Arsenic

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Pathogenesis and Pathophysiology. Although arsenic is rapidly absorbed through the mucous membranes and the skin, although the most common route is ingestion. Arsenic rapidly leaves the bloodstream for storage in the liver, kidneys, intestines, spleen, lymph nodes, and bones, and within 2 weeks it is deposited in the hair, remaining there for years. It also remains in the bones for extended periods of time. Excretion through the kidneys and feces is slow. A single dose may require up to 10 days to be excreted. Pathways involved in oxidative metabolism are sensitive to arsenic toxicity. Arsenic also prevents the transformation of thiamine into acetyl-CoA, causing patients to become clinically thiamine deficient. Organic arsenicals release the poison slowly and are therefore less likely to produce acute symptoms than the elemental form. Neuropathological findings in patients with fatal arsenic encephalopathy include cerebral congestion, multiple hemorrhagic lesions throughout the white matter, and areas of necrosis. Decreased numbers of myelinated fibers are seen in the peripheral nerves, and degenerative changes, consisting of swelling, granularity, and a reduction in the number of axons, are present.

Epidemiology and Risk Factors. Occupational and job-related sources of arsenic are listed in Iable39-1 . The National Institute for Occupational Safety and Health (NlOSH) estimates that about 900,000 workers have potential daily exposure to arsenic.

Clinical Features and Associated Findings. Acute toxicity is associated with a sudden rise in temperature accompanied by headache, vertigo, nausea and vomiting, nervousness, and apprehension. Convulsions are common. Tendon reflex changes are variable and are frequently exaggerated. Nystagmus, paralysis, or incontinence may also be observed. Kernig's sign is often positive with neck stiffness. Mee's lines (white lines in the nails) usually appear 2 to 3 weeks after acute exposure to arsenic (Fig. 39-1 (Figure Not Available) ). Encephalopathy with marked excitement followed by lethargy, and coma occur, and signs of acute peripheral neuropathy can develop within hours. In patients with fatal acute poisoning, death ensues within a few days. With subacute and chronic

Figure 39-1 (Figure Not Available) Double set of Mees' lines in a patient with arsenic intoxicatiReprinted from Chhuttani PN, Chopra JS. Arsenic poisoning. In Vinken PJ, Bruyn GW, Cohen MM, Klawans HL [eds]: Intoxications of the Nervous System. Handbook of Clinical Neurology, Vol 36. Amsterdam, Elsevier, 1979, p. 202, with kind permission from Elsevier Science-NL, Sara Burgerhartstraat 25, 1055 KV Amsterdam, The Netherlands.)

arsenic encephalitis, continuous progressive headaches, physical and mental fatigue, vertigo, restlessness, mild somnolence, and focal paresis develop. Spinal cord involvement leads to weakness, sphincter disturbances, motor and sensory impairment, and trophic changes. Optic neuritis manifested by cloudy vision and visual field defects may also be observed subacutely but can be delayed for as long as 2 years. Generally, a mixed sensory and motor neuropathy develops within 7 to 10 days after ingestion of toxic amounts of arsenic, and patients often complain of severe burning in the soles of the feet (Fig. 39-2 (Figure Not Available) ). Long-standing cognitive changes have been reported.

Differential Diagnosis and Evaluation. Arsenic intoxication is suggested when a patient presents with severe abdominal pain, dermatitis, painful peripheral neuropathy, and seizures. A history of arsenic exposure and toxic levels in the hair, urine, or nails confirm the diagnosis. Arsenic is poorly tolerated in the presence of alcohol. Therefore, patients with alcohol-related disease may be at greater risk for developing associated arsenic neuropathy. Although hair and nails may be useful, urinary arsenic is the major biomarker; Iabje39:2. shows the threshold levels. Because high urinary arsenic levels may also be seen after the consumption of seafood, it is important to obtain a dietary history at the time of testing. Arsenic toxicity may occur even when blood and urine concentrations are normal.

Management. In patients with acute oral ingestion of arsenic, gastric lavage with electrolyte replacement is recommended. Also, excretion of absorbed arsenic can be enhanced by chelation using dimercaprol (British antilewisite [BAL]), D-penicillamine, or dimercaptosuccinic acid

Figure 39-2 (Figure Not Available) Hyperkeratosis of the skin of soles with exfoliation in a patient with peripheral neuropathy and arsenic intoxicfRepr/nted from Chhuttani PN, Chopra JS: Arsenic poisoning. In Vinken PJ, Bruyn GW, Cohen MM, Klawans HL [eds]: Intoxications of the Nervous System. Handbook of Clinical Neurology, Vol 36. Amsterdam. Elsevier, 1979, p. 202, with kind permission from Elsevier Science-NL, Sara Burgerhartstraat 25, 1055 KV Amsterdam, The Netherlands.)

(DMSA). Chelators essentially reverse or prevent the attachment of heavy metals to various essential body chemicals. While chelation may alleviate the acute symptoms, there is no evidence indicating that it improves chronic symptoms such as peripheral neuropathy or encephalopathy. In fact, once neuropathy occurs, BAL treatment is not considered effective. Intravenous fluids for dehydration and morphine for abdominal pain should also be given. In alcoholics who develop arsenic encephalopathy, vitamins should be administered to replace nutritional deficits.

Prognosis and Future Perspectives. Prognosis with severe arsenic poisoning is poor, with a mortality rate of 50 to 75 percent, usually within 48 hours. Intoxication during pregnancy carries a particularly poor prognosis.

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