Ghai Essential Pediatrics8th

B

Figs 25.55A and B: Infantile scabies. (A) Multiple papulovesicular lesions on soles; (B) nodular lesions of genitalia

•Malathion, 0.5% water based lotion, applied on dry hair for 6 hr. Has residual effect, so second application is not needed.

Petrolatum (twice daily for7-10 days) isused, withgood results, for eyelash infestation. The petrolatum covers the lice and their nits, preventing respiration. The dead lice are removed mechanically with a pair of tweezers.

Popular Urticaria

Papular urticaria is due to bites of arthropods such as mosquitoes and fleas. An initial itchy urticaria! weal that

Fig. 25.56: Papular urticaria: Papule with a central hemorrhagic punctum

develops at the site of bite evolves into a firm pruritic papule, which persists for several days. The lesion often has a central hemorrhagic punctum (Fig. 25.56) and may be surmounted by a tiny vesicle.

Complications. Secondary infection, eczematization, hyperpigmentation and hypopigmentation, particularly in darkly pigmented individuals are not uncommon. New bites by the same species often causes a recrudescence of activity in existing and even healed lesions.

Prevention of repeated insect bites through use of protective clothings,judicious use ofinsect repellents and treatmentofpets with infestationisrecommended.Topical steroids combined with topical antibiotics may help with individual lesions. Oral antihistaminics help in reducing pruritus and hypersensitivity reaction.

Pityrasis Alba

Ill-defined hypopigmented macules with fine scales are seen on face, in children 2-6-yr-old. The lesions are asymptomatic and clear up spontaneously after a few months or in some cases 2-3 yr. The family is reassured regarding the benignnatureoftheillness. Mild emollients may be useful in some cases.

Suggested Reading

Bhutani LK, Khanna N. Bhutani's Color Atlas of Dermatology, 5th edn. Mehta Publishers, New Delhi, 2006

Grichnik JM, Rhodes AR, Sober AJ. In: Fitzpatrick's Dermatology in General Medicine, Wolff K, eds. McGrawhill Medical, New York; 2008: 1099-109

Khanna N. Illustrated Synopsis of Dermatology and Sexually Trans­ mitted Diseases. 4 edn. Elsevier, New Delhi, 2011

Accidents, poisoning, vehicular trauma and falls are an important cause of childhood mortality and morbidity. Toddlers are especially predisposed as they are mobile, inquisitive and cannot differentiate between harmful and harmless things. It is important to implement strategies involving careful supervision and interventions to reduce incidence of accidents and poisoning, especially in children less than 5-yr-old.

A poison is any agent of self-injury absorbed into the body through epithelial surfaces. Toxins are poisons produced by a natural biological process. Venoms are toxins that are injected by a bite or sting to cause their effect. An accident is a sudden unexpected event of an afflictive or unfortunate character by chance occurrence.

POISONING

Poisoning in children in developing countries is usually caused by ingestion of pesticides and plants while pharmaceuticals and chemicals form the major cause of poisoning in the developed world. Common causes of poisoning in children are household products including kerosene oil, drugs (particularly barbiturates), chemicals (corrosives)andpesticides (organophosphatecompounds). Majority of poisons are ingested by children at home and include products that are familiar and visually appealing due to glossy packaging. Nontoxic household items (like nail polish, shampoo, ink) are also consumed by toddlers. Two distinct patterns of poisoning are observed. While children younger than 11 yr usually have accidental poisoning, toxic exposures in adolescents are primarily intentional (suicide, abuse) or occupational.

Databases on toxicology, hazardous chemicals, environmental health and toxic releases are available at

www.toxnet.nlm.nilz.gov.

Diagnosis

Identification of poisoning in children requires a high index of suspicion since history of ingestion of a chemical

P Ramesh Menon

isuncommon. Clues topoisoningare shown in Table26.l. Clinicalfeaturesmaysimulatecommonconditions (Tables 26.2 and 26.3). Figure 26.1 depicts the approach to a child with suspected poisoning.

Table 26.1 : Clues to poisoning in children

Acute onset of symptoms (e.g. encephalopathy) in a otherwise healthy child*

Unexplained multisystem involvement Metabolic acidosis

Acute renal failure; acute liver failure

Arrhythmias in a child with no known cardiac illness

• High index of suspicion in children between 1 and 3 yr of age

Table 26.2: Clinical clues to nature of poisoning

i = Increased; J.= Decreased

Assess general condition, need for advanced life support Initial management to reduce and eliminate continued exposure

History

nme, route, duration and circumstances (location and intent) of exposure

Name and amount of drug, chemical or toxin; bite/sting involved

nme of onset, nature and severity of symptoms nming of first aid measures

Family history of diseases and drug therapy

Examination

Heart rate, blood pressure, temperature, peripheral perfusion, respiratory rate, Sp02

Specific pointers: Evaluation of clinical signs (Table 26.2) Identifying toxidromes (Table 26.3)

Fig. 26.1: Approach to a child with suspected poisoning

Bedside Screening Tests

Blood Tests

Measurement of anion gap and osmolal gap detects accumulation of unmeasured ions and osmotically active agents in blood. Blood appears chocolate color in patients with methemoglobinemia. This turns pink on addition of potassium cyanide.

Urine should be examined for abnormal color. In phenol poisoning, urine turns smoky dark green on standing. Oxalate crystals suggest the possibility of ethylene glycol poisoning. Ketones in urine suggest exposure to acetone, salicylate or isopropyl alcohol.Ferric chloride test may help in identifying the incriminated toxin and requires the addition of 5-10 drops of freshly prepared 10% ferric chloride solution to 10 ml of boiled and acidified urine. Change of color to red suggests exposure to salicylates; purple green color indicates phenothiazine overdose and violet suggests phenol exposure.

Early suspicion and appropriate management are essential. General measures should be instituted imme­ diately, since early treatment is associated with improved outcomes.

Principles

All patients are treated as medical emergencies. Based on the child's general condition, triage is done. If the child is brought in the pre-toxic phase, decontamination is the highest priority and treatment is based on history. The maximum potential toxicity based on greatest possible

Table 26.4: Laboratory pointers to identification of toxins

exposure should be assumed. During toxic phase, the time between the onset of poisoning and peak effects, management is basedprimarilyon clinicalandlaboratory findings. Resuscitation and stabilization are the first priority. During resolution phase, supportive care and monitoring should continue until clinical and laboratory abnormalities have resolved.

Components of management include: (i) provision of basic life support and supportive care; (ii) prevention of further poison absorption; (iii) enhancement of poison elimination; (iv) administration of antidotes; and (v) pre­ vention of re-exposure.

Basic Life Support

Airway. This includes airway maintenance, establishment of breathing and restoration of circulation. Establishing airway may be difficult in children with poisoning due to caustic and thermal upper airway injuries, neck and facial injuries or angioedema. In a child with altered mental status, respiratory depression and pupillary constriction, a trial of naloxone should be given before intubation. Bag and mask ventilation is associated with a higher risk of aspiration. The risk of aspiration is minimized by aspirating gastric contents prior to intubation, use of the Sellick maneuver during intubation and synchronized mechanical ventilation.

Breathing. Adequacy of breathing should be assessed by respiratory effort, chest movement, air entry and oxygen saturation.

Circulation. Shock, particularly noted in poisoning due to cardiotoxic agents and in children with cardiopulmonary diseases, is managed initially with fluid boluses, repeated if needed, undermonitoringfor fluidoverload. Dopamine is thevasopressorofchoiceif shock remains unresponsive, except in poisoning due to tricyclic antidepressant or monoamine oxidase inhibitors where its use is avoided. Hypotension may be refractory to these measures in patients with exposure to myocardial depressants or vasodilators, and in presence of concomitant visceral injury, pulmonary embolism, ruptured aortic aneurysm, sepsis or severe acidosis.

Supportive Therapy

The goals of supportive therapy include maintenance of homeostasisandpreventionandtreatmentofcomplications. Indications for admission to intensive care unit include:

(i) evidence of severe poisoning, coma, respiratory depression, hypotension, cardiac conduction abnor­ malities, arrhythmias, hypothermia or hyperthermia;

(ii)needforantidote or enhanced elimination therapy; and

(iii)progressive clinical deterioration.

Prevention of Further Absorption of Poison

These measures target preventing absorption of the toxin and depend upon the site androute ofpoisoning, patient's age and general condition (Table 26.5).

Table 26.5: Methods to decrease the absorption of toxins

Dilution

Gastric emptying: Emesis, gastric lavage Binding agents: Activated charcoal, others Cathartics

Whole bowel irrigation Endoscopic or surgical removal

Dilution This involves washing with water to reduce the duration of exposure to the toxin. The mechanism depends upon the site of exposure. In patients with corrosive burns and poisoning with organophosphorus (readily absorbed from the skin), all clothes should be removed and the contaminated area washed with liberal amount of water and soap. It is important to emphasize that neutralization of an agent using alkali for acid exposure or vice versa is harmful and contraindicated. Skin cleaning is done irrespective of duration of exposure to the toxin. Lubricants like grease or cream may cause poison to stick on to the skin.

Oral and ocular mucosa is washed with plenty of water. Eyes should be irrigated with lids fully retracted for at least 20 min. In patients with corrosive ingestion, liberal amounts of water or clear fluid are given orally as soon as possible. Thisis contraindicatedinpoisoning due to tablets

as it may increase their absorption.

Gastrointestinal decontamination In the past, a regimentedapproachto decontamination was used, which consisted of gastric emptying by emesis or orogastric

lavage, followed by adsorption of residual poison within the gut by nonabsorbable agents, preferably activated charcoal. A cathartic, such as sorbitol was used to hasten the excretion of charcoal. However, there is no evidence of actual benefit with this approach. Gastric emptying remains a cardinal principle in management of poisoning by toxin ingestion and the desired outcome is the prevention of continued absorption of poison from the gut into bloodstream. The procedure of choice for decontamination, if needed, is activated charcoal. Administration of syrupofipecac may remove 30to40% of ingested toxin when administered within one hour of the ingestion. However, ipecac induced emesis and cathartics are no longer recommended as gastric emptying procedures.

Gastric lavage may be considered in situations where a potentially lethal toxin has been ingested within the last hour. Gastric lavage is preferred in patients below 6-month-old, impaired level of consciousness, seizures, absent gag reflex or mercury chloride poisoning. The procedure is contraindicated in children with corrosive poisoning. Gastric lavage is performed with a large tube with multiple lateral holes at the distal end and funnel at theproximalend.The size of the tube is selected according to age 28 Fr neonates, 36 Fr older children; narrow tubes are ineffective in removing solids. Before gastric lavage is performed, the gag reflex is ensured; if absent, the patient is first intubated. The child is kept in lateral decubitus position with head end lowered. Lavage is done with 15 ml/kg of normal saline until clear fluid is drained.

Activated charcoal should be instilled after the lavage iscompleted.Activatedcharcoal isproducedby destructive distillation of organic materials like wood, coconut and petroleum and treatment of the distillate at high temperatures (about900°C)usingsteam. The latter process increases the adsorptive capacity of charcoal by increasing its surface area, removing adsorbed material and reducing the particle size. Its total adsorptive surface is 1600 to 1800 m2 per g of activated charcoal, making it an ideal binding agent.

Activated charcoal is an effective nonspecific adsorbent and should be considered in all cases of poisoning. It should be avoided in patients with corrosive ingestion, ileus, intestinalhemorrhage and patient with unprotected airway at risk of aspiration. Activated charcoal, available as 400 mg tablet, is used in a dose of 1-2 g/kg and should be crushed, made into slurry and administered. Under most circumstances, a single dose is effective, with the greatest benefit being within an hour of ingestion. Repeat administration is indicated in patients with massive ingestion of toxin or desorption of toxin from activated charcoal (Table 26.6). Causes of nonresponse include ingestion of toxin not adsorbed by activated charcoal, ingestion of additional substances, delayed toxic effects and secondary complications including surgical causes.

Poisoning, Injuries and Accidents

Table 26.6: Indications for repeat doses and nonresponse to charcoal

Interruption of enteroCyclic antidepressants, diazepam,

Superactive charcoal, with thrice the adsorptive area, has been tried in some situations. Carbonized resin and modified silica gel are as effective as activated charcoal in adsorbing methanol, ethylene glycol, kerosene and turpentine in vitro. Other binding agents including attapulgite, bentonite, fuller's earth and kaolin pectin are less effective. Burnt toast possesses little, if any, adsorption capacity and has been abandoned. Cholestyramine is effective in paracetamol and digitalis toxicities but is less well tolerated. Routine use of cathartics either alone or with activated charcoal is not recommended.

Whole bowel irrigation with polyethylene glycol has been used in patientswithpoisoning and drugoverdosage.This is the only procedure which decontaminates beyond the pyloruswithoutinducingemesisorcausingfluid overload and dyselectrolytemia. It is, however, not a substitute for activated charcoal. It is particularly useful following ingestion of sustained release drugs, slowly dissolving agents, ingestedcrackvialsanddrugpacks. The procedure is not helpful in the management of ingestion of rapidly absorbed drugs, liquids, parenteral drugs and caustics. Whole bowel irrigation can be achieved with adminis­ tration of 500 ml per hour of polyethylene glycol over 4-6 hr.

Enhancing Elimination

Procedures directed towards enhancing elimination are indicated in patients with significant delay following poisoning or when methods to prevent absorption are ineffective or not applicable. Specific indications are provided in Table 26.7. Methods used commonly to enhance drug elimination include the following.

Table 26.7: Indications for enhancing elimination of toxins

Ingestion of drug or poison whose removal is enhanced by >30%, and:

Intense exposure with severe or lethal toxicity Toxin with serious, delayed effects

Impaired natural removal mechanism, or

Deteriorating condition, as suggested by hypotension, coma, metabolic acidosis, respiratory depression, dysarrhythmia or congestive cardiac failure

Manipulation of pH and diuresis. The rate of elimination of ingested substances can be increased by increasing glomerular filtration or by altering urine pH for toxins excreted by kidneys.Alkalization of urine may be used in patients with poisoning due to weak acids like salicylate, phenobarbital and herbicides. This is achieved by administration of sodium bicarbonate at a dose of 1-2mEq/kg given every 3-4 hr, targeting urine pH between 7 and 8. Sodium bicarbonate also reduces the toxicity of tricyclic antidepressants, quinine and some antiarrythmic drugs. Acidification of urine to enhance elimination of weak bases is not advised.

Dialysis. The indications of dialysis are given in Table 26.8. Peritoneal dialysis enhanceselimination ofcompoundslike alcohol, lithium and salicylates. It is more effective in children than adults due to presence of larger peritoneal surface in relation to body surface area. It has the disadvantages of gradual removal of toxinsanddecreased efficacy in hypotensive subjects. The procedure may be used as a temporizing measure before hemodialysis or hemoperfusion.

Hemodialysis is preferred for removal of compounds like bromide, chloral hydrate, ethanol, methanol, ethylene glycol, lithium and salicylates. In addition to removing toxins, it also rapidly corrects metabolic abnormalities and fluid overload. The procedure carries risk of possible elimination of agents like folinic acid and ethanol, administered therapeutically during acute poisoning.

Hemoperfusion is the procedure of circulating blood through a cartridge with a large surface area coated with activated charcoal or carbon. The procedure has the advantage of being not limited by protein binding and is the preferred method for elimination of carbamazepine, phenobarbital, phenytoin and theophylline. Substances whichare not adsorbedby activatedcharcoal,likealcohol, lithium and many heavy metals, are not removed. The procedure may be associated with complications like thrombocytopenia, leukopenia and hypocalcemia.

Exchange transfusion removes poisons affecting the red blood cells, as in methemoglobinemia or arsenic induced hemolysis. The elimination of heavy metals is enhanced by chelation and removal of carbon monoxide can be increased by hyperbaric oxygen.

Table 26.8: Indications of dialysis in a patient with suspected poisoning

Administration of Antidotes

Antidotescounteractthe effects of poisons by neutralizing them (antibody-antigen reactions, chelation, chemical binding) or by antagonizing their physiologic effects (activation of opposingnervous system activity, provision of metabolic or receptor substrate). Antidotes may reduce morbidity and mortality significantly, but are potentially toxic. Their safe use requires correct identification of specific poisoning or toxidrome. Table 26.9 enlists antidotes used commonly for management of poisonings.

Prevention of Re-exposure

Poisoning is a preventable illness. The best approach to prevent poisoning in children is to limit the access of poison. Alcoholic beverages, medications, products used for automotives, household cleaning and petcare, fuels and toiletry products, nonedible plants, medications and vitamins should be kept out of reach or locked inside childproof cabinets.Poison prevention education should be an integral part of all well child visits. Counseling parents and other caregivers about potential poisoning risks, howto 'poison-proof' achild'senvironment and steps to be taken if a poisoning occurs diminishes the likelihood of serious morbidity or mortality from an exposure. Adolescents with suicidal poisoning or drug addiction need proper counseling before discharge.

COMMON POISONINGS

Acetaminophen (Paracetamol)

This is the most common and safest analgesic and antipyretic used in children. The toxic dose is usually >200mg/kgin children below12-yr-old.Hepatic damage after paracetamol overdose usually begins at >150 mg/ kg and occurs due to formation of a highly reactive intermediate, N-acetyl-p-benzoquinoneimine. This is normally detoxified by endogenous glutathione.Overdose of paracetamol results in depletion of glutathione, allowing the intermediate metabolite to damage hepatocytes. The stages of paracetamol toxicity are as follows:

Stage I (12-24 hr): Nausea, vomiting and cold sweats

Stage II (24-48 hr): Clinical recovery with biochemical evidence of hepatorenal injury; elevation of hepatic transaminases to above 1000 IU/1 is associated with serious hepatic damage

Stage III (48-96 hr): Peak hepatotoxicity

Prolonged coma

Hepatic and renal failure; serious underlying illness Correlation between plasma concentration and toxicity Plasma levels in fatal range

Removal of toxin or its toxic metabolite possible by dialysis (e.g. barbiturates, chloral hydrate, ethylene glycol, theo­ phylline, salicylates, heavy metals)

Stage IV (7-8 days): Recovery is heralded by return of consciousness and improvement in the hepatic function tests. Histological recovery may take up to 3 months.

Death may occur within 2-7 days of ingestion. Overdosage is treated with N-acetylcysteine used orally within16 hrafteringestionatdosesindicatedinTable 26.9. Once hepatic failure occurs, the agent is contraindicated. Supportivetreatmentincludescorrectionofhypoglycemia,

maintenanceofhydration,electrolytebalance,treatmentof coagulopathy, hemodialysis for acute renal failure and management offulminanthepatic failure.

The following are poor prognostic factors in patients with hepatic failure due to paracetamol: blood pH <7.3, prothrombin time >100 sec, grade III or more hepatic encephalopathy, elevated serumbilirubin >4 mg/dl and

SGOT >1000 IU/1. A ratio of factor VIII to factor V >30 is associated with poor outcome.

Organophosphorus Compounds

Pesticides andinsecticidesare the most common cause of poisoning throughoutthe tropics and are associated with a highmortalityrate. Pesticidesincludeinsecticides herbi­ cides, fungicides, nematocides, rodenticides and fumi­ gants. Chronic exposure may be dietary or non-dietary. Aggregate exposure refers to total exposure to a single pesticide through food, water and nondietary exposure. Cumulativeexposureis the summated exposureto multi­ plepesticideswithacommonmodeofaction.Childrenare at higher risk inview of higherbody surface areaand high bodymassratio,absorptionofpesticidethroughintactskin and mucosa and higher minute ventilation rates in young children resulting in increased pulmonary exposure.

Clinical features appear when cholinesterase activity falls to 25-30% of normal. Symptoms of excessive para­ sympathetic activity including blurred vision, headache, giddiness,nausea,paininthechest,profusesalivationand sweating occur within a few hours. Pupils are constricted and papilledema may occur. At low doses of organo­ phosphates, muscarinic symptoms may be most prominent. In more severe intoxication, nicotinic and central muscarinic activity may predominate. Thus,

0.05 mg/kg IV; repeat dose titrated to effect

150 mEq/1 + 40 mEq KCl/1 of 5% dextrose

Loading dose of 15 mg/kg followed by 10 mg/kg q 12 hr for 4 doses, then 15 mg/kg q 2 hr until ethylene glycol levels are <20 mg/di; dialysis is required in presence of renal failure or ethylene glycol level >50 mg/di; fomepizole is given q 4 hr during dialysis to prevent washout

25-50 mg/kg IM (maximum 2000 mg) every 12 hr (maximum 2500 mg in young children); adjust dose in

tachycardiaand hypertensionareimportantsignsofsevere poisoning. Carbamates are less toxic than organo­ phopsphorus pesticides. Death is usually due to respiratory failure.

Intermediatesyndromeoccursduetoprolongedcholin- •f esterase inhibition and causes chronic effects, muscle necrosis and delayed sensory polyneuropathy. Definitive diagnosis of organophosphate poisoning can be made by estimation of red cell cholinesterase activity, before administrationofcholinesterasereactivator.Redcellacetyl­ cholinesterase is considered a satisfactory marker of synaptic function and atropine needs in patients with organophosphoruspoisoning,andisthereforeamarkerof severity. Patients with red cell enzyme activity of at least

30%havenormalmusclefunctionandnoneedforatropine; in contrast, patients with less than 10% of normal activity have grossly deranged muscle function and need high doses of atropine.

Treatment includes reduction of dermal contact and gastric emptying. Gastric decontamination should be considered only after the patient has been fully resus­ citated and stabilized. Atropine sulphate is the primary antidote and is given at 0.05 mg/kg IV; the dose is repea­ ted after 15 min and thenevery hour until atropinization (maximum 1 mg/kg in 24 hr). Atropine is a competitive antagonist of muscarinic receptors, reverses the peri­ pheral symptoms of excessive secretions and airway resistanceandarreststheearlyphaseofconvulsionswhen given within 5 minof exposure. Infusions of atropine are reported to be better than repeated bolus doses. Glyco­ pyrrolate is a reasonable alternative for mildly affected victims as an anti-sialogogue or as a peripheral parasympatholytic. This agent does not cross the blood

- Essential Pediatrics

brain barrier and is ineffective for those with central nervous system involvement.

Pralidoxime aldoxime methiodide (2-PAM) hydrolytically cleaves the organophosphate from the enzyme acetyl­ cholinesterase restoring enzymatic function. It is often highly effective in reversing nicotinic effects of pesticides including muscle fasciculations, weakness and respiratory depression. It is not given in carbamate poisoning. Common untoward effects include dizziness, transient diplopia and blurred vision. Dose adjustment is required in individuals with renal insufficiency since it is excreted almost entirely unchanged by the kidneys. Rapid IV administration can causelaryngospasm and rigidity. Hypertension is the most serious untoward effect at higher doses.

Patients must be carefully observed after stabilization for changes in atropine needs, worsening respiratory function because of intermediate syndrome and recurrent cholinergic features occurring with fat-soluble organ­ ophosphorus compounds.

Toxicity with diethyltoluamide (DEET), the component of most insect repellant creams, may occur through covered skin surfaces or ingestion. Seizures are the most severe manifestation but are usually self limited.

Hydrocarbon Poisoning

Aliphatic hydrocarbons, including kerosene, turpentine, lubricating oils and tar,have the greatest risk of aspiration and pulmonary symptoms. Aromatic compounds include benzene compounds and have mainly neurological and hepatic toxicity. The type of toxicity with a hydrocarbon depends on its volatility, viscosity or surface tension. The lower the viscosity, higher is the risk of pulmonary aspiration. Substances with low viscosity and volatility (e.g. mineral oil, kerosene, furniture polish) have a higher risk of aspiration. Substances with high volatility and low viscosity (e.g. benzene derivatives like toluene, xylene used in solvents and degreasers, gasoline, naphtha in lacquerdiluent)may also act as toxinsthroughinhalation, manifesting with neurological depression.

Kerosene and paraffin oils are often kept in unsafe containers (e.g. soft drinkandbeer bottles) and are a major cause of accidental ingestion among young children. Kerosene toxicity has also been noted following appli­ cation of kerosene on the skin of neonates, indicating that transdermal absorption can also result in toxic effects. Intravenous kerosene injections have been reported among IV drug abusers, causing major injury tothelungs.

Respiratory symptoms, as a result of chemical pneumo­ nitis, restlessness, fever and abdominal distension are common.Convulsions and coma may occur. Radiological changes, which might occur within one hour include basilar infiltrates, emphysema, pleural effusion and pneumatoceles. Ingestion of 30 ml is lethal.

Management is symptomatic with preservation of the airway in unconscious patients. Gastric emptying is

contraindicated and is done only when large quantities of turpentine have been ingested or the hydrocarbon product contains benzene, toluene, halogenated hydro­ carbons,heavymetals,pesticidesor aniline dyes.Mortality ranges from 2 to 10% and is higher in malnourished children. Death may ensue within 24 hours. Avoiding oil and milk at home as antidotes should be emphasized. Steroids have no role in treatment.

For DDT poisoning, phenobarbitone is given for convulsions. Cholestyramine, an anion exchange resin should be administered to all symptomatic patients of DDT poisoning.

Iron Intoxication

Ingestion of tablets of ferrous sulfate may cause acute poisoning, characterized by gastrointestinal toxicity, followed by a period of relative stability (up to 48 hr),and then circulatory shock with metabolic acidosis and myocardial dysfunction. Hepatic fibrosis and gastric scarring are longterm effects. Gastrointestinal symptoms can be seen at doses of 15 to 30 mg/kg. Significant toxicity is uncommon at amounts less than 50 mg/kg. The lethal oral dose isbetween200 and 500 mg/kg of elemental iron. The toxic dose isnotabsolute andfatal reactions have been reported with small amounts. Peak serum iron levels of >500 µg/dl may result in severe toxicity. Vomiting, diarrhea, serum glucose greaterthan150mg/dl,leukocyte count greater than 15,000/mm3 and the finding of radio­ opaque material on abdominal radiograph correlate with an elevated serum iron level greater than 300 µg/dl. The child may develop complications within a few hours or after a latent period of 1-2 days.

Treatment includes gastric emptying, followed by stomach wash with sodium bicarbonate. IV sodium bicarbonate (3 ml/kg diluted twice with 5% dextrose) is given for treatment of acidosis. Fluid resuscitation may be necessary. Iron is chelated with IV infusion of deferoxa­ mine (dose 15 mg/kg/hr) until the serum iron is <300 µg/ dl or until 24 hr after the child has stopped passing 'vine rose' colored urine. In case of renal failure, dialysis may be required to remove deferoxamine iron complexes.

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 urinaryretention. Treatment is by gastric lavage and physostigmine at a dose 0.1 mg/kg (max 2 mg) IV slowly.

Unconventional poisons and toxins include herbal or shrub products, inhalational agents, polychlorinated biphenyls, polycyclic aromatic hydrocarbons, paraben in plastics and packaged food.

Information sources on poisoning are available at: www.cehn.org and www.ace.orst.edu/info/nptm

HELP CENTRE

National Poison Information Centre

All India Institute of Medical Sciences, New Delhi Telephone +91 11 26589321, 26593677

Email: npicaiims@hotmail.com, npicaiims20l0@gmail.com Website: www.aiims.edu/aiims/departments/NPIC/NPIC intro.htm

ENVENOMATION

Snake Bites

Snake bites cause 125,000 deaths annually worldwide, chiefly in young adults in rural areas in tropical climates. About400 of 3000 snakespeciesworldwideare poisonous, chiefly belonging to the Elapidae (cobra, krait, coral snake, death adders, sea snake) and Viperidae (rattlesnake, saw scale, Russell viper) families. The venom of these snakes contains neurotoxins, cardiotoxins, hemotoxins or cytotoxins that cause: (i) neurotoxicity (sea snake, cobra, mamba, coral snake) with ptosis, diplopia and bulbar palsyprogressing to dysarthriaand generalizedweakness; (ii) coagulopathy (viper, Australian elapids) with gum bleeding, epistaxis or intracranial bleeding; (iii) rhabdo­ myolysis (Russell viper, sea snake, some Australian elapids) with muscle pain, tenderness, dark urine with acute tubularnecrosis; (iv) hypotension and/or shock due to vasodilation, myocardial toxicity and/or hypovolemia with bleeding; and (v) tissue necrosis (viper and cobra) with pain, tenderness, swelling, bleeding and blisters at the location of the bite. Initial symptoms are nonspecific, such as nausea, vomiting, abdominal pain and headache.

Management. Management of snake bite is directed at reducing the spread of venom and expediting transfer to thehospital,summarizedby the mnemonic 'Do it RIGHT' (R for reassuring the patient, I to Immobilize the limb in a functional position below the level of heart, G and H to Get to the Hospital immediately and T to Tell the doctor of any symptoms during transit). The wound is cleansed thoroughly without using alcohol. Pressure immobi­ lization to decrease venous outflow may delay systemic absorption of venom that contains primarily neurotoxins but is not recommended for venoms with cytotoxins since this may worsen local necrosis. Incision and suction by mouth or using mechanical devices are ineffective.

The evaluation of the patient in the hospital should take into account common syndromes caused by snake bites. Identification of the snake requires knowledge of local snake fauna, venom kit testing and clinical syndrome. Fang bites are often obvious for cobra and viper bites due to local tissue necrosis, but are easily missed in bites by Australian elapids. Since most snake bites do not cause envenomation, a large proportion of patients only require observation.

Clinical and laboratory assessment and management should focus on supportive care for specific syndromes.

Poisoning, Injuries and Accidents -

Continuous attention to vital signs and fluid status is important, with central pressure monitoring for patients with shock. Serial evaluation for serum creatine kinase and electrolytes, and urine dipstick for myoglobinuria helpsdetectrhabdomyolysis.Patientswiththiscomplication benefit from plasma volume expansion with isotonic saline, avoiding nephrotoxic medications, and ensuring diuresistargetingurinepH of 6.5. Patientswith established renal failure may require short-term dialysis. Patients with poisoning by snakes with neurotoxic venom require close monitoringforsignsofmuscleweaknessand development of hypoxia; severe cases require mechanical ventilation for airway protection or respiratory paralysis.

The whole blood clotting test is a useful bedside screen­ ing test for coagulopathy. The failure of blood to clot in a clean dry glass tube after 20 min suggests severe hypo­ fibrinogenemia, caused usually by vipers (and not cobra or krait). Antivenom administration reverses this abnor­ mality and improves other changes such as elevated internationalnormalizedratio,prolonged activated partial thromboplastin time, severe thrombocytopenia and low fibrinogen. Patients with life-threatening hemorrhage despite antivenom use may requirewhole blood or fresh frozen plasma.

The administration of adequate amounts of antivenom is the only specificmanagementfor envenomation.Its use depends upon availability and an individualized assess­ ment of risk-benefit ratio. Administration of antivenom is indicated in patients with neurological signs, sponta­ neous bleeding and/or incoagulable blood; it should also beconsideredforrhabdomyolysis,persistenthypotension, renal failure and/or severe local tissue destruction. Pre­ paration, dosing and administration should follow pro­ duct information guidelines and do not differ between adults and children. To prevent allergic reactions, anti­ venom is administeredslowly (over 1 hr) with continuous monitoring; epinephrine (0.01 mg/kg intramuscularly) may be necessary if a reaction develops.

Suggested Reading

Simpson ID. The pediatric management of snakebite: National protocol. Indian Pediatrics 2007;44:173-6

Warrell, DA.Guidelines for the management of snake-bites. World Health Organization 2010

www.who.int/neglected-cliseases/diseases/snakebites/en/ index.html; www.toxinology.com

Scorpion Sting

Scorpion sting is an important hazard in tropical regions, particularly in dry rural areas in south and central India. Envenomation by 30 of 1500 known species of scorpions (Buthidae or Scorpionidae family)can resultin neurotoxicity, cardiovascular toxicity or respiratory dysfunction. Severe excruciating pain radiating along corresponding derma­ tomes and life-threatening systemic effects may be noted. Scorpion venom is more potent than snake venom or

- Essential Pediatrics

cyanide and mortality is high, deaths occurring chiefly in patients with delayed diagnosis or therapy.

Scorpion venom is a complex mixtures of mucopoly­ saccharides, hyaluronidase, phospholipase, acetyl­ cholinesterase, serotonin, histamine, protease inhibitors, histamine releasers and neurotoxins. The neurotoxin causes incomplete inactivation ofsodium channels during depolarization of neurons, resulting in membrane hyperexcitability, repetitive uncontrolled firing of axons, enhanced release of neurotransmitters at synapses and neuromuscular junction, excessive neuromuscularactivity andautonomicdysfunction. The venom of the Asian black scorpion has high concentrations of noradrenaline and acetylcholine, which account for localized burning and algesia, respectively. Hemodynamicchangesaresecondary to transient cholinergic effects and secondary prolonged adrenergic effects and/or severe inflammatory response syndrome.

Neurotoxicityafterenvenomation is categorized intofour clinical grades, including local pain and paresthesias at the sting site without inflammation (Grade I); local symptoms and remote pain and paresthesias(radiatingproximally up the affected limb or generalized) with agitation (Grade II); cranial nerve dysfunction (blurred vision, involuntary conjugate,slowandrovingeye movements; slurred speech, tongue fasciculations, hypersalivation) or somatic neuromuscular dysfunction (restlessness, fasciculations, alternating opisthotonos and emprosthotonos) in an alert individual (Grade III) and presence of both cranial nerve dysfunctionandsomaticskeletalneuromusculardysfunction (Grade IV). An 'autonomic storm' is a common presen­ tation, with transient parasympathetic activity (vomiting, profuse sweating, hypersalivation,bradycardia,ventricular premature contraction, priapism and hypotension) and prolonged sympathetic (cold extremities, hypertension, tachycardia, pulmonary edema and shock) stimulation. Many patients show hypertension and/or left ventricular dysfunction at presentation. The onset and progression of symptoms is rapid with maximum severity within 5 hr. Children show earlier onset of symptoms (15-30 min in infants) and are more likely to require intensivesupportive care.

The management of scorpion stings involves relief of pain (paracetamol or ibuprofen), wound cleaning and tetanus prophylaxis. These patients may be discharged after observation for 4 hr to ensure lack of symptom progression.

Severe cases with restlessness, muscle fasciculations, hypersalivation,cranialnerve dysfunction and rovingeye movements require monitoring for respiratory distress, hyperthermia, rhabdomyolysis or multiple organ failure. Fluid balance should be maintained to correct losses due to vomiting, sweating and salivation. Oral secretions should be suctioned frequentlyandtheneedforintubation and mechanical ventilation anticipated in patients who cannot maintain airway or develop pulmonary edema.

Midazolam infusion helps provide sedation and relief from muscle spasticity. Intravenous fentanyl is preferred tomorphine of pain relief, since it does not cause histamine release. Prazosin is useful in the management of vasoconstriction and hypertension associated with a­ receptor stimulation, since it reduces preload without causing tachycardia and increase in myocardial oxygen demand. Patients with left ventricular dysfunction due to hypertension may benefit from sodium nitroprusside infusion or use of an angiotensin converting enzyme inhibitor.

Scorpion antivenom reverses the excitatory effects of the venom and neutralizes circulating unbound venom to minimize parasympathetic stimulation. Its use reduces the duration of symptoms and the need for benzo­ diazepines. Scorpion-specific F(ab') equine antivenom should be administered as early as possible to patients with Grade III or IV neurotoxicity. While specific anti­ venom is not available in India, nonspecific antivenom can be procured. Goat-derived antivenom carries risks of anaphylaxis and delayed serum sickness.

Suggested Reading

Bawaskar HS, Bawaskar PH. Scorpion sting: update. J Assoc Physicians India 2012;60:46-55

www.toxinology.com

INJURIES AND ACCIDENTS

Injuries and accidents are a leading causes of death in children who survive beyond their first birthday and represent amajor epidemic of non-communicable disease throughout the world. WHO estimates suggest that over 10% ofthosekilleddueto any type ofaccidentarechildren. Most accidents occur in the age group of 2-5 yr, mostly in boys. India has among the highest rates of road traffic accidents in the world. Burn injuries are second only to motor vehicle accidents as the cause of accidental death in children 1-4-yr-old.

Details of epidemiology are available at http//whqlib doc.who.int/publications/924156220X.pdf.

Epidemiology of Injury

The agent-host-environment model used to describe the epidemiology of communicable diseases can be extended to childhood injuries (Fig. 26.2).

Injuries are of 2 types, unintentional and intentional. Unintentional injuries can be broadly divided into three categories: injuries at home, sports injuries and road injuries.Intentionalinjuriessuch as homicide and suicide are rare in children but not uncommon in adolescents.

Injury Control

Injurycontroloperatesin3phases: prevention,minimization of damage, and post injury care. In planning injury prevention strategies, 3 principles deserve emphasis.