Infective Endocarditis

Infective Endocarditis: colonization of heart valves with microbiologic organisms leading to the formation of friable, infected vegetations and frequently valve injury.

Pathogenesis:

Bacteremia is a prerequisite for IE. They may derive from an infection elsewhere in the body; IV drug abuse; dental or surgical procedures; or micro-injuries to gut, urinary tract, oropharynx, or skin.

Predisposing factors:

• Cardiac congenital anomalies (e.g. tight shunts, VSD, ASD)

• Previously damaged valves (e.g. rheumatic heart disease)

• Prosthetic valves

• Indwelling catheters

• Neutropenia

• Immunosuppressed states

Clinical features:

Acute endocarditis: (highly virulent organisms e.g. S. Aureus)

• Affects normal and abnormal heart  severe septicaemia, destruction of valves and high mortality (>50% even + treatment) – sudden complete failure (zero CO).

• Severe febrile illness, high swinging temperature, rapidly changing heart murmurs, severe HF.

Sub-acute endocarditis: (caused by moderate to low virulent organisms e.g. S. viridans)

• Affects abnormal or previously injured valve, causing less valvular destruction than acute IE.

• Persistent fever (of unknown origin at first) general malaise, loss of weight.

Complications:

Three distinct sets of processes bring about the presentation and complications of IE.

Embolism: mostly bland ( infarction) but in acute IE, may be infected and cause metastatic abscesses.

• Cerebral emboli (20%) – may be fatal

• Renal emboli (50%) – less severe.

Mycotic aneurysm can occur when an infected embolus gradually erodes the wall of the vessel – may rupture.

Direct injury:

• To valves – insufficiency or stenosis with CHF.

• To myocardium and aorta – ring abscess, perforation.

Immune complex mediated: circulating IC can cause

• Skin vasculitis to purpuric haemorrhages

• Joint involvement with arthralgia

• Renal injury – glomerulonephritis can result in nephritic syndrome, renal failure or both.

Category: Pathology Notes