Combined antipyretic therapy: another potential source of chronic acetaminophen toxicity.
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Biomedical subjects
Publications and source records attributed to H C Mofenson.
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OBJECTIVE: To present a child who developed gastric ulcers and duodenal erosions after ingestion of hydrogen peroxide 3% and delineate the epidemiology, medical outcomes, and toxicity of exposures to this agent managed by a poison control center. METHODS: A retrospective chart review of exposures to hydrogen peroxide 3% reported to the Long Island Regional Poison Control Center from January 1992 to April 1995 was conducted. Data extracted included age, route of exposure, amount of agent, symptoms, therapy, and medical outcome. RESULTS: There were 670 exposures to hydrogen peroxide 3% of 81,126 total exposures reported during the 40 months. Most exposures were by oral route (77%), occurred in children < 17 years old (67%), and were asymptomatic (85.6%). All but one exposure resulted in a benign outcome. One child, who presented with bloody emesis, developed multiple gastric ulcers and duodenal erosions after ingestion of hydrogen peroxide 2-4 oz. CONCLUSIONS: Exposure to hydrogen peroxide 3% is usually benign, however, severe gastric injury may occur following small ingestions in children. Patients who report persistent vomiting or bloody emesis require medical evaluation and consideration of endoscopy to evaluate gastrointestinal injury.
CASE REPORT: A case of severe lead poisoning following ingestion of an imported clothing accessory is reported. The child presented with abdominal pain, vomiting, and anemia but did not develop encephalopathy. RESULTS: Prompt removal of the object in conjunction with whole bowel irrigation and chelation therapy led to a favorable outcome.
STUDY OBJECTIVE: It is often taught that acetaminophen-induced liver dysfunction occurs only after a latent period of 24 to 48 hours. This study was designed to evaluate the temporal profile of transaminase levels in patients with acetaminophen-induced hepatotoxicity. DESIGN: Prospective data collection using standard poison control center data sheets. PARTICIPANTS: Hospitalized patients with acetaminophen exposure who were reported to the Long Island Poison Control Center between January 1993 and June 1994. Patients who presented within 24 hours of ingestion and in whom increased aspartate aminotransferase (AST) levels developed during hospitalization were included in the data analysis. Patients who presented more than 24 hours after ingestion, who had ingested another potentially hepatotoxic agent, or who had ingested acetaminophen over a period of more than 2 hours were excluded. RESULTS: Of 1,825 patients with reported acetaminophen exposure, 779 had potentially toxic ingestions and were examined in an emergency department. Of 291 patients with toxic acetaminophen levels who were admitted, 36 (12%) had increased levels of AST at some point during hospitalization. All received oral N-acetylcysteine within 2.5 hours of presentation. In 11 of 19 patients who met all inclusion criteria (58%), AST levels were noted to be increased in the 24 hours after ingestion. The median peak AST level was 422 IU/L (range, 74 to 8,538 IU/L). AST levels peaked within 48 hours in 4 patients (21%) and within 72 hours in 18 patients (95%). Six of eight patients with peak AST levels greater than 1,000 IU/L had increased transaminase levels during the 24 hours after acetaminophen ingestion. CONCLUSION: Acetaminophen poisoning may cause the serum transaminase level to increase during the 24 hours after ingestion.
We present a case of ingestion of a commonly used stool fixative containing 675 mg of mercuric chloride per 15 mL vial. Early chelator therapy with dimercaprol and aggressive hydration were initiated and the patient remained asymptomatic. Safety packaging of this product is recommended.
We report four cases of poisoning with amatoxin-producing mushrooms in suburban Long Island. All occurred when amateur mushroom hunters picked mushrooms from neighboring lawns. Two patients presented 30 hours post ingestion with evidence of acute hepatic dysfunction. One survived, after treatment with charcoal and penicillin; the other, a 90-year-old woman with prior cardiac disease soon developed shock and subsequently died. The other two patients were admitted 18 hours after ingestion of Lepiota chlorophyllum and received prompt charcoal hemoperfusion. Both did well, although one had a mild elevation of transaminases. Although most reports of amatoxin poisoning originate in Europe, these cases confirm that amatoxin-producing mushrooms, including Lepiota chlorophyllum, may be found in northeastern American suburbs. Such patients who present prior to 24 hours after ingestion should receive charcoal hemoperfusion if a lethal dose (> 50 g of mushroom) has been eaten.
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This is a case of magnesium intoxication in a neonate produced by an oral magnesium cathartic. A review of the literature revealed there are very few cases that have been reported of magnesium toxicity due to cathartics. There is no recommended dose for magnesium cathartics in neonates or data on their safety. A review of the management of magnesium intoxication is presented.
This is the fourth reported case of acute pancreatitis associated with acetaminophen overdose. The patient had ingested the smallest amount of acetaminophen (9.75-13 g) that has been reported to produce acute pancreatitis. This patient also suffered liver and renal impairment and developed an ileus and ascites. Despite late therapy and laboratory tests that indicated a poor prognosis the patient made a complete recovery without sequelae.
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