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Basics ⬇

Outline

BASICS

Overview!!navigator!!

  • Pb toxicosis (plumbism) affects the nervous, musculoskeletal, GI, hematopoietic, and renal systems
  • Horses are less susceptible to plumbism than cattle or dogs. Lead intoxication in horses is relatively uncommon in the USA
  • Acute (rare) and chronic forms result from exposures to Pb-contaminated forages in habitats adjacent to mines and smelters or environments with buildings or fences built prior to 1977 (with Pb pipes) and coated with Pb-based paints
  • Ingestion of Pb from Pb-acid batteries, soil contaminated with Pb-containing products, or the ashes of combusted older buildings also poses a risk of Pb intoxication to horses
  • Lead binds to sulfhydryl groups and mimics calcium, thereby disrupting heme synthesis, neurotransmission, and vitamin D metabolism

Signalment!!navigator!!

  • No breed predilections
  • Young, growing foals are most susceptible as they absorb 10–20% of ingested Pb
  • Pregnant and lactating mares also have enhanced GI absorption of Pb and transfer Pb to the fetus or neonate

Signs!!navigator!!

  • Peripheral neuropathies including abnormal lip and tongue movements, laryngeal hemiplegia (“roaring”) or paralysis, dysphagia, esophageal obstruction (“choke”), aspiration pneumonia
  • Anorexia
  • Depression
  • Weight loss
  • Weakness
  • Ataxia
  • Muscle fasciculations
  • Hyperesthesia
  • Lameness and swollen joints (young, growing horses or Pb-containing foreign bodies near joint surfaces)
  • Colic, diarrhea
  • Anemia
  • Seizures
  • Death

Causes and Risk Factors!!navigator!!

  • Acute exposures to >500–750 mg/kg
  • Chronic exposures to 1.7–7 mg/kg/day
  • Habitats near smelting or mining operations
  • Housing in or around barns or fences built prior to 1977 that contain Pb-lined pipes and/or walls painted with Pb-based paints
  • Premises contaminated with Pb-containing batteries, shot, solder, gasoline, oil, or ashes of combusted older buildings
  • Diets deficient in calcium, zinc, iron, or vitamin D
  • Trauma from Pb-containing objects

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Laryngeal hemiplegia or paralysis (“roaring”), esophageal obstruction (“choke”), and EIPH not associated with plumbism—physical examination, endoscopy, radiography, no identified sources of Pb exposure, history of trauma
  • Rabies and other viral encephalitides
  • Equine motor neuron disease and equine degenerative myeloencephalopathy
  • Fumonisin B1 intoxication (“moldy corn poisoning” or equine leukoencephalomalacia)
  • Botulism
  • Intoxications by Centaurea sp.
  • Arsenic toxicosis

CBC/Biochemistry/Urinalysis!!navigator!!

  • Anemia
  • Nucleated red blood cells
  • Basophilic stippling and Howell–Jolly bodies
  • Proteinuria (uncommon)

Other Laboratory Tests!!navigator!!

  • Antemortem—whole-blood concentrations of Pb >0.35 ppm in the presence of appropriate clinical signs, alterations in erythrocyte ALAD activity (decreased), zinc protoporphyrin concentrations (increased), and increased urinary excretion of coproporphyrin and uroporphyrins (ALAD and porphyrin analyses not performed in many veterinary diagnostic laboratories)
  • Postmortem—concentrations of Pb in liver or kidney >10 ppm on a wet-weight basis (>5 ppm in chronic cases), bone concentrations of Pb >40 ppm on a dry-matter basis in chronic cases

Imaging!!navigator!!

  • Radiography to detect Pb-containing objects in the GI tract of small foals or around joints
  • Radiographic visualization of “Pb lines” at epiphyseal plates of long bones in young, growing horses

Other Diagnostic Procedures!!navigator!!

  • Endoscopy to diagnose laryngeal hemiplegia or to visualize Pb-containing foreign bodies in the stomach
  • Measurement of 24 h urinary excretion of Pb following chelation therapy (logistically challenging)

Pathologic Findings!!navigator!!

  • Gross—inconsistent gross pathologic changes in horses, aspiration pneumonia, and emaciation in chronic cases
  • Histologic—peripheral neuropathy with segmental degeneration of axons and myelin in distal motor fibers, pulmonary changes consistent with aspiration pneumonia, reports of renal tubular disease in chronic cases

Treatment ⬆ ⬇

TREATMENT

  • Prevent further Pb exposure
  • Administer sulfate-containing cathartics to bind Pb in GI tract (decrease absorption) and to increase elimination of Pb
  • Enhance urinary Pb excretion with chelation
  • Control pain and hyperexcitability
  • Treat aspiration pneumonia with appropriate antibiotics and NSAIDs
  • Provide supportive care for dehydration, circulatory shock, and dysphagia

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Sodium or magnesium sulfate administered by nasogastric tube (250–500 mg/kg)
  • Dimercaprol (British anti-Lewisite) to chelate intracellular and extracellular Pb at a dimercaprol loading dose of 4–5 mg/kg given by deep IM injection, followed by 2–3 mg/kg every 4 h for 24 h and then 1 mg/kg every 4 h for 2 days; adverse reactions include tremors, convulsions, and coma
  • Ca-EDTA to chelate Pb at a dosage of 75 mg/kg/day divided into 2 or 3 equal treatments and administered for 5 days by slow IV infusion as a 6.6% solution in normal saline or 5% dextrose (1.1 mL of 6.6% EDTA solution/kg); if deemed necessary, retreatment with Ca-EDTA after a 2 day “rest”; adverse effects include depletion of zinc and essential electrolytes
  • In cattle, thiamine hydrochloride at dosages of 2–10 mg/kg twice daily IM for 2 weeks is used; but dosage and efficacy not clearly established in horses
  • Flunixin meglumine at 0.55–1.1 mg/kg IV every 12–24 h and/or butorphanol tartrate at 0.02–0.1 mg/kg IV every 3–4 h up to 48 h for abdominal discomfort
  • Xylazine hydrochloride at 0.3–1.1 mg/kg IV alone (higher dosage) or with butorphanol at 0.01–0.02 mg/kg IV (lower dosage of xylazine) for sedation or control of severe pain
  • Diazepam administered to adults (25–50 mg IV) or foals (0.05–0.4 mg/kg IV) for hyperesthesia, muscle tremors, and seizures (can repeat in 30 min)
  • Appropriate fluid therapy as necessary

Contraindications/Possible Interactions!!navigator!!

  • Chelators may deplete essential cations and electrolytes
  • Sedatives in ataxic horses
  • Cautious use of NSAIDs in GI and renal disease or dimercaprol if renal disease is present

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

  • Identification and removal of Pb source
  • Proper disposal of or limited access to Pb sources
  • Recheck Pb concentration in whole blood 2 weeks after final chelation dose; repeat chelation if >0.35 ppm
  • Monitor serum electrolytes and supplement as needed
  • Provide supportive treatment as needed

Patient Monitoring!!navigator!!

  • Monitor hemogram and whole-blood Pb concentrations
  • Periodic neurologic assessments

Prevention/Avoidance!!navigator!!

  • Prevent exposure to habitats near smelters or mines
  • Avoid use of Pb-containing paints
  • Clean up Pb-contaminated pastures, paddocks, or soil

Possible Complications!!navigator!!

  • Aspiration pneumonia
  • Concurrent exposure to other toxic metals

Expected Course and Prognosis!!navigator!!

Long-term neurologic deficits possible following removal from Pb source and partial recovery of neurologic function.

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Other metal intoxications
  • Laryngeal hemiplegia
  • EIPH
  • Esophageal obstruction

Age-Related Factors!!navigator!!

Young, growing horses.

Zoonotic Potential!!navigator!!

N/A

Public Health Importance!!navigator!!

Appropriate regulatory agencies should be notified of Pb-contaminated matrices that could potentially poison children, e.g. soil or water.

Pregnancy/Fertility/Breeding!!navigator!!

Lead can cross the placenta and, potentially, have adverse effects on the fetus.

Abbreviations!!navigator!!

  • ALAD = d-aminolevulinic acid dehydratase
  • Ca-EDTA = calcium disodium ethylenediaminetetraacetic acid
  • EIPH = exercise-induced pulmonary hemorrhage
  • GI = gastrointestinal
  • NSAID = non-steroidal anti-inflammatory drug

Suggested Reading ⬆ ⬇

Casteel SW. Metal toxicosis in horses. Vet Clin North Am Equine Pract 2001;17:517–527.

Gwaltney-Brant S.Lead. In: Plumlee KH, ed. Clinical Veterinary Toxicology. St. Louis, MO: Mosby, 2004:204–210.

Kruger K, Saulez MN, Nesser JA, Soldberg K. Acute lead intoxication in a pregnant mare. J S Afr Vet Assoc 2008;79(1):50–53.

Author(s) ⬆

Author: Tim J. Evans

Consulting Editors: Wilson K. Rumbeiha and Steve Ensley