current best practices and guidelines-indications for surgical intervention in infective...

7/21/2019 Current Best Practices and Guidelines-Indications for Surgical Intervention in Infective Endocarditis

1/23

Current best practices and guidelinesIndications for surgical intervention

in infective endocarditis

Lars Olaison, MD, PhD

a,*, Gosta Pettersson, MD, PhD

b

aDepartment of Infectious Diseases, Sahlgrenska University Hospital,

S-416 85 Goteborg, SwedenbThe Cleveland Clinic Foundation, Thoracic and Cardiovascular Surgery/F25,

9500 Euclic Avenue, Cleveland, OH 44195, USA

The role of surgery in active infective endocarditis (IE) has been expand-

ing since the first report of successful ventricular septal repair and removal

of tricuspid vegetation in 1961 and the first successful valve replacement

during active IE in 1965 [1,2]. The reduction of mortality in IE during thelast three decades from 25% to 30% to 10% to 20% may be due chiefly to

more aggressive surgical intervention in cases with congestive heart failure

(CHF), complicated invasive infections with abscesses and aneurysms, and

prosthetic valve infections. For IE caused by Staphylococcus aureus in par-

ticular, a reduction of mortality from 50% to 60% to 15% to 30% has been

achieved.

The results of surgery depend upon many factors. The general preopera-

tive condition of the patient, antibiotic treatment, timing of surgery, peri-

operative management, surgical techniques (including choice of methodsfor reconstruction), postoperative management, and follow-up are all

important determinants of outcome. Considerations of the indications for

surgery, the timing, and evaluation of the patients ability to withstand the

contemplated operation are all highly dependent upon the experience of

both the surgeons and their institutions. These are complicated decisions,

requiring sound judgment based upon extensive clinical experience. New

problems have emerged that are associated with an increasing number of

patients in intensive care units (ICUs) and other hospital settingsincluding

Infect Dis Clin N Am 16 (2002) 453475

This work was supported by grants from the Swedish Heart and Lung Foundation and the

National Board of Health and Welfare, Sweden.

* Corresponding author.

E-mail address: [email protected] (L. Olaison).

0891-5520/02/$ - see front matter 2002, Elsevier Science (USA). All rights reserved.

PII: S 0 8 9 1 - 5 5 2 0 ( 0 1 ) 0 0 0 0 6 - X


2/23

chronic hemodialysiswho develop nosocomial endocarditis. This group of

patients has high mortality and is often considered inoperable [3,4], but

some can be salvaged by judicious surgical intervention.Published experience of surgical treatment during active endocarditis

from the 1990s reported mortality rates of 8% to 16%, with actuarial

survival at 5 years of 75% to 76% and at 10 years of 61% [510]. Pre-

operative New York Heart Association (NYHA) classification, age, and

preoperative renal failure are common predictors of operative mortality

in logistic regression analyses. Aggressive disease of shorter duration, most

often being acute endocarditis caused by S. aureus, is associated with higher

mortality.

A series of illustrations have been included to illustrate some of our gen-eral concepts (Figs. 17). The figures illustrate some typical pathologies as

well as surgical principles and options.

Fig. 1. Operative specimen from a fatal case ofS. aureus aortic valve endocarditis affecting a

valve with preexisting calcific aortic valve stenosis. The vegetations and the invasive lesion are in

the typical location underneath a commissure, in this case between the right and noncoronary

cusps. There is destruction and perforation of the right cusp through to the pericardium,

resulting in the fatal tamponade. The conduction bundle is located under the central fibrous

body (CFB) and is not destroyed.

454 L. Olaison, G. Pettersson / Infect Dis Clin N Am 16 (2002) 453475


3/23

Timing of surgery

The duration of antibiotic therapy before the operation appears to have

no influence on operative mortality [911]. It is, however, considered impor-tant to have adequate antibiotic coverage during operation to kill bacteria

entering the circulation during the surgical debridement. In a Swedish 5-year

national study 223 patients underwent cardiac surgery during treatment, one

third during the first 5 days and 52% during the first 10 days of treatment.

Treatment mortality was equal (8.5%) for patients subjected to surgery with-

in the first 10 days and after 10 days (data from the National Swedish Endo-

carditis Registry).

Some authors have found operation during the acute phase of endocar-

ditis to be associated with a higher risk of persistent or early recurrentprosthetic valve endocarditis (PVE) [12,13]. Others did not find an increased

recurrence rate [14], particularly not after surgery for mitral valve endocar-

ditis [13,1518]. In addition to the postoperative antibiotic treatment, radi-

cal debridement and the method of reconstruction utilized are important

determinants of the risk for persistent and recurrent infection, as illustrated

by the improving early and late results over the last decade.

Fig. 2. Aortic valve endocarditis caused by S. aureus not responding to antibiotic treatment.

Surgery disclosed extensive periaortic cellulitis with infection and necrosis (white arrows)

involving the space between the aortic root and the wall of the right atrium (RA), spreading

anteriorly in the epicardial fat.

455L. Olaison, G. Pettersson / Infect Dis Clin N Am 16 (2002) 453475


4/23

Indications for surgery

The indications for surgery are defined more precisely today than in the

past [13,14] due to increased experience and the refinement of echocardio-

graphy, particularly the introduction of transesophageal imaging.

Surgery is necessary in approximately 25% to 30% of cases during the

acute phase of infection, and in another 20% to 40% in later or secondary

phases [1921]. In general, the prognosis is better after early surgery under-

taken before the cardiac pathology and the general condition of the patient

have deteriorated too severely [2023]. The final outcome has little relation

Fig. 3. Prosthetic aortic valve endocarditis. Complete heart block developed two days

preoperatively. (A) shows the right atrial (RA) view of the infection invading the triangle of

Koch with destruction of the atrioventricular (AV) node (white arrows) anterior to the coronary

sinus (CS). (B) displays the full extent of the circumferential horseshoe abscess after

debridement. The process originally started anteriorly, underneath the right coronary artery

(RCA) where the cavity was communicating with the circulation, irrigated by blood and

eventually endothelialized. To the left and posterior the infection is still active and destructive,eventually penetrating into the floor of the right atrium and the triangle of Koch to cause

destruction of the AV node and complete heart block. The left ventricular outflow tract is well

preserved with stay sutures placed in the two trigones on either side of the base of the anterior

mitral leaflet (MV). (C) demonstrates the reconstruction of the heart with an autologous

pericardial patch to reconstruct the free wall of the right atrium and an aortic homograft to

reconstruct the left ventricular outflow tract. Monofilament polypropylene sutures are used.

LVOT left ventricular outflow tract; TV tricuspid valve.



5/23

Fig. 3 (continued)



6/23

to the duration and intensity of antibiotic therapy prior to surgery [5,24,25].

This observation is important to remember with regard to the decision to

perform early surgery.The decision to undertake surgery should be based on careful daily clin-

ical evaluations, microbiological tests (including follow-up blood cultures

during antibiotic treatment), and the information provided by repeated

echocardiographic examinations.

Indications for surgery, ranked with respect to degree of urgency, are

presented in Table 1. These can be divided into the following categories,

according to the phase of the disease and the objectives of the operation.

Congestive heart failure

Moderate and severe (NYHA class III or IV) or progressive heart failure

due to valvular dysfunction are the most common and best validated indica-

Fig. 4. (A) and (B): Even in the presence of advanced pathology, including annular destructionand development of periaortic cavities, the left ventricular outflow tract is most often well

preserved. (A) and (B) show two cases in which the Ross operation (pulmonary autograft

reconstruction of the left ventricular outflow tract and homograft replacement of the

pulmonary valve) has been used for aortic valve endocarditis. The removal of the pulmonary

artery (the autograft) provides unparalleled exposure of the left ventricular outflow tract and

the pathology. The autograft allows insertion of living tissue into the infected area with minimal

use of foreign material.



7/23

tions for surgery in patients with IE, being the main indication in 22% to

71% in different series [8,15]. Acute onset of aortic insufficiency is tolerated

poorly, and heart failure secondary to aortic regurgitation is generally con-

sidered to be severe and likely to progress rapidly. Congestive heart failure

(CHF) may also develop acutely from rupture of infected mitral chordae,

perforation of native or bioprosthetic valve leaflets and cusps, valve obstruc-tion, or sudden development of intracardiac shunts from fistulous tracts or

prosthetic valve dehiscence.

A progressive worsening of valvular regurgitation and ventricular dys-

function may also lead to more gradual onset of CHF despite appropriate

antibiotic therapy. Mild CHF at the time of initial diagnosis may progress

to severe CHF during treatment, usually within the first month of therapy.

CHF in IE carries a worse prognosis with medical therapy alone, but also

constitutes a surgical risk factor. Delaying cardiac surgery, thus allowing

more severe cardiac decompensation to develop, dramatically increasesoperative mortality: from 6% to 11% for patients without CHF to 17% to

33% for patients with CHF [26]. In addition, delay exposes the patient to the

risk of perivalvular extension of the infection with increased likelihood of

serious secondary complications.

Four studies from the 1970s and 1980s have compared medical and com-

bined medical and surgical treatment of CHF in IE. All showed a reduction

Fig. 4 (continued)



8/23

of mortality with surgery, from 56% to 86% to 11% to 35%, although no

correction was made for interfering underlying conditions [2730]. In two

Swedish studies mortality rates for surgically treated versus non-surgicallytreated decompensated patients were 9% versus 20% and 10% versus 27%

(P< 0.05), respectively. The greatest benefit of early surgery was noted in

patients with new heart failure at entry who underwent surgery on median

treatment day 4 [9,31]. The infected valve plays an important role. Aortic

regurgitation with tachycardia and early closure of the mitral valve as a sign

of uncompensated ventricular overload is an urgent indication for surgery as

well as acute aortic or mitral regurgitation with progressive heart failure.

Aortic insufficiency due to pre-existing valve disease may be treated conser-

vatively if the patient remains compensated, but new-onset, moderate, orsevere aortic regurgitation due to IE usually requires surgery. Mitral regur-

gitation is usually better tolerated and has a better prognosis because the left

atrium and the pulmonary vascular bed can better accommodate the regur-

gitant volume than the left ventricle alone, as occurs in aortic regurgitation.

Fig. 5. (A) and (B): Double (aortic and mitral) valve endocarditis with typical location of

secondary kissing/jet lesion on the anterior mitral leaflet seen from the aortic side. The

indication for surgery was congestive heart failure due to severe regurgitation through both

valves. (B): Mitral lesions of this size and location are repaired with a patch of autologous

pericardium.



9/23

Cardiac decompensation may occur when the chordae tendinae rupture, but

the left ventricle often adapts to the overload.

Right-sided IE requires surgery less often because tricuspid or pulmonic

regurgitation is well tolerated as long as the pulmonary vascular resistance is

not significantly elevated.

The risk of development of acute heart failure is also related to virulentpathogens, such as S. aureus, hemolytic streptococci group AC, F, and G,

or Streptococcus pneumoniae, but any microorganism may cause this com-

plication if treatment is delayed long enough.

Periannular extension of infection

Peri-annular and para-annular abscesses can be difficult to diagnose with

certainty, even with transesophageal echocardiogram (TEE). The sensitivity

for the diagnosis of abscesses in a French multicenter study of perivalvularabscesses was 36% and 80%, respectively, using transthoracic echocardio-

graphy (TTE) and TEE [32]. In other studies of TEE the sensitivity was

76% to 100% for defining periannular extension of IE while retaining a spe-

cificity of 95% [3335]. Extension beyond the leaflets is common, occuring

in 10% to 40% of all episodes of native valve endocarditis (NVE). This

complication occurs more commonly with aortic IE than with mitral or

Fig. 5 (continued)



10/23

tricuspid infection. In PVE it is even more common, occurring in 56% to

100% of all patients.Extension of infection to deep tissue begins as cellulitis and eventually

progresses to abscess formation. Hemodynamic pressure effects on perival-

vular tissue weakened or destroyed by infection will result in formation of

pseudoaneurysms. Drained abscesses are converted to pseudoaneurysms

or blood-filled cavities when the pus and necrotic material are washed away

by the flow of blood. The same infectious process can be in different stages

of activity, working its way around the circumference of the valve in a horse-

shoe fashion [36]. Destruction of the aortic or mitral annulus will result in

partial or circumferential ventriculo-aortic or atrio-ventricular separation,respectively. If an abscess breaks through to another heart chamber, a fistula

is formed. A rupture through to the pericardium is a catastrophe, usually

fatal. In aortic valve endocarditis, the peri-valvular invasion often begins

under the commissures. From there, annular destruction spreads around the

root on top of the interventricular septum and underneath the pulmo-

nary artery into areas previously occupied by periaortal and epicardial

Fig. 6. The patient presented with stroke and cerebral infarct. Vegetation and perforation in the

medial scallop of the posterior mitral leaflet causing 34+ mitral regurgitation. Surgery was

postponed for one week. The valve pathology was debrided and the valve repaired with the use

of an autologous pericardial patch.



11/23

fat. Proximal tissue loss caused by invasion and necrosis of ventricular

musculature is less common, but when it occurs surgical reconstruction pre-

sents a more difficult problem. If the infectious process enters into the triangleof Koch, inflammation or destruction of the atrioventricular node and

bundle of His often results in heart block.

Aortic valve involvement and intravenous drug abuse are the only known

independent risk factors for perivalvular abscesses [37]. Development of new

AV-block on ECG during the course of endocarditis carries an 77% positive

predictive value for abscess formation, but has a relatively low sensitivity of

42% [38]. Acute surgery is beneficial in most of these patients because delay

may compromise cardiac function with a resultant higher perioperative risk

[39, 40]. In a recent series of 25 patients with aortic valve abscesses 20 (80%)underwent surgical intervention. Mortality for surgically treated patients

was 30% as compared to 100% for patients without surgery. S aureus was

isolated in 73% of the fatal cases [41]. The presence of annular abscesses

was not an adverse predictor of early mortality in a series presented by

Bauernschmitt et al.; provided the surgical procedures were radical, the

abscess cavities were completely resected and approximately normal hemo-

dynamics could be restored [6]. Early reinfection rate was low (2%) despite

insertion of mechanical valves. For patients with large abscesses at the aortic

root, however, a radical resection carries the risk of destruction of the con-duction system with resultant postoperative AV-block.

A small number of patients may be treated successfully without surgical

intervention, especially those who do not have heart block, echocardio-

graphic evidence of progression during therapy, valvular dehiscence, or

insufficiency. These patients should be monitored closely with serial TEE

and followed at least 2 months after completion of antimicrobial therapy

with repeated TEE [26,42,43]. The significance of residual cavities after

microbiologic cure of endocarditis for long-term prognosis and risk of

recurrent endocarditis remains unresolved. A larger-sized cavity, recentendocarditis, significant valvular regurgitation, and younger age are factors

that favor corrective surgery in such cases.

Vegetations and risk of systemic embolization

A vegetation can be visualised by echocardiography in 13% to 78% of IE

episodes; this is not per se an indication for surgery [44]. Clinically signifi-

cant embolic events are common, with a cumulative incidence (including

pretreatment and post-treatment) ranging from 10% to 50% [4447]. In thepre-antibiotic era, cerebral embolism was one of the major causes of death,

being second only to progressive heart failure. In modern times, emboli are

directly responsible for about 25% of fatalities and for a substantial propor-

tion of irreversible sequelae after microbiological cure. Three quarters of

clinically diagnosed emboli occur before antibiotic treatment begins; thus

only one quarter of all emboli are potentially preventable [48].



12/23

Up to 50% to 65% of embolic events involve the central nervous system,

the majority involving the distribution of the middle cerebral artery. When

considering that the brain receives approximately 14% of the cardiac output,but accounts for about 50% of clinical embolic events, it is apparent that

many emboli to other sites must remain undiagnosed.

The risk for clinically apparent emboli during treatment was 14% and

21%, respectively, among patients with definite vegetations or larger-sized

(10 mm) vegetations at the start of therapy in two series from the Mayo

Clinic and Goteborg, Sweden, while absence of vegetations indicated a risk

of 11% and 8% in the same series [31,44]. The series were performed to a

large extent with utilization of the less sensitive TTE technique. These are

the only studies that report the changing incidence of embolism over timeduring antibiotic treatment. They show that the frequency of embolism

decreases after only one week of treatment (Fig. 8).

Attempts have been made to grade different risk factors to predict the risk

of embolization for an individual patient. In the Mayo study mentioned

above, the strongest risk factor (irrespective of vegetation size) was atrial

fibrillation, followed in rank order by S. aureusetiology, history of previous

Fig. 7. (A) and (B): Composite graft endocarditis with mediastinal abscess surrounding the

graft, perivalvular leak and valve thrombosis. (B) illustrates the circumferential pathology. Note

successfully that the left ventricular outflow tract is well preserved. The patient was re-operated

with complete debridement of the infected necrotic tissue as well as all foreign material and

reconstructed with an aortic homograft.



13/23

embolism, short symptom duration, mitral valve location, and older age. In

the Swedish study, the rank order of risk factors was PVE (which was not

studied in the Mayo Clinic patients), followed by S. aureus etiology, older

age, short symptom duration, mitral valve location, and a history of pre-

vious embolism.

Many studies have tried to use the echocardiographic charcteristics of thevegetations and other pathological findings to identify a sub-group of

patients who might benefit from early surgery to prevent embolism. Con-

flicting results of correlation between vegetation size and embolization have

been seen in studies using TEE. In one study mitral vegetations 10 mm in

diameter were associated with the highest rate of embolism (25%). The

highest embolic rate (37%) was seen in the subset of patients with mitral

vegetations attached to the anterior rather than the posterior leaflet. The

mechanical stress of broad and abrupt leaflet excursions may give rise to

fragmentation and embolization of the vegetation [49]. Vegetation size>20 mm predicted embolic events in another TEE study [50]. Two other

studies, however, failed to demonstrate this relationship, possibly due to

relatively small numbers of patients [45,47]. A recent study using TEE com-

bined with careful clinical examinations and investigations to detect silent

emboli found a significantly higher incidence of embolism associated

with vegetations 10 mm (60%), mobile vegetations (62%), and in particular

Fig. 7 (continued)



14/23

with the combination of severely mobile and large vegetations (15 mm)

(83%) [46].S. aureusinfection was a risk factor, while mitral localization had

no association to risk of embolic event.

In one study, large vegetations independently predicted embolic events

only in the viridans streptococci group, while staphylococcal infections car-

ried a high risk of embolization that was independent of vegetation size [44].

When should preventive removal of vegetations by means of surgery berecommended? Traditional indications for surgery to avoid embolization

in IE patients have been two or more major embolic events during therapy.

Every patient should be considered in light of the specific risk factors for

embolization mentioned above. The duration of antibiotic treatment should

also strongly influence the decision because the risk of embolism decreases

rapidly after the first week of effective treatment.

Table 1

Indications for surgery in patients with infective endocarditis

Indication Evidence basedEmergency indication for cardiac surgery (same day)

1. Acute AR with early closure of mitral valve A

2. Rupture of a sinus Valsalva aneurysm into the right heart chamber A

3. Rupture into the pericardium A

Urgent indication for cardiac surgery (within 12 d)

4. Valvular obstruction A

5. Unstable prosthesis A

6. Acute AR or MR with heart failure, NYHA IIIIV A

7. Septal perforation A

8. Evidence of annular or aortic abscess, sinus or aortic true or falseaneurysm, fistula formation, or new onset conduction disturbances A

9. Major embolism + mobile vegetation >10 mm + appropriate antibiotic

therapy 15 mm + appropriate antibiotic therapy 7 d C

AStrong evidence or general agreement that cardiac surgery is useful and effective;

B Inconclusive or conflicting evidence or a divergence of opinion about the usefulness/efficacy

of cardiac surgery, but weight of evidence/opinion of the majority is in favor; C Inconclusive

or conflicting evidence or a divergence of opinion; lack of clear consensus on the basis of

evidence/opinion of the majority. AR

aortic regurgitation; MR

mitral regurgitation;NYHANew York Heart Association classification.



15/23

Urgent surgery is recommended during the first 10 to 14 days of treatment

in cases of recurrent embolism after a second embolic complication. Surgery

should also be considered seriously after an initial embolic episode when

echocardiography shows a remaining large, mobile vegetation. Vegetations

localized on the anterior mitral leaflet might carry a higher risk of embolism,even if the last published series failed to show any correlation [46].

Should surgery be recommended when echocardiography reveals large,

mobile vegetations but embolization has not yet occurred? If the patient has

significant heart failure or severe valvular dysfunction, the decision is clear

because surgerywill achieve a two-fold objective. However, when valvular dys-

function is modest, the surgical indication is unclear. In general, the authors

do not recommend surgery solely to prevent embolization. If a large, mobile

vegetation is located on the mitral valve, the decision to operate is somewhat

favored because in this situation it is often possible to perform conservativedebridement of the vegetation and valve repair without valve replacement.

Persistent bacteremia

Persistent bacteremia in the absence of an extracardiac source of bacter-

emia indicates a failure of antibiotic therapy, provided treatment is given

Fig. 8. Incidence of embolic events per 1000 treatment days during treatment of infective endo-

carditis in Goteborg [30] and the Mayo Clinic [41]. (From Alestig K, Hogevik H, Olaison L.

Infective endocarditis: a diagnostic and therapeutic challenge for the new millenium. Scand

J Infect Dis 2000;32:34356. Copyright 2000 Taylor & Francis [31]).



16/23

according to accepted recommendations. The time considered necessary to

identify such a failure is considered to be at least 7 days after initiation of

antibiotic therapy. Provided that all efforts have been made to exclude meta-static foci, the most plausible cause is intracardiac suppurative disease, which

requires surgical intervention. Fever during treatment should not automat-

ically be regarded as synonymous with persistent bacteremia or suppurative

disease; it must be analyzed in terms of persistent and recurrent fever. Fever

persisted more than one week or recurred, despite effective antibiotic treat-

ment, in 57% of 193 episodes in a study of IE treatment. Persistent fever was

caused by a complicating cardiac infection in 56% of the episodes. On the

other hand, recurrent fever, which occurred most commonly during the third

and fourth weeks of treatment, was caused by hypersensitivity reactions tob-lactam antibiotics in the majority of episodes [51,52].

Valve obstruction

Mechanical obstruction of prosthetic valves or the native mitral valve by

large vegetations or thrombi is an urgent indication for surgery, particularly

if the valve is a mechanical valve prosthesis.

Fungal endocarditis

The earliest reported intracardiac surgical intervention for active IE was

in 1961 in a patient with Candida albicans endocarditis [1]. Candida and

Aspergillus species cause the majority of fungal IE cases. Amphotericin B,

still the only fungicidal agent available, has poor penetration into vegeta-

tions and surgery is usually needed. Most cases of fungal IE are complicated

with bulky vegetations, metastatic infections, perivalvular infections, or

embolization to large blood vessels [53,54]. Virtually all complicated cases

need surgery. In uncomplicated episodes caused by Candidaspecies, a num-

ber of case reports of NVE and PVE patients who are not valve replacement

candidates suggests that medical therapy alone may be successful, although

long-term suppressive therapy of at least 2 years with imidazoles is usually

employed [53,54].Aspergillus endocarditis carries a mortality risk of 90% to

100% without surgery.

Unstable prosthesis

The development of a rocking prosthesis or a rapidly progressive para-

valvular leak are urgent indications for valvular surgeryespecially duringthe early postoperative periodin a patient with early PVE.

Difficult-to-treat organisms

Pseudomonas aeruginosa is a rare agent of IE, and is in most cases con-

nected with intravenous drug abuse. Isolated right-sided pseudomonal IE



17/23

can generally be managed successfully with antibiotics with or without sur-

gery. Medical therapy alone has rarely been effective in left-sided IE; valve

replacement is indicated for the optimal chance of achieving cure [55].Coxiella burnetti, which causes Q-fever, is a strict intracellular pathogen.

Patients with previously damaged aortic or mitral valves or prosthetic valves

might acquire IE. Eradication of the organism with medical therapy alone is

unlikely, and reinfection of prosthetic material after surgical replacement

is common. Valve replacement is recommended only for CHF, PVE, or

uncontrolled infection [56]. To prevent reinfection of prosthetic material

some experts recommend that antimicrobial therapy be continued long-

term, possibly indefinitely [57].

Brucellaeare intracellular gram-negative bacilli that can cause IE compli-cated by development of valve destruction, perivalvular abscesses, and

CHF. Few patients have been cured with antimicrobial therapy alone; most

require valve replacement for cure [58].

Staphylococcus lugdunensis is a coagulase-negative staphylococci that

often causes a destructive course of infection with a frequent need for valve

replacement.

No effective antimicrobial agent available

In the rare case that no effective antimicrobial agent is available, IE

usually is caused by fungi or vancomycin-resistant enterococci. In such cases

surgery provides the only means capable of eradicating the infection.

Prosthetic valve endocarditis

Perivalvular invasive infections are common in PVE, especially when the

infection arises within 12 months after surgery or involves an aortic prosthe-

sis [59]. The microbial etiology of early PVE is dominated by coagulase-

negative staphylococci and S. aureus, accounting for about 30% and 20%of the cases, respectively [12]. In nearly all these patients, infection spreads

behind the site of attachment of the valve prosthesis, resulting in valve ring

abscesses and valve dehiscence in 60% of cases. If murmurs suggestive of

valve dysfunction, moderate to severe CHF, persistent fever 10 days, or

new ECG conduction abnormalities appear as signs of an invasive infection,

surgical treatment results in higher survival rates, less relapses, less rehospi-

talization for valve surgery, and less delayed mortality due to IE than med-

ical treatment alone [5962]. The rate of recrudescent PVE after surgery is

reported to be 6% to15%, and repeat surgery is required for recurrent PVEor prosthesis dysfunction in the new prosthesis in 18% to 26% of patients

[59,6365]. These figures indicate that these operations are very demanding

technically. Radical debridement and reconstruction are often needed,

requiring highly experienced surgeons. Multiple studies have shown that

PVE caused by S. aureus is most effectively treated with early surgery and

antibiotics [13,62].



18/23

There are a few subsets of patients in whom medical therapy alone may

be effective for PVE. These patients usually have late-onset of infection (12

months after prosthesis insertion), infection by viridans streptococci,HACEK(Haemophilus spp, Actinobacillus acinetocomitans, Cardiobacterium

hominis, Eikenella spp, Kingella kingae) or enterococci and absence of evi-

dence of invasive infection. Early antibiotic treatment improves the

chances of cure without complications in these patients with late-onset PVE

[42,66].

Additional issues related to surgical decision making in the acute phase

Neurological complications

Evaluation and management of patients with neurologic symptoms

represents another difficult and controversial area. The incidence of neuro-

logic complications differs in the literature from 15% to 40% [11,46,48]. Neu-

rologic complications include transient ischemic attack (TIA), embolic

stroke with or without hemorrhage, ruptured mycotic aneurysms, meningi-

tis, and non-focal encephalopathy.

The cardiac surgeon has two concerns: the first is related to the immedi-

ate risk of intracranial bleeding during cardiopulmonary bypass [67], andthe second is related to the risk associated with short- and long-term antico-

agulation.

Benefits versus risks should be carefully analyzed [68]. TIA or embolic

stroke without hemorrhage is the most common complication, constituting

62% of pathologically proven episodes in one study [48]. Hemorrhage from

rupture of a mycotic aneurysm or septic arteritis artery occurs less often but

entails a higher operative risk and a higher risk associated with anticoagula-

tion. Since the majority of patients with infective endocarditis and cerebral

symptoms have neither bleeding nor mycotic aneurysms, it is not possible togive firm recommendations about the necessary preoperative evaluation.

There is a consensus regarding the recommendation that a preoperative

CT scan of the brain be performed on every patient with neurologic symp-

toms to clarify the nature and extent of any cerebral lesion and to identify

hemorrhagic infarcts and other bleeding. In patients with intracranial bleed-

ing identified on CT scan 10% to 50% will have a ruptured mycotic aneur-

ysm [69,70]. Cerebral angiography is recommended in these patients. A

ruptured mycotic aneurysm should be resected, clipped, or embolized before

cardiac operation [69].Ting et al. [71] have shown that operative mortality increased in the pre-

operative presence of a hemorrhagic infarct but not in the presence of an

ischemic infarct. In the absence of a hemorrhagic infarction, valve replace-

ment can be performed at least 72 hours after the accident, with a low risk of

perioperative stroke [67]. However, a recent multicenter retrospective study

in Japan showed that there remains an increased risk of exacerbation of the



19/23

neurological deficits for weeks, but that this risk lessens with time irrespec-

tive of the type of lesion [68].

Patients with a recent hemorrhagic infarction clearly have an increasedrisk of intracranial bleeding during surgery [71]. The current recommenda-

tion is to allow an interval of 2 to 3 weeks between the neurologic event and

cardiac operation based on small published series [69,72].

Parrino et al. found diffuse encephalopathy to be associated with poor

outcome, focal deficit associated with 21% mortality, and 18% risk of dete-

rioration of the neurological deficit. The question remains, however, if

delaying surgery does anything other than select out hardier patients [73].

As a basic rule, operations should be delayed in unconcious patients and

patients unable to follow simple commands until neurological improvementhas been demonstrated.

Extracardiac invasive infections

Extra-cardiac lesions are not always explained by emboli. Some are due

to mycotic aneurysms, infectious arteritis, and other septicemic processes. In

the case of diagnosis of a visceral abscess (most often splenic), this should be

treated before cardiac surgery [74].

Extra-cardiac manifestations (most often in the form of stroke) often

precede the cardiac manifestations of IE. A high index of suspicion for

the diagnosis of IE is important in such circumstances, to prevent missing the

opportunity of early detection.

Age

Increased age is another risk factor. The population is becoming older;

the fact that a 9-fold increased rate of endocarditis has been reported for

patients older than 65 years is important [44,75]. Age per se is not a contra-

indication for surgery. Coronary angiography before surgery can be usefulin elderly patients, in patients with previous coronary grafting, and in

patients with advanced pathology and abscesses that may necessitate com-

plex repairs. The increased risk of emboli during catheter manipulation in

the aortic root should be considered.

Drug abuse

Intravenous drug abuse (IVDA) is associated, among other complica-

tions, with increased risk of blood-borne viral disease, non-compliance withmedical regimens, and recurrent endocarditis. The predominance of isolated

right-sided involvement in IE in this group with lower hemodynamic pres-

sures implies a less aggressive infection with excellent short-term prognosis

despite the frequent isolation ofS. aureusin blood cultures. Heart surgery is

seldom indicated. The frequency of left-sided involvement in IVDA has,

however, been relatively high33% and 39%in two series from Denmark



20/23

and Sweden, respectively [76] (data from the National Swedish Endocarditis

Registry). In the Swedish 5-year study involving 138 cases of IE in IVDA,

left-sided involvement as compared to isolated right-sided involvementnecessitated heart surgery in 35% versus 6% of the episodes. Mortality rates

for the two groups were 21% and 0%, respectively. The indications for surgical

intervention in patients with IVDA with left-sided endocarditis are the same as

for non-users, while the indications for surgical intervention in isolated tricus-

pid endocarditis are very limited. Furthermore, the hazards of overdosing and

underdosing anticoagulant therapy in this group of patients must be kept in

mind when surgery and surgical technique is considered. In an article by Math-

ew et al., the overall 5-year survival rate was 70% for 80 surgically treated

patients with IVDA, while 5-year event-free survival was only 52%; the eventswere recurrent endocarditis, stroke, bleeding, and systemic embolism [77].

References

[1] Kay JH, Bernstein S, Feinstein D, et al. Surgical cure ofCandida albicansendocarditis with

open-heart surgery. New Engl J Med 1961;264:90710.

[2] Wallace AG, Young WG, Osterhout S. Treatment of acute bacterial endocarditis by valve

excision and replacement. Circulation 1965;31:4503.

[3] Gouello JP, Asfar P, Brenet O, et al. Nosocomial endocarditis in the intensive care unit: ananalysis of 22 cases. Crit Care Med 2000;28(2):37782.

[4] McCarthy JT, Steckelberg JM. Infective endocarditis in patients receiving long-term

hemodialysis. Mayo Clin Proc 2000;75(10):100814.

[5] Alexiou C, Langley SM, Stafford H, et al. Surgery for active culture-positive endocarditis:

determinants of early and late outcome. Ann Thorac Surg 2000;69:144854.

[6] Bauernschmitt R, Jakob HG, Vahl C-F, et al. Operation for infective endocarditis: results

after implantation of mechanical valve. Ann Thorac Surg 1998;65:35964.

[7] Haydock D, Barratt Boyes B, Macedo T, et al. Aortic valve replacement for active

infectious endocarditis in 108 patients. A comparison of freehand allograft valves with

mechanical prostheses and bioprostheses. J Thorac Cardiovasc Surg 1992;103:1309.

[8] McGiffin DC, Galbraith AJ, McLachlan GJ, et al. Aortic valve infection. Risk factors fordeath and recurrent endocarditis after aortic valve replacement. J Thorac Cardiovasc Surg

1992;104:51120.

[9] Olaison L, Hogevik H, Myken P, et al. Early surgery in infective endocarditis. Q J Med

1996;89:267378.

[10] dUdekem Y, David TE, Feindel CM, et al. Long-term results of surgery for active

endocarditis. Eur J Cardiothorac Surg 1997;11:4652.

[11] Agnihotri AK, McGiffin DC, Galbraith AJ, et al. The prevalence of infective endocarditis

after aortic valve replacement. J Thorac Cardiovasc Surg 1995;110:170820.

[12] Chastre J, Trouillet JL. Early infective endocarditis on prosthetic valves. Eur Heart J

1995;16(Suppl B):328.

[13] Wolff M, Witchitz S, Chastang C, et al. Prosthetic valve endocarditis in the ICU.Prognostic factors of overall survival in a series of 122 cases and consequences for

treatment decision. Chest 1995;108:68894.

[14] Verheul H, Renee B, Vanden Brink A, et al. Effects of changes in management of active

infective endocarditis on outcome in a 25-year period. Am J Cardiol 1993;72:6827.

[15] Aranki S, Santini F, Adams D, et al. Aortic valve endocarditis. Determinants of early

survival and late morbidity. Circulation 1994;90(SII):17582.



21/23

[16] Edwards MB, Ratnatunga CP, Dore CJ, et al. Thirty-day mortality and long-term survival

following surgery for prosthetic endocarditis: a study from the UK heart valve registry. Eur

J Cardiothorac Surg 1998;14:5664.

[17] Horstkotte D, Piper C, Wiemer M, et al. Emergency heart valve replacement after acute

cerebral embolism during florid endocarditis. Med Klin 1998;93:28493.

[18] Aranki SF, Adams DH, Rizzo RJ, et al. Determinants of early mortality and late survival

in mitral valve endocarditis. Circulation 1995;92(SII):1439.

[19] Delahaye F, Ecochard R, de Gevigney G, et al. The long term prognosis of infective

endocarditis. Eur Heart J 1995;16(Suppl B):4853.

[20] Jault F, Gandjbakhch I, Rama A, et al. Active native valve endocarditis: determinants of

operative death and late mortality. Ann Thorac Surg 1997;63:173741.

[21] Larbalestier R, Kinchla N, Aranki S, et al. Acute bacterial endocarditis: optimizing

surgical results. Circulation 1992;86(SII):6874.

[22] Middlemost S, Wisenbauch T, Meyerowitz NC, et al. A case for early surgery in native left

sided endocarditis complicated by heart failure: results in 203 patients. J Am Coll Cardiol

1991;18:6637.

[23] Rocchioli C, Chastre J, Lecompte Y, et al. Prosthetic valve endocarditis. The case for

prompt surgical management. J Thorac Cardiovasc Surg 1986;92:7849.

[24] dAgostino RS, Miller DC, Stinson EB. Valve replacement in patients with native valve

endocarditis: what really determines operative outcome? Ann Thorac Surg 1985;40:42938.

[25] Soma Y, Handa S, Iwanaga S. Medical treatment or surgical intervention? A coopera-

tive retrospective study on infective endocarditistiming of operation. Jpn Circ J 1991;55:

799803.

[26] Bayer AS, Bolger AF, Taubert KA, et al. Diagnosis and management of infective endo-

carditis and its complications [AHA scientific statement]. Circulation 1998;98:293648.[27] Croft CH, Woodward W, Elliot A, et al. Analysis of surgical versus medical therapy in

active complicated native valve endocarditis. Am J Cardiol 1983;51:16505.

[28] Griffin FM, Jones G, Cobbs CG. Aortic insufficiency in bacterial endocarditis. Ann Intern

Med 1972;76:238.

[29] Mills J, Utley J, Abbott J. Heart failure in infective endocarditis. Predisposing factors,

course and treatment. Chest 1974;66:1517.

[30] Richardson JV, Karp RB, Kirklin JW, et al. Treatment of infective endocarditis: a 10-year

comparative analysis. Circulation 1978;58:58997.

[31] Alestig K, Hogevik H, Olaison L. Infective endocarditis: a diagnostic and therapeutic

challenge for the new millenium. Scand J Infect Dis 2000;32:34356.

[32] Choussat R, Thomas D, Isnard R, et al. Perivalvular abscesses associated with endo-carditis: clinical features and prognostic factors of overall survival in a series of cases.

Perivalvular abscesses French multicentre study. Eur Heart J 1999;20:1701.

[33] Daniel W, Mugge A, Martin R, et al. Improvement in the diagnosis of abscesses asso-

ciated with endocarditis by transesophageal echocardiography. N Engl J Med 1991;324:

795800.

[34] Erbel R, Rohmann S, Drexler M, et al. Improved diagnostic value of echocardiography in

patients with infective endocarditis by transesophageal approach: a prospective study. Eur

Heart J 1988;9:4353.

[35] Rohman S, Seifert T, Erbel R, et al. Identification of abscess formation in native-valve

infective endocarditis using transesophageal echocardiography: implications for surgical

treatment. Thorac Cardiovasc Surg 1991;39:27380.[36] Pettersson G, Carbon C. The Endocarditis Working Group of the International Society of

Chemotherapy. Recommendations for the surgical treatment of endocarditis. Clin

Microbiol Infect 1998;4:3S3446.

[37] Omari B, Shapiro S, Ginzton L, et al. Predictive risk factors for periannular extension

of native valve endocarditis: clinical and echocardiographic analyses. Chest 1989;96:

12739.



22/23

[38] Blumberg EA, Karalis DA, Chandrasekaran K, et al. Endocarditis-associated paraval-

vular abscesses: do clinical parameters predict the presence of abscess? Chest 1995;107:

898903.

[39] Baumgartner FJ, Omari BO, Robertson JM, et al. Annular abscesses in surgical

endocarditis: anatomic, clinical, and operative features. Ann Thorac Surg 2000;70:4427.

[40] Knosalla C, Weng Y, Yankah AC, et al. Surgical treatment of active infective aortic valve

endocarditis with associated periannular abscess11 year results. Eur Heart J 2000;21:

4907.

[41] Lerakis S, Robert Taylor W, Lynch M, et al. The role of transesophageal echocardio-

graphy in the diagnostic management of patients with aortic perivalvular abscesses. Am J

Med Sci 2001;321:1525.

[42] Truninger K, Attenhofer Jost CH, Seifert B, et al. Long term follow up of prosthetic valve

endocarditis: what characteristics identify patients who were treated successfully with

antibiotics alone? Heart 1999;82:71420.

[43] Vlessis AA, Hovaguimian H, Jaggers J, et al. Infective endocarditis: ten-year review of

medical and surgical therapy. Ann Thorac Surg 1996;61:121722.

[44] Steckelberg JM, Murphy JG, Ballard D, et al. Emboli in infective endocarditis: the

prognostic value of echocardiography. Ann Intern Med 1991;114:63540.

[45] De Castro S, Magni G, Beni S, et al. Role of transthoracic and transesophageal

echocardiography in predicting embolic events with active infective endocarditis involving

native cardiac valves. Am J Cardiol 1997;80:10304.

[46] Di Salvo G, Habib G, Pergola V, et al. Echocardiography predicts embolic events in

infective endocarditis. J Am Coll Cardiol 2001;37:106976.

[47] Heinle S, Wilderman N, Harrison K, et al. Value of transthoracic echocardiography in

predicting embolic events in active infective endocarditis. Am J Cardiol 1994;74:799801.[48] Heiro M, Nikoskelainen J, Engblom E, et al. Neurologic manifestations of infective

endocarditis. A 17-year experience in a teaching hospital in Finland. Arch Intern Med

2000;160:27817.

[49] Rohman S, Erbel R, Gorge G, et al. Clinical relevance of vegetation localization by

transesophageal echocardiography in infective endocarditis. Eur Heart J 1992;13:44652.

[50] Werner GS, Schulz R, Fuchs JB, et al. Infective endocarditis in the elderly in the era of

transesophageal echocardiography: clinical features and prognosis compared with younger

patients. Am J Med 1996;100:907.

[51] Olaison L, Hogevik H, Alestig K. Fever, C-reactive protein and other acute phase reactants

during treatment of infective endocarditis. Arch Intern Med 1997;157:88592.

[52] Olaison L, Belin L, Hogevik H, et al. Incidence of betalactam-induced delayedhypersensitivity and neutropenia during treatment of infective endocarditis. Arch Intern

Med 1999;159:60715.

[53] Moyer D, Edwards JE. Fungal endocarditis. In: Kaye D, editor. Infective endocarditis.

New York: Raven Press; 1992. p. 299312.

[54] Nguyen MH, Nguyen ML, Yu VL, et al.Candidaprosthetic valve endocarditis: prospective

study of six cases and review of the literature. Clin Infect Dis 1996;22:2627.

[55] Wieland M, Lederman MM, Kline-King C, et al. Left-sided endocarditis due to

Pseudomonas aeruginosa: a report of 10 cases and review of the literature. Medicine

(Baltimore) 1986;65:1809.

[56] Raoult D, Marrie T, Q fever. Clin Infect Dis 1995;20:48995.

[57] Levy PY, Drancourt M, Etienne J, et al. Comparison of different antibiotic regimensfor therapy of 32 cases of Q fever endocarditis. Antimicrob Agents Chemother 1991;35:

5337.

[58] Jacobs F, Abramowicz D, Vereerstraten P, et al. Brucella endocarditis: the role of

combined medical and surgical treatment. Rev Infect Dis 1990;12:7404.

[59] Calderwood SB, Swinski LA, Karchmer AW, et al. Prosthetic valve endocarditis. Analysis

of factors affecting outcome of therapy. J Thorac Cardiovasc Surg 1986;92:77683.



23/23

[60] Gordon SM, Serkey JM, Longworth DL, et al. Early onset prosthetic valve endocarditis:

the Cleveland Clinic experience 19921997. Ann Thorac Surg 2000;69:138892.

[61] Tornos P, Almirante B, Olona M, et al. Clinical outcome and long-term prognosis of late

prosthetic valve endocarditis: a 20-year experience. Clin Infect Dis 1997;24:3816.

[62] Yu VL, Fang GD, Keys TF, et al. Prosthetic valve endocarditis: superiority of surgical

valve replacement versus medical therapy only. Ann Thorac Surg 1994;58:10737.

[63] Jault F, Gandjbakheh I, Chastre JC, et al. Prosthetic valve endocarditis with ring abscesses.

Surgical treatment and long-term results. J Thorac Cardiovasc Surg 1993;105:110613.

[64] Lytle BW, Priest BP, Taylor PC, et al. Surgical treatment of prosthetic valve endocarditis.

J Thorac Cardiovasc Surg 1996;111:198207.

[65] Pansini S, di Summa M, Patane F, et al. Risk of recurrence after reoperation for prosthetic

valve endocarditis. J Heart Valve Dis 1997;6:847.

[66] Sett SS, Hudon MP, Jamieson WR, et al. Prosthetic valve endocarditis. Experience with

bioporcine prosthesis. J Thorac Cardiovasc Surg 1993;105:42834.

[67] Horstkotte D, Weist K, Ruden H. Better understanding of the pathogenesis of prosthetic

valve endocarditisrecent perspectives for prevention strategies. J Heart Valve Dis 1998;7:

3135.

[68] Eishi K, Kawazoe K, Kuriyama Y, et al. Surgical management of infective endocarditis

associated with cerebral complications. Multi-center retrospective study in Japan. J Thorac

Cardiovasc Surg 1995;110:174555.

[69] Gillinov AM, Shah RV, Curtis WE, et al. Valve replacements in patients with endocarditis

and acute neurologic deficit. Ann Thorac Surg 1996;61:112530.

[70] Hart RG, KaganHallet K, Joerns SE. Mechanisms of intracranial hemorrhage in infective

endocarditis. Stroke 1987;18:104856.

[71] Ting W, Silverman N, Levitsky S. Valve replacement in patients with endocarditis andcerebral septic emboli. Ann Thorac Surg 1991;51:1822.

[72] Matsushita K, Kuriyama Y, Sawada T, et al. Hemorrhagic and ischemic cerebrovascular

complications of active infective endocarditis of native valve. Eur Neurol 1993;33:26774.

[73] Parrino PE, Kron IL, Ross SD, et al. Does a focal neurologic deficit contraindicate

operation in a patient with endocarditis? Ann Thorac Surg 1999;67:5964.

[74] Trouillet JL, Hoen B, Battik R, et al. Splenic involvement in infectious endocarditis.

Association for the Study and Prevention of Infectious Endocarditis. Rev Med Interne

1999;20:25863.

[75] Hogevik H, Olaison L, Anderson R, et al. Epidemiological aspects of infective endocarditis

in an urban populationa 5-year prospective study. Medicine (Baltimore);1995;74:32439.

[76] Faber M, FrimodtMoller N, Espersen F, et al. Staphylococcus aureus endocarditis inDanish intravenous drug users: high proportion of left-sided endocarditis. Scand J Infect

Dis 1995;27:4837.

[77] Mathew J, Abreo G, Namburi K, Narra L, Franklin C. Results of surgical treatment for

infective endocarditis in intravenous drug users. Chest 1995;108:737.


current best practices and guidelines-indications for surgical intervention in infective...

Documents