Pulmonary and Critical Care Pearls |

A 43-Year-Old Man With a Large Recurrent Right-Sided Pleural Effusion* FREE TO VIEW

Ruxana T. Sadikot, MD; Joseph L. Fredi, MD; Richard W. Light, MD, FCCP
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*From the Departments of Medicine, Saint Thomas Hospital and Vanderbilt University School of Medicine, Nashville, TN.

Correspondence to: Ruxana T. Sadikot, MD, T1217 Medical Center North, Pulmonary and Critical Care Division, Vanderbilt University School of Medicine, Nashville, TN 37232-2650; e-mail: RTSadikot@POL.net

Chest. 2000;117(4):1191-1194. doi:10.1378/chest.117.4.1191
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A 43 -year-old white man developed a febrile illness for 2 to 3 weeks that was associated with retrosternal chest pain radiating to the back in May 1997. The patient was treated with a course of oral antibiotics with some improvement. However, several weeks later, he developed exertional shortness of breath and pedal edema. He denied orthopnea or paroxysmal nocturnal dyspnea. He had gained 30 lb in weight.

His medical history was significant for type II diabetes, for which he used glyburide. He had a 10-pack-year history of smoking and had quit 10 years ago. His alcohol intake was modest, and he denied use of illicit drugs. He worked as a mechanic assembling computers. There was no history of travel abroad. There was no history of tuberculosis (TB) or TB contact.

In June 1997, he was seen by his local physician, who obtained posteroanterior and lateral chest radiographs and told him that “his lung was partially collapsed.” He was treated with diuretics, but when a chest radiograph revealed persistence of the effusion in December 1997, a thoracentesis was performed and the fluid was found to be a lymphocyte-predominant exudate. A pleural biopsy was nondiagnostic. Over the next 15 months, the patient had fluctuating edema, abdominal fullness, and dyspnea on exertion; at times, he was unable to walk > 25 feet. In April 1999, at which time the effusion occupied > 75% of the hemithorax (Fig 1 ), a thoracoscopy revealed normal pleura. A CT scan showed no masses or lymphadenopathy. An echocardiogram showed a normal ejection fraction, although the study was technically difficult due to the patient’s obesity. When the effusion recurred after thoracoscopy, he was referred to our facility for further evaluation. Medications at this time included furosemide, 80 mg bid; lisinopril, 20 mg qd; and metolazone, 2.5 mg qd.

He was healthy appearing and afebrile, with a pulse rate of 100 beats/min, BP of 110/74 mm Hg with no paradoxus, and a respiratory rate of 15 breaths/min. Jugular venous pressure was increased to 6 cm above the sternal angle, but the waveform was difficult to assess. Chest examination showed dullness to percussion and reduced breath sounds on the right side. Heart sounds were distant, with no murmurs, gallops, or rub. The abdomen was distended with a palpable liver but no ascites. Extremities showed 3+ edema to mid-calf with no clubbing or cyanosis.

CBC, electrolytes, liver function tests, renal functions, and thyroid function tests were all within normal limits. A repeat thoracentesis was performed, which showed an amber-colored fluid with protein of 4.0 g/dL, lactate dehydrogenase (LDH) of 303 U/L (serum protein and LDH were 6.4 U/L and 505 U/L, respectively), glucose of 128 mg/dL, and an amylase < 30 U/L. A cell count of the pleural fluid revealed RBC count of 5,650 cells/μL and WBC count of 450 cells/μL, with 81% lymphocytes, 13% neutrophils and 6% monocytes. A diagnostic test was performed.

What was the diagnostic test, and what is the diagnosis?

Diagnostic test: Right and left heart catheterization.

Diagnosis: Constrictive pericarditis.

In 1669, Richard Lower described the physiology of constrictive pericarditis and cardiac tamponade. The clinical/pathologic features were described by Norman Chevers in 1842. He stated that “the adhesive matter that deposited around the heart led to embarressment of cardiac filling; the patient then becomes incapable of muscular exertion and always liable to dropsy and other serous effusions.”

Worldwide, TB remains the most common cause of constrictive pericarditis. However, in the western world, no definite etiology is established for a high percentage of the cases of constrictive pericarditis, and many of these may be due to an inapparent viral infection. Postsurgical pericarditis is now an important cause of constrictive pericarditis. Other causes include chronic renal failure treated with hemodialysis, connective tissue diseases, neoplastic pericardial infiltration, incomplete drainage of purulent pericarditis, and fungal infections. It has also been reported as a complication of myocardial infarction. The patient described had initially presented with a febrile illness and pericardial chest pain. We suspect a viral etiology is most likely for his constrictive pericarditis.

Clinical features of constrictive pericarditis are due to impaired cardiac filling, which leads to reduced diastolic compliance and cardiac output. The symptoms of constrictive pericarditis are similar to congestive heart failure, with dyspnea, fatigue, weight gain, and edema being the most common. Physical signs include a raised venous pressure that increases during inspiration (Kussmaul’s sign). The x and y descents are normally preserved. Peripheral edema, ascites, enlarged liver, and an audible third heart sound or pericardial knock are other important physical signs. Chest radiograph shows calcification of the pericardium in 50%, which is more evident on the lateral view. CT and MRI of the chest are often helpful in delineating the thickened pericardium, especially when the chest radiograph does not show calcified pericardium.

Right and left heart catheterization is required to confirm the diagnosis. Normal cardiac filling is bimodal. A surge of venous return occurs at the onset of ventricular ejection marked by the x descent and a small drop in the intrapericardial pressure; a second surge occurs in the diastole when the tricuspid valve opens and the y descent is inscribed. In constrictive pericarditis, early diastolic filling is faster than normal; consequently, the ventricular diastolic pressure is characterized by a dip in early diastole. The ventricles are completely filled by the end of the rapid-filling phase. Diastasis therefore persists for the remainder of the diastole. This pattern is described as a “square-root sign” or “the dip and the plateau pattern.” These signs may be obscured, especially in the presence of tachycardia and dehydration. The term “occult constrictive pericarditis” has been used to describe patients whose hemodynamics and left ventricular systolic function are normal at baseline, with a characteristic response to rapid fluid infusion. In cases where the hemodynamics are unremarkable in the baseline state, a fluid challenge with 1,000 mL of normal saline solution over 6 to 8 min may unmask these findings. In the case described, a fluid challenge test revealed findings suggestive of constrictive pericarditis (Table 1 ).

The treatment of constrictive pericarditis is surgical resection of the pericardium, which is most commonly done by median sternotomy. At times it may be nearly impossible to remove the pericardium because of tight adhesions between the pericardium and the epicardium. Incomplete removal is associated with poor outcomes. Striking hemodynamic improvement is apparent in some patients immediately after pericardiectomy, as in the present case where there was an immediate increase in cardiac output and a dramatic regression of edema within a few days.

Pleural effusions are often associated with constrictive pericarditis. In a retrospective study conducted by Tomaselli et al, 60% of their patients (18 of 30) with constrictive pericarditis were found to have a pleural effusion. The authors did not specify the size of the effusion in their series. In 12 cases, the effusion was bilateral and symmetrical. In the remaining six patients, the effusion was unilateral on the left in three and on the right in three. Sporadic reports of large unilateral effusions secondary to constrictive pericarditis have appeared. Pleural effusions in constrictive pericarditis may develop as a result of congestive heart failure and diastolic dysfunction. In most cases of constrictive pericarditis, systemic venous hypertension results in ascites that is disproportionate to the edema. It is possible that the fluid from the abdomen moves into the chest, particularly the right side through the diaphragmatic defects similar to that in hepatic hydrothorax and Meig’s syndrome (ovarian fibroma, ascites, and right-sided pleural effusion). Although a radionuclide scan was not performed to demonstrate the movement of ascitic fluid into the chest, we believe that this was the case in our patient.

The diagnosis of pericardial constriction may be problematic and delayed, as in the present patient. Constrictive pericarditis often masquerades as liver disease, the Budd-Chiari syndrome, or malignancy. It can also present as an unexplained pleural effusion, as in the above case. A combination of increased jugular venous pressure, peripheral edema, and disproportionate ascites are important clinical clues.

The patient underwent a pericardiectomy. Prior to pericardiectomy, the cardiac output was 3.5 L/min and it increased after pericardiectomy to 8.5 L/min. Within 3 days, all edema had disappeared. Four weeks after pericardiectomy, the patient was edema-free off diuretics, and a chest radiograph documented that the right pleural effusion had disappeared.

Clinical Pearls

  1. A large pleural effusion can be the presenting manifestation of constrictive pericarditis.

  2. Elevated jugular venous pressure, peripheral edema, and disproportionate ascites are important clinical findings.

  3. Chest radiograph will reveal a calcified pericardium in only 50% of cases.

  4. CT may be helpful in delineating a thickened pericardium.

  5. Left and right heart catheterization are required to establish a definite diagnosis. When baseline hemodynamics are nondiagnostic, a fluid challenge may help establish the diagnosis.

Baim DS, Grossman W. Cardiac catheterization, angiography and intervention. 5th ed. Baltimore, MD: Williams and Wilkins, 1996

Blake S. The clinical diagnosis of constrictive pericarditis. Am Heart J 1983; 106:432–433

Bush CA, Stang JM, Wooley CF, et al. Occult constrictive pericardial disease: diagnosis by rapid volume expansion and correction by pericardiectomy. Circulation 1977; 56:924–930

Lorrel BH, Braunwald E. Heart disease: a text book of cardiovascular medicine. Philadelphia, PA: WB Saunders, 1997

Masui T, Finck S, Higgins C. Constrictive pericarditis and restrictive cardiomyopathy evaluation with MR imaging. Radiology 1992; 182:369–373

Oki T, Tatabata T, Yamada H, et al. Right and left ventricular wall motion velocities as diagnostic indicators of constrictive pericarditis. Am J Cardiol 1998; 81:465–470

Tomaselli G, Gamsu S, Stulbarg MS. Constrictive pericarditis presenting as pleural effusion of unknown origin. Arch Intern Med 1989; 149:201–203

Supported in part by the Saint Thomas Foundation, Nashville, TN, and by grant HL 07123, from the National Institutes of Health.

Figure Jump LinkFigure 1. Chest radiograph revealing large right-sided pleural effusion.Grahic Jump Location
Table Graphic Jump Location
Table 1. Cardiac Catheterization Data at Baseline and After Fluid Challenge*

RAP = right atrial pressure; RVEDP = right ventricular end-diastolic pressure; PAP = pulmonary arterial pressure; PCWP/LVEDP = pulmonary capillary wedge pressure/left ventricular end-diastolic pressure.


Figure Jump LinkFigure 1. Chest radiograph revealing large right-sided pleural effusion.Grahic Jump Location


Table Graphic Jump Location
Table 1. Cardiac Catheterization Data at Baseline and After Fluid Challenge*

RAP = right atrial pressure; RVEDP = right ventricular end-diastolic pressure; PAP = pulmonary arterial pressure; PCWP/LVEDP = pulmonary capillary wedge pressure/left ventricular end-diastolic pressure.


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