Historical Perspectives

The heart is surrounded by a fibroserous sac known as the pericardium, a term derived from the Greek words peri, “around,” and kardia, “heart.” It was a Greco‐Roman physician, Claudius Galen, who first described and named this anatomical structure in 160 AD. He was also the first to recognize the deleterious effects of a pericardial effusion on cardiac function. In 1653 the Parisian surgeon Jean Riolan recommended aspiration of the pericardial fluid in patients with effusions and proposed trepanning of the sternum to provide exposure to the pericardium [1]. In 1749, when the first comprehensive book on cardiac anatomy, physiology, and pathology was published by Jean‐Baptiste Senac, a French physician, there was a full chapter dedicated to the pericardium and its diseases [2].

The pericardium was involved in one of the first documented successful interventions on the heart. In 1896 a patient who was dying from cardiac tamponade after suffering a stab wound to the chest was taken to the operating room by Ludwig Rehn. Rehn evacuated the clot in the pericardium and successfully repaired the cardiac laceration [3]. Some years later in 1913, Rehn published the first report of successful pericardiectomy for pericarditis [4]. His successes stimulated the pursuit of surgical approaches for the management of cardiac and pericardial diseases.

Embryology and Anatomy

In the human embryo, between weeks 5 and 7 of gestation, the pericardial cavity is created from the subdivision of the embryonic coelom [5]. Fusion of the pleuropericardial membranes with the foregut mesenchyme posteriorly divides the thoracic cavity into a ventral pericardial cavity and two dorsolateral pleural cavities. Abnormal development of the pleuropericardial membranes results in defects in the pericardial wall [6].

The pericardium is a bilayered sac consisting of a thick stiff outer fibrous layer and a thin inner serous layer. The fibrous outer capsule is mainly made up of collagen and elastin fibers and the serous layer of a thin elastic membrane of mesothelial cells, which envelop the inner aspect of the fibrous pericardium (serous parietal pericardium) and also the myocardium (serous visceral pericardium or epicardium). Between the two layers of the serous pericardium there is a potential space known as the pericardial cavity, which is normally lubricated by a thin layer of fluid (pericardial fluid) (Figure 41.1).

Within the pericardial cavity there are two recesses, the transverse and oblique sinuses, representing reflections of the serous pericardium between the great vessels at the base of the heart (Figure 41.2) [7]. The transverse sinus lies behind the aorta and main pulmonary artery and the oblique sinus resides behind the left atrium in the region between all four pulmonary veins. In order to provide structural support to the heart and prevent excessive cardiac motion within the thoracic cavity, the pericardium is connected to the undersurface of the sternum by the superior and inferior sternopericardial ligaments and to the posterior mediastinal structures by loose connective tissue. Also, the pericardium is attached to the central tendon of the diaphragm.

The main vascular arterial supply to the pericardium is provided by the pericardiophrenic artery, a branch of the internal mammary artery, and the venous drainage is via the pericardiophrenic veins, which are tributaries of the brachiocephalic veins. The phrenic nerves provide the sensory enervation and the sympathetic trunks the vasomotor enervation.

Diseases of the Pericardium

Pericardial disease is defined as a structural or functional abnormality of the visceral or parietal pericardium that may, or may not, have a significant impact on cardiac function. The International Congenital Heart Surgery Nomenclature and Database Project described 12 types of disease processes affecting the pericardium. They were classified as effusive pericarditis (pericardial effusion), constructive pericarditis, cardiac tamponade, postoperative pericardial effusion, postoperative cardiac tamponade, postpericardiotomy syndrome, congenital defect, neoplastic process, benign mass, pericardial cyst, pneumopericardium, and chylopericardium [8, 9]. Each group will be discussed briefly with common causes, diagnosis, and medical and surgical treatments.

Effusive Pericarditis

Effusive pericarditis (pericardial effusion) is defined as an inflammatory stimulation of the pericardium that results in the accumulation of appreciable amounts of pericardial fluid. Causes include viral, uremic, tuberculous, bacterial, neoplastic, traumatic, drug induced, and idiopathic. Pericardial effusion may be serous, purulent, or hemorrhagic. Of note is that postoperative pericardial effusions are classified separately.

Pericardial effusions can be diagnosed based on the history and physical examination, electrocardiogram, chest roentgenography, echocardiogram, computed tomogram (CT), and/or magnetic resonance imaging (MRI). The clinical presentation is determined by the primary etiology and the speed of accumulation of the pericardial fluid. If the effusion develops slowly it can be asymptomatic, while a relatively smaller but rapidly accumulating effusion can present with severe hemodynamic compromise. Large effusions may cause cough and dyspnea owing to compression of adjacent lung tissue and on auscultation distant heart sounds are present. In pericarditis there may be a friction rub, which is best heard on the left border of the sternum or in the midclavicular line, between the second and the fourth intercostal space. Large effusions are usually related to neoplastic, tuberculous, or uremic processes.

On chest roentgenogram an enlarged cardiac silhouette can be observed in the presence of a large effusion, but a normal cardiothoracic ratio does not rule out smaller effusions (Figure 41.3). The diagnosis is best confirmed by echocardiogram, which also documents cardiac filling and ventricular function, determining the presence or absence of cardiac tamponade physiology (Figure 41.4). Specifically, the echocardiogram can assess for restriction of right atrial or right ventricular filling, and increased respirophasic variation indicating that the effusion is compromising cardiac function. CT can easily detect pericardial effusions and is also useful in identifying the characteristics of the fluid (blood, chyle, transudate, etc.). Low voltage on the electrocardiogram (ECG) is a typical finding in patients with pericardial effusions.

Viral effusions are often, but not always, associated with other signs and symptoms of an acute viral infection. Common causative viruses include Coxsackie virus, adenovirus, enteric cytopathic human orphan (ECHO) virus, influenza virus, mumps virus, varicella virus, Epstein–Barr virus, and human immunodeficiency virus [10, 11]. They can be small or large effusions and cause a pericardial friction rub, which is the most common physical finding. Patients with renal disease develop uremic effusions. Approximately 20% of uremic patients requiring chronic dialysis will develop a pericardial effusion during their lifetime [12]. The association between uremia and pericardial effusions has been well described and is recognized as one of the indicators of end‐stage renal disease. However, the specific causes of uremic pericarditis remain unclear [13]. Idiopathic pericardial effusions are quite common in the pediatric population, representing up to 37% of cases in some series [14]. In these patients there is no identifiable cause for the pericardial process.

Bacterial pericarditis can be primary, resulting from contiguous spread of bacteria from a mediastinal and/or pleural source, or secondary, resulting from septicemic spread from a remote source. Staphylococcus aureus is the most common organism identified, followed by Haemophilus influenza type B. Other bacteria responsible for purulent pericarditis include Pseudomonas aeruginosa, Neisseria meningitides, Salmonella species, Neisseria gonorrhoeae, Listeria monocytogenes, Escherichia coli, Brucella, Yersinia, and Gemella morbillorum. Tuberculosis may be associated with a serosanguineous pericardial effusion with predominance of lymphocytes. Purulent pericardial effusions can be life‐threatening and may require emergency interventions.

Although primary tumors of the pericardium are rare, neoplastic pericardial effusions are frequently observed in patients with neoplastic diseases and may result from local tumor invasion of the pericardium or from metastatic seeding. Occasionally, they can develop from metastatic spread to the pericardial fluid itself. Blunt or penetrating trauma, including cardiac massage during resuscitation, may cause a hemorrhagic pericardial effusion. Minoxidil, anticoagulants, thrombolytics, drugs causing a lupus‐like syndrome such as chlorpromazine (Thorazine), hydralazine, isoniazid, minocycline, methyldopa, procainamide, and quinidine can be the causes of drug‐induced pericardial effusion [15].

The management of pericardial effusions includes both medical and surgical options. In the absence of hemodynamic compromise, some of the pericardial effusion may resolve with medical management without the need for fluid analysis or drainage. Idiopathic or viral effusions often have a benign course and tend to improve with bed rest and the use of nonsteroidal anti‐inflammatory drugs such as indomethacin or salicylates [16]. Steroids may occasionally be needed for recurrent or refractory cases.

Uremic effusions are frequently managed with nonsteroidal anti‐inflammatory agents and diuretics. In these patients dialysis can also effectively treat the pericardial effusion. Uremic effusion can be quite large and may lead to cardiac tamponade requiring urgent drainage. Drainage is also indicated if the effusion persists after a two‐week course of aggressive dialysis [17, 18].

Bacterial pericarditis should be managed with both antimicrobial therapy and surgical drainage, which has been shown to reduce the mortality and morbidity associated with this illness [19, 20]. Tuberculosis is the most common cause of constrictive pericarditis, therefore patients with tuberculous pericarditis may benefit from early pericardiectomy. Neoplastic pericardial effusions are often asymptomatic requiring no specific treatment, but, when symptomatic, they can be managed by palliative pericardiocentesis or extended catheter drainage [21]. In recurrent cases a subxiphoid pericardiostomy and tube drainage are the preferred option. For the management of chronic recurrent malignant effusions, the intrapericardial delivery of sclerosing agents (tetracycline or bleomycin) has been used with apparent success, but no controlled trials are available [22–25].

The most common surgical techniques used in the management of pericardial effusions consist of pericardiocentesis, subxiphoid pericardiostomy, and video‐assisted thoracoscopy. Pericardiocentesis involves placing a needle 1–2 cm below the xiphoid process, at a 45‐degree angle with the skin, directed toward the tip of the left scapula, and then advancing it into the pericardial space (Figure 41.5). This is preferably done with echocardiographic guidance. Once the needle is in the pericardial space, a guide wire is inserted through it and a drainage catheter is advanced. The drainage catheter is then connected to a closed drainage system. The pericardial fluid should be sent for cell count, chemistry, culture, and cytology. Pericardiocentesis will not be effective in cases with loculated effusions.

If the aspirated fluid is grossly bloody, it is important to rule out intracardiac placement of the needle. Therefore, an aliquot of 3–5 mL is drawn onto a clean sponge to document clotting: blood withdrawn from the pericardial space will not clot because of fibrinolysis. The risk of cardiac injury can be reduced by performing the procedure under echocardiographic guidance. Prior to proceeding with pericardiocentesis, it is important to be aware of the patient’s coagulation parameters at the time of the procedure to avoid bleeding complications.

The subxiphoid pericardiostomy (pericardial window; Figure 41.6) is usually performed under general anesthesia. In patients who may not tolerate general anesthesia, the case can be performed with sedation and local anesthesia. Given the risk of decompensation during intubation, consideration should be given to prepping and draping prior to induction of anesthesia. The procedure entails a short vertical midline incision, extending from the xiphisternal junction to just below the xiphoid process. Then the linea alba is divided and the sternum retracted, allowing for visualization of the anterior pericardium. In patients with significant effusion, immediately on pericardial entry there is a fluid outrush, which should be associated with a rise in systemic blood pressure and a decrease in the heart rate. In the event of any cardiac injury and massive bleeding, the opposite will occur [26]. An advantage to this approach is that a piece of pericardium can be excised and sent to the pathology lab for examination. A pericardial drainage tube can be placed through a separate skin incision and secured at skin level. This procedure may be performed with transesophageal echocardiographic guidance to ensure complete drainage, particularly in patients with concern for loculations. A sucker also may be gently advanced more superiorly in the pericardial space to break up loculations if needed. Complications of subxiphoid pericardiostomy are rare, but include bleeding, infection, incisional hernia, anesthetic complications, and cardiac injury [27].

Video‐assisted thoracoscopic surgery is another potential strategy for the creation of a pericardial window (Figure 41.7) [28]. With the patient in a right lateral decubitis position and through three small incisions in the left chest, endoscopic instruments are inserted in the pleural space. Under single‐lung ventilation a thoracoscope and two thoracoscopic instruments are inserted, allowing for bimanual dissection. Once the phrenic nerve is visualized, the pericardium is grasped and a window is created, allowing for drainage of the pericardial fluid into the pleural space, carefully avoiding proximity to the phrenic nerve. Evaluation of any metastases to pleural cavity or pericardium can also be made. This technique should be considered in posterior loculated effusions that may not be amenable to a subxiphoid approach. Of course, an open thoracotomy approach also can be used to create a pericardial window.

Constrictive Pericarditis

Constrictive pericarditis is defined as an inflammatory process of the fibrous and serous layers of the pericardium that leads to pericardial thickening and compression of the cardiac chambers, ultimately resulting in a significant reduction in cardiac function [9]. Although tuberculous pericarditis remains the leading cause of constrictive pericarditis worldwide, its incidence has declined in western countries [29]. Presently, idiopathic constrictive pericarditis is the most common etiology in the western world, followed by postcardiotomy and postmediastinal irradiation.

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