Endocarditis: Pathology review

Two people came into the cardiology ward.

One of them was 25 year old Darren, who came in with a fever, chills and fatigue.

On the clinical examination, his fingernails had splinter hemorrhages and the palm of his hands had some erythematous flat lesions.

There were also some track marks on his forearm.

The other one is 75 year old Anna, who also had a fever and the same splinter hemorrhages and erythematous flat lesions that we previously saw.

On auscultation, a heart murmur was heard.

On her history, she said she was at the dentist 2 weeks ago.

Okay, so both people likely have endocarditis, or inflammation of the inner layer of the heart.

Remember that the heart’s wall is made up of three layers, the epicardium being the outermost layer, then the myocardium, and the endocardium, which is the layer that gets inflamed.

The inflammation can affect the heart valves, the mural endocardium or even prosthetic valves!

The most common cases of endocarditis are due to a microbial infection, and this is called infective endocarditis but in some cases, endocarditis can also be non-infective.

For non-infective endocarditis, the first step is usually damage to the endocardium.

Damage exposes the underlying collagen and tissue factor, which causes platelets and fibrin to adhere, which forms tiny blood clots.

This is called Nonbacterial Thrombotic Endocarditis or NBTE.

Tiny clots and fibrin can develop into vegetation, especially on the heart valves which damages them and makes it harder for them to open or close.

Although the exact cause of NBTE is unknown, it’s thought that a proinflammatory state where cytokines levels are elevated can increase clot formation.

This can happen with hypercoagulable states, like when there’s a malignancy, especially pancreatic adenocarcinoma.