Page 245 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

220 CHAPTER 1

VetBooks.ir pain, and because severe rhabdomyolysis may lead also on the mandible and ribs and in sites of tendon
insertion and periarticular tissues. They may also
to renal compromise, correcting fluid imbalance
and inducing diuresis are essential. Horses affected
roughened coat. Poor growth and weight loss can
with the chronic form of this condition are bet- have a stiff gait, intermittent lameness and a dry and
ter off exercising daily than being rested, and their occur as well, and abnormal bones are susceptible to
diet should be assessed and adjusted accordingly fractures. Teeth may appear mottled and brown dis-
to include balanced minerals and vitamins, high- coloured, and with hypoplastic enamel. Some teeth
quality hay (other than alfalfa) and a minimum of may be missing.
carbohydrates. Limb deformities should be treated
according to the location of the deformity, its sever- Differential diagnosis
ity and the age of the animal. Hypertrophic osteopathy; nutritional second-
ary hyperthyroidism; osteomyelitis; OA; septic
FLUORIDE TOXICOSIS arthritis.

Definition/overview Diagnosis
This condition is a rare event in horses and refers This is based mainly on clinical signs and history
to skeletal abnormality caused by chronic fluorine of possible exposure. Fluoride in urine and bone
intake above the critical levels. Although both acute can be determined, and analysis of water and feed
and chronic forms have been reported, chronic fluo- is advisable. Radiographs may reveal abnormal bone
ride toxicosis appears to be more common. appearance such as thickening and increased density
of the bones.
Aetiology/pathophysiology
Common sources of fluoride include contaminated Management
forage from nearby industrial plants, drinking A reduction of the toxic effects of fluoride can be
water containing excessive amounts of fluoride, attempted by using substances such as aluminum
feed supplements with high fluoride concentra- sulphate, aluminum chloride and calcium carbon-
tion and vegetation grown on soils rich in fluo- ate, but dietary restriction of fluoride-containing
ride. Fluoride accumulates in the bone and teeth substances and removing affected animals from
throughout the horse’s life and it is therefore a the source of the fluoride are the main options for
cumulative poison. It is almost fully absorbed from treatment.
the gastrointestinal tract, and approximately half is
rapidly excreted in the urine; the rest accumulates Prognosis
in calcified developing tissues (i.e. bones and teeth) The prognosis appears to be poor if intermittent
and therefore young growing animals are more sus- lameness is present. The teeth never recover from
ceptible. Excessive amounts of fluoride affect teeth the discolouration.
during development by causing ameloblastic and
odontoblastic damage, which results in defective HYPERTROPHIC OSTEOPATHY
mineralisation. The pathophysiology of the bone
damage is not clear, but the results include abnor- Definition/overview
mal osteogenesis, production of abnormal bone, Hypertrophic osteopathy is a non-contagious con-
accelerated remodelling and, occasionally, acceler- dition usually demonstrated clinically by bilateral
ated bone resorption. symmetric proliferation of vascular connective tis-
sue and subperiosteal bone of the distal extremities.
Clinical presentation The condition is also referred to as Marie’s disease,
Affected horses may have exostosis formation, espe- hypertrophic osteodystrophy and hypertrophic pul-
cially on the third metacarpal/metatarsal bones, but monary osteoperiostitis.