**4. Pericardial effusion**

The triad of severe pericarditic chest pain: a pericardial friction rub, widespread ST segment, and T-wave abnormalities; and PR segment depression typical of acute pericarditis is an uncommon clinical presentation of tuberculous pericarditis, accounting for only 3–8% of patients who present with tuberculous pericarditis [9]. The pericardial effusion begins as soon as the tubercle bacillus enters the pericardium and develops slowly and insidiously. Is characterized pathologically by polymorphonuclear leukocytosis with abundant bacilli and granuloma formation, and is usually present with nonspecific systemic symptoms, such as fever, night sweats, fatigue, and weight loss. Chest pain, cough, and breathlessness are uncommon symptoms [10].

TB pericarditis should be considered in the evaluation of all cases of pericarditis without a rapidly self-limited course.

#### **4.1 Diagnosis of pericardial effusion**

ECG is abnormal in most cases of tuberculous pericardial effusion, usually in the form of nonspecific ST-T-wave changes. The presence of microvoltage (complexes <5 mm in limb leads and <10 mm in precordial leads) suggests a large pericardial effusion [11]. Chest radiograph usually shows an enlarged cardiac shadow in more than 90% of cases and demonstrates features of active pulmonary TB in 30% of cases and pleural effusion in 40–60% of cases (**Figure 1**) [12]. The advent and

**33**

**Figure 1.**

*Tuberculous Pericarditis*

almost 100% of cases [14].

*DOI: http://dx.doi.org/10.5772/intechopen.85822*

accessibility of echocardiography have made it possible to diagnose the pericardial effusion when suspected; however, it does not determine the etiology. The presence of fibrinous strands on the visceral pericardium is typical but not specific for a tuberculous pathogenesis (Video 1, https://bit.ly/2JNuQdB) [13]. Computed tomography of the chest shows typical changes in mediastinal lymph nodes (enlargement >10 mm with matting and hypodense centers and sparing of hilar lymph nodes) in

The pericardial fluid is bloodstained in 80% of cases of tuberculous pericarditis,

but malignant disease and the late effects of penetrating trauma may also cause bloody pericardial effusion, so confirmation of TB as the cause is important [15]. 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's criteria (whereby an exudate is defined as having one or more of the following: pleural fluid protein divided by serum protein >0.5, pleural fluid lactate dehydrogenase [LDH] divided by serum LDH >0.6, and/ or pleural fluid LDH level > 66% of the upper limit of normal for serum LDH) [16]

**4.2 Direct methods for the diagnosis of tuberculous pericarditis**

is the most reliable diagnostic tool for identifying pericardial exudates.

The definitive diagnosis of tuberculous pericarditis should be established as soon as possible, by searching for the acid-alcohol bacilli resistant in sputum, lymph nodes, or pericardial fluid [17]. Culture of tubercle bacilli from pericardial fluid can be improved by inoculation of the fluid into double-strength liquid Kirchner

*Chest X-ray in front of a merchant marine patient who consulted due to progressive dyspnea for months of evolution. In the consultation, he presented signs of cardiac tamponade, so an echocardiogram (Video 1, https:// bit.ly/2JNuQdB) was performed with an evacuating pericardiocentesis of 3 liters of hematopurulent fluid.* 

*Bacteriological isolation was not obtained, but there was increased ADA activity.*

### *Tuberculous Pericarditis DOI: http://dx.doi.org/10.5772/intechopen.85822*

*Inflammatory Heart Diseases*

**4. Pericardial effusion**

without a rapidly self-limited course.

**4.1 Diagnosis of pericardial effusion**

**3. Pathogenesis of tuberculous pericarditis**

Tubercle bacilli access the pericardium via three mechanisms: (1) retrograde lymphatic spread from mediastinal, paratracheal, and peribronchial lymph nodes [3], (2) hematogenous spread (dominant in immunocompromised hosts) [4], and (3) direct contiguous spread from adjacent structures such as the lungs, pleura, and spine (infrequent) [3]. When the guest is immunocompetent, tuberculous pericardial disease is localized to the pericardial space. Usually in a paucibacillary condition, tubercle proteins trigger an important cell-mediated hypersensitivity response with T-helper cell (subtype 1) predominant cytokine release, leading to an inflammatory exudative effusion and its hemodynamic sequelae [5, 6]. The immune response to the viable acid-fast bacilli penetrating the pericardium is responsible for the morbidity associated with tuberculous pericarditis. In patients with dysfunctional immunity as occurred in HIV/AIDS, there is evidence that mycobacterial replication is active, bacillary loads are high, and the clinical manifestations of tuberculous pericarditis are related to the impact of the infectious and virulent

nature of the Mtb itself in addition to the hemodynamic sequelae [4–7].

filling, and generating the clinical syndrome of constrictive pericarditis [8].

ST segment, and T-wave abnormalities; and PR segment depression typical of acute pericarditis is an uncommon clinical presentation of tuberculous pericarditis, accounting for only 3–8% of patients who present with tuberculous pericarditis [9]. The pericardial effusion begins as soon as the tubercle bacillus enters the pericardium and develops slowly and insidiously. Is characterized pathologically by polymorphonuclear leukocytosis with abundant bacilli and granuloma formation, and is usually present with nonspecific systemic symptoms, such as fever, night sweats, fatigue, and weight loss. Chest pain, cough, and breathlessness are uncommon symptoms [10]. TB pericarditis should be considered in the evaluation of all cases of pericarditis

constrictive pericarditis, and a combination of effusion and constriction.

Tuberculous pericarditis presents clinically in three forms: pericardial effusion,

The triad of severe pericarditic chest pain: a pericardial friction rub, widespread

ECG is abnormal in most cases of tuberculous pericardial effusion, usually in the form of nonspecific ST-T-wave changes. The presence of microvoltage (complexes <5 mm in limb leads and <10 mm in precordial leads) suggests a large pericardial effusion [11]. Chest radiograph usually shows an enlarged cardiac shadow in more than 90% of cases and demonstrates features of active pulmonary TB in 30% of cases and pleural effusion in 40–60% of cases (**Figure 1**) [12]. The advent and

There are four pathological stages of tuberculous pericarditis: (1) fibrinous exudation, initial polymorphonuclear leukocytosis, abundant mycobacteria, and early granuloma formation with loose organization of macrophages and T cells; (2) serosanguineous effusion with a predominantly lymphocytic exudate with monocytes and foam cells; (3) absorption of effusion with organization of granulomatous caseation and pericardial thickening caused by fibrin, collagenosis, and, ultimately, fibrosis; and (4) constrictive scarring. The fibrosis generated between the visceral pericardium and the parietal pericardium can calcify and adhere to the myocardium, generating a cuirass around the heart, preventing the correct diastolic

**32**

accessibility of echocardiography have made it possible to diagnose the pericardial effusion when suspected; however, it does not determine the etiology. The presence of fibrinous strands on the visceral pericardium is typical but not specific for a tuberculous pathogenesis (Video 1, https://bit.ly/2JNuQdB) [13]. Computed tomography of the chest shows typical changes in mediastinal lymph nodes (enlargement >10 mm with matting and hypodense centers and sparing of hilar lymph nodes) in almost 100% of cases [14].
