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Acute Arsenic Poisoning: An ICU Nurse's Guide

⚕️ Medical Disclaimer: This content is for educational purposes only and is intended for licensed healthcare professionals. It does not constitute medical advice and should not replace clinical judgment, facility protocols, or physician orders. Always verify medications, doses, and procedures with your institution's guidelines.

Part of the ICU Emergencies Hub — browse every related guide in one place.

This article was created with AI assistance.

Updated July 2026  |  More ICU nursing guides →

Scope note: Educational overview for licensed ICU and ED nurses — not a treatment protocol. Chelation, antidote, and dysrhythmia decisions belong to the provider, toxicology, and your regional Poison Control Center (1-800-222-1222 in the U.S.). Follow local protocol and your scope of practice.

Acute arsenic poisoning is rare, and that rarity is the danger: it is easy to miss because its first act looks like severe gastroenteritis or sepsis. But arsenic is one of the classic homicidal and industrial poisons, and a patient with unexplained profound GI losses, shock, and a widening QT interval — especially with a suggestive history — may be arsenic-poisoned. The ICU nurse's role is to resuscitate the massive fluid losses, watch the heart for the lethal dysrhythmia arsenic causes, and support the patient through chelation while toxicology confirms the diagnosis.

How arsenic injures

Arsenic poisons cellular energy production, binding to sulfur-containing groups on enzymes throughout the body and crippling the cell's ability to make ATP. Nearly every organ that depends on high energy turnover suffers: the gut lining sloughs, the heart's electrical system destabilizes, capillaries leak, and later the nerves and marrow fail. Inorganic arsenic (the toxic form) comes from pesticides and rodenticides, some industrial and mining exposures, contaminated well water (usually chronic), certain folk and traditional remedies, and deliberate poisoning.

The clinical picture: an evolving illness

Acute arsenic poisoning unfolds over hours to weeks, and the ICU nurse may meet it at any stage.

PhaseWhat you may see
Early (minutes–hours)Metallic taste, garlicky breath, vomiting, and severe "rice-water" diarrhea; profound volume loss, third-spacing, hypotension and shock
Cardiac (hours–days)QT prolongation, torsades de pointes and other ventricular dysrhythmias, myocardial dysfunction, ongoing hypotension
Delayed (days–weeks)Painful, ascending sensorimotor peripheral neuropathy; encephalopathy; bone-marrow suppression (pancytopenia); hepatic and renal injury; later, Mees' lines on the nails
The heart is the acute killer. Massive GI losses cause shock and electrolyte derangement, and arsenic itself prolongs the QT interval — the combination sets up torsades de pointes. Put the patient on continuous cardiac monitoring, track the QT/QTc, and keep potassium and magnesium repleted to the high-normal range. Correcting the electrolytes is one of the most protective nursing-facing interventions you can influence.

Confirming it

The diagnosis is a clinical suspicion confirmed by testing. A 24-hour urine arsenic is the standard for acute inorganic exposure; a random urine or blood level may help early, but blood arsenic clears quickly. An important pitfall: eating seafood loads the urine with harmless organic arsenic (arsenobetaine) and can produce a high total level that does not mean poisoning — speciation or a seafood-free interval sorts this out. Because arsenic is radio-opaque, an abdominal X-ray can sometimes show ingested material. Hair and nail testing document remote or chronic exposure but do not guide acute care.

Treatment: resuscitate, protect the heart, chelate

The first job is aggressive fluid resuscitation for the rice-water losses — these patients can lose liters and go into hypovolemic shock — along with correcting electrolytes and treating dysrhythmias. Chelation is started early in significant poisoning and is toxicology-directed.

AgentRouteNote
Dimercaprol (BAL)Deep IMOften first in the acutely ill patient who cannot take oral meds
Succimer (DMSA)OralUsed once the patient can tolerate oral therapy / for continued chelation
DMPS (unithiol)Oral/IV (availability varies)Used in some centers/regions for arsenic
Dialysis does not clear arsenic well in patients with working kidneys — chelation is the mainstay — but hemodialysis is used when the kidneys fail so that chelator-bound complexes can be removed. Don't assume "poison equals dialysis." Confirm the plan with toxicology.

Nursing cautions with the chelators

Dimercaprol is a painful deep IM injection in a peanut-oil base (screen for peanut allergy), can cause fever and hypertension, and is avoided in G6PD deficiency. Succimer is oral with GI and hepatic effects and a strong sulfur smell. Chelation courses are guided by repeat urine levels, and therapy continues until the burden falls.

What the ICU nurse monitors

Hemodynamics and strict intake/output for the ongoing GI losses; continuous ECG with QT/QTc surveillance and aggressive K+/Mg2+ repletion; neuro checks for the encephalopathy and the emerging painful neuropathy (which may need long-term rehab and pain management); serial CBCs for marrow suppression; and renal and hepatic function. As with all metal poisonings, the exposure must be identified and stopped, and because deliberate poisoning is on the differential, unexplained cases may involve public health or law enforcement — document carefully and follow your facility's process.

Your role in one line: Resuscitate the rice-water losses, guard the QT with continuous monitoring and aggressive electrolyte repletion, support the patient through chelation, and keep looking for the source — arsenic hides behind a gastroenteritis that shocks the patient and then stops the heart.

Related guides

For related metal and toxin exposures and the complications arsenic shares, see lead poisoning, mercury poisoning, and organophosphate poisoning. For the dysrhythmia and kidney threads, see torsades de pointes and acute kidney injury and CRRT.

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