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Chapter 114: Metals and Metalloids

D. Adam Algren

INTRODUCTION

Metal and metalloid poisoning, although uncommon, can result in morbidity and mortality if unrecognized. Toxicity results from occupational, recreational, or environmental exposures and results in multi-system organ involvement.

LEAD POISONING

Clinical Features

Lead poisoning manifests with signs and symptoms affecting a variety of organ systems (Table 114-1).

Table 114-1

Clinical Features of Lead Poisoning

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Table 114-1

Clinical Features of Lead Poisoning
System Clinical Manifestations
Central nervous Acute toxicity: encephalopathy, seizures, altered mental status, papilledema, optic neuritis, ataxia
Chronic toxicity: headache, irritability, depression, fatigue, mood and behavioral changes, memory deficit, sleep disturbance
Peripheral nervous Paresthesias, motor weakness (classic is wrist drop), depressed or absent deep tendon reflexes, sensory function intact
GI Abdominal pain (mostly with acute poisoning), constipation, diarrhea, toxic hepatitis
Renal Acute toxicity: Fanconi’s syndrome (renal tubular acidosis with aminoaciduria, glucosuria, and phosphaturia)
Chronic toxicity: interstitial nephritis, renal insufficiency, hypertension, gout
Hematologic Hypoproliferative and/or hemolytic anemia; basophilic stippling (rare and nonspecific)
Reproductive Decreased libido, impotence, sterility, abortions, premature births, decreased or abnormal sperm production

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 complete blood count (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. The differential diagnosis of toxicity is broad and includes meningitis, encephalitis, metabolic abnormalities, hypoxia, drug intoxications, arsenic, mercury, and carbon monoxide poisoning.

Emergency Department Care and Disposition

  1. Address life-threatening problems with advanced airway management and fluid resuscitation.

  2. Decontaminate the GI tract with whole-bowel irrigation using polyethylene glycol solution in those with retained lead flecks in the GI tract. Larger foreign bodies may require endoscopic or surgical removal.

  3. Treat seizures aggressively with benzodiazepines, followed by barbiturates and/or propofol, and/or general anesthesia. Avoid lumbar puncture in the setting of lead-induced encephalopathy as this can precipitate herniation.

  4. Chelation therapy is the mainstay of treatment and often must be started empirically (Table 114-2). Dimercaprol (BAL) can only be administered intramuscularly and is contraindicated in those with peanut allergies.

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

Table 114-2

Guidelines for Chelation Therapy in Lead-Poisoned Patients*

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Table 114-2

Guidelines for Chelation Therapy in Lead-Poisoned Patients*
Severity (Blood Lead Level [μg/dL]) Dose

  • Encephalopathy

  • Dimercaprol, 75 mg/m2 (or ...

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