Call for Abstracts The American Pediatric Society, The Society for Pediatric Research, and the Ambulatory Pediatric Association announce that the abstract deadline for the 1993 annual meeting (May 3-6, 1993, Washington [DC] Sheraton Hotel) is January 5, 1993. For further information, contact the APS/SPR Association Headquarters, 141 Northwest Point Blvd, PO Box 675, Elk Grove Village, IL 60009-0675 ([708] 427-0205; fax, [708] 427-1305), or the APA Headquarters, 6728 Old McLean Village Dr, McLean, VA 22101 ([703]

556-9222).

Clinical and

Lead Encephalopathy in Saudi Arabian Children Sir.\p=m-\Leadis probably the most ancient metallic poison known to man. Because of the wide dissemination of lead into our environment and its common use for various purposes, both See also pp

acute and chronic forms of lead

poisoning are frequently encountered.1,2 Ancient physicians depended heavily on lead as a major ingredient in the recipes they used in the treatment of

Laboratory Data on

No./Sex/ mo

1/M/1Í

10 Saudi Children With Lead

Hématologie

Patient

Age,

1259, 1275, and 1278.

Symptoms Vomiting,

Lead, µ /L 5.10

µ

FEP,

/L

25.38

their patients. In recent years, infants have been reported to fall victim to a new form of lead poisoning. Several reports from the Middle East and other countries have incriminated the faith healers who use home remedies containing lead in the treatment of childhood diseases.3-5 Patients and Methods.\p=m-\Duringthe period 1984 to 1988, 10 Saudi infants and young children (six boys and four girls) aged between 8 and 48 months were seen at the King Fahad National Guard Hospital in Riyadh, Saudi Arabia, for lead encephalopathy. Blood samples were drawn in a lead-free vacutainer containing sodium heparin for lead determina¬ tions and ethylenediaminetetraacetic acid

Encephalopathy*

Data

CSF

I-

Hb, g/L

80

MCV, MCH, RDW, fL

pg

74

22

%

Ret, xlO"3

BS

110

+

Pb Lines

Protein,

g/L

Outcome

1.61

Survived with

sequelae

seizures,

coma, anemia

2/F/24

Vomiting,

13.25

24.78

91

74

23

40

Died

5.00

46.70

76

58

14

50

Survived

3.40

8.50

88

70

22.6

30

+

0.80

Survived

12.20

18.22

95

81

25

20

+

2.08

Survived

3.40

18.40

76

69

22

70

+

1.61

Survived

6.90

15.12

85

70

22

18.3

30

+

1.54

Died

6.40

28.32

87

68

21

27.7

20

+

2.50

10.04

110

66

22

19.1

30

+

3.00

14.56

86

60

19



50

+

seizures, coma, anemia

3/M/14

Vomiting,

seizures,

fever, 4/M/15

anemia

Vomiting,

seizures,

irritability,

anemia 5/F/9

Vomiting,

seizures, anemia

6/M/13

Vomiting,

seizures, coma, anemia

7/F/12

Vomiting,

seizures, coma, anemia

8/M/8

Vomiting,

Survived

seizures, coma, anemia

9/F/48

Vomiting,

1.85

Survived

seizures, anemia

10/M/1Í

Seizures,

Survived

anemia *FEP indicates free erythrocyte protoporphyrin; Hb, hemoglobin; MCV, mean corpuscular volume; MCH, mean corpuscular hemoglobin; RDW, red blood cell distribution width; Ret, reticulocyte; BS, basophilic stippling; Pb, lead; CSF, cerebrospinal fluid; plus sign, positive; and minus sign,

negative.

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0.45±0.28. Coarse

pling

The effect of chelation

therapy on

free

eryth¬

rocyte protoporphyrin (FEP; line with squares) and lead levels (lines with circles) in three pa¬ tients. For both lead and FEP

values, day 1 represents pretreatment values; day 5, posttreatment

values.

for hématologie study and free erythrocyte protoporphyrin (FEP) values. The blood lead level was determined using atomic ab¬ sorption spectrophotometry (model 703 equipped with a graphite furnace and HGA-600 programmer, Perldn Elmer Ine, Norwalk, Conn).6 All glassware was washed with acid and with deionized wa¬ ter, and the reagents were kept in airtight containers. Free erythocyte protoporphy¬ rin levels were estimated using the method of Lonola et al.7 Cerebrospinal fluid protein was estimated with the Astra Automated

stat/routine system analyzer (Beckman In¬

Ine, Fullerton, Calif). Results.—The clinical symptoms and laboratory findings for the 10 pa¬ tients are presented in the Table. Their mean (±SD) age was 18±12 months (range, 8 to 48 months). The mean blood lead level in this group was 6.10±3.75 µ /L (range, 2.50 to 13.25 µ /L). Mean FEP levels were 21.00±11.12 µ /L (range, 8.50 to 46.70 µ /L). Anemia was ob¬ served in all (mean hemoglobin level, 87±10 g/L). Hypochromasia and microcytosis were noticed in all but one. This finding probably reflects an iron deficiency-associated anemia. Mea¬ surement of red blood cell distribu¬ tion width in four children showed all values to be higher than normal, which may also reflect the associated iron deficiency, the reticulocytosis, or both. Mean reticulocyte count was strument

basophilic stip¬

observed in nine of 10 infants, lead lines in six, and elevated cerebrospinal fluid protein values (mean, 1.58±0.43 g/L) in all six pa¬ tients who underwent lumbar punc¬ ture; pleocytosis was seen in none. Three children presented with clin¬ ical, biochemical, and radiological findings consistent with rickets, in the absence of nutritional deficiency or lack of exposure to sunlight. One child developed moderate hyperuricemia. The source of lead was the same in all but one patient: an orange granular powder known as Farouk with a lead content of 2310 ppm and other ele¬ ments such as potassium, calcium, and magnesium in variable proportions. This powder is usually used for rub¬ bing the gums of children in an attempt to enhance teeth eruption. One infant was allowed to inhale lead-containing fumes (Galena) in a practice referred to as Bakhoor, in¬ tended to chase the devils and cure various illnesses. Al Kohol is a cos¬ metic powder, black or gray, found to have a high lead content (5% to 92%), used as eye mascara or as an astrin¬ gent applied to the umbilical cord stump of the newborn. Bint Al Zahab (lead content, 82.5%) is used to treat colic. Such products are freely avail¬ able in the market in this part of the world and were identified as a source of poisoning in infants and children. Children with encephalopathy were treated with a 5-day course of dimercaprol (2,3-dimercapto-lpropanol) (British Anti-Lewisite, Beeton Dickinson Microbiology Systems, Cockeysville, Md) and calcium disodium ethylenediaminetetraacetic acid. Four milligrams per kilogram of British Anti-Lewisite was given intra¬ muscularly every 4 hours, and 70 mg/kg of ethylenediaminetetraacetic acid per day was given in doses ad¬ ministered every 4 hours.8 Intrave¬ nous diazepam was the anticonvul¬ sant of choice in most cases (0.1 to 0.15 was

mg/kg). Paraldehyde was occasion¬ ally administered rectally, intrave¬ nously, or intramuscularly for intrac¬ table seizures (300 mg/kg rectally and 150 mg/kg through other routes).

Two (20%) of our 10 infants died. One of the eight survivors was left with apparent neurological sequelae and seven survive with no gross neurological or mental deficits at the time of this writing. A similar death

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incidence (25%) was reported from Kuwait among children with enceph¬ alopathy caused by liberal use of Ko¬ hol.4 The Figure illustrates the FEP and lead values before and after chelation therapy in three of our 10 patients. Blood lead level was noted to drop rapidly after therapy, unlike the FEP level, which reacted in a variable and unpredictable manner. Comment.—Lead encephalopathy is a serious and potentially fatal pe¬ diatrie emergency. Several reports910 have shown that the incidence of this condition in the Western world has significantly decreased. This is not the case, however, in many of the Third World countries. Prior to 1960, a blood lead level of 2.90 µ / L was not considered dangerous; in 1975, a level of 1.45 µ /L was designated by the Centers for Disease Control (Atlanta, Ga) as one that required treatment. This was further reduced to 1.20 µ /L11 in 1985, and to 0.50

µ

/L

in

a

report

in

1991,u

as a

threshold level for lead poisoning. In most of our patients, the body lead burden was relatively high, consis¬ tent with the levels reported to cause encephalopathy.13 Two of our pa¬ tients, however, displayed their symptoms at levels of 2.50 and 3.00 µ /L. These low values may be due to the method used in our labo¬ ratories to measure lead levels. When inorganic standards are used, values for lead in blood will be systemically low. This probably indicates that all values in the 10 patients were underestimated. In conclusion, our study, as well as several other reports from the Middle East, were able to show that lead poi¬ soning continues to represent a major public health hazard to a certain seg¬ ment of the population that is at risk. The main victims in all the studies were infants and young children who received home-made medications and cosmetic agents. Until preventive measures become fully effective in eradicating all practices resulting in lead poisoning in children, physi¬ cians should be suspicious when faced with intractable seizures, unex¬

plained rickets, or hyperuricemia, es¬ pecially when associated with anemia or basophilic stippling. Eliminating predisposing factors, removal of lead from the environment, and identify¬ ing and treating individuals at risk before neurologic symptoms develop

expected to decrease morbidity and death from lead poisoning. HASSAN M. YAISH, MD Pediatric Hematology/ are

Oncology Department of Pediatrics Henry Ford Hospital, K-13

2799 W Grand Blvd Detroit, MI 48202 GULZAR A. NIAZI, PHD Department of Medical Education ABDULLAH AL SOBY, MBBCH Department of Pediatrics King Fahad National Guard

Hospital

PO Box 22490 Riyadh 11426 Saudi Arabia 1. Fernando NF, Healy MA, Aslam M, Davis SS, Hussein A. Lead poisoning and traditional practices: the consequences for world health\p=m-\astudy in Kuwait. Public Health. 1981;95:250-260. 2. Needleman HL. The persistent threat of lead: medical and sociological issues. Curr Probl

Pediatr. 1988;18:702-744. 3. Ali AR, Smales ORC, Aslam M. Surma and lead poisoning. BMJ. 1978;2:915-916. 4. Shaltout A, Yaish SA, Fernando N. Lead encephalopathy in infants in Kuwait. Ann Trop Pediatr. 1981;1:209-215. 5. Rahman H, Al-Khayat A, Menon N. Lead poisoning in infancy: unusual causes in the UAE. Ann Trop Pediatr. 1986;6:213-217. 6. Baselt RC. Analytical Procedures for Therapeutic Drug Monitoring and Emergency Toxicology. Davis, Calif: Biochemical Publications; 1980. 7. Lonola AA, Joselow M, Tamane T. Zinc protoporphyrin: a sensitive fluormetric screening test for lead poisoning. Clin Chem. 1975;21:23-28. 8. Piomelli S, Rosen JF, Chisolm J Jr, Graef W. Management of childhood lead poisoning. J Pediatr. 1984;105:523-532. 9. Working Party on Lead in the Environment, Department of Health and Social Security. Lead and Health. London, England: Her Majesty Sta-

tionery Office;

1980. 10. Centers for Disease Control. Preventing Lead Poisoning in Young Children. Atlanta, Ga: Centers for Disease Control, US Dept of Health and Human Services; 1978. 11. Centers for Disease Control. Preventing Lead Poisoning in Young Children. Atlanta, Ga: Centers for Disease Control, US Dept of Health and Human Services; 1985. Publication 99-2230. 12. Rhein R. US lowers lead limits. BMJ.

1991;303:943. 13. Selbert SM, Henretig FM, Pearce J. Lead encephalopathy. Clin Pediatr. 1985;24:280-285.

Lead Poisoning in Young Children in Washington, DC: A Crisis That Remains to Be Addressed Sir.\p=m-\TheCenters for Disease Control, Atlanta, Ga, have recently lowered the

acceptable blood lead concentration in young children from 1.20 \g=m\mol/ Lor less to 0.50 \g=m\mol/L or less.1 Lead values of 0.50 to 1.20 \g=m\mol/L have

been shown to be associated with decreased intelligence and impaired neurobehavioral development.2,3 Specific social and medical interventions are now deemed necessary in this lead concentration range for exposed children.1 Although the incidence of toxic levels of lead in young children, using the new criteria, is not well established, it is expected to have a sigSee also pp 1257, 1275, and 1278.

nificant

munity.

impact In

on

the medical

com-

addition, federal, state,

and local health care resources will be adversely affected. In this report, we describe the incidence of lead poisoning in 2837 young inner-city children from the General Pediatric Ambulatory Clinic at Children's Hospital in Washington, DC. Materials and Methods.\p=m-\Intravenous blood specimens were randomly studied for lead concentrations from 2837 young children aged 9 months to 3 years, as part of the physical examination in our outpa¬ tient clinic. We also determined free eryth¬

rocyte protoporphyrin (FEP)

centration (r=.16). Only slightly better correlation was seen for lead concen¬ trations of 1.20 µ /L or higher

(r=A7).

Comment.—Our findings confirm those of others regarding the lack of usefulnessofFEPasa screening test for lead concentration between 0.50 and 1.20 µ /L.4·5 In our survey, 547 pa¬ tients (19.3%) had lead concentrations between 0.50 and 1.15 µ /L. This is a significant number of new patients requiring medical and /or social inter¬ vention on the part of an already stressed health care system. At the present time, the Lead Poisoning Pre¬ vention Program of the District of Co¬ lumbia Commission of Public Health intervenes only when children have a blood lead concentration of 0.96

µ /L or higher. Therefore, our study indicates that 502 (85%) of 590 children with lead poisoning will not receive adequate intervention. Clearly, additional resources are needed to deal with this medical crisis. NADER RIFAI, PHD

CHRISTINE FASER, MD GEORGE COHEN, MD

concentra¬

MURIEL WOLF, MD Louis DEPALMA, MD The George Washington University Medical Center Children's National Medical Center 111 Michigan Ave NW Washington, DC 20010

tions in these

patients to investigate their usefulness as predictors of blood lead values below 1.20 µ /L. Blood lead and FEP concentrations were determined with atomic absorption spectrometry and fluo-

rometry, respectively. Results.—Of the samples studied, 590 (20.8%) had lead concentrations of 0.50 µ /L or more, of which only 43 (1.5%) had lead values of 1.20

µ /L or more. All subjects were divided into subgroups as deter¬ mined by magnitude of blood lead concentration (Table). In addition, these subgroups were correlated with FEP results. For lead values higher than or equal to 0.50 µ /L but lower than 1.20 µ / there was a very poor correlation with FEP conBlood Lead and Free

1. Centers for Disease Control. Preventing Poisoning in Young Children. Atlanta, Ga: Department of Health and Human Services, Centers for Disease Control; 1991. 2. Davis JM, Svendsgaard DJ. Lead and child

Lead

development.

Nature. 1987;329:297-300. 3. Mushak P, Davis JM, Crochetti AF, Grant LD. Prenatal and postnatal effects of low level

lead exposure: integrated summary of a report to the US Congress on childhood lead poisoning. Environ Res. 1989;50:11-36. 4. Truk DS, Schonfeld DJ, Cullen M, Rainey P. Sensitivity of erythrocyte protoporphyrin as a screening test for lead poisoning. N Engl J Med.

Erythrocyte Protoporphyrin (FEP) Concentrations on Patient Subgroups

Based

Mean±SD

Blood Lead

No. of

Croups, µ /L

Specimens

1.20

43

1.50±0.60

1.34±2.02

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Lead encephalopathy in Saudi Arabian children.

Call for Abstracts The American Pediatric Society, The Society for Pediatric Research, and the Ambulatory Pediatric Association announce that the abst...
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