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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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valvular disease


Mark Boyko, CCFP-EM R3

one night at the foot
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
At first glance…
  • Moving both sides of body (barely)
  • Not speaking to you
  • GCS 9

-Hgb 108

-WBC 14

-Lytes N

-EKG pacer spikes

ddx 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
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?

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
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
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
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
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
HACEK Organisms
  • Haemophilus aphrophilus
  • Actinobacillus actinomycetemcomitans
  • Cardiobacterium hominis
  • Eikenella corrodens
  • Kingella kingae
hacek organisms1
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
GROUP #2 Injection Drug Users (IDU’s)

#1 Staph

#2 Strep

#3 Pseudomonas

#4 Serratia

#5 Fungal (Candida, Apergillis)

group 3 prosthetic valve
GROUP #3 Prosthetic Valve

#1 Staph Epidermidis (50%)

#2 Streptococcus

ie risk factors
IE Risk Factors
  • Prior episode IE
  • Prosthetic Valve (same risk mechanical vs biological)
  • Recent invasive procedures
  • Structural Heart Disease (congenital and acquired valvular)
  • IDU
idu s
  • 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
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
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
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
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.
  • Usually normal, but can have new conduction disturbances
      • BBB
      • AV dissociation
diagnosis of ie
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
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
Osler’s Triad
  • Pneumonia, endocarditis, meningitis
  • Streptococcus pneumoniae is the culprit
  • Often associated with alcohol abuse, mortality is extremely high
empiric treatment
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
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

summary ie
  • Suspect it
  • Exam the hands of your patient
  • Always draw blood cultures x3 before administering antibiotics
  • Order an echo if concerned
antibiotic prophylaxis
Antibiotic Prophylaxis

Guidelines 2007

patients at highest risk
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
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
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 presentation1
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
  • Revolves around management of mitral regurgitation
  • Nitrates and Diuretics for CHF
  • IABP as bridging therapy
  • Definitive treatment is surgical repair
aortic stenosis1
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
Scarey Symptoms
  • A ngina
  • S OB
  • S yncope
  • S udden death (not really a symptom!)

“Classic Triad”:

CP, CHF, Syncope

classic characteristics
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
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