Bladder and Urethra - Clinical Tree

The bladder and urethra normally function as a coordinated unit to store and discharge urine from the body. Both structural and functional disorders of the bladder or urethra can be responsible for bleeding, incontinence, infection, discomfort, pain, and obstruction that can cause upper tract deterioration to the point of compromising renal function. This chapter focuses on the major diseases and dysfunctional conditions of the bladder and urethra as a unit and the management of such problems.

The bladder and upper urethra are composed of bundles of smooth muscle fibers arranged in a reticular lattice, the outermost bundles being more circular and the inner bundles more longitudinal in orientation at the bladder neck. The smooth muscle bundles blend into the striated muscle of the external urethral sphincter, which is derived from the pelvic diaphragm. The bladder is lined by transitional epithelium, which is sensitive to irritants such as bacterial toxins and various urinary crystals. The urethra and trigone are especially sensitive, and the presence of any irritant in these areas can create significant discomfort.

Proper function of the lower urinary tract depends on intact autonomic and somatic nervous innervation. The detrusor muscle of the bladder is innervated by both sympathetic and parasympathetic fibers. Storage functions are mediated by the sympathetic component, which arises from spinal levels T10–L1. The chemical mediator of this process is norepinephrine, which acts on β-adrenergic receptors in the fundus of the bladder and causes muscle relaxation for low-pressure storage of urine. The same sympathetic stimulus acts on the β-adrenergic receptors of the trigone, bladder neck, and proximal urethra to increase internal sphincter activity and promote continence during urine storage by maintaining outlet resistance. The external urinary sphincter, innervated by the pudendal nerve, progressively increases its tone as the bladder fills, providing additional resistance. As the child develops, the external sphincter may be consciously contracted at times of urgency or stress to prevent the unwanted passage of urine. Properly coordinated function of the external urinary sphincter relies on an intact sacral reflex arc, which should be well developed in normal infants but is variably functional in infants with spinal cord abnormalities or pelvic lesions.

The sensation of bladder fullness initiates a response in toilet-trained children that causes them to discharge their urine. When ready, the parasympathetic nervous system, via acetylcholine, causes cholinergic fibers of the detrusor to contract, resulting in a widened and shortened proximal urethra, eliminating its resistance to outflow. With relaxation of the volitional external sphincter, the bladder empties by sustained and complete contraction of the detrusor, leaving a residual urine volume of <5 mL.

Spinal pathways connect the sacral micturition center with three areas in the brain stem, collectively referred to as the pontine micturition center. This center functions to inhibit urination during storage and to produce external sphincter relaxation during the voiding phase. Above this level are areas of cerebral cortex that oversee and modulate the autonomic process. It is the mature, integrated function of all these components that produces urinary continence.

Toilet training is, in large part, a learned phenomenon. It requires adequate recognition by the brain that micturition would be socially unacceptable in a given situation. With maturation, the bladder gains capacity, allowing for longer intervals between voiding. The approximate bladder capacity in milliliters may be estimated for an infant by the formula 38 + 2.5 × Age (months). For older children, the formula [Age (years) + 2] × 30 can be utilized. Infants void 20 times per day, which decreases to about 10 times per day by age 3 years. The child also learns to resist the urge to void by voluntary contraction of the external sphincter until the detrusor contraction passes and the bladder once again relaxes. Thus, toilet training depends on the development of voluntary cooperation between detrusor and sphincter functions. At times, this process can become dysfunctional. Finally, full bladder control relies on the child developing volitional control over the spinal micturition reflex to be able to initiate or inhibit detrusor contractions. Most children attain day and night continence by 4 years of age.

Urinary incontinence may be in part due to immaturity of the bladder and its nervous system connections. The usual sequence of bladder development is linked to bowel development and is as follows: (1) control of bowel at night, (2) control of bowel during the day, (3) control of bladder during the day, and (4) control of bladder at night.

Childhood Incontinence

Incontinence is the term used for the unintentional loss of urine after toilet training is achieved. The following definitions are clinically useful :

Enuresis or nocturnal enuresis: intermittent incontinence while sleeping
Primary nocturnal enuresis: never been continent at night
Secondary nocturnal enuresis: nighttime incontinence following a dry period of at least 6 months
Daytime incontinence: daytime wetting after toilet training
Overactive bladder—Urinary urgency, usually accompanied by frequency and nocturia with or without incontinence in the absence of infection
Stress incontinence: urine leakage due to physically stressful activities such as coughing
Urgency incontinence: unintentional loss of urine when bladder urgency occurs

The discussion of incontinence is divided into sections on nocturnal enuresis and daytime incontinence, realizing that some children have both. The current recommendation for children with nocturnal enuresis and daytime incontinence is to focus on daytime treatment first followed by nocturnal enuresis therapy.

Nocturnal Enuresis

About 15–20% of children at 5 years of age continue to have bed wetting. As so many children still wet at night before this age, it is considered within the range of normal and not termed nocturnal enuresis. After age 5, night wetting resolves at the rate of about 15% each year. By age 15 years, it has resolved in 99% of children.

Etiology

Children with monosymptomatic nocturnal enuresis are, in general, physically and emotionally similar to their peers. The difference lies in their inability to awaken during sleep when their bladder is full or contracts. The etiology of this disorder is likely complex and several factors should be considered.

Genetic

Family history is significant. If both the parents had enuresis, close to 80% of their offspring will as well. If one parent was affected, 44% of the offspring are affected. If neither parent has a history, only 15% of their children have this problem.

Psychological

Psychological stress can induce nocturnal enuresis in certain children. Secondary nocturnal enuresis often raises this concern. Common factors include divorce, changing homes, birth of a new sibling, trouble at school, or just starting school.

Developmental

As children grow, bladder capacity increases significantly each year at a proportion greater than urine volume produced. Volitional control over bladder and sphincter also may mature at variable rates and may be related to subtle delays in perceptual abilities or fine motor skills.

Urodynamic

Studies show that enuretic episodes occur when the bladder is full, and they simulate normal awake voiding. Although nocturnal enuretic patients have more nighttime unstable bladder contractions, these are at low pressure and do not cause leakage.

Night wetting appears to occur in three ways: wetting associated with significant restlessness and visceral and somatic activity (deep respirations), wetting with a quick contraction and minimal movement, and wetting with no central nervous system response (parasomnia).

Sleep Disorders

Parents of children with nocturnal enuresis are generally convinced that these children sleep deeply and are difficult to arouse. However, this is probably not true. Enuretic patients sleep no more deeply than age-matched controls, wet in all stages of sleep, and show no different awakening patterns. Wetting episodes occur as the bladder fills throughout the night.

Antidiuretic Hormone

Antidiuretic hormone (ADH) is released from the pituitary in a circadian rhythm so that levels are higher at night and thus diminish urine output. Some children may undersecrete ADH at night resulting in bed wetting. Although some patients follow this pattern, others do not; the altered circadian patterns appear to normalize with maturation.

Evaluation

The screening evaluation should include a history, physical examination, and urinalysis. If these are normal, then no other testing is needed because organic disease rarely causes monosymptomatic nocturnal enuresis. Any associated anomaly or problem such as urinary tract infection (UTI), sacral anomalies, or complex enuresis patterns warrant radiographic investigation.

Treatment

The treating physician should recognize enuresis as a symptom and not a disease. Realizing that there may be more than one cause permits the physician to consider more than one treatment option. Specific treatment is generally discouraged before the age of 7 years. Certain measures are sensible in all nocturnal enuretic patients: void just before getting into bed, avoid excessive fluid intake during the evening hours, and avoid caffeine after 3:00 p.m.

Enuretic Alarms

Wetting alarms are devices that fit in the underwear of the patients. When moistened, an alarm is sounded. This type of conditioning therapy requires a motivated patient and parents. A variety of products are available with either an audio alarm, a vibrating alarm, or both. In our experience, the best alarm is simply one that is easy to set up and is able to wake the child. The parent may need to help arouse the child, take him or her to the bathroom, and reset the alarm. This may occur multiple times each night, particularly at the onset of therapy. In two studies, wetting alarms were shown to give the best long-term results when compared with other treatments. The length of treatment to achieve dryness varied between 18 nights and 2.5 months. Relapse may occur in 20–30% of treated children, but re-treatment can be successful.

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