1. VALVULAR DISEASE Mark Boyko, CCFP-EM R3

2. 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

3. At first glance… Moving both sides of body (barely) Not speaking to you GCS 9

4. Labs -Hgb 108 -WBC 14 -Lytes N -EKG pacer spikes

6. REPORT: Multiple ischemic areas consistent with embolic stroke

7. 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

8. 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

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

10. Infective Endocarditis (IE)

11. Question Which age group is most commonly affected? a) < 30 yrs b) 31-60 yrs c) >60 yrs

12. 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

13. 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.

14. 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

15. Question Which microbe causes most cases of IE overall?

16. 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

17. 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)

18. Question Can you name at least 3 organisms in the HACEK group? …. Alternatively…. Which NHL team first drafted famous Czeck goaltender Dominik Hasek?

19. HACEK Organisms Haemophilus aphrophilus Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella kingae

20. 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

21. GROUP #2 Injection Drug Users (IDU’s) #1 Staph #2 Strep #3 Pseudomonas #4 Serratia #5 Fungal (Candida, Apergillis)

22. GROUP #3 Prosthetic Valve #1 Staph Epidermidis (50%) #2 Streptococcus

23. IE Risk Factors Prior episode IE Prosthetic Valve (same risk mechanical vs biological) Recent invasive procedures Structural Heart Disease (congenital and acquired valvular) IDU

24. IDU’s Right-sided IE Tricuspid > Pulmonary valve PE more common Less likely to have peripheral embolic findings High recurrance rate

25. Question Rank the cardiac valves in order of decreasing incidence of IE

26. Answer Aortic Mitral Tricuspid Pulmonary

27. Valves LEFT-SIDED valves are more commonly hit! However, when all cases of right-sided IE are analyzed, the vast majority occur in IDUs

28. 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!

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

30. 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)

31. 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

32. Question Which of the following lesions are painful? a) Osler’s Nodes b) Janeway Lesions c) Splinter hemorrhages d) Roth spots

33. 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.

34. Osler Nodes (Ouch!)

35. Janeway Lesions

36. Splinter Hemorrhages

37. Roth’s Spots

38. EKG Usually normal, but can have new conduction disturbances BBB AV dissociation

39. 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.

42. Blood Culture Key to the diagnosis Draw 3 samples total, 3 different sites –2 different sites at time 0 –3 rd separate site at time 1hr 90-95% will be positive if truly IE

43. 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.

47. Question When is the highest risk for IE after prosthetic valve surgery? a) 0-6mos b) 6mos-3yrs c) 3-10yrs d) >10yrs

48. Question What is Olser’s Triad?

49. Osler’s Triad Pneumonia, endocarditis, meningitis Streptococcus pneumoniae is the culprit Often associated with alcohol abuse, mortality is extremely high

50. Empiric Treatment Native 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

51. 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

52. SUMMARY - IE Suspect it Exam the hands of your patient Always draw blood cultures x3 before administering antibiotics Order an echo if concerned

53. Antibiotic Prophylaxis Guidelines 2007

54. 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

55. 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

56. 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

60. 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

61. 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

62. 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

64. Management Revolves around management of mitral regurgitation Nitrates and Diuretics for CHF IABP as bridging therapy Definitive treatment is surgical repair

65. AORTIC STENOSIS

66. Aortic Stenosis Most common valvular lesion among elderly patients “critical” AS is 50mmHg Asymptomatic period can last 10-20yrs Once symptomatic, life expectancy only 1- 3yrs

67. Scarey Symptoms A ngina S OB S yncope S udden death (not really a symptom!) “Classic Triad”: CP, CHF, Syncope

68. 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

69. 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

70. 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

72. Thanks!