By Patrick J. Sullivan, DVM, DABVP (Avian Practice)
MSPCA-Angell West, Waltham
Heavy metal toxicosis is one of the most common toxic diseases for which companion avian species present. Lead and zinc are over-represented in this category, although other metals such as mercury and cadmium may also be seen. This article will focus mainly on lead and zinc, as many of the symptoms can be quite similar.
Exposure to heavy metals can come from a number of different sources, including, but not limited to; paint, plaster, galvanized wire, fishing weights, bullets/ammunition, costume jewelry, stained glass, bells or other toys, twist ties, and linoleum. Diagnosis of heavy metal toxicity is based on a number of factors, the first being a thorough history. Clinical signs can vary greatly based on the amount of metal ingested and the species of bird. Toxicity may become a more likely differential if the owner reports any chewing on walls or baseboards, new toys or enclosures, or construction that could aerosolize lead paint. Ingestion of a large amount of metal may cause acute symptoms or death while chronic ingestion of smaller amounts may present as worsening neurologic symptoms or weight loss.
Clinical Signs/Hematologic Changes:
As previously mentioned, acute presentation is usually secondary to ingestion of a large amount of metal. Common clinical signs include weakness, depression, regurgitation, abnormally colored droppings, and neurologic signs, which may be quite pronounced. Ingestion of smaller amounts of metal over a longer period of time may yield a more chronic presentation of symptoms. Weight loss, chronic regurgitation and increasing paresis or neurologic deficits are the most commonly seen symptoms. Microcytic anemia, thought to be the result of increased fragility of RBC, as well as hematuria and heterophilia, are changes typically seen on the hemogram. Biochemical changes can include some or all of the following: elevated aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), and uric acid.
Lead is rapidly absorbed through the GI tract following breakdown in the acidic environment of the stomach after which it binds to RBC and is distributed throughout the body. The majority of lead is stored in the bone marrow (94%), with a small amount circulating in the blood (4%), and an even smaller amount (2%) remaining in soft tissue, including nervous tissue. Once in the erythropoietic system, lead denatures multiple enzymes in the hemoglobin synthesis pathway; these changes are thought to be the main cause of the microcytic anemia commonly seen in affected animals.
Radiographs, serum zinc and lead testing and tissue sampling are all helpful in obtaining a diagnosis. Radiographs can be very helpful when metallic objects are identified in the gastrointestinal tract, but the absence of these objects on a radiograph does not rule out the presence of heavy metal in the body. Non-radiographically visible forms of metal may include paint chips, gaseous fumes or mobilized lead stores in the bone marrow. Serum zinc and blood lead levels are probably the most commonly used indicators of both intoxication and response to treatment. Atomic absorption spectrophotometry is the gold standard for testing small amounts (0.2ml) of whole blood or serum, although it requires sending samples to an outside laboratory. Many practices will begin chelation therapy while waiting for results, which can take 1-3 days, or more. Another option is to use an in-house testing kit such as the LeadCare testing kit. The downside to this kit is that it has a high end cut off, making it difficult to track progress if the initial value is quite high. Tissue testing is typically not performed on live animals, but rather used to help diagnose flock health issues.
Patients should be stabilized prior to treatment if possible. This includes rehydration, heat therapy and gavage feeding. NSAIDs are frequently used to reduce inflammation around peripheral nerves and help to lessen neurologic signs. Antibiotics are used on a case by case basis, primarily to rule out secondary infection. Chelation therapy is the most important aspect of treatment, with these medications being the most commonly used:
- Calcium EDTA – Calcium disodium salt of ethylene diaminetetraacetic acid. Typical treatment protocol consists of 5 days of treatment by intramuscular injection, followed by 3 days off to prevent excessive calcium binding. This protocol has been adopted from mammalian protocols to be as renal protective as possible, although the risk of renal damage is much lower in avian species. CaEDTA does not cross the blood brain barrier and should not be given to treat central nervous system signs.
- D- penicillamine – This medication, given orally, can be combined with CaEDTA in hospital. Significant side effects involving the hepatic and renal system have been seen when using this drug in human medicine, but these side effects do not seem to occur nearly as frequently in avian patients. This drug can be used to treat central nervous system signs as it does cross the blood brain barrier.
- DMSA – Meso 2,3 – dimercaptosuccinic acid is an oral chelating agent that is very effective in treating both lead and zinc toxicity. This drug does not chelate lead from the bone marrow, which may lengthen the course of treatment.
The main indicators of improvement are cessation or reduction in clinical signs and reduction of the serum lead level to below 20ug/dL. Multiple rounds of treatment are often needed to achieve remission, and some neurologic symptoms may not fully resolve regardless of treatment length. Surgical removal of metallic, foreign bodies as well as bulking agents used to move metal through the GI tract can be used on an individual basis, potentially reducing chelation time. A 2009 study found that the administration of grit, either fine or coarse, promoted a decrease in the amount of time it took for birds to pass metallic foreign bodies from the GI tract, when surgery was not an option.
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