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Poisonings (Contd…


An analgesic and antipyretic Oil of wintergreen •Contains methyl salicylate •very toxic yet is available over the counter for oral and topical use •Smells great and children may drink it Don’t keep this drug around

Risk factors/ etiology •Salicylates uncouple oxidative phophorylation and increase the metabolic rate, resulting in tachypnea, tachycardia, fever, hypoglycemia •Krebs cycle inhibited causing a metabolic acidosis •Damage to hepatocytes occurs, causing liver toxicity, prolonged PT, platelet inhibition and prolonged BT

Presentation/ physical examination Mild salicylate ingestion •Vomiting, hyperpnea, fever, lethargy, mental confusion Severe salicylate ingestion •Convulsions, coma, respiratory and cardiovascular collapse Chronic salicylate ingestion •Hyperventilation, dehydration, bleeding disorders, seizures, coma

Three phases of salicylate ingestion Phase1 Respiratory alkalosis from direct stimulation of the respiratory center Potassium and sodium bicarbonate excreted in the urine Lasts 12 h in an adolescent , but may not be evident in a small child

Phase 2 “Paradoxical aciduria” 12 – 34 h after salicylate ingestion in the adolescent Begins shortly after salicylate ingestion in the young child Aciduria may lead to hypovolemia

Phase 3 Metabolic acidosis, dehydration, hypokalemia 4 – 6 h after ingestion of salicylates in an infant and ≥ 24 h after ingestion in an adolescent Metabolic acidosis results from lactic acidosis Hyperpnea is secondary to acidosis rather than to stimulation of respiratory centers

•WBC, hematocrit, platelets increased •BUN, creatinine also increased •Na+, K+ •Blood glucose •ABG show a metabolic acidosis with respiratory compensation in children and a respiratory alkalosis alone in adolescents; or mixed ABG disorder

In acute overdose, salicylate serum level is predictive of the clinical course at 6 h after ingestion Serum level should be plotted on the Done’s nomogram

Done’s Nomogram

•If the serum salicylate level is < 35 mg/dl, asymptomatic •If at 6 h after ingestion, the salicylate level is 35 – 70 mg/dl, mild to moderate toxicity •Salicylate level between 70 and 100 mg/dl , severe toxicity •Salicylate level > 100 mg/dl, potentially fatal

Treatment Gastric decontamination performed Patient hydrated To enhance the excretion of salicylate the intravenous route should be used to administer bicarbonate Urine pH should be raised to a pH of 7.0 – 7.5 Hemodialysis required in severe cases of salicylate toxicity (salicylate level > 100 mg/dl)

Complication/ follow-up Causes of death from •Respiratory failure •Cerebral edema •Hemorrhage •Cardiovascular collapse

A colorless, odorless gas produced from the combustion of carbon-containing fuel Risk factors/ etiology •Affinity of CO to hemoglobin is 250 times that of oxygen •Results in the formation of carboxyhemoglobin, decreasing the oxygen carrying capacity of blood

Presentation/ physical examination
Symptoms depend on the carboxyhemogloin levels 0-10%: None 11-20%: Mild headache 21-30%: Throbbing headache, irritability 31–40%: Severe headache, lethargy, nausea, vomiting 41–50%: Confusion, syncope, tachycardia, tachypnea 51-60%: Syncope, coma, seizures

Diagnostic tests •Presence or absence of the classic cherry-red skin color no diagnostic value •Carboxyhemoblobin level and ABG analysis should be obtained •Urinalysis for myoglobin (Severe CO poisoning may have muscle breakdown) •CBC and electrolytes

Treatment •Patient should be removed from the environment •100% supplemental oxygen or hyperbaric oxygen in severe cases, administered until the carboxyhemoglobin level is ≤ 5% •Urine output should be >1ml/kg/h Complications/follow-up Behavior changes, memory loss, blindness in 10-30% of cases, even after a single exposure

Acids: batteries, toilet bowel cleaners, metals etc. Bases: dishwashing detergent, Liquid Plummer etc. Risk factors/ etiology •Acids coagulate proteins, resulting in tissue necrosis, and alkalis produce liquefaction necrosis with the risk of perforation if the burn located in the intestinal tract •Serious injuries tend to occur with a pH <2 or >12

Presentation/ physical examination •Burns of mucous membranes may be visualized •Patient may drool and refuse to swallow secondary to pain •Esophageal strictures may be found •Acids may be responsible for delayed gastric emptying from pylorus scarring Diagnostic tests CBC, Abdominal radiograph

Treatment •Caustic should be removed by flushing copiously with water •Emesis and gastric lavage contraindicated in caustic patients •Activated charcoal not used •Endoscopy completed in the first 24 h if the patient is symptomatic or the history is suggestive of burns from caustic ingestion •Use of steroid controversial and prophylactic antibiotics do not seem to improve outcome

•An alkaloid extracted from Erythroxylon coca •Supplied as a hydrochloride salt in crystalline form •Absorbed from the nasal mucosa •Detoxified in the liver and excreted in the urine •Half-life approximately 1 h Risk factors/ etiology •All coacaine not “pure” as drugs such as PCP, heroin, or amphetamines may be added or sbstituted for cocaine •May be snorted (nasal application), injected, or smoked

Presentation •Euphoria •CNS stimulation, ie, restlessness, excitement, agitation, increased motor activity, increased respiratory rate, and hypertension Later, •Hypotension with seizure, coma, and respiratory depression •Chest pain secondary to myocardial injury that ranges from angina pectoris to myocardial infarction •Nausea, insomnia, and emaciation in the chronic user

Physical examination •There may be a perforated nasal septum from snorting Diagnostic tests •Urine drug screen •If smuggling suspected, a flat-plate abdominal radiograph will show opaque densities within the bowel highlighted by a gas halo

Treatment •Activated charcoal indicated only when “body packing” suspected •Intensive supportive therapy applied to the clinical manifestations •Half-life for cocaine is appox 1 h and prognosis is good if adequate support Complications/ follow-up •Hypertension may lead to a CVA •Chronic cocaine users may develop a cardiomyopathy that leads to depressed cardiac function and death

Carbon compounds that become liquid at room temperature Risk factors/ etiology •Found in fuels, solvents, household cleaners, and polishes •Aspiration of hydrocarbons may cause a chemical pneumonitis

Presentation •Cough, emesis, and fever •Symptoms may be delayed for 6 h Physical examination •SOB, wheezing, rales, dullness to percussion and respiratory difficulty Diagnostic tests •CXR may show and infiltrate

Treatment Gastric lavage contraindicated, unless a risk of severe poisoning, eg, CNS involvement If gastric lavage is necessary, endotracheal intubation Patients who remain asymptomatic after 6 h and have a negative CXR may be discharged Antibiotics not indicated unless a secondary bacterial infection Corticosteroid not beneficial

Complication/ follow-up Recovery in most cases, but course may include •Lethargy, seizures, and coma •Pneumothorax, pleural effusions, secondary infections •Respiratory failure and death

Acetylesterase inhibitors that may be ingested, inhaled, or absorbed through the skin Commonly found in insecticides Used as nerve gases in chemical warfare agents Presentation/ physical examination •Muscarinic, nicotnic, and CNS signs and symptoms

Muscarinic symptoms: salivation, lacrimation, urination, defecation, GI cramping, and emesis Nicotinic symptoms: cramps, fasciculations, twitching, weakness, and areflexia, and paralysis of voluntary muscles, including respiration, occurs after the muscarinic effects Nicotinic symptoms not seen in mild poisoning CNS symptoms: anxiety, ataxia, dizziness, headache, convulsions, coma

Diagnostic tests: •History of exposure and clinical presentation •Odor of insecticide •Decreased RBC cholinesterase Treatment: •ABC’s •Gastric lavage and activated charcoal •If exposure via skin, wash with soap and water and contaminated clothing placed in a plastic bag •Health-care workers should take precautions not to get organophosphate on their skin Atropine (for muscarinic symptoms) Pralidoxime (for nicotinic symptoms)

•Most common cause of death form poisoning in childhood •Severity of the poisoning depends on the amount of elemental iron ingested •Adult preparations responsible for serious poisonings

Presentation/ Physical examination Iron poisoning occurs in four stages: •Stage 1: occurs 30 min - 6 h after ingestion, nausea, vomiting, diarrhea and abdominal pain; hemorrhagic gastroenteritis in more serious iron ingestion •Stage 2: occurs 6 – 12 h after ingestion, relative clinical improvement mistaken for recovery (honeymoon phase) •Stage 3: occurs 24- 48 h after ingestion, severe poisoning, progressive circulatory collapse (shock), hepatorenal failure, bleeding, metabolic acidosis, and coma •Stage 4: occurs 1-2 months after ingestion and causes GI scarring and obstruction and pyloric stenosis

Diagnostic tests •Based on history and development of symptoms •Serum iron levels obtained •Serum iron levels >500 ug/dl severe poisoning •Iron is radiopaque and iron tablets may be seen on plain abdominal films •Children’s multivitamins may not be visualized on X-ray because of their low iron concentration

Treatment •Syrup of ipecac may be used to remove iron tablets from stomach if there is no evidence of gastroenteritis •Whole bowel irrigation used to flush tablets from the intestine •If tablets continue to adhere to the gastric mucosa, then they must be removed by endoscopy or surgery •Treatment is supportive and includes airway and fluids if the patient is in shock

Antidote is deferoxamine (IV) administered 1)To symptomatic patients and those with hypotension and lethargy regardless of the serum iron level and total iron binding capacity (TIBC) 2)If the serum iron is greater than TIBC 3)If the serum iron level is >350 ug/dl The urine turns “vin rose” when free iron binds with deferoxamine Treatment should continue until the patient is symptom free

Complication/ follow- up Iron is corrosive to the GI mucosa, and may cause hypotension and metabolic acidosis and coagulopathies Drowsiness and coma Toxic ingestions may result in death

A chronic disorder often seen in children who are near environmental exposure risk, such as ingestion of paint chips or plaster from old buildings Presentation/ physical examination •Depends on blood lead level and age of the child •Most asymptomatic ; picked up on routine screen •Anorexia, apathy, lethargy, anemia, decreased play activity, aggressiveness, and poor coordination

Diagnostic tests •Elevated blood lead levels •increase in free erythrocyte protoporphyrin and •increased lead excretion in the urine after administration of a chelating agent such as Calcium EDTA •Minimal lead screening should be done for patients who are 6 months – 6 years old age •Blood lead levels of >10 ug/dl are abnormal •Sideroblastic anemia •X-ray shows lead lines at the metaphyses of the long bones and radiopaque foreign material within the small bowel

Treatment The goal of management is to eliminate or remove the child from the source of lead

*DMSA, Meso-2,3dimercaptosuccinic acid **BAL, Dimercaprol



Complications/ follow-up: Encephalopathy after 36 weeks of actively ingesting lead (<3 years)

•Used as sedatives , for allergies, for antinausea, and for motion sickness •Found in some cold medication such as liquid cough medication Presentation/physical examination •Drowsy or •Insomnia, nervousness, restless •Children may be hyperactive and hallucinations •Tonic clonic seizures •Anticholinergic effects such as flushed skin, fever, tachycardia, fixed dilated pupils

Treatment •Activated charcoal unless a sustained release antihistamine, in which case, whole bowel irrigation •Seizures should be controlled •Supportive therapy Complication/ follow up: •Death from uncontrolled seizures leading to coma and cardiopulmonary arrest

•Mild to moderate toxicity mimics alcohol intoxication •Severe toxicity results in CNS problems including lethargy and coma Physical examination •Constricted pupils, confusion, hypotension, poor coordination, respiratory depression, coma

Treatment: •ABC’s •Gastric lavage •Multiple doses of activated charcoal •IV fluids and forced diuresis and alkalinization for long-acting barbiturate intoxication •In severe cases, hemodialysis Complications/ follow- up •Shock or cardiopulmonary arrest leading to early deaths •Aspiration pneumonia or pulmonary edema leading to later deaths

Presentation/physical examination •CNS and heart systems affected •Drowsiness, delirium, hallucination, disorientation, seizures, coma, hypertension, later, hypotension, and arrhythmias Diagnostic tests •ECG to check for QRS widening and QT and QTc prolongation

Treatment •Supportive therapy •Activated charcoal •Sodium bicarbonate to treat and prevent dysrhythmias (Lidocaine if not responding) •Hypotension treated with fluids and NE •Seizures resolves without treatment •Symptomatic patients should be monitored in ICU •Patients completely asymptomatic after 6 h of observation may be discharged home Complications/ follow-up •Seizures and arrhythmias