Diagnosis

Thoracic radiographic changes are variable and will depend on the size of the PDA and any consequential left-sided heart failure. Cardiomegaly, shifting of the cardiac apex to the left, a ductus aneurysmal bump, and pulmonary over-circulation are all common radiographic findings. If the patient presents in left-sided heart failure, pulmonary venous congestion and pulmonary edema will be present.

Diagnosis is usually confirmed with echocardiography using a right parasternal short axis or left parasternal cranial window (Fig. 48-1). Initially, there may be no changes in chamber size or myocardial contractility but eventually the consequences of left to right shunting may result in dilatation of the left atrium, aorta, and main pulmonary artery and dilatation and hypertrophy of the left ventricle, all recognizable on echocardiography (Fig. 48-2). Left ventricular systolic function may become impaired. If a left-to-right shunting PDA is identified, Doppler studies can be performed and will show characteristic high velocity turbulent flow from the aorta, through the ductus and into the main pulmonary artery (Fig. 48-3). This PDA peak velocity will decrease if pulmonary pressures increase, prior to exceeding systemic pressures. However, note that this decrease may be reactive pulmonary hypertension as a consequence of the pulmonary over-circulation and closure of the PDA may resolve the mild pulmonary hypertension when assessed after surgery. Mild increase of velocity in the left ventricular outflow tract and mild aortic and pulmonic insufficiency may also be recognized. Mitral regurgitation is secondary to the left-sided dilation and may be significant.

Thorough echocardiography should be performed in cats because concurrent, but unspecified, congenital heart defects may be present; these were found in 29% of cats in one study.⁷

If the diagnosis of suspected PDA cannot be confirmed by echocardiography, or the presence of other congenital heart anomalies is suspected, cardiac catheterization and angiocardiography may be helpful, but this investigative procedure is rarely required to confirm diagnosis of PDA.

ECG is non-specific; it usually shows tall R waves and wide P waves due to atrial enlargement. Arrhythmias such as atrial fibrillation, supraventricular or ventricular arrhythmias, and ventricular premature complexes may be present.

Treatment

Patients with CHF and pulmonary edema at the time of diagnosis should be treated for several days with furosemide and angiotensin-converting enzyme (ACE) inhibitors before proceeding to anesthesia and surgery. In patients that are older at the time of diagnosis, with a small PDA, conservative management may be appropriate, although generally surgery is still recommended.

Intrapericardial cysts

Intrapericardial ‘cysts’ are rarely reported.10–14 These are usually not true cysts but encapsulated adipose tissue or organizing cystic hematomas. The cyst may be attached to the apex of the pericardium by a pedicle. They may arise if a PPDH containing herniated omentum or falciform fat closes before birth, trapping the fat within the pericardial sac. Cystic changes of herniated and incarcerated liver tissue may also occur in association with PPDH in cats. Intrapericardial cysts cause clinical signs either directly associated with their presence, or due to an associated effusion causing cardiac tamponade. Diagnosis can usually be made by radiography (Fig. 48-4) and/or ultrasound examination of the cranial abdomen and heart. Treatment is by subtotal pericardectomy (see Box 48-4), removal of the cyst (and pedicle if present), and repair of the PPDH (Chapter 45, 45.4.3) if present.

Congenital pericardial defects are very rare. Clinical signs may develop if the size of the defect is such that a portion of the heart can herniate through the defect, as cardiac function will then be compromised. This condition is treated by subtotal pericardectomy.

Pericardial effusion

The commonest acquired pericardial disease in both cats and dogs is pericardial effusion (PE), but the incidence, presentation and underlying causes have differences between these species. Clinically significant PE is very uncommon in cats, and this species rarely presents with cardiac tamponade. In both species PEs remain asymptomatic if the effusion is small and the pericardium remains slightly compliant, or if a larger effusion accumulates slowly allowing the pericardial sac to accommodate to some extent. Cardiac tamponade results when the amount of fluid (or cyst/mass) reaches a volume such that it exerts a pressure equal to or greater than normal cardiac diastolic pressures. The heart is compressed externally and cannot fill effectively during diastole. Right ventricular filling is reduced first, and may progress to compromise left ventricular filling and cardiac output. Systemic venous pressure and capillary hydrostatic pressure increase whilst cardiac output is reduced. Cats with cardiac tamponade usually develop pleural effusion and present with tachypnea and increased respiratory effort.

PE in cats is most commonly part of a more generalized disease (Box 48-1). Myocardial disease is the commonest underlying cause.¹⁵ Small volume clinically insignificant PEs have been reported in approximately 45% of cats with CHF,^16,17 while PEs are rarely reported in dogs with CHF. The other most frequent underlying cause of PE in cats is feline infectious peritonitis. The commonest causes of PE in dogs are idiopathic hemorrhagic pericardial effusion (IPHE), which is unreported in the cat, and cardiac-related neoplasia. In dogs, hemangiosarcoma, usually of the right side of the heart, is the most common neoplastic cause of PE, aortic body tumors also occur with some frequency, mesotheliomas occur less commonly, and other tumors are also reported. These tumors are rarely diagnosed as a cause of PE in cats; lymphoma is the most common underlying tumor associated with the effusion.

The classic radiographic appearance of PE is general cardiomegaly (globoid heart) and sharp borders to the cardiac silhouette (Fig. 48-5). If the PE has accumulated rapidly without time for adaptation, cardiac tamponade may occur without the classic radiographic signs being present. Pleural effusion is usually present in cats with significant PE and may partly obscure the cardiac silhouette.

A definitive diagnosis of PE is made by echocardiography, which allows cardiac disease or mass lesions to be excluded. The pericardial fluid is seen as an anechoic/slightly anechoic circular region surrounding the heart, within the thin hyperechoic line representing the pericardium. Although an uncommon cause of PE in cats, mass lesions affecting the heart may be seen on ultrasound examination. A thorough examination of the heart should be performed prior to pericardiocentesis because masses are most likely to be identified whilst surrounded by fluid (Fig. 48-6).

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