Chapter 114. Metals and Metalloids

Metal poisoning often results from occupational, recreational, or environmental exposure and results in a combination of neurologic, cardiovascular, gastrointestinal, hematologic, and renal findings.

Clinical Features

Lead is the most common cause of chronic metal poisoning and manifests as signs and symptoms affecting a variety of organ systems (Table 114-1).

Diagnosis and Differential

Suspect lead poisoning in any individual demonstrating a combination of abdominal pain, nausea, vomiting, and neurologic symptoms (particularly children with encephalopathy), especially in the setting of anemia. A CBC may demonstrate normocytic or microcytic anemia with hemolysis and basophilic stippling; however, hematologic findings are neither sensitive nor specific for lead poisoning. Lead toxicity is confirmed by an elevated blood lead level, though results are often not immediately available. Radiographs may identify metaphyseal long bone lead lines, radiopaque material in the GI tract, or retained bullet fragments.

Emergency Department Care and Disposition

1. Address life-threatening ventilatory and circulatory problems through advanced airway management and fluid resuscitation. Avoid lumbar puncture in the setting of lead induced encephalopathy as this can precipitate herniation.

2. Decontaminate the GI tract with whole-bowel irrigation using polyethylene glycol solution in those with retained lead in the GI tract.

3. Chelation therapy is the mainstay of treatment and often must be started empirically (Table 114-2).

4. Admit patients requiring parenteral chelation therapy or those who cannot avoid further environmental lead exposure. Arrange follow up for patients started on succimer.

Clinical Features

Arsenic is used in a variety of insecticides and herbicides as well as mining and smelting processes. Acute ingestion results in a profound vomiting and diarrhea within hours of exposure. Hypotension and tachycardia may develop secondary to hypovolemia and direct myocardial dysfunction. Encephalopathy, pulmonary edema, and acute renal failure have been described. Chronic poisoning causes peripheral neuropathy, malaise, and confusion. Skin findings include alopecia, hyperpigmentation, keratoses, and transverse white nail lines (Mees lines).

Diagnosis and Differential

An exposure history is most useful in identifying arsenic poisoning. However, consider the diagnosis in patients with hypotension preceded by profound vomiting and diarrhea. An ECG may show QT-interval prolongation. The diagnosis is confirmed by demonstrating an elevated 24-hour urine arsenic level. Other diagnoses to consider include septic shock, encephalopathy, peripheral neuropathy, Addison disease, and lead, thallium, or mercury poisoning.

Emergency Department Care and Disposition

1. Support the ABCs: endotracheal intubation may be required to protect the airway; treat hypotension with volume resuscitation and vasopressors, but avoid over resuscitation that may result in pulmonary or cerebral edema. Manage dysrhythmias according to ACLS/PALS protocols, but avoid agents that prolong the QT interval (class IA, IC and III antidysrhythmics). Magnesium sulfate or isoproterenol should be considered for treatment of torsades de pointes.

2. Decontaminate the gastrointestinal tract with whole-bowel irrigation using polyethylene glycol solution in those with radiopaque GI fragments.

3. Treat symptomatic patients empirically with chelation therapy (Table 114-3) using dimercaprol (BAL) IM. Succimer (DMSA) PO is preferred for clinically stable patients who can tolerate oral intake.

4. Hospitalize symptomatic patients. Discharge stable patients with subacute or chronic poisoning if follow-up is ensured.

Mercury poisoning can result from exposure to elemental, inorganic, or organic mercury compounds.

Clinical Features

Elemental mercury exposure is most likely to occur after contact with a broken thermometer, and mercury is primarily absorbed via inhalation (especially with heating or vacuuming). Ingestions of elemental mercury are nontoxic in those with normal GI tracts. Vapor exposure results in cough, fever, dyspnea, vomiting, and headache. Acute lung injury can progress to respiratory failure. Inorganic mercury is used as a disinfectant and in manufacturing. Ingestion of inorganic mercury results in corrosive injury to the GI tract, with vomiting, diarrhea, abdominal pain, and GI bleeding early, followed by acute renal failure. Organic mercury is found in some fungicides and pesticides and can be absorbed when ingested. Poisoning tends to occur with chronic exposures and results in profound central nervous system dysfunction.

Diagnosis and Differential

A history of exposure to mercury is key to diagnosis and is confirmed by an elevated 24-hour urine mercury level when toxicity is due to elemental or inorganic mercury; an elevated whole blood mercury level is necessary in cases of organic mercury exposure. The differential diagnosis is extensive and includes causes of metal fume fever (elemental), encephalopathy or tremor (elemental/inorganic/organic). Consider alternative causes of corrosive gastroenteritis (ingestion of iron, arsenic, phosphorus, acids, and alkalis) if mercury salt ingestion is suspected.

Emergency Department Care and Disposition

1. Support the ABCs with airway management and crystalloid infusion.

2. Consider gastric lavage in cases of inorganic mercury ingestion or activated charcoal in cases of organic mercury ingestion.

3. Begin chelation therapy prior to confirming the diagnosis (Table 114-4). Dimercaprol (BAL) is preferred for elemental and inorganic mercury poisonings. Succimer (DMSA) is the agent of choice in organic mercury poisonings and in cases of mild or chronic elemental/inorganic mercury toxicity.

4. Admit patients with respiratory symptoms following mercury vapor exposure and those with inorganic mercury ingestions.

Less common toxic heavy metals include bismuth, cadmium, chromium, cobalt, copper, silver, thallium, and zinc. Unique manifestations and treatments of these exposures are outlined in Table 114-5.