Treatment

Acute arsenical toxicity is a life-threatening illness requiring aggressive management. The first task is to ensure adequate respiratory and circulatory function. Hypotension and dysrhythmias are the chief causes of death. Hypotension, usually due to volume depletion, should be managed initially with crystalloid volume replacement. Invasive hemodynamic monitoring followed by further crystalloid and pressor therapy with dopamine or norepinephrine may be required. Overhydration should be avoided because pulmonary and cerebral edema can occur. Cardiac monitoring should be instituted. Ventricular tachycardia and fibrillation may be treated with lidocaine, bretylium, and electrical defibrillation as necessary. Isoproterenol, magnesium, and overdrive pacing therapies should be considered for torsade de pointes dysrhythmias. Drugs that prolong the QTc, including classes IA (procainamide, quinidine, disopyramide), iC, and III antidysrhythmics should be avoided. Potassium, calcium, and magnesium levels should be monitored and corrected as necessary to prevent further prolongation of the QT c with possible exacerbation of torsade de pointes dysrhythmias.

Gastric lavage with a large-bore orogastric tube should be performed in all cases of acute ingestion, and activated charcoal (1 g/kg of body weight) and a cathartic should be instilled. Activated charcoal poorly adsorbs arsenic but may be effective if coingestants were taken. Whole-bowel irrigation should be considered if abdominal radiographs reveal intestinal radiopaque materials consistent with arsenic. Seizures can be treated with benzodiazepines, phenobarbital, phenytoin, and general anesthesia as necessary.

Initial management of chronic toxicity should be directed toward prevention of further arsenic absorption and gastrointestinal decontamination, if appropriate. In cases of suspected homicidal intent, patients should be advised to avoid food and drinks prepared by others, and visitor contact with hospitalized patients should be monitored carefully.

Chelation therapy with BAL should be instituted immediately in all cases of known or suspected acute arsenical poisoning. BAL doses range 3 to 5 mg/kg intramuscularly every 4 h for 2 days followed by 3 to 5 mg/kg every 6 to 12 h. In severe, life-threatening toxicity, BAL therapy should be continued until the clinical condition stabilizes and DMSA, the less toxic oral chelating agent, can be substituted. In cases of suspected chronic toxicity with stable symptoms, therapy may be withheld pending diagnosis. DMSA is the preferred chelating agent in these patients. 19 It is given according to the dosing regimen for lead, but therapy may be required beyond the initial 19-day regimen. D-Penicillamine does not effectively chelate arsenic and should no longer be used. 20 During chelation, intermittent 24-h urinary arsenic levels should be measured and therapy continued until the urine level falls below 0.05 mg/L per 24 h. Hemodialysis can remove small amounts of arsenic (2 to 4.5 mg) in patients with acute renal failure but is not indicated otherwise. 21

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