A cardiology case (video): Infective endocarditis of a prosthetic mitral valve -Transesophageal echocardiography
This is a case of a 32 years old female with a history of mitral valve replacement (with a bileaflet mechanical valve) 3 years before, presenting with fever and a cerebrovascular stroke.
( Echo images are courtesy of dr Abdallah Almaghraby )
To watch the video in full screen click on the symbol  at the lower right corner
Infective endocarditis (IE) is a microbial infection of the endocardium or implanted intracardiac materials (eg prosthetic valves, conduits), or pacing electrodes, and indwelling catheters. The most typical pathologic feature of IE is a mobile vegetation associated with valve leaflets. Vegetations are composed of fibrin, platelets, debris, and bacteria. Left-sided lesions are more common than right-sided lesions (the latter are common in intravenous drug
use and congenital abnormalities).
Infective endocarditis (IE) is a serious disease carrying potential for high morbidity and mortality, in part due to the difficulty in establishing an accurate diagnosis early in the course of the disease.
The incidence of IE in the general population is approximately 3-4 cases in 100.000 people per year.
The most common microorganism involved is staphylococcus aureus , the next most common are streptococci of the oropharyngeal cavity (mostly streptococcus viridians), followed in order of frequency by enterococcus, coagulase-negative staphylococci, other streptococcal species, microorganisms of the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium hominis, Eikenella corrodens, Kingella) group, non HACEK Gram-negative bacteria, and fungi.
Pathogenesis of IE
In most cases, an injury to the endothelium is involved, being the result of turbulent blood flow at the site of a preexisting cardiac lesion. This results in the deposition of platelets and fibrin on the site and these early deposits are called nonbacterial thrombotic endocarditis. In case of a microorganism present in the blood, for example due to a dental procedure, or an infection, the microorganism can enter these thrombotic deposits and grow, resulting in the development of vegetations, composed of fibrin, platelets, debris, and bacteria and also often in invasion and destruction of cardiac structures, such as valve tissue, or occasionally invasion of the adjacent myocardium (formation of an abscess).
Heart conditions predisposing to endocarditis
Conditions that predispose to the development of IE by order of frequency include degenerative valve disease , presence of a prosthetic heart valve, intravenous narcotic drug use, rheumatic heart disease and congenital heart disease.
Conditions predisposing to endocarditis (if significant bacteremia also occurs) are classified according to their relative risk for endocarditis and are the following:
Cardiac conditions with a relatively high or intermediate risk for IE
Indwelling right heart catheters for hyperalimentation are associated with high risk for IE, but indwelling right heart catheters for other purposes pose an intermediate risk
Hypertrophic obstructive cardiomyopathy (intermediate risk)
Congenital heart disease with low risk for IE: an uncorrected atrial septal defect and surgically corrected congenital lesions without a prosthesis >6 months after surgery
Aortocoronary bypass surgery (negligible risk)
A cardiac transplant with valve regurgitation due to a structurally abnormal valve
Antibiotic prophylaxis is also recommended before implantation of pacemakers, or implantable defibrillators (ICDs), to avoid infection of the device.
Clinical manifestations of IE
The most typical presentation of IE is the presence of fever and a new murmur (in about 85%) of cases. However, fever may be absent in the elderly, uremic, or immunosuppressed. A murmur may be absent with right-sided or mural infection or with infection of an intracardiac device. Nonspecific symptoms such as malaise, fatigue and night sweats are common. Dyspnea is also common.
Congestive heart failure occurs in up to 55% of cases.
Neurologic symptoms and findings, are usually indications of an embolic complication and may include clinically apparent cerebral emboli (20%), rupture of a mycotic aneurysm (< 5%), meningitis, or brain abscess (< 5%).
Additional possible manifestations of IE, are due to embolic or immune complex phenomena and include mucosal petechiae (in about 20% -30% of cases), Osler’s nodes (painful, tender red nodules on the pads of fingers or toes: 10% -20%), splinter hemorrhages (dark red linear streaks under the nails in about 10% -20%), an arterial embolism (the clinical picture depends on the site of embolism,see below), Janeway lesions (these are more rare, they are red, macular, nontender lesions on the fingers, palms, or soles, observed in < 5% of IE cases), splenomegaly (in about 30% of cases), and Roth’s spots (retinal hemorrhages: < 5%). These classic physical findings are not sensitive and (also not specific) for the diagnosis of IE.
Systemic embolization occurs in about 20% - 40% of cases of IE and may result in manifestations of an acute stroke (cerebral emboli), or it can mimic peritonitis (embolization to the spleen, kidney, or bowel), a pulmonary embolism (from IE involving the right side of the heart), an acute coronary syndrome (coronary artery emboli), or it may result in a cold extremity with reduced or absent pulse (embolization of a peripheral artery).
In summary, the clinical picture of IE is highly variable, ranging from subtle and slowly progressive symptoms to acute severe congestive heart failure due to severe valvular regurgitation. IE can be divided into acute and subacute.
The major diagnostic criteria can be summarized as
A more detailed description of the major clinical diagnostic criteria is the following:
• A positive blood culture for infective endocarditis, as defined by the recovery of a typical microorganism from two separate blood cultures in the absence of a primary focus.
(Typical microorganisms include viridans streptococci, community-acquired staphylococcus aureus or enterococcus species, streptococcus bovis, HACEK group, abiotrophia species and granulicatella species), or
• A persistently positive blood culture, for a microorganism consistent with IE from either blood samples obtained more than 12 hours apart, or all three, or a majority of four or more separate blood samples, with the first and last obtained at least 1 hour apart, or
• A positive serological test for Q fever, with an immunofluorescence assay showing phase 1 IgG antibodies at a titre >1 : 800, or
-An oscillating intracardiac mass on a cardiac valve or its supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation, or
-An abscess, or
-New partial dehiscence of a prosthetic valve, or
-New valvular regurgitation.
The minor criteria are:
Predisposing cardiac lesion
IV drug use
Vascular phenomena (arterial embolic, septic pulmonary infarcts, Janeway lesions),
Immunologic phenomena (such as Osler nodes, Roth spots, glomerulonephritis, or a positive rheumatoid factor)
Microbiologic evidence (positive blood cultures not meeting major criteria or evidence of active infection with an organism consistent with infective endocarditis)
Some echocardiographic findings, that can be observed in infective enocarditis (IE):
An abscess, on echocardiography, is a thickened, nonhomogeneous area near a valve with echodense or echolucent appearance. Evidence of flow into the region is supportive for the diagnosis, but not mandatory.
Perforation of a valve leaflet is defined as interruption of tissue continuity of valve leaflet with demonstration of flow with color flow doppler, through the defect.
Dehiscence of a prosthetic valve is shown by demonstration of paravalvular regurgitation by transthoracic or transesophageal echocardiography, with or without a rocking motion of the prosthesis.
Pseudoaneurysm is a perivalvular cavity communicating with the cardiovascular lumen and in echocardiography it appears as a pulsatile perivalvular echo-free space (an echolucent cavity) with color-Doppler detected entering this space.
A valve aneurysm is a saccular outpouching or bulging of valvular tissue (meaning that a portion of the valvular tissue protrudes outward).
Treatment of IE
According to the latest guidelines, the best management of IE can be achieved via an "endocarditis team", a multidisciplinary collaboration among cardiologists, cardiac surgeons, and infectious
disease specialists (Although, this is not always quite possible).
In IE, prompt initiation of parenteral antibiotic therapy is important, because the rate of complications, such as embolization, decreases rapidly within several days, after initiation of proper antibiotic treatment. In severely ill patients with IE initial empirical antibiotic treatment (before pathogen identification) should start immediately after obtaining three separate blood cultures at 30 minute time intervals. When the pathogen is identified the antibiotic regimen can change according to the specific microorganism and its antibiotic subsceptibility. Generally in IE the duration of antibiotic treatment is usually about 4-6 weeks. Repeat sets of blood cultures
after the initiation of antibiotic treatment are obtained every 48 hours, until the resolution of bacteremia is confirmed.
Indications for surgery in IE include:
Heart failure with pulmonary edema or cardiogenic shock, or signs and symptoms of heart failure, or valve dysfunction with echocardiographic signs of poor haemodynamic tolerance.
Findings suggesting that the infection cannot be controlled or is allready uncontrolled such as persisting positive blood cultures despite appropriate antibiotic therapy and adequate control of septic metastatic foci, or
local findings of uncontrolled infection such as abscess, false aneurysm, fistula, or an enlarging vegetation,
After an embolic episode in a patient with IE involving a native or prosthetic aortic or mitral valve with persistent vegetations >10 mm despite appropriate antibiotic therapy.
IE involving an aortic or mitral valve (native or prosthetic) with very large vegetations >30 mm (this is a relative-class IIa-indication for surgery).
Therapy of I E caused by some common specific microorganisms
For patients allergic to beta-lactam antibiotics (penicillines, cephalosporines) : Use for 4 weeks Vancomycin 30 mg/kg/day i.v. in 2 doses.
or in allergic patients Vancomycin (4 weeks) + Gentamycin (2 weeks), dosages as above
For staphylococcus (Methicillin-resistant) endocarditis of prosthetic valves, or allergy to penicillin, instead of Flucloxacillin, or Oxacillin use Vancomycin, with the same other 2 drugs. Treatment duration is the same.
Alternative treatment (in penicillin-allergic patient or resistant strain of enterococcus):Vancomycin + Gentamycin, both for 6 weeks (Dosages as usual, see above).
(Pediatric doses of antibiotics in IE: Penicillin G 200,000 U/kg/day i.v. in 4–6 divided doses, Amoxicillin 300 mg/kg/day i.v. in 4–6 divided doses ,
Rifampin 20 mg/kg/day i.v. or orally in 3 equally divided doses)
Treatment for HACEK group microorganisms. These are slow growing fastidious gram negative bacilli. They are susceptible to ceftriaxone, other third-generation cephalosporins and quinolones. Standard treatment is ceftriaxone 2 g/day ( treatment duration in native valve enodcardis is 4 weeks and in prosthetic valve endocarditis is 6 weeks.
For Gram-negative bacteria that do not belong to the HACEK group the recommended treatment is early surgery plus long-term (at least 6 weeks) therapy with bactericidal combinations of beta-lactams and aminoglycosides. A quinolone or cotrimoxazole may be added to the above treatment.
In cases of pocket infection : erythema (redness), pain, local warmth, purulent discharge, or erosion of the skin.
In cases of endocarditis: fever is the most common symptom, fatigue, malaise, loss of appetite are common, and local signs of pocket infection may be present. A septic pulmonary embolus may occur.
In the majority of patients, CDRIE must be treated by complete hardware (device and leads) removal and prolonged antibiotic therapy (i.e. before and after hardware removal). The same treatment is also recommended in presumably isolated pacemaker or defibrillator pocket infection (i.e infection at the site, where the battery of the device has been implanted).Before reimplantation of the device a re-evaluation of the indication for implantation is necessary, because in some cases, reimplantation is not necessary. The new device should be implanted on the contralateral side. Immediate reimplantation should be avoided, because there is a significant risk of new infection. Blood cultures should be negative for at least 72 hours before placement of a new device. The decision on the timing of reimplantation needs a consideration of several factors such as persistent bacteremia, persistent vegetation and how dependent is the patient from the pacemaker or the implantable cardioverter defibrillator. When there is evidence of remnant valvular infection, implantation should be delayed for at least 14 days. Temporary pacing should be avoided if possible, because it is a risk factor for subsequent cardiac device infection. In a pacing-dependent patient, temporary use of active fixation leads connected to an external device can be a "bridging strategy", until the placement of a new permanent device is considered safe.
I recommend this video (by 123sonography) showing echocardiography in native valve endocarditis Link:
Echo in Endocarditis-Prof. Thomas Binder
Hoen B, Duval X. Infective endocarditis. N Engl J Med 2013; 368:1425–1433
Li JS, Sexton DJ, et al: Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis, Clin Infect Dis 2000;30:633–638