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VALVULAR DISEASE. Mark Boyko, CCFP-EM R3. One night at the Foot…. 64yo male found down at home… -HR 111 -BP 109/67 -RR 12 -Temp 38.6 -O2 88% -Glucose 22. At first glance…. Moving both sides of body (barely) Not speaking to you GCS 9. Labs. -Hgb 108 -WBC 14 -Lytes N

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Mark Boyko, CCFP-EM R3

One night at the Foot…

64yo male found down at home…

-HR 111

-BP 109/67

-RR 12

-Temp 38.6

-O2 88%

-Glucose 22

At first glance…

  • Moving both sides of body (barely)

  • Not speaking to you

  • GCS 9


-Hgb 108

-WBC 14

-Lytes N

-EKG pacer spikes

REPORT: Multiple ischemic areas consistent with embolic stroke

DDx Embolic Stroke ?

  • Valvular disease (infective or sterile)

  • Prosthetic valves

  • A fib / Arrythmia

  • MI / Mural thrombus

  • Cardiac tumours

  • Cardiomyopathy (amyloid, sarcoid)

  • Antiphospholipid Ab, pro-thrombotic states

  • R-sided emboli with PFO

  • Carotid plaques

You decide to..

  • Treat for aspiration pneumonia secondary to stroke

  • Intubate for decreased GCS

  • Off to ICU, neuro consult

  • Carotid dopplers N

  • Echo of heart reveals vegetations on mitral valve

  • Blood Cultures later reveal +Strep Bovis


  • Due to his blood culture, what further (non-acute) examination does this patient require in the future?

Infective Endocarditis (IE)


Which age group is most commonly affected?

a) < 30 yrs

b) 31-60 yrs

c) >60 yrs


  • Turbulent flow is the biggest enemy, it denudes the endothelium over time

  • IDU’s  there is often talc mixed in with the drug injection, in addition to cocaine-induced ischemia, causing damage to valves

  • A vegetation begins as platelets and thrombin, and may be sterile at first. But it is a perfect home for a bacteria present in the bloodstream

Transient Bacteremia

  • A brief period where the bacterial count in the bloodstream is <10 organisms/mL blood.

  • This should only last 30min or so, and for most people this is not a problem. However, for people with valvular disease, it is.

Acute vs Subacute IE

  • Historically IE classified as acute (rapid onset, hemodynamic compromise) or subacute, but best viewed as a continuum

  • Acute is lethal in days if left untreated

  • For us…

    • Acute: if they are sick and this is a rapid change

    • Subacute: grumbling along last few weeks


Which microbe causes most cases of IE overall?

Microbiology of IE

  • Overall, #1 cause is Staph Aureus

  • However, many causitive agents, the microbiology of IE is best classified by:

    • Native valve, non-IDU

    • IDU’s

    • Prosthetic Valves

GROUP #1 Native Valve, Non IDU

#1 Streptococcus Viridans (40%)

#2 Staph Aureus (30%)

#3 Enterococci (10%)

#4 HACEK group

*Culture Negative 5% (Coxiella Burnetti, Bartonella)


Can you name at least 3 organisms in the HACEK group?

…. Alternatively…. Which NHL team first drafted famous Czeck goaltender Dominik Hasek?

HACEK Organisms

  • Haemophilus aphrophilus

  • Actinobacillus actinomycetemcomitans

  • Cardiobacterium hominis

  • Eikenella corrodens

  • Kingella kingae

HACEK Organisms

  • Just remember they are GRAM Negative organisms, difficult to culture

  • Collectively, cause 5-10% of IE in people that are not IDU’s

GROUP #2 Injection Drug Users (IDU’s)

#1 Staph

#2 Strep

#3 Pseudomonas

#4 Serratia

#5 Fungal (Candida, Apergillis)

GROUP #3 Prosthetic Valve

#1 Staph Epidermidis (50%)

#2 Streptococcus

IE Risk Factors

  • Prior episode IE

  • Prosthetic Valve (same risk mechanical vs biological)

  • Recent invasive procedures

  • Structural Heart Disease (congenital and acquired valvular)

  • IDU


  • Right-sided IE

  • Tricuspid > Pulmonary valve

  • PE more common

  • Less likely to have peripheral embolic findings

  • High recurrance rate


  • Rank the cardiac valves in order of decreasing incidence of IE


  • Aortic

  • Mitral

  • Tricuspid

  • Pulmonary


  • LEFT-SIDED valves are more commonly hit!

  • However, when all cases of right-sided IE are analyzed, the vast majority occur in IDUs

What about Pacemakers?

  • Rare, but can get IE

  • Right-sided vegetations (on either valves or pacer leads)

  • Seen from 0-20 months post insertion

  • Look for hematomas, cellulitis at site

  • Be suspicious!


  • What percent of people with IE will have a murmur at some point during the course of their illness?

Clinical Presentation

  • Fever 80%

  • General malaise 40%

  • Skin manifestations 20-50%

  • Splenomegaly if present for weeks 20%

  • Murmur 30-80% (but almost all will have a murmur at some point during their course of illness)

Better way to remember things…

  • Bacteremia-related symptoms

    • Fever, chills, SIRS

  • Cardiac symptoms

    • Chest pain, SOB, CHF

  • Embolic Phenomenon

    • CNS, cardiac, pulmonary, GI, renal, DERM


Which of the following lesions are painful?

a) Osler’s Nodes

b) Janeway Lesions

c) Splinter hemorrhages

d) Roth spots

Dermatologic Findings in IE

  • These are immune-complexes (bacteria + Ig + fibrin) that have become lodged in distal arterioles, just under the skin.

  • Usually only seen in sub-acute IE because it takes time for them to develop.

Osler Nodes (Ouch!)

Janeway Lesions

Splinter Hemorrhages

Roth’s Spots


  • Usually normal, but can have new conduction disturbances

    • BBB

    • AV dissociation

Diagnosis of IE

  • DUKE Criteria

  • Not straight-forward, but sensitivity ~90%

  • We cannot make the diagnosis of IE in the ER! But you must be suspicious.

  • Requires blood cultures to come back, echo to be done, and monitoring over course of an admission.

Blood Culture

  • Key to the diagnosis

  • Draw 3 samples total, 3 different sites

    • 2 different sites at time 0

    • 3rdseparate site at time 1hr

  • 90-95% will be positive if truly IE


  • TTE ~60% sensitive for vegetations

  • TEE ~ 80% sensitive for vegetations

  • If TTE negative but clinical suspicion remains high, make sure you get a TEE

  • NPV value for IE with a normal TEE without prosthetic valves ~100%

  • All patients need one within 12hrs, but if they are acutely decompensating order one STAT.


When is the highest risk for IE after prosthetic valve surgery?

a) 0-6mos

b) 6mos-3yrs

c) 3-10yrs

d) >10yrs


What is Olser’s Triad?

Osler’s Triad

  • Pneumonia, endocarditis, meningitis

  • Streptococcus pneumoniae is the culprit

  • Often associated with alcohol abuse, mortality is extremely high

Empiric Treatment

Native Valve

  • Ceftriaxone 2g IV, plus

  • Gentamicin 1mg/kg IV q8hrs


  • Native valve regimen, plus

  • Vancomycin 15mg/kg IV q12hr

    Prostethic Valve

  • IDU regimen, plus

  • Rifampin 300mg PO TID

Surgical Intervention ?

  • Significant valve incompetance (ongoing CHF)

  • Uncontrolled sepsis despite proper Abx

  • Abscess or new conduction disturbance

  • Severe embolic phenomenon

  • Unstable prosthetic

    *Okay to perform surgery in acute setting


  • Suspect it

  • Exam the hands of your patient

  • Always draw blood cultures x3 before administering antibiotics

  • Order an echo if concerned

Antibiotic Prophylaxis

Guidelines 2007

Patients at Highest Risk

  • Prosthetic cardiac valve

  • Previous infective endocarditis

  • Congenital heart disease (CHD)

    • Unrepaired or within 6mos of repair

  • Cardiac transplantation with valvular defects

Procedures Requiring Prophylaxis

1. ANY dental work

2. Bronchoscopy

3. Skin infection & procedure

*99% of our ER procedures are safe, but use in abscess drainage


  • Dental/Resp/Esophagael

  • Amoxil 2g PO 30-60min prior

    • *some data that 2hrs post-procedure beneficial is missed initial dose

  • Penicillin Allergy: Clindamycin 600mg PO

Papillary Muscle Rupture

  • Very rare (<1% of all MI), but very lethal

  • 80% mortality within 24hrs of rupture without surgical intervention

  • Most often associated with mitral valve regurgitation

  • Timing: From onset of MI to 7 days post-MI

  • Requires urgent cardiac surgery


  • Think about it in your inferior MI’s  disruption of flow in the right coronary artery or circumflex

  • Posteromedial papillary muscle has single blood supply, once cut off, it is vulnerable

Clinical Presentation

  • Tip-offs:

    • New Murmur

    • Respiratory failure / pulmonary edema (esp if no hx CHF)

    • Within hours to 7 days of an inferior MI

  • Seen more commonly in the older patient with his/her first MI

  • Management

    • Revolves around management of mitral regurgitation

    • Nitrates and Diuretics for CHF

    • IABP as bridging therapy

    • Definitive treatment is surgical repair


    Aortic Stenosis

    • Most common valvular lesion among elderly patients

    • “critical” AS is <0.8cm2 or when pressure gradient across valve is >50mmHg

    • Asymptomatic period can last 10-20yrs

    • Once symptomatic, life expectancy only 1-3yrs

    Scarey Symptoms

    • A ngina

    • S OB

    • S yncope

    • S udden death (not really a symptom!)

      “Classic Triad”:

      CP, CHF, Syncope

    Classic Characteristics

    • Harsh, mid-systolic murmur (later in systole, more severe)

    • Radiation to carotids

    • Decreased pulse amplitude

    • ‘Parvus et Tardus’

    • Narrow Pulse Pressure

    • Brachial-radial delay

    • Louder if patient leans forward


    • These patients are PRE-LOAD dependent

    • They have NO CARDIAC RESERVE (essentially, a fixed CO)

    • Medical management is a spit in the ocean, they need surgery

    Acute Management

    • Fluids (even if in CHF, you’ll have to balance diuresis)

    • Blood transfusion

    • Restore NSR

    • AVOID Nitroglycerin, vasodilators. This may kill them

    • Inotropes?  If you’re stuck, you are stuck

    • Call CCU for IABP


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