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TB Pericarditis
Epidemiology
Incidence low secondary to low incidence of TB in general Occurs in 1-2% of patients with pulmonary TB One Spanish study found 4.4% of pulmonary TB patient s had pericarditis Keep in mind that Spanish (and South African) figures on incidence far exceed that in the USA A Mayo clinic study found 2% cases of pericarditis in pulmonary TB patients as apposed to a similar study at Mayo fifty years ago However, parts of the USA have high immigrant populations where TB pericarditis rates are much higher, as established at Baylor in 1990.
Pathogenesis
TB pericarditis is usually associated with TB somewhere else in body Usually represent reactivation disease thus a primary infective location usually not found 4 Stages
Effusive
Serosangiouness fluid with leukocytes and high protein and tubercle bacilli found in low concentration Pressures consistent with cardiac tamponade are found
Pathogenesis
Absorptive
50% of patients will reabsorb this fluid without treatment Healing with fibrosis and calcification and overall thickening of visceral pericardium Pressures consistent with constrictive pericarditis are found Patients who have continued elevation of pressures after pericardiocentesis have effusive-constrictive pericarditis
Constrictive
Restrictive Cardiomyopathy
nondilated rigid ventricle severe diastolic dysfunction and restrictive filling History of infiltrative disease
amyloidosis sarcoidosis
bundle branch block, ventricular hypertrophy, pathologic Q waves, or impaired atrioventricular conduction strongly favors restrictive cardiomyopathy Decreased myocardial tissue velocity by doppler Pro-BNP elevated Independent Ventricular action 2/2 stiff myocardium and septum
Tissue Doppler:
Myocardial velocity is shown by arrows in row C.
Constrictive Pericarditis
scarring with the consequent loss of elasticity of the pericardial sac impairment of ventricular filling affecting all four cardiac chambers Equalization of pressures in severe constriction Inspiratory decrease in Mitral E velocity
Constrictive Pericarditis
majority of ventricular filling occurs rapidly in early diastole ie: rapid and deep Y descent on RA tracings.
Constrictive Pericarditis
Suggested by history prior pericarditis Tuberculosis connective tissue disease Malignancy Trauma cardiac surgery Pro-BNP normal as myocardium not stretched Thickened pericardium on Chest CT or calcification on CXR
Constrictive Pericarditis
Pericardial Calcification on CXR
Cardiac Tamponade
Pericardial fluid enlarging around the heart Acute vs Subacute Equalization of pressures measured by catheterization
Blunting of y descent
Clinical Manifestations
Cough Dyspnea Chest pain Night sweats Orthopnea Weight loss
Physical Exam
Fever Tachycardia hypotension increased JVD
Kussmauls Sign
Loss of the expected inspiratory decline of jugular venous pressure Also seen in right heart failure and severe venous congestion Seen in tamponade and constrictive physiology
Physical Exam
Pulsus Paradoxus
Seen in tamponade, not in restrictive cardiomyopathy, and only in severely constrictive pericarditis Effusive constrictive disease can produce tamponade like features. Inflate cuff and start to deflate slowly, the first Korotkoff sound will be heard only during expiration. Then the first Korotkoff sound will be heard during inspiration and expiration. The difference in pressures when this occurs is the measured pulsus paradoxus. Tamponade
Inspiration increases RV filling which pushes on LV thus decreasing LVEDV which decreases SV and SBP
Constrictive Pericarditis
Inspiration has no effect on ventricular filling because they are shielded by fibrotic pericardium Inspiration lowers pulmonary venous pressures, thereby decreasing gradient of flow into LV.
Studies
CXR
Electrical Alternans
Studies
ECHO
Tamponade or Effusive-Constrictive
Remember that tamponade is clinical diagnosis Compression of RA Collapse of RV in diastole Increased respiratory variation of TV/MV flow
Constrictive
Pericardial thickening Dilated atria and vena cava
Studies
Cardiac Catheterization
Tamponade
Equalization of increased RA, PCW, RV and LV pressures throughout respiratory cycle Considerable respiratory variation
Constrictive
equalization of increased RA and PCW pressures, but CW pressures drop during inspiration, therefore not equal throughout respiratory cycle Intra-cardiac pressures have little respiratory variation
Effusive Constrictive
Similar to tamponade but constrictive features unmasked when fluid is removed
Differential Diagnosis
Malignancy Hemopericardium
Viral infections Radiation Connective tissue disorders Sarcoidosis Post-myocardial infarction Uremia
Diagnosis
There is no good diagnostic test!! PPD
Negative tests in non-HIV patient suggest it is not TB pericarditis Exudative, high protein fluid AFB present in only 40-60% patients Culture improves these figures somewhat Yield of diagnosis is only between 5 and 29%
Pericardiocentesis
Pericardial Biopsy
Adenosine Deaminase
In high endemic regions results are quite helpful with Sensitivity 91%, Specificity 68% in one South African study of 110 patients (they used a cut-off value of 30U/L)
Treatment
Medications
INH (300 mg orally once daily) Rifampin (600 mg orally once daily) Pyrazinamide (15 to 30 mg/kg per day up to 2 g/day given as a single dose) Ethambutol (15 to 20 mg/kg orally once daily)
8 weeks of four drug regimen followed by 18 weeks of INH and Rifampin daily Prednisone 60mg x 4 weeks, 30mg x 4 weeks, 15mg x 2 weeks, 5mg x 1 week
This was shown to decrease repeat pericardiocentesis, improve JVD by exam and decrease mortality
Pericardiectomy
Reserved for patients with recurrent effusions and continued elevation of CVP Better tolerated in patients that have not progressed to constrictive pericarditis
References
Sagrista-Sauleda, J, Permanyer-Miralda, G, Soler-Soler, J. Tuberculous pericarditis: Ten year experience with a prospective protocol for diagnosis and treatment. J Am Coll Cardiol 1988; 11:724. Strang, JIG, Kakaza, HSS, Gibson, DG, et al. Controlled trial of prednisolone as adjuvant in treatment of tuberculous constrictive pericarditis in Transkei. Lancet 1987; 2:1418. Up-to-date