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 auscultatory 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 2 nd 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.

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.