TREATMENT OF LEAD ENCEPHALOPATHY WITH BAL (2.3-DIMERCAPTOPROPANOL)

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Abstract
BAL is apparently effective in lowering the mortality rate in children with severe lead encephalopathy. The severity of the residua of severe lead encephalopathy may also be reduced by BAL treatment. No conclusive effects of therapy could be demonstrated in subacute mild cases of lead encephalopathy. The toxic effects of BAL in this series have been limited to nausea and vomiting which were never severe enough to contraindicate continuation of treatment. There was no evidence of exacerbation of symptoms in mild cases of lead poisoning treated with BAL. As has previously been shown, BAL administration increases the urinary excretion of lead for a limited time, and this effect can be repeated in the same patient after an interval. The concentrations of lead in blood fall spontaneously following removal of children with lead poisoning from their source of exposure by admission to the hospital. The rate of decrease in blood lead is not influenced by BAL administration. The case histories of nine patients with severe lead encephalopathy treated with BAL are summarized below: Case No. 1: J. B., a 3 yr. old Negro girl, was admitted to BCH. She began to sit up at 8 mo. of age, walked at 11 mo. and talked in sentences at 1½ yr. For some time before admission, she had been seen to eat paint off the wall at home. Three weeks before admission, she had rubella, and 4 days before admission began to have fever and persistent vomiting, became drowsy and remained so until admission. On admission she did not respond to ordinary stimuli. When a lumbar puncture was performed, she had a convulsion which persisted for some minutes, after which she became comatose and remained so for 4 days. Physical examination: she was seen to have a stiff neck, papilledema, and weakness of the left arm and leg. Laboratory examinations revealed albuminuria, glycosuria, and anemia with basophilic stippling of the erythrocytes. Blood lead concentration was 0.15 mg./100 gm. blood. Cerebrospinal fluid protein was 78 mg./100 cc. Roentgenogram of long bones revealed a dense line at the metaphyseal ends. BAL treatment was begun shortly after admission and continued for 10 days. On the 5th day, she began to respond to stimuli, and a bilateral squint was noted at this time. On the 6th day, she was able to take fluids by mouth. Until about the 14th day, it was thought that she could not see but at the time of discharge, 21 days after admission, she had apparently recovered except for a residual weakness of the left leg, and VI and VII left cranial nerve pareses. Eight months after discharge, the left leg paresis was no longer detectable, but slight left facial weakness was still present. She had developed frequent convulsive seizures which were controlled by phenobarbital as long as it was continued. She was not seen again for 3 yr., at which time she had had 3 convulsions which occurred 3 mo. after phenobarbital had been discontinued. She is still a severe behavior problem, hyperactive, restless and distractible. She appears duller than her age of 6 yr., but is physically normal except for a slight left facial paralysis. She was placed on anticonvulsant therapy and has had no further convulsions. Psychometric examination revealed an I.Q. of 62. Case No. 2: N.D., a 2 yr. old white girl, was admitted to HLH. For the year prior to admission, she had been eating paint from the walls. For 1 wk. prior to admission, she had been vomiting and was anorexic. Three hours before admission, she developed severe generalized convulsions which continued up to admission, following which she lapsed into coma. Physical examination revealed a comatose child with a right-sided hemiplegia, who was slightly dehydrated. Laboratory examination revealed slight albuminuria, glycosuria, hematuria and casts in the urine. Hgb. was 8 gm./100 cc. blood, and there was basophilic stippling of the erythrocytes. Blood lead concentration was 0.33 mg./ 100 gm. blood. Cerebrospinal fluid protein was 81 mg./l00 cc., and there were 11 lymphocytes/cmm. Roentgenograms of long bones revealed evidences of heavy metal deposition. She remained comatose throughout her hospitalization. Twenty-four hours after admission, BAL therapy was begun without any change in her condition, and she died on the 3rd hospital day. Case No. 3: A. S., an 18 mo. old Negro girl, was admitted to BCH with a severe left-sided convulsion. She had walked and said a few words at 1 yr. For 5 mo. prior to admission, she had been in the habit of going to the window sill and chewing paint off the wood. For 1 mo. before admission, she had been vomiting intermittently. Four days prior to admission, she became fretful, listless and anorexic, and was vomiting forcefully after each feeding. On the day of admission, she was taken to the HLH Dispensary and while waiting to be seen had a severe left-sided convulsion, which lasted 10 mm. and recurred shortly afterwards. She was admitted to BCH in this condition. Laboratory examination on admission revealed the following: Urine was normal, Hgb. was 8.0 gm./100 cc. blood, RBC count 4.7 million/cmm., WBC count was 12.4 thousand/cmm., and basophilic stippling of the erythrocytes was noted. Cerebrospinal fluid pressure was 310 mm. H2O, and the fluid contained protein 105 mg./100 cc. and 66 lymphocytes/cmm. Blood lead concentration was 0.21 mg./100 gm. blood. Roentgenograms of long bones revealed changes consistent with a diagnosis of lead deposition (Fig. 2). On admission she was placed on BAL therapy. Subsequent blood and urine lead determinations are shown in chart 2. For 3 days after admission, she continued to convulse in spite of large doses of [SEE FIG. 2. IN SOURCE PDF]anticonvulsant drugs, and thereafter she was semicomatose until the 5th day when she began to recognize people, and she then improved throughout the remainder of her hospital stay. At the time of her discharge 1 mo. later, she appeared well except for left hemi-paresis. Since discharge she has...
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