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Published by nasibdin
Management of poisoning
Management of poisoning

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Published by: nasibdin on Mar 28, 2013
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By: nasibdin

most of which have been developed since world war II. .000 synthetic chemicals. Children today are at risk of exposure to more than 80. Substance involved in poisoning vary widely between different countries*.Poisoning: Acute poisoning remains one of the most common medical emergencies in the world*.

2-children’s metabolic pathways. especially in the first months.* Children’s hand-to-mouth behavior and their play close to the ground further magnify their exposures. are immature. they have a time to develop multistage chronic disease that may be due to early exposures.Children are uniquely vulnerable to chemical pollutants for several resons: 1-they have proportionally greater exposures to many environmental pollutants than adults. & their development processes are uniquely sensitive to disruption by chemical pollutants.* 3-children are growing & developing. . 4-because children have many further years of life.

-classification: Blood lead level (µ/dl) Chemical poisoning: 1. Exposure is especially common in countries that still permit lead gasoline*.Lead exposure occurs worldwide.Lead poisoning: Action recommended No immediate concern Environmental survay Remove from lead sources Survey the community &education about the risk Bring to medical attention 0-9 10-19 20-24 25-54 55-69 >70 Or symptomatic ““ ““ Emegency hospitalization EDTA test Treat with EDTA or DMSA “ “ with BAL and EDTA . Anther major sources of exposure is lead-based paint.

include lower intelligence and poor school performance. may be precede by behavior changes or lead colic. ataxia. characterized by vomiting. -encephalopathy is the most serious manifestation. abdominal pain. constipation.-Pathophysiology: The high toxicity of lead result from its avidity for the sulfhydryl (sh) group of proteins. papilledema. seizures. -encephalopathy include persistence vomiting. -Neurobehavioral abnormalities. . -in absence of clear sings of encephalopathy are usually nonspecific & vague. & coma. -Clinical manifestation: The probability of severe symptoms increase as the exposure to lead and blood lead levels rise. lead irreversibly binds to the SH group of protein and thus impairs its function. demonstrated at low levels of lead exposure by epidemiological studies.

-Diagnosis: of critical importance in the diagnosis is an accurate environmental history. is strongly suggestive. particularly of exposure to lead-containing paint. -Treatment: -(Table)*. when present. -blood lead test. . History of pica. ”symptoms nonspecific”.

& produces a neurological syndrome. .swordfish). readily penetrates the CNS. & chelation therapy when appropriate. -Management: Removal from the source of poisoning.Mercury: -inorganic: can cause dermatitis. -organic: fat-soluble. tremor. gingivitis. decontamination. stomatitis.( fish "tuna.2. Even low dose exposure has been shown to be hazardous to developing fetal brain. aggressive stabilization & supportive care.

-Drug poisoning: 1. which immediate conjugated with glutathione to form harmless substance. Where it can be unintentionally ingested by young children or taken in an intentional over dose by adolescents. only small amount (4%) of a dose is metabolized by hepatic cytochrome P450 to NAPQI.paracetamol (acetaminophen): Most widely used analgesic & commonly available in the home. when therapeutic doses are administrated. -pathophysiology: The toxicity results from the formation of highly reactive intermediate metabolite (NAPQI). When hepatic store of glutathione are depleted to less than 70% of normal. the NAPQI metabolite can combine with hepatic macromolecules to produce hepatocellular damage. (acute toxic dose:>20mg/kg in children younger than 12yr) .

. I II III IV 72 – 96hr 4days2wk Peak liver function abnormality-anorexianausea-vomiting. hepatic enzymes-oliguria. child pass through four stages of toxicity: Stage Time after ingestion ½ . PTT.clinical & laboratory manifestation: if untreated.48hr Characteristics Anorexia-nausea-vomiting-malaise-pallordiaphoresis. .-Repeated administration of over dose may lead to hepatic injury or failure in some children. Resolution of hepatic dysfunction Or complete liver failure.24hr 24 . Resolution of above. Rt upper quadrant abdominal pain-elevated bilirubin.

NAC serves as precursor for glutathione synthesis. Start: 14mg/kg 70mg/kg every 4hr for 17 dose. -Liver function test. -Treatment: Can be stated within 1-2 hr of the ingestion. activated charcoal administration should be considered.-can measured at 4hr or more after ingestion to determine the severity of over dose. The antidote for paracetamol poisoning is N-acytylcysteine (NAC). .

and inhibiting amino acid synthesis also decrease platelet adhesiveness & increase pulmonary capillary permeability. as in case of over dose. now usually in therapeutic situations. -Pathophysiology: Effect directly or indirectly affect most organ systems by uncoupling oxidative phosphorlation. . Acute toxic dose: more than 150mg/kg.2-Aspirin (salicylates): Salicylate toxicity. -clinical & laboratory manifestation: Young children are more susceptible to toxic effects because they are less able to buffer the acid load produced by salicylates. inhibition kerbs cycle enzymes.

restlessness. -Coma may occur develop secondary to cerebral edema. -cardiovascular collapse. caused by the accumulation of lactic acid & other metabolic acids. Salicylate directly stimulate the respiratory center. -Pulmonary edema or hemorrhage may develop in more sever cases.& death may occur.& confusion are common. result respiratory alkalosis with compensatory alkaluria*. -CNS changes. agitation. nausea & vomiting occur secondary to gastric irritation. Heapatotoxicity occur after chronic exposure or very large dose. Dehydration & progressive metabolic acidosis.acute salicylate ingestion. leading to hyperventilation & hyperpnea. -after .

-Treatment: -initial treatment gastric decontamination with active charcoal. K & electrolytes level.-Investigation: urine PH. glucose. -urine excretion of unmetabolized salicylate. (need large quantities of K &bicarbonate). (important rout of elimination in overdose). -In sever cases dialysis may be required. -urine PH should be raised to at least 7-7. Liver function test.5”iv bicarbonate”. (not useful for chronic exposure). . volume/hr Plasma PH. -rehydration & correction of electrolyte abnormalities.

Iron: One of the most common causes of childhood poisoning death.Iron corrosive to the gastrointestinal mucosa. causing metabolic acidosis. lead to abnormal liver function & coagulopathies. It accumulates in the mitochondria & tissues to produce cellular damage & systemic toxicity.*** . The potential severity of exposure is based on the amount of elemental iron ingested.3. -Drowsiness &coma may develop indirect or direct by effect of iron in the CNS. -Sever poisoning may cause hepatic necrosis.Pathophysiology: . . -Reduce peripheral perfusion & mitochondrial damage lead to accumulate of lactic acid. -Cause venodilation & increase permeability leading to hypotension. -Toxic dose: more than 60mg/kg.

-Clinical &laboratory manifestation: -Nausea. . 3-liver function test. -Investigation: 1-serum iron after 4hr: -less than 500µg/dl ---. 2-blood gas level. 4-abdominal radiography (iron radiopaque).low risk toxicity.significant toxicity. vomiting. -Hematemesis & bloody diarrhea in more serious poisoning. -Gastric scaring & pyloric stenosis can develop 2-4wk after large ingestion. -more than 500µg/dl ---. serum glucose. diarrhea & abdominal pain are the hallmark of iron poisoning and usually develop within 30min-6hr after ingestion.

2-gatric lavag is inefficiency. dilute phospho-soda(1:4). 5-Deferoxamine. if serum iron greater than 500µg/dl(iv). 4-oral bicarbonate (2%). 3-activited charcoal “dose not absorbed iron“. ”specific chelator of iron” . until child symptom free. poorly absorbed iron salts.Treatment: 1-good supportive & symptomatic care. and magnesium hydroxide react with iron to form less soluble.

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