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Infective Endocarditis and Valvular Disease

Infective Endocarditis and Valvular Disease. Geoff Lampard PGY-1 Ian Walker. Outline. What will be covered. What will not be covered. The rest……. Infective Endocarditis Aortic Stenosis What murmurs need workup?. Doctor! I gotta fever!. 55 yo male Fever of 24 hours

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Infective Endocarditis and Valvular Disease

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  1. Infective Endocarditis and Valvular Disease Geoff Lampard PGY-1 Ian Walker

  2. Outline What will be covered What will not be covered The rest…… • Infective Endocarditis • Aortic Stenosis • What murmurs need workup?

  3. Doctor! I gotta fever! • 55 yo male • Fever of 24 hours • No focal symptoms • Past history includes mechanical aortic valve for symptomatic AS • Faint I/VI SEM but "that's not new"

  4. the making of the beast a 4 step process • 1. Endocardial injury • 2. Sterile thrombus formation • 3. Transient bacteremia and seeding • 4. Maturation

  5. epidemiology Epidemiology has changed dramatically over the past 50 years 2-10 episodes/100,000 patient years in general population 1-3/1000 in IVDU M>F Mean age ≈ 60 Mortality is steadily increasing

  6. which valves? • Mitral valve • Aortic valve • Multivalvular • Right sided endocarditis (mostly IVDU)

  7. IE risk factors 1. Structural valvular lesion or prosthetic valve (75%) Also: Prior IE Invasive Procedure/Line IVDU Age

  8. 2 very different presentations 1. AcuteIE • acute fever • CHF +/- hemodynamic instability • peripheral signs of embolism 2. Subacute Bacterial Endocarditis (SBE) • Fever (85%), malaise (80%) • Murmur is unpredictable • Others: weakness, myalgias, back pain, dyspnea, chest pain, cough, headaches. • Commonly misdiagnosed as viral illness • Check their hands and eyes!

  9. The Duke – simplified! Reported sensitivity/specificity of Duke Criteria 95%/99%

  10. Duke criteria – echocardiographic findings Oscillating intracardiac mass Abscess New partial dehiscence of prosthetic valve New valvular regurgitation (new murmur insufficient)

  11. vascular phenomena Janeway lesions and splinter hemorrhages Also: Conjunctival hemorrhages Major arterial emboli

  12. vascular phenomena Mycotic aneurysms with intraventricular hemorrhage Septic pulmonary infarcts

  13. immunologic phenomena – eponymous potpourri! Osler nodes and Roth spots Glomerulonephritis and elevated rheumatoid factor Much more likely to occur in SBE

  14. making the call • Investigations • Echo (TTE vs TEE) • Blood Cultures • >3 different sites, 1st and last >1 hr apart • Let your lab know that you are considering IE • ECG • RF/CRP/ESR • Urinalysis • CXR

  15. TTE or TEE? Both have a role, but common practice differs from guidelines TTE TEE Sn/Sp : 93% / 96% 1st choice modality for: Medium to high pretest probability When TTE less sensitive (obesity, lung hyperinflation, valve prosthesis) • Sn/Sp : 46% / 95% • Ideal for low pretest probability patients, children In practice in Calgary, TTE first unless acutely ill

  16. some antibiotic principles • Long durations required • Parenteral preferred • Stable SBE:forgo antibiotics until cultures return • Acute IE: obtain cultures first, then treat • Think of 3 treatment groups: • NVE • IVDU • PVE

  17. aortic valve vegetation and perforation 1. Native Valve Endocarditis S. Aureus Streptococcus spp.(esp. viridansand bovis) Enterococci (>80% enterococcus faecalis) HACEK group (5-10%) Persistently culture negative spp

  18. HACEK group – can you name them? Haemophilusspecies Actinobacillusactinomycetemcomitans Cardiobacteriumhominis Eikenellacorrodens KingellaKingae colony of actinobacillus actinomycetemcomitans

  19. s. aureus 2. IVDU associated endocarditis S. Aureus(70%) Polymicrobial Streptococcus spp. Pseudomonusaeruginosa Must also consider fungal species (candida, aspergillus)

  20. staph epidermidis 3. Prosthetic Valve Endocarditis Early Staph epidermidis Staph aureus Streptococcus spp. Late (>1year) same as NVE

  21. which drug should you start? Rosen’s Keep it simple! vs: Vancomycin 15mg/kg IV q12h and Gentamicin 1mg/kg IV q8h

  22. I suspect IE. What next? • All suspected cases should be admitted • Hold antibiotics until cultures return for SBE • Treat Acute IE. But get cultures first! • Unstable? 2x cultures 20 minutes apart • Sick? 3x cultures 1 hrapart • PVE and fever NYD? Admit.

  23. complications CHF and cardiogenic shock Embolisation CNS Spleen Kidneys Lungs Liver Intracardiac Abscess Death! 20-30% at 1 year

  24. the IV drug user • 79% of IVDU IE is right sided • 70% s. aureus • Only 35% will have a murmur on admission • Septic pulmonary emboli: hallmark of disease • 80% of tricuspid valve IE will have CXR findings on presentation

  25. what about prostheses? • Risk is highest in the 1styear • Low threshold for admission of Fever NYD + admission • Aggressive organisms • High risk of dehiscence • TTE very low sensitivity • Pacemakers can get infected too!

  26. who needs emergent surgery? • Practically speaking, CHF + cardiogenic shock is only true indication for emergent surgery. • Consult cardiac surgeon early for: • CHF or severe valvular dysfunction likely to precipitate CHF • Invasive valvular complications on echo • Pseudomonas, fungi, or MDR organisms • High risk of embolism • PVE

  27. prophylaxis – simpler than you think! • Amoxicillin PO 2g (adults) 50mg/kg (children) 30-60 minutes pre-procedure • Allergic? Try Clindamycin 600mg PO

  28. aortic stenosis A few handy principles

  29. key definitions

  30. who gets it? By far 3 most common causes: Calcific degeneration Bicuspid aortic valve Rheumatic disease

  31. pathophysiology • High pressure gradients (afterload) lead to concentric LVH • Angina: Concentric LVH maintains CO but impairs coronary reserve • CHF/Dyspnea: Increased LVEDP lead to pulmonary congestion • Syncope: unclear; may be vasovagal response

  32. how do they present? SAD symptoms on exam SEM @ RUSB, radiating to carotids S4, soft S2 in late disease Parvus et tardusdespite powerful apex beat Crescendo peaks later as severity increases and may disappear • Early: asymptomatic • Later: angina, CHF (dyspnea) • Latest: exertionalsyncope • Long asymptomatic period, then rapid deterioration

  33. principles of management • There are no set rules in decompensated AS • They are preload dependent with a fixed cardiac output • A surgical disease; medical management is a bridge only

  34. and the CHF patient with AS? • Vasodilation has a narrow therapeutic range • BiPAP, nitrates, and diuretics should be used cautiously • Use something titratable! • Evidence exists for Na-nitroprusside in ICU setting • Inotropic support for cardiogenic shock • Call CCU! They need definitive treatment.

  35. what lies beyond….. • Early involvement of CCU is critical • Interventional options are definitive • Valvuloplasty • IABP • TAVI (transcatheter aortic valve implantation) • Surgical aortic valve replacement

  36. which murmurs need workup? • Incidental murmurs are common in the ED • AHA 2006 Guidelines: • Diastolic • Continuous • Holosystolic • Late systolic • Ejection clicks • Radiation to neck or back

  37. if you remember nothing else • Suspect IE in patients with fever/malaise and structural valvular disease • Examine hands, feet,and eyes! • 3 blood cultures, 3 different sites, at least 1hr apart • Admit all suspected IE. If acute, obtain fast cultures and treat empirically (Vanco + Gent). • If SBE and stable, delay ABx until cultures return • Amoxil 2g prophylaxis for oral procedures

  38. … and for aortic stenosis • AS is a surgical disease • They are preload dependent with a fixed cardiac output • Medical management may hinder more than help • Get CCU involved quickly for decompensating patients

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