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ACUTE RHEUMATIC FEVERBurhanuddin IskandarPediatric
CardiologyPediatric Department,Medical Faculty, Hasanuddin
University/ WS Hospital Makassar
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ETIOLOGY1.Immunologic Streptococcus Beta hemolytic group A
2. Predisposing factors - Family history - Socio economic status
- Age 5 -15 years ( peak 8 years)
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PATHOLOGY Inflammatory lesion : heart, brain, joints, skin
Aschoff bodies (in atrial myocardium) : characteristic ? Central
necrosis surrounded by lymphocy tes, plasma cells, and large
mononuclear and giant multinucleate cell
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Aschoof Body : the cells are large, multinucleotide
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CLINICAL MANIFESTATIONS HistoryStreptococcal pharyngitis, 1-5
wks (ave 3 wks) before onset; chorea 2-6 mosPallor, easy
fatigability, epistaxis, abdominal pain
Positive family history
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2. Carditis 50 % of cases, usu within first 3 wksDiagnosis
requires presence of 1 of 4:- organic heart murmur- pericarditis
(friction rub, pericard effusion, chest pain, ECG changes) -
cardiomegaly on chest X ray- congestive heart failure
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Jones criteria (updated 1992)Mayor criteria
1. Arthritis* Affects 70 % of cases* Large joints : knee, ankle,
elbow, wrist* Often > 1 joints, simultaneously or in succession,
migratory* Swelling, heat, redness, severe pain, tenderness, motion
: not specific
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Evidence of antecedent Group A Streptococcal infectionPositive
throat culture or rapid streptococcal antigen tests for group A
:less reliable (recent and chronic infect)Streptococcal antibody
tests : most reliableASTO : 80% Anti-DNA se BAnti hyaluronidase
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Diagnosis of rheumatic fever Based on
2 major criteria or + ASTO 1 major + 2 minor
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ExeptionsChorea may occur as the only manifestations of
RFIndolent carditis may be the only manifestationOccasionally
patients with RF recurrencesmay not fulfill the Jones criteria
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Differential diagnosis of RFJuvenile rheumatoid
arthritisCollagen vascular diseasesVirus associated acute
arthritis
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Note
* Rheumatic fever is a clinical syndrome for which no specific
diagnostic test exist !* No symptom, sign or lab test result is
pathognomonic, although several combinations of them are
diagnostic* Only carditis can cause permanent cardiac damage. Signs
of mild carditis disappear rapidly in weeks but severe carditis may
last for 2-6 months. Chorea and arthritis usually subside without
permanent damage.
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Management of RFBenzathin penicillin G 0.6 1.2 M units IM for
eradication and prophylaxisBed restAcetosal for mild casesPrednison
for severe casesAntiinflammatory agents not needed for isolated
chorea
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Recommended anti-inflammatory
agents_______________________________________________________________________________________
Arthritis Mild Moderate Severe alone carditis carditis
carditis__________________________________________________
Prednisone 0 0 0 2-6 wk*
Aspirin 1-2 wk 3-4 wk# 6-8 wk 2-4
mo___________________________________________________
* Prednisone should be tapered and aspirin started during the
final week# Aspirin may be reduced to 60 mg/kg/dayDosagesPrednisone
: 2mg/kg/day, in 4 divided dosesAspirin : 100 mg/kg/day, in 4-6
divided doses
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Bed rest and indoor
ambulation____________________________________ Arthritis Mild
Moderate Severe Alone Carditis Carditis
Carditis__________________________________________________________
Bed rest 1-2 wk 3-4 wk 4-6 wk as long as HF +Indoor ambulation
1-2 wk 3-4 wk 4-6 wk 2-3
mo_________________________________________________________
ESR: important for duration of restriction of activities.Full
activity : ESR normal, except significant cardiac involvement _
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Mild carditis : questionable cardiomegalyModerate carditis :
definite but mild cardiomegalySevere carditis : marked cardiomegaly
or HF (heart failure)
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PreventionIdeally prophylaxis is indefiniteBenzathin Penicillin
(600,000-1,200,000 U) every 28 days, min till age 21-25
ysSulfadiazine 0.5 g 1x daily (BW < 27 kg),1 g 1X (BW >27
kg)Penicillin V 2 x 250 mg /dayErythromycin 2 X 250 mg /day
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DEMAM REMATIK
KARDITIS (+)
SEMBUH
KARDITIS (-)
PENYAKIT JANTUNG
REMATIK
REAKTIVASI
SEMBUH
REAKTIVASI
3 6 bulan
Bising masih ada
Bising -
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Thank YouNO PAIN NO GAIN
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RHEUMATIC HEART DISEASEAffects Mitral valve 75 %Aortic valve 25
%Tricuspid valve rarePulmonary valve never
Stenosis and regurgitation usually occur together
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Mitral stenosisPrevalenceMost common valvular involvement in
adultRequires 5-10 years from the initial attack
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Pathology- Thickening of the leaflets and fusion of the
commisureCalcification results overtimeDilated and hypertrophied LA
and right sided heartPulmonary venous hypertension pulmonary
congestion and edema and fibrosis of the alveolar walls,
hypertrophy of the pulmonary arterioles, loss of lung
compliance
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Stenotic Mitral ValveCommisures are fused and valve
thickened
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Clinical manifestationsMild MS : asymptomaticMore severe :
dyspnea with/out exertion : orthopnea, nocturnal dyspnea or
palpitation
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Physical ExaminationsIncreased RV impulse along the LSBWeak
peripheral pulse with narrow pulse pressurePulmonary hypertension :
loud S1 at apex and narrow split S2, accentuated P2Mid
diastolic/presystolic murmur
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ECG : RAD, LAH, RVH (due to PH)
CXR :Enlarged LA and RV, MPA segment prominentPulmonary venous
congestion
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Treatment of MSProphylactic antibioticRestriction of activity
depends on severitySymptomatic patients (dyspnea on exertion,
pulmonary edema, paroxysmal dyspnea) : baloon or surgery
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MITRAL REGURGITATIONMost common in RHDPathology Mitral valve
leaflets are shortened because of fibrosis. When degree of MR
increases, dilatation of LA and LV results, mitral ring becomes
dilated
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Mitral Valve involvement
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Echocardiography
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Clinical manifestations * Asymptomatic during childhood * Rare :
fatigue, palpitation
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Physical examinationHeaving, hyperdynamic apical impulse in
severe MRS1 normal or diminished. S2 may split (shortening of LV
ejection, early aortic closure)Pansystolic murmur at apex left
axilla
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ECGNormal in mild casesLVH or LV dominance, with or without
LAH
CXRLA and LV enlargedPulmonary congestion pattern in CHF
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TreatmentProphylactic antibioticNo restriction of activity in
mild casesSurgical : intractable CHF, progressive cardiomegaly,
pulmonary hypertension
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AORTIC REGURGITATIONLess common than MR. Mostly associated with
mitral valve disease.
Pathology* Semilunar cusps are deformed and shortened.* Valve
ring is dilated* Commisures usually are fused
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Aortic Valvulitis
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Clinical Manifestations
Mild regurgitation : asymptomaticMore severe : reduced exercise
tolerance test
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Physical Examination
Precordium may be hyperdynamic. Diastolic thrill at 3 LICSS1
decreased, S2 may be normal or singleHigh pitched diastolic
cresendo murmur at 3 LICS or 4 LICS Systolic murmur at 2 RICS due
to relative AS Severe AS : middiastolic murmur at apex
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ECGNormal in mild casesSevere : LVH, LAHCXRCardiomegaly
(LVH)Dilated ascending aorta
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TreatmentProphylactic antibioticsMild cases : no restriction in
activitySurgical : in anginal pain or dyspnea on exertion,
significant cardiomegaly
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Thank YouNO PAIN NO GAIN
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