Lead Poisoning

Also known as: plumbism — saturnism

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 usually occurs following ingestion of paint, lead weights, lead shot and used oil and batteries.

Absorbed lead enters blood and soft tissues and eventually redistributes to bone. The degree of absorption can vary, and in ruminants, particles of lead lodged in the reticulum can dissolve slowly and lead to chronic lead poisoning.

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.

Clinical signs

Lead poisoning is most common in young animals. Clinical signs are associated with the gastro-intestinal and nervous systems.

In cattle actue signs include: ataxia, blindness, salivation, bruxism, muscle tremors and convulsions.

The chronic disease is characterised by: anorexia, rumen stasis and colic, followed by diarrhoea, blindness, head pressing and death.

Dogs can show gastrointestinal signs such as anorexia, diarrhoea and vomiting. Hysterical barking, jaw champing, salivation, blindness, ataxia and convulsions may also develop.

Horses usually show chronic signs such as weight loss, colic, depression, laryngeal paralysis and dysphagia.

Birds often show the acute form of poisoning: depression, lethargy, regurgitation, vomiting, diarrhoea, ataxia and wing and leg weakness.

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.

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.

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.

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 hepatitis may appear similar to lead poisoning.

Treatment

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. Thiamine alleviates clinical manifestations and reduces tissue deposition of lead. Combined Ca-EDTA and thiamine treatment appears to produce the most beneficial response.

Succimer (meso 2,3-dimercaptosuccinic acid, DMSA) is a chelating agent that has proven to be effective in dogs and is also useful in birds. Fewer side effects have been associated with DMSA as compared with Ca-EDTA.

Cathartics such as magnesium sulfate or a rumenotomy may be useful to remove lead from the GI tract.

Barbiturates or tranquilizers may be indicated to control convulsions.

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.