THE JOURNAL OF UROLOGY
Vol. 76, No. 1, July 1956 Printed in U.S.A.
A CLINICAL STUDY OF THE MOTOR PARALYTIC BLADDER IN POLIOMYELITIS B. G. CLARKE
From the Department of Urology, Tufts University School of Medicine, Boston, Mass.
Urinary retention has been reported as occurring in 4 to 42 per cent of patients with poliomyelitis in five epidemics upon which reports are available. 1- 5 In spite of the relative frequency of the complication there is little material in the literature upon which to base an understanding of the physiologic disturbances which occur. With this consideration in mind clinical data have been collected and analyzed from 13 cases. Six of the patients were observed by the author; the records of the other 7 were made available through the kindness of Dr. Edward C. Curnen. Urinary retention was found in 13 of 117 hospitalized cases observed in the present study, an incidence of 11 per cent. MATERIAL
The patients were seen during two epidemics: one in southern New England in 1949 and one in eastern Maine in 1952. Table 1 indicates that the bladder paralysis occurred during the acute, febrile phase of the illness. Among the 6 cases personally observed in 1952, urinary retention appeared concurrently with somatic paralyses in 3 patients, a day before appearance of skeletal muscle paralysis in 2 patients, and 4 days after the first skeletal muscle paralysis in 1. Distinct evidence of ileus was seen simultaneously with urinary retention in 5 of the 6 patients. In all the patients (cases 9-12) who were able to report their subjective reactions, the urinary retention was accompanied by mild to severe desire to void and suprapubic distress. No interference with bladder sensation was apparent. In the younger patients and in one of the adults (case 13) who had severe encephalitis, bladder distention, usually accompanied by overflow incontinence, were the usual presenting signs. Large residual urine volumes The study was aided by a grant from the Charlton Research Fund, Tufts University School of Medicine. Accepted for publication January 26, 1956. Acknowledgements: Dr. Edward Curnen, professor of pediatrics, University of North Carolina School of Medicine, has permitted inclusion of certain patients under his care in the study. Dr. Clyde Deming, professor emeritus of urology, Yale University School of Medicine; Dr. Derek Denny-Brown, professor of neurology, Harvard Medical School; and Dr. Reed Nesbit, professor of urology, University of Michigan, have advised in their fields of special interest, during various stages of the study. Dr. H. E. MacMahon, professor of pathology, Tufts University School of Medicine, reviewed the microscopic sections. 1 Duursma, S. A.: Disturbances of bladder function caused by poliomyelitis. Nederl. tijdschr. v. geneesk, 89: 216, 1945. (Abstract No. 8665, A Bibliography of Infantile Paralysis, 1880-1949, National Foundation for Infantile Paralysis, Inc., 2nd ed. Edited by M. Fishbein, M. Salmonsen, and L. Hektoen. Philadelphia: J. B. Lippincott, 1951.) 2 McDonald, S. F.: Signs and symptoms of the acute stage of anterior poliomyelitis in the 1931-32 epidemic. M. J. Australia, 1: 1-5, 1933. 3 Toomey, J. A.: The intestine and urinary bladder in poliomyelitis. Am. J. Dis. Child, 45: 1211-1215, 1933. 4 Tunevall, G.: Poliomyelitic bladder paralysis. Nord. med., 38: 880-885, 1948. (Abstract iii 9930, see footnote 1, p. 66.) 5 Wright, B. W.: Urinary complications in epidemic of poliomyelitis. J. Urol., 35: 618629, 1936. 66
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B. G. CLARKE
were obtained. In only one patient (case 2) was anal sphincter weakness observed although cases 9-13 were observed with particular reference to this point. Among the patients who survived, recovery from micturitional disturbances occurred during the subsidence of skeletal muscle paralyses of the extremities. DISCUSSION
In the present study, bladder paralysis occurring during acute poliomyelitis was a self-limited motor disturbance, unaccompanied by disturbances in vesical sensation in subjects able to report them. It appeared during the acute febrile phase of the disease at about the same time as the skeletal muscle paralyses and subsided when beginning skeletal muscle recovery was evident. In the younger subjects the micturitional disorders appeared to be milder, as also has been noted by vVright, 5 and responded favorably in most cases to administration of parasympathomimetic drugs as ::mggested by La,vson and Garvey, 6 or to other simple measures. In the older patients, a small, ind·welling Foley type catheter was left in place until the patient began to recover from the acute illness. It was considered that in the sick patients the use of an indwelling catheter was safer than intermittent catheterization accompanied by repeated urethral trauma and the recurring discomfort of bladder distention. In the two patients who died, kidneys and bladder were examined at autopsy 2 and 5 days after establishment of catheter drainage. Microscopic sections showed no evidence whatever of pyelonephritis although mild inflammatory changes were seen in the tunica propria of the bladder. A number of mechanisms have been suggested as the possible cause of urinary retention in acute poliomyelitis. It has been suggested7 that urinary retention may reflect loss of voluntary micturitional ability as a result of abdominal muscle weakness. Although this must be a contributing factor if it exists, only 6 of our 13 patients displayed abdominal muscle weakness during the course of their disease. It has also been suggested8 that the virus of poliomyelitis may act directly on the ganglia within the muscle wall of the bladder. Histologic study of these ganglia by a standard method 9 in the 2 patients who died during the fifth and ninth days of their disease (cases 11 and 13) failed to disclose any abnormality of these structures. Toomey's cystometric studies3 and our clinical observations indicate that the urinary retention of poliomyelitis is the result of detrusor weakness without sensory loss. Nesbit, Lapides and Baum10 have proposed the term motor paralytic bladder for this type of disorder. 6 Lawson, R. B. and Garvey, F. K.: Paralysis of the bladder in poliomyelitis. J.A.M.A., 135: 93-94, 1947. 7 Selverstone, B.: Personal communication, 1953. 8 Toomey, J. A., Pilcher, J. D. and Rossman, P. T.: Effects of poliomyelitic virus on the urinary bladder of rabbits. J. Pediat., 23: 166-167, 1943. 9 Swenson, 0., Mac~Iahon, H. E., Jaques, W. E. and Campbell, J. S.: A new concept of the etiology of megaloureters. New Eng. J. Med., 246: 41-46, 1952. 10 Nesbit, R. M., Lapides, .T. and Baum, W. C.: Fundamentals of Urology. Ann Arbor, jVIich.: J. E. Edwards, 1953.
STFDY OF J\IOTOH l',UULYTIC BL,\DDloft Ii': l'OLIOMYJ<;LITIS
The observations of Bodian, 11 Goodpasture, 12 8abin/3 and others indicate that poliomyelitis is a generalized encephalomyeliti:-; with wide di:-;tribution of lesion:-; of varying degrees of severity and reversibility, many of them clinically unapparent, throughout the spinal cord, brain stern, and brain. It seems reasonable to conclude that the urinary retention, when it occurs in this disease, simply reflec:tt:J motoneuron changes, usually reversible, in the lateral columns of the sacral segments of the spinal cord, from which originate the parasympathetic motor nerves of the bladder. If this type of motor paralytic bladder is untreated it ,Yill overflow, decornpensate, and become atonie. 10 Three cases have been reported by \Vright5 in which a chronic, hypotonic type of bladder developed. Keyes 14 obscn·ed a patient in whom this situation eventuated in a fatal pyelorwphritis. SUMMARY
In 1;3 patients, bladder paralysis appeared concmTently with peripheral, skeletal muscle paralysis during the acute, febrile stage of poliomyelitis. Distribution of peripheral paralyses had 110 relationship to segmental location of bladder motor imierYation. Among the adults capable of de:ocribing sensation, micturitional disturbances assumed the form of painful urinary retention. Large volumes of residual urine were obtained. lleus of varying degrees of i,ever .. ity developed concurrently with difficulty voiding. In 2 patients who died, no histologic abnormality of the muscle, nerves ur ganglia of the bladder wall could he found. Paralysis of the abdorninal striated muscles was present in only half of the patients. In t:Jluviving patients, normal bladder function returned during defervescence and beginning recovery of skeletal muscle paralyses. In the younger patients, simple measures such as manual expression of the bladder, ~1dministration of parasy1npathomimetic drug8, or one or two catheterizations sufficed for treatment. In the adults, indwelling catheter drainage during the phase of bladder paralysis was used suece8sfully until return of normal bladder function. 11. Bodian, D.: Poliomyelitis: Xcurop;cthologic observu.t.ions in rclaiion to motor symptoms . .J.A.J\LA .. 134: 11481154, Hl47. 12 Coodpastmc, E. W.: The pathology of poliomyelitis. J.A.J\l.A., 117: 273-·27fi, JD41. 13 Sabin, A. B.: Pathology and pathogenesis of human poliomyelitis. J.A.M.A., 120: 506-511. HJ42. 14 l(eyes, B. L.: Severe visccrnl complications inn.cute an Leri or poliomyelitis . .J. Pediat 10: 2:n-235, rn3i.