Cardiac Path Online
Pathology of Pericardial Disease
pericardium provides an enclosed lubricated space for the heart and
functions to fix the heart in the chest cavity relative to adjacent
Pericardial pathophysiology is often manifested in a spectrum of distinct cardiac and systemic disease states.
The pericardial response to injury typically involves a spectrum of inflammation with both acute and chronic features and/or fluid accumulation.
Recent advances in imaging methods have refined the diagnosis and therapy of pericardial disease.
The diseases of the pericardium include inflammatory conditions and effusions. Important features of these lesions have been briefly discussed:
Pericarditis is usually secondary to disorders involving the heart, or adjacent mediastinal structures/
(Example: Myocardial infarct , trauma, radiation, tumour or infections).
Rarely, it may be due to systemic abnormalities (uremia, diabetes mellitus, chronic nephritis, severe anemia , autoimmune disease).
Acute pericarditis is most often of viral origin.
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 :
It may occur in several forms:
This form 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 (Example: Coxsackie).
Microscopically, there is scant epicardial or pericardial acute and chronic inflammatory infiltrates.
Fibrinous and Serofibrinous Pericarditis:
This 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.
Purulent (suppurative) 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.
Example: Pneumonia, empyema, lung abscess, subphrenic abscess, liver abscess etc or during cardiotomy.
Most common causative organisms are Staphylococci, Streptococci, and Pneumococci.
Purulent 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.
It usually organizes and may produce mediastinopericarditis or constrictive pericarditis.
This 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.
This 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.
Accordingly, chronic pericarditis may be of the following types:
1. Adhesive pericarditis :
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.
2. Adhesive Mediastinopericarditis :
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 dilation.
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.
Occasionally, 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 disease.
II- Pericardial Effusion:
Visit related post -Pathology of Pericardial Effusion
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