Smith’s General Urology - part 7 pdf

NEUROPATHIC BLADDER DISORDERS / 451 b. Hypertonic bladder—The problem with patients in this category is more serious because the bladder is spas- tic with reduced capacity and the sphincter is hypotonic. Virtually constant dribbling can result. The cystogram will reveal heavy trabeculation of the bladder, often with reflux and advanced hydroureteronephrosis. Anticholinergic med- ication should be given, and an indwelling catheter should be inserted for several months. Once upper urinary tract dilatation has improved and the bladder has been restored to a more spheric shape, intermittent catheterization may be reinstituted. With time and care, many of these chil- dren develop a more balanced type of bladder behavior. Continence may be gained without compromising the upper urinary tract. Most of these patients will not require urinary diversion if they are carefully followed up and if the parents actively participate in their care. B. SURGICAL TREATMENT If the bladder is of the spastic type with diminished capac- ity, there are several surgical options short of actual urinary diversion. Sacral nerve block during urodynamic evalua- tion helps in determining whether sacral nerve root section would be beneficial. This helps in cases of spastic bladder but not in cases of poorly compliant, fibrotic bladder. Sec- tioning the S3 nerves reduces intravesical pressures, improves storage, and reduces the risk of reflux or obstruc- tion of the ureters. For the patient with a mildly spastic bladder and rea- sonable storage capacity (>200 mL), urinary incontinence might be controlled via electrostimulation of the pelvic floor. Many of these patients have intact nerves to the sphincter. These can be stimulated to enhance sphincter tone and inhibit voiding. If the bladder has a limited capacity with poor compliance and poor contractility, aug- mentation cystoplasty followed by intermittent self-cathe- terization is the treatment of choice. If the refluxing patient has recurrent fever (equivalent to pyelonephritis) despite the presence of an indwelling catheter or if incontinence cannot be controlled because of poor detrusor compliance, urinary diversion must be con- sidered. Nonrefluxing continent reservoirs offer the most favorable long-term outlook for preservation of the upper urinary tract. 3. Control of Urinary Incontinence In the Hospital Urinary incontinence is one of the most distressing aspects of neurovesical dysfunction, especially when the bladder has otherwise adequate function. The problem is minimized in men who are hospitalized because supervision is available, bathrooms are nearby, and a bedside urinal is always avail- able. Women have a greater problem because they must use a bedpan or may require an indwelling catheter. Catheters have associated risks and do not always control leakage asso- ciated with spastic bladder. No simple, satisfactory solution to this problem has been devised for women. After Discharge After discharge from the hospital, most men with spastic bladders rely on a condom catheter for protection against leakage and for practical urine collection. The only excep- tion is patients who are predictably dry between catheter- izations. The condom catheter attaches to the penis with- out pressure and has a conduit to a leg bag. The adhesives are nonirritating and long lasting. Problems involved in keeping these catheters in place are limited to noncircum- cised patients and those with large suprapubic fat pads that shorten the length of the shaft of the penis. Circumcision or placement of a penile prosthesis will correct for these limitations. Urethral compression by means of a Cunningham clamp is occasionally preferred by patients. This protects only against low-pressure leakage, however, and if it is applied too tightly, a urethral diverticulum may develop. Other types of external collection devices are available (McGuire urinal, Texas catheter), but with advancements in adhesive glues for condom catheters and use of penile pros- theses, the other methods are being used less frequently. Neurostimulation Extensive research continues to be conducted on methods of restoring complete voluntary control over the storage and evacuation functions of the bladder. Sacral and puden- dal nerve anatomy has been determined so that surgical exposure of these nerves and their branches is possible. An electrode can be placed for selective stimulation of the bladder, levator, and urethral or anal sphincters. A number of possibilities exist for neurostimulation or rhizotomy, but only a few are practical. Urodynamic evaluation of bladder function following a nerve block or during neurostimula- tion can help determine the therapeutic value of these treatments. Single or multiple electrodes can be placed on selected nerves and coupled to a subcutaneous receiver. The desired function (continence or evacuation) can be selected. Usu- ally, one or the other is needed in any one patient. Much will change in this approach as technologic advances become adapted to the increased understanding of bladder physiology. Striking successes are also being seen with elec- troevacuation in highly selected patients. COMPLICATIONS OF NEUROPATHIC BLADDER The principal complications of the neuropathic bladder are recurrent urinary tract infection, hydronephrosis secon- dary to ureteral reflux or obstruction, and stone formation. 452 / CHAPTER 27 The primary factors contributing to these complications are the presence of residual urine, sustained high intravesi- cal pressures, and immobilization, respectively. Incontinence in neuropathic disorders may be passive, as in flaccid lesions when outlet resistance is compromised, or may be the result of uninhibited detrusor contractions, as in spastic lesions. Infection Infection is virtually inevitable with the neuropathic blad- der state. During the stage of spinal shock that follows cord injury, the bladder must be emptied by catheterization. Sterile intermittent catheterization is recommended at this stage, but for practical purposes or for the sake of conve- nience, a Foley catheter is often left indwelling. Chronic catheter drainage guarantees infection regardless of any pre- ventive measures taken. Nevertheless, a recent clinical trial of colonization of the bladder with nonpathogenic Esche- richia coli showed some promise; it significantly reduced the episodes of infection in a group of spinal cord injury patients with neurogenic bladder (Darouiche et al, 2001). The upper urinary tract is usually protected from infec- tion by the integrity of the ureterovesical junction. If this becomes incompetent, infected urine will reflux up to the kidneys. Decompensation of the ureterovesical junction results from the high intravesical pressures generated by the spastic bladder. It is most important that these cases be treated aggressively with an intensive program of self-cath- eterization and anticholinergic medication. The Credé maneuver should not be used. A number of infective complications can result from the presence of a chronically indwelling Foley catheter. These include cystitis and periurethritis resulting from mechanical irritation. A periurethral abscess may follow, with formation of a fistula via eventual rupture of the abscess through the perineal skin. Drainage may also take place through the urethra, with the end result being a ure- thral diverticulum. Infection may travel up into the pros- tatic ducts (prostatitis) or seminal vesicles (seminal vesiculi- tis) and along the vas into the epididymis (epididymitis). A. TREATMENT OF PYELONEPHRITIS Episodic renal infection should be treated aggressively with appropriate antibiotics to prevent renal loss. The source and cause of infection should be eliminated if possible. B. TREATMENT OF EPIDIDYMITIS This condition is a complication of either dyssynergic voiding or an indwelling catheter. Treatment consists of appropriate antibiotics, bed rest, and scrotal elevation. The indwelling catheter should be removed or replaced with a suprapubic catheter. Preferred long-term management is to place the patient on an intermittent self-catheterization program. Rarely, ligation of the vas is required. Hydronephrosis Two mechanisms lead to back pressure on the kidney. Early, the effect of trigonal stretch secondary to residual urine and detrusor hypertonicity becomes compounded by evolving trigonal hypertrophy. The combination causes abnormal pull on the ureterovesical junction, with increased resistance to the passage of urine. A “functional” obstruction results, which leads to progressive ureteral dilatation and back pressure on the kidney. At this stage, this condition can be relieved by continuous catheter drainage or by combined intermittent catheter drainage and use of anticholinergics. A delayed consequence of trigonal hypertrophy and detrusor spasticity is reflux due to decompensation of the ureterovesical junction. The causative factor appears to be a combination of high intravesical pressure and trabecula- tion of the bladder wall. The increased stiffness of the ure- terovesical junction weakens its valve-like function, slowly eroding its ability to prevent reflux of urine during forceful bladder contractions. When ureteral reflux is detected by cystography, previ- ous methods of bladder care must be radically adjusted. An indwelling catheter may manage the problem temporarily. However, if the reflux persists after a reasonable period of drainage, antireflux surgery must be considered. In addi- tion, measures to reduce high intravesical pressure are needed (bladder augmentation, sacral rhizotomy, trans- urethral resection of the bladder outlet, or sphincterot- omy). Progressive hydronephrosis may require nephros- tomy. Urinary diversion is a last resort, which should be avoidable if the patient is followed up regularly. Calculus A number of factors contribute to stone formation in the bladder and kidneys. Bed rest and inactivity cause demin- eralization of the skeleton, mobilization of calcium, and subsequent hypercalciuria. Recumbency and inadequate fluid intake both contribute to urinary stasis, possibly with increased concentration of urinary calcium. Catheteriza- tion of the neurogenic bladder may introduce bacteria. Subsequent infection is usually due to a urea-splitting organism, which causes the urine to become alkaline, with reduced solubility of calcium and phosphate. A. BLADDER STONES Because these stones are usually soft, they can be crushed and will wash out through a cystoscope sheath. Occasion- ally, they are large and need to be removed via a suprapu- bic cystotomy. B. URETERAL STONES Virtually all ureteral stones can now be removed by ante- grade or retrograde retrieval methods or by extracorporeal shock wave lithotripsy (ESWL). NEUROPATHIC BLADDER DISORDERS / 453 C. RENAL STONES In a patient with neurogenic bladder, kidney stones gener- ally are the result of infection; if the infection is untreated, the stones become the source of persistent renal infection and eventual renal loss. Most of the stones in the renal pel- vis can be removed by either a percutaneous endoscopic procedure or ESWL. Occasionally, a large staghorn stone may require open surgery. Renal Amyloidosis Secondary amyloidosis of the kidney is a common cause of death in patients with neuropathic bladder. It is a result of chronic debilitation in patients with difficult decubitus ulcers and poorly controlled infection. Fortunately, due to better medical care, this is an uncommon finding today. Sexual Dysfunction Men who have had traumatic cord or cauda equina lesions experience varying degrees of sexual dysfunction. Those with upper motor lesions fare well, with the majority hav- ing reflexogenic erectile capability. Dangerous elevations in blood pressure can occur with erections in patients with high thoracic or cervical lesions. Problems of quality of erection or premature detumescence are found with all levels of injury. Patients with lower motor lesions are, as a rule, impotent, unless the lesion is incomplete. There is a high degree of variability in the sexual capabilities of patients with all levels of spinal injury. Fortunately, sexual function can be restored to most patients by oral sildenafil, transurethral medications, a vacuum erection device, intra- cavernous injection, or a penile prosthesis. Often, patients with spinal injury lose the ability to ejaculate even with preservation of functional erections. This is a result of lost coordination between reflexes nor- mally synchronized through higher center regulation. Patients may have the capability to ejaculate after an erec- tion, but are either unable to trigger this sexual event or are unable to trigger it in proper sequence. Techniques using vibratory stimulation of the penis or transrectal electrical stimulation have been developed to accomplish semen col- lection in patients with “functional infertility.” Autonomic Dysreflexia Autonomic dysreflexia is sympathetically mediated reflex behavior triggered by sacral afferent feedback to the spinal cord. The phenomenon is seen in patients with cord lesions above the sympathetic outflow from the cord. As a rule, it occurs in rather spastic lesions above T1 but on occasion in lesions of mild spasticity or those as low as T5. Symptoms include dramatic elevations in systolic or dia- stolic blood pressure (or both), increased pulse pressure, sweating, bradycardia, headache, and piloerection. Symp- toms are brought on by overdistention of the bladder. Immediate catheterization is indicated and usually brings about prompt lowering of blood pressure. Oral nifedipine (20 mg) has been shown to alleviate this syndrome when given 30 minutes before cystoscopy (Dykstra, Sidi, and Anderson, 1987) or electroejaculation (Steinberger et al, 1990). The acute hemodynamic effect can be managed with a parenteral ganglionic blocking agent or alpha-adre- nergic blockers (Barrett and Wein, 1987). Sphincterotomy and peripheral rhizotomy have been used by some to pre- vent recurring autonomic dysreflexia. PROGNOSIS The greater threat to the patient with a neuropathic blad- der is progressive renal damage (pyelonephritis, calculosis, and hydronephrosis). Advances in the management of the neuropathic bladder, together with better follow-up of patients at regular intervals, have substantially improved the outlook for long-term survival. REFERENCES Andersson KE: The overactive bladder: Pharmacologic basis of drug treatment. Urology 1997;50(6A suppl):74. Artibani W: Diagnosis and significance of idiopathic overactive blad- der. 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Giannantoni A et al: Intravesical capsaicin versus resiniferatoxin in pa- tients with detrusor hyperreflexia: A prospective randomized study. J Urol 2002;167:1710. Gosling JA, Dixon JS: Anatomy of the bladder and urethra. In: Chish- olm GP, Fair WR (editors): Scientific Foundations of Urology. Year Book Medical, 1990. Gosling JA et al: Decrease in the autonomic innervation of human de- trusor muscle in outflow obstruction. J Urol 1986;136:501. Hackler RH: A 25-year prospective mortality study in the spinal cord injured patient: Comparison with the long-term living paraple- gic. J Urol 1977;117:486. Hackler RH, Hall MK, Zampieri TA: Bladder hypocompliance in the spinal cord injury population. J Urol 1989;141:1390. Jackson S: The patient with an overactive bladder—Symptoms and quality-of-life issues. Urology 1997;50(6A suppl):18. Janig W, Koltzenburg M: Pain arising from the urogenital tract. In: Maggi CA (editor): Nervous Control of the Urogenital System. Harwood Academic Publishers, 1993. Jayanthi VR et al: The nonneurogenic bladder of early infancy. J Urol 1997;158(3 Pt 2):1281. Joseph DB et al: Clean, intermittent catheterization of infants with neurogenic bladder. Pediatrics 1989;84:78. Lepor H et al: Muscarinic cholinergic receptors in the normal and neu- rogenic human bladder. J Urol 1989;142:869. Light JK, Beric A, Wise PG: Predictive criteria for failed sphincterot- omy in spinal cord injury patients. J Urol 1987;138: 1201. McGuire EJ, Cespedes RD, O’Connell HE: Leak-point pressures. Urol Clin North Am 1996;23:253. McGuire EJ, Savastano JA: Long-term follow-up of spinal cord injury patients managed by intermittent catheterization. J Urol 1983; 219:775. McLorie GA et al: Determinants of hydronephrosis and renal injury in patients with myelomeningocele. J Urol 1988;140:1289. Mollard P, Mouriquand P, Joubert P: Urethral lengthening for neuro- genic urinary incontinence (Kropp’s procedure): Results of 16 cases. J Urol 1990;143:95. Nickell K, Boone TB: Peripheral neuropathy and peripheral nerve in- jury. Urol Clin North Am 1996;23:491. Rivas DA, Figueroa TE, Chancellor MB: Bladder autoaugmentation. Tech Urol 1995;1:181. Rudy DC, Awad SA, Downie JW: External sphincter dyssynergia: An abnormal continence reflex. J Urol 1988;140:105. Satoh K: Localization of the micturition center at dorsolateral pontine tegmentum of the rat. Neurosci Lett 1978;8:27. Schmidt RA: Advances in genitourinary neurostimulation. Neurosur- gery 1986;19:1041. Schulte-Baukloh H et al: Efficacy of botulinum-a toxin in children with detrusor hyperreflexia due to myelomeningocele: prelimi- nary results. Urology 2002;59:325. Sidi AA, Reinberg Y, Gonzalez R: Comparison of artificial sphincter implantation and bladder neck reconstruction in patients with neurogenic urinary incontinence. J Urol 1987;138:1120. Smith AR, Hosker GL, Warrell DW: The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine: A neurophysiological study. Br J Obstet Gynaecol 1989;96:24. Steers WD, De Groat WC: Effect of bladder outlet obstruction on micturition reflex pathways in the rat. J Urol 1988;140:864. Steinberger RE et al: Nifedipine pretreatment for autonomic dysre- flexia during electroejaculation. Urology 1990;36:228. Stone AR: Neurourologic evaluation and urologic management of spi- nal dysraphism. Neurosurg Clin North Am 1995;6:269. Sullivan MP, Comiter CV, Yalla SV: Micturitional urethral pressure profilometry. Urol Clin North Am 1996;23:263. Tanagho EA, Schmidt RA: Electrical stimulation in the clinical man- agement of the neurogenic bladder. J Urol 1988;140:1331. Tanagho EA, Schmidt RA, Orvis BR: Neural stimulation for control of voiding dysfunction: A preliminary report in 22 patients with serious neuropathic voiding disorders. J Urol 1989;142:340. Thomas TM, Karran OD, Meade TW: Management of urinary in- continence in patients with multiple sclerosis. J R Coll Gen Pract 1981;31:296. Van Kerrebroeck PE: The role of electrical stimulation in voiding dys- function. Eur Urol 1998;34(suppl 1):27. Vorstman B et al: Nerve crossover techniques for urinary bladder rein- nervation: Animal and human cadaver studies. J Urol 1987;137: 1043. Watanabe T, Rivas DA, Chancellor MB: Urodynamics of spinal cord injury. Urol Clin North Am 1996;23:459. Weiss JM: Pelvic floor myofascial trigger points: Manual therapy for interstitial cystitis and the urgency-frequency syndrome. J Urol 2001;166:2226. 455 28 Urodynamic Studies Emil A. Tanagho, MD, & Donna Y. Deng, MD Urodynamic study is an important part of the evaluation of patients with voiding dysfunctions—dysuria, urinary incontinence, neuropathic disorders, and so on. Formerly, the examiner simply observed the act of voiding, noting the strength of the urinary stream, and drawing inferences about the possibility of obstruction of the bladder outlet. In the 1950s, it became possible to observe the lower uri- nary tract by fluoroscopy during the act of voiding; and in the 1960s, the principles of hydrodynamics were applied to lower urinary tract physiology. The field of urodynam- ics now has clinical applications in evaluating voiding problems resulting from lower urinary tract disease. The nomenclature of the tests used in urodynamic studies is not yet settled, and the meanings of urodynamic terms are sometimes overlapping or confusing. In spite of these difficulties, urodynamic tests are extremely valuable. Symptoms elicited by the history or by physical, endo- scopic, or even radiographic examination often must be investigated further by urodynamic tests so that therapy can be devised that is based on an understanding of the altered physiology of the lower urinary tract. As is true of many high-technology testing procedures (eg, electrocardiography, electroencephalography), urody- namic tests have the greatest clinical validity when their interpretation is left to the treating physician, who should either supervise the study or be responsible for correlating all of the findings with personal clinical observations. FUNCTIONS RELEVANT TO URODYNAMICS & TESTS APPLICABLE TO EACH Urodynamic study of the lower urinary tract can provide useful clinical information about the function of the uri- nary bladder, the sphincteric mechanism, and the voiding pattern itself. Bladder function has been classically studied by cys- tography and fluoroscopy. Urodynamic studies use cys- tometry. Conventional radiographic studies and urody- namic studies can, of course, be usefully combined. Sphincteric function depends on 2 elements: the smooth muscle sphincter and the voluntary sphincter. The activity of both elements can be recorded urodynamically by pressure measurements; the activity of the voluntary sphincter also can be recorded by electromyography. The act of voiding is a function of the interaction between bladder and sphincter, and the result is the flow rate. The flow rate is one major aspect of the total function of the lower urinary tract. It is generally recorded in millili- ters per second as well as by total urine volume voided. The simultaneous recording of bladder activity (by intralu- minal pressure measurements), sphincteric activity (by electromyography or pressure measurements), and flow rate reveals interrelationships among the 3 elements. Each measurement may give useful information about the nor- mality or abnormality of one specific aspect of lower uri- nary tract function. A more complete picture is provided by integrating all 3 lower tract elements in a simulta- neously recorded comparative manner. This comprehen- sive approach may involve synchronous recordings of vari- able pressures, flow rate, volume voided, and electrical activity of skeletal musculature around the urinary sphinc- ter (electromyography), along with fluoroscopic imaging of the lower urinary tract. The multiple pressures to be recorded are quite variable and usually include intravesical pressure, intraurethral pressure at several levels, intra- abdominal pressure, and anal sphincteric pressure as a function of muscular activity of the pelvic floor. The techniques of urodynamic study must be tailored to the needs of specific patients. Each method has advantages and limitations depending on the requirements of the study. In one patient, results of a single test might be suffi- cient to establish the diagnosis and suggest appropriate ther- apy; in another, many more studies might be necessary. ■ PHYSIOLOGIC & HYDRODYNAMIC CONSIDERATIONS URINARY FLOW RATE Because urinary flow rate is the product of detrusor action against outlet resistance, a variation from the normal flow rate might reflect dysfunction of either. The normal flow rate from a full bladder is about 20–25 mL/s in men and 25–30 mL/s in women. These variations are directly Copyright © 2008, 2004, 2001, 2000 by The McGraw-Hill Companies, Inc. Click here for terms of use. 456 / CHAPTER 28 related to the volume voided and the person’s age. Obstruction should be suspected in any adult voiding with a full bladder at a rate of less than 15 mL/s. A flow rate less than 10 mL/s is considered definite evidence of obstruc- tion. Occasionally, one encounters “supervoiders” with flow rates far above the normal range. This may signify low outlet resistance but is of less concern clinically than obstruction. Outlet Resistance Outlet resistance is the primary determinant of flow rate and varies according to mechanical or functional factors. Functionally, outlet resistance is primarily related to sphincteric activity, which is controlled by both the smooth sphincter and the voluntary sphincter. The smooth sphincter is rarely overactive in women; we have never seen an example of it in any of our urodynamic eval- uations. Overactivity of the smooth sphincter is rarely seen in men also but it may occur in association with hypertro- phy of the bladder neck due to neurogenic dysfunction or distal obstruction. However, such cases must be critically evaluated before this conclusion is reached. Increased voluntary sphincteric activity is not uncom- mon. It is often neglected as a primary underlying cause of increased sphincteric resistance. It is manifested either as lack of relaxation or as actual overactivity during voiding. The normal voluntary sphincter provides adequate resis- tance, along with the smooth sphincter, to prevent escape of urine from the bladder; if the voluntary sphincter does not relax during detrusor contraction, partial functional obstruction occurs. Overactivity of the sphincter, resulting in increased outlet resistance, is usually a neuropathic phe- nomenon. However, it can also be functional, resulting from irritative phenomena such as infection or other fac- tors—chemical, bacterial, hormonal, or, even more com- monly and often not appreciated, psychological. Mechanical Factors Mechanical factors resulting in obstruction to urine flow are the easiest to identify by conventional methods. In women, they may take the form of cystoceles, urethral kinks, or, most commonly, iatrogenic scarring, fibrosis, and compression from previous vaginal or periurethral operative procedures. Mechanical factors in men are well known to all urologists; the classic form is benign prostatic hypertrophy. Urethral stricture from various causes and posterior urethral valves are other common causes of uri- nary obstruction in men, and there are many others. Normal voiding with a normal flow rate is the product of both detrusor activity and outlet resistance. A high intravesical pressure resulting from detrusor contraction is not necessary to initiate voiding, because outlet resistance has usually dropped to a minimum. Sphincteric relaxation usually precedes detrusor contraction by a few seconds, and when relaxation is maximal, detrusor activity starts and is sustained until the bladder is empty. Variations in Normal Flow Rate The sequence just described is not essential for normal flow rates. The flow rate may be normal in the absence of any detrusor contraction if sphincteric relaxation is assisted by increased intra-abdominal pressure from straining. Per- sons with weak outlet resistance and weak sphincteric con- trol can achieve a normal flow rate by complete voluntary sphincteric relaxation without detrusor contraction or straining. A normal flow rate can be achieved in spite of increased sphincteric activity or lack of complete relaxation if detrusor contraction is increased to overcome outlet resistance. Because a normal flow rate can be achieved in spite of abnormalities of one or more of the mechanisms involved, recording the flow rate alone does not provide insight into the precise mechanisms by which it occurs. Distinction between patterns of flow can be difficult. For practical pur- poses, if the flow rate is adequate and the recorded pattern and configuration of the flow curve are normal, these vari- ations may not be clinically significant except in rare cases. Nomenclature The study of urinary flow rate itself is usually called uro- flowmetry. The flow rate is generally identified as maxi- mum flow rate, average flow rate, flow time, maximum flow time (the time elapsed before maximum flow rate is reached), and total flow time (the aggregate of flow time if the flow has been interrupted by periods of no voiding) (Figure 28–1). The flow rate pattern is characterized as continuous or intermittent, etc. Pattern Measurement of Flow Rate A normal flow pattern is represented by a bell-shaped curve (Figure 28–1). However, the curve is rarely com- pletely smooth; it may vary within limits and still be nor- mal. Flow rate can be determined by measuring a 5 sec- onds’ collection at the peak of flow and dividing the amount obtained by 5 to arrive at the average rate per sec- ond. This rough estimate is useful, especially if the flow rate is normal and the values are above 20 mL/s. In modern practice, the flow rate is more often recorded electronically: The patient voids into a container on top of a measuring device that is connected to a trans- ducer, the weight being converted to volume and recorded on a chart in milliliters per second. Figure 28–2 is an example of such a recording from a normal man. The gen- eral bell-shaped curve is quite clear, and the tracing shows all of the values discussed previously: total flow time, maxi- mum flow time, maximum flow rate, average flow rate, and total volume voided. Occasional supervoiders can URODYNAMIC STUDIES / 457 exceed the limits of the chart, but this is usually not of clin- ical concern (Figure 28–3). A possible variation in the bell appearance is seen in Figure 28–4. The overall appearance of the flow curve may disclose unsuspected abnormalities. In Figure 28–5, for example, flow time is greatly prolonged. Maximum flow rate may not be low, but the average flow rate is very low—though the maximum flow rate is at one point within the normal range. Such fluctuation in flow rate is most commonly related to variations in voluntary sphincteric activity. In Figure 28–6, this pattern is extreme: Maximum flow rate never exceeds 15 mL/s, and average flow rate is about 10 mL/s, which is indicative of obstruction. (Again, this fluctu- ation in pattern probably reflects sphincteric hyperactivity.) The flow rate pattern reveals a great deal about the forces involved. For example, if the patient is voiding without the aid of detrusor contractions—primarily by straining—this can be easily deduced from the pattern of the flow rate. Figure 28–7 shows an example of intermit- tent voiding, primarily by straining, with no detrusor activity, and at a rate that sometimes does not reach the usual peaks. With experience, one becomes expert at detecting the mechanisms underlying abnormalities in flow rate. For example, in Figure 28–5, the maximum flow rate is in the normal range, the average flow rate is slightly low, and the curve has a general bell pattern, yet brief partial intermittent obstructions to flow can be readily interpreted as due to overactivity of the voluntary sphincter, a mild form of detrusor/sphincter dyssynergia (see discussion following). Flow rates in mechanical obstruction are totally differ- ent, classically in the range of 5–6 mL/s; flow time is greatly prolonged, and there is sustained low flow with minimal variation (Figure 28–8). Figure 28–9 is a striking example of a curve for a patient with benign prostatic hypertrophy. No simultaneous studies are needed with such a pattern, since the pattern is obviously one of mechanical obstruction. Figure 28–1. Uroflowme- try. Basic elements of maxi- mum flow, average flow, total flow time, and total volume voided. Figure 28–2. Classic normal flow rate, with peak of about 30 mL/s and average of about 20 mL/s. On the horizontal scale, one large square equals 5 s. 458 / CHAPTER 28 Figure 28–3. Flow rate of “supervoider.” Maxi- mum flow rate exceeds limits of chart. Tracing shows fast buildup and complete bladder emptying of large volume of urine in a very short period. On the horizontal scale, one large square equals 5 s. Figure 28–4. Normal flow rate with some variation in appear- ance of curve. Note rapid pressure rise but progressive increase to maximum, followed by a sharp drop. There is also fluctuation in ascending limb of tracing. On the horizontal scale, one large square equals 5 s. URODYNAMIC STUDIES / 459 Figure 28–7. Classic flow rate due to ab- dominal straining with no detrusor activity. See effect of spurts of urine with complete interruption between them; patient cannot sustain increased intra-abdominal pressure. On the horizontal scale, one large square equals 5 s. Figure 28–8. Flow rate in a case of urinary obstruction showing very low average flow rate (not above 5 or 6 mL/s). Prolonged duration of flow is associated with incomplete emptying. On the horizontal scale, one large square equals 5 s. Figure 28–9. Classic low flow rate of bladder outlet obstruction (benign prostatic hypertrophy), markedly prolonged flow time, and fluctuation due to attempt at improving flow by increasing intra-abdominal pressure. On the horizontal scale, one large square equals 5 s. Figure 28–5. Rather low flow rate (not exceeding 10 mL/s), yet at one point the peak reaches 27–32 mL/s. Note again fluctuation in flow. On the horizontal scale, one large square equals 5 s. Figure 28–6. Very low flow rate of short duration and small volume. Note that maximum flow is not above 15 mL/s; however, flow average is less than 10 mL/s, and flow is almost completely interrupted in the middle. On the horizontal scale, one large square equals 5 s. [...]... 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