Various clinical symtpoms of rheumatic heart disease

The major clinical manifestations by which rheumatic fever can be recognized are polyarthritis, carditis, chorea, erythema marginatum, and subcutaneous nodules.


The classic attack of rheumatic fever appears as an acute migratory polyarthritis accompanied by sings and symptoms of an acute febrile illness.

The large joints of the extremities are most frequently affected, but no joint is impervious to the inflammatory process; one may find arthritis of the hands and feet but only rarely of the spine or of the sternoclavicular or temporomandibular joints, joint effusions occur but are not persistent.

As pain and swelling subside in one joint, others tend to become involved. Although such “migratory” involvement is characteristic, it is not invariable, and several large joint may be inflamed at one time.

To be acceptable as a criterion for the diagnosis of rheumatic fever, the polyarthritis should involve two or more joints, should be associated with at least two minor manifestations.

Such as fever and elevation of sedimentation rate, and should be associated with high titer of antistreptolysin O or some other streptococcal antibody.

There is nothing distinctive about the arthritis of rheumatic fever, and other causes of migratory polyarthritis that may be associated only coincidentally with high streptococcal antibody levels must, of course, be excluded.

Acute rheumatic carditis

Acute rheumatic carditis first becomes manifest by the appearance of the heart murmurs of either mitral or aortic regurgitation, the former most frequently.

Signs and symptoms of pericarditis and of congestive heart failure may supervene in more severe cases. Death may result from heart failure during the acute stage of the disease, or permanent valvular damage may be sustained which results ultimately in serious disability.

Carditis may vary from a fulminating, fatal course to a low-grade, in apparent inflammation. It is well to bear in mind that the vast majority of patients with carditis do not have symptoms referable to the heart.

The latter occur only in more severe cases when heart failure or pericardial effusions produce characteristic symptoms. For this reason, unless extra cardiac manifestations, such as polyarthritis and chorea, are present.

Patients whose rheumatic fever is manifested only by carditis are frequently not diagnosed and later life may be discovered to have rheumatic heart disease without a define history of rheumatic fever.

When carditis is manifest, there is usually tachycardia disproportionate to the degree of fever, gallop rhythms are often heard, and the heart sounds may become fetal in character due to the loss of the muscular quality of the first heart sound. Occasionally,arrhythmias and a pericardial friction rub may be present.

Prolongation of the conduction time may lead to dropped beats with varing degrees of heart block. Prolongation of the PR interval and other changes in the electrocardiogram are very common, but these findings, in the absence of clinical manifestations of carditis, have a benign prognosis.

Therefore, changes in the electrocardiogram alone, unassociated with significant murmurs or cardiac enlargement, do not by themselves constitute an acceptable criterion for the diagnosis of rheumatic carditis. Pericarditis may cause percordial pain, and a friction rub may be audible.

A definite clinical diagnosis of carditis can be made if one or more of the following can be demonstrated:

• The appearance of , or change in the character of organic heart murmurs,

• Definite increase in heart size demonstrated b radiogram or fluoroscopy

• Pericardial friction rub or effusion best demonstrated by echocardiography, or

• Signs of congestive heart failure. Rheumatic carditis is almost always associated with a significant murmur.

The most common murmurs of acute rheumatic carditis are those due to mitral and aortic regurgitation caused by valvular inflammation. The former is usually a high-pitched holosystolic bolwing murmur.

W which must be carefully distinguished from the functional low-pitched, musical, apical flow murmur commonly heard with increased cardiac output in children and other thin-chested individuals.

When more severe, mitral inflammation and left ventricular diatation may produce , in addition to a blowing systolic murmur, a very low pitched, vibratory middiastolic murmur which often follows an accentuated third heart sound-the so-called carey coombs murmur.

Aortic regurgitation murmurs are often associated with those of mitralorigin, and in acute rheumatic fever, occasionally cooing or screeching (“seagull”) murmurs are heard that reflect the turbulence formed around swollen and distorted valves during the acute inflammatory phase of carditis.

| Investigation procedures rheumatic heart disease | How Does Rheumatic Heart Disease Occur | How to Treat acute attack and importance of secondary prevention | Various pathogenesis of rheumatic heart disease |


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