Diagnostic value of pericardial fluid analysis in the dog

The physical, chemical, and cytologic characteristics of 50 pericardial effusions were reviewed to determine their value to the clinician for distinguishing a variety of pericardial disorders in the dog. Pericardial fluid analysis allowed identification of chylous and bacterial pericardial effusions. Overlap in the ranges of RBC counts, nucleated cell counts, and protein concentrations between dogs with neoplastic and nonneoplastic disorders precluded identification of the cause of the effusion. Of 19 neoplastic effusions, 74% were not detected on the basis of cytologic findings and 13% of 31 nonneoplastic effusates were falsely reported as positive or suspect for a neoplasm. It was concluded that pericardial fluid analysis, including cytologic examination, did not reliably distinguish neoplastic from nonneoplastic disorders.     

Cardiac troponins I and T in dogs with pericardial effusion

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are sensitive and specific markers for myocardial ischemia and necrosis. Dogs with pericardial effusion frequently have myocardial ischemia and necrosis, and these changes are more severe in dogs with hemangiosarcoma (HSA). We investigated the utility of using serum cTnI and cTnT concentrations to identify the idiopathic pericardial effusion from that associated with HSA. Blood samples for measurement of cTnI and cTnT concentrations were collected before pericardiocentesis in 37 dogs with pericardial effusion. Eighteen dogs had a mass consistent with HSA, 6 dogs had idiopathic pericardial effusion, 1 dog had mesothelioma, and 1 dog had a heart base tumor. No final diagnosis was achieved for 11 dogs. Dogs with pericardial effusion had significantly higher serum concentrations of cTnI (P < .001) but not cTnT (P = .16) than did normal dogs. Dogs with HSA had significantly higher concentrations of cTnI (2.77 ng/dL; range: 0.09-47.18 ng/dL) than did dogs with idiopathic pericardial effusion (0.05 ng/dL; range: 0.03-0.09 ng/dL) (P < .001). There was no difference in the concentration of cTnT between dogs with HSA and those with idiopathic pericardial effusion (P = .08). Measurement of cTnI may be useful in helping to distinguish between idiopathic pericardial effusion and pericardial effusion caused by HSA.     

Biochemical analysis of pericardial fluid and whole blood in dogs with pericardial effusion

Studies evaluating pericardial fluid analysis in dogs to determine the etiology of pericardial effusions have yielded conflicting results. The purpose of this prospective study was to compare acid-base status, electrolyte concentrations, glucose, and lactate of pericardial fluid to peripheral blood from dogs with pericardial effusion and to compare these variables between dogs with neoplastic and nonneoplastic pericardial effusion. Acid-base status, electrolyte concentrations, glucose, hematocrit, urea nitrogen, and lactate concentrations were evaluated in peripheral blood samples and in pericardial effusion samples of 41 client-owned dogs with pericardial effusion. Common abnormal findings in the peripheral blood of dogs with pericardial effusion included hyperlactatemia (n = 38 [of 41]; 93%), hyponatremia (n = 25/41; 61%), hyperglycemia (n = 13/41; 32%), and hypermagnesemia (n = 13/41; 32%). Bicarbonate, sodium, ionized calcium, glucose, and hematocrit were all significantly lower in the pericardial fluid compared with peripheral blood, whereas lactate, chloride, and PCO2 were significantly higher in the pericardial fluid. When comparing the concentrations of variables in the pericardial fluid of dogs with neoplasia (n = 28) to those without neoplasia (n = 13), pH, bicarbonate, and chloride were significantly lower in dogs with neoplasia, whereas lactate, hematocrit, and urea nitrogen were significantly higher in the pericardial fluid of dogs with neoplasia. The difference between peripheral and pericardial glucose concentrations was significantly larger in dogs with neoplasia than in dogs without neoplasia. Although differences between variables in dogs with neoplastic and nonneoplastic pericardial effusion were documented, clinical relevance is likely limited by the degree of overlap between the 2 groups.     

Immunohistochemical characterisation of the lesions of canine idiopathic pericarditis

Pericardial tissue was obtained from 14 dogs with idiopathic pericarditis, and from three dogs with pericardial effusion associated with neoplastic disease, for histopathological assessment and characterisation of infiltrating leucocytes by immunohistochemistry. The major pathological change was extensive pericardial fibrosis which was generally accompanied by a mixed inflammatory response that was of greatest intensity at the cardiac surface of the tissue. Perivascular lymphoplasmacytic aggregates were present at the pleural surface and within the fibrosed pericardium. There were no features that clearly distinguished the samples from dogs with neoplastic disease from dogs with idiopathic pericarditis. The pericardial infiltrates were dominated by MAC 387+ monocyte-macrophages and plasma cells expressing immunoglobulin (Ig)A or IgG. CD3+ T lymphocytes and major histocompatibility complex (MHC) class II+ macrophages were less common, although the perivascular aggregates were mixtures of T and B lymphocytes and a proportion of fibroblasts expressed MHC class II. There was no vascular pathology or deposition of immunoglobulin or complement within vessel walls. These findings are consistent with an immune response dominated by humoral effector mechanisms (Th2 immunity) but do not clearly support a primary immune-mediated pathogenesis for idiopathic pericarditis.     

DIAGNOSTIC PNEUMOPERICARDIOGRAPHY IN DOGS WITH SPONTANEOUS PERICARDIAL EFFUSION

To evaluate the diagnostic accuracy of pneumopericardiography, diagnostic pneumopericardiograms from 39 dogs with spontaneous pericardial effusion of various etiologies were reviewed. Diagnoses were confirmed by surgical biopsy, necropsy, or follow-up evaluation. Thirty-two of 39 studies (82%) were considered diagnostic. There were one false-positive and six false-negative studies. Fifteen of 16 studies (94%) in dogs with idiopathic sanguinous pericardial effusion were negative (i.e., similar to those in normal dogs). Seven of 12 right atrial hemangiosarcomas (58%), six of six heartbase neoplasms (100%), and two of two pericardial cysts (100%) were outlined. Studies in two cases of infective pericarditis revealed abnormal findings, while a negative study was obtained in one patient with pericardial mesothelioma. Lateral positions were most valuable in idiopathic effusions and for outlining heartbase neoplasms. The left lateral recumbent position was particularly important for outlining hemangiosarcomas. Pericardial cysts were profiled best in ventral or dorsal recumbent positions. This study documents the high diagnostic potential of technically adequate pneumopericardiograms in the etiologic diagnosis of pericardial effusion in the dog.     

Idiopathic pericarditis in dogs: no evidence for an immune-mediated aetiology

OBJECTIVE: To ascertain whether specific immunological changes are associated with canine pericardial effusion due to idiopathic pericarditis. METHODS: In this prospective study, serum antinuclear antibody and serum and pericardial fluid immunoglobulin (Ig) G, Ig M and Ig A concentrations were measured in dogs with pericardial effusion due to idiopathic pericarditis or pericardial neoplasia. The secretory index relative to albumin concentration was calculated in order to distinguish between Ig actively secreted into the pericardial fluid and that derived from the blood accumulating within the pericardial sac. Statistical analysis was performed comparing the results obtained between the two groups of dogs. RESULTS: Only three dogs were antinuclear antibody positive; two of these dogs had idiopathic pericarditis and one had neoplasia. Mean serum Ig M and Ig A concentrations were lower than the reference values in both groups, and the secretory indices for Ig M and Ig A were greater than 1.0. However, there was no significant difference with respect to any Ig measurement between the two groups of dogs (P>0.1). CLINICAL SIGNIFICANCE: The results of the present study do not support the hypothesis that canine idiopathic pericarditis has a significant 'immune-mediated' aetiology or immunological features that distinguish it from the pericardial changes associated with local neoplastic disease.     

Long-term survival of 23 dogs with pericardial effusions

Twenty-three dogs with pericardial effusions were identified from case records made between 1992 and 2000. Fourteen of the 23 were diagnosed with idiopathic pericardial effusions, and three of these were treated successfully by one pericardiocentesis. In the remaining 11 cases the pericardial effusion recurred; six cases were managed long-term by either two (three cases), three (two cases), or 11 repeated pericardiocenteses, and the remaining five were treated by pericardiectomy. The median survival time of the six dogs treated by repeated pericardiocentesis was five years and nine days.     

Thoracoscopic partial pericardiectomy in 13 dogs

Thirteen dogs with cardiac tamponade resulting from pericardial effusion were prospectively evaluated to determine feasibility and outcome of thoracoscopic partial pericardiectomy. A lateral thoracoscopic approach allowed adequate exposure to remove a 4- to 5-cm-diameter section of pericardium in all dogs. Complete resolution of cardiac tamponade occurred in all dogs for which there was follow-up (11 dogs). Ten of 13 dogs (76.9%) had neoplastic pericardial effusion. One of these dogs remains alive at 220 days postoperatively and is asymptomatic. The mean survival of the remaining 9 patents with neoplastic effusion was 128 days (range, 14-544 days; median, 38 days). Three of 13 patients (23.1%) had idiopathic pericardial effusion. Two of these dogs remain alive at 585 and 1,250 days postoperatively. One dog with idiopathic pericardial effusion developed cardiomyopathy and was euthanized 18 days after the procedure. Results indicate that the procedure was technically successful in all dogs. No anesthetic complications occurred. Procedural complications included phrenic nerve transection (1 dog), lung laceration (1 dog), and moderate intraoperative bleeding (1 dog). No adverse clinical manifestations of the complications were apparent. We conclude that thoracoscopic partial pericardiectomy is technically feasible and offers several advantages over conventional open thoracic surgical pericardiectomy.     

Percutaneous balloon pericardiotomy as a treatment for recurrent pericardial effusion in 6 dogs

Percutaneous balloon pericardiotomy (PBP) has been performed in people and in a small number of dogs as a treatment for recurrent pericardial effusion with tamponade (PET). We performed this technique on 6 dogs with recurrent PET (5 with heart base tumors and 1 with no identifiable mass). Under general anesthesia and fluoroscopic guidance, a balloon-dilating catheter (diameters 14-20 mm) was introduced percutaneously at the 5th intercostal space through a sheath-introducing catheter, positioned across the parietal pericardium, and inflated 3 times. No dog experienced serious complications. The procedure was considered successful in 4 of 6 dogs. One dog is still alive without recurrence of PET 1 year after the procedure. Three dogs died of unrelated disease without recurrence of PET 5. 19, and 32 months after the procedure. The procedure was not beneficial in 1 dog that was euthanized 9 weeks later because of recurrence of pleural and abdominal effusion thought to be secondary to PET. One dog may have temporarily benefited but developed symptomatic PET 6 months after PBP. PBP appears to be a safe, economical, and potentially effective palliative treatment for recurrent PET and is a reasonable, less invasive alternative to surgery for dogs with recurrent PET, especially effusions caused by heart base tumors and possibly idiopathic pericardial effusion. Premature closure of the stoma is a potential cause for long-term failure and was thought to have been responsible for the recurrence of clinical signs in 2 dogs.     

Use of pericardial fluid pH to distinguish between idiopathic and neoplastic effusions

Pericardial effusion (PE) resulting from neoplasia usually is associated with a poor prognosis, whereas idiopathic PE frequently has a good prognosis. This study examined the utility of pH measurement to distinguish between these 2 etiologies. Dogs were classified as having idiopathic PE (n = 12) if pericarditis was diagnosed on histopathology (n = 4) or if no historical, physical, or echocardiographic evidence of recurrent PE was present for at least 6 months after pericardiocentesis (n = 8). Dogs were classified as having neoplastic PE (n = 25) if pericardial or myocardial neoplasia was detected on histopathology (n = 11) or a discrete mass associated with the right atrium, right ventricle, or the aorta was visualized on echocardiography (n = 14). Samples of PE were centrifuged and the supernatant pH was measured with a portable pH meter. The lowest pH (6.40) was found in a dog with idiopathic PE and the highest pH (7.85) was found in a dog with neoplastic PE. However, data from the 2 groups overlapped in 33 out of 37 (89%) instances, and median pH from the idiopathic and neoplastic groups was not significantly different (7.40 and 7.47, respectively; P = 0.28; difference in medians = -0.7; 95% CI, -0.26-0.06). Because of the degree of overlap, our data provide little justification for the use of pH measurement as a diagnostic test in cases of PE.     

Vascular endothelial growth factor concentrations in body cavity effusions in dogs

Vascular endothelial growth factor (VEGF) has potent angiogenic, mitogenic, and vascular permeability enhancing properties specific for endothelial cells. VEGF is present in high concentrations in inflammatory and neoplastic body cavity effusions and has been implicated in the pathogenesis of neoplastic and inflammatory effusion formation. In this study, VEGF was quantitated by solid-phase enzyme-linked immunoadsorbent assay (ELISA) in samples of pericardial, pleural, and peritoneal effusions (N = 38) from dogs (N = 35) with neoplastic and non-neoplastic diseases. VEGF was detected in 37 of 38 effusions (median, 754; range, 18-3,669 pg/mL) and was present in much higher concentrations than in previously established normal concentrations for canine plasma (median, < 1 pg/mL; range, < 1-18 pg/mL) or in those previously noted in the plasma of dogs with hemangiosarcoma (HSA; median, 17 pg/mL; range, < 1-67 pg/mL). In 4 dogs with HSA, the concurrent plasma VEGF concentration was much lower than in the abdominal effusion (P = .029). No significant correlation was demonstrated between VEGF effusion concentration and effusion total protein content or nucleated cell count. Mean VEGF concentrations were significantly higher in pericardial (median, 3,533; range, 709-3,669 pg/mL) and pleural effusions (median, 3,144; range, 0-3,663 pg/mL) compared to peritoneal effusions (median, 288; range, 18-2,607 pg/mL; P < .05). There was no marked difference demonstrated between effusions associated with malignant and nonmalignant diseases. Further studies are necessary to elucidate the role of VEGF in body cavity effusion formation in dogs.     

Flow cytometric analysis of effusions in dogs and cats with the automated haematology analyser ADVIA 120

Samples were aspirated from 12 thoracic effusions, 10 abdominal effusions and four pericardial effusions in 17 dogs and nine cats. They were analysed cytometrically with the ADVIA 120 flow cytometer and the results were compared with the results of cytological examinations of May-Grünwald-Giemsa-stained smears. The conventional cytology revealed a purulent or pyogranulomatous inflammation in 12 of the animals, lymphoma in six, malignant histiocytosis in two, and an unspecified carcinoma in two; two animals had a chylous effusion, two had a modified transudate, and one dog had an idiopathic pericardial haemorrhage. The flow cytometric analysis was based on cellular volume, peroxidase staining intensity and the determination of nuclear lobularity, and made it possible to identify predominant cell lineages and cell debris, which were shown in characteristic cytograms. Inflammatory effusions, monocytic proliferation and lymphoma were easily detected, but carcinoma cells and mesothelial cells were classified as 'mononuclear blasts'.     

Septic pericarditis in a Yorkshire Terrier

Objective: To describe a novel case management strategy for a small breed dog diagnosed with septic pericarditis. Case summary: An 8‐year‐old spayed female Yorkshire Terrier presented for evaluation of pericardial effusion and persistent hypoglycemia. The dog had been hospitalized at a primary care facility for acute onset of vomiting, lethargy, inappetance, and painful abdominal distension. Pericardial effusion was detected and upon referral, cytologic examination revealed a suppurative exudate with Gram‐positive and Gram‐negative bacteria. The dog was treated with pericardiocentesis and placement of an indwelling pericardial catheter. Subtotal pericardiectomy was performed and a thoracotomy tube was utilized postoperatively. A penicillin‐susceptible Bacteroides species was cultured from the pericardial fluid and was treated with a 6‐week course of antibiotics. The dog was discharged from the hospital and clinical signs have not recurred in over 2 years. New or unique information provided: Septic pericarditis, an uncommon cause of canine pericardial effusion, has been described primarily in large breed dogs and in association with bacterial infection secondary to Hordeum grass (foxtail) awn migration. This case was unique in that the dog was a small breed with no evidence of foreign body penetration or other precipitating cause for the pericarditis. In a novel management plan, an indwelling pericardial catheter was employed to stabilize the dog before subtotal pericardiectomy.     

Septic pericardial effusion associated with pulmonary and pericardial botryomycosis in a dog

The authors report a case of septic pericardial effusion resulting in cardiac tamponade associated with intrathoracic botryomycosis in a dog. Septic pericarditis and a pulmonary mass were diagnosed, and subtotal pericardiectomy and lobectomy of the affected pulmonary areas were carried out. Histopathology of the excised tissue showed changes supportive of botryomycosis--namely a pyogranulomatous inflammation with neutrophils centred around amorphous homogeneous eosinophilic material and club-like bodies containing Gram-positive bacterial cocci present in the centre. The patient recovered well following surgery and antibiotic therapy. To the authors' knowledge, this is the first report of pulmonary botryomycosis in the dog and the first report of this condition presented with pericardial involvement and cardiac tamponade in any species.     

Idiopathic hemorrhagic pericardial effusion with organized thrombi in a dog

A dog was examined because of cardiac tamponade secondary to pericardial effusion. Masses adjacent to the right atrial and ventricular walls were revealed by echocardiography. Pericardectomy and biopsies of the masses established the diagnosis of idiopathic hemorrhagic pericardial effusion with organized thrombi. The dog was healthy 3 months after surgery. These organized thrombi mimicked cardiac neoplasia echocardiographically, and such a possibility should be included in the list of differential diagnoses of cardiac masses.     

Renal failure associated with pericardial effusion in a dog.

Signs of heart failure due to cardiac tamponade developed in a young dog with previously unrecognized renal disease. The uremic syndrome was considered the likely cause of the effusive pericarditis found at necropsy. In a review of necropsy records from 150 dogs with renal disease, 11 had pericardial lesions.     

Successful therapy of coumatetralyl rodenticide induced pericardial effusion with pericardiocentesis in a dog

A 5-year-old, intact male, golden retriever was presented with an acute onset of lethargy and respiratory distress. The dog was diagnosed as having rodenticide intoxication with pericardial effusion. Pericardiocentesis was successfully performed and was followed with a blood transfusion. This case suggests that rodenticide intoxication might cause pericardial effusion in dogs.     

Idiopathic hemorrhagic pericardial effusion in eight dogs

Idiopathic hemorrhagic pericardial effusion was diagnosed in 8 dogs. The patients were typically males of large or giant breeds and a wide age range was represented. In all dogs clinical features of acute or chronic cardiac tamponade and right-sided heart failure were present. The pericardial effusion in each case was identified by thoracic radiography, electrocardiography, and echocardiography. Cytologic examination of the fluid did not allow differentiation from hemorrhagic effusions caused by neoplasia. Bacterial and fungal cultures were negative in 5 dogs. In 6 cases, a presumptive diagnosis was based on the absence of cardiac masses on 2-dimensional echocardiography, contrast pericardiography, or both. The condition was managed successfully by partial pericardiectomy in 5 cases. The definitive diagnosis in each case was established by gross cardiac examination at surgery or necropsy and by histologic examination of tissues. Blood vessels and lymphatics of the parietal and visceral pericardia appeared to be the primary targets of the disease process.