Rheumatic Fever and Endocarditis Flashcards
RF is an autoimmune disease assocaited with ___ ___ infection
streptococcus pyogenes (Group A strep) infection.
sub-Saharan Africa and south central Asia, indigenous
populations in Australia and New Zealand represent
the world’s highest prevalence
RF Pathophysiology
delayed immune-mediated host response
when they look at acute and chronci tissue lesions of RF there’s no bacteria.
• bacteria are absent from the acute and chronic
tissue lesions of rheumatic fever
• molecular mimicry
- poorly understood. theres many factors including genetics, specific host, envrinoment, and pathogen subtype of group A strep
Jones Criteria for RF
2 major or 1 major and 2 minor criteria, + evidence of recent strep infection.
Jones criteria Major and minor criteria
Major: CPCES
Minor: FAAPP
major:
• Carditis: All layers of cardiac tissue are affected (pericardium,
myocardium, endocardium)
• Polyarthritis: Migrating arthritis that typically affects the knees, ankles, elbows and wrists.
• Chorea: Also known as Syndenham´s chorea, or “St. Vitus´ dance”. There
are abrupt, purposeless movements
• Erythema marginatum: A non-pruritic rash that commonly affects the trunk and proximal extremities, but spares the face. The rash typically migrates from central areas to periphery, and has well-defined borders.
• Subcutaneous nodules: Usually located over bones or tendons; painless and firm.
•Minor Criteria:
• Fever
• Arthralgia
• Previous rheumatic fever or rheumatic heart disease
• Acute phase reactants: Leukocytosis, elevated ESR
and CRP
• Prolonged P-R interval on ECG
ECG findings of RF
• Prolonged P-R interval on ECG
what are some “evidences” of preceding streptococcal infection?
- incerased antistreptolysin O or strep antibodies
- positive throat culture for GRoup A strep
- rapid strep dest that’s positive
- recent scarlet fever.
acute carditis manifests as an acute ___. MOst often resulting in ___ ___ followed by ___ ___.
acute carditis manifests as an acute VALVULITIS. MOst often resulting in MITRAL REGURG followed by AORTIC REGURG.
• LV dysfunction is thought to be secondary to valvular
dysfunction (rather than myocarditis)
• valvulitis can be subclinical, only to manifest years
later (often as MS)
• __ ___ is the hallmark cardiac
lesion in acute rheumatic fever carditis
• underlying pathology is controversial:
• __ lesions
• __ ___ prolapse due to annular dilatation and
chordal elongation
• MITRAL REGURGITATION is the hallmark cardiac
lesion in acute rheumatic fever carditis
• underlying pathology is controversial:
• verrucous lesions
• anterior leaflet prolapse due to annular dilatation and
chordal elongation
treatment of acute carditis
treatment; there is no good evidence.
- usually treated with steroids
note: mild MR can go into a cycle resulting in recurrent carditis especially if they have recurrent rheumatic fever
chronic rheumatic heart disase can happen if rheumatic fever continues/a lot of infections into adult hood.
in younger patients, mitral valve regurgitation is a bigger maifestation, but in older population is ____.
in younger patients, mitral valve regurgitation is a bigger maifestation, but in older population is MITRAL STENOSIS.
- additionally, you’d see aoritc valve regurgitation and less common involvement of tricuspid and pulmonic vavles.
outline 3 characteristic echo findings on the mitral valve due to rheumatic fever
- commissural fusion
- leaflet thickening/calcification: “hockey sticking”
- ALSO SEEN IN AORTIC VALVE - subvalvular thickening
- restricted leaflet motion
- mitral regurgitation ( most common in pediatric)
- mitral stenosis
primary prevention of rhrumatic fever
- accurate recognition and proper antibiotic treatment of GAS pharyngitis
- throat culture or a rapid antigen detection test
- prompt treatment with Abx
secondary prophylaxis of rheumatic fever (involving patients that have had rheumatic fever but now we wanna reduce the chances of rheumatic heart disease/prevent another round of rheumatic fever happening again)
if someone has had rheumatic fever with carditis, the duration of treatment/prophylaxis is over 10 years, sometimes life long.
types of endocarditis
- infective (usually of heart valve)
- non bacterial thrombotic endocarditis
- rheumatic endocardidits: already covered but due to rheumatic Strep A fever.
risk factors for Infective endocarditis (IE)
main organisms that cause infective endocarditis
staph A, viridans strep, and enterococci
clnical presentation of IE
to assess infective endocarditis, we use the ___ criteria
duke criteria.
____ is considered a first-line modality when suspecting
IE complications (perforation, abscess), prosthetic
valve endocarditis, S. aureus bacteremia, intracardiac
devices, and when TTE images are suboptimal
TEE (echocardiography) is considered a first-line modality when suspecting
IE complications (perforation, abscess), prosthetic
valve endocarditis, S. aureus bacteremia, intracardiac
devices, and when TTE images are suboptimal
an acute cardiac complication of IE would be heart failure of ___ block
AB block
systemic acute complications of iE
neuro: stroke, brain abscess
septic emboli: kidney, spleen, etc.
metastatic infection: vertebral osteomyelitis, septic arthritis, splenic or psoas abscess
systemic immune reaction; globerulonephritis
treatment of IE
treatment duration will depend on pathogen, left vs right side. typically lasts 4-6 weeks.
- if you have a high suscpicion of IE, empirically treat before blood culture return. then use targeted treatment when blood cultures are available.
- ABx depends on the bug and if the valve is native or prosthetic.
• NATIVE VALVE: Empiric tx: Depends on clinical
scenario, but typically vancomycin + ceftriaxone (cover
staph/strp/enterococcus)
• PROSTHETIC VALVE: Empiric tx: vancomycin +
gentamycin + rifampin
Additionally, you might need to consider surgery. if there is valve dysfunction causing heart failure, highly resistant organisms, heart block, persistent infection, recurrent embolit or persistent/enlarging vegetations or severe valve regurgitation,.
indications for surgical repairation of Infectious endocarditis
chronic complications of IE
what is marantic endocarditis and how is it caused? what part of the heart do the clots affect?
an endocarditis that involves thrombi interwoven with strands of firbin, immune complexes and mononuclear cells “white thrombus”. Usually on aortic or mitral valves.
caused by
- pancreatic adenocarcinoma/cancer
- SLE
- APLA
- RA
- SEpsis
- Burns
antibiotic prophylaxis conditions for IE
- we don’t give antibiotics to everyone. But, we would give it to them if they have a prostehtic cardiac valve, previous IE, congenital heart disease, or cardiac transplantation.
treatment of marantic endocarditis
- Treatment: LMWH
- Treat underlying disorder (ex/ lupus, RA, treat cancer)
