Endocarditis, infectious I33.0

The internist Sir William Osler first described infective endocarditis 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 (Roth spots) were first described by the Swiss physicist and pathologist Moritz Roth (1839 - 1914) (Harris 2018).

A 1907 paper by Max Hermann Friedrich Löhlein (1877 - 1921) of Leipzig can be found in which he first described the Löhnlein nephritis named after him in the context of infective endocarditis. This had already been described as a "hemorrhagic nephritis" by Harbitz in 1899 (Sebastian 2018).

In 1909, the oral cavity was postulated as a portal of entry for germs, and in 1923, the association between invasive dental treatments and endocarditis was recognized (Al- Nawass 2021).

The first prophylactic treatments with penicillin occurred in the 1940s. The American Heart Association (AHA) subsequently published guidelines on antibiotic prophylaxis for the first time in 1955 (Cahill 2017).

Infective endocarditis (IE) is defined as endocarditis caused by an infectious stray focus in the area of the endocardium or the heart valves (Herold 2022), which is always life-threatening and often accompanied by a septic clinical picture (Mewis 2006). IE is a multisystem disease (Holland 2017), as the clinical manifestation can affect any organ system (Hubers 2020).

IE is differentiated into the following 4 forms:

• endocarditis of the native valves and congenital structural anomalies
• IE acquired nosocomially e.g. through catheters etc.
• prosthesis or implant associated IE
• Endocarditis in drug addicts (Knirsch 2014).

The disease may present as:

• infective endocarditis
• Mixed form: In this case, an additional infectious inflammation occurs on the floor of an abacterial endocarditis (Herold 2022).

IE is a rarely occurring disease (Cahill 2017). However, it represents the most common form of endocardial disease (Hellmich 2017). The incidence of the community-acquired form is approximately 2 - 5 cases per 100,000 population annually in industrialized countries (Renz- Polster 2008). Kasper (2015) gives an incidence of 4 - 7 cases per 100,000 population. The sex ratio between m: w is 2: 1 (Herold 2022).

The incidence is significantly higher in the elderly, as well as in the first 6 - 12 months after valve replacement (Kasper 2015).

Risk factors are:

• Immunodeficiency
• previous endocarditis
• post heart valve surgery (Renz- Polster 2008)
• congenital heart defects (Knirsch 2014)
• chronic rheumatic heart disease (the most common predisposition [Kasper 2015])
• pre-damaged valve apparatus
• Dialysis patients
• drug addicts (Renz- Polster 2008)

The causes of endocarditis may be:

Infectious by e.g.:

• Staphylococci in approx. 45 - 65 %.
• Streptococci in approx. 30 %
• Enterococci < 10 % ( Herold 2022 / Kasper 2015)
• Pneumococci
• Rare pathogens such as Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Coxiella burnetii, Chlamydia, Eikenella corrodens, Kingella Kingae, Mycoplasma, Legionella, pathogens of the HACEK group (Herold 2022)
• Fungi, with approx. 1 % very rarely occurring (Herold 2022), mostly caused by Candida spp. and Aspergillus spp. (Knirsch 2014).

Note: However, in 10-30% of patients, the pathogen cannot be isolated in blood culture (Herold 2022).

Pathogens that frequently cause endocarditis early after cardiac valve replacement are:

• methicillin-resistant Staphylococcus aureus
• coagulase-negative staphylococci
• gram-negative pathogens (Herold 2022)

In endocarditis with native valves or occurring late after valve disruption, the predominant pathogens are:

• Methicillin-sensitive Staphylococcus aureus
• Enterococcus faecalis
• different streptococcal species (Herold 2022).

The main entry sites are: the oral cavity, the skin and the upper respiratory tract (Kasper 2015). Recently, the number of people suffering from streptococcal - endocarditis is decreasing, while the disease is now more frequently caused by staphylococci and rare pathogens. The cause is thought to be the increasing number of prosthetic materials such as venous catheters, heart valves, pacemakers, endoprostheses, etc. (Herold 2022). Of note is the clustered occurrence of endocarditites in atopic dermatits (Grabczynska SA et al. 1999, Park BW et al. 2019).

Predisposing factors for infective endocarditis include:

• Congenital heart defects both non-operated, and (palliative) operated.
• rheumatic fever (now plays a minor role in industrialized countries
• piercing
• tattoo
• dermatological diseases that can cause bacteremia such as acne, severe erysipelas, ulcus curis, necrotizing fasciitis, severe atopic dermatitis
• Procedures such as:
  • dental interventions
  • cardiac surgery
  • catheter interventional (Knirsch 2014)

Prerequisites for the development of IE are primarily 3 factors:

• preexisting damage of the valve apparatus (this is NOT found in 15 - 35 %)
• thrombotic vegetations
• transient bacteremia (Mewis 2006)

Mostly subtle lesions of the endocardium precede the infection (Renz- Polster 2008). Platelet-fibrin thrombi form at these sites, especially in the region of congenital or acquired pre-damaged valves, which is referred to as non-bacterial endocarditis (Herold 2022). Infection can then occur at these sites as part of bacteremia (Renz- Polster 2008).

This so-called transitory bacteremia occurs frequently. It can even occur during tooth cleaning. However, the invading bacteria usually circulate in the blood for only a few minutes, as they are very quickly rendered harmless by normal bactericides. On the other hand, they find an ideal place to settle at already existing endothelial alterations (Herold 2022).

The infection can lead, for example, to destruction of the valve apparatus and abscesses of the valve ring. If detachment of the vegetations occurs, septic emboli in the brain, kidneys or coronary arteries occur (Renz- Polster 2008).

The peak age of the disease is now 60-70 years, whereas it used to be around 40 years (Mewis 2006).

IE may manifest as valvular, chordal, or parietal disease of the endocardium (Mewis 2006).

Most commonly, infective endocarditis affects the valves of the left ventricle with > 85 %:

- isolated aortic valve 55 - 60 %

- isolated mitral valve 25 - 30 %

- combined aortic and mitral valve 15 %.

- Right ventricular endocarditis (mostly of the tricuspid valve in 10 - 15 % [Mewis 2006]).

Multiple valve involvement is found in approximately 25% of patients.

The clinical course can be very variable, up to fulminant courses with septic clinical picture and signs of multi-organ failure (Renz-Polster 2008).

Basically, one can differentiate between an acute and a subacute course:

• Acute course: This course has increased in frequency (Herold 2022). Pathogens are usually Staphylococcus aureus, pneumococci, gram-negative rods. In this case, a septic clinical picture is found with rapid onset of heart failure and a heart murmur (Knirsch 2014).
• Subacute course, also known as endocarditis lenta: Predominantly triggered by streptococci (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. The subacute course shows an insidious course in 80 % with non-specific symptoms such as fever, fatigue, myalgias, arthralgias and clinical signs of heart failure. In about 20%, specific symptoms are found in the form of a new-onset heart murmur and skin manifestations in the form of Roth's spots, splinter hemorrhages (splinter hemorrhages), Osler's nodules, Janeway 's spots (Knirsch 2014).

Leading symptoms in infective endocarditis are the typical leading symptoms:

• Bacteremia
• Emboli
• fever (found in about 90%)
• Heart murmur (usually a pre-existing heart murmur changes its character)
• splenomegaly (Herold 2022)

Other symptoms may include:

Tachycardia

General symptoms such as:

• Loss of appetite
• Arthralgias
• Weight loss
• General weakness
• Sweating tendency

Cardiac symptoms such as:

• increasing signs of heart failure

Cutaneous symptoms such as:

• Petechiae (in up to 30%).
• Splinter (splinter) hemorrhage under the nails
• Osler's nodules (dull, reddish, lentil-sized nodules, especially of the fingers and toes, due to immune complex vasculitis).
• Janeway lesions (indolent hemorrhagic lesions in the area of the palm or soles of the feet)
• drumstick fingers (rare)
• Clock glass nails (rare)

Bacterial microemboli:

• micro-embolism in the area of the retina
• embolic herd encephalitis with passive hemiparesis

Renal involvement due to immune complex deposition on the glomerular basement membrane (Kasper 2015) with e.g:

- proteinuria

- hematuria

- glomerular focal nephritis (almost regularly present)

- renal infarcts in embolic events

- Acute diffuse glomerulonephritis (rarely present) (Herold 2022).

Embolic renal infarcts with:

• Hematuria
• Flank pain

Rarely:

• Renal dysfunction (Kasper 2015).
• Splenomegaly
• Ocular changes such as - Roth spots (hemorrhages into the retina).

Infective endocarditis triggered by drug use is confined to the tricuspid valve in 50% and results in symptoms such as:

• Fever
• no or at most a faint heart murmur
• no peripheral manifestation
• septic pulmonary embolism with
• cough
• pleuritic thoracic pain
• pyopneumothorax (Kasper 2015)

The diagnosis of IE is still a challenge today. The most important techniques in diagnosis are blood cultures and echocardiography (Holland 2016).

For diagnosis, one should

- Obtain a history of any risk factors, such as vitiation, i.v. drug use, etc.

- Obtain clinical symptoms, e.g., fever, heart murmur

- Obtain laboratory findings

- Draw blood cultures repeatedly (minimum is 3 aerobic and 3 anaerobic) (Herold 2022).

Itis obligatory to take blood cultures repeatedly both before starting antibiosis and during the course for targeted antibiosis (Renz- Polster 2008).

According to the ESC guideline, the diagnosis of infective endocarditis is made according to the simplified and modified Duke criteria. These criteria are based on clinical, laboratory chemistry, imaging findings, and major or minor criteria (Knirsch 2022). Sensitivity and specificity are around 80%. Subsequent modifications have resulted in a sensitivity for pediatric patients of nearly 90% (Knirsch 2022). For prosthetic valve endocarditis, the sensitivity is also 90% (Saha 2022).

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)

If the Duke criteria are not met, IE cannot be ruled out. This is only the case if (Girndt 2022):

- Resolution of symptoms after ≤ 4 days of antibiotic therapy.

or

- Existence of a clear alternative diagnosis

or

- the criteria of a possible IE are not fulfilled

or

- Lack of pathological evidence at surgery or autopsy after ≤ 4 days of antibiotic therapy (Knirsch 2022).

Transthoracic echocardiography (TTE)

In children, noninvasive TTE should always be performed initially; in adults, the decision should be made on an individual basis (Knirsch 2014). However, vegetations < 2 mm cannot be imaged with this method. In approximately 20% of adults, the technique cannot be used due to emphysema or body structure (Kasper 2015). The sensitivity of TTE is approximately 70% (Mgbojikwe 2019). If the examination findings are positive, TEE is recommended for more accurate diagnosis (Knirsch 2014).

Transesophageal echocardiography (TEE).

TEE can be used to detect:

- endocarditic vegetations (the sensitivity for vegetations is 99%, which is higher than that of 4D- CT at 91% [Mgbojikwe 2019]).

- abscesses

- valve destruction

- Fistula or dehiscence of prosthetic valves

- Pseudoaneurysms (Knirsch 2014).

However, a negative finding does not exclude IE. In this case, a short-term repeat examination is recommended (Knirsch 2014). Overall, up to 30% of cases cannot be visualized by echocardiography. In this case, newer imaging modalities are indicated such as 4-dimensional computed tomography (4D- CT), fluorodeoxyglucose positron emission tomography (FDG- PET), and leukocyte scintigraphy (Mgbojikwe 2019).

Cardiac computed tomography.

Cardiac CT is used particularly in patients in whom the anatomy cannot be clearly delineated on echocardiography. CT is equivalent, if not superior, in visualizing paravalvular anatomy and complications such as paravalvular abscesses and mycotic aneurysms (Cahill 2017).

4-Dimensional Computed Tomography (4D- CT).

This examination method is increasingly used in the diagnosis of IE. It represents a non-invasive useful alternative to TEE. In particular, it can be used to visualize abscesses and pseudoaneurysms. The sensitivity for vegetations is 91%, which is lower than TEE (Mgbojikwe 2019). Patients with cardiac arrhythmias or tachycardias are less suitable for this type of examination, as they often present technical problems with image acquisition (Mgbojikwe 2019).

Fluorodeoxyglucose positron emission tomography (FDG- PET).

FDG- PET can be used to detect IE early, even when echocardiography is still negative. The examination is generally more sensitive than echocardiography in detecting IE in implanted devices, such as pacemakers, implanted defibrillators, cardiac resynchronization devices, etc. In particular, pseudoaneurysms and IE of the prosthetic aortic valve can be well visualized. Sensitivity is 97%, and 91% in patients with prosthetic valves. Specificity is 95% (Mgbojikwe 2019). A recent study demonstrated that an18F-fluorodeoxyglucose positron emission tomography/computed tomography (18 F- FDG- PET/CT ) scan has a sensitivity of 93% in endocarditis of a prosthetic valve, but only a sensitivity of 22% in native valves (Rajani 2020).

Leukocyte scintigraphy

This can increase the sensitivity of Duke criteria. The study is particularly useful in patients with prosthetic valves or implanted electrical cardiac devices (Mgbojikwe 2019).

Typically, there are:

- elevated 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 immunologic findings such as:

- anti-endothelial antibodies

- anti-sarcolemmal antibodies

- other immune phenomena are possible (Herold 2022)

- Blood cultures: If possible, 3 - 5 separately taken blood cultures should be prepared, taken from the cubital vein, not from indwelling catheters (Herold 2022).

Blood cultures are negative in 5 - 15% of patients (Kasper 2015). Most commonly, this is due to initiation of antibiotics before blood cultures are taken, but it may also be IE caused by microorganisms that are difficult to isolate by conventional microbiological techniques. In the case of IE caused by microorganisms, highly specialized assays, serological tests, and polymerase chain reaction (PCR) can ultimately detect the causative agent in up to 60% of cases (Holland 2016).

Infective endocarditis should always be considered in cases of indeterminate fever combined with a heart murmur (Herold 2022).

Complications can occur in all organs, especially in the form of:

- Cardial:

- heart valve rupture

- heart valve perforation

- myocardial abscess

- Concomitant myocarditis

- Embolism of the coronary vessels

- Pericardial effusion (Herold 2022)

- Lungs:

- Pulmonary edema (Herold 2022)

- pulmonary embolism

- pneumonia

- Pleural effusions

- Empyema (Holland 2016)

- Spleen:

- septic splenic rupture (Herold 2022)

- Splenic infarcts (often detectable on autopsy, but had usually remained clinically occult [Holland 2016])

- Renal:

- renal insufficiency

- renal infarction

- renal abscess

- glomerulonephritis

- Renal biopsies were always pathologic during active IE, even if there was no renal disease clinically (Holland 2016)

- Neurovascular damage such as.

- aneurysms

- abscesses

- intracerebral microbleeds (detectable in up to 80% but usually asymptomatic)

- cerebral emboli (Holland 2016)

- Skin manifestations:

- petechiae

- Osler nodules

- Janeway lesions

- skin infarcts (Holland 2016)

- Eyes:

- Endophthalmitis (especially with S. aureus IE)

- Roth spots (Holland 2016).

In up to 60% of patients with Streptococcus gallolyticus / bovis - endocarditis, colon tumors such as carcinomas, polyps are found. Therefore, these patients should definitely be colonoscoped in the free interval (Herold 2022).

Since IE is a life-threatening disease, therapy should be started immediately after the initial blood cultures are taken, even if the pathogen is not yet known at that time (Herold 2022).

To cure IE, all bacteria in the vegetations must be eliminated (Kasper 2015).

Treatment is always carried out by an interdisciplinary team, the so-called "endocarditis team", consisting of cardiologists, cardiac surgeons, infectiologists and microbiologists, if necessary also together with neurosurgeons, neurologists and radiologists (Herold 2022).

Therapy consists of symptomatic and microbial therapy (for the latter, see "Internal therapy").

Symptomatic therapy

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

- antipyretic therapy

- antiarrhythmic therapy

- pacemaker therapy

- treatment of cardiac insufficiency

- treatment of renal insufficiency, etc. (Knirsch 2014).

Systemic anticoagulation is generally not recommended. Patients who are anticoagulated due to pre-existing conditions should be switched to heparin so that any surgical intervention that may become necessary can be performed at any time. If severe embolisms occur, an individual risk-benefit assessment with regard to anticoagulation is required (Knirsch 2014).

In the case of previously unknown pathogen, therapy for ambulatory acquired endocarditis and native valves and prosthetic valves > 12 mon postoperatively should consist of:

- Ampicillin 12 g / d i. v., divided into 4 - 6 single doses (ED), the maximum dose is 12 g / d

plus

- (Flu) cloxacillin or oxacillin 12 g / d i. v., distributed over 4 - 6 ED, maximum dose 12 g / d

plus

- Gentamicin 3 mg / kg bw / d i. v. or i. m. as ED, the valley level is < 2.0 mg / l

The duration of therapy should be 4 - 6 weeks (Herold 2022) and should be performed under inpatient conditions (Knirsch 2014).

If the prosthetic heart valve surgery less than 12 mon. ago, recommend:

- Vancomycin 30 mg / kg bw / d i. v., distributed over 2 ED, therapy duration ≥ 6 weeks, the valley level is between 15 - 20 mg / l

plus

- Gentamicin 3 mg / kg bw / d i. v. or i. m. as ED, duration of therapy 2 weeks, the valley level is < 2.0 mg / l

plus

- Rifampicin 900 - 1,200 mg / d i. v. or orally, distributed over 2 - 3 ED, duration of therapy ≥ 6 weeks, maximum dose: 1,200 mg / d (Herold 2022 / Knirsch 2014)

- Enterococci

Enterococci are usually resistant to oxacillin and cephalosporins. They are inactivated but not killed by penicillin, ampicillin, and vancomycin. To kill enterococci, additional treatment with aminoglycosides such as gentamicin or streptomycin is needed in addition to penicillin, ampicillin, and vancomycin (Kasper 2015).

- 1. beta- lactam-sensitive strains:

- Ampicillin 300 mg / kg bw / d, distributed over (4) - 6 ED, duration of therapy 4 - 6 weeks, maximum dose 12 g / d

- plus

- Gentamicin 3 mg / kg bw / d, distributed over 3 ED, duration of therapy 4 - 6 weeks, the valley level is < 2.0 mg / l (Knirsch 2014).

- 2. beta- lactam resistant strains:

- Vancomycin 40 mg / kg bw / d, distributed over 2 - 3 ED, duration of therapy 6 weeks, the valley level is between 15 - 20 mg / l

- plus

- Gentamicin 3 mg / kg bw / d, spread over 2 - 3 ED, duration of therapy 6 weeks, the valley level is < 2.0 mg / l (Knirsch 2014).

- Staphylococci

- 1. methicillin-sensitive staphylococci:

- Native valves:

- Oxacillin 200 mg / kg bw / d, distributed over 4 - 6 ED, duration of therapy 4 - 6 w., maximum dose 12 g / d

- plus

- Gentamicin 3 mg / kg bw / d, distributed over 3 ED, duration of therapy 3 - 5 days, valley level is < 2.0 mg / l (Knirsch 2014).

- Prosthetic valves:

- Oxacillin 200 mg / kg bw / d, distributed over (4) - 6 ED, duration of therapy ≥ 6 weeks, maximum dose 12 g / d

- plus

- Rifampicin 20 mg / kg bw / d, distributed over 3 ED, duration of therapy ≥ 6 weeks, maximum dose 1,200 mg / d

- plus

- Gentamicin 3 mg / kg bw / d, distributed over 3 ED, duration of therapy 2 weeks, valley level is < 2.0 mg / l (Knirsch 2014).

- 2. methicillin-resistant staphylococci or patients with beta-lactam intolerance:

- Native and prosthetic valves:

- Vancomycin 40 mg / kg bw / d, distributed over 2 - 3 ED, duration of therapy ≥ 6 days, the valley level is between 15 - 20 mg / l

- plus

- Rifampicin 20 mg / kg bw / d, distributed over 3 ED, duration of therapy ≥ 6 days, the valley level is between 1,200 mg / d

- plus

- Gentamicin 3 mg / kg bw / d, spread over 3 EDs, duration of therapy 2 days, trough level is < 2.0 mg / l (Knirsch 2014)

- Gram-negative rods

Here, there is often resistance to penicillin. Treatment should therefore be with ceftriaxone 100 mg / kg bw / d, therapy duration 4 weeks (Knirsch 2014).

- Fungi

Since IE caused by fungi is very rare, there are only case reports on this, the therapy is empirical. It is usually carried out with amphotericin B, azole antifungals or echinocandins (Knirsch 2014).

In the course of IE, approximately 50% of patients require surgery (Rajani 2020).

Patients should therefore be presented to a cardiothoracic surgeon at an early stage in order to decide, among other things, on a necessary valve replacement for infection control (Herold 2022).

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)

However, the surgical risk is increased in the active phase of IE compared with elective surgery (Knirsch 2014).

Before the era of antibiotics , infective endocarditis was almost always fatal. But even today, the prognosis of endocarditis remains serious, as it is associated with considerable morbidity and mortality. In almost half of the cases, cardiac surgery is required to repair the valves (Lechner 2020).

In the acute form, for example, the prognosis is extremely poor without immediate treatment (Herold 2022).

According to Renz-Polster (2008), mortality is around 25 % even with adequate treatment. Mortality can now be reduced to < 10 % by a multidisciplinary endocarditis team (Herold 2022). Cahill (2017) describes mortality after one year as 30%. The prognosis for children is slightly better, with a mortality rate of < 10% (Knirsch 2014).

The prognosis is unfavorable from the outset in patients with e.g.:

- Post heart valve surgery

- cyanotic congenital heart disease

- acute course of the disease and concomitant heart failure

- Infection with gram-negative pathogens, fungi (Herold 2022), Staphylococcus aureus, MRSA, vancomycin-resistant enterococci = VRE (Knirsch 2014)

- Left heart endocarditis (Herold 2022)

- Age < 3 years

- insulin-dependent diabetes mellitus

- Delayed diagnosis

- Occurrence of complications, in particular e.g.:

- Renal insufficiency

- cardiac insufficiency

- septic shock

- apoplexy (Knirsch 2014).

- Sonographic findings such as:

- pulmonary hypertension

- premature mitral valve closure

- Increase in left ventricular end-diastolic pressure (LVEDP)

- perianular complications

- severe prosthetic valve dysfunction

- large vegetations > 10 mm (Knirsch 2014).

Recurrence occurs in 2 - 6 % of patients (Rajani 2020).

The most common cause of death is cardiac decompensation as a result of myocardial damage or valve destruction (Herold 2022).

Prophylaxis

Patients should receive an endocarditis identification card and endocarditis prophylaxis in appropriate risk constellations (Herold 2022).

These risk constellations include:

- post heart valve replacement

- congenital heart defect

- significant residual defects in prosthetic materials

- valve diseases after heart transplantation

- history of IE (Knirsch 2014).

In addition, patients should be educated about good dental hygiene, avoiding intravenous drug use, and body piercings or tattoos (Rajani 2020).

Follow-up

Most complications occur within the first 12 months (Rajani 2020).

There should be close outpatient checks by the "endocarditis team" (Herold 2022), ideally at 1, 3, 6, 12 month intervals (Rajani 2020).

These examinations include:

- clinical examination

- resting ECG

- transthoracic echocardiography

- laboratory chemical controls (if necessary)

- in clinically conspicuous patients with fever, renewed blood cultures are always necessary (Knirsch 2014)

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