Pericardial effusion: causes and clinical outcomes in dogs (Proceedings)

Pericardial effusion is a fairly common acquired heart disease in dogs, and prevalence has been reported to be 0.43% (or 1 dog per 233 cases) of dogs presenting to a referral veterinary hospital, and accounts for approximately 7% of dogs with clinical signs of cardiac disease.1 It is a multi-etiologic disorder (including infectious, inflammatory, and neoplastic causes) with a wide spectrum of prognoses ranging from good to grave.2 Careful echocardiographic evaluation for cardiac masses is necessary, and localization of the mass to specific anatomic regions such as the heart base or right atrium is very critical to provide prognostic value.

The most common presenting complaint of dogs with pericardial effusion is collapse, weakness, syncope, or lethargy. Dogs may present with abdominal distension and ascites secondary to cardiac tamponade. Heart sounds are muffled, and lung sounds may also be muffled if there is pleural effusion. Femoral pulses are weak, and sometimes pulsus paradoxis may be palpated when the pulse is stronger during exhalation and weaker during inhalation. If there is cardiac tamponade, the animal may have signs of cardiogenic shock including pale mucous membranes, cold extremities, hypotension, tachycardia, and collapse. These cases require immediate triage for emergency diagnostics and treatment.

Initial triage of a dog with cardiovascular collapse includes a brief triage echocardiogram to assess if there is significant pericardial effusion as a cause of the collapse, as well as an abdominal scan for free abdominal fluid in cases of hemoabdomen. An intravenous catheter should be placed and shock doses of fluids given. Immediate pericardiocentesis is necessary in dogs with low output heart failure and collapse. The animal is placed in left lateral recumbency, and echocardiography is used to define the most optimal site for pericardiocentesis at the right 5-6th intercostal spaces, where there is greatest amount of pericardial fluid the furthest away from the heart and great vessels. In animals that are stable and do not have signs of cardiac tamponade, it is advisable to postpone pericardiocentesis until a detailed echocardiogram is done, as long as it is within a relatively short period of time.

Echocardiography is necessary to diagnose presence and severity of pericardial effusion and a detailed echocardiogram is needed for diagnosis of cardiac masses. Masses are typically classified as right atrial (infiltrating the right atrium or auricle) or heart base (adherent to the ascending aorta), and other less common masses may be located on the pericardium or ventricles. Cardiac tamponade is diagnosed when there is diastolic collapse of the right atrium and/or right ventricle, and indicates that the pericardial effusion is hemodynamically compromising and requires timely pericardiocentesis. Very mild pericardial effusion may be seen with severe right heart disease such as dilated cardiomyopathy or severe tricuspid regurgitation, but is hemodynamically insignificant. Absence of a mass places idiopathic pericarditis, mesothelioma, or infectious causes as highest differentials.

Fluid analysis and cytology is necessary to diagnose infectious causes of pericardial effusion, but is not usually helpful to diagnose neoplastic causes or to differentiate idiopathic pericarditis from neoplastic causes. Most pericardial effusion is classified as hemorrhagic, and often there is mesothelial reactivity. Lymphoma is one neoplastic etiology that may be reliably diagnosed by fluid analysis. Over-interpretation of mesothelial hyperreactivity as mesothelioma based on fluid cytology has been common in the past.

Approximately 50% of idiopathic pericarditis cases have recurrent pericardial effusion. In cases of recurrent pericardial effusion without an identifiable mass, subtotal pericardectomy is necessary, and histopathologic evaluation of the pericardium is necessary (often with special immunohistochemical stains) for differentiation of idiopathic pericarditis from mesothelioma. Subtotal pericardectomy is curative for idiopathic pericarditis. Partial pericardectomy is indicated for dogs with heart base masses, as it relieves cardiac tamponade and is associated with a significant prolongation of survival time (median survival time of 730 days pericardectomy versus 42 days without pericardectomy).3 Pericardectomy is not recommended for dogs with hemangiosarcoma, unless it is combined with mass resection. In dogs with right auricular hemangiosarcoma, surgical resection is a feasible option, followed by chemotherapy. In a small study of 23 dogs with surgically resected right atrial or right auricular hemangiosarcoma, administration of chemotherapy increased survival time (MST with chemotherapy and surgery 175 days versus 42 days with surgery alone).4 No studies have evaluated whether chemotherapy alters survival time in dogs that do not have surgical mass resection. In the author's experience, recurrent acute hemorrhage and cardiac tamponade is common in dogs with cardiac hemangiosarcoma, and usually is lethal before the animal succumbs to metastatic disease.

Retrospective study of 107 dogs with pericardial effusion

The speaker has recently authored a recent retrospective study evaluating 107 dogs diagnosed with pericardial effusion that underwent pericardectomy or necropsy. Surgery and/or necropsy identified 66 dogs with cardiac masses and 41 dogs without a mass. The location of masses included: 38 right atrial masses, 23 heart base masses, 2 concurrent right atrial and heart base masses, 2 pericardial masses, and 1 right ventricular mass. Echocardiography by a board certified cardiologist or supervised cardiology resident identified 53 of 66 dogs with cardiac masses, including 32 of the 38 dogs with right atrial masses and 17 of the 23 dogs with heart base masses. Echocardiography was sensitive (80%) and specific (100%) for detection of a cardiac mass, and was equally sensitive (84%) and specific (100%) for distinguishing right atrial masses from all other etiologies, or distinguishing heart base masses from all other etiologies (sensitivity 74% and specificity 98%). Of the 12 dogs which echocardiography missed masses on initial examination, only 4 dogs had repeated echocardiograms, which identified cardiac masses. This increased the sensitivity of echocardiography to detect a cardiac mass to 88%. This illustrates the importance of repeating echocardiograms in dogs with recurrent pericardial effusion to identify masses that were not evident on the initial examination. Eight of the 12 dogs with masses that were missed on the first echocardiographic examination had a small volume of pericardial effusion at the time of the echocardiogram.

Etiology of pericardial effusion

Neoplasia was the most common cause of pericardial effusion (71% of dogs). Hemangiosarcoma was the most common etiology of pericardial effusion (34%), followed by idiopathic pericarditis (20%), mesothelioma (14%), chemodectoma (8%), thyroid adenocarcinoma (6%), infective pericarditis (5%), lymphoma (3%), sarcoma (2%), and 1 case of each of the following: carcinomatosis, ruptured left atrium secondary to severe mitral regurgitation, sterile foreign body, and granuloma. 33% of cases of mesothelioma had discrete cardiac masses, most often of the heart base (4/5) and rarely of the right atrium (1/5). A majority of right atrial masses were hemangiosarcoma (35/40 dogs, 88%), followed by 1 case (2.5%) of each: neuroendocrine tumor, thyroid adenocarcinoma, mesothelioma, lymphoma, and sarcoma. Heart base masses were most often neuroendocrine tumors (40%), followed by thyroid adenocarcinoma (25%), mesothelioma (20%), and hemangiosarcoma (15%). 1 dog had concurrent right atrial hemangiosarcoma and a neuroendocrine heart base mass. The pericardial masses were caused by one case each of lymphoma and a granuloma. The right ventricular mass was an undifferentiated sarcoma. 3 of 5 cases of infective pericarditis were caused by fox tail foreign bodies with secondary bacterial infections.

Half of dogs with pericardial effusion had evidence of right heart failure, with equal occurrence of ascites or pleural effusion (50% and 47% respectively), with fewer dogs having concurrent ascites and pleural effusion (33%). There was no difference in occurrence of bicavitary effusion, pleural effusion, or ascites between neoplastic and non-neoplastic causes (P= 1, P= 0.84, and P= 0.93 respectively). Cardiac tamponade was subjectively suspected on echocardiography in 39% of dogs. A globoid shaped heart was identified in 50% of dogs on thoracic radiographs, giving a poor sensitivity for detection of pericardial effusion. Pulmonary metastases were only identified on thoracic radiographs in 33% of dogs with confirmed pulmonary metastases on necropsy or thoracotomy. There was a suspicion of a right atrial or heart base mass on thoracic radiographs in 10 of 63 dogs with masses, with a specificity of 100%. The most common electrocardiographic abnormalities included: electrical alternans (28%), sinus tachycardia (28%), dampened QRS complexes < 1 mv (19%), and ventricular arrhythmia (13%). Other less common abnormalities included: supraventricular tachycardia (3%), atrial premature complexes (2%), atrial fibrillation (2%), ST segment elevation (2%), high grade second degree atrioventricular block (1%), and right bundle branch block (1%).

59 dogs had complete necropsies. The metastatic rate was not different between dogs with hemangiosarcoma (56.6%), mesothelioma (62.5%), thyroid adenocarcinoma (50%), or chemodectoma (66.6%) (P = 1 for all comparisons). 21.6% of dogs with right atrial hemangiosarcoma also had splenic hemangiosarcoma. All dogs with lymphoma had metastatic disease. The most common organ of metastasis for all neoplastic cases was the lung (18 dogs; 31%). In dogs with cardiac hemangiosarcoma, the most common organs of metastasis included: lungs (40%), spleen (27%), liver (27%), and kidney (13%). The most common organs of metastasis in dogs with mesothelioma included: intrathoracic lymph nodes (63%), lungs (25%), and pleura (13%). In dogs with neuroendocrine tumors, 50% of metastasis involved the lungs, followed by the spleen (17%) and liver (17%). The most common organ of metastasis for dogs with thyroid adenocarcinoma was the pericardium (33%), followed by equal metastatic rate to the following organs: lung, transcoelomic, and myocardium (each 25%).

Survival analysis

Based on echocardiographic classification, dogs with no cardiac mass lived longer (MST 10.1 months) than dogs with echocardiographic evidence of a cardiac mass (MST 0.5 months, P= 0.0001) Dogs with a heart base mass diagnosed by echocardiography lived longer (MST 5.2 months) compared to dogs with a right atrial mass diagnosed by echocardiography (MST 0.03 months, P= 0.0002) All deaths recorded were caused by the specific etiology of the pericardial effusion and not due to other systemic disease. Regarding specific etiologies of pericardial effusion, dogs with non-neoplastic etiologies lived longer (MST 24.83 months) than dogs with neoplastic etiologies (MST 0.63 months, P < 0.0001). Dogs with hemangiosarcoma had shorter survival (MST 0.07 months) than all other neoplastic etiologies combined (MST 5.17 months, P= 0.0001). Survival time of dogs with mesothelioma was not different from dogs with heart base masses including chemodectoma, ectopic thyroid, or non-specific etiology (MST 6.5 months vs. MST 5.17 months respectively, P= 0.51).

References

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Dunning D, Monnet E, Orton EC, Salman MD. Analysis of prognostic indicators for dogs with pericardial effusion: 46 cases (1985-1996). J Am Vet Med Assoc. 1998;212:1276-80.

Ehrhart N, Ehrhart EJ, Willis J, Sisson D, Constable P, Greenfield C et al. Analysis of factors affecting survival in dogs with aortic body tumors. Vet Surg.2002.Jan.-Feb.;31.(1):44.-8. 2002;31:44-48.

Weisse C, Soares N, Beal MW, Steffey MA, Drobatz KJ, Henry CJ. Survival times in dogs with right atrial hemangiosarcoma treated by means of surgical resection with or without adjuvant chemotherapy: 23 cases (1986-2000). J Am.Vet Med Assoc.2005.Feb.15.;226.(4):575.-9. 2005;226:575-79.