COMMON POISON IN CHILDREN

BY Click to edit Master subtitle style DY BATUBO, NIMISOERE P

4/19/12

INTRODUCTION
v

Poisoning are substances that results in toxicity when in contact with the body by altering the normal physiology of the body. Toxicity result in 2 ways

1. exposure to excess amounts of normally nontoxic substances 2. exposure to substances that are poisonous at all doses
v

Route of poisoning
v

injection, inhalation, or exposure of body surfaces (eg, skin, eye, mucous membranes) Ingestion

4/19/12

Epidemiology

Poisoning in children: general principles

Ascertain the nature and time of poisoning. Contact the local Poison Centre for advice (if available). Assess the patient following the principles of ABC (Airway, Breathing, and Circulation). If airway protection is impaired, the patient requires intubation. Induced emesis is no longer recommended and is contraindicated with volatile substances. Consider gastric emptying and administration of activated charcoal Remove contaminated clothing and wash patient with soap and water Send samples for lab investigation (urea, electrolytes, blood glucose.) Urine and gastric aspirates should be saved for later toxicology analysis (where available). Measure relevant drug levels (paracetamol and salicylate 4/19/12 and others if available).

GROUP OF POISONS
v

Household chemicals e.g bleach, drain cleaner

Hydrocarbons kerosene

Inhaled poisons CO, cyanide, lead

Medicines aspirin/salicylate, paracetamol, iron, theophylline

Pesticides- paraguat, organophosphate

Toxic plant- mushroom

Household chemicals
v

Children frequently ingest household substances and most of these are non-toxic. However, some products contain alcohol which may cause seizures and hypoxia Household solutions of bleach contain approximately 10% hypochlorite Commonly, they cause nausea, vomiting and diarrhoea. Less than 100ml of household bleach is unlikely to cause serious problems Ingestion of small quantities of strong alkalis such as drain cleaner containing sodium hydroxide may cause devastating injuries. Oesophageal injury is most common and evolves over the course of a few days. Ingestion causes immediate burning pain, swelling of the lips, and depending on the quantity ingested, salivation, haematemesis, dyspnoea, stridor or shock.
4/19/12

The burn injury is classified by endoscopy:

Hydrocarbons (Paraffin, white spirit)

Most of the hydrocarbons are petroleum distillates, containing a variable amount of saturated and unsaturated aliphatic (open-chain) and aromatic(cyclic) hydrocarbons. The aliphatics are not readily absorbed from the gastrointestinal tract and therefore cause minimal systemic toxicity. Paraffin, petrol, thinners, diesel and benzene are low viscosity aliphatic-based petroleum distillates The aromatic hydrocarbons are well absorbed, and therefore may cause systemic toxic affects but are less inclined to aspiration-related complications. The main hazard of accidental ingestion of the aliphatic hydrocarbons (paraffin) is that of chemical pneumonitis characterised by ventilation/perfusion imbalance and hypoxia This can occur even in the absence of vomiting or impaired consciousness and as little as 1ml aspirated hydrocarbon can result in a chemical pneumonitis. Signs 4/19/12 and symptoms appear after 30 minutes of ingestion but may be delayed for 8 hours. A non-productive cough,

The clinical picture generally deteriorates over the first 24 hours. A temperature that persists or only develops after 24 hours usually suggests a secondary infection

Abnormalities on the chest film may be seen within 30 minutes after aspiration even in the absence of clinical signs or symptoms. Common radiological findings of chemical pneumonitis include bilateral perihilar infiltrates which progress to form patchy infiltrates and later become large areas of consolidation. Diagnosis of kerosene poisoning can be made even in the absence of specific laboratory parameters if there is a positive history of exposure (ingestion) supported by compatible respiratory and neurological findings.

Investigations such as full blood count, serum, electrolytes, urea and creatinine, as well as liver function test are done 4/19/12 management and to monitor complications in other to aid

Management of kerosene poisoning

ABC principles 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. If asymptomatic after 8 hours and the chest film is normal, the patient may be discharged. Symptomatic patients should be x-rayed on admission. Emesis and gastric lavage is contra-indicated as it increases the risk of aspiration. The use of milk is not recommended but clear fluids are not contra-indicated. Oxygen should be administered to all patients with respiratory signs or symptoms. Other respiratory support modalities should be instigated as required, according to standard indications. Corticosteroid therapy may increase the risk of secondary bacterial infection and has not been shown to be of any 4/19/12 benefit.

Inhaled poisons
v

Carbon monoxide Carbon monoxide is produced through incomplete combustion processes. It is colourless, tasteless and nonirritant. The commonest sources of carbon monoxide poisoning are smoke inhalation, poorly maintained domestic gas appliances and deliberate inhalation of car exhaust fumes (less common in children) Carbon monoxide causes tissue hypoxia by the interruption of electron transport in the mitochondria. It also reduces oxygen delivery by competing with O2 for binding to Hb and altering the shape of the HbO2 dissociation curve (making it less sigmoidal, a shift to the left). Its affinity for Hb is >200-fold that of O2 Carbon monoxide causes injury by hypoxia, with symptoms referable to tissues with greatest oxygen consumption, notably the heart and brain
4/19/12 Patients present with hypoxia without cyanosis. Skin and

Anaemia, increased metabolic rate (e.g. children) and underlying ischaemic heart disease all increase susceptibility to CO. Neurological recovery depends on the duration of hypoxic coma.

Management of carbon monoxide poisoning

Pulse saturation monitoring does not distinguish between HbO2 and COHb and will read falsely high. Arterial blood gases should be done. PO2 may be normal but any evidence of metabolic acidosis indicates serious poisoning (useful even in the absence of COHb measuring facilities.) COHb measurements are diagnostic but not always available.

Treat according to ABC principles. Apply tight-fitting mask with 100% oxygen. This reduces the half life of COHb from 320 mins (in room air) to 80 minutes. Intubation and ventilation may be necessary in severe 4/19/12 cases.

Cyanide poisoning

Most commonly seen in victims of smoke inhalation as a combustion product of polyurethane foams. Cyanide derivates are also used in industrial processes and fertilizers. Children may ingest amygdalin, a cyanogenic glycoside contained in kernels of almonds and cherries. Cyanide acts by irreversibly blocking mitochondrial electron transport. HCN gas can lead to cardiorespiratory collapse and arrest within a few minutes. Patients surviving to reach hospital are unlikely to have suffered significant poisoning. Early signs include dizziness, chest tightness, dyspnoea, confusion and paralysis, followed by cardiovascular collapse, apnoea and seizures. Management of cyanide poisoning Do not attempt mouth to mouth resuscitation as the skin will be contaminated.

4/19/12

Lead Poisoning 3.3.1 Introduction Lead is a ubiquitous metal that has been used by humans for more than 3 millennia. Its toxic effects on humans are well documented in history. Early reports of toxicity in adult metal workers suggest that 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 severe symptoms that require emergency management Research suggests that the primary source of lead exposure for most children are; deteriorating lead-based paint, lead contaminated dust, and lead contaminated residential soil. Children get lead in their bodies when they put lead objects in their mouth especially if they swallow the lead object. They can even get lead poison on their fingers from touching a dusty or peeling lead object and then putting their fingers in their mouth or eating food afterward. Tiny amounts of lead can also be inhaled. Lead can be found in drinking water in homes whose pipes were 4/19/12 contaminated with lead solder, although while new building codes

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 the protoporphyrin molecule; the result is a decrease in heme production. Because heme is essential for cellular oxidation, deficiencies have far-reaching effects. The effects of lead poisoning on the brain are manifold and include delayed 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 can 4/19/12 even affect different parts of the body. Overtime, even low levels

Vincent's gingivostomatitis, an infection due to fusiform spirochactes, characteristically destroys the interdental papillae. A thick, felted, greenish-grey slough is formed and halitosis is present. In patients exposed to lead compounds, a stippled blue line can be observed running along the edge of the gum, especially opposite 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 by inhibiting the enzyme pyrmidine 5' nucleotidase, causing accumulation of denatured RNA in red cells, the RNA giving an appearance called basophilic stippling on the ordinary (Romanowsky) stain. The anaemia may be hypochromic or predominantly haemolytic, and the bone marrow may show ring sideroblasts. Free erythrocyte protoporphyrin is raised. Chronic lead poisoning in children may cause intellectual disability, seizure disorders, aggressive behavior disorders, developmental regression, 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-ethyl 4/19/12 or tetra-methyl lead (in leaded gasoline) may develop toxic

Investigations/Diagnosis

Lead poisoning is suspected in patients with characteristic symptoms. 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. An abdominal x-ray should be taken to look for lead particles, which are radiopaque. X-rays of long bones are taken in children. Horizontal, metaphyseal lead bands representing lack of RBC remodeling and increased Ca deposition in the zones of provisional calcification in children's long bones are somewhat specific for poisoning with lead or other heavy metals but are insensitive. Normocytic or microcytic anemia suggests lead toxicity, particularly when the reticulocyte count is elevated or RBC basophilic stippling occurs; however, sensitivity and specificity are limited. Diagnosis is definitive if the PbB level is 10 g/dL.
4/19/12

N/B

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

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 do not 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 4/19/12

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 in saline or glucose solution and infused i.v. over 1 hour twice daily for 3-5 days. The urinary excretion of Pb is promptly increased, but declines quickly as the metal is removed from accessible sites (primarily bone). A second course of CaNa2EDTA may be repeated after 5-7 days allowing time for Pb to redistribute to extracellular sites. 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, gradually decreasing over next few days; Calcium EDTA 50mg/kg/day in divided 4 hourly doses IV/IM. Oral penicillamine 40 mg/kg/day when the child recovered.
4/19/12 PROGNOSIS

Medicines

Children frequently ingest medicines. Dangerous substances for children include salicylates, paracetamol, iron, theophylline and tricyclic antidepressants.

Aspirin / Salicylate poisoning

Commonly ingested by children. Also probably the commonest drug to be ingested deliberately in overdose. Oil of wintergreen is 98% methyl salicylate. Its primary toxic effect is by uncoupling of oxidative phosphorylation. Patients present with restlessness, hyperventilation, tinnitus, deafness, tachycardia, nausea, vomiting, sweating, hyperthermia and dehydration. Pulmonary oedema, acute renal failure, hypokalaemia, hypoglycaemia and hypothrombinaemia may also develop. In adults there is an early increase in respiration rate causing a respiratory alkalosis that precedes the later 4/19/12 development of metabolic acidosis. However this is not

Paracetamol overdose Paracetamol ingestion is common but seldom leads to severe toxicity in children due to the diluted concentration of the paediatric syrup formulation. The children at risk are those with glutathione depletion, such as children with cystic fibrosis, adolescents with eating disorders and those also on enzyme inducing 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 and tenderness, 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 4/19/12

If the initial levels indicate no treatment, repeat after 4 hours to check 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 theEnhanced risk treatment line. Where levels are not available, liver damage should be assumed after ingestion of a single dose of more than 150mg/kg paracetamol. Acetylcysteine is the antidote of choice and is usually given iv. Oral methionine may be used if the patient is allergic to acetylcysteine and is also a suitable alternative in remote areas if vomiting is not a problem. Oral acetylcysteine and carbocysteine have also been used. Monitor urea and electrolytes, PT and LFT. Give vitamin K but avoid giving fresh frozen plasma unless there is active bleeding. The PT is the best indicator of the severity of live 4/19/12 failure.

Iron poisoning

Ingestion of more than 20mg/kg of elemental iron is considered potentially toxic and the lethal dose is estimated at about 180mg/kg. Iron is extremely irritant. The clinical features can be divided into three 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) during which 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 pyloric obstruction have been reported.
4/19/12

Management of iron overdose

A patient with serum iron >90mmol/l may be treated with a chelating agent. If <20mg/kg are ingested, treatment is supportive. Patients with iron level below 54mmol/l and who remains asymptomatic 6 hours post ingestion would not be expected to develop significant toxicity and require no active treatment. For ingestion of between 20-60mg/kg elemental iron, gastric emptying may be considered if within one hour of ingestion. Whole bowel irrigation may be used in patients with ingestion of more than 60mg/kg and more than one hour post ingestion. It is especially 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 dose 4/19/12 80mg/kg)

Theophylline poisoning This type of poisoning is rare but serious. Most preparations are slow release so that problems develop 12-24 hours 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, metabolic acidosis, hyperglycaemia, hypotension and seizures.

Management of theophylline poisoning

Gastric lavage should be considered if ingestion occurred within 12 hours. Repeated administration of activated charcoal to prevent further absorption and enhance systemic clearance. (May be difficult in the presence of nausea and vomiting).
4/19/12 Whole bowel irrigation is considered if a slow-release preparation is

Tricyclic antidepressants Cardiovascular toxicity is the main cause of death in tricyclic antidepressant overdose. It is caused by the blockade of noradrenaline uptake as well as the anticholinergic, membranestabilising 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 and therefore gastric lavage should be attempt as late as 12 hours post ingestion. 4/19/12

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 therefore not that frequently seen in the paediatric population. It is the most toxic herbicide known, producing multi-organ failure. After oral ingestion, patients develop a severe gastroenteritis with oral, oesophageal and gastric ulceration. Depending on the dose ingested, multi-organ failure may develop within 48-72 hours. As little as 10ml may be fatal. Those who survive the initial phase develop pulmonary fibrosis as a response to the acute alveolitis in the first phase. This leads to respiratory failure and patients die of anoxia.

5.1.2 Management of paraquat poisoning 4/19/12

Activated charcoal may be used if Fullers earth is not available. Mix with saline and a laxative like lactulose to prevent constipation. Repeat every 4 hours until paraquat is no longer detected in the urine. If neither is available, careful gastric emptying may be done but be aware of possible pharyngeal and oesophageal ulceration and perforation Haemoperfusion or dialysis may be used (if available). Appropriate management of respiratory complications includes PEEP/CPAP. Low FiO2 should be used as high concentrations of oxygen lead to worse pulmonary toxicity. Paraquat accumulates in the lung where it generates superoxide anions through the reaction with oxygen. 5.2 Organophosphate poisoning 5.2.1 Introduction Organophosphate poisoning (OP) remains an issue in developing countries. In one study, 35% of OP poisoned victims were children. The organophosphates and carbamates are cholinesterase 4/19/12

OP poisoning causes: Muscarinic effects hypersecretion, vomiting, diarrhoea, constrictedpupils, bronchoconstriction and urinary incontinence. Nicotinic effects muscular weakness, fasciculations and respiratory muscle weakness (may override muscarinic effect and cause tachycardia, hypertension and mydriasis). CNS effects irritability, seizures, coma (and accompanying respiratory depression).

5.2.2 Management of organophosphate poisoning

ABC Patient may require intubation (avoid suxamethonium because ofprolonged effect) Gastric lavage, activated charcoal. 4/19/12

TOXIC PLANT and conclusion 6.1 MUSHROOM POISONING 6.1.1 Introduction

Mushroom poisoning refers to the severe and often deadly effects of various toxins that are found in certain types of mushrooms. Mushrooms are fungi, Saprophytic in nature, use organic material from dead plants and animals. Severity of mushroom poisoning depends on type of mushroom eaten; early diagnosis and correct treatment. Fatalities due to mushroom poisoning are increasing worldwide, more than 90% of deaths resulting from ingestion of amatoxin containing species. If necessary expert knowledge is present, consuming wild mushrooms is relatively safe. However tragic deaths or illnesses can occur if toxic mushrooms are ingested unintentionally.
4/19/12 Ingestion of high doses of Amanita phalloides for suicidal purpose

6.1.2 Clinical manifestations Clinical manifestations of Amanita phalloides are the result of the cyclopeptide toxins, Phalodin and alpha Amantinin. Phalodin is cyclic heptapeptide that interrupts the actin polymerizationdepolymerization cycle and impair cell membrane function. It has limited GI absorption and cause gastroenteritis like effects. Alpha Amantinin produces deleterious effects on liver and kidney when circulating in the blood. Clinical features occur in four phases. Latent phase lasts for 0.5- 12 hours. Gastroenteritis phase includes diarrhoea, vomiting, abdominal pain during which patient becomes severely dehydrated. During the phase of temporary improvement, patient feels well for 68 hours. During Hepatic and Renal phase (4th and 5th day) patient lapses into hepatic coma and renal failure ending in death. 6.1.3 Diagnosis /Investigation: Patients history and initial symptoms are important in diagnosis. It
4/19/12

6.1.4 Management of mushroom poisoning The therapy includes: stabilization of the patient with the correction of hypoglycaemia and electrolyte imbalance, substitution with coagulation factors Fresh Frozen Plasma (FFP) and red cells and the treatment of septic complications, decontamination, which consists of gastric levage, the administration of activated charcoal and laxatives as well as the forced diuresis, and Therapy with high doses of penicillin or ceftazidime and of silibinin. Silibinin is the most promising new treatment for Amanita mushroom 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 considered as final option depending on availability and affordability.
4/19/12

CONCLUSION

Prevention of childhood poisoning is vital. There must be adequate supervision, safe placement of medications, child safe cabinets and containers, blister packaging and education. Most paediatric cases are not severe. Recognition of potentially life-threatening ingestions is important so that appropriate early treatment can be instituted. Aggressive supportive care is vital.

4/19/12