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Emergency and Acute Medicine – Arsenic Toxicity
Overview And Definition
Arsenic toxicity may present as either an acute poisoning or a chronic exposure syndrome. Acute cases most often follow intentional ingestion, malicious poisoning, or dosing errors, with a potentially lethal dose near 2 mg/kg. Chronic toxicity develops from prolonged low-level exposure, typically through contaminated water or food, occupational contact, or traditional remedies containing arsenic. Ingestion is the most common exposure route, although inhalation of arsine gas can also result in toxicity.
Sources And Mechanism Of Injury
In emergency care, acute presentations usually involve intentional ingestion, most commonly sodium arsenate found in insecticides in the United States. Globally, environmental contamination of food and water is the predominant source. Arsenic exists in inorganic, organic, elemental, and gaseous forms, with inorganic arsenic responsible for most clinically significant poisonings. Pentavalent arsenic disrupts oxidative phosphorylation and is converted in vivo to trivalent arsenic, which binds sulfhydryl groups, interferes with cellular metabolism, impairs hemoglobin synthesis, and induces DNA damage.
Clinical Manifestations
Neurologic involvement includes altered mental status, encephalopathy, seizures, and peripheral neuropathy. Early neuropathy is often sensory, progressing to sensorimotor deficits with ongoing exposure. Cardiovascular effects include QTc prolongation, ventricular dysrhythmias, acute hypotension, or chronic hypertension. Pulmonary findings range from noncardiogenic pulmonary edema to hemorrhagic bronchitis, particularly following large ingestions or inhalational exposure. Gastrointestinal symptoms are prominent, featuring severe nausea, vomiting, abdominal pain, and profuse watery diarrhea that may resemble rice-water stools. A garlic-like odor to the breath or excreta may be present. Chronic exposure is associated with dermatologic changes, nail abnormalities, alopecia, endocrine dysfunction, anemia, vascular disease, and increased malignancy risk.
Diagnostic Evaluation
Diagnosis is based on clinical suspicion supported by laboratory testing. A spot urine arsenic level is useful for initial assessment, while definitive diagnosis requires a 24-hour urine collection with arsenic speciation to distinguish inorganic from organic forms. Serum arsenic levels are generally unhelpful due to rapid clearance. Additional evaluation includes complete blood count, renal and hepatic function tests, electrolytes, creatine phosphokinase for rhabdomyolysis, and urinalysis. Abdominal radiographs may identify radiopaque material following acute ingestion.
Differential Diagnosis
Acute arsenic poisoning can resemble severe gastroenteritis, cholera, appendicitis, toxic shock, encephalopathy, or other toxic ingestions. Chronic exposure should be considered in patients with unexplained peripheral neuropathy, Raynaud-like phenomena, hyperkeratotic skin lesions, vasculitic symptoms, or nonspecific wasting.
Initial Stabilization And Emergency Care
Management begins with airway, breathing, and circulation support, continuous cardiac monitoring, and aggressive isotonic fluid resuscitation for hypotension. Seizures are treated with benzodiazepines, and respiratory failure may require ventilatory support. Antiarrhythmic agents that prolong the QT interval should be avoided. Renal failure and severe metabolic derangements warrant early specialty consultation.
Decontamination And Definitive Treatment
Early gastrointestinal decontamination may be considered within the first hour of ingestion, though activated charcoal does not effectively bind arsenic. Whole bowel irrigation is indicated when radiopaque material is identified. Dermal exposures require immediate skin decontamination. Chelation therapy is recommended for symptomatic patients or those with significantly elevated levels and should be initiated in consultation with a medical toxicologist or poison center. Dimercaprol and oral succimer are the primary chelating agents. Hemodialysis is not routinely effective for arsenic removal but may be necessary in patients with renal failure and should be continued concurrently with chelation when indicated.
Disposition And Follow-Up
Patients with symptomatic arsenic toxicity require hospital admission, often to an intensive care unit. Asymptomatic patients with low urinary arsenic levels may be discharged with appropriate follow-up and confirmation of environmental safety. Individuals with suspected chronic exposure should undergo outpatient evaluation, repeat urine testing, and long-term surveillance.
Key Clinical Insights And Diagnostic Traps
Arsenic toxicity produces a wide range of systemic findings, frequently delaying recognition. Acute poisoning should be considered when gastrointestinal distress is accompanied by neurologic abnormalities, while chronic exposure should be suspected in patients with peripheral neuropathy and characteristic skin or nail changes. Early consultation with a poison center or medical toxicologist is critical to determine the need for chelation therapy and to avoid missed or delayed treatment.
Overview And Definition
Arsenic toxicity may present as either an acute poisoning or a chronic exposure syndrome. Acute cases most often follow intentional ingestion, malicious poisoning, or dosing errors, with a potentially lethal dose near 2 mg/kg. Chronic toxicity develops from prolonged low-level exposure, typically through contaminated water or food, occupational contact, or traditional remedies containing arsenic. Ingestion is the most common exposure route, although inhalation of arsine gas can also result in toxicity.
Sources And Mechanism Of Injury
In emergency care, acute presentations usually involve intentional ingestion, most commonly sodium arsenate found in insecticides in the United States. Globally, environmental contamination of food and water is the predominant source. Arsenic exists in inorganic, organic, elemental, and gaseous forms, with inorganic arsenic responsible for most clinically significant poisonings. Pentavalent arsenic disrupts oxidative phosphorylation and is converted in vivo to trivalent arsenic, which binds sulfhydryl groups, interferes with cellular metabolism, impairs hemoglobin synthesis, and induces DNA damage.
Clinical Manifestations
Neurologic involvement includes altered mental status, encephalopathy, seizures, and peripheral neuropathy. Early neuropathy is often sensory, progressing to sensorimotor deficits with ongoing exposure. Cardiovascular effects include QTc prolongation, ventricular dysrhythmias, acute hypotension, or chronic hypertension. Pulmonary findings range from noncardiogenic pulmonary edema to hemorrhagic bronchitis, particularly following large ingestions or inhalational exposure. Gastrointestinal symptoms are prominent, featuring severe nausea, vomiting, abdominal pain, and profuse watery diarrhea that may resemble rice-water stools. A garlic-like odor to the breath or excreta may be present. Chronic exposure is associated with dermatologic changes, nail abnormalities, alopecia, endocrine dysfunction, anemia, vascular disease, and increased malignancy risk.
Diagnostic Evaluation
Diagnosis is based on clinical suspicion supported by laboratory testing. A spot urine arsenic level is useful for initial assessment, while definitive diagnosis requires a 24-hour urine collection with arsenic speciation to distinguish inorganic from organic forms. Serum arsenic levels are generally unhelpful due to rapid clearance. Additional evaluation includes complete blood count, renal and hepatic function tests, electrolytes, creatine phosphokinase for rhabdomyolysis, and urinalysis. Abdominal radiographs may identify radiopaque material following acute ingestion.
Differential Diagnosis
Acute arsenic poisoning can resemble severe gastroenteritis, cholera, appendicitis, toxic shock, encephalopathy, or other toxic ingestions. Chronic exposure should be considered in patients with unexplained peripheral neuropathy, Raynaud-like phenomena, hyperkeratotic skin lesions, vasculitic symptoms, or nonspecific wasting.
Initial Stabilization And Emergency Care
Management begins with airway, breathing, and circulation support, continuous cardiac monitoring, and aggressive isotonic fluid resuscitation for hypotension. Seizures are treated with benzodiazepines, and respiratory failure may require ventilatory support. Antiarrhythmic agents that prolong the QT interval should be avoided. Renal failure and severe metabolic derangements warrant early specialty consultation.
Decontamination And Definitive Treatment
Early gastrointestinal decontamination may be considered within the first hour of ingestion, though activated charcoal does not effectively bind arsenic. Whole bowel irrigation is indicated when radiopaque material is identified. Dermal exposures require immediate skin decontamination. Chelation therapy is recommended for symptomatic patients or those with significantly elevated levels and should be initiated in consultation with a medical toxicologist or poison center. Dimercaprol and oral succimer are the primary chelating agents. Hemodialysis is not routinely effective for arsenic removal but may be necessary in patients with renal failure and should be continued concurrently with chelation when indicated.
Disposition And Follow-Up
Patients with symptomatic arsenic toxicity require hospital admission, often to an intensive care unit. Asymptomatic patients with low urinary arsenic levels may be discharged with appropriate follow-up and confirmation of environmental safety. Individuals with suspected chronic exposure should undergo outpatient evaluation, repeat urine testing, and long-term surveillance.
Key Clinical Insights And Diagnostic Traps
Arsenic toxicity produces a wide range of systemic findings, frequently delaying recognition. Acute poisoning should be considered when gastrointestinal distress is accompanied by neurologic abnormalities, while chronic exposure should be suspected in patients with peripheral neuropathy and characteristic skin or nail changes. Early consultation with a poison center or medical toxicologist is critical to determine the need for chelation therapy and to avoid missed or delayed treatment.
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