Acute Primary Tuberculous Pericarditis

Acute Primary Tuberculous Pericarditis

Hsien-Kuo Chin, Yee-Phoung Chang and Chia-Shen Chao

Acute primary tuberculous (TB) pericarditis is a rare but life-threatening condition. It may lead to diastolic heart

failure in constrictive pericarditis. A 77-year-old man suffered from exertional dyspnea for 3 weeks. He had

received percutaneous transluminal coronary angioplasty (PTCA) with stent for left anterior descending artery

lesion 3 weeks prior to this admission. As dyspnea on exertion persisted, he was admitted to our hospital for possible

coronary arterial bypass grafting. No significant in-stent restenosis was found during recatheterization. Meanwhile,

bilateral pleural effusions were found, but they were negative for TB cultures and polymerase chain reaction (PCR).

Thickening of pericardium with large amount of pericardial effusion was noted during echocardiographic examination

3 weeks after admission. Emergent pericardiotomy was done for cardiac tamponade and biopsy. Acute primary TB

pericarditis was diagnosed and antituberculous chemotherapy plus adjuvant corticosteroid treatment were given.

The patient was discharged 2 weeks later in fair condition. Unfortunately, one month later he was readmitted due to

constrictive pericarditis. Pericardiectomy was done. After a full course of anti-TB therapy for 9 months, the patient

kept well after follow-up for one year.

Key Words: Cardiac tamponade � Corticosteroid � Pericardiectomy � Primary tuberculous pericarditis

INTRODUCTION

Acute pericarditis1 (< 3 months) is dry, fibrinous or

effusive, independent of its etiology. Most cases of acute

pericarditis are viral or idiopathic. Other causes are un-

common, including bacterial infection, tuberculosis, ur-

emic pericarditis, myocardial infarction, previous cardiac

surgery, complication after radiotherapy, cancer, and in-

flammatory diseases, etc. Each year, there are approxi-

mately 9 million new cases of tuberculosis worldwide,

and 3 million die from the disease. Tuberculosis (TB) is

a serious problem in developing countries, which ac-

count for 95% of worldwide TB cases, and 99% of

worldwide TB mortality. TB has not been on the list of

the leading causes of death in Taiwan since 1985. How-

ever, the incidence of TB in Taiwan remains high. Ac-

cording to a report from the Center for Disease Control

of Taiwan in 2002, the incidence and mortality rate of

TB were 74.6 and 5.68 per 100,000 population, respec-

tively.2 Pulmonary involvement accounted for 77.8% of

cases, with TB and isolated extra-pulmonary involve-

ment only accounting for 22%.3 Cardiac tamponade and

constrictive pericarditis are major lethal complications

of TB pericarditis.4 Apart from antituberculous chemo-

therapy with/without corticosteroid therapy, pericar-

diectomy may be the optimal therapy for TB pericarditis.

As the incidence of TB in Taiwan remains high and the

symptoms of TB pericarditis are nonspecific, a high sus-

picion of TB pericarditis should always be kept in mind

when encountering a patient with pericardial effusion.

CASE REPORT

A 77-year-old man, a retired bank manager, suffered

from chest oppression about 3 weeks prior to this admis-

sion. Percutaneous transluminal coronary angioplasty

Acta Cardiol Sin 2007;23:56�61 56

Case Reports Acta Cardiol Sin 2007;23:56�61

Received: September 12, 2006 Accepted: December 14, 2006Division of Cardiovascular Surgery, Department of Surgery, Kao-hsiung Armed Forces General Hospital, Kaohsiung, Taiwan.Address correspondence and reprint requests to: Dr. Chia-ShenChao, No. 2, Chung-Cheng 1st Road, Kaohsiung 802, Taiwan.Tel: 886-7-749-4963; Fax: 886-7-749-3207; E-mail: [email protected]

with stent for left anterior descending artery lesion was

done under the diagnosis of coronary artery disease with

congestive heart failure at another hospital three weeks

previous. But exertional dyspnea persisted. Under the

suspicion of in-stent restenosis, the patient was admitted

to our hospital for possible coronary arterial bypass

grafting surgery on June 13, 2005.

The patient had had history of hypertension and dia-

betic mellitus for more than 10 years, and he had been

taking medication regularly. He had no habit of smoking

or drinking. Poor appetite, malaise and loss of body

weight were noted in recent weeks. No fever was found.

There was no jugular vein engorgement. Bilateral basal

rales of lungs and pitting edema of both legs were noted.

On the day of admission, echocardiography revealed im-

paired left ventricle (LV) systolic function. Bilateral

blunt costophrenic angles (left side more prominent than

the right) were noted on chest radiography (Figure 1).

Hepatic vein and inferior vena cava engorgement was

noted in abdominal sonography. Pulmonary hypertension

(pulmonary arterial pressure: 41/23 mmHg), high central

venous pressure (21 mmHg) and low cardiac index (1.81

L/min/m2) were found after Swan-Ganz catheterization

measurement. No in-stent restenosis and patency of left

circumflex coronary artery & right coronary artery were

found in cardiac catheterization. Proximal LAD 50%

narrowing was the same as previous. The symptoms im-

proved after the use of inotropic agents. Intermittent low

grade fever (37~38 �C) was found during hospitaliza-

tion, but there were negative results in all the cultures of

sputum, pleural effusion and blood.

On July 6, a follow-up echocardiography revealed

severe hypokinesia of the right ventricle (RV) free wall

with preserved LV systolic function. Tumor of the pe-

ricardium with large pericardial effusion was noted, too.

Thickening of the pericardium was confirmed in a chest

computed tomography (Figure 2). Pericardial window

thru minimal thoracotomy was arranged. Unfortunately,

cardiac tamponade occurred (blood pressure: 80/50

mmHg, heart rate: 138/min and respiratory rate: 30/min,

SpO2: 87%), emergent pericardiotomy via subxyphoid

approach was done. Caseous-like turbid fluid, about 150

cc, was drained (Figure 3). Bilateral thoracic intubations

57 Acta Cardiol Sin 2007;23:56�61


Figure 2. Chest computed tomography revealed thickened

pericardium, large amount of pericardial effusion with right ventricle

compression and bilateral pleural effusions (left side more prominent

than the right).

Figure 3. Pleural effusion (A) revealed light yellowish color, while

pericardial effusion (B) was caseous-like turbid fluid.

Figure 1. Chest radiography, performed on the day of admission,

showed bilateral blunt costophrenic angles (left side more severe than

the right).

were performed, and a large amount of clear transudate

was drained. The vital signs became stable after the pro-

cedures. The patient was sent to intensive care unit for

recovery. The systolic function of RV and LV were

found normal by echocardiography 2 weeks later.

Numerous acid-fast bacilli were identified in the

specimen from the pericardium (Figure 4). The TB-

polymerase chain reaction (PCR) test of pericardial effu-

sion was positive. Negative finding of acid-fast stain in

sputum and pleural effusion was found. The TB-PCR

test was negative, too. Cultures of sputum and pleural ef-

fusion also yielded negative findings. Four combined

antituberculous chemotherapy (EMB 800 mg + isoniazid

320 mg + pyrazinamide 1000 mg + rifampin 480 mg per

day) plus adjuvant corticosteroid therapy (prednisolone

60 mg per day) were given. The fever subsided on the

next day of regimen. The patient was discharged in good

condition. Dyspnea on exertion (New York Heart As-

sociation Function Class II~III) developed again one

month later. He was re-admitted to our ward under the

impression of constrictive pericarditis on September 5,

2005. Pericardiectomy was done (Figure 5). Numerous

acid-fast bacilli were found in the excised pericardium.

The symptom of exertional dyspnea was absent after

pericardiectomy. After a full course of anti-TB therapy

for 9 months, the patient kept well after one year fol-

low-up.

DISCUSSION

The incidence and mortality of TB pericarditis in de-

veloping countries are still high. The mortality rate in

untreated acute effusive TB pericarditis can approach up

to 85%,1 and was reduced to 3~11% in patients5 who re-

ceived oral medication. In Taiwan, the incidence of

tuberculosis has remained high in recent years. The cli-

nical manifestations in patients with TB pericarditis

usually are nonspecific. Dyspnea, jugular vein disten-

sion, fever (usually < 39 �C), cough, tachycardia, leg

edema and chest tightness or pain were the most com-

monly found clinical manifestations.5 Combined intra-

and extrapulmonary TB had a significantly higher in-

cidence of high fever and a longer duration of fever.

Low-voltage QRS and inverted T-waves were the cha-

racteristic findings of electrocardiogram in TB peri-

carditis in one previous report,4 but this was not seen in

our patient. Although isolated extra-pulmonary involve-

ment only accounted for 22% of cases with TB, pleural

effusion was found in 63% of cases with TB pericardtis.5

Clinicians should have a high index of suspicion of TB

pericarditis when encountering a patient with pericardial

effusion in Taiwan, especially if co-existent pleural effu-

sion is noticed.

The diagnosis is made by the identification of Myco-

bacterium tuberculosis in the pericardial fluid or tissue,

and/or the presence of caseous granulomas in the pe-

ricardium.6 PCR can identify DNA of Mycobacterium

tuberculosis rapidly from only 1 �L of pericardial fluid.7

High adenosine deaminase activity and interferon gam-

ma concentration in pericardial effusion are also di-

agnostic. Pericardial biopsy enables rapid diagnosis with

better sensitivity than pericardiocentesis (100 vs. 33%).

Various antituberculous drug combinations and treat-

ment duration of different lengths (6, 9, 12 months) have

been applied.4,8-10 Although corticosteroids are capable


Hsien-Kuo Chin et al.

Figure 4. Numerous acid-fast bacilli were identified from pericardial

material tissue under microscope.

Figure 5. Thickened pericardium with fibrotic change and some

calcification.

of suppressing inflammatory reaction in TB pericar-

ditis,4,10 the use of corticosteroids will inevitably further

compromise the immunity in vulnerable elderly suffer-

ing from TB pericarditis.4 Despite the use of steroids

remaining controversial, a meta analysis of patients with

effusive and constrictive TB pericarditis11,12 suggested

that tuberculosis treatment combined with steroids might

be associated with fewer deaths,13 and less frequent need

for pericardiocentesis or pericardiectomy.10,14 In our pa-

tient, the fever subsided rapidly after the use of pred-

nisolone. High-dose prednisolone (1-2 mg/kg per day)

should be given, since rifampicin induces its liver me-

tabolism. The dose is maintained for 5-7 days and is

progressively tapered to discontinue in 6-8 weeks.1

Since cardiac tamponade and constrictive pericar-

ditis are two major lethal complications of TB peri-

carditis, can we predict or prevent these conditions?

Based on the echocardiographic findings, TB peri-

carditis has been categorized into: (1) early stage, when

only pericardial effusion is found, and (2) advanced

stage, when fibrin strand formation or fibrosis with

thickening of pericardium reflecting constrictive peri-

carditis is detected. An early report indicated that car-

diac tamponade developed in approximately 50% of

patients who did not received adequate treatment in the

first 3 months after the diagnosis of TB pericarditis.5

Yang et al. reported their 14 years’ experience, in-

dicating that 37.5% of patients with early-stage TB pe-

ricarditis developed constrictive pericarditis, while

among patients with advanced-stage disease, 85.7%

subsequently developed pericardial constriction.5 From

the study of Suwan and Potjalongsilp, cardiac tam-

ponade in the early stage of TB pericarditis was the

most predictive factor for subsequent constrictive pe-

ricarditis,12 and the degree of fibrosis of pericardium

before treatment was the most important determinant of

developing constriction.15

In early-stage patients with minimal pericardial effu-

sion, pericardiocentesis with biopsy can be done to

confirm the diagnosis. If cardiac tamponade develops,

creation of a pericardial window should be done. If con-

strictive pericarditis presents, pericardiectomy is the

treatment of choice. The operative mortality for peri-

cardiectomy is around 2.3%. As a poor hemodynamic

result after complete pericardiectomy relates to the pre-

operative degree of constriction and resultant cardio-

myopathy,16 the long-term survival after pericardiectomy

for constrictive pericarditis is related to LV systolic

function, renal function and pulmonary artery pressure;17

early pericardiectomy is recommended when constrictive

pericarditis is diagnosed, or when conditions suggests a

high possibility of developing constrictive pericarditis.18

In conclusion, clinicians in Taiwan should maintain

a high index of suspicion for TB pericarditis when a

patient develops an unexpected pericardial effusion. De-

spite the use of steroids remaining controversial, tubercu-

losis treatment combined with steroids is recommended

if no clear contraindication is present. In patients with

advanced-stage TB, if there is cardiac tamponade in the

early clinical stage, or if severe fibrosis of the peri-

cardium and constrictive pericarditis develop, early pe-

ricardiectomy will be the optimal treatment.

REFERENCES

1. Bernhard M, Petar MS, Arsen DR, et al. Guidelines on the

Diagnosis and Management of Pericardial Diseases. Executive

summary. The Task Force on the Diagnosis and Management of

Pericardial Diseases of the European Society of Cardiology. Eur

Heart J 2004;25:587-610.

2. Center for Disease Control Taiwan, R.O.C. Available at: URL:

http//203.65.7.83/ch/dt/Show Publication.ASP

3. Lin YS, Huang YC, Chang LY et al. Clinical characteristics of

tuberculosis in children in the north of Taiwan. J Microbiol

Immunol Infect 2005;38:41-6.

4. Fowler NO. Tuberculous pericarditis. JAMA 1991;266(1):99-

103.

5. Yang CC, Lee MH, Liu JW, et al. Diagnosis of tuberculous

pericarditis and treatment without corticosteroids at a tertiary

teaching hospital in Taiwan: a 14-year experience. J Microbiol

Immuno Infect 2005;38:47-52.

6. Spodick DH. Infectious pericarditis. In: Spodick DH, Ed. The

pericardium: a comprehensive textbook. New York: Marcel

Dekker; 1997. p. 260-90.

7. Seino Y, Ikeda U, Kawaguchi K, et al. Tuberculosis pericarditis

presumably diagnosed by polymerise chain reaction analysis. Am

Heart J 1993;126:249-51.

8. Koh KK, Kim EJ, Cho CH, et al. Adenosine deaminase and

carcinoembryonic antigen in pericardial effusion diagnosis,

especially in suspected tuberculous pericarditis. Circulation

1994;89(6):2728-35.

9. Sagrista-Sauleda J, Permanyer-Miralda G, Soler-Soler J. Tu-

berculous pericarditis: ten year experience with a prospective

protocol for diagnosis and treatment. J Am Coll Cardiol 1988;

11(4):724-8.

59 Acta Cardiol Sin 2007;23:56�61


10. Strang JI, Kakaza HH, Gibson DG, et al. Controlled clinical trial

of complete open surgical drainage and of prednisolone in

treatment of tuberculous pericardial effusion in Transkei. Lancet

1988;2(8614):759-64.

11. Mayosi BM, Ntsekhe M, Volmink JA, et al. Interventions for

treating tuberculous pericarditis. Cochrane Database Syst Rev

2002;(4):CD000526.

12. Ntsekhe M, Wiysonge C, Volmink JA, et al. Adjuvant cor-

ticosteroids for tuberculous pericarditis: promising, but not pro-

ven. Q J Med 2003;96:593-9.

13. Strang JI, Nunn AJ, Johnson DA, et al. Management of tu-

berculous constrictive pericarditis and tuberculous pericardial

effusion in Transkei: results at 10 years follow-up. Q J Med

2004;97(8):525-35.

14. Strang JI. Rapid resolution of tuberculous pericardial effusion

with high dose prednisone and antituberculous drugs. J Infect

1994;28:251-4.

15. Suwan PK, Potjalongsilp S. Predictors of constrictive pericarditis

after tuberculous pericarditis. Br Heart J 1995;73(2):187-9.

16. McCaughan BC, Schaff HV, Pihler JM, et al. Early and late results

of pericardiectomy for constrictive pericarditis. J Thorac Car-

diovasc Surg 1985;89(3):340-50.

17. Bertog SC, Thambidorai SK, Parakh K, et al. Constrictive pe-

ricarditis: etiology and cause-specific survival after pericar-

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Hsien-Kuo Chin et al.

Case Reports Acta Cardiol Sin 2007;23:56−61

急性原發性結核心包膜炎

金憲國張一方趙家聲高雄市國軍高雄總醫院外科部心臟血管外科

急性原發性結核心包膜炎是一十分罕見但卻致命的一種狀況，它通常導致侷限性心包膜炎

進而造成舒張性心衰竭。我們報告一位 77歲男性在住院前三個月因冠心症合併心衰竭接受左前降支支架置放術。後因氣喘而到本院求診，要求進行冠狀動脈繞道手術。心導管攝影

顯示除左前降支之支架外無明顯病兆。住院後反覆有兩側肋膜積水，積水之所有結核檢查

皆呈陰性。3 週後於心臟超音波檢查發現心包膜有增厚情形且合併大量心包膜液，因為造成心包填塞而從劍突施予緊急心包膜切開術。經組織病理診斷為急性原發性結核心包膜炎，

我們給予抗結核菌藥物合併類固醇輔助治療後病情明顯好轉並於幾天後出院。病患於一個

月後因侷限性心包膜炎而施予心包膜截除術。病患在九個月的抗結核藥物治療後，追蹤至

今滿一年仍保持良好狀態。

關鍵詞：心包填塞、類固醇、心包膜截除術、原發性結核心包膜炎。

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Acute Primary Tuberculous Pericarditis