Postpericardiotomy Syndrome

Updated: Dec 27, 2017
  • Author: M Silvana Horenstein, MD; Chief Editor: Howard S Weber, MD, FSCAI  more...
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Overview

Background

Postpericardiotomy syndrome (PPS) is a febrile illness secondary to an inflammatory reaction involving the pleura and pericardium. [1, 2, 3, 4] It is more common in patients who have undergone surgery that involves opening the pericardium (in the United States, the estimated frequency varies from 2% to 30% of these patients). However, postpericardiotomy syndrome has also been described following myocardial infarction (Dressler syndrome) and as an unusual complication after percutaneous procedures such as coronary stent implantation, [5] after implantation of epicardial pacemaker leads [6] and transvenous pacemaker leads, [7, 8, 9, 10, 11] and following blunt trauma, [12] stab wounds, [13] and heart puncture. [14]

Pericardial effusions often accompany the syndrome and may develop into early or late postoperative cardiac tamponade [15] and even recurrent cardiac tamponade. [16] The syndrome is also characterized by pericardial or pleuritic pain, friction rubs, pleural effusions, pneumonitis, and abnormal ECG and radiography findings (see Workup).

PPS usually occurs as a single episode; however, it can recur years later. [17] It is uncommon in patients younger than 2 years, [18]  but the frequency increases in children and adults to as much as 30%. It is more common after repair of tetralogy of Fallot, repair of atrial and ventricular septal defects, [19] and after cardiac transplantation. [20]

It is essential that clinicians diagnose and adequately treat PPS as well as recognize and treat impending or manifest cardiac tamponade.

 

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Pathophysiology

Postpericardiotomy syndrome is often associated with the development of antiheart antibodies, leading to an inflammatory reaction within the pericardial space. [21]  Various viral agents, including coxsackie B, adenovirus, and cytomegalovirus, have been present in approximately two thirds of patients with postpericardiotomy syndrome, suggesting an autoimmune response associated with a viral infection. However, a prospective study found no evidence to support a viral etiology for postpericardiotomy syndrome. [22] This study suggested that the use of viral titers in the setting of cardiopulmonary bypass and recent blood transfusions is unreliable.

The etiology may be multifactorial; a systematic review found that the inflammatory response and perioperative bleeding and coagulation may play a role in the development of postpericardiotomy syndrome. [23]  Factors that were associated with a higher risk of this condition included the following [23] :

  • Lower levels of preoperative interleukin 8, platelets, and hemoglobin
  • Higher postoperative complement conversion products
  • Younger age
  • Red blood cell transfusions
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Etiology

The precise etiology of postpericardiotomy syndrome is not known. Postpericardiotomy syndrome is postulated to be an autoimmune response involving autoantibodies which target antigens exposed after the percardium has been damaged. [21]

In a study of patients who had developed postpericardiotomy syndrome after transplantation, an increased proportion of activated helper T cells (CD4+/25+) and cytotoxic T cells (Leu-7+/CD8+) was found. This led the investigators to conclude that, in this population, postpericardiotomy syndrome was possibly secondary to cell-mediated immunity. [20]

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Prognosis

Most cases of postpericardiotomy syndrome resolve within a few weeks. Rarely, symptoms may occur for more than 6 months.

Relapse may occur after tapering anti-inflammatory medications; it is estimated to occur in 10-15% of patients. Most recurrences occur within 6 months of the initial insult.

Morbidity/mortality

Postpericardiotomy syndrome usually manifests as a mild, self-limited inflammatory illness. Life-threatening pericardial tamponade can develop due to a rapidly increasing pericardial effusion. [3, 4] Tamponade occurs in less than 1% of patients with postpericardiotomy syndrome. Elevation of cardiac filling pressures, progressive limitation of ventricular diastolic filling, and reduction of stroke volume and cardiac output characterize cardiac tamponade.  This also correlates with the rapidity of pericardial effusion accumulation, because slow accumulation of even large pericardial effusions may not result in clinical signs and symptoms of tamponade. This is directly related to the ability of the pericardial space to enlarge significantly over an extended time period, thereby accomodating the fluid volume, and not resulting in cardiac tamponade.

A study that evaluated 822 patients undergoing nonemergent valve surgery found postpericardiotomy syndrome in 119 (14.5%), with a 20.9% incidence of reoperation for tamponade at 1 year in patients who developed the syndrome compared to 2.5% in those who did not, but also having similar 1-year mortality (4.2% vs 5.5%, respectively). [23]  Patients with postpericardiotomy syndrome also had longer median hospital stays (13 days vs 11 days, respectively) and were more likely to have had preoperative therapy for pulmonary disease without corticosteroids. [23]

Carriage of the Mediterranean Fever (MEFV) gene may affect the severity of postpericardiotomy syndrome. In a study of 86 patients who underwent cardiac surgery, of whom 45 developed this condition and 41 did not, investigators found a significantly lower rate of mutation carriage in patients with severe postpericardiotomy syndrome (4.8%) relative to those with mild-moderate postpericardiotomy syndrome (25%) (P <0.05).<ref>24</ref>​ However, the rate of MEFV mutation carriage between the groups with and without postpericardiotomy syndrome was similar.

Complications

Cardiac tamponade is a life-threatening complication of postpericardiotomy syndrome. Emergent pericardiocentesis and drainage of the pericardial effusion is necessary. As noted earlier, tamponade occurs in approximately 1% of patients with postpericardiotomy syndrome.

Constrictive pericarditis occurs late postoperatively in fewer than 0.5% of patients but may not be related to postpericardiotomy syndrome. The high prevalence of postpericardiotomy syndrome and quite low prevalence of constriction suggests that a direct association is unlikely. With constriction, the pericardium becomes thickened and adherent to the heart and restricts filling of the ventricles. A pericardiectomy may be required for treatment.

Patients with pain from the inflammatory response may demonstrate splinting during breathing. This can result in hypoxemia. Monitor oxygen saturation by pulse oximetry in patients presenting with these findings.

Coronary artery bypass grafting is an unusual procedure in children. Occlusion of the graft is reported as a rare, but fatal, complication of postpericardiotomy syndrome.

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