Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online: 341
  • Home
  • Print this page
  • Email this page

 Table of Contents  
Year : 2018  |  Volume : 4  |  Issue : 2  |  Page : 160-168

Standardized approach to pericardial effusion management

1 Department of Surgery, Summa Health, Akron, OH, USA
2 Summa Health Medical Group, Cardiothoracic Surgery Specialists, Akron, OH, USA

Date of Submission11-Dec-2017
Date of Acceptance16-Feb-2018
Date of Web Publication30-Aug-2018

Correspondence Address:
Dr. Sarah Eapen
525 East Market Street, Akron, Ohio 44304
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJAM.IJAM_91_17

Rights and Permissions

The purpose of this review is to provide evidence-based, standardized recommendations on intervention for pericardial effusions. The appropriate management strategy is determined by effusion etiology. Pericardiocentesis under echocardiographic or fluoroscopic guidance is recommended for acute viral or idiopathic pericardial effusions. Due to recurrence risk, indwelling pericardial catheter placement is recommended for malignant pericardial effusions. Intrapericardial instillation of sclerosing or antineoplastic agents and percutaneous balloon pericardiotomy are alternative strategies. If less invasive options are not feasible or successful, pericardiotomy may be considered. Wide anterior pericardiectomy is indicated for relapse after repeated drainage. Potential procedural risks and therapeutic benefits are considered in determining the approach to intervention.
The following core competencies are addressed in this article: Practice-based learning and improvement, Medical knowledge, and Patient care.

Keywords: Management, pericardial effusion, pericardiocentesis, pericardiotomy

How to cite this article:
Eapen S, Firstenberg M. Standardized approach to pericardial effusion management. Int J Acad Med 2018;4:160-8

How to cite this URL:
Eapen S, Firstenberg M. Standardized approach to pericardial effusion management. Int J Acad Med [serial online] 2018 [cited 2022 Dec 10];4:160-8. Available from: https://www.ijam-web.org/text.asp?2018/4/2/160/240144

  Introduction Top

Since the first subxiphoid surgical drainage was described by Larrey in 1829, significant advancements have been made in the management of pericardial effusion.[1] Kopecky et al. followed with the first report of successful percutaneous pericardiocentesis in 1986.[2] Despite technological progress, the approach to pericardial effusion varies by etiology, hemodynamic impact, physician experience, and institutional protocol. Common etiologies of pericardial effusion include infection, malignancy, pericardial injury, metabolic disorders, connective tissue disease, and myopericardial and aortic disease.[3],[4],[5] Management of pericardial effusion is directed by the underlying etiology. In the presence of acute pericarditis, medical management with nonsteroidal anti-inflammatory drugs (NSAIDs) is indicated.[3],[4],[6],[7],[8]

Therapeutic interventions for pericardial effusion include pericardiocentesis, indwelling pericardial catheter placement, intrapericardial instillation of sclerosing or antineoplastic agents, pericardiotomy, and wide anterior pericardiectomy.[4],[5],[7],[8],[9],[10],[11],[12],[13] Pericardiocentesis is recommended for acute viral or idiopathic pericardial effusions and may be performed under echocardiographic or fluoroscopic guidance.[4],[7],[8],[9],[10],[11],[13] Indwelling pericardial catheter placement is advised for malignant pericardial effusions, with or without instillation of sclerosing or neoplastic agents.[7],[8],[13] Pericardiotomy or wide anterior pericardiectomy may be considered if less invasive interventions are unsuccessful or in cases of recurrence.[3],[4],[5],[7],[8],[9],[12],[13] Clinical stability is considered in addition to etiology in determining the need for intervention.[9],[10] The purpose of this review is to provide evidence-based, standardized recommendations on intervention. The underlying pathophysiology, clinical presentation, and appropriate diagnostic evaluation preceding intervention will be described as well.

  Pathophysiology Top

Pericardial fluid is an ultrafiltrate of plasma which accumulates secondary to increased production or decreased reabsorption.[6],[14] 10–50 ml of fluid are typically contained within the pericardial sac.[7],[9],[10],[14] Inflammation leads to increased production of pericardial fluid, while increased systemic venous pressure decreases reabsorption of pericardial fluid.[9] Disease processes associated with increased systemic venous pressure include congestive heart failure and pulmonary hypertension.[7] The effects of this process can be magnified by the presence of blood, especially in the setting of antiplatelet or anticoagulation therapy. Even a small amount can increase oncotic effects, drawing fluid into the pericardial sac.

The pericardial pressure–volume curve is J-shaped.[7],[15],[16] An initial increase in volume within the pericardium results in a minimal increase in pressure.[7],[10],[15],[16] Further increase in volume raises pericardial pressure significantly and may lead to acute cardiac tamponade.[7],[10],[15],[16] The pressure–volume response is also dependent upon the rate of fluid accumulation.[7],[10],[15],[16] Slow accumulation allows for gradual pericardial distension without the development of tamponade until later stages.[7],[10],[15],[16]

Increased intrapericardial pressure impairs diastolic filling, thereby decreasing stroke volume and compromising cardiac output.[9],[10],[11],[15],[16] Cardiac output is initially preserved by tachycardia, which is stimulated by increased adrenergic tone.[6],[10],[15],[16] The hemodynamic spectrum of pericardial effusion ranges from preclinical fluid accumulation to shock.[11],[16] In the preclinical stage, pericardial pressure equals right atrial pressure, but is lower than the left atrial pressure.[11],[16] With progression, the left and right ventricular diastolic, right atrial, and pulmonary wedge pressures equalize with pericardial pressure.[10],[15],[16] Consequently, a significant reduction in cardiac output and blood pressure occurs, leading to shock and death without intervention.[11],[15],[16] Such pathophysiologic changes can occur even in the setting of an open pericardium after cardiac surgery.

  Classification Top

Classification of pericardial effusions considers onset, size, distribution, and composition. Hemodynamic impact and cardiac cycle phase are significant as well.[4],[7] Onset may be acute at <1 month, subacute at 1–3 months, or chronic at >3 months.[4],[7] Size is most accurately estimated at end diastole.[4],[10] Effusions are described as small if <10 mm, moderate if 10–20 mm, large if 20–25 mm, and very large if >25 mm with cardiac compression.[4],[5],[10] Effusion distribution is either loculated or circumferential.[4],[7],[10] Small effusions tend to be located posterior to the left ventricle due to gravity dependence.[7] They may also be found adjacent to the right atrium due to lower pressure in the cardiac cycle facilitating fluid accumulation.[7] Moderate-to-large effusions tend to be circumferential.[7] Isolated anterior pericardial fluid is unusual, except in cases of prior surgery or chronic pericarditis causing pericardial scarring.[7] Depending on the presence of plasma ultrafiltrate, purulence, blood, chyle, or air, effusion composition may be described as transudative or exudative.[7] The hemodynamic impact of pericardial effusions ranges from no impact to cardiac tamponade.[7] Finally, the cardiac cycle phase in which the effusion occurs allows for differentiation between physiologic and pathologic effusions.[10] Physiologic effusions are visualized during systole only, whereas pathologic effusions are present throughout the cardiac cycle.[10]

  Etiology Top

In developing countries, tuberculous pericarditis is the most common etiology of pericardial effusion.[3],[7],[8],[10],[12],[13] Concomitant HIV infection promotes effusion development in these cases, leading to more aggressive disease with greater myocardial involvement.[7],[12],[13],[17] Tuberculosis is the cause of pericardial effusion development in over 85% of patients with an HIV coinfection.[17] Failure to treat tuberculous pericarditis is associated with an 85% mortality rate and a 30%–50% risk of progression to constrictive pericarditis.[4],[7] Tuberculous pericarditis develops secondary to an immune response to antigens within the pericardium.[17] A tuberculous etiology should be suspected in immigrants from endemic areas presenting with subacute, moderate-to-large pericardial effusions.[7],[17] Associated low-grade fever, night sweats, and unintentional weight loss may be present as well.[4],[7] Definitive diagnosis requires demonstration of Mycobacterium tuberculosis bacilli in pericardial fluid or tissue.[4],[7],[10],[12]

In developed countries, etiology differs by clinical setting. The most common inpatient causes of pericardial effusions in developed countries are iatrogenic, neoplastic, and uremic pericarditis.[4],[5],[8],[10] In the outpatient setting, idiopathic and viral pericarditis are responsible for most effusions.[4],[5],[8],[10] Neoplastic effusions may develop secondary to primary cardiac malignancies, such as mesothelioma or angiosarcoma.[4],[10] More commonly, pericardial effusions develop in the setting of lung and breast cancer, lymphoma, and leukemia.[4],[10]

Effusions develop in congestive heart failure, cirrhosis, and nephrotic syndrome due to chronic sodium and water retention, reduced lymphatic drainage, and consequent high systemic venous pressures.[5],[8],[10] Metabolic causes include hypothyroidism, renal failure, and severe protein deficiency.[4],[7],[10] Connective tissue and autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus, also have been implicated.[4],[8] Effusion may develop secondary to pericardial injury following myocardial infarction, pericardiotomy, and traumatic pericarditis as well.[4],[7],[10]

Clinical findings may suggest the underlying etiology of pericardial effusion. The presence of inflammatory signs is associated with acute idiopathic pericarditis.[8] In the absence of inflammatory signs, tamponade may delineate etiology.[8] With chronic idiopathic pericardial effusions, both inflammatory signs and tamponade are typically absent.[8] With neoplastic pericardial effusions, inflammatory signs are absent, but tamponade frequently occurs.[8] Hemorrhagic pericardial effusions develop secondary to both idiopathic pericarditis and malignancy.[8] The complex spectrum of pericardial effusions, their presentations, and differentiating characteristics is beyond the scope of this review.

  Clinical Presentation Top

Clinical findings of pericardial effusion depend on the presence of inflammation and tamponade. Inflammatory signs, predictive for acute pericarditis, include fever, chest pain, and pericardial friction rub.[3],[4],[6],[8] Diffuse and sometimes subtle ST-wave changes on electrocardiogram (ECG) can mimic acute coronary syndrome.[4],[17],[18] The associated risk for misdiagnosis potentially leads to inappropriate or delayed therapy.[18] Initially, patients may be asymptomatic with elevated intrapericardial pressure secondary to fluid accumulation.[8] With progression, clinical tamponade and associated signs and symptoms develop. Classic findings described by Beck's triad include hypotension, jugular venous distension, and diminished heart sounds.[19]

Additional signs of tachycardia and pulsus paradoxus may be seen.[5],[7],[10],[11],[20],[21] Sinus tachycardia develops as physiologic compensation for decreased stroke volume to maintain cardiac output.[6],[10],[15],[16] Pulsus paradoxus is defined as an inspiratory decrease in systolic blood pressure of 10 mmHg or greater with inspiration.[4],[5],[6],[10],[20] It occurs with an increase in pericardial pressure >10–12 mmHg and resultant compression of the right atrium and ventricle.[5],[11] It is also predictive of cardiac tamponade severity.[6] Alternative causes of pulsus paradoxus include constrictive pericarditis, right ventricular infarct, chronic obstructive pulmonary disease exacerbation, and pulmonary embolism.[10]

Kussmaul sign, which describes elevated jugular venous pressure during inspiration, may be seen in cardiac tamponade with pericardial constriction.[6] ECG findings of cardiac tamponade include low QRS voltages and electrical alternans.[4],[6],[11] Potential symptoms include chest pain, dyspnea, and orthopnea.[4],[7],[8],[11] When severe, tamponade leads to hemodynamic compromise and shock.[8]

Clinical presentation also depends on the rate of fluid accumulation, as described by the pericardial pressure–volume curve.[7],[14],[15],[16] With rapidly accumulating fluid, small volumes lead to rapid increases in pericardial pressure.[7],[14],[16] Cardiac tamponade subsequently develops when the maximum pericardial reserve volume is exceeded.[14],[16] With slowly accumulating fluid, a large volume of fluid may accumulate over days to weeks before significant changes in pericardial pressure and associated signs and symptoms develop.[7] Even a small amount of loculated fluid can cause localized compressive effects, especially when involving the lower pressure right-sided chambers or vena cava.

  Diagnostic Imaging Top

Chest X-ray is the initial diagnostic imaging study performed for pericardial effusion, given associated symptoms of chest pain and dyspnea.[10],[13] Although the sensitivity and specificity of X-ray are low, findings of cardiomegaly with clear lung fields are consistent with pericardial effusion.[4],[6],[8],[11] On lateral X-ray images, the presence of pericardial fluid is indicated by lucent lines within the cardiopericardial shadow, described as an epicardial halo.[4] Enlargement of the cardiac silhouette does not occur until at least 200 ml of pericardial fluid have accumulated.[6]

In cases of suspected pericardial effusion, echocardiography is the most reliable and cost-effective diagnostic imaging modality.[4],[7],[8],[10],[11],[12],[13],[22],[23] An echocardiogram characterizes the size, location, and hemodynamic impact of an effusion.[8],[22] It may identify concomitant cardiac or paracardial disease and detect elevated pericardial pressure before hemodynamic deterioration occurs.[4],[5],[8] Disadvantages of echocardiogram include operator dependence and false positive findings of pericardial effusion in the presence of adjacent pathology.[8]

Measurement of the total echo-free space in the anterior and posterior pericardial sac during diastole in millimeters corresponds with effusion severity.[4],[8] Mild, moderate, and severe pericardial effusions are <10 mm, 10–20 mm, and >20 mm, respectively.[4],[8] Hemodynamic compromise is more likely in the presence of a moderate-to-severe pericardial effusion.[8] Other suggestive echocardiographic findings include right atrial and ventricular collapse, which occurs when pericardial pressure exceeds intracardiac pressure.[4],[6],[8],[10],[21]

Altered mitral and tricuspid flow may also occur during respiration, which is assessed with Doppler echocardiogram.[7],[8],[10],[21] A >30% decrease in mitral inflow and a >60% increase in tricuspid inflow during inspiration is specific for tamponade.[10] Inferior vena cava (IVC) plethora is a sensitive finding with a high negative predictive value for tamponade.[7],[10],[24] It is defined by an IVC diameter >2.1 cm and <50% decrease with inspiration.[6],[10],[24] The specificity of IVC plethora is limited by the number of conditions associated with IVC dilation.[10] For this reason, the clinical significance of IVC plethora is its negative predictive value, with a normal IVC diameter on echocardiography making tamponade unlikely.[10]

Computed tomography (CT) and magnetic resonance imaging (MRI) are alternative imaging modalities used to characterize pericardial effusions.[12] Rarely are these modalities first-line diagnostic tests searching for pericardial disease. Instead, these tests are performed to evaluate other causes of cardiopulmonary pathology, such as pulmonary embolism, pleural effusion, and aortic dissection. Pericardial effusions may be an unexpected or incidental finding. Typically, these alternatives may be considered in cases of a limited echocardiogram or for procedural planning.[10],[23] Advantages include a larger field of view, allowing for assessment of the entire mediastinum, lungs, and adjacent structures.[7],[8],[12] They facilitate detection of loculated effusions, pericardial thickening, and masses.[7],[12] CT and MRI also provide information regarding spatial distribution, which evaluates complex pericardial effusions.[8],[12]

CT density measurements and MRI signals characterize pericardial fluid more effectively than echocardiogram.[7],[12] Effusion composition is estimated by the degree of CT attenuation in Hounsfield units (HU).[8],[10],[25] Less than 10 HU are consistent with a transudative effusion.[8],[10],[25] Pericardial effusions are typically low density at 0–20 HU.[8],[25] The presence of hemorrhage or bacterial infection increases the density of pericardial effusions.[8],[10],[25] 10–60 HU suggest an exudative effusion while >60 HU are likely hemorrhagic.[10],[25] CT contrast enhances visualization of pericardial inflammation and calcification.[10],[23] However, evaluation of pericardial thickness is limited without ECG gating due to cardiac motion artifact.[10] Disadvantages of CT for pericardial assessment include overestimation of effusion size, lack of hemodynamic insight, and requirement for iodinated contrast and ionizing radiation.[4],[10]

MRI evaluates both cardiac morphology and function.[10],[12],[23],[26] It is superior to CT in characterizing pericardial effusions and masses with combined T1- and T2-weighted imaging.[12],[26] In contrast to CT, it does not require iodinated contrast or ionizing radiation.[12],[26] The addition of gadolinium may be used to enhance pericardial inflammation for the detection of pericarditis.[12],[26] MRI limitations include overestimation of effusion size, cost, and availability.[4],[26] Using MRI to distinguish tissue characteristics can also help separate pericardial effusions from other forms of pericardial pathology, such as constrictive pericarditis.[12],[22],[26]

  Medical Management Top

If an effusion develops secondary to an underlying disease process, resolution occurs with appropriate medical treatment of that process.[3],[8] Pericardial effusions are associated with a known disease process in approximately 60% of cases.[27] In the presence of inflammatory signs suggestive of pericarditis or elevated inflammatory markers, medical management with NSAIDs is appropriate.[3],[4],[6],[7],[8],[13],[17],[21],[23] Ibuprofen is the anti-inflammatory drug of choice in pericarditis given its favorable side effect profile and broad dosage range.[4],[7] Aspirin is preferred post-myocardial infarction due to the need for antiplatelet therapy.[6] Indomethacin and ketorolac may be used as an alternatives, although indomethacin is avoided in coronary artery disease since it reduces coronary blood flow.[4],[6] Azathioprine and methotrexate are considered in cases of intolerance or contraindication to NSAIDs.[4],[7] Proton-pump inhibitors are initiated in conjunction with NSAID therapy for gastric protection.[4],[6]

Colchicine is used in the treatment of acute and relapsing pericarditis.[4],[8],[13],[23] Recurrence risk is reduced by colchicine use and steroid avoidance.[6],[8],[13],[23] In cases of recurrent inflammation, combination therapy with NSAIDs and colchicine is recommended.[4],[7] The most common adverse effect leading to discontinuation of colchicine is diarrhea, which occurs in 8% of patients.[6],[13] Other less common side effects include hepatotoxicity, myotoxicity, and bone marrow suppression.[6] Early high-dose corticosteroids are associated with the development of complicated pericarditis.[23] For this reason, systemic corticosteroid therapy is limited to pericarditis secondary to connective tissue disease, autoimmune disease, and uremia.[4] Treatment of tuberculous pericarditis consists of a 6-month course of the standard 4-drug tuberculosis regimen.[12] Associated constrictive pericarditis requires pericardiectomy.[12] Acute viral or idiopathic pericarditis is typically managed on an outpatient basis.[8] Inpatient management should be considered in the presence of severe pericardial effusion, tamponade, anticoagulation, fever greater than >38°C, and anticoagulation.[8] These factors are clinical predictors of poor prognosis.[8]

  Indications for Pericardial Drainage Top

Considerations before pericardial drainage include clinical presentation, hemodynamic stability, echocardiogram findings, and risk-to-benefit ratio of intervention. Drainage may be performed on an emergent, urgent, or elective basis. Urgent drainage is indicated for cardiac tamponade.[4],[5],[6],[11] If hemodynamically stable, drainage is recommended within 12–24 hours of diagnosis.[11] Emergent drainage by pericardiocentesis is necessary in tamponade with associated hemodynamic shock.[4],[11] Indications for emergent surgical drainage include type A aortic dissection, postmyocardial infarction ventricular free wall rupture, trauma, and purulent effusions causing sepsis with hemodynamic instability.[11]

When associated with mechanical problems such as dissection or ventricular rupture, drainage can result in uncontrolled or fatal hemorrhage without the ability to immediately manage the precipitating cause. In theory, pericardial drainage has both diagnostic and therapeutic value. In practice, the diagnostic yield of pericardial drainage is 7% in the absence of tamponade and hemodynamic compromise.[8] Given this diagnostic limitation and the potential procedural risks, pericardial drainage is not performed on a routine basis in the setting of hemodynamic stability.[8] Elective pericardiocentesis is appropriate in cases of purulent, tuberculous, and neoplastic pericarditis as well as massive chronic idiopathic pericardial effusion.[5],[6],[8],[11] Examination of pericardial fluid in the setting of underlying malignancy delineates effusion secondary to neoplastic pericardial involvement from postthoracic irradiation effusion.[8] Patients with massive chronic idiopathic pericardial effusion are at risk for the development of sudden tamponade.[5],[8] For this reason, pericardiocentesis should be performed even if asymptomatic.[5],[8]

Elective surgical drainage is performed when the effusion cannot be reached safely by needle or catheter percutaneously.[11] Other indications include purulent pericardial fluid, intrapericardial bleeding, and clotted hemopericardium.[4],[5],[11] Advantages of open surgical drainage include facilitation of pericardial biopsy, hematoma evacuation, loculation break up, and drainage tube placement.[11] Disadvantages include potential complications of general anesthesia such as hypotension with large effusions or tamponade.[11] The requisite 6 cm to 8 cm incision and possible xiphoid process resection bear morbidity as well.[11]

If cardiac tamponade is diagnosed in a facility with limited experience in pericardial effusion drainage and the patient is clinically stable, urgent transfer to a specialized institution is recommended.[11] Contraindications to drainage in a primary care facility include uncorrected thrombocytopenia with platelets <50,000/mm3, uncorrected coagulopathy, and anticoagulation with an international normalized ratio (INR) >1.5.[4],[11] Drainage in this setting is also not recommended with small, posterior, and loculated pericardial effusions.[4],[11]

Patients in tamponade may have an associated coagulopathy and/or thrombocytopenia, presumed to be from hepatic congestion. In addition, many patients will also present with acute hemorrhagic pericarditis in the setting of antiplatelet or anticoagulation therapy. While such laboratory abnormalities could result in treatment delay, they further indicate the severity of the problem and may encourage immediate drainage. Despite concern for bleeding in the setting of antiplatelet and anticoagulation therapy, uncontrolled bleeding is encountered rarely. Delayed drainage to allow for reversal of iatrogenic coagulopathy is reasonable in stable patients. However, immediate drainage should be pursued at the first sign of hemodynamic instability or organ system dysfunction.

  Pericardial Drainage Procedures Top

Selection of the appropriate pericardial drainage procedure depends on effusion etiology. Simple pericardiocentesis is sufficient in most cases of acute viral or idiopathic pericarditis.[8] These effusions are typically self-limited, resolving within days to weeks, and rarely relapsing.[8] Pericardiocentesis performed under echocardiographic guidance is associated with a >95% success rate.[4],[7],[10],[28] It is the procedure of choice in unstable patients due to expeditious performance at bedside.[4],[9],[10] Feasibility varies by effusion location, with >90% success with anterior effusions and <60% success with small, posterior effusions.[7] The overall complication rate of pericardiocentesis is 4.7%.[28] Severe complications include myocardial and coronary vessel laceration or perforation.[4],[7] Avoiding lateral needle movements while approaching the effusion may reduce this risk.[11] Other potential complications include arrhythmia, pneumothorax, air embolism, and peritoneal cavity puncture with abdominal visceral injury.[4],[7]

Echocardiographic and fluoroscopic guidance improve the safety of pericardiocentesis, limiting the incidence of major complications to 1%–1.6%.[4],[7],[10],[11],[13] Imaging guidance allows for the identification of effusion size and distribution.[6],[11],[13],[22] The optimal location for pericardiocentesis is closest to the largest amount of pericardial effusion.[11],[13] The majority of patients require a subxiphoid or intercostal (apical) approach.[11]

Neoplastic pericardial effusions are commonly associated with breast and lung cancer, lymphoma, and leukemia.[5],[7] Given the associated poor prognosis, treatment goals include improvement in symptoms and quality of life.[5],[7] Selection of the approach to intervention should consider cancer stage, prognosis, likelihood of success, potential risks, and availability.[5],[7] With malignant pericardial effusion and tamponade, pericardiocentesis provides symptom relief, but is associated with a 40%–50% recurrence risk.[5],[8] This conservative approach to drainage may be appropriate in terminally ill patients.[5],[8] Drainage of >1 liter of pericardial fluid is not recommended.[11] For the remaining effusion, prolonged catheter drainage should be considered.[11]

Indwelling pericardial catheter placement is an alternative for malignancy-associated tamponade, associated with a 75% success rate.[8],[13] Catheter removal is considered safe when drainage is <20–30 ml/day, which requires 4.8 days on average.[7],[8],[11],[13] Intrapericardial catheter placement reduces the risk of effusion recurrence by inducing inflammation, thereby promoting pericardial adherence and obliterating the pericardial space.[7],[8],[13] Effusion recurrence rates with and without prolonged drainage are 12% and 52%, respectively.[11] Factors independently correlated with recurrence of tamponade at 1 year include incomplete drainage, absence of prolonged drainage, effusion loculation, and malignancy.[11] Another option for malignant effusion management is instillation of sclerosing and antineoplastic agents.[8] This approach is avoided in nonterminal patients and is associated with potential risk of constrictive pericarditis.[8]

Percutaneous balloon pericardiotomy has been described as an alternative to open surgical pericardiotomy.[4],[7],[8],[13] It is associated with a >80% success rate and has been applied in malignant pericardial effusion management.[6],[7],[8] In this approach, subxiphoid pericardiocentesis is used to access the pericardial space under echocardiographic or fluoroscopic guidance.[7],[8],[13] A guide wire and balloon catheter are then sequentially advanced into the pericardial space.[8] The balloon is inflated, creating a window to facilitate pericardial drainage.[8] Potential complications of this approach include pericardial bleeding, pneumothorax, and pleural effusion.[8],[13]

If less invasive options are not feasible or fail, open surgical pericardiotomy should be considered.[4],[5],[7],[13] This approach has an 80%–90% success rate.[8] However, compared to less invasive options, it is associated with greater morbidity and mortality.[8] Open surgical drainage for symptomatic pericardial effusion is associated with a significantly higher complication rate compared to pericardiocentesis at 26.4% and 4.9%, respectively.[29] In comparison, pericardiocentesis is associated with a higher rate of effusion recurrence.[9],[29] This necessitates repeated intervention more often than open surgical drainage at 28.9% and 2.8%, respectively.[14],[29] Length of hospitalization is significantly shorter following pericardiocentesis compared to surgical drainage.[29] There is no significant difference in 30-day mortality and long-term survival, except for malignant pericardial effusions.[9],[29] Given these competing factors, the decision for percutaneous pericardiocentesis or open surgical drainage considers complication risks and definitive procedural benefits.[29]

A 12-year retrospective study of 1281 patients at a quaternary referral center compared postprocedural outcomes of patients requiring intervention for pericardial effusion.[9] Outcomes of interest included in-hospital morbidity and mortality, 30-day effusion reaccumulation, and procedural success.[9] Morbidity outcomes included postprocedural hemodynamic instability and major bleeding.[9] Hemodynamic instability was defined as either a systolic blood pressure <100 mmHg or vasopressor requirement within 48 hours of the procedure.[9] Major bleeding was defined as a reduction in hemoglobin of 2 g/dl or the requirement of blood transfusion within 48 hours of the procedure.[9] Procedural success was defined as drainage resulting in resolution of tamponade or associated symptoms.[9]

In this patient population, selection for pericardiotomy was found to be more common in effusions secondary to cardiac surgery.[9] Following surgery, pericardial effusions are more likely to be loculated than circumferential, which may account for this finding.[9] In comparison, pericardiocentesis was performed more frequently for effusions related to procedural trauma, such as coronary perforation with cardiac ablation or device implantation.[9] Procedural success and in-hospital mortality rates were found to be comparable.[9] Preprocedural factors associated with higher mortality rates included higher New York Heart Association class, effusion etiology other than cardiac surgery, higher heart rate, lower blood pressure, and lower platelets.[9]

Effusion reaccumulation was found to be more common in patients who underwent pericardiocentesis.[9] Preprocedural factors associated with effusion reaccumulation included cardiac tamponade, large drainage volume, underlying neoplasm, and absence of drain placement.[9] The 24% reaccumulation rate demonstrated in this study may have been reduced with pericardial drain placement, which was associated with a 10% absolute risk reduction in reaccumulation rate.[9] All patients in the study population who required intervention for reaccumulation underwent surgical pericardiotomy.[9] These patients were found to have greater postprocedural risk of hemodynamic instability and major bleeding at 6.3% and 4.9%, respectively.[9]

The risk of postprocedural instability was attributed to the hemodynamic effects of general anesthesia induction and intubation necessary for surgical pericardiotomy.[9] Anesthetic agents cause venodilation in patients with tamponade who are preload dependent.[9] In addition, positive pressure ventilation increases intrathoracic pressure, thereby compromising venous return.[9] The compensatory sympathetic response to tamponade is reduced by anesthetic agents as well.[9] These factors may account for the higher rates of hemodynamic instability following pericardiotomy.[9] Overall, both percutaneous pericardiocentesis and surgical drainage were found to be highly successful in the management of pericardial effusions with relatively low complication rates in this study.[9]

In the setting of malignant pericardial effusion, pericardiotomy has a 19.4% 30-day mortality rate.[8] For this reason, indwelling pericardial catheter placement, instillation of sclerosing and antineoplastic agents, and percutaneous pericardiotomy are initially preferred.[11] Purulent pericarditis is rare, but universally fatal if untreated.[4] It is associated with systemic infection, diabetes mellitus, and cirrhosis.[8] The mortality rate of purulent pericarditis in treated patients is 40%, attributed to cardiac tamponade, constriction, and sepsis.[4] Although pericardiocentesis may be attempted, surgical drainage by pericardiotomy is preferred.[4],[5],[8] Intraoperative echocardiography may be used to guide pericardiotomy, specifically in cases of posterior or loculated pericardial effusions.[22] Surgical mortality in purulent pericarditis approaches 8%.[4]

Massive chronic idiopathic pericardial effusions are typically >20 mm and have been present for more than 3 months.[3],[8] In 29%–33% of these effusions, sudden evolution to tamponade occurs despite long-term clinical stability.[3],[6],[7],[8],[13] Factors implicated in the progression to tamponade include acute pericarditis, tachyarrhythmia, and hypovolemia.[4],[8] Pericardiocentesis is recommended in these cases, both therapeutically for cardiac tamponade and prophylactically in asymptomatic patients.[3],[8] If relapse occurs after a second pericardiocentesis, surgical drainage with pericardiotomy or wide anterior pericardiectomy is indicated.[3],[4],[5],[7],[8],[13] Surgical intervention should especially be considered with echocardiographic findings of right atrial and ventricular collapse in this context.[3],[7] Aside from recurrence, other indications for pericardiectomy include chronic permanent constriction, resistance to medical therapy, and severe steroid toxicity.[4],[7],[12],[13]

  Prognostic Considerations Top

The prognosis of pericardial effusions is determined by etiology, severity, and duration. Acute viral and idiopathic pericarditis are associated with a good prognosis and low complication rates.[7],[8] However, idiopathic effusions large in size and chronic in nature are associated with a 30%–35% risk of cardiac tamponade.[4],[7] Large, subacute idiopathic effusions are at increased risk of progression to tamponade when right-sided chamber collapse is present on echocardiogram.[4],[6],[7] In these cases, preventative drainage is recommended.[4],[6],[7] In comparison, neoplastic pericardial effusions with positive cytology are associated with a poor prognosis.[8] In cases of purulent pericarditis, early diagnosis and treatment improve prognosis.[8]

Surveillance is determined by the presence of symptoms, echocardiogram stability, etiology, and intervention.[7] Mild idiopathic effusions do not require specific monitoring given good prognosis.[7] Patients with idiopathic effusions require an echocardiogram every 6 months for moderate effusions and every 3–5 months for large effusions.[7] Early complications include effusion recurrence and progression to tamponade.[7] Late complications include the development of constrictive pericarditis.[7] Patients at increased complication risk are those with effusions secondary to bacterial infection, irradiation, and pericardial injury.[7]

There are 3 independent predictors of postoperative mortality in patients undergoing surgical intervention for pericardial effusion.[14] These include underlying malignancy, thoracic invasion on CT, and tamponade on echocardiogram.[14] The prognosis of lung cancer is worse than that of breast cancer, hematologic malignancy, and other solid tumor malignancy.[14] Malignant thoracic invasion on CT is characterized by a pericardial or pulmonary mass.[14] Echocardiographic findings of tamponade and cardiac chamber collapse are the final predictive factors correlating with poor survival.[14] In patients with these risk factors, minimally invasive alternatives to open surgical drainage are strongly considered.[14]

  Conclusion Top

The appropriate management strategy for pericardial effusions is determined by etiology. For acute viral or idiopathic pericardial effusions, pericardiocentesis is recommended. Echocardiographic and fluoroscopic guidance improve the success and safety of intervention. For malignant effusions, indwelling pericardial catheter placement is advised over pericardiocentesis due to risk of recurrence. Alternative strategies include intrapericardial instillation of sclerosing or antineoplastic agents and percutaneous balloon pericardiotomy. Surgical pericardiotomy is considered if less invasive options are not feasible or successful. With relapse after repeated drainage, wide anterior pericardiectomy is indicated. The selection process is guided by consideration of potential procedural risks and their bearing on intended therapeutic benefits. Currently, there is limited data available to guide pericardial effusion management. Further studies are needed to facilitate development of evidence-based recommendations for intervention in the future.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

Ethical conduct of research

The literature review for this research was conducted ethically.

  References Top

Larrey, EL. New surgical procedure to open the pericardium in the case of fluid in the cavity. Clin Chir 1829;36:303-37.  Back to cited text no. 1
Kopecky SL, Callahan JA, Tajik AJ, Seward JB. Percutaneous pericardial catheter drainage: Report of 42 consecutive cases. Am J Cardiol 1986;58:633-5.  Back to cited text no. 2
Imazio M, Mayosi BM, Brucato A, Markel G, Trinchero R, Spodick DH, et al. Triage and management of pericardial effusion. J Cardiovasc Med (Hagerstown) 2010;1:928-35.  Back to cited text no. 3
Maisch B, Seferović PM, Ristić AD, Erbel R, Rienmüller R, Adler Y, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; the task force on the diagnosis and management of pericardial diseases of the European Society of Cardiology. Eur Heart J 2004;25:587-610.  Back to cited text no. 4
Soler-Soler J, Sagristà-Sauleda J, Permanyer-Miralda G. Management of pericardial effusion. Heart 2001;86:235-40.  Back to cited text no. 5
Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, et al. Pericardial disease: Diagnosis and management. Mayo Clin Proc 2010;85:572-93.  Back to cited text no. 6
Imazio M, Adler Y. Management of pericardial effusion. Eu Heart J 2013;34:1186-97.  Back to cited text no. 7
Sagristà-Sauleda J, Mercé AS, Soler-Soler J. Diagnosis and management of pericardial effusion. World J Cardiol 2011;3:135-43.  Back to cited text no. 8
Horr SE, Mentias A, Houghtaling PL, Toth AJ, Blackstone EH, Johnston DR, et al. Comparison of outcomes of pericardiocentesis versus surgical pericardial window in patients requiring drainage of pericardial effusions. Am Journal Cardiol 2017;120:883-90.  Back to cited text no. 9
Vakamudi S, Ho N, Cremer PC. Pericardial effusions: Causes, diagnosis, and management. Prog in Cardiovasc Dis 2017;59:380-8.  Back to cited text no. 10
Ristić AD, Imazio M, Adler Y, Anastasakis A, Badano LP, Brucato A, et al. Triage strategy for urgent management of cardiac tamponade: A position statement of the European Society of Cardiology working group on myocardial and pericardial diseases. Eur Heart J 2014;35:2279-84.  Back to cited text no. 11
Mayosi BM, Burgess LJ, Doubell AF. Tuberculous pericarditis. Circulation 2005;112:3608-16.  Back to cited text no. 12
Imazio M, Spodick DH, Brucato A, Trinchero R, Adler Y. Controversial issues in the management of pericardial diseases. Circulation 2010;121:916-28.  Back to cited text no. 13
Mirhosseini SM, Fakhri M, Mozaffary A, Lotfaliany M, Behzadnia N, Aval ZA, et al. Risk factors affecting the survival rate in patients with symptomatic pericardial effusion undergoing surgical intervention. Interact Cardiovasc and Thorac Surg 2013;16:495-500.  Back to cited text no. 14
Shabetai R. Pericardial effusion: Haemodynamic spectrum. Heart 2004;90:255-6.  Back to cited text no. 15
Spodick DH. Acute cardiac tamponade. N Engl J Med 2003;349:684-90.  Back to cited text no. 16
Ntsekhe M, Mayosi BM. Tuberculous pericarditis with and without HIV. Heart Fail Rev 2013;18:367-73.  Back to cited text no. 17
Spodick DH. Electrocardiogram in acute pericarditis: Distributions of morphologic and axial changes by stages. Am J Cardiol 1974;33:470-4.  Back to cited text no. 18
Beck C. Two cardiac compression triads. J Am Med Assoc 1935;104:714-6.  Back to cited text no. 19
Kussmaul A. Uber schwielige mediastino-perikarditis und den paradoxen. Puls Berl Klin Wochenschr 1873;10:433-5.  Back to cited text no. 20
Fowler NO. Cardiac tamponade. A clinical or echocardiographic diagnosis? Circulation 1993;87:1738-41.  Back to cited text no. 21
Cheitlin MD, Armstrong WF, Aurigemma GP, Beller GA, Bierman FZ, Davis JL, et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: Summary article: A report of the American College of Cardiology/American Heart Association task force on practice guidelines (ACC/AHA/ASE committee to update the 1997 guidelines for the clinical application of echocardiography). Circulation 2003;108:1146-62.  Back to cited text no. 22
Cremer PC, Kumar A, Kontzias A, Tan CD, Rodriguez ER, Imazio M, et al. Complicated pericarditis: Understanding risk factors and pathophysiology to inform imaging and treatment. J Am Coll Cardiol 2016;68:2311-28.  Back to cited text no. 23
Himelman RB, Kircher B, Rockey DC, Schiller NB. Inferior vena cava plethora with blunted respiratory response: A sensitive echocardiographic sign of cardiac tamponade. J Am Coll Cardiol 1988;12:1470-7.  Back to cited text no. 24
Tomoda H, Hoshiai M, Furuya H, Oeda Y, Matsumoto S, Tanabe T, et al. Evaluation of pericardial effusion with computed tomography. Am Heart J 1980;99:701-6.  Back to cited text no. 25
McRee CW, Mergo P, Parikh P, Pollak A, Shapiro BP. Modern advances in cardiovascular imaging: Cardiac computed tomography and cardiovascular MRI in pericardial disease. Future Cardiol 2014;10:769-79.  Back to cited text no. 26
Sagristà-Sauleda J, Mercé J, Permanyer-Miralda G, Soler-Soler J. Clinical clues to the causes of large pericardial effusions. Am J Med 2000;109:95-101.  Back to cited text no. 27
Tsang TS, Enriquez-Sarano M, Freeman WK, Barnes ME, Sinak LJ, Gersh BJ, et al. Consecutive 1127 therapeutically echocardiographically guided pericardiocenteses: Clinical profile, practice patterns, and outcomes spanning 21 years. Mayo Clin Proc 2002;77:429-36.  Back to cited text no. 28
Saltzman AJ, Paz YE, Rene AG, Green P, Hassanin A, Argenziano MG, et al. Comparison of surgical pericardial drainage with percutaneous catheter drainage for pericardial effusion. J Invasive Cardiol 2012;24:590-3.  Back to cited text no. 29


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Clinical Present...
Diagnostic Imaging
Medical Management
Indications for ...
Pericardial Drai...
Prognostic Consi...

 Article Access Statistics
    PDF Downloaded108    
    Comments [Add]    

Recommend this journal