Endocarditis: Pathology review

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Endocarditis: Pathology review

ETP Cardiovascular System

ETP Cardiovascular System

Introduction to the cardiovascular system
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
Fetal circulation
Cardiac muscle histology
Artery and vein histology
Arteriole, venule and capillary histology
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Cardiac work
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Electrical conduction in the heart
Cardiac conduction velocity
ECG basics
ECG rate and rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG normal sinus rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
Aortic dissection
Vasculitis
Behcet's disease
Kawasaki disease
Hypertension
Hypertensive emergency
Renal artery stenosis
Coarctation of the aorta
Cushing syndrome
Conn syndrome
Pheochromocytoma
Polycystic kidney disease
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
Hypertriglyceridemia
Hyperlipidemia
Chronic venous insufficiency
Thrombophlebitis
Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Truncus arteriosus
Transposition of the great vessels
Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Atrial septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications
Cardiomyopathies: Clinical
Congenital heart defects: Clinical
Valvular heart disease: Clinical
Infective endocarditis: Clinical
Pericardial disease: Clinical
Chest trauma: Clinical
Hypertension: Clinical
Pulmonary hypertension
Aortic aneurysms and dissections: Clinical
Raynaud phenomenon
Peripheral vascular disease: Clinical
Heart failure: Clinical
Coronary artery disease: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Fascia, vessels and nerves of the upper limb
Vessels and nerves of the forearm
Vessels and nerves of the hand
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Fascia, vessels, and nerves of the lower limb
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Ventilation
Ventilation-perfusion ratios and V/Q mismatch
Gas exchange in the lungs, blood and tissues
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Trypanosoma cruzi (Chagas disease)
Yellow fever virus
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Arteriovenous malformation
Cerebral circulation

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Questions

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A 36-year-old man presents to the emergency department with fever, chills, and cough of three days duration. The patient uses intravenous heroin regularly and reports he last used heroin earlier today. He is currently living in a homeless shelter. Temperature of 38.7 °C (101.6 °F), pulse is 105/min, respirations are 22/min, blood pressure is 100/63 mmHg, and oxygen saturation is 91% on room air. On physical examination, the patient appears disheveled. Erythematous lesions are noted on the chest and arms bilaterally. Rales are appreciated in the lungs bilaterally, and a holosystolic murmur is appreciated at the left lower sternal border. Laboratory values are demonstrated below:  
 
 Laboratory value  Result 
Complete Blood Count, Serum 
 Hemoglobin  12.5 g/dL 
 Hematocrit  40.5% 
 Leukocyte count  18,100 /mm3 
 Platelet count  250,000/mm3 
Inflammatory Markers, Serum 
ESR                 44 mm/hr 
 CRP  18 mg/L 
Electrolytes, Serum 
                  Sodium                131 mEq/L 
               Potassium                 3.6 mEq/L 
                 Chloride                 94 mEq/L  
              Bicarbonate                 20 mEq/L 
                 Calcium                8.4 mg/dL 
Blood is drawn and sent for culture, and the patient is started on empiric antibiotics. Three days later, 3 of 4 blood cultures obtained on admission grow Gram-positive, coagulase-positive bacteria. Which of the following is the most common initial site of infection in this patient?   

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)