Pericardial Effusion

Article Author:
Daniel Willner
Article Editor:
John Kiel
Updated:
12/19/2018 7:17:21 AM
PubMed Link:
Pericardial Effusion

Introduction

A pericardial effusion refers to the accumulation of fluid in the pericardial sac surrounding the heart. The pericardial sac is composed of the thin visceral pericardium which consists of a single layer of cells adherent to the cardiac epicardium and the thicker and fibrous parietal pericardium composed of collagen and elastin which is adherent to the lungs, diaphragm, sternum, great vessels, and other mediastinal structures surrounding the heart. In a healthy individual, the pericardial sac contains between 15 mL and 50 mL of serous fluid.[1][2][3]

Etiology

The etiology of a pericardial effusion varies widely and can be divided into several categories:

  • Infectious: Pericardial effusion may be due to infection with a multitude of viral,  bacterial, fungal, and even parasitic pathogens. Viral pericarditis leading to effusion is the most common cause in the developed world. In developing areas, pericardial effusion due to Mycobacterium tuberculosis is quite prevalent. Bacterial and parasitic etiologies are less common. 
  • Idiopathic: Many cases of pericardial effusion are idiopathic.
  • Inflammatory/ rheumatologic: Numerous auto-immune disorders including Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), and Sjogren's Syndrome can cause a pericardial effusion.
  • Neoplastic: Both metastatic disease and primary cardiac tumors can cause pericardial effusions. Lung cancer is the most common cause of a malignant pericardial effusion.
  • Trauma: Blunt, penetrating and iatrogenic injury to the myocardium, aorta or coronary vessels can lead to accumulation of blood within the pericardial sac.
  • Cardiac: Pericarditis, post-myocardial infarction (referred to as Dressler's syndrome) or other cardiac event can lead to subsequent pericardial effusion
  • Vascular: Aortic dissection can all lead to pericardial effusion.
  • Other: There are numerous additional etiologies of pericardial effusion including radiation, chronic kidney disease (CKD) and renal failure, congestive heart failure, cirrhosis, hypothyroidism leading to myxedema, ovarian hyperstimulation syndrome, and drug-induced.

Epidemiology

Pericardial effusion is possible across all ages and populations. The predominant etiology of the effusion varies by demographic characteristics such as age, geography, and comorbidities. There is little data regarding the prevalence and incidence of pericardial effusions. In patients undergoing echocardiograms for other etiologies, the prevalence and incidence of pericardial effusion was 3 and 9% in a 6 year window in a large Italian hospital [1]

Pathophysiology

Pericardial effusion is due to the accumulation of fluid within the pericardial sac. This fluid may be transudative, exudative, or sanguineous and may contain infectious organisms or malignant cells. It may be due to infection, inflammation, or direct filling of the pericardial sac by blood from a defect in the myocardium (iatrogenic or traumatic injury or cardiac wall rupture) or backfilling from an ascending aortic dissection that dissects into the pericardium. Enough fluid may accumulate to cause cardiac tamponade via impaired venous blood return and decreased stroke volume. In the acute setting, only 100 ml to 150 mL of fluid is necessary to cause cardiac tamponade. In the chronic setting, the pericardial effusion may become one to two liters in size before it causes cardiac tamponade as long as the accumulation is gradual and the parietal pericardium has adequate time to stretch and accommodate the increased volume.[4][5][6]

History and Physical

The clinical presentation of pericardial effusion is along a spectrum from a clinically irrelevant, incidental finding to life-threatening cardiac tamponade. This wide variation is due in large part to the variable rate of accumulation of the pericardial fluid. Acute accumulation may cause impaired cardiac filling and decreased cardiac output with as little as 100 mL of fluid while chronic, and slow accumulation may lead to significant effusions of one to two liters that produce no significant hemodynamic effects. 

  • History: In patients with pericardial effusion due to pericarditis patients often present with chest pain and dyspnea with symptoms that improve while sitting upright and worsen while laying flat due to the inflamed pericardium contacting adjacent structures. Patients may also present with symptoms that are not specific for pericardial effusion including dyspnea, edema, and fatigue. Other important elements of the history include questions regarding recent illnesses, malignancy, history of TB and vaccination status, auto-immune disorders, history of chronic kidney disease (CKD) or renal failure, or history of CHF, hypothyroidism, or liver disease.
  • Physical exam: Pericardial effusion leading to pericardial tamponade should be on the differential for patients in cardiac arrest or with vital sign abnormalities including hypotension and tachycardia. The classic teaching of Beck's Triad (hypotension, jugular venous distension (JVD), and muffled heart sounds) is only found in a minority of patients. Other physical exam findings unique to pericardial effusion include Ewart's sign (dullness to percussion at the base of the left inferior scapular border in conjunction with tubular breath sounds and egophony). The physical exam of patients with a concern for cardiac tamponade should also include evaluation for pulsus paradoxus, which refers to a relative drop in systolic blood pressure by more than 10 mmHg during inspiration due to the collapse of the right atrium and ventricle. This leads to bowing of the interventricular septum and augmented compression of the left side of the heart with decreased filling volumes and subsequent decreased stroke volume and systolic blood pressure.

While both history and physical exam are critical components of the evaluation for pericardial effusion and cardiac tamponade, the standard of care now includes additional modalities such as echocardiography to confirm the diagnosis.

Evaluation

There are several tests which can aid in evaluating a patient in whom pericardial effusion is the differential diagnosis.[7][8][9]

  • Chest X-ray: The chest X-ray may can not directly identify pericardial effusion. If there is a significant, chronic effusion, then the heart may appear boot shaped, and radiology may comment on a "water bottle sign" or water bottle shaped heart. There may also be evidence of pulmonary edema, engorgement of the pulmonary vessels, and/or pleural effusions on chest x-ray - none of which are sensitive or specific for pericardial effusion.
  • ECG: The ECG findings vary from normal to non-specific ST segment changes for small effusions. For large effusions or tamponade, the ECG may demonstrate electrical alternans which is a specific but not a sensitive finding. Electrical alternans refer to QRS complexes of varying heights corresponding to a back and forth motion of the heart within the pericardial sac as it swings on its anchored base during the cardiac cycle. If the pericardial effusion is due to pericarditis, then the ECG may show PR depressions or diffuse ST elevations.
  • Echocardiography: Transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) is the diagnostic modality of choice when evaluating for pericardial effusion. Echocardiography provides a dynamic assessment of the pericardial effusion allowing for quantification of the size of the effusion and determination of whether there is evidence of cardiac tamponade physiology. Pericardial effusion is identified as anechoic fluid surrounding the heart. In cases of hemopericardium with a clot, pyogenic effusions, or exudative effusions there may be hypoechoic clot or debris visible within the anechoic pericardial fluid. There are numerous criteria for the diagnosis of cardiac tamponade by TTE or TEE. Right atrial free-wall collapse or inversion during systole, right ventricular free wall collapse during diastole, increased septal bowing into the left ventricle during inspiration and the right ventricle during exhalation, a dilated inferior vena cava (IVC) without respiratory variation in a spontaneously breathing patient in sinus rhythm, and increased flow across the mitral valve during exhalation and the tricuspid valve during inspiration are all potentially indicative of intrapericardial pressures that are greater than intracardiac pressures and potential pericardial tamponade. It is important to note that some of these echo findings are sensitive but not specific while others are specific but not sensitive for cardiac tamponade.
  • CT/MRI: Pericardial effusion can also be identified on CT or MRI of the chest or heart however this is not the diagnostic modality of choice.

Treatment / Management

Treatment for pericardial effusion ranges from watchful waiting for emergent intervention and depends largely on the suspected etiology. Small effusions without evidence of hemodynamic compromise are watched with serial echocardiography if deemed necessary or determined to be small enough that no follow-up is necessary. Large effusions may receive a diagnostic pericardiocentesis to evaluate the etiology or drained to provide symptomatic relief if the patient has associated symptoms such as dyspnea, chest discomfort, pulmonary or lower extremity edema, or decreased exercise tolerance. Effusions that have accumulated rapidly enough or have grown to such a size as to cause hemodynamic instability or collapse are managed emergently at the bedside, the cardiac catheterization lab, or the operating room. Techniques for drainage include needle pericardiocentesis via subxiphoid or anterior thoracic approach with or without placement of a pericardial drain for serial evacuation, percutaneous balloon pericardiotomy, emergent thoracotomy and pericardiotomy, and surgical pericardial window via subxiphoid, anterior mini-thoracotomy, or video-assisted thoracoscopic surgery (VATS) approach. The type of intervention chosen is based on the etiology of the pericardial effusion, the clinical status of the patient at the time of the intervention, and the patient's expected clinical course.[10][11]

Pearls and Other Issues

  • Pericardial effusion is a relatively commonly encountered pathology
  • The etiology is widely varied
  • The effusion can range from incidental to life threatening
  • The diagnostic modality of choice is ultrasound, although other modalities can provide critical information
  • Management is driven by the size of the effusion and clinical status of the patient
  • Cardiothoracic surgeons are the consultant of choice in patients who are diagnosed with a pericardial efffusion

Enhancing Healthcare Team Outcomes

Pericardial effusions are common. Unlike chronic effusions, acute effusions in symptomatic patients need emergent treatment. The management of pericardial effusions is by a multidisciplinary team that includes a cardiologist, radiologist, and a cardiac surgeon. While aspiration can help relieve symptoms and hemodynamic compromise in most patients, those occurring after a malignancy may require a pericardial window that can be done either open or via thoracoscopy. symptomatic pericardial effusions that are not properly treated carry a very high mortality.



References

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