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-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
Question
• Due to his blood culture, what further (non-acute) examination does this patient require in the future?
Infective Endocarditis (IE)
Question
Which age group is most commonly affected?
a) < 30 yrsb) 31-60 yrsc) >60 yrs
Pathophysiology
• 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
Question
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)
Question
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
IDU’s
• Right-sided IE• Tricuspid > Pulmonary valve• PE more common• Less likely to have peripheral embolic
findings• High recurrance rate
Question
• Rank the cardiac valves in order of decreasing incidence of IE
Answer
• Aortic• Mitral• Tricuspid• Pulmonary
Valves
• 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!
Question
• 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
Question
Which of the following lesions are painful?
a) Osler’s Nodesb) Janeway Lesionsc) Splinter hemorrhagesd) 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
EKG
• 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– 3rd separate site at time 1hr
• 90-95% will be positive if truly IE
ECHO
• 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.
Question
When is the highest risk for IE after prosthetic valve surgery?
a) 0-6mosb) 6mos-3yrsc) 3-10yrsd) >10yrs
Question
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 TreatmentNative Valve• Ceftriaxone 2g IV, plus• Gentamicin 1mg/kg IV q8hrs IDU• 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
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
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 work2. Bronchoscopy3. Skin infection & procedure
*99% of our ER procedures are safe, but use in abscess drainage
Prophylaxis
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
How?
• 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
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
Remember…
• 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
Thanks!