11/16 Inflammation and Infection in Heart - Corbett Flashcards
infective endocarditis
what is it
microbial infection of endocardial surface of heart
- heart valves
- mural endocardium
- septal defect
requires formation of vegetations (composed of thrombotic debris and microorganisms)
risk factors for IE
- age > 60
- male sex
- poor dentition/dental infections
- structural heart disease
- valvular HD
- congenital HD
- IV drug use
- prosthetic vale
- intravascular devices
what about healthcare assoc endocarditis?
associated with intravascular devices
- central, peripheral indwelling catheters
- pacemaker wires
- implatable defibs
- chemotx lines
principal org: Staph aureus
HIGH MORTALITY
special cases
- prosthetic valves : infection leading to valve compromise (ex. ring abscess)
- coag neg Staph, Staph aureus
- HACEK bacteria
- IVDA: tricuspid valve (often also see pulm manifestations)
- S. aureus is more common etiologic pathogen
pathophysiology:
how does it form? (consider the elements involved)
- nonbacterial thrombotic endocarditis forms : sterile fibrin-platelet vegetation
- platelets adhere to injured endocardium
- platelet-fibrin thrombus forms the vegetation
- bacteremia/fungemia that predisposes heart to IE
- acquired through an obvious infection: dental/surgical procedure, contaminated needle, break in epithelial barrier
- ability of a bacteria to cause inf dependent on:
- access to circ
- ability to survive in bloodstream (reason why Gram+ are more common in IE!)
- adherence to endothelium
IE
clinical presentation
acute vs subacute
- basics
- organisms
- timecourse
acute IE
- systemic toxicity
- rapidly destructive to native valve
- virulent organism
- Staph aureus
- Strep pyogenes
- rapidly fatal if untreated
subacute IE
- indolent nature
- structural or congenital HD
- common organism
- Strep viridans
- Enterococci
- can live up to a year untreated
IE
clinical spectrum
acute vs subacute
- symptoms
acute IE
- acute onset of high grade fevers and chills
- rapid onset of CHF
- rapid valve failure
- history of antecedent procedures or illicit drug use
subacute IE
- fever/chills
- nonspecific fatigue
- weight loss
- “flu-like” sx
fever present in 90%
clinical dx
new regurgitant murmur
+
recurrent/unremitting fever
=
ENDOCARDITIS until proven otherwise
endocarditis physical findings
85% pt have MURMUR
petechiae (20-40%: skin, palate)
nail bed hemorrhage (“splinter” hemm, not with IVDU)
rare findings
- retinal hemorrhage
- “Roth spots”
- immune-mediated vasculitis
- painless palm or sole lesions
- “Janeway lesions”
- painful fingertip nodules
- “Osler nodes”
complications of endocarditis (that may present as sx)
cardiac complications (50%)
- valvular insufficiency
- CHF
neuro complications (40%)
- freq, most severe
- ischemic/hem stroke/TIAs
- silent cerebral embolism, mycotic aneurysm
- incr risk for vegetations that are large/mobile/mitral valve and/or Staph aureus infection
septic emboli (25%)
- common w/ IV drug use
- emboli to kidneys, lungs
systemic immune rxn
myocarditis
disease of myocardium
- inflammatory infiltrate of myocardium with necrosis and/or degen of adjacent myocytes
- manifests in otherwise healthy person, can result in reapidly progressive (often fatal) HF and arrhythmia
clinical presentation: VARIED
- often in young
- sx
- chest pain and palpitations with ECG changes
- ventricular arrhythmias
- life-threatening cardiogenic shock
causes
- cardiotropic viuses are most common cause of myocarditis in US
- Parvovirus B19
- HHV6
- Coxsackie A, B
- H1N1 flue
- Borrelia species: Lyme myocarditis
- Typanosoma cruzi (Chagas disease)
pathogenesis of viral myocarditis
acute → subacute → chronic phases
acute viral inf
flowchart
Lyme carditis
Lyme disease: multisystem illness caused by Vorrelia burgdorferi
common signs:
- erythema migrans rash
- rheumatologic
- neurologic manifestations
in Lyme carditis…
- Lyme spirochetes invade tissues of heart
- most commonly recognized clinical feature: atrioventricular block
- sx: palpitations, syncope, chest pain, dyspnea; muscle aches, fever, fatigue, erythema migrans
Chagas Disease
cause: protozoan Trypanosoma cruzi
myocardial involvement in most infected individs (approx 10% of pt die during acute attach)
chronic immune mediated myocarditis which can progress to cardiac insufficiency in 10-20yrs
acute rheumatic fever
- autoimune disease that develops as a sequela of Group A beta-hemolytic streptococcal inf (most typically: pharyngitis)
- nonsuppurative infl lesions of
- heart (rheymatic crditis)
- joints (polymigratory arthritis)
- subcutaneous tissue (erhythma marginatum)
- CNS (Sydenham chorea)
affects moslty children (80% of cases: 5-15yr)
3% of GABHS (grp A beta hemolytic strep) → acute rheumatic fever
- presents 2-4wk after strep infection
five major manifestations of acute rheumatic fever
JONES CAFE PAL
- carditis and valvulitis (50-70%)
- polyathritis (35-66%)
- Syndenham chorea (10-30%; F >>> M)
- Erythema marginatum and subcutaneous nodules (uncommon, <1 0%)
ARF: what happens in the heart?
Aschoff nodules
pathgnomonic for rheumatic heart disease
