Page 1127 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1102 CHAPTER 10

VetBooks.ir signs that have been seen. Death can occur within of ingested lead, versus 1–2% in adults, based on the
increased calcium requirement of younger animals.
a few hours of the onset of clinical signs and is often
Ingestion of forage containing more than 80 ppm
accompanied by violent convulsions.
lead may cause chronic lead poisoning. Chronic lead
Diagnosis exposure results in slowly developing toxic manifes-
Diagnosis is based on clinical signs and known tations, which are primarily neurological (peripheral
exposure to metaldehyde. Clinicopathological tests, neuropathy) or haematopoietic (anaemia). Exposure
including CSF analysis, are non-diagnostic and post- to high levels of lead may result in overt CNS toxic-
mortem lesions are non-specific. Metaldehyde test- ity, as lead enters the brain at a dose-dependent rate
ing can be carried out on stomach contents or serum. following absorption. Lead deposition in the CNS
results in acute cerebellar haemorrhage and oedema
Management from capillary dysfunction.
The primary aim of treatment is to control convul-
sions, because there is no antidote available. Mineral Clinical presentation
oil or activated charcoal may be beneficial soon after In horses, lead poisoning is manifested as a combina-
ingestion to minimise absorption. Supportive care tion of central and peripheral nerve dysfunction, GI
in addition to treatment for any dehydration or aci- upset and interference with haematopoiesis. Clinical
dosis is also warranted. signs commonly seen are laryngeal hemiplegia, dys-
phagia (with associated secondary aspiration pneu-
Prognosis monia), ataxia, muscle fasciculations, hyperaesthesia,
Horses that recover do not seem to suffer from any weight loss and depression. The mild to moderate
sequelae. anaemia seen with chronic poisoning is primar-
ily due to disruption of haemoglobin synthesis. An
LEAD TOXICOSIS increase in nucleated RBCs out of proportion to the
anaemia suggests lead poisoning, especially when
Definition/overview accompanied by basophilic stippling.
Lead toxicosis is a rare cause of neurological disease
in horses and is associated with inadvertent ingestion Differential diagnosis
of lead. EMND; anticholinesterase insecticide toxicity
(organophosphates and carbamates).
Aetiology/pathophysiology
Lead is regarded as a global contaminant. The most Diagnosis
likely sources of lead for horses are contamination Definitive diagnosis of lead poisoning is based on
from nearby mines and smelting operations, dis- detection of a blood lead concentration greater than
carded lead-acid batteries and ashes remaining after 0.35 ppm in an animal with appropriate clinical signs.
combustion of older buildings. Lead-based paints Greater than 10 ppm lead in liver and kidney samples
on buildings were a major source of contamination, is also compatible with lead poisoning. Supportive
but these are likely only to be found on buildings analyses include urinary lead concentrations before,
built before 1960 in most countries. The majority of and 6–12 hours after, chelation therapy is initiated.
ingested lead is finely divided and highly available. It
is solubilised in the acidic environment of the stom- Management
ach and readily absorbed from the proximal small Treatment is aimed at enhancing urinary excretion
intestine. Atomic similarities mean that bivalent lead with chelation therapy. Calcium disodium ethyl-
acts like calcium once absorbed. In mammals, most enediaminetetraacetic acid (EDTA) will accelerate
lead from chronic exposure is dynamically bound in excretion from blood and soft tissues, but does little
the bone matrix. The toxic dose depends on the age of to lead that is stored in bone. A 6.6% solution of cal-
the animal, with younger animals absorbing 10–20% cium disodium EDTA is prepared in 5% dextrose