Page 1 of 2: Q: Earliest valvular lesion in rheumatic fever is?

manipalguy · Credits: 15905 My Scrapbook

earliest valvular lesion in rheumatic fever is
1.MS
2MI
3.AS
4.AR
answer given in medicine buster book is AR .... is it right???

cnn · Credits: 77713 My Scrapbook My Reading List 262569 Books

MI

anandkumar_m · Credits: 3208 My Scrapbook

Hi pal
any reference??

docsab · Credits: 238 My Scrapbook

Harri says: 40-60% patients of rheumatic fever have evidence of carditis with features like sinus tachycardia, murmur of mitral regurgitation, S3 gallop, pericardial friction rub, and cardiomegaly.

swazamight · Credits: 3151 My Scrapbook

Commonest is an acute valvulitis leading to MR

pajitmenon · Credits: 1107 My Scrapbook

to all would be pg's....
most common is the pansystolicmm of MR in acute pancarditis eg. ac.rheumatic fever.
all the best

CLINICAL MANIFESTATIONS OF ACUTE RHEUMATIC FEVER

After a latent period of 1-5 weeks, the clinical manifestations of rheumatic fever becomes manifest. Certain manifestations have been designated as major manifestations & include carditis, arthritis, chorea, subcutaneous nodules & erythema marginatum. Other nonpathognomic signs & symptoms are called minor manifestations. The laboratory signs are included in this category.

Major Manifestations-

Carditis has always been the first & most important element
to be considered in establishing the diagnosis of rheumatic fever since it may result in the only significant sequelae of the disease. Carditis is the rheumatic inflammatory process, which involves the endocardium, myocardium &pericardium. The incidence of carditis in rheumatic fever in developing parts of the world has been reported to be much higher varying from 64% to 80% compared to West (40-51%).

The confirmation of carditis during initial attack of rheumatic fever solely depends upon auscutatory recognition of mitral and/or aortic valvar incompetence.

The pansystolic murmur of high frequency [because of high systolic pressure gradient between Left ventricle (LV) & Left atrium (LA) more than 100 mm Hg] begins with first heart sound & as pressure gradient persists after aortic closure, murmur is detected beyond 2nd heart sound. The murmur is heard at apex &extends towards axilla because it is the LV which transmits vibratory activity generated by the turbulent regurgitant flow to the chest wall. The murmur occasionally can propagate to the sternal border due to predominant involvement of posterior leaflet. This classical description may not be present if murmur is soft & then is better detected in left lateral position during full expiration.these r all seen in MR.In addition, often apical mid diastolic murmur is heard, due to additional volume of blood in left atrium contributed by regurgitant flow across mitral valve. This murmur originally was described by Dr. Carry Coombs of Bristol in 1924. This murmur is only heard in the presence of mitral regurgitation & is low pitched as turbulence is caused by the increased flow without a pressure gradient. The mid diastolic murmur as an isolated murmur would never be present as an isolated finding with the initial attack of rheumatic carditis but may be an earliest manifestation of mitral stenosis.

Rarely a basal diastolic murmur of aortic regurgitation can be encountered in first attack of acute rheumatic fever.

Myocarditis – Myocarditis in the absence of valvulitis is never rheumatic in origin. Myocardial involvement in acute rheumatic carditis unequivocally does exist but it is not significant from clinical stand point of view except for its probable role in mitral annulus dilation and it may lead to congestive heart failure. There is no way to prove presence of myocarditis except cardiomegaly on X-ray chest. Even myocardial biopsy has not shown to confirm the presence of myocardial involvement.

Pericarditis - As with myocarditis in acute rheumatic fever, pericarditis is never encountered in the absence of valvar involvement. The precordial pain of pericarditis automatically directs attention to heart but from practical standpoint it is not hemodynamically significant and never causes cardiac tamponade.

The onset of carditis in majority of children older than 6 years of age is rather abrupt and in 76% of the cases occurs during first week. In children younger than 6 years the onset of carditis is often insidious and it may take several weeks until an unequivocal diagnosis can be made. During this period children are chronically ill with low grade fever and pain in joints. The incidence and severity of carditis in this group is often greater.

Role of echocardiography

Echocardiography is the only new diagnostic tool, which significantly contributes in confirming the presence of rheumatic carditis.

Initially echocardiography was used to differentiate the murmur of mitral regurgitation from systolic murmur caused by VSD, obstructive cardiomyopathy and mitral valve prolapse. It is now established that more than leaflet edema, the mitral annular dilation and secondary chordal elongation permits the apical portion of the anterior leaflet to prolapse back into the left atrium resulting in characteristic jet of regurgitant flow that passes over the posterior leaflet striking on posterior left-atrial wall.

Recent experience suggests that silent mitral regurgitation can be demonstrated by doppler evaluation in patients presenting with isolated rheumatic polyarthritis. Silent but pathologic mitral regurgitation that cannot be heard can be differentiated from physiologic if

Regurgitant flow is holosystolic
Regurgitant flow should extend back to left-atrial wall.
Regurgitant flow should have mosaic pattern on color flow.
Regurgitant flow should be confirmed in more than one plane.
There now appears to be enough experience to add echocardiographic demonstration of silent-valve regurgitation as an additional minor manifestation. It is also important to demonstrate this echocardiographic evidence of pathologic regurgitation in patients presenting with polyarthritis to decide about future penicillin prophylaxis.

2. Polyarthritis

Polyarthritis has always been the "Achilles heel" of Jones criteria. The list of disorders which can mimic rheumatic polyarthritis includes juvenile rheumatoid arthritis, post viral arthritis, and systemic lupus. At the onset of polyarthritis, a given diagnosis is difficult to establish.

Rheumatic arthritis can be present with wide range of severity and duration. The pain can be so severe that patient may refuse to walk and will scream with pain when hardly touched, even by bed clothing. On the other hand, pain may be so mild that it is often not recalled a week later. The pain can last less than 24 hours or recur off and on for weeks.

Rheumatic arthritis is a migrating polyarthritis and involvement of single joint is extremely unusual. It usually involves larger joints- knees, ankles, elbow and wrist-joint. Characteristically the pain far exceeds the objective findings which may well be the reason Dr. Jones originally chose polyarthralgia rather than polyarthritis as a major manifestation. The 1955 modification which Dr. Jones personally endorsed has required only minimal objective findings to establish the presence of arthritis. Limitation of voluntary motion and tenderness to touch are acceptable and both are usually present. Though Feinstain described rheumatic joints as typically red, hot or swollen, this is not usually seen. Redness is uncommon and when present with rheumatic arthritis- usually only a small area of mild erythema is encountered. Any joint that is markedly inflammed and swollen should be considered septic. If this is associated with pericarditis the first consideration should be that it is infectious mandating immediate confirmation and intervention. If patient fails to respond to aspirin on a dosage of 100 mg/kg within 48 hours, one can exclude rheumatic arthritis.

There is a lower incidence of carditis in patients with classical sever migratory polyarthritis as compared to those who have milder joint manifestation.

Arthralgia is an extremely common complaint in all patients with rheumatic fever especially during recurrence and is probably neglected because of its nonspecific nature.

Nevertheless it does at times precede severe carditis and deserves better recognition.

3. Chorea (Sydenham chorea)

This is a late manifestation of acute rheumatic fever whose incidence has apparently shown a decline. Earlier reports showed an incidence of 52% as against 15-20% in the more recent surveys. This is of interest since in areas where rheumatic fever is still a common affliction, the incidence of chorea is equal to west where the disease has shown a decline.

The latent period of chorea varies from 1 to 6 months. It is more common in females and is characterised by non-repetitive, purposeless involuntary movement often associated with muscle weakness signs of incoordination, Nervous milking grip, positive pronator sign, hanging knee jerk, alternating contraction & relaxation of pupils and emotional instability. It may be associated with carditis but laboratory signs of rheumatic activity have usually subsided.

4. Erythema marginatum and subcutaneous nodules

Although erythema marginatum has been traditionally regarded as major manifestation of acute rheumatic fever - its validity is indeed questionable because of the following facts

It is an uncommon finding.
It cannot be correlated with other signs of rheumatic activity.
It is nonspecific and can occur with drug reactions, glomerulonephritis and sometimes without apparent reason.
It is however often associated with carditis and in such instance it serves to confirm the diagnosis of rheumatic fever. If seen as an isolated finding it can by no means serve as an evidence of acute rheumatic fever. It is an irregular circinate evanescent red rash with normal central stain without itch.

Subcutaneous nodules are late and relatively uncommon manifestations of an active rheumatic fever and are almost always associated with severe carditis. These appear on wrist, elbow, knees, ankles and skull.

The inclusion of these two signs as major manifestations of acute rheumatic fever independent of other major manifestations are thus somewhat erroneous and it is preferable to designate them as secondary major manifestations of acute rheumatic fever.

Minor manifestations-

Clinical manifestations –

Fever – It is usually present during first week to ten days of rheumatic fever and is rarely above 390 C. If patient’s temperature elevation persistently exceeds 390 C, other cause should be sought. In particular, in the presence of rheumatic heart disease superimposed infective endocarditis should be the first consideration.

Arthralgia –Arthralgia is an extremely common complaint in rheumatic fever. It commonly precedes an acute attack of carditis.

Laboratory minor manifestations-

Laboratory data which can be helpful in the diagnosis of acute rheumatic fever are of two kinds :

Evidence of streptococcal infection and
Tests for the presence of rheumatic activity.
The proof of streptococcal infection can be based on

A positive throat culture for group A b hemolytic streptococcus. Although old literature quotes throat culture to be positive in 25%, with the common use of antibiotics in almost every febrile child this figure is nowadays hardly ever attained.
The most useful and practical test for detecting a preceding streptococcal infection is a rise in antistreptolysinO titre. The rise occurs in a week, reaches a peak in 3-5 weeks and subsides in 2-6 months. It can be detected in about 80% of cases of acute rheumatic fever because it remains elevated far longer than other signs.
It must be understood that a low ASO titre does not exclude the diagnosis of rheumatic fever if other criteria are fulfilled and on the other hand too much reliance on a solely elevated ASO titre can result in unnecessary treatment.

Test for presence of rheumatic activity:

Erythrocyte sedimentation rate
The elevation of ESR is due to increase in plasma fibrinogen secondary to inflammation. The magnitude of elevation of ESR is often directly proportional to the severity of the disease except in patients with heart failure whose liver may not produce enough fibrinogen.

Elevation of ESR is fairly good index of rheumatic activity. ESR remains elevated for about 4-8 weeks and it may remain high in severe carditis. Also it may remain high longer in presence of anemia.

ESR is useful in deciding how long a child should remain in bed or when to modify suppressive therapy.

C-reactive protein – It is not usually present in blood. It appear promptly in the course of any inflammatory reaction. It becomes normal much more readily than ESR and is a helpful adjunct in proving rheumatic activity because of its transient nature and rapid disappearance from blood. ESR is preferable to CRP especially for the follow up of rheumatic activity. CRP is not influenced by anemia or CHF so in the presence of other criteria and normal ESR, CRP is a good indication of rheumatic process. But in the absence of other criteria, normal ESR and elevated CRP suggest non-rheumatic etiology.
Leukocyte changes are of little help in rheumatic fever due to its variability.
Electrocardiogram in rheumatic fever
The most characteristic feature in acute rheumatic fever is conduction disturbances most commonly in the form of 1st degree heart block (a prolonged PR interval) which occurs in 24 – 40%. Dr. Jones in 1944 recommended repeat tracings to demonstrate a variation in atrioventricular conduction which is more valuable. The PR interval usually returns to normal after the disease becomes inactive and it can occur with or without carditis. In acute rheumatic pericarditis, ST elevation or inversion is present.

annie · Credits: 642 My Scrapbook

hi guys
i think the ans is AR

cnn · Credits: 77713 My Scrapbook My Reading List 262569 Books

my ref---------------1)harrison as shown by Docsab(in acute cases-earliest)
2)an mcq book(with some mistakes) based on harrison gives this q & ans given there is alsoMI

manipalguy · Credits: 15905 My Scrapbook

hi pajit menon... its request.. instead of just copying the whole stuff from a cd rom just try to answer the questions in a brief form... and kindly just mention the book and page no. where u took this reference... this will be appreciated more !!! thanks

anuj · Credits: 4672 My Scrapbook

ya bit tough to read here na.... we aRE still use to read books ..not cds wiase bhia finally wht the nswer till date i belive it to be ar......

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