Infective endocarditis

Infection most commonly involves heart valves (either native or prostatic) but may also occur on the low-pressure side of a VSD, damaged mural endocardium or on intra-cardiac devices.
Classification
Temporal – acute, sub acute
Site of infection – right Vs left, Valvular Vs non valvular
Cause of infection – bacterial, fungal, rickettsial, culture negative
Predispostion – congenital defects, prostatic valves, drug abuse
Definition and classification

Incidence – 2.6-7:100,000 in the western world. Increasing among elderly.
Predisposition – congenital heart disease, rheumatic heart disease, IV drug abuse, intra-cardiac devices.
16-30% of all cases involve prostatic valves.
The risk for IE on prostatic valve is greatest during the first 6-12 month after surgery.
Epidemiology

Clinical manifestation
Cardiac manifestations
Murmur 80-85%
CHF 30-40%
Arrhythmia
Pericarditis
Coronary emboli
Non cardiac manifestations
Fever 80-90%
Chills 40-75%
Anorexia, weight loss, malaise 25-50%
Back pain 7-15%
Arterial emboli 20-50%
Splenomegaly 15-50%
Clubbing 10-20%
Neurologic manifestations 20-40%
Peripheral manifestations 2-15%
Petechiae 10-40%
Laboratory manifestations
Anemia 70-90%
Leukocytosis 20-30%
Microscopic hematuria 30-50%
Elevated ESR 60-90%
Elevated CRP >90%
Elevated RF 50%
Decreased complement 5-40%

Clinical manifestations

Diagnosis – Duke criteria
Definite IE: Histology or culture of a cardiac vegetation, an embolized vegetation, or intracardiac abscess from the heart finds microorganisms.
Active endocarditis: One of these combinations of clinical criteria
2 major clinical criteria
1 major and 3 minor criteria
5 minor criteria
Possible IE:
1 major and 1 minor criteria
3 minor criteria

Etiology

Treatment

B. quintana and B. henselae are the most common bartonella spp. implicated in endocarditis.
Native valves > prostatic valves
60% aortic valve
Sub-acute endocarditis, mild non specific symptomes lasting for months to years,
Positive blood cultures 25% (6 weeks of incubation)
Diagnosis – sierology, PCR
Treatment – aminoglycosides for at least 2 weeks
Bartonella endocarditis

C. brunetti
Gram neg cocco-bacillus
Primary sources – cattle, sheep and goats
Incidence – 24-54 cases per years in the USA. 70% male, April - June.
Acute Q fever
Incubation 3 – 30 days
Hepatitis (40%), pneumonia (17%), pneumonia + hepatitis (20%), isolated fever (14%), CNS involvement (2%), pericarditis or myocarditis (1%).
Symptoms: fatigue, photophobia, headache, sweats, nausea, vomiting, diarrhea, cough, rash.
Lab: normal WBC, thrombocytosis during recovery.
CXR: rounded opacities
Chronic Q fever
Almost always implies endocarditis usually in patients with previous valvular disease, immunosuppression or CRF
Valvular vegetations 12% in TTE
Hepatomegaly, splenomegaly, elevated RF, elevated ESR, elevated CRP.
Diagnosis: PCR, Sierology (IgG >1:800 phase I = chronic disease. IgG >1:800 phase II = acute disease).
Treatment
Acute disease – doxycycline 100mg bid for 14 days
Chronic disease – doxycycline 100mg bid + hydroxychloroquine 200mg bid for 18 mo.
second line rifampin + doxycycline or ciproxin
Q fever

Main complications of left-sided valve infective endocarditis and their management
HF is the most frequent and among the most severe complications of IE. Unless severe co-morbidity exists, the presence of HF is an indication for early surgery in NVE and PVE, even in patients with cardiogenic shock.
Heart failure in infective endocarditis
HF is the most frequent complication of IE and represents the most common indication for surgery in IE. HF is observed in 42–60% of cases of NVE and is more often present when IE affects the aortic rather than the mitral valve.
Valvular regurgitation in native IE may occur as a result of mitral chordal rupture, leaflet rupture (flail leaflet), leaflet perforation or interference of the vegetation mass with leaflet closure. A particular situation is infection of the anterior mitral leaflet secondary to an infected regurgitant jet of a primary aortic IE.
Clinical presentation of HF may include dyspnea, pulmonary edema and cardiogenic shock. Echocardiography is also useful to evaluate the hemodynamic consequences of valvular dysfunction, measurement of pulmonary artery pressure, detection of pericardial effusion and assessment and monitoring of left ventricular systolic function and left and right heart filling pressures.
B-type natriuretic peptide has potential use in the diagnosis and monitoring of HF in IE. Both elevated levels of cardiac troponins and B-type natriuretic peptide are associated with adverse outcomes in IE. Moderate to severe HF is the most important predictor of in-hospital, 6-month and 1-year

Uncontrolled infection
Perivalvular extension of IE is the most frequent cause of uncontrolled infection and is associated with a poor prognosis and high likelihood of the need for surgery. Perivalvular complications include abscess formation, pseudoaneurysms and fistulae
Pseudoaneurysms and fistulae are severe complications of IE and are frequently associated with very severe valvular and perivalvular damage. The frequency of fistula formation in IE has been reported to be 1.6%, with S. aureus being the most commonly associated organism (46%).
Despite high rates of surgery in this population (87%), hospital mortality remains high (41%). Other complications due to major extension of infection are less frequent and may include ventricular septal defect, third-degree atrio-ventricular block and acute coronary syndrome.
Perivalvular extension should be suspected in cases with persistent unexplained fever or new atrio-ventricular block. Therefore an electrocardiogram should be performed frequently during continuing treatment, particularly in aortic IE. TOE, MSCT and PET/CT are particularly useful for the diagnosis of perivalvular complications, while the sensitivity of TTE is <50%.
Persisting infection
Perivalvular extension in infective endocarditis
Embolic events in infective endocarditis
Embolic events are a frequent and life-threatening complication of IE related to the migration of cardiac vegetations. The brain and spleen are the most frequent sites of embolism in left-sided IE, while pulmonary embolism is frequent in native right-sided and pacemaker lead IE. Stroke is a severe complication and is associated with increased morbidity and mortality. Conversely, embolic events may be totally silent in 20–50% of patients with IE, especially those affecting the splenic or cerebral circulation, and can be diagnosed by non-invasive imaging. Thus systematic abdominal and cerebral CT scanning may be helpful. However, contrast media should be used with caution in patients with renal impairment or hemodynamic instability because of the risk of worsening renal impairment in combination with antibiotic nephrotoxicity.
Overall, embolic risk is very high in IE, with embolic events occurring in 20–50% of patients. However, the risk of new events (occurring after initiation of antibiotic therapy) is only 6–21%. A study from the ICE group demonstrated that the incidence of stroke in patients receiving appropriate antimicrobial therapy was 4.8/1000 patient-days in the first week of therapy, falling to 1.7/1000 patient-days in the second week, and further thereafter.

Neurological complications
Symptomatic neurological events develop in 15–30% of all patients with IE and additional silent events are frequent. Stroke (ischaemic and haemorrhagic) is associated with excess mortality. Rapid diagnosis and initiation of appropriate antibiotics are of major importance to prevent a first or recurrent neurological complication. After a first neurological event, cardiac surgery, if indicated, is generally not contraindicated, except when extensive brain damage or intracranial haemorrhage is present.
Infectious aneurysms
Other complications of infective endocarditis
Splenic complications
Myocarditis and pericarditis
Heart rhythm and conduction disturbances
Musculoskeletal manifestations
Acute renal failure

Surgery

Patient population: relatively young, low rate of comorbidities.
Microbiology: high rate of Streptococcal infections, low rate of Staphylococcal.
In real-life: patients are older, more comorbidities, and more virulent bacteria, higher rate of complications are expected.
Rate of embolism: ~30% (60% cerebral).
Higher risk during first wk after diagnosis.
Points for discussion

Prophylaxis

Non-specific prevention measures to be followed in high-risk and intermediate-risk patients

Recommendations for prophylaxis of infective endocarditis in the highest-risk patients according to the type of at-risk procedure

Recommendations for antibiotic prophylaxis for the prevention of local and systemic infections before cardiac or vascular interventions

49y male
Staphylococcus aureus NVE
3 weeks of IV antibiotics
Undergoing MVR due to ruptured chorda and CHF
How long will you treat following the surgery?
Case

How do you count the duration of therapy?
It is reasonable that the counting of days for the duration of antimicrobial therapy begin on the first day on which blood cultures are negative
If operative tissue cultures are positive, antimicrobial course is reasonable after valve surgery