Endocarditis & Cardiac Infections Flashcards
layers lining the heart (from outermost to innermost)
- pericardium (outermost layer): composed of:
-fibrous pericardium
-serous pericardium (parietal layer)
-pericardial space
-serous pericardium (visceral layer; aka epicardium) - myocardium (muscle layer)
- endocardium (inner endothelial lining covering trabeculae)
pericarditis - overview
*inflammation of the lining around the heart (pericardium)
pericarditis - etiologies
*often idiopathic
*VIRAL INFECTIONS (coxsackie B
*other infectious causes (bacteria, fungi, parasites)
*malignancy
*cardiac surgery
*thoracic radiotherapy (early)
*MI (postcardiac injury syndrome)
*autoimmune diseases (SLE, rheumatoid arthritis)
*renal failure (uremia)
pericarditis - clinical presentation
*sharp chest pain
-aggravated by inspiration
-relieved by sitting up & LEANING FORWARD
*PERICARDIAC FRICTION RUB on auscultation
*can be complicated by a pericardial effusion
*classic presentation: YOUNG ADULT, usually male, with CHEST PAIN
pericarditis - diagnosis
*diagnosed by physical exam, echocardiogram, EKG, and pericardiocentesis (if pericardial effusion):
-PE: sharp chest pain, pericardial friction rub
-echo:
-EKG: widespread/diffuse ST-segment elevation and/or PR depression
pericarditis - treatment
*anti-inflammatories if viral (NSAIDs, colchicine)
*antibiotics if bacterial
myocarditis - overview
*inflammation of the heart muscle itself (inflammation of myocardium)
*major cause of sudden cardiac death in adults < 40 yo
myocarditis - etiologies
*VIRAL (coxsackie B, echoviruses)
*parasitic
*bacterial
*toxins
*rheumatic fever
*drugs
*autoimmune
myocarditis - clinical presentation
*highly variable
*classically presents in younger adults
*heart failure signs predominant (dyspnea, pulmonary edema, peripheral edema, dyspnea on exertion)
*fever, dyspnea, chest pain, arrythmias *persistent tachycardia out of proportion to fever
myocarditis - diagnosis
*echocardiogram: low EF, decreased heart wall movements
*serologies for likely causes
*possibly biopsy
myocarditis - treatment
*supportive, using anti-inflammatories
COVID-19 myocarditis
*virus binds its spike to membrane ACE2 (found in higher concentrations on male > female cells)
*combination of direct myocardial cell infection & damage from inflammatory response
*estimated that COVID has > 15-fold risk of myocarditis compared to other viruses
*vaccine was also implicated
*can cause life-threatening arrhythmias
infective endocarditis (IE) - overview
*infection of the lining membranes of the heart or its valves
*usually caused by a BACTERIAL infection
*most commonly infects sites of pre-existing lesions (rheumatic heart disease, unrepaired congenital heart disease, mitral valve prolapse, etc)
*associated with IV DRUG USE
*increasing incidence of healthcare-associated IE (dialysis patients, central lines, cardiac devices, prosthetic valves)
infective endocarditis (IE) - right vs. left side heart valve disease
*in non-drug users, left-sided disease dominates (mitral valve, aortic valve)
*IV drug use:
-mean age ~30 yo
-RIGHT-sided tricuspid valve disease much more common & considered a hallmark
-note: can have left-sided valve disease as well
infective endocarditis (IE) - etiologies (pre-antibiotic era)
*viridans streptococci predominate
*rheumatic heart disease is key risk factor
*subacute processes key to diagnoses:
-glomerulonephritis
-splenomegaly
-Osler’s nodes and roth spots
infective endocarditis (IE) - etiologies (in US)
*STAPH AUREUS predominates, causing a rapid/acute disease course
-median age > 50yo
*risk factors include: IVDU, CIEDs, prosthetic valves
*diagnosis: modified Duke Criteria
infective endocarditis (IE) - pathophysiology
- damaged endothelium exposes collagen & matrix molecules
- platelets & fibrin adhere to these exposed molecules → sterile vegetation forms (nonbacterial thrombotic endocarditis)
- circulating bacteria seed this vegetation following a transient bacteremia
- lots of bacteria densely pack in to vegetation:
-keep bacteria in circulation
-circulating bacteria continue to feed the thrombus
-more platelets and fibrin deposit
-growing, increasingly friable thrombus develops - developing complications: ring abscess, myocarditis, and vegetation emboli
infective endocarditis (IE) - pathophysiology of vegetation
*only certain bacteria or strains of bacteria have virulence factors that allow them to attach and infect the endothelium/sterile vegetations
*the vegetation is building progressive layers around the core:
-quorum sensing in the core: gene expression alterations in areas of high bacteria density; allows simultaneous upregulation of genes for virulence factors & more
-BIOFILMS: bacteria which stick to each other & a surface and coat themselves in a difficult-to-penetrate extracellular matric
most common cause of infective endocarditis
STAPH AUREUS > streptococci
infective endocarditis (IE) - modified duke criteria (MAJOR criteria)
- valve culture/histopathology (during heart surgery)
- blood culture criteria: 2 blood cultures with typical organisms (Staph aureus, viridans strep, etc)
- echo criteria:
-vegetation or abscess
-prosthetic valve dehiscence
-new valvular regurgitation
infective endocarditis (IE) - modified duke criteria (MINOR criteria)
- predisposing heart condition or IVDU
- fever > 100.4
- embolic phenomena (vegetation broke off and traveled to another organ, including brain)
- immunologic phenomena (immune complex deposition, glomerulonephritis, Roth spots)
- blood culture not meeting major criteria
infective endocarditis (IE) - Osler’s Node
*example of an immunologic phenomenon seen in infective endocarditis
*PAINFUL, RAISED, violaceous lesions on finger or toe pads
*immune-mediated vasculitis
infective endocarditis (IE) - Janeway Lesions
*example of an embolic phenomenon seen in infective endocarditis
*macules
*micro abscesses with neutrophil infiltration of capillaries (septic emboli to skin)
infective endocarditis (IE) - Roth Spots
*example of an immunologic phenomenon seen in infective endocarditis
*retinal hemorrhagic lesions with central clearing (pale centers)
*can be seen in other conditions
infective endocarditis (IE) - Duke Scoring
*definite endocarditis: 2 major criteria OR 1 major + 3 minor OR 5 minor OR positive culture from tissue OR coxiella anti-phase 1 IgG titer > 1:800
*possible endocarditis: 1 major criteria + 1-2 minor OR 3 minor
*rejected endocarditis: firm alternative diagnosis OR resolution of manifestations after antibiotic therapy for 4 days OR no pathological evidence at surgery or on autopsy
infective endocarditis (IE) echocardiogram principles (when to perform transthoracic vs transesophageal)
*transesophageal (TEE) is better if there is vegetation on a prosthetic valve or an abscess
*transthoracic (TTE) is generally sufficient for a right-sided infective endocarditis
*if high concern, do a TEE
*if see IE or TTE, and there are concerns for complications, then do a TEE
infective endocarditis (IE) - antibiotic treatment principles
*static organisms in stasis at the center of the vegetation
*antibiotic penetration:
-vancomycin: concentrates on periphery and has poor penetration inward
-beta lactams: do perfuse inward, but with steep concentration gradient
-homogenous diffusion through the whole lesions: tobramycin, fluoroquinolones, daptomycin
*CIDAL > STATIC, MAX OUT THE DOSES
infective endocarditis (IE) - antibiotic regimen
*at least 10 days of IV antibiotics, followed by long-term oral antibiotics course
*make sure that the antibiotics you choose cover the infectious organism
causes of culture-negative endocarditis
*candida
*coxiella
*bartonella
*chlamydia species
*brucella
*legionella
*fungi
*acid-fast bacilli
dental prophylaxis for infective endocarditis
*people with risk factors sometimes now receive prophylactic antibiotics prior to dental procedures to prevent development of endocarditis (usually amoxicillin)
*guidelines restrict the prophylaxis to those with:
-previous IE
-prosthetic heart valve or prosthetic material used for heart repair
-UNREPAIRED cyanotic heart disease
-completely repaired congenital heart disease in 6 months post-surgery
-congenital heart disease with residual deficits
-cardiac transplant patient with valvuloplasty
rheumatic fever & heart disease - epidemiology
*mostly in age 5-14 years old
*pretty common
*acute rheumatic fever leading to rheumatic heart disease: 2 to 3 weeks after group A strep throat infection (or occasionally skin infections)
acute rheumatic fever - J❤️NES Criteria
*JOINTS: large joint arthritis/arthralgia
*❤️ (heart): rheumatic carditis with inflammation of cardiac tissue, especially the mitral and aortic valves & heart walls
*NODULES: subcutaneous nodules (hard and painless on extensor surfaces)
*Erythema marginatum (evanescent rash with ring margin)
*Sydenham chorea (involuntary irregular movements of limbs and face)
rheumatic heart disease - pathophysiology
*carditis: molecular mimicry
-strep M protein & other antigens cause cross-reaction for nervous system and heart tissue
-Aschoff bodies: intense inflammation in the heart leads to nodules of T cells and macrophages
-inflammation causes valve leaflets to fuse together, chordae to shorten, and rigidity
*rheumatic heart disease: chronic heart disease due to persistent damage to heart valve from the immune response & repeat infections
-MITRAL VALVE most commonly affected (classically, MITRAL STENOSIS)
rheumatic heart disease - prevention & treatment
*prevented by penicillin treatment of strep throat
*if develop rheumatic fever, need ongoing penicillin to prevent recurrent acute rheumatic fever and worsening rheumatic heart disease
aortitis - overview & symptoms
*inflammation of aorta itself; seeding of an atherosclerotic plaque or aneurysm sac by vaso vasorum
*symptoms: vary; back pain, fever, dissection
aortitis - etiologies
*non-typhoidal Salmonella
*SYPHILIS
*staphylococcus & strep pneumo
*TB
aortitis - diagnosis & treatment
*dx: CTA or MR angiogram
*tx: ? antibiotics & surgical management
Lemierre’s Syndrome
*infectious thrombophlebitis of internal jugular
*classically presents in young & healthy patients with prolonged tonsillitis, progressing to sepsis; septic emboli to lung is common
*FUSOBACTERIUM NECROPHORUM most common pathogen
*tx with antibiotics usually
CIED infections
*infections of cardiac IEDs, at time of implantation or through bacteriemia
*s/s: local inflammation/erythema or erosion at pocket, bacteremia, FUO
*organisms: CoNS, S. aureus, gram negatives
*dx: TEE, blood cultures, culture of pocket/leads
*tx: ICR removal and 2-6 weeks of antibiotics like IE treatment
