The bladder has flexible muscular walls three layers thick. As urine fills the bladder, these walls expand; they contract to expel urine. Although the bladder can hold about a pint of urine, the urge to urinate usually starts when it is about half full. The wall of the bladder wall has three principal tissue layers or coats:
- Mucous membrane (mucosa)--transitional epithelium (urothelium); lines the bladder, ureters, and urethra
- Epithelial layer - contains no blood vessels or lymphatic
- Basement membrane - lies beneath epithelial layer; single layer of cells separating the epithelial layer from the lamina propria; a sheet of extracellular material serving as a filtration barrier and supporting structure for the mucosal layer
- Submucous coat (lamina propria) - areolar connective tissue; interlaced with the muscular coat. This layer contains blood vessels, nerves, and in some regions, glands. A tumour which has spread to this layer can metastasize to the rest of the body via the lymphatics and blood vessels.
- Muscular coat (muscularis propria) -three layers: inner longitudinal, middle circular, and outer longitudinal
- Serous coat (serosa) - a reflection of the peritoneum which covers only the superior surface and the upper part of the lateral surfaces
- Adventitia - in areas on bladder where there is no serosa, the connective tissue between organs merges
- Perivesical fat - layer of fat surrounding bladder outside of serosa/adventitia
Neuroanatomy of bladder function
The brain is the master control of the entire urinary system. The micturition control centre is located in the frontal lobe of the brain. The primary activity of this area is to send tonically inhibitory signals to the detrusor muscle to prevent the bladder from emptying (contracting) until a socially acceptable time and place to urinate is available. Certain lesions or diseases of the brain, including stroke, cancer, or dementia, result in loss of voluntary control of the normal micturition reflex. The signal transmitted by the brain is routed through two intermediate steps (the brainstem and the sacral spinal cord) prior to reaching the bladder.
Within the brainstem is a specialized area known as the pons, a major relay centre between the brain and the bladder. The pons is responsible for coordinating the activities of the urinary sphincters and the bladder so that they work in synergy. The mechanical process of urination is coordinated by the pons in the area known as the pontine micturition centre (PMC). The PMC coordinates the urethral sphincter relaxation and detrusor contraction to facilitate urination. The conscious sensations associated with bladder activity are transmitted to the pons from the cerebral cortex. The interaction of a variety of excitatory and inhibitory neuronal systems is the function of the PMC, which is characterized by its inborn excitatory nature. The PMC functions as a relay switch in the voiding pathway. Stimulation of the PMC causes the urethral sphincters to open while facilitating the detrusor to contract and expel the urine.
The PMC is affected by emotions, which is why animals may be incontinent when excited or scared. The ability of the brain to control the PMC is part of the social training that animals experience during growth and development. Usually the brain takes over the control of the pons at age 3-4 months, which is why most cats and dogs undergo toilet training at this age. When the bladder becomes full, the stretch receptors of the detrusor muscle send a signal to the pons, which in turn notifies the brain. Animals perceive this signal (bladder fullness) as a sudden desire to urinate. Under normal situations, the brain sends an inhibitory signal to the pons to inhibit the bladder from contracting until a suitable place is found. When the PMC is deactivated, the urge to urinate disappears, allowing the animal to delay urination until finding a socially acceptable time and place. When urination is appropriate, the brain sends excitatory signals to the pons, allowing the urinary sphincters to open and the detrusor to empty.
Spinal cord control
The spinal cord functions as a long communication pathway between the brainstem and the sacral spinal cord. When the sacral cord receives the sensory information from the bladder, this signal travels up the spinal cord to the pons and then ultimately to the brain. The brain interprets this signal and sends a reply via the pons that travels down the spinal cord to the sacral cord and, subsequently, to the bladder. In the normal cycle of bladder filling and emptying, the spinal cord acts as an important intermediary between the pons and the sacral cord. An intact spinal cord is critical for normal micturition. If spinal cord injury has occurred, the animal will demonstrate symptoms of urinary frequency, urgency, and urge incontinence but will be unable to empty its bladder completely. This occurs because the urinary bladder and the sphincter are both overactive, a condition termed detrusor sphincter dyssynergia with detrusor hyperreflexia (DSD-DH).
The sacral spinal cord is the terminal portion of the spinal cord situated at the lower back in the lumbar area. This is a specialized area of the spinal cord known as the sacral reflex centre. It is responsible for bladder contractions. The sacral reflex centre is the primitive voiding centre. In infants, the higher centre of voiding control (the brain) is not mature enough to command the bladder, which is why control of urination in neonates and young animals comes from signals sent from the sacral cord. When urine fills the infant bladder, an excitatory signal is sent to the sacral cord. When this signal is received by the sacral cord, the spinal reflex centre automatically triggers the detrusor to contract. The result is involuntary detrusor contractions with coordinated voiding. As the animal's brain matures and develops, it gradually dominates the control of the bladder and the urinary sphincters to inhibit involuntary voiding until complete control is attained. Voluntary continence usually is attained by age 3-4 months. By this time, control of the voiding process has been relinquished by the sacral reflex centre of the sacral cord to the higher centre in the brain.
If the sacral cord becomes severely injured (eg, spinal tumour, trauma, herniated disc), the bladder may not function. Affected animals may develop urinary retention, termed detrusor areflexia. The detrusor will be unable to contract, so the patient will not be able to urinate and urinary retention will occur.
Peripheral nerves form an intricate network of pathways for sending and receiving information throughout the body. The nerves originate from the main trunk of the spinal cord and branch out in different directions to cover the entire body. Nerves convert the internal and external environmental stimuli to electrical signals so that the body can understand stimuli as one of the ordinary senses (ie, hearing, sight, smell, touch, taste, equilibrium). The bladder and the urethral sphincters are under the influence of their corresponding nerves. The autonomic nervous system (ANS) lies outside of the central nervous system. It regulates the actions of the internal organs (eg, intestines, heart, bladder) under involuntary control. The ANS is divided into the sympathetic and the parasympathetic nervous system. Under normal conditions, the bladder and the internal urethral sphincter primarily are under sympathetic nervous system control. When the sympathetic nervous system is active, it causes the bladder to increase its capacity without increasing detrusor resting pressure (accommodation) and stimulates the internal urinary sphincter to remain tightly closed. The sympathetic activity also inhibits parasympathetic stimulation. When the sympathetic nervous system is active, urinary accommodation occurs and the micturition reflex is inhibited.
The parasympathetic nervous system functions in a manner opposite to that of the sympathetic nervous system. In terms of urinary function, the parasympathetic nerves stimulate the detrusor to contract. Immediately preceding parasympathetic stimulation, the sympathetic influence on the internal urethral sphincter becomes suppressed so that the internal sphincter relaxes and opens. In addition, the activity of the pudendal nerve is inhibited to cause the external sphincter to open. The result is facilitation of voluntary urination.
Like the ANS, the somatic nervous system is a part of the nervous system that lies outside of the central spinal cord. The somatic nervous system regulates the actions of the muscles under voluntary control. Examples of these muscles are the external urinary sphincter and the pelvic diaphragm. The pudendal nerve originates from the nucleus of Onuf and regulates the voluntary actions of the external urinary sphincter and the pelvic diaphragm. Activation of the pudendal nerve causes contraction of the external sphincter and the pelvic floor muscles, which occurs with activities such as Kegel exercises. Difficult or prolonged vaginal delivery may cause temporary neurapraxia of the pudendal nerve and cause stress urinary incontinence. Conversely, suprasacral-infrapontine spinal cord trauma can cause over-stimulation of the pudendal nerve that results in urinary retention.
During the filling phase, the bladder accumulates increasing volumes of urine while the pressure inside the bladder remains low. The pressure within the bladder must be lower than the urethral pressure during the filling phase. If the bladder pressure is greater than the urethral pressure (resistance), urine will leak out. The filling of the urinary bladder depends on the intrinsic viscoelastic properties of the bladder and the inhibition of the parasympathetic nerves. Thus, bladder filling primarily is a passive event. Sympathetic nerves also facilitate urine storage in the following ways: Sympathetic nerves inhibit the parasympathetic nerves from triggering bladder contractions. Sympathetic nerves directly cause relaxation and expansion of the detrusor muscle. Sympathetic nerves close the bladder neck by constricting the internal urethral sphincter. This sympathetic input to the lower urinary tract is constantly active during bladder filling.
As the bladder fills, the pudendal nerve becomes excited. Stimulation of the pudendal nerve results in contraction of the external urethral sphincter. Contraction of the external sphincter, coupled with that of the internal sphincter, maintains urethral pressure (resistance) higher than normal bladder pressure. The combination of both urinary sphincters is known as the continence mechanism. The pressure gradients within the bladder and urethra play an important functional role in normal micturition. As long as the urethral pressure is higher than that of the bladder, animal will remain continent. If the urethral pressure is abnormally low or if the intravesical pressure is abnormally high, urinary incontinence will result. As the bladder initially fills, a small rise in pressure occurs within the bladder (intravesical pressure). When the urethral sphincter is closed, the pressure inside the urethra (intraurethral pressure) is higher than the pressure within the bladder. While the intraurethral pressure is higher than the intravesical pressure, urinary continence is maintained.
The storage phase of the urinary bladder can be switched to the voiding phase either involuntarily (reflexively) or voluntarily. Involuntary reflex voiding occurs in young animals when the volume of urine exceeds the voiding threshold. When the bladder is filled to capacity, the stretch receptors within the bladder wall signal the sacral cord. The sacral cord, in turn, sends a message back to the bladder indicating that it is time to empty the bladder. At this point, the pudendal nerve causes relaxation of the levator ani so that the pelvic floor muscle relaxes. The pudendal nerve also signals the external sphincter to open. The sympathetic nerves send a message to the internal sphincter to relax and open, resulting in a lower urethral resistance. When the urethral sphincters relax and open, the parasympathetic nerves trigger contraction of the detrusor. When the bladder contracts, the pressure generated by the bladder overcomes the urethral pressure, resulting in urinary flow. These coordinated series of events allow unimpeded, automatic emptying of the urine.
As the young animal's brain matures, the PMC also matures and gradually assumes voiding control. When the young aniaml reaches about 3-4 months old, this primitive voiding reflex becomes suppressed and the cerebral cortex assume control of bladder function.
Delaying voiding or voluntary voiding
In a healthy adult animal, the PMC functions as an on-off switch that is activated by stretch receptors in the bladder wall and is, in turn, modulated by inhibitory and excitatory neurologic influences from the brain. When the bladder is full, the stretch receptors are activated. The animal perceives the activation of the stretch receptors as the bladder being full, which signals a need to void. When an animal cannot find an appropriate place to urinate, the brain bombards the PMC with a multitude of inhibitory signals to prevent detrusor contractions. At the same time, the animal may actively contract the levator muscles to keep the external sphincter closed or initiate distracting techniques to suppress urination. Thus, the voiding process requires coordination of both the ANS and somatic nervous system, which are in turn controlled by the PMC located in the brainstem.
If a problem occurs within the nervous system, the entire voiding cycle is affected. Any part of the nervous system may be affected, including the brain, pons, spinal cord, sacral cord, and peripheral nerves. A dysfunctional voiding condition results in different symptoms, ranging from acute urinary retention to an overactive bladder or to a combination of both. Urinary incontinence results from a dysfunction of the bladder, the sphincter, or both. Bladder overactivity (spastic bladder) is associated with the symptoms of urge incontinence, while sphincter underactivity (decreased resistance) results in symptomatic stress incontinence. A combination of detrusor overactivity and sphincter underactivity may result in mixed symptoms.
Lesions of the brain above the pons destroy the master control centre, causing a complete loss of voiding control. The voiding reflexes of the lower urinary tract—the primitive voiding reflex—remain intact. Affected individuals show signs of urge incontinence, or spastic bladder (medically termed detrusor hyperreflexia or overactivity). The bladder empties too quickly and too often, with relatively low quantities, and storing urine in the bladder is difficult. This is relatively rare in cats. Typical examples of a brain lesion are stroke, brain trauma, and brain tumors.
Spinal cord lesions
Diseases or injuries of the spinal cord between the pons and the sacral spinal cord also result in spastic bladder or overactive bladder. Animals with paraplegic or quadriplegic have lower extremity spasticity. Initially, after spinal cord trauma, the individual enters a spinal shock phase where the nervous system shuts down. After 6-12 weeks, the nervous system reactivates. When the nervous system becomes reactivated, it causes hyperstimulation of the affected organs. For example, the legs become spastic.
These animals experience urge incontinence. The bladder empties too quickly and too frequently. The voiding disorder is similar to that of the brain lesion except that the external sphincter may have paradoxical contractions as well. If both the bladder and external sphincter become spastic at the same time, the affected animal will sense an overwhelming desire to urinate but only a small amount of urine may dribble out. The medical term for this is detrusor-sphincter dyssynergia because the bladder and the external sphincter are not in synergy. Even though the bladder is trying to force out urine, the external sphincter is tightening to prevent urine from leaving.
Table 1. The causes of spinal cord injuries include trauma and neurological tumours.
|Disorder||Drug||Dosage (cats and dogs)||Mode of action||Side effects|
|Estrogen-responsive incontinence||Diethylstilboestrol||initially 0.1-1.0 mg/day for 3-5 days, then 1.0mg/week||unknown bone marrow toxicity|
|Testosterone-responsive incontinence||Testosterone cypionate||200mg/month||Unknown||none noted in dogs|
|post-prostatic or post-urethral disease (urethral incompetence)||Phenyl-propanolamine||12.5-50.0mg PO tid||sympathomimetic alpha receptor stimulation and increased urethral resistance||minimal|
|Urge incontinence||Propantheline||7.5-30 mg PO tid||Anticholinergic||urine retention|
|Functional urethral obstruction (Sympathetic)||Phenoxybenzamine||2.5-30 mg PO once daily||Sympatholytic: alpha receptor blockage and decreased urethral resistance||Postural hypotension, tachycardia|
|Prazosin (Minipress)||1.0-5.0 mg PO once daily as above||as above|
|(Somatic)||Diazepam 2.0-10 mg PO tid||Skeletal muscle relaxation and decreased external sphincter resistance|
|Sedation||Dantolene (Dantrium)||3-15mg/kg daily||Generalised muscle weakness, hepatotoxicity|
|Detrusor atony||Bethanecol 5-15 mg PO tid||cholinergic: stimulation of detrusor contractions||abdominal discomfort due to increased intestinal peristalsis|
|Detrusor atony with urethral resistance||Bethanecol and phenoxybenzamine||as above||Stimulation of detrusor contraction and decreased urethral resistance||as above|