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Mean age infective endo

· mean ages 49 – 67 due to prevalence of prosthetic heart valves and degenerative valve disease

Rf for IE

o Rheumatic heart disease
o Intravenous drug abuse (usu get R sided endocarditis)
o AV fistulas, hemodialysis shunts
o Hardware
§ Pacemaker
§ Prosthetic heart valve
o Unrepaired and repaired congenital heart disease
§ patent ductus arteriosus
§ ventricular septal defect
§ coarctation of aorta
§ hypertrophic obstructive cardiomyopathy
§ bicuspid aortic valve
§ tetrology of fallot
o Degenerative heart disease
§ calcified mitral annulus
§ astherosclerosis
§ post-myocardial infarction
§ Mitral valve prolapse (with regurgitation)

Pathophysiology of IE

Classic lesion is vegetation– microtrauma, platelet aggregation, sterile thrombus on which microorganisms colonize
o thrombus forms due to trauma, inflammation, abN turbulence
o colonization from transient bacteremia

Bacteria in IE


-Congenital valve disease/MV prolapse


-IVDU


- Prosthetic valves


- Poor, nutritionally disadvantage


-Culture negative


-Long-term indwelling IV/ICD/pacemaker


-Immunosuppressed


-Cancer patient

Congenital valve disease/MV prolapse – Strep, staph, enterococcus
o IVDU – Staph, pseudomonas, fungus (Candida, Aspergillus)
o Prosthetic valves – CNS, staph, strep, gram –ve, fungi
o Poor, nutritionally disadvantaged – Bartonella
o Culture negative – HACEK (Hemophilus, Actinobacillus, Cardiobacterium, Eikanella corrodens, Kingella)
o Long-term indwelling IV/ICD/pacemaker – fungus (Candida, Aspergillus)
o Immunosuppressed – fungus (Candida, Aspergillus)
o Cancer patient – strep bovis

S/S for IE

Classic triad rare – fever, anemia, new murmur
· most commonly non-specific s/s – fever, malaise
· murmur may be difficult to hear if tricuspid (IVDU)
· Periphal Stigmata of Infective Endocarditis
· Vasculitic lesions present in 35% cases
o Osler’s nodes: painful erythematous nodules on finger tips from immune complex related vasculitis
o Janeway’s lesions: painless erythematous, flat, macular lesions on palms/soles that blanch with pressure related to emboli to skin
o Roth spots: retinal hemorrhages with pale center surrounded by halo
o Flame shaped retinal hemorrhages
o Splinter hemorrhages – proximal part of finger nailbed
o Petechiae

· Lab investigations

o Need 3 blood cultures with 3rd drawn 1h apart from 1st. Must be drawn from 3 separate sites. Positive in >90%.
o WBC, CRP, ESR all non-specific
o may have microscopic hematuria(embolic kidney lesions)
· Echo
o TTE – 60% sensitive
o TEE – almost 100% sensitive

How do you diagnose IE?

Duke criteria established for risk stratification
o sensitivity 95%, specificity 99%



o Definite endocarditis need one of the following:
§ 2 major criteria
§ 1 major + 3 minor
§ 5 minor



o Possible endocarditis needs one of the following:
§ 1 major + 1 minor
§ 3 minor



o Rejected endocarditis needs one of the following:
§ Alternate diagnosis is made
§ Resolution of clinical manifestations after 4 days of abx
§ Clinical criteria of definite or possible endocarditis not met

What is dukes criteria?

Major Criteria


Positive blood cultures (of typical pathogens) from at least two separate cultures


Evidence of endocardial involvement by echocardiography, such as the following:


Endocardial vegetation


Paravalvular abscess


New partial dehiscence of prosthetic valve


New valvular regurgitation


Minor Criteria


Predisposition: Predisposing heart condition or IV drug use


Fever: ≥38° C


Vascular phenomena: Arterial emboli, septic pulmonary infarcts, mycotic aneurysm, conjunctival hemorrhages, or Janeway lesions


Immunologic phenomena: Osler's nodes, Roth's spots, and rheumatoid factor


Microbiologic evidence: Single positive blood culture (except for coagulase-negative staphylococcus or an organism that does not cause endocarditis)


Echocardiogram findings: Consistent with endocarditis, but do not meet major criteria

Dukes criteria mneumonic

BE FEVEER
(*BE - Bacterial Endocarditis)

Major:
B = blood culture +ve >2 times 12 hr part
E = Endocardial involvement from Echo*
*VADR (vegetation, abcess perivalvular, dehiscense prosthetic valve, regurgitation)

Minor:
F = Fever ≥38° C
E = Echo findings (not fulfilling a major)
V = Vascular findings – janeway, septic emboli…
EE = Evidences from microbiological AND immunology (2 evidences)
Eg osler nodes (immunologic) single +ve BC (microbiologic)
R = Risk factors/predisposing factors - drug abuse, valvular diseases

Initial Management:

Native valve


-pen 5mil q4 + nafcilin 2g q4 OR


Vanco 15mg/kg q12 + Gent 1mg/kg q8h



Native +IVDU


-vanc



prostethic


-Vanc + gent

IE prophylaxis in ED? dont need for.....

Do not give it for suturing, ETT intubation, delivery, catheter placement, foley in the absence of infection.

· When would you CONSIDER giving prophylaxis in the ED?

When the patient has one of the underlying conditions in Table 3 and is going to have a procedure done through infected tissue. For example:
o Dental injection tor I&D. Manipulation of the periapical region of the teeth… ? replacing an avulsed tooth
o I&D of an abcess under infected skin
o There are no resp or GI procedures that ED docs do that involve incision of respiratory mucosa BUT if they are going for the procedure after the ED as an inpatient

· The following are taken from the AHA 2008 update of infective endocarditis in Circulation 116(15) p1736

+prosthetic cardiac valve/porsthetic material used


+previous IE


+CHD


- unrepeaired cyanotic


- repeaired with prosthetic material - only first 6mo after


- repaired but defects near prosthetic part(stops endothel)


+cardiac transplant patients with valulopathy




so need abx if


-dental


-respiratory


-infected skiln/msk



not for GI or GU procedures

What antibiotic regimen would you use?

oral


- amox 2g/50mg/kg 30-60m before



not oral


- Amp 2g/50mgkg IV/IM


- cefazolin/ceftriaxone 1g 50mgkg IV/IM



allergic pen/amp


-cephalexin 2g 50mgkg


-clinda 600mg 20mgkg


-azithro/clarithro 500mg 15mgkg



allergic not oral


-cefazolin/ceftriax


-clinda



· If the patient is already on antibiotics, select an antibiotic from another class

Whats the bug in rheumatic fever and what causes it?

caused by untreated group A Strep pharyngitis, pathogenesis unknown
o ASOT (anti-streptolysin O titer) positive in all patients
· Pathophysiology unknown: ?abnormal immunological response which leads to cross reactivity with heart valves, joints, skin, CNS

Whats Jones criteria?

Major Manifestations (MNEMONIC “SPACE”)


-Arthritis - polyarthritis


-Carditis


-Nodules – subQ nodules


-Erythema marginatum


-Sydenham chorea



Minor Manifestations (Mnemonic FA CE P)


-Arthralgias


-Fever


-Increased erythrocyte sedimentation rate or C- -reactive protein


-Prolonged P-R interval



OR



Dr. Jones is the FACEpr of cMENSA



· migratory polyarthritis most common s/s large joints with pain out of proportion for physical findings
· carditis involves – murmur, cardiomegaly, pericardial effusion, CHF
· chorea (St. Vitus’ dance) – random, rapid, purposeless movements of upper extremities/face; rare
· erythema marginatum – painless smoke ring of erythema on trunk and proximal extremities




need evidence of antecedent Strep infection plus 1 major and 2 minor or 2 major criteria

Treatment of RF

Prevention: treat GAS strep throat with penicillin 300mg pot id x 10 days



o Acute event:
o Pharyngitis: penicillin 300mg po tid x 10 days OR banzathing penicillin 1.2million units x 1 IM



o Carditis:
§ Bed rest to prevent failure
§ Mild to moderate treat with ASA
· Adult
o 90-100 mg/kg/d PO divided q6-8h for 2 wk initially, then 60-70 mg/kg/d for 6 wk; not to exceed 3.6-5.4 g/d



· Pediatric
o 60-90 mg/kg/d PO divided q6-8h for 8 wk; adjust according to serum levels



§ Severe: diuretics
§ Severe: prednisone 40mg po daily x 3 weeks then taper OR 1mg/kg in peds x 3 weeks then taper



o Chorea: treated with IVIG, steroids, plasmaphoresis



o Prophylaxis against Strep infections with bid penicillin x 5 years

Should we treat strep pharyngitis?

10million Rx - 10% diarhea, 0.24% severe allergic rxn


ABx reduced symptoms by 12hrs



COchrane 2006


NNT to prevent peritonsilar abcess 50-225


NNT to prevent otitis >200



NNT 5million to prevent rheumatic heart disease


24,000 will get a severe allergic reaction



abx dont prevent glomerulonephritis



Isolation period: 24 hours after initiation of antibiotics



(20-30% age 5-15); only 5-15% o

MV Prolapse......aaannnddd GO

· common congenital malformation seen most often in young women
· usually asymptomatic



o may have chest pain, palpitations (PVCs)
· complications – endocarditis, dysrhythmias, sudden death



· associated with Marfan’s, Ehlers-Danlos



· murmur – midsystolic click followed by late systolic crescendo



· Tx – BB for palpitations/chest pain, usually just reassurance

Mitral Stenosis:

· most common cause rheumatic heart disease – latency period 20 years
· s/s left heart failure
o exertional dyspnea
o orthopnea
o hemoptysis
· murmur – loud S1 with opening snap and low-pitched rumbling diastolic
· Complications – a fib, embolic events, frequent respiratory infections

Mitral Regurgitation:

Mitral Regurgitation:
· acute and chronic



o acute – catastrophic event resulting from rupture of chordae tendinae/papillary muscle/perforation of valve leaflet; due to MI/endocarditis/trauma
§ regurgitant volume 3 - 4x that of forward flow resulting in pulmonary edema and peripheral vascular collapse
§ murmur – crescendo-decrescendo ending before S2
§ Tx – emergency Echo and cath; NTG/morphine/diuretics for pulmonary edema, IABP if ¯ BP



o Chronic – usually due to rheumatic disease, may be MV prolapse or connective tissue disorders
§ regurgitant volume small with L ventricle compensation
§ usually develop a fib
§ murmur – high-pitched holosystolic
§ tx – diuretics, salt restriction, digoxin; sx if debilitating

Aortic Stenosis:

Aortic Stenosis:
· cause


-age < 65 congenital bicuspid valve, rheumatic heart disease;


-age > 65 calcific degeneration



· significant obstruction of LV outflow when valve area <1cm; compensatory LV hypertrophy



· Classic triad – exertional dyspnea (LV failure), angina, exertional syncope
· life expectancy 5 years with above symptoms; 2 years if CHF
· murmur – rasping crescendo-decrescendo systolic radiating into carotids
· carotid pulse diminished intensity (parvus) and slow rising (tardus)
· Tx – gentle fluid resus, inotropes, IABP; all need sx referral

Aortic Regurgitation:

Aortic Regurgitation:
· acute and chronic
o acute – usually associated with fulminant endocarditis, aortic dissection, trauma, connective tissue disease



§ results in flash pulmonary edema
§ murmur – short soft diastolic
§ Tx – afterload reduction, diuretics, IABP; needs sx



o chronic – rheumatic heart disease or bicuspid aortic valve, connective tissue disease



§ results in LV hypertrophy
§ murmur – high-pitched blowing diastolic
§ associated s/s – waterhammer carotid pulse, nail pulsations (Quincke’s sign) and head bobbing



§ tx – afterload reduction, GTN, digoxin; sx when LV failure

Tricuspid Stenosis and Regurgitation:

· stenosis – almost always rheumatic, usually coexists with mitral and aortic valve disease
o s/s – fatigue, edema, ascites, hepatosplenomegaly
o tx – fluid and salt restriction; sx later
· regurgitation – usually due to pulmonary HTN; may be caused by rheumatic heart disease, R sided endocarditis, trauma
o s/s – dyspnea, painful hepatomegaly, ascites, peripheral edema
o murmur – high-pitched pansystolic, S3
o tx – fluid and salt restriction; sx later

Complications of Prosthetic Valves:

· embolization
· valve obstruction - from thrombus formation (loss of metallic click of mechanical valve), tissue growth
· endocarditis
· hemolytic anemia
· primary valve failure – calcification of biologic valve (40% in 10y), strut failure of mechanical valve, paravalvular regurg, prosthesis dehiscence
· hemorrhage – from anti-coagulation