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Tuberculous pericarditis
Tuberculous pericarditis is a form of pericarditis. It is a condition in which the pericardium surrounding the heart is infected by the bacterial species Mycobacterium tuberculosis.[1] Tuberculous pericarditis accounts for a significant percentage of presentations of tuberculosis worldwide.[2] The condition has four stages of disease which manifests with clinical presentations ranging from acute pericarditis to overt heart failure.[3] Tuberculous pericarditis is an under-diagnosed condition.[3] Diagnosis often requires a range of diagnostic tools, including pericardiocentesis, biochemical tests, and imaging.[3][4] Treatment of this disease is similar to treatment of pulmonary tuberculosis.[1][4] Alternative treatment options to reduce cardiac complications are also available.[3][5] EpidemiologyTuberculous pericarditis is a condition that accounts for 1-2% of presentations of tuberculosis outside of the lungs.[2] It is found in people of all ages and typically affects males more frequently than females.[4] Tuberculosis is also one of the leading causes of effusive pericarditis worldwide.[6] In tuberculosis-endemic regions, tuberculous pericarditis accounts for 50-90% of cases of effusive pericarditis, depending on HIV status.[6] In developed countries, it only accounts for about 4% of cases.[6] Tuberculous pericarditis is a deadly disease with a mortality rate of up to 40% in the first 6 months after diagnosis.[6] PathogenesisTuberculous pericarditis is caused by infection with the bacterial species Mycobacterium tuberculosis.[1] Bacteria enter the body through inhalation and are ingested by white blood cells called macrophages.[1] Surviving bacteria multiply and can spread to other areas of the body. This can occur through the lymphatic system, blood, or via direct spread from infected tissues.[1][3] Infection of the pericardium is assisted by a variety of inflammatory and fibrotic mediators. These mediators include IL-10, IL-1β, IL-6, IL-8, interferon-γ induced protein, and tumor necrosis factor.[3] These mediators then accumulate in the pericardial fluid leading to inflammation and fibrosis.[3] Certain individuals have an increased risk of infectious spread to the pericardium. This includes people with immunosuppression, HIV/AIDS, chronic kidney disease, and diabetes, amongst others.[2][4] There are four stages of tuberculous pericarditis following infection by Mycobacterium tuberculosis: [3]
Signs and SymptomsTuberculous pericarditis commonly presents with symptoms similar to both pulmonary tuberculosis and heart failure.[4] These symptoms include: [4]
Indications of pericarditis or heart failure may also be seen on physical exam. These signs include increased heart rate, decreased blood pressure, pericardial friction rub, ascites, and lower extremity edema.[2] The clinical presentation depends on the stage of disease. The dry stage presents with features resembling acute pericarditis (chest pain, pericardial friction rub, diffuse ST-segment elevation on EKG, etc.).[4] The effusive, adsorptive, and constrictive stages typically present with features of heart failure (shortness of breath, ascites, peripheral edema, etc.).[4] DiagnosisTuberculous pericarditis is an under-diagnosed condition with up to 15-20% of people with the disease never being formally diagnosed.[3] It is difficult to diagnose because definitive diagnosis requires culturing Mycobacterium tuberculosis from aspirated pericardial fluid.[4] This can be achieved via pericardiocentesis, which has both therapeutic and diagnostic utility.[3] Pericardial biopsy is another method of obtaining samples, although this method is invasive and is used less frequently.[5][6] Culturing pericardial fluid is currently the most widely used diagnostic test for tuberculous pericarditis.[3] However, this process is lengthy and may take up to 3 weeks to receive results.[3] Biochemical tests are another method for diagnosis, as these are much less time consuming. Adenosine deaminase (ADA) is the most widely used biochemical test.[3] Other options include Xpert MTB/RIF and IFN-γ, but these tests are costly and therefore less available.[3] When collecting pericardial fluid is not possible, the Tygerberg scoring system helps the clinician to decide whether pericarditis is due to tuberculosis or another cause.[5] In tuberculosis-endemic regions, ≥6 points is highly predictive of tuberculous pericarditis: [5]
Radiography is another method used to aid in the diagnosis of tuberculous pericarditis. This imaging can help identify effusions, calcifications, and thickening around the heart.[4] Echocardiography is the first-line imaging modality for diagnosis of pericarditis.[4] Chest X-Ray, CT scans, and MRI are also widely used options.[4] ManagementThere are three main goals in the management of tuberculous pericarditis. These goals are to kill the active infection, reduce heart strain and associated symptoms, and prevent future cardiac complications.[3] Elimination of the infection is through the same therapy used in pulmonary tuberculosis. This therapy consists of a 2-month regimen of rifampin, isoniazid, pyrazinamide, and ethambutol followed by 4-months of rifampin and isoniazid.[1][4] However, recent research has yet to evaluate the definitive length of anti-tuberculosis treatment required for tuberculous pericarditis.[7] Reducing heart strain and improving symptoms is achieved primarily through pericardiocentesis.[3] This procedure helps to reduce fluid accumulation around the heart.[3] Constrictive pericarditis is the main long-term complication of tuberculous pericarditis that requires management.[5] Corticosteroids have long been thought to help reduce the risk of future cardiac complications.[3][7] Colchicine is a drug thought to reduce the recurrence of constrictive pericarditis, although evidence is limited.[5] The use of fibrinolytics and ACE inhibitors are also options to help reduce pericardial fibrosis.[5] Pericardiectomy may be indicated in severe cases,[2] as open surgical drainage of fluid around the heart may reduce risk of future fluid accumulation.[7] References
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