ACUTE RHEUMATIC
FEVER
BY
[Link] VAISHNAVI
MD PAEDIATRICS JR 1
Rheumatic fever is an immunological
disorder initiated by group A beta hemolytic
streptococci.
Antibodies produced against selected
streptococcal cell wall proteins and sugars
react with the connective tissues of the body
as well as the heart and result in rheumatic
fever
Age and sex:
The incidence of rheumatic fever following
streptococcal throat infection is 0.3% in the
general population and 1 to 3% in presence
of epidemics of streptococcal pharyngitis.
Commonly affects those between 5 and 15
Epidemiolog years
y Although the sexes are nearly equally
affected
Mitral valve disease and chorea is more
common in girls
Aortic valve involvement is often seen in
boys.
Poor socioeconomic conditions
Predisposin Unhygienic living conditions
g factors
Overcrowding
Rheumatic fever appears to be the result of
the host's unusual response at both the
cellular and humoral level to Streptococci
Following streptococcal sore throat there is a
Etiopathoge latent period of 10 days to several weeks
before the onset of rheumatic fever.
nesis Streptococcal cell wall proteins as well as
carbohydrates may induce production of
antibodies that are capable of reacting with
human connective tissue, resulting in
rheumatic fever.
Only heart valves are permanently
damaged during an episode of
rheumatic fever.
All other affected tissue typically heal
without residua: Pericarditis, chorea
and arthritis resolve completely
without constriction, long term
neurologic consequences or joint
disability, respectively.
Acute phase reactants:
The leukocyte count usually lies
Laboratory
between 10000 to 15000/cu mm.
manifestation
s The ESR is elevated during acute
rheumatic fever and remains so for 4
to 10 weeks in almost 80% patients.
C-reactive protein is elevated in all patients
of acute rheumatic fever, and subsides
rapidly if the patient is treated with
corticosteroids.
While absence of raised C reactive protein is
against the diagnosis of rheumatic fever, its
presence is non-specific.
Prolonged PR interval:
Prolonged PR interval can get
prolonged in many infections, nor is
diagnostic of carditis
These include evidence of recent
streptococcal infection.
Elevated levels of antistreptolysin 0 (ASO)
indicate previous streptococcal infection and
not rheumatic fever.
Essential A basal ASO titer of 50 U / dL that goes up to
Criteria 250 U / dL is indicative of recent
streptococcal infection.
Rising titer of ASO is a strong evidence for
recent infection.
Positive throat culture for streptococci, at
diagnosis of rheumatic fever, is uncommon.
The recent revision of Jones criteria
now includes echocardiographic
findings for the diagnosis of rheumatic
carditis.
Echocardiog Features suggestive of rheumatic
raphy carditis include
Annular dilatation
Elongation of the chordae to the
anterior leaflet of the mitral valve
causing a prolapse
Bed rest is generally recommended for
acute rheumatic fever.
Prolonged bed rest (>2- 3 weeks) is
TREATMENT
seldom necessary unless there is
clinically apparent carditis with heart
failure.
Penicillin:
After obtaining throat cultures, the
patient should receive penicillin.
A single injection of benzathine
penicillin is given when the diagnosis of
rheumatic fever is made.
TREATMENT
ALTERNATIVE
Penicillin V (250 mg four times a day for
10 days)
Erythromycin (250 mg four times a day
for 10 days) is given to those with
penicillin allergy.
Suppressive Therapy
Aspirin
corticosteroids
Carditis with congestive cardiac failure: use steroids
Carditis without congestive cardiac failure: One may use either
steroids or aspirin, however, steroids are preferred
If the patient does not have carditis, it is preferable to use aspirin.
The total duration of course for the suppressive agent, aspirin or
steroids, is 12 weeks.
Aspirin : 90-120 mg/kg/ day (in 4 divided doses) for 10 weeks, and
then tapered in the next two weeks.
Alternatively, prednisolone (2 mg/kg daily; maximum dose 60 mg) is
given for three weeks and then tapered gradually in next 9 weeks
Surgical replacement of the mitral
and/or aortic valve is sometimes
indicated, if the patient is
deteriorating despite aggressive
decongestive measures.
Acute hemodynamic overload due to
mitral or aortic regurgitation is the
main cause of mortality due to
rheumatic fever.
The patient as well as the parents are
reassured about the self-limiting
course of the disease.
The signs and symptoms of chorea do
Manageme not respond well to anti-inflammatory
nt of chorea agents or steroids.
Supportive measures such as rest in a
quiet room and medications such as
haloperidol, diazepam and
carbamazepine are effective
Prevention (i) prompt identification of sore throat
of (ii) rapid confirmation of a
Rheumatic streptococcal etiology
Fever (iii) availability of penicillin.
Long-acting benzathine penicillin.
Secondary Dose is 1.2 million units once every 3
prevention weeks or 0.6 million units every
alternate week
Mitral valve involvement manifests
predominantly as mitral regurgitation
(MR) and much less commonly as
RHEUMATIC mitral stenosis (MS).
HEART Aortic valve and tricuspid valve
DISEASE involvement presents as aortic (AR)
and tricuspid regurgitation (TR),
respectively
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