However, in penicillin-resistant cases, aminoglycoside treatment must be given for at least 2 weeks and short-term therapy regimens are not recommended. There is very limited experience with daptomycin. IE due to S. The same holds true for penicillin intermediate MIC 0. In cases with meningitis, penicillin must be avoided because of its poor penetration of the cerebrospinal fluid, and should be replaced with ceftriaxone or cefotaxime alone or in association with vancomycin according to the antibiotic susceptibility pattern.
IE due to group B streptococci was once associated with the peripartum period, but it now occurs in other adults, especially the elderly. Group B, C, and G streptococci and S. Gentamicin should be given for 2 weeks. Antibiotic recommendations include penicillin G, ceftriaxone or vancomycin for 6 weeks, combined with an aminoglycoside for at least the first 2 weeks. Staphylococcus aureus is usually responsible for acute and destructive IE, whereas CoNS produce more protracted valve infections except S.
Of note, the addition of an aminoglycoside in staphylococcal native valve IE is no longer recommended because it increases renal toxicity. For penicillin-allergic patients with MSSA IE, penicillin desensitization can be attempted in stable patients since vancomycin is inferior to beta-lactams and should not be given.
If beta-lactams cannot be given, where available, daptomycin should be chosen and given in combination with another effective antistaphylococcal drug to increase activity and avoid the development of resistance. Some experts have recommended a combination of high doses of cotrimoxazole plus clindamycin as an alternative for S. Other differences in comparison with NVE include the overall duration of therapy, the use of aminoglycosides and the addition of rifampin after 3—5 days of effective antibiotic therapy once the bacteraemia has been cleared.
Although the level of evidence is poor, adding rifampin to the treatment of staphylococcal PVE is standard practice, although treatment may be associated with microbial resistance, hepatotoxicity and drug interactions. Methicillin-resistant S. MRSA are usually resistant to multiple antibiotics, leaving only vancomycin and daptomycin to treat severe infections. However, vancomycin-intermediate S. Daptomycin is a lipopeptide antibiotic approved for S. Importantly, daptomycin needs to be administered in appropriate doses and combined with other antibiotics to avoid further resistance in patients with IE.
First, enterococci are highly resistant to antibiotic-induced killing, and eradication requires prolonged administration up to 6 weeks of synergistic bactericidal combinations of two cell wall inhibitors ampicillin plus ceftriaxone, which synergize by inhibiting complementary PBPs or one cell wall inhibitor with aminoglycosides Table Second, they may be resistant to multiple drugs, including aminoglycosides [high-level aminoglycoside resistance HLAR ], beta-lactams via PBP5 modification and sometimes beta-lactamases and vancomycin.
Ampicillin or amoxicillin might be preferred since MICs are two to four times lower. Gentamicin resistance is frequent in both E. Streptomycin may remain active in such cases and is a useful alternative. There have been two important advances in recent years. First is the demonstration, in several cohort studies of E. It is also safer, without any nephrotoxicity. Second, the total daily dose of gentamicin can be given in a single daily dose instead of the two or three divided doses recommended up to now, and the length of the treatment for non-HLAR E.
Beta-lactam and vancomycin resistance are mainly observed in E. Since dual resistance is rare, beta-lactam might be used against vancomycin-resistant strains and vice versa. Varying results have been reported with quinupristin—dalfopristin not active against E. Again, these situations require the expertise of an ID specialist. HACEK Gram-negative bacilli are fastidious organisms and the laboratory should be made aware that infection with these agents is under consideration, as specialist investigations may be required see also section 5.
Because they grow slowly, standard MIC tests may be difficult to interpret. Some HACEK-group bacilli produce beta-lactamases, and ampicillin is therefore no longer the first-line option. Quinupristin—dalfopristin is not active against E. In vitro bactericidal tests and monitoring of serum antibiotic concentrations may be helpful. Because of their rarity and severity, these conditions should be discussed by the Endocarditis Team or with an ID specialist.
Antibiotic treatment of blood culture-negative infective endocarditis adapted from Brouqui et al.
Abbreviations and acronyms
The presented durations are based on selected case reports. In the case of central nervous system involvement, sulfadiazine 1. Trimethoprim is not active against T. Treatment of IE should be started promptly. Three sets of blood cultures should be drawn at min intervals before initiation of antibiotics. Whether the infection affects a native valve or a prosthesis [and if so, when surgery was performed early vs.
The place of the infection community, nosocomial, or non-nosocomial healthcare-associated IE and knowledge of the local epidemiology, especially for antibiotic resistance and specific genuine culture-negative pathogens Table Proposed antibiotic regimens for initial empirical treatment of infective endocarditis in acute severely ill patients before pathogen identification a.
Outpatient parenteral antibiotic therapy OPAT is used to consolidate antimicrobial therapy once critical infection-related complications are under control e. Criteria that determine suitability of outpatient parenteral antibiotic therapy for infective endocarditis adapted from Andrews et al. Surgical treatment is required in approximately half of the patients with IE because of severe complications. Surgery is justified in patients with high-risk features that make the possibility of cure with antibiotic treatment unlikely and who do not have co-morbid conditions or complications that make the prospect of recovery remote.
Age per se is not a contraindication to surgery. Early consultation with a cardiac surgeon is recommended in order to determine the best therapeutic approach. Each case must be individualized and all factors associated with increased risk identified at the time of diagnosis. Frequently the need for surgery will be determined by a combination of several high-risk features.
In other cases, surgery can be postponed to allow 1 or 2 weeks of antibiotic treatment under careful clinical and echocardiographic observation before an elective surgical procedure is performed. Indications and timing of surgery in left-sided valve infective endocarditis native valve endocarditis and prosthetic valve endocarditis. HF is the most frequent complication of IE and represents the most common indication for surgery in IE.
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 dyspnoea, pulmonary oedema and cardiogenic shock. Identification of surgical candidates and timing of surgery decisions should preferably be made by the Endocarditis Team. Surgery is also indicated in patients with severe acute aortic or mitral regurgitation without clinical HF but with echocardiographic signs of elevated left ventricular end-diastolic pressure e.
Surgery must be performed on an emergency basis, irrespective of the status of infection, when patients are in persistent pulmonary oedema or cardiogenic shock despite medical therapy.
Urgent surgery should also be performed in patients with severe aortic or mitral insufficiency with large vegetations, even without HF. In patients with well-tolerated New York Heart Association class I or II severe valvular regurgitation and no other reasons for surgery, medical management with antibiotics under strict clinical and echocardiographic observation is a good option, although early surgery may be an option in selected patients at low risk for surgery.
Elective surgery should be considered depending on the tolerance of the valve lesion and according to the recommendations of the ESC Guidelines on the management of valvular heart disease. Uncontrolled infection is one of the most feared complications of IE and is the second most frequent cause for surgery. Infection due to resistant or very virulent organisms often results in uncontrolled infection. The definition of persisting infection is arbitrary and consists of fever and persisting positive cultures after 7—10 days of antibiotic treatment. Persisting fever is a frequent problem observed during treatment of IE.
Usually, temperature normalizes within 7—10 days under specific antibiotic therapy. Persisting fever may be related to several factors, including inadequate antibiotic therapy, resistant organisms, infected lines, locally uncontrolled infection, embolic complications or extracardiac site of infection and adverse reaction to antibiotics.
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 defined in Table Pseudoaneurysms and fistulae are severe complications of IE and are frequently associated with very severe valvular and perivalvular damage.
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. Indeed, perivalvular extension is frequently discovered on a systematic TOE.
However, small abscesses can be missed, even using TOE, particularly those in a mitral location when there is co-existent annular calcification. The results of surgery when the reason for the procedure is uncontrolled infection are worse than when surgery is performed for other reasons.
In some cases of IE, antibiotics alone are insufficient to eradicate the infection. Surgery has been indicated when fever and positive blood cultures persist for several days 7—10 days despite an appropriate antibiotic regimen and when extracardiac abscesses splenic, vertebral, cerebral or renal and other causes of fever have been excluded.
However, the best timing for surgery in this difficult situation is unclear. Recently it has been demonstrated that persistent blood cultures 48—72 h after initiation of antibiotics are an independent risk factor for hospital mortality. Signs of locally uncontrolled infection include increasing vegetation size, abscess formation, false aneurysms, and the creation of fistulae. Rarely when there are no other reasons for surgery and fever is easily controlled with antibiotics, small abscesses or false aneurysms can be treated conservatively under close clinical and echocardiographic follow-up. Surgery is indicated in fungal IE, , in cases of multiresistant organisms e.
MRSA or vancomycin-resistant enterococci or in the rare infections caused by Gram-negative bacteria. In NVE caused by S. Finally, surgery should be performed in patients with PVE and S. Unless severe co-morbidity exists, the presence of locally uncontrolled infection is an indication for early surgery in patients with IE. 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. However, contrast media should be used with caution in patients with renal impairment or haemodynamic instability because of the risk of worsening renal impairment in combination with antibiotic nephrotoxicity. Echocardiography plays a key role in predicting embolic events, 72 , , — although prediction remains difficult in the individual patient.
Several factors are associated with increased risk of embolism, including the size and mobility of vegetations, 72 , , — the location of the vegetation on the mitral valve, 72 , — the increasing or decreasing size of the vegetation under antibiotic therapy, 72 , particular microorganisms S. Several factors should be taken into account when assessing embolic risk. In a recent study of patients with IE, the 6-month incidence of new embolism was 8.
Whatever the risk factors observed in an individual patient, it must be re-emphasized that the risk of new embolism is highest during the first days following initiation of antibiotic therapy and rapidly decreases thereafter, particularly beyond 2 weeks, 58 , 72 , , although some risk persists indefinitely while vegetations remain present, particularly for very large vegetations. Avoiding embolic events is difficult since the majority occur before admission. The exact role of early surgery in preventing embolic events remains controversial.
The value of early surgery in an isolated large vegetation is controversial. A recent randomized trial demonstrated that early surgery in patients with large vegetations significantly reduced the risk of death and embolic events compared with conventional therapy. Finally, the decision to operate early for prevention of embolism must take into account the presence of previous embolic events, other complications of IE, the size and mobility of the vegetation, the likelihood of conservative surgery and the duration of antibiotic therapy.
The main indications and timing of surgery to prevent embolism are given in Table Surgery undertaken for the prevention of embolism must be performed very early, during the first few days following initiation of antibiotic therapy urgent surgery , as the risk of embolism is highest at this time. The risk of embolism is highest during the first 2 weeks of antibiotic therapy and is clearly related to the size and mobility of the vegetation, although other risk factors exist.
The decision to operate early to prevent embolism is always difficult and specific for the individual patient. Governing factors include the size and mobility of the vegetation, previous embolism, type of microorganism and duration of antibiotic therapy. Clinical presentation is variable and may include multiple symptoms or signs in the same patient, but focal signs predominate and ischaemic strokes are most commonly diagnosed. Vegetation length and mobility also correlate with embolic tendency. Successful management of IE requires a combined medical and surgical approach in a substantial proportion of patients.
Following a neurological event, the indication for cardiac surgery often remains or is strengthened, but must be balanced with perioperative risk and postoperative prognosis. Randomized studies are not possible and cohort studies suffer from bias that can only be partly compensated for by statistical methods. If urgent cardiac surgery is needed, close cooperation with the neurosurgical team and the Endocarditis Team is mandatory.
Table 23 and Figure 4 summarize the recommended management of neurological complications in IE. Cerebral imaging is mandatory for any suspicion of neurological complication of IE. CT scanning, with or without contrast agent, is most often performed. The higher sensitivity of MRI, with or without contrast gadolinium enhancement, allows for better detection and analysis of cerebral lesions in patients with neurological symptoms, and this may have an impact on the timing of surgery 89 see section 5. In patients without neurological symptoms, cerebral MRI often detects lesions that may change the therapeutic strategy; in particular, the indications and timing of surgery.
The lack of association with parenchymal haemorrhage and the absence of postoperative neurological complications in patients with microbleeds suggest that microbleeds should not be interpreted as active bleeding and should not lead to postponed surgery when this is indicated. 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 mycotic aneurysms result from septic arterial embolism to the intraluminal space or vasa vasorum or from subsequent spread of infection through the intimal vessels.
Infectious aneurysms are typically thin walled and friable and, as such, exhibit a high tendency to rupture and haemorrhage. No predictor of rupture has been identified and, in contrast to non-infectious aneurysms, size does not appear to be a reliable predictor of potential rupture. Clinical presentation is highly variable i.
Cerebral CT and MRI both reliably diagnose infectious aneurysms with good sensitivity and specificity. Owing to the lack of randomized trials, there is no widely accepted standard management for infectious aneurysms. Thus management should be provided by an Endocarditis Team and tailored to the individual patient. Some infectious aneurysms may resolve during antibiotic treatment, while others require surgical or endovascular intervention depending on the occurrence of rupture and the location in the artery bed, as well as the clinical status of the patient.
Regarding intracranial infectious aneurysms, ruptured aneurysms must be treated immediately by surgical or endovascular procedures. Unruptured infectious aneurysms should be followed by serial cerebral imaging under antibiotic therapy. If the size of the aneurysm decreases or resolves completely, surgical or endovascular intervention is usually unnecessary.
However, if the size of the aneurysm increases or remains unchanged, it is likely that the patient will require intervention. On the other hand, if the infectious aneurysm is voluminous and symptomatic, neurosurgery or endovascular therapy is recommended. Splenic infarcts are common and very often asymptomatic.
Persistent or recurrent fever, abdominal pain and bacteraemia suggest the presence of complications splenic abscess or rupture. Although splenic emboli are common, splenic abscesses are rare. Persistent or recurrent fever and bacteraemia suggest the diagnosis. Recently PET has proved useful for the diagnosis of splenic metastasic infection in patients with IE.
Splenectomy may be considered for splenic rupture or large abscesses, which respond poorly to antibiotics alone, and should be performed before valvular surgery unless the latter is urgent. Rarely, splenectomy and valvular surgery are performed during the same operative time. Percutaneous drainage is an alternative for high-risk surgical candidates. Cardiac failure may be due to myocarditis, which is frequently associated with abscess formation or immune reaction. Ventricular arrhythmias may indicate myocardial involvement and imply a poor prognosis.
The inflammatory response, HF, periannular complications or infection itself can cause pericardial effusion, which could be a sign of more severe IE. Rarely, ruptured pseudoaneurysms or fistulae may communicate with the pericardium, with dramatic and often fatal consequences. Purulent pericarditis is rare and may necessitate surgical drainage. Conduction disorders are uncommon complications of IE. Conduction abnormalities mainly first-, second-, and third-degree atrio-ventricular blocks, rarely bundle branch blocks are due to spread of the infection beyond the endocardium, from valves to the conduction pathways, and are generally associated with perivalvular complications.
In a study of patients with IE and complete atrio-ventricular block, pathology workup revealed the presence of an infection, frequently accompanied by abscesses and fistulae, affecting the conduction pathways; in cases of paroxysmal atrio-ventricular block, inflammation was observed at this level, which would explain the reversibility of the event. The occurrence of conduction abnormalities during electrocardiographic monitoring in patients with endocarditis can therefore alert physicians to the appearance of perivalvular complications. In the case of embolization of vegetation fragments into a coronary artery, the resulting myocardial ischaemia can be the substrate for the onset of tachyarrhythmias.
Atrial fibrillation can be observed in patients with IE and may be present before IE or occur as a complication of IE. Atrial fibrillation has been reported to be more frequent in the elderly and to be associated with a poor prognosis. However, there is no specific study on this situation and no international consensus for the care of these patients. The management of anticoagulation therapy in these patients should be taken on an individual basis by the Endocarditis Team. Musculoskeletal symptoms arthralgia, myalgia, back pain are frequent during IE. The prevalence of IE in vertebral osteomyelitis is higher , in the presence of Streptococcus viridans IE.
Acute renal failure is a common complication of IE and may worsen the prognosis of IE. The onset of renal dysfunction is independently associated with increased risk of in-hospital death , and postoperative events. Haemodialysis may be required in some patients with advanced renal failure and is associated with high mortality.
Imaging with nephrotoxic contrast agents should be avoided when possible in patients with haemodynamic impairment or previous renal insufficiency. Few studies have evaluated the utility of operative risk scores in the setting of IE. Risk scores specific to IE surgery have been developed: i from the Society of Thoracic Surgeons database using 13 patients and ii an additional NVE risk score from a single centre using patients by De Feo et al.
However, the relevance of these findings is limited by the small number of patients involved. Similar to previous studies, preoperative use of inotropes or an intra-aortic balloon pump, prior coronary artery bypass surgery and renal failure requiring dialysis were independent predictors of operative and long-term mortality. Finally, although no single operative risk score is perfect, preoperative assessment of operative risk is of utmost importance. Although the theoretical indications for surgery in IE are clear Table 22 , their practical application relies largely on the clinical status of the patient, the patient's co-morbidities and the patient's operative risk.
Exceptions arise when there are aortic vegetations that may be dislodged during catheterization or when emergency surgery is necessary. In these situations, high-resolution CT may be used to rule out significant coronary artery disease in haemodynamically stable patients. If a primary focus of infection likely to be responsible for IE has been identified, it must be eradicated before cardiac surgical intervention unless valve surgery is urgent.
In any case, it should be eradicated before the end of antibiotic therapy. Intraoperative TOE is most useful to determine the exact location and extent of infection, guide surgery, assess the result and help in early postoperative follow-up. The two primary objectives of surgery are total removal of infected tissues and reconstruction of cardiac morphology, including repair or replacement of the affected valve s.
Where infection is confined to the valve cusps or leaflets, any method to repair or replace the valve may be used. However, valve repair is favoured whenever possible, particularly when IE affects the mitral or tricuspid valve without significant destruction. Isolated or multiple ruptured chordae may be replaced by polytetrafluoroethylene neo-chordae. More extensive destruction of a single leaflet or the presence of an abscess is not necessarily a contraindication for valve repair.
The need for a patch to achieve a competent valve, whether pericardial, tricuspid autograft or a flipped-over mitral patch, has not been associated with worse results in terms of recurrence of IE or mitral regurgitation when performed by experienced surgeons. To avoid paravalvular leaks in complex cases with locally uncontrolled infection, total excision of infected and devitalized tissue should be followed by valve replacement and repair of associated defects to secure valve fixation.
Mechanical and biological prostheses have similar operative mortality. The use of foreign material should be kept to a minimum. Small abscesses can be closed directly, but larger cavities should be allowed to drain into the pericardium or circulation. In aortic IE, replacement of the aortic valve using a mechanical or biological prosthesis is the technique of choice. However, experience with aortic valve repair in this setting is still very limited and there is no evidence that repair is associated with improved outcomes compared with replacement.
A monoblock aorto-mitral homograft has been suggested as a surgical option for extensive bivalvular IE. Cardiac transplantation may be considered in extreme cases where repeated operative procedures have failed to eradicate persistent or recurrent PVE.
Postoperative patient management should follow the usual recommendations after valvular surgery but should also take into account the specificities of IE. Among the most frequent complications are severe coagulopathy requiring treatment with clotting factors, re-exploration of the chest for bleeding or tamponade, acute renal failure requiring haemodialysis, stroke, low cardiac output syndrome, pneumonia and atrio-ventricular block following radical resection of an aortic root abscess with the need for pacemaker implantation. Following in-hospital treatment, the main complications include recurrence of infection, HF, need for valve surgery and death.
In these cases, molecular methods including strain-typing techniques should be employed. Thus, although variable, the time between episodes is usually shorter for relapse than for reinfection. Generally speaking, a recurrence caused by the same species within 6 months following the initial infection represents relapse, whereas later events suggest reinfection. Factors associated with an increased rate of relapse are listed in Table Relapses are most often due to insufficient duration of original treatment, suboptimal choice of initial antibiotics or a persistent focus of infection.
When the duration of therapy has been insufficient or the choice of antibiotic incorrect, relapse should be treated for a further 4—6 weeks depending on the causative microorganism and its antibiotic susceptibility remembering that resistance may develop in the meantime. Patients with previous IE are at risk of reinfection, and prophylactic measures should be very strict.
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Reinfection is more frequent in IVDAs especially in the year after the initial episode , , in PVE, in patients undergoing chronic dialysis , and in those with multiple risk factors for IE. The type of valve implanted has no effect on the risk of recurrent IE. A first episode of IE should not be seen as an ending once the patient has been discharged. Residual severe valve regurgitation may decompensate left ventricular function, or valve deterioration may progress despite bacteriological cure, usually presenting with acute HF. After completion of treatment, recommendations for surgery follow conventional guidelines.
Patients should be educated about the signs and symptoms of IE after discharge. They should be aware that recurrence could occur in IE and that new onset of fever, chills or other signs of infection mandate immediate evaluation, including procurement of blood cultures before empirical use of antibiotics. To monitor the development of secondary HF, an initial clinical evaluation and baseline TTE should be performed at the completion of antimicrobial therapy and repeated serially, particularly during the first year of follow-up.
Good oral health maintenance, preventive dentistry and advice about skin hygiene, including tattoos and skin piercing, are mandatory. Deficiencies in dental surveillance contribute to the continuous gradual increase in the incidence of IE. Compared with an age- and sex-matched general population, patients surviving a first episode of IE have a significantly worse survival.
Patients with IE must be informed of the risk of recurrence and educated about how to diagnose and prevent a new episode of IE. The need for late valve surgery is low. Early PVE is defined as IE occurring within 1 year of surgery and late PVE as IE occurring beyond 1 year, because of significant differences between the microbiological profiles observed before and after this time point. What is important is not the time from the valve replacement procedure to the onset of IE, but whether IE is acquired perioperatively and which microorganism is involved.
The pathogenesis of PVE differs according to both the type of contamination and the type of prosthetic valve. In cases with perioperative contamination, the infection usually involves the junction between the sewing ring and the annulus, leading to perivalvular abscess, dehiscence, pseudo-aneurysms and fistulae. For example, in late bioprosthetic PVE, infection is frequently located on the leaflets of the prosthesis, leading to vegetations, cusp rupture and perforation.
PVE has recently been reported after transcatheter aortic bioprosthetic valve implantation, which should be managed in the same manner as other prosthetic valves. The consequence of PVE is usually new prosthetic regurgitation. Less frequently, large vegetations may cause prosthetic valve obstruction, which can be diagnosed by TOE and sometimes by TTE or fluoroscopy. Clinical presentation is frequently atypical, particularly in the early postoperative period, in which fever and inflammatory syndromes are common in the absence of IE.
However, persistent fever should trigger the suspicion of PVE. However, both are more frequently negative in PVE. A negative echocardiogram is frequently observed in PVE 2 and does not rule out the diagnosis, but identification of a new periprosthetic leak is a major criterion, in which case an additional imaging modality could be considered such as CT or nuclear imaging.
Staphyloccoci and enteroccoci are the most common agents in prosthetic valve implantation endocarditis. Several factors have been associated with poor prognosis in PVE, , , — including older age, diabetes mellitus, healthcare-associated infections, staphylococcal or fungal infection, early PVE, HF, stroke and intracardiac abscess.
Among these, complicated PVE and staphylococcal infection are the most powerful markers. These patients need aggressive management, consisting of antibiotic therapy and early radical surgery. An exception is S. Radical debridement in these cases means removal of all infected foreign material, including the original prosthesis, and any calcium remaining from previous surgery.
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Homografts, stentless xenografts or autografts may be considered in aortic PVE, and homograft or xenograft root replacement is indicated for any abnormality of the aortic root that distorts the aortic sinuses. Alternatively, a valved Dacron conduit can be used. The best therapeutic option in PVE is still debated. Other groups have reported similar data. Therefore a surgical strategy is recommended for PVE in high-risk subgroups identified by prognostic assessment, i. Emergency surgery is indicated only in cases with refractory congestive HF leading to pulmonary oedema or shock, as in NVE.
Conversely, patients with uncomplicated non-staphylococcal and non-fungal late PVE can be managed conservatively. These forms of PVE must be managed aggressively. Patients with uncomplicated, non-staphylococcal late PVE can be managed conservatively with close follow-up. Infection of cardiac implantable electronic devices CIEDs is a severe disease associated with high mortality. Local device infection is defined as an infection limited to the pocket of the cardiac device and is clinically suspected in the presence of local signs of inflammation at the generator pocket, including erythema, warmth, fluctuance, wound dehiscence, erosion, tenderness or purulent drainage.
However, the possibility of intraoperative contamination of the lead tip cannot be excluded in these patients. The pocket may become infected at the time of implantation, during subsequent surgical manipulation of the pocket or if the generator or subcutaneous electrodes erode through the skin. Pocket infection may track along the intravascular portion of the electrode to involve the intracardiac portion of the pacemaker or implantable cardioverter defibrillator. Alternatively, the pocket or intracardiac portion of the electrode may become infected as a result of haematogenous seeding during a bacteraemia secondary to a distant infected focus.
The consequence may be formation of vegetations, which can be found anywhere from the insertion vein to the superior vena cava, on the lead or on the tricuspid valve, as well as on the right atrial and ventricular endocardium. Several factors have been associated with CIED infections. The factors associated with an increased risk of infection include the type of intervention, , device revisions, the site of intervention, the amount of indwelling hardware, the use of pre-procedural temporary pacing, failure to administer perioperative antimicrobial prophylaxis, fever within the 24 h before implantation and operator experience.
Clinical presentation is frequently misleading, with predominant respiratory and rheumatological symptoms as well as local signs of infection. Fever is frequently blunted, particularly in elderly patients. As in other forms of IE, echocardiography and blood cultures are the cornerstones of diagnosis. Echocardiography plays a key role in CDRIE and is helpful for the diagnosis of both lead vegetations and tricuspid involvement, quantification of tricuspid regurgitation, sizing of vegetations and follow-up after lead extraction.
Several prognostic features may be better defined on TTE than on TOE, such as pericardial effusion, ventricular dysfunction and pulmonary vascular pressure estimations. In addition, the sensitivity of TOE for left-sided involvement and for perivalvular extension of infection is superior to that of TTE. Considering their complementary role, it is recommended to perform both investigations in suspected CDRIE. Intracardiac echocardiography was recently found to be feasible and effective in cardiac device patients and to have a superior sensitivity for the detection of vegetations in cardiac devices.
The Duke criteria are difficult to apply in these patients because of lower sensitivity. CDRIE must be treated by prolonged antibiotic therapy associated with complete hardware removal. Antimicrobial therapy for CDRIE should be individualized and based on culture and susceptibility results if possible see section 7. Daptomycin, approved for right-side IE and bacteraemia attributable to S. There are no clinical trial data to define the optimal duration of antimicrobial therapy. The duration of therapy should be 4—6 weeks in most cases. In the case of definite CDRIE, medical therapy alone has been associated with high mortality and risk of recurrence.
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