Proceedings Fourth Annual Meeting of the American Academy of Pediatrics

American Academy of Pediatrics Proceedings FOURTH

ANNUAL

MEETING OF

OF

THE

AMERICAN

ACADEMY

PEDIATRICS

J U N E 11 AND 12, 1934

R o u n d Table Conference on Heart Disease Leader:

Dr. Hugh

MeCulloeh,

St. L o u i s .

Assistant:

Dr. Stanley

Gibson, Chicago. The Round Table discussion on Heart Disease, held in Room 940, Wade Park Manor Hotel, Cleveland, Ohio, convened at 9:30 A.~., June 12, Dr. Hugh MeCulloch, presiding. CHAIRMAN M c C U L L O C t t . - - I t was decided to take up the subject at this meeting from the standpoint of symptoms and physical signs and treatment of heart conditions, in order to make it a part of the two conferences preceding this one. At the first conference, conducted by Dr. Morse two years ago, the general subject of rheumatic fever, its relation to heart disease, and some of the forms of heart disease common in that condition were diseussecL Last year, rheumatic fever was taken up without much consideration of heart disease. In order to round out the subject a little more fully, this conference will deal with symptoms, physical signs, and treatment of congenital heart disease and rheumatic, or infectious, heart disease. Dr. Gibson and I will discuss these two subjects separately and when we are finished, a general discussion will be in order. DR. S T A N L E Y G I B S O N . - - I t requires considerable courage to undertake a discussion of congenital heart disease, inasmuch as it is a more or less obscure condition. I t has been obscure partly at least because there has not been as much work done on congenital heart disease as on other forms of heart disease. There are a number of reasons for this neglect. First, the adult cardiologist sees a relatively small number of cases of congenital hear~ disease, as the majority do not survive to the age where they come under his observation. Second, the pediatrician rarely is primarily, or often even secondarily, a cardiologist, and hence he is not likely to make an intensive study of these cases. Another reason why congenital heart disease has been more or less neglected is because treatment i s unsatisfactory. Conditions with more therapeutic promise are naturally of more interest to the clinician. In regard to the etiology of congenital heart disease, it is fairly well agreed that the chief cause is developmental. The cause of the error in development is unknown. One f a c t stands out clearly, however, and t h a t is, the cause of the malformation in 545

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congenital heart disease is the same as other congenital malformations.

From 15 Sometimes these defects, such as harelip, cleft palate, or deformity of the ears, are obvious- on physical examination; in other instances the malformations involving internal organs are revealed only at autopsy. A much less frequent and less important cause is fetal disease. Rheumatic infection occurring during pregnancy may be transmitted to the baby, though this occurrence i s extremely rare. Myocardial disease is another cause of maldevelopment, and syphilis has been considered the most important factor in this group. Certainly~ from the clinical standpoint there is no unusual association between congenital syphilis and congenkal heart disease. The symptomatology of congenital heart disease is extremely variable. We see unmistakable signs of the condition in many children who are normally developed, have a good color, and are able to play as actively as other children. On the other hand, some of these children are poorly developed, blue, breathless, and able to lead only the quietest sort of life. To account for this great variation in the clinical picture) one must have a knowledge of the nature of the defects in congenital heart disease, and the alteration in blood flow resulting from their presence. There are three defects far more common than any others. I n 1Vlunde A b b o t t ' s series of 1,000 cases, she found open foramen ovale in 290 case% e i t h e r alone or in conjunction with other defects. Next most frequent was interventricular septal defect, occurring 257 times. Open ductus arteriosus was third with 242 cases. The above defects allow a communication between the two sides of the heart or the great vessels, thai is, b e t w e e n the arterial and venous circulation. I t is generally agreed that the pressure on the left side of the heart is higher than on the right side; hence, if any one of the above lesions exists in pure form, blood is shunted from the left %0 the right side of the heart;. There is, therefore, no failure of aeration of the blood, in fact, ~ portion of the arterial blood is again returned to the lungs. If, however, something occurring in the pulmonary circuit, pneumonia for example, causes the pressure on the right side of the heart to be raised above that on the left, a reversal of flow results, and venous blood is shunted into the arterial stream. I t is this mixture of venous with arterial blood which is chiefly responsible for the presence of cyanosis in congenital heart d~sease. Although open foremen ovale is the most frequent congenital lesion, it is not the most important clinically. I n fact, if the opening is small, it is unrecognizable clinically~ imposes no appreciable handicap, and is compatlb]e with the usual span of llfe; even when the opening is large, recognition of the condition is difficult as there are usually no symptoms. Sir Thomas Lewis says be knows no direct physical signs by which it may be recognized. Mande Abbott, however, feels that in a child of slender build, who is pale, and in whom one hears a late diastolic or early systolic murmur localized at the third or fourth left interspace, the presence of defect in the auricular septum should be suspected. I n defect of the mterventricular septum, the diagnosis may be made with a good degree of accuracy. The murmur is characteristic: i t is harsh in quality, systolic in time, reaches the maximum in the third and fourth interspaces at the left sternal margin, and usually widely transmitted in all directions. A thrill is often present; the heart is usually little or not at all e n l a r g e d ; there is no cyanosls, and the child is usually able to exercise fairly freely. Open duetus arteriosus affords the most spectacular findings and is in typical cases the easiest of all congenital lesions to diagnose. I t is characterized by a most extraordinary murmur. This murmur is usually continuous, very harsh in character, %o 20 per cent of congenital cardiac patients show other congenital defects.

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and variously described as humming top, machinery, or rolling thunder in type; it ~s maximal in the first and second teft interspaees and is widely transmitted. In addition to the characteristic murmur, x-ray examination may reveal widening of the cardiac shadow in the second and third left interspaces, due to dilatation of the pulmonary artery which is present in these cases. As already emphasized, the lesions described ahoy% when existing in pure form, result in a shunting of blood from the arterial to the venous circulation, and hence do not produce eyanosis. Very often~ however~ these lesions are complicated by some other anomaly , particularly of the right side of ~he heart, which causes the pressure in the pulmonary circuit to be constantly higher than t h a t on the left side. Under such circumstances venous blood from the right side of the heart mingles with the arterial blood, and i f this admixture is large in amount, cyanosis results. I n the group of cases in which eyanosis is present, diagnosis is difficult because in the great majority of cases a combination of lesions r a t h e r than a single lesion is present. The younger the child, the more difficult the diagnosis because a great variety of lesions may produce cyanosis~ I t is a well-known fact, however, that not many of the. combinations of lesions producing eyanosis in early life allow of long survival. One combination which does permit a longer span of life is known as the tetralogy of :Fallot. It consists of pulmonary stenosis, defect in the interventrieular septum, dexter position of the aorta so that the aorta overrides the defect in the septum, and hypertrophy of the right ventricle. I f then one encounters a child from six to ten years of age who presents the typical picture of breathlessness, cyanosis, and clubbing of the fingers with physical signs of congenital heart disease, the condition most likely present is the tetralogy of Fallot. The physical signs are not in themselves conclusive. A s~stolic murmur is present over the preeordium, due perhaps partly to the defect in the interventrieuIar septum and partly to the pulmonary stenosis. The most characteristic finding is the x-ray silhouette of the heart. I t has been described as the Coe~'-e~-~abo.t, or wooden-shoe-shaped type of heart, in which there i s a broadening of the cardiac shadow, with a very blunt apex. This change of shape is due chiefly to hypertrophy of the right ventriel% whictl tends to envelop the smaller ]eft ventricle. Transposition of the great vessels and complete absence of the cardiac septa are interesting conditions in that, while they produce a high degree of eyanosis and have a very serious prognosis~ murmurs over the heart may be altogether lacking. These cases of arterial-venous and venous-arterial shunt comprise the greater proportion of cases of congenital heart disease. There is, howcver~ a third group in which no slmnt exists~ but in which some anomaly of the heart or vessels may be present which results in more or less cardiac strain. From the clinical standpoint the most important condition in this group is coarctation Of the aorta. Coarctatiou of the aorta may be either of the infantile or adult type. I n the infantile type there is a diffuse narrowing of the isthmus of the aorta, and there are usually other associated anomalies in the heart which render the condition incompatible with long life. Hence this condition, rarely encountered except in infancy, cannot be diagnosed during llfe. The adult type of coaretation occurs more often, i s compatible with an active life, and can be diagnosed i f one is on the alert for it. IX consists of a sudden narrowing of the aorta in" the region of the duetus arteriosus, muet~ as i f a Iigature had been tied tightly aronnd it. Because of this constriction, the blood pressure in the upper extremities is elevated, often to 200 or more. The increased pressure may cause headache, dizziness, ringing in the cars, or nosebleed.

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T h e circulation b e y o n d t h e p o i n t of c o a r c t a t i o n m u s t be carried on chiefly t h r o u g h t h e d e v e l o p m e n t of a collateral circulation. H e n c e t h e r e is decreased or a b s e n t p u l s a t l o a in t h e f e m o r a l a n d dorsalis p e d i s a r t e r i e s ; t h e blood p r e s s u r e in the legs is low or c a n n o t b e m e a s u r e d at all. I n a s m u c h as t h e i n t e r c o s t a l a r t e r i e s m u s t a i d in c a r r y i n g t h e collateral circulation, t h e y a r e f r e q u e n t l y so l a r g e t h a t t h e i r t h r o b b i n g can be felt, especially in t h e i n t e r s c a p u l a r r e g i o n a n d i n t h e axillae. T h e s e e n l a r g e d arteries f r e q u e n t l y p r o d u c e e r o s i o n s of t h e ribs w h i c h are d e m o n s t r a b l e on x - r a y e x a m i n a t i o n and, w h e n p r e s e n t , serve to clinch t h e d i a g n o s i s in d o u b t f u l cases. E x a m i n a t i o n of t h e h e a r t itself m a y show somc e n l a r g e m e n t , a n d a systolic murm u r over t h e p r e c o r d i u m w i t h t r a n s m i s s i o u t o w a r d t h e neck is u s u a l l y present. 9C o a r c t a t i o n of t h e a o r t a is i n t h e m a j o r i t y of i n s t a n c e s overlooked d u r i n g life. T h e n u m b e r of r e p o r t e d cases a t a u t o p s y , however~ i n d i c a t e s t h a t it is n o t a rare condition. I f in children with h i g h blood p r e s s u r e t h e c o n d i t i o n of t h e circulation in t h e lower e x t r e m i t i e s were i n v e s t i g a t e d , no d o u b t a good m a n y cases would be discovered. I h a v e seen two children w i t h t h i s condition. O n e child h a d h a d a h e m i p l e g i c a t t a c k , a n d t h e blood p r e s s u r e i n t h e course of a r o u t i n e e x a m i n a t i o n w a s f o u n d to be 200. T h e f e m o r a l p r e s s u r e w a s u n o b t a i n a b l e . X - r a y p i c t u r e s revealed scalloping of t h e ribs. The second child h a d developed n e p h r i t i s i n the course of scarlet fever. Blood p r e s s u r e was 180 a n d p e r s i s t e d as t h e n e p h r i t i s improved. T h e r e w a s a loud systolic m u r m u r over t h e p r e c o r d i u m . I n t h i s case also t h e f e m o r a l p r e s s u r e w a s u n o b t a i n a b l e , a n d x - r a y e x a m i n a t i o n showed erosion of t h e ribs. T h e p r o g n o s i s in c o n g e n i t a l h e a r t disease m u s t be d e t e r m i n e d by a v a r i e t y of f a c t o r s . I n t h e i n f a n t s who a r e cyanotic f r o m b i r t h , t h e outlook is u s u a l l y grave. I n t h o s e i n f a n t s who ha~e cyanotic spells or who become p e r s i s t e n t l y cyanotic in t h e first f e w years, t h e r e is u s u a l l y a sufficient h a n d i c a p to t h e circulation to m a k e t h e outlook bad. On t h e other h a n d , t h e r e are m a n y children w i t h u n q u e s t i o n e d s i g n s of c o n g e n i t a l h e a r t disease who h a v e good color, develop n o r m a l l y , a n d are a b l e to exercise freely. So f a r as t h e h a n d i c a p to t h e c i r c u l a t i o n is concerned, these children could c a r r y on indefinltely. T h e r e is a n o t h e r h a z a r d , however, w i t h w h i c h all children w i t h c o n g e n i t a l cardiac a n o m a l i e s m u s t cope, a n d t h a t is a c o m p l i c a t i n g i n f e c t i o n . P n e u m o n i a , tuberculosis, or especially s u b a c u t e b a c t e r i a l e n d o e a r d i t i s m a y c a u s e death. S t a t i s t i c s reveal the s u r p r i s i n g f a c t t h a t a l m o s t 20 p e r cent of p a t i e n t s w i t h c o n g e n i t a l h e a r t d e f e c t s s u c c u m b to b a c t e r i a l endocarditis. We, as p e d i a t r i c i a n s , are a p t to f o r g e t t h i s f a c t , b e c a u s e m a n y do n o t develop b a c t e r i a l e n d o c a r d i t i s u n t i l t h e y are b e y o n d t h e pediatri~ age. L a r g e l y because of the likelihood of complications, t h e p r o g n o s i s m u s t be g u a r d e d even i n t h e a p p a r e n t l y mild cases. I s h o u l d like to quote f r o m M a u d e A b b o t t ' s s t a t i s t i c s to b r i n g to m i n d t h e s e r i o u s n e s s of c o n g e n i t a l h e a r t disease. I n 40 cases i n which p a t e n t f o r a m e n evale w a s t h e p r i m a r y lesion, t h e a v e r a g e a g e at d e a t h w a s t w e n t y - n i n e y e a r s ; i n u n c o m p l i c a t e d open d u c t u s arterlosus, t w e n t y - f o u r y e a r s ; a n d in i n t e r v e n t r i c u l a r septal defect, f o u r t e e n a n d o n e - h a l f years. Y e t t h e above lesions a r e r e g a r d e d as a m o n g t h e m i l d e s t c o n g e n i t a l cardiac anomalies. I n t h e t e t r a l o g y of F a l l o t t h e a v e r a g e d u r a t i o n o f life w a s a b o u t twelve years~ a n d in e o a r c t a t i o n of t h e a o r t a t h e a v e r a g e w a s t h i r t y - t h r e e years. L i t t l e need be said r e g a r d i n g t r e a t m e n t . Since we d o n o t know t h e cause of t h e condition, we c a n n o t p r e v e n t it. W e c a n n o t b y s u r g i c a l m e t h o d s correct t h e a n o m alous c o n d i t i o n ; therefore, t h e t r e a t m e n t is chiefly supportive. One should s t r e s s t h e i m p o r t a n c e of k e e p i n g these c h i l d r e n free, so f a r as possible, f r o m u p p e r r e s p i r a t o r y

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infections or contagious disease, as they do not stand infection well. Moreover, the danger of bacterial endocarditis is always to be kept in mind, and it is more likely to occur if they contract an infection which lowers their resistance. Where a choice is possible, a warm, sunny, equable climate is desirable. So far as the child's activities are concerned, it is my experience that there is much less .difficulty in controlling the child with the congenital than the one with the acquired cardiac disease. The child with congenital heart disease has grown up with his handicap; since he has learned from the age of beginning to walk that i f he tries to do too much, he becomes fatigued; from infancy he has been accustomed to a quiet life. The rheumatic child has known what it is to romp and play and take part in games, and he does not so readily adapt himself t o a more quiet existence. In closing I should like also to mention tile importance of proper mental hygiene. The cardiac child should be taught to make the necessary adjustments to enable him to lead a life that is happy and useful. CHAIRMAN McCULLOCH.--~t is very fortunate that we have been able to h e a r this presentation of congenital heart disease because it is not often discussed other than by ease reports. From a pediatric standpoint, congenital heart disease is extremely important, and all of us see many children who require expert or adequate opinion as to their management. They form a fairly large percentage of a pediatric cardiac practice. There are two other types of heart disease that do not concern us as pediatricians in any great degree. One is syphilitic heart disease and the other, degenerative heart disease associated with recessive growth of body tissue. The fourth major type of heart disease is due to rheumatism and might be considered as infectious heart disease. I t has always seemed wise to me to describe infectious heart disease as C,rheumatic heart d i s e a s e " because by far the largest number of cardiac children have rheumatism in some f o r m or other. According to a strict terminology, infectious heart disease would probably be more correct because in that way one could include the few cases not of a rheumatic nature but due to various sflbacute bacterial infections, such as StreFtoooocazs viridans, pneumococcus, meningococcus, and gonococcus, and the occasional organism present in a newborn child or during infancy which produces heart disease as a part of a generalized infection. Even those cases of cardltis occurring in early infancy in which rheumatic fever is either obscure or entirely absent should be included as rheumatic in nature because at autopsy one can show the process in the valves and in the muscles to be identical with rheumatic heart disease that is easily recognized in later life. Therefore, as I present the subject this morning, I have in mind the picture of rheumatism and rheumatic heart disease. Changes in the heart and other parts of the body in rheumatic heart disease consist of two different processes: ~irst, the exudutive manifestas of rheumatic fever, characterized by changes in the wandering or labile elements of the body t i s s u e - - f o r instance, edema, vascular injury, capillary dilatation, the laying down of fibrin, the infiltration of polynuelear leucocytes, local heat and so forth. Second, the proliferative manifestations, characterized by changes in the fixed tissue elements of the body, such us overgrowth of epithelioid cells, infiltration of the plasma and round cells, and the formation of scar tissue. I n the heart the first process manifests itself by first a myodardial injury consisting of edema, cloudy swelling, f a t t y infiltration, leucocyte infiltration and in severe cases, a certain degree of necrosis of the cardiac muscle cells; and, second, a valvulitis characterized by the same changes that occur in the acutely inflamed

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joint--edema, capillary injury, and cellular infiltration of the valve~ resulting in thickening an([ loss of elasticity; and third, a n acute or subaeute serofibrinous periearditis. I n the second process there is an acute, subacute, or chronic change producing, first, myocarditis with Aschoff's nodules comparable to the rheumatic nodules found elsewhere in the body, a myocarditis existing over a longer period of time and resulting in a chronic fibrosing interstitial lesion; second, chronic fibrotic scars in the valves preceded by, o1' associated with, rheumatic verruca on the valves; and third, an obliterating pericardltis. I t is easy to describe these two processes theoretically as being separate and distinct. We know, however, that many times these two processes are present in the same child, and each of them may be recognized. I am going to describe the individual lesions in rheumatic heart disease in as controversial a manner as possible with the idea. of provoking discussion later on. Pericarditis may be extensiv% with the whole pericardium involved, or localized in patches, and it is rarely suppurative in younger children. The fluid in acute serefibrinous pericarditis rarely persists; while the clinical picture may be extremely serious and it is common to find the hospital internes despairing of the p a t i e n t ' s life, the condition is rarely fatal undm" proper care. The clinical picture of acute serofibrinous pericarditis bears a very strong resemblance to that of acute lobar pneumenia, and many times in the early stages it is diagnosed as acute lobar pneumonia. The course of the attack also resembles in many varied details an acute lebar pneumonia. I t is worthy of note, too~ that in many instances the lesion in the pericardium improves as satisfactorily and as completely as the infiltration in the lung in pneumonia. Acute serofibrinous periearditis should be suspected whenever there are spells of fever occurring in a rheumatic child witheut other obvious causes, especially if there is no "acute infection in the nose and throat. At times attacks of fever may occur in the rheumatic child without pericarditis, but this condition should always be suspected whenever the temperature rises. When the rheumatic child complains of pain in the chest during a period of fever, serofibrineus pericarditls should be suspected. Usually the friction rub can be heard, but in some instances the lesion may be in some p a r t of the pericardium where the friction rub is not audible. The diagnosis ef chronic adhesive pericarditis is rarely made during life because these children have very few symptoms and the physical signs are not recognized or may be absent. I t should be suspected in those children who have chronic heart disease with markefl precordial deformity and pulsation, especially when there is congestive failure out of proportion to the degree of injury to the myocardium and when all of the usual remedies for the relief of congestive failure fail. Young children with thin, elastic chest walls do not show the same fixation of the heart that older children and adults de. I t has also been our observation that Broadbent's sign is not a very satisfactory physical sign for the detection ef chronic adhesive pericarditis because the chest wall and mediastinal tissues are so very elastic that the tug of the heartbeat is net against a semirigid or fixed structure and also because the lesion is rarely confined to the diaphragm. :Pericarditis of one form or another occurs mere frequently than is usually recognized in children with rheumatic fever. The acute forms are associated with fever, pain in the chest, cough, and prostration. The principal physical sign is a perieardial friction rub somethnes not heard for several days after the onset of fever; it may be present only for a day or so because the fluid accumulates rapidly and tends to separate the layers of the pericardimn causing the disappearance of the

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rub. The friction rub is best and most often heard close to the sternal border as a hlgh-pitched, superficial to-and-fro scratching sound; occasionally, it may be felt rather faintly in this same area. Myoearditis in rheumatic fever is by f a r the most important lesion i n the heart, and I would like t o place particular emphasis on it in this discussion. I t is roost important because it occurs to some degree in every child with rheumatic heart disease and in every attack~ whether of the cyclic exudative or of the continuous proliferative type of rheumatic fever, and becanse the alternate function of the heart and circulation depends largely on the nature and severity of this lesion. The principal result of myocarditis is an enlargement of the heart from thickening of the walls, with or without hypertrophy of the cells and weakening of the muscle tone, resulting in dilatation of the chambers with increasing failure. The enlargement of the heart may be very slight and in most cardiac children amounts to no more than 1 or 2 centlmeters' increase in size above the normal as measured on the chest wall or by x-ray cardiac silhouette) but the determination of any degree of enlargement is of greatest significance and importance. The absence of e~rdiac enlargement renders of little value all other physical signs, including the famous systolic apieM murmur. Cardiac enlargement and myocardltis are associated with two other important physical signs, taehycardia and increased force of cardiac contraction revealed by palpating the cardiac impulse on the chest wall when the child is at rest or lying supine. The increased force of the cardiac impulse may be localized to the apex area but is usually widespread over the whole precordium. In severe forms of myocurditis the great loss of muscle tone and filling of. the chambers result in a high systemic and pulmonary venous pressure and greater or less degree of congestive failure in one or both circulatory systems. Occasionally disturbaaees of mechanism may occur as a result of myocardial changes when they are present, and they m a y be accepted as evidence of myoearditis. The common disturbauces are: auricular fibrillation, a~ricnlar arLd ventricular extrasystoles (premature contractions) and heart-block. These lesions occur very infrequently, however, in childrem It may be posslble to determine some degree of delay in cardiac aurieuloventrieular conduction in severe cases, but in the usual cardiac child there is no delay and no disturbances of mechanism. An important symptom of acute myoearditis is vomiting. I would like to emphasize this symptom. I t occurs frequently during an acute toxic myocarditis from diphtheria, scarlet fever, as well as during the. attacks of an acute myoearditis from rheumatic level'. u is important because it is the result of the myoearditis and is not due to indigestion, distention, or overdosing with various drugs which are supposed t o irritate the gastric mucous membrane, notably digitalis. I t is the common reason for discontinuing digitalis in the treatment of a cardiac child, whereas many times the vomiting is due to acute myocarditis present as a part of the rheumatic fever. It is vitally important to the patient, as far as his immediate care and ultimate prognosis are concerned, to know how well the heart can function under the existing circumstances; that is, whether the heart can mechanicaIly force the blood through the peripheral circulation to meet the degree of activity required of the patient. In children there is rarely any factor to interfere with this circulation through the peripheral vessels except the efficiency of the pump itself and the condition of the myocardium. In the presence of signs of congestive failure, the child's activity nmst be reduced to a point where the signs and symptoms of cardiac distress dis'~ppear, either by providing physical and mental res~ or by the use and Md of various drugs. I t should be pointed out that congestive cardiac failure occurs in children as a

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late event in the course o2 rheumatic heart disease, in either the acute or chronic form of the disease, and that when it occurs, either very extensive or severe injuries in the myocardium have also occurred. The early signs of congestive failure, such as breathlessness, edema, and venous filling, therefore, do not occur so frequently in children and then only late in the course of heart disease. The degree of breathlessness, edema, and venous filling may be noted~ but it is more important to know the amount of effort required to produce these conditions. Breathlessness may be recognized either as a subjective symptom or by measuring the vital capacity of the respiration. Edema may be estimated by noting the location and degree of pitting in the superficial dependent parts of the body. Venous filling may be measured by noting the level of inclination of the body required to fill the neck veins; by measuring the venous pressure in the peripheral veins, especially those of the forearm by means of the Moritz cannula or one of its modifications; or by an air tambour and by noting the level at which the veins empty, fill, and pulsate in relation to the level of the right auricle. Myoearditis in young cMldren with rheumatic heart disease usually involves all parts of the myocardinm~ both auricles and ventricles, and the right and left sides of the hea~'t, i%r t h i s reason, signs of distress from the right side of the heart, which account for the increased force of the cardiac impulse on the chest wall, are present in an unusual degree as a result of the myocarditis. There is a high incidence of mitral stenosis in rheumatic heart disease in early life so that the additional strain on the right side of the heart because of increased pulmonary pressure present in mitral stenosis increases the frequency of peripheral venous congestion in children. The arrest of the inflammatory process in the myocardinm determines the future of the p a t i e n t ' s welfare and if the attacks of rheumatic infection subside and further injury ceases; if the present injury is repaired without the formation of too much scar tissue; and if too much cardiac muscle tissue is not destroyed over a period of time, recovery takes place, cardiac function is restored to normal or nearly normal limits, and the ehild~ as the saying goes~ outgrows the heart trouble. I t is important to emphasize, therefore, the p a r t the myocardial lesion plays in rheumatic heart disease. To summarize this rather briefly, in cardiac children the usual signs of myocardltis anil activity of cardiac muscle infection are three: first, tachycardia; second~ enlargement os the heart; and third, increased force of the cardiac impu]se on the chest wall. The later signs of myocarditis and loss of cardiac muscle tone are those associated with congestive failure: breathlessness, edema, and increased venous-filling. Endocardltis is purposely brought up for discussion last because there is so little opportunity for controversial discussion on this point. ]~ndocardltis occurs either on the valve cusps or on the mural endocardium most frequently Of the left auricle, rarely in the right ventricle or the r i g h t auricle. The mitral valve is most frequently involved; next in order are the aortic, the tricuspid, and the pulmonary valves. The pulmonary valve is most freqnent]y involved in the unusual forms of subacute bacterial endocarditis due to such organisms as staphylococci, menlngococci, and pneumoeocci. The endocarditis due to StreTtovo.oc~s v i v i d a ~ usually occurs on the seat of an old rheumatic or a congenital malformation~ and, therefore~ the mitral valve is more frequently involved. The lesion in these various valves should be termed '~valvulitis ~' rather than C~endocardltis,,, both to distinguish it from the mural endocarditis and because the lesion i a the valve is not confined to the endocardinm alone but really involves the

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structures underneath the endocardium as well as the endothelial layer itself. The lesion in the mltral valve may or may not be associated with stenosis and this important condition should be indicated. I n either the exudative or the proliferative type of rheumatic process, there is thickening, increased vascularization, and cellular infiltration in whatever valve is involved. I n the proliferative lesion there are verrucae along the line of closure which resemble in every respect rheumatic nodules. During life it is not possible always to differentiate the type of lesion occurring in the valve because the physical signs are the same in each instance. Those physical signs usually are a systolic murmur heard near the apex of the heart and occasionally along the sternal border toward the base. There is also some change in the quality of the first sound at the apex, principally a lengthening of t h e sound together with stone lowering of its pitch. I t is usually louder tharL normal. In more advanced eases of mitral valvulitis, a presystolie .thrill can be felt a t the apex. The apex impulse is very forceful and can be described as thrusting. The difficulty in diagnosing these valvular lesions during life is in differentiating those with true structural stenosis of the valve from those with a functional but transient stenosis. At autopsy I have noted t h a t those valves with changes corresponding to the exudative lesions in the rest of the body are thickened and inelastic and must~ to some extent, interfere with the column of blood as it passes through the valve orifice. Such patients during life give the same physical signs as occur in individuals with actual anatomic narrowing of the valve leaflet due to fibrous tissue infiltration of the proliferative type. I n the first instance, however, the lesion is a transient one which may and o f t e n does disappear, whereas, the latter type~ the changes being permanent and due to the formation of scar tissue, is o f t e n progressive. Aortic valvulitis is common, occurring in a very h r g e proportion of rheumatic children with o r g a n i c heart disease. This lesion is very frequently overlooked because its physical signs are inconspicuous compared with those associated with mitral stenosis. Since a patient with mitral stenosis~ i f he has congestive failure, will also have murmurs along the sternal border resembling aortic insuffieiency, the presence of the latter lesion is often overlooked. Aortic insufficiency can be recognized more easily by studying the conditions in the peripheral circulation than from any direct examination of the heart. The high pulse pressure, the low diastolic pressure, and the pulse changes in the peripheral vessels indicate when this lesion is present. Another important point is that the diastolic murmur in aortic insufficiency may be absent or very f a i n t during the first few days after admission to the hospital, when the patient has a f a s t rate and is decompensated. AS the patien~ improves, the diastolic murmur appears along the sternal border. The other valve lesions have no common interest since they are rarely seen in ordinary cardiac practice. The various measures for the treatment of cardiac children could be divided into three major groups: first, measures directed toward controlling the recurring infection; second, those directed toward improving the general nutrition and hygiene, both mental and physical; and third, those directed toward the care of the heart itself. Measures directed toward controlling recurring infection are the same as those used in any group of children that we, as pediatricians, are working with and for. The question to be settled in nearly every instance, is whether or not the tonsils should be removed. 3/lost of us are agreed t h a t tonsils should be removed in those children who have a history of attacks of tonsillitis or who show physical signs of active or recurring tonsillitis. The .commonest and most hnportant probIem, however, is that most children, even after satisfactory tonsilleetomyi continue to have many recurring and severe respiratory infections. With the tonsil question settled, either by their removal or by being allowed to remain, the care of that child has

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j u s t b e g u n b e c a u s e so o f t e n t h e r e is extensive i n f e c t i o n elsewhere i n the nose a n d t h r o a t ; u n l e s s t h i s is cared f o r a n d controlled, no benefit will regult f r o m tonsilleetomy. R h e m n a t i e children a r e o f t e n in c o n t a c t w i t h n l e m b e r s of t h e f a m i l y a n d other i n d i v i d u a l s who h a v e a c u t e i n f e c t i o n s or who are carrier% a n d it is m o s t i m p o r t a n t to b r e a k off t h e s e c o n t a c t s as m u c h as possible. tYieasures f o r i m p r o v i n g t h e g e n e r a l n u t r i t i o n a r e also v e r y i m p o r t a n t . P r o p e r b a l a n c e of f o o d elements a n d the p r o v i s i o n of v i t a m i n s r e l a t e d to n u t r i t i o n a n d =res i s t a n c e to i n f e c t i o n p l a y a n i m p o r t a n t r6Ie in t h e recovery of cardiac children. B e s i d e s food, such f a c t o r s as s u n l i g h t , outdoor a c t i v i t y , t h e c h i l d ' s daily routine, t h e a m o u n t of v e n t i l a t i o n in t h e sleeping room, w h a t he does in school, t h e c o n t a c t s he m a k e s w i t h friends, a n d t h e a m o u n t of noise a n d m e n t a l c o n f u s i o n should be inv e s t i g a t e d a n d controlled for these children. T h e s e t h i n g s are p a r t i c u l a r l y import a n t f o r t h o s e children who p r o b a b l y will live u n d e r t h e h a n d i c a p of a p h y s i c a l restriction. T h e detailed r e g u l a t i o n of t h e d a i l y r o u t i n e in t h e s e children should be p l a n n e d a n d enforced. M a n y cardiac children a r e b e i n g t r a n s p o r t e d to w a r m e r climates, a p p a r e n t l y w i t h g r e a t success in t h e control of t h e i r r h e u m a t i c fever. T h e r e is only a little to be said a b o u t m e a s u r e s t o w a r d t h e control of the disease in t h e h e a r t itself, a n d t h e r e is very little t h a t c a n be done. Salicylates are of no benefit i n h e a r t disease except in so f a r as t h e y relieve t h e s y m p t o m s of a c u t e r h e u m a t i c fever. I n order to control t h e s y m p t o m s i n d i c a t i n g a m y o c a r d i a l lesion such as t a c h y e a r d i a , cardiac en]argement~ a n d t h e i n c r e a s e d force of t h e b e a t on t h e chest wall, t h e s e children should be p u t at r e s t u n t i l t h e i r b a s a l cardiac r a t e is slow; w e h a v e a r b i t r a r i l y chosen 100 p u l s e b e a t s p e r m i n u t e as t h e u p p e r l i m i t which t h e y m u s t n o t exceed. T h e p u l s e r a t e should r e t u r n r a t h e r p r o m p t l y to this r e s t i n g level following exercise. P a t i e n t s should be k e p t at r e s t u n t i l t h e c a r d i a c size is d e c r e a s i n g , or h a s r e a c h e d n o r m a l limits, or is s t a t i o n a r y . Sa long as t h e h e a r t c h a n g e s or seems to b e i n c r e a s i n g i n size, one n m s t a s s u m e t h a t t h e r e is a n active m y o c a r d i a l lesion a n d absolute rest should b e continued. The cardiac impulse should be quiet p a r t i c u l a r l y w h e n t h e p a t i e n t s a r e at rest. D u r i n g periods of congestive failure, absolute rest is a l w a y s indicated, a n d ~t is at this t i m e t h a t v a r i o u s d r u g s m a y be of help. Such d r u g s as digitalis, those b e l o n g i n g to t h e x a n t h i n e group, of which t h e r e are a considerable n u m b e r , metrazol~ a n d m a n y o t h e r p r e p a r a t i o n s c a n be used f o r t h e relief of edema, venous filling, a n d r e s t o r a t i o n of c a r d i a c muscle function. M a n y other details in t h e t r e a t m e n t of congestive f a l ] u r e v a r y with t h e individual p h y s i c i a n , a n d h e learns which ones are b e s t s u i t e d f o r t h e p a r t i c u l a r case. I a m p a r t i c u l a r l y a n x i o u s to e m p h a s i z e one p r i n c i p l e in m a n a g i n g cardiac cases. W e s h o u l d cease t r y i n g to r e s t r i c t cardiac children as m u c h as possible, b u t i n s t e a d we should t r y to keep t h e i r a c t i v i t y u p t o . a s h i g h a level as is c o n s i s t e n t w i t h adeq u a t e p r o t e c t i o n o f t h e i r cardiac f u n c t i o n . T h e m i s t a k e is so o f t e n m a d e of p u t t i n g a child to bed, k e e p i n g h i m quiet, a n d p l a c i n g too m u c h e m p h a s i s on t h e presence of a systolic m u r m u r a t t h e a p e x i n s t e a d of b r i n g i n g h i m u p as close as possible to his cardiac f u n c t i o n b y t r y i n g to b u i l d h i m up a n d a d j u s t i n g h i m to a n o r m a l w a y of living. DISCUSSION DR. W I L L I A M B. M c I L W A I N E (PET'ER.SBURG, W A . ) . - - I s there a n y definite p r o o f t h a t s t r e p t o c o c c u s i n f e c t i o n causes r h e u m a t i s m ? W o u l d it be possible to find a locality where streptococcus i n f e c t i o n s do n o t exist a n d see w h e t h e r or n o t children there h a v e r h e u m a t i s m ? Could t h e s e a t t a c k s of r h e u m a t i c f e v e r b e due to a l l e r g y ? Is a l l e r g y in connection w i t h r h e u m a t i s m b e i n g s t u d i e d ?

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I have ~ little g i r l with i n f e c t i o n in t h e p o s t n a s a l s p a c e who, a f t e r e a t i n g crabs, h a d a n a c u t e a t t a c k of r h e u m a t i s m w i t h swelling in h e r ankles~ knees, ~md w r i s t joints. T h e d i a g n o s i s of a c u t e r h e u m a t i c f e v e r was m a d e b y a cardiologist. A f t e r w a r d she w a s p r o v e d t o be allergic. Could a definite d i a g n o s i s be m a d e b e t w e e n f u n c t i o n a l a n d o r g a n i c cardiac murm u r s ? I t h i n k i f we can l e a r n at this m e e t i n g how to d e t e r m i n e w h e t h e r a d i s t i n c t systolic m u r m u r in five- or six-year children is f u n c t i o n a l or w h e t h e r it is organi% this g r o u p would have achieved s o m e t h i n g o u t s t a n d i n g . DR. H E R M A N S C H W A R Z (N]~w YORK CITY).--]: w a n t to t a k e issue a b o u t the d i s t i n c t i o n b e t w e e n cardiologists a n d p e d i a t r i c i a n s . I t h i n k a p e d i a t r i c i a n should k n o w more a b o u t h e a r t disease i n children t h a n a cardiologist~ but~ u n f o r t u n a t e l y , m a n y t i m e s he does not. I have been v e r y m u c h i n t e r e s t e d in a s t u d y of r h e u m a t i s m a n d in collaboration w i t h Dr. :Louis Gross a n d others have tried to r e p r o d u c e it in t h e animal. Needless to say, we have b e e n u n s u c c e s s f u l , a n d to m y k n o w l e d g e it h a s as y e t n o t been accomplished. I h a v e h a d a n o p p o r t u n i t y to s t u d y so-called " a c q u i r e d " congenital h e a r t disease in t h e f e t u s e s of p r e g n a n t w o m e n who h a v e h a d active r h e u m a t i c h e a r t disease d u r i n g t h e i r p r e g n a n c y , n o t i n g w h a t effect i i f a n y , t h e m o t h e r ' s condition h a d on t h e f e t a l h e a r t . ~Poynten, y e a r s ago, h a d one such case, a n d a b o u t a y e a r ago I saw a n i n f a n t who died at b i r t h a n d who h a d a d i s t i n c t va]vulitis on histologic examination. T h a t b r i n g s up t h e question of acquired h e a r t disease in i n f a n t s . I feel t h a t in i n f a n c y we have m o r e r h e u m a t i s m t h a n we suspect. T h e earliest proved case I have seen was in a s e v e n t e e n - m o n t h - o l d b a b y in w h o m t h e disease h a d never been suspected d u r i n g life. T h e i n f a n t h a d r e m a r k a b l e r h e u m a t i c n o d u l e s (Asehoff bodies) t h r o u g h o u t t h e e n t i r e hear~ muscle a n d on t h e valves. T h e i m p o r t a n t p o i n t is w h e t h e r or n o t cardiac disease in a given p a t i e n t is progressive. W h e n I a m a s k e d b y m o t h e r s a b o u t theh" c h i l d r e n ' s cardiac m u r m u r s , I o f t e n c a n n o t be c e r t a i n w h e t h e r there is a definite valvulitis, t h o u g h I c a n u s u a l l y s t a t e t h a t f o r all i n t e n t s a n d p u r p o s e s t h e s e m u r m u r s do n o t m e a n p r o g r e s s i v e h e a r t disease a n d t h a t t h e y do n o t call f o r a c u r t a i l m e n t of t h e c h i l d ' s activities. I t h i n k t h a t so-called f u n c t i o n a l cardiac m u r m u r s are m o s t o f t e n due to some mild b u t nonp r o g r e s s i v e o r g a n i c involvement. I t is i m p o r t a n t to m a k e a d i a g n o s i s of p r o g r e s s i v e h e a r t disease. I n t h e d a y s b e f o r e the i n t r o d u c t i o n of the von P i r q u e t test, m o r e tuberculosis was f o u n d a t a u t o p s y t h a n was clinically s u s p e c t e d ; so t h e s t o r y n o w goes for r h e u m a t i s m . I f t h e r e were a t e s t for r h e u m a t i s m s i m i l a r to t h e yon P i r q u e t test f o r tuberculosis, we would be s u r p r i s e d as to t h e f r e q u e n c y o f r h e u m a t i c fever in e a r l y life. Y o u c a n n o t d i a g n o s e r h e u m a t i s m in i n f a n c y or e a r l y childhood w i t h o u t t h e presence of either r h e u m a t i c nodules or o r g a n i c h e a r t disease. L a s t y e a r at the M o u n t Sinai H o s p i t a l , in t h e p o s t m o r t e m e x a m i n a t i o n of six h u n d r e d h e a r t s , definite evidence of r h e u m a t i s m was f o u n d in a b o u t 10 per c e n t of t h e p a t i e n t s in w h o m t h e r e h a d b e e n no clinical s y m p t o m s of t h e disease. ]: believe t h a t every case of r h e u m a t i s m or chorea ~s associated w i t h some cardiac involvement. I have followed a b o u t seventy-five c a s e s of chorea f r o m five to fifteen y e a r s ; f o u r t e e n of these ][ have w a t c h e d f o r fifteen y e a r s ; a b o u t t h i r t e e n , f o r twelve y e a r s ; a n d t h e r e are nine t h a t now h a v e a t e n - y e a r follow-up. I n t h a t period every one o f t h e s e p a t i e n t s h a s h a d some definite evidence to p o i n t t o w a r d an o r g a n i c c a r d i a c involvement, as i n d i c a t e d b y either x - r a y e x a m i n a t i o n , the e l e c t r o c a r d i o g r a m , or a definite m u r m u r . One of t h e m o s t i m p o r t a n t t h e r a p e u t i c m e a s u r e s is t h e p r e v e n t i o n of u p p e r res p i r a t o r y infection~ w h i c h c e r t a i n l y seems to r e a c t i v a t e a r h e u m a t i c condition. I t is m o s t i m p o r t a n t , too, to p r e v e n t scarlet f e v e r in a r h e u m a t i c p a t i e n t . T h e question

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of giving salicylates has never seemed very i m p o r t a n t to me; they t e n d to stop pain and lower temperature b u t certainly do not help the rheumatism. Equally unimp o r t a n t to m e is the question of tonsillectomy. One sees innumerable cases which have started long after the tonsils have been removed; once clinical m a n i f e s t a t i o n s of r h e u m a t i s m have occurred, it usually makes little difference whether the tonsils are removed or not; in fact, tonsillectomy m a y at times be a sufficient reason to reactivate a quiescent infection. C H A I R M A N ~ c C U L L O C H . - - T h o s e questions are all difficult to answer. A great deal is being done in various cardiac centers at the present time to determine whether or n o t allergy is the n a t u r e of r h e u m a t i c fever. W e will not go into a discussion of this point too much; we w a n t to confine this conference principally to the h e a r t and heart disease rather t h a n to rheumatic f e v e r . Dr. Schwarz has answered your question about functional m u r m u r s . I think myself t h a t a child who has a systolic m u r m u r at the apex probably has h a d r h e u m a t i s m or has it a t t h a t time. The answer i n each Case can be found by det e r m i n i n g whether or not a n y of the other signs are present. I f the child has tachycardia, cardiac enlargeraent, or a n increased force to the cardiac beat with or without a systolic murmur, he h a s , surely, r h e u m a t i c heart disease. I f there is a systoliz m u r m u r without those three conditions, the chances are that no matter what the m u r m u r sounds like, the child does not have heart disease. I think it would

be best to disregard systolic m u r m u r s a n d pay more attentio~ to other cardiac signs. DR. S T A N L E Y N I C H O L S (ASBU~Y PANE, N. f f . ) . - - A r e there a n y statistics on the m o r t a l i t y of cases of idiopathic hypertrophy in congenital cardiac patients available~ Are children with congenital heart disease who are operated on for recurrent tonsillitis and such things prone to develop a bacterial infection later~. Dr. Clinic in an tients

l~aliner, who does the research work in our postgraduate Children's H e a r t in New York, m i g h t present some results on a s t u d y carried on this winter, effort to prevent a bacterial endocarditis in n o t only congenital cardiac pab u t in other patients likely to develop bacterial endocarditis.

I a m interested in the points for the diagnosis of myocarditis. Acute myocarditis is rarely reported in New York. I would like to know the actual experience in rheumatic patients when they are moved to Florida a n d other southern states. Do they do better.~ I would also like to know w h a t digitalis can be expected to do in cases of congenital heart disease with heart failure. DR. M. M. M A L I N E I ~ (BI~OO]~LYN, N. Y . ) . - - I have seen several cases of aortic stenosls of t h e congenital type, described by Maude A b b o t t as '~subaortic s t e n o s i s . " The characteristics of acquired aortic stenosis are present, namely, a systolic thrill and m u r m u r in the second right intercostal space. We have never had a case diagnosed aortic coarctation in the clinic of the New York P o s t g r a d u a t e Hospital. Recently the New York Heart Association published a book, Criteria fo~ the

C~aes~fivatio~ a|

Diaqgnosis of Hea~'t D~se~se.

The diagnosis of an organic valvular lesion rests on two i m p o r t a n t signs, namely, hypertrophy of the heart and a characteristic m u r m u r . If a case presents a typical m u r m u r b u t no a p p a r e n t enlargement of the heart, the lesion should be classified as functional rather t h a n organic h e a r t disease. One m u s t not be misled by a short, soft, systolic sound frequently heard over the precordium, which is merely the resonance of the booming first heart s o u n d . I f one m u s t s t r a i n the ears to hear a murmur, ignore it, while a persistent, loud m u r m u r o v e r the apex, with or w i t h o u t concomitant demonstrable cardiac hypertrophy, means organic heart disease.

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Several years ago, I used epinephrine as a means of testing these questionable heart cases. A small subcutaneous injection of from 5 to 10 minims of epinephrine (1-1,000 solution) served t o accentuate the organic murmurs. Unfortunately, however, it is rather difficult for the average physician to ascertain slight degrees of hypertrophy of the heart, even with the aid of x-ray pictures. The usual 5-foot x-ray plate is of little value; direct ~uoroscopy is the best method to observe the size and position of the heart. Dr. Nichols asked about the prophylaxis of recurring rheumatic states and the prevention of subaeute bacterial endocarditis in children with heart disease. We have isolated and cultured a Stre~OleOw~a~ vtrr obtained from the blood of several children with subacute bacterial endocardltis complicating chronic rheumatic valvular heart disease. The filtrate of this broth culture with the addition of bacteriophage was used for intravenous injection in a group of twelve children with a possible congenital, or rheumatic heart disease. This filtrate) when used intravenous]L prevents the so-called upper respiratory infections. We had hoped that i f we could stimulate a resistance to these infections and bring about an immunity to subacute bacteria] endocarditls, which kills most of the cardiac patients, we would accomplish a great deal. r will hastily smnmarize the group of children treated. Each child received a total of fifty-four injections of progressively increasing amounts of filtrate at biweekly intervals. The results did not meet our hopeful expectations. During the period of treatment, the majority of children developed their customary upper respiratory infections. One contracted chorea. Another developed acute rheumatic fever complicated by pancarditis terminating in death. Still another became decompensated and died. None of the patients had a positive blood culture at any time. So in general, the rheumatic manifestations were not prevented by the filtrate. Whether an immunity to subacute bacterial endocardltis has been established in these children, time alone will tell. I n discussing the results, we are of the opinion that perhaps rheumatic conditions are not so much due to a streptococcic organism as we are at present inclhmd t0 believe. DR. MAURICE T. BRIGGS (Lu MASS.).--No one has said very much about nosebleeds or joint pains. I f cardiac chl]dren have nosebleeds or joint pains, it is wise to have bed rest for a more or less indeterminate period even though there is no fever or the heart does not at the time show any definite involvement. I n regard to the prognosis of heart disease, we have followed the congenital cases for a long period. There were about twenty fivo in the series t h a t were found still alive after fifteen and twenty years. Some of them had apparently outgrown the disease entirely. They had all been examined by x-ray originally and also when they were checked a f t e r the lapse of fifteen or twenty years. I t was concluded that when no enlargement is revealed by x-ray examination and there is no eyanosis, the prognosis of congenital heart disease is fairly good. One patient was a tennis champion who played for the Massachusetts state championship, t i e had been definitely diagnosed originally as having congenital cardiac disease. One~ a truck driver, had had an original diagnosis of congenital heart disease and was found later to be not only driving a truck but also taking care of the heavy lifting and work necessary with such a strenuous job. I n regard to the prognosis of infectious heart disease, I studied this year eighty patients who had been in our clinic. In this group who had had infectious heart disease over five years, many showed quite a surprising improvement. Last winter I had a case of fetal endomyocarditis. I found there had been four cases at the Boston Children's Hospital and reports of fourteen in the literature.

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DR. G I B S O N . - - I did n o t s a y m u c h i a m y d i s c u s s i o n a b o u t m u r m u r s a n d t h e i r differentiation. W h e n a child h a s a h e a r t m u r m u r , t h e p a r e n t i m m e d i a t e l y a s k s w h e t h e r it is serious, a n d we m u s t do our best to give a correct opinion. I n m o s t i n s t a n c e s one can d i f f e r e n t i a t e b e t w e e n o r g a n i c a n d f u n c t i o n a l m u r m u r s . O r g a n i c m u r m u r s in children are due either to c o n g e n i t a l or r h e u m a t i c h e a r t disease. I f one keeps i n m i n d t h e location a n d t h e n a t u r e of t h e lesions of c o n g e n i t a l h e a r t disease, h e will a p p r e c i a t e t h a t p r a c t i c a l l y all t h e m u r m u r s , except those of open d u c t u s a r t e r i o s u s , are systolic in t i m e a n d have t h e i r m a x i m u m i n t e n s i t y above t h e apex. I n r h e u m a t i c h e a r t disease the m i t r a l a n d aortic valves are m o s t f r e q u e n t l y involved. M i t r a l i n v o l v e m e n t gives a systolic m u r m u r m a x i m u m at t h e apex, t r a n s nlitted to t h e left. Sometimes, of. course~ t h e r e is also a m i t r a l diastolic m u r m u r at t h e apex. A o r t i c involvement, in children a t l e a s t , produces a b a s a l diastolic m u r m u r due to t h e presence of valve insufficiency. I n general, it m a y be said t h a t a n o r g a n i c systolic m u r m u r a t t h e a p e x or a diastolic m u r m u r at t h e b a s e is suggestlve of r h e u m a t i c h e a r t disease, while a n o r g a n i c m u r m u r , s y s t o l i c in t i m e a n d m a x i m u m at t h e base, s u g g e s t s c o n g e n i t a l h e a r t disease. I n .differentiating f u n c t i o n a l f r o m o r g a n i c m u r m u r s , one m u s t consider t h e h i s t o r y of t h e case, also t h e location a n d q u a l i t y of t h e m u r m u r s . F u n c t i o n a l m u r m u r s a r e s e l d o m m a x i m u m at t h e a p e x b u t a r e u s u a l l y h e a r d b e s t in the second lef.t interspace, s o m e t i m e s in t h e t h i r d or f o u r t h l e f t i n t e r s p a c e . T h e y a r e p r a c t i c a l l y a l w a y s systolic in t i m e . T h e y are u s u a l l y s o f t e r t h a n o r g a n i c m u r m u r s a n d are seldom widely t r a n s m i t t e d . T h e y c h a n g e v e r y a p p r e c i a b l y u p o n c h a n g e o f position, or u p o n c h a n g e of h e a r t rate. T h e y m a y be quite loud a t one e x a m i n a t i o n a n d scarcely a u d i b l e at a s u b s e q u e n t one. O f t e n t i m e s t h e y d i s a p p e a r at a b o u t t h e age of p u b e r t y . A b s e n c e of c a r d i a c e n l a r g e m e n t or other evidence of h e a r t disease is also a n import a n t p o i n t i n differentiation. I n r e g a r d to t h e q u e s t i o n s a b o u t c o n g e n i t a l i d i o p a t h i c h y p e r t r o p h y , the d i a g n o s i s is n o t o f t e n m a d e except a t autopsy. A s f a r as I know, t h e p r o g n o s i s is always v e r y bad. Of course, t h e n a m e " c o n g e n i t a l i d i o p a t h i c h y p e r t r o p h y " is a c o n f e s s i o n o f our i g n o r a n c e of t h e condition. I t h a s b e e n r e c e n t l y shown, however, t h a t g l y c o g e n s t o r a g e i n t h e h e a r t muscle i s t h e e s s e n t i a l p a t h o l o g y in a considerable n u m b e r of these cases. C o n c e r n i n g operations on children w i t h c o n g e n i t a l h e a r t disease, I feel t h a t ope r a t i o n m a y be u n d e r t a k e n s a f e l y except in t h e h i g h l y cyanotic cases. I n f a c t , 1V[aude A b b o t t e m p h a s i z e s t h e i m p o r t a n c e of r e m o v a l of tonsils a n d adenoids~ or other loci of infection, w h e n indicated, w i t h t h e idea of l e s s e n i n g t h e d a n g e r of. a b a c t e r i a l endoearditis. I t seems to me t h a t w h e n c o n g e s t i v e f a i l u r e occurs in t h e course of c o n g e n i t a l h e a r t disease, d i g i t a l i s w o u l d be i n d i c a t e d j u s t as it is in other f o r m s of h e a r t disease. I w a s m u c h i n t e r e s t e d in t h e s t a t e m e n t a b o u t o u t g r o w i n g c o n g e n i t a l h e a r t disease. I c a n conceive t h a t t h e f o r a m e n ovale or d u e t u s arteriosus, m i g h t be late in closing, a n d so in e a r l y i n f a n c y yield a m u r m u r w h i c h would d i s a p p e a r later. I t is q u i t e t r u e t h a t we s o m e t i m e s see eases of u n d o u b t e d c o n g e n i t a l h e a r t disease in w h i c h t h e m u r m u r is v e r y f a i n t , or a t t i m e s a b s e n t altogether, b u t I would be s o m e w h a t h e s i t a n t in s a y i n g t h a t t h e c h i l d h a s o u t g r o w n t h e condition. r

DR. PHILIP h a s no p r e v i o u s I see no r e a s o n be a n s w e r e d b y

ROSENBLUlVl ( C ~ r c A G O ) . - - I f we h e a r a m u r m u r in a p a t i e n t who h i s t o r y o f h e a z t disease, no real c a r d i a c e n l a r g e m e n t , or disability, for g e t t i n g excited a b o u t it. I t is o f t e n a q u e s t i o n t h a t can only o b s e r v i n g t h e p a t i e n t o v e r a l o n g p e r i o d of time.

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I was happy to h e a r . D r . McCuEloch's remarks about myocarditis bec'mse just recently I saw brought into the clinic for general examination a cl~ild, who was quite breathless; no one could At this breathlessness into the picture. Ttle etfild had endocarditis and also real inyocarditis. The breathlessness wa% no doubt, due to that. We do not make the diagnosis of myocarditis nearly as often as it is present 9 Adhesive pericardltls has always been a problem in diagnosis. The diagnosis is not made as often as it is found at autopsy. We will have to make the diagnosis earlier in order to take advantage of any operative procedure such as cardiolysis. It seems to prolong llfe. a little, though it will take some experience to say which patients should be operated upon and when. So far as the pulse rate is concerned, [Dr. Wiggers, of Cleveland~ has shown that in aortic insufficiency, a slightly rapid pulse i'ate is compensatory; w e must take this into consideration when we are taking the pulse rate. After digitalis is given to children with decompensated hearts without any effect, we have stopped it~ especially where there is marked edema or generalized anasarca. Instead, we put them to bed and give amnmnlum chloride and after twenty-four or forty-eight hours, we give salyrgan. After the salyrgan has had its effect, we then begin digitalis. We previously wondered why sudden death sometimes occurred in these patients when large doses of digitalis were given early. The digitalis was excreted into the fluids and was concentrated there so that when salyrgan was given the digitalis was taken up into the blood stream and poisoning resulted. A small dose of morphine repeated will ofted do as nmeh as digitslis in the beginning~ and it makes the patient more comfortable. I think if this is kept in mind the results will be more satisfactory. DR. MARGARET NICHOLSON (X/V'ASIHNGTON, 1). C . ) . - - I n the ea,pillary bed of the eyanosed clubbed finger tips o f the congenital cardiac patients, there is an increase in number and size and a eImnge in shape of the capillaries. When the cyanosis disappears, does the capillary bed return to normal.~ DR. W. AMBROSE McGEE (RICHMOND, V a . ) . - - W h e n a child develops a. systolic murmur at the apex and has an unexplained fever of one-half to one degree, ! feel the safest thing to do is to put the child to bed until the fever subsides. While the child may have a normal apex impulse and no cardiac enlargement (as shown by the x-ray examination) and not a very rapid pulse rate and when all such reasonable tests, as tuberculin skin test, are negative, and there are no apparent feel of infection, it seems advisable to class him as a poe,ential rheumatic patient. By keeping him in bed, the only damage done is that particular child might miss some pleasures of. life and time from school; but h e might be very materially damaged if he is allowed to remain up when running an undetermined fever. In attempting to separate the functibual from the organic murmur% I feel that if the Schilling diffm'ential blood count comes within the normal range~ %hat test would show there was probably an absence of infection or tissue derangement. As l'heumatie patients improve, or those children who have unexplained fevers improve, the, shift to the left. in the Schilling differential count decreases, but it does,*tot usually return to normal for a long time. The ordinary differential blood couut (Ehrlich) will frequently appear normal when the Schilling differential blood count is far from normal. CHAIRMAN MoCULLOCI~.- Dr. Patton, now at the Rockefeller Institute~ has studied the time of closure, of the various fetal cardiac foramina after birth. I t is generally believed that these openings, such as thd foramen ovale, close rather quick]2#

560

TItE JOURNAL OF PEDIATRICS

a f t e r b i r t h , as soon as p o s t n a t a l circu]atiou is established, t i e w a s able to show in v a r i o u s a n a t o m i c studies t h a t t h e closure t a k e s place m u c h l a t e r t h a n t h a t . T h e f o r a m e n oval% for example, closes completely a n d p e r m a n e n t l y s o m e w h e r e b e t w e e n the f o u r t h a n d s i x t h m o n t h s of p o s t n a t a l life. I h a v e seen several i n f a n t s who h a d p r e s e n t a t b i r t h r a t h e r loud m u r m u r s w h i c h I t h o u g h t were due to a p a t e n t f o r a m e n ovale. W h e n t h e children r e a c h e d t h e a g e of six m o n t h s to one year, t h o s e m u r m u r s were lost, W h e t h e r or n o t one could call t h a t o u t g r o w i n g c o n g e n i t a l h e a r t disease~ I do n o t k n o w ; b u t so f a r as t h e m u r m u r is concerned, it would be called o u t g r o w i n g it. DR. G I B S O N . - - I

should like to a s k Dr. iKcCulloch a n u m b e r of q u e s t i o n s :

I n t h e a b s e n c e of a f r i c t i o n r u b how is one g o i n g to tell w h e t h e r t h e s y m p t o m s are due to m y o c a r d i a l i n v o l v e m e n t alone, or to a c o m b i n a t i o n of m y o c a r d i t i s a n d pericarditis ? I n w h a t p e r c e n t a g e of cases of active r h e u m a t i c h e a r t disease do y o u find electrocardiographic changes? Do you believe in t h e use of d i g i t a l i s in t h e p r e s e n c e of active c a r d i a c i n f e c t i o n ? H o w o f t e n do you find p e r i p h e r a l s i g n s of aortic insufficiency i n t h e a b s e n c e o f the aortic diastolic m u r m u r ? W h a t do y o u t h i n k of t h e value of the s e d i m e n t a t i o n r a t e in d e t e r m i n i n g w h e n a child is convalescent? C H A I R M A N 1 V i c C U L L O C t I . - - E p i s t a x l s is a v e r y i m p o r t a n t s i g n of r h e u m a t i c fever a n d h e a r t disease. All children who h a v e e p i s t a x i s do n o t have r h e u m a t i c h e a r t d i s e a s e ; b u t w h e n t h e y do h a v e r h e u m a t i c h e a r t disease, it is a v e r y c o m m o n s y m p t o m , p a r t i c u l a r l y i n t h o s e i n d i v i d u a l s who h a v e r h e u m a t i c nodules a n d prol i f e r a t i v e r h e u m a t i c changes. I do n o t know w h a t m i g h t be t h e cause of t h i s epistaxis. Our children have been e x a m i n e d repeatedly, a n d in m o s t i n s t a n c e s a s m a l l ulcer h a s b e e n f o u n d on t h e s e p t u m . However, t h e r e m u s t be m o r e t h a n t h a t to cause e p i s t a x i s in t h i s disease w i t h such r e g u l a r i t y . I t m a y be a s i g n of t h e capillary i n j u r y t h a t occurs i a r h e m n a t i c fever, a n d t h e i n j u r y to t h e vessels in t h e n a s a l m u c o s a m a y allow blood to escape. I believe it is n o t g e n e r a l l y recognized a m o n g p e d i a t r i c i a n s as one o f t h e causes o f epistaxis. E v e r y p a t i e n t w i t h Pericarditls , p a r t i c u l a r l y of t h e chronic adhesive type, h a s m o r e or less m y o e a r d i t i s as well. I t m a y be q u i t e difficult to decide w h e t h e r t h e m y o c a r d i a l f a i l u r e or t h e p e r i c a r d i t i s is r e s p o n s i b l e f o r t h e c o n g e s t i o n a n d edema. A f t e r v a r i o u s m e a s u r e s f o r t h e control of congestive f a i l u r e h a v e b e e n tried w i t h o u t effect, t h e r e comes a t i m e w h e n y o u feel t h a t s u c h a p a t i e n t h a s more t h a n j u s t o r d i n a r y c a r d i a c failure. T h i s is p a r t i c u l a r l y t r u e in children in w h o m congestive f a i l u r e is r a t h e r rare. Those p a t i e n t s who show considerable e n l a r g e m e n t of t h e liver o u t o f p r o p o r t i o n to e d e m a elsewhere in t h e b o d y a n d who show precordial def o r m i t y w i t h m a r k e d precordial p u l s a t i o n s u g g e s t v e r y s t r o n g l y t h e d i a g n o s i s of chronic adhesive pericarditis. I t is difficult to d i s t i n g u i s h betweer~ t h e f a i l u r e resulti n g f r o m m y o c a r d i t i s as c o n t r a s t e d to t h a t r e s u l t i n g f r o m t h e adhesiOns in t h e pericardium. I a m n o t able to a n s w e r t h e second question. W e have m a d e a l a r g e n u m b e r o f e l e c t r o c a r d i o g r a m s of r h e u m a t i c p a t i e n t s . I t is difficult to recognize i m p o r t a n t changes. D u r i n g t h e v e r y active s t a g e s of m y o e a r d i t i s electrocardiographic c h a n g e s occur, especially p r o l o n g a t i o n of t h e A - V conduction time. O t h e r t h a n t h a t , t h e other c h a n g e s a r e v e r y s l i g h t or v e r y i n f r e q u e n t .

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Two things which I felt were on the horizon have come up for discussion today. One is the diagnosis of systolic murmurs at the apexl the other, the use of digitalis in the treatment of cardiac disease. Those subjects would require a morning for discussion. I have always felt, as Dr. Rosenblum states, that there are many things that can be used in cardiac children suffering from infection before digitalis is tried. From the studies I have c~rried on, I believe patients are frequently not benefited by the use of digitalis and occasionally are definitely injured by it. Dr. Schwarz sMd that most of the patients are suffering from actual infection in the heart muscle, and during that time digitalis may do as much harm as good. These patients should be put to bed first, given complete rest, the diet attended to, theocalcin, ammonium chloride and salyrgan, and other remedies, and then digitalis given later, i f the others fail. We, too, have had such a case as Dr. Rosenblum described. The patient s with moderate edema~ was given a lot of digitalis~ and after about five days complete heart-block developed suddenly. The drug was discontinued and the block disappeared within about forty-eight hours. Salyrgan was tried, in just the reverse order from his description, with a very prompt diuresis. The patient was greatly improved in about twenty-four hours~ whereas, the digitalis had caused a great deal of harm. I n regard to the periphera ! signs of aortic insufficiency, I disagree with Dr. Gibson. I think they are present very early and in considerable degree in most cases of aortic insufficiency. When the patient is admitted to the hospital with a moderate degree of congestive fMlure (and mos~ of them have mitral stenosis), it is very easy to overlook the diastolic murmur along the sternal border, whereas, under those same conditions the peripheral vascular signs are very easy to recognize. The blood pressure must be taken and the peripheral pulse noted in all cases of congestive failure even though the diastolic murmur is not heard. A good many of these patients show the diastolic murmur several days later as they begin to improve. One explanation may be that the heart sounds are simpler, the closer study helps to analyze the various murmurs present~ and t h a t the ear can appreciate the diastolic murmur along the sternal border; but it is a very common observation that these patients with aortic insufficiency are not diagnosed in the first few days of admission to the hospital. I f one is familiar with the size of aortic insufficiency in heart disease, the lesion will usually be recognized. I would like to emphasize, therefore, the value of these peripheral vascular signs. A pulse rate of 100 is an arbitrary level at which one can decide whether the patient has an active infections but there are many notable exceptions to that rule. There are many individual v.ariations in pulse rate. Some patients with a very acute myocarditis may have a bradycardia of 80-70 beats and a normal mechanism. I n ambulatory cardiac children, it. has proved an extremely useful guide and can be used in the same way as the body temperature reading. I would hesitate to keep in bed a child who has no more than 0.4 ~ of fever. We have appIied a rule in our cardiac .clinic that the patient with an active infection must consistently show a temperature as high as 100 ~ F. or more or must show a daily variation of at least 1.5 ~ between the lowest point and the highest point in the period of observation~ which is usually one weeki in other words, 99.4" or 99 ~ above the normal of 98.6 ~ would hardly be described as fever. For guidance in managing ambulatory cardiac patients, especially when an active rheumatic fever is suspected, these two signs are extremely useful.

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T h e s e d i m e n t a t i o n r a t e of blood cells is b e i n g used to d e t e r m i n e activity of t h e i n f e c t i o n a n d offers a very h e l p f u l m e t h o d of r e c o g n i z i n g activity. I t is g o i n g to be a very gre~lt help i f we g e t some test, s u c h as t h e s e d i m e n t a t i o n rate, which is fairly easy to carry ont. Dr. M c G e e

also mentioned blood counts as a help in determining an acute infec-

tion. The average ambulatory cardiac child has a very variable leucocyte count even w h e n t h e count is t a k e n u n d e r c a r e f u l l y controlled c o n d i t i o n s ; it is of v e r y little help in t h e o r d i n a r y clfild. I n a c u t e m y o c a r d i t i s we f o u n d some c h a n g e in t h e n u m b e r of m a t u r e a n d i m m a t u r e cells p r e s e n t i n t h e count.

DI~. E. B. S H A W (SA~ ~r~.~NClSCO, C A L I ~ . ) . - - ] l a s scarlet fever a n y etiologic significance in r h e u m a t i c carditls~. M a n y c a r d i o l o g i s t s m a k e quite a p o i n t of this in t h e i r case histories, b u t I h a v e n e v e r been i m p r e s s e d w i t h t h e evidence t h a t scarlet fever i n i t i a t e s r h e u m a t i c f e v e r or t h a t it h a s m o r e t h a n chance relation to it. E v e r y g o o d p e d i a t r i c i a n m u s t be able to express a n a u t h e n t i c opinion r e g a r d i n g cardiac d i a g n o s i s in childhood; it is d o u M y i m p o r t a n t t h a t the cardiologist who sees childhood c a r d i a c p r o b l e m s have some b r e a d t h of p e d i a t r i c t r a i n i n g . I f only we h a d b e t t e r c r i t e r i a for early d i a g n o s i s ! There is u s u a l l y no difficulty in w o r k i n g a d i a g n o s i s o f v a l v u l i t i s ; a n y one c a n h e a r a m u r m u r . B u t m o s t of us h a v e h a d t h e experience of seeing a child t h r o u g h a series of m i l d i n f e c t i o n s , n o t p a r t i c u l a r l y s u g g e s t i n g r h e u m a t i s m , a n d later discovering, w i t h o u t k n o w i n g i t s precise t i m e of origin, s i g n s of a n a c u t e valvulitis. I n r h e u m a t i c fever, as in childhood tuberculosis, we a r e u n a b l e to detect clinical evidence of first i n f e c t i o n a n d a r e able to m a k e c l i n i c a l d i a g n o s i s only w i t h the a p p e a r a n c e of e x u d a t i v e p h e n o m e n a . As Dr. Schwarz s u g g e s t s , w h a t we need is a P i r q u e t t y p e of t e s t for r h e u m a t i c fever, s o m e t h i n g b y which to pick t h e i n d i v i d u a l who is i n f e c t e d a n d who b e c a u s e o f his altered rea c t i v i t y m a y develop severely c r i p p l i n g lesions as a r e s u l t of s e c o n d a r y i n f e c t i o n s . A final p o i n t m a y a p p e a r f a n t a s t i c . E n g l e b a c h h a s s u g g e s t e d t h a t h y p o t h y r o i d ism i n t h e m o t h e r is a cause of c o n g e n i t a l defects, s u c h as f a i l u r e of f u s i o n of t h e s e p t a in f e t a l life. I n a small n u m b e r of cases I h a v e t h o u g h t t h a t t h e a s s o c i a t i o n of m a t e r n a l t h y r o i d d i s t u r b a n c e s a n d c o n g e n i t a l h e a r t disease in t h e i n f a n t were c o m m o n e r t h a n could be a t t r i b u t e d to p u r e chance. I n cases of p a t e n t septum~ etc., d i a g n o s e d e a r l y in life, is t h e r e s a y r a t i o n a l e in g i v i n g t h y r o i d e x t r a c t to t h e i n f a n t .r DI~. I ~ I C ~ I O L S . - - M y s u g g e s t i o n to m y c a r d i a c s t a f f is t h a t we follow t h e doubtf u l cases f o r one or two years. I t h o r o u g h l y a g r e e w i t h Dr. G i b s o n a n d Dr. MeCulloeh t h a t , in c e r t a i n l y t h e l a r g e m a j o r i t y of cases, we c a n tell (even i f we h a v e to follow t h e m six m o n t h s or a y e a r ) w h i c h a r e the f u n c t i o n a l a n d which a r e t h e o r g a n i c cases. W e eanllot o f f h a n d do t h a t in a f e w m i n u t e s , b u t we can, certainly, in t h e g r e a t m a j o r i t y , b y saying, ~ W e will w a t c h t h i s child six m o n t h s or a y e a r . " This b r i n g s u p Dr. M e G e e ' s story of t h e p o t e n t i a l group. I hope t h a t some one here h a s t h e facilities a n d t h e staff to follow a l a r g e g r o u p of p o t e n t i a l cardiac p a t i e n t s . W e would all like to do t h a t , b u t we have m o r e a c t u a l cardiac p a t i e n t s on h a n d t h a n we h a v e time to accommodate. I f some one w o u l d do t h a t f o r a n u m b e r of years, it m i g h t give u s a lot of d a t a t h a t we would all like to have. I w o u l d like to r e g i s t e r a p r o t e s t a g a i n s t t h e i d e a o f p u t t i n g all cardiac children to bed, u n l e s s t h e y are p r o v e d to h a v e p r o g r e s s i v e h e a r t disease. 1)1%. G I ' B S O N . - - I do n o t know of azLy r e l a t i o n s h i p b e t w e e n h y p o t h y r o i d i s m a n d c o n g e n i t a l h e a r t disease. I t is a well-known f a c t t h a t c o n g e n i t a l h e a r t d i s e a s e is u n u s u a l l y f r e q u e n t in m o n g o l o i d i n f a n t s . A s f a r as I know, this is t h e only condition w i t h w h i c h c o n g e n i t a l cardiac a n o m a l i e s seem to be especially associated.

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Concerning the relationship of scarlet fever to rheumatic h e a r t disease, I think t h a t scarlet fever serves to activate rheumatic infection r a t h e r t h a n being itself the cause of carditis. C H A I R M A N M c C U L L O C H . ~ I n a few instances, scarlet fever seems to be the first evidence of a rheumatic activity. It is als0 true t h a t m a n y rheumatic children who have scarlet fever show activity of infection to a considerable degree. DR. M A L I N E R . - - I have noticed the presence of a peculiar m u r m u r in suspected cases of adherent pericarditis. This m u r m u r is of a very h i g h pitch~ located a t the apex, usually occurring in late systole, and is superimposed upon the concomitant systolic m u r m u r of the associated mitral valve lesion. Since this sound suggests the bleating of a lamb, I call it the " b l e a t " ram.tour. M y explanation is t h a t the m u r m u r is due to a stretching of the pericardia] adhesions d u r i n g the systolic corn traction of the ventricles. DR. B R I G G S . - - T h e question arises whethcr epistaxis means a n y t h i n g in rheumatic fever. We feel very strongly t h a t epistaxis means a b e g i n n i n g of rheumatic fever and t h a t it is a definite danger signal. Some observers, Dr. Coburn and others, feel t h a t the early incipient stage of recurrent rheumatic fever is purpuric in character. Sometimes it shows in the nose, sometimes in eechymotic axeas and in a purpuric rash. This is the stage where rest is required as it is the earliest stage of rheumatic fever. I t indicates a definite r e t u r n of cardiac s y m p t o m s if rest is disregarded a n d the liberal use of salicylates is not followed. (The remainder of the discussion follo~ved the talks of Dr. McCu]loch and Dr. Gibson repeated before tlie second Round Table discussion on H e a r t Disease, Tuesday afternoon.) DR. W I L L I A M M. C H A M P I O N you use ?

(CLE57ELAIqD)O m o ) . - - W h a t f o r m of digitalis do

C H A I R M A N McCULLOCI-I.--We use the dry leaf of digitalis recommended by the American H e a r t Association and administer it in units based on the child's body weight. The tincture of digitalis is quite satisfactory. The tablets are easily taken~ and the dry l e a f does not deteriorate. DR. P A U L G. A L B R E C H T (CLEVELAND) OHIO).--]~ should like to inquire about exercise f o r cardiac patients. I have a p a t i e n t who has been in bed for almost a year with rheumatism. During t h a t time she has been very irritable and restless. W h a t is the ultimate prognosis? C H A I R M A N McCULLOCI-I.--My conception of that sort of child is t h a t she is suffering f r o m an active infection and when it will terminate is ent!rely problematical. Until it does terminate, one m u s t continue t h a t child's entire rest in bed with whatever other measures one might feel like using. DtL A L B R E C H T . - - H a v e you usdd sodimn cacodylate with a n y success at all? CHAIRMAN McCULLOCH.--No. DR. O R V I L L E L. B A L D W I N (CoLUmBUS, OHIo).--tIow long do you keep patients in bed a f t e r acute rheumatic fever, a f t e r the fever has subsided and there is j u s t a moderate heart involvement? C H A I R M A N M e C U L L O C H . - - I f one can establish a r u l e - - a f t e r a child has had an attack of exudative rheumatic fever~ with joint pains a n d fever, we believe t h a t a period of a b o u t three weeks is usually long enough to keep t h a t child entirely

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at r e s t in bed, i f b y t h a t t i m e he shows a n o r m a l p u l s e r a t e or one t h a t is below a level of a b o u t 100 b e a t s per m i n u t e , t h e s t a n d a r d a r b i t r a r i l y established. The child should also be free of fever, or at l e a s t t h e t e m p e r a t u r e should be below 100 ~ F. a n d v a r y i n g n o t m o r e t h a n 1.5 ~ I% over a p e r i o d of o b s e r v a t i o n ; he should also be f r e e of other s y m p t o m s , such as j o i n t p a i n s . I f t h e child is, however, sufferi n g f r o m a p r o l i f e r a t i v e t y p e of r h e u m a t i c fever, I t h i n k t h a t t h a t period o f rest s h o u l d be l e n g t h e n e d to c o n s i d e r a b l y m o r e t h a n t h r e e weeks. I t t a k e s l o n g e r f o r t h e child w i t h p~oliferative r h e u m a t i c fever to a t t a i n a slow pulse r a t e a n d to lose his fever. Such children u s u a l l y require f r o m two to t h r e e m o n t h s ' rest a f t e r t h e c e s s a t i o n of their s y m p t o m s b e f o r e t h e y c a n b e allowed out of bed. I t also dep e n d s s o m e w h a t on t h e season o f t h e year. W h e n t h e child is g e t t i n g over a n a t t a c k of r h e u m a t i c fever in t h e spring, we u s u a l l y keep h i m in bed a g r e a t deal longer t h a n we would i f he were g e t t i n g over a n a t t a c k d u r i n g t h e s u m m e r o1" f a l l f o r t h e r e a s o n t h a t r h e u m a t i c fever is more active a n d t h e child is m o r e a p t to have a r e l a p s e during the spring and early summer months. I n h a n d l i n g cardiac children, especially t h e a m b u l a t o r y group, we have a d o p t e d a policy o f k e e p i n g t h e child as n e a r l y up to his l i m i t of activity as possible; i n s t e a d o f p u t t i n g h i m to bed in d a y s of doubt, we a s s u m e t h a t he should be allowed a c t i v i t y u p to t h e p o i n t w h e r e he is n o t distressed. U n d e r those eondltions I believe t h e children a r e m u c h h a p p i e r , a n d their recovery is really as rapid, i f n o t m o r e so, t h a n w h e n t h e y are confined to bed. DR. E L I ! ~ R I E D M A N (B0s,r~)N, l ~ A s s . ) - - W h a t is t h e value of theoealcin i n t h e a c u t e s t a g e of e n d o c a r d i t i s ? T h e P - R interval, in m y experience, is n o t p r o l o n g e d u s u a l l y in r h e u m a t i c h e a r t d i s e a s e in children as it is d e s c r i b e d in adults. I n a d u l t s the P - R i n t e r v a l is v e r y f r e q u e n t l y prolonged. I n children w i t h a c u t e r h e u m a t i c fever, t h e P - R i n t e r v a l was n o t prolonged. I s t h e r e a n y difference b e t w e e n t h e m y o c a r d i t i s in d i p h t h e r i a a n d the m y o c a r d i t i s in o t h e r toxic cases? I n m y o c a r d i t i s due to d i p h t h e r i a , very o f t e n t h e r e is l e f t or r i g h t axis deviation a n d c h a n g e s in t h e P-I~ interval. I t h i n k we do n o t see t h a t o f t e n in myocardi~is f r o m other conditions. T h e p o i n t you s t r e s s e d a b o u t a b d o m i n a l p a i n as a sign of m y o e a r d i t i s is part i c u l a r l y t r u e in d i p h t h e r i a because it is a v e r y c o m m o n s y m p t o m a n d is very o f t e n m i s t a k e n b y t h e g e n e r a l p r a c t i t i o n e r for g a l l b l a d d e r disease. H o w o f t e n do y o u g e t cerebral embolism in m y o c a r d i t i s , especially in diphtheria.? I h a v e seen j u s t one case a n d I wondered w h e t h e r y o u h a d occasion to see others. I p r e s u m e t h e embolism w a s due to m u r a l t h r o m b o s i s following t h e f o u r t h or fifth week of t h e illness. C H A I R M A N M c C U L L O C I = [ . - - A good m a n y y e a r s ago we were t r y i n g to find some d r u g other t h a n digitalis t h a t m i g h t h a v e some effect on t h e m y o c a r d i u m in c a r d i a c children who were sick over a long period of t i m e a n d who seemed to be p r o g r e s s i n g r a p i d l y t o w a r d a f a t a l outcome in s p i t e of all t h e efforts we were m a k i n g . A t t h a t t i m e we h a d u s e d d i u r e t l n f o r i t s d i u r e t i c effect f o r t h e relief of edema, b u t we were seeking a d r u g t h a t m i g h t h a v e some effect on t h e m y o c a r d i u m for t h e relief o f t h e edema. W e also believed t h a t some of t h e s e children did n o t do well as a result o f the n u t r i t i o n a l c h a n g e s e x i s t i n g in t h e m y o e a r d i u m a n d t h a t n u t r i t i o n a l disorders a n d deficiencies o c c u r r i n g e a r l y in i n f a n c y m a y d e t e r m i n e i n some degree t h e incidence o f r h e u m a t i c fever. W e ~ h o n g h t these children m i g h t have a calcium deficiency in

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the heart muscle along with other signs of calcium disturbance. Since theoealcin is a combination of theobromin and calcium salicy]at% we thought it might be helpful for rheumatic children. We have had a large number of children who have received theocalcin over a period of several weeks or months at a time to determine whether or not it has any beneficial effect in the child who does not have edema. I am of the opinion that these children are benefited by it as much or more than any other single drug that can be used. How it works, I do not know beyond this explanation. I t has been rather unusual to find a definite prolongation of the P-I~ interval in children with rhemnatic fever and myocarditis. The myocarditis in diphtheria is distin.zily different from the myocarditis that occurs from any other form of an infection. I think those patients are in a class by themselves. I t is truly a toxic myocarditis. In the milder cases the evidence of myocarditis is extremely slight~ and by any ordinary microscopic examination, there is no evidence of a lesion. In the severer forms there is actual necrosis of cardiac muscle cells, particularly in the sinus nodes and the auricles. That type of myocarditis, however, is separate from the other types and is much more acute. Yon mentioned the importsmce of abdominal paln and vomiting in children with acute myocarditis, and I am very glad to rcemphasize it. I n the treatment of this condition, we have been impressed by the value of intravenous glucose in controlling the vomiting and abdominal pain. The glucose can be given intravenously in very large amounts. We usually give enough insulin to combine about half the glucose. I t is interesting to note that many of these patients with pain ask for the glucose injections for relief. I t is a very satisfactory form of treatment~ and, again, we are not certain as to just how it works. All cardiac children of this type have a low blood sugar content, and it is probable that their glycogen storage throughout the bl()od is somewhat low and the glucose they receive does no more than restore that substance. We have never observed cerebral embolism i n a child with diphtheritic myocarditis. I do not know what would cause it. I rather agree with you that it might be due t o different factors. DR. E L I ~ R I E D M A N . - - T h e r e are fifteen cases of hemiplegia following myocarditis reported in the literature. What do you think is the cause Of the abdominal pain? Is it all due to congestion of the liver, or is it nerve pain through vagus stimulation? CHAIRMAN M c C U L L O C H . ~ r t may be due to the acutely engorged liver with distention of the capsule, but it can be observed in Children who do not have congestive failure~ whose livers are not very much enlarged. DR. THOMAS A. FOSTER (PoR~.LA~D, M~.).--You spoke of chorea in connection with rheumatic fever. IIas it been your experience that chorea does the same thing to the myocardium and endocardimn that rheumatic fever does? The more I see the infection which I think is rheumatic fever of childhood the less I think it has t o do with chorea or that chorea has to do with rheumatic fever. CHAIRMAN )/IcCULLOCH.~My feeling is that chorea is a manifestation of rheums~tic fever in the brain; that chorea is a form of encephalitis due to rheumatic fever in the same way that a lesion in the lung or a lesion in the myoeardinm or a lesion in the joint may occur. Chorea itself does not cause the myocardial lesion, but they are a joint offspring of a common parent which is the rheumatic state.

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DR. W I L L I A M M. C H A M P I O N (CLEVELAND, O n l o ) . - - I I o w about an en!~'ephalitis in those cases you are now calling real choreas? Did you ever see t h a t suggestive movement of chorea? W h y not encephalitis? C H A I R M A N M c C U L L O C I I . - - T h e r e are children who may have had encephalitis ai some time in their lives when the disease was not recognized a:ad as a result, the child has clumsy athctoid movements all the time. Some of those children for various reasons such as physical strainj fatigue, or infections m a y become mildly choreic, a n d they, too, m a y not be rheumatic in nature. They are not very common, however. W h e n I say t h a t chorea is a f o r m of encephalitis due to rheumatic fever, it is essentially different from the ordinary forms of encephalitis because chorea rarely ever leaves any residual effect in the brain provided t h a t one did not exist before the attack. Effects such as paralysis or m e n t a l disturbances do not last longer t h a n a few weeks in these children. A t autopsy when the brain is examined, it is very rare, except in very acute cases, to find a n y morpholqgic change in the brain itself such as you find in a t r u e encephalitis. DR. I ~ O S T E R . - - I s the percentage of heart involvement as great with chorea as with any type of rheumatic infection? C H A I R M A N M c C U L L O C K . - - I think it is. I f you examine those patients over a long enough period of time, for example, if you follow them into adult life, nearly every one of them shews signs of r h e u m a t i c fever in some form later on. Also in working out the family relationships of rheumatic fever, it h a s been quite interesting to note t h a t a good m a n y parents, especially mothers who have had chorea i n childhood, have a rheumatic child with heart disease. T h a t is a quite common occurrence. DR. C H A M P I O N . ~ T H e : U n i v e r s i t y Hospitals of Cleveland consist of Lakeside Hospital, Babies and Childrens Hospital, Materni~ty Hospital, and Rainbow Hospital. The last named is out in the country about ten miles f r o m the m a i n group. I t is a convalescent hospital for both pediatric and orthopedic children. Dr. N o r m a n C. Wetzel is the visiting pediatrist in charge of the cardiac cases. I-Ie has been u s i n g the sedimentation r a t e to determine when to let a child up. You have not mentioned this test, and I am wondering what you think about it for this purpose. C H A I R M A N M c C U L L O C H . - - I , personally, have not been using this test at all, although I am familiar with it and have been noting the results of other workers who h a v e been reporting, apparently, t h a t it is very favorable a n d a very s a t i s f a c t o r y t e s t to use. It m a y be a little difficult but, apparently, it is very satisfactory to indicate a loss of rheumatic activity. A n d a n y such test, of course, will be of extreme value because it is very difficult under conditions t h a t you have at Rainbow Hospital w i t h convalescent children to say when the rheumatic infection is no longer active; a n y s u c h t e s t would be very welcome. DI~. C H A M P I O N . - - F r o m m y observation the sedimentation r a t e seems to be a n excellent way of determining when the'cardiac infection has become qulescent. Some children are kept in bed longer a n d some a shorter time t h a n they Would have .been before the use of this test. The n e t result, however, seems to be very m u c h better. DR. E. S. W E G N E R (LIncOLN, N E B . ) . - - W h a t is t h e : v a l u e of blb0d l~reSsure r e a d i n g s in determining activity of the rheumatic i n f e c t i o n ? Do you give a n y a t tentiorL to blood pressure readings in determining when to allow these patients more exercise?

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C H A I R M A N M c C U L L O C H . - - T h e blood p r e s s u r e is n o t c h a n g e d except in cases with aortic insufficiency. T h e o r d i n a r y p a t i e n t w i t h r h e u m a t i c f e v e r h a s no c h a n g e in his systolic or diastolic blood pressure. I n eases w i t h aortic insuffieiency~ t h e blood p r e s s u r e m a y b e of some value in d e t e r m i n i n g w h e n t h e p a t i e n t is r e a d y for exercise. W e believe t h a t a pulse p r e s s u r e of 50 m i l l i m e t e r s of m e r c u r y should be t h e m a x i m u m b e f o r e a c t i v i t y is allowed. A child with m o r e t h a n 50 m i l l i m e t e r s o f p u l s e p r e s s u r e s h o u l d be k e p t in bed. DR. E. R. 5 ~ c C L U S K E u ( P I ~ S B V a ~ H , P A , ) . - - Y o u spoke of t h e r h e u m a t i c state. S t u d e n t s have p i g e o n h o l e d all o f these r h e u m a t i c conditions as s e p a r a t e entities a n d give v e r y little t h o u g h t to t h e r h e u m a t i c state. I should like to a s k :Dr. Gibson a b o u t so-called i d i o p a t h i c h y p e r t r o p h y . Could c o n g e n i t a l a t e l e c t a s i s of t h e ] u n g be a f a c t o r in h y p e r t r o p h y , or m a y o v e r f u n e t i o n o f t h e i n f a n t i l e a d r e n a l g l a n d be i m p o r t a n t ? C H A I R M A N M o C U L L O C H . - - T h e question of the r h e u m a t i c s t a t e was t a k e n up l a s t year. I feel v e r y definitely, as you do, t h a t we m u s t l e a r n to recognize h e a r t disease only as a p a r t o f a r h e u m a t i c state. ~ ' R h e u m a t i s m ~' is a g e n e r a l t e r m u s e d to include m a n y lesions t h r o u g h o u t t h e body~ a n d I t h i n k t h e t e r m should be used in the s a m e w a y t h a t one recognizes tuberculosis in children. T h e lesion in t h e heaz't f r o m r h e u m a t i s m is r e a l l y s o m e t h i n g c o m p a r a b l e to t h e lesion in t h e l u n g of tuberculosis. I t is only one p h a s e of t h i s disease s t a t e t h a t m i g h t be p r e s e n t in a n ind i v i d u a l a t a g i v e n time. This idea will g r a d u a l l y seep t h r o u g h to medical s t u d e n t s in d u e time. DR. l Y [ c C L U S K Y . - - I f o u n d it very h a r d to g e t it across. DR. G I B S O N . - - T h e r e is one t h i n g I would like to ask you, Dr. 1VicCul]oeh. Y o u said t h a t in cases of serofibrinous p e r i e a r d i t i s you m i g h t h a v e complete recovery. H o w a r e you g o i n g to b e s u r e of t h a t ? C H A I R M A N M c C U L L O C H . - - W e have a good m a n y children who have h a d att a c k s of a c u t e serofibrinous p e r i c a r d i t i s who s e e m to be p e r f e c t l y ~vell a f t e r several y e a r s or in w h o m n o t h i n g was f o u n d in t h e p e r i c a r d i u m w h e n t h e y came to a u t o p s y later f r o m h e a r t disease. DR. G I B S O N . - - W e h a v e recently reviewed s e v e n t y - t h r e e a u t o p s i e s at t h e C h i l d r e n ' s M e m o r i a l H o s p i t a l . I n these a u t o p s i e s we m a d e p a r t i c u l a r n o t e as to the presence or absence of p e r i c a r d i t i s . Since we h a d only t e n eases w i t h o u t evidences of perlcarditis at a u t o p s y , I ~eel tha~ t h e very g r e a t m a j o r i t y of children, i f one c a n n o t prove it d u r i n g life, do have p e r i c a r d i t i s as s h o w n at a u t o p s y . O u t o f t h e t e n children who did n o t h a v e periearditis, f o u r o f t h e m died a n o n c a r d i a e death. W e t h o u g h t t h e y m i g h t h a v e developed a p e r i c a r d i t i s i f t h e y h a d lived l o n g enough. W e h a v e n o t h a d t h e experience of h a v i n g been able to m a k e a definite d i a g n o s i s of pericaxditis a n d t h e n f a i l i n g to find it at a u t o p s y . I a m v e r y m u c h i n t e r e s t e d in y o u r findings. C H A I R M A N M c C U L L O C H . ~ D i d those six p a t i e n t s who died a cardiac d e a t h a n d who showed no p e r i e a r d i t l s have a n y t h i n g in t h e i r h i s t o r y or in their.: previous exami n a t i o ~ to i n d i c a t e t h a t t h e y h a d a n a t t a c k of p e r i c a r d i t i s ? DR. G I B S O N . - - W e did n o t accept a n y t h i n g f o r a d i a g n o s i s of p e r i c a r d i t i s unless we c o u l d hear a f r i c t i o n rub. W e felt t h a t w a s t h e only t h i n g we could be sure about. I a m q u i t e s u r e we did n o t h e a r a f r i c t i o n r u b in a n y one o f those six cases.

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TI~E JOURNAL OF PEDIATRICS

C H A I R M A N M c C U L L O C H . - - W e have h a d several children in whom we have h e a r d a f r i c t i o n r u b and in whom at a u t o p s y no evidence of pericarditis could be found. I am ~nterested in your s t a t e m e n t a b o u t the large n u m b e r of p a t i e n t s who were f o u n d to have pericarditis when examined at autopsy. T h a t has been our experience, too. Most of those who die a cardiac death have pericarditis. DR. G I B S O N . - - I n a little less t h a n h a l f o f the cases we heard perieardial friction. Of course, they did not r u n their entire course in the hospital; they m a y have had the pericardial friction b e f o r e they came in, b u t there was a wide discrepancy between the n u m b e r of friction r u b s heard and those t h a t actually had pericarditis. The m e e t i n g adjourned at 5"15 o'clock.