Treatment and outcome
While it was appreciated that pulmonary parenchymal disease could be the underlying problem in this dog, the immediate threat
was the severe pulmonary hypertension. Thus, the therapeutic plan included steps to reduce pulmonary vascular resistance and
pressure. Therapy included 40% cage oxygen, sildenafil citrate (we decided to administer a dosage of 1.5 mg/kg orally b.i.d.
and gradually increased it over five days to 6 mg/kg every four to six hours), and heparin (100 U/kg subcutaneously q.i.d.).
Repeated echocardiographic studies were done to assess the effectiveness of the therapy. While some peak right ventricular
systolic pressure measurements were as low as 50 mm Hg, the pressure never consistently remained reduced, and the dog did
not improve clinically. After five days of continuous oxygen therapy, increasing doses of sildenafil (maximum dose of 6 mg/kg
orally four to six times a day), heparin, amoxicillin (24 mg/kg b.i.d., added on Day 3), and furosemide (3 mg/kg t.i.d., added
on Day 4), the dog was euthanized.
A complete necropsy was performed. The lungs were mottled and rubbery, and the lung peripheries were firmer than the hilar
portions. No thrombi were present in the pulmonary arteries. The heart was dilated with a hemorrhagic right auricle. The kidneys
were grossly normal. Histologically, the kidneys showed scattered interstitial areas that were infiltrated with lymphoid cells.
Pulmonary alveoli were filled with neutrophils and macrophages, and some contained fibrin. Many of the smaller pulmonary arteries
were thickened because of smooth muscle cell proliferation (Figure 3). The right ventricular wall had scattered foci of interstitial fibrosis and degenerate myocytes. Cultures of the pulmonary
parenchyma were not done. The pathologic diagnoses were cardiomyopathy and suppurative interstitial pneumonia.
3. A photomicrograph of a specimen from the lung of the dog in Case 1. The two pulmonary arteries in this section demonstrate
advanced arteriosclerosis. There is marked thickening of the tunica media and tunica adventitia. The thickening of the tunica
media is due to proliferation of muscle fibers, and there is increased fibrous tissue in the tunica adventitia. The vascular
thickening is presumably an important factor in the development of pulmonary hypertension (hematoxylin-eosin).
A 13-year-old, 68-lb (30.9-kg), spayed female Labrador retriever was presented to the referring veterinarian with a history
of gagging, retching, coughing, and respiratory stridor. The dog had been receiving a heartworm preventive, and the most recent
antigen test result (obtained 22 months before presentation) had been negative. A thoracic radiographic examination had revealed
only small, diffuse pulmonary calcifications. The referring veterinarian had concluded that the dog had chronic bronchitis
and laryngeal paralysis. Treatment included enrofloxacin and aminophylline. The dog improved initially but had returned three
months later with worsening respiratory signs. An electrocardiographic examination had showed occasional right-ventricular-originating
premature beats. Laboratory testing had revealed a low serum thyroxine concentration, so levothyroxine sodium had been added
to the therapeutic plan.
Seven months after the initial presentation for the respiratory problem, arytenoid lateralization was performed to alleviate
the respiratory obstruction. For 10 days after the surgery, the dog had profound weakness, respiratory stridor, cardiac arrhythmia,
and one syncopal episode. Three weeks after the surgery, the dog was referred to the Veterinary Teaching Hospital at Virginia
Tech for evaluation of the cardiac arrhythmia. At the time of referral, the dog was being treated orally with levothyroxine
(0.016 mg/kg b.i.d.), procainamide (16 mg/kg t.i.d.), theophylline (9.7 mg/kg b.i.d.), dexamethasone (0.008 mg/kg every 48
hours), and carprofen (2.4 mg/kg b.i.d.).
Initial examination, diagnostic tests, and treatment
On physical examination, the dog's rectal temperature was 101.6 F (38.7 C), its pulse rate was 180 beats/min, and its pulse
quality was weak. The dog was panting heavily. No heart murmurs or abnormal pulmonary sounds were auscultated. The results
of an echocardiographic examination were normal. An electrocardiographic examination revealed occasional right ventricular
premature beats. The cardiac silhouette was normal on thoracic radiographs, but there was a mild, diffuse interstitial lung
pattern that was considered a secondary complication to respiratory compromise. The radiographs also showed numerous radiopaque,
small nodules primarily in the cranial lung lobes that were thought to be age-related calcification. The results of a complete
blood count were normal.
Since the clinical signs in this dog were not entirely attributable to the cardiovascular system, a consult from the surgery
service was requested to evaluate the laryngeal paralysis and the prior surgery. The dog was anesthetized for a brief period,
and visual inspection of the laryngeal area revealed bilateral obstruction and substantial laryngeal and perilaryngeal swelling.
The surgical procedure had not successfully reduced the laryngeal obstruction, so a right arytenoid lateralization was performed
within 48 hours of presentation to the teaching hospital.