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Standards of Care October 2002 (Vol 4, No 9)

Pericardial Effusion

by Mark Rishniw, BVSc, MS, DACVIM

    Introduction

    Pericardial effusion has two basic presentations—acute collapse and more chronic development of ascites and right heart failure. In both cases, there is accumulation of fluid within the pericardial space, with a consequent increase in intrapericardial pressure. This results in diastolic compression of the heart, predominantly the thinner, more compliant right ventricle, because the pressure within the ventricular chamber is lower than the pressure within the pericardial space. A compressed right ventricle cannot fill appropriately. In acute situations, this results in markedly decreased cardiac output from the right side (and subsequently, the left side) and collapse. If the pericardial fluid build-up is slower, neurohormonal mechanisms compensate for the slowly decreasing cardiac output and retain fluid to increase venous filling pressure of the right ventricle. As the venous filling pressure exceeds venous capacitance, right heart failure develops.

    
Pericardial disorders do not cause left heart failure (pulmonary edema). Additionally, those that do not involve fluid deposition within the pericardial space rarely cause emergency complications. Cytologic and biochemical analyses of pericardial fluids are of limited diagnostic value.

    Cardiac tamponade can occur with pericardial effusions. This is characterized by equalization of intracardiac and extracardiac diastolic pressures and is often seen echocardiographically as a diastolic collapse of the right ventricle or atrium. Tamponade can be acute or chronic and results in signs of output failure or right heart failure.

    
Common causes of chronic acquired pericardial effusion include neoplasia (hemangiosarcoma [HSA], heart-base tumors, mesotheliomas) and idiopathic hemorrhagic peritonitis. Feline infectious pericarditis (FIP) can cause clinically significant pericardial effusions in cats. Acute cardiac tamponade can occur with trauma, neoplasia, HSA, and left atrial rupture in dogs with severe mitral regurgitation.

    Diagnostic Criteria

    Historical Information

    
Gender Predisposition: Male dogs may be predisposed to heart-base tumors (e.g., chemodectomas).

    
Age Predisposition: Middle-aged to older dogs are predisposed to pericardial effusion. 


    Breed Predisposition:  

    • HSAs: German shepherds and golden retrievers.
    • Chemodectomas: Brachycephalic breeds.
    • Idiopathic effusions: Large breeds (Great Danes, St. Bernards, Great Pyrenees, golden retrievers).

    Owner Observations:
    Sudden collapse or weakness if acute; ascites, distended abdomen, or “weight gain” if chronic.

    Other Historical Considerations/Predispositions:
    Rarely, atrial rupture with preexistent severe mitral valve disease; rarely in hunting dogs with grass seed migration; cats with FIP.

    Physical Examination Findings

    
In most cases, severe acute effusions produce cardiac tamponade. Severe chronic effusions can also lead to tamponade. Signs listed below attributable to tamponade are indicated.

    
Acute and Chronic

    • Muffled heart sounds.
    • Weak femoral pulses and pulsus paradoxus (tamponade).
    • Sinus tachycardia.

    
Acute

    • Collapse or sudden weakness (tamponade).
    • Dyspnea, tachypnea (tamponade).

    
Chronic

    • Jugular venous distention and jugular pulses (± tamponade).
    • Ascites (± tamponade).

    
Laboratory Findings

    
Acute

    • Prerenal azotemia.
    • Schistocytosis (in some cases of HSA).
    • Hypoxemia.

    Chronic

    • Often unremarkable.
    • Prerenal azotemia if severe.
    • Dilutional hypokalemia and hyponatremia (secondary to congestive heart failure [CHF]) if severe.

    Other Diagnostic Findings

    
Radiography

    • Acute: Loss of normal cardiac shape; heart may not be markedly enlarged because of limited pericardial distensibility but may look more “rounded.”
    • Chronic:
      - Large globoid cardiac silhouette (“basketball-shaped”).
      - Pulmonary interstitial pattern due to compression of the lungs, not pulmonary edema.
      - ± Pleural effusion: Will generally not obscure the cardiac silhouette entirely.
      - Hepatomegaly.
      - Loss of abdominal detail due to ascites.
      - Gas-filled bowel loops or hepatic lobes can be seen within the pericardial space in cases of pericardio-peritoneal diaphragmatic hernia (PPDH). Absence of viscera from their normal abdominal location may also be noted in these cases.

    
Electrocardiography

    • Sinus tachycardia is most common; other arrhythmias are rare. Atrial premature contractions (APCs) and ventricular premature contractions (VPCs) can be seen with HSAs.
    • Decreased amplitude of QRS complexes: not pathognomonic.
    • Electrical alternans: Beat-to-beat changes in QRS amplitude, most often of the R wave, but can be seen in Q or S waves.
    • Arrhythmias: VPCs and APCs are the most common arrhythmias; usually associated with preexistent cardiac disease or myocardial hypoxia in acute pericardial disease.

    
Echocardiography

    • Hypoechoic pericardial region can be seen; this is the fluid within the pericardial space.
    • The heart is more mobile within the pericardial sac and “bounces” around.
    • Diastolic collapse of the right atrium and/or right ventricle can often be seen.
    • Left ventricular measurements are often decreased due to “underloading” of the left heart. Interventricular septum and left ventricular free wall can be thicker than normal (pseudohypertrophy).
    • Masses or clots may be seen within the pericardial space or attached to the epicardium. Pericardial fluid assists in visualizing these, so pericardiocentesis should be done after careful echocardiographic evaluation unless the condition is imminently life threatening. Additionally, tumors are often located in regions not seen with routine views, so expertise in echocardiography is desired to rule out masses.
    • HSAs are most commonly seen on the right auricle, right atrioventricular groove, or right atrium; chemodectomas are usually attached to the ascending aorta; mesotheliomas cannot be identified echocardiographically.
    • Doppler echocardiography of the outflow tracts can document pulsus paradoxus and decreased right and left ventricular outflow velocities (usually of little diagnostic value).
    • Abdominal viscera, displaced into the pericardial space (e.g., with PPDH) may appear as soft-tissue structures alongside the heart, without pericardial fluid.

    
Pericardial Fluid Analysis

    • Most commonly serosanguineous, with a packed cell volume lower than blood. Often described as “port wine” in appearance.
    • Rarely has neoplastic cells (most tumors are not exfoliative).
    • Often has reactive mesothelial cells.
    • If septic, will have neutrophilia with toxic change ± bacteria/fungi.
    • Usually does not clot on exposure to air; fluid is rapidly defibrinated within the pericardial space.
    • Fluid pH is of little diagnostic utility.

    Summary of Diagnostic Criteria

    • Echocardiography: Fluid space surrounding the heart, with accompanying cardiac findings.
    • Radiography: Globoid cardiomegaly.
    • Physical examination: Ascites if chronic, collapse if acute; muffled heart sounds.

    Differential Diagnosis

    • Echocardiography is the most discriminative diagnostic test.
    • Muffled heart sounds may be present in obese animals and animals with pleural effusion or an intrathoracic mass. Radiography and echocardiography will discriminate these differentials.
    • Increased pulmonary interstitial patterns can be misdiagnosed as pulmonary edema. However, pericardial diseases do not cause pulmonary edema because pulmonary blood flow and plasma volume are reduced, resulting in pulmonary vascular hypotension. The interstitial patterns are due to compression of pulmonary parenchyma.
    • Ascites can occur with many cardiac and noncardiac causes; echocardiography will rule out pericardial and cardiac disease.
    • Low-amplitude electrocardiographic complexes may occur with pleural effusion, obesity, or improper electrocardiographic calibration.
    • Pleural fluid can present as a hypoechoic region surrounding the heart on echocardiographic examination. Careful echocardiographic examination will help discriminate pleural from pericardial effusions.
    • Fluid obtained during attempted pericardiocentesis can be pleural fluid, pericardial fluid, or blood. Examining the fluid for clot formation after extraction of a small volume will rule out blood. Contrast pneumo-pericardio-echocardiography (injection of a small bolus of air into the pericardial space during echocardiographic examination) will help identify the location of the catheter to identify the thoracic compartment being aspirated. Air should not be injected if the catheter is within the ventricle.
    • Mesotheliomas cannot be differentiated from an idiopathic effusion without special histopathological techniques. However, continued patient malaise and relatively rapid or persistent recurrence is suggestive of mesothelioma.

    Key To Costs

    On The News Front: Pericardial Effusion

    Treatment Recommendations

    Initial Treatment

    
Diuretics are contraindicated in pericardial effusions.

    Pericardiocentesis $$

    • 
Treatment of choice. This should be performed once the echocardiographic examination has been performed and potential tumors have been identified.
    • Performed with patient under local anesthesia in most cases.
    • Catheter is introduced into the right side after identifying landmarks to minimize the risk of lacerating coronary vessels. It can also be performed from the left side.
    • A small amount of fluid is aspirated initially to confirm correct placement.
    • Electrocardiographic or echocardiographic monitoring during placement is advisable.

    Surgery $$$

    • If the pericardial effusion is due to profuse hemorrhage, emergency surgery to arrest the hemorrhage may be attempted while the pericardium is being emptied via catheter. However, this is generally a heroic and unsuccessful measure.
    • In cases of PPDH that cause severe respiratory compromise (uncommon), surgical reduction of the hernia is recommended. A transabdominal approach is often sufficient in these cases, which retains the integrity of the pleural space and allows normal ventilation during surgery.

    
Fluid Therapy $
    With acute collapse, plasma volume should be expanded rapidly, if possible, especially if pericardiocentesis and echocardiography are not immediately available (fluids can be administered during the echocardiographic examination). This increases venous filling pressure and improves cardiac output. A large-breed dog can easily accommodate 500–1000 ml in 20 minutes. The patient will evacuate the fluid after pericardiocentesis by increased diuresis.

    Alternative/Optional Treatments/Therapy

    Pericardiectomy

    • Can be performed in cases of recurrent pericardial effusion. With idiopathic hemorrhagic pericarditis, recurrence after two pericardiocenteses may warrant pericardiectomy.
    • Is generally the treatment of choice with heart-base tumors after emergency pericardiocentesis.

    
Glucocorticoids
    Oral or intrapericardial glucocorticoids have been recommended for idiopathic hemorrhagic pericardial effusion, but benefits have not been documented.

    
Chemotherapy

    • HSAs may respond to cytoreductive surgery and chemotherapy, although no studies have examined survival in the subset of patients with cardiac HSA.
    • Adriamycin is commonly used.
    • Best results might be in cases in which surgical removal of the HSA is feasible.
    • Chemotherapy is of no value with heart-base tumors and of questionable value with mesotheliomas (intrapericardial cisplatin has been recommended).

    
Surgery
    Cytoreductive surgery after patient stabilization may be attempted in selected cases of HSA that have tumors restricted to accessible and respectable areas. Most HSAs have metastases at time of diagnosis. Consent for intraoperative euthanasia should be obtained prior to surgery in the event that metastases are observed during surgery. Chemodectomas are intimately associated with the aortic wall and cannot be removed but can be “de-bulked” if they are compressing the great vessels. However, bleeding complications can result.

    Relative Frequency: Pericardial Effusion

    Supportive Treatment

    • 
Diuretics: After pericardiocentesis, in cases of chronic pericardial effusion and right heart failure, diuretics may be administered to hasten the evacuation of the ascites. However, patients will generally mobilize and evacuate the ascites within 48–72 hours after successful pericardiocentesis without additional diuretics.
    • Thoracocentesis/abdominocentesis: Pleural and abdominal fluid can be manually evacuated. Pleural fluid can be removed during catheter withdrawal after pericardiocentesis. Ascites is usually allowed to resolve spontaneously.

    Patient Monitoring

    • 
If chemotherapy is instituted, appropriate hematologic and clinical signs should be monitored.
    • Repeat echocardiography can be performed after apparent recovery to ensure lack of subclinical recurrence. Monitoring of clinical signs is also possible, but echocardiography allows more rapid identification of recurrence prior to redevelopment of patient discomfort.
    • In cases of mesothelioma and HSA, thoracic radiography may be used to monitor for pulmonary metastases.

    Diagnostic and Therapeutic Algorithm: Pericardial Effusion
    Causes of Pericardial Effusions: Pericardial Effusion

    Home Management

    
Observation for recurrence of clinical signs (ascites, breathlessness, collapse).

    Milestones/Recovery Timeframes

    • 
With successful pericardiocentesis in acute cases, immediate recovery is anticipated. Rapid recurrence (within minutes) of collapse suggests rapid re-effusion and portends a grave prognosis.
    • With chronic effusions, diuresis is anticipated over the following 72 hours with resolution of the ascites.
    • With mesotheliomas, recurrence is generally relatively rapid (within weeks of initial therapy).
    • HSAs treated with pericardiocentesis alone generally have recurrence of clinical signs within a few days to weeks. Repeated pericardiocentesis may allow a few months’ survival.
    • HSAs treated more aggressively may have slightly longer survival (weeks to months).
    • Chemodectomas treated with pericardiectomy will survive for months to years.
    • In cases of atrial rupture, the prognosis is grave and surgical repair of the atrial tear is generally not possible.

    Treatment Contraindications

    • 
Diuretics are contraindicated in the treatment of pericardial effusion. They can be used as adjunctive therapy to help resolve the ascites once the pericardial effusion has been drained.
    • Pericardiectomy may be contraindicated in cases of HSA, because it removes the limits of hemorrhage volume. With HSAs, the pericardial fluid is due to hemorrhage, not effusion. Hemorrhagic events after pericardiectomy would occur into the much larger pleural space, with likely fatal consequences. If tumor removal is to be attempted, pericardiectomy will also be necessary.

    Prognosis

    Favorable Criteria

    • Rapid resolution of clinical signs without recurrence.
    • Idiopathic hemorrhagic pericarditis.
    • Chemodectoma.
    • Infectious pericarditis with appropriate antimicrobial therapy.

    
Unfavorable Criteria

    • Mesothelioma.
    • HSA.
    • Atrial rupture secondary to severe mitral valve disease.
    • Rapid re-effusion after initial pericardiocentesis (within minutes to hours) is suggestive of a diagnosis of the conditions listed above.

    Kienle RD: Pericardial disease and cardiac neoplasia, in Kittleson MD, Kienle RD (eds): Small Animal Cardiovascular Medicine. St Louis, Mosby, 1998, pp 413–432.

    Sisson D, Thomas WP: Pericardial disease and cardiac tumors, in Fox PR, Sisson D,
    Moise NS (eds): Textbook of Canine and Feline Cardiology, ed 2. Philadelphia, WB
    Saunders, 1999, pp 679–701.

    Ware WA, Hopper DL: Cardiac tumors in dogs: 1982–1995. J Vet Intern Med 13(2):95–103, 1999.

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