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

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] 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

#### **Figure 1.**

*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.*

culture medium, resulting in a 75% yield, compared with a 53% yield with conventional culture [18]. Pericardial biopsy specimens may also be used to diagnose tuberculous pericarditis. The polymerase chain reaction (PCR) has also been suggested for detecting *M. tuberculosis* DNA in pericardial fluid [19]. The probability of obtaining a definitive bacteriological result is greatest when pericardial fluid and biopsy specimens are examined early in the effusive stage [18].

#### **4.3 Indirect methods for the diagnosis of tuberculous pericarditis**

The difficulty of carrying out the diagnosis of tuberculous pericarditis, associated with its high mortality without proper treatment, has led to the use of indirect methods. Indirect methods such as dosing activity of adenosine deaminase (ADA) in the pericardial fluid, with cut-off levels between 30 and 60 U/L of ADA activity, are suggestive of tuberculous pericarditis [20]. In areas of the high endemic level of tuberculosis, a cut-off level of ADA activity <35 presents a sensitivity of 90% and a specificity of 74% for diagnosis [21]. The utility of ADA activity in pericardial fluid was also demonstrated in HIV-positive patients, although in patients with severe CD4 lymphocyte depletion, the ADA levels observed are lower [22].

Very high levels of ADA in pericardial fluid have strong association with constrictive pericarditis [23].

The measurement of interferon gamma (IFN-γ) levels in the pericardial fluid also helps early diagnosis. Cut-off values >200 pg/L have a sensitivity of 92% and specificity of 100% for the diagnosis of TB [21].

In summary, the "definitive" diagnosis of tuberculous pericarditis is based on the presence of the tubercle bacillus in the pericardial fluid or proving it in the pericardium biopsy and "probably" when there is evidence of tuberculosis elsewhere in the body and the presence of unexplained pericarditis, with high levels of ADA or good response to pharmacological treatment.

#### **5. Treatment**

Pharmacological treatment increases survival in tuberculous pericarditis, even in HIV-positive patients [24]. A regimen that includes rifampicin, isoniazid, pyrazinamide, and ethambutol for at least 2 months, followed by rifampicin and isoniazid (up to 6 months), proved to be effective in extrapulmonary tuberculosis [25]. Treatments beyond 6 months do not show better results, increasing cost and decreasing tolerance [26].

The treatment associated with corticosteroids would not be justified at present, given that the evidence for its use is not the best [27]. Although the results are inconclusive, adding corticosteroids to treatment may have benefits on morbidity and re-experiences, but randomized controlled trials with sufficient numbers of HIV-positive and HIV-negative patients are needed [28].

It is obvious that if pericarditis is associated with severe pericardial effusion, with hemodynamic compromise, the first treatment option associated with antituberculous treatment is drainage by subxiphoid puncture or by minimal thoracotomy.

### **6. Constrictive pericarditis**

It is the most feared complication of tuberculous pericarditis; it is described in about 30% of patients, even in spite of antituberculous treatment and the use of

**35**

*Tuberculous Pericarditis*

experienced observers [30].

low voltage.

**6.2 Treatment**

6 months.

**8. Conclusions**

in this pathology.

of tuberculous pericarditis.

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

**6.1 Diagnosis of constrictive pericarditis**

dilation of the superior vena cava [12].

**7. Effusive-constrictive pericarditis**

corticosteroids [29]. The clinical presentation can be variable, from asymptomatic patients and stress design to heart failure with preserved function, liver failure (due to retrograde passive congestion) with ascites, and generalized edema. The presence of pericardial knock, associated with protodiastolic murmur, splitting of the second heart sound, and Kussmaul's sign (paradoxical increase in jugular venous pressure in inspiration), is frequent in constrictive pericarditis but difficult to detect by non-

Sometimes we can see a calcium shell surrounding the heart in the chest X-ray, but it is not the most frequent [31]. Other nonspecific radiographic findings are

In the electrocardiogram there are no specific signs, either atrial fibrillation, nonspecific alterations of repolarization (changes in the T wave), or complexes with

The Doppler echocardiogram may show thickening of the pericardium; the presence of fibrin; restrictive transmitral filling pattern, associated with normal size of the cavities, in the absence of ventricular hypertrophy; and valvular insufficiency.

The treatment must include antituberculous medication for 6 months. Consider pericardiectomy in all patients once antibiotic treatment has been instituted [32]. Surgery should be performed early if the patient presents hemodynamic deterioration (despite antituberculous treatment) [33] or if they present pericardial calcifi-

It is the presence of increased intrapericardial pressure due to effusion and constriction of the visceral pericardium, which does not improve with pericardiocentesis. The signs and symptoms are similar to those of constrictive pericarditis. The treatment is pericardiectomy associated with antituberculous treatment for

Tuberculous pericarditis is a rare pathology in developed countries but frequent in developing countries. There is difficulty in the diagnosis due to low bacteriological and histological results. The usefulness of indirect methods for diagnosis should be taken into account, especially in patients with torpid pericarditis. The presence of positive serology for HIV can modify the clinical presentation and the outcome

There is still a lack of sustainable evidence for the use of systemic corticosteroids

Pharmacological treatment should be performed for at least 6 months in all patients with tuberculous pericarditis, regardless of drainage or pericardiectomy.

cations, which are markers of chronicity of the disease [34].

corticosteroids [29]. The clinical presentation can be variable, from asymptomatic patients and stress design to heart failure with preserved function, liver failure (due to retrograde passive congestion) with ascites, and generalized edema. The presence of pericardial knock, associated with protodiastolic murmur, splitting of the second heart sound, and Kussmaul's sign (paradoxical increase in jugular venous pressure in inspiration), is frequent in constrictive pericarditis but difficult to detect by nonexperienced observers [30].
