Arsenic poisoning
Inorganic arsenic poisoning presents acutely with vomiting, profuse diarrhea, garlic-odor breath, and QT prolongation, and chronically with skin pigmentation, hyperkeratosis, and peripheral neuropathy. The mechanism is sulfhydryl-group binding that inhibits lipoic acid and the pyruvate dehydrogenase complex. It is treated with fluid resuscitation and chelation, dimercaprol or succimer, which reverses the systemic illness far better than the neuropathy.
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What this article covers
- Overview
What it is: poisoning by inorganic arsenic, absorbed by ingestion or inhalation, producing an acute gastrointestinal and cardiac syndrome followed, in survivors, by a delayed neuropathy and characteristic skin disease.
- Epidemiology
Occupational exposure predominates in industrialized settings: smelting and metal-refining, wood-preservative and pesticide manufacturing, and glass and semiconductor work carry chronic low-level exposure.
- Risk factors
Occupational exposure: smelting, wood-preservative manufacturing, herbicide application, and mining and glass work.
- Pathophysiology
The target is the sulfhydryl group: trivalent arsenite binds vicinal thiol groups on proteins, inactivating enzymes broadly.
- Clinical features
Acute ingestion, first hours: severe nausea, vomiting, and profuse watery, rice-water-like diarrhea with cramping; a garlic odor may be detectable on the breath.
- Differential diagnosis
Guillain-Barre syndrome: also causes ascending, areflexic weakness, but cerebrospinal fluid shows albuminocytologic dissociation, nerve conduction shows demyelinating rather than axonal change, and…
- Diagnosis
The diagnosis is established by a compatible exposure history and clinical picture together with an elevated arsenic level, most reliably a 24-hour urine collection, the test of choice for recent exposure.
- Management
First, airway, breathing, and circulation, with continuous cardiac monitoring for QT prolongation and torsades de pointes.
- Complications
Hypovolemic shock, within hours of large acute ingestion, from third-space fluid loss.
- Prognosis
Survival from acute ingestion depends chiefly on how quickly shock is corrected and whether torsades de pointes occurs; prompt resuscitation and monitoring make early death largely preventable.
- Prevention
Eliminate or control the exposure source, remediating contaminated groundwater or industrial sites and enforcing occupational controls in smelting, wood-preservative, and herbicide manufacturing.
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