11.4.6 Infectious endocarditis

Nosology 

 

Infective endocarditis is a rare disease (prevalence 3-10/100,000/year), but its mortality remains dramatic: 20% in hospital and 40% at one year [3]. Despite advances in antibiotic therapy and surgery, these figures remain stable because patients are getting older, the pathogens are more virulent and the medical context is becoming more complex (haemodialysis, diabetes, immunosuppression, intravascular prostheses, pacemakers, intravenous drugs). In 72% of cases, the disease affects a native valve with degenerative pathology, and in 20% of cases it affects a prosthetic valve [10]. The risk of endocarditis for the latter is 0.4-0.6%/year [4]. The pathogens involved have evolved over the last twenty years and currently have the following profile [9,10].

 

*Haemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella.

 

Clinical features include persistent fever, petechiae (40% of cases), heart failure, the presence of a murmur on auscultation and emboli (50% of cases) [10]. The majority of cerebral emboli are silent. Diagnosis is based on blood cultures (2 separate samples) and echocardiography. If the transthoracic examination is inadequate, transesophageal echocardiography (sensitivity and specificity > 90%) is performed (Figure 11.32) and possibly a CT scan, which is less susceptible to artefacts caused by prosthetic material. In doubtful cases, PET scan will show areas of high metabolic activity around the prosthesis [2]. Blood cultures are negative in 10-20% of cases, mostly due to previous antibiotic therapy; for certain pathogens, specific serology may help to overcome this problem. The Duke criteria are useful in assessing the likelihood of endocarditis (Table 11.4) [5].

 

 

 Antibiotic treatment

 

Antibiotic treatment is started as soon as the causative organism is identified. If clinical and echocardiographic findings are positive but blood cultures are negative, empirical treatment is required (Table 11.5) [1,3,4,11].

 

In 48% of cases of endocarditis, treatment leads to surgery to resect the infected structure, repair the valvular insufficiency or fistula, control the infection and prevent embolism. The degree of failure is such that surgery is often performed as an emergency within 48 hours after haemodynamic restoration and antibiotic coverage; once the indication has been established, delay is detrimental, except in the case of stroke (risk of intracranial haemorrhage) [2]. Indications for surgery are divided into three categories [1,4].

• Haemodynamic decompensation.
  • Severe mitral or aortic regurgitation (often acute).
  • Severe valve obstruction (obstructed winglets).
  • Fistula resulting in cardiogenic shock.
• Uncontrolled infection.
  • Abscess, pseudoaneurysm (increasing in volume), complete AV block.
  • Vegetation.
  • Infection of prosthetic devices (mechanical valve, bioprosthesis, Dacron tube).
  • Persistence of infection despite antibiotic treatment (fever, positive blood cultures).
• Prevention of emboli
  • Aortic or mitral mobile vegetation > 10 mm with embolic event, abscess or cardiac decompensation.
  • Aortic or mitral mobile vegetation > 15 mm.
  • Tricuspid vegetation > 20 mm.

Valve repair is always preferable to prosthesis replacement in this setting, but is not always possible given the degree of valve destruction and extent of the lesion. If aortic reconstruction is required, a homograft is preferred. If the valve is infected, removal of the implanted device (pacemaker, catheter, etc) is recommended [7]. In-hospital mortality is 17%; 10-year survival is 40-60%, much lower than for elective valve surgery on a clean valve [6].

 Prophylactic treatment

High velocity jets and the presence of prosthetic material are a cause of endothelial lesions leading to platelet and fibrin deposition; in the presence of bacteraemia, organisms can easily colonise these lesions and develop a focus of endocarditis [7]. This phenomenon is a high-risk situation requiring antibiotic prophylaxis in the event of surgery that could lead to bacteraemia [2,7,8].

• Presence of prosthetic material; the risk of endocarditis is highest with mechanical prostheses and foreign components (rings, tubes, patches, implanted material); it is lowest with bioprostheses; it is lowest with homografts. Endoprostheses such as TAVI carry the same risk as other prostheses. The presence of high velocity blood flow is an additional risk factor.
• Cyanotic congenital heart disease.
• Congenital heart disease with prosthetic material during the first 6 months after implantation or for life in the presence of high-velocity shunt/regurgitation.
• Heart transplant recipients with valvular insufficiency due to structural damage.
• History of endocarditis.

Low-velocity non-cyanogenic heart disease (ASD, PFO, coarctation), low mechanical stress valve disease (Barlow's disease, ischaemic or functional MI, dynamic subaortic obstruction) and functional insufficiencies are low-risk lesions that do not require prophylaxis, except where justified by the surgical procedure [1,4].

Although antibiotic prophylaxis is necessary in high-risk cases, recent recommendations favour a more balanced attitude between the risks associated with antibiotics, which are significant, and the benefits of prophylaxis, which are not very significant [1,4]. Prophylaxis is therefore no longer systematically recommended for all operations, unless it is part of the surgical procedure itself. A few comments are in order [7].

• Antibiotic prophylaxis for dental surgery is only justified in cases of gingival effraction, perforation of the mucosa, periapical surgery or dental abscess.
• Genitourinary or digestive endoscopic procedures (cystoscopy, gastroscopy, TEE, colonoscopy, etc.) do not require prophylaxis in the absence of active infection.
• With the exception of tonsillectomy, prophylaxis is no longer recommended for operations on the respiratory tract in the absence of active infection.
• Prophylaxis is no longer recommended in aortic stenosis, mitral stenosis, bicuspid aortic valve without haemodynamic consequences, coarctation of the aorta, mitral valve prolapse, functional insufficiency or obstructive cardiomyopathy, unless routine treatment is justified by the operation itself.