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.

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 yrs

b) 31-60 yrs

c) >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 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

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) 0-6mos

b) 6mos-3yrs

c) 3-10yrs

d) >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 work

2. Bronchoscopy

3. 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!