Objective—To quantitatively compare 3 commonly
used treatments for navicular syndrome (NS) in horses:
heel-elevation shoeing alone, heel-elevation shoeing
and phenylbutazone administration, heel-elevation
shoeing and injection of the distal interphalangeal
joint (DIPJ) with triamcinolone acetonide (TA), and all
3 treatments in combination.
Animals—12 horses with NS.
Procedure—A force plate was used to measure
baseline peak vertical ground reaction force (PVGRF)
of the forelimbs. Each horse's forelimbs were shod
with 3° heel-elevation horseshoes; PVGRF was measured
24 hours and 14 days after shoeing. Fourteen
days after shoeing (following data collection),
phenylbutazone (4.4 mg/kg, IV, q 12 h) was administered
(5 treatments). Two hours after the fifth treatment,
PVGRF was measured; TA (6 mg) was injected
into the DIPJ of the forelimb that generated the lower
baseline PVGRF. Fourteen days later, PVGRF was
measured. Phenylbutazone was administered as
before, and PVGRF was measured. Percentage body
weight of force (%BWF) was calculated from PVGRF
measurements and used for comparisons.
Results—14 days after shoeing, mean %BWF in both
forelimbs significantly increased from baseline; additional
administration of phenylbutazone significantly
increased %BWF applied from the more lame forelimb.
Compared with shoeing alone, there was no significant
change in %BWF after injection of the DIPJ
with TA in shod horses.
Conclusions and Clinical Relevance—Heel-elevation
shoeing alone and in combination with phenylbutazone
administration quantitatively decreased lameness
in horses with NS. Although not significant, additional
DIPJ injection with TA resulted in further quantitative
decrease in lameness, compared with that
achieved via shoeing alone. (Am J Vet Res
Objective—To evaluate dogs with sudden acquired retinal degeneration syndrome (SARDS) for evidence of pituitary gland, adrenal gland, and pulmonary neoplasia and antiretinal antibodies and to evaluate dogs with neoplasia for antiretinal antibodies.
Animals—57 clinically normal dogs, 17 with SARDS, and 53 with neoplasia.
Procedure—Thoracic radiography, ultrasonography of adrenal glands, and contrast-enhanced computed tomography of pituitary glands were performed in 15 dogs with SARDS. Western blot analysis was performed on sera of all dogs; recoverin (23 kd) and arrestin (48 kd) retinal antibodies were used as positive controls.
Results—Neoplasia was not detected via diagnostic imaging in dogs with SARDS. Western blot analysis revealed bands in all dogs ranging from > 48 to < 23 kd. Prominent bands with equivalent or greater density than 1 or both positive controls at the 1:1,000 dilution, and present at the 1:3,000 dilution, were detected in 28% of clinically normal dogs, 40% of dogs with neoplasia, and 41% of dogs with SARDS. No bands in dogs with SARDS had a consistent location of immune activity, and none were detected at the 23-kd site. The area around the 48-kd site had increased immune activity in all 3 groups.
Conclusions and Clinical Relevance—The etiology of SARDS in dogs does not appear to be similar to cancer-associated retinopathy in humans on the basis of absence of differential antibody activity against retinal proteins. Although dogs with SARDS often have clinical signs compatible with hyperadrenocorticism, neoplasia of the adrenal glands, pituitary gland, or lungs was not detected.