Lead Poisoning: Introduction - The Merck Veterinary Manual

Lead Poisoning: Introduction

In veterinary medicine, lead poisoning is most common in dogs and cattle. Lead poisoning in other species is limited by reduced accessibility, more selective eating habits, or lower susceptibility. In cattle, many cases are associated with seeding and harvesting activities when used oil and battery disposal from machinery is handled improperly. Other sources of lead include paint, linoleum, grease, lead weights, lead shot, and contaminated foliage growing near smelters or along roadsides. Lead poisoning is also encountered in urban environments, and renovation of old houses that have been painted with lead-based paint has been associated with lead poisoning in small animals and children.

Pathogenesis:

Absorbed lead enters the blood and soft tissues and eventually redistributes to the bone. The degree of absorption and retention is influenced by dietary factors such as calcium or iron levels. In ruminants, particulate lead lodged in the reticulum slowly dissolves and releases significant quantities of lead. Lead has a profound effect on sulfhydryl-containing enzymes, the thiol content of erythrocytes, antioxidant defenses, and tissues rich in mitochondria, which is reflected in the clinical syndrome. In addition to the cerebellar hemorrhage and edema associated with capillary damage, lead is also irritating, immunosuppressive, gametotoxic, teratogenic, nephrotoxic, and toxic to the hematopoietic system.

Clinical Findings:

Acute lead poisoning is more common in young animals. The prominent clinical signs are associated with the GI and nervous systems. In cattle, signs that appear within 24-48 hr of exposure include ataxia, blindness, salivation, spastic twitching of eyelids, jaw champing, bruxism, muscle tremors, and convulsions.

Subacute lead poisoning, usually seen in sheep or older cattle, is characterized by anorexia, rumen stasis, colic, dullness, and transient constipation, frequently followed by diarrhea, blindness, head pressing, bruxism, hyperesthesia, and incoordination. Chronic lead poisoning, which is occasionally seen in cattle, may produce a syndrome that has many features in common with acute or subacute lead poisoning.

GI abnormalities, including anorexia, colic, emesis, and diarrhea or constipation, may be seen in dogs. Anxiety, hysterical barking, jaw champing, salivation, blindness, ataxia, muscle spasms, opisthotonos, and convulsions may develop. CNS depression rather than CNS excitation may be evident in some dogs. In horses, lead poisoning usually produces a chronic syndrome characterized by weight loss, depression, weakness, colic, diarrhea, laryngeal or pharyngeal paralysis (roaring), and dysphagia that frequently results in aspiration pneumonia.

In avian species, anorexia, ataxia, loss of condition, wing and leg weakness, and anemia are the most notable signs.

Lesions:

Animals that die from acute lead poisoning may have few observable gross lesions. Oil or flakes of paint or battery may be evident in the GI tract. The caustic action of lead salts causes gastroenteritis. In the nervous system, edema, congestion of the cerebral cortex, and flattening of the cortical gyri are present. Histologically, endothelial swelling, laminar cortical necrosis, and edema of the white matter may be evident. Tubular necrosis and degeneration and intranuclear acid-fast inclusion bodies may be seen in the kidneys. Osteoporosis has been described in lambs. Placentitis and accumulation of lead in the fetus may result in abortion.

Diagnosis:

Lead levels in various tissues may be useful to evaluate excessive accumulation and to reflect the level or duration of exposure, severity, and prognosis and the success of treatment. 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.

Hematologic abnormalities, which may be indicative but not confirmatory of lead poisoning, include anemia, anisocytosis, poikilocytosis, polychromasia, basophilic stippling, metarubricytosis, and hypochromia. Blood or urinary δ-aminolevulinic acid and free erythrocyte protoporphyrin levels are sensitive indicators of lead exposure but may not be reliable indicators of clinical disease. Radiologic examination may be useful to determine the magnitude of lead exposure.

Lead poisoning may be confused with other diseases that cause nervous or GI abnormalities. In cattle, such diseases may include polioencephalomalacia, nervous coccidiosis, tetanus, hypovitaminosis A, hypomagnesemic tetany, nervous acetonemia, arsenic or mercury poisoning, brain abscess or neoplasia, rabies, listeriosis, and Haemophilus infections.

In dogs, rabies, distemper, and hepatitis may appear similar to lead poisoning.

Treatment:

If tissue damage is extensive, particularly to the nervous system, treatment may not be successful. In livestock, calcium disodium edetate (Ca-EDTA) is given IV or SC (110 mg/kg/day) divided into 2 treatments daily for 3 days; this treatment should be repeated 2 days later. 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 (2-4 mg/kg/day SC) alleviates clinical manifestations and reduces tissue deposition of lead. Combined Ca-EDTA and thiamine treatment appears to produce the most beneficial response.

d-Penicillamine can be administered PO to dogs (110 mg/kg/day) for 2 wk. However, undesirable side effects such as emesis and anorexia have been associated with this treatment. d-Penicillamine is not recommended for livestock. Succimer (meso 2,3-dimercaptosuccinic acid, DMSA) is a chelating agent that has proven to be effective in dogs (10 mg/kg, PO, tid for 10 days) and is also useful in birds. Fewer side effects have been associated with DMSA as compared with Ca-EDTA.

Cathartics such as magnesium sulfate (400 mg/kg, PO) 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 (50 mg/kg, PO, sid) have been used in combination with DMSA.

Mobilization of lead at parturition, excretion of lead into milk, and lengthy withdrawal times in food-producing animals raise considerable controversy regarding the rationale for treatment from both public health and animal management perspectives.