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Aggressive Approach in the Treatment of Acute Lead Encephalopathy with an Extraordinarily High Concentration of Lead

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Aggressive Approach in the Treatment of Acute Lead Encephalopathy with an Extraordinarily High Concentration of Lead ARTICLE Aggressive Approach in the Treatment of Acute Lead Encephalopathy With an Extraordinarily High Concentration of Lead Robert A. Gordon, PharmD; Gerard Roberts, MD; Zubair Amin, MD; Robert H. Williams, PhD; Frank P. Paloucek, PharmD, ABAT Objective: To report a case of a 3-year-old child with Conclusions: In this case, aggressive gut decontami- an extraordinarily massive lead concentration, 26.4 µmol/L nation with whole bowel irrigation and triple chela- (550 µg/dL), following environmental exposure to lead tion therapy with British anti-Lewisite, EDTA, and oral paint in the home. succimer was well tolerated and seemed effective for rapidly deleading the child. The extent to which her Literature Review: The relevant literature concern- lead concentration increased while being treated with ing the treatment of lead encephalopathy was reviewed oral succimer alone necessitated further chelation with during the treatment of this child and preparation of the EDTA. Further evaluation is necessary to determine if manuscript. To our knowledge, the landmark article writ- triple chelation therapy is an appropriate method for ten by Julian Chisolm in 1968 is the only recent article severe lead intoxication, and if the use of whole bowel that reported similarly high levels of lead concentra- irrigation should be considered in heavy metal intoxi- tion. This case, however, is the first in which 3 chelat- cation. ing agents were used for the treatment of lead encepha- lopathy. We also reviewed the literature on the use of whole bowel irrigation in heavy metal intoxications. Arch Pediatr Adolesc Med. 1998;152:1100-1104 generally accepted that low-income hous- Editor’s Note: The unusually severe problem reported in this case ing areas are at high risk for lead poison- study should serve as a stark reminder that lead poisoning might ing, yet higher income areas are not im- be decreasing, but it’s certainly not gone. mune to the risks of lead poisoning.2,6-8 We Catherine D. DeAngelis, MD report a case of severe lead encephalopa- thy with extraordinary concentrations of lead in a 3-year-old child following envi- ronmental exposure. EAD POISONING in children remains a significant prob- REPORT OF A CASE lem. Although many sources of lead (ie, gasoline, sol- CLINICAL FINDINGS dered seams of food and bev- Lerage cans, and seals on wine bottles, and A 3-year-old girl was transferred to our paint) have been eliminated, lead is still hospital with a history of progressively present in many residences.1-4 Buildings worsening visual acuity, difficulty walk- constructed in the United States prior to ing and speaking, abdominal pain, and From the Department of 1977 are exempt from legislation that pro- vomiting. She previously had been admit- Pharmacy Practice, College of hibits the use of lead-based paint. The act ted to the emergency department of a lo- Pharmacy (Drs Gordon and of 1977 only restricted lead-based paint in cal hospital with nonspecific abdominal Paloucek), the Departments new residential homes and paint sold in pain, nonbilious, nonbloody vomiting, and of Medicine (Dr Roberts and interstate commerce. Consequently, build- frequent soft bowel movements for 3 days. Paloucek) and Pediatrics ings constructed prior to 1980 may have The child was dehydrated and her com- (Drs Roberts and Amin), a large amount of peeling or chipped paint plete blood cell count revealed a micro- College of Medicine, University of Illinois, Chicago; and the with high lead content, putting children cytic, hypochromic anemia. She was given Department of Pathology, living there at high risk of lead intoxica- fluids by mouth and was sent home with 1,3,4 University of Illinois Hospital tion. As renovations of old buildings a prescription for ferrous sulfate solution and Clinics, Chicago increase, there is additional risk of ex- and instructions for follow-up with her pri- (Dr Williams). posure to lead in the dust and dirt.5 It is mary care physician. During the next 2 ARCH PEDIATR ADOLESC MED/ VOL 152, NOV 1998 1100 ©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 28.98 (600) 24.15 (500) g/dL) µ 19.32 (400) mol/L ( µ 14.49 (300) 9.66 (200) 4.83 (100) Lead Concentration, 0 12345678910 11 12 13 14 15 16 17 18 19 20 21 22 23 Time, d Whole-Bowel Irrigation Intramuscular British Anti-Lewisite Intravenous EDTA Oral Succimer Oral Zinc Figure 1. The blood lead concentration vs the duration of treatment up to the last treatment course. days her abdominal pain and vomiting continued. She blood smear demonstrated hypochromia and anisopoi- also became lethargic, sometimes difficult to awaken, and kilocytosis with prominent basophilic stippling. developed an unsteady gait. The mother also noticed a deviation in the child’s left eye and a deterioration in her TREATMENT COURSE hand-eye coordination. On subsequent evaluation at the local emergency department, she was more lethargic and Because of the exceptionally high concentrations of lead had a heart rate of 60/min. Her laboratory findings in- in this child and other evidence indicating excessive lead cluded hemoglobin, 7.7 g/dL; mean corpuscular vol- exposure, it was decided by the toxicology service that ume, 55.9 fL; red cell distribution width, 0.24; and a white the potential benefits of attempting intensive 3-drug che- blood cell count of 12.33109/L, with 0.82 neutrophils. lation therapy and whole bowel irrigation outweighed the Cerebrospinal fluid analysis revealed a white blood cell unknown risks. The initial chelation therapy consisted count of 5.03109/L, with 0.24 neutrophils and 0.62 lym- of the administration of 4 mg/kg of British anti-Lewisite phocytes; and a red blood cell count of 4.431012/L. Her (BAL) intramuscularly every 4 hours. Whole bowel ir- serum ammonia level was 38 µmol/L; alanine amino- rigation (WBI) with polyethylene glycol was performed transferase, 53 U/L. Noncontrast computed tomogra- at 20 mL/kg per hour via nasogastric tube and contin- phy of the head showed normal findings. A blood lead ued for 3 days until the abdominal radiograph essen- concentration was also drawn at this time, but was sent tially showed no abnormalities. Calcium disodium EDTA to an outside laboratory for testing. The child was given therapy was started 4 hours after BAL, at 50 mg/kg per 1 dose of ceftriaxone disodium, 100 mg/kg, and was trans- day intravenously, and was subsequently increased to 75 ferred to our facility. mg/kg per day on the second day and continued at this The child’s medical history included one hospital dosage through the first treatment course. When WBI was admission for bronchiolitis, and the mother described be- completed, oral succimer was administered at 200 mg 3 havior consistent with pica. The mother denied that the times daily for 5 days, followed by 200 mg 2 times daily child had ingested paint chips or other lead-containing for 14 days. The patient’s blood lead concentration fell products, but did indicate that they had lived for the from 25.4 µmol/L (550 µg/dL) to 3.38 µmol/L (70 µg/ past 3 years in an older apartment building that had not dL) during the first 5 days of the treatment course been well maintained. The child had received limited (Figure 2). It then increased sharply to 4.78 µmol/L (99 medical care in the past and was not seen regularly by a µg/dL) 2 days after the BAL and EDTA treatments were physician. stopped. Calcium disodium EDTA treatment was re- The child was difficult to awaken and unable to walk. started at 50 mg/kg per day for another 5 days, which She opened her eyes only in response to pain. Her vital resulted in a drop in blood lead concentration to 3.71 signs were temperature, 36.8°C; heart rate, 67 beats per µmol/L (77 µg/dL) the day after completion. The admin- minute; respirations, 18/min; and blood pressure, 95/31 istration of oral succimer was continued and the patient mm Hg. Her right pupil was 4 to 5 mm in diameter and had serial blood lead concentrations 2 and 4 days after had a sluggish reaction to light. Her left pupil was 5 to 6 discontinuation of the second treatment course of cal- mm in diameter and deviated to the right. Her Glasgow cium disodium EDTA. Blood lead concentrations were Coma Scale score was 8. Her blood lead concentration 3.18 µmol/L (66 µg/dL) and 3.96 µmol/L (82 µg/dL), re- was 26.4 µmol/L (550 µg/dL). An abdominal radio- spectively, and we reinstituted treatment with a third graph showed opaque areas that resembled paint chips course of calcium disodium EDTA at 50 mg/kg per day throughout the gastrointestinal tract and dense areas along for 5 days. An oral zinc sulfate supplement was also ad- the iliac crest that resembled lead lines (Figure 1). Her ministered at 100 mg/d at this time. Blood lead concen- ARCH PEDIATR ADOLESC MED/ VOL 152, NOV 1998 1101 ©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 Figure 2. Radiographic findings of the long bones in the legs (left) and hands (right) showing areas of increased lead density of “lead lines.” trations at completion of the third course and 2 days af- lead poisoning or who are asymptomatic but have blood ter completion were 2.51 µmol/L (52 µg/dL) and 3.33 lead concentrations greater than 3.38 µmol/L (.70 µg/dL) µmol/L (69 µg/dL), respectively.
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