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1ST YEAR SYSTEMS: Cardiovascular > Infective endocarditis > Flashcards

Infective endocarditis Flashcards

1
Q

define infective endocarditis

A

Heart has 3 layers: epicardium, myocardium and endocardium.

Endocarditis - infection involving the endocardial surface

Valvular structures- native and prosthetic valves

Chordae tendineae

Sites of septal defects

Mural endocardium- posterior wall of the LA becomes rough and wrinkled

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2
Q

incidence of infective endocarditis

A

low incidence 3-10/100,000

affects males more than females but when females contract it they have a worse prognosis

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3
Q

risk factors for native valve IE

A 
Mitral valve disease
Rheumatic heart disease
Congenital heart disease
Degenerative  heart disease
Asymmetrical septal hypertrophy
Intravenous Drug abusers
Alcoholic cirrhosis
Diabetic mellitus
Indwelling medical devices
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4
Q

what is mitral valve prolapse

A

Mitral valve prolapse is a condition in which the two valve flaps of the mitral valve do not close smoothly or evenly, but instead bulge (prolapse) upward into the left atrium

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5
Q

prevalence of mitral valve prolapse

A

high prevalence 2-4% of general population
20% are young female

52/100,000 who have MVP and a systolic murmur develop IE

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6
Q

Congenital heart disease

A

10-20% of endocarditis case in young adults

ventricular septal defect, bicuspid aortic valve, patent ductus arteriosus

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7
Q

how does endothelium become infective due to mechanical endothelium disruption?

A

Mechanical endothelial disruption exposures extracellular matrix protein → production of tissue factors.

Deposition of fibrin and platelets→ Non-bacterial thrombotic endocarditis (NBTE).

NBTE facilitates bacterial adherence and infection.

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8
Q

how can an endothelial valve become damaged?

A

Turbulent blood flow (Venturi effect-low pressure )

electrodes

catheters

inflammation (rheumatic carditis)

degenerative valve disease (ECHO - 50% of asymptomatic patients >60yrs)

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9
Q

Venturi effect?

A

there’s a reduction in fluid pressure when a fluid flows through constricted area of pipe. High velocity but low pressure

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10
Q

how does a normal valve become inflamed?

A

Inflammation of endothelial cell → expression of integrins (β1 family)

integrin acts like a hook that binds circulating fibronectin binding proteins on staph aureus

Adherent organisms trigger active internalisation into valve endothelial cells.

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11
Q

examples of invasive procedures that can cause bacteraemia

A

Dental procedures requiring manipulation - gingival /periapical region

Dental procedures -perforation of oral mucosa

GU and GI surgery

Intravascular catheters

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12
Q

non-invasive activities that can lead to bacteraemia?

A

(chewing and tooth brushing)-low grade bacteraemia of short duration but with high incidence.

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13
Q

pathophysiology of infective endocarditis

A

valvular endothelium - platelet-fibrin deposition - nonbacterial thrombotic endocarditis - adherence - colonisation = vegetation

mucous membranes - trauma - bacteremia - adherence - colonisation - vegetation

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14
Q

causative organisms of IE

A 
Viridans group streptococci
Staphylococcus aureus
Enterococci 
Coagulase-negative staphylococci				
Haemophils parainfluenzae
Strep bovis
Fungi
Brucella species
Culture-negative Haemphilus species
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15
Q

acute vs subacute

A 
acute = days/weeks
subacute = weeks to months
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16
Q

mode of acquisition of IE

A

IVDU - IV drug users
healthcare
community

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17
Q

Classification:- localisation of IE

A

+/- intra-cardiac material

L sided native valve IE
L sided prosthetic valve IE (PVE)

R sided IE
Device related IE (permanent pacemaker/cardioverter -defib)

18
Q

how can you tell if a patient has active infective endocarditis

A

IE with persistent fever (>38 °C) and positive blood cultures

active inflammatory morphology found at surgery

patient still under antibiotic therapy

histopathological evidence of active IE

19
Q

why is IE difficult to diagnose

A

it’s not a uniform disease
syndrome diagnosis determined by presence of multiple findings ie

Presence or absence of pre-existing cardiac disease

causative microorganisms

presence or absence of complication

underlying patient characteristics

mode of presentation

20
Q

atypical presentation of IE occurs in which patients?

A

elderly

immunocompromised

21
Q

diagnosis of acute IE

A

fever, embolic signs/symptoms (stroke, splenic infarct) or decompensated HF

22
Q

diagnosis of subacute IE

A

fever, non-specific constitutional symptoms or palpitation and immunologic/vascular phenomena.

23
Q

common symptoms of IE

A

fever/chills
night sweats, malaise, fatigue, anorexia, weight loss

weakness, arthralgia, headache (may be non-specific or embolic)

SOB

24
Q

Clinical signs of IE

A 
cardiac murmur (regurgitant murmur) with signs of HF
janeway lesions

immune complex depostion:- olser nodes, roth spot

meningeal signs
splinter haemorrhage
cutaneous infarcts
vasculitis rash

25
Q

what are janeway lesions

A

painless, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles

indicative of infective endocarditis

26
Q

what are olser nodes

A

small, painful nodular lesion found on pads of fingers or toes

27
Q

what are roth spots

A

Retinal haemorrhage with a white or pale centre

28
Q

in diagnosis of IE often use high index of suspicion - give some examples

A

new regurgitant murmur
embolic events of unknown origin
sepsis of unknown origin
fever

29
Q

investigations carried out for IE

A

Blood culture- Timing. 3 sets and sites 30mins apart. +/- cultures

Echocardiography

FBC.ESR/CRP- elevated acute inflammatory markers

urea and electrolytes- renal failure

Urinalysis- +ve for blood

ECG: PR interval prolongation ≥200ms

CXR: Pulmonary congestion or abscess.

Further Imaging for subgroups – MSCT (multi-slice CT - accuracy similar to ECHO but superior perivalvular abscess), MRI, 18F-FDG -PET/CT and Leukocyte SPECT/CT –detect silent vascular phenomena/ endocardial lesions

30
Q

preferred imaging option for possible IE in native valve?

A

repeat ECHO (TTE +TOE)/microbiology

imaging for embolic events
cardiac CT

31
Q

preferred imaging option for possible IE in mechanical valve?

A

repeat ECHO (TTE +TOE)/microbiology

'’F-FDG -PET/CT or Leukocyte SPECT/CT

cardiac CT

imaging for embolic events

32
Q

What is an ECHO good at detecting in IE

A

vegetation

abscess

pseudoaneurysm

intracardiac fistula

valvular perforation or aneurysm

new partial dehiscence of prosthetic valve (surgical complication)

33
Q

what is 18F-FDG PET/CT good at detecting?

A

abnormal activity around the site of the prosthetic valve implantation (if it has been implanted for >3 months)

34
Q

cardiac CT is good at detecting what in IE?

A

definitive paravalvular lesions

35
Q

what do you need to diagnose definite IE?

A 
2 major criteria 
or
1 major + 3 minor 
or
5 minor criteria
36
Q

IE rejection criteria

A

Resolution of endocarditis syndrome with antibiotics therapy for ≤ 4 days.

37
Q

treatment of IE

A

Three sets of blood culture (taken 30min apart ) before initiating IV antibiotics

PVE-Prosthetic valve Endocarditis –treat for 6weeks

NVE-Native Valve Endocarditis – treat for 2-6 weeks

38
Q

what does treatment of IE depend on?

A

Whether the patient has received previous antibiotic therapy

Whether the infection affects a native valve or a prosthesis [and if so, when surgery was performed (early vs. late PVE)].

The place of the infection (community, nosocomial, or non-nosocomial healthcare-associated IE) and knowledge of the local epidemiology, especially for antibiotic resistance and specific genuine culture-negative pathogens.

39
Q

Antibiotics to treat community acquired native or late prosthetic valves endocarditis

A 
ampicillin 
with
flucloxacillin or oxacillin
with
gentamicin

vancomycin
with
gentamicin (for penicillin allergic patients)

40
Q

Antibiotics to treat early PVE or hospital/ non-hospital acquired endocarditis

A 
vancomycin 
with 
gentamicin
with 
Rifampin - only recommended for PVE
41
Q

complications and indications for surgery

A

Heart failure in IE: valvular regurgitation- leaflet perforation etc
42-60% of Native Valve Endocarditis(NVE)
Aortic IE> Mitral IE

Uncontrolled Infection: Perivalvular abscess
More common in Aortic IE (10-40%) in NVE
56-100% of Prosthetic valve endocarditis (PVE)
Mortality rate 41%

Prevention of systemic embolism: migration of cardiac vegetation to brain/spleen from left-IE Size and mobility of vegetation.
Pulmonary embolism are the results of right sided IE.

42
Q

antibiotic prophylaxis is limited to which patients?

A

those at highest risk of IE undergoing the highest risk dental procedures, patients with previous IE, patients with congenital heart disease, patients with a prosthetic valve, including a transcatheter valve or a prosthetic material used for cardiac valve repair

good oral hygiene
aseptic measures during venous catheter manipulation

disinfection of wounds

discourage piercing/tattooing

1ST YEAR SYSTEMS: Cardiovascular (39 decks)

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