History
Acute toxicity following ingestion, inhalation, or absorption of inorganic arsenic produces a burning sensation in the mouth and throat. This is followed, usually somewhat later, by severe gastrointestinal distress with copious and severe diarrhea and vomiting. Vertigo, delirium, coma, and often convulsions are seen as the toxicity is manifest. Circulatory collapse and renal and hepatic failure ensue, and hemolysis usually occurs 4-6 hours after onset of evidence of toxicity. Acute symptoms typically develop hours after exposure to inorganic arsenic. Inhalation of arsine gas produces headache, malaise, weakness, dizziness, dyspnea, and GI distress more rapidly.
The typical picture in subacute arsenic toxicity includes the onset of gastrointestinal symptoms—nausea, vomiting, and diarrhea—which may be intermittent but in retrospect are associated with ingestion of hot or cold beverages. For a layperson's account of an experience with arsenic poisoning, read "My Husband Poisoned Me" by Ellen Harris in the March 2000 issue of McCall's Magazine, pages 68-73.
Chronic exposure effects should be suspected when a patient presents with a distal sensorimotor neuropathy accompanied by skin hyperpigmentation. History of drinking well water is an additional clue. Bae et al have written on the role of a rice cooking technique associated with arsenic toxicity in Bangladesh. [3]
Physical
Heavy metal poisonings have many similarities, making clinical distinctions between them difficult at times. Arsenic is more likely than other heavy metals to produce a dramatic gastroenteric picture when ingested. Inhalation of arsine gas produces clinical features whose onset is dependent on the degree of exposure. The initial complaints may be vague, with headache, malaise, weakness, dizziness, and dyspnea. Later, the features are the same as those seen in inorganic arsenic ingestion. The cutaneous manifestations are rather different depending on the heavy metal exposure.
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Cutaneous: Hyperpigmentation of the skin of the face or extremities is in a "raindrop" distribution. The skin has a peculiar bronze tint. A patient described by Kyle and Pease had pigmentation of the buccal mucosa resembling the hyperpigmentation of Addison disease. [19] Oral herpetiform lesions or a diffuse macular rash may be present, as may brawny, nonpruritic desquamation and patchy alopecia as well as hyperkeratosis of the palms and soles. Mees lines are transverse, 1-2 mm white striations in the fingernails, which may be deformed or fall out within 2-3 weeks of exposure. The Mees lines are actual arsenic deposits. Because of the availability of sulfhydryl groups in keratin, arsenic can be measured in hair and fingernail samples. Arsenic can be detected in hair samples as early as 30 hours after ingestion and as late as 9 years after ingestion. Thallium toxicity can be suspected in case of hair loss and fingernail loss, but thallium is more likely to produce hyperglycemia.
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Neurological: Paresthesias and numbness, usually in a symmetric stocking-glove distribution, and muscle weakness are a result of peripheral neuropathy. The onset and progression may be mistaken for Guillain-Barré syndrome. [11] This problem may persist long after arsenic exposure stops. Fatigue and weakness are major complaints. The neuropathy is not seen acutely but develops over the weeks subsequent to exposure in acute or subacute toxicity. In regular, long-term arsenic exposure, the presenting complaint is frequently a sensory neuropathy with features that resemble an alcoholic neuropathy. [20] Burning paresthesias in glove and stocking distribution, early loss of stretch reflexes, and later weakness are seen. In severe toxicity, flaccid paralysis may appear in the lower extremities, then the upper extremities. This is maximal about 4 weeks after acute exposure. Again, the clinical picture resembles Guillain-Barré syndrome.
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Hematologic: Anemia with leukopenia is seen frequently; splenomegaly may be apparent. Granulocytopenia and an increase in the eosinophil count often occur.
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Systemic complaints of regional subcutaneous edema are present in arsenic intoxication. The eyelids in particular, and legs less frequently, become quite edematous.
