Pathology of infectious endocarditis

2021-01-28 12:00 AM

Infectious endocarditis in injecting drug users: common in young men without heart disease, the skin is often the source of infection, the tricuspid valve is most often damaged.


Infectious endocarditis is an infection of the endocardium that damages primarily the heart valves, but the endothelium of the major blood vessels is also damaged in the general clinical setting. The disease is caused by many pathogens and many different entryways eventually localized in the endocardium, lesions characterized by ulcers and warts, especially the heart valves, led by the mitral valve and then to the aortic valve. The tricuspid valve is less common and is typically localized (intravenous hydrocephalus).


Infectious endocarditis mostly occurs in infected patients, common age <50, more men than women, 60-80% of patients with a history of heart disease before mainly heart valve disease, 30 % due to low; infectious endocarditis often met the mitral valve leading to the aortic valve, 10-20% due to congenital heart disease. For example the disease also has ductus arteriosus, ventricular septal defect, quadriplegic Fallot, aortic stenosis; 10-30% mitral valve prolapse. Degenerative heart disease is also the basis of endocarditis, especially calcified aortic stenosis in the elderly, rarer than asymmetric septal hypertrophy, Marfan syndrome, syphilis stenosis and 20 - 40% have no heart disease before.

Infectious endocarditis in injecting drug users: common in young men without heart disease, the skin is often the source of infection, the tricuspid valve is most often damaged.

Endocarditis in patients with artificial valves accounts for 10-20%, most of them are men, the aortic valve is more common than the mitral valve, the damage is usually next to the valve on the artificial valve stitch with the valve ring. The disease usually occurs in the first week or in the first year after surgery (accounting for 1-2% of cases), the incidence decreases to 1% in the following years.


Harmful bacteria

Most cases of the pathogenic bacteria are streptococci, usually group D streptococcus, less susceptible to conventional penicillin. Hemolytic streptococci (causing partial hemolysis) and hemolytic streptococcus (again very sensitive to Penicillin, in addition to endocarditis due to streptococcus (currently, staph bacteria are also most common bacteria due to sepsis after abortion (this type is usually severe, high mortality due to antibiotic resistance). In addition, endocarditis caused by bacilli Salmonella and Brucella can also be encountered.

Way in

Table: Causes and entry of bacteria in infectious endocarditis.

Road of entry               



Teeth, mouth

Extractions, U granules stick to streptococcus


Ear, nose and throat

Pharyngitis, ear infections, tonsillectomy, sinusitis

Bridge-D, streptococcus


Urinary catheterization, cystoscopy, urinary surgery

Streptococcus D, staphylococcus aureus, bacillus Gr (-)


Abortion, childbirth, endometritis

Staphylococci, interconnected D


Burns, skin diseases



Gallbladder inflammation, digestive tumours

Bridge D, streptococcus, staphylococcus

The catheter



Shunt hemodialysis


Bacillus Gr (-), staph

Using drugs


Bacillus Gr (-)

Heart surgery



Mechanism of pathogenesis

Endothelial damage

The location of the bacteria in the theoretical endothelial lesion is usually located opposite the endothelial injury according to Venturi's law.


Bacterial immobilization and proliferation depend on:

Serum natural bacterial resistance: complement protection - the rarity of Gram (-) bacteria due to natural sensitivity to the complement.

The presence of agglutination antibodies creates colonies

Adhesion properties can be attributed to the involvement of slime secreted by certain bacteria such as staph.

Staphylococcus aureus -> hemolytic streptococci -> Pseudomonas aeruginosa

Immune manifestations


Duration of infection.

Existence of antibody stimulation.


People distinguish two main subjects as follows:

Malignant acute endocarditis

Rapid progression, appearing on a benign endocardium, this form is severe, often causes rapid death and in the context of sepsis. Pathological lesions are ulcers, erosions, eventually perforation of valves, ligaments can be ruptured, ulcers can cause abscesses in some organs such as liver, spleen, and kidneys. This can be called malignant because it was 100% fatal before antibiotics.

Jaccoud-Osler infection subacute endocarditis

The ulcerative lesion occurs on the heart valve disease, congenital heart. Pathogenic bacteria are detected by blood culture or autopsy with pus culture in the area of ​​injury. Before antibiotics, this was a serious illness, with 100% mortality, but since antibiotics mortality has decreased but still a serious illness.

Clinical symptoms

Initial stage

Usually begins with unexplained fever in patients with heart disease, so if the patient has heart disease and has an unexplained fever for more than 10 days, accompanied by weakness, loss of appetite, pallor of the patient, think inflammation. infectious subacute endocardium (Osler). Probe diagnostic by:

Find your way into the bacteria.

Urine tests for protein and leukocytes.

For many blood cultures, antibiotics should not be given to make blood cultures negative.

Sometimes it can begin with a stroke with hemiplegia or visceral infarction.

Full-play stage

Usually, after a few weeks the symptoms gradually clear up:

Fever and weakness: Fever fluctuates with chills or fever wave type, the temperature of 39-40 degrees alternating with no fever, so thermocouple every 3 hours, fever often with blue skin, anaemia, thinning.

Hearing heart: Pre-existing heart disease usually does not change. The more common sequence is aortic regurgitation, mitral regurgitation, mitral stenosis, tricuspid and pulmonary valve disease are rarer. Congenital heart disease can be seen as the ductus arteriosus, ventricular septal defect, pulmonary artery stenosis, aortic stenosis, aortic stenosis, quadruple Fallot.

The finger drumstick is very valuable for diagnosing fever heart disease, but this sign is often late, in addition to bleeding under the skin, mucous membranes can also be encountered.

Big spleen: 2 - 4cm below the ribs, very valuable for diagnosis, especially when combined with heart disease with fever.

Kidney: The classic is gross or microscopic hematuria; Proteinuria occurs in 70% of cases.

Other signs of evidence: Clogged arteries such as:

Cerebral embolism causes hemiplegia.

Blockage of the limb causes pain, pale, cold skin.

Splenic embolism causes pain in lower left ribs, rapid spleen.

Mesenteric embolism: Abdominal pain.

Renal vascular obstruction: Severe low back pain, hematuria, usually reflex anuria in the first 3 hours.

Lung infarction: Chest pain, coughing up blood, difficulty breathing.

Meningitis, meningitis.

Occlusion of the eye conjunctiva.


Complete blood count: Anemia, increased leukocytes.

Blood sedimentation increased.

Electrocardiogram, chest X-ray.

Fundoscopy: Retinal artery occlusion.

Residue Addis.


Blood urea usually increases> 0.5g / liter.

Protein electrophoresis: increased globulin.

Blood cultures: 9 times in 3 consecutive days, at high temperature and in many different environments.

Echocardiography: Currently considered a test with high diagnostic sensitivity, in addition to allowing monitoring of disease progression. With a 2-plane ultrasound technique, one can determine the presence of warped lesions on heart valves, ultrasound can detect ligament rupture or heart valve perforation. If erosive lesions are found, a definitive diagnosis in spite of blood transplants (-), but no warp lesions do not rule out the diagnosis.

Implementing the quadrants

Applying Duke clinical diagnostic standard 1994.

Two main standards

Positive blood cultures:

Specific bacteria were isolated in two separate blood cultures.

Positive blood cultures exist.

Evidence of endocardial damage.

Positive ultrasound.

New valve opening appears.

Six sub-criteria

Favourable factors: Heart disease, intravenous medication.

Fever> 38 degrees.

Cardiac valve manifestations: embolism, swelling, haemorrhage, Janeway signs.

Immune manifestations: Glomerulonephritis, Osler nodules, Roth markers, rheumatoid factor.

Microbiological evidence: Positive blood cultures but inadequate key criteria, serological markers for acute infection.

Echocardiography: Signs of infectious endocarditis but no major signs.

Applying the diagnosis

Pathological criteria:

Bacteria: Blood cultures or warts cause embolism or abscesses in the heart.

Pathological lesions: Warts, abscesses in the heart are determined by histology

Clinical standards:

A diagnosis of endocarditis is confirmed when:

2 main standards, or

1 primary standard and 3 sub-standards, or

5 sub-standards.

Clinical form

Subacute infectious endocarditis with negative blood cultures

Subacute, subacute infectious endocarditis with blood cultures 9 times for 3 consecutive days is negative, but bacteria can be found on cadaver dissection lesions.

Characteristics of subacute endocarditis with cultured negative blood cultures are:

Common in patients with damage to the aortic valve.

Often accompanied by visceral changes.

Often accompanied by anaemia, leukopenia, increased γ globulin.

The disease is often severe, with high mortality despite aggressive treatment. Why are blood cultures negative? The cause is unknown, but there are some comments as follows:

In the spleen, there is an encapsulation of bacteria.

Some patients accompanied by scarlet fever, scattered lupus erythematosus.

Globulin usually increases.

Streptococcus group D

Common in 10-15% of cases, the disease often occurs after genital-urinary infections, the disease responds to high-dose Penicillin in combination with Gentamycin, the disease tends to recur.

Can be caused by staph

Skin, urinary and genital infections.

Common lesions on the tricuspid valve.

Clinical manifestations of irreversible heart failure.

High mortality despite aggressive treatment.

Renal body

This accounts for 8-12% of cases.

Clinical manifestations with hematuria, high blood urea, edema and hypertension, poor prognosis.

Subacute endocarditis in congenital heart disease

Commonly seen is staphylococcus.

Endocarditis on closed or open-heart surgery

Expression 3-5 days early after surgery, most commonly staphylococcus and other bacteria.

The principles of treatment

Internally medical treatment

Mainly using antibiotics and usually depending on the antibiotic treatment.

Surgical treatment

Depending on the hemodynamic status that indicated intervention.

Preventive treatment

Absolutely sterile surgical instruments, examination tools or antibiotics for patients with acquired heart disease or congenital heart disease during surgical or surgical intervention.

Progression and prognosis

Without antibiotics, the mortality rate was 100%, the prognosis has improved since the antibiotic was available, but the mortality rate is still high at 20-40%. The prognosis of the disease depends on the following factors:

Age> 70.

No bacterial entry was found.


Expression of severe kidney, embolism or early heart failure.

Negative blood cultures.

Relapse after 2 months despite radical treatment.

Progression: Usually clears in early treatment. However, sequelae of diseases such as chronic nephritis with hyperuricemia, stroke with hemiplegia, the prognosis depend on pre-existing heart disease and some deaths due to renal failure or embolism.


Internally medical treatment

Eradication treatment: Mainly with antibiotics. It is necessary to use antimicrobial antibiotics with high, early, continuous and prolonged doses, and use of synergistic antibiotics including the role of subclinical to help select the right drug. It is necessary to determine the bacterial sensitivity based on an antibiotic by determining the minimum inhibitory concentration (MIC), the minimum bactericidal concentration (MBC) of the antibiotic and the kill bacteria alone or in combination.

Penicillin G-sensitive Streptococci with MIC of ≤ 0.1ug / ml: use one of the following regimens:

Regimen A: PNC G 12-18 million / day, IV every 4 hours for 4 weeks.

Regimen B: PNC G is the same as regimen A combined with Gentamycin at 1 mg/kg IV every 8 hours, both for 2 weeks.

Regimen C: Ceftriaxone 2g IV IV or TB 1 time / day for 4 weeks.

Regimen D: Vancomycin 15 mg/kg IV every 12 hours for 4 weeks.

PNC-sensitive streptococci have 0.1 ug / ml <MIC <0.5ug / ml:

Regimen E: PNC G 18 million VND / day, IV every 4 hours for 4 weeks. Gentamycin 1 mg/kg IV combination every 8 hours for the first 2 weeks.

Or use regimen D if the patient is allergic to PNC.

Enterococci or Penicillin sensitive streptococci with MIC ≤ 0.5ug / ml or modified Streptococci viridians:

Regimen F: Penicillin G 18-30 million VND / day or Ampicillin 12 g / day by TN injection every 4 hours. Combine with Gentamycin 1 mg / kg IV every 8 hours. Use both types for 4-6 weeks.

Regimen G: Vancomycin 15 mg / kg IV every 12 hours. Combining Gentamycin as regimen F. Both types are used for 4-6 weeks.

Staph is also sensitive to methicillin in patients with natural heart valves:

Regimen H: Nafcillin or Oxacillin 2 g IV every 4 hours for 4-6 weeks. May be combined with or without Gentamycin 1 mg/kg time IV every 8 hours for the first 3-5 days.

The regimen I: Cefazolin 2 g, IV every 8 hours, for 4-6 weeks, with or without Gentamycin as in H.

Regimen J: Vancomycin 15 mg/kg IV every 12 hours for 4-6 weeks with or without Gentamycin as an H regimen.

Staphylococci are resistant to Methicillin or Corynebacterium in natural valves:

K regimen: vancomycin as J regimen, with or without a combination of Gentamycin as with staphylococcal H regimen but continued Gentamycin for 4-6 weeks with Corynebacterium.

For patients with artificial heart valves:

Streptococci or Enterococci: F or G regimen.

Due to Streptococci: PNC or vancomycin for 6 weeks with Gentamycin in the first 2 weeks or longer.

Due to Enterococci: PNC or vancomycin, combined with 1 aminoglycoside for 6-8 weeks.

Staphylococcus still sensitive to Methicillin: HI or J regimen for 6-8 weeks, combining Gentamycin for the first 2 weeks and Rifampicin 300mg orally every 8 hours for 4-6 weeks.

Methicillin-resistant staphylococci: J regimen for 6-8 weeks, a combination of gentamycin for the first 2 weeks and Rifampicin 300mg orally every 8 hours during the course.

With HACEK bacteria:

Regimen L: use regimen C.

Some special cases:

Cephalosporine of another generation can be used to replace Cefazoline.

Streptomycin can replace Gentamycin with a dose of 7.5 mg/kg TB every 12 hours.

When blood cultures are not available: If there is no artificial heart valve: use antibiotics according to the F or G regimen. If an artificial heart valve is available: regimen K. If injecting drugs: regimen J.

Negative blood cultures: if the clinical response is good: continue treatment as above. If there is no clinical response after 7-10 days of treatment: use a special culture method or longer, look for other pathogens such as Brucella, Legionella, Chlamydia, Rickettsia, fungus ... Simultaneously apply a combination treatment regimen of all three types of antibiotics: vancomycin + Gentamycin + Rifampicin. If after 3 weeks still does not help stop antibiotics. Treatment of sugar into bacteria and treatment of complications

Surgical treatment:


Heart failure is due to damage to the aortic valve or the artificial heart valve.

Organ pulp has large size> 10 cm.

Severe cardiac valve ventilation even when heart failure is present.

Persistent infection persists despite taking appropriate antibiotics for 8-10 days.

Brain stroke recurs in many places.

Aortic septal abscess or aortic valve ring abscess.

Endocarditis recurs after 6 months.

Damage to the Valsalva sinus or atrioventricular region.

Fungal endocarditis.

On the artificial heart valve soon after valve replacement <2 months.


This is the most effective treatment. It is necessary to examine the oral or ENT system. Pay attention to high-risk subjects such as artificial heart valve replacement. Thoroughly sterilized surgical instruments.

Prophylactic antibiotics in infectious endocarditis

Source of risk


Antibiotic first choice

Oral, amygdala


Amoxicillin 500mg / 6 hours TM; if the risk is very high: PNC G 10-20 million VND / day or Amoxicillin 0.5g / 6 hours + Gentamycin 1mg / kg / 12 hours.

Genital urinary

Bowel cocci

Amoxicillin 1g / 4 hours or Amoxicillin 0.5g / 6 hours + Gentamycin 1 mg / kg / 12 hours.



Dicloxacillin 1.5 g / day; Pristinamycin 2 g/ day


LCK, enteric cocci, anaerobic type

Amoxicillin 1g / 4 hours + Gentamycin + Metronidazole 500 mg / 12 hours


Enteric cocci, anaerobic gut bacteria

The risk is too high: Amoxicillin + Gentamycin + Metronidazole

Heart surgery


Cefazoline 2 g + Gentamycin 1.5 mg / kg IV before surgery, 8 hours after and 16 hours after surgery.