Metal poisoning often results from occupational, recreational, or environmental exposure and results in a combination of neurologic, cardiovascular, gastrointestinal, hematologic, and renal findings.
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).
Table Graphic Jump Location Table 114-1 Common Manifestations of Lead Poisoning ||Download (.pdf)
Table 114-1 Common Manifestations of Lead Poisoning
|Central nervous system||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 system||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 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 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
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.
Decontaminate the GI tract with whole-bowel irrigation using polyethylene glycol solution in those with retained lead in the GI tract.
Chelation therapy is the mainstay of treatment and often must be started empirically (Table 114-2).
Admit patients requiring parenteral chelation therapy or those who cannot avoid further environmental lead exposure. Arrange follow up for patients started on succimer.
Table Graphic Jump Location Table 114-2 Guidelines for Chelation Therapy in Lead-Poisoned Patients* ||Download (.pdf)
Table 114-2 Guidelines for Chelation Therapy in Lead-Poisoned Patients*
|Severity [blood lead level (micrograms/dL)]||Dose|
|Encephalopathy||Dimercaprol, 75 milligrams/m2 (or 4 milligrams/kilogram) IM every 4 h for 5 d|
|Edetate calcium disodium, 1500 milligrams/m2/d, for 5 d as a continuous IV infusion started 4 h after dimercaprol|
| Adults: blood lead >100||and|
| Children: blood lead >69||Edetate calcium disodium (as described above)|
|Edetate calcium disodium (alone)|
|Succimer (as described below)|
Adults: blood lead 70 to 100