CASE REPORT SUBACUTE LEAD POISONING IN A HEIFER B. R. BLAKLEY*
Introduction Treatment Lead poisoning is one of the most common On June 5, calcium disodium edetate2 was toxicoses encountered in farm animals (10). given intravenously at 110 mg/kg and reIt has been reported in several species includ- peated six hours later. In addition, 225 g of ingthe horse (6, 9), cat (13), pig (11), sheep magnesium sulfate3 mixed with 14 litres of (1), dog (17), guinea pig (4) and avian spe- water was given orally. On June 6 and 7, the cies such as waterfowl (15). Lead toxicosis is same treatment was repeated. By June 7, the often encountered in adult cattle raised on fecal material contained copious quantities of pasture (2, 13). oil. On June 8, 225 g of MgSO4 and 14 litres of water were given orally again. The animal History and Clinical Findings was anorexic from admission and since little On June 5, 1974 a 700 pound, 15 month old improvement could be noticed by June 11, Holstein heifer was admitted into the Large Ani- the rumen was lavaged to remove oil persistmal Clinic, Western College of Veterinary Medi- ing in the rumen. In addition, 14 litres of cine. The owner reported that he had found the water and 180 ml of 10% dioctol sodium sulfoanimal separated from the herd containing succinate were given orally. On June 12, the about 18 cattle of various ages. The pasture animal received 225 g of MgSO4 and 14 litres contained a large number of old cars, various of Ringers solution orally, plus 4 litres of debris and two 45 gallon drums of used crank- rumen fluid from a fistulated steer. Increased case oil. Upon admission, the animal was lung sounds were detected over the ventral clinically weak, depressed and moderately de- areas of the lungs. Penicillin procaine G was hydrated. It exhibited head pressing, excess administered intramuscularly at a dosage of salivation, grinding of teeth and rumen stasis. 5000 IU/kg. On June 16, the animal still had The heifer was reluctant to move and would not improved clinically, therefore, it was killed stand motionless for long periods. When forced and submitted for post mortem examination. to move, it had a stiff gait. The menace reflex was depressed upon admission and absent by the second day. The oculomotor and palpebral Pathology There was marked emaciation of the entire reflexes were slightly depressed. Rectal temperature, respiratory and heart rates were animal. The anterior lobes and lower half of within the normal range. A tentative diagnosis the diaphragmatic lobes of the lungs were of lead poisoning was made and treatment gangrenous. The upper diaphragmatic lobes were edematous. The digestive tract contained initiated. only scant quantities of ingesta. It had an odor of oil with droplets of oil present in the Laboratory Findings and Diagnosis Blood samples taken for hematology and ingesta. The kidneys were hyperemic. The serum electrolytes were within normal limits. brain had malacic areas at the tips of the Urinalysis revealed a specific gravity of 1.048, cerebral gyri. Histopathological examination of the kidney a pH of 6.0 and a trace of ketones. Initial revealed glomerular edema and tubular neblood and fecal lead levels of 0.60 ppm and 790 ppm respectively confirmed the diagnosis phrosis. In the brain, perivascular edema was of lead poisoning. Thereafter blood, fecal (Fig- present and in the malacic areas there were ure 1) and rumen samples (Figure 2) were gliosis and neuronal degeneration. Chemical analysis of the liver and the kidcollected daily six days and analyzed for lead' ney cortex for lead revealed levels of 22.1 to ascertain the response to treatment. ppm (wet weight) and 24.5 ppm respectively. *Veterinary Physiological Sciences, Western A diagnosis of lead toxicity and gangrenous of
College Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N OWO. lLaboratory Section 66, Report #5 of the Consolidated Mining and Smelting Company of Can-
2Havidote, Haver-Lockhart Laboratories, Calgary, Alberta. 3Anachemia Chemicals Ltd., Lachine, Quebec.
ada Ltd., 1967.
[11 CAN. VET. JOUR., vol. 17, no. 12, December, 1976
-X
CANADIAN VETERINARY JOURNAL .72g
disodium edetate forms a complex with lead and is excreted as a non-toxic and nonionizable disodium salt (9). Continued treatment .56 after the first day produced only a slight re.48 duction in the blood lead concentration. This zE .40 apparent refractory level may be overcome by 01 32 using intermittent dosages (6). However, the blood levels in this animal (Figure 1) show ° 24 evidence of a refractory period in spite of the ? .16 intermittent treatment with calcium disodium .08 edetate. An ante mortem diagnosis of lead poisoning 6 10 11 7 8 June S 9 can be best confirmed by determination of FiGuRE 1. Blood lead levels during the course lead levels in the blood (19). Hatch and Funof treatment. nell (8) state that the kidney is the most reliable post mortem specimen. 1800 The most prominent gross pathology lesions Rumen and Fecol Leod Concentrations 1600 involve the digestive system (evidence of oil) Rumen teod levels Fecal lead levels and malacic areas in the brain. Christian and 1400 Tryphonas (3) have shown that these malacic 1200 areas are confined to the tips of the cerebral 0 in1000 gyri. Degenerative changes seen on a histological level involve liver, kidney and brain. ° 800 s Inclusion bodies are common in the liver and 600 kidney (14). Tubular nephrosis was seen in X \x\~~~~~~~~~~~~~ L' 400 the kidney, which was consistent with the findings of Zook et al (17) and Wilson and -"'200 Lewis (16) in dog. Centrilobular necrosis may be seen in the liver (16). Segmental demyeliJune 5 6 7 8 11 9 10 nation and axonal degeneration has been reFIGURE 2. Rumen and fecal lead levels during ported by Fullerton (4). Other body systems the course of treatment. or components affected include chromosomes (12) mitochondria (5), hemopoetic (18) and aspiration pneumonia was made at post mor- Ca/P balance (11). tem examination. The gangrenous aspiration pneumonia which occurred is a plausible sequel in an animal Discussion with impaired nervous control, especially the The signs exhibited by the animal were typ- swallowing reflexes. This may have contributed ical for the subacute syndroms (2). Blood and to the aspiration of rumen contents resulting Henderson (2) report that muscular tremors in an aspiration pneumonia and a grave progand hyperesthesia are not uncommon. How- nosis. ever, these particular signs were absent in this animal. Moderate success has been achieved using Summary A case of subacute lead poisoning due to calcium disodium edetate to treat lead toxiingestion of used crankcase oil in a 15 month coses (9). Hammond and Sorensen (7) obtained favourable recovery rates with this anti- old Holstein heifer is described. Clinical and dote after about five to 16 days of treatment. laboratory findings, treatment, response and Secondary complications (aspiration pneu- gross and histopathology are presented. monia) may have prevented recovery in this case. Lead levels in the rumen dropped ra- Resume pidly during the treatment (Figure 2). After L'auteur decrit un cas d'empoisonnement the lavage, the rumen levels were low. Fecal subaigu par le plomb, chez une taure Holstein concentrations initially increased following ag6e de 15 mois qui avait ingere de la vieille treatment. This was probably due to passage de l'huile 'a moteur. Il presente aussi les obof the lead contaminated rumen contents down servations clniques de ce cas, les resultats the gastrointestinal tract. The blood levels d'epreuves de laboratoire, la r6ponse au traiteshowed a dramatic drop on the first day of ment, ainsi que les l6sions macroscopiques et treatment from 0.61 to 0.37 ppm. Calcium histologiques. .64
E
Blood Leod Concentration
\
c
-0
o-
-
c
a,
.
312
LEAD POISONING
Acknowledgments The assistance of Dr. D. L. Hamilton and Dr. C. S. Sisodia is gratefully appreciated.
References 1. ALLCROFT, R. Lead poisoning in cattle and sheep. Vet. Rec. 63: 583-590. 1951. 2. BLOOD, D. C. and J. A. HENDERSON. Veterinary Medicine, 3rd Edition. pp. 759-764. London: Bailliere, Tindall & Cassell. 1968. 3. CHRISTIAN, R. G. and L. TRYPHONAS. Lead poisoning in cattle. Brain lesions and hematologic changes. Am. J. vet. Res. 32: 203-215. 1971. 4. FULLERTON, P. M. Chronic peripheral neuropathology produced by lead poisoning in guinea-pigs. J. Neuropath. exp. Neurol. 25: 214-236. 1966. 5. GOYER, R. A. and R. KRALL. Ultrastructural transformation in mitochondria isolated from kidneys of normal and lead intoxicated rats. J. Cell. Biol. 41: 393-400. 1969. 6. HAMMOND, P.B. and A. L. ARONSON. Lead poisoning in cattle and horses in the vicinity of a smelter. Ann. N.Y. Acad. Sci. 111: 595611. 1964. 7. HAMMOND, P. B. and D. K. SORENSEN. Recent observations on the course and treatment of bovine lead poisoning. J. Am. vet. med. Ass. 130: 23-25. 1967. 8. HATCH, R. C. and H. S. FUNNELL. Lead levels in tissues and stomach contents of poisoned cattle: A fifteen-year survey. Can. vet. J. 10: 258-262. 1972. 9. HOLM, L. W., J. D. WHEAT, E. A. RHODE and G. FIRCH. The treatment of chronic lead poisoning in horses with calcium di-
313
sodium ethylene diaminetetraacetate. J. Am. vet. med. Ass. 123: 383-388. 1953.
10. JUBB, K. V. F. and P. C. KENNEDY. Pathology of Domestic Animals. Vol. 2, 2nd Edition. pp. 388-391. New York: Academic Press. 1970. 11. LINK, R. P. and R. R. PENSINGER. Lead toxicosis in swine. Am. J. vet. Res. 27: 759763. 1966. 12. MURO, L. A. and R. A. GOYER. Chromosome damage in experimental lead poisoning. Archs Path. 87: 660-663. 1969. 13. PRIESTER, W. A. and H. M. HAYES. Lead poisoning in cattle, horses, cats and hogs as reported by 11 colleges of veterinary medicine in the United States and Canada from July, 1968, through June 1972. Am. J. vet. Res. 35: 567-572. 1974. 14. THOMSON, R. G. Reliability of acid-fast inclusions in the kidneys of cattle as an indication of lead poisoning. Can. vet. J. 13: 88-89. 1972. 15. TRAINER, D. R. and R. A. HuNT. Lead poisoning of waterfowl in Wisconsin. J. Wildl. Mgmt 29: 95-103. 1965. 16. WILSON, M. R. and G. LEWIS. Lead poisoning in dogs. Vet. Rec. 75: 787-791. 1963. 17. ZOOK, B. C., J. L. CARPENTER and E. B. LEEDS. Lead poisoning in dogs. J. Am. vet. med. Ass. 155: 1329-1342. 1969. 18. ZOOK, B. C., J. L. CARPENTER and R. M. ROBERTS. Lead poisoning in dogs. Occurrence, source, clinical pathology, and electroencephalography. Am. J. vet. Res. 33: 891902. 1972. 19. ZOOK, B. C., L. KOPITO, J. L. CARPENTER, D. V. CRAMER and H. SHWACHMAN. Lead poisoning in dogs: Analysis of blood, urine, hair and liver for lead. Am. J. vet. Res. 33: 903-909. 1972.
Introduction Treatment Lead poisoning is one of the most common On June 5, calcium disodium edetate2 was toxicoses encountered in farm animals (10). given intravenously at 110 mg/kg and reIt has been reported in several species includ- peated six hours later. In addition, 225 g of ingthe horse (6, 9), cat (13), pig (11), sheep magnesium sulfate3 mixed with 14 litres of (1), dog (17), guinea pig (4) and avian spe- water was given orally. On June 6 and 7, the cies such as waterfowl (15). Lead toxicosis is same treatment was repeated. By June 7, the often encountered in adult cattle raised on fecal material contained copious quantities of pasture (2, 13). oil. On June 8, 225 g of MgSO4 and 14 litres of water were given orally again. The animal History and Clinical Findings was anorexic from admission and since little On June 5, 1974 a 700 pound, 15 month old improvement could be noticed by June 11, Holstein heifer was admitted into the Large Ani- the rumen was lavaged to remove oil persistmal Clinic, Western College of Veterinary Medi- ing in the rumen. In addition, 14 litres of cine. The owner reported that he had found the water and 180 ml of 10% dioctol sodium sulfoanimal separated from the herd containing succinate were given orally. On June 12, the about 18 cattle of various ages. The pasture animal received 225 g of MgSO4 and 14 litres contained a large number of old cars, various of Ringers solution orally, plus 4 litres of debris and two 45 gallon drums of used crank- rumen fluid from a fistulated steer. Increased case oil. Upon admission, the animal was lung sounds were detected over the ventral clinically weak, depressed and moderately de- areas of the lungs. Penicillin procaine G was hydrated. It exhibited head pressing, excess administered intramuscularly at a dosage of salivation, grinding of teeth and rumen stasis. 5000 IU/kg. On June 16, the animal still had The heifer was reluctant to move and would not improved clinically, therefore, it was killed stand motionless for long periods. When forced and submitted for post mortem examination. to move, it had a stiff gait. The menace reflex was depressed upon admission and absent by the second day. The oculomotor and palpebral Pathology There was marked emaciation of the entire reflexes were slightly depressed. Rectal temperature, respiratory and heart rates were animal. The anterior lobes and lower half of within the normal range. A tentative diagnosis the diaphragmatic lobes of the lungs were of lead poisoning was made and treatment gangrenous. The upper diaphragmatic lobes were edematous. The digestive tract contained initiated. only scant quantities of ingesta. It had an odor of oil with droplets of oil present in the Laboratory Findings and Diagnosis Blood samples taken for hematology and ingesta. The kidneys were hyperemic. The serum electrolytes were within normal limits. brain had malacic areas at the tips of the Urinalysis revealed a specific gravity of 1.048, cerebral gyri. Histopathological examination of the kidney a pH of 6.0 and a trace of ketones. Initial revealed glomerular edema and tubular neblood and fecal lead levels of 0.60 ppm and 790 ppm respectively confirmed the diagnosis phrosis. In the brain, perivascular edema was of lead poisoning. Thereafter blood, fecal (Fig- present and in the malacic areas there were ure 1) and rumen samples (Figure 2) were gliosis and neuronal degeneration. Chemical analysis of the liver and the kidcollected daily six days and analyzed for lead' ney cortex for lead revealed levels of 22.1 to ascertain the response to treatment. ppm (wet weight) and 24.5 ppm respectively. *Veterinary Physiological Sciences, Western A diagnosis of lead toxicity and gangrenous of
College Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N OWO. lLaboratory Section 66, Report #5 of the Consolidated Mining and Smelting Company of Can-
2Havidote, Haver-Lockhart Laboratories, Calgary, Alberta. 3Anachemia Chemicals Ltd., Lachine, Quebec.
ada Ltd., 1967.
[11 CAN. VET. JOUR., vol. 17, no. 12, December, 1976
-X
CANADIAN VETERINARY JOURNAL .72g
disodium edetate forms a complex with lead and is excreted as a non-toxic and nonionizable disodium salt (9). Continued treatment .56 after the first day produced only a slight re.48 duction in the blood lead concentration. This zE .40 apparent refractory level may be overcome by 01 32 using intermittent dosages (6). However, the blood levels in this animal (Figure 1) show ° 24 evidence of a refractory period in spite of the ? .16 intermittent treatment with calcium disodium .08 edetate. An ante mortem diagnosis of lead poisoning 6 10 11 7 8 June S 9 can be best confirmed by determination of FiGuRE 1. Blood lead levels during the course lead levels in the blood (19). Hatch and Funof treatment. nell (8) state that the kidney is the most reliable post mortem specimen. 1800 The most prominent gross pathology lesions Rumen and Fecol Leod Concentrations 1600 involve the digestive system (evidence of oil) Rumen teod levels Fecal lead levels and malacic areas in the brain. Christian and 1400 Tryphonas (3) have shown that these malacic 1200 areas are confined to the tips of the cerebral 0 in1000 gyri. Degenerative changes seen on a histological level involve liver, kidney and brain. ° 800 s Inclusion bodies are common in the liver and 600 kidney (14). Tubular nephrosis was seen in X \x\~~~~~~~~~~~~~ L' 400 the kidney, which was consistent with the findings of Zook et al (17) and Wilson and -"'200 Lewis (16) in dog. Centrilobular necrosis may be seen in the liver (16). Segmental demyeliJune 5 6 7 8 11 9 10 nation and axonal degeneration has been reFIGURE 2. Rumen and fecal lead levels during ported by Fullerton (4). Other body systems the course of treatment. or components affected include chromosomes (12) mitochondria (5), hemopoetic (18) and aspiration pneumonia was made at post mor- Ca/P balance (11). tem examination. The gangrenous aspiration pneumonia which occurred is a plausible sequel in an animal Discussion with impaired nervous control, especially the The signs exhibited by the animal were typ- swallowing reflexes. This may have contributed ical for the subacute syndroms (2). Blood and to the aspiration of rumen contents resulting Henderson (2) report that muscular tremors in an aspiration pneumonia and a grave progand hyperesthesia are not uncommon. How- nosis. ever, these particular signs were absent in this animal. Moderate success has been achieved using Summary A case of subacute lead poisoning due to calcium disodium edetate to treat lead toxiingestion of used crankcase oil in a 15 month coses (9). Hammond and Sorensen (7) obtained favourable recovery rates with this anti- old Holstein heifer is described. Clinical and dote after about five to 16 days of treatment. laboratory findings, treatment, response and Secondary complications (aspiration pneu- gross and histopathology are presented. monia) may have prevented recovery in this case. Lead levels in the rumen dropped ra- Resume pidly during the treatment (Figure 2). After L'auteur decrit un cas d'empoisonnement the lavage, the rumen levels were low. Fecal subaigu par le plomb, chez une taure Holstein concentrations initially increased following ag6e de 15 mois qui avait ingere de la vieille treatment. This was probably due to passage de l'huile 'a moteur. Il presente aussi les obof the lead contaminated rumen contents down servations clniques de ce cas, les resultats the gastrointestinal tract. The blood levels d'epreuves de laboratoire, la r6ponse au traiteshowed a dramatic drop on the first day of ment, ainsi que les l6sions macroscopiques et treatment from 0.61 to 0.37 ppm. Calcium histologiques. .64
E
Blood Leod Concentration
\
c
-0
o-
-
c
a,
.
312
LEAD POISONING
Acknowledgments The assistance of Dr. D. L. Hamilton and Dr. C. S. Sisodia is gratefully appreciated.
References 1. ALLCROFT, R. Lead poisoning in cattle and sheep. Vet. Rec. 63: 583-590. 1951. 2. BLOOD, D. C. and J. A. HENDERSON. Veterinary Medicine, 3rd Edition. pp. 759-764. London: Bailliere, Tindall & Cassell. 1968. 3. CHRISTIAN, R. G. and L. TRYPHONAS. Lead poisoning in cattle. Brain lesions and hematologic changes. Am. J. vet. Res. 32: 203-215. 1971. 4. FULLERTON, P. M. Chronic peripheral neuropathology produced by lead poisoning in guinea-pigs. J. Neuropath. exp. Neurol. 25: 214-236. 1966. 5. GOYER, R. A. and R. KRALL. Ultrastructural transformation in mitochondria isolated from kidneys of normal and lead intoxicated rats. J. Cell. Biol. 41: 393-400. 1969. 6. HAMMOND, P.B. and A. L. ARONSON. Lead poisoning in cattle and horses in the vicinity of a smelter. Ann. N.Y. Acad. Sci. 111: 595611. 1964. 7. HAMMOND, P. B. and D. K. SORENSEN. Recent observations on the course and treatment of bovine lead poisoning. J. Am. vet. med. Ass. 130: 23-25. 1967. 8. HATCH, R. C. and H. S. FUNNELL. Lead levels in tissues and stomach contents of poisoned cattle: A fifteen-year survey. Can. vet. J. 10: 258-262. 1972. 9. HOLM, L. W., J. D. WHEAT, E. A. RHODE and G. FIRCH. The treatment of chronic lead poisoning in horses with calcium di-
313
sodium ethylene diaminetetraacetate. J. Am. vet. med. Ass. 123: 383-388. 1953.
10. JUBB, K. V. F. and P. C. KENNEDY. Pathology of Domestic Animals. Vol. 2, 2nd Edition. pp. 388-391. New York: Academic Press. 1970. 11. LINK, R. P. and R. R. PENSINGER. Lead toxicosis in swine. Am. J. vet. Res. 27: 759763. 1966. 12. MURO, L. A. and R. A. GOYER. Chromosome damage in experimental lead poisoning. Archs Path. 87: 660-663. 1969. 13. PRIESTER, W. A. and H. M. HAYES. Lead poisoning in cattle, horses, cats and hogs as reported by 11 colleges of veterinary medicine in the United States and Canada from July, 1968, through June 1972. Am. J. vet. Res. 35: 567-572. 1974. 14. THOMSON, R. G. Reliability of acid-fast inclusions in the kidneys of cattle as an indication of lead poisoning. Can. vet. J. 13: 88-89. 1972. 15. TRAINER, D. R. and R. A. HuNT. Lead poisoning of waterfowl in Wisconsin. J. Wildl. Mgmt 29: 95-103. 1965. 16. WILSON, M. R. and G. LEWIS. Lead poisoning in dogs. Vet. Rec. 75: 787-791. 1963. 17. ZOOK, B. C., J. L. CARPENTER and E. B. LEEDS. Lead poisoning in dogs. J. Am. vet. med. Ass. 155: 1329-1342. 1969. 18. ZOOK, B. C., J. L. CARPENTER and R. M. ROBERTS. Lead poisoning in dogs. Occurrence, source, clinical pathology, and electroencephalography. Am. J. vet. Res. 33: 891902. 1972. 19. ZOOK, B. C., L. KOPITO, J. L. CARPENTER, D. V. CRAMER and H. SHWACHMAN. Lead poisoning in dogs: Analysis of blood, urine, hair and liver for lead. Am. J. vet. Res. 33: 903-909. 1972.
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