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Infective Endocarditis

Recognition and diagnosis. Does the patient really have endocarditis? First, there are a group of patients who are at particular risk. In any of these patients, endocarditis should always be high on your concern and I think many of these groups will be familiar to you but there’s one at the end that is new. First, the patients with damaged natural valves and I think all of you are aware that in the past it was mainly congenital heart defects – patients with rheumatic valvular disease. This is less common today. Patients with mitral valve prolapse. Not all of them but ones with certain characteristics, particularly on echocardiogram and when they have persistent murmurs associated with this not uncommon congenital lesion. Asymptomatic septal hypertrophy syndrome and degenerative calcified valves in the elderly patient population all constitute a risk factor as a damaged natural valve endocarditis infective endocarditis, endocarditis, heart valve infection

Intravenous drug users and patients who have prosthetic heart valves. Those who are considered having early prosthetic valves, meaning those less than 60 days of valve replacement can develop endocarditis. I use 60 days because it’s one of the more useful and accepted ways of dividing

But the point is there’s disturbing news here because there are more and more of these patients in our population and a fairly recent article by Fones from the University of Pittsburgh in the annals of 1993 reported on patients with prosthetic heart valves who were followed one year after a

This allows us to go into a new group of patients who I think we have to consider very seriously as patients at particular risk. Patients in the hospital setting, there’s a fourth group that we have to be aware of. Not just those with prosthetic valves but those with malignancies. There are increasing reports, most recently from the University of Pittsburgh, about patients with solid organ transplants who develop endocarditis – those with

They have a disturbingly high mortality – well over 50% in any of the series of those patients that I described. It’s attributed (1) to not recognizing and (2) to the host who is often immunologically impaired and (3) to the nature of the organisms that they get – Staph aureus being particularly important and fungal infections. So I think we also have to be aware that when I say "patients in a hospital setting" we have to enlarge our

One, in the hospital. So bacteremic episodes occurring in patients with prosthetic valves, intravascular devices and this includes AV fistula or 

Now, what I’d like to do is talk to you a minute about the diagnosis of the disease. I think you are all aware of the fact that there is news here. Durack and his group at Duke University offered new criteria for assessment in the American Journal of Medicine article that they published in 1994 and since then there have been many, many series reported from other institutions assessing the validity and the usefulness of these new criteria.

As you know, the classic diagnostic criteria that most of us remember, the Von Rheim criteria which Petersdorf published in medicine the journal in 1977 and they were assigned by Von Rheim. Conceptual categories based on our understanding of the pathophysiology of this disease. A documented persistent worse state of bacteremia, an active endocardiopathology and predisposing heart disease with vascular phenomenon that may be embolic or maybe immunologically mediated and that’s kind of how we grew up.

The Duke or the Durack modifications are interesting because they kind of try to model encarditis after rheumatic heart disease which is a disease we still don’t really understand that much about. So there are major criteria and minor criteria and I think at some point we might have to think about this as maybe the flaw in this whole new way of thinking about the disease.

This is the Von Rheim criteria and you’ll notice there are "definite", "probable", "possible" and "rejected" categories and, again, this was to put series together so as to compare experiences with endocarditis so that you’re very kind of sure that the patient has the disease that you’re reporting.

Some of the differences or modifications was that the Durack criteria were finally recognizing IV drug users as a risk factor. As I said, this was published in 1994 and I think we’ve all recognized that. That would be a minor criteria in this and you can change the categories. So that there was definite, not only autopsy or surgical, evidence of infection or a pathology from an embolic event but he loosened it up and allows clinical criteria and that gets to the two major, one major and three minor, five minor criteria and then possible or rejected and eliminates probable. The only point I want to make about this is these new criteria imply that fewer patients will be rejected from the diagnosis and this has implications not only for the series that you would include these patients in but for treatment of these patients. So we may well be treating more patients for endocarditis if we use these criteria than actually have the disease but that may be the safest way.

Also what the Duke criteria do is recognize certain organisms as highly likely to be associated and correlated with having endocarditis and I think this is an extremely useful thing that these modifications offer. (1) That Strep viridans and Strep bovis and the HACEK’s group – Hemophilus, saprophilous, Actinobacillus, Cardiobacterium hominis, Eikenella and Kingella – all mouth organisms – are so highly correlated with endocarditis that when you see just two blood cultures positive for these organisms coming from the community, there really is almost nothing else it could be. So you don’t need maybe perhaps as many documented blood cultures as for the other organisms. He also includes in this, community acquired Staph aureus and enterococcal bacteremia without a known focus.

The other thing that I think is extremely important that the Durack criteria offer is some comment about the echocardiogram. As the echocardiogram got more and more refined, all of us were using the echocardiogram not as it was initially meant to be, which was as an add on, a helpful aspect of the kind of damage, how much damage, but as a diagnostic tool. What the Duke criteria do is they say, "Okay, we acknowledge that this has a role in diagnosis but be careful out there." Major determinants, he’s very clear about this and they have a lot of background data to support it is that he will allow the echocardiogram to be used for endocardial involvement only if it fits certain criteria for the echocardiologist. It has to be an oscillating intracardiac mass on the valve in the anticipated location of a patient with endocarditis or on a supporting structure or an annular abscess or if there’s a prosthetic valve, a new partial dehiscence.

All the other things that our echocardiologists say, "Well, this could be endocarditis" those go down into minor or not relevant including a thickened valve, a non-oscillating mass, fibrinous threads. Those don’t carry the same weight as these very specific echocardiogram determinants. So you have to be careful when your echocardiologist gets a request for an echocardiogram saying "rule out endocarditis". They’re going to look very hard, which 

Introduction

Infective endocarditis - an uncommon disease but a critical consideration in diagnosis of the febrile patient

the febrile, bacteremic patient

Issues of treatment: Begin with recognition and diagnosis then medical management then role of valve surgery - indications

Recognition

Does the patient "really" have endocarditis

The groups at risk

patients with damaged natural heart valves intravenous drug users patients with prosthetic valves

<60 days after valve replacement

> 60 days after valve replacement

and new groups

the immunosuppressed patients

hospitalized patients - nosocomial endocarditis, with or without prosthetic valves

Diagnosis - challenge clinically and standardization helpful for comparing series

Classic criteria -von Reyn

based on pathophysiologic features

predisposing heart disease, persistent bacteremia,

vascular phenomena, evidence of active intracardiac pathology

 

Newly suggested criteria - Durack - Duke Criteria

case definition includes Echocardiographic findings and sets up

system of major and minor clinical criteria

 

Major criteria

1. "Classic" - pathologic confirmation by examination/culture of the heart valves

or of embolic material

2. Duke additions

persistent bacteremia 

Echocardiographic findings 

new regurgitant murmur

persistent bacteremia

formally acknowledges certain microorganisms that are highly

associated with endocarditis

 

HACEK group, streptococcus viridans and streptococcus bovis - 2 blood cultures Staphylococcus aureus and Enterococcus - if community acquired, no

focus - 2 blood cultures

other organisms - 2 or more blood cultures separated by 12 hrs, 3 or more blood

cultures at least 1 hr between 1 st and last culture

Echocardiography

Trans thoracic / Trans esophageal

major criteria: an oscillating mass located where vegetations typically occur,

abscess or new prosthetic dehiscence

minor criteria: less clear - less useful

"consistent with" - non oscillating targets, new valvular fenestrations, nodular valvular thickening

and formally includes intravenous drug use as a predisposing condition but changes categories of certitude - definite/probable/possible/rejected- definite/possible/rejected

and definite not only pathologic documentation - of valve or embolic tissue but allow clinical criteria - a combination of major and minor criteria and relegates vascular phenomena to minor criteria

Medical Management

I. Antibiotics

properties - penetration into fibrin/platelet aggregates and cidal in this milieu route - reliable levels IV preferred

duration - longer untreated ? more complex the vegetation organisms in different metabolic states does this mean duration of symptoms should dictate length of therapy? choices -

Streptococcus viridans, bovis

penicillin 4 million units every 4 hrs IV alone for 4 wks

or

penicillin 2-4 million units every 4 hrs IV + gentamicin 1 mgm/kgm every 8 hrs for 2 wks then penicillin alone for 2 wks

or

penicillin 2-4 million units every 4 hrs IV + gentamicin 1 mgm/kgm every 8 hrs for 2 wks only (?)

alternatives

Vancomycin or

Cefotaxime or Ceftriaxone ? alone

 

Enterococcus fecalis, faecium

ampicillin 2 gms every 4 hrs (or penicillin 4 million units every 4 hrs IV ?) + gentamicin 1 mgm/kgm every 8 hrs alternatives

vancomycin 1 gm every 12 hrs + gentamicin 1 mgm/kgm every 8 hrs

 

Staphylococcus

aureus

oxacillin 2 gms every 4 hrs IV may choose to use

gentamicin for first 3-5 days

alternate

Vancomycin 1 gm every 12 hrs IV

MRSA

Vancomycin 1 gm every 12 hrs with

gentamicin for first 3-5 days and ? rifampin

coagulase negative staphylococcus Vancomycin 1 gm every 12 hrs with gentamicin for first 3-5 days and ? rifampin

HACEK organisms

cefotaxime 2 gins every 6 hrs IV or ceftriaxone 2 gms every day

alternative

ampicillin 2 gms every 4 hrs IV + gentamicin 1 mgm/kgm every 8 hrs hospital or home?

 

II. The Host

if native valve - will do "better" than infection of prosthetic valve

if tricuspid valve only - will do "better" than left sided valve involvement

III. The Microorganism

Streptococcus

Enterococcus

Staphylococcus aureus

Problems: VREF, pseudomonas aeruginosa

fungus - candida, aspergillus

IV. Complications

of the antibiotics

fever - IV site, drug; allergic reaction; toxicity

of the disease

fever - persistent

annular or septal abscess/distant abscess other heart failure embolization

 

The Role of Valve Surgery During Treatment of Active Infection

Why

eradicate infection; correct hemodynamic defect; remove locus of emboli

Indications

persistent or relapsing infection; congestive heart failure; embolization

Who

persistent or relapsing infection native valve endocarditis - rarely

prosthetic valve (particularly early), IV drug user - not rare congestive heart failure/embolization

can Echocardiography help in risk assessment? presence of vegetation and size alone - not sufficient valve position - microorganism - associated LV failure possibly duration of symptoms

Procedures

Valve replacement 

Reconstruction 

Valve repair