Bladder Function and Dysfunction

Question 1

ureter peristaltic contractions

Answer 1

• There are various pacemaker cells that initiate spontaneous action potentials that lead to the peristaltic contractions. Similar to situation for the heart, there are multiple areas of intrinsic potential pacemaker activity along the entire collecting system, but the fastest one dominates the slower, secondary areas of latent pacemaker activity. In the renal collecting system, the areas of fastest pacemaker activity are in the kidney calyces.
• The ureteral peristaltic waves push boluses of urine forward toward the bladder until the urine exits the ureter and enters the bladder at the ureterovesical junction (UVJ). The ureteral pressure pushing the bolus forward must be greater than the pressure encountered at the UVJ in order for the urine to enter the bladder. Because the bladder normally stores urine at low pressure, urine enters the bladder easily.

Question 2

hydronephrosis

Answer 2

• There are various pacemaker cells that initiate spontaneous action potentials that lead to the peristaltic contractions. Similar to situation for the heart, there are multiple areas of intrinsic potential pacemaker activity along the entire collecting system, but the fastest one dominates the slower, secondary areas of latent pacemaker activity. In the renal collecting system, the areas of fastest pacemaker activity are in the kidney calyces.
• The ureteral peristaltic waves push boluses of urine forward toward the bladder until the urine exits the ureter and enters the bladder at the ureterovesical junction (UVJ). The ureteral pressure pushing the bolus forward must be greater than the pressure encountered at the UVJ in order for the urine to enter the bladder. Because the bladder normally stores urine at low pressure, urine enters the bladder easily.

Question 3

bladder smooth muscle

Answer 3

The bladder is composed of smooth muscle arranged in a rather diffuse, random arrangement. The smooth muscle is NOT arranged in the classic inner circular and outer longitudinal layers as seen in the bowel.

Question 4

bladder body

Answer 4

The body of the bladder is distensible and allows accommodation of urine as the bladder fills with urine. The bladder base is relatively fixed in place and is the location where urine enters and leaves the bladder

Question 5

bladder base

Answer 5

The bladder base consists of the trigone and bladder neck (area where bladder and urethra connect).

Question 6

bladder outlet

Answer 6

The bladder outlet is a conceptual term that includes all the anatomic structures involved urinary continence and the exit of urine from the bladder: bladder base + urethra + external (striated) sphincter which surrounds the urethra.

Question 7

smooth or internal sphincter

Answer 7

• Bladder neck + proximal urethra are often termed the “smooth” or “internal” sphincter
• The bladder neck/proximal urethra contribute to urinary continence in men and women (more so in males, however), but it is not the primary zone of urinary continence in either.

Question 8

external urethral sphincter or rhabdosphincter

male

Answer 8

• surrounds urethral smooth muscle
• slow twitch fibers
• In both men and women, the periurethral muscles that compose the pelvic floor (the levator ani muscles, which are under conscious control) augment the action of the rhabdosphincter. The periurethral muscles of the pelvic floor are composed of both fast and slow-twitch skeletal muscle
• The striated sphincter in the male exists at the membranous urethra just distal to the apex of the prostate where the urethra passes through the pelvic floor musculature

Question 9

external urethral sphincter

female

Answer 9

• surrounds urethral smooth muscle
• slow twitch fibers
• In both men and women, the periurethral muscles that compose the pelvic floor (the levator ani muscles, which are under conscious control) augment the action of the rhabdosphincter. The periurethral muscles of the pelvic floor are composed of both fast and slow-twitch skeletal muscle
• In the female, the rhabosphincter is at the level of the mid-urethra

Question 10

male urethra

Answer 10

The male urethra is long and has 4 distinct divisions:

(1) the bladder neck/prostatic urethra
(2) membranous urethra (area of the external sphincter)
(3) the bulbar urethra at the penile base
(4) pendulous urethra (penile shaft).

• The primary zone of male continence is the membranous urethra.
• The bladder neck/prostatic urethra forms a secondary zone of continence and is a secondary sphincter that closes during ejaculation, but also has a basal tone that promotes urinary continence.
• The male with often remain continent after resection of the prostate or bladder neck whereas destroying the external sphincter will typically lead to urinary incontinence (involuntary loss of urine).
• Mother Nature has designed the male urethra to perform

(1) sexual function (ejaculation)
(2) urinary storage. It is important to be mindful that in lower mammals (and in certain humans, I suppose…), the release of urine is heavily involved in sexual/reproductive function as well—marking territory, social dominance, attracting mates, etc. Therefore, nature has made the male continence mechanisms robust.

Question 11

female urethra

Answer 11

• The precise mechanism of female continence is still subject to significant debate.
• The female urethra is significantly shorter and is fused to the anterior wall of the vagina with its distal meatus visible at the vaginal introitus. There is no true anatomic plane between the female urethra and vaginal wall. The anterior vaginal wall (with its supporting fascia) forms a fundamental support of the female urethra contributing to female continence. This is why women with vaginal prolapse (laxity of the vaginal walls) often suffer concurrently from urinary incontinence.
• Female continence is thought to occur through a combination of 3 mechanisms which seem to converge most strongly at the area of the middle of the female urethra (“the mid-urethral complex”):

(1) The tone of the female external sphincter which occupies the mid-to-distal urethra
(2) the firm supportive “hammock” provided to the urethra by the anterior vaginal wall and its fascia,
(3) strong apposition (coaptation) of the anterior and posterior walls of the urethral lumen (“viscous seal”). Damage to these mechanisms by childbirth, nerve injury, or loss of estrogen can lead to involuntary loss of urine.

Examples:

• Vaginal childbirth can cause damage to the pudendal nerves promoting loss of innervation to the external sphincter and weak pelvic floor muscles leading to incontinence risk.
• Vaginal childbirth (and loss of estrogen) can lead to tearing and laxity of the anterior vaginal wall leading to poor urethral support and increasing incontinence risk.
• Loss of estrogen (post-menopause) can lead to atrophy of the well vascularized, spongy tissue of the female urethra leading to poor coaptation of the urethral walls increasing incontinence risk.

Question 12

Reasons why urinary incontinence has an earlier onset in the female population

Answer 12

The fundamental differences between men and women with regard to the anatomic urethral configuration, the physiologic mechanisms of continence, and the different roles of the male/female genital tracts (i.e. vaginal childbirth).

Question 13

Detrusor Autonomic Physiology

Answer 13

• The entire detrusor is rich is muscarinic acetylcholine (Ach) receptors. The release of acetylcholine (Ach) onto the bladder detrusor muscle results in contraction of the detrusor muscle. o

• M2 and M3 are the subtypes of Ach receptors on the detrusor and both are targets for antimuscarinic drugs used to treat conditions in which the detrusor muscle is overactive (“overactive bladder”).
• Despite that M2 receptors are more common on the detrusor muscle, it is the M3 receptors that lead to bladder contractions.
• The exact role of bladder M2 receptors are still being studied.

•Typically, the bladder outlet relaxes when the detrusor muscle contracts to allow efficient voiding. This relaxation is thought to occur because a different nitric oxide based system is activated leading to smooth muscle relaxation in this region. This is still an area of ongoing research.

Question 14

Bladder Body Autonomic Physiology

Answer 14

• The bladder body (dome) is rich in Beta-adrenergic receptors. Release of norepineprine (NE) onto these receptors causes direct relaxation of the detrusor muscle, promoting urine storage.
• The relaxation is mediated primarily by Beta-3 adrenergic receptors which occurs via a cAMP-mediated relaxation of the smooth muscle (discussed below).
• The bladder Beta-3 receptors are the target for Beta-3 agonists used to treat overactive detrusor mucle (“overactive bladder”).

Question 15

Bladder Base Autonomic Physiology

Answer 15

• The bladder base and proximal urethra (part of the bladder outlet) are rich in Alpha-adrenergic receptors. Release of NE onto these receptors (Alpha-1 receptors) promotes constriction of the smooth muscle of the bladder neck, promoting urine storage.
• The bladder neck in males has significantly higher concentrations of Alpha receptors in the bladder neck than females.

-The reason: the male bladder neck must contract during ejaculation to ensure the ejaculate exits via the urethra. Failure to do so results in retrograde ejaculation into the bladder which can negatively affect male fertility.

Question 16

Answer 16

Question 17

During normal voiding there is both ______ contraction and relaxation of the ______ _______.

Answer 17

During normal voiding there is both detrusor contraction and relaxation of the bladder outlet.

Question 18

Bladder Function

Answer 18

1. Storage
2. Emptying

• The normal micturition cycle involves a complex interplay between the autonomic and somatic nervous systems and the end organs involved (bladder, urethra, pelvic floor musculature). The normal micturition cycle involves the exertion of conscious control over autonomic reflexes controlling urine storage and emptying. If output from the cerebral cortex is lost (and the brainstem/spinal cord is intact), the bladder will cycle itself by pure reflex control.

Question 19

Bladder Function - Storage

Answer 19

Storage:

• Bladder must store adequate and increasing volumes of urine at low pressure (therefore must be highly compliant and have adequate capacity)
• When the bladder fails to store urine properly, it typically results in the involuntary loss of urine, otherwise known as urinary incontinence.

Question 20

Bladder Function - Emptying

Answer 20

Emptying:

• Efficient bladder emptying requires synchronous activation of the entire detrusor (otherwise all the urine would flow into the non-contracting part, as occurs with large bladder diverticulae in certain diseases).
• Efficient emptying also requires the ability to properly and adequately relax the bladder outlet (i.e. reduce the resistance to urine flow)
• Failure to empty the bladder efficiently can result in high Post Void Residuals (PVRs)—that is the volume of urine that remains inside the bladder after emptying. Ideally, the PVR of a healthy person should be zero or negligible. The PVR can be measured with a small ultrasound device called a bladder scanner or can be done by catheterizing the bladder immediately after voiding.
• Taking this to the extreme, certain problems result in complete failure to empty the bladder, a condition referred to as urinary retention. It is important to identify these patients because the urine can back up into the kidneys resulting in dilated ureters (hydronephrosis) which can ultimately lead to renal failure, which is potentially life threatening.

Question 21

Bladder Filling (Storage)

Answer 21

• Laplace’s Law relates bladder wall tension (T) to bladder pressure (Pves) and radius (R): T= Pves(R/2d), where R=bladder radius and d= bladder wall thickness. Bladder thickness is often ignored since it is normally small compared to radius (volume), yielding T= P(R/2). Therefore, as the bladder distends (increases in radius), wall tension increases.

-This is important because the afferent nerves controlling bladder function actually sense wall tension and send this information to higher centers controlling the decision to void.

• Compliance = ΔV/ΔP, where ΔV= volume change, ΔP=pressure change.

• This is important because compliance influences wall tension during filling. Therefore compliance can alter how the bladder afferent nerves sense bladder filling and thus alter the threshold for micturition.
• For example, patients with thickened, non-compliant bladders will often complain of the need to urinate frequently which is, at least in part, thought to be due to the increased wall tension at lower filling volumes.

Question 22

Bladder Compliance Alterations

Answer 22

• Compliance is altered by two components:

(1) the collagen and elastin content of the bladder (which is altered by disease states)
(2) the intrinsic tone of the detrusor muscle, called tonus (which can also be affected in disease).

• Physiologic filling occurs at low pressure (<10cm H2O) due to the normally high compliance of the bladder.

Question 23

Voiding Mechanism - Intravesicular Pressure

Answer 23

• P_ves = P_det + P_abd
• P_det = P_ves - P_abd

Question 24

Voiding Mechanisms

Answer 24

• Voiding is achieved by a combination of 2 events:

(1) relaxation of the bladder outlet
(2) contraction of the detrusor muscle.

• There is often a great deal of emphasis on detrusor contractility, but relaxation of the bladder outlet is just as important.
• Some patients with atonic (non-contractile) bladders are able to void by voluntary relaxation of the bladder outlet and abdominal straining (valsalva maneuvaer) and/or manual compression of the bladder (this is known as Crede voiding).

Question 25

The same flow rate of urine can be achieved with multiple different combinations of detrusor pressure and urethral resistance

Answer 25

• depends on the patient’s unique physiology and disease state
• Therefore, a low Pdet does not always imply impaired contractility of the bladder, esp. in females who typically void at low pressures. Normal flow can be achieved with a low Pdet so long as urethral resistance is low. Many women are able to void by relaxation of the urethra and pelvic floor such that a detrusor contraction is barely detectable.
• Conversely, patients with a high urethral resistance due to obstruction (for example, a large prostate) can void with a near normal flow rate so long as they can generate high detrusor pressure to overcome the high urethral resistance.

Question 26

The unique properties of smooth muscle that allow the bladder to store large and variable amounts of urine and empty efficiently.

Answer 26

• Smooth muscle is able to shorten by over two thirds it length whereas skeletal muscle can only shorten to 1/3 its length. This permits the bladder to accommodate significantly greater volumes of urine than could ever be achieved with skeletal muscle.
• Smooth muscle contractions are slow, maintained contractions that utilize ATP slowly (i.e. smooth muscle is very efficient) as compared to skeletal muscle. This allows the bladder to contract for extended periods of time with little use of energy such that it can empty to completion despite varying degrees of fullness.

Question 27

Bladder Contraction

Answer 27

• Similar to other smooth muscles, the process of excitation-contraction coupling is required for bladder contractions.
• Because smooth muscle hydrolyzes ATP slowly, it contracts (and relaxes) slowly and maintains its tension over a longer period of time (with less use of ATP) as compared to skeletal muscle. This property is critical to proper bladder emptying as the distended bladder must be able to maintain its tension until the bladder has completely emptied through the comparatively small opening of the bladder outlet.

-The situation is analogous to squeezing out the contents of a large syringe which has a small opening. One has to squeeze the syringe and maintain the tension for a significant period of time until the fluid has emptied. Squeezing harder does little to make it empty faster since the increased pressure is simply transmitted to the wall of the container as the flow rate stays relatively constant.

Question 28

Bladder Relaxation

Answer 28

•Activation of detrusor Beta-3 receptors leads to activation of adenylate cyclase and the accumulation of cytosolic cAMP which relaxes the detrusor muscle.

Question 29

Neural Control of the Lower Urinary Tract

Answer 29

•Three sets of nerves innervate the lower urinary tract - all contain afferent and efferent fibers

1. Pelvic Parasympathetic Nerves (nervi efferents)
   - excite the detrusor and relax the proximal urethra
2. Lumbar Sympathetic Nerves
   - inhibit detrusor and contract bladder base and urethra

•Pudendal Nerve

-excite /relax the striated urethral sphincter

Question 30

Pelvic Parasympathetic Nerves

Answer 30

• excite the detrusor and relax the proximal urethra
• pelvic splanchnic nerves
• Parasympathetic preganglionic neurons are located in the sacral spinal cord (S2-S4) in the sacral parasympathetic nucleus. This area of the spinal cord is often called the Sacral Micturition Center (SMC).
• They travel through the pelvic nerves to release acetylcholine (Ach) on postganglionic neurons located in the perivesical plexus and within the bladder wall itself (intramural ganglia)
• The post ganglionic neurons also release Ach which causes detrusor contraction. The proximal urethral relaxation is mediated by the parasympathetic nervous system, but it is likely not mediated by Ach (rather it is probably nitric oxide).

Question 31

Lumbar Sympathetic Nerves

Answer 31

• inhibit detrusor and contract bladder base and urethra
• hypogastric plexuses and nerves
• Sympathetic preganglionic fibers arise in spinal cord levels T10 to L2 and synapse in the sympathetic chain ganglia and inferior mesenteric ganglia where Ach is released. The postganglionic fibers travel in the hypogastric nerves to the target organs where norepinephrine (NE) is released.
• Note that some fibers also synapse on the intramural bladder ganglia (mentioned above) and also inhibit parasympathetic transmission in these ganglia
• The NE causes smooth muscle of the detrusor to relax, and it causes constriction of the smooth muscle of the bladder neck / proximal urethra (bladder outlet)

Question 32

Pudendal Nerve

Answer 32

• excite / relax the striated urethral sphincter
• Motor neuron nuclei are located in Onuf’s nucleus in the sacral cord levels S2-S4
• They travel through the pudendal nerve to release Ach onto the nicotinic Ach receptors on the striated external sphincter muscle (rhabdosphincter, discussed above) causing contraction.

-Because the external sphincter is composed of skeletal muscle, neuromuscular transmission occurs via the nicotinic Ach receptor as opposed to the muscarinic Ach receptor on the detrusor.

• The constriction of the external sphincter can be consciously augmented by contracting the adjacent muscles of the pelvic floor (levator ani muscles).

• The motor neuron nuclei are also located in the sacral spinal cord levels S2-4 and are actually adjacent to nuclei controlling the external sphincter (Onuf’s nucleus).
• Note that the external urethral sphincter is under BOTH unconscious reflex control AND conscious control. Without conscious input, the external sphincter will reflexively relax during voiding, but one can consciously constrict the external sphincter when postponing micturition or even during voiding to abort micturition (but, ouch, that stings!).
• Typically, the pelvic floor muscles also contract when consciously contracting the external sphincter. Conversely, the muscle groups often relax together as well.

Question 33

Affferent Pathways

Answer 33

• The sensory neurons in the pelvic (parasympathetic) and pudendal (somatic) nerves have cell bodies in the sacral dorsal root ganglia, and those in the hypogastric (sympathetic) nerve have cell bodies in the lumbar dorsal root ganglia. All synapse on second order neurons in the spinal cord which carry signals to higher levels.
• A-delta fibers (large, myelinated) in the detrusor smooth muscle sense wall tension and a full bladder (bladder proprioception).
• C-fibers (small, unmyelinated) in the bladder mucosa also sense wall stretch (bladder volume) and sense nociceptive stimuli (pain and temperature).
• Irritation increases discharge of all sensory pathways at a lower pressure threshold, especially the C-fibers, which appear to be recruited in inflammation –> ultimately leads to bladder irritability. o
• The irritation produced by a bladder infection leads to firing of the afferent nerves at lower bladder filling volumes resulting in the typical symptoms of urinary frequency and urgency.
• Additionally, urination is typically painful (dysuria) due to activation of the C-fibers.

Question 34

Filling and Storage Reflexes

Answer 34

• A somewhat involved set of neurologic events control normal urine storage and voiding.
• An important theme to recognize is that conscious control is exerted on these reflexes to allow voluntary control over the decision to store and release urine.
• Interruption or disease of the pathways controlling micturition can lead to dysfunctional voiding.

Question 35

Guarding Reflex (Storage)

Answer 35

• The guarding reflex is based solely on spinal pathways and causes the bladder to reflexively store urine.

-This reflex requires an intact spinal cord and is modulated by higher brain centers.

• Filling stimulates low level firing of the afferent fibers in the bladder which synapse in the sacral and lumbar spinal cord
• Reflex sympathetic outflow from the hypogastric nerve releases NE onto the detrusor and intramural ganglia of the bladder resulting in:

(1) inhibits detrusor contraction (relaxation of the smooth muscle) via Beta-3 adrenergic receptors
(2) contracts the smooth muscle of the bladder neck and urethra (“the smooth sphincter”) via the alpha-1 adrenergic receptors
(3) inhibits parasympathetic transmission in intramural parasympathetic ganglia (i.e. blocks Ach-induced detrusor contractions)

• Reflex sacral somatic outflow via the pudendal nerve tonically contracts the external striated sphincter (rhabdospincter) with bladder filling. Additionally, basal efferent outflow from the pons also promotes the resting basal tone of the external urinary sphincter.

Question 36

Spino-Bulbo-Spinal Reflex (Voiding)

Answer 36

• Reflexive voiding is controlled by brainstem nuclei located in the pons called the pontine micturition center (PMC).
• Recent evidence demonstrates the PMC actually has two divisions: one controlling storage and one controlling micturition. However, the general area is still typically referred to as the pontine micturition center (PMC).
• The PMC is tonically inhibited by output from the cerebral cortex allowing conscious control over the decision to void. If input from the cortex is lost (brain death, stroke), then the PMC is still able to reflexively empty the bladder. Thus, voiding can be voluntary or involuntary, but both depend upon an intact spinal cord and brainstem (pons).
• Thus, voluntary voiding is initiated by voluntarily releasing cortical inhibition on the PMC thereby allowing the voiding reflex to occur

Question 37

PMC

Answer 37

• The PMC receives afferent input originating from fibers in the pelvic nerves which synapse on second order neurons in the spinal cord which carry the signals to the PMC. Bladder filling triggers intense firing of the afferent nerves. The intense firing eventually reaches a critical threshold at which the PMC decides to initiate the voiding reflex. So long as the cerebral cortex and the circuits connecting it to the PMC are intact, the PMC remains inhibited and its decision-making capacity is suppressed leaving the ultimate decision to the cortex (primarily the frontal cortex). As we have all experienced, when the bladder becomes increasingly full it becomes harder and harder to suppress this voiding reflex and the sensory information starts to intrude upon other cerebral activities (attention to lecture, exams, trying to perform urologic surgery!…)

Question 38

When threshold for voiding has been reached…

Answer 38

…the inhibition on the PMC is released and the PMC sends efferent signals to BOTH the lumbar and sacral cord which does the following:

(1) inhibits the pudendal nerve tonic contraction of the striated sphincter = relaxation of the external spincter. This is especially important. The external urethral sphincter (recall–the primary zone of continence in men and women) is highly dependent upon supraspinal brainstem input to properly relax during voiding.
(2) inhibits the hypogastric n. lumbar sympathetic outflow which aborts the guarding reflex discussed above.
(3) stimulates parasympathetic excitatory outflow from the sacral micturition center (SMC) which travels through the pelvic nerves to the bladder, bladder neck and proximal urethra. This contracts the detrusor muscle and relaxes the smooth muscle of the bladder neck and proximal urethra.

•In the absence of cortical inhibition (for example, in the human infant), the PMC will make the decision to void and initiate the voiding reflex on its own.

Question 39

Set of Events Resulting in Micturition

Answer 39

1. The first event of voiding is relaxation of the external striated sphincter (rhabdosphincter)
2. Next, there is detrusor contraction
3. Lastly, there is relaxation of the smooth sphincter (bladder neck and proximal urethra) with funneling of the bladder neck and flow of urine.

Question 40

Secondary Urethra-to-Bladder Reflex (a.k.a. “Barrington reflex”, “The augmentation reflex”)

Answer 40

• This secondary urethra-to-bladder reflex is much more well defined in lower mammals (cats and rats), but it is thought to play a role in human voiding as well.
• Note that this is the mechanism by which stress urinary incontinence can sometimes trigger urge incontinence—the trickle of urine into the proximal urethra can trigger involuntary bladder contractions leading to urgency and urge incontinence.

Question 41

Urodynamics

Answer 41

•a test in which tiny catheters are placed into the bladder and rectum (or vagina) so that the pressure in the bladder (Pves) and abdominal cavity (Pabd) can be measured simultaneously as the bladder is filled and during voiding.

-Remember, the pressure generated by the bladder (Pdet) is calculated by subtracting the abdominal pressure from intravesical pressure: Pdet = Pves-Pabd.

• The urine flow rate is also measured during voiding.
• Additionally, EMG electrodes are placed in the perineum near the external urinary sphincter to assess sphincter contractions during urine storage and voiding.
• Urodynamics can provide a wealth of information about the lower urinary tract including the following:

1. Bladder capacity and compliance
2. Bladder sensation (proprioception)
3. The detrusor pressure at which the bladder stores and empties urine and the urinary flow rate produced by the voiding detrusor pressure.
4. Determine if the bladder is obstructed by examining the pressure-flow relationship during micturition
5. Determine if the bladder exhibits detrusor overactivity (involuntary contractions, aka “overactive bladder”) which can lead to involuntary loss of urine
6. Determine the presence of a weak urinary sphincter and the intravesical pressure at which incontinence occurs due to the weak sphincter.

Question 42

Wein Classification

Answer 42

Failure to Store Urine:

Due to a problem of the outlet

Due to a problem of the bladder

Due to both problem of both bladder and outlet (mixed)

Failure to Empty Urine:

Due to a problem of the outlet

Due to a problem of the bladder

Due to both problem of both bladder and outlet (mixed)

Question 43

Urinary Incontinence

Answer 43

•involuntary loss of urine

1. Detrusor Overactivity
2. Urethral Incompetence
3. Overflow Incontinence

Question 44

Detrusor Overactivity

Answer 44

• Various disease processes can lead to bladder contractions that occur involuntarily which can lead to loss of urine. The medical term for this is detrusor overactivity (which is the currently accepted terminology endorsed by the International Continence Society). This is often called “overactive bladder” in lay terminology and by the pharmaceutical industry.
• Patients will typically report urge incontinence—that is an immediate need to urinate which they are unable to suppress.

-Typically, they will report leaking on the way to toilet or not making to the toilet in time.

• In addition to the incontinence, patients will often report urinary urgency (the immediate sensation to urinate which is difficult to postpone—“I have to run to the toilet”) and urinary frequency (urinating very often) because the overactive bladder is contracting despite attempts to inhibit it.
• According to the Wein classification, this is failure to store urine due to the bladder.

Question 45

Urethral Incompetence

Answer 45

• Various disease processes can lead to a loss of the normal function of the bladder outlet. This is also termed sphincteric incompetence, but it is important to realize that the problem is not always due to a problem with the urethral sphincter itself, but is often the overall function of the bladder outlet (which is urethra + bladder neck). This is especially true in women where urinary continence involves the complex interplay of the urethral sphincter, support of the anterior vaginal wall, and the overall ability of the urethral walls to close.
• Patients will typically report stress incontinence. The symptoms are loss of urine with straining, coughing, laughing, or physical activity (“I cough or sneeze and urine squirts out”).
• In men, stress incontinence typically occurs after surgery on the prostate which can damage the nerves to the external sphincter leading to poor urethral function.
• In women, vaginal childbirth can damage the nerves to the sphincter and also lead to poor anterior vaginal/urethral support leading to poor urethral function. Addtionally, after menopause, the loss of estrogen can lead to urethral atrophy and poor urethral coaptation (closure) resulting in stress incontinence as well.

•According to the Wein classification, this is failure to store urine due to the outlet

Question 46

Overflow Incontinence

Answer 46

• (aka “Paradoxical Incontinence”)
• This type of incontinence is often called paradoxical incontinence because failure of the bladder to empty results in the urinary incontinence.
• The non-emptying bladder becomes completely distended with urine and the intravesical pressure increases to the point that it overcomes urethral resistance and urine trickles continuously out of the urethra.

-Note that this situation typically leads to simultaneous bilateral hydronephrosis and can compromise renal function so it needs to be addressed in an urgent manner.

• The symptoms of overflow incontinence are continuous urinary leakage. This typically occurs in patients with impaired bladder sensation (neurologic injury, chronic bladder obstruction) because an acutely distended bladder is quite painful and patients with a sensate bladder will seek treatment before reaching the point of overflow incontinence.
• Overflow incontinence is seemingly paradoxical because the bladder fails to empty urine which leads to incontinence (“failure to store”). However, one must realize that the primary problem is failure of the bladder to empty. Even though incontinence is occurring, the bladder’s failure to empty is the fundamental problem.
• So in the Wein classification, this is a failure of the bladder to empty.
• This failure to empty can be due to the bladder, the outlet, or both. Two examples are discussed below:
• A bladder that is unable to contract (areflexic bladder) due to neurologic injury can lead to overflow incontinence (failure to empty due to the bladder)
• Urinary retention due to a large, obstructing prostate gland can also lead to urinary retention with overflow incontinence (failure to empty due to the outlet)

Question 47

Other Incontinence

Answer 47

•There are other types of incontinence that exist, but the above account for the majority encountered on a routine basis. Additionally, one must be aware that stress and urge incontinence often occur together. This is called mixed incontinence. This is why it is important to perform a thorough history and physical to identify all the components of the incontinence.

Question 48

Answer 48

Question 49

Evaluation of Urinary Incontinence

Answer 49

The standard evaluation for urinary incontinence includes 5 basic steps:

1. Identify and treat reversible causes
2. Identify complicating factors that need specialized treatment / evaluation (for example, spinal cord injury with complex voiding dysfunction, prior urologic surgery, etc…)
3. Exclude overflow incontinence by checking a post-void residual (PVR)
4. Distinguish the primary problem as urge or stress incontinence
5. Trial of initial therapy for urge or stress incontinence

• Patients who fail initial treatment, have overflow incontinence, or who have complicating factors are typically referred for urologic evaluation and urodynamic testing.

Question 50

Patterns of Neurogenic Voiding Dysfunction

Answer 50

• Neurogenic voiding dysfunction is disruption of normal urine storage and emptying due to neurologic injury. All patients with significant neurologic injury should be evaluated by and under the care of a urologist.
• Certain neurologic injuries can lead to hydronephrosis and lead to long term renal damage. The leading cause of death among spinal cord injury patients who survive the initial trauma used to be renal failure. Due to advances in urologic management, this is no longer the case. The leading causes are now pneumonia, pulmonary emboli and sepsis.
• The bladder dysfunction in neurologic injury can change over time so regular urologic surveillance of these patients is recommended.
• The involvement of a urologist in the care of patients with neurogenic voiding dysfunction is important to preserving renal function, quality of life, and prolonging the lifespan.
• It is important to understand that neurologic injury at different levels of the neuraxis usually leads to common, distinct patterns of voiding dysfunction. It is these general patterns that are important to know. Ultimately, each patient will have a unique situation depending upon the level of injury and degree of spinal injury (for example, complete vs. partial cord transaction).
• Basic patient evaluation:

o History and physical including a neurologic and genitourinary exam

o Measurement of PVR

o Urodynamic evaluation

o Renal ultrasound to evaluate for possible hydronephrosis

o Check of renal function (BUN/creatinine)

Question 51

Typical Patterns of Voiding Dysfunction

Answer 51

• detrusor overactivity
• detrusor areflexia
• detrusor sphincter dyssnergia

Question 52

Detrusor Overactivity

Answer 52

•involuntary bladder contractions which lead to urinary frequency, urgency and possibly urge incontinence.

Question 53

Dterusor Arelexia

Answer 53

• the bladder fails to contract.
• The patient is unable to void and experiences urinary retention with possible overflow incontinence.
• Sensate—the patient can sense the full bladder (bladder proprioception intact), but cannot void
• Insensate—the patient does not sense the full bladder (impaired bladder proprioception) and cannot void

Question 54

Detrusor Sphincter Dyssynergia

Answer 54

• the bladder contracts, but the outlet fails to relax resulting in inefficient bladder emptying and high post-void residuals.
• This is also typically accompanied by simultaneous detrusor overactivity. The patient complains of frequency, urgency, possible small amounts of urge incontinence, but also exhibits high post-void residuals due to the inefficient emptying.

Question 55

Lesions Above Brainstem

Answer 55

• These typically lead to detrusor overactivity.
• The patient complains of urinary frequency, urgency, and urge incontinence and nocturia. This is thought to be due to impairment of the tonic cortical inhibition on the PMC (i.e. the PMC decides to initiate voiding because there is less cortical inhibition over it).
• Examples:
• stroke,
• Parkinson’s disease
• brain tumor
• many other processes above the brainstem

•Wein classification: failure to store due to the bladder

Question 56

Lesions of the Brainstem

Answer 56

• Brainstem lesions (if the patient survives) often result in complex and variable voiding dysfunction which we will not cover in this class.
• The tipoff to a brainstem lesion is to notice simultaneous lesions of the cranial nerve nuclei (difficult swallowing—glosspharyngeal n., and/or hoarse voice–recurrent laryngeal branch of vagus n.)
• Example:

-brainstem stroke

Question 57

Spinal Cord Injury

Answer 57

• Initially there is a period of spinal shock with decreased spinal excitability at and below lesion.
• The spinal shock nearly always leads to an areflexic, non-contractile bladder with a closed bladder outlet (both bladder neck and external spincter)—failure to empty due to both the bladder and the outlet. The result is failure to empty with overflow incontinence until the spinal shock resolves.
• The initial spinal shock usually lasts weeks to months. After recovery, the long term lesion will be unmasked. Since neural tissue regenerates slowly it can take up to 2 years for the final voiding pattern to emerge even after the initial spinal shock rresolves. It is important to monitor these patients for the first few years after the injury.

Question 58

Suprasacral SCI (above S2)

Answer 58

•spinal cord lesions above the sacral cord typically result in detrusor sphincter dyssynergia. There is loss of coordinated voiding because the communication between the PMC and voiding centers in the sacrum (sacral micturition center) are lost.

-Recall that control of the urinary sphincter is especially dependent upon input from the PMC. Therefore, the bladder contracts and attempts to empty by primitive spinal reflexes, but the urinary sphincter fails to relax and in fact contracts with increases in with bladder contractions.

• This results in discoordinated and inefficient voiding and also typically results in detrusor overactivity because of the loss of inhibition from the higher brain centers.
• The patient will have high post-void residuals, but may also leak due to urge incontinence.
• Patients with intact sensation will also report urinary frequency and urgency symptoms.
• Examples:
• thoracic vertebral gunshot wound with damage to lumbar or thoracic cord
• multiple sclerosis with demyelination of the thoracic cord

•Note that these patients can have a mixed problem according to the Wein classification:

1. failure to empty due to the outlet (non-relaxing sphincter)
2. failure to store due to the bladder (detrusor overactivity with urge incontinence)

Question 59

Sacral SCI (below S2)

Answer 59

• Typically results in detrusor areflexia with a fixed external sphincter.
• The bladder fails to contract and the striated sphincter retains residual resting tone which is not under voluntary control.
• The result is urinary retention with overflow incontinence.
• Typically bladder sensation is also impaired.
• Examples:
• upper lumbar crush injury with damage to sacral cord
• spina bifida with meningomyelocele

•According to the Wein classification the primary problem is failure to empty due to the bladder

Question 60

Obstructive Uropathy

Answer 60

• According to the Wein classification the fundamental problem is failure to empty due to the outlet.

Question 61

Chronic Obstructive Uropathy

Answer 61

• Chronic blockage of the urinary tract produces characteristic symptoms of obstructive lower urinary tract symptoms. This includes the following:

• Weak and intermittent (starts and stops) urinary stream
• Urinary hesitancy (takes a long time for stream to start)
• Straining to void (patient performs valsalva maneuver while voiding to increase the intravesical pressure during voiding)
• Sensation of incomplete emptying—the patient does not feel completely empty after voiding

•Other irritative voiding symptoms also typically develop that include:

• Urinary urgency with possible urge incontinence. The chronic obstruction leads to a compensatory thickening of the detrusor muscle. For poorly understood reasons, thick-walled bladders have the tendency to develop detrusor overactivity. This leads to bothersome urinary urgency, frequency, and urge incontinence.
• Urinary frequency and nocturia (getting up at night to urinate). The obstruction leads to incomplete emptying of the bladder which reduces its functional capacity leading to frequent urination.

• The best analogy here is to imagine a 2 liter soda bottle. If you only empty out 1 liter from it, then it can only refill with 1 liter. Thus, the incomplete emptying has reduced the functional capacity to only 1 liter despite that the total capacity is 2 liters. This is why a patient with an enlarged prostate and a large capacity bladder will often report frequent urination and voiding small amounts of urine.

Question 62

Prolonged Urinary Obstruction –> Changes in the Urinary Tract

Answer 62

• Bladder hypertrophy—the bladder becomes thick-walled and hypercontractile to force urine past the obstruction. The result is higher voiding pressures to allow continued emptying. The patient often experiences urinary urgency because the thickened bladder leads to detrusor overactivity due to a poorly understood mechanism.
• In the late stage of obstructive uropathy, as the obstruction progresses, the bladder will typically decompensate and fail to empty resulting first in elevated post-void residuals. In this phase of the disease the bladder is no longer able to sustain enough power to empty completely. Left untreated, the incomplete emptying gradually worsens until it decompensates into urinary retention with hydronephrosis. This can progress to renal failure in some cases. The chronically decompensated bladder (after many years of obstruction) often has poor sensation and contracts poorly even after the obstruction is relieved.

Question 63

Male Obstructive Uropathy

Answer 63

The most common source of male obstructive uropathy is benign prostatic hyperplasia (BPH). This is due to a testosterone-mediated physical enlargement of the transition zone of the prostate (which surrounds the urethra). Mechanical obstruction of the bladder outlet results.

• By age 75, greater than 50% of men report some degree of obstructive urinary symptoms
• By age 51-60, 50% of autopsies show evidence of BPH, by age 80, the incidence rises to >90%

• Other common sources of male urinary obstruction include urethral strictures (scarring of the urethra), dysfunction of the male bladder neck, and neurogenic voiding dysfunction

Question 64

Female Obstructive Uropathy

Answer 64

• Women with urethral obstruction will typically report the same symptoms as men, but women do not get BPH since they do not have a prostate.
• Common causes in women include neurogenic voiding dysfunction, prior anti-incontinence surgery (sling is too tight), severe vaginal prolapse due to acute angulation/ kinking of the urethra, female bladder neck dysfunction (rare) or ppelvic floor muscle dysfunction, and female urethral strictures (which are very rare).