Tuberculous pericarditis overview: Difference between revisions
No edit summary |
No edit summary |
||
| (One intermediate revision by the same user not shown) | |||
| Line 8: | Line 8: | ||
== Overview == | == Overview == | ||
Tuberculous pericarditis was first discovered by Rokitansky, an English scientist, in 1852. Tuberculous pericarditis is the result of hematogenous or [[lymphatic]] spread of mycobacterium tuberculosis to the [[pericardium]]. This causes acute [[inflammation]] of the [[pericardium]] and we may have [[Polymorphonuclear cells|polymorphonuclear]] ([[PMN]]) and [[leukocytes]] infiltration in the [[pericardium]]. This may lead to [[pericardial effusion]] and [[fibrinous]] changes of the [[pericardium]]. The visceral [[pericardium]] thickens with [[fibrin]] deposition (changes of [[constrictive pericarditis]]). There are four pathologic stages of involvement: stage 1 is presence of diffuse [[fibrin]] deposition, [[granulomas]] and abundant [[mycobacterium]]. Stage 2 is development of [[serous]] or [[Serosanguineous discharge|serosanguineous]] [[pericardial effusion]] with a predominantly [[Lymphocyte|lymphocytic]] [[exudate]] with [[monocytes]] and [[foam cell]]s. Stage 3 is absorption of the effusion with organization of granulomatous [[caseation]] and thickening of [[pericardium]] secondary to deposition of [[fibrin]] and [[collagen]]. Stage 4 is development of [[constrictive pericarditis]]. The [[pericardial space]] is obliterated by dense adhesions with marked thickening of [[parietal]] layer and replacement of [[granulomas]] by [[fibrous tissue]]. Conditions associated with tuberculous pericarditis include [[pulmonary TB]], [[HIV]], [[malignancy]], [[chemotherapy]], and [[diabetes mellitus]]. On gross [[pathology]], thickened [[pericardium]], shaggy [[hemorrhage]], and [[exudate]] are characteristic findings of tuberculous pericarditis. On microscopic histopathological analysis, [[Acid-fast bacillus|acid fast bacilli]] is characteristic findings of tuberculous pericarditis. The [[prevalence]] of tuberculous pericarditis is approximately 1-2% of patients with [[pulmonary tuberculosis]]. [[Patients]] of all age groups may develop tuberculous pericarditis. The [[incidence]] of tuberculous pericarditis increases with age. Tuberculous pericarditis commonly affects [[elderly]]. Tuberculous pericarditis usually affects individuals of the [[black]] race. [[Men]] are more commonly affected by tuberculous pericarditis than [[female]]. Since the [[prevalence]] of tuberculous pericarditis may follow [[tuberculosis]] [[prevalence]], The majority of tuberculous pericarditis cases are reported in South Africa, Indonesia, Nigeria, Pakistan, India, and China. [[Patients]] with tuberculous pericarditis may have a positive [[history]] of [[pulmonary TB]], [[HIV]] infection, any [[Immunocompromised|Immune system dysfunction]], [[elderly]], [[black]] race, [[male]] gender, and living/traveling to [[TB]] endemic areas. Common [[symptoms]] of tuberculous pericarditis include [[fever]], [[weight loss]], [[night sweat]], [[cough]], [[breathlessness]], [[chest pain]], [[Malaise (patient information)|malaise]], and [[ankle edema]]. Patients with tuberculous pericarditis usually appear [[Cachexia|Cachectic]]. They may have [[fever]], [[tachycardia]], [[pulsus paradoxus]], [[hypotension]], [[tachypnea]], [[JVP]] distension, [[kussmaul's sign]], [[lymphadenopathy]], [[ankle edama]], [[pleura]] dullness, decreased [[breath sounds]], [[pericardial]] knock, [[pericardial rub]], fine/coarse [[crackles]] upon auscultation of the lung, [[hepatomegaly]], [[Ascites, pleural effusion, and benign ovarian tumor.|ascites]], distant [[heart sounds]], displaced point of maximal impulse (PMI) suggestive of [[cardiomegaly]], [[friction rub]], and [[Heart sounds#Fourth heart sound S4|S4]]. A 2 months course of [[isoniazid]], [[pyrazinamide]], [[rifampicin]], and [[ethambutol]] followed by 4months course of [[isoniazid]] and [[rifampicin]] is shown to be effective for treatment of tuberculous pericarditis. Short course chemotherapy is beneficial in [[HIV]] infected patients. The mainstay of treatment for tuberculous pericarditis is medical therapy. [[Pericardiectomy]] is usually reserved for [[patients]] resistance [[constrictive pericarditis]]. | |||
==Historical Perspective== | ==Historical Perspective== | ||
Tuberculous pericarditis was first discovered by Rokitansky, an English scientist, in 1852. | |||
==Classification== | ==Classification== | ||
| Line 15: | Line 17: | ||
==Pathophysiology== | ==Pathophysiology== | ||
Tuberculous pericarditis is the result of hematogenous or [[lymphatic]] spread of mycobacterium tuberculosis to the [[pericardium]]. This causes acute [[inflammation]] of the [[pericardium]] and we may have [[Polymorphonuclear cells|polymorphonuclear]] ([[PMN]]) and [[leukocytes]] infiltration in the [[pericardium]]. This may lead to [[pericardial effusion]] and [[fibrinous]] changes of the [[pericardium]]. The visceral [[pericardium]] thickens with [[fibrin]] deposition (changes of [[constrictive pericarditis]]). There are four pathologic stages of involvement: stage 1 is presence of diffuse [[fibrin]] deposition, [[granulomas]] and abundant [[mycobacterium]]. Stage 2 is development of [[serous]] or [[Serosanguineous discharge|serosanguineous]] [[pericardial effusion]] with a predominantly [[Lymphocyte|lymphocytic]] [[exudate]] with [[monocytes]] and [[foam cell]]s. Stage 3 is absorption of the effusion with organization of granulomatous [[caseation]] and thickening of [[pericardium]] secondary to deposition of [[fibrin]] and [[collagen]]. Stage 4 is development of [[constrictive pericarditis]]. The [[pericardial space]] is obliterated by dense adhesions with marked thickening of [[parietal]] layer and replacement of [[granulomas]] by [[fibrous tissue]]. Conditions associated with tuberculous pericarditis include [[pulmonary TB]], [[HIV]], [[malignancy]], [[chemotherapy]], and [[diabetes mellitus]]. On gross [[pathology]], thickened [[pericardium]], shaggy [[hemorrhage]], and [[exudate]] are characteristic findings of tuberculous pericarditis. On microscopic histopathological analysis, [[Acid-fast bacillus|acid fast bacilli]] is characteristic findings of tuberculous pericarditis. | Tuberculous pericarditis is the result of hematogenous or [[lymphatic]] spread of mycobacterium tuberculosis to the [[pericardium]]. This causes acute [[inflammation]] of the [[pericardium]] and we may have [[Polymorphonuclear cells|polymorphonuclear]] ([[PMN]]) and [[leukocytes]] infiltration in the [[pericardium]]. This may lead to [[pericardial effusion]] and [[fibrinous]] changes of the [[pericardium]]. The visceral [[pericardium]] thickens with [[fibrin]] deposition (changes of [[constrictive pericarditis]]). There are four pathologic stages of involvement: stage 1 is presence of diffuse [[fibrin]] deposition, [[granulomas]] and abundant [[mycobacterium]]. Stage 2 is development of [[serous]] or [[Serosanguineous discharge|serosanguineous]] [[pericardial effusion]] with a predominantly [[Lymphocyte|lymphocytic]] [[exudate]] with [[monocytes]] and [[foam cell]]s. Stage 3 is absorption of the effusion with organization of granulomatous [[caseation]] and thickening of [[pericardium]] secondary to deposition of [[fibrin]] and [[collagen]]. Stage 4 is development of [[constrictive pericarditis]]. The [[pericardial space]] is obliterated by dense adhesions with marked thickening of [[parietal]] layer and replacement of [[granulomas]] by [[fibrous tissue]]. Conditions associated with tuberculous pericarditis include [[pulmonary TB]], [[HIV]], [[malignancy]], [[chemotherapy]], and [[diabetes mellitus]]. On gross [[pathology]], thickened [[pericardium]], shaggy [[hemorrhage]], and [[exudate]] are characteristic findings of tuberculous pericarditis. On microscopic histopathological analysis, [[Acid-fast bacillus|acid fast bacilli]] is characteristic findings of tuberculous pericarditis. [[Pericardiocentesis]] is the gold standard test for the [[diagnosis]] of tuberculous pericarditis. [[Pericardial]] [[biopsy]] must be performed when we can't find [[acid fast bacilli]] in sputum or [[pericardial fluid]]. Finding [[acid fast bacilli]] on [[pericardiocentesis]] is confirmatory for tuberculous pericarditis. | ||
==Causes== | ==Causes== | ||
| Line 42: | Line 44: | ||
===Physical Examination=== | ===Physical Examination=== | ||
Patients with tuberculous pericarditis usually appear [[Cachexia|Cachectic]]. They may have [[fever]], [[tachycardia]], [[pulsus paradoxus]], [[hypotension]], [[tachypnea]], [[JVP]] distension, [[kussmaul's sign]], [[lymphadenopathy]], [[ankle edama]], [[pleura]] dullness, decreased [[breath sounds]], [[pericardial]] knock, [[pericardial rub]], fine/coarse [[crackles]] upon auscultation of the lung, [[hepatomegaly]], [[Ascites, pleural effusion, and benign ovarian tumor.|ascites]], distant [[heart sounds]], displaced point of maximal impulse (PMI) suggestive of [[cardiomegaly]], [[friction rub]], and [[Heart sounds#Fourth heart sound S4|S4]]. | |||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
Laboratory findings consistent with the [[diagnosis]] of tuberculous pericarditis include mild [[anemia]], normal [[leukocyte]] count, [[exudate]] [[pericardial effusion]], [[mycobacterium tuberculosis]] bacilli in [[pericardial effusion]], and positive [[HIV]] test. | |||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
An [[ECG]] may be helpful in the [[diagnosis]] of tuberculous pericarditis. Findings on an [[ECG]] suggestive of tuberculous pericarditis include low voltage [[QRS]], absence of [[ST segment elevation]] which we usually see in [[acute pericarditis]], [[inverted T wave]], [[atrial fibrillation]], and [[electrical alternans]]. | |||
===X-ray=== | ===X-ray=== | ||
An [[x-ray]] may be helpful in the [[diagnosis]] of tuberculous pericarditis. Findings on an [[x-ray]] suggestive of tuberculous pericarditis include [[pericardial calcification]], [[pericardial]] thickening, [[pericardial effusion]], and evidence of [[pulmonary TB]]. | |||
===Echocardiography and Ultrasound=== | ===Echocardiography and Ultrasound=== | ||
[[Echocardiography]]/[[ultrasound]] may be helpful in the [[diagnosis]] of tuberculous pericarditis. Findings on an [[echocardiography]]/[[ultrasound]] suggestive of tuberculous pericarditis include pericardial effusion, , pericardial thickening, increased [[right ventricular]] dimensions, decreased [[left ventricular]] dimensions, abnormal septal motion, flattening of the [[left ventricular]] posterior wall during [[diastol]], dilated [[inferior vena cava]], and dilated [[atrium]]. | |||
===CT scan=== | ===CT scan=== | ||
[[CT scan]] may be helpful in the [[diagnosis]] of tuberculous pericarditis. Findings on [[CT scan]] suggestive of tuberculous pericarditis include calcification of the [[pericardium]], thickened [[pericardium]], [[pericardial effusion]], and back flow of blood into the [[IVC]] and [[hepatic veins]] (in contrast [[CT scan]]). | |||
===MRI=== | ===MRI=== | ||
[[MRI]] may be helpful in the [[diagnosis]] of tuberculous pericarditis. Findings on [[MRI]] suggestive of tuberculous pericarditis include [[pericardial effusion]], [[pericardial]] thickening, [[Mediastinum|mediastinal]] and [[tracheobronchial]] [[lymphadenopathy]] (with hilar sparing), and bowing of the [[interventricular septum]] toward the left ventricle during diastole. | |||
===Other Imaging Findings=== | ===Other Imaging Findings=== | ||
There are no other imaging findings associated with tuberculous pericarditis. | |||
===Other Diagnostic Studies=== | ===Other Diagnostic Studies=== | ||
Other diagnostic studies for tuberculous pericarditis include [[PPD skin test]], [[interferon-gamma assay]], [[smear]] and [[culture]] of [[pericardial]], [[sputum]], and [[gastric fluid]], [[pericardial]] [[biopsy]], and [[lymph node]] [[biopsy]]. | |||
==Treatment== | ==Treatment== | ||
===Medical Therapy=== | ===Medical Therapy=== | ||
A 2 months course of [[isoniazid]], [[pyrazinamide]], [[rifampicin]], and [[ethambutol]] followed by 4months course of [[isoniazid]] and [[rifampicin]] is shown to be effective for treatment of tuberculous pericarditis. Short course chemotherapy is beneficial in [[HIV]] infected patients. | |||
===Surgery=== | ===Surgery=== | ||
The mainstay of treatment for tuberculous pericarditis is medical therapy. [[Pericardiectomy]] is usually reserved for [[patients]] resistance [[constrictive pericarditis]]. | |||
===Primary Prevention=== | ===Primary Prevention=== | ||
There are no established measures for the [[primary prevention]] of tuberculous pericarditis. | |||
===Secondary Prevention=== | ===Secondary Prevention=== | ||
There are no established measures for the [[secondary prevention]] of tuberculous pericarditis. | |||
==References== | ==References== | ||
Latest revision as of 16:24, 19 December 2019
|
Tuberculous pericarditis Microchapters |
|
Differentiating Tuberculous pericarditis from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Tuberculous pericarditis overview On the Web |
|
American Roentgen Ray Society Images of Tuberculous pericarditis overview |
|
Risk calculators and risk factors for Tuberculous pericarditis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Fahimeh Shojaei, M.D., Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.
Overview
Tuberculous pericarditis was first discovered by Rokitansky, an English scientist, in 1852. Tuberculous pericarditis is the result of hematogenous or lymphatic spread of mycobacterium tuberculosis to the pericardium. This causes acute inflammation of the pericardium and we may have polymorphonuclear (PMN) and leukocytes infiltration in the pericardium. This may lead to pericardial effusion and fibrinous changes of the pericardium. The visceral pericardium thickens with fibrin deposition (changes of constrictive pericarditis). There are four pathologic stages of involvement: stage 1 is presence of diffuse fibrin deposition, granulomas and abundant mycobacterium. Stage 2 is development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells. Stage 3 is absorption of the effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen. Stage 4 is development of constrictive pericarditis. The pericardial space is obliterated by dense adhesions with marked thickening of parietal layer and replacement of granulomas by fibrous tissue. Conditions associated with tuberculous pericarditis include pulmonary TB, HIV, malignancy, chemotherapy, and diabetes mellitus. On gross pathology, thickened pericardium, shaggy hemorrhage, and exudate are characteristic findings of tuberculous pericarditis. On microscopic histopathological analysis, acid fast bacilli is characteristic findings of tuberculous pericarditis. The prevalence of tuberculous pericarditis is approximately 1-2% of patients with pulmonary tuberculosis. Patients of all age groups may develop tuberculous pericarditis. The incidence of tuberculous pericarditis increases with age. Tuberculous pericarditis commonly affects elderly. Tuberculous pericarditis usually affects individuals of the black race. Men are more commonly affected by tuberculous pericarditis than female. Since the prevalence of tuberculous pericarditis may follow tuberculosis prevalence, The majority of tuberculous pericarditis cases are reported in South Africa, Indonesia, Nigeria, Pakistan, India, and China. Patients with tuberculous pericarditis may have a positive history of pulmonary TB, HIV infection, any Immune system dysfunction, elderly, black race, male gender, and living/traveling to TB endemic areas. Common symptoms of tuberculous pericarditis include fever, weight loss, night sweat, cough, breathlessness, chest pain, malaise, and ankle edema. Patients with tuberculous pericarditis usually appear Cachectic. They may have fever, tachycardia, pulsus paradoxus, hypotension, tachypnea, JVP distension, kussmaul's sign, lymphadenopathy, ankle edama, pleura dullness, decreased breath sounds, pericardial knock, pericardial rub, fine/coarse crackles upon auscultation of the lung, hepatomegaly, ascites, distant heart sounds, displaced point of maximal impulse (PMI) suggestive of cardiomegaly, friction rub, and S4. A 2 months course of isoniazid, pyrazinamide, rifampicin, and ethambutol followed by 4months course of isoniazid and rifampicin is shown to be effective for treatment of tuberculous pericarditis. Short course chemotherapy is beneficial in HIV infected patients. The mainstay of treatment for tuberculous pericarditis is medical therapy. Pericardiectomy is usually reserved for patients resistance constrictive pericarditis.
Historical Perspective
Tuberculous pericarditis was first discovered by Rokitansky, an English scientist, in 1852.
Classification
There is no established system for the classification of Tuberculous pericarditis.
Pathophysiology
Tuberculous pericarditis is the result of hematogenous or lymphatic spread of mycobacterium tuberculosis to the pericardium. This causes acute inflammation of the pericardium and we may have polymorphonuclear (PMN) and leukocytes infiltration in the pericardium. This may lead to pericardial effusion and fibrinous changes of the pericardium. The visceral pericardium thickens with fibrin deposition (changes of constrictive pericarditis). There are four pathologic stages of involvement: stage 1 is presence of diffuse fibrin deposition, granulomas and abundant mycobacterium. Stage 2 is development of serous or serosanguineous pericardial effusion with a predominantly lymphocytic exudate with monocytes and foam cells. Stage 3 is absorption of the effusion with organization of granulomatous caseation and thickening of pericardium secondary to deposition of fibrin and collagen. Stage 4 is development of constrictive pericarditis. The pericardial space is obliterated by dense adhesions with marked thickening of parietal layer and replacement of granulomas by fibrous tissue. Conditions associated with tuberculous pericarditis include pulmonary TB, HIV, malignancy, chemotherapy, and diabetes mellitus. On gross pathology, thickened pericardium, shaggy hemorrhage, and exudate are characteristic findings of tuberculous pericarditis. On microscopic histopathological analysis, acid fast bacilli is characteristic findings of tuberculous pericarditis. Pericardiocentesis is the gold standard test for the diagnosis of tuberculous pericarditis. Pericardial biopsy must be performed when we can't find acid fast bacilli in sputum or pericardial fluid. Finding acid fast bacilli on pericardiocentesis is confirmatory for tuberculous pericarditis.
Causes
Common cause of tuberculous pericarditis is lymphatic or hematogenous spread of mycobacterium tuberculosis to the pericardium.
Differentiating Tuberculous pericarditisfrom Other Diseases
Epidemiology and Demographics
The prevalence of tuberculous pericarditis is approximately 1-2% of patients with pulmonary tuberculosis. Patients of all age groups may develop tuberculous pericarditis. The incidence of tuberculous pericarditis increases with age. Tuberculous pericarditis commonly affects elderly. Tuberculous pericarditis usually affects individuals of the black race. Men are more commonly affected by tuberculous pericarditis than female. Since the prevalence of tuberculous pericarditis may follow tuberculosis prevalence, The majority of tuberculous pericarditis cases are reported in South Africa, Indonesia, Nigeria, Pakistan, India, and China.
Risk Factors
Common risk factors in the development of tuberculous pericarditis include immunodeficiency (AIDS, malignancy, chemotherapy, diabetes and elderly), TB exposure, male gender, and African-American race.
Screening
There is insufficient evidence to recommend routine screening for tuberculous pericarditis.
Natural History, Complications, and Prognosis
Diagnosis
Diagnostic Study of Choice
Pericardiocentesis is the gold standard test for the diagnosis of tuberculous pericarditis. Pericardial biopsy must be performed when we can't find acid fast bacilli in sputum or pericardial fluid. Finding acid fast bacilli on pericardiocentesis is confirmatory for tuberculous pericarditis.
History and Symptoms
Patients with tuberculous pericarditis may have a positive history of pulmonary TB, HIV infection, any Immune system dysfunction, elderly, black race, male gender, and living/traveling to TB endemic areas. Common symptoms of tuberculous pericarditis include fever, weight loss, night sweat, cough, breathlessness, chest pain, malaise, and ankle edema.
Physical Examination
Patients with tuberculous pericarditis usually appear Cachectic. They may have fever, tachycardia, pulsus paradoxus, hypotension, tachypnea, JVP distension, kussmaul's sign, lymphadenopathy, ankle edama, pleura dullness, decreased breath sounds, pericardial knock, pericardial rub, fine/coarse crackles upon auscultation of the lung, hepatomegaly, ascites, distant heart sounds, displaced point of maximal impulse (PMI) suggestive of cardiomegaly, friction rub, and S4.
Laboratory Findings
Laboratory findings consistent with the diagnosis of tuberculous pericarditis include mild anemia, normal leukocyte count, exudate pericardial effusion, mycobacterium tuberculosis bacilli in pericardial effusion, and positive HIV test.
Electrocardiogram
An ECG may be helpful in the diagnosis of tuberculous pericarditis. Findings on an ECG suggestive of tuberculous pericarditis include low voltage QRS, absence of ST segment elevation which we usually see in acute pericarditis, inverted T wave, atrial fibrillation, and electrical alternans.
X-ray
An x-ray may be helpful in the diagnosis of tuberculous pericarditis. Findings on an x-ray suggestive of tuberculous pericarditis include pericardial calcification, pericardial thickening, pericardial effusion, and evidence of pulmonary TB.
Echocardiography and Ultrasound
Echocardiography/ultrasound may be helpful in the diagnosis of tuberculous pericarditis. Findings on an echocardiography/ultrasound suggestive of tuberculous pericarditis include pericardial effusion, , pericardial thickening, increased right ventricular dimensions, decreased left ventricular dimensions, abnormal septal motion, flattening of the left ventricular posterior wall during diastol, dilated inferior vena cava, and dilated atrium.
CT scan
CT scan may be helpful in the diagnosis of tuberculous pericarditis. Findings on CT scan suggestive of tuberculous pericarditis include calcification of the pericardium, thickened pericardium, pericardial effusion, and back flow of blood into the IVC and hepatic veins (in contrast CT scan).
MRI
MRI may be helpful in the diagnosis of tuberculous pericarditis. Findings on MRI suggestive of tuberculous pericarditis include pericardial effusion, pericardial thickening, mediastinal and tracheobronchial lymphadenopathy (with hilar sparing), and bowing of the interventricular septum toward the left ventricle during diastole.
Other Imaging Findings
There are no other imaging findings associated with tuberculous pericarditis.
Other Diagnostic Studies
Other diagnostic studies for tuberculous pericarditis include PPD skin test, interferon-gamma assay, smear and culture of pericardial, sputum, and gastric fluid, pericardial biopsy, and lymph node biopsy.
Treatment
Medical Therapy
A 2 months course of isoniazid, pyrazinamide, rifampicin, and ethambutol followed by 4months course of isoniazid and rifampicin is shown to be effective for treatment of tuberculous pericarditis. Short course chemotherapy is beneficial in HIV infected patients.
Surgery
The mainstay of treatment for tuberculous pericarditis is medical therapy. Pericardiectomy is usually reserved for patients resistance constrictive pericarditis.
Primary Prevention
There are no established measures for the primary prevention of tuberculous pericarditis.
Secondary Prevention
There are no established measures for the secondary prevention of tuberculous pericarditis.