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19 Cardiopulmonary Bypass and Mechanical Circulatory Assistance in…
a
Fig. 19.4 Volume rendered images (a, b) show extensive pericardial calcication (*) along the
right atrioventricular groove and over the right ventricular (RV) free wall and RV outow tract.
(LV: left ventricle; RA: right atrium)
b
approach should only be offered two patients with satisfactory respiratory functions. A thorough assessment of respiratory status is thus essential to decide on the
optimal surgical strategy.
19.2 Mechanical Circulatory Support
Intra-aortic balloon counterpulsation is commonly used in adult patients with acute
left ventricular dysfunction after myocardial infarction, valvular heart surgeries or
cardiac surgery. Rarely, it has also been used to treat ventricular dysfunction in
patients undergoing pericardiectomy for chronic constrictive pericarditis [5–14, 20,
22, 25, 27, 28, 30]. When the medical management fails to maintain the cardiac
output, the option left is to assist the failing heart by mechanical circulatory assistance. Intra-aortic balloon counterpulsation facilitates recovery of left ventricular
function in various ways. It decreases the left ventricular end-diastolic and left atrial
pressure, thus helps the systemic ventricle and indirectly the pulmonary ventricle by
the phenomenon of ventricular interdependence. It helps in maintaining coronary
perfusion pressure and decreases afterload to ventricle with decrease in need for
vasopressor agents [5–14].
The main advantage of balloon counterpulsation over left atrial-aortic assist
devices is the ease of application [5–14, 20, 22, 25, 27, 28, 32]. Literature documents sporadic use of other mechanical assist devices like axial ow pumps and
veno-arterial extracorporeal membrane oxygenation [19, 26].
19.2 Mechanical Circulatory Support
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325
Use of intra aortic balloon counterpulsation is limited in children with chronic
constrictive pericarditis [26]. This is due to the technical difculties like unavailability of suitable sizes, difculty in vascular access for insertion of balloon, and
importantly the inability to track rapid heart rates and narrow pulse pressures of
children in shock. Moreover, complications like renal failure, ischemia of the limbs
and mesentery are greater for smaller children because of inappropriate lengths of
the balloons [26].
Pediatric balloon catheters and pumping consoles have greatly evolved and
devices suitable even for the smallest child are commercially available. There were
early concerns of achieving effective counterpulsation in the highly elastic and distensible aorta of young children, which have been proved baseless. However,
another major concern that has hindered the widespread use of an intra-aortic balloon in children is that they are more likely to have dysfunctional right ventricle and
pulmonary function and may not benetted with an intra-aortic balloon. In such
scenarios, extracorporeal membrane oxygenation and left ventricular assist devices
are the prevalent means of mechanical circulatory assistance [12, 22, 26].
Lots of clinical analysis and judgement is required to decide the timing of deployment of intraaortic balloon counterpulsation therapy. In patients who suddenly deteriorate after pericardiectomy and not responding to maximum medical therapy, the
decision to initiate intra-aortic balloon counterpulsation is relatively straightforward. In cases of progressive deterioration of ventricular function and unresponsiveness to adequate inotropic support, the decision making process is tedious [12].
The insertable lengths of commercially available intra-aortic balloon catheters
are 16.5cm, 22.1cm and 25.8cm for 25cm3, 34cm3 and 40cm3 balloons respectively. Intraaortic balloon therapy can be initiated in pediatric patients with preserved right ventricular and pulmonary function and requiring mechanical
circulatory assistance fullling the above-mentioned mandate, albeit with 57%
(n=4) dying despite use of balloon support. In our three previous investigations on
547 (n= 395, 30, and 122) consecutive patients undergoing pericardiectomy for
chronic constrictive pericarditis between January 1985 and December 2015, the
cumulative occurrence of low cardiac output syndrome and hospital mortality was
36.5% (n= 200) and 6.9% (n=38), respectively. Twenty-two (4%) deaths were
primarily due to low cardiac output syndrome. Among the 547 patients, 298 (54.5%)
were younger than 20years. The youngest patient was 10months old, weighing
9 kg. Left ventricular assist devices and extracorporeal membrane oxygenation
were not used for any patient following pericardiectomy in published literature [5–14].
There are few case reports and series of patients whom were treated with intraaortic balloon support for a failing circulation following pericardiectomy [5–14, 20,
25, 27, 32]. In 2018, we published reports of two patients aged 18- and 19-years
undergoing total pericardiectomy for chronic calcic pericarditis with systemic
ventricular failure who were successfully treated using intra-aortic balloon counterpulsation [12]. Subsequent to the last publication, we have employed intra-aortic
balloon counterpulsation successfully in seventeen more patients undergoing total
pericardiectomy for calcic chronic constrictive pericarditis (unpublished).
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19 Cardiopulmonary Bypass and Mechanical Circulatory Assistance in…
From our experience we found that post pericardiectomy patients benet from
intra-aortic balloon counterpulsation when they have systemic ventricular failure, in
the same way as adult patients after surgery for other acquired heart diseases.
However we do not advocate widespread use of balloon pumping after pericardiectomy without an exhaustive search for adequacy of pericardiectomy, and exclusion
of any other surgically correctable causes like signicant coronary artery disease,
signicant mitral and/or tricuspid regurgitation, or other rectiable issues [12, 20,
21, 25, 27, 32].
Specic indications, proper time of intervention, and factors that can predict a
successful outcome with use of mechanical assist devices after pericardiectomy can
only be dened after randomised studies or systematic reviews of larger patient
population [29, 31, 33].
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BW, Blackstone EH, Lauer MS, Klein AL. Constrictive pericarditis: aetiology and causespecic survival after pericardiectomy. J Am Coll Cardiol. 2004;43:1445–52.
2. Copeland JG, Stinson EB, Griepp RB, Shumway NE.Surgical treatment of chronic constrictive pericarditis using cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1975;69:236–8.
3. Culliford AT, Lipton M, Spencer FC. Operation for chronic constrictive pericarditis do the
surgical approach and degree of pericardial resection inuence the outcome signicantly? Ann
Thorac Surg. 1980;29:146–52.
4. Copeland JG, Riley JE, Fuller J. Pericardiectomy for effusive constrictive pericarditis after
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5. Chowdhury UK, Subramaniam G, Kumar AS, Airan B, Singh R, Talwar S, etal. Pericardiectomy
for constrictive pericarditis: clinical, echocardiographic and haemodynamic evaluation of two
surgical techniques. Ann Thorac Surg. 2006;81:522–30.
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Operative Tech Thorac Cardiovasc Surg. 2008;13:14–25.
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output syndrome following pericardiostomy and pericardiectomy for massive pericardial effusion and chronic constrictive pericarditis: myths and realities at 100 years. Int J Clin Case Stud
Rep. 2019;2(1):46–60. (Invited article)
8. Chowdhury UK, Narang R, Malhotra P, Choudhury M, Choudhury A, Singh SP.Indications,
timing and techniques of radical pericardiectomy via modied left anterolateral thoracotomy
(UKC’s modication) and total pericardiectomy via median sternotomy (Holman and Willett)
without cardiopulmonary bypass. J Prac Cardiovasc Sci. 2016;2:17–27.
9. Chowdhury UK, Kumari LS.Pericardiectomy for chronic constrictive pericarditis: where are
we after 100 years? World J Surg Surg Res. 2018;1:1027–30.
10. Chowdhury UK, Kumari L. Surgery for Chronic Constrictive Pericarditis, Tuberculous
Pericarditis and Effusive-Constrictive Pericarditis. Invited Chapter: Cardiological Society of
India, 2018 (Invited chapter 64), pp.1–10.
11. Chowdhury UK, Kumari LS, Hasija S. Surgery for chronic constrictive pericarditis, tuberculous pericarditis and effusive-constrictive pericarditis. Cardiological Society of India, 2018.
Essentials of Postgraduate Cardiology, Evangel Publishers, Invited Chapter 64, pages 1–10.
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12. Chowdhury UK, Jena JK, Hasija S, Kumari LS.Successful use of intra-aortic balloon counterpulsation for systemic ventricular failure following total pericardiectomy for calcic chronic
constrictive pericarditis. World J Ped Cong Heart Surg. 2020;11(4):NP203–6.
13. Chowdhury UK, George N, Singh S, Sankhyan LK, Sengupta S, Ray R, Vaswani P, Kalaivani
M.Total pericardiectomy via modied left anterolateral thoracotomy without cardiopulmonary bypass. Ann Thorac Surg. 2021; https://doi.org/10.1016/j.athoracsur.2020.10.045.
14. Cameron J, Oesterle SN, Baldwin JC, Hancock EW.The etiologic spectrum of constrictive
pencarditis. Am Heart J. 1987;113:354–60.
15. Carson TJ, Murray GF, Wilcox BR, Starek PJK.The role of surgery in tuberculous pericarditis.
Ann Thorac Surg. 1974;17:163–7.
16. DeValeria PA, Baumgartner WA, Casale AS. Current indications, risks, and outcome after
pericardiectomy. Ann Thorac Surg. 1991;52:219–24.
17. George TJ, Arnaoutakis GJ, Beaty CA, Kilic A, Baumgartner WA, Conte JV.Contemporary aaetiologies, risk factors and outcomes after pericardiectomy. Ann Thorac Surg. 2012;94:445–51.
18. Gopaldas RR, Dao TK, Caron NR, Markley JG.Predictors of in-hospital complications after
pericardiectomy: a nationwide outcomes study. J Thorac Cardiovasc Surg. 2013;145:1227–33.
19. Gaines WE, Pierce WS, Prophet GA, Holtsman K.Pulmonary circulatory support: a quantitative comparison of four methods. J Thorac Cardiovasc Surg. 1984;88:958–64.
20. Ha JW, Oh JK, Schaff HV, Ling LH, Higano ST, Mahoney DW, Nishimura RA.Impact of left
ventricular function on immediate and long-term outcomes after pericardiectomy in constrictive pericarditis. J Thorac Cardiovasc Surg. 2008;136:1136–41.
21. Johnson TL, Baughman WB, Josephson RA.Worsening tricuspid regurgitation following pericardiectomy for constrictive pericarditis. Chest. 1993;104:79–81.
22. Kiley S, Soa J, Machuca T.Venoarterial ECMO for recovery from right ventricular failure
after pericardiectomy. SOCCA Post Session 2017 (Abstact), No. 1344.
23. Ling LH, Oh JK, Schaff HV, Danielson GK, Mahoney OW, Seward JB, Tajik JA.Constrictive
pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy. Circulation. 1999;100:1380–6.
24. Ling LH, Oh JK, Breen JF, Schaff JV, Danielson GK, Mahoney DW, Seward JB, Tajik
AJ.Calcic constrictive pericarditis: is it still with us? Ann Intern Med. 2000;132:444–50.
25. Omoto T, Minami K, Varvaras D, Böthig D, Körfer R.Radical pericardiectomy for chronic
constrictive pericarditis. Asian Cardiovasc Thorac Ann. 2001;9(4):286–90.
26. Pinkney KA, Minich LL, Tani LY, Di Russo GB, Veasy LG, McGough EC, Hawkins
JA.Current results with intraaortic balloon pumping in infants and children. Ann Thorac Surg.
2002;73(3):887–91.
27. Ruiz-Cano MJ, Fernandez-Ruiz M, Sanchez V, Lopez-Medrano F. Constrictive pericarditis
due to Candida albicans: an unexpected cause of pericardial effusion after heart transplantation. Rev Clin Esp. 2012;212:551–7.
28. Romeo FJ, Guzzetti E, Arias A, Belziti C, Marenchino R.New-onset liver failure: pitfalls of an
unusual diagnosis. Arch Cardiovasc Imaging. 2015;3:e33652.
29. Szabo G, Schmack B, Bulut C, Soos P, Weymann A, Stadtfeld S, etal. Constrictive pericarditis: risks, aetiologies and outcomes after total pericardiectomy: 24 years of experience. Eur J
Cardiothorac Surg. 2013;44:1023–8.
30. Senni M, Redeld MM, Ling LH, Danielson GK, Tajik AJ, Oh JK.Left ventricular systolic
and diastolic function after pericardiectomy in patients with constrictive pericarditis. J Am
Coll Cardiol. 1999;33:1182–8.
31. Tokuda Y, Miyata H, Motomura N, Araki Y, Oshima H, et al. Outcome of pericardiectomy for constrictive pericarditis in Japan: a nationwide outcome study. Ann Thorac Surg.
2013;96:571–6.
32. Wood JA.Tuberculous pericarditis; a study of fortyone cases with special reference to prognosis. Am Heart J. 1951;42:737–45.
33. Zhu P, Mai M, Wu R, Lu C, Fan R, Zheng S.Pericardiectomy for constrictive pericarditis:
single-Centre experience in China. J Cardiothorac Surg. 2015;10:34.
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Chapter 20
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Specic Disease Entities
20.1 Purulent/Bacterial Pericarditis
20.1.1 Denition
Purulent pericarditis is dened as a localized infection of pericardial space producing uid that is macroscopically or microscopically purulent [75–83].
20.1.2 Incidence, Aetiology andPathophysiology
Presently, among patients with purulent pericarditis 20–25% have an underlying
primary source of infection, e.g. pneumonia, acute pyelonephritis, skin infection, or
meningitis. About 80% of cases have multiple aetiology, including history of recent
thoracic surgery, chest trauma, malignancy, chronic renal failure, HIV infection or
other immunosuppressive conditions, and alcohol abuse. Direct spread from an
intrathoracic infective focus, e.g. pulmonary, esophageal, mediastinal, chest trauma,
extension from a sub-diaphragmatic suppurative focus, oral sepsis or hematogenous
(staphylococcus) spread during bacteremia account for most cases [75–83,
155–168].
In the antibiotic era, the most common agents are staphylococcus aureus
(20–30%), gram-positive infections, e.g. pneumococcal, meningococcal, streptococci (40–45%), and gram-negative bacilli (i.e. Hemophilus inuenza, Brucella
melitenesis, Neisseria gonorrhea, Neisseria meningitides, Salmonella species). The
incidence of hospital- acquired bacterial infections has increased, and fungal pathogens have become more common (upto 20%) in patients with a predisposing factor
including hyperalimentation, prolonged antibiotic therapy, malignancy, steroid
administration, immunosuppression, burns and following cardiac surgery [33, 102,
Ltd. 2023
U. K. Chowdhury, L. K. Sankhyan, Surgical Treatment of Chronic Constrictive
Pericarditis, https://doi.org/10.1007/978-981-99-5808-5_20
329© The Author(s), under exclusive license to Springer Nature Singapore Pte
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103, 112, 155–168]. After thoracic surgery, methicillin-resistant staphylococcus
aureus and anaerobic organisms are more common.
20 Specic Disease Entities
20.1.3 Clinical Features
The clinical ndings are high-grade fever with chills and rigor, but this may be
absent in debilitated patients. The disease may take a fulminant course with rapid
development of tamponade and may remain undiagnosed because the associated
illnesses may dominate the clinical picture.
20.1.4 Investigations
Blood picture includes leukocytosis with a marked leftward shift. Pericardial uid
examination shows leukocytosis, low glucose, high protein and elevated lactic
dehydrogenase [112, 216].
Chest radiography may show an enlarged cardiac silhouette. Gas-producing
organisms may produce an air-lled interface. The electrocardiogram may show
ST-T wave changes of acute pericarditis and low voltage if a large effusion is present. Echocardiography demonstrates pericardial effusion with or without adhesions
[112, 170].
20.1.5 Management
In the author’s opinion, based on 40years of experience, management of purulent
pericarditis should include identication of the foci of infection, control of infection, and early total/radical pericardiectomy via left anterolateral thoracotomy to
prevent later constrictive pericarditis. A median sternotomy approach is not recommended, for chances of infection within the cancellous bone [22–24, 28].
20.2 Tuberculous Pericarditis
20.2.1 Epidemiology
Tuberculous pericarditis is a life-threatening form of extrapulmonary tuberculosis,
which presents as either pericardial effusion or constrictive pericarditis [14–19, 167,
170–180]. In developing countries which account for 86% of world’s population,
20.2 Tuberculous Pericarditis
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tuberculosis is the most common etiological factor comprising 60%–80% of cases
of signicant pericardial effusion and constrictive pericarditis [113, 115, 116, 144,
146]. The disease is increasing in prevalence, because of resurgence of multi-drug-
resistant tuberculosis in developing countries, and accounts for 3 million deaths
annually [217]. According to postmortem studies conducted more than 100years
ago, tubercular pericarditis was present in 2.5% to 11% of people dying of tuberculosis and 1% in deaths due to other reasons [14–19, 128–130, 136, 164, 171, 172,
174, 175].
There has been a steady decline in the prevalence of tuberculosis in industrialised
countries from 10% in the middle of the last century to 1–5% in recent times [104,
139–142, 144, 148, 216]. Published literature documents a wide variation in the
prevalence of tubercular pericardial effusion from 10% in Turkey, 26% in areas of
UK with a large immigrant Asian and Caribbean population, 27% in Pakistan, 37%
in Kuwait, 60% in India, and 70% in South Africa [5, 45, 98, 105, 144–148]. The
criterions used for diagnosing tuberculous pericardial effusion may be one of the
major factors responsible for such variation.
In HIV infected persons living in tuberculosis endemic areas, tuberculosis is
most common cause (>90%) of large pericardial effusion. In a study conducted in
Malawi, more than 90% of patients with pericardial tuberculosis were found to have
HIV infection [14–18, 34, 36, 117, 139, 140, 144–148].
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20.2.2 Pathogenesis
Retrograde lymphatic spread of mycobacterium tuberculosis from peribronchial,
paratracheal, or mediastinal lymph nodes is the commonest reason for pericardial
involvement [136, 137, 174–176]. The lymphatic drainage of pericardium is primarily to the anterior and posterior mediastinal and bronchial lymph nodes.
Contiguous spread of tuberculosis to pericardium due to direct contact with
lesions in the lung, pleura, rib cage, diaphragm or peritoneum is less frequent and
hematogenous spread is rare [127, 128, 136, 137, 164–168, 171–174]. In an autopsy
study on pericardial tuberculosis, Schepers and colleagues noted associated pulmonary tuberculosis in 75% to 90%, and extrapulmonary involvement in 25% to 50%
of cases [175].
The scarce presence of tubercle bacilli in the pericardial uid collected from
immunocompetent patients with tuberculous pericarditis is an evidence of the pericardium’s avid immunologic activity [175]. This active immune response is cited as
the reason for the pathologic changes noted in tuberculous pericarditis. Delayed
hypersensitivity response is induced by the antigens of the mycobacterium, stimulating lymphocytes to release lymphokines that activate macrophages and induce
formation of granulomatous lesions. The cytokine prole points to a hypersensitivity response caused by TH-1 lymphocytes [5, 6]. The antimyolemmal and antimyosin antibodies cause cytolysis and contribute to development of exudative tubercular
pericarditis [112].
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The literature documents four pathological stages of tuberculous pericarditis.
• First is a stage of brinous exudation with polymorphonuclear leukocytosis,
presence of mycobacteria, and early granuloma formation associated with loose
organization of T-cells and macrophages.
• Next is the stage of serosanguinous effusion which is a lymphocytic exudate with
foam cells and monocytes.
• Later the effusion is absorbed, granulomatous caseation forms, and pericardial
thickens due to deposition of brin and collagen leading to brosis.
• Constricting scarring with or without calcication: the brosis of parietal and
visceral pericardium may become calcied, which impedes diastolic lling,
causing constrictive pericarditis [203].
20 Specic Disease Entities
20.2.3 Clinical Characteristics
Tuberculous pericarditis usually presents in one of three forms: pericardial effusion
(60%–80%), effusive-constrictive pericarditis (15%–20%), or constrictive pericarditis (5%–70%), depending on the reporting centres in different parts of world [14–
22, 55–57, 77–83, 113–116, 144–149, 155, 156].
,
20.2.4 Tuberculous Pericardial Effusion
Tuberculous pericardial effusion has an insidious onset with fever, night sweats,
weight loss and fatigue. Other symptoms include chest pain, breathlessness, cough,
and right upper abdominal pain [14–20, 33, 34, 36, 37, 57, 167, 170–172]. In some
patients, constrictive pericarditis result in clinical features mimicking heart failure.
Presence of pericardial friction rub and increased area of cardiac dullness on percussion are two signs that favour a clinical diagnosis of pericardial effusion over
chronic constrictive pericarditis [21, 22, 144–149, 167, 170–172, 174–176,
181–185].
20.2.5 Non-calcic andCalcic Constrictive Pericarditis
Despite early initiation of antitubercular and steroid therapy, the rst presentation of
tuberculous pericarditis may be pericardial constriction, with an incidence varying
from 5% to 80% as described in published literature [14–28, 46, 47, 75, 79, 106,
112–116, 128, 149, 155, 167, 174–188]. The clinical presentation is a spectrum,
starting from asymptomatic patients to features of severe pericardial constriction
like ‘ascites precox’, pedal oedema and hepatomegaly [14–28, 46, 47, 75–83,
20.2 Tuberculous Pericarditis
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112–116, 128, 149, 155, 167, 174–176, 180, 186–188]. The diastolic lift (pericar-
dial knock) that coincides with a high-pitched early diastolic sound and sudden
inspiratory split of [156] are found in 21%, 45% and 36% of patients respectively
[171–173]. According to literature, the incidence of pericardial calcication in
patients with constrictive pericarditis of tubercular aetiology vary from 5% to 76%
[14–28, 46, 47, 75, 79, 106, 112–116, 128, 149, 155, 167, 174–176, 180, 186–188].
In a study conducted at a tertiary referral centre in North India, among 395 patients
undergoing pericardiectomy for constrictive pericarditis between 1985 and 2004,
we observed 4.8% incidence of calcied pericardium, of which 88.9% of cases had
tubercular etiology [23].
Area of maximum pericardial calcication occurs over the right atrium and right
ventricle followed by diaphragmatic surface, and atrio-ventricular grooves. This
could be possibly explained by the displacement of uid by vigorous left ventricular
contraction during resorption of primary pericardial effusion, which preferentially
gravitates towards the right side of the heart. Later calcium and minerals are slowly
deposited in the inspissated uid causing calcication which are sometimes as
dense as bone [14–17, 28, 46, 47, 75–79, 106, 112–116, 128, 149, 155, 167, 174–
176, 180, 186–188].
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20.2.6 Effusive-Constrictive Pericarditis
This is mixed form of tuberculous pericarditis which is common in India and other
Asian countries. Clinical signs of pericardial effusion along with a diastolic knock
and early third heart sound may be present in these cases. Often the cardiopericardial silhouette on chest X-ray is larger than in those with purely constrictive pericarditis. It is characterised by located effusion between thickened pericardial
membranes, which can be visualised on echocardiogram [14–28, 55, 56, 73, 118,
119, 178, 179, 182, 183, 189–191].
20.2.7 A Systematic Approach totheDiagnosis ofTuberculous
Pericardial Effusion
The most difcult part in evaluation of tuberculous pericarditis is establishing a
bacteriological or histological diagnosis [112–115, 118, 119]. Pericardiocentesis is
recommended in all cases of suspected tuberculous pericardial effusion [103, 112–
115, 118, 119, 192]. Tuberculous pericardial effusion shows typically exudative,
hemorrhagic, leukocytosis with predominant lymphocytes and monocytes and a
high protein count.
Light’s criteria dene exudate as a uid having one or more of the following:
uid protein/serum protein >0.5, uid lactate dehydrogenase/serum lactate
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20 Specic Disease Entities
dehydrogenase >0.6, uid lactate dehydrogenase level>2/3 of the upper limit of
normal for serum lactate dehydrogenase [112–115, 118, 119].
The variability of detection of tubercle bacilli ranges from 0 to 42% in different
series [7, 8, 36–39, 106–109, 175, 177]. Culturing of tubercle bacilli in modied
Kirchner culture results in 75% yield compared with a 53% yield with conventional
culture. When pericardial uid is scanty or inaccessible for evaluation, pericardial
biopsy (surgical/pericardioscopy) and histological examination is more appropriate
test [26, 27, 34]. The sensitivity of pericardial biopsy as a diagnostic test for tuberculosis ranges from 10% to 64%. The probability of obtaining a denite bacteriologic result is greater in the early effusive stage [45, 181, 182, 204, 207].
Polymerase chain reaction can detect DNA or RNA of mycobacterium tuberculosis in pericardial uid [1, 7, 8, 14, 46, 47, 106–109, 127–130, 132, 149]. However
current evidence suggests that polymerase chain reaction is prone for false positive
results and less sensitive than established methods [107, 120–122, 153]. Serum anti-
body test against specic tuberculoprotein epitopes is another diagnostic test, which
also does not have a signicant advantage over existing methods [131, 132].
Ng and colleagues have demonstrated the limited use of tuberculin skin test in
nonendemic areas [131, 132]. In tuberculosis endemic areas, tuberculin skin testing
lacks any diagnostic value, because of the likelihood of cross sensitization from
myocobacteria [131, 132]. Another suggested method is an enzyme-linked immunospot test that detects T-cells specic for myocardium tuberculosis antigen in other
body uids. However, its clinical signicance is not studied in detail [35].
Reuter and associates have developed a diagnostic index score to assess the probability of tuberculosis in patients with pericarditis from endemic areas (Table20.1)
[144–148]. Independent predictors of tuberculous pericarditis (with diagnostic
index score) are: fever (1), night sweats (1), weight loss (2), serum globulin
level>40g/L (3), and peripheral leucocyte count <10×109/L (3). A total score of
≥6 indicates tuberculous pericarditis with 86% sensitivity and 85% specicity. This
scoring system has a better diagnostic efciency than culture of pericardial uid or
pericardial histology [144–148].
Non-specic ST-T wave changes are seen in virtually all cases of tuberculous
pericardial effusion [193]. A prolonged PR-interval and an ST-segment elevation
are noted in 9% to 11% of cases. The presence of microvoltage (complexes <5mm
in limb leads and<10mm in precordial leads) suggests a large pericardial effusion.
Atrial brillation is usually present.
Table 20.1 Tuberculous
pericarditis diagnostic index
[144–148]
Variables Score
Weight loss 1
Night sweats 1
Fever 2
Leucocyte count <10×109/L 3
Serum globulin >40g/L 3
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