3 dogs were examined because of a sudden onset of signs of pain (1 dog) or paraparesis (2 dogs).
Neurologic findings consisted of myelopathy affecting the lumbar intumescence (1 dog) and T3-L3 myelopathy (2 dogs). In all dogs, MRI revealed spinal cord compression caused by L3-4 disk herniation. All dogs underwent routine surgical decompression of the intervertebral disk herniation. During MRI and decompressive surgery, physiologic variables were monitored. Immediately after surgery, all dogs were paraplegic with pelvic limb neurologic dysfunction consistent with myelopathy affecting the L4 through caudal spinal cord segments.
TREATMENT AND OUTCOME
Within 24 hours after surgery, repeated MRI in all dogs revealed hyperintensity in the spinal cord gray matter of the lumbar intumescence on T2-weighted images. In the absence of neurologic improvement, dogs were euthanized at 3, 91, and 34 days after surgery. Postmortem microscopic examination of each dog's spinal cord at the lumbar intumescence revealed necrosis of the gray matter with relative white matter preservation suggestive of an ischemic injury.
Dramatic neurologic deterioration following decompressive surgery for intervertebral disk herniation in dogs may be associated with the development of poliomyelomalacia secondary to ischemia. In these 3 dogs, ischemia developed despite probable maintenance of normal spinal cord blood flow and perfusion during anesthesia. To exclude other causes, such as compression or hemorrhage, MRI was repeated and revealed hyperintensity of the spinal cord gray matter on T2-weighted images, which microscopically corresponded with ischemic neurons and neuronal loss.
Objective—To determine the effect of long-term
administration of enalapril on renal function in dogs
with severe, compensated mitral regurgitation.
Design—Randomized controlled trial.
Animals—139 dogs with mitral regurgitation but
without overt signs of heart failure.
Procedure—Dogs were randomly assigned to be
treated with enalapril (0.5 mg/kg [0.23 mg/lb], PO,
q 24 h) or placebo, and serum creatinine and urea
nitrogen concentrations were measured at regular
intervals for up to 26 months.
Results—Adequate information on renal function
was obtained from 132 dogs; follow-up time ranged
from 0.5 to 26 months (median, 12 months). Mean
serum creatinine and urea nitrogen concentrations
were not significantly different between dogs receiving
enalapril and dogs receiving the placebo at any
time, nor were concentrations significantly different
from baseline concentrations. Proportions of dogs
that developed azotemia or that had a ≥ 35% increase
in serum creatinine or urea nitrogen concentration
were also not significantly different between groups.
Conclusions and Clinical Relevance—Results suggest
that administration of enalapril for up to 2 years
did not have any demonstrable adverse effects on
renal function in dogs with severe, compensated
mitral regurgitation. (J Am Vet Med Assoc 2002;221:
Animals—124 dogs with compensated mitral valve regurgitation (MR).
Procedures—Dogs randomly assigned to receive enalapril or placebo were monitored for the primary endpoint of onset of CHF for ≤ 58 months. Secondary endpoints included time from study entry to the combined endpoint of CHF-all-cause death; number of dogs free of CHF at 500, 1,000, and 1,500 days; and mean number of CHF-free days.
Results—Kaplan-Meier estimates of the effect of enalapril on the primary endpoint did not reveal a significant treatment benefit. Chronic enalapril administration did have a significant benefit on the combined endpoint of CHF-all-cause death (benefit was 317 days [10.6 months]). Dogs receiving enalapril remained free of CHF for a significantly longer time than those receiving placebo and were significantly more likely to be free of CHF at day 500 and at study end.
Conclusions and Clinical Relevance—Chronic enalapril treatment of dogs with naturally occurring, moderate to severe MR significantly delayed onset of CHF, compared with placebo, on the basis of number of CHF-free days, number of dogs free of CHF at days 500 and study end, and increased time to a combined secondary endpoint of CHF-all-cause death. Improvement in the primary endpoint, CHF-free survival, was not significant. Results suggest that enalapril modestly delays the onset of CHF in dogs with moderate to severe MR.