Toxicology – Arsenic Poisoning

Sources

Arsenic exposure may occur from:

• Contaminated groundwater or food
• Certain traditional or nonstandard medicines
• Some pesticides and industrial products
• Pigments and manufacturing processes
• Contaminated occupational environments

Inorganic arsenic is generally responsible for the most significant systemic toxicity.

Typical Presentation

A patient with substantial arsenic exposure may develop severe gastrointestinal illness followed by cardiovascular and neurologic toxicity. Chronic exposure can produce characteristic skin changes and a painful stocking-glove peripheral neuropathy.

A garlic-like odor on the breath has traditionally been described but is neither sensitive nor specific.

Clinical Features

Acute poisoning may cause:

• Severe nausea and vomiting
• Profuse watery diarrhea
• Abdominal pain
• Dehydration
• Tachycardia
• Hypotension and shock
• Altered mental status
• Seizures
• Peripheral neuropathy, sometimes developing after the initial illness
• Cardiac dysrhythmias and QT prolongation
• Cardiovascular collapse in severe cases

Chronic poisoning may cause:

• Hyperkeratosis, especially of the palms and soles
• Abnormal skin pigmentation
• Peripheral neuropathy
• Metabolic abnormalities, including increased risk of diabetes
• Cardiovascular disease
• Increased risk of several cancers, particularly skin, lung, and bladder cancers

Mechanism of Action

Arsenic disrupts cellular energy production. Inorganic arsenic can inhibit enzymes such as pyruvate dehydrogenase, interfering with formation of acetyl-CoA and ATP.

It can also impair:

• Oxidative phosphorylation
• Glucose metabolism
• Other essential enzyme systems

The result is widespread cellular dysfunction affecting the gastrointestinal, cardiovascular, neurologic, and other organ systems.

Management

Treatment includes:

• Immediate removal from the exposure source
• Aggressive supportive care
• IV fluids and cardiovascular stabilization
• Correction of electrolyte abnormalities
• ECG monitoring in significant acute poisoning

Chelation may be required for clinically important poisoning. Agents include:

• Dimercaprol (BAL) in selected severe acute cases
• Succimer (DMSA)
• DMPS, where available

Chelation decisions should be made with a medical toxicologist or poison center because the preferred agent depends on the type and severity of exposure.

Key Points

• Acute arsenic poisoning often begins with severe GI symptoms and can progress to shock, dysrhythmias, and neurologic injury.
• Painful stocking-glove neuropathy is an important clue.
• Chronic exposure can cause hyperkeratosis and characteristic pigmentation changes.
• Arsenic interferes with cellular energy production.
• Chronic inorganic arsenic exposure is associated with increased cancer risk.
• Groundwater contamination remains an important source of arsenic exposure worldwide.