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New Zealand Veterinary Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/tnzv20
Lead poisoning in dogs B.J. McLeavey
a
a
100 Lincoln Road, Christchurch Published online: 23 Feb 2011.
To cite this article: B.J. McLeavey (1977) Lead poisoning in dogs, New Zealand Veterinary Journal, 25:12, 395-396, DOI: 10.1080/00480169.1977.34466 To link to this article: http://dx.doi.org/10.1080/00480169.1977.34466
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
1977
395
NEW ZEALAND VETERINARY JOURNAL
Lead poisoning in dogst B. J. McLeavey·
N.l.
~el.
J. 15:
.l\l5·/\
INTRODUCfION
Lead poisoning in dogs is insidious in onset, difficult to diagnose. and frequently overlooked. It is more prevalent in the older and more run-down areas in cities, where deteriorating paint. old lead plumbing, and untidy yards present many op portunities for dogs to acquire toxic amounts. My own practice is situated in one of the olderareas of Christchurch and, overthe II years covered by this paper, I have confirmed 107 casesoflead poisoning.
Downloaded by [Tufts University] at 08:50 10 December 2014
SYMPTOMS
There are two main categories - abdominal and nervous. The abdominal symptoms which may, or may not, precede nervous symptoms include abdominal pain, vomiting, anorexia, diarrhoea. loss of weight and poor coat. It is not possible to test all dogs with these symptoms for lead poisoning, but I always test any dog with recurrent attacks of any of these symptoms where a cause cannot be found, or where the dog has failed to respond to symptomatic treatment. For example a IS-month-old dog was presented with a history of acute vomiting which led me to suspect a foreign body. I was unable to confirm this by palpation or x-ray so I put the dog onto symptomatic treatment. Over the next week the dog suffered repeated attacks of severe abdominal pain and eventually I carried out a laparotomy. When I found nothing significant I realised it was probably a case of lead poisoning so I took a blood sample for analysis and treated the dog for lead poisoning. The dog made a rapid recovery and the blood test subsequently confirmed the diagnosis. The nervous symptoms include convulsions, extreme ner vousness. aggressivness. and change in temperament. Wherever possible I have tested all dogs presented to me with any of the above symptoms. The severity of the symptoms in this group vary considerably as the following histories show. Case 1: A 6-month-old pomeranian was presented with a history of inappetance and continual scratChing since a young puppy. The dog was extremely timid and nervous, so I took blood and urine for lead analysis. These were positive and after treatment the scratching stopped and the appetite and temperament im proved markedly. Case 2: A 3-month-old pup was presented for routine vaccina tion. As it had an extremely aggressive temperament I took a blood sample for testing and this was positive. Case 3: An IS-month-old labrador suddenly became aggressive towards its owner who was currently painting the house. Case 4: A 3-year-old corgi suddenly collapsed in severe con vulsions while being exercised. This history nearly always in dicates lead poisoning. DIAGNOSIS
A final diagnosis of lead poisoning can only be made after confirmation of elevated lead levels in the animal's tissues. The most reliable test is the estimation oflead levels in the blood. For accurate analysis 10 mls of unclotted blood is required. It must be collected into lead-free containers such as the MAF "oxalate". or the BD heparinised. vacutainers. Urine levels can be useful but. in many cases with elevated blood levels, the urine
t
Presented to the NZV A Conference 1977. * 100 lincoln Road. Christchurch.
levels will be negative or within the normal range. Urine levels taken before, and after, treatment will show a massive increase in levels in cases oflead poisoning and can be of use where blood levels cannot be obtained. In the dead animal, liver is the most useful organ for testing, but it must be collected carefully so that there is no contamination from extraneous lead. The interpretation of the test results can present problems. I have taken the following levels as being the minimum amounts consistent with a diagnosis of lead poisoning, where the clinical signs and history would support it - Blood 0.4 mgj1; Urine 0.75 mg/l: Liver 5.0 mg/kg. A useful aid to diagnosis in the clinic is the examination of blood smears for nucleated red blood cells. Fresh smears stained with Jenner-Giemsa readily show the nucleated red blood cells. A level of 10 NBC's per 100 WBC's in the absence of anaemia is strong evidence ofle-ad poisoning in dogs and I usually give these dogs some treatment while awaiting the lead analysis. These smears will frequently show basophilic stippling of the eryth rocytes which is also common in cases of lead poisoning. CASE RESULTS
The cases submitted for testing came from three main groups:(I) Dogs exhibiting nervous symptoms. (2) Dogs exhibiting abdominal symptoms. (3) Random cases. This group includes dogs submitted for routine treatments with no symptoms of lead poisoning; dogs submitted for routine treatments with excessively nervous or aggressive temperaments; all autopsies where the cause of death was not apparent on gross pathology. Three hundred and sixty seven cases were submitted for testing. and 107 of these had toxic levels of lead present. There were 169 cases completely negative for lead and 91 dogs had lead present but below the toxic level. Some of the latter group subsequently returned with toxic levels which shows that these dogs had continuing access to lead. Age groups. The majority of cases of lead poisoning occur in young an imals. This reflects the propensity for pups to lick and chew anything within reach. Out of 107 positives, 62.6% occurred in dogs under 12 months and 41 % in dogs under 6 months of age. These figures are similar to those obtained in an American survey where. in 216 cases, Sl% were under 12 months and 53% under 5 months of age. Symptoms When examined in relation to symptoms. 63.2% of the positive cases had nervous symptoms. Abdominal symptoms were predominant in 26.4% of cases and 10.4 %of the positives were from the random group. In an earlier NZ survey, involving 19 cases. 63.2% also showed nervous symptoms and 36.S% ab dominal. It is interesting that from all the dogs examined with nervous symptoms where I was able to obtain a test, 36.2% were positive for lead poisoning. SEASONAL INCIDENCE
I nan American survey 63 %ofcases occurred in the spring and summer months. This was attributed to the increased outdoor activity of dogs at this time of year. when increased amounts of lead were absorbed as a result of the higher levels of vitamin D present in the months with the most sunlight. In my own cases the
NEW ZEALAND VETERINARY JOURNAL
396
reverse occurred with 64.5% in the autumn and winter months. I feel that in Christchurch dogs spend quite a lot of their time outside in the winter but tend to stay closer to the house where the soil and water is often contaminated. Licking soil off their feet or drinking the contaminated water is likely to be a source of lead in these cases.
Downloaded by [Tufts University] at 08:50 10 December 2014
SOURCES
I have not kept separate records of sources, but despite one American report where the source was determined in only 30% of cases. I find in practice that the source can be found in almost every case. In the majority of cases the source is present in the dog's home environment. I have had a number of cases in pups where contaminated soil is the source. Old flaking paint, especially near feeding bowls, is very common. Linoleum con tains appreciable amounts oflead and, in one case, a dog which was fed on the surface of old linoleum, and used to lick the area clean afterwards, eventually developed severe convulsions. Contaminated water is a fairly common source. One dog threw fits every time it rained. The owner noticed it drinking from rain water pools close to the house. This water had an elevated lead level. In another case the dog only drank from the shower base: the base was terrazo which had cracked and been puttied up with red lead putty. The owner ofanother dog was a compositer who handled lead all day: when he returned home the dog used to lick his hands clean. Other regular sources are old lead pipes and batteries and poorly glazed pottery when used as drinking bowls. If the owner cannot suggest a source I find it wen worthwhile to visit the property. In one case, for example, two pups were presented in convulsions. The owner stated that, as his dogs were kept in a netting run during the day and in the house at night, there was no possibility of lead poisoning. On visiting the property I found one end of the pen was a shed wan with flaking paint which was scattered widely in the pen, especially in the feeding area. CONCURRENT DISEASE AND PRECIPITATING FACTORS
In a 1956 survey at Wallaceville, during a distemper outbreak, when the causes of mortality in young dogs was being studied, 17 out of 27 dogs with lead poisoning were complicated by dis temper. In my own cases. 29 dogs had elevated lead levels on autopsy but only 2 were complicated by distemper. In one case two littermates with blood lead levels of2.5 mg/kg had concurrent salmonellosis. Workers using salmonella-resis tant strains of mice have shown a decreased resistance to sal monella when lead was being ingested. Exercise is the most important precipitating factor in lead convulsions. Classically the dogs collapse in severe convulsions while being taken for a run by their owners. Unless vigorous treatment is instituted as soon as possible these dogs will die. I always advise owners of dogs with suspected lead poisoning not to exercise their dogs until the test results are known. In two cases this advice was ignored and the dogs threw severe convulsions, one dog dying before it reached the clinic. Stress precipitated convulsions in one dog, which threw severe convulsions after its kennel was blown apart during a hurricane. TREATMENT
The two main aims of treatment are to reduce the lead levels in the dog's tissues and then remove the source oflead, or prevent access to it. Lead is removed from the body by chelating agents which combine with the lead. rendering it highly soluble so that it can be excreted through the kidneys. The most important agents in veterinary practice are Ca EDTA or Ca versenate. usually given intravenously or subcu taneously. The recommended dose is 75 mg/kg daily for three days and I usually repeat this in two weeks. So long as there is no further access to lead. this course is sufficient. The drug may be
VOL.2S
given intravenously asa 10% solution, but, for subcutaneous use, it should be diluted with saline to a 4% solution as it is very painful when used this way. The recommended dose of 75 mg/kg can be attained by giving 2 mljkg of the 4% solution. I never use the oral tablets because, if the dog still has access to lead. they can increase the absorption of lead from the gut. The dog presented in severe convulsions, is to my mind, a clinical challenge and requires careful and intensive treatment if it is going to survive. I start treatment by giving a tranquilliser, followed immediately by a short-acting barbiturate to control the convulsions. The barbiturate must be given very carefully because it is easy to give it too rapidly in order to control the convulsions and kill the dog in the process. To achieve a sufficient length ofanaesthesia, I then give ijv pentobarbitone in small doses and repeat it during treatment until the dog is able to wake up without convulsions. As soon as a satisfactory plane ofanaesthesia has been attained I collect a blood sample for later analysis. I then connect the dog to an i/v drip using lactated ringers to which I add sufficient dextrose to make a 10% solution; this helps to reduce any cerebral oedema which may be present. Because most dogs in this condition have complete anuria it is important to run the drip long enough to establish a good urine flow before administering the Ca EDTA. This not only helps reduce the lead levels rapidly, but also reduces the toxicity of the Ca EDTA which is excreted unchanged through the kidneys and can cause a nephrosis. Steroids will increase this toxicity and should not be used. When the urine flow is satisfactory, which usually takes about half-an-hour, I then administer the Ca EDT A i/v and I also give another of the chelating agents, BAL, intramuscularly. This drug is not as effective as Ca EDTA but it does reduce the toxicity of Ca EDTA. It is used at a dose rate of 8mg/kg i/m. I then keep the drip going for a further 15-30 mins and allow the dog to wake up slowly while keeping a close watch on it. The dog is then given Ca EDTA for the next two days and the course is repeated in two weeks. There is a rapid reduction of lead levels with the use of Ca EDTA for the first three days and then the level stabilises, even if the treatment is continued. Some idea of the speed of lead removal is given by the following case. An 8-mondt-old dog weighing 8 kg was admitted in severe convulsions. I treceived the treatment outlined above and serial blood and urine samples were taken. TIME BLOOD URINE DRIP mi. mg/I mg/l 7.30 pm 1.0 0.9 o 8.20pm 0.6 0 1000 + Ca EDTA &BAL 8.50 pm not sampled 2.5 9.20 pm 0.06 1.8 1300 10.20 pm 0.2 1.9 2.30 pm 0.4 0.7 (next day) These figures show the initial dilution by the drip and then the rapid removal of the lead. The dog passed 280 ml of urine in the first hour and a half after the administration of the antidotes and this removed 0.46 mg oflead. By the time the dog was sent home the next afternoon the blood levels were less than halfthe initial figure 21 hours before. While most dogs will recover on this treatment, some will remain timid and nervous because the lead damages the small capillaries in the brain causing death of the surrounding neurones. To conclude, lead poisoning has been a fairly common con dition in my practice. Diagnosis is based on an examination of the history, symptoms. home environment, blood smears and blood analysis. Identification and removal ofthesource. coupled with careful treatment. will result in a clinical cure in most cases.
New Zealand Veterinary Journal Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/tnzv20
Lead poisoning in dogs B.J. McLeavey
a
a
100 Lincoln Road, Christchurch Published online: 23 Feb 2011.
To cite this article: B.J. McLeavey (1977) Lead poisoning in dogs, New Zealand Veterinary Journal, 25:12, 395-396, DOI: 10.1080/00480169.1977.34466 To link to this article: http://dx.doi.org/10.1080/00480169.1977.34466
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
1977
395
NEW ZEALAND VETERINARY JOURNAL
Lead poisoning in dogst B. J. McLeavey·
N.l.
~el.
J. 15:
.l\l5·/\
INTRODUCfION
Lead poisoning in dogs is insidious in onset, difficult to diagnose. and frequently overlooked. It is more prevalent in the older and more run-down areas in cities, where deteriorating paint. old lead plumbing, and untidy yards present many op portunities for dogs to acquire toxic amounts. My own practice is situated in one of the olderareas of Christchurch and, overthe II years covered by this paper, I have confirmed 107 casesoflead poisoning.
Downloaded by [Tufts University] at 08:50 10 December 2014
SYMPTOMS
There are two main categories - abdominal and nervous. The abdominal symptoms which may, or may not, precede nervous symptoms include abdominal pain, vomiting, anorexia, diarrhoea. loss of weight and poor coat. It is not possible to test all dogs with these symptoms for lead poisoning, but I always test any dog with recurrent attacks of any of these symptoms where a cause cannot be found, or where the dog has failed to respond to symptomatic treatment. For example a IS-month-old dog was presented with a history of acute vomiting which led me to suspect a foreign body. I was unable to confirm this by palpation or x-ray so I put the dog onto symptomatic treatment. Over the next week the dog suffered repeated attacks of severe abdominal pain and eventually I carried out a laparotomy. When I found nothing significant I realised it was probably a case of lead poisoning so I took a blood sample for analysis and treated the dog for lead poisoning. The dog made a rapid recovery and the blood test subsequently confirmed the diagnosis. The nervous symptoms include convulsions, extreme ner vousness. aggressivness. and change in temperament. Wherever possible I have tested all dogs presented to me with any of the above symptoms. The severity of the symptoms in this group vary considerably as the following histories show. Case 1: A 6-month-old pomeranian was presented with a history of inappetance and continual scratChing since a young puppy. The dog was extremely timid and nervous, so I took blood and urine for lead analysis. These were positive and after treatment the scratching stopped and the appetite and temperament im proved markedly. Case 2: A 3-month-old pup was presented for routine vaccina tion. As it had an extremely aggressive temperament I took a blood sample for testing and this was positive. Case 3: An IS-month-old labrador suddenly became aggressive towards its owner who was currently painting the house. Case 4: A 3-year-old corgi suddenly collapsed in severe con vulsions while being exercised. This history nearly always in dicates lead poisoning. DIAGNOSIS
A final diagnosis of lead poisoning can only be made after confirmation of elevated lead levels in the animal's tissues. The most reliable test is the estimation oflead levels in the blood. For accurate analysis 10 mls of unclotted blood is required. It must be collected into lead-free containers such as the MAF "oxalate". or the BD heparinised. vacutainers. Urine levels can be useful but. in many cases with elevated blood levels, the urine
t
Presented to the NZV A Conference 1977. * 100 lincoln Road. Christchurch.
levels will be negative or within the normal range. Urine levels taken before, and after, treatment will show a massive increase in levels in cases oflead poisoning and can be of use where blood levels cannot be obtained. In the dead animal, liver is the most useful organ for testing, but it must be collected carefully so that there is no contamination from extraneous lead. The interpretation of the test results can present problems. I have taken the following levels as being the minimum amounts consistent with a diagnosis of lead poisoning, where the clinical signs and history would support it - Blood 0.4 mgj1; Urine 0.75 mg/l: Liver 5.0 mg/kg. A useful aid to diagnosis in the clinic is the examination of blood smears for nucleated red blood cells. Fresh smears stained with Jenner-Giemsa readily show the nucleated red blood cells. A level of 10 NBC's per 100 WBC's in the absence of anaemia is strong evidence ofle-ad poisoning in dogs and I usually give these dogs some treatment while awaiting the lead analysis. These smears will frequently show basophilic stippling of the eryth rocytes which is also common in cases of lead poisoning. CASE RESULTS
The cases submitted for testing came from three main groups:(I) Dogs exhibiting nervous symptoms. (2) Dogs exhibiting abdominal symptoms. (3) Random cases. This group includes dogs submitted for routine treatments with no symptoms of lead poisoning; dogs submitted for routine treatments with excessively nervous or aggressive temperaments; all autopsies where the cause of death was not apparent on gross pathology. Three hundred and sixty seven cases were submitted for testing. and 107 of these had toxic levels of lead present. There were 169 cases completely negative for lead and 91 dogs had lead present but below the toxic level. Some of the latter group subsequently returned with toxic levels which shows that these dogs had continuing access to lead. Age groups. The majority of cases of lead poisoning occur in young an imals. This reflects the propensity for pups to lick and chew anything within reach. Out of 107 positives, 62.6% occurred in dogs under 12 months and 41 % in dogs under 6 months of age. These figures are similar to those obtained in an American survey where. in 216 cases, Sl% were under 12 months and 53% under 5 months of age. Symptoms When examined in relation to symptoms. 63.2% of the positive cases had nervous symptoms. Abdominal symptoms were predominant in 26.4% of cases and 10.4 %of the positives were from the random group. In an earlier NZ survey, involving 19 cases. 63.2% also showed nervous symptoms and 36.S% ab dominal. It is interesting that from all the dogs examined with nervous symptoms where I was able to obtain a test, 36.2% were positive for lead poisoning. SEASONAL INCIDENCE
I nan American survey 63 %ofcases occurred in the spring and summer months. This was attributed to the increased outdoor activity of dogs at this time of year. when increased amounts of lead were absorbed as a result of the higher levels of vitamin D present in the months with the most sunlight. In my own cases the
NEW ZEALAND VETERINARY JOURNAL
396
reverse occurred with 64.5% in the autumn and winter months. I feel that in Christchurch dogs spend quite a lot of their time outside in the winter but tend to stay closer to the house where the soil and water is often contaminated. Licking soil off their feet or drinking the contaminated water is likely to be a source of lead in these cases.
Downloaded by [Tufts University] at 08:50 10 December 2014
SOURCES
I have not kept separate records of sources, but despite one American report where the source was determined in only 30% of cases. I find in practice that the source can be found in almost every case. In the majority of cases the source is present in the dog's home environment. I have had a number of cases in pups where contaminated soil is the source. Old flaking paint, especially near feeding bowls, is very common. Linoleum con tains appreciable amounts oflead and, in one case, a dog which was fed on the surface of old linoleum, and used to lick the area clean afterwards, eventually developed severe convulsions. Contaminated water is a fairly common source. One dog threw fits every time it rained. The owner noticed it drinking from rain water pools close to the house. This water had an elevated lead level. In another case the dog only drank from the shower base: the base was terrazo which had cracked and been puttied up with red lead putty. The owner ofanother dog was a compositer who handled lead all day: when he returned home the dog used to lick his hands clean. Other regular sources are old lead pipes and batteries and poorly glazed pottery when used as drinking bowls. If the owner cannot suggest a source I find it wen worthwhile to visit the property. In one case, for example, two pups were presented in convulsions. The owner stated that, as his dogs were kept in a netting run during the day and in the house at night, there was no possibility of lead poisoning. On visiting the property I found one end of the pen was a shed wan with flaking paint which was scattered widely in the pen, especially in the feeding area. CONCURRENT DISEASE AND PRECIPITATING FACTORS
In a 1956 survey at Wallaceville, during a distemper outbreak, when the causes of mortality in young dogs was being studied, 17 out of 27 dogs with lead poisoning were complicated by dis temper. In my own cases. 29 dogs had elevated lead levels on autopsy but only 2 were complicated by distemper. In one case two littermates with blood lead levels of2.5 mg/kg had concurrent salmonellosis. Workers using salmonella-resis tant strains of mice have shown a decreased resistance to sal monella when lead was being ingested. Exercise is the most important precipitating factor in lead convulsions. Classically the dogs collapse in severe convulsions while being taken for a run by their owners. Unless vigorous treatment is instituted as soon as possible these dogs will die. I always advise owners of dogs with suspected lead poisoning not to exercise their dogs until the test results are known. In two cases this advice was ignored and the dogs threw severe convulsions, one dog dying before it reached the clinic. Stress precipitated convulsions in one dog, which threw severe convulsions after its kennel was blown apart during a hurricane. TREATMENT
The two main aims of treatment are to reduce the lead levels in the dog's tissues and then remove the source oflead, or prevent access to it. Lead is removed from the body by chelating agents which combine with the lead. rendering it highly soluble so that it can be excreted through the kidneys. The most important agents in veterinary practice are Ca EDTA or Ca versenate. usually given intravenously or subcu taneously. The recommended dose is 75 mg/kg daily for three days and I usually repeat this in two weeks. So long as there is no further access to lead. this course is sufficient. The drug may be
VOL.2S
given intravenously asa 10% solution, but, for subcutaneous use, it should be diluted with saline to a 4% solution as it is very painful when used this way. The recommended dose of 75 mg/kg can be attained by giving 2 mljkg of the 4% solution. I never use the oral tablets because, if the dog still has access to lead. they can increase the absorption of lead from the gut. The dog presented in severe convulsions, is to my mind, a clinical challenge and requires careful and intensive treatment if it is going to survive. I start treatment by giving a tranquilliser, followed immediately by a short-acting barbiturate to control the convulsions. The barbiturate must be given very carefully because it is easy to give it too rapidly in order to control the convulsions and kill the dog in the process. To achieve a sufficient length ofanaesthesia, I then give ijv pentobarbitone in small doses and repeat it during treatment until the dog is able to wake up without convulsions. As soon as a satisfactory plane ofanaesthesia has been attained I collect a blood sample for later analysis. I then connect the dog to an i/v drip using lactated ringers to which I add sufficient dextrose to make a 10% solution; this helps to reduce any cerebral oedema which may be present. Because most dogs in this condition have complete anuria it is important to run the drip long enough to establish a good urine flow before administering the Ca EDTA. This not only helps reduce the lead levels rapidly, but also reduces the toxicity of the Ca EDTA which is excreted unchanged through the kidneys and can cause a nephrosis. Steroids will increase this toxicity and should not be used. When the urine flow is satisfactory, which usually takes about half-an-hour, I then administer the Ca EDT A i/v and I also give another of the chelating agents, BAL, intramuscularly. This drug is not as effective as Ca EDTA but it does reduce the toxicity of Ca EDTA. It is used at a dose rate of 8mg/kg i/m. I then keep the drip going for a further 15-30 mins and allow the dog to wake up slowly while keeping a close watch on it. The dog is then given Ca EDTA for the next two days and the course is repeated in two weeks. There is a rapid reduction of lead levels with the use of Ca EDTA for the first three days and then the level stabilises, even if the treatment is continued. Some idea of the speed of lead removal is given by the following case. An 8-mondt-old dog weighing 8 kg was admitted in severe convulsions. I treceived the treatment outlined above and serial blood and urine samples were taken. TIME BLOOD URINE DRIP mi. mg/I mg/l 7.30 pm 1.0 0.9 o 8.20pm 0.6 0 1000 + Ca EDTA &BAL 8.50 pm not sampled 2.5 9.20 pm 0.06 1.8 1300 10.20 pm 0.2 1.9 2.30 pm 0.4 0.7 (next day) These figures show the initial dilution by the drip and then the rapid removal of the lead. The dog passed 280 ml of urine in the first hour and a half after the administration of the antidotes and this removed 0.46 mg oflead. By the time the dog was sent home the next afternoon the blood levels were less than halfthe initial figure 21 hours before. While most dogs will recover on this treatment, some will remain timid and nervous because the lead damages the small capillaries in the brain causing death of the surrounding neurones. To conclude, lead poisoning has been a fairly common con dition in my practice. Diagnosis is based on an examination of the history, symptoms. home environment, blood smears and blood analysis. Identification and removal ofthesource. coupled with careful treatment. will result in a clinical cure in most cases.
