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Anatomy : 

Anatomy The urinary bladder is a smooth muscle chamber composed of two main parts: (1) the body, the major part, collects urine (2) the neck, a funnel-shaped extension of the body, passing inferiorly and anteriorly into the urogenital triangle and connecting with the urethra

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The lower part of the bladder neck is also called the posterior urethra because of its relation to the urethra. The smooth muscle of the bladder is called the detrusor muscle.

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On the posterior wall of the bladder, lying immediately above the bladder neck, is a small triangular area called the trigone. The trigone can be identified by the fact that its mucosa, the inner lining of the bladder, is smooth, in contrast to the remaining bladder mucosa, which is folded to form rugae.

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At the lowermost apex of the trigone, the bladder neck opens into the posterior urethra, and the two ureters enter the bladder at the uppermost angles of the trigone. Each ureter, as it enters the bladder, courses obliquely through the detrusor muscle and then passes another 1 to 2 centimeters beneath the bladder mucosa before emptying into the bladder.

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The bladder neck (posterior urethra) is 2 to 3 centimeters long, and its wall is composed of detrusor muscle interlaced with a large amount of elastic tissue. The muscle in this area is called the internal sphincter.

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Its natural tone normally keeps the bladder neck and posterior urethra empty of urine and, therefore, prevents emptying of the bladder until the pressure in the main part of the bladder rises above a critical threshold.

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Beyond the posterior urethra, the urethra passes through the urogenital diaphragm, which contains a layer of muscle called the external sphincter of the bladder.

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This muscle is a voluntary skeletal muscle, in contrast to the muscle of the bladder body and bladder neck, which is entirely smooth muscle. The external sphincter muscle is under voluntary control of the nervous system and can be used to consciously prevent urination even when involuntary controls are attempting to empty the bladder.

Innervation of the Bladder : 

Innervation of the Bladder The principal nerve supply of the bladder is by way of the pelvic nerves, which connect with the spinal cord through the sacral plexus, mainly connecting with cord segments S-2 and S-4. Coursing through the pelvic nerves are both sensory nerve fibers and motor nerve fibers. The sensory fibers detect the degree of stretch in the bladder wall. Stretch signals from the posterior urethra are especially strong and are mainly responsible for initiating the reflexes that cause bladder emptying.

Innervation of the urinary bladder and its sphincters : 

Innervation of the urinary bladder and its sphincters

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The motor nerves transmitted in the pelvic nerves are parasympathetic fibers. These terminate on ganglion cells located in the wall of the bladder. Short postganglionic nerves then innervate the detrusor muscle. In addition to the pelvic nerves, two other types of innervation are important in bladder function. Most important are the skeletal motor fibers transmitted through the pudendal nerve to the external urethral sphincter. These are somatic nerve fibers that innervate and control the voluntary skeletal muscle of the sphincter.

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Also, the bladder receives sympathetic innervations from the sympathetic chain through the hypogastric nerves, connecting mainly with the L-2 segment of the spinal cord. These sympathetic fibers stimulate mainly the blood vessels and have little to do with bladder contraction. Some sensory nerve fibers also pass by way of the sympathetic nerves and may be important in the sensation of fullness and, in some instances, pain.

Blood supply : 

Blood supply The bladder is supplied by the superior and inferior vesical arteries which are branches of anterior trunk of internal iliac artery. The veins that drain the bladder form a plexus on the infero-lateral surface before ending in the internal iliac vein. Most of the lymph from the urinary bladder ends in the external iliac nodes.

The Cystometrogram : 

The Cystometrogram When there is no urine in the bladder, the intravesicular pressure is about 0, but by the time 30 to 50 milliliters of urine has collected, the pressure rises to 5 to 10 centimeters of water. Additional urine—200 to 300 milliliters— can collect with only a small additional rise in pressure; this constant level of pressure is caused by intrinsic tone of the bladder wall itself. Beyond 300 to 400 milliliters, collection of more urine in the bladder causes the pressure to rise rapidly.

Normal cystometrogram, showing also acute pressure waves(dashed spikes) caused by micturition reflexes. : 

Normal cystometrogram, showing also acute pressure waves(dashed spikes) caused by micturition reflexes.

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Superimposed on the tonic pressure changes during filling of the bladder are periodic acute increases in pressure that last from a few seconds to more than a minute. The pressure peaks may rise only a few centimetres of water or may rise to more than 100 centimeters of water. These pressure peaks are called micturition waves in the cystometrogram and are caused by the micturition reflex.

Micturition Reflex : 

Micturition Reflex As the bladder fills, many superimposed micturition contractions begin to appear. They are the result of a stretch reflex initiated by sensory stretch receptors in the bladder wall, especially by the receptors in the posterior urethra when this area begins to fill with urine at the higher bladder pressures.

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Sensory signals from the bladder stretch receptors are conducted to the sacral segments of the cord through the pelvic nerves and then reflexively back again to the bladder through the parasympathetic nerve fibers by way of these same nerves.

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When the bladder is only partially filled, these micturition contractions usually relax spontaneously after a fraction of a minute, the detrusor muscles stop contracting, and pressure falls back to the baseline. As the bladder continues to fill, the micturition reflexes become more frequent and cause greater contractions of the detrusor muscle.

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Once a micturition reflex begins, it is “self-regenerative.” That is, initial contraction of the bladder activates the stretch receptors to cause a greater increase in sensory impulses to the bladder and posterior urethra, which causes a further increase in reflex contraction of the bladder; thus, the cycle is repeated again and again until the bladder has reached a strong degree of contraction.

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Once a micturition reflex has occurred but has not succeeded in emptying the bladder, the nervous elements of this reflex usually remain in an inhibited state for a few minutes to 1 hour or more before another micturition reflex occurs. As the bladder becomes more and more filled, micturition reflexes occur more and more often and more and more powerfully.

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Once the micturition reflex becomes powerful enough, it causes another reflex, which passes through the pudendal nerves to the external sphincter to inhibit it. If this inhibition is more potent in the brain than the voluntary constrictor signals to the external sphincter, urination will occur. If not, urination will not occur until the bladder fills still further and the micturition reflex becomes more powerful.

Facilitation or Inhibition of Micturition by the Brain : 

Facilitation or Inhibition of Micturition by the Brain The micturition reflex is a completely autonomic spinal cord reflex, but it can be inhibited or facilitated by centers in the brain. These centers include (1) strong facilitative and inhibitory centers in the brain stem, located mainly in the pons, and (2) several centers located in the cerebral cortex that are mainly inhibitory but can become excitatory

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The micturition reflex is the basic cause of micturition, but the higher centers normally exert final control of micturition as follows: 1. The higher centers keep the micturition reflex partially inhibited, except when micturition is desired. 2. The higher centers can prevent micturition, even if the micturition reflex occurs, by continual tonic contraction of the external urethral sphincter until a convenient time presents itself. 3. When it is time to urinate, the cortical centers can facilitate the sacral micturition centers to help initiate a micturition reflex and at the same time inhibit the external urethral sphincter so that urination can occur.

Abnormalities of Micturition : 

Abnormalities of Micturition

Irritative Voiding Symptoms : 

Irritative Voiding Symptoms Urgency is the sudden desire to void in inflammatory conditions such as cystitis or in hyperreflexic neuropathic conditions such as neurogenic bladders resulting from upper motor neuron lesions. Dysuria painful urination associated with inflammation. The pain is typically referred to the tip of the penis in men or to the urethra in women.

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Frequency is the increased number of voids during the daytime, and nocturia is nocturnal frequency. Adults normally void five or six times a day and once at most during the nighttime hours. Increased frequency may result from increased urinary output or decreased functional bladder capacity.

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Diabetes mellitus, diabetes insipidus, excess fluid ingestion, and diuretics (including caffeine and alcohol) are a few of the causes of increased urinary output. Decreased functional bladder capacities may result from bladder outlet obstruction (increased residual urine volume results in a lower functional capacity), neurogenic bladder disorders (spasticity and reduced compliance), extrinsic bladder compression (uterine fibroids, radiation-induced fibrosis, pelvic neoplasms), or psychological factors (anxiety).

Obstructive Voiding Symptoms : 

Obstructive Voiding Symptoms Hesitancy is a delay in the initiation of micturition. results from the increased time required for the bladder to attain the high pressure necessary to exceed that of the urethra in the obstructed setting. Decreased force of stream results from the high resistance the bladder faces and is often associated with a decrease in caliber of the stream. Intermittency is the interruption of the urinary stream Postvoid dribbling the uncontrolled release of the terminal few drops of urine. Obstructive symptoms are most commonly due to benign prostatic hyperplasia, urethral stricture, or neurogenic bladder disorders, prostatic or urethral carcinoma and foreign body are other causes.

Incontinence : 

Incontinence Urinary incontinence is the involuntary loss of urine. Total incontinence, patients lose urine at all times and in all positions. Stress incontinence is the loss of urine associated with activities that result in an increase in intra-abdominal pressure (coughing, sneezing, lifting, exercising). Uncontrolled loss of urine preceded by a strong urge to void is known as urge incontinence. Chronic urinary retention may result in overflow incontinence.   The evaluation and treatment vary with each of the categories.

Medications causing urinary incontinence: Sedatives Diuretics Anticholinergics Antipsychotics Alpha antagonists

Bladder sphincter dyssynergia (detrusor sphincter dysynergia (DSD), neurogenic detrusor overactivity (NDO) : 

Bladder sphincter dyssynergia (detrusor sphincter dysynergia (DSD), neurogenic detrusor overactivity (NDO) It is a consequence of a neurological pathology such as spinal injury or multiple sclerosis that disrupts central nervous system regulation of the micturition reflex resulting in dys-coordination of the bladder musculature and the external urethral sphincter. Instead of the urethral muscle relaxing completely during voiding, it dyssynergically contracts causing the flow to be interrupted and the bladder pressure to rise. On cystography there is an irregular appearance of the bladder outline due to muscular contraction against the unrelaxed bladder sphincter.

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Symptoms Symptomatically, people with this condition generally experience daytime and night time wetting, urinary retention, and often have a history of urinary tract and bladder infections. Constipation and encopresis are often associated with this condition. Diagnosis Strictly DSD can only be diagnosed from an CMG trace or x-ray findings

Urodynamic studies : 

Urodynamic studies It is the investigation and assessment of the bladder and lower urinary tract. It measures the intravesical pressure during bladder filling (filling cystometrogram) and the relationship between intravesical pressure and urinary flow rate during voiding (micturition cystometrogram).

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We now have four channel recording of abdominal pressure(Pabd), total bladder pressure(Pves) (< 30cmH2O), subtracted true intravesical (detrusor) pressure(Pdet = Pves – Pabd) and flow rate(normal peak flow rate for males is 20–25 mL/s and for females 20–30 mL/s).

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The filling volume and voiding volume will be recorded a note is made on the patient’s awareness of bladder sensation, the capacity before a strong desire to void is appreciated, the compliance of the bladder (the volume change for a given pressure), the contractility of the detrusor (eg. spontaneous contractions before complete filling).

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After the bladder is filled with contrast medium, a video-radiological screening is possible, detecting abnormalities of the structure and visualising the bladder contraction and sphincter mechanisms. These can be interpreted alongside the pressure-flow measurements. In this way, the assessment of neurotrophic bladder dysfunction has become much more detailed and accurate.

Neurologic disorders causing urinary disturbences: : 

Neurologic disorders causing urinary disturbences: With regard to the neurologic diseases that cause bladder dysfunction, multiple sclerosis, usually with urinary urgency, is by far the most common. degenerative diseases (Parkinson disease and multiple system atrophy) for 14 percent, spinal cord disorders account for 12 percent of cases, and frontal lobe lesions for 9 percent.

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Complete destruction of the cord below T12 conus lesions trauma, myelodysplasias, tumor, venous angioma, and necrotizing myelitis. bladder is paralyzed for voluntary and reflexactivity no awareness of the state of fullness; voluntary initiation of micturition is impossible; the tonus of the detrusor muscle is abolished and the bladder distends as urine accumulates until there is overflow incontinence; voiding is possible only by the Crede´ maneuver, i.e.,lower abdominal compression and abdominal straining. Usually the anal sphincter and colon are similarly affected, and there is “saddle” anesthesia and abolition of the bulbocavernosus and anal reflexes as well as the tendon reflexes in the legs. The cystometrogram shows low pressure and no emptying contractions. Management: catherisation & anticholinergics

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Disease of the sacral motor neurons in the spinal gray matter autonomic bladder , autonomous bladder the anterior sacral roots, or peripheral nerves innervating the bladder lumbosacral meningomyelocele and the tethered cord syndrome. a lower motor neuron paralysis of the bladder. sacral and bladder sensation are intact. Various causes pertain in cauda equina disease, the most frequent being compression by epidural tumor or disc, neoplastic meningitis, and radiculitis from herpes or cytomegalovirus. a hysterical patient can suppress motor function and suffer a similar distention of the bladder.

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Interruption of sensory afferent fibers atonic bladder as in diabetes and tabes dorsalis (tabetic bladder). motor nerve fibers unaffected Although a flaccid (atonic) paralysis of the bladder may be purely motor or sensory, as described above, in most clinical situations there is interruption of both afferent and efferent innervation, as in cauda equina compression or severe polyneuropathy. Neuropathies affecting mainly the small fibers are the ones usually implicated (diabetes, amyloid, etc.), but urinary retention also occurs in certain acute neuropathies such as Guillain-Barre´ syndrome. Treatment includes intermittent self catheterisation

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Upper spinal cord lesions, above T12 reflex neurogenic (spastic) bladder, automatic bladder multiple sclerosis and traumatic myelopathy, which are the commonest causes; myelitis, spondylosis, arteriovenous malformation (AVM), syringomyelia, and tropical spastic paraparesis If the cord lesion is of sudden onset, the detrusor muscle suffers the effects of spinal shock. At this stage, urine accumulates and distends the bladder to the point of overflow. As the effects of spinal shock subside, the detrusor usually becomes reflexly overactive (detrusor hyperreflexia), and since the patient is unable to inhibit the detrusor and control the external sphincter, urgency, precipitant micturition, and incontinence result. Incomplete lesions result in varying degress of urgency in voiding.

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With slowly evolving processes involving the upper cord, such as multiple sclerosis, the bladder spasticity and urgency worsen with time and incontinence becomes more frequent. In addition, initiation of voluntary micturition is impaired and bladder capacity is reduced. Bladder sensation depends on the extent of involvement of sensory tracts. Bulbocavernosus and anal reflexes are preserved. The cystometrogram shows uninhibited contractions of the detrusor muscle in response to small volumes of fluid.

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Some patients can still control urination in this condition by stimulating the skin (scratching or tickling) in the genital region, which sometimes elicits a micturition reflex. Management: Decompress the rectum or bladder - reverses the effects of unopposed sympathetic outflow. Terazosin/ spinal anesthetic may be used as prophylaxis.

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Mixed type of neurogenic bladder. In diseases such as multiple sclerosis, subacute combined degeneration, tethered cord, and syphilitic meningomyelitis, bladder function may be deranged from lesions at multiple levels, i.e., spinal roots, sacral neurons or their fibers of exit, and higher spinal segments. The resultant picture is a combination of sensory, motor, and spastic types of bladder paralysis.

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Stretch injury of the bladder wall, as occurs with anatomic obstruction at the bladder neck and occasionally with voluntary retention of urine, as in hysteria. Repeated overdistention of the bladder wall often results in varying degrees of decompensation of the detrusor muscle and permanent atonia or hypotonia, although the evidence for this mechanism is uncertain. The bladder wall becomes fibrotic and bladder capacity is greatly increased. Emptying contractions are inadequate, and there is a large residual volume even after the Crede´ maneuver and strong contraction of the abdominal muscles. As with motor and sensory paralyses, the patient is subject to cystitis, ureteral reflux, hydronephrosis and pyelonephritis, and calculus formation.

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Frontal lobe incontinence. Often the patient, because of his confused mental state, ignores the desire to void and the subsequent incontinence. There is also a supranuclear type of hyperactivity of the detrusor and precipitant evacuation.   Nocturnal enuresis, or urinary incontinence during sleep, due presumably to a delay in acquiring inhibition of micturition.

Therapy of Disordered Micturition : 

Therapy of Disordered Micturition Goals in treatment: Preservation of upper urinary tract Maintain adequate bladder capacity with good compliance Promote low-pressure micturition Avoid bladder over-distension Prevent urinary tract infection Minimize use of Foley catheter Choose therapy that minimizes patient risks while maximizing social, emotional, and vocational acceptability

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Anti incontinent measures: Pelvic floor exercises. Vaginal weights. Biofeedback. Electrical stimulation. Bladder training. In the case of a flaccid paralysis, bethanechol (Urecholine) produces contraction of the detrusor by direct stimulation of its muscarinic cholinergic receptors. In spastic paralysis, the detrusor can be relaxed by propantheline (15 to 30 mg three times daily), which acts as a muscarinic antagonist, and by oxybutynin (Ditropan, 5 mg two to three times daily), which acts directly on the smooth muscle and also has a muscarinic antagonist action.

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Atropine, which is mainly a muscarinic antagonist, only partially inhibits detrusor contraction. More recently, alpha1 sympathomimetic blocking drugs such as terazosin, doxazosin, and tamsulosin have been used to relax the urinary sphincter and facilitate voiding. Their widest use has been in men with prostatic hypertrophy, but they may be beneficial in patients with dyssynergia of the sphincter from neurologic disease.

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Often the patient must resort to intermittent self-catheterization, which can be safely carried out with scrupulous attention to sterile technique (washing hands, disposable catheter, etc.). Some forms of chronic antibiotic therapy and acidification of urine with vitamin C (1000 g/day) are practical aids, but their use has gone through cycles of popularity based on various studies with differing results. In selected paraplegic patients, the implantation of a sacral anterior root stimulator may prove to be helpful in emptying the bladder and achieving continence.

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