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VALVULAR DISEASE

Date post: 10-Feb-2016
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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 - PowerPoint PPT Presentation
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VALVULAR DISEASE Mark Boyko, CCFP- EM R3
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Page 1: VALVULAR DISEASE

VALVULAR DISEASE

Mark Boyko, CCFP-EM R3

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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

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At first glance…

• Moving both sides of body (barely)• Not speaking to you• GCS 9

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Labs

-Hgb 108-WBC 14-Lytes N-EKG pacer spikes

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REPORT: Multiple ischemic areas consistent with embolic stroke

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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

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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

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Question

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

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Infective Endocarditis (IE)

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Question

Which age group is most commonly affected?

a) < 30 yrsb) 31-60 yrsc) >60 yrs

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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

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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.

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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

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Question

Which microbe causes most cases of IE overall?

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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

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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)

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Question

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

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

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HACEK Organisms

• Haemophilus aphrophilus• Actinobacillus actinomycetemcomitans• Cardiobacterium hominis• Eikenella corrodens• Kingella kingae

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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

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GROUP #2 Injection Drug Users (IDU’s)

#1 Staph#2 Strep#3 Pseudomonas#4 Serratia#5 Fungal (Candida, Apergillis)

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GROUP #3 Prosthetic Valve

#1 Staph Epidermidis (50%)#2 Streptococcus

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IE Risk Factors

• Prior episode IE• Prosthetic Valve (same risk mechanical vs

biological)• Recent invasive procedures• Structural Heart Disease (congenital and

acquired valvular)• IDU

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IDU’s

• Right-sided IE• Tricuspid > Pulmonary valve• PE more common• Less likely to have peripheral embolic

findings• High recurrance rate

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Question

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

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Answer

• Aortic• Mitral• Tricuspid• Pulmonary

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Valves

• LEFT-SIDED valves are more commonly hit!

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

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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!

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Question

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

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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)

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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

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Question

Which of the following lesions are painful?

a) Osler’s Nodesb) Janeway Lesionsc) Splinter hemorrhagesd) Roth spots

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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.

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Osler Nodes (Ouch!)

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Janeway Lesions

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Splinter Hemorrhages

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Roth’s Spots

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EKG

• Usually normal, but can have new conduction disturbances

• BBB• AV dissociation

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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.

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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

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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.

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Question

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

a) 0-6mosb) 6mos-3yrsc) 3-10yrsd) >10yrs

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Question

What is Olser’s Triad?

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Osler’s Triad

• Pneumonia, endocarditis, meningitis• Streptococcus pneumoniae is the culprit• Often associated with alcohol abuse,

mortality is extremely high

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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

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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

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SUMMARY - IE

• Suspect it• Exam the hands of your patient• Always draw blood cultures x3 before

administering antibiotics• Order an echo if concerned

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Antibiotic Prophylaxis

Guidelines 2007

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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

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Procedures Requiring Prophylaxis

1. ANY dental work2. Bronchoscopy3. Skin infection & procedure

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

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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

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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

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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

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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

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Management

• Revolves around management of mitral regurgitation

• Nitrates and Diuretics for CHF• IABP as bridging therapy• Definitive treatment is surgical repair

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AORTIC STENOSIS

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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

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Scarey Symptoms

• A ngina• S OB• S yncope• S udden death (not really a symptom!)

“Classic Triad”:CP, CHF, Syncope

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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

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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

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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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Thanks!


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