Disease Association and Clinical Assessment of Feline Pericardial Effusion
Records were reviewed from 83 cases to determine the main causes and clinical significance of feline pericardial effusion. The most common causes included hypertrophic cardiomyopathy with congestive heart failure, neoplasia, and systemic infection. Most cases had concurrent or secondary pleural effusion or pulmonary edema, with clinical signs of respiratory disease. However, several cases appeared to be affected solely by pericardial effusion rather than pulmonary pathology. Feline pericardial effusion remains an infrequent diagnosis, but its clinical relevance and association with severe cardiac and extracardiac disease warrant diagnostic evaluation.
Introduction
Pericardial effusion accumulates around the heart and, when severe enough, can cause cardiac tamponade—a phenomenon in which diastolic compliance and cardiac preload are decreased to the point of diminished cardiac output. The myocardial thickness and intraventricular pressure of the right heart are less than those of the left heart. Therefore, the right heart is generally affected before the left, resulting in impaired venous return and increased systemic venous pressure. In cats, the elevated hydrostatic pressures create predominantly pleural effusion, although ascites is sometimes noted. The combination of effusions and decreased cardiac output impair both cardiovascular function and the general health of the animal.1
Pericardial effusion is rare in cats, with cardiac tamponade being rarer still. However, pericardial effusion has been reported secondary to some of the most common feline diseases, including hypertrophic cardiomyopathy (HCM), neoplasia, and feline infectious peritonitis (FIP).2 In one study, causes were diagnosed based on necropsy results,2 but no such report has been made using an antemortem data set. Case reports of less common diagnoses or clinical progression have been sporadic, but no recent compilation of clinical signs and findings from a substantial number of cases has been available.3–10
Antemortem diagnosis and comparison of severity, clinical signs, and disease progression are needed to better understand the significance of feline pericardial effusion. The current study had two main objectives: 1) to compare the presence of pericardial effusion to clinical signs and clinical findings, and 2) to determine the etiological frequency of pericardial effusion diagnosed on antemortem or postmortem examination.
Materials and Methods
Data were collected by retrospective analysis of patient records from January 1, 1999 through December 31, 2005 at one institution and from January 1, 1990 through December 31, 2005 at a second institution. Computerized and hard-copy patient records for all cats seen at the two institutions were reviewed. Inclusion criteria consisted of 1) the presence of pericardial effusion; 2) a single etiological diagnosis without evidence of concurrent disease that could pathophysiologically contribute to respiratory or cardiovascular signs; and 3) either a full antemortem diagnostic report or a necropsy report. A complete antemortem diagnostic report included client-reported history, physical examination findings, laboratory results, findings from thoracic radiographs, and an echocardiographic report. Additional diagnostics results were not required unless they were necessary to confirm a diagnosis. Additional antemortem data available on some cases included pericardiocentesis, thoracocentesis, fluid cytological evaluation, FIP polymerase chain reaction (PCR), feline coronavirus titers, fine-needle aspiration of mass lesions with cytological evaluation, and thoracotomy with surgical biopsy and histopathology. A postmortem report that met inclusion criteria consisted of a notation of pericardial effusion on the necropsy report, a single etiological diagnosis, and a gross weight of the heart.
Medical records were reviewed, and information on signalment, clinical signs, and clinical findings was recorded. Clinical signs were defined as abnormal events noted by the owner. Such signs included cough, increased respiratory effort, and tachypnea (i.e., respiratory rate >30 breaths per minute at rest). Clinical findings were defined as abnormal results from physical examination or diagnostic tests; they included muffled heart sounds, jugular pulse or distension, and pleural effusion or pulmonary edema identified on thoracic radiography. Etiological diagnoses were ranked in order of prevalence within three data sets: those found on antemortem examination, postmortem examination, or a combination of the two.
Results
During the 15 years covered by the study, 62 cats had antemortem diagnoses of pericardial effusion, with 44 of these cases meeting inclusion criteria. During this same time period, 57 cases of pericardial effusion were identified on postmortem examination without documented evidence of pericardial effusion on antemortem evaluation. Thirty-nine of these cases met inclusion criteria; therefore, a total of 83 cases were included in the study.
Most (45) of the cases were domestic shorthairs, but other represented breeds included domestic longhair (n=15), Persian (n=5), Himalayan (n=4), domestic medium hair (n=4), Burmese (n=3), Siamese (n=3), Abyssinian (n=2), Maine Coon (n=1), and Manx (n=1). Age at diagnosis ranged from 0.8 to 16 years (mean 6.28 years, median 6 years). Cats <1 year of age presented with peritoneopericardial diaphragmatic hernia (n=2), FIP (n=1), primary mitral valve disease (n=1), or pulmonic stenosis (n=1).
All cats in the antemortem data set had a complete blood count, serum biochemical profile, thoracic radiography, and echocardiography. Other tests performed to definitively prove or exclude diagnoses included thoracocentesis with fluid cytology (n=26), coagulation profile (n=19), pericardiocentesis with fluid cytology (n=11), feline coronavirus titer (n=10), FIP PCR (n=6), fine-needle aspiration (n=3), and thoracotomy with surgical biopsy and histopathology (n=3).
Clinical signs were noted by the owner for 37 of the 44 cats in the antemortem data set. Reported clinical signs included tachypnea (n=33), increased respiratory effort (n=8), and cough (n=5). The antemortem clinical findings reported by the clinician included pleural effusion (n=29), jugular pulse or distension (n=8), muffled heart sounds (n=8), and pulmonary edema (n=5).
Congestive heart failure (CHF) from various cardiac pathologies was the most common cause (n=30) of pericardial effusion in the antemortem data set. Pathologies associated with CHF included HCM, unclassifiable cardiomyopathy, mitral valve disease, dilated cardiomyopathy (DCM), and pulmonic stenosis [see Table]. The second most common cause was neoplasia, which was found in two cases of lymphoma, two cases of thymoma, and one case of mesothelioma. The remaining causes included FIP, peritoneopericardial diaphragmatic hernia, hypoalbuminemia, disseminated intravascular coagulation (DIC), pericarditis, and systemic infection and inflammation [see Table].
Neoplasia was the most common (n=11) cause reported in the postmortem data set, with lymphoma and adenocarcinoma as the only two types identified at necropsy. Congestive heart failure (n=7) due to HCM, DCM, or unclassifiable cardiomyopathy was the second most frequent postmortem diagnosis. The remaining cases had systemic infection and inflammation, FIP, trauma, DIC, pericarditis, renal failure, and myocardial necrosis [see Table].
The most frequently diagnosed etiology in the combined antemortem and postmortem data set (n=83) was CHF (n=37), which was primarily caused by HCM and unclassifiable cardiomyopathy. Neoplasia was the second most common (n=16) diagnosis, consisting primarily of lymphoma and adenocarcinoma [see Table].
Discussion
The retrospective nature of this study limited the authors’ ability to analyze disease progression and changes in clinical signs associated with improvement or worsening of pericardial effusion. The clinical evaluations recorded on either antemortem or postmortem records were performed by clinicians and veterinary students of variable skill levels, and thus may have inherent variation and error. The authors also relied on the accuracy and interpretation of those same medical findings and reports, which may have led to some errors in the interpretation of the data.
The current study was modeled after a previous retrospective study, published by Rush et al. in 1990, that was based solely on postmortem cases.2 The authors’ additional antemortem evaluation allowed assessment of the potential importance of clinical signs such as tachypnea, increased respiratory effort, and cough as well as clinical findings such as muffled heart sounds, jugular pulse or distension, pleural effusion, and pulmonary edema.
Rush et al. stated that the time from death to necropsy may have altered the pericardial effusion and thereby skewed its recorded prevalence.2 The antemortem data set provided the authors with information that could not have been altered in the postmortem time period, adding an extra degree of clarity to the findings. Some clinical findings such as electrocardiographic changes (including Q wave attenuation and electrical alternans) were inconsistently recorded and were thus omitted from evaluation.
The authors found a very low frequency of pericardial effusion on either antemortem or postmortem evaluation. It is impossible to accurately estimate the prevalence among cats presented for antemortem evaluation at the two institutions during the study period, given the large number of variables involved in such a calculation. However, the authors identified only 57 postmortem cases among the 5560 cats necropsied over the study period, which suggests a prevalence at necropsy of approximately 1.0%. This is approximately half of the previously reported prevalence.2
The majority of the cases were domestic shorthairs, which is consistent with the total breed presentation to the two hospitals. The authors did not determine whether any of the other breeds were over- or under-represented. The ages at the time of diagnosis were evenly distributed over a substantial range, which was likely a result of the considerable variation in causes.
Pericardial effusion and cardiac tamponade initially and most commonly cause evidence of right-sided heart failure in cats. Cats with cardiac tamponade usually are presented with clinical signs of respiratory disease, while dogs with tamponade typically are presented with ascites.11 This is consistent with the antemortem data set in this study, in which pleural effusion was noted in 62.2% (n=23) of cats with clinical signs; both pleural effusion and pulmonary edema were present in 8.1% (n=3) of cases. Pulmonary edema alone was noted in 5.4% (n=2) of cases.
No pulmonary or pleural pathology was reported in 24.3% (n=9) of the clinically affected cats; however, all nine of these cats were tachypneic, and two of them had increased respiratory effort (although none had a cough). These nine cats may have been clinically affected solely by the presence of pericardial effusion, but most clinical cases probably had concurrent or secondary pleural effusion and/or pulmonary edema.
In the combined data set, 25.3% (n=21) of cats had abdominal effusion, which is less than the 30% previously noted for necropsy cases.2 This discrepancy may have been a result of missed diagnoses of ascites on the antemortem evaluations, earlier detection of pericardial effusion (with less severe cardiac tamponade and right-sided heart failure), or chance. The authors also do not know the impact of postmortem changes on the production of effusions.
Because the amount of pericardial effusion or severity of cardiac tamponade was not measured, the authors could not evaluate the degree of pericardial disease associated with the development of clinical signs or findings. The clinical signs that were consistent with pericardial effusion could also have been associated with many other disease processes, including (but not limited to) pulmonary, pleural, and acid-base disorders. Decreased heart sounds can be a clinical finding in animals with pericardial effusion, systolic dysfunction, decreased left ventricular filling, obesity, pulmonary disease, or pleural pathology. Jugular pulse or distension is indicative of a disease affecting the right heart, thereby causing increased right-sided filling pressures. Cardiac tamponade associated with pericardial effusion causes an increased right ventricular diastolic pressure and subsequent backup of pressure through the venous system. Other causes of right-sided heart failure, such as primary tricuspid valve insufficiency or right ventricular hypertrophy, can result in similar findings.
The frequency of pericardial effusion associated with CHF was considerably lower (17.9) in this study than in a previous report (28.8%).2 This difference could potentially be the result of earlier antemortem detection of congestive heart disease and improved therapeutic management of CHF before death. An antemortem diagnosis of heart failure may also have precluded some owners from requesting or permitting a necropsy.
Subclinical amounts of pericardial effusion have been reported previously in 41.6% to 47% of cats with CHF;12,13 this is greater than the percentage observed in the current study. This difference may be related to the retrospective nature of this study, in which pathologists performing the necropsies may not have documented trivial amounts of pericardial effusion. Therefore, this study may not have included mild cases of subclinical disease that had been documented in previous reports.
In the authors’ study, HCM was the most common cardiomyopathy and the most common cause of CHF associated with pericardial effusion identified on postmortem examination. This finding is consistent with the literature, although HCM was more frequent in this study (51.7%) than in previously reported studies (47.4%).2 No correlation has been suggested between degree of left ventricular hypertrophy and degree of left-sided CHF (determined by the comparison of left atrial diameter and aortic root diameter) in cats with HCM;14 therefore, a correlation between the degree of left ventricular hypertrophy and formation of pericardial effusion is unlikely.
During the period covered by this study, 769 cases of HCM were diagnosed on antemortem evaluation at the two institutions. The 17 cases of pericardial effusion associated with HCM suggest a 2.2% prevalence of pericardial effusion in cats with HCM. In several cases, the antemortem diagnosis of restrictive cardiomyopathy could not be confirmed, because sufficient test results (including diastolic filling pressures) were not available for definitive diagnosis. Therefore, the authors categorized these cases as unclassified cardiomyopathy.
Neoplastic causes were identified on necropsy much more frequently in this study (28.2%) than in the previous report (18.2%).2 All cancer cases diagnosed on necropsy were confirmed with histopathology. The cancers in the antemortem evaluation were diagnosed by various methods. Two cases of lymphoma were diagnosed by echocardiography and cytology of pleural effusion; a case of thymoma was diagnosed with surgical biopsy; a second case of thymoma was identified by echocardiography and confirmed at necropsy; and a case of mesothelioma was identified on echocardiography and confirmed at necropsy.
The frequencies of infection (15.4%) and FIP (12.8%) that the authors reported were similar to those reported previously (15.2% and 13.8%, respectively).2 These findings were consistent with recent epidemiological trends suggesting that FIP prevalence has not substantially decreased in the pet population.15 The frequency of renal failure that the authors reported (5.1%) was also similar to that reported previously (7.6%).2
Conclusion
Feline pericardial effusion is relatively rare and often subclinical. When present, it usually signals a more severe primary disease process, such as HCM, neoplasia, or systemic infection. Therefore, a diagnosis of pericardial effusion suggests the need for further diagnostic tests, including echocardiography, to elucidate the underlying cause. Clinical signs and findings are most commonly associated with concurrent pulmonary edema or pleural effusion, although tachypnea and increased respiratory effort from pericardial effusion can be seen in the absence of other effusive diseases or pulmonary pathology. Prospective studies are needed to evaluate the management and long-term prognosis of cats with pericardial effusion.
