Acute serofibrinous pericarditis.

The viruses typically causing this disease

produce a relatively mild inflammatory reaction that is associated with focal
damage to the adjacent myocardium. The response varies from a small amount
of serous fluid with mononuclear cells and fibrinogen to a large, neutrophil-rich,
bloody effusion. The tissue damage is the result of:
1. Direct cellular damage by the infecting virus
2. Destruction of viral-infected cells by sensitized T-lymphocytes
3. Antibody-dependent, cell-mediated cytotoxicity (null cell-dependent).
Mild fibrosis and occasional adhesions between visceral and parietal surfaces
may mark the healing of viral pericarditis. However, such a fibrotic reaction
rarely gives rise to a constrictive pericarditis. The disease is self limiting and
rarely fatal.
Acute purulent pericarditis. The bacteria typically causing this disease produce
a relatively strong rapidly progressing purulent reaction. The purulent material
contains large numbers of polymorphonuclear leukocytes in a large volume of
effusion. The tissue damage is the result of:
1. Toxin and enzyme production by the bacteria
2. Myocardial damage
3. Rapidly progressing cardiac tamponade
Healing is associated with extensive fibrosis that may progress to a chronic,
constrictive pericarditis. The mortality rate exceeds 50%.
Chronic pericarditis. This is most commonly caused by M. tuberculosis. About
5% of patients with pulmonary tuberculosis will have pericardial involvement.
The early granulomatous stages are associated with large pericardial effusions
(> 300 ml) that are typically serosanguinous and contain a predominance of
mononuclear cells. As the disease evolves, the inflammatory process becomes
chronic; fusion of the parietal and visceral pericardium may result, yielding
constrictive pericarditis and circulatory failure.

CLINICAL SYMPTOMS AND SIGNS:

Acute serofibrinous pericarditis gives rise to:
a. Chest pain - rapid in onset, persistent for several hours to days. It is
worse during
inspiration and recumbency but improves with leaning forward. The
pain is usually in the
upper abdominal region overlying the stomach and may be sharp, dull,
constricting and/or
crushing making clinical differentiation from myocardial infarction
difficult. Radiation of
pain to the left trapezius ridge is particularly characteristic.
 b. Fever - not prominent
c. Malaise
d. Pericardial friction rub - this is usually a triphasic sound that resembles
scratching or the
crunch of footsteps on cold snow.
Acute purulent pericarditis gives rise to:
a. Little, if any, chest pain
b. Prominent fever and chills from the severe underlying infection
c. Cardiac tamponade which leads to:
(1) Dyspnea
(2) Agitation
(3) Orthopnea
(4) Cough
d. Pericardial friction rub - occurs in less than 50% of patients.
Chronic pericarditis is generally due to M. tuberculosis and the symptoms are
those of tuberculosis. These include:
a. Fever
b. Night sweats
c. Weight loss
d. Fatigue
e. Progressive circulatory failure due to:
(1) Slowly progressing dyspnea
(2) Ascites
(3) Edema
In general all types of pericarditis may result in:
a. Abnormal heart sounds other than those due to pericardial friction
b. Pericardial effusion that causes:
(1) Decreased or muffled heart sounds
(2) An area of dullness to percussion at the tip of the left scapula
(Ewart's sign)
(3) Pulsus paradoxes
(4) Cervical venous pressure increase with inspiration (Kussmaul's
sign)
(5) Abnormal EKG
TREATMENT:
The treatment includes bed rest, control of pain with non-steroidal anti-
inflammatory agents and anti-microbial therapy based on the species of the
infecting agent and its sensitivity pattern.