Infective Endocarditis and Valvular Disease

Geoff Lampard PGY-1 Ian Walker

Outline

What will be covered

Infective Endocarditis

Aortic Stenosis

What murmurs need workup?

What will not be covered

The rest……

Doctor! I gotta fever!

55 yo male

Fever of 24 hours

No focal symptoms

Past history includes mechanical aortic valve for symptomatic AS

Faint I/VI SEM but "that's not new"

the making of the beast

1. Endocardial injury

2. Sterile thrombus formation

3. Transient bacteremia and seeding

4. Maturation

a 4 step process

epidemiology

• Epidemiology has changed dramatically over the past 50 years

• 2-10 episodes/100,000 patient years in general population• 1-3/1000 in IVDU

• M>F

• Mean age ≈ 60

• Mortality is steadily increasing

which valves?

1. Mitral valve

2. Aortic valve

3. Multivalvular

4. Right sided endocarditis (mostly IVDU)

IE risk factors

1. Structural valvular lesion or prosthetic valve (75%)

Also:

• Prior IE

• Invasive Procedure/Line

• IVDU

• Age

2 very different presentations

1. Acute IE acute fever CHF +/- hemodynamic

instability peripheral signs of

embolism

2. Subacute Bacterial Endocarditis (SBE)

Fever (85%), malaise (80%) Murmur is unpredictable Others: weakness, myalgias,

back pain, dyspnea, chest pain, cough, headaches.

Commonly misdiagnosed as viral illness

Check their hands and eyes!

The D

uke

– sim

plifi

ed

!

Reported sensitivity/specificity of Duke Criteria 95%/99%

Major

Pathologic Criteria• Typical bugs from 2 cultures

OR• Typical bug from persistently

positive cultures OR• Single c. burnetti (culture or

IgG titre)

Echo Criteria• New regurgitation OR• Positive echo (1 of 3 criteria)

Minor

Risk factors

Fever

Vascular phenomena

Immunologic phenomena

Microbiological findings

Duke criteria – echocardiographic findings

1. Oscillating intracardiac mass2. Abscess3. New partial dehiscence of prosthetic valve4. New valvular regurgitation (new murmur insufficient)

vascular phenomena

• Janeway lesions and splinter hemorrhages• Also:

• Conjunctival hemorrhages

• Major arterial emboli

vascular phenomena

• Mycotic aneurysms with intraventricular hemorrhage• Septic pulmonary infarcts

immunologic phenomena – eponymous potpourri!

• Osler nodes and Roth spots• Glomerulonephritis and elevated rheumatoid factor• Much more likely to occur in SBE

making the call

Investigations Echo (TTE vs TEE) Blood Cultures

>3 different sites, 1st and last >1 hr apart Let your lab know that you are considering IE

ECG RF/CRP/ESR Urinalysis CXR

TTE or TEE?

TTE

Sn/Sp : 46% / 95%

Ideal for low pretest probability patients, children

TEE

Sn/Sp : 93% / 96%

1st choice modality for: Medium to high pretest

probability

When TTE less sensitive (obesity, lung hyperinflation, valve prosthesis)

Both have a role, but common practice differs from guidelines

In practice in Calgary, TTE first unless acutely ill

some antibiotic principles

Long durations required

Parenteral preferred

Stable SBE: forgo antibiotics until cultures return

Acute IE: obtain cultures first, then treat

Think of 3 treatment groups: NVE IVDU PVE

1. Native Valve Endocarditis

1. S. Aureus2. Streptococcus spp.(esp. viridans and bovis)3. Enterococci (>80% enterococcus faecalis)4. HACEK group (5-10%)5. Persistently culture negative spp

aortic valve vegetation and perforation

HACEK group – can you name them?

• Haemophilus species

• Actinobacillus actinomycetemcomitans

• Cardiobacterium hominis

• Eikenella corrodens

• Kingella Kingae

colony of actinobacillus actinomycetemcomitans

2. IVDU associated endocarditis

1. S. Aureus (70%)2. Polymicrobial3. Streptococcus spp.4. Pseudomonus aeruginosaMust also consider fungal species (candida, aspergillus)

s. aureus

3. Prosthetic Valve Endocarditis

Early1. Staph epidermidis2. Staph aureus3. Streptococcus spp.Late (>1year) same as NVE

staph epidermidis

which drug should you start?

Rosen’s Keep it simple!vs:

Vancomycin 15mg/kg IV

q12h

and

Gentamicin 1mg/kg IV q8h

I suspect IE. What next?

All suspected cases should be admitted

Hold antibiotics until cultures return for SBE

Treat Acute IE. But get cultures first! Unstable? 2x cultures 20 minutes apart Sick? 3x cultures 1 hr apart

PVE and fever NYD? Admit.

complications

1. CHF and cardiogenic shock

2. Embolisation1. CNS

2. Spleen

3. Kidneys

4. Lungs

5. Liver

3. Intracardiac Abscess

4. Death! 20-30% at 1 year

the IV drug user

79% of IVDU IE is right sided

70% s. aureus

Only 35% will have a murmur on admission

Septic pulmonary emboli: hallmark of disease 80% of tricuspid valve IE will have CXR findings on presentation

what about prostheses?

Risk is highest in the 1st year

Low threshold for admission of Fever NYD + admission Aggressive organisms High risk of dehiscence

TTE very low sensitivity

Pacemakers can get infected too!

who needs emergent surgery?

Practically speaking, CHF + cardiogenic shock is only true indication for emergent surgery.

Consult cardiac surgeon early for: CHF or severe valvular dysfunction likely to

precipitate CHF Invasive valvular complications on echo Pseudomonas, fungi, or MDR organisms High risk of embolism PVE

prophylaxis – simpler than you think!

Amoxicillin PO 2g (adults) 50mg/kg (children) 30-60 minutes pre-procedure

Allergic? Try Clindamycin 600mg PO

High Risk Procedures• Now ONLY dental procedures• Oral sutures

High Risk Patients• Prosthetic Valves• Prior IE• Congenital HD• Unrepaired cyanotic HD• 1st 6 months post-CHD

repair• Repaired CHD with defects

at repair site• Cardiac transplant with valve

regurgitation

aortic stenosisA few handy principles

key definitions

Severe <1cm2 or gradient >40mmHg

Moderate 1.0-1.5cm2

Mild >1.5cm2

Normal valve area >3cm2

who gets it?

By far 3 most common causes:

• Calcific degeneration

• Bicuspid aortic valve

• Rheumatic disease

pathophysiology

High pressure gradients (afterload) lead to concentric LVH

1. Angina: Concentric LVH maintains CO but impairs coronary reserve

2. CHF/Dyspnea: Increased LVEDP lead to pulmonary congestion

3. Syncope: unclear; may be vasovagal response

how do they present?

SAD symptoms

Early: asymptomatic

Later: angina, CHF (dyspnea)

Latest: exertional syncope

Long asymptomatic period, then rapid deterioration

on exam

SEM @ RUSB, radiating to carotids

S4, soft S2 in late disease

Parvus et tardus despite powerful apex beat

Crescendo peaks later as severity increases and may disappear

principles of management

There are no set rules in decompensated AS

They are preload dependent with a fixed cardiac output

A surgical disease; medical management is a bridge only

and the CHF patient with AS?

Vasodilation has a narrow therapeutic range

BiPAP, nitrates, and diuretics should be used cautiously Use something titratable!

Evidence exists for Na-nitroprusside in ICU setting

Inotropic support for cardiogenic shock

Call CCU! They need definitive treatment.

what lies beyond…..

Early involvement of CCU is critical

Interventional options are definitive Valvuloplasty IABP TAVI (transcatheter aortic valve

implantation) Surgical aortic valve replacement

which murmurs need workup?

Incidental murmurs are common in the ED

AHA 2006 Guidelines: Diastolic Continuous Holosystolic Late systolic Ejection clicks Radiation to neck or back

if you remember nothing else

Suspect IE in patients with fever/malaise and structural valvular disease

Examine hands, feet, and eyes!

3 blood cultures, 3 different sites, at least 1hr apart

Admit all suspected IE. If acute, obtain fast cultures and treat empirically (Vanco + Gent).

If SBE and stable, delay ABx until cultures return

Amoxil 2g prophylaxis for oral procedures

… and for aortic stenosis

AS is a surgical disease

They are preload dependent with a fixed cardiac output

Medical management may hinder more than help

Get CCU involved quickly for decompensating patients