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CARDIAC MANIFESTATIONS OF POLIOMYELITIS
323 13 it would 110 assessed as moderate in relation to the oilier forms of interstitial myocarditis. In none did it show the severity seen, for example, in Fiedler’s isolated
CARDIAC MANIFESTATIONS OF POLIOMYELITIS
myocarditis.
MAX J. Fox M.D. ASSOCIATE PROFESSOR, MARQUETTE UNIVERSITY SCHOOL MEDICINE ; PRECEPTOR, UNIVERSITY OF WISCONSIN SCHOOL
OF OF
MEDICINE
LOUIS SENNETT M.D. CLINICAL INSTRUCTOR, DEPARTMENT OF INTERNAL MEDICINE,
MARQUETTE
UNIVERSITY SCHOOL OF MEDICINE
JOSEPH F. KUZMA M.D. PROFESSOR AND DIRECTOR OF DEPARTMENT OF PATHOLOGY,
MARQUETTE
UNIVERSITY SCHOOL OF MEDICINE
POLIOMYELITIS is no longer looked upon as a disease of the central nervous system only. It is now generally accepted that the myocardium may be involved, but the recognition of cardiac lesions is relatively recent, dating from the observations published by Saphir and Wile in 1942. Since that time several clinical and electrocardiographic studies of the condition have appeared, most of which were well reviewed by Weinstein and Shelokov (1951). Our purpose here is to describe the electrocardiographic findings in 189 cases of poliomyelitis and the pathological appearances of necropsy material from 70 fatal cases of bulbar poliomyelitis.
In cases with inflammation the myoca-rdial fibres show variation in tlie intensity of staining, coupled with fragmentation and separation. The larger interstitial areas about muscle huncllos are widened and appear as a palo eosinophilic mesh containing variable numbers of inflammatory cells. Most often small groups of fewer than a dozen cells are irregularly distributed without constant relation to the interstitial vessels. The predominant polymorphonuclear loucocytes are accompanied by both lymphocytes and histiocytes. Occasionally the inflammatory cells form larger populations that can readily be seen on low-powor examination and in these they are seen in long anastomosing cellular patterns about muscle bundles (fig. 1). Interstitial oedema Interstitial infiltrations within the muscle may be severe. bundies are seen along individual fibres which now and then show fragmentation and necrosis (fig. 2). The changes are seen most often in the subendocardial areas where minor interstitialhamorrhages are most frequent ; but the epicardial tissues also commonly show a reaction with a great increase in monocytes immediately beneath the surface. In one case a coronary vessel was surrounded by prominent inflammatory
cells,
chiefly
polymorphonuclears (fig. 3). DISCUSSION
The incidence of electrocardiographic abnormalities in this study (32-4%) represents an approximate median between those reported by other workers-namely, Weinstein and Shelokov (1951), 30% ; Gefter et al. (1947), 14-2% ; Manning and Yu (1950), 77% ; and Bradford and Anderson (1950), 12.9%. The wide difference between some of these figures probably reflects differing criteria of abnormality in the electrocardiogram, plus the inclusion of sinus tachycardia as an abnormality in one paper (Manning) and not in another (Bradford). ST depression and/or T-wave changes were seen in 90% of our cases showing electrocardiographic abnormalities, compared with 80%reported by Bradford and Anderson, and Yu, and only 25% by Gefter 57-7% by et al. This difference again is probably attributable to varying definition of ST and T-wave abnormality. In all these studies, including our own, the most frequentt E.C.G. abnormalities were ST and T-wave Changes in conduction, whether suprachanges. ventricular or ventricular, were unusual.
ELECTROCARDIOGRAPHY
Sanborn Viso machine, electrocardiograms taken on admission, one week later, and on discharge. In most cases, the standard limb leads, the angmented unipolar leads, and the six conventional V chest leads were employed. The criteria of interpretation were essentially those of Katz (1946) and Sokolow and Friedlander (1949). In several cases, in which the illness
Using the
were
Manning
mild and the patient was discharged early only one or two tracings were obtained. In 189 cases, 412 electrocardiograms were taken, and 61 patients (32-4%) were found to have definite abnormalities as follows : was
The electrocardiographic changes were noted as early the first day of illness, and usually during the first week. Lead AVF disclosed the earliest and sometimes the only abnormality. Of the 9 patients with bulbar as
involvement 3 had
abnormal
electrocardiograms.
Clinical evidence indicative of myocarditis was obtained in 4 cases. In 2 there was a grade-II apical systolic murmur ; in 1 a grade-I apical systolic murmur ; and in 1 (a child of ten
years) tic-toe heart tones.J
HISTOLOGY
Our
histological
observations
were
made
on
routine
necropsy material from 70 cases of bulbar poliomyelitis. The mean age of the patients was twenty years ; 25 of
the 38 showing myocarditis were over the age of ten ; , and the two sexes seemed to be affected equally. there no was constant Alacroseopically significant finding, petechial haemorrhages being the change most often encountered. The colour and consistence of the heart were not altered. On microscopy, an interstitial inflammatory reaction was evident in about half the cases (38). In 25 of these it was irregular, slight, and easily overlooked, while in
’
Fig. I-Myocardium showing separation of muscle bundles and individual fibres. About the larger interstitial vessels there is a cell infiltration. The pattern is diffuse ( X )60).
324
Fig. 2-The myocardial- fibres
in the centre show fragmentation-necrosis and this is associated with the presence of-polymorphonuclear and histiocytic cells. Interstitial oedema between the fibres ( x 470).
Fig. 3-Coronary artery showing adventitial inflammatory reaction, principally lymphocytic. Polymorphonuclear cells and histiocytes present but sparse ( x )30).
We did not observe the prolongation of QTC found by Joos and Yu (1950) in 5 of 23 cases. These workers noted only 1 case of T-wave abnormality ; but inspection of tracings included in their paper to illustrate the QTC phenomenon reveals definite involvement of T in AVF, which, fifty days later, had reverted towards normal.
A review of 70 autopsied cases of poliomyelitis revealed interstitial inflammatory reactions in about half of the cases. Because
the non-specific characteristics of the the findings, diagnosis of myocarditis complicating poliomyelitis remains a clinical problem, in which the electrocardiogram serves as a supplement. The possibility of selective " cardiotropism by individual strains of the virus is commented upon.
The
myocarditis produced by poliomyelitis does not give rise to characteristic electrocardiographic changes. Those seen primarily in the ST and T-waves seem
to
"
are those often found in other diseases overtones. They are evident during the seven to ten days of illness, and subside with con valescence. Our data suggest that patients with bulbar involvement are no more liable than other poliomyelitis patients to develop E.C.G. abnormalities. with the observations of Bradford and Anderson (1950) but not with those of Manning and Yu (1950). From the clinical standpoint, the diagnosisof myocarditis complicating poliomyelitis leaves much to be desired, though persistent tachycardia is suggestive if it has no other evident cause. The lack of signs of myocarditis has been commented on by other investigators (Gefter et al. 1947). Weinstein and Shelokov (1951) have suggested that the mild form of myocarditis is probably hypoxic in origin whereas the severe form may be due to invasion of the heart by the virus. But patients without bulbar involvement, and therefore with nothing to produce hypoxia, may have myocarditis, while conditions known to produce chronic hypoxia, such as advanced pulmonary disease, are not ordinarily associated with myocarditis. It is, of course, conceivable that the three strains of poliomyelitis virus already recognised may be cardiotropic in different degree. To confirm or refute this explanation it would be necessary to ascertain the prevalence of myocarditis in different outbreaks caused by different strains of virus. are
transient, and
with first
systemic
REFERENCES
Bradford, H. A., Anderson, L. L. (1950) Ann. intern. Med. 32, 270. Gefter, W. I., and others (1947) Amer. Heart J. 33, 228. Joos, H. A., Yu, P. N. G. (1950) Amer. J. Dis. Child. 80, 22. Katz, L. N. (1946) Electrocardiography. Philadelphia. Manning, M. P., Yu, P. N. G. (1950) Amer. Heart J. 40, 336. Saphir, O., Wile, S. A. (1942) Amer. J. med. Sci. 203, 781. Sokolow, M., Friedlander, R. D. (1949) Amer. Heart J. 38, 665. Weinstein, L., Shelokov, A. (1951) New Engl. J. Med. 244, 281.
This agrees
SUMMARY
AND
INFECTION WITH PASTEURELLA SEPTICA IN A CHILD AGED THREE WEEKS
N. C. D. PIZEY M.B. Lond., F.R.C.S. FORMERLY
HOUSE-SURGEON, GREAT
Bollinger
HOSPITAL
ORMOND
and Kitt in 1878
FOR
SICK
CHILDREN,
STREET
were
the first to
study
describe, in wild boar, deer, and cattle in the neighbourhood of Munich, a disease then known as haemorrhagic and
septicaemia. Later they isolated an organism from these various animals so affected and showed that it was the same organism in each case. Various workers in ten years isolated similar organisms which were pathogenic to some In 1901 Lignieres grouped these domestic animals. organisms together and suggested the name Pasteurella. The specific names-e.g., aviseptica and feliscptica-have usually been given to denote the animals from which the organisms were derived. The organism in the case reported here has been labelled Pasteurella septica because its origin was not determined. The clinical picture produced by infection with the Pasteurella septica organisms appears to be very variable and to depend to a large extent on the animal infected. However, with most animals it is usually an acute
the following
CONCLUSION
A total of 412 electrocardiograms were taken on 189 cases of poliomyelitis. Electrocardiographic abnormalities were found in 32% of the patients. The most consistent abnormality was in the ST-T. The data presented conform, in the main, with those reported by other -investigators.
of
E.C.G.
.
CARDIAC MANIFESTATIONS OF POLIOMYELITIS
myocarditis.
MAX J. Fox M.D. ASSOCIATE PROFESSOR, MARQUETTE UNIVERSITY SCHOOL MEDICINE ; PRECEPTOR, UNIVERSITY OF WISCONSIN SCHOOL
OF OF
MEDICINE
LOUIS SENNETT M.D. CLINICAL INSTRUCTOR, DEPARTMENT OF INTERNAL MEDICINE,
MARQUETTE
UNIVERSITY SCHOOL OF MEDICINE
JOSEPH F. KUZMA M.D. PROFESSOR AND DIRECTOR OF DEPARTMENT OF PATHOLOGY,
MARQUETTE
UNIVERSITY SCHOOL OF MEDICINE
POLIOMYELITIS is no longer looked upon as a disease of the central nervous system only. It is now generally accepted that the myocardium may be involved, but the recognition of cardiac lesions is relatively recent, dating from the observations published by Saphir and Wile in 1942. Since that time several clinical and electrocardiographic studies of the condition have appeared, most of which were well reviewed by Weinstein and Shelokov (1951). Our purpose here is to describe the electrocardiographic findings in 189 cases of poliomyelitis and the pathological appearances of necropsy material from 70 fatal cases of bulbar poliomyelitis.
In cases with inflammation the myoca-rdial fibres show variation in tlie intensity of staining, coupled with fragmentation and separation. The larger interstitial areas about muscle huncllos are widened and appear as a palo eosinophilic mesh containing variable numbers of inflammatory cells. Most often small groups of fewer than a dozen cells are irregularly distributed without constant relation to the interstitial vessels. The predominant polymorphonuclear loucocytes are accompanied by both lymphocytes and histiocytes. Occasionally the inflammatory cells form larger populations that can readily be seen on low-powor examination and in these they are seen in long anastomosing cellular patterns about muscle bundles (fig. 1). Interstitial oedema Interstitial infiltrations within the muscle may be severe. bundies are seen along individual fibres which now and then show fragmentation and necrosis (fig. 2). The changes are seen most often in the subendocardial areas where minor interstitialhamorrhages are most frequent ; but the epicardial tissues also commonly show a reaction with a great increase in monocytes immediately beneath the surface. In one case a coronary vessel was surrounded by prominent inflammatory
cells,
chiefly
polymorphonuclears (fig. 3). DISCUSSION
The incidence of electrocardiographic abnormalities in this study (32-4%) represents an approximate median between those reported by other workers-namely, Weinstein and Shelokov (1951), 30% ; Gefter et al. (1947), 14-2% ; Manning and Yu (1950), 77% ; and Bradford and Anderson (1950), 12.9%. The wide difference between some of these figures probably reflects differing criteria of abnormality in the electrocardiogram, plus the inclusion of sinus tachycardia as an abnormality in one paper (Manning) and not in another (Bradford). ST depression and/or T-wave changes were seen in 90% of our cases showing electrocardiographic abnormalities, compared with 80%reported by Bradford and Anderson, and Yu, and only 25% by Gefter 57-7% by et al. This difference again is probably attributable to varying definition of ST and T-wave abnormality. In all these studies, including our own, the most frequentt E.C.G. abnormalities were ST and T-wave Changes in conduction, whether suprachanges. ventricular or ventricular, were unusual.
ELECTROCARDIOGRAPHY
Sanborn Viso machine, electrocardiograms taken on admission, one week later, and on discharge. In most cases, the standard limb leads, the angmented unipolar leads, and the six conventional V chest leads were employed. The criteria of interpretation were essentially those of Katz (1946) and Sokolow and Friedlander (1949). In several cases, in which the illness
Using the
were
Manning
mild and the patient was discharged early only one or two tracings were obtained. In 189 cases, 412 electrocardiograms were taken, and 61 patients (32-4%) were found to have definite abnormalities as follows : was
The electrocardiographic changes were noted as early the first day of illness, and usually during the first week. Lead AVF disclosed the earliest and sometimes the only abnormality. Of the 9 patients with bulbar as
involvement 3 had
abnormal
electrocardiograms.
Clinical evidence indicative of myocarditis was obtained in 4 cases. In 2 there was a grade-II apical systolic murmur ; in 1 a grade-I apical systolic murmur ; and in 1 (a child of ten
years) tic-toe heart tones.J
HISTOLOGY
Our
histological
observations
were
made
on
routine
necropsy material from 70 cases of bulbar poliomyelitis. The mean age of the patients was twenty years ; 25 of
the 38 showing myocarditis were over the age of ten ; , and the two sexes seemed to be affected equally. there no was constant Alacroseopically significant finding, petechial haemorrhages being the change most often encountered. The colour and consistence of the heart were not altered. On microscopy, an interstitial inflammatory reaction was evident in about half the cases (38). In 25 of these it was irregular, slight, and easily overlooked, while in
’
Fig. I-Myocardium showing separation of muscle bundles and individual fibres. About the larger interstitial vessels there is a cell infiltration. The pattern is diffuse ( X )60).
324
Fig. 2-The myocardial- fibres
in the centre show fragmentation-necrosis and this is associated with the presence of-polymorphonuclear and histiocytic cells. Interstitial oedema between the fibres ( x 470).
Fig. 3-Coronary artery showing adventitial inflammatory reaction, principally lymphocytic. Polymorphonuclear cells and histiocytes present but sparse ( x )30).
We did not observe the prolongation of QTC found by Joos and Yu (1950) in 5 of 23 cases. These workers noted only 1 case of T-wave abnormality ; but inspection of tracings included in their paper to illustrate the QTC phenomenon reveals definite involvement of T in AVF, which, fifty days later, had reverted towards normal.
A review of 70 autopsied cases of poliomyelitis revealed interstitial inflammatory reactions in about half of the cases. Because
the non-specific characteristics of the the findings, diagnosis of myocarditis complicating poliomyelitis remains a clinical problem, in which the electrocardiogram serves as a supplement. The possibility of selective " cardiotropism by individual strains of the virus is commented upon.
The
myocarditis produced by poliomyelitis does not give rise to characteristic electrocardiographic changes. Those seen primarily in the ST and T-waves seem
to
"
are those often found in other diseases overtones. They are evident during the seven to ten days of illness, and subside with con valescence. Our data suggest that patients with bulbar involvement are no more liable than other poliomyelitis patients to develop E.C.G. abnormalities. with the observations of Bradford and Anderson (1950) but not with those of Manning and Yu (1950). From the clinical standpoint, the diagnosisof myocarditis complicating poliomyelitis leaves much to be desired, though persistent tachycardia is suggestive if it has no other evident cause. The lack of signs of myocarditis has been commented on by other investigators (Gefter et al. 1947). Weinstein and Shelokov (1951) have suggested that the mild form of myocarditis is probably hypoxic in origin whereas the severe form may be due to invasion of the heart by the virus. But patients without bulbar involvement, and therefore with nothing to produce hypoxia, may have myocarditis, while conditions known to produce chronic hypoxia, such as advanced pulmonary disease, are not ordinarily associated with myocarditis. It is, of course, conceivable that the three strains of poliomyelitis virus already recognised may be cardiotropic in different degree. To confirm or refute this explanation it would be necessary to ascertain the prevalence of myocarditis in different outbreaks caused by different strains of virus. are
transient, and
with first
systemic
REFERENCES
Bradford, H. A., Anderson, L. L. (1950) Ann. intern. Med. 32, 270. Gefter, W. I., and others (1947) Amer. Heart J. 33, 228. Joos, H. A., Yu, P. N. G. (1950) Amer. J. Dis. Child. 80, 22. Katz, L. N. (1946) Electrocardiography. Philadelphia. Manning, M. P., Yu, P. N. G. (1950) Amer. Heart J. 40, 336. Saphir, O., Wile, S. A. (1942) Amer. J. med. Sci. 203, 781. Sokolow, M., Friedlander, R. D. (1949) Amer. Heart J. 38, 665. Weinstein, L., Shelokov, A. (1951) New Engl. J. Med. 244, 281.
This agrees
SUMMARY
AND
INFECTION WITH PASTEURELLA SEPTICA IN A CHILD AGED THREE WEEKS
N. C. D. PIZEY M.B. Lond., F.R.C.S. FORMERLY
HOUSE-SURGEON, GREAT
Bollinger
HOSPITAL
ORMOND
and Kitt in 1878
FOR
SICK
CHILDREN,
STREET
were
the first to
study
describe, in wild boar, deer, and cattle in the neighbourhood of Munich, a disease then known as haemorrhagic and
septicaemia. Later they isolated an organism from these various animals so affected and showed that it was the same organism in each case. Various workers in ten years isolated similar organisms which were pathogenic to some In 1901 Lignieres grouped these domestic animals. organisms together and suggested the name Pasteurella. The specific names-e.g., aviseptica and feliscptica-have usually been given to denote the animals from which the organisms were derived. The organism in the case reported here has been labelled Pasteurella septica because its origin was not determined. The clinical picture produced by infection with the Pasteurella septica organisms appears to be very variable and to depend to a large extent on the animal infected. However, with most animals it is usually an acute
the following
CONCLUSION
A total of 412 electrocardiograms were taken on 189 cases of poliomyelitis. Electrocardiographic abnormalities were found in 32% of the patients. The most consistent abnormality was in the ST-T. The data presented conform, in the main, with those reported by other -investigators.
of
E.C.G.
.