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CHRONIC PERICARDITIS – REPORT
CASES
Doina Butcovan¹, Catalina Arsenescu²,
Cleopatra Borza
Gr. Tinica², E. Sandica², V. Diaconescu²,
GIM Georgescu²
...
We report 8 cases of chronic pericarditis diagnosed at Cardiology Center
Iasi. The purpose of the study was to establish the disease and etiological
diagnosis. The study was made on multiple cardiac investigations and on
surgical biopsic specimens, obtained by making a pleuro-pericardial window
and using routine morphological techniques. We evidentiated 2 cases of
constrictive pericarditis and 6 cases of effusive-constrictive pericarditis.
We specified their aetiology, as well. The microscopical examination revealed
5 cases of fibrinous pericarditis with tendency to organisation and 2 cases
of calcified fibrotic pericardial thickening, all these morphological appearences
being unspecific for an aetiological agent; in a case, we evidentiated
a characteristic morphological aspect, corresponding to tuberculous pericarditis.
The study revealed the importance of establishing the etiological disease
diagnosis for indicating a target effective treatment. Key words: tuberculous
pericarditis, constrictive pericarditis, effusive-constrictive pericarditis.
INTRODUCTION
The chronic pericarditis is
a pericardial inflammatory disease caused by different etiological agents.
Silver (1) described two main forms: constrictive pericarditis and effusive-constrictive
pericarditis. Constrictive pericarditis is a fibrous thickening of the
pericardium with obliteration of the pericardial sac and the restriction
of the diastolic filling (1). It has the same causes as acute pericarditis:
idiopathic (42%), post-iradiation (31%), post-surgery (11%), post-infectious
(6%), connective tissue diseases (4%), neoplasms (3%), dialysis (2%), sarcoidosis
(1%), etc (2, 3). Clinical picture is often asymptomatic, but sometimes,
the patient may present, increased pulmonary venous pressure (dispnea with
ortopnea), increased systemic venous pressure (turgescent jugular veins,
pleural effusion, hepatomegaly, ascite and lower leg oedema) (3, 4). The
diagnosis is based on electrocardiography, X ray chest, echocardiography
and morphology, as well (5, 6). Morphologically, on pericardial biopsy
are evidentiated two subtypes of chronic pericarditis: adhesive pericarditis
(pericardial fibrosis and adhesions) and constrictive pericarditis (fibrous
thickening of the visceral pericardium associated with calcifications which
are present in 50% of cases)(5). This form have to be differentiated by
restrictive cardiomyopathy. Effusive-constrictive pericarditis is defined
as a form of constrictive pericarditis characterised clinically and hemodinamicaly
through signs of cardiac tamponade which is not resolved by pericardiocenthesis
(1). Pericardial effusion has between 50 ml and over 1000 ml, being caused
by the same etiological agents enumerated earlier (2, 3). Clinical picture
is dominated by cardiac tamponade and clinical examination revealed a paradoxus
pulsus (6). Morphologically, pericardial effusions may be serous, chilous
and hemorrhagic (5, 6). The recommended treatment consists in resection
of the epicardial fibrous tissue (7, 8).
MATERIALS AND METHODS
In 8 patients, 4 women and 4
men, with ages between 5 and 78 years, presenting with progressive dispnea
and malaise, and having a previous diagnosis of pleuro-pericarditis of
unknown aetiology, the repeated hospital admissions were indicated for
draining the pleuro-pericardial fluid.
The surgical biopsic specimens,
obtained through a pleuro-pericardial window, were fixed in buffered 10%
formalin for 12 hours and quite totally sampled. Samples were processed
using routine paraffin embedding, cutting (5 mm) and hematoxilin-eosin
(HE) and Van Gieson (VG) staining.
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¹ Department of Pathology - UMF – Iasi,
² Cardiology Center Iasi
RESULTS AND DISCUSSIONS
The study represents 8 report
cases of chronic pericarditis, of unknown cause, presenting for repeated
hospital admission for paracenthesis.
Physical examination, revealed the most common found
physical findings, as fever and tachycardy, cardiomegaly (50%), followed
by hepatomegaly. The pericardial friction rub was soft and distant heart
sounds were common. Pleural effusions and peripheral oedema were evident,
as well, while patients with constrictive pericarditis had inspiratory
swelling of the neck veins known as Kussmaul’s sign. Similar findings were
reported by Muir (9) in a study of 27 patients. Hepatomegaly was found
in 95%, jugular venous distention in 88%, ascites in 73%, oedema in 25%,
and a pericardial friction rub in 18%.
The laboratory tests were not
relevant for a specific agent. In circulating blood, we found only a mild
anaemia and an average total white blood cell count of 7.000, similar resulting
were reported by Hageman (10) in his study.
The chest X-ray, evidentiated
an enlarged cardiac silhouette in 50% of cases, comparative with 40 of
48 of patients described by Hageman (10), and 100 of 103 patients described
by Strang (8). Cardiomegaly was usually due to pericardial effusion or
effusive-constrictive pericarditis. We revealed in 5 cases an associate
pleural fluid reaction, predominant to the bases, while Muir (9) found
radiological evidence of pleural effusion in 2 of 35 patients in his series.
In our series of 8 patients, only 1 (12,5%) had an evidence of a right
micronodular apical sequel, while in the series of the Strang (8), 32%
of 19 cases had radiological evidence of active pulmonary tuberculosis.
Generally, the echocardiografic
findings were not specific. If, in the early fibrinous phase the echocardiogram
was normal, later, we found evidences of pericardial effusion with some
adhesions or pericardial thickening (6 cases), while Brisson (11) in his
series, of 13 from 17 patients, noted moderate or large effusions, 4 patients
having evidence of tamponade. In our series, the two remaining cases, had
constrictive pericarditis, as Symmers (2) who found similar pericardial
thickening to his cases. Computed tomographic scanning also gave us informations
concerning the cause of a pericardial effusion and thickening, in a case.
In our series of 8 patients,
pericardial fluid was examined in 3 cases. Acid-fast bacilli were not found
on stained smear. The fluid was usually an exudate, with a high protein
content. There was a fluid increased leukocyte count, with lymphocytes
and monocytes predominating, with slight elevation of polymorphonuclear
leukocytes. The fluid was serosanguineous in a case, and even grossly hemorrhagic
in another case. We didn’t find tubercle bacilli on stained smear; in this
case pericardial biopsy remained an important diagnostic tool. But, in
a case, we evidentiated characteristic tuberculous lesions on histologic
examination of the pericardium. Brisson (11) recommended a method based
on DNA amplification, that may be used on sputum, or lymph node biopsy
material, to provide a more rapid diagnosis. Virmani (5) appreciated, the
diagnosis is probable when there is evidence of pericarditis in a patient
with tuberculosis demonstrated elsewhere in the body. We had 2 cases with
history of pulmonary tuberculosis, with negative stained smears and cultures
of sputum for tubercle bacilli, while positive sputum cultures were found
in 11% of 184 patients in the study by Strang (8). Strang considers tuberculin
skin tests, chest roentgenograms, electrocardiograms, and differential
cell count in the pericardial fluid may be useful screening tests in patients
suspected of having tuberculous pericarditis. So, he evidentiated, in adults,
especially those more than 60 to 65 years old, as many as 30% of patients
with idiopathic pericarditis a positive skin test. In our study, a patient,
without tuberculous history and with negative skin test, responded very
well to tuberculostatics, demonstrating tuberculous etiology. Two cases
had a sepsis history and another one had evidences of chronic uraemia.
We couldn’t demonstrate a specific etiological agent, in a case, noted
as idiopathic case.
The surgically intervention
evidentiated a tickened fibrous pericardium and moderate effusion requiring
a pleuro-pericardial drainage and a pleuro-pericardial window. The histological
examination of the surgical biopsic specimen revealed different lesions,
illustrated by few photogrames: 5 cases of fibrinous pericarditis with
tendency to organisation (fig 1) ;
at these cases the persistence of the inflammation was demonstrated morphologically
by a hyperplastic mesothelial reaction (fig.2) ;
2 cases of constrictive pericarditis, demonstrated by fibrous calcified
pericardial thickening; in a case, we revealed a thick pericardium through
an extensive fibrosis enclosing multiple specific tuberculous granulomas
(fig. 3, 4) .
Medical treatment was the first
pattern of choice. Corresponding with Waller recommendations (4), for the
definite or probable cases of tuberculous pericarditis, the patients were
hospitalized and observed for evidence of cardiac tamponade. In tuberculous
pericarditis, a triple drug therapy is generally recommended for a minimum
of 9 months, with at least 6 months of therapy following culture conversion.
Hageman (10), also added a 40 to 60 mg dose of prednisone daily in divided
doses to antituberculous therapy when there is persistent or recurrent
pericardial effusion, despite therapy with antituberculous drugs. Using
adrenal corticosteroids he was able to avoid pericardial resection .
Surgical treatment was the second pattern of choice.
Symmers (2) recommended the placement of a pericardial window for both
diagnostic and therapeutic purposes in patients with chronic pericarditis.
If pericardial thickening is present, pericardiectomy was recommended by
Waller (4). Surgical resection of the pericardium was indicated early for
recurrent or life-threatening tamponade, or later when there was a continuing
elevation of systemic venous pressure after 4 to 6 weeks of drug therapy.
Waller reported that one third of patients presenting with hepatomegaly
and oedema responded to medical treatment; the others required surgical
treatment. In the latter case, continued venous pressure elevation may
be the result of cardiac tamponade, constrictive pericarditis, or effusive-constrictive
pericarditis. Since, the surgical mortality rate appears higher in the
late calcific stage of constrictive pericarditis, Muir (9) recommended
pericardial resection to be performed early. Pericardiectomy for all patients
with tuberculous pericarditis has been recommended by some authors (6,
7), as well.
CONCLUSIONS
The study revealed the importance of establishing the
etiological disease diagnosis for indicating a target effective treatment.
REFFERENCES
1. Silver MD. Pericarditis. In Silver MD. Gotlieb AI. Eds. Cardiovascular
Pathology. Churchill Livingstone 2001, 385-389.
2. Symmers WSC. The pericardium. In: Symmers WSC. Cardiovascular
System. Springer-Verlag, New York, 1980, 672-675.
3. Colin MB. Pericarditis. In: Colin MB Ed. Heart Pathology.
Churchill Livingstone 1980, 265-272.
4. Waller BF. Pericardial Disease. In: Waller BF. Pathology of the
Heart and great vessels, The Mosby Company, 1998, 1173-1178.
5. Virmani R. Tuberculous Pericarditis. In: Allen Burke and Renu Virmani.
Atlas of Cardiovascular Pathology. Ed. AFIP. Washington DC 1966: 104-106.
6. Blomm J. Pericarditis. In: Sternberg SS. Diagnostic Surgical Pathology.
Ed. Raven Press, 1944: 1216-1217.
7. Gilbert E. Pericarditis. In: Silverberg SG. Principles and Practice
of Surgical Pathology and Cytopathology. Ed. Churchill Livingstone 1997,
1318-1321.
8. Strang JIG, Kakaza HS, Gibson DG, et al. Controlled clinical trial
of complete open surgical drainage and of prednisolone in treatment of
tuberculous pericardial effusion. Lancet. 1988; 2: 759-764
9. Muir P, Nicholson F et al: Chronic relapsing pericarditis. Lancet
I: 804-7, 1989.
10. Hageman JH, D’Esopo ND, Glenn WL. Tuberculosis of the pericardium
on a long term analysis of forty-four proved cases. N Engl J Med. 1964;
270: 327-332
11. Brisson NA, Gicquel B, Le Cossier D. Rapid diagnosis of tuberculosis
by amplification of mycobacterial DNA in clinical samples. Lancet 1989;
2: 1069-1071
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