Changes

Jump to navigation Jump to search
1,235 bytes added ,  20:02, 11 July 2012
no edit summary
Line 1: Line 1: −
Also known as: '''''plumbism saturnism'''''
+
{{OpenPagesTop}}
 +
Also known as: '''''Plumbism Saturnism'''''
    
==Introduction==
 
==Introduction==
Lead poisoning is a condition caused by increased levels of lead in the body and is most common in dogs and cattle. It can also occur in birds, but disease in other animals is limited by reduced accessibility, selective eating habits or lower susceptibility.
+
Lead poisoning is a condition caused by increased levels of lead in the body and is most common in dogs and cattle. It can also occur in birds and chelonia, but disease in other animals is limited by reduced accessibility, selective eating habits or lower susceptibility.
    
Lead poisoning usually occurs following ingestion of '''paint, lead weights, lead shot and used oil and batteries'''.
 
Lead poisoning usually occurs following ingestion of '''paint, lead weights, lead shot and used oil and batteries'''.
Line 10: Line 11:  
Lead has a profound effect on antioxydant enzymes involved in the protection of erythrocytes and lead to '''capillary damage'''. Lead is also '''irritating, immunosuppressive, teratogenic, nephrotoxic and toxic to the haematopoietic system'''.
 
Lead has a profound effect on antioxydant enzymes involved in the protection of erythrocytes and lead to '''capillary damage'''. Lead is also '''irritating, immunosuppressive, teratogenic, nephrotoxic and toxic to the haematopoietic system'''.
   −
In young animals ingesting a large dose at once, there is '''malfunction of osteoclasts''' and increased density of the metaphysis on radiographs.
+
In young animals ingesting a large dose at once, it causes '''malfunction of osteoclasts''' and increased density of the metaphysis on radiographs.
   −
==Clinical signs==
+
==Clinical Signs==
 
Lead poisoning is most common in young animals. Clinical signs are associated with the '''gastro-intestinal and nervous systems'''.
 
Lead poisoning is most common in young animals. Clinical signs are associated with the '''gastro-intestinal and nervous systems'''.
   Line 26: Line 27:     
==Diagnosis==
 
==Diagnosis==
'''Haematology''' may show changes consistent but not pathognomonic for lead poisoning: normocytic, normochromic anaemia with basophilic stippling and nucleated erythrocytes out of proportion to the degree of anaemia.
+
'''Haematology''' may show changes consistent but not pathognomonic for lead poisoning: normocytic, normochromic [[:Category:Anaemia|anaemia]] with basophilic stippling and nucleated [[erythrocytes]] out of proportion to the degree of anaemia. The anaemia is sometimes polychromatic and anisocytic, indicating a regenerative process.
 +
 
 +
'''Biochemistry''': may reveal hepatic damage and elevations in ALP, ALT and [[bilirubin]] levels.
    
Measurement of '''lead levels''' in various tissues may be useful to evaluate excessive accumulation and to reflect the level of exposure, severity and prognosis. Concentrations of lead in the blood at 0.35 ppm, liver at 10 ppm, or kidney cortex at 10 ppm are consistent with a diagnosis of lead poisoning in most species.
 
Measurement of '''lead levels''' in various tissues may be useful to evaluate excessive accumulation and to reflect the level of exposure, severity and prognosis. Concentrations of lead in the blood at 0.35 ppm, liver at 10 ppm, or kidney cortex at 10 ppm are consistent with a diagnosis of lead poisoning in most species.
Line 32: Line 35:  
'''Post mortem''' examination may reveal evidence of gastroenteritis. In the nervous system, oedema and congestion of the cerebral cortex and flattening of the cortical gyri are present. Histologically, endothelial swelling, laminar cortical necrosis, and oedema of the white matter may be evident. There is also tubular necrosis and degeneration in the kidneys.
 
'''Post mortem''' examination may reveal evidence of gastroenteritis. In the nervous system, oedema and congestion of the cerebral cortex and flattening of the cortical gyri are present. Histologically, endothelial swelling, laminar cortical necrosis, and oedema of the white matter may be evident. There is also tubular necrosis and degeneration in the kidneys.
   −
'''Radiographs''' may be useful to reveal metal particles in the gastrointestinal tract.
+
'''Radiographs''' may be useful to reveal metal particles in the gastrointestinal tract. They are particularly recommended in birds where metal particles within the [[ventriculus]] should not be confused with grit.
 +
 
 +
Other diseases may '''mimic''' the clinical signs of lead poisoning and in cattle, polioencephalomalacia, nervous coccidiosis, [[tetanus]], [[hypovitaminosis A]], [[Hypomagnesaemia|hypomagnesemic tetany]], nervous [[Ketosis of Cattle|acetonemia]], arsenic or mercury poisoning, brain abscess or neoplasia, [[rabies]], [[listeriosis]], and [[:Category:Haemophilus species|''Haemophilus'']] infections should be considered.
   −
Other diseases may '''mimic''' the clinical signs of lead poisoning and in cattle, polioencephalomalacia, nervous coccidiosis, tetanus, hypovitaminosis A, hypomagnesemic tetany, nervous acetonemia, arsenic or mercury poisoning, brain abscess or neoplasia, rabies, listeriosis, and Haemophilus infections should be considered.
+
In dogs, rabies, [[distemper]], and [[Infectious Canine Hepatitis|hepatitis]] may appear similar to lead poisoning.
In dogs, rabies, distemper, and hepatitis may appear similar to lead poisoning.  
      
==Treatment==
 
==Treatment==
 
Treatment may not be successful if tissue damage, particularly to the nervous system, is excessive.
 
Treatment may not be successful if tissue damage, particularly to the nervous system, is excessive.
   −
In livestock, calcium disodium edetate (Ca-EDTA) is given IV or SC for 3 days. In dogs, a similar dose divided into 4 treatments/day is administered SC in 5% dextrose for 2-5 days. After a 1-wk rest period, an additional 5-day treatment may be required if clinical signs persist. No approved veterinary product containing Ca-EDTA is commercially available at present.
+
In livestock, calcium disodium edetate (Ca-EDTA) is given IV or SC for 3 days. In dogs, a similar dose divided into 4 treatments/day is administered SC in 5% dextrose for 2-5 days. After a one week rest period, an additional 5-day treatment may be required if clinical signs persist. No approved veterinary product containing Ca-EDTA is commercially available at present.
 +
 
 
Thiamine alleviates clinical manifestations and reduces tissue deposition of lead. '''Combined Ca-EDTA and thiamine''' treatment appears to produce the most beneficial response.
 
Thiamine alleviates clinical manifestations and reduces tissue deposition of lead. '''Combined Ca-EDTA and thiamine''' treatment appears to produce the most beneficial response.
   Line 50: Line 55:     
Chelation therapy, in combination with '''antioxidant treatment''', may limit oxidative damage associated with acute lead poisoning. Antioxidants such as n-acetylcysteine have been used in combination with DMSA.
 
Chelation therapy, in combination with '''antioxidant treatment''', may limit oxidative damage associated with acute lead poisoning. Antioxidants such as n-acetylcysteine have been used in combination with DMSA.
 +
 +
In chelonia it is possible to remove the ingested lead fragments from the stomach using endoscopically-guided forceps. This should be followed with two weeks medical therapy with Ca-EDTA.
    
{{Learning
 
{{Learning
|flashcards = [[Avian Medicine Q&A 25]]
+
|flashcards = [[Avian Medicine Q&A 25]]<br>[[Rabbit Medicine and Surgery Q&A 05]]<br>[[Reptiles and Amphibians Q&A 07]]<br>[[Reptiles and Amphibians Q&A 13]]
 
}}
 
}}
    
==References==
 
==References==
 +
Frye, FL & Williams, DL (1995) '''Self-Assessment Colour Review - Reptiles & Amphibians''' ''Manson''
    
Kahn, C. (2005) '''Merck Veterinary Manual''' 9th Edition ''Merck and Co''
 
Kahn, C. (2005) '''Merck Veterinary Manual''' 9th Edition ''Merck and Co''
Line 62: Line 70:     
Payne, J. (2010) '''Lead poisoning in Cattle and Sheep''' ''In Practice'' 32, 64-69
 
Payne, J. (2010) '''Lead poisoning in Cattle and Sheep''' ''In Practice'' 32, 64-69
 +
 +
 +
{{review}}
 +
 +
{{OpenPages}}
    
[[Category:Bones - Metabolic Pathology]]
 
[[Category:Bones - Metabolic Pathology]]
 
[[Category:Toxicology]]
 
[[Category:Toxicology]]
[[Category:To Do - Major]]
+
[[Category:Expert Review]]
[[Category:To Do - Manson]]
+
[[Category:Expert Review - Exotics]]
[[Category:To Do - Helen]]
+
[[Category:Alimentary Diseases - Cat]]
[[Category:To Do - Review]]
+
[[Category:Alimentary Diseases - Cattle]]
 +
[[Category:Alimentary Diseases - Birds]]
 +
[[Category:Alimentary Diseases - Horse]]
 +
[[Category:Neurological Diseases - Cat]]
 +
[[Category:Neurological Diseases - Cattle]]
 +
[[Category:Neurological Diseases - Birds]]
 +
[[Category:Neurological Diseases - Horse]]
Author, Donkey, Bureaucrats, Administrators
53,803

edits

Navigation menu