Pericardial Disease

7 Pericardial Disease

3. How is PPDH diagnosed?

Clinical signs associated with PPDH usually develop within the first year or so of life but can appear at any age (cases have been diagnosed between 4 weeks and 15 years of age). Some animals never have clinical signs and are diagnosed fortuitously. Clinical signs are usually gastrointestinal or respiratory. Vomiting, diarrhea, anorexia, weight loss, abdominal pain, cough, dyspnea, and wheezing are most often reported; shock and collapse can also occur. The physical examination may indicate muffled heart sounds on one or both sides of the chest, displacement or attenuation of the apical precordial impulse, an “empty” feel on abdominal palpation (with herniation of many organs), and, rarely, signs of cardiac tamponade.

Thoracic radiography is often diagnostic or highly suggestive of PPDH. Characteristic findings include enlargement of the cardiac silhouette with dorsal tracheal displacement, overlap of the diaphragmic and caudal heart borders, and abnormal fat or gas densities within the cardiac silhouette. On lateral view, a pleural fold is usually evident extending between the caudal heart shadow and the diaphragm ventral to the caudal vena cava. Gas-filled loops of bowel crossing the diaphragm into the pericardial sac, a small liver, or few organs within the abdominal cavity may also be observed. Echocardiography is useful in confirming the diagnosis in animals in which the diagnosis is equivocal. A gastrointestinal barium series is diagnostic if stomach or intestines are in the pericardial cavity. Fluoroscopy, nonselective angiography (especially if only falciform fat or liver has herniated), celiography, or pneumopericardiography also have been used in diagnosis. Electrocardiographic changes are inconsistent; decreased amplitude complexes and axis deviations caused by cardiac position changes sometimes occur.

12. What clinical manifestations are characteristic of cardiac tamponade?

Clinical findings in animals with cardiac tamponade reflect poor cardiac output and right-sided (most commonly) congestive heart failure. Congestive failure arises from compensatory volume retention and the direct effects of impaired cardiac filling. Right-sided signs predominate because of the right heart’s thinner walls and low pressures, although signs of biventricular failure may occur. Nonspecific clinical signs such as lethargy, weakness, poor exercise tolerance, or inappetence may be noted before obvious ascites develops. Rapid accumulation of even small volumes of fluid (50-100 ml) can cause acute tamponade, shock, and death. In such cases, pulmonary edema, jugular venous distention, and hypotension may be evident without signs of pleural and peritoneal effusions or radiographic cardiomegaly.

Historical findings of weakness, exercise intolerance, abdominal enlargement, tachypnea, syncope, and cough are typical. Significant loss of lean body mass occurs in some chronic cases. Jugular vein distention or positive hepatojugular reflux, hepatomegaly, ascites, labored respiration, and weakened femoral pulses are common physical examination findings. A palpable decrease in arterial pulse strength during inspiration (pulsus paradoxus) might be discernable in occasional cases. High sympathetic tone commonly produces sinus tachycardia, pale mucous membranes, and prolonged capillary refill time. The precordial impulse is palpably weak with a large pericardial fluid volume. Heart sounds are muffled in animals with moderate-to-large pericardial effusions. Lung sounds are muffled ventrally with pleural effusion. Although pericardial effusion does not cause a murmur, concurrent cardiac disease may do so. Fever may be associated with infectious pericarditis.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Pericardial Disease

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