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Lead toxicity

ISSN 2398-2950

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Introduction

  • Relatively rare poisoning.
  • Cause: ingestion of lead (must be ingested   →   poisoning needs HCl in stomach to make lead soluble).
  • Signs: gastrointestinal and neurological signs, weight loss.
  • Diagnosis: clinical signs, measurement of lead level in blood.
  • Treatment: calcium-EDTA, succimer.
  • Prognosis: good with early administration of chelating agents.

Presenting signs

  • Anorexia.
  • Vomiting Vomiting.
  • Seizures Seizures.
  • Hysteria.
  • Weight loss.
  • Onset may be acute or insidious

Age predisposition

  • Young animals (mean age = 2.7 years) more susceptible as absorb greater fraction of ingested lead.

Special risks

  • Owners of pets with confirmed lead poisoning should be warned of potential exposure to children from the same environmental source.
  • Owners should contact their local health department to obtain advice on testing for lead in the environment.

Pathogenesis

Etiology

  • The source of lead can be difficult to identify.
  • When found, paint is the most common source.
  • Other sources include contaminated soil, linoleum, putty and caulking materials, solder, plumbing materials, decorative glazes, lead shot, fishing sinkers, old toys, drapery weights, batteries, foil from wine bottles, drinking water from lead pipes, etc.
  • Often ingested during grooming.

Predisposing factors

General

  • Increased absorption in young animal especially if calcium-deficient.
  • Absorption depends, in part, on surface area of lead ingested.
  • Incidence is highest in the spring/summer and lowest in the fall/winter, although the cause of this seasonality is not known.
  • A positive correlate has been found in households living at or beneath the poverty level.

Pathophysiology

  • Interferes with thiol-containing enzymes.
  • Has adverse effect in nearly all tissues.
  • LD50 = 800-1000 mg/kg.
  • Anemia due to reduced marrow synthesis of hemoglobin, and increased RBC fragility/destruction.
  • Neurological signs result from CNS edema caused by capillary damage and segmental peripheral nerve demyelination.

Timecourse

  • Chronic: signs progress over weeks-months.
  • Acute: death within a few days.

Epidemiology

  • Anorexia, weight loss.
  • Vomiting.
  • Neurological signs, especially seizures and hysteria.

Diagnosis

Client history

  • Possible known access to old paint or other sources of lead.
  • Vomiting Vomiting.
  • Anorexia.
  • Seizures Seizures, hysteria.
  • Weight loss Weight loss.
  • Polyuria, polydipsia (uncommon).

Clinical signs

  • Anorexia.
  • Vomiting Vomiting.
  • Seizures Seizures.
  • Hysteria.
  • Lethargy.
  • Hyperesthesia.
  • Diarrhea.
  • Weight loss Weight loss.
  • Anemia Anemia: overview.
  • Paresis, paralysis.
  • Polyuria, polydipsia.
  • Blindness Blindness.
  • Abnormal gait, weakness.
  • Abdominal pain.
  • Nystagmus.
  • Regurgitation from megaesophagus.

Diagnostic investigation

Hematology, biochemistry

Radiography

  • May show 'lead line' on distal extremities (very rare in cats).
  • Radio-opaque foreign material in intestines.
  • Megaesophagus is an uncommon finding.

Blood lead analysis

  • Historically, blood lead levels > 35-40 ug/dl (> 0.35 - 0.4 ppm) were considered compatible with toxicosis.
  • Monitoring studies published in the last 10 years, however, have indicated toxicosis in animals with blood levels < 40 ug/dl. In these animals, lead levels have ranged from 12 34 ug/dl (Morgan, 1992).
  • A blood lead level > 15 ug/dl combined with typical clinical signs is now considered significant.

Confirmation of diagnosis

Discriminatory diagnostic features

  • History of potential access.
  • Combination of gastrointestinal and neurologic signs, especially in a young cat.

Definitive diagnostic features

  • Blood lead levels >35 ug/dl (0.35 ppm) with or without clinical signs.
  • Blood lead levels > 15 ug/dl with clinical signs.
  • Post-mortem findings: Liver lead level >5 ppm wet weight, > 10 ppm in the kidneys.

Differential diagnosis

Treatment

Initial symptomatic treatment

  • Remove ingested lead from intestine:
  • Prevent further exposure. Bathe cat to remove any lead dust from the hair coat.
  • Provide fluid and electrolyte support.
  • Control seizures with diazepam Diazepam, phenobarbital Phenobarbital, or propofol  Propofol.

Standard treatment

Administer antidote (chelation therapy):

  • Calcium-EDTA (Versenate) at 25 mg/kg QID x 5 days. Make solution of 1 gm versenate in 100 ml of 5% dextrose/water. Divide total milliliters into 20 doses and give SC QID over 5 days.

Not sodium-EDTA - chelates calcium   hypocalcemia. Do not exceed 5 days of treatment or may result in renal or gastrointestinal changes.

    • Calcium EDTA worsens the signs of toxicosis if lead is still present within the GIT.
    • Calcium EDTA also transiently increases blood lead levels as lead is mobilized into the blood stream.
    • Lead levels in the brain also transiently increase with EDTA therapy.
    • It is most beneficial in recumbent, comatose or vomiting animals that cannot be given oral medications.
    • Its onset of action is quite rapid, so it is very beneficial in animals with extremely high blood lead levels.
    • Requires hospitalization for 5 days.
  • Succimer (Chemet) 10 mg/kg PO TID x 10 days.
    • Does not require lead to be removed from the GIT tract prior to treatment, as chelation-enhanced absorption does not occur.
    • Also does not increase lead levels within the brain.
    • Side effects include vomiting, diarrhea, anorexia and elevated liver enzymes.
    • Onset is rapid.
    • Can be used on an outpatient basis.
    • Expensive.

Monitoring

  • Renal and hepatic function.
  • Urine 6 + 24 hours after treatment with EDTA (to confirm chelation/excretion lead).
  • Measure urine lead and urine lead: urine creatinine ratio 48 hours after onset of succimer therapy.

Subsequent management

Treatment

  • Improved clinical signs.
  • Blood levels of lead begin to drop within 2-3 days of starting treatment, but do not always correlate with an improvement in clinical signs.
  • Re-check blood levels 10-14 days after treatment to determine how far the blood lead level has dropped. This is particularly important in animals with original blood levels of > 100ug/dl, as one course of chelation therapy rarely returns their blood lead concentration to an acceptable level.

Monitoring

  • Improved clinical signs.
  • Blood levels of lead drop within 1-3 days of starting treatment. This does not correlate with improving clinical signs.
  • Recheck blood levels after 3-4 weeks and should be < 0.2 ppm.
  • If not repeat treatment.

Prevention

Control

  • Search the environment for the potential source of lead.
  • Warn parents of risk to children from same source, and encourage children to be tested.
  • Contact local health department for advice on testing the environment for lead, and for lead abatement recommendations.
  • Discourage pica Pica in young animals.

Outcomes

Prognosis

  • Generally good. Approximately 85-90% respond favorably to therapy.
  • Poor if neurological signs severe.

Expected response to treatment

  • Clinical improvement should be seen 24-48 hours.
  • After one course of therapy if blood lead levels are not < 35 ug/dl, repeat therapy. If blood lead levels after therapy are < 35 ug/dl, then monitor lead levels again in 2-3 weeks to make sure they continue to fall (or are not rising again).

Reasons for treatment failure

  • Delayed treatment.
  • Inadequate dosage or duration of therapy.
  • Failure to recognize that more than one course of therapy may be needed.
  • Premature termination of therapy due to expense.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Knight T E & Kumar M S (2003) Lead toxicosis in cats-a review. J Feline Med Surg (5), 249-255 PubMed.
  • Knight T E, Kent M & Junk E J (2001) Succimer for treatment of lead toxicosis in two cats. J Am Vet Med Assoc 218 (12), 1946-1948, 1936 PubMed.
  • Morgan R V (1994) Lead poisoning in small companion animals: an update (1987-1992). Vet Human Toxicol 36 (1), 18-22 PubMed.
  • Morgan R V, Moore F M, Pearce L K et al (1991) Clinical and laboratory findings in small companion animals with lead poisoning - 347 cases (1977-1986). J Am Vet Med Assoc 199 (1), 93-97 PubMed.
  • Morgan R V, Pearce L K, Moore L K et al (1991) Demographic data and treatment of small companion animals with lead poisoning - 347 cases (1977-1986). J Am Vet Med Assoc 199 (1), 98-102 PubMed.

Other sources of information

  • Carson T L, Osweiler G D (2002) Household and metal toxicants. In: Morgan RV, Bright RN, Swartout MS (eds):Handbook of Small Animal Practice. 4th Ed. WB Saunders, Philadelphia, pp. 1222-1229.

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