Tuberculous pericarditis is caused by Mycobacterium tuberculosis infection of the pericardium. It typically progresses through dry, effusive, absorptive, and constrictive stages. The effusive stage involves a serosanguineous pericardial effusion that is often lymphocytic. Left untreated, tuberculous pericarditis can lead to cardiac tamponade, pericardial constriction, and death. Diagnosis involves identifying M. tuberculosis through smear, culture or molecular testing of pericardial fluid, or demonstrating caseating granulomas on biopsy. Treatment consists of a standard antituberculosis regimen with corticosteroids to reduce mortality

1. Tuberculous Pericarditis
Dr Jay Bhanushali
MD Pulmonary Medicine PGY2
JNMC

2. Pericardium
• Double layered sac. Visceral Pericardium is serous membrane while Parietal pericardium is a
Fibrous membrane.
• Volume of pericardial Fluid ranges from 15-50ml in normal healthy population.
• Critical Functions
- Avoids over and sudden expansion of the heart during strenuous activities.
- Acts as a barrier for spread of infection from lungs and pleural cavity.

3. TB is an important cause of Pericardial Disease, it is present in 2 % of all autopsied
cases of Pulmonary TB. In India, TB is responsible of 2/3rd cases of constrictive
pericarditis.
• Acute Pericarditis (<6weeks)
• Chronic Pericardial Effusion
• Cardiac Tamponade
• Pericardial Constriction (>6months)
Reported Mortality in TB pericarditis is more than 80% during the acute phase of illness and still
more at a later stage due to constrictive pericarditis.

4. Pathogenesis of TB Pericarditis

5. Stages of TB Pericarditis
• Dry Stage
• Effusive Stage
• Absorptive stage
• Constrictive stage
(1) Dry Stage: Fibrinous exudation with initial polymorphonuclear leukocytosis, relatively abundant
mycobacteria, and early granuloma formation with loose organization of macrophages and T
cells.
(2) Effusive Stage: Serosanguineous effusion with a predominantly lymphocytic exudate with
monocytes and foam cells
(3) Absorptive Stage: Absorption of effusion with organization of granulomatous caseation and
pericardial thickening caused by fibrin, collagenosis, and ultimately, fibrosis.
(4) Constrictive stage: Constrictive scarring of the fibrosing visceral and parietal pericardium
contracts on the cardiac chambers and may become calcified, encasing the heart in a
fibrocalcific skin that impedes diastolic filling and causes constrictive pericarditis.

6. -Disease my progress sequentially from 1-4 or may present as any of the stages.
- Acute pericarditis appears to be a primary hypersensitivity response to tuberculoproteins, chronic
effusion and constriction , and reflects granuloma formation and fibrosis.
-The Exudative pericardial Fluid may contain PMN leucocytes in the initial 1-2 weeks but later it is
predominantly lymphocytic with high protein content. Pericardial Fluid may vary from 15ml to
3500ml !
• Tuberculous pericarditis presents clinically in 3 forms, namely, pericardial effusion, constrictive
pericarditis, and a combination of effusion and constriction.

7. Clinical Features of Pericardial disease
• Most common occurrence in middle age, but can occur in any age group.
• More common in immunocompromised patients.
• Clinical features depend on the stage and severity of the disease.
• It is insidious in onset and presents with Fever, malaise and weakness.
• Attention to diagnosis is drawn by presence of Pericardial Rub, vague chest pain, or cardiomegaly on CXR.
• Dypnea, non productive cough and weight loss are common symptoms.
• Chest Pain, Ankle oedema and Orthopnea occur in almost 70% of the patients.
• Chest Pain is typically pleuritic in nature and relieved by sitting up and leaning forward. Radiation of pain to
trapezius ridge through the phrenic nerve is Pathognomic of Pericardial Pain.
• Fever, Pericardial rub and systemic Congestive Failure are important signs that are commonly seen.

8. Pericardial Effusion
• Tuberculous pericardial effusion usually develops insidiously, presenting with nonspecific systemic
symptoms, such as fever, night sweats, fatigue, and weight loss. Chest pain, cough, and breathlessness
are common. Right upper abdominal aching owing to liver congestion has also been described.
• Sinus Tachycardia, Pulsus Paradoxus, Raised JVP, muffled heart sounds , Oedema, Hepatomegaly are
consistent clinical findings.
• Diagnosis of Pericardial Effusion
• The advent of echocardiography has made it possible to achieve an accurate, noninvasive method of
diagnosing the presence of a pericardial effusion. Imaging by CT scanning or MRI can also be used but is
seldom available in rural areas in the developing world.
• The chest radiograph, which shows an enlarged cardiac shadow in more than 90% of cases, demonstrates
features of active pulmonary TB in 30% of cases and pleural effusion in 40% to 60% of cases. The ECG is
abnormal in virtually all cases of tuberculous pericardial effusion, usually in the form of nonspecific ST-T–
wave changes.The presence of microvoltage (ie, complexes <5 mm in limb leads and <10 mm in
precordial leads) suggests a large pericardial effusion, and cardiac tamponade is unlikely in the absence
of ECG microvoltage. Echocardiographic findings of effusion with fibrinous strands on the visceral
pericardium are typical but not specific for a tuberculous pathogenesis.In addition to features of
pericardial disease (ie, pericardial effusion and thickening of the pericardium), CT of the chest shows
typical changes in mediastinal lymph nodes (ie, enlargement >10 mm with matting and hypodense
centers and sparing of hilar lymph nodes) in almost 100% of cases.

9. • The pericardial fluid is bloodstained in 80% of cases of tuberculous pericarditis. However,
because malignant disease and the late effects of penetrating trauma may also cause bloody
pericardial effusion, confirmation of TB as the cause is important.
• Tuberculous pericardial effusions are typically exudative and characterized by a high protein
content and increased leukocyte count, with a predominance of lymphocytes and monocytes.
Light’scriteria are the most reliable diagnostic tool for identifying pericardial exudates.
• A Smear of pericardial fluid rarely identifies AFB on ZN statining.
• Culture of Pericardial fluid grows MTB in 50-60% of cases with LJ media.
• Elevated ADA > 40 and interferon gamma >50pg/ml have high sensitivity and specificity for
Tuberculosis.
• MTB gene xpert has high diagnostic value.

10. Subcostal echocardiographic image of the heart showing a large pericardial effusion. The surface of the heart has a
shaggy appearance, with frond-like structures extending to the parietal pericardium. This appearance is typical of
tuberculous pericardial effusion.

12. Subacute Effusive Constrictive Pericarditis
• Also termed as Elastic pericarditis.
• It shows features of both Pericardial Effusion and Constriction.
• The fluid fibrin layer leads to relatively elastic compression of heart resembling “wrapping the
heart tightly with rubber bands”
• This stage can develop within weeks of TB Pericarditits.
• With ATT this stage resolves in a some patients but commonly progresses to Chronic Constrictive
Pericarditis.

13. Constrictive Pericarditis
Constrictive pericarditis is one of the most serious sequelae of tuberculous pericarditis, occurring in 30% to 60% of patients,
despite prompt antituberculosis treatment and the use of corticosteroids. TB is said to be the most frequent cause of
constrictive pericarditis. The clinical presentation is highly variable, ranging from asymptomatic to severe constriction. The
diastolic lift (pericardial knock) that coincides with a high-pitched early diastolic sound and sudden inspiratory splitting of
the second heart sound are subtle but specific physical signs, found in patients with constrictive pericarditis. These signs are
often missed by the inexperienced observer. Furthermore, if the investigation is not guided by clinical examination,
echocardiography has the potential to miss signs that are suggestive of this diagnosis.
Hearts with CCP, the inflow of blood is impeded due to thickened unyielding pericardium, especially in the late diastole.
Thus, patients usually present with symptoms of systemic and pulmonary venous congestion. Abdominal swelling [from
ascites or hepatomegaly] and peripheral oedema are the most common presenting symptoms. Dyspnoea and ortho- pnoea
are also present in nearly half the patients requiring surgical intervention. Cardiac output is mildly reduced at rest. These
patients have compensatory tachycardia to maintain cardiac output. Since more than 75 per cent of diastolic filling occurs in
the first 25 per cent of the diastole, shortening of diastole does not reduce stroke volume much but helps in augmenting
cardiac output.

14. • Other Clinical signs include raised JVP with rapid y descent, which further increases on inspiration
[Kussmaul's sign]. Pulsatile hepatomegaly, ascites, with an impalpable apex or systolic retraction
of the precordium [Broadbent's sign] are also seen commonly. In general, presence of
cardiomegaly, third and fourth heart sounds, significant mitral or tricuspid regurgitation, and
severe pulmonary hypertension favours the diagnosis of restrictive cardiomyopathy.
• Other atypical manifestations include clinical presentation with ascites that is disproportionate to
the peripheral oedema which may seem as a primary liver disease. Sometimes, patients may also
present with subtle signs, such as like fatigue, without obvious clinical findings of CCP. These
patients with "occult" constrictive pericarditis often manifest pericardial thickening on
radiological imaging. The clinical signs of constrictive pericarditis may become evident on fluid
challenge in such patients. These patients improve with pericardiectomy. Other patients may
present with congestive splenomegaly. Cardiac cirrhosis may also develop after many years of
hepatic venous congestion.
• The disease worsens gradually and in chronic cases, significant myocardial atrophy occurs due to
extension of inflammation and possibly disuse of cardiac muscle. These patients have suboptimal
results and higher mortality with pericardiectomy.

15. Diagnosis of Constrictive Pericarditis
• Echocardiography is particularly valuable in confirming the diagnosis of subacute constrictive
pericarditis. Typically, a thick fibrinous exudate is seen in the pericardial sac and is associated with
diminished movements of the surface of the heart, normal-size chambers, absence of valvular
heart disease, and absence of myocardial hypertrophy. Pericardial thickening is best visualized in
the anteriorly over the right ventricle free wall. TEE is superior in diagnosis of Pericardial
Thickening. >3mm thickness is highly sensitive and specific for CCP
• Pericardial Biopsy , Percutaneous or open for a tissue diagnosis is also done and is diagnostic in
about 70% of the cases. A normal histopathology biopsy does not exclude TB.
• Cardiac CT and MRI is useful, characteristic hallmark is pericardial thickening with or without
calcification. CT additionally shows mediastinal Lymphadenopathy which is seen frequently with
TB Pericardial disease.
• Cardiac Catheterization is an invasive method of diagnosis of CCP which has 100% sensitivity. In
CCP, RV systolic pressure increases with Inspiration while Left ventricular pressure simultaneously
decreases.

22. Cardiac Tamponade
• Cardiac Tamponade is accumulation of access fluid in the pericardial
space resulting in compression of all the chambers of the heart ,
impaired cardiac filling, reduction in stroke volume and epicardial
coronary artery compression with resultant myocardial ischaemia.
• It is a Clinical diagnosis intergrated with ECHO findings and Pulsus
Paradoxus
• Rate of Filling is more important than the volume of filling.

26. Pericardiocentesis

27. Treatment of Tuberculous Pericardial Disease.
• Once diagnosis of TB pericarditis is established, prompt initiation of antituberculosis treatment is
mandatory. Recommended therapy consists of four drug regimens consisting of isoniazid,
rifampicin, pyrazinamide and ethambutol or streptomycin for two months followed by isoniazid
,rifampicin and Ethambutol for next four months.
• Some physicians prefer to administer longer duration of treatment. However, no randomized
controlled trials have compared different durations of antituberculosis drug regimens in TB
pericarditis. Similar duration of treatment is recommended for HIV-seropositive patients.
• Pericardial TB is categorized as serious form of extra- pulmonary TB and is treated with Category I
DOTS treatment.

28. Role of Adjuvant Corticosteroid Treatment
In controlled clinical trials, the addition of prednisolone to antituberculosis treatment has been shown to
reduce mortality and the need for repeated pericardiocentesis in patients with TB pericarditis and
effusion. In active TB constrictive pericarditis, addition of prednisolone increased the rate of clinical
improvement, reduced the risk of death from pericarditis and the need for pericardiectomy, and was
associated with a higher proportion of patients with an overall favourable status.
Prednisolone 1mg/kg for 4 weeks , tapered over next 4 weeks. Duration can be increased depending on
the patient’s response.

29. Pericardiocentesis and Pericardiectomy
Pericardiocentesis is life saving in patients with cardiac tamponade and also provides an opportunity
to confirm the aetiology of the pericardial effusion. This can be performed percutaneously and by
open surgical drainage. The latter method abolishes the need for repeat pericardiocentesis but does
not reduce subsequent mortality or need for pericardiectomy (16). Furthermore, open surgical
drainage requires general anaesthesia unlike percutaneously performed procedure, but provides an
opportunity to obtain pericardial tissue for histopathological examination.
Chronic constrictive pericarditis requires pericardiectomy, which is preferably avoided in the
subacute stage when a plane of cleavage has not clearly developed. However, pericardiectomy can
be done after two to four weeks of chemotherapy and should not be unduly delayed if indicated.
Various approaches to pericardiectomy, i.e. median sternotomy, lateral thoracotomy, bilateral
thoracotomy, with or without use of cardio- pulmonary by pass; and anterior or total removal of
pericardium have been described depending on patient population or personal preferences.
Cardiopulmonary bypass is needed for more difficult cases with extensive calcification, coronary
involvement or large vessel involvement. Surgical mortality of pericardiectomy is still high,
especially in patients with calcification. Other poor predictors of outcome are long standing disease,
baseline functional class, low voltage ECG complex, significantly increased atrial pressure,
associated organ failure and myocardial involvement.

30. • Thank you.
SOURCE
- Harrisons Textbook of Internal Medicine
- Sharma Mohan textbook of TB
- Online for pictures