Pediatric emergency medicine trisk 3073 3073
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mitochondrial poison, particularly in the liver, with resulting changes in cellular
energy metabolism and the production of metabolic acidosis.
Clinical Considerations
The clinical effects of iron poisoning are classically divided into four phases.
Phase I represents the effects of direct mucosal injury and usually lasts 6 hours.
Vomiting, diarrhea, and GI blood loss are the prominent early signs; when severe,
the patient may lapse into early coma and shock caused by volume loss and
metabolic acidosis.
Phase II, which lasts from 6 to 24 hours after ingestion, is marked by
diminution of the GI symptoms. With appropriate therapy to replace fluid and/or
blood losses, the child may seem relatively well and often goes on to full
recovery without any subsequent symptoms. However, this remission may be
transient and may be followed by phase III, characterized by metabolic acidosis,
coma, seizures, and intractable shock. This phase is believed to represent
hepatocellular injury with consequent disturbed energy metabolism; elevated
levels of lactic and citric acids are noted in experimental iron poisoning before
cardiac or respiratory failure occurs. Jaundice and elevated transaminases are
noted in this phase. A phase IV has been described in survivors of severe iron
poisoning, marked by pyloric or duodenal stenosis resulting from scarring and
consequent obstruction.
Laboratory abnormalities often associated with severe iron intoxication include
metabolic acidosis, leukocytosis, hyperglycemia, hyperbilirubinemia and
increased liver enzymes, and a prolonged prothrombin time. If fluid loss is
significant, there will be hemoconcentration and elevated BUN. Abdominal films
may show radiopaque material in the stomach, but the absence of this finding
does not indicate a trivial ingestion.
Patients who arrive with severe early symptoms, including vomiting, diarrhea,
GI bleeding, depressed sensorium, or circulatory compromise merit urgent,
intensive treatment in the ED. The first priority is to obtain venous access.
Simultaneously, draw blood for CBC, blood glucose, electrolytes, BUN, liver
function tests, serum iron, and type and cross-match analyses. GI
decontamination is begun as detailed in the following section. Provide crystalloid
to support blood pressure. Start chelation therapy with IV deferoxamine
immediately in all severely poisoned patients. Obtain an abdominal radiograph as
soon as possible after GI decontamination to determine its efficacy and to
investigate for the presence of iron pill concretions.
