Infective endocarditis

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Acute endocarditis
)
Infective endocarditis
Other namesBacterial endocarditis
heart surgery[1]
Prognosis25% risk of death[6]
Frequency5 per 100,000 per year[6]

Infective endocarditis is an

backward blood flow in the heart, heart failure – the heart struggling to pump a sufficient amount of blood to meet the body's needs, abnormal electrical conduction in the heart, stroke, and kidney failure.[1][2][8][9]

The cause is typically a

The usefulness of

heart surgery is required.[1]
The number of people affected is about 5 per 100,000 per year.[6] Rates, however, vary between regions of the world.[6] Infective endocarditis occurs in males more often than in females.[1] The risk of death among those infected is about 25%.[6] Without treatment, it is almost universally fatal.[1] Improved diagnosis and treatment options have significantly enhanced the life expectancy of patients with infective endocarditis, particularly with congenital heart disease.[5]

Classification

Infective endocarditis is divided into the three categories of acute, subacute, and chronic based on the duration of symptoms.[12] Acute infective endocarditis refers to the presence of signs and symptoms of infective endocarditis that are present for days up to six weeks.[12] If these signs and symptoms persist for more than six weeks but less than three months, this is subacute infective endocarditis.[12] Chronic infective endocarditis refers to the presence of such signs and symptoms when they persist for more than three months.[12]

This classification is now discouraged, because the ascribed associations (in terms of organism and prognosis) were not strong enough to be relied upon clinically. The terms short incubation (meaning less than about six weeks) and long incubation (greater than about six weeks) are preferred.[14]

Culture results

Infective endocarditis may also be classified as culture-positive or culture-negative. By far the most common cause of "culture-negative" endocarditis is prior administration of antibiotics and can occur in up to 31% of cases.[15][16]

Sometimes

Chlamydia species. Due to delay in growth and identification in these cases, patients may be erroneously classified as "culture-negative" endocarditis.[18]

Heart side

Endocarditis can also be classified by the side of the heart affected:

Infection setting

Another form of endocarditis is

pacemakers, etc.[20]

Valve type

Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important. Prosthetic valve endocarditis can be early (within 1 year of surgery) or late (> 1 year following valvular surgery).[21]

  • Early prosthetic valve endocarditis is usually due to intraoperative contamination or postoperative bacterial contamination which is usually
    nosocomial
    in nature.
  • Late prosthetic valve endocarditis is usually due to community-acquired microorganisms.[20]

Prosthetic valve endocarditis is commonly caused by Staphylococcus epidermidis as it is capable of growing as a biofilm on plastic surfaces.[22] Cutibacterium acnes almost exclusively causes endocarditis on prosthetic heart valves.[17]

Signs and symptoms

Cause

Many microorganisms can cause infective endocarditis. These are generally isolated by blood culture, where the patient's blood is drawn and any growth is noted and identified. The term bacterial endocarditis (BE) commonly is used, reflecting the fact that most cases of IE are due to bacteria; however, infective endocarditis (IE) has become the preferred term.[27]

Bacterial

HACEK group of bacteria are also rare causes of infective endocarditis in North America.[29]

The viridans group includes S. oralis, S. mitis, S. sanguis, S. gordonii and S. parasanguis. The primary habitats for these organisms are the oral cavity and upper respiratory tract.[30] These bacteria are present in the normal oral flora and enter the bloodstream due to disruption of tissues in the mouth when dental surgical procedures are performed (tooth extractions) or genitourinary manipulation. Similarly, HACEK organisms are a group of bacteria that live on the dental gums and can be seen with people who inject drugs who contaminate their needles with saliva. Patients may also have a history of poor dental hygiene or pre-existing valvular disease.[31]

Staphylococcus bloodstream infections are frequently acquired in a health care setting where they can enter the bloodstream through procedures that cause breaks in the integrity of skin, such as surgery, catheterization, or during access of long term indwelling catheters or secondary to intravenous injection of recreational drugs.[citation needed
]

Enterococcus can enter the bloodstream as a consequence of abnormalities in the gastrointestinal or genitourinary tracts.[citation needed]

Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific.

Multiple case reports of infective endocarditis caused by unusual organisms have been published.

Tropheryma whipplei has caused endocarditis without gastrointestinal involvement.[37] Citrobacter koseri was found in an immunocompetent adult.[38] Neisseria bacilliformis was found in a person with a bicuspid aortic valve.[39]

Dental operations

One in eight cases of infective endocarditis is thought to be caused by S. viridans infection associated with dental procedures such as cleaning or tooth

antibiotics were regularly administered to patients with certain heart conditions as a precaution, although this practice has changed in the US, with new American Heart Association guidelines released in 2007,[40]
and in the UK as of March 2008 due to new NICE guidelines.

Fungal

Fungal endocarditis (FE) is often fatal and one of the most serious forms of infective endocarditis. The types of fungi most seen associated with this disease are:

immunocompromised patients. It forms biofilms around thick-walled resting structures like prosthetic heart valves and additionally colonizes and penetrates endothelial walls.[30] C. albicans is responsible for 24-46% of all the cases of FE, and its mortality rate is 46.6–50%.[41]

Other fungi demonstrated to cause endocarditis are Histoplasma capsulatum and Aspergillus.[35] Aspergillus contributes to roughly 25% of FE cases.[41] Endocarditis with Tricosporon asahii has also been reported in a case report.[42]

Risk factors

Risk factors for infective endocarditis are based on the premise that in a healthy individual,

bacteremia (bacteria entering the bloodstream) is cleared quickly with no adverse consequences.[43] However, if a heart valve is damaged, the bacteria can attach themselves to the valve, resulting in infective endocarditis. Additionally, in individuals with weakened immune systems, the concentration of bacteria in the blood can reach levels high enough to increase the probability that some will attach to the valve. Some significant risk factors are listed here:[12][43]

Pathogenesis

Drawing of endocarditis.

Damaged valves and

blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE). The platelet and fibrin deposits that form as part of the blood clotting process allow bacteria to take hold and form vegetations. As previously mentioned, the body has no direct methods of combating valvular vegetations because the valves do not have a dedicated blood supply. This combination of damaged valves, bacterial growth, and lack of a strong immune response results in infective endocarditis.[citation needed
]

Damage to the valves and endocardium can be caused by:[43]

  • Altered, turbulent blood flow. The areas that fibrose, clot, or roughen as a result of this altered flow are known as jet lesions. Altered blood flow is more likely in high pressure areas, so ventricular septal defects or patent ductus arteriosus can create more susceptibility than atrial septal defects.
  • Catheters, electrodes, and other intracardiac prosthetic devices.
  • Solid particles from repeated intravenous injections.
  • Chronic inflammation. Examples include
    auto-immune
    mechanisms and degenerative valvular lesions.

The risk factors for infective endocarditis provide a more extensive list of conditions that can damage the heart.

Diagnosis

Vegetation on the tricuspid valve by echocardiography. Arrow denotes the vegetation.

In general, the Duke criteria should be fulfilled in order to establish the diagnosis of endocarditis.[12][44] Although the Duke criteria are widely used, they have significant limitations.[12] For example, the sensitivity of the Duke criteria for detecting infective endocarditis decreases when prosthetic heart valves are present.[12]

As the Duke criteria rely heavily on the results of echocardiography, research has addressed when to order an

staphylococci
make the following estimates incorrect.

The blood tests

C reactive protein (CRP) and procalcitonin have not been found to be particularly useful in helping make or rule out the diagnosis.[50]

Ultrasound

Echocardiography is the main type of diagnostic imaging used to establish the diagnosis of infective endocarditis.[12] There are two main types of echocardiography used to assist with the diagnosis of IE: transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE).[12]

The transthoracic echocardiogram has a sensitivity and specificity of approximately 65% and 95% if the echocardiographer believes there is 'probable' or 'almost certain' evidence of endocarditis.[51][52] However, in endocarditis involving a prosthetic valve, TTE has a sensitivity of approximately 50%, whereas TEE has a sensitivity exceeding 90%.[12] The TEE also has an important diagnostic role when the TTE does not reveal IE but diagnostic suspicion remains high, since TEE is more sensitive for infective endocarditis and is better able to characterize infection-related damage to the heart valves and surrounding tissues.[12]

Guidelines support the initial use of TTE over TEE in people with abnormal blood cultures, a new heart murmur, and suspected infective endocarditis.

pacemaker).[12]

Modified Duke criteria

Established in 1994 by the Duke Endocarditis Service and revised in 2000, the Duke criteria are a collection of major and minor criteria used to establish a diagnosis of infective endocarditis.[44][55] According to the Duke criteria, diagnosis of infective endocarditis can be definite, possible, or rejected.[43] A diagnosis of infective endocarditis is definite if either the following pathological or clinical criteria are met:

One of these pathological criteria:

  • Histology or culture of cardiac vegetation, embolized vegetation, or intracardiac abscess from the heart finds microorganisms
  • Active endocarditis

One of these combinations of clinical criteria

  • Two major clinical criteria
  • One major and three minor criteria
  • Five minor criteria

Diagnosis of infective endocarditis is possible if one of the following combinations of clinical criteria is met:

  • One major and one minor criteria
  • Three minor criteria are fulfilled

Major criteria

Positive blood culture with typical IE microorganism, defined as one of the following:[43]

  • Typical microorganism consistent with IE from two separate blood cultures, as noted below:
    • Viridans-group streptococci
      , or
    • Streptococcus bovis including nutritional variant strains, or
    • HACEK
      group, or
    • Staphylococcus aureus, or
    • Community-acquired
      enterococci
      , in the absence of a primary focus
  • Microorganisms consistent with IE from persistently positive blood cultures defined as:

Evidence of endocardial involvement with positive echocardiogram is defined as

  • Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or
  • Abscess, or
  • New partial dehiscence of prosthetic valve or new valvular regurgitation (worsening or changing of preexisting murmur not sufficient)

Minor criteria

Updated (2023) Modified Duke Criteria for Infective Endocarditis: Infective endocarditis (IE) is a life-threatening condition and the Duke criteria (established in 1994 and revised in 2000) has been fundamental for the diagnosis of the disease. However, the landscape of micro-biology, diagnostics, epidemiology, and treatment for lE has evolved significantly over the years. The 2023 modified Duke criteria address these changes: https://medicalstudyhub.com/updated-2023-modified-duke-criteria-for-infective-endocarditis/

Risk

Among people who do not

use intravenous drugs and have a fever in the emergency department, there is a less than 5% chance of occult endocarditis. Mellors in 1987 found no cases of endocarditis nor of staphylococcal bacteremia among 135 febrile patients in the emergency room.[49] The upper confidence interval for 0% of 135 is 5%, so for statistical reasons alone, there is up to a 5% chance of endocarditis among these patients. In contrast, Leibovici found that among 113 non-selected adults admitted to the hospital because of fever there were two cases (1.8% with 95%CI: 0% to 7%) of endocarditis.[48]

Among people who do use intravenous drugs and have a fever in the emergency department, there is about a 10% to 15% prevalence of endocarditis. This estimate is not substantially changed by whether the doctor believes the patient has a trivial explanation for their fever.[47] Weisse found that 13% of 121 patients had endocarditis.[45] Marantz also found a prevalence of endocarditis of 13% among such patients in the emergency department with fever.[47] Samet found a 6% incidence among 283 such patients, but after excluding patients with initially apparent major illness to explain the fever (including 11 cases of manifest endocarditis), there was a 7% prevalence of endocarditis.[46] During the Opioid epidemic in the United States, hospitals observed an increase in stroke associated with infective endocarditis.[56]

Among people with staphylococcal bacteremia (SAB), one study found a 29% prevalence of endocarditis in community-acquired SAB versus 5% in nosocomial SAB.[57] However, only 2% of strains were resistant to methicillin and so these numbers may be low in areas of higher resistance.[citation needed]

Prevention

Not all people with heart disease require antibiotics to prevent infective endocarditis. Heart diseases have been classified into high, medium and low risk of developing IE. Those falling into high risk category require IE prophylaxis before endoscopies and urinary tract procedures. Diseases listed under high risk include:[58]

  • Prior endocarditis
  • Unrepaired cyanotic congenital heart diseases
  • Completely repaired congenital heart disease in their first 6 months
  • Prosthetic heart valves or valves repaired with any prosthetic material
  • Incompletely repaired congenital heart diseases
  • Cardiac transplant valvulopathy

Following are the antibiotic regimens recommended by the American Heart Association for antibiotic prophylaxis:[40]

Oral amoxicillin one hour before the procedure
Intravenous or intramuscular ampicillin one hour before the procedure
In patients allergic to penicillins
Azithromycin or clarithromycin orally one hour before the procedure
Cephalexin orally one hour before the procedure
Clindamycin orally one hour before the procedure

In the UK, NICE clinical guidelines no longer advise prophylaxis because there is no clinical evidence that it reduces the incidence of IE and there are negative effects (e.g. allergy and increased bacterial resistance) of taking antibiotics that may outweigh the benefits.[59]

Antibiotics were historically commonly recommended to prevent IE in those with heart problems undergoing dental procedures (known as dental antibiotic prophylaxis). There is, however, insufficient evidence to support whether antibiotics are effective or ineffective at preventing IE when given prior to a dental procedures in people at high risk.[60] They are less commonly recommended for this procedure.[61]

In some countries e.g. the US, high risk patients may be given prophylactic antibiotics such as

beta lactamase-producing bacteria) are used in prophylaxis.[citation needed
]

Treatment

High-dose antibiotics are the cornerstone of treatment for infective endocarditis. These antibiotics are administered by the intravenous (IV) route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adhering to them are supplied by blood vessels. Antibiotics are typically continued for two to six weeks depending on the characteristics of the infection and the causative microorganisms. Antibiotic treatment lowers the risk of embolic complications in people with infective endocarditis.[12]

In acute endocarditis, due to the fulminant inflammation, empirical antibiotic therapy is started immediately after the blood has been drawn for

streptococci) and the high rate of complications.[63] In cases of subacute endocarditis, where the person's hemodynamic status is usually stable, antibiotic treatment can be delayed until the causative microorganism can be identified.[citation needed
]

Viridans group

Enterococci are usually treated with a combination therapy consisting of penicillin and an aminoglycoside for the entire duration of 4–6 weeks.[64]

Some people may be treated with a relatively shorter course of treatment[64] (two weeks) with benzyl penicillin IV if infection is caused by viridans group streptococci or Streptococcus bovis as long as the following conditions are met:

  • Endocarditis of a native valve, not of a prosthetic valve
  • A MIC ≤ 0.12 mg/l
  • No complication such as
    arrhythmia
    , or pulmonary embolism occurs
  • No evidence of extracardiac complication like septic thromboembolism
  • No vegetations > 5 mm in diameter conduction defects
  • Rapid clinical response and clearance of bloodstream infection

Additionally, oxacillin-susceptible Staphylococcus aureus native valve endocarditis of the right side can also be treated with a short 2-week course of a

beta-lactam antibiotic such as nafcillin
with or without aminoglycosides.

Histopathology of a vegetation of bacterial endocarditis, taken from a valve repair, H&E stain. In a consistent clinical setting, neutrophils and fibrin is enough to diagnose a bacterial vegetation, even without visible bacterial colonies.

The main indication for surgical treatment is regurgitation or stenosis. In active infective endocarditis, the surgery should remove enough leaflet tissue to ensure eradication of the infectious process.[66] Subsequent valve repair can be performed in limited disease.[66] Replacement of the valve with a mechanical or bioprosthetic artificial heart valve is necessary in certain situations:[67]

  • Patients with significant valve stenosis or regurgitation causing heart failure
  • Evidence of hemodynamic compromise in the form of elevated end-diastolic left ventricular or left atrial pressure or moderate to severe pulmonary hypertension
  • Presence of intracardiac complications like paravalvular abscess, conduction defects or destructive penetrating lesions
  • Recurrent septic
    emboli
    despite appropriate antibiotic treatment
  • Large vegetations (> 10 mm)
  • Persistently positive blood cultures despite appropriate antibiotic treatment
  • Prosthetic valve dehiscence
  • Relapsing infection in the presence of a prosthetic valve
  • Abscess formation
  • Early closure of mitral valve
  • Infection caused by fungi or resistant Gram-negative bacteria.

The guidelines were recently updated by both the American College of Cardiology and the European Society of Cardiology. There was a recent meta-analysis published that showed surgical intervention at seven days or less is associated with lower mortality.[68]

Prognosis

Infective endocarditis is associated with 18% in-hospital mortality.[29] However, adult patients with congenital heart disease can have relatively lower mortality down to 5% due to younger age, right-sided endocarditis and management by multidisciplinary teams. As many as 50% of people with infective endocarditis may experience embolic complications.[12]

Epidemiology

In developed countries, the annual incidence of infective endocarditis is 3 to 9 cases per 100,000 persons.[43] Infective endocarditis occurs more often in men than in women.[12] There is an increased incidence of infective endocarditis in persons 65 years of age and older, which is probably because people in this age group have a larger number of risk factors for infective endocarditis. In recent years, over one-third of infective endocarditis cases in the United States was healthcare-associated.[43] Another trend observed in developed countries is that chronic rheumatic heart disease accounts for less than 10% of cases. Although a history of valve disease has a significant association with infective endocarditis, 50% of all cases develop in people with no known history of valvular disease.[citation needed]

History

Few diseases present greater difficulties in the way of diagnosis than malignant endocarditis, difficulties which in many cases are practically insurmountable. It is no disparagement to the many skilled physicians who have put their cases upon record to say that, in fully one-half the diagnosis was made post mortem.

— William Osler, 1885

Lazare Riviére first described infective endocarditis affecting the

systemic lupus erythematosus.[12] In 1944, physicians reported on the first successful use of penicillin to treat a case of infective endocarditis.[12]

References

  1. ^ a b c d e f g h i j k l m n o p q r "Infective Endocarditis – Cardiovascular Disorders". Merck Manuals Professional Edition. September 2017. Retrieved 11 December 2017.
  2. ^
    PMID 27886786
    .
  3. ^ "Endocarditis". Mayo Clinic. Retrieved June 4, 2022.
  4. ^ "Endocarditis". Cleveland Clinic. Retrieved 2022-06-09.
  5. ^
    PMID 36946284
    .
  6. ^ .
  7. .
  8. ^ .
  9. .
  10. .
  11. .
  12. ^ .
  13. ^ .
  14. .
  15. ^ "Endocarditis". The Lecturio Medical Concept Library. Retrieved 18 July 2021.
  16. PMID 26320109
    .
  17. ^ .
  18. .
  19. .
  20. ^ .
  21. .
  22. .
  23. ^ .
  24. .
  25. .
  26. ^ "Heart Valves and Infective Endocarditis". American Heart Association. Retrieved 18 July 2021.
  27. PMID 26320109
    .
  28. .
  29. ^ .
  30. ^ .
  31. ^ HACEK Group Infections at eMedicine
  32. ^ "Pseudomonas aeruginosa". Topics in Infectious Diseases Newsletter. August 2001. Archived from the original on July 24, 2008.
  33. PMID 15249410
    .
  34. .
  35. ^ .
  36. .
  37. .
  38. .
  39. .
  40. ^ .
  41. ^ .
  42. .
  43. ^ .
  44. ^ .
  45. ^ .
  46. ^ .
  47. ^ .
  48. ^ .
  49. ^ .
  50. .
  51. .
  52. .
  53. ^ a b c "UOTW #27 – Ultrasound of the Week". Ultrasound of the Week. 26 November 2014. Archived from the original on 9 May 2017. Retrieved 27 May 2017.
  54. ^ "UOTW #60 – Ultrasound of the Week". Ultrasound of the Week. 5 October 2015. Archived from the original on 9 May 2017. Retrieved 27 May 2017.
  55. PMID 10770721
    .
  56. .
  57. .
  58. .
  59. ^ "Prophylaxis against infective endocarditis: Antimicrobial prophylaxis against infective endocarditis in adults and children undergoing interventional procedures". NICE Clinical Guidelines. National Institute for Health Care and Excellence (UK). March 2008. Archived from the original on 2013-01-26. Retrieved 2013-04-30.
  60. PMID 35536541
    .
  61. ^ "Prophylaxis against infective endocarditis: antimicrobial prophylaxis against infective endocarditis in adults and children undergoing interventional procedures". National Institute for Health and Care Excellence (NICE). 2008.
  62. ^ "Drug Prescribing". SDCEP. Retrieved 2018-01-25.
  63. PMID 19207079
    .
  64. ^ .
  65. .
  66. ^ .
  67. .
  68. .

External links

Infective endocarditis at

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