Pericarditis
Inflammatory-Pericarditis
Usually an infective aetiology. As with non-inflammatory accumulation of fluid the main complication is the restriction of ventricular movement. Clinical signs seen are therefore those of circulatory failure along with pyrexia and a general depression.
Spread of infectious agent may be:
- Haematogenous; following generalised infection. Most often seen in cattle and pigs.
- Extension of infection form surrounding tissues; for example from the lungs, pleura, mediastinum.
- Extension of infection from myocardium; rare.
- Traumatic penetration of the pericardium;
- Foreign bodies from the oesophagus or reticulum in cattle; traumatic reticulo-peritonitis.
- Fractured ribs; E.g. RTAs in small animals, horses etc.
Pericarditis can be subdivided into two main categories:
Fibrinous pericarditis
Most common form. Grey strands of fibrin cover the epicardium and little fluid accumulates. Close apposition of the parietal and visceral pericardium layers allows adhesion formation within approximatley 7-10 days. Such adhesions may resolve with little residual pathology or may become focal or diffuse adhesive pericarditis lesions.
Fibrinous pericarditis produces a crackiling sound on auscultation.
Suppurative pericarditis
Purulent pericarditis indicates the presence of pyogenic organisms E.g. Staphs Usually occurs in cattle as a result of traumatic penetration of the pericardial sac with a sharp metallic object or wire. This is Traumatic reticulo-peritonitis → Traumatic Pericarditis Death usually occurs before organisation and a constrictive pericarditis can become apparent.
Sequalae of pericarditis:
- Resolution with no further clinical significance.
- Adhesion: organisation of fibrin. May lead to a bread and butter appearance.
- Constriction: gradual cardiac tamponade will occur.