In the latest Case Record of the Massachusetts General Hospital, a 34-year-old man was seen in the emergency department because of abdominal pain and vomiting after his wife had given him a powder to cause him to stop drinking alcohol. The substance was identified, diagnostic tests were performed, and management decisions were made.
Patients with exposures to poisons commonly present to emergency departments. Unintentional poisoning was second only to motor vehicle accidents as a cause of accidental injury or death for all ages in 2009 and accounted for more than 830,000 visits to the emergency department in 2010.
• What initial testing is useful in the care of a patient with suspected poisoning?
In most, if not all, poisoned patients, a blood chemistry panel should be obtained, along with an electrocardiogram to screen for abnormalities in the duration of the QRS complex and the QT interval, tests for the serum glucose level, and screening tests for serum acetaminophen, salicylate, and alcohol. A pregnancy test should be obtained in female patients of child-bearing age. Plain radiographs may provide additional information in cases of suspected ingestions of heavy metals, body packing (internal concealment of illicit drugs), and toxin-induced noncardiogenic pulmonary edema. The utility of toxicologic screening of the urine will hinge on the recognition of a toxidrome or the suspicion of a particular substance.
• What are the toxic effects of antimony ingestion?
Trivalent antimony (tartar emetic) has a potent emetic effect as aversive therapy for substance abuse, and is sold in some countries for this purpose. Doses of as little as 200 to 1200 mg can be fatal. Antimony is rapidly absorbed from the gastrointestinal tract and undergoes enterohepatic recirculation. Ninety percent of tartar emetic is excreted during the first day after ingestion, and the remaining 10% during a slower elimination phase of 16 days after ingestion. Similarly to arsenic, antimony is thought to inhibit the pyruvate dehydrogenase complex, thus preventing acetyl coenzyme A from entering the Krebs cycle with a subsequent lack of ATP production. Many organs can be affected, including the gastrointestinal tract, liver, kidneys, heart, and central nervous system. Antimony salts are gastrointestinal irritants with local effects on enterochromaffin cells, which release serotonin that subsequently acts on 5-hydroxytryptamine type 3 receptors to stimulate vomiting, which may be severe.
Morning Report Questions
Q: How is antimony poisoning treated?
A: Antimony is excreted in bile after conjugation with glutathione; therefore, the administration of N-acetylcysteine, a synthetic precursor of glutathione, is often recommended to enhance the secretion of antimony. Chelation may also be an important part of management. The goal of chelation is to form a stable complex between antimony and the sulfur donors, or dithiols, on the chelator, preventing the antimony from chelating host enzymes. Options are dimercaprol, DMPS (2,3-dimercapto-1-propanesulfonic acid), and DMSA (2,3-dimercaptosuccinic acid). A sensation of chest constriction, as well as anxiety and hypertension, may occur within 10 to 30 minutes after the administration of dimercaprol and typically will resolve in 30 to 50 minutes.
Q: What are the indicators of poor prognosis in acute liver failure?
A: The King’s College Hospital criteria remain the most used prognostic criteria for acute liver failure. For patients with acute liver failure not induced by acetaminophen, poor prognostic factors include a prothrombin time of more than 100 seconds or any three of the following criteria: drug toxicity or indeterminate cause, an age younger than 10 years or older than 40 years, a jaundice-to-coma interval of more than 7 days, a prothrombin time of more than 50 seconds (INR, greater than or equal to 3.5), and a serum bilirubin level of more than 300 micromoles per liter (17.5 mg per deciliter). A study of 165 patients with acute liver failure at King’s College Hospital showed that patients with an arterial ammonia level of more than 200 micromoles per liter (340.6 micrograms per deciliter) on admission to the ICU were at the highest risk for the development of intracranial hypertension, the main cause of death in patients with acute liver failure.