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Contents | Director | One | Two | Article | Topic 1 | Topic 2 | EKG | Rad 1 | Rad 2 Albany Medical Review - May 2002 |
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Case Report
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Ashit G. Patel, M.D. Vinay Sood, D.O.
This is a 50-year-old woman with a history significant for Hodgkin’s lymphoma diagnosed in 1970 and treated with chemo and radiation therapy. The patient originally presented with pleuritic chest pain, cough, and dyspnea of 3 weeks duration. She was admitted and treated for pneumonia and left pleural effusion, which was analyzed to be an exudate. Her condition improved and was discharged to home with follow-up with primary care provider (PCP) for further outpatient work-up. Shortly after discharge, patient progressively developed bilateral lower extremity swelling, dyspnea, and feeling of palpitations and irregular heart beat. She denied any chest discomfort, nausea, vomiting, diaphoresis, or dizziness. As a result, the patient was directed to Albany Medical Center for further work-up.
On physical examination, she was sitting up in bed in no acute distress with blood pressure of 110/88 and an irregular pulse of 142. She did not have an elevated jugular venous pressure, no palpable lymphadenopathy, breath sounds were decreased more at the right base then left base with bilateral rales from the base to the mid-lung fields. Her heart sounds were irregular and tachycardic with no audible murmur, gallops, or rubs. There was no hepatomegaly. She had 3+ bilateral pitting edema extending from her ankles to her knees. Chest X-ray showed a right greater then left-sided pleural effusion. The Electrocardiogram (ECG) showed a rapid atrial flutter with 2:1 block with no significant ST-T changes (Figure 1). M-mode echocardiogram revealed pericardial thickening, small pericardial effusion, and abnormal ventricular filling. 2-D echocardiogram showed left ventricle function was mild to moderately depressed and bilateral atrial enlargement. Synchronized cardioversion to convert the rapid rhythm was not attempted since a Trans-esophageal echocardiogram (TEE) showed a left atrial appendage clot. Based on the echocardiogram results chest CT scan was done, which showed a mild pericardial thickening with a small right pericardial calcification and a pericardial effusion. At this time a left and right heart cardiac catherization was performed. Results show equalization of pressures in all chambers forming the classic square root sign (Figure 2).
Thus her diagnosis of constrictive pericarditis was made based on dyspnea, lower extremity edema, bilateral pleural effusion, thickening of pericardium, atrial flutter, and hemodynamic changes seen on cardiac catherization. The patient was medically managed at this point with anti-arrhythmias and anticoagulation for atrial thrombus and discharged to home. Follow-up ECG and TEE was done as outpatient which showed patient to be in sinus rhythm with resolution of atrial thrombus. As a result, she under went an elective pericardectomy without any significant post-operative complications. Histopathology of the pericardial tissue showed calcification and scaring. Cultures were done but did not reveal any microorganisms. The etiology was attributed to previous exposure to radiation for treatment of her lymphoma. The patient is currently doing well.
Discussion Constrictive pericarditis occurs when a thickened, fibrotic, adherent pericardium restricts diastolic filling of all chambers of the heart. As time progresses the encasement of the heart by such a rigid and non-pliable pericardium results in certain distinctive pathophysiologic and hemodynamic changes. It basically leads to restricted diastolic filling of the heart that result in a diminished cardiac output and venous congestion. Constrictive pericarditis is an uncommon condition with multiple etiologies. At present, the largest number of cases is idiopathic in nature. Infection, most notably tuberculosis, remains as the leading known cause in third world countries.[1] [2] It is less frequent in developing nations secondary to availability of anti-Tb therapy. Other bacteria such as staphylococcal, pneumococcal, meningococcal, legionella, and haemophilus influenza are few of the others to consider since, in severe infection, these organisms typically can lead to a pyogenic pericarditis and subsequently to constrictive pericarditis. Viral infections such as coxsackie can also cause constrictive pericarditis. More recently, constrictive pericarditis after cardiac surgery has emerged as an important cause since studies have shown that approximately 60% of the patients develop post pericardectomy syndrome. [3] [4] [2] Neoplastic infiltration of the pericardium from breast and lung cancer, and lymphoma can also result in constrictive pericarditis. Radiation therapy, especially to mediastinal tumors (i.e. Hodgkin’s lymphoma such as in our patient) is well associated with constrictive pericarditis. Patients can develop an acute pericarditis following treatment that can progress to constrictive pericarditis years later, which is the likely mechanism in our patient. Connective tissue disease such as rheumatoid arthritis, dermatomyositis, and systemic lupus erythematosus are also rare etiologies to consider. Chronic renal failure treated with hemodialysis and renal transplant patients are often prone to development of acute pericarditis that can lead to constrictive pericarditis. Certain medications (hydralazine, cromolyn sodium, procanamide, penicillin, monoxide, phenylbutazone, methylsergide) have also been implicated. [1] [5] [6] Signs and Symptoms of constrictive pericarditis are nonspecific. Patient typically presents with complaints of dyspnea on exertion (85-95%), Jugular venous pulse rise (95-100%), abdominal distention secondary to ascites (65-75%), lower extremity edema (67%), and fatigue (25%). [5] [6] [7] [8] Weight loss is common in patients with tuberculous constrictive pericarditis. Chest pain is not a common finding but can see in 10-15% of patients if there is an active inflammatory process present. [7] Physical findings that are associated with constrictive pericarditis are dusky hue of the face secondary to venous congestion, tachycardia, and elevated jugular venous pressure (JVP). A prominent feature of the elevated JVP is the rapidly collapsing negative wave of the diastolic y descent (Friedrich’s sign). Other findings are, distant and muffled heart sounds, pericardial knock which indicates rapid end-diastolic ventricular filling, and pulsus paradoxus. Ascites is also an important finding. Ascites secondary to constrictive pericarditis is referred to as ascites praecox. It typically occurs early and before lower extremity or sacral edema. This is important in distinguishing ascites from congestive heart failure in which edema appears first and then ascites in the late phase of CHF. Atrial fibrillation is a common arrhythmia seen attributed to scarring or right atrium from the compression. Pleural effusion is also common finding, approximately 50% of the cases. [7] [8] [9] Previously difficult to distinguish from restrictive cardiomyopathy, constrictive pericarditis can now be diagnosed efficiently using chest X-ray (CXR), electrocardiogram (ECG), echocardiography (trans-thoracic and trans-esophageal), central venous and Doppler measurements, CT scan or MRI, and cardiac catheterization. Typical CXR in constrictive pericarditis shows a normal heart size and clear lung fields. Calcifications of the pericardium is usually seen when it is quite extensive and forms a shell like encasement around the apex of the heart. In a Mayo clinic series, the study reported calcifications of pericardium in 40% of the patients. ECG findings are generally non-specific. May see low voltage QRS complex, non-specific ST-T wave abnormalities, P-wave changes to suggest atrial enlargement, supra-ventricular tachyarrhythmias such as atrial fibrillation (35%), or atrial flutter (<5%). [7] [8] [9] Echocardiogram (M-mode, 2-dimensional, and Doppler velocities) combined can be used to make a diagnosis of constrictive pericarditis. With M-mode, may see pericardial thickening or flattening of posterior wall during diastole. You can look for apical pericardial calcifications, inferior vena cava and hepatic venous congestion, sudden stop in ventricular diastolic filling, and apical calcifications with 2-dimensional echocardiogram. Doppler velocities are used to measure the mitral inflow velocities. In constrictive pericarditis, the velocity decreases by more than 25% during inspiration. [5] [6] [10] Computed tomography (CT) and magnetic resonance imaging (MRI) is also used often to determine the extent of pericardial thickening, MRI being more sensitive then CT. Normal pericardium is usually 1-2mm thick. Right and Left heart cardiac catherization is considered to be the gold standard for the diagnosis of constrictive pericarditis. Typical findings are low resting cardiac output, elevated pulmonary capillary wedge pressure, and right ventricular end-diastolic pressure that is more than one-third of the systolic pressure. Plots of ventricular pressure versus time in patients with constrictive pericarditis shows a characteristic early diastolic dip (secondary to rapid filling of ventricles during early diastole) followed by a plateau (secondary to abrupt halt in filling due to non-compliant pericardium during mid-late diastole. Thus forming the classic dip and plateau waveform for right and left ventricle pressure tracing (square root sign). [5] [6] [11] Management of constrictive pericarditis is predominantly symptomatic. Patient is usually placed on bed rest, low sodium high protein diet, steroids, and NSAID’s. Curative treatment is pericardiectomy. However surgery is not indicated in early (NYHA class I) or severe (NYHA IV) constrictive pericarditis since risk of surgery out weighs the benefit. Siefert et al shows that patients in class II or III to have the best results following pericardiectomy and 80-90% of patients achieved a functional class of I or II post-pericardiectomy. Our patient would be characterized as post-radiation constrictive pericarditis in which case pericadiectomy has a higher complication rate and is considered an independent predictor of post-operative death. [12] Mayo Clinic studied 18 cases of post radiation constrictive pericarditis that underwent pericardiectomy between 1985 and 1995. The study showed there was a 50% 1-year and 30% 5-year mortality rate.
REFERENCES
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30.01.2002 |
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