VALVULAR DISEASE Mark Boyko, CCFP-EM R3. One night at the Foot… 64yo male found down at home…...
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Transcript of VALVULAR DISEASE Mark Boyko, CCFP-EM R3. One night at the Foot… 64yo male found down at home…...
![Page 1: 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.](https://reader035.fdocuments.net/reader035/viewer/2022062304/56649d4b5503460f94a2899a/html5/thumbnails/1.jpg)
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 yrs
b) 31-60 yrs
c) >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 Nodes
b) Janeway Lesions
c) Splinter hemorrhages
d) 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) 0-6mos
b) 6mos-3yrs
c) 3-10yrs
d) >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 work
2. Bronchoscopy
3. 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!