(b) PERICARDIAL ADHESION Etiology and Adhesion of the pericardium with the heart is more frequent in childhood than is generally supposed and is as a rule a condition resulting from plastic rheumatic pericarditis. Not rarely the pericardial adhesion develops slowly, wholly without symptoms, in older children with rheumatic polyarthritis; or it follows a valvular lesion of the heart without having previously caused the characteristic symptom-complex of pericarditis, and by its appearance makes compensation decidedly more difficult. In general the causes, of pericarclial adhesion are the same as those of pericarditis, rheumatism, chorea, scarlet fever and tuberculosis. It should be noted that symphy sis pericardii is found much more frequently at autopsy in childrem than is recent pericarditis itself. Very rarely does purulent pericarditis lead to adhesion of the layers of the pericardium.
So far as age is concerned, obliteration of the pericardium has been found by Nib-Lid and Hilter in newborn infants; by Bednar in a child of three months; Morel-Lavallee found it eighteen times in children out of 30 cases. Among 43 cases which came to autopsy Cerf found three in the first. decade of life and fifteen in the second decade.
Pathologic pericardial cavity is abolished and the heart is covered with a thick fibrous mass, which may reach 2 cm.
in thickness, even in small children. Just as in later life, so, too, in small children, adhesions of the outer surfaces of the pericardium may form with the sternum, ribs, lungs and diaphragm, results of an exter nal pericarditis, which is combined with internal pericarditis (medias tinopericarditis) as frequently as it occurs as an independent disease of the mediastinal cellular tissue. When the disease exists a long time, deposits of lime and of cartilage are found between the heart and neighboring organs in childhood. In fresher cases the intermediate layer joining the external and internal layers of the pericardium is still soft, fibrinous and easily separated. Tuberculous adhesions may be cartilaginous lumps or semifluid, salty or caseous masses of exudate.
In early childhood the heart is almost always decidedly hyper trophied with symphysis pericardii; when this has lasted some time, there is high-grade dilatation, frequently causing relative insufficiency of the arterial and venous valvular apparatus. Secondary fatty degen eration of the myocardium is rare in childhood. The functional dis turbance due to pericardial adhesion is very intense in children and is due to the arrest of growth of the child's heart primarily, depending upon obliteration of the pericardium.
Symptoms.—Taken altogether, two main groups of pericardial adhesions may be differentiated clinically: those which are associated with marked cardiac hypertrophy, usually of rheumatic origin; and those in which the heart only increases slightly in size, chiefly due to tuberculosis.
Whether the heart is hypertrophied or small, the most important physical signs are a systolic in-drawing of the chest wall over the entire precordial region and the absence of motility of the heart dulness with respiration and change of position. This systolic in-drawing of the thorax wall is of decided value if all the intercostal spaces entering into question are moved at the same time, especially if the region of the apex-beat and the base of the heart, as well as the xyphoid process, are all drawn in simultaneously with systole. This is observed with tuberculous obliteration chiefly, in which thick, lumpy adhesions be tween the pericardium and the chest wall occur. Under these condi tions Rantgen photographs rnay help in making the diagnosis, in which the immobility of the heart and the extrapericardial bands and adhesions can sometimes be recognized (see Fig. HS', Hochsinger's case).
A certain intensity of the cardiac power and the presence of adhe sions between the outer layer of the pericardium and its surroundings (chest wall, diaphragm, mecliastinura) are necessary for the appearance of this systolic in-drawing. The tuberculous forms show this condition more frequently than obliteration of the pericardium due to other causes.
Auscultation of the heart gives but few certain signs in support of the diagnosis. Weill observed fcetal rhythm of the heart sounds many times. Redupl:cation and splitting of the heart sounds, disappearance of the diastolic sound and a metallic character of the first sound have also been observed in pericardial adhesion in childhood. The last-men tioned symptom depends upon adhesion of the apex of the heart with the diaphragm and modification of the first heart sound from the vibra tion of air in the gastric cavity. With ineoniplete adhesion a pericardial friction murmur may also be heard, hes:des. As a result of dilatation insufficiency of the mitral and aortic valves, systolie anci diastolic mur murs may appear (Schoneich), which are of no decided value in diag nosis since they may be caused by the valvular lesions of endocarditis existing at the same time.