User:Ssturpin/Tuberculous pericarditis
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Tuberculous pericarditis is a condition in which the pericardium surrounding the heart is infected by the bacteria mycobacterium tuberculosis.[1] Tuberculous pericarditis accounts for a significant percentage of presentations of tuberculosis worldwide.[2] The condition has 4 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]
Epidemiology
[edit]Tuberculous 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]
Pathogenesis
[edit]Tuberculous pericarditis is caused by infection with a bacteria called mycobacterium tuberculosis.[1] This bacteria enters the body through inhalation and is 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 4 stages of tuberculous pericarditis that occur following infection with mycobacterium tuberculosis: [3]
Manifestation | Pathological Basis | Clinical Presentation | |
---|---|---|---|
Stage 1 | Dry stage |
|
|
Stage 2 | Effusive stage |
|
|
Stage 3 | Adsorptive stage |
|
|
Stage 4 | Constrictive stage |
|
|
Signs and Symptoms
[edit]Tuberculous pericarditis commonly presents with symptoms similar to both pulmonary tuberculosis and heart failure.[4] These symptoms include: [4]
- Fever
- Fatigue
- Night sweats
- Weight loss
- Shortness of breath
- Chest pain
- Cough
Indications of pericarditis or heart failure may also be seen on physical exam.[2] 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]
Diagnosis
[edit]Tuberculous pericarditis is an under-diagnosed condition with up to 15-20% of people with the disease never being formally diagnosed.[3] Definitive diagnosis of the disease requires presence of mycobacterium tuberculosis in the pericardial fluid or on histology slides.[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 than culturing fluid. 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, a European diagnostic scale may be used to help categorize the likelihood of tuberculous pericarditis.[6] In tuberculosis-endemic regions, ≥6 points is highly predictive of tuberculous pericarditis: [5][6]
- Fever = 2 points
- Night sweats = 1 point
- Loss of body mass = 1 points
- Globulin level > 40 g/L = 3 points
- Peripheral leukocyte count < 10 × 10^9/L = 3 points
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]
Management
[edit]There 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] 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] 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 to reduce long-term consequences.[2]
References
[edit]- ^ a b c d e f Agabegi, Steven; Agabegi, Elizabeth; Duncan, Mark; Chuang, Kelley (2023). Step-Up to Medicine (6 ed.). pp. 394–451. ISBN 9781260460636.
{{cite book}}
: CS1 maint: multiple names: authors list (link) - ^ a b c d e f Adefuye, Mayowa A; Manjunatha, Nisha; Ganduri, Vinutna; Rajasekaran, Kruthiga; Duraiyarasan, Shrimahitha; Adefuye, Bolanle O. "Tuberculosis and Cardiovascular Complications: An Overview". Cureus. 14 (8): e28268. doi:10.7759/cureus.28268. ISSN 2168-8184. PMC 9491794. PMID 36158349.
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: CS1 maint: unflagged free DOI (link) - ^ a b c d e f g h i j k l m n o p q r Isiguzo, Godsent; Du Bruyn, Elsa; Howlett, Patrick; Ntsekhe, Mpiko (2020). "Diagnosis and Management of Tuberculous Pericarditis: What Is New?". Current Cardiology Reports. 22 (1): 2. doi:10.1007/s11886-020-1254-1. ISSN 1523-3782. PMC 7222865. PMID 31940097.
- ^ a b c d e f g h i j k l m Feger, Joachim. "Tuberculous pericarditis | Radiology Reference Article | Radiopaedia.org". Radiopaedia. Retrieved 2023-12-04.
- ^ a b c d e f Naicker, Kishendree; Ntsekhe, Mpiko (2020-4). "Tuberculous pericardial disease: a focused update on diagnosis, therapy and prevention of complications". Cardiovascular Diagnosis and Therapy. 10 (2): 289–295. doi:10.21037/cdt.2019.09.20. ISSN 2223-3652. PMC 7225424. PMID 32420111.
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(help)CS1 maint: unflagged free DOI (link) - ^ a b c d e f g Dybowska, Małgorzata; Błasińska, Katarzyna; Gątarek, Juliusz; Klatt, Magdalena; Augustynowicz-Kopeć, Ewa; Tomkowski, Witold; Szturmowicz, Monika (2022-03). "Tuberculous Pericarditis—Own Experiences and Recent Recommendations". Diagnostics. 12 (3). doi:10.3390/diagnostics12030619. PMID 35328173.
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