Tuberculous pericarditis overview: Difference between revisions

Jump to navigation Jump to search
(New page: {{Tuberculous pericarditis}} {{Pericarditis}} {{CMG}}; '''Associate Editor-In-Chief:''' Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S. ==Overview== The incidence of [[tub...)
 
No edit summary
 
(8 intermediate revisions by 6 users not shown)
Line 1: Line 1:
__NOTOC__
{{Tuberculous pericarditis}}
{{Tuberculous pericarditis}}
{{Pericarditis}}
{{CMG}}; '''Associate Editor-In-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.


==Overview==
{{CMG}}; '''Associate Editor-In-Chief:''' {{Fs}}, [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.
The incidence of [[tuberculosis]] caused by ''[[Mycobacterium tuberculosis]]'' and its complications has significantly decreased in developed nations while it remains high in developing countries. Approximately one third of the world population is believed to be infected with [[tuberculosis]](TB)<ref name="pmid18810682">{{cite journal| author=Lönnroth K, Raviglione M| title=Global epidemiology of tuberculosis: prospects for control. | journal=Semin Respir Crit Care Med | year= 2008 | volume= 29 | issue= 5 | pages= 481-91 | pmid=18810682 | doi=10.1055/s-0028-1085700 | pmc= | url= }} </ref>. In 2006, the [[WHO]] estimated the global prevalence of active [[TB]]<ref>WHO. Global Tuberculosis control. WHO/HTM/TB/2008.393. Geneva: World Health Organization; 2008. Available online at http://www.who.int/tb/publications/global_report/2008/en/index.html (Accessed June 27, 2011)</ref> to be 14.4 million cases. [[TB]] accounts for 1.7 million deaths worldwide. One of the important complications of [[TB]] is [[pericarditis]] which is inflammation of the pericardial sac that encases the heart.
 
 
 
== 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==
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 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==
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 [[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]].
 
===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 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, [[Mediastinum|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.


==References==
==References==
{{reflist|2}}
{{reflist|2}}


[[Category:Cardiology]]
{{WikiDoc Help Menu}}
[[Category:Diseases involving the fasciae]]
{{WikiDoc Sources}}
[[Category:Inflammations]]
[[Category: (name of the system)]]
[[Category:Emergency medicine]]
[[Category:Infectious disease]]
 
{{WH}}
{{WS}}

Latest revision as of 16:24, 19 December 2019


Tuberculous pericarditis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Tuberculous pericarditis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Tuberculous pericarditis overview On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Tuberculous pericarditis overview

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Tuberculous pericarditis overview

CDC on Tuberculous pericarditis overview

Tuberculous pericarditis overview in the news

Blogs on Tuberculous pericarditis overview

Directions to Hospitals Treating Psoriasis

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.

References


Template:WikiDoc Sources