W3 Systemic Infective Endocarditis Flashcards

1
Q

Infective Endocarditis (IE)
What is it?
How is it classified? 3
What is the etiology? 4

A

—infection of the cardiac endothelium, seen as vegetations

Classified
—clinical course, or
—host substrate, or
—organism

Etiology
—pts have existing cardiac abnormalities
—MV prolapse w/ MR is leading
—rheumatic HDisease
—congenital HDisease

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2
Q

IE of the NATIVE valve
—which pathogen responsible for majority?
—which pathogens make up 3%?
—right sided IE due to what? Which pathogen?

A

—strep & staph (80%)

HACEK, gram neg, in normal flora of URT (3%)
—haemophilus
—actinobacillus
—cardiobacterium
—eiknella
—kingella

right sided IE
—IV drug users
—staph (60%)

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3
Q

IE of the PROSTHETIC valve
Responsible for how many cases?
When is the greatest risk
Which organism is causative for infection <2 months ?

A

10-20% of IE cases
—greatest risk w/i first 6mo after implantation
—w/i 2 months = staph
—>2 mo is typical of native valve IE

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4
Q

IE pathogenesis
Describe 3 main steps

What are 3 complications/progressions?

A
  1. Endothelial injury
    —immune complex deposition OR turbulent blood flow due to regurgitation lesions (valve disorders): left sided regurg valves more affected b/c higher pressure system
  2. Platelets + fibrin adhere to damaged tissue which is known as a non bacterial thrombotic endocarditis
  3. Bacteria in bloodstream INFECT this nidus forming a VEGETATION. Fibrin covers the organisms and protects them from host defences. They multiply.

bacteria comes from trauma to mucosa, skin surfaces (oropharyngeal, IV drug use, GI tract etc)

gram + more common

complications/progression
—vegetations can cause valve coaptation & rupture&raquo_space; worsening regurg
—vegetation can embolise&raquo_space; organ ischemia distally
—can extend into valve ring, conduction system, myocardium etc

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5
Q

IE
What are the clinical S/S for:
Acute: microorganism, disease course?
Subacute: microorganism, disease course?
What are the hallmark findings? 2

A

—subtle to fulminant CHF

acute&raquo_space; valve destruction in days to weeks (staph)
—explosive/rapid illness w/ high fever & rigours

subacute&raquo_space; evolves over weeks to months (strep viridans) in pts w/underlying disease
—low grade fever, fatigue, anorexia, weakness, myalgias, night sweats (can be mistaken for UTI or flu)

HALLMARK: fever & new murmur

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6
Q

IE: physical signs — 5

A
  1. New murmur w/ aortic > mitral > tricuspid
  2. Neuro: cerebral emboli, encephalopathy, meningitis
  3. These findings relating to emboli/immune complex (stigmata)
    —mucosal petechiae
    —splinter haemorrhages
    —osler nodes (painful, fingers/toes, “osler ouch”)
    —Roth spots (retinal hem)
    —Janeway lesions (erythematous, macular, non tender, palms/soles)
    —splenomegaly
  4. Fundoscopic exam chorioretinitis or endophthalmitis
  5. Systemic embolization
    —kidney (flank pain, hematuria, renal failure)
    —lung infarction (septic PE/pneumonia)
    —aneurysm
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7
Q

IE — what labs do you order? 4

A

—blood cultures to Isolde microorganism
—CBC: leukocytosis, normocytic-normochromic anemia
—elevated ESR, CRP (inflammation)
—UA w/ microhematuria

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8
Q

IE diagnostics, what would you see on
EKG
CXR
What is the best test sensitivity wise ?

A

EKG
—conduction disturbances
—prolonged PR interval

CXR
—signs of HF (pulm edema, effusions)

Transthoracic ECHO
—visualise valves for vegetation (65% sensitivity)

TEE
—>90% sensitivity and should be performed if IE is suggested
—detects vegetations, posterior valves, right side heart structures, perforations better than TTE

CT/MRI
—for pts w/ CNS complications
—detect metastatic infection

Cath
—To assess coronaries

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9
Q

IE
What is the Duke criteria?
Definite, possible and rejected
Major 4
Minor

A

DEFINITE
pathologic:
1. microorganisms found on culture or histologic examination of vegetation / a vegetation has embolised
2. Pathological lesions, vegetations or abscess confirmed by histo exam showing active endocarditis
🔑clinical:
—2 major
—OR 1 major and 3 minor
—OR 5 minor**

POSSIBLE
—1 major criterion, 1 minor criterion
—3 minor

REJECTED
—firm alt dx
—resolution of IE syndrome w/ abx therapy <4d
—no path evidence of IE at surgery/autopsy w/abx <4d
—does not meet criteria above

🔑MAJOR “BRET”
—Blood culture positive 🩸
—Regurgitation murmurNEW
—Endocardial involvement 💪🫀
—TEE positive for IE 😮

MINOR
—predisposition
—fever >38 C
—vasc phenomena: arterial emboli, pulm infarcts, intracranial haemorrhage, conjunctival hemorrhage,
—some microbiological evidence

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10
Q

IE: Duke Criteria
Major : “BRET”
Minor

A

MAJOR “BRET”
—blood culture for IE, 2 separate cultures
—regurgitation murmur (new)
—endocardial involvement
—TEE positive for IE

MINOR
—predisposition, IV drug use
—fever >38C
—vasc phenomena : major arterial emboli, septic pulm infarts, mycotic aneurysm, intracranial hem, conjunctival hem, Janeway lesions
—immunologic phenomena: glom.nephritis, Osler nodes, Roths,
—microbiological evidence

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11
Q

IE
Medical therapy
Surgery
ABX prophylaxis: what are the 4 risk groups
When should they all receive proph?
General rule for proph?

A

—abx should be bactericidal
—if fulminant, do not delay abx as you obtain cultures
—6w IV dosing to sterilise vegetation
anticoags do not prevent embolisation related to IE

Surgery
—abx + valve replacement and cardiac reconstruction = higher survival rates than abx alone
—debride infected tissue
—remove non viable tissue
—reconstruct affected area
—restore the valve

ABX prophylaxis: 2Ps, 2Cs
—Prosthetic heart valves
—Prior IE
—Cardiac transplantation pts that develop valvulopathy
—Congenital heart disease
amoxicillin or cephalexin w/PCN allergy

—if any of these risk groups receive dental procedures that involve gingival manipulation should receive proph abx

PROSTHETIC - PRIOR - POST - PROCEDURE - congenital

—recommended for procedures occurring in the context of infection
—tonsillectomy
—bronchoscope w/ incision of mucosa in pts w/ infection
—surgical procedure of skin/MSK

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12
Q

IE: abx proph

A
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13
Q

Syncope
SBP and MAP ?
Causes: 3

A

—as short as 6-8 secs can precipice syncope
—SBP <70 or
—MAP <40

Causes
—cardiac: structural vs arrhythmic

—non-cardiac: neurocardiogenic, carotid hypersensitivity, situational, orthostatic, subclavian steal syndrome, vertebrobasilar disease

—LOC: seizure, hypoglycaemia, hypoxemia, psychogenic

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14
Q

Syncope
Examination, what are you checking?
Diagnostics?

A

—BP and orthostatic BP
—HR
—carotid bruits, cardiac murmus, periph pulses, neuro

Diagnositcs
—EKG
—ECHO (structural)
—Head CT if LOC
—blood work for cardiac enzymes, CBC, chem panel

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15
Q

Syncope — etiology 4

A
  1. Neurocardiogenic
    —most common
    —autonomic overactivity triggered by stimuli (blood) 🩸 followed by fall in vasc resistance w/o rise in CO&raquo_space; prodromal SX
  2. Situational 😵‍💫
    —causes vagal reflex vasodilation which decreases blood return to the heart (peeing, pooping, playing an instrument, coughing)
  3. Carotid sinus syncope 🤵
    —uncommon
    —pressure on carotid sinus
    —shaving, turning head, tight collar
  4. Orthostatic 👵🏻
    —elderly people when standing
    —systolic drops >20mmHg (normal is 5-15)
    —dehydration, meds, diabetes, alcohol, varicose veins
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16
Q

Cardiac syncope
Characteristics
Two causes

Hospital admission?

A

—no prodromal SX
—sudden LOC w/o warning

  1. Mechanical/structural ⚙️ causes
    —w/exertion 🏃
    —hypertrophic obstructive cardiomyopathy
    —aortic stenosis
    —MI, PE, cardiac tamponade
  2. Electrical causes ⚡️
    —worst prognosis
    —arrhythmias r/t vent tachy, fib, torsades, heart block, sick sinus syndrome
    —scar from MI, depressed EF/HR
    —evaluate for prolonged QT (genetic or secondary to med/electrolyte imbalance)
    —Brugada syndrome
    —ARVD (Arrhythmogenic right ventricular dysplasia: genetic. With this condition, fat and/or fibrous tissue replaces damaged heart muscle in your right ventricle. Your right ventricle stretches out, becomes thin and contracts poorly. As a result, your heart has a weakened ability to pump blood.)

cardiac syncope carries a high 1 year mortality rate: 18-33% and high risk pts should be admitted to hospital

17
Q

Syncope — neuro evaluation

A
18
Q

Syncope — monitoring options outpatient

A

—holster for 48-72h
—event 2-4w
—ILR : pts w/ recurrent syncope
—electrophysiology study for pts w/ structural heart disease

19
Q

Syncope
What is the tilt table test?

A
20
Q

Syncope
Treatment 4

A
  1. Non-pharmacologic
    —behaviour change, avoid triggers
    —tilt training
    —counter-pressure maneuver can raise periph vasc resistance and BP
  2. Medical
    —correct electrolyte imbalances
    —discontinue QT prolong meds
    —anti-arrhythmias if vent. Tachy.
    —for autonomic dysfunction: Florinef to increase volume or midi drive to inc periph resistance
  3. Devices
    —pacemaker
    —defibrillators
  4. Surgical
    —for pts for mechanical cardiac causes from LVOT obstruction relating to HOCM or aortic stenosis