Historical Highlights

Galen was the first to describe pericardial disease in animals (circa 160 AD) and subsequently described in two patients the surgical drainage of purulent pericardial effusions.¹ This predated Lower’s 1669 description of pericarditis in humans.² There are apocryphal references of penetrating heart wounds being treated, usually by the removal of the offending object, without much information about how subsequent drainage of the pericardial space was dealt with. Francisco Romero, a Catalonian physician, was probably the first heart surgeon, earning this title when he performed open drainage of a pericardial effusion in 1801. He presented this work 15 years later, but it was silenced for being too aggressive.³ This predates the “birth of heart surgery” by almost 100 years, when Rehn first successfully sutured a heart wound in 1896.⁴

In 1929, Beck showed experimentally that constrictive pericarditis could be produced and treated surgically in laboratory animals^5,6 using Dakin’s solution. His observations of the extent of the adhesions formed (and the concomitant neovascular supply) probably contributed to his later procedures for ischemic heart disease.⁷ Pericardiectomy was then translated to clinical practice. By 1941, Blalock reported a series of 28 patients⁸ who had undergone this procedure.

This chapter focuses on many aspects of pericardial disease including cardiac tamponade, pericardial effusion, and pericarditis, with an emphasis on the surgical aspects of this disease.

Anatomy

The pericardium is a conical sac that encloses the heart and great vessels. It is located posterior to the body of the sternum, bounded by the second and sixth costal cartilages anteriorly and thoracic vertebrae 5 to 8 posteriorly. The ascending aorta, pulmonary artery, and the superior vena cava exit from the cephalad opening of the pericardium. The base is fused with the central tendon of the diaphragm. Loose connective tissue called the sternopericardial ligaments attaches the anterior surface of the pericardium to the posterior table of the sternum.

The pericardium is composed of an outer and inner membrane. A thick layer termed the fibrous pericardium is external, while a thin transparent membrane called the serous pericardium is internal. The serous pericardium is further divided into parietal and visceral layers. The former is fused to the fibrous portion, while the latter is reflected onto the epicardium. The visceral layer of the serous pericardium is in fact the epicardium of the heart, and thus is also in continuity with the adventitia of the coronary vessels. The thin layer of fluid between the two layers allows the heart to move in a near-frictionless environment.

By virtue of the anatomic reflection of the pericardium, two sinuses exist—the transverse and the oblique pericardial sinuses (Fig. 47-1). The transverse sinus is located behind the ascending aorta and pulmonary trunk. If the pericardium is opened anteriorly, one can place a finger easily into this space and go from right lateral to left lateral pericardium. The larger sinus is the oblique sinus, which cradles the heart. One can see this space when the heart is lifted toward the right shoulder. This is a blind cul-de-sac, bordered to the right by the inferior vena cava (IVC). This therefore prevents passage around the IVC without sharp dissection. The two sinuses lie in near continuity with only a thin layer of serous pericardium separating the two.

The arterial supply of the pericardium comes mainly from the internal thoracic arteries. Smaller branches of the bronchial, esophageal, and superior phrenic arteries also contribute to the blood supply. The visceral layer of the serous pericardium is supplied by the coronary arteries. Venous drainage flows into the internal thoracic veins and azygous system. Nervous supply comes from the vagus, phrenic, and sympathetic trunks.⁹

Embryology

The pericardium is derived, beginning the third week of gestation, from the progressive invagination of the intraembryonic coelomic cavity. This results in a creation of the visceral and parietal layers of the serous membrane, which will later become the serous pericardium. By the fourth week, with growth of the lung buds, pleuropericardial membranes are developed on each side. With continued growth and eventual fusion of the pleuropericardial membranes, the thoracic cavity becomes separated into the pericardial and two pleural cavities. This membrane will become the fibrous pericardium. It is the failure of these membranes to fuse which results in congenital defects of the pericardium.¹⁰

Epidemiology

The finding of a pericardial effusion is common in modern day cardiology and cardiothoracic surgical practices. The evolution and prevalence of noninvasive technology [i.e., echocardiography (ECHO)] has made the diagnosis of pericardial effusion both easier and apparently more frequent. Such incidental effusions are often discovered while patients are being evaluated for cardiac valvular disease. But many systemic processes other than cardiac can contribute to the development of pericardial effusions. All types of pericarditis (discussed later in this chapter) can lead to the development of effusions. Etiologies of pericarditis include infection, inflammation, immunologic disorders, malignancy, myxedema, uremia, pregnancy, aortic dissection, cardiac rupture, trauma, chylopericardium, postmyocardial infarction, cirrhosis, heart failure, and idiopathic.¹¹ Tuberculosis now is an uncommon cause of pericardial effusion but once was one of the more frequent etiologies of infective pericarditis. The clinical constellation of hemodynamic compromise, cardiomegaly, pleural effusion and large pericardial effusion were more common in those with tuberculosis than either malignancy or idiopathic causes.¹²

Multiple studies have shown the three most common etiologies for pericardial effusion to be neoplasia, uremia, and idiopathic.^13–15 Approximately 40 percent of these patients present with cardiac tamponade (discussed later).

Pathophysiology

The pathophysiology of pericardial effusion relates to the underlying cause. As described above, fluid naturally exists between the two layers of the serous pericardium. It is when this fluid accumulates in the pericardial space that the pericardial effusion can become pathologic. The production of fluid is balanced by the corresponding absorption of fluid by lymphatic channels. The parietal pericardium is drained by the anterior and posterior mediastinal lymph nodes; visceral pericardium is drained via the tracheal and bronchial lymph nodes.¹⁶ Pericardial mesothelial cells contain dense microvilli that facilitate ion and fluid exchange.¹⁷ Effusions arise when production exceeds reabsorption. Thus, effusions can arise from either overproduction or from underabsorption.

Clinical Features

A wide spectrum of clinical presentations exists for pericardial effusions. Many are asymptomatic and found incidentally by ECHO, this is especially true for elderly women.¹⁸ On the other end of the spectrum are those patients presenting in cardiac tamponade.

Symptoms of pericardial effusions may include dyspnea, fever, chest pain, or hemodynamic instability. Signs include a pericardial friction rub, EKG abnormalities, or pulsus paradoxus (described in cardiac tamponade section).

Posner et al. found that the initial presentation of cardiac tamponade was suggestive of malignancy, especially with very large effusions. Fever, pericardial friction rub, and improvement after starting nonsteroidal anti-inflammatory drugs are suggestive of idiopathic pericardial effusion.¹⁹ In 60 percent of patients, a known previous condition that could cause a pericardial effusion was present. The underlying condition was the cause in greater than 90 percent of these patients. The presence of inflammatory signs (chest pain, pericardial friction rub, fever, or EKG changes) was predictive for acute idiopathic pericarditis. Furthermore, a large effusion without tamponade or inflammatory signs was predictive of chronic idiopathic effusion. Tamponade without inflammatory signs was predictive of malignancy.²⁰

Diagnostic Modalities

Before the advent of ECHO, the diagnosis of a hemodynamically significant pericardial effusion was difficult and needed to be confirmed by physical exam. ECHO is now considered the gold standard for diagnosis of effusions (Fig. 47-2) and can help confirm the diagnosis of a hemodynamically significant effusion (tamponade). Importantly, a “negative” ECHO does not eliminate the possibility of tamponade. Cardiac catheterization can aid in the diagnosis of tamponade or pericardial constrictive disease, but does not impact the diagnosis of effusion.

Attention must be drawn to specific ECHO findings. Some patients with evidence of right atrial and ventricular collapse have no clinical evidence of tamponade. Levine et al.²¹ performed right-sided heart catheterization and pericardiocentesis on a group of patients with ECHO evidence of tamponade. Many patients had no hemodynamic evidence of tamponade. Systolic blood pressure was greater than 100 mm Hg in 94 percent. Pulsus paradoxus was present in only one-third of patients. Right atrial collapse had a positive predictive value of only 50 percent.

Treatment

Medical Therapy

The success of medical therapy for pericardial effusions depends on the underlying disease processes that cause the effusion to occur. If systemic signs of inflammation are present, a course of nonsteroidal anti-inflammatory agents or steroids should be started, unless evidence of hemodynamic compromise is suspected. Any underlying infection should be treated if known.

Medical therapy is most useful with malignant effusions. Chemotherapy or radiotherapy may be useful in preventing recurrence after aspiration of the fluid. Vaitkus et al. report a success rate of 78 percent in preventing recurrence after systemic chemotherapy was given. Radiation therapy also had good results, especially with radiosensitive tumors such as lymphoma, with success rates greater than 90 percent. Instillation of sclerosing agents (e.g., tetracycline or bleomycin) through an indwelling catheter also reduced recurrence in some small series.²²

Surgical Therapy

Surgical therapy of pericardial effusion consists of pericardiocentesis with or without catheter placement, pericardial window, and pericardiectomy. The indications and techniques will be described.

Pericardiocentesis or other modes of surgical drainage are indicated for patients with clinical aspects of cardiac tamponade, suspicion of infection, and in patients with large idiopathic chronic pleural effusions. Pericardiocentesis or drainage is not warranted in the initial management of asymptomatic patients with a large effusion. However, when large asymptomatic effusions persist for more than 3 months, the risk of tamponade without a specific inciting event approaches 30 percent.²³

Pericardiocentesis can be performed either in the catheterization laboratory (under fluoroscopic guidance) or at the bedside. It should be the initial therapy for those in overt tamponade when such a procedure can be easily and safely performed, and for those patients that are not in the immediate postoperative period. Once the decision is made to proceed with pericardiocentesis, the decision is to perform either simple aspiration or percutaneous catheter drainage. These authors favor the latter approach. With this approach, the subxiphoid area is infiltrated with 1 percent lidocaine for local anesthesia. An 18-gauge spinal needle is inserted to the left of the xiphoid process at a 45° angle toward the left shoulder. A “pop” is felt when the needle enters the pericardial sac. This can be aided with either fluoroscopic or ECHO guidance. An 8F pigtail catheter is then placed in the pericardial space using the Seldinger technique. Fluid should be aspirated and then sent for culture and cytology. If blood is withdrawn, it is placed in a small basin and observed. Clotted blood suggests that a cardiac chamber was entered. If ECHO is being used for guidance, a simple bubble study can be used to verify extracardiac positioning of the catheter needle. A follow-up CXR evaluates catheter placement and any evidence of pneumothorax. Techniques have also been described using an alligator clip attached to the needle and one lead of the EKG. When the myocardium is violated with the needle, a deflection will be noted on the EKG.

Pericardial drainage can also be achieved by creating a pericardial window. Surgical approaches include subxiphoid, left anterior thoracotomy, or thoracoscopy (VATS). General anesthesia is preferred for all approaches. Especially when tamponade is the presumptive diagnosis, the patient should be prepped and draped prior to induction of anesthesia since hypotension and hemodynamic instability may ensue, and rapid drainage may be necessary.

The subxiphoid approach consists of a 6- to 8-cm incision that starts at the junction of the sternum and xiphoid. The xiphoid process is either resected or split. An Army–Navy retractor is placed under the sternum. Dissection is continued under the sternum until the pericardium is identified and incised. The fluid is drained and sent for culture and cytology. The largest possible piece of pericardium is resected and any intrapericardial loculations are broken with finger dissection. A 28F right-angled chest tube is placed into the pericardial space through a separate stab incision. The surgical pericardial incision can be closed, left opened, or drained into the peritoneal space.

Pericardial drainage can be approached by left anterior thoracotomy. A double-lumen tube is not necessary for this approach. A small roll should be placed under the patient’s left shoulder, so that the patient is at a 30° angle from the table. A 6- to 8-cm incision is made in the infra-mammary crease with the nipple as its most medial aspect. Subcutaneous dissection is continued superiorly for one rib space. The fourth intercostal space is entered; the intercostal muscles are taken off the fifth rib medially and laterally. A sponge stick is used to push the lung away. The pericardium is identified and incised. The fluid is drained and sent for culture and cytology. The pericardium is resected anterior to the phrenic nerve, with the largest possible section being taken. The incision is closed after a 28F chest tube is placed through a separate stab incision. The pericardial space can be drained directly with the chest tube, or the tube can be left in the pleural space under the assumption that any reaccumulation of pericardial fluid will drain into the pleural space.

Thoracoscopy can be used to create a pericardial window. However, this approach does require placement of a dual lumen endotracheal tube and single lung ventilation. Patients with clinical tamponade often will not tolerate this approach. A port for the camera and two working ports are placed. The chest cavity is first inspected, including identification of the phrenic nerve. The pericardium is then incised anterior to the nerve and a large piece of pericardium is resected. Care is taken not to leave a defect so large that cardiac herniation may occur. A single 28F chest tube is left in the pleural space.

Outcomes/Prognosis

The outcomes and prognoses for pericardial effusions relate to the underlying disease process. Patients with malignant effusions have a median survival of 2 to 3 months.²⁴ A recent study by McDonald et al.²⁵ compared subxiphoid pericardial window to percutaneous catheter placement. No direct procedural mortality occurred in either group. However, the in-hospital mortality and recurrence rates were significantly higher in the percutaneous group. Allen et al. reviewed combined results in the literature, and similar results were noted.²⁶ Surgical drainage had mortality, complication, and recurrence rates of 0.6, 1.5, and 3.2 percent, respectively. Catheter drainage had rates of 1.9, 10.6, and 13.8 percent, respectively. Thus, despite the relatively short-term benefit of any procedure, compared with percutaneous approaches, surgical drainage may allow more patients to be discharged from the hospital.