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 encephalopathy. 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 encephalopathy with extraordinary concentrations of lead in a 3-year-old child following environmental 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

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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 12.3ϫ109/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 5.0ϫ109/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 4.4ϫ1012/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-

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©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 (Ͼ70 µg/dL) µmol/L (69 µg/dL), respectively. She was discharged into recommend removal of the child from the source of lead the care of the mother and grandmother to stay at a lo- and inpatient treatment with parenteral drug therapy.9 Pa- cation approved by the Illinois Department of Public tients who are asymptomatic with blood lead concentra- Health. Her medications on discharge from the hospital tions between 2.17 and 3.33 µmol/L (45 and 69 µg/dL) included oral succimer, zinc sulfate, and iron sulfate. The generally receive chronic outpatient treatments or are ad- child is being monitored by her local physician without mitted for parenteral drug therapy with calcium diso- further complications. dium EDTA.9 In 1991, meso-2,3-dimercaptosuccinic acid, or succimer, was added to the treatment options for mild COMMENT to moderate lead poisoning (2.17-3.33 µmol/L [45-69 µg/dL]), representing the only new agent for the treat- The treatment of acute lead encephalopathy has not ment of lead poisoning in more than 30 years.9,12 Besun- changed much in the last 20 years.9-11 The mainstay of treat- der et al13 and Graziano et al14 studied meso-2,3 dimer- ment is chelation therapy, which is frequently limited by captosuccinic acid in the short-term treatment of patients toxic reactions.10-12 The pharmacological action of BAL has with low to moderate blood lead concentrations and found proven useful for chelating several heavy metals, includ- it both efficacious and safe. Cory-Slechta15 used meso-2,3- ing lead.10-12 As BAL must be administered by deep intra- dimercaptosuccinic acid for long-term treatment in rats muscular injection every 4 hours, treatment is painful and and also found it to be both safe and effective.15 She does often difficult to adhere to, especially in children. Most of note that it may be effective as an adjunct treatment with the other adverse effects tend to be dose limiting, but do calcium disodium EDTA to further reduce total body lead not contraindicate the use of BAL unless the patient has burden. an allergy to peanut oil (the diluent in which BAL is pre- Extraordinarily high blood lead concentrations simi- pared) or is glucose-6-phosphate dehydrogenase– lar to the concentration found in our patient (26.4 µmol/L deficient.10-12 Calcium disodium EDTA (ethylenediamine- [550 µg/dL]), although infrequent, have been seen in chil- tetraacetic acid) has been available for the treatment of lead dren since 1968. Until the late 1960s, death rates for pa- poisoning for more than 50 years. Initial use revealed salt- tients seen with severe neurologic sequelae (ie, seizures specific problems.12 The current salt form (calcium diso- or coma) were reported to be approximately 25%, even dium EDTA) is now the specific agent approved for use after the development of calcium disodium EDTA.10,16 Prior in treating lead intoxication, but it still binds other metal to this, Foreman17 noted that encephalopathy secondary ions including zinc, copper, and manganese.12 Its major to lead poisoning, if left untreated, had a greater than 60% limiting toxicity is a dose- and infusion rate–related neph- mortality rate. It was not until the standard of medical prac- rotoxicity.12 In an effort to minimize toxic effects, we used tice included the concurrent administration of BAL and a 5-day continuous intravenous infusion for our patient. calcium disodium EDTA that this fatality rate started to In 1968, Chisolm10 recommended the use of BAL and cal- decrease. Other factors, such as the timeliness of the di- cium disodium EDTA together for the treatment of mod- agnosis of lead intoxication and the initiation of treat- erate to severe lead poisoning and found the combina- ment, probably also affected the percentage of deaths re- tion to be superior to either agent alone in lowering the lated to lead intoxication. Isolated case reports of child blood lead concentration. In 1992, O’Connor11 also stud- fatalities resulting from lead intoxication have been re- ied the combination of calcium disodium EDTA and BAL, ported since 1970 (eg, Alexander and Delves18, Hugelmyer corroborating the results found by Chisolm in 1968 that et al19), and notable features of those cases were inappro- gave us the current recommendations for the treatment priate diagnosis, delay in treatment, or both. of acute lead encephalopathy.9-11 Most current treatment Among the cases reported by Greengard et al16 in regimens for children who are symptomatic for chronic 1965, the blood lead concentrations that resulted in death

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 varied greatly (4.35-39.85 µmol/L [90-825 µg/dL]). It is lead concentration of 3.72 µmol/L (77 µg/dL). She was likely that most of these deaths are related to an acute also treated with BAL, calcium disodium EDTA, and oral ingestion as opposed to chronic intoxication. Extraor- succimer (triple chelation therapy). Three days into treat- dinarily high concentrations of lead (Ͼ14.49 µmol/L ment, her blood lead concentration was 0.43 µmol/L (9 [Ͼ300 µg/dL]) are most likely the result of an acute or µg/dL), and BAL therapy was subsequently discontin- acute-on-chronic ingestion. In light of the considerable ued. risk of encephalopathy and death in children with very As chelating agents are not free of significant ad- high blood lead concentrations, we elected at the outset verse effects (especially calcium disodium EDTA and to use a 3-drug chelation regimen. During her initial 5- BAL), the use of these agents must be carefully consid- day treatment course, the patient experienced a signifi- ered. With the addition of oral succimer, it may be ap- cant drop in her blood lead concentration, from 26.56 propriate to be aggressive initially and use these 3 agents to 3.38 µmol/L (550 to 70 µg/dL), and she showed dra- (BAL, calcium disodium EDTA, and succimer) simulta- matic improvement in neurologic status. Even though neously not only in those patients with extraordinarily oral succimer therapy was continued, her blood lead con- high blood lead concentrations or in those who are seen centration increased substantially once calcium diso- with frank encephalopathy, but in a select population (ie, dium EDTA and BAL therapy were stopped. Since her blood lead concentrations Ͼ7.24 µmol/L [Ͼ150 µg/ condition had improved so drastically, we decided to re- dL]). Further studies are necessary to assess the safety start a second treatment course of calcium disodium EDTA and efficacy of using 3 chelating agents in patients with without BAL in an effort to minimize toxic effects. Her blood lead concentrations greater than 7.24 µmol/L (Ͼ150 cognitive function improved rapidly and, with the help µg/dL), but a single-site study is not realistic. of physical therapy, she was able to walk well again. She The cost of the patient’s hospital stay was approxi- continued to have strabismus of the right eye, but was mately $30 000. Clearly, lead poisoning continues to be able to recognize objects and people. According to the a significant problem in terms of treatment cost and long- family, she was close to her baseline cognitive function term physical consequences that may haunt the patients prior to initial presentation. for the rest of their lives.2,4,30 In this child, aggressive simultaneous treatment with BAL, calcium disodium EDTA, and succimer was well tolerated; this treatment course efore the third treatment course of cal- may also be effective for other patients with extremely cium disodium EDTA was started, oral zinc high blood lead concentrations. Please note that this regi- supplementation was initiated. Following men is not approved for use in the treatment of lead en- this, the patient’s blood lead concentra- cephalopathy, and further evaluation is needed. Bone tion dropped significantly from 4.10 to 2.51 growth is very active in young children through adoles- µmol/LB (85 to 52 µg/dL). Zinc supplementation has been cence. As blood lead is the only lead in the body avail- reported to enhance the elimination of lead when given able for chelation, is it not theoretically possible to have in conjunction with calcium disodium EDTA in ani- an effect on the bony compartment and decrease the to- mals.20,21 tal body burden of lead with aggressive initial treat- Whole bowel irrigation has become a popular ment?31,32 This should be studied more closely, espe- method of gross removal of toxins in the gastrointesti- cially with the addition of succimer to long-term nal tract.22,23 In this case, the use of WBI removed most, outpatient management. The treatment we used for this if not all, of the lead chips present in the initial kidney, child was as follows: (1) Whole bowel irrigation with poly- ureter, and bladder, without causing any of the meta- ethylene glycol at 20 to 30 mL/kg per hour for the kid- bolic derangements seen with other forms of catharsis. ney, ureter, and bladder where lead chips were present. The effectiveness of this method in removing certain tox- (2) British anti-Lewisite at 4 mg/kg every 4 hours as an ins, especially those not bound to activated charcoal, and intramuscular injection for 3 to 5 days. (3) Calcium di- those found below the level of the pylorus, needs fur- sodium EDTA at 50 to 75 mg/kg per day 4 hours after ther investigation. Other forms of catharsis have been as- starting BAL therapy. (Note: We diluted the calcium di- sociated with significant metabolic abnormalities in fluid sodium EDTA to a concentration of 2 to 4 mg/mL 5% and electrolyte levels.22 To date, most studies and obser- dextrose in water, and infused it intravenously over 24 vations in the literature concerning WBI for gross re- hours). This was continued for a total of 5 days. (4) Once moval of toxins have not been associated with signifi- WBI was completed, we started oral succimer treatment cant metabolic derangement, and we found it safe, at 10 mg/kg every 8 hours for 5 days, and then 10 mg/kg effective, and supportive of that literature.24-28 Kaczo- twice daily for 14 days. (Note: Oral succimer treatment rowski and Wax29 report a case in which 44 L of poly- was started immediately in the younger sibling, as her ethylene glycol was used to remove a large iron concre- gastrointestinal tract was clear on presentation). (5) Zinc tion. This was infused over 5 days, and no metabolic supplementation was started during the third course of abnormalities were seen. chelation with calcium disodium EDTA. The child’s blood lead concentration at discharge The course of oral succimer treatment was contin- from the hospital was 3.33 µmol/L (69 µg/dL). In the ued after the patient was discharged from the hospital. course of her evaluation, the Illinois Department of Pub- The patient and her sister are being monitored by their lic Health inspected the home and found paint contain- pediatrician. Unfortunately, the family has relocated more ing a 10% lead base. The asymptomatic younger sister than once, making follow-up more difficult. The Illinois was admitted to the hospital shortly afterward with a blood Department of Public Health and the local police depart-

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/30/2021 ment have been involved to ensure that the children are the blood lead levels of lead poisoned children. Pediatrics. 1991;88:893-897. getting the necessary medical attention required. This situ- 9. Committee on Drugs. Treatment guidelines for lead exposure in children. Pedi- atrics. 1995;96:155-160. ation is probably not unusual in many cases of lead in- 10. Chisolm JJ. The use of chelating agents in the treatment of acute and chronic toxication. Families must often move away from the lead intoxication in childhood. J Pediatr. 1968;73:1-38. source of lead if it cannot be removed, which further con- 11. O’Connor M. CaEDTA vs CaEDTA plus BAL to treat children with elevated blood founds the efforts of the medical system to effectively treat lead levels. Clin Pediatr. 1992;31:386-390. patients. 12. Klaassen C. Heavy metals and heavy-metal antagonists. In: Hardman JG, Lim- bird LE, Molinoff PB, Ruddon RW, Goodman Gilman A, eds. Goodman and Gil- Efforts to increase public awareness of the dangers man’s The Pharmacological Basis of Therapeutics. New York, NY: McGraw-Hill of lead poisoning and to remove the sources of lead from Book Co; 1996:1650-1654, 1664-1667. the environment are clearly needed. Closer adherence to 13. Besunder J, Anderson R, Super D. Short-term efficacy of oral dimercaptosuc- the Title X mandate “The Residential Lead-Based Paint cinic acid in children with low to moderate lead intoxication. Pediatrics. 1995; Hazard Reduction Act of 1992” is imperative.2,4,7 Land- 96:683-687. 7 14. Graziano J, Lolacono N, Moulton T, Mitchell ME, Slavkovich MS, Zarate C. Con- rigan and Todd suggested adapting the guidelines of the trolled study of meso-2,3-dimercaptosuccinic acid for the management of child- Asbestos Hazard Emergency Response Act, which re- hood lead intoxication. J Pediatr. 1992;120:133-139. quires appropriate training for lead workers in the re- 15. Cory-Slechta D. Mobilization of lead over the course of DMSA chelation therapy moval of lead. Without safe and appropriate removal of and long-term efficacy. J Pharmacol Exp Therap. 1988;246:84-91. 16. Greengard J, Adams B, Berman E. Acute lead encephalopathy in young children. lead from its many sources in the environment, lead in- J Pediatr. 1965;66:707-711. toxication will continue to be a problem well into the 21st 17. Foreman H. Use of chelating agents in the treatment of metal poisoning. Fed Proc. century. 1961;20:191-196. 18. Alexander FW, Delves HT. Deaths from acute lead poisoning. Arch Dis Child. 1972; Accepted for publication May 22, 1998. 47:446-448. 19. Hugelmeyer CD, Moorhead JC, Horenblas L, Bayer M. Fatal lead encephalopathy We would like to make a special acknowledgment to following foreign body ingestion: case report. J Emerg Med. 1988;6:397-400. 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