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TEACHING TOPIC
Ingestion of an Unknown Substance
CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL,
Case 22-2012: A 34-Year-Old Man with Intractable Vomiting after
Ingestion of an Unknown Substance,
(https://www.nejm.org/action/doSecureKeyLogin?uuid=7684715&dateTime=201207280000&key=xBJkN7Hr41AZZX2DlpXcvg4jSWVIUF91188N28Kxsao%3D&uri=/doi/full/10.1056/NEJMcpc1111580?query=BUL)
W. Macias Konstantopoulos, M. Burns Ewald, and D.S. Pratt
CME Exam
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.
Clinical Pearls
- 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.