Endocarditis – causes, symptoms, diagnosis, treatment, pathology

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much more. Try it free today! Endocarditis means “inflammation of the
inner layer of the heart”. The heart wall’s made up of three layers,
the epicardium being the outermost layer, then the myocardium, and then the endocardium,
which is the layer that gets inflamed. It turns out that most cases of endocarditis
are due to a microbial infection of the endocardium. Any area of the heart that is exposed to turbulent
blood flow (such as a narrowed cardiac valve or a septal defect) could be affected by endocarditis. Turbulence of blood flow causes damage to
the endocardial lining. That damage exposes the underlying collagen
and tissue factor, which causes platelets and fibrin to adhere, which forms this tiny
thrombosis or blood clot. This is called Nonbacterial Thrombotic Endocarditis
or NBTE, and it’s nonbacterial because it happens even before the bacteria shows up. Then, a microbe has to first get into the
bloodstream, and that might happen if a person has an obvious open wound or an abscess, a
dental or surgical procedure, or injection with an infected needle or infected substance
usually while using illicit drugs. The valves are often affected because they
are often the site of turbulent blood flow. Most often the valves on the left side are
affected, the mitral valve and the aortic valve, sometimes due to predisposing conditions
like mitral valve prolapse and bicuspid aortic valves. Risk factors for developing endocarditis include
having prosthetic valves, having a congenital cardiac defect involving the valves, having
damage to the valves from rheumatic heart disease, and finally intravenous drug use
can put valves at risk. Although most cases of tricuspid valve endocarditis
are due to intravenous drug use, the majority of intravenous drug using patients with endocarditis
have left sided valvular endocarditis. Even without using intravenous drugs, there
are many opportunities for microbes to get into the bloodstream whether it’s through
brushing your teeth and having them slip into the gums, or having them slip in through your
gut or lungs, whatever the case they regularly make their way into the body. It’s not usually not a problem though, because
it’s a small amount and can easily be killed by our immune system, but occasionally they
float around in the blood for long enough to find an NBTE which serves as a perfect
location for them to attach to and set up an infection – called a vegetation. To attach to it a lot of bacterial species
use proteins on their surface called adhesins, that let them stick to the valve as well as
stick to one another. They also create an extracellular matrix around
themselves – called biofilm which allows them to literally stick together and from a large
clump of bacteria that can behave like a colony. Usually these guys stick to areas of lower
pressures, since it’s easier to adhere. So let’s take mitral valve regurgitation,
where blood flows backward from the higher pressure left ventricle to the lower pressure
left atrium. So in this case, vegetations will tend to
form on the lower pressure atrial surface. Not only that, though, they’ll form on the
edge of the opening, and this is because of the venturi effect. The venturi effect describes how fluid pressure
decreases as it flows through a narrowed opening, while its velocity increases. So as blood forces it’s way through the
opening, pressure is lower near the edges. If the person had aortic regurgitation, meaning
blood’s going from the higher pressure aorta to the lower pressure ventricle, then vegetations
would tend to be located on the lower pressure ventricular surface of the valve. Infective endocarditis used to be classified
into groups like acute and subacute based on how quickly the infection developed, but
nowadays the key is to identify that microbial cause of infection and to treat it as effectively
as possible. Viridans Streptococci is the most common cause. It’s virulence is low, it’s found in the
mouth, and they usually attack valves that have had some previous damage, usually resulting
in small vegetations which don’t destroy the valve. Staphylococcus aureus, on the other hand,
is a highly virulent bacteria that can be found on the skin, and this guy can infect
both damaged and healthy valves—often the tricuspid valve. S aureus causes large vegetations that can
destroy the valve, and is the bacteria most commonly contracted from intravenous drug
use. Next we have Staphylococcus epidermidis, which
is a bacteria that loves foreign prosthetic material, like prosthetic heart valves. One way that the bacteria gets into the body
is at the time of heart valve surgery and it literally sticks around on the valve. Another common point of entry into the body
though is through an infected intravenous catheter. Both of these scenarios usually happen in
a hospital, so this would be considered a nosocomial infection. Two other bacterial species are Enterococcus
faecalis and Streptococcus bovis which are both normally found in the gut flora. But, when somebody has severe colorectal disease,
like colorectal cancer or ulcerative colitis, these gut bacteria can migrate across the
gut lining and into the bloodstream, which becomes a setup for potential endocarditis. An even more unusual bacteria is Coxiella
burnetii which patients typically contract after exposure to infected animals like cows,
sheep, and goats. The bacteria initially causes a disease called
Q fever, but months or sometimes years after the initial Q fever, they can develop endocarditis,
but usually this is in high-risk people, like those that are immunocompromised, pregnant
women, and those with pre-existing heart valve defect, which makes it tricky to diagnose
unless there’s a reason to suspect it. Finally, a group of organisms that are less
commonly associated with endocarditis are the HACEK organisms. These guys are a group of gram-negative bacteria
that are also part of the normal flora of the mouth and throat. Each letter of HACEK stands for a different
genus—Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella. Finally, fungal endocarditis can also occur
but this happens mostly in intravenous drug using patients or patients in the intensive
care unit on multiple antibiotics. It’s important to remember fungi as routine
bacterial blood cultures won’t grow them. Now people with infective endocarditis almost
always have a fever, as well as a new heart murmur, that results from turbulent blood
flow past a damaged heart valve. Sometimes those vegetations can detach from
the valve, and little clumps of pathogens can float through the bloodstream—called
septic emboli. These guys can lodge under the fingernails,
causing splinter hemorrhages, or in the palms and soles of the feet, causing small painless,
flat, and erythematous lesions, called Janeway lesions. Separately there might be an immune reaction
with antigen-antibody complexes that form and deposit in different parts of the body. In the fingers and toes, these complexes can
lead to painful lesions called Osler’s nodes. In the eye these deposits can lead to Roth
spots, and in the kidney they can lead to glomerulonephritis (inflammation of the glomerulus
of the nephron). Diagnosing the cause of infective endocarditis,
typically involves getting multiple positive blood culture, which is literally growing
bacteria from a blood sample. Echocardiography can also be used to visualize
the heart and look for vegetations or more subtle clues like the way the valve’s moving. Depending on the organism that caused the
infection, a prolonged course of antibiotics will likely be used to try and wipe out the
infection but surgery might be needed for severe cases, especially when the valve dysfunction
causes heart failure or there are multiple emboli. It’s also important to prevent endocarditis
especially among high risk groups like for example those with prosthetic heart valves,
history of heart transplant and a history of endocarditis. Before dental procedures, sometimes these
people are recommended antibiotics, since remember that some of those microbes that
cause endocarditis live in the mouth. Finally, there’s Libman-Sacks endocarditis,
which is not infection-related. This one’s usually associated with systemic
lupus erythematosus, which is an autoimmune disease involving antigen-antibody complexes,
and in this case they settle in the endocardium and cause inflammation. These areas of inflammation can happen anywhere
on the valve surface or chordae tendineae, but typically happen on the mitral valve,
leading to mitral valve regurgitation. In this case, inflammation can also happen
on the atrial endocardium or ventricular endocardium. Alright, so to recap, endocarditis or inflammation
of the endocardium typically develops from bacterial infection—usually in this case
there’s first some damage or injury to the heart valves, which leads to thrombi which
serves as a place for bacteria to adhere to and cause inflammation. Sometimes, though, it can be nonbacterial,
one example being libman-sacks endocarditis, which is associated with Lupus—an autoimmune


  1. I liked the part on the venturi effect. You explained it well. It is an important aspect of developing endocarditis, and therefore it is good to completely understand it as a student. 👍😏

  2. Both endocarditis and myocarditis carry a roughly 1/4 risk of death, while pericarditis is anywhere from 1-40% if treated and nearly 100% if not.

  3. Some very important points have been left out, like Baker's score for diagnosing endocarditis, which antibiotics to use empiracally, more details on symptoms

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