DIAGNOSIS History of an exposure—occupational, hobby, environmental, or related to retained lead bullets—is the most important clue to making the diagnosis. The physician should focus on symptoms, developmental and dietary histories (in children), pica, any house or day-care remodeling, previous serum iron and blood lead levels, and possible lead toxicity in other family members. Occupational and hobby histories should be elicited, both for adults being evaluated and for children who may be exposed to lead secondarily from these adult activities.
The combination of abdominal or neurologic dysfunction with a hemolytic anemia should raise the suspicion of lead toxicity. Emergency physicians should consider the diagnosis in all children presenting with encephalopathy. Toxicity due to retained lead bullets has manifested in patients as long as several decades after being shot. Hyperthyroidism, pregnancy, fever, reinjury, or immobilization of the affected extremity can promote lead release after years of dormancy.
Laboratory studies in the emergency department (ED) should focus on evaluation for anemia and examination of bone radiographs in children for "lead bands" and abdominal radiographs for radiopaque material consistent with lead in the gastrointestinal tract. The anemia can be normocytic or microcytic, possibly with evidence of hemolysis such as an elevated reticulocyte count and increased serum free hemoglobin.
The peripheral smear may show basophilic stippling of the RBCs. Both anemia and basophilic stippling occur variably, and their absence does not rule out lead toxicity. Basophilic stippling of RBCs is nonspecific for lead toxicity, since it is also found in arsenic toxicity, sideroblastic anemia, and the thalassemias. In children, radiographs of long bones, especially of the knee, may reveal horizontal, metaphyseal lead bands, which represent failure of bone remodeling rather than deposition of lead.
The definitive diagnosis rests on finding an elevated PbB level, with or without symptoms. The PbB level is the best single test for evaluating lead toxicity, and levels of 10 pg/dL or more are considered toxic. Screening levels may be performed on fingerstick capillary blood, but because of the potential for environmental lead contamination, elevated levels always should be confirmed on a venous blood sample.8 Previously, a calcium disodium versenate (CaNa2-EDTA) provocation test was used to evaluate total-body lead stores and the need for chelation therapy when PbB levels were between 25 and 55 pg/dL. However, animal data demonstrating that one dose of CaNa2-EDTA redistributes lead to the brain, the technical difficulties in performing the test, the lowering of the toxic PbB level to 10 pg/dL or more, and the advent of dimercaptosuccinic acid (DMSA) as a safe and effective oral chelator raise concerns about the utility of the provocation test. Some major lead treatment centers have abandoned its use. Also, with the lowering of the toxic PbB level to 10 pg/dL or more, the erythrocyte protoporphyrin (EP) test can no longer be used to screen for lead toxicity because of its unacceptably low sensitivity at these lower PbB levels.9
DIFFERENTIAL DIAGNOSIS The differential diagnosis of lead toxicity includes causes of encephalopathy such as Wernicke's encephalopathy, withdrawal from ethanol and other sedative-hypnotic drugs, meningitis, encephalitis, human immunodeficiency virus (HIV) infection, intracerebral hemorrhage, hypoglycemia, severe fluid and electrolyte imbalances, hypoxia, arsenic, thallium, and mercury toxicity, and poisoning with cyclic antidepressants, anticholinergic drugs, ethylene glycol, or carbon monoxide. The abdominal pains can mimic sickle cell crisis or the hepatic porphyrias. Chronic lead toxicity can masquerade as depression, neurosis, hypothyroidism, polyneuritis, gout, iron deficiency anemia, and learning disability.
TREATMENT All patients with appropriate symptoms and an elevated PbB level are classified as lead toxic and should be treated.
Severe Toxicity Lead-induced encephalopathy rarely occurs now, but it remains a major cause of serious morbidity and mortality in lead-poisoned patients. In severely toxic patients, standard life support measures should be instituted and seizures treated with benzodiazepines, phenobarbital, phenytoin, and general anesthesia, if necessary. If abdominal films demonstrate radiopaque flecks consistent with lead, whole-bowel irrigation with a polyethylene glycol electrolyte solution should be instituted. The solution should be administered continuously at a rate of 500 to 2000 mL/h for adults and 100 to 500 mL/h for children until the abdominal radiograph is clear. It will not alter fluid or electrolyte balance in the patient. Larger lead bodies such as fishing sinkers may require surgical removal. Fluid administration should be controlled carefully to avoid worsening cerebral edema. Lumbar puncture may precipitate cerebral herniation and should be performed carefully, if at all, with the removal of a small amount of cerebrospinal fluid (CSF) only.
Chelation therapy should be instituted immediately (i.e. in the ED) prior to obtaining laboratory verification of the diagnosis. All chelating agents supply sulfhydryl groups to which the lead attaches. Dimercaprol (British anti-Lewisite, or BAL), 75 mg/m 2, should be administered intramuscularly first, followed 4 h later by CaNa2-EDTA, 1500 mg/m2 per 24 h, in a continuous intravenous infusion. BAL administration is continued every 4 h. BAL chelates intracellular as well as extracellular lead and may be administered to patients in renal failure because it is also excreted in the bile. It is mixed in peanut oil and must be given intramuscularly. CaNa2-EDTA chelates extracellular lead only and may exacerbate lead-induced CNS toxicity in patients with high PbB levels unless preceded by BAL therapy. Continuous intravenous infusion is the preferred method of delivery. CaNa 2-EDTA can cause renal toxicity, and patients should be adequately hydrated to promote diuresis and minimize the risk of this complication. It should not be used in patients with renal failure. Adverse effects of the chelating agents are listed in T§bieJ,78:3.
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