Introduction:
A major complication of tuberculosis (TB) is tuberculous pericarditis; the diagnosis can be challenging and is frequently postponed, leading to late complications such as constrictive pericarditis and increased mortality. Despite some optimistic developments in the fight against tuberculosis, such as the recent positive results of a phase 2b placebo-controlled trial of the M72/AS01E TB vaccine, much work still has to be done.
This is especially true in the case of tuberculous pericarditis (TBP), where a lack of knowledge on this severe form of extra-pulmonary tuberculosis (EPTB) has impeded the development of affordable, quick diagnostic procedures and host-directed medicines capable of preventing its crippling sequelae. Both at the immunological and clinical levels, the presence of HIV significantly adds to the illness process' complexity.
What Is the Epidemiology of Tuberculosis Pericarditis?
The WHO estimates 300,000 HIV-TB co-infected deaths and 1.3 million TB deaths in people without HIV in 2017 alone, making TB the most lethal infectious illness in the world. This number of deaths from TB and HIV co-infection may be underreported since, according to post-mortem studies of HIV-positive people in TB-endemic areas, 45.8 % of TB cases go untreated at the time of death, and 87.9 % of all deaths result from disseminated TB.
Depending on the level of TB endemicity in the area, the incidence of TBP varies. For instance, only four percent of 294 admissions for acute pericardial illness in a case series from Spain were attributable to TBP. According to various statistics, TB accounts for 64.9 to 70 % of pericardial effusions in Africa. According to a study that included 84 HIV-infected people with exuberant pericarditis, just three had a diagnosis other than TB; the HIV pandemic contributes to the high incidence of TBP seen particularly in Southern Africa.
The epidemiology of TBP (TB affecting organs other than the lungs) in children is currently poorly supported by fresh evidence. However, it is probably an underappreciated issue, given that EPTB makes up 21 to 44 % of all TB in children. Only one fatality out of 30 children with TBP was documented in the most recent retrospective observational study, and the cause of death was determined to be disseminated TB.
The authors admit that the lack of follow-up may have led to underestimating actual mortality. 10 % of children, according to the study, experienced constrictive pericarditis. In contrast, previous retrospective research of 44 pediatric TBP cases found no deaths and five (20 %) occurrences of constrictive pericarditis during follow-up.
What Is the Pathogenesis of Tuberculosis Pericarditis?
The pericardium can get infected with Mycobacterium tuberculosis (Mtb) bacteria through retrograde lymphatic spread, hematogenous dissemination, or, less frequently, direct contiguous spread from other nearby diseased structures like the lungs, pleura, and spine. Hematogenous dissemination is the most frequent method of Mtb transmission in HIV co-infected people, whereas, in HIV-uninfected TBP patients, PCF lymphocytes predominate CD4+ effector memory T cells, whereas, in HIV-infected patients, PCF lymphocytes are predominately CD8+ T cells. HIV viral load in HIV-positive TBP patients' PCF is higher than in their plasma and is inversely correlated with the percentage of PCF CD4+ T cells.
These results are significant because they doubt the belief that TBP is primarily a paucibacillary illness caused by a strong delayed-type hypersensitivity reaction to TB antigens. TBP is, in fact, multibacillary in at least certain patient groups, which has important implications for both results and assuring that the pericardium can be effectively penetrated by the present medication regimens.
The clinical manifestation of pericarditis is caused by one of two general mechanisms: either thickening of the pericardium with minimal or absent effusion impairing cardiac filling in diastole (constriction) or fluid accumulation within the pericardium compressing the heart chambers throughout the cardiac cycle (tamponade). Regardless of the underlying cause, heart failure syndrome is the most common clinical presentation of TBP. However, some patients with tamponade may also experience hemodynamic compromise with hypotension, tachycardia (increased heart rate), and shock.
What Are the Direct Methods for the Diagnosis of Tuberculous Pericarditis?
In 80 % of instances of tuberculous pericarditis, the pericardial fluid is blood-stained, but other conditions like malignancy and the long-term effects of trauma can also result in bloody pericardial effusions, making it crucial to rule out TB as the cause. Most tuberculous pericardial effusions are exudative, high protein, and have an elevated leukocyte count with a predominance of lymphocytes and monocytes.
The most accurate diagnostic method for identifying pericardial exudates is Light's criteria (where an exudate is defined as having one or more of the following: pleural fluid protein divided by serum protein is greater than 0.5, pleural fluid lactate dehydrogenase [LDH] divided by serum LDH is greater than 0.6, or pleural fluid LDH level is greater than 66 % of the upper limit of normal for serum LDH).
The definite diagnosis of tuberculous pericarditis should be made as soon as feasible by looking for acid-alcohol bacilli resistant in sputum, lymph nodes, or pericardial fluid. By inoculating the fluid into the double-strength liquid Kirchner culture media, the yield of tubercle bacilli from the pericardial fluid may be increased from 53 % to 75 %, an improvement over conventional culture.
The diagnosis of tuberculous pericarditis can also be made using pericardial biopsy samples. Using the polymerase chain reaction (PCR) to find DNA from M. tuberculosis in the pericardial fluid has also been recommended. When pericardial fluid and biopsy specimens are tested early in the effusive stage, the likelihood of getting a conclusive bacteriological result is highest.
What Is the Treatment Given for Tuberculous Pericarditis?
Even in individuals who are HIV positive, pharmacological therapy boosts survival in tuberculous pericarditis. Extrapulmonary tuberculosis responded well to a regimen consisting of Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol for at least two months, followed by Rifampicin and Isoniazid (up to six months). Treatments lasting more than six months do not produce superior outcomes while increasing cost and lowering tolerance.
Steroids are often added to the treatment regimen for TB pericarditis to reduce inflammation and minimize complications. The decision to use steroids depends on the severity of the pericarditis, the presence of certain clinical features, and individual patient factors. Prednisone is commonly used, and the dosage and duration of steroid therapy will be determined by the treating physician. The gradual tapering of steroids is generally recommended to avoid potential side effects associated with abrupt discontinuation. On the basis of a systematic review updated in 2002 that included four trials with a total of 469 participants reported that overall corticosteroids are associated with a beneficial effect and with fewer deaths especially on long term (2 years as mentioned in the study). Another and a more recent systematic review, meta‐analysis published in 2013, included six studies in patients with TB pericarditis showed that corticosteroid use was associated with a significant reduction in mortality.
Conclusion:
In wealthy nations, tuberculous pericarditis is a rare pathology but is common in underdeveloped nations. Low bacteriological and histological results make a diagnosis difficult. Particularly in patients with torpid pericarditis, it is important to consider the value of indirect diagnostic techniques. The clinical manifestation and prognosis of tuberculous pericarditis can be altered by HIV serology positivity.
