Endocarditis: Pathology review

Last updated: November 01, 2022

Endocarditis: Pathology review

Semiomed 2

Semiomed 2

Endocarditis: Pathology review
Endocarditis
Mitral valve disease
Aortic valve disease
Tricuspid valve disease
Pulmonary valve disease
Valvular heart disease: Pathology review
Atrial septal defect
Ventricular septal defect
Tetralogy of Fallot
Coarctation of the aorta
Supraventricular arrhythmias: Pathology review
Atrial flutter
Atrial fibrillation
Ventricular fibrillation
Ventricular tachycardia
Long QT syndrome and Torsade de pointes
Wolff-Parkinson-White syndrome
Atrioventricular block
Bundle branch block
Myocarditis
Trypanosoma cruzi (Chagas disease)
Cardiomyopathies: Pathology review
ECG cardiac infarction and ischemia
Angina pectoris
Stable angina
Unstable angina
Prinzmetal angina
Myocardial infarction
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Pericarditis and pericardial effusion
Recurrent pericarditis (NORD)
Pericardial disease: Pathology review
Cardiac tamponade
Hypertension
Hypertension: Pathology review
Heart failure: Pathology review
Aortic dissections and aneurysms: Pathology review
Aneurysms
Aortic dissection
Coronary artery disease: Pathology review
Buerger disease: Year of the Zebra
Peripheral artery disease: Pathology review
Raynaud phenomenon
Deep vein thrombosis
Chronic venous insufficiency
Gastroesophageal reflux disease (GERD)
Esophageal cancer: Year of the Zebra
Achalasia: Year of the Zebra
Esophageal disorders: Pathology review
Peptic ulcer
Zollinger-Ellison syndrome
Gastric cancer
Malabsorption syndromes: Pathology review
Celiac disease
Ulcerative colitis
Crohn disease
Inflammatory bowel disease: Pathology review
Colorectal cancer
Colorectal polyps and cancer: Pathology review
Diverticulosis and diverticulitis
Irritable bowel syndrome
Small bowel ischemia and infarction
Bowel obstruction
Hemorrhoid
Portal hypertension
Cirrhosis: Pathology review
Primary biliary cholangitis
Jaundice: Pathology review
Alcohol-associated liver disease
Ascending cholangitis
Acute cholecystitis
Chronic cholecystitis
Primary sclerosing cholangitis
Acute pancreatitis
Chronic pancreatitis
Pancreatitis: Pathology review
Pancreatic cancer
Pancreatic neuroendocrine neoplasms
Diabetes mellitus
Nephritic syndromes: Pathology review
Nephrotic syndromes: Pathology review
Alport syndrome
Fabry disease (NORD)
Acute pyelonephritis
Chronic pyelonephritis
Diabetic nephropathy
Membranous nephropathy
Polycystic kidney disease
Renal failure: Pathology review
Esophageal cancer
Diabetes mellitus: Pathology review

Transcript

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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.

Another situation where NBTE can happen is with systemic lupus erythematosus,

This is an autoimmune disease involving antigen-antibody complexes, and in this case they settle in the endocardium and cause inflammation, leading to a particular type of endocarditis, called Libman-Sacks endocarditis.

Remember that it’s associated with large vegetations, sometimes described as verrucous vegetations since they look like warts.

Now, infective endocarditis occurs when pathogens find their way to the endocardium, typically from the heart valves.

Every day, there are opportunities for pathogens like bacteria and fungi to get into the bloodstream, but this is not a problem because they are usually few in number and can easily be cleared by our immune system.

However, sometimes a larger quantity of microbes can get into the bloodstream, like if a person has an obvious open wound or an abscess, during a dental or surgical procedure, or use of infected needles.

These microbes can float around in the blood for long enough to reach the heart.

A particular site that’s prone to infections is the heart valve which is supplied by tiny blood vessels.

Now, most often the valves on the left side are affected, the most common being the mitral valve and than the aortic valve.

This is sometimes due to predisposing conditions, with the most common one in high- and middle-income countries being mitral valve prolapse and, less often, bicuspid aortic valves.

So on these valves bacterial colonies, clots and fibrin, can also form vegetations.

They usually present on the mitral or aortic valve, but what’s special here is that they can present on either surface of the valve, though most commonly, on the undersurface.

Let’s now go over the microbes that can cause endocarditis. Viridans Streptococci , especially Streptococcus sanguinis, is the most common cause.

They have low virulence, are found in the mouth, and they typically only affect valves that have had some previous damage, so think older patients or those with a history of heart valve disease after a dental procedure.

That’s because S. sanguinis uses special molecules on its surface, called dextrans, that bind to fibrin-platelet aggregates on damaged heart valves.

This usually results 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 it can infect damaged valves.

They are often introduced via surgical procedures, wounds, or intravenous drug use, and often affects the tricuspid valve.

S aureus causes large vegetations that can destroy the valves.

Next we have Staphylococcus epidermidis.

A high yield fact is that this bacteria loves foreign prosthetic material, like prosthetic heart valves and this could be your best clue on a test.

This bacteria is usually introduced into the body at the time of heart valve surgery and it literally creates an extracellular matrix around itself called biofilm which allows it to stick around on the valve.

Another common point of entry into the body is through an infected intravenous catheter.

Enterococcus is a part of the normal urogenital flora.

But following genitourinary catheterization or surgery, it can escape into the bloodstream and go on to cause enterococcal endocarditis on either damaged or healthy valves.

Another bacterial species is Streptococcus gallolyticus, previously known as Streptococcus bovis which is normally found in the gut flora.

But, when there’s colorectal bleeding, like with colorectal cancer, these gut bacteria can migrate across the gut lining and into the bloodstream, which can develop into endocarditis.

A high yield fact to remember is that in case of S gallolyticus endocarditis, we need to do a colonoscopy to look for colorectal cancer.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Management Considerations in Infective Endocarditis" JAMA (2018)
  4. "Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications" Circulation (2015)
  5. "2015 ESC Guidelines for the management of infective endocarditis" European Heart Journal (2015)
  6. "Poor oral hygiene as a risk factor for infective endocarditis–related bacteremia" The Journal of the American Dental Association (2009)
  7. "Clinical Presentation, Etiology, and Outcome of Infective Endocarditis in the 21st Century" Archives of Internal Medicine (2009)
  8. "2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease" Journal of the American College of Cardiology (2017)
  9. "Antibiotic prophylaxis for infective endocarditis: a systematic review and meta-analysis" Heart (2017)