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 factors1. Structural valvular lesion or prosthetic valve (75%)
Also:
• Prior IE
• Invasive Procedure/Line
• IVDU
• Age
2 very different presentations1. 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 Duke – simplified!
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)
MinorRisk factors
Fever
Vascular phenomena
Immunologic phenomenaMicrobiological findings
Duke criteria – echocardiographic findings1. 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 Endocarditis1. 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 endocarditis1. S. Aureus (70%)2. Polymicrobial3. Streptococcus spp.4. Pseudomonus aeruginosaMust also consider fungal species (candida, aspergillus)
s. aureus
3. Prosthetic Valve EndocarditisEarly1. 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.
complications1. CHF and cardiogenic shock
2. Embolisation1. CNS2. Spleen3. Kidneys4. Lungs5. 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