Common Poison in Children

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4/19/12

COMMON POISON INCHILDREN

BYDY BATUBO, NIMISOERE P



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INTRODUCTION

v Poisoning are substances that results in toxicity when incontact with the body by altering the normal physiology of

the body.

v Toxicity result in 2 ways

1. exposure to excess amounts of normally nontoxicsubstances

2. exposure to substances that are poisonous at alldoses

v Route of poisoning

v injection,

v inhalation, or

v exposure of body surfaces (eg, skin, eye, mucous membranes)

v Ingestion

Epidemiology



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Poisoning in children: general principles

v Ascertain the nature and time of poisoning.

v

Contact the local Poison Centre for advice (if available).v Assess the patient following the principles of ‘ABC’ (Airway,

Breathing, and Circulation). If airway protection is impaired,the patient requires intubation.

v Induced emesis is no longer recommended and iscontraindicated with volatile substances.

v Consider gastric emptying and administration of activatedcharcoal

v Remove contaminated clothing and wash patient with soap

and water

v Send samples for lab investigation (urea, electrolytes, bloodglucose.) Urine and gastric aspirates should be saved forlater toxicology analysis (where available).

v Measure relevant drug levels (paracetamol and salicylateand others if available).



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GROUP OF POISONS

v Household chemicals e.g bleach, drain cleaner

v Hydrocarbons – kerosene

v Inhaled poisons – CO, cyanide, lead

v Medicines – aspirin/salicylate, paracetamol, iron,theophylline

v Pesticides- paraguat, organophosphate

v Toxic plant- mushroom



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Household chemicals

v Children frequently ingest household substances and mostof these are non-toxic. However, some products contain

alcohol which may cause seizures and hypoxia

v Household solutions of bleach contain approximately 10%hypochlorite

v Commonly, they cause nausea, vomiting and diarrhoea.

Less than 100ml of household bleach is unlikely to causeserious problems

v Ingestion of small quantities of strong alkalis such as draincleaner containing sodium hydroxide may causedevastating injuries. Oesophageal injury is most common

and evolves over the course of a few days.

v Ingestion causes immediate burning pain, swelling of thelips, and depending on the quantity ingested, salivation,haematemesis, dyspnoea, stridor or shock.

v

The burn injury is classified by endoscopy:



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Hydrocarbons (Paraffin, white spirit)v Most of the hydrocarbons are petroleum distillates,

containing a variable amount of saturated and unsaturatedaliphatic (open-chain) and aromatic(cyclic) hydrocarbons.

v The aliphatics are not readily absorbed from thegastrointestinal tract and therefore cause minimal systemictoxicity. Paraffin, petrol, thinners, diesel and benzene arelow viscosity aliphatic-based petroleum distillates

v The aromatic hydrocarbons are well absorbed, and

therefore may cause systemic toxic affects but are lessinclined to aspiration-related complications.

v The main hazard of accidental ingestion of the aliphatichydrocarbons (paraffin) is that of chemical pneumonitischaracterised by ventilation/perfusion imbalance and

hypoxia

v This can occur even in the absence of vomiting or impairedconsciousness and as little as 1ml aspirated hydrocarboncan result in a chemical pneumonitis.

v Signs and symptoms appear after 30 minutes of ingestionbut ma be dela ed for 8 hours. A non- roductive cou h



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v The clinical picture generally deteriorates over the first 24hours. A temperature that persists or only develops after 24

hours usually suggests a secondary infection.v Abnormalities on the chest film may be seen within 30

minutes after aspiration even in the absence of clinicalsigns or symptoms.

v Common radiological findings of chemical pneumonitisinclude bilateral perihilar infiltrates which progress to formpatchy infiltrates and later become large areas of consolidation.

v Diagnosis of kerosene poisoning can be made even in theabsence of specific laboratory parameters if there is apositive history of exposure (ingestion) supported bycompatible respiratory and neurological findings.

v Investigations such as full blood count, serum, electrolytes,urea and creatinine, as well as liver function test are doneto aid management and to monitor complications in other



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Management of kerosene poisoning

v ABC principles

v Observe all asymptomatic patients for at least 8 hours.

Carefully examine patients for the development of respiratory signs. A chest film at 6 hours is recommended.

v If asymptomatic after 8 hours and the chest film is normal,the patient may be discharged.

v

Symptomatic patients should be x-rayed on admission.v Emesis and gastric lavage is contra-indicated as it increases

the risk of aspiration. The use of milk is not recommendedbut clear fluids are not contra-indicated.

v Oxygen should be administered to all patients withrespiratory signs or symptoms. Other respiratory supportmodalities should be instigated as required, according tostandard indications.

v Corticosteroid therapy may increase the risk of secondary

bacterial infection and has not been shown to be of anybenefit.



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n a e po sonsv Carbon monoxide

v Carbon monoxide is produced through incompletecombustion processes. It is colourless, tasteless and non-

irritant.v The commonest sources of carbon monoxide poisoning are

smoke inhalation, poorly maintained domestic gasappliances and deliberate inhalation of car exhaust fumes(less common in children)

v Carbon monoxide causes tissue hypoxia by the interruptionof electron transport in the mitochondria.

v It also reduces oxygen delivery by competing with O2 forbinding to Hb and altering the shape of the HbO2

dissociation curve (making it less sigmoidal, a shift to theleft). Its affinity for Hb is >200-fold that of O2

v Carbon monoxide causes injury by hypoxia, with symptomsreferable to tissues with greatest oxygen consumption,notably the heart and brain

v Patients present with hypoxia without cyanosis. Skin and



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v Anaemia, increased metabolic rate (e.g. children) andunderlying ischaemic heart disease all increasesusceptibility to CO. Neurological recovery depends on theduration of hypoxic coma.

Management of carbon monoxide poisoning

v Pulse saturation monitoring does not distinguish betweenHbO2 and COHb and will read falsely high.

v

Arterial blood gases should be done. PO2 may be normalbut any evidence of metabolic acidosis indicates seriouspoisoning (useful even in the absence of COHb measuringfacilities.) COHb measurements are diagnostic but notalways available.

v Treat according to ABC principles.

v Apply tight-fitting mask with 100% oxygen. This reduces thehalf life of COHb from 320 mins (in room air) to 80 minutes.

Intubation and ventilation may be necessary in severecases.



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Cyanide poisoning

• Most commonly seen in victims of smoke inhalation as acombustion product of polyurethane foams. Cyanide

derivates are also used in industrial processes andfertilizers. Children may ingest amygdalin, a cyanogenicglycoside contained in kernels of almonds and cherries.

• Cyanide acts by irreversibly blocking mitochondrial electrontransport.

• HCN gas can lead to cardiorespiratory collapse and arrestwithin a few minutes. Patients surviving to reach hospitalare unlikely to have suffered significant poisoning.

• Early signs include dizziness, chest tightness, dyspnoea,

confusion and paralysis, followed by cardiovascularcollapse, apnoea and seizures.

• Management of cyanide poisoning

• Do not attempt mouth to mouth resuscitation as the skin

will be contaminated.•



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• Lead Poisoning

• 3.3.1 Introduction

• Lead is a ubiquitous metal that has been used by humans for morethan 3 millennia. Its toxic effects on humans are well documentedin history. Early reports of toxicity in adult metal workers suggestthat they suffered from lead poisoning.

• Alternative name for lead poisoning is plumbism. Lead is a very

strong poison. A single high toxic dose of lead can cause severesymptoms that require emergency management

• Research suggests that the primary source of lead exposure formost children are; deteriorating lead-based paint, leadcontaminated dust, and lead contaminated residential soil.

Children get lead in their bodies when they put lead objects in theirmouth especially if they swallow the lead object. They can evenget lead poison on their fingers from touching a dusty or peelinglead object and then putting their fingers in their mouth or eatingfood afterward. Tiny amounts of lead can also be inhaled. Lead canbe found in drinking water in homes whose pipes werecontaminated with lead solder, although while new building codes



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• Pathophysiology

• Lead perturbs multiple enzyme systems. As in most heavy metals,any ligand with sulfhydryl groups is vulnerable.

• Perhaps the best-known effect is that on the production of heme.Lead interferes with the critical phases of the dehydration of aminolevulinic acid and the incorporation of iron into theprotoporphyrin molecule;

• the result is a decrease in heme production. Because heme isessential for cellular oxidation, deficiencies have far-reachingeffects.

• The effects of lead poisoning on the brain are manifold and includedelayed or reversed development, permanent learning disabilities,

seizures, coma, and even death.• Lead is primarily excreted in urine and bile, but the elimination

rate varies, depending on the tissue that absorbed the lead.

• Clinical Features

•

There are many possible symptoms of lead poisoning. Lead caneven affect different arts of the bod . Overtime, even low levels



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• Vincent's gingivostomatitis, an infection due to fusiformspirochactes, characteristically destroys the interdental papillae. Athick, felted, greenish-grey slough is formed and halitosis ispresent. In patients exposed to lead compounds, a stippled blue

line can be observed running along the edge of the gum, especiallyopposite those teeth showing gingivitis.4

• Lead Inhibits both haem and globin synthesis at a number of points. In addition, it interferes with the breakdown of RNA byinhibiting the enzyme pyrmidine 5' nucleotidase, causing

accumulation of denatured RNA in red cells, the RNA giving anappearance called basophilic stippling on the ordinary(Romanowsky) stain. The anaemia may be hypochromic orpredominantly haemolytic, and the bone marrow may show ringsideroblasts. Free erythrocyte protoporphyrin is raised.

• Chronic lead poisoning in children may cause intellectual disability,seizure disorders, aggressive behavior disorders, developmentalregression, chronic abdominal pain, and anemia.

• In children: Anemia may develop because lead interferes with the

normal formation of Hb. Children and adults who inhale tetra-ethylor tetra-methyl lead (in leaded gasoline) may develop toxic



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Investigations/Diagnosis

• Lead poisoning is suspected in patients with characteristicsymptoms. However, because symptoms are often nonspecific,

diagnosis is often delayed.• Evaluation includes CBC and measurement of serum electrolytes,

BUN, serum creatinine, plasma glucose, and PbB levels. Anabdominal x-ray should be taken to look for lead particles, whichare radiopaque. X-rays of long bones are taken in children.

Horizontal, metaphyseal lead bands representing lack of RBCremodeling and increased Ca deposition in the zones of provisionalcalcification in children's long bones are somewhat specific forpoisoning with lead or other heavy metals but are insensitive.Normocytic or microcytic anemia suggests lead toxicity,particularly when the reticulocyte count is elevated or RBCbasophilic stippling occurs; however, sensitivity and specificity arelimited.

• Diagnosis is definitive if the PbB level is ≥ 10 g/dL.μ

N/B

• Increase blood lead levels > 80<g/100ml.



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CONTROL AND MANAGEMENT

• Exposure to lead can be reduced by;

• Keeping homes as dust free as possible

• Washing hands before eating

•

Throwing out old painted toys if you donot know whether the paint contains lead

• Letting tap water run for a minute before

drinking or cooking with it• Wiping the rim and neck of the bottle with

a towel moistened with lemon juice,

vinegar, or wine before use if the



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• Chelation therapy is a procedure that can remove higher levels of lead that have built up in a person's body overtime. 1gm of CaNa2EDTA (calcium disodium edetate) is diluted to 200-300ml insaline or glucose solution and infused i.v. over 1 hour twice daily

for 3-5 days. The urinary excretion of Pb is promptly increased, butdeclines quickly as the metal is removed from accessible sites(primarily bone). A second course of CaNa2EDTA may be repeatedafter 5-7 days allowing time for Pb to redistribute to extracellularsites.

• In summary

• Identify source and prevent further ingestion.

• Decrease cerebral oedema -Dexamethasone 0.2-0.4mg/kg ±mannitol.

• Chelating agents -Dimercaparol 4mg/kg IM 4 hourly, graduallydecreasing over next few days; Calcium EDTA 50mg/kg/day individed 4 hourly doses IV/IM.

• Oral penicillamine 40 mg/kg/day when the child recovered.

• PROGNOSIS

M di i



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Medicines

• Children frequently ingest medicines. Dangerous substances forchildren include salicylates, paracetamol, iron, theophylline andtricyclic antidepressants.

Aspirin / Salicylate poisoning

• Commonly ingested by children. Also probably thecommonest drug to be ingested deliberately in overdose.Oil of wintergreen is 98% methyl salicylate.

• Its primary toxic effect is by uncoupling of oxidativephosphorylation.

• Patients present with restlessness, hyperventilation,tinnitus, deafness, tachycardia, nausea, vomiting,sweating, hyperthermia and dehydration. Pulmonaryoedema, acute renal failure, hypokalaemia,hypoglycaemia and hypothrombinaemia may alsodevelop. In adults there is an early increase in respiration

rate causing a respiratory alkalosis that precedes the laterdevelo ment of metabolic acidosis. However this is not



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• Paracetamol overdose

• Paracetamol ingestion is common but seldom leads to severetoxicity in children due to the diluted concentration of the

paediatric syrup formulation. The children at risk are those withglutathione depletion, such as children with cystic fibrosis,adolescents with eating disorders and those also on enzymeinducing agents such as anticonvulsants.

• The liver is the main target organ in paracetamol poisoning.

Patients are generally asymptomatic up to 24 hours post ingestion.• Mild nausea, vomiting and anorexia may occur. Hepatic necrosis

becomes apparent in 24-36 hours with right subchondral pain andtenderness, jaundice, vomiting and acute liver failure.

•

Confusion and encephalopathy develop over 36-72 hours.• Oliguria and renal failure may occur from acute tubular necrosis in

the absence of liver failure.

• Lactic acidosis may be seen early or late.

•

Management of paracetamol poisoning



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• If the initial levels indicate no treatment, repeat after 4 hours tocheck for delayed absorption.

• All patients on or above the ‘Normal treatment line’ should be

given N-acetylcysteine.• Patients on enzyme-inducing drugs should be treated if above

the‘Enhanced risk treatment line’.

• Where levels are not available, liver damage should be assumedafter ingestion of a single dose of more than 150mg/kgparacetamol.

• Acetylcysteine is the antidote of choice and is usually given iv. Oralmethionine may be used if the patient is allergic to acetylcysteineand is also a suitable alternative in remote areas if vomiting is not

a problem. Oral acetylcysteine and carbocysteine have also beenused.

• Monitor urea and electrolytes, PT and LFT.

• Give vitamin K but avoid giving fresh frozen plasma unless there isactive bleeding. The PT is the best indicator of the severity of livefailure.

Iron poisoning



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Iron poisoning

• Ingestion of more than 20mg/kg of elemental iron is consideredpotentially toxic and the lethal dose is estimated at about180mg/kg.

• Iron is extremely irritant. The clinical features can be divided intothree phases (not always very clear)

• . Patients present with vomiting, diarrhoea, abdominal pain,haematemesis and rectal bleeding in the early phase (0-2 hours).

•

This is followed by a period of stabilisation (up to 12 hours) duringwhich a deceptive recovery occurs.

• This is followed by a life-threatening period during which coma,fits, jaundice, hepatic failure renal failure, clotting abnormalities,hypoglycaemia and cardiovascular collapse may occur.

• Patients alive 72 hours after ingestion usually make a full recovery.

• Late complications of gut stricture, gastric fibrosis and pyloricobstruction have been reported.

Management of iron overdose•

A patient with serum iron >90mmol/l may be treated with a



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• A patient with serum iron >90mmol/l may be treated with achelating agent.

• If <20mg/kg are ingested, treatment is supportive. Patients withiron level below 54mmol/l and who remains asymptomatic 6 hours

post ingestion would not be expected to develop significanttoxicity and require no active treatment.

• For ingestion of between 20-60mg/kg elemental iron, gastricemptying may be considered if within one hour of ingestion. Wholebowel irrigation may be used in patients with ingestion of more

than 60mg/kg and more than one hour post ingestion. It isespecially useful if a slow release preparation has been ingested.Charcoal is of no benefit as iron does not bind to it.

•

•

Desferrioxamine chelates iron and is the recommended treatment.• Give 1 gram im every 6-12 hours for children (2g for adolescents).

(100mg of desferrioxamine binds 8.5mg of elemental iron).

• If the patient is hypotensive, give desferrioxamine iv at a rate of 15mg/kg/hour, until the serum iron falls (maximum daily dose80mg/kg)

Theophylline poisoning



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• Theophylline poisoning

• This type of poisoning is rare but serious.

• Most preparations are slow release so that problems develop 12-24hours after ingestion.

• Features of acute ingestion reflect the local irritant GI effects –nausea, vomiting, haematemesis and diarrhoea.

• The child may be hyperactive with dilated pupils, hypereflexia,hypotonia and myoclonus.

• There may also be severe hypokalaemia, arrhythmias, metabolicacidosis, hyperglycaemia, hypotension and seizures.

Management of theophylline poisoning

• Gastric lavage should be considered if ingestion occurred within 1-2 hours.

• Repeated administration of activated charcoal to prevent furtherabsorption and enhance systemic clearance. (May be difficult inthe presence of nausea and vomiting).

• Whole bowel irrigation is considered if a slow-release preparation is

• Tricyclic antidepressants



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• Tricyclic antidepressants

• Cardiovascular toxicity is the main cause of death in tricyclicantidepressant overdose. It is caused by the blockade of noradrenaline uptake as well as the anticholinergic, membrane-

stabilising and alpha-blocking effects.• Nervous system toxicity includes drowsiness, agitation,

hallucinations, hyperreflexia, myoclonus, rigidity, convulsions,respiratory depression and coma.

• Anticholinergic effects include flushing, dry mouth, dilated pupils,hyperpyrexia and bladder/bowel paralysis.

• Cardiovascular toxicity includes sinus tachycardia, hypotension,conduction abnormalities and arrhythmias.

• Respiratory complications include respiratory depression,

aspiration pneumonia, ARDS and pulmonary oedema.

• Management of tricyclic overdose

• Gastric emptying is delayed by tricyclic antidepressants andtherefore gastric lavage should be attempt as late as 12 hours post

ingestion.



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• Pesticides

5.1 Paraquat

5.1.1 Introduction

• Paraquat ingestion remains a problem in a large number of countries. Most of these cases are intentional suicide attempts(73% in a Malaysian study) or occupational exposure and thereforenot that frequently seen in the paediatric population. It is the mosttoxic herbicide known, producing multi-organ failure.

• After oral ingestion, patients develop a severe gastroenteritis withoral, oesophageal and gastric ulceration. Depending on the doseingested, multi-organ failure may develop within 48-72 hours. Aslittle as 10ml may be fatal.

• Those who survive the initial phase develop pulmonary fibrosis asa response to the acute alveolitis in the first phase. This leads torespiratory failure and patients die of anoxia.

•

5.1.2 Management of paraquat poisoning

• Activated charcoal may be used if Fuller’s earth is not available



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• Activated charcoal may be used if Fuller s earth is not available.Mix with saline and a laxative like lactulose to preventconstipation. Repeat every 4 hours until paraquat is no longerdetected in the urine.

•

If neither is available, careful gastric emptying may be done but beaware of possible pharyngeal and oesophageal ulceration andperforation

• Haemoperfusion or dialysis may be used (if available).

• Appropriate management of respiratory complications includesPEEP/CPAP. Low FiO2 should be used as high concentrations of oxygen lead to worse pulmonary toxicity. Paraquat accumulates inthe lung where it generates superoxide anions through the reactionwith oxygen.

•

5.2 Organophosphate poisoning• 5.2.1 Introduction

• Organophosphate poisoning (OP) remains an issue in developingcountries. In one study, 35% of OP poisoned victims were children.

•

The organophosphates and carbamates are cholinesteraseinhibitors thereb elicitin choliner ic si ns and s m toms. The

• OP poisoning causes:



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OP poisoning causes:

• Muscarinic effects – hypersecretion, vomiting, diarrhoea,constrictedpupils, bronchoconstriction and urinary incontinence.

•

• Nicotinic effects – muscular weakness, fasciculations andrespiratory muscle weakness (may override muscarinic effect andcause tachycardia, hypertension and mydriasis).

•

• CNS effects – irritability, seizures, coma (and accompanyingrespiratory depression).

•

5.2.2 Management of organophosphate poisoning

• ABC

• Patient may require intubation (avoid suxamethonium becauseofprolonged effect)

•

Gastric lavage, activated charcoal.

TOXIC PLANT and conclusion



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TOXIC PLANT and conclusion

6.1 MUSHROOM POISONING

6.1.1 Introduction

•

Mushroom poisoning refers to the severe and often deadly effectsof various toxins that are found in certain types of mushrooms.

• Mushrooms are fungi, Saprophytic in nature, use organic materialfrom dead plants and animals.

•

Severity of mushroom poisoning depends on type of mushroomeaten; early diagnosis and correct treatment.

• Fatalities due to mushroom poisoning are increasing worldwide,more than 90% of deaths resulting from ingestion of amatoxincontaining species.

• If necessary expert knowledge is present, consuming wildmushrooms is relatively safe.

• However tragic deaths or illnesses can occur if toxic mushroomsare ingested unintentionally.

• Ingestion of high doses of Amanita phalloides for suicidal purpose

• 6 1 2 Clinical manifestations



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6.1.2 Clinical manifestations

• Clinical manifestations of Amanita phalloides are the result of thecyclopeptide toxins, Phalodin and alpha Amantinin. Phalodin iscyclic heptapeptide that interrupts the actin polymerization-

depolymerization cycle and impair cell membrane function. It haslimited GI absorption and cause gastroenteritis like effects. AlphaAmantinin produces deleterious effects on liver and kidney whencirculating in the blood.

• Clinical features occur in four phases.

• Latent phase lasts for 0.5- 12 hours.

• Gastroenteritis phase includes diarrhoea, vomiting, abdominal painduring which patient becomes severely dehydrated.

• During the phase of temporary improvement, patient feels well for

6–8 hours.

• During Hepatic and Renal phase (4th and 5th day) patient lapsesinto hepatic coma and renal failure ending in death.

• 6.1.3 Diagnosis /Investigation:

• Patient’s history and initial symptoms are important in diagnosis. It

• 6.1.4 Management of mushroom poisoning



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6.1.4 Management of mushroom poisoning

• The therapy includes:

• stabilization of the patient with the correction of hypoglycaemiaand electrolyte imbalance, substitution with coagulation factors

Fresh Frozen Plasma (FFP) and red cells and the treatment of septiccomplications,

• decontamination, which consists of gastric levage, theadministration of activated charcoal and laxatives as well as theforced diuresis, and

• Therapy with high doses of penicillin or ceftazidime and of silibinin.Silibinin is the most promising new treatment for Amanitamushroom poisoning.

• Impending hepatic failure needs supportive measures including

lactulose, low protein diet, vitamin K and fresh frozen plasma.

• Haemodialysis/Plasma Pharesis may be helpful in some cases. If response is not satisfactory liver transplantation can be consideredas final option depending on availability and affordability.



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CONCLUSION

• Prevention of childhood poisoning is vital. There must beadequate supervision, safe placement of medications, child

safe cabinets and containers, blister packaging andeducation.

• Most paediatric cases are not severe. Recognition of potentially life-threatening ingestions is important so thatappropriate early treatment can be instituted.

• Aggressive supportive care is vital.

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Common Poison in Children