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Clinical Summary

Arsenic, a tasteless and odorless metalloid, is well absorbed by multiple routes of administration. Although arsenic exists in both inorganic and organic species, only the inorganic form is responsible for toxicity. Contaminated soil and water with inorganic arsenic are the primary sources of exposure to the general population. Chronic arsenic poisoning due to contaminated water continues to be a global health issue.

Arsenic inhibits multiple enzymes critical to the production of ATP. It inhibits pyruvate dehydrogenase complex, decreases the citric acid cycle, and decreases gluconeogenesis. Acute arsenic poisoning typically starts with acute onset of nausea, vomiting, abdominal pain, and “rice water” diarrhea. Acute encephalopathy, acute renal failure, lung injury, and death may occur. Later findings in survivors include alopecia, rash, Mees lines, and neuropathy. Chronic toxicity results in dermatologic changes such as hyperpigmentation or hypopigmentation. Hyperkeratosis may occur on the skin, particularly the palms and soles. Peripheral vascular disease (blackfoot disease) may occur. Arsenic is a known carcinogen and is associated with skin and lung cancers.

Management and Disposition

After an acute ingestion, an abdominal radiograph may demonstrate radiopaque material in the GI tract. Supportive care with maintenance of electrolytes is important. A 24-hour urine collection in a metal-free container is the optimal method for determining arsenic burden. However, the acutely ill patient will likely require chelation before urine results are available. Chelation is usually initiated with intramuscular dimercaprol (British anti-Lewisite [BAL]). Succimer, an oral analog of BAL, may be useful in subacute poisoning. Patients with suspected acute arsenic poisoning should be admitted to an intensive care unit.


  1. When a nonselective heavy metal urine test is performed for possible arsenic exposure, the measured arsenic typically reflects the presence of nontoxic organic species from dietary sources such as seafood rather than toxic inorganic species. As such, urine should either be speciated, or the patient advised to refrain from seafood prior to urine collection.

  2. Intravenous arsenic trioxide is approved by the US Food and Drug Administration for treatment of acute promyelocytic leukemia unresponsive to other therapies.

  3. Arsenic is one of the few heavy metals that is directly cardiotoxic due to its blockade of delayed rectifier channels. Torsade de pointes has been described in the setting of acute arsenic poisoning.

FIGURE 17.77

Chronic Arsenic Poisoning. Hyperpigmentation of the skin is a clinical finding from chronic arsenic poisoning. (Photo contributor: Lawrence B. Stack, MD.)

FIGURE 17.78

Chronic Arsenic Poisoning. Hyperpigmentation and hypopigmentation along with hyperkeratosis are findings on the palms of patients with chronic arsenic poisoning. (Photo contributor: Lawrence B. Stack, MD.)

FIGURE 17.79

Chronic Arsenic Poisoning. The patchy hair loss seen in this photograph is from chronic arsenic poisoning. (Photo contributor: Selim Suner, MD, MS.)


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