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Endocarditis and Valvular Heart Disease

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Endocarditis

Native:  non-viridans  strep,  strep viridans, enterococci,  staph aureus

Prosthetic:  coagulase neg. staph (early <60 days postop), Staph Aureus (>60 days post op), Non-viridans strep, enterococci

IVDA/Immunocompromised:  staph aureus, strep, gram-negative bacilli

 

Fever/Anemia/Murmur

Change in mental status due to embolization

Ptechiae, splinter hemorrhages, osler noders (palmar surface of fingertips; tender), janeway lesions (flat macular lesions on the palms; painless), Roth’s spots (pale c red halo)

Can present with microscopic hematuria (up to 50% of the time)

 

Get three sets blood cultures from three different sites.  Better if separated by time.

 

Rheumatic Fever

Jones criteria (major)-carditis, polyarthritis, chorea, erythema marginatum (smoke ring of erythema), Sub-Q nodules

Antistrep antibodies stay positive 4-6 weeks post infxn

 

Native:  PCN G and Naf and Genta or Vanco/Genta

Prosthetic:  Naf, Genta, Rifampin or Vanco/Genta/Rifampin

 

 

virtually all bacteria have been implicated 2. vast majority cause by gram positive organisms a. viridans streptococci most common for abnormal native heart valve IE b. staph aureus most common in injection drug users (normal native valves) and in PV IE c. staph epidermidis (coag – staph) relatively common in PV IE 3. fungal organisms in PV IE, immunosuppressed hosts, and indwelling vascular catheters 4. remember the fastidious gram neg bacilli that can cause endocarditis: HACEK organisms that will grow very slowly in culture a. Haemophilus parainfluenza, Haemophilus aphrophilus b. Actinobacillus actinomycetemcomitans c. Cardiobacterium hominum d. Eikenella corrodens e. Kingella kingae

Complications A. embolic phenomenon 1. seen in 22-50% of cases 2. mitral vegetations have highest rate (25%) – especially anterior leaflet (37%) – followed by aortic (10%) 3. most cases occur within first two weeks of treatment 4. staph and fungus embolize most frequently 5. CNS most common site (65%) and most of these lodge in MCA 6. Splenic infarct common (40% of left sided IE) but only 5% of these go on to abscess formation 7. ECHO finding risk factor for embolization: vegetations >1 cm in diameter B. periannular infection/abscess 1. very common with prosthetic valve IE (56-100%) 2. 10-40% incidence in native valve IE (AV >MV or TV) 3. AV conduction block may result 4. myocardial fistulae can occur leading to intracardiac shunts 5. prosthetic valve dehiscence leading to CHF 6. rupture into the pericardium also a concern – tamponade or purulent pericarditis may result 7. most will need surgery C. acute valvular insufficiency with acute CHF 1. perforation of valve 2. rupture of chordae tendinae 3. dehiscence of prosthetic valve 4. paravalvular leak D. valve obstruction from bulky vegetation 1. fungus is frequent pathogen in this setting 2. less common complication VII. Prophylaxis A. Recommended for whom? 1. High risk a. prosthetic heart valve b. h/o endocarditis c. complex cyanotic CHD (transposition, Tetralogy of Fallot) 2. Moderate risk a. Other congenital heart disease b. Acquired valvular dysfunction (e.g. RHD) c. MVP with regurgitation (or thickened leaflets) d. Hypertrophic cardiomyopathy 3. Not recommended a. isolated secundum ASD b. Surgical repair of ASD, VSD, or PDA c. MVP without regurgitation d. Previous CABG e. “functional” or “physiologic” heart murmurs f. pacemakers and implanted defibrillators B. For which ED procedures? 1. dental procedure causing gingival bleeding 2. insertion of FC when UTI is present – controversial 3. I&D of abscess 4. Bronchoscopy C. Which antibiotics: 1. Oral or respiratory procedures b. amoxacillin 2 g po one hr pre-procedure (15 mg/kg for children) c. NPO: ampicillin 2 g IV or IM within 30’ pre-procedure d. PCN allergic: clindamycin 600 mg, or cephalexin 2 g, clarithromycin/azithromycin 500 mg po 1 hr pre-procedure e. NPO/PCN allergy: clindamycin 600 mg IV or cephazolin 1 g IV/IM within 30’ pre-procedure 2. GU procedures a. high risk: ampicillin 2 g and gentamicin 1.5 mg/kg IV/IM within 30’ of procedure; 6 hr later, ampicilling 1 g iv/im or amoxacillin 1 g po; substitue single dose of vanco if PCN allergy b. moderate risk: amoxacillin 2 g po one hr pre-procedure or ampicillin 2 g IV/IM within 30’ of procedure 3. Skin/soft tissue abscess (non-oral) a. dicloxacillin or cephalexin single dose one hr pre – procedure b. vancomycin for those NPO or PCN- allergic SELECTED REFERENCES 1. Wilson WR, Karchner AW, Dajani AS, et al: Antibiotic treatment of adults with infective endocarditis due to steptococci, enterococci, staphylococci, and HACEK microorganisms: American Heart Association. JAMA 1995;274:1706. 2. Bayer AS, Bolger AF, Taubert KA, et al: Diagnosis and management of infective endocarditis. Circulation 1998;98:2936. 3. Dajani AS, Taubert KA, Wilson W, et al: Prevention of bacterial endocarditis: recommendations by the American Heart Association. JAMA 1997;277:1794. 4. Bayer AS: Infective endocarditis. Clin Infect Dis 1993;17:313. 5. Anonymous. Management of infective endocarditis. Drug & Therapeutics Bulletin. Apr. 2002 404):26-30. 6. Barnes PD, Crook DW. Culture negative endocarditis. Journal of Infection. 1997; 35(3):209-13. 7. Delahaye F, Hoen B, McFadden E, et al. Treatment and Prevention of infective endocarditis. Expert Opinion on Pharmacotherapy. 2002; 3(2):131-45 8. Giessel BE, Koenig CJ, Blake RL Jr. Management of bacterial endocarditis. American Family Physician. Mar 2000 61(6):1725-32. 9. Hoesley CJ, Cobbs CG. Endocarditis at the millennium. Journal of Infectious Diseases. Mar. 1999 179 Suppl 2:S360-5. 10. Keys TF. Infective endocarditis: prevention, diagnosis, treatment, referral. Cleveland Clinic Journal of Medicine. May 2000 67(5):353-60. 11. Mauri L, de Lemos JA, O’Gara PT. Infective Endocarditis. Current Problems in Cardiology, Sep. 2001 26(9):562-610.Farmer JA, TorreG. Endocarditis. Current Opinion in Cardiology. Mar 1997 12(2:123-30 12. Pawsat DE, Lee JY. Inflammatory disorders of the heart. Pericarditis, myocarditis, and endocarditis. Emergency Medicine Clinics of North America. Aug. 1998 16(3):665- 81. 13. Piper C, Korfer R, Horstkotte D. Prosthetic valve endocarditis. Heart (British Cardiac Society) May 2001 85(5):590-3. 14. Stamboulian D, Carbone E. Recognition, management and prophylaxis of endocarditis. Drugs Nov. 1997 54(5):730-44.

Prophylaxis

(1) a prosthetic valve of any kind, (2) a history of prior IE, or (3) a history of congenital cyanotic heart disease

EASE trial just reported shows early surgery should be the path instead of intial medical management

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Valvular Heart Disease

Prosthetic Valves

Mechanical

Last ~20 yrs, SEM murmur

Bioprosthetics

human, porcine, or bovine

8-10 yrs

anticoagulation optional, usually aspirin

 

Both types are prone to thromboembolism.

Valves may fail leading to acute regurgitation

Paravalvular leak from disruption from annulus, can result from endocarditis

Endocarditis

Hemolysis

Get CBC, LDH, PT/PTT, ESR, Blood CX,

 

Aortic valves are lower risk for clot than mitral

The peak incidence of thromboembolism is during the first 3 months after surgery, probably reflecting the lack of endothelialization of the newly implanted prosthetic materials and delay in achieving therapeutic anticoagulation in the early days after operation

 

 

Mitral Valve Prolapse

can be associated with chest pain, palpitations, and hyperventilation in females.

May need b-blockers, dental prophylaxis,

Mitral Stenosis

from rheumatic heart disease, congenital, or left atrial myxomas

exertional dyspnea, hemoptysis, CHF sx

Can lead to a-fib, embolization

Mitral Regurgitation

acute is from ruptured chordae or papillary muscle dysfunction

chronic is most commonly from rheumatic or MVP, also Marfan’s

rate control, diuretics, anticoagulate

These patients need afterload reduction

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Aortic Stenosis

congenital bicuspid valve, rheumatic heart disease, calcific aortic stenosis.

DOE, angina, exertional syncope, CHF, sudden death

Harsh systolic murmur

Symptomatic patients are at risk for sudden death, refer for valve surgery.

Most common cause in ICUs is senile calcific disease Causes LVH which predisposes to subendocardial ischemia

tachycardia decreases diastolic filling and therefore decreases coronary blood flow

Pts present with exertional dyspnea, angina, syncope, may progress to heart failure

Diuresis, IVF, and venodilators can all cause deterioration

avoid hypotension

Unload trial would say nitroprusside is a good move

OVERVIEW

Obstruction can be

  • supravalvular
  • valvular (most common)
  • subvalvular

SEVERITY ASSESSMENT

  • appearance
  • mobility
  • gradient
    — continuous wave Doppler allows peak velocity to be measured -> peak gradient can be calculated using Bernoulli equation
    — peak gradient = 4 x peak velocity across the narrowing squared
    — normal peak gradient < 10mmHg, critical > 70mmHg
    — gradient measurements are very dependent on ventricular function so can be misleading.
  • area
    — normal 2.5-5.5 cm2
    — critical < 0.92 cm2
  • dimensionless severity index = ratio of LVOT velocity/aortic valve velocity (V1/V2)
    — provides a dimensionless measurement of aortic stenosis which is independent of Q
    — < 0.25 implies a valve area of 0.75cm2 (severe AS)
  • complications:
    — LV hypertrophy or dilation
    — LV systolic and diastolic dysfunction
    — post-stenotic dilation

CATEGORIES OF AORTIC STENOSIS SEVERITY (From Vahanian et al, 2010)

Aortic
sclerosis		 Mild Moderate Severe
Aortic jet velocity (m/s) <2.6 2.6–3.0 3–4 >4
Mean gradient (mmHg) — <30 (25) 30–50 (25–40) >50 (40)
AVA (cm2) — >1.5 1.0–1.5 <1.0
Indexed AVA (cm2/m2) >0.9 0.6–0.9 <0.6
Velocity ratio >0.50 0.25–0.50 <0.25

Above from Life in the Fast Lane CCC

Aortic Insufficiency

acutely from infective endocarditis, dissection, trauma

chronic from rheumatic heart disease, bicuspid valve, marfan’s

widened pulse pressure

try judicious use of nitro or nitroprusside

reduce bradycardia to decrease diastolic filling and therefore degree of regurg

never use IABP

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Withholding Anticoagulation

much more dangerous in mitral and tricuspid

can hold aorta anti-coag 2 days before surg and drift INR t to <=1.5

then restart

for mitral/tricusp bridge with heparin until procedure

(Emerg Med Clin 2011;29:801)

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Which Valve has been Replaced?

http://www.raddaily.com/whitepaperarticle.php?articleTitle=Cardiac+Valves:+Assessment+and+Identification

valve-ap-edit valve-lat-edited

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