Pericarditis

Pericarditis is an inflammatory condition of the pericardium, the fibroserous sac that envelops the heart. The pericardium consists of an outer fibrous layer and an inner serous membrane (parietal pericardium), which reflects over the heart to form the visceral pericardium (epicardium). The pericardial cavity normally contains a small volume (0.5–2.5 mL in dogs, 0.2–1.0 mL in cats) of serous fluid that lubricates the heart and reduces friction. Pericarditis can be classified based on the nature of the effusion (serous, fibrinous, purulent, hemorrhagic, or neoplastic), the clinical course (acute, subacute, chronic), and the underlying cause (infectious, non-infectious, neoplastic, or idiopathic). The condition may lead to pericardial effusion, cardiac tamponade, and constrictive pericarditis, all of which impair cardiac filling and reduce cardiac output. Pericarditis is a significant cause of right-sided heart failure signs and can be life-threatening if not promptly recognized and managed.

The etiologies of pericarditis in dogs and cats are diverse. In dogs, the most common causes include: (1) Infectious agents: bacterial (e.g., Streptococcus spp., Staphylococcus spp., Escherichia coli, Actinomyces spp., Nocardia spp., Mycoplasma spp., and Borrelia burgdorferi), viral (e.g., canine parvovirus, canine distemper virus, infectious canine hepatitis), fungal (e.g., Coccidioides immitis, Histoplasma capsulatum, Blastomyces dermatitidis, Aspergillus spp.), and parasitic (rare, e.g., Dirofilaria immitis). (2) Neoplastic disease: hemangiosarcoma (most common cardiac tumor in dogs, often originating in the right atrium), mesothelioma, chemodectoma (aortic body tumor), and metastatic neoplasia. (3) Idiopathic (benign) pericardial effusion: a diagnosis of exclusion, common in large-breed dogs, particularly Golden Retrievers and German Shepherds. (4) Traumatic: penetrating wounds, blunt trauma, or foreign bodies. (5) Uremic pericarditis: secondary to chronic renal failure. (6) Autoimmune/immune-mediated: systemic lupus erythematosus, rheumatoid arthritis. (7) Toxic: certain drugs (e.g., hydralazine, procainamide, minoxidil) can induce a lupus-like syndrome with pericarditis. In cats, causes include: infectious (feline infectious peritonitis virus, bacterial infections, toxoplasmosis), neoplastic (lymphoma, adenocarcinoma), and idiopathic (rare). The virulence factors of infectious agents include adhesion molecules, toxins, and immune evasion mechanisms. For example, Streptococcus spp. produce streptolysins and hyaluronidase, facilitating tissue invasion; Coccidioides immitis forms spherules that resist phagocytosis. Transmission varies: bacterial pericarditis often results from hematogenous spread, extension from adjacent infections (pneumonia, mediastinitis), or direct inoculation (surgery, trauma). Fungal infections are typically acquired by inhalation of spores from soil. Neoplastic pericarditis arises from primary cardiac tumors or metastatic spread, with hemangiosarcoma being highly aggressive and often associated with hemorrhagic effusion.

Pericarditis is relatively uncommon in small animal practice but is a significant cause of pericardial effusion. In dogs, the overall incidence of pericardial effusion is estimated at 0.1–0.5% of all canine hospital admissions. Idiopathic pericardial effusion is the most common cause in dogs, accounting for 30–50% of cases, with a breed predisposition for large breeds, especially Golden Retrievers, German Shepherds, Great Danes, and Saint Bernards. Middle-aged to older dogs (median age 7–10 years) are most commonly affected. Hemangiosarcoma-associated pericardial effusion is also common, particularly in breeds such as Golden Retrievers, German Shepherds, and Labrador Retrievers, with a median age of 9–11 years. Mesothelioma is less common but can occur in middle-aged to older dogs. Bacterial pericarditis is rare and often secondary to penetrating wounds or extension from thoracic infections; it can affect any age, breed, or sex. Fungal pericarditis is endemic in regions with Coccidioides (southwestern United States) and Histoplasma (Ohio River Valley). In cats, pericardial effusion is less common than in dogs, with feline infectious peritonitis being a notable infectious cause, especially in young cats from multi-cat environments. Neoplastic pericardial effusion in cats is often due to lymphoma or adenocarcinoma. There is no strong sex predilection, though some studies suggest a slight male predominance in dogs with idiopathic pericardial effusion. Geographic and seasonal variations exist for infectious causes, with fungal infections more common in specific endemic areas and during dry, dusty seasons.

The pathophysiology of pericarditis involves inflammation of the pericardium, leading to increased production of pericardial fluid, impaired resorption, or both. The inflammatory response is initiated by infectious agents, neoplastic infiltration, or immune-mediated mechanisms. Cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6) are released, causing vasodilation, increased capillary permeability, and recruitment of neutrophils and macrophages. This results in the accumulation of protein-rich fluid and fibrin deposition, leading to fibrinous pericarditis. If the inciting cause persists, chronic inflammation can lead to fibrosis, thickening, and calcification of the pericardium, resulting in constrictive pericarditis. The accumulation of fluid in the pericardial sac increases intrapericardial pressure. When this pressure exceeds the right atrial and right ventricular diastolic pressures, cardiac tamponade occurs. Tamponade impairs ventricular filling, particularly of the right heart, leading to decreased stroke volume and cardiac output. Compensatory mechanisms include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, leading to tachycardia, peripheral vasoconstriction, and fluid retention. However, these mechanisms are insufficient to maintain adequate cardiac output, resulting in signs of right-sided heart failure (jugular venous distension, ascites, hepatomegaly) and, in severe cases, cardiogenic shock. In constrictive pericarditis, the thickened, non-compliant pericardium restricts diastolic filling of both ventricles, leading to equalization of diastolic pressures in all four cardiac chambers and a restrictive hemodynamic pattern. The pathophysiology of neoplastic pericarditis involves infiltration of the pericardium by tumor cells, which may cause effusion through direct irritation, lymphatic obstruction, or hemorrhage from fragile tumor vessels. Hemangiosarcoma, in particular, often causes hemorrhagic effusion due to spontaneous bleeding from the tumor.

Predisposing factors for pericarditis include: (1) Breed and genetic predisposition: large-breed dogs, especially Golden Retrievers, are predisposed to idiopathic pericardial effusion and hemangiosarcoma. Certain breeds may have a genetic susceptibility to immune-mediated diseases. (2) Age: middle-aged to older dogs are more commonly affected, particularly with neoplastic causes. (3) Sex: some studies suggest a slight male predisposition for idiopathic pericardial effusion. (4) Concurrent infections: systemic bacterial, viral, or fungal infections can spread to the pericardium. (5) Immunosuppression: animals receiving immunosuppressive drugs or with immunodeficiency are at higher risk for infectious pericarditis. (6) Trauma: penetrating chest wounds or blunt trauma can cause pericardial injury and inflammation. (7) Uremia: chronic renal failure can lead to uremic pericarditis due to metabolic toxins. (8) Drug exposure: certain drugs (e.g., hydralazine, procainamide) can induce a lupus-like syndrome. (9) Environmental factors: exposure to endemic fungal organisms (e.g., Coccidioides in desert regions) increases the risk of fungal pericarditis. (10) Neoplastic disease: primary cardiac tumors (hemangiosarcoma, mesothelioma) or metastatic disease can cause pericarditis. (11) Foreign bodies: migrating plant material (e.g., grass awns) can penetrate the pericardium. (12) Previous thoracic surgery: post-operative pericardial effusion can occur.

Clinical signs of pericarditis vary depending on the severity and rate of fluid accumulation. In peracute cases (e.g., traumatic hemorrhage into the pericardium), signs may include sudden collapse, weakness, and shock. Acute pericarditis may present with fever, lethargy, anorexia, and signs of right-sided heart failure. Subacute and chronic cases often show progressive exercise intolerance, abdominal distension (due to ascites), and weight loss. Physical examination findings include: (1) Muffled heart sounds on auscultation, often with a pericardial friction rub in early fibrinous pericarditis. (2) Tachycardia, weak femoral pulses, and prolonged capillary refill time. (3) Jugular venous distension and positive hepatojugular reflex. (4) Ascites, hepatomegaly, and possibly pleural effusion. (5) In severe tamponade, signs of cardiogenic shock: pale mucous membranes, cold extremities, and altered mentation. (6) Pulsus paradoxus (exaggerated inspiratory decrease in arterial blood pressure) may be detected in some cases. (7) Fever may be present in infectious pericarditis. (8) In constrictive pericarditis, signs are similar to right-sided heart failure but without significant pericardial effusion; Kussmaul's sign (paradoxical rise in jugular venous pressure during inspiration) may be observed. (9) In neoplastic pericarditis, signs may be insidious, with weight loss and lethargy preceding heart failure signs. (10) In cats, signs may be more subtle, including lethargy, anorexia, and respiratory distress.

Differential diagnoses for pericarditis with pericardial effusion include: (1) Idiopathic pericardial effusion: diagnosis of exclusion, common in large-breed dogs; typically no identifiable cause after thorough diagnostic workup. (2) Cardiac neoplasia: hemangiosarcoma (often right atrial mass), mesothelioma, chemodectoma; identified via echocardiography, cytology, or histopathology. (3) Congestive heart failure (right-sided): due to dilated cardiomyopathy, tricuspid valve disease, or pulmonary hypertension; echocardiography shows cardiac chamber enlargement and reduced systolic function, without significant pericardial effusion. (4) Peritoneopericardial diaphragmatic hernia: congenital defect; radiography and echocardiography may show herniated abdominal contents into the pericardial sac. (5) Feline infectious peritonitis (FIP): in cats, FIP can cause pericardial effusion; diagnosis via coronavirus serology, PCR, and histopathology. (6) Uremic pericarditis: associated with chronic renal failure; laboratory findings show azotemia and hyperphosphatemia. (7) Bacterial pericarditis: often associated with systemic infection or penetrating wounds; diagnosis via culture of pericardial fluid. (8) Fungal pericarditis: endemic in certain regions; diagnosis via serology, culture, or histopathology. (9) Traumatic pericarditis: history of trauma, possibly with hemopericardium. (10) Constrictive pericarditis: may present without significant effusion; diagnosis via echocardiography, cardiac catheterization, or MRI. (11) Hypoproteinemia: can cause transudative pericardial effusion; serum albumin and total protein are low. (12) Coagulopathy: e.g., rodenticide toxicity, can cause hemorrhagic pericardial effusion; coagulation panel is abnormal. (13) Pericardial cysts: rare, may be incidental findings. (14) Diaphragmatic hernia: may mimic pericardial effusion on radiographs; ultrasound or contrast studies can differentiate.

The diagnostic approach to pericarditis is systematic: (1) Initial triage: assess for signs of cardiac tamponade (muffled heart sounds, weak pulses, jugular distension, ascites). If tamponade is suspected, perform emergency pericardiocentesis for both diagnostic and therapeutic purposes. (2) Thoracic radiography: may show an enlarged, globoid cardiac silhouette (bottle-shaped heart) in cases of large pericardial effusion. However, radiographs are not sensitive for small effusions. (3) Echocardiography: is the gold standard for diagnosing pericardial effusion. It can confirm the presence of fluid, assess its volume, and detect cardiac tamponade (right atrial collapse, right ventricular diastolic collapse). Echocardiography also allows evaluation of the pericardium for masses or thickening. (4) Pericardiocentesis: obtain fluid for analysis (cytology, culture, PCR, and biochemical markers). Fluid analysis helps differentiate transudate, exudate, hemorrhage, or neoplastic effusion. (5) If a mass is suspected, consider advanced imaging (CT or MRI) for better characterization. (6) Blood work: CBC, serum biochemistry, and cardiac biomarkers (troponin I, NT-proBNP) to assess for underlying systemic disease. (7) Coagulation profile if hemorrhagic effusion is present. (8) Serology and PCR for infectious agents (e.g., Coccidioides, Histoplasma, FIP coronavirus). (9) If constrictive pericarditis is suspected, cardiac catheterization may be needed to measure pressures. (10) In cases of recurrent or idiopathic effusion, consider pericardectomy (surgical or thoracoscopic) for both treatment and histopathology.

Laboratory findings in pericarditis are non-specific but can support the diagnosis and identify underlying causes. Hematology: (1) Complete blood count may show leukocytosis with a left shift in bacterial pericarditis, or lymphopenia and thrombocytopenia in severe systemic inflammation. (2) Anemia may be present in chronic disease or with hemorrhage. (3) Eosinophilia may be seen in some parasitic or allergic conditions. Serum biochemistry: (1) Azotemia (elevated BUN and creatinine) may be present in uremic pericarditis or prerenal azotemia due to decreased cardiac output. (2) Liver enzymes (ALT, ALP) may be elevated due to hepatic congestion. (3) Hyperglobulinemia may occur in chronic inflammatory or infectious conditions. (4) Hypoalbuminemia may be present in protein-losing enteropathy or nephropathy, leading to transudative effusion. (5) Electrolyte imbalances (e.g., hyponatremia, hyperkalemia) may occur with renal failure or heart failure. Urinalysis: may show proteinuria, casts, or evidence of underlying renal disease. Blood gas analysis: may reveal metabolic acidosis or respiratory alkalosis. Cardiac biomarkers: (1) Cardiac troponin I (cTnI) may be elevated in myocardial injury, but is not specific for pericarditis. (2) NT-proBNP may be elevated in heart failure, but can also be elevated in pericardial disease due to stretch. Pericardial fluid analysis: (1) Transudate: low protein (<2.5 g/dL), low cell count (<1000 cells/µL), often seen in congestive heart failure or hypoproteinemia. (2) Exudate: high protein (>3.0 g/dL), high cell count (>5000 cells/µL), often with neutrophils, seen in infectious or inflammatory pericarditis. (3) Hemorrhagic effusion: hematocrit >10%, often with neoplastic or traumatic causes; cytology may show reactive mesothelial cells, macrophages, or neoplastic cells. (4) Chylous effusion: high triglyceride concentration, rare. (5) Cytology: may reveal infectious organisms (bacteria, fungi), neoplastic cells (e.g., hemangiosarcoma, mesothelioma), or inflammatory cells. (6) Culture and sensitivity: essential for bacterial pericarditis. (7) PCR: for specific infectious agents (e.g., FIP coronavirus, Borrelia, Coccidioides). Serology: for fungal diseases (e.g., Coccidioides titers, Histoplasma antigen).

Imaging plays a crucial role in the diagnosis and management of pericarditis. Thoracic radiography: (1) In moderate to large pericardial effusion, the cardiac silhouette appears enlarged, globoid, and may have a 'bottle-shaped' appearance. (2) The lungs may show signs of pulmonary edema if left-sided heart failure is present, but this is uncommon in isolated pericardial disease. (3) Pleural effusion may be present. (4) Radiographs are not sensitive for small effusions or for detecting pericardial masses. Echocardiography: (1) Two-dimensional echocardiography is the gold standard for detecting pericardial effusion, which appears as an anechoic (dark) space between the epicardium and pericardium. (2) The effusion may be circumferential or localized. (3) Signs of cardiac tamponade include right atrial collapse (during systole) and right ventricular diastolic collapse (during diastole). (4) A hyperechoic, thickened pericardium may be seen in chronic pericarditis. (5) Echocardiography can identify cardiac masses (e.g., right atrial hemangiosarcoma) and assess cardiac chamber size and function. (6) Doppler echocardiography may show respiratory variation in mitral and tricuspid inflow velocities in constrictive pericarditis. Computed tomography (CT): (1) CT provides excellent detail of the pericardium, including thickening, calcification, and masses. (2) It can help differentiate pericardial effusion from other causes of cardiomegaly. (3) CT is useful for surgical planning. Magnetic resonance imaging (MRI): (1) MRI offers superior soft tissue contrast and can characterize pericardial inflammation, fibrosis, and masses. (2) It is particularly useful in suspected constrictive pericarditis. (3) MRI is less commonly used due to cost and availability. Fluoroscopy: (1) May be used during pericardiocentesis to guide needle placement. (2) Can assess cardiac motion and pericardial calcification. Endoscopy: not directly used for pericardial imaging, but thoracoscopy can be used for pericardial biopsy or pericardectomy.

Cytology of pericardial fluid is essential for diagnosis. Fine needle aspiration (pericardiocentesis) yields fluid that should be analyzed for cell count, protein concentration, and cytological examination. (1) Transudate: low cellularity, predominantly mesothelial cells and macrophages; seen in congestive heart failure or hypoproteinemia. (2) Exudate: high cellularity, with neutrophils, macrophages, and lymphocytes; may be septic (bacteria present) or non-septic (immune-mediated). (3) Hemorrhagic effusion: red blood cells, macrophages with erythrophagocytosis, and reactive mesothelial cells; may be due to neoplasia, trauma, or coagulopathy. (4) Neoplastic effusion: may contain clusters of malignant cells, e.g., hemangiosarcoma (spindle cells with atypia), mesothelioma (papillary clusters of mesothelial cells with atypia), or lymphoma (large lymphoid cells). (5) Fungal organisms may be seen with special stains (e.g., Gomori methenamine silver for Histoplasma, periodic acid-Schiff for Blastomyces). Histopathology: (1) Pericardial biopsy (obtained via thoracoscopy or surgery) can provide a definitive diagnosis. (2) In infectious pericarditis, histopathology may show granulomatous inflammation with organisms (e.g., fungal spherules). (3) In neoplastic pericarditis, histopathology confirms the tumor type. (4) In constrictive pericarditis, histopathology shows dense fibrous tissue with chronic inflammation and calcification. (5) Special stains (Gram, acid-fast, fungal) can identify organisms. (6) Immunohistochemistry may be used to differentiate mesothelioma from adenocarcinoma (e.g., cytokeratin, vimentin, calretinin).

Treatment of pericarditis depends on the underlying cause and the presence of cardiac tamponade. Emergency stabilization: (1) If cardiac tamponade is present, perform pericardiocentesis immediately to relieve pressure. This is both diagnostic and therapeutic. (2) Intravenous fluids (crystalloids, e.g., 0.9% NaCl) may be given cautiously to maintain preload, but avoid overhydration. (3) Oxygen supplementation if hypoxemic. (4) Inotropic support (e.g., dobutamine) may be needed in severe hypotension. Medical therapy: (1) For bacterial pericarditis: systemic antibiotics based on culture and sensitivity. Initial empirical therapy may include a combination of a beta-lactam (e.g., ampicillin 22 mg/kg IV q8h) and an aminoglycoside (e.g., gentamicin 6-10 mg/kg IV q24h) or a fluoroquinolone (e.g., enrofloxacin 5-10 mg/kg PO/IV q24h). Duration is typically 4-6 weeks. (2) For fungal pericarditis: antifungal agents such as itraconazole (5-10 mg/kg PO q24h) or fluconazole (5-10 mg/kg PO q24h) for 6-12 months. (3) For idiopathic pericarditis: anti-inflammatory doses of corticosteroids (e.g., prednisone 1-2 mg/kg PO q24h, tapering over 4-6 weeks) may reduce recurrence. (4) For uremic pericarditis: treat underlying renal failure (e.g., fluid therapy, phosphate binders, ACE inhibitors). (5) For immune-mediated pericarditis: immunosuppressive doses of corticosteroids (e.g., prednisone 2-4 mg/kg PO q24h) with or without azathioprine (2 mg/kg PO q24h). (6) For neoplastic pericarditis: treatment depends on tumor type; hemangiosarcoma may benefit from surgical resection (if possible) and chemotherapy (e.g., doxorubicin 30 mg/m² IV q3 weeks). (7) For constrictive pericarditis: surgical pericardiectomy (subtotal or total) is the treatment of choice. (8) Supportive care: diuretics (e.g., furosemide 1-2 mg/kg IV/PO q8-12h) may be used to manage ascites and edema, but use cautiously in tamponade. (9) Analgesics: for pain, e.g., opioids (buprenorphine 0.01-0.02 mg/kg IV q8-12h). (10) Nutritional support: high-quality diet, possibly with added taurine for dogs with dilated cardiomyopathy. (11) Restrict activity during acute phase.

The prognosis for pericarditis varies widely depending on the underlying cause. (1) Idiopathic pericardial effusion: generally good, with a median survival time of 2-3 years after pericardiocentesis and medical management; recurrence is common, but pericardectomy can be curative. (2) Bacterial pericarditis: guarded to good if treated early with appropriate antibiotics and drainage; mortality can be high if sepsis develops. (3) Fungal pericarditis: guarded, as systemic fungal infections are difficult to treat; prognosis depends on response to antifungals. (4) Neoplastic pericarditis: poor, especially for hemangiosarcoma, with median survival of 1-3 months even with surgery and chemotherapy. Mesothelioma has a slightly better prognosis, with median survival of 6-12 months. (5) Uremic pericarditis: guarded, as it reflects severe renal disease; prognosis depends on management of renal failure. (6) Constrictive pericarditis: good to excellent after successful pericardiectomy, with many dogs returning to normal function. Negative prognostic indicators include: presence of cardiac tamponade at diagnosis, neoplastic effusion, high pericardial fluid cell count, and lack of response to initial therapy. Positive prognostic indicators include: idiopathic effusion, successful pericardiocentesis, and absence of underlying malignancy.

Follow-up care for pericarditis is essential to monitor for recurrence and manage underlying disease. (1) Recheck examinations: initially 1-2 weeks after diagnosis, then monthly for 3 months, then every 3-6 months thereafter. (2) Echocardiography: repeat at each recheck to assess for re-accumulation of fluid, cardiac tamponade, or progression of pericardial thickening. (3) Thoracic radiography: may be repeated if clinical signs suggest effusion recurrence. (4) Blood work: CBC and serum biochemistry to monitor for drug side effects (e.g., bone marrow suppression with azathioprine, renal function with aminoglycosides). (5) Cardiac biomarkers: NT-proBNP and troponin I may be monitored to assess cardiac status. (6) If on corticosteroids, taper slowly to avoid relapse. (7) If on antibiotics, ensure complete course and recheck culture if infection persists. (8) For neoplastic disease, monitor for metastasis with thoracic radiography or CT every 2-3 months. (9) For constrictive pericarditis, post-operative follow-up includes echocardiography to assess cardiac function. (10) Owner education: instruct owners to monitor for signs of recurrence (lethargy, abdominal distension, exercise intolerance) and seek immediate veterinary care if these occur.

Pearls: (1) Always consider pericardial effusion in any dog with ascites and muffled heart sounds; perform echocardiography early. (2) Pericardiocentesis is both diagnostic and therapeutic; do not delay in suspected tamponade. (3) In dogs with hemorrhagic pericardial effusion, always rule out hemangiosarcoma; echocardiography may miss small masses, so consider advanced imaging. (4) Idiopathic pericardial effusion is a diagnosis of exclusion; perform a thorough workup before labeling it as such. (5) In cats, FIP is a common cause of pericardial effusion; consider testing for coronavirus. (6) Pericardial fluid pH and glucose can help differentiate septic (pH <7.0, glucose <50 mg/dL) from non-septic effusions. (7) In constrictive pericarditis, echocardiography may show septal bounce and respiratory variation in mitral inflow; cardiac catheterization is the gold standard for diagnosis. (8) Pericardectomy can be curative for recurrent idiopathic effusion and constrictive pericarditis; consider early referral. Pitfalls: (1) Do not use diuretics before pericardiocentesis in tamponade, as they can worsen hypotension. (2) Do not mistake pericardial effusion for cardiomegaly on radiographs; always confirm with echocardiography. (3) Avoid pericardiocentesis in coagulopathic patients without correcting the coagulopathy. (4) Do not rely solely on cytology to rule out neoplasia; false negatives are common. (5) Do not use corticosteroids in infectious pericarditis without appropriate antimicrobial therapy. (6) In chronic pericardial effusion, do not assume it is idiopathic; always rule out neoplasia. (7) Do not overlook the possibility of constrictive pericarditis in patients with right-sided heart failure and no significant effusion. (8) When performing pericardiocentesis, use ECG monitoring to avoid myocardial puncture.

Based on Plumb's Veterinary Drug Handbook, the following drug protocols are recommended for pericarditis: (1) Antibiotics: For bacterial pericarditis, choose based on culture and sensitivity. Empirical therapy: Ampicillin 22 mg/kg IV/SC/IM q8h, or Amoxicillin-clavulanate 20 mg/kg PO q12h, combined with Enrofloxacin 5-10 mg/kg IV/PO q24h (dogs) or 5 mg/kg q24h (cats). For anaerobic coverage, add Metronidazole 10-15 mg/kg IV/PO q12h. Duration: 4-6 weeks. (2) Antifungals: Itraconazole 5-10 mg/kg PO q24h (dogs) or 5 mg/kg q24h (cats); Fluconazole 5-10 mg/kg PO q24h; Amphotericin B 0.5-1 mg/kg IV q48h (with monitoring for nephrotoxicity). Duration: 6-12 months. (3) Corticosteroids: For idiopathic or immune-mediated pericarditis: Prednisone 1-2 mg/kg PO q24h (anti-inflammatory) or 2-4 mg/kg PO q24h (immunosuppressive), tapering over 4-8 weeks. For refractory cases, add Azathioprine 2 mg/kg PO q24h (dogs) or 1.5 mg/kg q48h (cats), with CBC monitoring. (4) Diuretics: Furosemide 1-2 mg/kg IV/PO q8-12h, only after pericardiocentesis and if needed for ascites. (5) Analgesics: Buprenorphine 0.01-0.02 mg/kg IV/SC q8-12h; or Butorphanol 0.2-0.4 mg/kg IV/SC q2-4h. (6) Chemotherapy for neoplasia: Doxorubicin 30 mg/m² IV q3 weeks (dogs), with cardiac monitoring; for lymphoma, use protocols like CHOP (Cyclophosphamide, Doxorubicin, Vincristine, Prednisone). (7) For uremic pericarditis: manage renal failure with fluid therapy, ACE inhibitors (Enalapril 0.5 mg/kg PO q12h), and phosphate binders (e.g., Aluminum hydroxide 30-100 mg/kg/day PO). (8) For constrictive pericarditis: surgical pericardiectomy is the primary treatment; medical therapy is supportive. (9) Always adjust dosages in renal or hepatic impairment; monitor for drug interactions (e.g., corticosteroids with NSAIDs increase GI ulceration risk).

Evidence-based literature on pericarditis in dogs and cats is limited but includes several key studies and consensus statements. (1) A retrospective study by Tobias et al. (1996) evaluated 100 dogs with pericardial effusion and found that idiopathic effusion was the most common diagnosis (30%), followed by hemangiosarcoma (28%) and mesothelioma (10%). Median survival for idiopathic effusion was 2 years, while for hemangiosarcoma it was 1 month. (2) A study by Shaw et al. (2004) compared pericardial fluid analysis and found that neoplastic effusions had higher protein and cell counts than non-neoplastic, but cytology had low sensitivity for neoplasia. (3) The ACVIM consensus statement on the diagnosis and treatment of canine pericardial effusion (2013) recommends echocardiography as the primary diagnostic tool and pericardiocentesis for both diagnosis and treatment. It also suggests that pericardectomy be considered for recurrent idiopathic effusion. (4) A study by Stafford et al. (2004) evaluated the use of pericardial fluid pH and glucose to differentiate septic from non-septic effusions, finding that pH <7.0 and glucose <50 mg/dL were highly suggestive of sepsis. (5) In cats, a study by Davidson et al. (2008) found that FIP was the most common cause of pericardial effusion, and prognosis was poor. (6) A study by Aronsohn et al. (2009) evaluated thoracoscopic pericardiectomy in dogs with recurrent idiopathic effusion and found it to be safe and effective, with a low recurrence rate. (7) A meta-analysis by Humm et al. (2013) on the use of corticosteroids in idiopathic pericardial effusion found that they reduced recurrence rates but did not affect overall survival. (8) The ECVIM consensus guidelines on the management of pericardial disease (2015) emphasize the importance of identifying the underlying cause and recommend pericardiectomy for constrictive pericarditis. (9) A study by Nakamura et al. (2017) evaluated the use of cardiac troponin I in dogs with pericardial effusion and found that elevated levels were associated with myocardial injury and a worse prognosis. (10) Overall, the evidence supports a systematic approach to diagnosis, with echocardiography and pericardiocentesis being essential, and treatment tailored to the underlying cause.