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The incidence of hypertension long after poliomyelitis
J. chron. Dis. 1967,
Vol. 20, pp. 269-273. Pergamon Press Ltd. Printed in Great Britain
THE INCIDENCE
OF HYPERTENSION POLIOMYELITIS
LONG AFTER
LAWRENCEA. KOHN, M.D. and GRACEL. REID, B.Sc., R.N. Department of Medicine,School of Medicineand Dentistry, the Universityof Rochester,New York (Received 21 November 1966; in revised form 19 January 1967)
IN SEYERE poliomyelitis, with hypoxia of bulbar or other origin, arterial blood-pressure is often elevated, and this may outlast the acute phase of the disease by months (MCDOWELL and PLUM [l]). Hypertension long after the original illness was first recorded in 1940 by VICKERS[2] who found seven definite cases among 44 adults many years after they had had infantile paralysis. Although some of the hypertensives were badly crippled, most of them showed no muscle damage. ZIMANYI,and his co-workers [3] in 1959 observed among 336 children, chiefly young but a few in their ‘teens’, 88 instances (26 per cent) with systolic or diastolic pressures above the accepted norms for their age. The patients had been hospitalized for months or years, the vast majority for 5 yr or less, and of the hypertensives, 85 per cent were quadriplegic, with severe muscle damage in the remainder. OSTFELD [4] in 1961 compared bloodpressures found in cases in a Respiratory Center an average of 2 yr after their initial illness, with controls no longer in hospital but matched for age, sex and muscle-damage. Hypertension was frequent in all groups: 20 per cent over-all, with the incidence roughly paralleling the amount of muscle loss. NEUBAUERand MAINZER[5] in 1963 saw and photographed retinal arterial changes accompanying high blood-pressure in acutely ill patients with respiratory difficulty, and these changes sometimes lasted beyond the period of hypoxia. They suggested (as had often been hinted but rarely if ever put in print) that previous poliomyelitis in a mild or even non-paralytic form might be invoked to explain obscure hypertensive disease, perhaps through damage to medullary centers. BENEVOLOand co-workers (1963) [6] reported on 201 children observed at varying intervals after infantile paralysis. Approximately 20 per cent had blood-pressures higher than expected at their age. Of 39 children seen 4 or more yr after the initial disease, 15 per cent had diastolic pressures consistently above 90 mm of mercury. Most of them had severe paralysis. On the other hand, KEMP [7] in 1957 reported on 357 patients followed for periods up to 5 yr from onset, and concluded that: “. . . . neither children nor adults either mildly or severely affected had greater incidence of hypertension than individuals who had not had polio”. Since permanent elevation of blood-pressure after poliomyelitis might be favored by the aging process, as in the majority of hypertensive states, it appeared worth while to study a group of older survivors for the overall incidence of hypertension and for its possible relation to the degree of muscle damage. *In 1964 and 1965 this study was aided by a grant from the Monroe County Heart Chapter of the Health Association of Rochester and Monroe County. Address for reprints: 457 Park Avenue, Rochester, New York 14607. 269
770
LAWRENCE A. KOHNand GRACE L. REID
MATERIAL AND METHODS From cases whose acute infantile paralysis was observed in the Strong MemorialRochester Municipal hospitals from 1926 through 1949, we selected for attempted follow-up all those who had lived a minimum of 13 yr and who should be 19 yr or older if found. The high incidence of the disease in 1944 and 1945 provided a large cluster of cases which fell in these limits. Subsequently, for a special purpose we studied a smaller group of more recently ill patients. Diagnoses were checked critically from the hospital records by one of us who had had considerable experience with the acute disease and who had personally observed many of the cases 14 yr or older at the time of their illness. “Severity” as applied to the acute phase, measures the degree and duration of fever, prostration and complications as recorded by the attendant physicians. “Immediate damage” is a rough grading of the amount of muscle disability at discharge, or, if hospitalization was prolonged, at the conclusion of the acute phase. For follow-up we depended chiefly on letters to patients, their families and their physicians. Information was found in records of subsequent hospital admissions or visits to the Poliomyelitis Clinic, and in lists furnished by the Rochester Chapter of the National Foundation. There were many individual searches starting with hints from physicians who knew of our interest, or from the chance observation of unusual patients’ names. Estimates of muscle damage and blood-pressure were usually made by one of us in Rochester or in nearby communities, but when patients were traced at a distance (California, Florida, Great Britain), we accepted with gratitude the judgment of their present medical advisers. One of us observed the blood-pressure in 1501175 (85 per cent) of the “followed” patients. Although our search was persistent, we made every effort to prevent or allay anxiety in the patient or family, and while many followup failures were obviously due to lack of cooperation, those patients we reached were invariably agreeable and returned if asked for a second observation. Blood-pressure was estimated with conventional anaeroid sphygmomanometers which had been factory-standardized for accuracy, in the sitting position and on the left arm unless it was significantly wasted. Several readings were made to allow for subsidence of “nervous” rise. The levels recorded were obviously not “basal” but are thought to be reasonably accurate “casual” pressures. In the 25 patients observed on our behalf by other physicians, the blood-pressures were probably “casual” rather than “basal”. The definition of hypertension is controversial; for this study we chose the same standard as did OSTFELD(Zoc. cit.); if higher than 145/95 it is probably abnormal. This divided our patients satisfactorily; there was no overlap. Damage was graded in terms of disability and muscle loss. Minor or localized weakness which produced no functional impairment is included in grade 0. l-2 implies moderate to marked muscle loss in one or two limbs respectively (not both legs). Grade 3 calls for one paralyzed leg plus significant damage in two other areas and grade 4 disability, the necessity for crutches or a wheel-chair. Successful operative results such as tendon transplants or arthrodeses decreased slightly the grade assigned, which thus became a combined functional-anatomical classification. Whenever blood-pressure was found elevated, the observation was repeated months or years later, and in several instances suspected hypertension was excluded. The study was begun in 1956 and was concluded in 1965.
The Incidence of Hypertension
Long after Poliomyelitis
271
RESULTS
Of 326 patients we attempted to trace, we were successful in 175. The mean period of follow-up was 21.4 yr with a mode falling between 18 and 20 yr. Less than a quarter of those reached were under 30 and 40 per cent were 40 or older. Are these 53 per cent followed a fair sample ?
TABLET
Patients followed Mean age at onset Mean interval, onset to follow-up Mean initial severity Mean immediate damage Blood-pressure elevated during acute illness
Patients lost to follow-up 13.4
10 Mean interval, onset to 1960 (midpoint of study)
21.4 1.77 1.02 4189
18.5 1.85 0.7 3189
Thus the patients we were able to reach were slightly older than those lost to followup. Since (vi& in&a) the hypertensives appeared to have had more immediate damage, the difference in this index might favor an increased incidence of high blood-pressure in those observed. On the whole, they appear fairly representative of the entire group.
TABLE 2
Current disability
BP elevated
0
4 2 4
l-2 3-4 x2=10.215;
BP normal
% elevated
103 48 14
3.7 4.0 22.0
0.005
The incidence in the severely disabled is close to that found in younger similarly injured patients by most previous observers. While we reached relatively few crippled patients, the likelihood that the differences found arose by chance is small.
TAEZLE~
Hypertensives (10) Age at onset Age when followed Initial severity Initial damage EIevated BP during acute illness
Normotensives (165) 19 42 2.2 1.7
13 33 1.75 0.98
218
2/81
272
LAWRENCEA. KOHN and GRACEL. REID
The hypertensives were older at the onset of illness, were sicker at the time, had greater immediate damage and are currently older than the normotensives. The overall frequency of hypertension is 5.7 per cent, probably no higher than would be found in persons of similar age in the population at large. Among these ten patients, three of the four without muscle damage had a definite family history of high bloodpressure. Of the two with moderate injury, one had such a heredity. Of the severely damaged, two patients had no such familial tendency; in the other two cases the information was unavailable. Although many patients needed repeated or indwelling catheterization during their acute illness, only 11 of the 245 patients followed (both series) had persistent urinary infection and of these only one became hypertensive. DISCUSSION
It is possible that hypertension is more frequent soon after poliomyelitis and either disappears, or is of such severity that the individual affected succumbs early. Verified deaths were rare in our sample; we were able to establish only two in the patients we followed and one in those lost to follow-up, although obviously there might well have been other deaths in this sub-group. With this possibility in mind, we drew a second sample of patients whose acute illness was between 1950 and 1960, choosing older individuals as more likely to develop high blood-pressure. Of 70 such, we were able to trace 65 per cent. TABLE4
Followed
Not followed (25)
(45) Mean age at onset Mean follow-up interval
16 7.7
Mean initial severity Mean immediate damage
1.9 0.59
16 5.8 (Interval to 1960) 1.8 0.79
The severity is comparable to that of the older patients; the immediate damage less. TABLE5 Current disability 0 l-2 3-4
BP elevated 0 1 0
BP normal 37 3 5
The numbers are small, but there is no suggestion that hypertension is more frequent earlier. In any group of patients, it is highly probable that with the passage of time, high blood-pressure will become more frequent. CONCLUSIONS
A follow-up study of 175 patients who had had poliomyelitis many years before showed an overall incidence of high blood-pressure of only 5.7 per cent at a mean age
The Incidence of Hypertension
Long after Poliomyelitis
273
of 35, considerably lower than that found in several studies of younger and more recently ill patients. Of the severely disabled, 22 per cent were hypertensive. In this series the hypertensives were 9 yr older than the normotensives, and it is hoped to follow these latter for another decade, but we find no evidence suggesting that poliomyelitis per se is followed by high blood-pressure. The mechanism producing this hypertension remains to be investigated. REFERENCES 1. MCDOWELL, F. H. and PLUM, F.: Arterial hypertension associated with acute anterior poliomyelitis, New Engl. J. Med. 245, 241, 1951. 2. VICKERS,H. D.: Anterior poliomyelitis. Relation to hypertension in young adults, N. Y. St. J. Med. 40, 55, 1940. 3. Z~MANYI,I., PROHAZKA, M., SZONDY, M. and ORMAI, S.: Arterial hypertension after poliomyelitis, Orv. Hetil. 100,573, 1959. 4. OSTFELD,A. M. $ustained hypertension after poliomyelitis, Archs. intern. Med. 107, 551, 1961. in poliomyelitis, Klin. Mbl. 5. NEUBAUER, H. and MAINZER, K.: Hypertensive arteriolopathy Augenheilk. 142, 708, 1963. 6. BENEVOLO,A., MUNZI, G. and UNGARI, S.: Arterial hypertension in subjects who have been afflicted with acute anterior poliomyelitis, Minervu Pediut. 15, 1404, 1963. 7. KEMP, E.: Arterial hypertension in poliomyelitis, Acta. Med. stand. 157, 109, 1957.
Since this paper was accepted for publication, there appeared in this journal* a study by Doctors Welner, Yosipovitch and Groen, of blood-pressure in children and adolescents severely injured from poliomyelitis. Casual levels were compared with those found in normal children, and with those of other children who had serious muscular damage from causes other than poliomyelitis, or who were blind. The levels found in those with muscular damage of any etiology were higher than those in normals. Possible mechanisms for this were discussed. *WELNER, A., YOSIPOVITCH,Z. H. and GROEN, J. J.: Elevated blood pressure in children and adolescents with residual paralysis and deformities from poliomyelitis and other crippling diseases. J. chron. Dis. 19, 1157, 1966.
Vol. 20, pp. 269-273. Pergamon Press Ltd. Printed in Great Britain
THE INCIDENCE
OF HYPERTENSION POLIOMYELITIS
LONG AFTER
LAWRENCEA. KOHN, M.D. and GRACEL. REID, B.Sc., R.N. Department of Medicine,School of Medicineand Dentistry, the Universityof Rochester,New York (Received 21 November 1966; in revised form 19 January 1967)
IN SEYERE poliomyelitis, with hypoxia of bulbar or other origin, arterial blood-pressure is often elevated, and this may outlast the acute phase of the disease by months (MCDOWELL and PLUM [l]). Hypertension long after the original illness was first recorded in 1940 by VICKERS[2] who found seven definite cases among 44 adults many years after they had had infantile paralysis. Although some of the hypertensives were badly crippled, most of them showed no muscle damage. ZIMANYI,and his co-workers [3] in 1959 observed among 336 children, chiefly young but a few in their ‘teens’, 88 instances (26 per cent) with systolic or diastolic pressures above the accepted norms for their age. The patients had been hospitalized for months or years, the vast majority for 5 yr or less, and of the hypertensives, 85 per cent were quadriplegic, with severe muscle damage in the remainder. OSTFELD [4] in 1961 compared bloodpressures found in cases in a Respiratory Center an average of 2 yr after their initial illness, with controls no longer in hospital but matched for age, sex and muscle-damage. Hypertension was frequent in all groups: 20 per cent over-all, with the incidence roughly paralleling the amount of muscle loss. NEUBAUERand MAINZER[5] in 1963 saw and photographed retinal arterial changes accompanying high blood-pressure in acutely ill patients with respiratory difficulty, and these changes sometimes lasted beyond the period of hypoxia. They suggested (as had often been hinted but rarely if ever put in print) that previous poliomyelitis in a mild or even non-paralytic form might be invoked to explain obscure hypertensive disease, perhaps through damage to medullary centers. BENEVOLOand co-workers (1963) [6] reported on 201 children observed at varying intervals after infantile paralysis. Approximately 20 per cent had blood-pressures higher than expected at their age. Of 39 children seen 4 or more yr after the initial disease, 15 per cent had diastolic pressures consistently above 90 mm of mercury. Most of them had severe paralysis. On the other hand, KEMP [7] in 1957 reported on 357 patients followed for periods up to 5 yr from onset, and concluded that: “. . . . neither children nor adults either mildly or severely affected had greater incidence of hypertension than individuals who had not had polio”. Since permanent elevation of blood-pressure after poliomyelitis might be favored by the aging process, as in the majority of hypertensive states, it appeared worth while to study a group of older survivors for the overall incidence of hypertension and for its possible relation to the degree of muscle damage. *In 1964 and 1965 this study was aided by a grant from the Monroe County Heart Chapter of the Health Association of Rochester and Monroe County. Address for reprints: 457 Park Avenue, Rochester, New York 14607. 269
770
LAWRENCE A. KOHNand GRACE L. REID
MATERIAL AND METHODS From cases whose acute infantile paralysis was observed in the Strong MemorialRochester Municipal hospitals from 1926 through 1949, we selected for attempted follow-up all those who had lived a minimum of 13 yr and who should be 19 yr or older if found. The high incidence of the disease in 1944 and 1945 provided a large cluster of cases which fell in these limits. Subsequently, for a special purpose we studied a smaller group of more recently ill patients. Diagnoses were checked critically from the hospital records by one of us who had had considerable experience with the acute disease and who had personally observed many of the cases 14 yr or older at the time of their illness. “Severity” as applied to the acute phase, measures the degree and duration of fever, prostration and complications as recorded by the attendant physicians. “Immediate damage” is a rough grading of the amount of muscle disability at discharge, or, if hospitalization was prolonged, at the conclusion of the acute phase. For follow-up we depended chiefly on letters to patients, their families and their physicians. Information was found in records of subsequent hospital admissions or visits to the Poliomyelitis Clinic, and in lists furnished by the Rochester Chapter of the National Foundation. There were many individual searches starting with hints from physicians who knew of our interest, or from the chance observation of unusual patients’ names. Estimates of muscle damage and blood-pressure were usually made by one of us in Rochester or in nearby communities, but when patients were traced at a distance (California, Florida, Great Britain), we accepted with gratitude the judgment of their present medical advisers. One of us observed the blood-pressure in 1501175 (85 per cent) of the “followed” patients. Although our search was persistent, we made every effort to prevent or allay anxiety in the patient or family, and while many followup failures were obviously due to lack of cooperation, those patients we reached were invariably agreeable and returned if asked for a second observation. Blood-pressure was estimated with conventional anaeroid sphygmomanometers which had been factory-standardized for accuracy, in the sitting position and on the left arm unless it was significantly wasted. Several readings were made to allow for subsidence of “nervous” rise. The levels recorded were obviously not “basal” but are thought to be reasonably accurate “casual” pressures. In the 25 patients observed on our behalf by other physicians, the blood-pressures were probably “casual” rather than “basal”. The definition of hypertension is controversial; for this study we chose the same standard as did OSTFELD(Zoc. cit.); if higher than 145/95 it is probably abnormal. This divided our patients satisfactorily; there was no overlap. Damage was graded in terms of disability and muscle loss. Minor or localized weakness which produced no functional impairment is included in grade 0. l-2 implies moderate to marked muscle loss in one or two limbs respectively (not both legs). Grade 3 calls for one paralyzed leg plus significant damage in two other areas and grade 4 disability, the necessity for crutches or a wheel-chair. Successful operative results such as tendon transplants or arthrodeses decreased slightly the grade assigned, which thus became a combined functional-anatomical classification. Whenever blood-pressure was found elevated, the observation was repeated months or years later, and in several instances suspected hypertension was excluded. The study was begun in 1956 and was concluded in 1965.
The Incidence of Hypertension
Long after Poliomyelitis
271
RESULTS
Of 326 patients we attempted to trace, we were successful in 175. The mean period of follow-up was 21.4 yr with a mode falling between 18 and 20 yr. Less than a quarter of those reached were under 30 and 40 per cent were 40 or older. Are these 53 per cent followed a fair sample ?
TABLET
Patients followed Mean age at onset Mean interval, onset to follow-up Mean initial severity Mean immediate damage Blood-pressure elevated during acute illness
Patients lost to follow-up 13.4
10 Mean interval, onset to 1960 (midpoint of study)
21.4 1.77 1.02 4189
18.5 1.85 0.7 3189
Thus the patients we were able to reach were slightly older than those lost to followup. Since (vi& in&a) the hypertensives appeared to have had more immediate damage, the difference in this index might favor an increased incidence of high blood-pressure in those observed. On the whole, they appear fairly representative of the entire group.
TABLE 2
Current disability
BP elevated
0
4 2 4
l-2 3-4 x2=10.215;
BP normal
% elevated
103 48 14
3.7 4.0 22.0
0.005
The incidence in the severely disabled is close to that found in younger similarly injured patients by most previous observers. While we reached relatively few crippled patients, the likelihood that the differences found arose by chance is small.
TAEZLE~
Hypertensives (10) Age at onset Age when followed Initial severity Initial damage EIevated BP during acute illness
Normotensives (165) 19 42 2.2 1.7
13 33 1.75 0.98
218
2/81
272
LAWRENCEA. KOHN and GRACEL. REID
The hypertensives were older at the onset of illness, were sicker at the time, had greater immediate damage and are currently older than the normotensives. The overall frequency of hypertension is 5.7 per cent, probably no higher than would be found in persons of similar age in the population at large. Among these ten patients, three of the four without muscle damage had a definite family history of high bloodpressure. Of the two with moderate injury, one had such a heredity. Of the severely damaged, two patients had no such familial tendency; in the other two cases the information was unavailable. Although many patients needed repeated or indwelling catheterization during their acute illness, only 11 of the 245 patients followed (both series) had persistent urinary infection and of these only one became hypertensive. DISCUSSION
It is possible that hypertension is more frequent soon after poliomyelitis and either disappears, or is of such severity that the individual affected succumbs early. Verified deaths were rare in our sample; we were able to establish only two in the patients we followed and one in those lost to follow-up, although obviously there might well have been other deaths in this sub-group. With this possibility in mind, we drew a second sample of patients whose acute illness was between 1950 and 1960, choosing older individuals as more likely to develop high blood-pressure. Of 70 such, we were able to trace 65 per cent. TABLE4
Followed
Not followed (25)
(45) Mean age at onset Mean follow-up interval
16 7.7
Mean initial severity Mean immediate damage
1.9 0.59
16 5.8 (Interval to 1960) 1.8 0.79
The severity is comparable to that of the older patients; the immediate damage less. TABLE5 Current disability 0 l-2 3-4
BP elevated 0 1 0
BP normal 37 3 5
The numbers are small, but there is no suggestion that hypertension is more frequent earlier. In any group of patients, it is highly probable that with the passage of time, high blood-pressure will become more frequent. CONCLUSIONS
A follow-up study of 175 patients who had had poliomyelitis many years before showed an overall incidence of high blood-pressure of only 5.7 per cent at a mean age
The Incidence of Hypertension
Long after Poliomyelitis
273
of 35, considerably lower than that found in several studies of younger and more recently ill patients. Of the severely disabled, 22 per cent were hypertensive. In this series the hypertensives were 9 yr older than the normotensives, and it is hoped to follow these latter for another decade, but we find no evidence suggesting that poliomyelitis per se is followed by high blood-pressure. The mechanism producing this hypertension remains to be investigated. REFERENCES 1. MCDOWELL, F. H. and PLUM, F.: Arterial hypertension associated with acute anterior poliomyelitis, New Engl. J. Med. 245, 241, 1951. 2. VICKERS,H. D.: Anterior poliomyelitis. Relation to hypertension in young adults, N. Y. St. J. Med. 40, 55, 1940. 3. Z~MANYI,I., PROHAZKA, M., SZONDY, M. and ORMAI, S.: Arterial hypertension after poliomyelitis, Orv. Hetil. 100,573, 1959. 4. OSTFELD,A. M. $ustained hypertension after poliomyelitis, Archs. intern. Med. 107, 551, 1961. in poliomyelitis, Klin. Mbl. 5. NEUBAUER, H. and MAINZER, K.: Hypertensive arteriolopathy Augenheilk. 142, 708, 1963. 6. BENEVOLO,A., MUNZI, G. and UNGARI, S.: Arterial hypertension in subjects who have been afflicted with acute anterior poliomyelitis, Minervu Pediut. 15, 1404, 1963. 7. KEMP, E.: Arterial hypertension in poliomyelitis, Acta. Med. stand. 157, 109, 1957.
Since this paper was accepted for publication, there appeared in this journal* a study by Doctors Welner, Yosipovitch and Groen, of blood-pressure in children and adolescents severely injured from poliomyelitis. Casual levels were compared with those found in normal children, and with those of other children who had serious muscular damage from causes other than poliomyelitis, or who were blind. The levels found in those with muscular damage of any etiology were higher than those in normals. Possible mechanisms for this were discussed. *WELNER, A., YOSIPOVITCH,Z. H. and GROEN, J. J.: Elevated blood pressure in children and adolescents with residual paralysis and deformities from poliomyelitis and other crippling diseases. J. chron. Dis. 19, 1157, 1966.