THREE CASES OF MYOCARDITIS
IN
CHILDREN
LESS
THAN
ONE YEAR OF AGE
By Carolyn M. McCue, M.D.
Departrnents of Pediatrics and Pathology, Medical College of Virginia, Richmond, Virginia
710
PEnwrlucs, May 1958
T
HE SURGE of interest in eliciting anex-act diagnosis in all types of congenital
heart disease has led to increased interest in other cardiac conditions in infancy with
which the diagnosis might be confused. It
is the purpose of this report to present three
cases of myocarditis in patients in whom
the diagnosis has been made before 1 year of age. Since most of the cases previously reported have occurred in older subjects,
attention should be drawn to the fact that the diagnosis can and should be made even in younger children. Two patients (Cases 1 and 2) are now living and getting along well. Serial electrocardiograms are shown.
Case 3 is presented with a complete patho-logic report as well as correlative electro-cardiograms.
In 1899, Fiedler described a condition of isolated myocarditis.1 The first case
re-ported in a child was in 19012 but since that time reports of the disease have been occur-ring with great frequency and well over 100 have been reported in children.3 An ex-tensive study made by Saphir, Wile and Reingold in 1944 emphasizes the
patho-logic aspects. These authors were aware that the condition may be associated with a great many disease states. Not only rheu-matic fever and diphtheria, but particularly poliomyelitis was condemned along with tuberculosis, pneumonias, nephritis and
many other infections. The patients
in-cluded children from 8 days to 16 years of age and it is interesting to note that 18 of these children were less than 1 year of age. In routine pathologic examination of
1,420
necropsies in a pediatric hospital, an incidence of myocarditis of 6.83% was noted. Vischer5 has reported an incidence ofmyo-carditis of only 3% in 800 necropsies from
an-other center. The idiopathic or Fiedler’s type of myocarditis has been the type most
fre-quently described; however, a recent
epi-demic in Johannesburg, South Africa, in-volving 10 children of whom 6 died, was
thought to be due to a Coxsackie virus.
Electrocardiograms in two cases revealed
flat T waves and ventricular tachycardia.
While definite bacteriologic or viral agents have been identified in some types of myocarditis, as better facilities become
available for virus study, perhaps a more definitive diagnosis can be made in many cases. Certainly the epidemic of
myocardi-tis described by Stoeber7 in which 140 newborn infants in Munich became ill weighs in favor of an infectious agent.
More extensive studies of primary myo-cardial diseases in infancy and childhood
have been presented by Rosenbaum, Nadas and Neuhauser3 and by Nadas.8 They re-port 10 cases of idiopathic myocarditis with necropsy findings and 19 other cases in which death did not occur but the patients were believed to have suffered from this same disease. Electrocardiographic and
clinical features are carefully described. Most of the patients were 6 months of age
or older.
Conlin and Mantz9 reported two cases of myocarditis in infants less than 1 year of
age. They found references to 26 cases in infants less than 22 months of age. Very few electrocardiograms are available
espe-cially in the younger age group where sud-den death often occurred before a diagno-sis of myocarditis was obtained and, there-fore, no electrocardiogram was made.
The clinical manifestations of
711
tis include primarily cardiac enlargement
without significant murmur,
electrocardio-graphic abnormalities, particularly of the
T waves and S-T segments, with an
essen-tially normal blood pressure and no other
evidence of rheumatic or congenital heart
disease. Such a condition may represent
either myocarditis or endocardial
fibro-elastosis. One of the main features in the
differential diagnosis between these two
conditions has been the age group,
myo-carditis being rare in infants less than 1
year of age and endocardial fibroelastosis
being more frequent before 6 months of
age. Most of the patients in either group show evidence of congestive heart failure
and are acutely ill at the time they are first
examined. Clinically, it is very difficult to
differentiate between the two groups.
Cardiac disease and enlargement in
chil-dren less than
2
years of age have received particular interest in the literature. In a roentgenographic study of 1,000 newborn infants 16 cases of cardiac enlargement were discovered.bO In seven of these infants who died no evidence of myocarditis was recorded and it was not recognized in those who survived. The same authors studied200 necropsies of newborns. They found 29
instances in which the heart weighed more
than 25 gm. Ten of these patients had pul-monary disease, six had erythroblastosis,
eight had congenital heart disease and five
had miscellaneous other abnormalities, but
none had myocarditis. Many cases have
been reported of myocarditis in the older
childhood group but relatively few in those less than 1 year of age. It seemed
worth-while, therefore, to present these cases
be-cause the patients became ill before 1 year
of age, and because electrocardiographic
records are available.
Case 1
CASE
REPORTS
HISTORY: CC. was first admitted to the
hospital on June 4, 1956, at the age of 6
months, with the chief complaint of mild
con-vulsive spells, suggesting petit mal, since 2%
months of age. Cyanosis was present during these spells. Preceding infections consisted of
a mild cold at 2 months of age during which
time he had not been acutely ill, but had
seemed weak and had had rapid respirations.
PHYSICAL FINDINGS: The weight had
in-creased from 3,580 gm at the time of birth to
8,180 gm at the time of admission to the
hos-pital. Body temperature was normal, pulse 136, respirations 66, blood pressure 105/70 in the
arm and 130/70 in the leg. There was a faint but high-pitched systolic murmur at the third
left intercostal space. No thrill was palpable.
There was no evidence of cardiac failure nor
of acute distress and no cyanosis or clubbing
was present.
LABORATORY FINDINGS : The concentration
of hemoglobin was 12.4 gm/100 ml and the
leukocvte count 7,300/mm3. Roentgenogram
demonstrated a huge heart with generalized
enlargement and cardiothoracic ratio of 77%. The lungs appeared normal. The
electrocardio-gram is shown in Figure 1.
COURSE: An initial diagnosis of endocardial
fibroelastosis was made and, because the elec-troencephalogram was mildly abnormal,
treat-ment with trimethadione (Tridione#{174}) was
be-gun. Digitalis or its derivatives were not
ad-ministered.
When re-examined 2 months later on
Au-gust 15 the electrocardiogram was markedly
improved (Fig. 2). On August 21 he became
suddenly ill with a severe respiratory infection
accompanied by symptoms of congestive car-diac failure with enlarged liver, dyspnea and a
dusky appearance. He improved with
admin-istration of antibiotics and oxygen and was doing very well without digitalis. The
cardio-thoracic ratio decreased to 60%. Treatment
with trimethadione was continued and
tetracy-cline administered. There were no further acute illnesses until the development of an
acute respiratory infection in March, 1957. The
electrocardiogram (Fig. 3) had T waves in-verted in all the precordial leads. He was
digitalized and his progress has been good
since that time. Electrocardiogram in June, 1957, is presented in Figure 4.
Case 2
HISTORY: J.C., a female infant, who had
appeared well previously, developed wheezing,
1 U 11]. aVr aV1 aVf
1]. aVr
Vi V2 V3 V4 VS V6
I-a’
.YL
LVR V14R
4 and 8 months. There was no cyanosis or
evi-dence of congestive cardiac failure.
PHYSICAL FINDINGS: At the age of 8 months
the infant appeared normally developed. The
body weight was 7.6 kg, pulse 180 and
respira-tions 40. The blood pressure was 80/50 in the arm and 110/70 in the leg. The heart sounds were rapid and the pulmonary second sound
was accentuated. There were no cardiac
mur-murs and no cyanosis. The inferior edge of the
liver was palpable 2 cm inferior to the costal
margin.
LABORATORY FINDINGS: The leukocvte count
was 14,800,’mm3 with 33% polvmorphonuclear
111
F’[G. 1. Electrocardiogram of patRnt CC. (Case 1)
on June 12, 1956. Cardiac rate 1:37/nun. T waves inverted in leads II, III, aVf and all chest leads
except V and V.;; diphasic 1’ in latter. Extensive T wave abnormalities especiaI1 in chest leads.
leukocvtes, 61% lymphocytes, 1% eosinophils,
1% basophils, and 4% monocvtes. The
concen-tration of hemoglobiii was 12 gm/100 ml and
the sedimentation rate was 7 mm in 1 hour.
Roentgenogram of the chest demonstrated
en-largement of 1)0th right and left ventricles with a cardiothoracic ratio of 65%. The
electrocar-diogram demonstrated that the PR interval was
.04 second and the QRS interval .04 second. There were diphasic T waves and depression
of the ST segment in leads a\’l, \4, V.
COURSE: Because cardiac failure seemed
im-pending, digitalis and antil)iotics were
admin-istered. By the age of 14 months considerable
aVi
a
VfFIG. 2. Electrocardiogram of patient C.C. (Case 1) on August 15, 1956. Cardiac rate 120/mm. Com-pared to tracing of June 12, 1956, the T waves are still inverted in III, aVf and chest leads on the right
aVi
V6
Vi V2 V3 V4 V5
V3R
.V6
1 ii
,
: aVx’. .“ .
- . .
.-
I LI 1 . . .1..
---.-..
,- -‘ . Vii
;
--I IL-
p
t-1
)-+-V5
.
V3
..; .V-
,-;; .V;R V4R V6R V6R
Fic. :3. Electrocardiogram of patient CC. (Case 1) on August 21, 1956. Cardiac rate 166/mm. Negative T wave in leads II, III, and aVf and all chest leads. Compared to previous tracing T waves are again
inverted in II, V- aiXi V.. This is definitely al)nOrnlal and reSeilll)les Figure 1.
growth ill height and weight had occurred but and digitalis and weighed 1 1 kg. No abnormal the cardiothoracic ratio remained about 60%. physical findings were noted except for slight
The electrocardiogram demonstrated definite evidence of cardiac enlargement. No murmurs
evidence of improvement, the abnormalities in were heard. The cardiothoracic ratio was 0.55.
the ST segments in V.1 and V3 being minimal. The electrocardiogram demonstrated a rate of When last examined at the age of 2:3 110 per minute, PR interval of .12 second and
months, the child was entirely asymptomatic. QRS complex of .04 second. There were no She had continued to receive oxvtetracvcline abnormalities of ST segments or T waves.
Ad-1 11 11]. aVr aVi aVt
r -
-Fic. 4. Electrocardiogram of patient CC. (Case 1) on June 20, 1957.
Cardiac rate 120/mill. T waves still low across precordium but upright
I
ii
aVi aVfaVr
-
-1_i
1
i
-V3 V4
-.
iLi_J
Vi V2
Fic. 5. Electrocardiogram of Patient AK. (Case :3). Cardiac rate 190/mimi. T wave changes in leads
I, II, a\r, a\’l, \‘, \, and V.; are suggestive of strain in left ventricle or nuvocardial abnormality.
VS V6
ministration of digitalis was discontinued after 1 ear, without recurrence of symptoms.
Case 3
HIsToR : AK. , a second child! ol \Oulug
par-ents, \‘as l)orn by cesarean section and
veighed 3,120 gun at the time of birth. He was apparently well until approximatel 4 months
of age when a moderately severe episode of diarrhea occurred. He recovered completely
l)ut had fairly frequent attacks of
nasopharv-gitis during the ensuing winter months. At 8
months of age rapid and rather grunting breathing was noted when he was awake but not during sleep. A roentgenograni of the chest made because of the abnormal breathing
indi-cated that the heart was enlarged. He was
ad-mitted! to the hospital for further stud at 9 months of age.
PHYSICAL FINDINGS: The infant was a
well-developed and well-nourished white male who
(lidi not appear acutely
ill.
The respirator rate was 96 per minute and! the character of therespirations WaS grunting. The tonsils were slightly enlarged. Temperature was :37.5#{176}C and pm1se 120 per minute. The heart soundls ‘ere of good quality and only modlerate en-largement was detected clinically.
LABORATORY FINDINGS : The concentration
of hemoglobin was 12.6 gm/100 ml and the
leukocyte count was 12,250/mm with 99% lymphocytes aiii I % polvmorphonuclear leuko-cvtes. Urinalysis \VL5 negative. Roentgenograrn
of tile chest ShOwed! a carcliothoracic ratio of .70
‘ith SOIfle congestion in 1)0th hilar audI trtlllk
areas. Eiectrocardiogranl showed a rate of 165
minute with ST segment an(i T ave changes suggestive of left ventricular strain, or
rrlyocardlial abnormality.
COURSE: He was dischargedl from the
hospi-tal and received no medlication. \Vhen seen for
the first time by the author, the infant was 10 months of age. Slight cyanosis had been noted!
during the precedling week and breathing hadl
been a little more labored than previously. The parelits statedl that he hadi become x’er ill iii
the afternoon. At the time of admission to
tile hospital the temperature was :39#{176}C,blood pressure was not obtainable, respirator rate
was 100 per Illillute and Pulse rate 185 per minute. There was no diefihlite cyanosis. The
liver was enlarged!. No murmurs could l)e heard. The concentration of hemoglobin was
11.9 gm, 100 nh and! tile leukocvte count
18,850, Illm. Lanatoside C was administered but tile Clhild! died 2 IlhillUtes later. An
dee-F
----
* Nccropsy performed by Dr. Gordon Hennigar.
trocard!iogram madle just before death showed
p1roxysm1l auricular tachvcardia andl evidlellce
of left ventricular strain (Fig. 5).
NECROPSY:#{176} Gross Findings: The body was
that of a well-developed and well-nourished infant. Significant findings were as follows:
The inferior margin of the liver was palpable
5 cm inferior to the right costal margin. It
weighed 350 gm (normal 274 gm) and ap-peared congested. One hundred twenty-five milliliters of straw colored fluid were present
111 the rigilt pleura! cavity, 50 ml in the left
pleural cavity and 400 ml in the pericardial
cavity. The heart weighed 150 gm compared
with a normal weight for this age of 39 gm. The left ventricle was markedly dilated and
hvpertrophied with flattened, densely scarred
716
MYOCARDITIS
hypertrophied and the right ventricular cavity
was encroached upon by the hypertrophied
dilated interventricular septum. The valves
ap-peared normal. Some compression atelectasis and slight edema of the lungs were present.
Microscopic Findings: There were focal
areas of lymphocytic infiltration in the myo-cardium, endocardial fibrosis of the left yen-tricle, and vacuolization of muscle fibers in the subendocardial layer of the left ventricle. Best’s carmine stain revealed the vacuoles to contain
glvcogen (Fig. 6). The lungs were the seat of
minimal interstitial bronchopneumonia. There
was mild centrilobuiar atrophy and minimal
fatty infiltration of the liver.
The probable causes of death were con-sidered to be ventricular fibrillation and
car-diac decompensation. Anatomic diagnosis was Fiedler’s myocarditis, generalized venous con-gestion and minimal fatty infiltration of liver.
DISCUSSION
These three cases illustrate the fact that
the symptoms of acute myocarditis in in-fancy may vary greatly from one case to another and may vary in the same case
over a brief period of time. The consistent
findings in these and other cases are marked cardiac enlargement with charac-teristic electrocardiographic changes as il-lustrated, associated with absence of
sig-nificant cardiac murmur and presence of a normal blood pressure. Most of the
pre-viously reported cases have occurred in
children with evidence of cardiac failure
when first examined by a physician. It is notable that none of the three children described here was recognized as severely ill when first examined. In the first instance
electrocardiograms and roentgenogram of the chest would probably not have been made if epileptic episodes had not
oc-curred. The severity of the electrocardio-graphic changes at that time suggested fibroelastosis. The course of the disease with improvement in the electrocardiogram
and recurrence on two occasions certainly supports the diagnosis of myocarditis. The child has been greatly improved while re-ceiving digitalis during the last few months.
The two episodes of acute cardiac failure
accompanied acute respiratory infections and the first one improved dramatically
even
without administration of digitalis when oxygen and antibiotics were given.In the
second
case
the
child
developed
marked cardiac enlargement and tachy-cardia with rapid respirations but never developed frank cardiac failure. It was our belief that cardiac failure was averted in this case by the prompt use of digitalis.
The excellent response to this drug and to antibiotics over the last year has been most
gratifying. The entirely normal
electrocar-diogram at the present time and excellent clinical course made discontinuation of
digitalis therapy possible and she has
con-tinued to be asymptomatic for about 3
months since cessation of such therapy.
In the third case the child was first recog-nized to have a large heart and rapid pulse and respiratory rates at 9 months of age but
the diagnosis was not suspected until he
suddenly developed cardiac failure one month later, with rapid progression to death within a few hours. There was not time for
digitalis to be effective in this case. It is
pos-sible that its use several weeks sooner might
have been far more beneficial. The patho-logic changes, however, in this case were
very extensive throughout the heart muscle
and any change in the course of the disease that could have been made by administra-tion of medication is purely conjecture.
In the light of our present knowledge it
would seem wise when cases of this type are recognized, to advise prompt digitaliza-tion, adequate antibiotic therapy to con-trol any immediate infections, and moderate
restriction of activity for a brief period.
Nadas8 and his associates have emphasized
the value of digitalis. The two patients who
survived received prophylactic antibiotics for many months to minimize infections. Because infections have precipitated car-diac failure in some cases it would seem
(lesiral)ie to administer antibiotics for at
least a year. It is interesting to note that the cardiac size has decreased during the
SUMMARY
A brief
discussion
of the historic
aspects
of myocarditis in children is given. Three cases are presented as myocarditis, showing cardiac enlargement, absence of
significant murmurs,
marked
electrocardio-graphic changes and normal bloodpres-sure.
In
two
of the
cases
the
electrocardio-grams improved and the size of the heart
decreased as the patients made clinical im-provement during a 12- to 18-month period. In the third patient, who died, pathologic
reports are presented as well as
electrocar-diographic records.
Although myocarditis is not frequently found in children less than 1 year of age,
its presence must be suspected in children
with the findings mentioned and appropri-ate therapy begun promptly.
ACKNOWLEDGMENT
Sincere thanks are extended to Drs. Robert Hoffman, William Spencer, and
Sarah Jones, who referred these patients
for study.
REFERENCES
1. Fiedler, A.: Uber akute interstitielle Myo-kaditis. Zentralbl. inn. Med., 21:212, 1900.
2. Zuppinger, H.: Uber Herztod bei anschei-nend bedeutungslosen oberfl#{228}chl Ce-schw#{252}rsprocessen. Wien. kim. Wchn-schr., 14:799, 1901.
3. Rosenbaum, H. D., Nadas, A. S., and Neuhauser, E. B. D.: Primary mo-cardial disease in infancy and child-hood. Am.
J.
Dis. Child., 86:28, 1953. 4. Saphir,0.,
Wile,
S. A., and Reingold,I. M.: Mvocarditis in children. Am.
J.
Dis. Child., 67:294, 1944.
5. Vischer, M.: Beitrage zur Myokarditis im Kindersalter, in Czerny, A., editor: Ab-haudlungen aus der Kinderheilkunde und ihren Grenzgebieten. Berlin, Kar-ger, 1924.
6. Javett, S. W.,
et
a!.:
Mvocarditis in the newborn infant.J.
Pediat., 48:1, 1956. 7. Stoeber, E.: Weitere Untersuchungen#{252}berepidemische Myocarditis (Schwie-lenherz) des Sauglings. Ztschr. Kinderh., 71:319, 592, 1952.
8. Nadas, A. S. : Pediatric Cardiology. Phila-delphia, Saunders, 1957, p. 214. 9. Conlin, C.
J.,
and Mantz, F. A. : Isolatedmyocarditis in infants.
J.
Pediat., 42: 414, 1953.10. Green, H., and Apley,
J.
: Study of cardiac enlargement in infancy with case reports of reversible enlargement. PDi.mIcs, 5:249, 1950.SUMMARIO
IN
INTERLINGUA
Tres
Casos
De
Myocarditis
in Patientes
Pediatric
De
Minus
Que
Un
Anno
De
Etate
Le prime patiente esseva studiate al etate de 6 menses a causa de episodios convulsive. Ilie habeva nunquam parite acutemente malade. Le examine physic revelava absentia de cya-nose, normal pression de sanguine, e soimente
un leve e basse murmure systolic al tertie
in-terspatio sinistre. Le corde esseva multo grande. Extense alterationes del unda T esseva contatate
in le electrocardiogramma.
Le stato clinic del patiente se meliorava. Etiam le electrocardiogramma se meliorava sin administration de digitalis. Duo menses e de novo 9 menses plus tarde ille experientiava disfallimento cardiac con acute infection respi-ratori. Al secunde de iste duo occasiones, le patiente esseva digitaiisate. Depost ilie se ha
mantenite ben pro plus que 6 menses. Un ieve ailargamento cardiac persiste.
Le secunde patiente disveloppava le prime de quatro sever episodios de apparente bron-chitis a! etate de 4 menses. Quando iste pa-tiente-un puera-habeva 8 menses, ii esseva recognoscite que su corde esseva multo grande. Nulle murmures esseva audite, e le pression del sanguine esseva normal. Congestive disfalli-mento cardiac non occurreva, sed a causa de simile anormalitates electrocardiographic, le diagnose de myocarditis esseva formulate. Le
patiente esseva tractate con digitalis e anti-bioticos e depost se ha tenite continuemente ben. Quando le administration de digitalis esse-va cessate 1 anno plus tarde, le svmptomas non retornava. Le dimensiones cardiac ha decres-cite, sed ilios es non ancora normal. Le electro-cardiogramma es marcatemente meliorate.
718
MYOCARDITIS
audite. Quando primo vidite le vespere de su morte, le patiente habeva un electrocardio-gramma que monstrava marcate alterationes del undas T con tension sinistro-ventricular. Digi-talis esseva administrate per via intravenose, sed le patiente moriva intra alicun horas. Le
studios pathologic monstrava typic mvocarditis
idiopathic.
Iste patientes non pareva acutemente malade
(1uando illes esseva primo portate al consulta-tion medical. Le symptomas de presentation
non es uniforme, sed allargamento cardiac sin
murmure significative e marcate alterationes
electrocardiographic esseva constatate in omne le casos. Le electrocardiogrammas ha un
im-portantissime function diagnostic. Es formulate
le opinion que prompte digitalisation es de valor e deberea esser mantenite durante circa un anno, insimul COfl administrationes quoti-dian de antibioticos pro prevenir infectiones. Le prognose non es si mal como on credeva in le passato.
OUTBREAK OF ASEPTIC MENINGITIS WITH EXANTHF:M, J. F. Galpine et ci. (Brit. \l. j., 1 :319, February 8, 1958.)
The aseptic type of meningitis has been found to be due to a variety of viruses:
Poliomyelitis; Coxsackie B virus; and ECHO virus type 6. In the last few years out-breaks of aseptic meningitis associated with a rash and fouhid to he due to ECHO
viruis type 9 have been reported from various parts of the world. Tile present report
concerns an outbreak of this type in Coventty, England, in the autumn of 1956 and covers 51 cases admitted to hospital. ECHO virus type 9 was isolated from the feces of 19 out of 27 patients so examined. Eighteen of tihese showed fourfold or greater rises in antibody titer against ECHO virus type 9 during the course of their illness. Tile illness was characterized by fever of 101 to 10.3#{176}Fand the usual signs of
menin-gitis. An erythematous rash was observed in about one-half of tile patients. It always
involved the face and was frequently limited to the cheeks only. It often spread to
the neck, shoulders and tipper trunk but was rarely generalized. Occasionally it
he-came petechial and this, with the predominance of poiymorphonuciear leukocytes ill
the cerebrospinal fluid, made occasional confusion with meningococcal meningitis
possible. Pleocytosis did not commonly exceed 500/mm’. No complications were
