Scand J Urol Nephrol 12: 189-190. 1978
LEAD POISONING TREATED WITH HAEMODIALYSIS Robert Smith Pedersen From t h e Ikpcirtt?ient c!fNc,phro/ogy. Acilhorg S y g r l i i ~ s9000 . Aulhorg,
1)c~ritirtirL
Scand J Urol Nephrol Downloaded from informahealthcare.com by Queen's University on 01/06/15 For personal use only.
(Submitted for publication January 30. 1977)
A h s t r w t . A 27-year-old woman ingested as an abortifa-
cient 40 grams of litharge (PbO). She was treated with EDTA infusion and haemodialysis. The half-life of lead in the blood was 9 hours during combined haernodialysis and EDTA infusion and 96 hours when EDTA was given alone. Signs and symptoms attributable to acute lead intoxication were mild.
infused in a daily dose of 2 g for 5 days. After a 4-day interval the infusions were resumed. now f o r 6 days with a daily dose of 1.2 g. Using injectable furosemide, the urinary output was maintained at about 2 litres per day. Apart from slight discomfort and colic she felt quite well. She was not pregnant. It1i.e.stigutioti.s
Acute lead intoxication is rare, but is often serious. In a search of the literature Karpathin (1961) found only seven cases published over 20 years. Opinion with regard t o treatment is divided. While some workers (Chisholm, 1968) recommended combined dimercaprol (BAL) and edathamil calcium-disodium (EDTA), Others have considered BAL to the contra-indicated (Moeschlin, 1972). Little experience has been gained of treating lead intoxication with peritoneal dialysis or haemodialysis, Mehbod 1967) reported that t h e amount of lead removed by peritoneal dialysis exceeded the renal excretion of lead and that this difference was increased by use of EDTA. Though combined haemodialysis and EDTA treatment was shown to be effective in vifro, it produced n o demonstrable clinical improvement in lead encephalopathy (Smith, King & Margolin, 1965). The present case is published because the course of lead intoxication was mild. possibly as a result of
Haerno-analysis showed anaemia. which was most severe on the second day but was still present after 7 weeks. During the first week the levels of bilirubin, alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase in the serum were slightly elevated. All values normalized during the second week. The renal function, a s expressed by the serum creatinine level and clearance of "'Cr-EDTA, was normal. Transient proteinuria, maximum 0.9 g/day. was found during an episode of urinary tract infection. During 9 hours of haemodialysis the concentration o f lead in whole blood fell from I360 to 680 pg/l. Ten hours later it was 690 pg/l and after 7 weeks it was only 280 pg/l. In the urine the concentration of lead immedia t e b before haemodialysis was I I 500 d l . Three urine samples collected during haemodialysis contained. respectively,46s0. 4600 and I 650 pg/I (,+, I),
LEAD I N WHOLE5tOOD mcg per l/ter
LEAD rN URINE m g per liter
I
10000
When the infusion of EDTA was interrupted, the mean concentration of lead in the urine over a 4-day period was 510 pg/l. Resumption of EDTA treatment produced a rise to I020 pg/l.
Scand J Urol Nephrol Downloaded from informahealthcare.com by Queen's University on 01/06/15 For personal use only.
DISCUSSION Colic and vomiting occur frequently in lead intoxication (Riedl, 1941; Bastrup-Madsen. 1950; Mellemgaard & Soerensen. 1955). Anaemia is equally frequent (Bastrup-Madsen; Mellemgaard & Soerensen; Wade & Burnum, 1955). Lead has been shown to inhibit the formation of the porphyrin portion of heme in immature rabbit erythrocytes and in mature duck erythrocytes (Erikson, 1955). Acute anaemia may develop after intravenous injection of lead (Brookfield, 1928), Presumably by direct action of lead on erythrocytes (Berk, Tschudy, Shipley, Waggoner & Berlin, 1970). Haemolytic anaemia with appreciable jaundice is rarely seen (Davidson, 1932; Beattie. Briggs, Canovan, Doyle, Mullin & Watson, 1975). Hepatic damage as a rule i s slight (Karpathin), but serious cases after intravenous injection of lead have been described (Beattie et al.). Signs of renal damage are haematuria (Bastrup-Madsen) and proteinuria (Karpathin). Histologic study of the kidneys has shown regeneration of the tubular epithelial cells (Beattie et al.). The proteinuria in the case here reported was caused partly by infection in the urinary tract. Since the lead concentration in the dialysis bath was not measured. the amount of lead removed by haemodialysis is not known. In in l i t r o experiments (Smith et al.) lead clearance was 31 ml/min. During haemodialysis the concentration of lead in the blood halved over 9 hours. When haemodialysis was terminated but EDTA infusion continued, the half-life of lead in the blood was 96 hours. The reason for this great difference may be partly that the lead moved, in the initial phase of the intoxica-
Suitid
J Urol Nephrol I 2
tion. from the blood to depots from which it was later released. During the second period of EDTA treatment, release of lead from depots led to doubling of the lead concentration in the urine. A depot effect alone, however. could scarcely explain the great difference in the half-life of lead in the blood. Haemodialysis seemed to be effective therapy. REFERENCES Bastrup-Madsen. P. 1950. Dimercaprol in acute lead poisoning. Loricer ii, 17 I . Beattie, A. D.. Briggs, J . D., Canovan, J . S . F., Doyle. D.. Mullin, P. J . &Watson. A. A. 1975. Acute lead poisoning. Q J M e d 174. 275. Berk, P. D.. Tschudy. D. P.. Shipley. L. A , , Waggoner. J . G. & Berlin, N . 1. 1970. Hematologic and biochemical studies in a case of lead poisoning. A m e r J M c c l 4 8 . 137. Brookfield, R. W. 1928. Blood changes occuring during the course of treatment of malignant disease by lead with special reference to punctate basophilia and the platelets. J Puih Bnct 31. 277. Chisholm. J . J. 1968. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood.JPediutr73. 1. Davidson. L. S. P. 1932. Macrocytic haemolytic anaemia. Q J M e d I . 543. Erikson, L. 1955. Lead intoxication. I . The effect of lead on the in vitro biosynthesis of heme and free erythrocyte porphyrins. Scund J Cliri Lnh In\$est 7. 80. Karpathin. S. 1961. Lead poisoning after taking Pb Acetate with suicidal intent. Arch /%\'iron Hecrlth 2 . 679. Mehbod, H . 1967. Treatment of lead intoxication. J A M A 201, 152.
Mellemgaard. K. & Soerensen. G. 19.55. A case of acute lead poisoning treated with ethylenediamine tetraacetate. Ugeskr Laegr 117, 177. Moeschlin, S. 1972. Lead (Pb). In: Klinik rtncl Tliercrpic, der Vergifrrtngen, 7th edition. pp. 3654. Georg Thieme Verlag. Stuttgart. Riedl, L. 1941. An unusual case of lead intoxication. Wieri Me11 Wschr 91, 697. Smith, H. D.. King. L. & Margolin. E. G. 1965. Treatment of lead encephalopathy. A m J Dis Child 109. 327. Wade. J . F. & Burnum, J . F. 1955. Treatment of acute and chronic lead poisoning with disodium calcium versenate. Ann Intern M e d 4 2 . 25 I .
LEAD POISONING TREATED WITH HAEMODIALYSIS Robert Smith Pedersen From t h e Ikpcirtt?ient c!fNc,phro/ogy. Acilhorg S y g r l i i ~ s9000 . Aulhorg,
1)c~ritirtirL
Scand J Urol Nephrol Downloaded from informahealthcare.com by Queen's University on 01/06/15 For personal use only.
(Submitted for publication January 30. 1977)
A h s t r w t . A 27-year-old woman ingested as an abortifa-
cient 40 grams of litharge (PbO). She was treated with EDTA infusion and haemodialysis. The half-life of lead in the blood was 9 hours during combined haernodialysis and EDTA infusion and 96 hours when EDTA was given alone. Signs and symptoms attributable to acute lead intoxication were mild.
infused in a daily dose of 2 g for 5 days. After a 4-day interval the infusions were resumed. now f o r 6 days with a daily dose of 1.2 g. Using injectable furosemide, the urinary output was maintained at about 2 litres per day. Apart from slight discomfort and colic she felt quite well. She was not pregnant. It1i.e.stigutioti.s
Acute lead intoxication is rare, but is often serious. In a search of the literature Karpathin (1961) found only seven cases published over 20 years. Opinion with regard t o treatment is divided. While some workers (Chisholm, 1968) recommended combined dimercaprol (BAL) and edathamil calcium-disodium (EDTA), Others have considered BAL to the contra-indicated (Moeschlin, 1972). Little experience has been gained of treating lead intoxication with peritoneal dialysis or haemodialysis, Mehbod 1967) reported that t h e amount of lead removed by peritoneal dialysis exceeded the renal excretion of lead and that this difference was increased by use of EDTA. Though combined haemodialysis and EDTA treatment was shown to be effective in vifro, it produced n o demonstrable clinical improvement in lead encephalopathy (Smith, King & Margolin, 1965). The present case is published because the course of lead intoxication was mild. possibly as a result of
Haerno-analysis showed anaemia. which was most severe on the second day but was still present after 7 weeks. During the first week the levels of bilirubin, alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase in the serum were slightly elevated. All values normalized during the second week. The renal function, a s expressed by the serum creatinine level and clearance of "'Cr-EDTA, was normal. Transient proteinuria, maximum 0.9 g/day. was found during an episode of urinary tract infection. During 9 hours of haemodialysis the concentration o f lead in whole blood fell from I360 to 680 pg/l. Ten hours later it was 690 pg/l and after 7 weeks it was only 280 pg/l. In the urine the concentration of lead immedia t e b before haemodialysis was I I 500 d l . Three urine samples collected during haemodialysis contained. respectively,46s0. 4600 and I 650 pg/I (,+, I),
LEAD I N WHOLE5tOOD mcg per l/ter
LEAD rN URINE m g per liter
I
10000
When the infusion of EDTA was interrupted, the mean concentration of lead in the urine over a 4-day period was 510 pg/l. Resumption of EDTA treatment produced a rise to I020 pg/l.
Scand J Urol Nephrol Downloaded from informahealthcare.com by Queen's University on 01/06/15 For personal use only.
DISCUSSION Colic and vomiting occur frequently in lead intoxication (Riedl, 1941; Bastrup-Madsen. 1950; Mellemgaard & Soerensen. 1955). Anaemia is equally frequent (Bastrup-Madsen; Mellemgaard & Soerensen; Wade & Burnum, 1955). Lead has been shown to inhibit the formation of the porphyrin portion of heme in immature rabbit erythrocytes and in mature duck erythrocytes (Erikson, 1955). Acute anaemia may develop after intravenous injection of lead (Brookfield, 1928), Presumably by direct action of lead on erythrocytes (Berk, Tschudy, Shipley, Waggoner & Berlin, 1970). Haemolytic anaemia with appreciable jaundice is rarely seen (Davidson, 1932; Beattie. Briggs, Canovan, Doyle, Mullin & Watson, 1975). Hepatic damage as a rule i s slight (Karpathin), but serious cases after intravenous injection of lead have been described (Beattie et al.). Signs of renal damage are haematuria (Bastrup-Madsen) and proteinuria (Karpathin). Histologic study of the kidneys has shown regeneration of the tubular epithelial cells (Beattie et al.). The proteinuria in the case here reported was caused partly by infection in the urinary tract. Since the lead concentration in the dialysis bath was not measured. the amount of lead removed by haemodialysis is not known. In in l i t r o experiments (Smith et al.) lead clearance was 31 ml/min. During haemodialysis the concentration of lead in the blood halved over 9 hours. When haemodialysis was terminated but EDTA infusion continued, the half-life of lead in the blood was 96 hours. The reason for this great difference may be partly that the lead moved, in the initial phase of the intoxica-
Suitid
J Urol Nephrol I 2
tion. from the blood to depots from which it was later released. During the second period of EDTA treatment, release of lead from depots led to doubling of the lead concentration in the urine. A depot effect alone, however. could scarcely explain the great difference in the half-life of lead in the blood. Haemodialysis seemed to be effective therapy. REFERENCES Bastrup-Madsen. P. 1950. Dimercaprol in acute lead poisoning. Loricer ii, 17 I . Beattie, A. D.. Briggs, J . D., Canovan, J . S . F., Doyle. D.. Mullin, P. J . &Watson. A. A. 1975. Acute lead poisoning. Q J M e d 174. 275. Berk, P. D.. Tschudy. D. P.. Shipley. L. A , , Waggoner. J . G. & Berlin, N . 1. 1970. Hematologic and biochemical studies in a case of lead poisoning. A m e r J M c c l 4 8 . 137. Brookfield, R. W. 1928. Blood changes occuring during the course of treatment of malignant disease by lead with special reference to punctate basophilia and the platelets. J Puih Bnct 31. 277. Chisholm. J . J. 1968. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood.JPediutr73. 1. Davidson. L. S. P. 1932. Macrocytic haemolytic anaemia. Q J M e d I . 543. Erikson, L. 1955. Lead intoxication. I . The effect of lead on the in vitro biosynthesis of heme and free erythrocyte porphyrins. Scund J Cliri Lnh In\$est 7. 80. Karpathin. S. 1961. Lead poisoning after taking Pb Acetate with suicidal intent. Arch /%\'iron Hecrlth 2 . 679. Mehbod, H . 1967. Treatment of lead intoxication. J A M A 201, 152.
Mellemgaard. K. & Soerensen. G. 19.55. A case of acute lead poisoning treated with ethylenediamine tetraacetate. Ugeskr Laegr 117, 177. Moeschlin, S. 1972. Lead (Pb). In: Klinik rtncl Tliercrpic, der Vergifrrtngen, 7th edition. pp. 3654. Georg Thieme Verlag. Stuttgart. Riedl, L. 1941. An unusual case of lead intoxication. Wieri Me11 Wschr 91, 697. Smith, H. D.. King. L. & Margolin. E. G. 1965. Treatment of lead encephalopathy. A m J Dis Child 109. 327. Wade. J . F. & Burnum, J . F. 1955. Treatment of acute and chronic lead poisoning with disodium calcium versenate. Ann Intern M e d 4 2 . 25 I .
