Endocarditis lentaI33.0

The term "endocarditis" was coined by Bouillaud in 1841 for the vegetations found on the heart valves (Schaub 1960).

The internist Sir William Osler first described the clinic and pathology of infective endocarditis lenta in 1885 (Al- Nawass 2021). The mucosal nodules on the tips of the fingers and toes, the so-called "Osler nodules," which can occur in the course of endocarditis lenta, also bear his name (Schuchart 2021).

Roth spots, also known as Roth 's spots, were first described by the Swiss physician Moritz Roth in 1872. However, they did not receive the name "Roth spots" until 6 years later by Moritz Litten (Ruddy 2022). They are retinal hemorrhages (hemorrhages) , which have a characteristic morphology.

Streptococcus viridans was identified as the causative agent of E. lenta by Schott- Müller in 1903 (Schaub 1960).

Endocarditis lenta describes a form of infective endocarditis characterized by a subacute course (Knirsch 2014).

After World War I and World War II, E. lenta was diagnosed with great frequency, especially among soldiers returning home from captivity. From about 1950, the number of cases gradually decreased (Fritze 2013).

Nowadays, approximately 50% of patients with E. lenta have a history of a recent instrumental procedure (Füssle 2001) such as tooth extraction, endoscopies, tonsillectomy, bladder catheterization (Suerbaum 2012)

The incidence of E. lenta has recently decreased (Herold 2022).

The typical pathogen of an E. lenta is Streptococcus viridans (Herold 2022) with approx. 80 % (Lohr 2002). This is a less virulent pathogen (Knirsch 2014).

Other pathogens may include:

- Streptococcus (44%)

- coagulase-negative staphylococci (27 %)

- less frequently by enterococci, pathogens of the HACEK-group such as Haemophilus / Aggregatibacter, Actinobacillus /Aggregatibacter, Cardiobacterium, Eikenella and Kingella or by fungi (Knirsch 2014).

The main ports of entry are the oral cavity, skin, and upper respiratory tract (Kasper 2015).

Predisposing factors for E. lenta are:

- pre-damaged valves (present in > 90% of cases [Lohr 2002]).

- congenital heart defects both non-operated and (palliative) operated

- rheumatic fever (now playing a minor role in industrialized countries)

- piercing

- tattoo

- dermatological diseases that can cause bacteremia such as acne

- surgical procedures such as:

- dental interventions

- cardiac surgery

- catheter interventional (Knirsch 2014).

E. lenta occurs when the pathogens attach to pre-damaged heart valves during transient bacteremia. So-called vegetations, consisting of bacteria, platelets and fibrin, form on the heart valves. They form starting points for bacteremic attacks and also for embolic infarcts in the brain, spleen, lungs, kidneys (Füssle 2002).

For more details see Endocarditis, infectious

Predilection sites of E. lenta are in descending order: mitral valve, aortic valve, tricuspid valve, pulmonary valve (Lohr 2002).

The subacute course shows nonspecific symptoms such as:

- Fever

Most often, these are subfebrile temperatures that can last for weeks (Suerbaum 2012). The fever is typically not as high as in the acute course of infective endocarditis. It usually does not exceed a temperature of 39.4 degrees C. In older, severely debilitated patients and in patients with renal failure, only subfebrile temperatures are predominantly found (Kasper 2015).

- Fatigue

- Myalgias

- arthralgias (Füssle 2002)

- Clinical signs of heart failure such as:

- Dyspnea

- cardiac arrhythmias

- edema (Erdmann 2009)

- weight loss

- anemia (Füssle 2001)

- Night sweats (Angstwurm 2014)

Only in about 20% of patients are specific symptoms found in the form of a new-onset heart murmur, skin manifestations in the form of Roth's spots (are detected in up to 80% of patients with E. lenta (Ruddy 2022), splinter hemorrhages, Osler nodules (Knirsch 2014), and emboli in the brain, spleen, lungs, kidneys (Füssle 2002).

Diagnosis of endocarditis lenta is sometimes relatively late because of the weeks- or months-long course, unless major embolic events occur (Vilcant 2022).

According to the ESC guideline, the diagnosis is made according to the simplified and modified Duke criteria.

Main criteria are:

1. blood culture positive for IE:

- 1. a. Typical pathogens in at least 2 separate blood cultures such as.

- Streptococcus bovis, Staphylococcus viridans or HACEK- group

or

- Staphylococcus aureus "community-acquired".

or

- Enterococci without primary focus (Knirsch 2022)

or

- 1. b. pathogens compatible with IE in multiple positive blood cultures:

- at an interval of > 12 hours in at least 2 blood cultures

- or

- regardless of spacing in 3 or the majority of ≥ 4 blood cultures

- or

- 1. c. a single culture positive for Coxiella burnetii or an increase in the phase I IgG antibody titer to > 1: 800 (Knirsch 2022).

2. positive imaging for IE:

- 2. a. Echocardiographic evidence of:

- Valve perforation or aneurysm.

- vegetation

- New onset dehiscence on a prosthetic valve.

- Pseudoaneurysm, intracardiac fistula, abscess (Knirsch 2022)

Or

- 2. b. F- FDG PET / CT or SPECT / CT:

- abnormal activity in the position of a prosthetic valve after implantation > 3 months (Knirsch 2022)

or

- 2. c. Cardiac computed tomography:

- Evidence of a paravalvular lesion (Knirsch 2022).

Ancillary criteria are:

- 3. a. predispositions such as Z. n. IE, history of known cardiac defect, i. v. drug abuse, etc. (Knirsch 2022)

- 3. b. > 38 degrees C fever (Knirsch 2022)

- 3. c. Vascular phenomena (including those detected on imaging) such as:

- septic pulmonary infarcts

- arterial embolism

- intracranial hemorrhage

- mycotic aneurysms

- Janeway lesions

- conjunctival hemorrhage (Knirsch 2022)

- 3. d. Occurrence of immunologic changes such as:

- Osler nodules

- glomerulonephritis

- rheumatoid factors

- Roth spots (Knirsch 2022)

- 3. e. Microbiological evidence by:

- Positive blood cultures, but not meeting the major criteria.

or

- Serological evidence of active infection by pathogens compatible with IE (Knirsch 2022).

The diagnosis is considered confirmed in the presence of:

- 2 main criteria

- or

- 1 major criterion and 3 minor criteria

- or

- 5 secondary criteria (Knirsch 2022)

or

- Pathologic criteria for the definite presence of an IE are met such as:

- histological evidence of IE

or

- microbiological evidence of IE

or

- histological preparation with evidence of active endocarditis (Knirsch 2022).

There is a suspected diagnosis of:

- 1 major criterion and 1 minor criterion.

- or

- 3 minor criteria (Knirsch 2022)

For more details on the diagnosis see Duke criteria and Endocarditis, infective

Imaging includes the following examinations:

- Transthoracic echocardiography (TTE)

- Transesophageal echocardiography (TEE)

- Cardiac computed tomography

- 4-dimensional computed tomography (4D- CT)

- Fluorodeoxyglucose positron emission tomography (FDG- PET)

- Leukocyte scintigraphy

For more information, especially details on the examinations , see Endocarditis, Infectious

- Increased inflammatory parameters such as CRP, ESR (a normal ESR speaks against an infectious inflammation [Herold 2022]), leukocytes, as well as an infectious anemia (Renz- Polster 2008)

- thrombocytopenia

- Concomitant immunological findings (Herold 2022)

The main focus of the diagnosis of E. lenta is the cultivation of the pathogens from blood cultures, including biochemical differentiation (Suerbaum 2012).

For more details, see also Endocarditis, infectious

Differentially, all diseases that cause chronic inflammation and / or diseases that cause B- symptoms can be considered (Angstwurm 2014).

- Destruction of the affected heart valve in the form of obstruction or destruction (Füssle 2001)

- Arterial emboli in brain, spleen, lungs, kidneys (Füssle 2002)

- glomerulonephritis

- Osler nodules

- Roth spots

Roth spots are exudative, edematous hemorrhagic lesions of the retina (Vilcant 2022).

Treatment of E. lenta consists primarily of antibiosis in addition to symptomatic treatment.

Symptomatic therapy

Depending on the symptoms, it may consist of, for example:

- antipyretic therapy (if necessary)

- antiarrhythmic therapy

- pacemaker therapy

- treatment of heart failure (Knirsch 2014)

- treatment of possible embolisms

Systemic anticoagulation is generally not recommended in patients with E. lenta. If the patient is anticoagulated due to pre-existing conditions, a switch to heparin should be made so that any surgical intervention that may become necessary can be performed at any time. In the case of severe embolisms, an individual risk-benefit assessment is required with regard to anticoagulation (Knirsch 2014).

S. a. Endocarditis, infectious

If the most common pathogen is Streptococcus viridans, therapy should be carried out as follows:

- Benzylpenicillin (Penicillin G) 20 million I. E. / d i. v., divided into 3 - 4 single doses, therapy duration 2 - 4 weeks

- plus

- Gentamicin 3 mg / kg bw / d i. v., divided into 3 single doses, duration of therapy 2 - 4 weeks (Lemmer 2007), the valley level is < 2.0 mg / l (Knirsch 2014).

If other pathogens are involved, the therapy must be adjusted taking into account the resistogram (Braun 2017).

S. a. Endocarditis, infectious

The indication for surgical measures is not as generous in E. lenta as in infective endocarditis (Braun 2017).

Urgent surgical indications are:

- Vegetations > 10 mm (here, the embolism risk increases up to 60%).

- emboli

- persistent valve vitium

- hemodynamically relevant valve vitium

- heart failure

- paravalvular abscess

- AV blockages (Herold 2022)

S. a. Endocarditis, infectious

If left untreated, E. lenta is always lethal within months (Füssle 2002).

With appropriate early therapy, the course of heart failure determines the prognosis (Bob 2001).

Endocarditis prophylaxis should be given to patients with prosthetic or reconstructed heart valves before and after surgical or diagnostic procedures for prophylaxis (Braun 2017).

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