Case:

A 38-year-old man is brought to the emergency department by EMS due to sudden-onset vomiting, diarrhea, and abdominal pain. The EMTs report a garlic-like odor on the patient’s breath. His family found an open container of an old pesticide in his shed, which they believe he was using earlier today. Upon arrival, he’s pale, diaphoretic, confused, and noted to be hypotensive (BP 82/40) and tachycardic (HR 132). His abdomen is diffusely tender on exam. Despite receiving IV fluids, the patient remains hypotensive. An initial ECG shows a prolonged QT interval, and labs reveal a high-anion-gap metabolic acidosis with elevated lactate. Given the history, acute onset of severe GI symptoms, refractory hypotension, and cardiac conduction abnormalities, a toxic ingestion was suspected.

Questions:

1. What is arsenic, and what are common sources of exposure?
2. What are the key clinical features of acute arsenic toxicity?
3. What is the management of acute arsenic poisoning?
4. How does chronic arsenic toxicity present, and how does it differ from acute?

Background:

• Arsenic is a naturally occurring metalloid element, often referred to as the “king of poisons”.[1]
• It exists in both inorganic and organic forms, and in multiple valence states.
• Inorganic arsenic (trivalent (As³⁺) arsenite and pentavalent (As⁵⁺) arsenate) is highly toxic, whereas arsenic incorporated into and “organified” by seafood (such as arsenobetaine) are less harmful.[2]
• Trivalent arsenic acts by inhibiting pyruvate dehydrogenase, preventing acetyl-CoA production and interfering with aerobic respiration by inhibiting the tricarboxylic acid  (TCA) cycle.[3]
• Common sources include contaminated groundwater, rice or grain, seafood, mining, and arsenic-based pesticides, often containing lead arsenate (likely the type of pesticide that was involved in this case), which were common throughout the 20th century. 
• It can also affect cardiac repolarization by inhibiting the availability of the delayed-rectifier potassium channels, prolonging the QTc interval.[4]
• The pentavalent form is rapidly reduced to the trivalent form, with the same effects. 
• Arsenic is often tasteless and odorless, can be absorbed through mucus membranes, and can induce a distinct “garlic” odor when inhaled; specifically the arsine gas form.[5,6] 
• Arsenic can freely cross the placenta, but studies have yielded conflicting results regarding its accumulation in breast milk.[7,8]
• Arsenic trioxide continues to be used in the treatment of acute promyelocytic leukemia (APML) by inducing cellular apoptosis through a variety of mechanisms.[9]

Epidemiology: 

• Globally, chronic exposure to arsenic through drinking water or consumption of soil-derived foods (eg. rice) from arsenic-laden regions remains a major health concern.
• The pentavalent form (As⁵⁺) is the form most seen in the environment.[1] For instance, millions of people in Bangladesh and India have developed chronic arsenic toxicity due to cross-contamination from arsenic-laden wells.[10,11] 
• In the United States, while everyday exposure is uncommon, arsenic can be found in well water or through specific occupations such as mining, smelting, or semiconductor production.[5] 
• Historically, it has been used in rodenticides.[12] 
• Although rare, acute arsenic poisoning does occur, typically from intentional ingestions or accidental exposure in workplaces.
• Organic arsenic (arsenobetaine) is typically encountered through the consumption of seafood and is considered non-toxic.[13]

Clinical Presentation:

Acute Arsenic Toxicity: When inorganic arsenic is ingested, GI symptoms (diarrhea, vomiting, etc.) are the first to appear, and may be seen within 10 minutes of ingestion. Some will present with a garlic-like odor or report a metallic taste. The diarrhea is often reported to be “cholera-like” and described as “rice water” stool. Arsenic-induced GI mucosal injury can lead to sloughing and resulting GI bleeding. 

• Due to significant GI losses, patients can frequently develop hypotension/hypovolemic shock (especially in large ingestions/exposures), requiring aggressive fluid resuscitation and potential use of vasopressors. The profound hypovolemia can lead to acute kidney injury (acute tubular necrosis) and acute liver injury.[14]
• Arsenic is associated with dysrhythmias and myocardial dysfunction, with sinus tachycardia being the most common dysrhythmia seen. Other EKG changes can include QT prolongation, T-wave flattening, ST depression, and QRS widening. Cases of polymorphic ventricular tachycardia (torsades de pointes) and ventricular fibrillation have been reported in acute poisoning.[15] These dysrhythmias are often worsened by significant electrolyte disturbances. A majority of the morbidity from acute arsenic exposure is secondary to dysrhythmias and resulting cardiovascular collapse.
• Rarer presentations of acute arsenic toxicity include acute respiratory distress syndrome (ARDS), muscle cramping, rhabdomyolysis, unilateral facial nerve palsy, exfoliative dermatitis, phrenic nerve paralysis, or even fever (sepsis mimic).[16–20]

Chronic Arsenic Toxicity: Chronic exposure to arsenic, usually through contaminated water, food, or occupational inhalation, presents differently. 

• The hallmark of chronic exposure is dermatologic findings, ranging from diffuse hyperpigmentation (often described as a bronzed or “raindrop” pattern of dark spots) and hyperkeratosis of the palms and soles.[5] A subtle finding is Mees’ lines (transverse white bands on the fingernails), which occur in a minority of cases and occasionally appear approximately 4–6 weeks after exposure.[5] 
• Arsenic is carcinogenic, and chronic exposure is associated with the development of a variety of cancers involving the liver, skin, and lungs.[5] 
• It has also been found to be associated with the development of atherosclerosis, cardiovascular disease, hepatomegaly, and cirrhosis.[5]
• Chronic exposure may also cause peripheral neuropathy, which can manifest as numbness, tingling, or burning in the hands and feet. It can progress to weakness, often in a stocking-glove distribution, and rarely has presented similarly to Guillain–Barré.[21]

Diagnosis:

• Diagnosing arsenic poisoning in the ED is often difficult because symptoms can be non-specific, there is no point-of-care test available, and blood levels are inaccurate due to rapid redistribution from the blood into tissues.[5] Therefore, in the ED, this is largely a clinical diagnosis, aided by a thorough history and high clinical suspicion. 
• The combination of severe gastroenteritis with hemodynamic instability or cardiovascular collapse after a possible exposure should raise an alarm.
• The most important diagnostic tool is a thorough history, specifically asking about well-water use, seafood consumption, occupational exposures (e.g., mining, metal refining), and pesticide/rodenticide use.
• The differential diagnosis for acute arsenic poisoning is broad; it can masquerade as infectious gastroenteritis (e.g., severe cholera, dysentery), other toxins (such as other heavy metals or organophosphates), and could even be mistaken for sepsis or Guillain–Barré syndrome.[5]

Laboratory Findings: While awaiting specific arsenic levels, certain lab abnormalities can support the diagnosis of acute arsenic. 

• An anion-gap metabolic acidosis with elevated lactate is commonly seen in severe arsenic poisoning due to inhibition of oxidative phosphorylation (arsenic blocks pyruvate dehydrogenase, inducing lactic acidosis).[3] 
• Hypokalemia and acute renal injury are common, likely due to GI losses and resulting hypovolemia.5 Liver enzymes might be mildly elevated. Pancytopenia may also be seen.
• ECG: An ECG may demonstrate QT or QRS interval prolongation, and potentially the development of torsades de pointes.[4]
• Confirmatory testing: The definitive diagnosis is made by detecting elevated arsenic levels in a 24-hour urinary concentration. A total arsenic level >50 µg/L or 100 mcg total in a 24-hour urine is considered positive. 
• While a 24-hour urine level is not likely feasible in the ED, a spot urine level can be sent, and if the level is markedly elevated with other clinical symptoms, then it is strongly suggestive of a significant arsenic exposure.[5]

Diagnostic Pitfalls: 

• Seafood consumption (fish, shellfish, seaweed) over the past few days can lead to elevated urinary total arsenic due to the presence of arsenobetaine, which is a non-toxic organic form of arsenic.[13,23]

Imaging: 

• Occasionally, an abdominal X-ray may show radiopaque material, as some arsenic compounds (e.g., arsenic trioxide) are radiopaque.[24,25]

Management:

• For this case, we will focus on the management of acute arsenic toxicity, which in the ED centers on decontamination, rapid stabilization, aggressive fluid and electrolyte repletion, and early antidotal therapy (chelation).Resuscitation and Supportive Care:Treat an acute arsenic-poisoned patient as you would any critically ill patient: start with the ABCs. These patients may not provide a clear story of arsenic ingestion; therefore, they will present with undifferentiated altered mental status or a sepsis-like syndrome and should be managed as such until further information is obtained that may push you in the direction of a toxic ingestion. 
  • Ensure the airway is protected, especially in cases where mentation may be altered, and there is profuse vomiting. 
  • Aggressively replace intravascular volume and replete electrolytes, as the majority of dysrhythmias are secondary to electrolyte derangements. 
  • Obtain serial EKGs to monitor intervals. Treat any significant dysrhythmias in accordance with ACLS protocols. Avoid class IA and III antiarrhythmics (like procainamide, amiodarone) if possible, as many of these can further prolong the QT interval.[5] 
  • If seizures occur, treat with benzodiazepines.

Decontamination:

• GI decontamination with activated charcoal is unlikely to provide any true benefit, as arsenic is poorly absorbed by charcoal. But if there is concern for co-ingestants, then activated charcoal may be more beneficial and its use should be discussed with the local poison center. 
• If abdominal imaging was obtained and showed radiopaque objects in the GI tract, whole bowel irrigation with polyethylene glycol could be considered but should be discussed with a local poison center, as GI losses could potentially already be significant.[27]

Chelation Therapy:

• The cornerstone of treatment for arsenic poisoning is chelation therapy. Chelation is most effective when started early, ideally within hours of exposure. Therefore, you should not wait for definitive lab confirmation if the patient is critically ill and you strongly suspect arsenic toxicity.
• In one case series, 75% of patients who had BAL chelation initiated within 6 hours survived, compared to only 45% who were treated after 9 hours.[28]
• The primary chelating agents for arsenic are Dimercaprol (BAL, “British Anti-Lewisite”) and Succimer (DMSA, 2,3-dimercaptosuccinic acid.[5] 
• Dimercaprol is a dithiol chelator that binds arsenic (especially trivalent arsenite) and forms a complex that can be renally excreted. It is given via intramuscular injection, and is dosed at 3–5 mg/kg IM every 4 to 6 hours.[29]
• While there is often limited availability of BAL, another potential option is succimer, a water-soluble analog of dimercaprol, that is often used for subacute toxicity, less severe cases, or after initial stabilization with BAL. A typical regimen is 10 mg/kg PO every 8 hours for 5 days, then every 12 hours for 2 more weeks.[5] Succimer is generally well tolerated, but oral dosing may be impractical in a vomiting, critically ill patient. 
• Dimercaptopropanesulfonic acid (DMPS), which can be administered intramuscularly, at 3 to 5 milligrams/kg every 4 hours, for 2 days, then followed by oral succimer.[5] DMPS is not approved for marketing in the United States. 
• In some cases, providers transition a patient from BAL to oral succimer after a few days of treatment, once the patient can tolerate oral meds. If IM chelators are unavailable, patients should be stabilized and, when able to tolerate PO intake, started on succimer treatment.

Disposition

• All patients with acute arsenic poisoning should be admitted for confirmatory testing and treatment. 
• Continuous cardiac monitoring, aggressive fluid/electrolyte management, and frequent reassessments are required. 
• Consult medical toxicology or a regional poison center early; they can assist with chelator procurement and ongoing management. 
• If there is any suspicion of an intentional poisoning (suicidal or homicidal), involve psychiatry and potentially law enforcement/public health authorities as needed. 
• Once stabilized, ensure proper follow-up. 
• Patients recovering from acute arsenic poisoning should have an outpatient follow-up to monitor for the development of long-term associated complications, such as hepatic fibrosis, portal hypertension, hepatic angiosarcomas, hyperkeratosis, or squamous cell carcinoma, though these are less likely, unless there is continued or repeated exposure. If the exposure was environmental, public health officials should be notified to prevent additional exposures.

Case Follow-up:

Clinical Pearls: 

• Acute arsenic exposure can present with “rice water” diarrhea, vomiting, hypotension, dysrhythmias (QT prolongation), garlic odor, lactic acidosis, and encephalopathy
• Dimercaprol (IM) is the first-line chelator for severe cases, and succimer (oral) is an effective alternative for more stable patients 
• Chronic arsenic exposure presents with skin changes (hyperpigmented spots, palmoplantar keratosis) and peripheral neuropathy.

References:

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