworkshops for automobile, lead storagebatteries or for manufacture of lead typesetsfor printing presses. Caustic soda poisoningused to be observed frequently in children offamilies, which prepared washing soap fordomestic or commercial purposes in their ownhouses. Insecticides, medicines, naphthalene

balls and kerosene are common householdthings 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 aremore common in those wandering infields.Also pesticides are more common inrural set up. The poor are driven by starvationto experiment on roots and fruits thus leading

to poisoning.


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Time relationship:

. Accidental poisoning is likely when

normal routine in the house isdisturbed such as during periodichouse painting, packing and

unpacking at the time of change ofresidence, going for vacation etc.


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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.


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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.


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Important causes of childpoisoning 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%).


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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.


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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 likeexpression, pallor, cyanosis,hypothermia, sweating, respiratorysymptoms, CVS symptoms, CNSs m toms.


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Poisoning severity Grades

None(0)- no symptoms orsigns/vague symptoms judged

not to be related to poisoning. Minor(1)- Mild, transient &

spontaneously resolving

symptoms.


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Moderate(2)- pronounced orprolonged symptoms.

Severe(3)- severe or lifethreatening symptoms.


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Diagnosis of Poisoning

Cardiac arrythmias. Tricyclicantidepressants, amphetamine, aluminiumphosphide, 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.


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Basic Management of a

poisoned patient

Antidotes are available for very fewcommonly encountered poisons, and

treatment is usually non-specific andsymptomatic. In such casesmanagement consists of emergencyfirst aid and stabilization measures,

appropriate treatment to reduceabsorption, measures to enhance lifesupport followed by psychiatriccounseling.


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Identification of Poison

Identify the poison by careful historyand helpful clues. Determine what,

when and how much of the poisonwas ingested or inhaled. Find thesupporting evidence for yourdiagnosis from the nature of the

symptoms and physical signs. Somecommon toxidromes based on certainsigns and symptoms :

P il R C i P ibl t Oth


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Pupils Resp Consciousness

Possible agent Otherassociations

Pinpoint Coma

Coma

Coma

Organophosphorusinsecticides,carbamates

Opioids

Phenothiazines

Cholinergic:bradycardia,wheeze,salivation

Hypotension,

hypothermia

Cardiacarrhythmia

Dilated Agitation At opine Anticholine g


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Dilated Agitation,hallucination

Coma

Coma

Agitation,hallucination

Atropine

Tricyclic

antidepressants

Sedatives,barbiturates

Theophylline,amphetamines

Anticholinergic; fever, drymucousmembranes,

flushing,urinaryretention

Cardiac

arrhythmia,seizure

,hypotension

Hypotension,hypothermia,hyporeflexia

Seizures,tachcardia,hypertension

, acidosis

N l C U i A id i


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Normal Coma

Coma

Uremia

Salicylates

Acidosis,hyperkalemia

Tinnitus,agitation,

diaphoresis,alkalosisfollowed byacidosis


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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.


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Emergency Stablization Measures

The unconscious patient should be transportedin the headdown semiprone position to minimizethe risk of inhalation of gastric contents. A clearairway is established and ventilation ismaintained. Potentially serious abnormalitiessuch as metabolic acidosis, hyperkalemia and

hypoglcymia may require correction as a matterof urgency. Neurological assessment is made bycalculating the Glasgow Coma Score (GCS).


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Many drugs and poisons can cause grand malconvulsions, which, if repeated, should becontrolled with intravenous diazepam.

Hypotension with peripheral circulatory failure istreated first by correction of hypoxia and acidosis,and by elevation of the foot end of the bed. Ifadequate perfusion is not restored by thesemeasures, the circulating volume should be

increased by administration of a plasma expanderintravenously. Cardiac arrhythmias are oftenimproved or abolished by correction of hypoxia,acidosis and electroyte imbalance


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Initial resuscitation

stabilization

Includes airway- proper positioning head tilt andchin lift, suction of secretions from oropharynx,falling back of tongue is prevented by suitableairway tube.

Breathing- oxygen via a mask, when gag/coughreflects is absent- ET tube inserted. if necessarypositive pressure ventilation with ABGmonitoring, respiratory stimulants for severerespiratory depression.

Circulation- proper IV access, maintenance offluid & electrolyte balance, IV drugs fortreatment.


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Symptomatic & supportive

Management

Hemodynamic support- elevation of footend of the bed, oxygen administration, IVfluids, blood products.

Cardiac dysrrhythmias- correction ofhypoxia, acidosis, hypokalemia, ECG,treatment with antiarrhythmic drugs.

Convulsions- correction ofhypoglycemia/hypocalcemia/hypoxia/cerebral edema and other metabolic defects,anticonvulsant therapy.


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Continued

Management of hypothermia- cover with ablanket, thermo neutral environmentmaintenance, pre warmed IV fluids andinspired gases.

Management of pulmonary edema-administer 100% oxygen, intermittent

positive pressure ventilation, IVaminophylline(5-8mg/kg), IVfrusemide(1-2 mg/kg).


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Continued

Management of stress ulcers- NGintubation, cold saline wash,

administration of antacids, H2-receptor antagonists.

Management of pain- analgesics

(preferably- narcotics).


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Removal of Toxin

The aim of decontamination procedures isto reduce the absorption of poison. It canbe achieved by:

Eye decontamination. Ocular exposure tosolvents, e.g., hydrocarbons, detergents, andalcohol, or corrosive agents, e.g., acid or alkalisrequire immediate local decontamination. Thisis achieved by copious irrigation withneutralizing solution (e.g., normal saline orwater) for at least 30 minutes. Do not use acidor alkaline irrigating solution.


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Dermal decontamination. Absorption oforganophosphorus and relatedcompounds through cutaneous routecan prove to be a fatal as oral routeabsorption. Cutaneous absorptiondepends on several factors such as lipid

solubility, skin condition, location,caustic effect, physical conditions


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Remove all contaminated clothes and irrigate thewhole body including nail, groin, skinfolds withwater or saline as soon as possible after exposureand continue irrigating for at least 15 minutes.Water should not be used to decontaminate skinin exposures to sodium and phosphorus. Incertain cases, specific agents may be indicated forskin decontamination (e.g., mineral oil for

elemental sodium, Neosporin for super glue andcalcium gluconate for hydrofluoric acid).


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Gut decontamination. This includes (i) gastricevacuation; (ii) adsorbent administration; and(iii) catharsis. Emesis is the preferred method ofemptying the stomach in conscious children.Vomiting can be induced by (a) tickling the fauceswith a finger, feather or a leafy twig of a tree; (b)administration of copious draughts of warmwater; (c) gurgling with non-detergent soap; or

(d) saline emetics in warm water. To preventaspiration in small children, the head should bekept low.


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Syrup of ipecac may be used for inducingemesis in children older than 6 months in asingle dose of 10 mL for 6-12 months age,

and 15 mL for children above 1 year ofage. The dose may be repeated in 20minutes for those more than 1 year of age.

Induction of vomiting is contraindicatied

in corrosive or kerosene poisoning and incomatose patients or those with absentgag reflex.


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Gastric Lavage. If the vomiting

does not occur quickly, gastric

lavage should be done promptly toremove the poison. In asymptomatic but alert patient with

minor ingestion, activated charcoalalone by mouth is sufficient forgastrointestinal decontamination


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The child is kept in the left lateral positionwith the head hanging over edge of thetable and the face down. A large single

lumen tube with multiple distal ports isnecessary. A restraint is required for mostchildren and mouth gag is placed in themouth before the procedure. The catheter

is passed gently and free end is dippedunder water to make sure that thecatheter is not in the airway.


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Generally tap water is used for lavage andfour or five washes are done. The volumeof each aliquot should be at least 10-15mL/kg. After the fluid has been instilled, itshould be removed by gravity drainage ortube suction. Catheter is pinched before it

is finally withdrawn or suction ismaintained during withdrawal to preventaspiration.


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Gastric lavage should not beperformed in children with poor gagreflex or corrosive ingestion. Inkerosene poisoning, lavage may bedone very cautiously if the child hasconsumed a large gulp of kerosene

and is brought quickly to thehospital, otherwise it is better toavoid stomach wash.


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Adsorbent administration

An agent capable of binding to atoxic agent in the GIT is known as

adsorbent. Activated charcoal is themost widely used adsorbent. It iscreated by subjecting carbonaceousmaterial e.g., wood, coal etc. tosteam at 600-900 degree Celsius andacid.


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For the comatosed patient (Grade 3 or 4)with potentially serious overdose, gastriclavage is followed by administration of

activated charcoal via an orogastric ornasogastric tube within 1-2 hours ofingestion. Dose of activated charcoaladministered should be atleast 10 timesthe dose of ingested toxic material. In

asymptomatic patient presenting early orwithout reliable history, 15-30 gram ofcharcoal may be used.


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Catharsis

Laxative and purgatives may be given inpoisoning with substances which do notcause corrosive action on gastrointestinalmucosa. Increased motility of the gut mayreduce absorption. Commonly usedcathartics include sorbitol and mannitol (1-

2 g/kg), and magnesium or sodium sulfate(200-300 mg/kg). Do not give magnesiumsalt cathartics in cases with renal failure.


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Specific Antidotal Therapy

The antidotes may be physiological, chemical orphysical. Chemical antidotes combine with thepoison and render it innocuous. Physiologicalantidotes counteract the effects of the poison onthe metabolism and physiological functions of thebody and thus prevent its harmful effects.Physical antidotes prevent the contact of thepoisonous substance with the target organ or

adsorb the toxic components, thus preventingtheir toxicity.


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Specific antidotes may be life saving butunfortunately they are not often availableand are effective for less than 5% of

poisoning cases. When obtainable, theymust be given without delay for maximumprotective action.

Antidotes now considered obsolete includeuniversal antidote for ingested poisons,

acetazolamide for modification of urinarypH, ascorbic acid for methemoglobinemia,castor oil as cathartic, nalorphine foropiates, sodium chloride for emesis andtannins for alkaloids.


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Promotion of Excretion ofToxin

The efficiency of regimens forenhancement of drug elimination from

the body can be predicted to a largeextent if the physio-chemical properties,disposition and pharmacokinetics of thesubstance are known. The fluid intake isincreased to promote glomerularfiltration and excretion of poison throughthe urine.


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Forced diuresis:Diuresis alone has relatively littleeffect on drug elimination because at best the renalclearance is only proportional to the urine flow rate.In the case of drugs which are weak organic acidsand bases, a much greater effect on clearance canbe obtained by manipulation of the urine Ph. Thelipid solubility and hence tubular reabsorption ofsuch acidic and basic drugs is decreased in alkalineand acid urine respectively. Theoretically for each

change of one unit in urine pH, the renal clearancecould change by a factor of 10. Urine pH is thereforemuch more important than urine flow rate.


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In practices, forced alkaline diuresis is restrictedlargely to poisoning with phenobarbitone andsalicylate, although much of the effect in loweringplasma salicylate concentrations result from

haemodilution rather than increased urinaryexcretion. Raise the urinary pH to 7.5 for weakacids (e.g., barbiturates, salicylates) with 1.4percent sodabicarb. Maintain urinary pH to 5.5-6.5 (forced acidic diuresis) in poisoning withweak bases e.g., tricyclic antidepressant andpheytoin, with ammonium chloride 4 gadministered every two hourly through Rylestube


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Any form of forced diuresis is potentiallydangerous. Forced diuresis is

contraindicated in patients with cardiacand renal impairment; complicationsinclude water intoxication, disturbances ofacid-base and electrolyte balance, leftventricular failure with pulmonary oedemaand cerebral oedema.


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Hemodialysis, hemo-perfusion andperitoneal dialysis. Drugs which canbe removed reasonably effectively byhemoperfusion and haemodialysisinclude barbiturates, carbamazepine,salicylates, theophylline, dapsone,

most antibiotics, lithium, chloralhydrate, methanol and ethyleneglycol.


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Peritoneal dialysis is much less effective and it isused rarely. It has the advantage that is doesnot require special facilities but may becomplicated by fluid and electrolyteabnormalities, perforations, peritonitis andadhesions.

Dialysis is not useful in poisoning with digitalis,antihistaminics, belladonna alkaloids, opiates,etc.


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Supportive Therapy

Keep the airway open, give oxygenfor inhalation and be prepared forintermittent positive pressure

respiration. Fluid and electrolytebalance is maintained. Circulatoryfailure should be managed to sustainlife. Anemia is treated with packed

cell transfusion.


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Severe convulsions and statusepilepticus are treated with

diazepam or midazolam. Renal failureis managed as per standard protocol;dialysis may be needed. Infectionsare treated with antibiotics. Feverand pain are relived with antipyreticsand analgesics.


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Prevention of Poisoning

Protection of the child from thepoisonous substances. The poisonoussubstances should be kept in secure

places out of reach of the child. Thepoisonous substances should bereplaced in their proper place. Potentialhousehold poisons should not betransferred to empty containersotherwise used for innocuous food orbeverages.


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Drugs should be dispensed in the originalcontainer. The word poison should beexhibited prominently on the containers of

potential poisonous substances. Keroseneoil and caustic soda should not be storedin tumblers or beverage bottles. Thecontainers should not be left on the

ground. Kerosene bottles and stovesshould be kept out of reach of the childrenin the kitchen.


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Education of parents about potentialhousehold poisons.

Need for parental supervision of toddlers

behavior should be emphasized. Safety regulations by the State should beenforced.

Establishment of poison control centers to

collect, compile and disseminateinformation on poisons and theirmanagement. These should promoteresearch on prevention and treatment.


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Some Specific Poisons

and Antidotes


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KEROSENE POISONING

Epidemiology

Clinical features

Investigation

Treatment


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Epidemiology

Accidental33 to 60% in India & otherdeveloping countries

Reasons for high incidence

1. Extensive use for cooking & lighting inlow socioeconomic status

2. Stored in soft drink bottles, beer

bottles within reach of children


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Clinical features

Age1 to 3 years

more than 70% symptomatic within

10 hours

SYMPTOMS

RS

breathlessness, coughCNS convulsions, coma

GPE fever, restlessness, cyanosis

GI vomiting, diarrhea


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Lab Investigations

BloodLeukocytosis

X Ray changes

Changes appear within one hour- commonly right basal infiltrates- emphysema- pleural effusion- pneumatocoeles

Severity score


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Severity score

PARAMETERS ABSENT PRESENT OTHERS

FEVER 0 1 0

SEVERE

MALNUTRITION

0 1 0

RESP. DISTRESS 0 2 4CNS SYMPTOMS 0 2 4

>4

Significant 8 Risk of death is increased

Management


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Management

Avoid emetics

Avoid gastric lavageIn case of massiveamount 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 hrsIV qid

Kanamycin10-15mg/Kg/24 hrs - IM bd

SteroidsNot helpful


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Complications

Pneumothorax

Pneumatocoeles

Pleural effusion

Bronchopneumonia

Coma

Organophosphorus


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Organophosphorus(insecticides and pesticides)

Poisoning Organic phosphate insecticides cause

irreversible inhibition of the enzyme

cholinesterase. As resultacetylcholine accumulates in varioustissues. Excessive parasympatheticactivity occurs. These agents areabsorbed by all routes including skinand mucosa.


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Symptoms manifest quickly usually withina few hours and include weakness, blurredvision, headache, giddiness, nausea, and

pain in chest. These patients haveexcessive secretion in the lungs and theysweat profusely. Salivation is marked.Pupils are constricted and papilledema

may occur. Muscle twitching, convulsionsand coma occur in severe cases. Reflexesare absent and sphincter control is lost.


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Treatment

If the insecticide was in contact with skinor eyes, these are thoroughly washed.Stomach wash is done.

Atropine sulphate: 0.03 to 0.04 mg/kg IV(atropine sulphate is usually available inampules 1 in 1,000 or 1 mg/mL). Otherstrengths may also be available. Repeat

half the dose in 15 minutes and ifnecessary every hour (until signs oftoxicity appear), subject to a maximum of1 mg/kg in 24 hours.


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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 injectmorphine, theophylline, aminophylline orchlorpromazine. Intravenous fluids shouldonly be given with caution. No oral

tranquilizers are administered. Artificialrespiration may be necessary to sustainlife.


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Iron Intoxication

Ingestion of a number of tablets of ferroussulphate may cause acute poisoning.Lethal dose is 300 mg/kg of iron. Severe

vomiting and diarrhea occur. These maycontain blood due to extensivegastrointestinal bleeding. The child may gointo severe shock, hepatic and renal failurewithin a few hours or after a latent periodof 1 to 2 days


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Treatment

Vomiting should be induced and stomachshould be washed with sodiumbicarbonate solution. Shock is corrected byinfusion of fluids parenterally. Three mL of7.5 percent sodium bicarbonate solutionper kg of body weight are diluted with 3times its volume of 5 percent glucosesolution and injected intravenously for

treatment of acidosis. This dose may berepeated after an hour if acidosis ispersisting.


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Iron salts are chelated withdesferrioxamine IV at 15mg/kg/hour until

the serum iron is


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Salicylate Poisoning

Ingestion of 150 mg/kg of salicylatescauses intoxication. Salicylate level of 50-80 mg/dL causes moderate symptoms.Severe symptoms are associated withblood levels above 80 mg/dL.

Initially, there is a respiratory alkalosis,because of hyperventilation induced bysensitization of the respiratory center by

salicylates. Kidneys compensate for thisalkalsis by increasing the excretion ofsodium and potassium bicarbonate


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Metabolic acidosis supervenesquickly due to disturbances ofoxidative phosphorylation andreduction of hepatic glycogen withresultant ketonemia. The patients aretreated with adequate replacement

of fluids to restore renal function.


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Urine is alkalinized by administering1-2 mEq/kg of sodium bicarbonate athalf hourly intervals for 4 hours topromote excretion of urine, becausein alkaline urine, salicylates do notdiffuse back into the tubular cells

from the lumen. Potassium saltsshould be given (3-5 mEq/kg/day) toreplace the potassium losses

Acetaminophen


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Acetaminophen

(paracetamol)

It is safe in pharmacological doses.Overdosage may cause hepaticdamage. Acetaminophen overdosageis treated with acetylcysteine to beused orally within 16 hours afteringestion in a loading dosage of 140

mg/kg diluted to 5 percent solutionorally followed by 70 mg/kg q 4h foranother 16 doses.


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Hydrocarbon Poisoning

These may be divided into aliphaticor aromatic compounds. Aliphatichydrocarbons include kerosene,turpentine, lubricating oils, tar andhave greatest risk of aspiration andpulmonary symptoms. Aromatic

compounds have mainly neurologicaland hepatic toxicity and includebenzene compounds.


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Type of toxicity with a hydrocarbondepends on its volatility, viscosity orsurface tension. The lower isviscosity, more is the risk ofpulmonary aspiration. Mineral spirit,kerosene and furniture polish have

both low volatility and viscosity andthus carry a higher risk of aspirationpneumonia.


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Benzene derivates, toluene and xylene arecomponents of various solvents anddegreasers. These are highly volatile but

have low viscosity. Inhalation is theprimary route of toxicity which manifestswith CNS symptoms. Gasoline and naphthaare constituents of lighter fuel and lacquerdiluent and primarily cause depression ofthe central nervous system (CNS).


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Turpentine oil is highly volatile but has lowviscosity also. Toxicity results from inhalation andgastrointestinal absorption. They can also causeCNS toxicity.

Halogenated hydrocarbons are used as solventsand spot removers. Freon is used as a refrigerant.

Toxic exposure to hydrocarbons may result incardia, gastrointestinal, neurological, pulmonary,

renal, hepatic, metabolic and hematologicalmanifestations.


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Induced emesis or gastric lavage iscontraindicated for kerosene oilpoisoning. It is done only when large

quantities of turpentine have beeningested or the hydrocarbons productcontains benzene, toluene,

halogenated hydrocarbons, heavymetals, pesticides or aniline dyes.Other specific modalities includingsteroids and antibiotics are not

efficacious.


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Carbon Monoxide Poisoning

Carbon monoxide poisoning results frominhalation of fire smoke, automobileexhaust, fumes from faulty gas stoves and

ingestion of paint and varnish removers.Clinical manifestations include headache,cyanosis, convulsions, and coma. Patientsare administered 100 percent oxygen andif carboxyhemoglobin levels are above 40percent, hyperbaric oxygen therapy isconsidered.


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Pyrethrin Poisoning

Pyrethrin is an active ingredient of variousmosquito and fly repellant strips. Theseinsecticides quickly inactivate the insect.

Mammals are relatively resistant to theseagents and most cases of toxicity withthese agent occur because of allergicreactions. Ingestion of these repellantstrips does not lead to significantsymptoms.

Lead Poisoning


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Lead Poisoning

Exposure to lead occurs from old

lead based deteriorated housepaint (in old houses) and dust andsoil contaminated with lead suchas from leaded gasoline, lead

electrode plates from oldautomobile batteries, adulteredfood, folk remedies, broken leadtypesets scattered around old

printing establishments. Food maybe adulterated with coloredmetallic salts or the black collyriumused as surma may contain aproportion of black oxide of lead.

Lead Poisoning


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Lead Poisoning

Chronic lead intoxication occurs

usually in children who eat non-edible substances (pica) andmanifests as pain in abdomen andresistant anemia. Lead is deposited

in the bones. Acute infections maymobilize lead from storage areas inbones and cause acute leadpoisoning leading to acute lead

encephalopathy.


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In these cases the child may be left withneurological sequelae. Lead inhibitssulfhydryl enzymes and formation of

heme. Heme precursors such as porphyrinsaccumulate in the blood and are excretedin the urine. Screening for leadintoxication is done by measuring zincprotoporphyrin or blood lead levels.


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Treatment

In symptomatic children, therapy isusually started with dimercapol (BAL) (75mg/m2 every 4 hourly IM). BAL may bestopped after 48 hours, while calciumdisodium edetate is used for another 3days but at a lower dosage of 50 mg/kg or1000 mg/M2 per 24 hours by continuousIV infusion.


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Maximum daily dose should not exceed500 mg/kg. Stop BAL when blood leadlevel falls below 60 microgram/dL. Give a

second course of edetate alone if bloodlead rebounds to 45-69 microgram/dL. Asecond course of edetate in combinationwith BAL is recommended for reboundlead level of >70 microgram/dL. Wait for5-7 days in between the two courses.


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Barbiturate Poisoning

Clinical features include hypoxia,depression of respiration, pulmonary

complications and kidney failure.Peripheral vascular bed is dilated;shock which may sometimes bedelayed may occur


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Treatment

Hypoxia is managed by oxygen inhalationand maintenance of open air way.Circulatory collapse is treated with fluids

and plasma. Patients do not respond toepinephrine.

Urine is alkalinized to facilitate excretionof barbiturates. Mannitol is given. This

causes osmotic diuresis. In severe casesperitoneal dialysis may be necessary toremove barbiturates.


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Alcohol Poisoning

Ethyl alcohol 0.75-1 mL/kg is givenIV followed by 0.5 mL/kg every 4

hours. Three mL of 7.5% sodiumbicarbonate solution diluted 1 in 4 isgiven IV. Dialysis should be done.


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Cyanide Poisoning

Sodium nitrite 2.5 to 5 mL of 3.5percent solution is given IV everyminute followed by sodiumthiosulfate 2.5 mL of 25 percentsolution every minute subject to amaximum of 50 mL. Amylnitritecapsules (10mg/kg) may be

inhaled.


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Opium Morphine) Poisoning

Respiratory depression occurs and pupilsare constricted; patients are excessively

drowsy.


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Treatment:-Stomach wash is done.

Specific antidote for opium poisoning isnaloxone given IV in a dose of 0.03

mg/kg/dose. If there is no response in 2minutes the same dose may be repeated.Naloxone can also be given by continuousinfusion (20-40 microgram/kg/h).Analeptics may be used and oxygen isadministered by inhalation.

Dhatura Belladonna) Poisoning


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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 0.02mg/kg (maximum 2 mg) IV slowly.Dose may be increased andrepeated after 20 minutes.


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Isoniazid INH) Intoxication

Toxic effects of INH may be (i)directly due to the drug i.e., jaundice,

SLE, arthralgias, altered sensorium,hemolysis and hypersensitivityreactions; or (ii) due to pyridoxinedepletion i.e., convulsions, peripheral

neuropathy, demyelination andinhibition of phenytoin metabolism.Lethal doses are>50 mg/kg.


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Gastric lavage is indicated. Patients aregiven 1 g of pyridoxine (vit. B6) for eachgram of INH ingested. If amount ofingested INH is not known, administer 70mg/kg of pyridoxine intravenously. Thedose may be repeated if seizures recur.Use diazepam or phenobarbitone tocontrol seizures. In severe cases with

seizures not responding to treatmenthemodialysis may be necessary to savelife.


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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


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Preventing childhood

poisoning

Education is the major component ofany poison prevention programme.

Keep medicines, insecticides, etcout of the reach and sight of yourchildren.

Never store food & cleaning products

together. Store medicine andchemicals in original containers.


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The label should be read before using thedrug. No drug should be given or taken inthe dark. Drugs after their expiry date

should be disposed in a safe manner.Avoid taking medicine in your childspresence. Never suggest that medicine iscandy.

Children should be taught not to eat plantsor berries.

L i


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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 ingredientscontained in it.

The Pharmacy Act-1948

The object of this act is to allow only the registeredpharmacists to prepare, mix or dispense any

medicine on prescription of a medical practitioner.


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The Drugs and Magic remedies Act-1954.

To ban advertisements procuringabortion/increase of sexualpotency/treatment of veneraldiseases/correction of menstrualdisorders.


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poisoning.ppt

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