Poisoning in Pediatrics - PDF

Shared using Xodo PDF Reader and Editor Poisoning Dr.Enas M. Alshemmary C.A.B.P. - M.B.Ch.B.  Shared using Xodo PDF Reader and Editor Objectives - General principles in poisoning; * Clinical manifestations * Etiology and epidemiology * Laborat...

Shared using Xodo PDF Reader and Editor Poisoning Dr.Enas M. Alshemmary C.A.B.P. - M.B.Ch.B.  Shared using Xodo PDF Reader and Editor Objectives - General principles in poisoning; * Clinical manifestations * Etiology and epidemiology * Laboratory and imaging studies * Treatment * Prognosis * Prevention - Selected compounds commonly involved in pediatric poisoning (Acetaminophen, iron, aspirin) * Clinical and laboratory manifestations * Treatment  Shared using Xodo PDF Reader and Editor Etiology and epidemiology  The most common agents ingested by young children include cosmetics, personal care products, cleaning solutions, and analgesics.  Most ingestions in young children are unintentional, with intentional ingestions becoming more common in children 13 and older.  Shared using Xodo PDF Reader and Editor Clinical manifestations  Any child who presents with unexplained symptoms including altered mental status, seizure, cardiovascular compromise, or metabolic abnormality should be considered to have ingested a poison until proven otherwise.  A history and physical examination by someone who understands the signs and symptoms of various ingestions often provide sufficient clues to distinguish between toxic ingestion and organic disease.  Shared using Xodo PDF Reader and Editor Laboratory and imaging studies 1. Laboratory studies helpful in initial management include  Specific toxin-drug assays.  Measurement of arterial blood gases, electrolytes, and glucose.  Calculation of the anion gap. 2. Electrocardiogram (ECG) should be part of the initial evaluation in all patients suspected of ingesting toxic substances. 3. Urine screens for drugs of abuse or to confirm suspected ingestion of medications in the home may be revealing.  Shared using Xodo PDF Reader and Editor Screening Laboratory Clues in Toxicological Diagnosis Shared using Xodo PDF Reader and Editor  Shared using Xodo PDF Reader and Editor Treatment The four foci of treatment for poisonings are I. Supportive care II. Decontamination III. Enhanced elimination IV. Specific antidotes  Shared using Xodo PDF Reader and Editor I. Supportive Care Supportive care is the mainstay of treatment in most cases. Prompt attention must be given to ABC  Protecting and maintaining the airway.  Establishing effective breathing.  Supporting the circulation. This management sequence takes precedence over other diagnostic or therapeutic procedures. If the level of consciousness is depressed and a toxic substance is suspected, glucose (1 g/kg intravenously), 100% oxygen, and naloxone should be administered.  Shared using Xodo PDF Reader and Editor II. Decontamination The majority of poisonings in children are from ingestion, although exposures can also occur by inhalational, dermal, and ocular routes. The goal of decontamination is to minimize absorption of the toxic substance. Decontamination should not be routinely employed for every poisoned patient.  Shared using Xodo PDF Reader and Editor  Careful decisions regarding the utility of decontamination should be made for each patient and should include: i. Consideration of the toxicity and pharmacologic properties of the exposure. ii. Route of the exposure. iii. Time since the exposure. iv. Risks vs benefits of the decontamination method.  Shared using Xodo PDF Reader and Editor GI decontamination should never supplant excellent supportive care and should not be employed in an unstable or persistently vomiting patient. *Methods of GI decontamination include; 1. Induced emesis with ipecac 2. Gastric lavage 3. Activated charcoal 4. Whole-bowel irrigation (WBI). Of these, only activated charcoal and WBI are likely to be of clinical benefit.  Shared using Xodo PDF Reader and Editor Activated charcoal Single-dose activated charcoal decreases drug absorption when used within 1 hour of ingestion; however, it has not been shown to improve outcome. Thus it should be used selectively in the management of a poisoned patient. Charcoal is ineffective against  Alcohols  Caustics: alkalis and acids  Cyanide  Heavy metals (e.g., lead)  Hydrocarbons  Iron  Lithium  Shared using Xodo PDF Reader and Editor Whole-bowel irrigation Whole-bowel irrigation using polyethylene glycol (GoLYTELY) as a non absorbable cathartic may be effective for toxic ingestion of sustained-release or enteric- coated drugs. There is theoretical benefit in its use for potentially toxic ingestions of  Iron  Lead  Zinc  Packets of illicit drugs.  Shared using Xodo PDF Reader and Editor III. Enhanced Elimination 1. Multiple-dose activated charcoal; should be considered only if a patient has ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine, or theophylline. 2. Alkalinization of urine; may be helpful for salicylate or methotrexate ingestion. 3. Dialysis; may be used for substances that have a low volume of distribution, low molecular weight, low protein binding, and high degree of water solubility, such as methanol, salicylates , theophylline, and lithium.  Shared using Xodo PDF Reader and Editor IV. Specific Antidotes Poison Antidote Comment Opiates Naloxone Naloxone causes no respiratory depression Organophosphates Atropine Physiological: blocks acetylcholine Pralidoxime Specific: disrupts phosphate-cholinesterase bond (2 PAM; Protopam) Acetaminophen N-Acetylcysteine Most effective within 16 hr of ingestion Benzodiazepine Flumazenil Possible seizures, arrhythmias, DO NOT USE FOR UNKNOWN INGESTIONS β-Blocking agents Glucagon Carbon monoxide Oxygen Half-life of carboxyhemoglobin is 5 hr in room air but 1.5 hr in 100% O2 Cyclic Sodium bicarbonate antidepressants Iron Deferoxamine Lead Edetate calcium disodium(EDTA)  Shared using Xodo PDF Reader and Editor Prognosis Most poisonings result in minimal or no toxicity, or have minor effects. Intentional ingestions result in a much higher rate (5.2%) of major effects or death compared with unintentional ingestions (0.2%). Adolescents are more likely to have a moderate, major, or fatal effect (17.3%) from ingestion compared to younger children under 6 years (1.1%).  Shared using Xodo PDF Reader and Editor Prevention Properly educating parents regarding safe storage of medications and household toxins is necessary for preventing ingestions. If a child has ingested poison, a poison control center should be called.  Shared using Xodo PDF Reader and Editor Acetaminophen  Acetaminophen (N-acetyl-para-aminophenol APAP) is the most widely used analgesic and antipyretic in pediatrics, available in multiple formulations, strengths, and combinations.  APAP is commonly available in the home, where it can be unintentionally ingested by young children, taken in an intentional overdose by adolescents and adults, or inappropriately dosed in all ages.  APAP toxicity remains the most common cause of acute liver failure in the United States, and is the number 1 cause of intentional poisoning death in the United States.  Shared using Xodo PDF Reader and Editor  The single acute toxic dose of APAP is generally considered to be  >200 mg/kg in children.  >7.5-10 g in adolescents and adults.  Repeated administration of APAP at supratherapeutic doses (>90 mg/kg/day for consecutive days) can lead to hepatic injury or failure in some children, especially in the setting of fever associated with dehydration, poor nutrition, and other conditions that serve to reduce glutathione stores.  Shared using Xodo PDF Reader and Editor Clinical and Laboratory Manifestations Classically, 4 general stages of APAP toxicity have been described  Shared using Xodo PDF Reader and Editor Laboratory assessment;  Serum APAP level  Liver function test  PT, PTT, INR  If a toxic ingestion is suspected, a serum APAP level should be measured 4 hr after the reported time of ingestion  Shared using Xodo PDF Reader and Editor Treatment 1. Supportive care (ABC…) 2. The antidote N-Acetylcysteine (NAC) which most effective within 16 hr of ingestion.  Shared using Xodo PDF Reader and Editor Iron The severity of an exposure is related to the amount of elemental iron ingested.  Ferrous sulfate contains 20% elemental iron  Ferrous gluconate 12%  Ferrous fumarate 33%  Shared using Xodo PDF Reader and Editor Toxic dose  Pediatric patients who ingest >40 mg/kg of elemental iron should be referred to medical care for evaluation, although moderate to severe toxicity is typically seen with ingestions of >60 mg/kg.  Symptomatic patients and patients with a large exposure by history should have serum iron levels drawn 4-6 hr after ingestion.  Shared using Xodo PDF Reader and Editor Clinical and Laboratory Manifestations; Iron toxicity is classically described in 4, often overlapping, stages.  Shared using Xodo PDF Reader and Editor Treatment 1. Close clinical monitoring, combined with aggressive supportive and symptomatic care, is essential to the management of iron poisoning. 2. Activated charcoal does not adsorb iron, and Whole-bowel irrigation (WBI) remains the decontamination strategy of choice. 3. Deferoxamine, a specific chelator of iron, is the antidote for moderate to severe iron intoxication  Shared using Xodo PDF Reader and Editor Aspirin (Salicylates) The incidence of salicylate poisoning in young children has declined dramatically. Acute toxic dose The acute toxic dose of salicylates is generally considered to be >150 mg/kg. More significant toxicity is seen after ingestions of >300 mg/kg, and severe, potentially fatal, toxicity is described after ingestions of >500 mg/kg.  Shared using Xodo PDF Reader and Editor Clinical and Laboratory Manifestations Salicylate ingestions are classified as acute or chronic;  Early signs of acute salicylism include nausea, vomiting, diaphoresis, and tinnitus.  Moderate salicylate toxicity can manifest as tachypnea and hyperpnea, tachycardia, and altered mental status.  Signs of severe salicylate toxicity include mild hyperthermia, coma, and seizures  Chronic salicylism can have a more insidious presentation,and patients can show marked toxicity (e.g. altered mental status, noncardiogenic pulmonary edema, acidemia) at significantly lower salicylate levels than in acute toxicity.  Shared using Xodo PDF Reader and Editor Laboratory; 1. BGA. 2. Liver function test. 3. Electrolyte. 4. Blood glucose. 5. Salicylate level. 6. Serum and urine pH. 7. CXR.  Shared using Xodo PDF Reader and Editor  Classically, laboratory values from a patient poisoned with salicylates reveal a primary respiratory alkalosis and a primary, elevated anion gap metabolic acidosis.  Early in the course of acute salicylism, respiratory alkalosis dominates and the patient is alkalemic.  As the respiratory stimulation diminishes, the patient will move toward acidemia.  Hyperglycemia (early) and hypoglycemia (late) have been described.  Shared using Xodo PDF Reader and Editor Treatment 1. For the patient who presents soon after an acute ingestion, initial treatment should include gastric decontamination with activated charcoal. 2. Initial therapy focuses on aggressive volume resuscitation and prompt initiation of sodium bicarbonate therapy in the symptomatic patient, even before obtaining serum salicylate levels.  Shared using Xodo PDF Reader and Editor 3. The primary mode of therapy for salicylate toxicity is urinary alkalinization.  Alkalinization is achieved by administration of a sodium bicarbonate infusion at approximately 1.5 times maintenance fluid rates.  The goals of therapy include a urine pH of (7.5 – 8), a serum pH of (7.45 - 7.55). 4. In cases of severe toxicity, dialysis may be required Shared using Xodo PDF Reader and Editor