The patient began receiving oxygen, and monitoring was begun with a continuous electrocardiogram (ECG) immediately after the
collapsing episode. The patient was treated with pantoprazole (1 mg/kg intravenously once daily) and dolasetron (0.5 mg/kg
intravenously once daily). Because of the concern of both neurologic disease and cardiac disease and because the patient did
not appear clinically dehydrated despite vomiting episodes, fluid therapy was not initiated on presentation until further
diagnostics could be performed.
Vitals, including mentation assessment, were performed every six hours with respiratory rate and effort being monitored every
two hours. The patient had two more episodes of vomiting overnight. An intermittent tachyarrhythmia was noted on telemetry
by a technician during one of the vomiting episodes, but the tachyarrhythmia had resolved by the time the veterinarian was
notified and evaluated the ECG.
PROGRESSION OF NEUROLOGIC SIGNS
Ten hours after presentation, the patient was laterally recumbent and no longer able to ambulate without assistance. The dog
could bear weight on all four limbs but would immediately lie down without support. Conscious proprioception was absent in
both hindlimbs with decreased reflexes and forelimb rigidity. Evaluation by a neurologist confirmed an upper motor neuron
spinal cord lesion with nonambulatory pelvic limb paresis. The lesion was localized to the T3-L3 spinal cord, although diffuse
cerebrocortical disease was also suspected because of the dull mentation.
At this time, differential diagnoses included autoimmune or infectious myelitis and encephalitis, primary or metastatic neoplasia,
or a vascular accident to the spinal cord and possibly brain.
ADDITIONAL DIAGNOSTIC TESTS
Thoracic radiography revealed mild left-sided cardiomegaly with a vertebral heart score of 12 (normal for dogs = 8.7 to 10.7)
without evidence of congestive heart failure. The pulmonary parenchyma was unremarkable and mild hepatomegaly was appreciated
on the included portion of the abdominal cavity.
At this time, the patient developed ventricular and supraventricular ectopy. Frequent isolates of ventricular premature complexes,
isolated supraventricular premature complexes, and periods of accelerated idioventricular rhythm were noted on the ECG. The
arrhythmias converted to sinus rhythm without intervention. Because of the combination of both neurologic and cardiovascular
abnormalities, systemic disease was suspected.
An echocardiogram, abdominal ultrasonography, and magnetic resonance imaging with cerebrospinal fluid collection were recommended,
but unfortunately, the patient's condition rapidly declined. Because of the severity of the patient's clinical signs, the
rapid progression, and the cost associated with further diagnostic tests, the owners elected euthanasia and consented to an
educational postmortem examination.