Pericarditis is usually secondary to
disorders involving the heart, or adjacent mediastinal structures (Eg:
Myocardial infarct, trauma, radiation, tumour or infections).
Rarely, it may be due to systemic
abnormalities (uremia, diabetes mellitus, chronic nephritis, severe
anemia , autoimmune disease).
HISTOPATHOLOGY REPORTING OF PERICARDIAL SPECIMEN
Classification of Pericarditis on the basis of etiological
a) Bacterial b) Viral c) Other infections
Rheumatic fever b) Other connective tissue disorder
a) Uremic b) Myxedema c) Gout.
Traumatic (including after cardiac surgery)
Acute pericarditis is most often of
Chronic pericarditis is seen in
tuberculosis and fungal infections, which on healing may lead to
damaging adhesion. Terminal pericarditis is seen in chronic
debilitating diseases e.g. Uremia,
Acute Pericarditis :
N Engl J Med 2004; 351:2195-2202, Nov 18, 2004
It may occur in several forms:
Serous pericarditis :
usually consists of 50 to 200 ml of slowly accumulating exudates
characteristically produced by nonbacterial involvement, including
rheumatic fever, systemic lupus erythematosus, tumours, uremia
and primary viral infection (Eg. Coxsackie). Microscopically, there is
scant epicardial or pericardial acute and chronic inflammatory
Fibrinous and serofibrinous
is the most common clinical form, seen in myocardial infarct with a
pericardial friction rub. Exudate may be completely resolved or be
organized causing adhesive pericarditis.
This is due
to bacteria, fungus or parasitic infection. Infection reaches by
direct extension, by hematogenous or lymphatic route from the
neighbouring areas of infection e.g. Pneumonia, empyema, lung abscess,
subphrenic abscess, liver abscess etc or during cardiotomy.
causative organisms are Staphylococci, Streptococci, and Pneumococci.
pericarditis is composed of 400 to 500 ml of a thin to creamy pus with
erythematous, granular serous surfaces.
The patient presents
with fever, rigor and a friction rub.
organizes and may produce mediastinopericarditis or constrictive
is composed of an exudates of blood admixed with
fibrinous to suppurative effusion. Most commonly it follows cardiac
surgery or is associated with tuberculosis or malignancy. It usually
organizes with or without calcification.
form is due to tuberculosis (by direct extension from neighbouring
lymphnodes) or less commonly, mycotic infection. This type most
frequently, causes fibrocalcific constrictive pericarditis.
Acute pericarditis may heal by
resolution or by pericardial fibrosis ranging from a thick, pearly,
nonadherent epicardial plaque , to thin delicate adhesion to massive
adhesions. In some cases the cause is unknown.
chronic pericarditis may be of the following types:
Chronic pericarditis with adhesion
between parietal and visceral pericardium is called adhesive
pericarditis. These are mostly seen in rheumatic disease. Less
commonly, it may be due to infection by pyogenic bacteria,
tuberculosis etc. In some cases, the cause is unknown.
Here, the pericardial sac is
obliterated due to adhesion between two layers of pericardium as well
as between parietal pericardium and surrounding mediastinal
structures, chest wall & diaphragm. The heart thus contracts against
all the surrounding attached structures leading to hypertrophy and
There is marked thickening of the
parietal pericardium with less involvement of visceral pericardium
causing constriction of great vessels entering and leaving heart.
The pericardial space is obliterated by
a dense fibrous tissue, which is often calcified.
Cardiac hypertrophy and dilation cannot
occur because of the dense enclosing scar and the heart becomes
smaller. Tuberculosis is the most common cause.
it may be due to pyogenic infection and in some, the cause is unknown
but never rheumatic.
The patients of pericarditis may
develop ascites and due to long standing ascites, liver & spleen are
coated with fibrin.
Later, there is fibrosis of the liver
(cardiac cirrhosis). Pleura may be involved similarly.
This polyserositis is known as Pick’s
A Clearer View of Effusive–Constrictive Pericarditis.
N Engl J Med 2004; 350:435-437, Jan
Engl J Med 2004; 350:469-475, Jan 29, 2004.