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or Spinal Cord Concussion
TIIE JOURNAL OF UROLOGY
Vol. 81, No. 5, May 1959
Printed
1·n
U.S.A.
REVERSIBLE :;\;EUROGENIC BLADDER FOLLOWING CEREBRAL SPINAL CORD CO:;\/CUSSIO~ EDWARD E. SHEV
AND
During the initial and over-all evaluation and treatment of the injured patient, assessment of function of the bladder may include little more than a single urethral catheterization. If the urine is not bloody, scant attention is given to this system during the next 24 hours. Disturbed bladder function may be overlooked for days or even weeks. Constipation may be the first sign of dysfunction of the associated nerve pathways to bowel and bladder. Overt manifestations of serious injuries to the head and spinal column usually engage the physician's continued observation to the neglect of concurrent urinary and fecal retention following the trauma. These disturbances in function of the bladder and bowd arc presumably due to concussion of the ccrebrospinal axis and are indistinguishable from those attributable to irreversible damage to the brain and spinal cord, especially during the early stages. There are few reports in the literature specifically concerning the status of bladder and bowel following concussion of the el'rebrospinal axis. Detailed descriptions of the neurogenic bladder secondary to various dcgrel's and types of permanent damage to the brain and spinal cord have been reported. 1- 6 These reviews possess a related rather than a direct bearing upon the present report. During the past year, 1\e have seen six cases of "revr;rsible ncnrogcniu bladder." CollaboraAccepted for publication October 31, 19.58. 1 Schwartz . .J. W.: The earlv treatment of the neurogenic bladder. Mil. Snr1s.," 115: 411-414, 1954. 2 Boshes, B., Zivin, I. and Tigay, E. L.: Recent methods of management of spinal cord and cauda equina injuries. Neurology, 4: 690-704, 1954. ' Prather, G. C. and l\Iayfield, F. H. : lnj uries of the Spinal Cord. Springfield, Ill.· Charles C Thomas, l\)53. 4 Emmett, J. L.: N eurogenic vesical dysfunction (cord bladder) and neuromuscula,r ureteral dysfunction. In Urology, vol. 2, edited by Campbel!. Philadelphia: W. B. Saunders Co., HJ54, pp. 12851383. 5 Naffziger, H. C. and Adams, J. E.: Spinal cord trauma. In Clinical Neurology, vol. 3, edited by A. B. Baker. New York: Roeber-Harper, 1955, pp. 1422-1448. 6
Bors, E.: Neurogenic, bladder. Urol Survey, 7:
177-250, Hl.57.
653
ALEX L. FINKLE
tion between the neurologist and urologist Jed to concepts of diagnosis and treatment which are reported here. CASE REPORTS
Case 1. J\'I. P., a 26-year-old ,,-hitc woman, was injured as a passenger in a sports car that was involved in a head-on collision witb another vehicl8 September 9, 1955. The mechanism of injury was a "jack-knife" flexion of her head on to the chest, producing instantaneo1rn m the mid-posterior neck. She did not lose consciousness. She suffered extensive bruises of tl1e head, neck, legs and anterior ehest wall. Diffu8e headaches and dizziness developed within hours. For 21 days, constant Sayre head traction was applied at a small general hospital to which slie had been admitted within one-half hour after the accident. "-\.pparently, little attention wn,s paid to her urinary status, since subsequrnt review of the hospital records disclosed that no hours after advoiding had occurred until J mission. Not until 22 hours latl'r and three unsuccessful attempts to void did she succeed, Intervals of six to 28 hours then elapsed between voidings during the next three >"1·ec-ks prior to ber transfer to a hospital in San Francisco, September 30, 1955. During her original hospitalization, enrrnas "·ere necessary every two or three days. Dr. R. V\T agner, hPr attending invited a neurological consultation, Ortoher ,1, 195,5. During this examination, thr patil'nt complained of "feeling incomplete emptying of tbc: bladder after urinating." A mild degree of abdominal distention mIB still prl'scnt in spite of ''effective encrnas" which overcame six of constipation. Physical examination l'enaled unequal pupils, intact function of thl' cranial nerves, rigidity of the neck due to muscle spasrn and absent superficial abdominal reflexe,. , \n electroencephalographie recording, Octobl'r 1955, disclosed a generalized slmY pattern. l'rological consultation was requcsk,l October 13, 1955. Forced oral hydr,1.tion wrts orc!Necl so
654
EDWARD E. SHEY AND ALEX L. FINKLE
that bladder function could be assessed: 500 cc water was drunk one hour before she voided 500 cc urine on a commode. Immediate urethral catheterization recovered 130 cc residual urine. (A specimen of the residual urine was cultured for bacteria, but none grew.) Cystometry performed the following day revealed a bladder capacity of 1000 cc with a flattened curve representing intravesical pressure. Urethral catheterization recovered 520 cc residual urine from the atonic bladder. A bladder training program consisting of hourly fluid intakes and of sitting on the toilet every 90 minutes to attempt urination was instituted. Urecholine, 10 mg., was administered orally, twice daily, for three weeks. During this time, cystometric studies revealed improved bladder tone; smaller amounts of residual urine were recoverable by urethral catheter than previously. Within five months the cystometric patterns had returned to normal; there was no residual urine and no regulations of fluid intake or scheduled urination were necessary. Gradual recovery of superficial abdominal and deep tendon reflexes was also complete by this time. No further urinary difficulties were reported at the time the patient was last contacted, two years after the accident. Case 2. M. E., a 25-year-old white man, was walking when struck by an automobile December 1956. He was unconscious for four hours. Roentgenologic examinations disclosed a crack in the lateral masses of C-5, C-6 and on the anterior superior border of L-5. Generalized bruises were also sustained. Weakness and multiple episodes of unconsciousness occurred within one week after the injury. Continued weakness after dismissal from the hospital led the patient to renew medical care; he was hospitalized elsewhere December 15, 1956. Dr. A. Zipser, the patient's internist, requested urological consultation after the nurses reported that the patient had urinated only three times daily; each urination was 900 to 1100 cc in volume. (Urination had normally occurred 10 times a day because the patient habitually maintained a fluid intake of over six quarts daily.) When the infrequent urinations were noted during hospitalization, urethral catheterization was performed December 17, 1956; 920 cc residual urine was recovered. Enemas were necessary every third day, despite the fact that the patient was ambulatory while in the hospital.
Examination was negative except for emotional instability and depressed superficial abdominal and cremasteric reflexes. Laboratory data were not significant. Results of an electroencephalogram, December 17, 1956, were within normal limits. Cystography and cystometry revealed poor detrusor tone, smooth bladder contour, vesical capacity 1550 cc and 450 cc residual urine. Indwelling urethral catheterization was begun; urecholine, 5 mg., thrice daily, was administered orally. Without instruction or encouragement, prodigious fluid intake was maintained by the patient and more than five liters of urine were excreted daily during the next 96 hours. (Restricted intake one afternoon produced a urinary specific gravity of 1.016, thus ruling out diabetes insipidus.) After these four days of indwelling urethral catheterization, cystometry disclosed marked improvement of detrusor tone and decline in bladder capacity to 400 cc. The urethral catheter was removed and urecholine was maintained for three additional days. Urinations then varied in quantity from 400 to 900 cc. The patient refused to adhere to any regularity of fluid intake and output. About one week after bladder evaluation had been made, chills and fever developed, owing to urinary infection. Antibiotics controlled the infection within two days, but 20 days later, a recurrence took place and was again readily overcome by use of antibiotics. Three weeks later epididymo-orchitis constituted the final infectious problem. A cystometric study on January 16, 1957 demonstrated a poorer bladder status than that 10 days previously: bladder capacity was 700 cc and there was 250 cc residual urine. Urecholine had not been taken by the patient as ordered. When the final cystometric study was performed February 7, 1957, bladder capacity was 850 cc and no residual urine was found. The patient said that he was urinating three to five times daily, "about one-half quart each time," without difficulty. Sexual intercourse was reported as normal. Case 3. A. E., a 31-year-old white man, was injured as a pedestrian when struck by an automobile February 10, 1957. Although badly dazed, at and just after, the time of the injury, he was not unconscious. No bony injuries were sustained, but generalized bruises occurred. Within the first month following the accident, the patient was constipated but had no overt urinary dif-
REVERSIBLE NEUROGENIC BLADDER
ficulty. The constipation improved gradually, without treatments, within 60 days after the injury. In the second month after the accident, urinary dribbling supervened and urological consultation was sought by his general practitioner, Dr. T. Diller. Concurrently with the dribbling, severe urinary urgency gradually developed; if the patient could not urinate promptly, he would soil his clothes. At the time of the first urological evaluation, March 28, 1957, the patient was observed to void 150 cc urine, just after which catheterization recovered 90 cc residual urine. Cystoscopy, cystography and cystometry three days later disclosed hyperemia of the verumontanum, prostatic urethra and floor of the bladder. An irritable, spastic bladder of 275 cc capacity was noted. Cystograms showed a spastic bladder; after the patient voided the opaque material, residual urine of 140 cc was present, as was suggested radiographically by the presence of residual dye within the bladder. Despite use of voluntary gluteal muscle exercises and the periodic administration of banthine, 50 mg., taken orally twice daily, urinary urgency and consequent episodes of incontinence continued. These complaints were corroborated by four cystometric demonstrations of autonomous, spastic detrusor tone at monthly intervals. The most recent cystometric study was performed February 17, 1958 at which time the only improvement was absence of residual urine. Incomplete voluntary control of the external urethral sphincter was observed during urination. Prostatic examination revealed a boggy consistency of the gland; microscopically, the expressed prostatic secretion contained 10 to 20 leukocytes per high power field. These findings were consistent with prostatitis, which doubtless aggravated the erratic, uncontrollable discharge of urine. Case 4. E. J., a 32-year-old colored man, was resting in the rear seat of an automobile parked near a highway April 19, 1957, when his vehicle was struck by a heavy truck. He was hospitalized immediately. He urinated once within 10 hours after the accident, but not thereafter; an indwelling Foley catheter was left in place during 13 days of hospitalization. During that time his bowels were evacuated twice, each time by an enema. After transfer to a San Francisco hospital, the urethral catheter was removed and the
655
patient urinated only once in 24 hours. Catheterizations were performed twice on May 5, 1957, which recovered 780 cc and 1100 cc respectively. Urological evaluation was requested by Dr. W. Garner, the attending general practitioner. Physical examination disclosed the absence of superficial abdominal and also of the cremasteric reflexes. Urinalysis at the time of admission to the San Francisco hospital showed 2-plus proteinuria, 3 to 5 white blood cells, numerous erythrocytes and a few bacteria. Bony fractures of the body of C-6 and of the transverse process of L-5 were noted radiologically. On May 7, 1957, cystoscopy demonstrated a slightly enlarged, boggy and hyperemic verumontanum and prostatic urethra. Bladder capacity was 900 cc. Cystometry revealed sluggish detrusor tone, with pronounced plateau between 400 to 800 cc in response to 50 cc instillations of fluid. Voluntary attempts to produce maximal increase in intra-abdominal and intravesical pressure resulted in poor response. Cystograms demonstrated an atonic bladder of large capacity with smooth contour. After the patient voided the radiopaque dye, 110 cc residual urine was measured and also demonstrated by roentgenograms. On the basis of the diagnosis of post-traumatic neurogenic bladder, secondary to spinal cord concussion, indwelling urethral catheterization was maintained for six days. For the first two days, the patient received urecholine, 5 mg. orally, three times daily. On the next three days, the dosage was 10 mg. orally, thrice daily. On May 16, a cystometry was performed again and disclosed an irritable bladder of 400 cc capacity, with high intravesical pressure in response to initial increments of fluid. Maximal increase in intravesical pressure by straining was only 16.25 cm., H~O. On this date superficial abdominal and cremasteric reflexes could be elicited for the first time. Only 50 cc residual urine was present. Cystometric and cystographic studies were performed again on June 6 and July 12, 1957. A smoother response to stretching of the detrusor was noted with 50 cc increments of fluid. Bladder capacity was 500 cc. Maximal voluntary increase in intra-abdominal pressure produced an intravesical pressure of 38 cm., H20. In June, 70 cc residual urine was noted; however, no residual was found in July 1957. The patient had never experienced difficulty in sexual function. Cystometric and cystographic studies m
656
EDWARD E. SHEY AND ALEX L. FINKLE
November 1957 and February 1958 were normal. However, cremasteric and superficial abdominal reflexes were still poor in February 1958. Case 5. G. M., a 37-year-old white truck driver, was knocked unconscious "momentarily" when another truck crossed the highway's center line and turned over the vehicle driven by the patient, December 12, 1955. He was rushed to a nearby hospital immediately after the accident. During 24 hours of hospitalization, urinations were "infrequent." However, while on a 200-milc bus trip to San Francisco, just after leaving that hospital, urinary urgency suddenly occurred and led to precipitate incontinence three times within four hours, while the bladder "kept feeling full." Upon arrival to the hospital in San Francisco, December 13, 1955, roentgenologic examination corroborated the lack of bony injury. An electroencephalogram disclosed no abnormalities. On the next day cystography revealed a smooth bladder contour, but cystometry demonstrated a spastic, irritable curve consistent with the "spastic phase of neurogenic bladder." Since urinalysis and prostatic evaluation were negative, the vesical spasticity ,vas attributed to the recovery phase of cerebral or distal spinal cord concussion. The cystogram was normal December 16, 1955 and, as was the case when this study was first done, only 5 cc residual fluid was present after the patient voluntarily expelled 350 cc fluid from the bladder. At the time of the last visit, six weeks after the accident, there were no urinary difficulties. Urinalysis was negative. No residual urine was found by urethral catheterization. Further studies were not possible because the patient moved to another part of the country. Case 6. L. l\1., a 42-year-old white woman, received a "whiplash" injury on June 14, 1953 when her parked car was struck from the rear. She complained regularly of low cervical pain, which radiated to the left shoulder. In June 1954, extensive neurological studies were perfom1ed, including cervical myelograms; the latter showed incomplete compression of the spinal cord between C-5 and C-6. No attention had been paid to bladder function at that time. In August 1957, neurological re-evaluation was done, revealing an incomplete BrownSequard syndrome at level of the low cervical region. Right-sided Babinski reflex, patellar
clonus and left-sided sensory changes, including impairment of the position sense, were found. It was noted at this time that her bladder habits had altered over the previous three years. Prior to her accident, the patient would void from four to six times daily, but subsequent to the trauma, urination occurred only once every 16 to 40 hours, without a preceding sensation of distention or intra-abdominal pressure. Between the hospitalizations in 1954 and 1957, she had one additional admission for an unrelated, minor orthopedic ]')rocedure. Later review of the nurses' notes for this admission disclosed that urinations took place only once during each 18 to 36 hours. Urological evaluations performed since August 1957 have shown an atonic neurogenic bladder consistent with an upper motor neuron lesion. Catheterizations have produced residual urines ranging from 300 to 750 cc. Passive fillings of the bladder revealed vesical capacity up to 1200 cc. With active filling of the bladder by urine, post-voiding catheterizations indicated a total vesical capacity of up to 1500 cc. Treatments have varied from courses of parasympathomimetic (urecholine) and parasympatholytic (donnatal) agents, without signal success. :\fild urinary antiseptics, chemotherapeutic and antibiotic agents have been used periodically, as necessary. During the past six months, the patient has shown slight vesical improvement, and has voided 125 to 400 cc urine every six to twelve hours. This change in the patient's condition may perhaps be attributable, at least in part, to a training pro~ gram of regulated fluid intake and timed urinary voidings. DISCUSSION
The bladder disturbance observed in whiplash or other types of reversible cerebral or spinal cord injury varies from the permanent "neurogenic bladder" only in the duration of dysfunction. Normal or comparably pre-traumatic bladder function is eventually recovered. Bors 6 presents a concise classification of neurogenic bladder based on the type of lesion, its extent (complete or incomplete), localization in regard to the co nus (central or "upper"; peripheral or "lower" motor neuron) and ratio of residual urine to bladder capacity. Thus, an initial stage and a stage of recovery following the damage to the brain and/or spinal cord constitute the fundamental considerations of classi-
657
REVERSIBLE NEUROGENIC BLADDER
fication. The three phases of vesical recovery cited by Prather and Mayfield 3 and McLellan 7 are, according to Bors, 6 " .•• transitional stag:s of a single continuous process, namely, recovery". Cystometric findings in each stage of recovery are reviewed by Mullenix. 8 In our cases of reversible neurogenic bladder it became clear that the "third stage" was not reached, although the first two stages of bladder dysfunction due to spinal cord trauma were evident. In cases 1 and 6 of our series, unbalanced bladder function persisted for many weeks during which slow and erratic (rather tha~ progressive) improvement occurred. Complete recovery of bladder function eventually took place in five of our six patients. After 2!,i years of observation, improvement is still occurring in our sixth patient. It is recognized that the initial episode of posttraumatic distention of the bladder in the unconscious patient may lead, per se, to a slowly resolving vesical atony. 1 However, that situation would seem entirely different from the "reversible neurogenic bladder" of cerebral or spinal cord concussion, wherein loss of superficial abdominal and cremasteric reflexes, as well as other neurological signs, may be noted. Moreover, indwelling urethral catheterization should suffice to overcome promptly the atony of mechanical overdistention of the bladder within several days. Until 20 years ago, when Munger 9 wrote of the ever-increasing incidence of "cord bladder " the subject was hardly recognized. Munro 10 r~emphasized the problem several years later. Carpenter11 referred briefly to this phenomenon in 1952. However, even as recently as 1957, a symposium on severe trauma neglected the "reversible neurogenic bladder."12-14 7 ~cLellan, F. C.: The Neurogenic Bladder. Sp[mgfield1 Ill.: Charles C. Thomas Co., 1939. Mullemx, R. B.: Cystometry in the study of traumatic neurogenic bladder. J. Urol., 55: 470-
482, 1946.
'. Munger, A. D.: The urologic-orthopedic viewpomt on the cord bladder. J. Urol. 37: 54-59 1937 10 Munro, D.: Cervical cord injilries. New' Eng: J. Med., 229: 919-933, 1943. : 1 Carpenter, M. B.: En passant injury of the spmal cord. U. S. Armed Forces Med. J. ·3: 14411456, 1952.
'
12 McCarroll, H. R.: Orthopedic management of the severely injured patient. J. A. M.A. 165·
1913-1916, 1957. ' . 13 DeWeerd, J. H.: Care of the severely injured patient: Urologic aspects. J. A. M.A. 165: 19161921, 1957. ' 14 White, J. C.: Care of the severely injured
In short, "reversible neurogenic bladder" deserves renewed interest and study. Prognosis depends upon early diagnosis. TREATMENT
Our therapeutic program is as follows: 1) A size 16 or I8F, indwelling urethral catheter is inserted and is connected to gravity ("straight") drainage. The catheter is changed every five days. The catheter is clamped for 30 to 60 minute intervals within 24 hours after the patient is fully conscious and co-operative. This provides estimates of vesical capacity as "spinal shock" dissipates. It should be noted whether severe trauma of the abdominal wall distorts perception of sensation of fullness of the bladder. If immediate indwelling catheterization has been overlooked or has not been feasible, this is done as soon as the attending physician becomes aware of the bladder dysfunction. 2) Liberal fluid intake should be ordered. One glass of water, imbibed "on the hour," reminds the patient of this all-important factor in the care of the neurogenic bladder. Other fluids may be taken, ad libitum, in addition to the water. 3) Urination should be attempted by the patient at specific intervals, usually every I!,~ hours, as soon as the urethral catheter is removed. This "re-education of detrusor tone" compliments the clampings of the catheter described in Principle 1. 4) Urecholine, 5 to 20 mg., every three to five hours, is administered orally. Dosages and intervals between medication are determined by the completeness of bladder emptying and rate of recovery of detrusor function. Usually a trial is made with 10 mg. dosages of urecholine, every five hours, while the patient is awake, for a period of five days. Withholding this medication for the succeeding five days ordinarily suffices as empirical estimation of the efficacy of such parasympathomimetic agents. 5) Mandelamine, 0.5 to 1.0 gm., every six hours, is provided orally. This is probably desirable in counteracting the inevitable cystitis and urethritis secondary to indwelling catheterization. The drug is prescribed in successive fiveday courses until residual urine is less than 30 cc. If indwelling catheterization does not promote patient: Neurosurgical injuries. J. A. M.A. 165: 1924-1930 1957.
'
658
EDWARD E. SHEY AND ALEX L. FINKLE
prompt return of vesical function, cystography and cystometry (and perhaps cystoscopy) may be performed to provide base-line data. Irrigation of the ind,velling catheter has not been recommended because generous fluid intake should serve to keep the bladder free of detritus and minimize the infection. Should irrigation be desired, a "closed system" described by Bors, 6 using a saline irrigant controlled by the patient, is preferred. In most instances of reversible neurogenic bladder, function should sufficiently improve within several weeks to warrant removal of the urethral catheter. Re-educating the bladder to a habit-pattern of urination is accomplished by regulating frequency of fluid intake, clampings of the catheter and (later) scheduled micturitions. Use of urecholine or like agents during the re-educational process is optional. Since no impairment of sexual function accompanied "reversible neurogenic bladder" in our patients, no comments seemed warranted. SUMMARY
Trauma to the cerebrospinal axis produces dysfunctions of the bladder and bowel probably
far more frequently and seriously than is generally documented. After consciousness is recovered, a persistent absence of superficial abdominal (and cremasteric) reflexes should lead to an investigation of possible vesical and rectal disturbances. Six personally supervised cases of "reversible neurr,genic bladder" secondary to cerebral or spinal cord contusion are reviewed. Discussion of the manifestations and mechanisms of disturbed vesical function is presented. A therapeutic regimen, based essentially upon decompression of the erratic bladder and upon augmentation of detrusor tonicity is offered. Disturbed expulsion of urine and feces as aftermaths of cerebrospinal trauma simulate irreversible injury. Recovery of nsical function is directly proportionate to the extent of the central nervous tissue changes, early diagnosis and efficacy of promptly instituted treatment. Sincere thanks are profferred to Dr. Ernest Bors, Long Beach, Cal., for his perusal of this report and for the helpful comments that he rendered.
516 Sutter St., San Franci:sco 2, Cal. (E. E. S.)
Vol. 81, No. 5, May 1959
Printed
1·n
U.S.A.
REVERSIBLE :;\;EUROGENIC BLADDER FOLLOWING CEREBRAL SPINAL CORD CO:;\/CUSSIO~ EDWARD E. SHEV
AND
During the initial and over-all evaluation and treatment of the injured patient, assessment of function of the bladder may include little more than a single urethral catheterization. If the urine is not bloody, scant attention is given to this system during the next 24 hours. Disturbed bladder function may be overlooked for days or even weeks. Constipation may be the first sign of dysfunction of the associated nerve pathways to bowel and bladder. Overt manifestations of serious injuries to the head and spinal column usually engage the physician's continued observation to the neglect of concurrent urinary and fecal retention following the trauma. These disturbances in function of the bladder and bowd arc presumably due to concussion of the ccrebrospinal axis and are indistinguishable from those attributable to irreversible damage to the brain and spinal cord, especially during the early stages. There are few reports in the literature specifically concerning the status of bladder and bowel following concussion of the el'rebrospinal axis. Detailed descriptions of the neurogenic bladder secondary to various dcgrel's and types of permanent damage to the brain and spinal cord have been reported. 1- 6 These reviews possess a related rather than a direct bearing upon the present report. During the past year, 1\e have seen six cases of "revr;rsible ncnrogcniu bladder." CollaboraAccepted for publication October 31, 19.58. 1 Schwartz . .J. W.: The earlv treatment of the neurogenic bladder. Mil. Snr1s.," 115: 411-414, 1954. 2 Boshes, B., Zivin, I. and Tigay, E. L.: Recent methods of management of spinal cord and cauda equina injuries. Neurology, 4: 690-704, 1954. ' Prather, G. C. and l\Iayfield, F. H. : lnj uries of the Spinal Cord. Springfield, Ill.· Charles C Thomas, l\)53. 4 Emmett, J. L.: N eurogenic vesical dysfunction (cord bladder) and neuromuscula,r ureteral dysfunction. In Urology, vol. 2, edited by Campbel!. Philadelphia: W. B. Saunders Co., HJ54, pp. 12851383. 5 Naffziger, H. C. and Adams, J. E.: Spinal cord trauma. In Clinical Neurology, vol. 3, edited by A. B. Baker. New York: Roeber-Harper, 1955, pp. 1422-1448. 6
Bors, E.: Neurogenic, bladder. Urol Survey, 7:
177-250, Hl.57.
653
ALEX L. FINKLE
tion between the neurologist and urologist Jed to concepts of diagnosis and treatment which are reported here. CASE REPORTS
Case 1. J\'I. P., a 26-year-old ,,-hitc woman, was injured as a passenger in a sports car that was involved in a head-on collision witb another vehicl8 September 9, 1955. The mechanism of injury was a "jack-knife" flexion of her head on to the chest, producing instantaneo1rn m the mid-posterior neck. She did not lose consciousness. She suffered extensive bruises of tl1e head, neck, legs and anterior ehest wall. Diffu8e headaches and dizziness developed within hours. For 21 days, constant Sayre head traction was applied at a small general hospital to which slie had been admitted within one-half hour after the accident. "-\.pparently, little attention wn,s paid to her urinary status, since subsequrnt review of the hospital records disclosed that no hours after advoiding had occurred until J mission. Not until 22 hours latl'r and three unsuccessful attempts to void did she succeed, Intervals of six to 28 hours then elapsed between voidings during the next three >"1·ec-ks prior to ber transfer to a hospital in San Francisco, September 30, 1955. During her original hospitalization, enrrnas "·ere necessary every two or three days. Dr. R. V\T agner, hPr attending invited a neurological consultation, Ortoher ,1, 195,5. During this examination, thr patil'nt complained of "feeling incomplete emptying of tbc: bladder after urinating." A mild degree of abdominal distention mIB still prl'scnt in spite of ''effective encrnas" which overcame six of constipation. Physical examination l'enaled unequal pupils, intact function of thl' cranial nerves, rigidity of the neck due to muscle spasrn and absent superficial abdominal reflexe,. , \n electroencephalographie recording, Octobl'r 1955, disclosed a generalized slmY pattern. l'rological consultation was requcsk,l October 13, 1955. Forced oral hydr,1.tion wrts orc!Necl so
654
EDWARD E. SHEY AND ALEX L. FINKLE
that bladder function could be assessed: 500 cc water was drunk one hour before she voided 500 cc urine on a commode. Immediate urethral catheterization recovered 130 cc residual urine. (A specimen of the residual urine was cultured for bacteria, but none grew.) Cystometry performed the following day revealed a bladder capacity of 1000 cc with a flattened curve representing intravesical pressure. Urethral catheterization recovered 520 cc residual urine from the atonic bladder. A bladder training program consisting of hourly fluid intakes and of sitting on the toilet every 90 minutes to attempt urination was instituted. Urecholine, 10 mg., was administered orally, twice daily, for three weeks. During this time, cystometric studies revealed improved bladder tone; smaller amounts of residual urine were recoverable by urethral catheter than previously. Within five months the cystometric patterns had returned to normal; there was no residual urine and no regulations of fluid intake or scheduled urination were necessary. Gradual recovery of superficial abdominal and deep tendon reflexes was also complete by this time. No further urinary difficulties were reported at the time the patient was last contacted, two years after the accident. Case 2. M. E., a 25-year-old white man, was walking when struck by an automobile December 1956. He was unconscious for four hours. Roentgenologic examinations disclosed a crack in the lateral masses of C-5, C-6 and on the anterior superior border of L-5. Generalized bruises were also sustained. Weakness and multiple episodes of unconsciousness occurred within one week after the injury. Continued weakness after dismissal from the hospital led the patient to renew medical care; he was hospitalized elsewhere December 15, 1956. Dr. A. Zipser, the patient's internist, requested urological consultation after the nurses reported that the patient had urinated only three times daily; each urination was 900 to 1100 cc in volume. (Urination had normally occurred 10 times a day because the patient habitually maintained a fluid intake of over six quarts daily.) When the infrequent urinations were noted during hospitalization, urethral catheterization was performed December 17, 1956; 920 cc residual urine was recovered. Enemas were necessary every third day, despite the fact that the patient was ambulatory while in the hospital.
Examination was negative except for emotional instability and depressed superficial abdominal and cremasteric reflexes. Laboratory data were not significant. Results of an electroencephalogram, December 17, 1956, were within normal limits. Cystography and cystometry revealed poor detrusor tone, smooth bladder contour, vesical capacity 1550 cc and 450 cc residual urine. Indwelling urethral catheterization was begun; urecholine, 5 mg., thrice daily, was administered orally. Without instruction or encouragement, prodigious fluid intake was maintained by the patient and more than five liters of urine were excreted daily during the next 96 hours. (Restricted intake one afternoon produced a urinary specific gravity of 1.016, thus ruling out diabetes insipidus.) After these four days of indwelling urethral catheterization, cystometry disclosed marked improvement of detrusor tone and decline in bladder capacity to 400 cc. The urethral catheter was removed and urecholine was maintained for three additional days. Urinations then varied in quantity from 400 to 900 cc. The patient refused to adhere to any regularity of fluid intake and output. About one week after bladder evaluation had been made, chills and fever developed, owing to urinary infection. Antibiotics controlled the infection within two days, but 20 days later, a recurrence took place and was again readily overcome by use of antibiotics. Three weeks later epididymo-orchitis constituted the final infectious problem. A cystometric study on January 16, 1957 demonstrated a poorer bladder status than that 10 days previously: bladder capacity was 700 cc and there was 250 cc residual urine. Urecholine had not been taken by the patient as ordered. When the final cystometric study was performed February 7, 1957, bladder capacity was 850 cc and no residual urine was found. The patient said that he was urinating three to five times daily, "about one-half quart each time," without difficulty. Sexual intercourse was reported as normal. Case 3. A. E., a 31-year-old white man, was injured as a pedestrian when struck by an automobile February 10, 1957. Although badly dazed, at and just after, the time of the injury, he was not unconscious. No bony injuries were sustained, but generalized bruises occurred. Within the first month following the accident, the patient was constipated but had no overt urinary dif-
REVERSIBLE NEUROGENIC BLADDER
ficulty. The constipation improved gradually, without treatments, within 60 days after the injury. In the second month after the accident, urinary dribbling supervened and urological consultation was sought by his general practitioner, Dr. T. Diller. Concurrently with the dribbling, severe urinary urgency gradually developed; if the patient could not urinate promptly, he would soil his clothes. At the time of the first urological evaluation, March 28, 1957, the patient was observed to void 150 cc urine, just after which catheterization recovered 90 cc residual urine. Cystoscopy, cystography and cystometry three days later disclosed hyperemia of the verumontanum, prostatic urethra and floor of the bladder. An irritable, spastic bladder of 275 cc capacity was noted. Cystograms showed a spastic bladder; after the patient voided the opaque material, residual urine of 140 cc was present, as was suggested radiographically by the presence of residual dye within the bladder. Despite use of voluntary gluteal muscle exercises and the periodic administration of banthine, 50 mg., taken orally twice daily, urinary urgency and consequent episodes of incontinence continued. These complaints were corroborated by four cystometric demonstrations of autonomous, spastic detrusor tone at monthly intervals. The most recent cystometric study was performed February 17, 1958 at which time the only improvement was absence of residual urine. Incomplete voluntary control of the external urethral sphincter was observed during urination. Prostatic examination revealed a boggy consistency of the gland; microscopically, the expressed prostatic secretion contained 10 to 20 leukocytes per high power field. These findings were consistent with prostatitis, which doubtless aggravated the erratic, uncontrollable discharge of urine. Case 4. E. J., a 32-year-old colored man, was resting in the rear seat of an automobile parked near a highway April 19, 1957, when his vehicle was struck by a heavy truck. He was hospitalized immediately. He urinated once within 10 hours after the accident, but not thereafter; an indwelling Foley catheter was left in place during 13 days of hospitalization. During that time his bowels were evacuated twice, each time by an enema. After transfer to a San Francisco hospital, the urethral catheter was removed and the
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patient urinated only once in 24 hours. Catheterizations were performed twice on May 5, 1957, which recovered 780 cc and 1100 cc respectively. Urological evaluation was requested by Dr. W. Garner, the attending general practitioner. Physical examination disclosed the absence of superficial abdominal and also of the cremasteric reflexes. Urinalysis at the time of admission to the San Francisco hospital showed 2-plus proteinuria, 3 to 5 white blood cells, numerous erythrocytes and a few bacteria. Bony fractures of the body of C-6 and of the transverse process of L-5 were noted radiologically. On May 7, 1957, cystoscopy demonstrated a slightly enlarged, boggy and hyperemic verumontanum and prostatic urethra. Bladder capacity was 900 cc. Cystometry revealed sluggish detrusor tone, with pronounced plateau between 400 to 800 cc in response to 50 cc instillations of fluid. Voluntary attempts to produce maximal increase in intra-abdominal and intravesical pressure resulted in poor response. Cystograms demonstrated an atonic bladder of large capacity with smooth contour. After the patient voided the radiopaque dye, 110 cc residual urine was measured and also demonstrated by roentgenograms. On the basis of the diagnosis of post-traumatic neurogenic bladder, secondary to spinal cord concussion, indwelling urethral catheterization was maintained for six days. For the first two days, the patient received urecholine, 5 mg. orally, three times daily. On the next three days, the dosage was 10 mg. orally, thrice daily. On May 16, a cystometry was performed again and disclosed an irritable bladder of 400 cc capacity, with high intravesical pressure in response to initial increments of fluid. Maximal increase in intravesical pressure by straining was only 16.25 cm., H~O. On this date superficial abdominal and cremasteric reflexes could be elicited for the first time. Only 50 cc residual urine was present. Cystometric and cystographic studies were performed again on June 6 and July 12, 1957. A smoother response to stretching of the detrusor was noted with 50 cc increments of fluid. Bladder capacity was 500 cc. Maximal voluntary increase in intra-abdominal pressure produced an intravesical pressure of 38 cm., H20. In June, 70 cc residual urine was noted; however, no residual was found in July 1957. The patient had never experienced difficulty in sexual function. Cystometric and cystographic studies m
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EDWARD E. SHEY AND ALEX L. FINKLE
November 1957 and February 1958 were normal. However, cremasteric and superficial abdominal reflexes were still poor in February 1958. Case 5. G. M., a 37-year-old white truck driver, was knocked unconscious "momentarily" when another truck crossed the highway's center line and turned over the vehicle driven by the patient, December 12, 1955. He was rushed to a nearby hospital immediately after the accident. During 24 hours of hospitalization, urinations were "infrequent." However, while on a 200-milc bus trip to San Francisco, just after leaving that hospital, urinary urgency suddenly occurred and led to precipitate incontinence three times within four hours, while the bladder "kept feeling full." Upon arrival to the hospital in San Francisco, December 13, 1955, roentgenologic examination corroborated the lack of bony injury. An electroencephalogram disclosed no abnormalities. On the next day cystography revealed a smooth bladder contour, but cystometry demonstrated a spastic, irritable curve consistent with the "spastic phase of neurogenic bladder." Since urinalysis and prostatic evaluation were negative, the vesical spasticity ,vas attributed to the recovery phase of cerebral or distal spinal cord concussion. The cystogram was normal December 16, 1955 and, as was the case when this study was first done, only 5 cc residual fluid was present after the patient voluntarily expelled 350 cc fluid from the bladder. At the time of the last visit, six weeks after the accident, there were no urinary difficulties. Urinalysis was negative. No residual urine was found by urethral catheterization. Further studies were not possible because the patient moved to another part of the country. Case 6. L. l\1., a 42-year-old white woman, received a "whiplash" injury on June 14, 1953 when her parked car was struck from the rear. She complained regularly of low cervical pain, which radiated to the left shoulder. In June 1954, extensive neurological studies were perfom1ed, including cervical myelograms; the latter showed incomplete compression of the spinal cord between C-5 and C-6. No attention had been paid to bladder function at that time. In August 1957, neurological re-evaluation was done, revealing an incomplete BrownSequard syndrome at level of the low cervical region. Right-sided Babinski reflex, patellar
clonus and left-sided sensory changes, including impairment of the position sense, were found. It was noted at this time that her bladder habits had altered over the previous three years. Prior to her accident, the patient would void from four to six times daily, but subsequent to the trauma, urination occurred only once every 16 to 40 hours, without a preceding sensation of distention or intra-abdominal pressure. Between the hospitalizations in 1954 and 1957, she had one additional admission for an unrelated, minor orthopedic ]')rocedure. Later review of the nurses' notes for this admission disclosed that urinations took place only once during each 18 to 36 hours. Urological evaluations performed since August 1957 have shown an atonic neurogenic bladder consistent with an upper motor neuron lesion. Catheterizations have produced residual urines ranging from 300 to 750 cc. Passive fillings of the bladder revealed vesical capacity up to 1200 cc. With active filling of the bladder by urine, post-voiding catheterizations indicated a total vesical capacity of up to 1500 cc. Treatments have varied from courses of parasympathomimetic (urecholine) and parasympatholytic (donnatal) agents, without signal success. :\fild urinary antiseptics, chemotherapeutic and antibiotic agents have been used periodically, as necessary. During the past six months, the patient has shown slight vesical improvement, and has voided 125 to 400 cc urine every six to twelve hours. This change in the patient's condition may perhaps be attributable, at least in part, to a training pro~ gram of regulated fluid intake and timed urinary voidings. DISCUSSION
The bladder disturbance observed in whiplash or other types of reversible cerebral or spinal cord injury varies from the permanent "neurogenic bladder" only in the duration of dysfunction. Normal or comparably pre-traumatic bladder function is eventually recovered. Bors 6 presents a concise classification of neurogenic bladder based on the type of lesion, its extent (complete or incomplete), localization in regard to the co nus (central or "upper"; peripheral or "lower" motor neuron) and ratio of residual urine to bladder capacity. Thus, an initial stage and a stage of recovery following the damage to the brain and/or spinal cord constitute the fundamental considerations of classi-
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REVERSIBLE NEUROGENIC BLADDER
fication. The three phases of vesical recovery cited by Prather and Mayfield 3 and McLellan 7 are, according to Bors, 6 " .•• transitional stag:s of a single continuous process, namely, recovery". Cystometric findings in each stage of recovery are reviewed by Mullenix. 8 In our cases of reversible neurogenic bladder it became clear that the "third stage" was not reached, although the first two stages of bladder dysfunction due to spinal cord trauma were evident. In cases 1 and 6 of our series, unbalanced bladder function persisted for many weeks during which slow and erratic (rather tha~ progressive) improvement occurred. Complete recovery of bladder function eventually took place in five of our six patients. After 2!,i years of observation, improvement is still occurring in our sixth patient. It is recognized that the initial episode of posttraumatic distention of the bladder in the unconscious patient may lead, per se, to a slowly resolving vesical atony. 1 However, that situation would seem entirely different from the "reversible neurogenic bladder" of cerebral or spinal cord concussion, wherein loss of superficial abdominal and cremasteric reflexes, as well as other neurological signs, may be noted. Moreover, indwelling urethral catheterization should suffice to overcome promptly the atony of mechanical overdistention of the bladder within several days. Until 20 years ago, when Munger 9 wrote of the ever-increasing incidence of "cord bladder " the subject was hardly recognized. Munro 10 r~emphasized the problem several years later. Carpenter11 referred briefly to this phenomenon in 1952. However, even as recently as 1957, a symposium on severe trauma neglected the "reversible neurogenic bladder."12-14 7 ~cLellan, F. C.: The Neurogenic Bladder. Sp[mgfield1 Ill.: Charles C. Thomas Co., 1939. Mullemx, R. B.: Cystometry in the study of traumatic neurogenic bladder. J. Urol., 55: 470-
482, 1946.
'. Munger, A. D.: The urologic-orthopedic viewpomt on the cord bladder. J. Urol. 37: 54-59 1937 10 Munro, D.: Cervical cord injilries. New' Eng: J. Med., 229: 919-933, 1943. : 1 Carpenter, M. B.: En passant injury of the spmal cord. U. S. Armed Forces Med. J. ·3: 14411456, 1952.
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12 McCarroll, H. R.: Orthopedic management of the severely injured patient. J. A. M.A. 165·
1913-1916, 1957. ' . 13 DeWeerd, J. H.: Care of the severely injured patient: Urologic aspects. J. A. M.A. 165: 19161921, 1957. ' 14 White, J. C.: Care of the severely injured
In short, "reversible neurogenic bladder" deserves renewed interest and study. Prognosis depends upon early diagnosis. TREATMENT
Our therapeutic program is as follows: 1) A size 16 or I8F, indwelling urethral catheter is inserted and is connected to gravity ("straight") drainage. The catheter is changed every five days. The catheter is clamped for 30 to 60 minute intervals within 24 hours after the patient is fully conscious and co-operative. This provides estimates of vesical capacity as "spinal shock" dissipates. It should be noted whether severe trauma of the abdominal wall distorts perception of sensation of fullness of the bladder. If immediate indwelling catheterization has been overlooked or has not been feasible, this is done as soon as the attending physician becomes aware of the bladder dysfunction. 2) Liberal fluid intake should be ordered. One glass of water, imbibed "on the hour," reminds the patient of this all-important factor in the care of the neurogenic bladder. Other fluids may be taken, ad libitum, in addition to the water. 3) Urination should be attempted by the patient at specific intervals, usually every I!,~ hours, as soon as the urethral catheter is removed. This "re-education of detrusor tone" compliments the clampings of the catheter described in Principle 1. 4) Urecholine, 5 to 20 mg., every three to five hours, is administered orally. Dosages and intervals between medication are determined by the completeness of bladder emptying and rate of recovery of detrusor function. Usually a trial is made with 10 mg. dosages of urecholine, every five hours, while the patient is awake, for a period of five days. Withholding this medication for the succeeding five days ordinarily suffices as empirical estimation of the efficacy of such parasympathomimetic agents. 5) Mandelamine, 0.5 to 1.0 gm., every six hours, is provided orally. This is probably desirable in counteracting the inevitable cystitis and urethritis secondary to indwelling catheterization. The drug is prescribed in successive fiveday courses until residual urine is less than 30 cc. If indwelling catheterization does not promote patient: Neurosurgical injuries. J. A. M.A. 165: 1924-1930 1957.
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EDWARD E. SHEY AND ALEX L. FINKLE
prompt return of vesical function, cystography and cystometry (and perhaps cystoscopy) may be performed to provide base-line data. Irrigation of the ind,velling catheter has not been recommended because generous fluid intake should serve to keep the bladder free of detritus and minimize the infection. Should irrigation be desired, a "closed system" described by Bors, 6 using a saline irrigant controlled by the patient, is preferred. In most instances of reversible neurogenic bladder, function should sufficiently improve within several weeks to warrant removal of the urethral catheter. Re-educating the bladder to a habit-pattern of urination is accomplished by regulating frequency of fluid intake, clampings of the catheter and (later) scheduled micturitions. Use of urecholine or like agents during the re-educational process is optional. Since no impairment of sexual function accompanied "reversible neurogenic bladder" in our patients, no comments seemed warranted. SUMMARY
Trauma to the cerebrospinal axis produces dysfunctions of the bladder and bowel probably
far more frequently and seriously than is generally documented. After consciousness is recovered, a persistent absence of superficial abdominal (and cremasteric) reflexes should lead to an investigation of possible vesical and rectal disturbances. Six personally supervised cases of "reversible neurr,genic bladder" secondary to cerebral or spinal cord contusion are reviewed. Discussion of the manifestations and mechanisms of disturbed vesical function is presented. A therapeutic regimen, based essentially upon decompression of the erratic bladder and upon augmentation of detrusor tonicity is offered. Disturbed expulsion of urine and feces as aftermaths of cerebrospinal trauma simulate irreversible injury. Recovery of nsical function is directly proportionate to the extent of the central nervous tissue changes, early diagnosis and efficacy of promptly instituted treatment. Sincere thanks are profferred to Dr. Ernest Bors, Long Beach, Cal., for his perusal of this report and for the helpful comments that he rendered.
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