available These findings include (i) microcytic anemia; (ii) elevated EP level, especially if higher than 250 mcg/dL (conversely, a normal or minimally elevated EP level, less than 50 mcg/dL, would make lead encephalopathy caused by chronic lead paint exposure unlikely); (iii) basophilic stippling of peripheral erythrocytes or, if feasible, of red blood cell precursors on bone marrow examination; (iv) glycosuria; (v) aminoaciduria; (vi) radiopaque flecks on abdominal radiographs; and (vii) dense metaphyseal bands on radiographs of knees and wrists (lead lines— Fig 102.11 ) Abnormalities on examination of cerebrospinal fluid (CSF) are also indicative of lead encephalopathy, including a lymphocytic pleocytosis, elevated protein level, and increased pressure The treatment of lead poisoning involves relocation of the child to a lead-free environment, consideration of chelation therapy, and appropriate supportive care Symptomatic patients are at risk of developing encephalopathy with subsequent death or neurologic sequelae In addition, asymptomatic patients with high BLL (especially higher than 100 mcg/dL) are also at significant risk for developing CNS involvement and might require urgent treatment Routine chelation is not indicated for children with BLL less than 45 mcg/dL The specific chelating drugs commonly used for symptomatic lead intoxication are edetate calcium disodium (CaNa2 EDTA) and 2,4-dimercaptopropanol (British Anti-Lewisite [BAL]; Table 102.16 ) Side effects of CaNa2 EDTA include local reactions at injection sites, fever, hypercalcemia, and renal dysfunction manifested by rising BUN and abnormal urine sediment with proteinuria, hematuria, and/or epithelial cells The major side effects of BAL include nausea and vomiting, so for the first day or two of BAL therapy, it is prudent to maintain the patient on IV fluids and clear liquids or nothing by mouth BAL is formulated in peanut oil, is given only by IM injection, and also induces hemolysis in patients with G6PD deficiency Its use is hazardous if the patient has severe hepatic dysfunction, and it forms a toxic complex if given concurrently with iron Succimer (dimercaptosuccinic acid [DMSA]) has been approved for pediatric use in cases in which BLL exceeds 45 mcg/dL ( Table 102.16 ) This water-soluble analog of BAL may be taken orally, and several studies have found such use to be as effective as CaNa2 EDTA given parenterally FIGURE 102.11 Knee radiograph demonstrating increased calcium deposition at metaphysis— the so-called “lead lines.” (Reprinted from Henretig FM A toddler in status epilepticus In: Osterhoudt KC, Perrone J, DeRoos F, et al., eds Toxicology Pearls Philadelphia, PA: Hanley & Belfus; 2004:S2–S5 Copyright © 2004 Elsevier With permission.) Asymptomatic children with BLL of 45 to 69 mcg/dL should have urgent referral and treatment with oral DMSA (typically a 19-day course) or parenteral CaNa2 EDTA for days ( Table 102.15 ) If the BLL is higher than 69 mcg/dL, combination therapy is initiated with both BAL and CaNa2 EDTA; the BAL may be discontinued in many cases after to days, but CaNa2 EDTA is continued for days For symptomatic patients or those with high BLLs (>69 mcg/dL), CaNa2 EDTA should always be started hours after BAL due to the risk of worsening lead encephalopathy when CaNa2 EDTA is given alone in these patients Provide adequate hydration to promote urine output Symptomatic children without frank encephalopathy should receive chelation therapy with a combination of BAL for to days and CaNa2 EDTA for days Supportive care includes close monitoring for signs of encephalopathy and, again, maintenance of urine flow In the event of BAL or CaNa2 EDTA shortage, succimer may be an adequate substitute, although the evidence in support of its use for severe intoxication or encephalopathy is purely observational Patients with encephalopathy require combination chelation therapy with higher-dose CaNa2 EDTA and BAL for days, as well as intensive supportive care Fluid therapy is critical to achieve adequate urine flow to excrete the lead– chelate complexes; however, fluid overload can exacerbate cerebral edema Seizures commonly occur in acute encephalopathy and should be controlled with anticonvulsant drugs (see Chapter 72 Seizures ) Hypothetical concerns have been raised about the use of phenobarbital in lead encephalopathy (i.e., synergistic disturbances in porphyrin metabolism), but its clinical use has not been associated with any noticeable deleterious effect Recent advances have been made in the management of cerebral edema and increased intracranial pressure (see Chapter 122 Neurosurgical Emergencies ), but have not been evaluated in controlled fashion in the context of lead encephalopathy TABLE 102.16 GUIDELINES FOR CHELATION THERAPY OF LEAD POISONING Condition, BLL Regimen a Comment Encephalopathy BAL 450 mg/m2 /day + 75 mg/m2 IM every hrs for days Continuous infusion, or 2–4 divided IV doses, for days (start hrs after BAL) 50–75 mg/m2 every hrs for 3–5 days (see text) Continuous infusion, or 2–4 divided IV doses, for days (start hrs after BAL) 350 mg/m2 TID for days, then BID for 14 days CaNa2 EDTA 1,500 mg/m2 /day Symptomatic, BAL 300–450 mg/m2 /day and/or BLL >70 CaNa2 EDTA 1,000–1,500 mg/m2 /day Asymptomatic, BLL 45–69 Succimer 700–1,050 mg/m2 /day or CaNa2 EDTA, 1,000 mg/m2 Continuous infusion, or 2–4 divided IV doses, for /day days a Doses expressed in mg/kg: BAL 450 mg/m2 (24 mg/kg), 300 mg/m2 (18 mg/kg); CaNa2 EDTA 1,000 mg/m2 (25–50 mg/kg), 1,500 mg/m2 (50–75 mg/kg); Succimer 350 mg/m2 (10 mg/kg) BLL, blood lead level (mcg/dL); BAL, British Anti-Lewisite; IM, intramuscular; IV, intravenous Adapted from American Academy of Pediatrics, Committee on Drugs Treatment guidelines for lead exposure in children Pediatrics 1995;1996:155–160; Henretig FM Lead In: Goldfrank LR, Flomenbaum NE, Lewin NA, et al., eds Goldfrank’s Toxicologic Emergencies 9th ed New York: McGraw-Hill; 2009 Pesticides CLINICAL PEARLS ... intramuscular; IV, intravenous Adapted from American Academy of Pediatrics, Committee on Drugs Treatment guidelines for lead exposure in children Pediatrics 1995;1996:155–160; Henretig FM Lead In: Goldfrank