Diagnosis of lead toxicosis is based upon a combination of clinical signs, hematology, biochemical analysis, radiology, toxicologic
analysis and, in some cases, post-mortem evaluation. A hypochromic regenerative anemia arising from the premature destruction
and decreased production of red-blood cells may be noted. Red-blood cells may also contain cytoplasmic vacuoles and basophilic
stippling (hemoglobin precipitation) although they may not be easily observed. Biochemical parameters that might be altered
in cases of lead intoxication include elevations in LDH and AST activity, total protein, uric acid and CK activity. Blood
and tissue lead analysis are useful diagnostic tools; however, ante-mortem measurement of tissue levels is not routinely performed
in live birds. Whole-blood samples should be submitted in heparinized tubes since the majority of lead is found in the RBCs.
Radiographs may be useful if metallic densities are noted in the gastrointestinal tract (Photo 1). However, the absence of
identifiable metal densities in the GI tract with appropriate clinical signs does not rule out lead intoxication.
If blood lead levels are greater than 20 microgram/dl (0.2 ppm) and documented clinical signs are consistent with lead toxicosis,
then lead poisoning is a very likely diagnosis. Blood levels greater than 50 microgram/dl in most species are considered to
be diagnostic, although, clinical signs have been correlated with blood lead levels as low as 15 microgram/dl (0.15 ppm).
As mentioned previously, chickens appear to be more resistant to lead toxicosis than other species and may appear normal even
with blood lead levels as high as 800 microgram/dl (8.0 ppm). Tissue (fresh frozen kidney, liver, brain and bone) levels 3
to 6 ppm or higher are considered significant. Elevated protoporphyrin levels (PP) or decreased aminolevulinic acid dehydrogenase
(ALAD) activity may be detected in some, but not all, birds and may not correlate well with clinical signs.
Pathologic lesions associated with lead intoxication include demyelination of peripheral nerves, focal areas of vascular damage
in the cerebellum, vascular necrosis, multifocal myocardial degeneration, renal nephrosis (with degeneration and necrosis
of tubular epithelial cells), hemosiderosis in the spleen and other organs, arrested mitotic activity in the proventricular
epithelial cells and testicular degeneration.
Therapeutic goals for managing heavy metal intoxication should concentrate on stabilizing the patient's condition, removing
the source of intoxication from the GI tract, removing lead from the tissues of the patient and prevention of further exposure
to the toxicant. Supportive care includes administration of fluid (Lactated ringer's solution IV or subcutaneously with dextrose),
corticosteroids (the use of corticosteroids is controversial) to relieve cerebral edema, control of seizures with diazepam
(0.5 to 1.0 mg/kg q 8-12 hours as needed), iron replacement therapy in severe cases of anemia and chelation with calcium ethylenediaminetetraacetate
(CaEDTA) (Calcium Disodium Versonate, Riker Laboratories, Northridge, CA, USA) (30-35 mg/kg q 12 hours for 5-10 days), D-Penicillamine
(Cuprimine, Merck, Rahway, NJ, USA) (55 mg/kg PO q 12 hours for one to two weeks) or dimercaptosuccinic acid (DMSA) (25-35
mg/kg q 12 hours). Although acute necrotizing nephrosis associated with administration of CaEDTA has not been documented in
avian species, chelation therapy with CaEDTA is most commonly limited to five days with a rest period of five to seven days
between additional treatments. Clinical signs associated with CaEDTA toxicosis include polydipsia, polyuria, proteinuria and
hematuria. Nephrotoxicity was not observed in a study that compared two heavy metal chelators in a group of cockatiels receiving
chelation therapy (40 mg/kg q 12h for 21 days) for lead or in two studies in which falcons receiving undiluted CaEDTA at a
does of 50 mg/kg IM q 12h for 2-23 consecutive days or 100 mg/kg IM q 12h for 5-25 consecutive days depending upon the falcons
blood lead concentration. It has been suggested that D-Penicillamine may increase the absorption of lead from the GI tract
despite the thought that it is a better chelating agent than CaEDTA. Combining CaEDTA and D-Penicillamine for several days
until the symptoms dissipate followed by a three-to six-week treatment period with D-Penicillamine alone has been suggested
as the best regimen for lead toxicity. Endoscopy, bulk diets, binding agents and even flushing of the GI tract with the patient
under general anesthesia may assist in the removal of lead from the gastrointestinal tract. Surgery may be necessary if the
lead particles cannot be removed with other methods.