Urinary incontinence in women

Stress incontinence

Increasing age, parity, vaginal delivery, and episiotomy are associated with stress incontinence in women.[7][11][14][15][16] This is due to weakening and stretching of muscles and connective tissue during delivery, as well as damage to pudendal and pelvic nerves.[16]
Excess weight, especially in those with a BMI over 25, increases pressure on pelvic tissues, causing chronic strain, stretching, and weakening of the muscles, nerves, and other pelvic structures.[3]
Women with urinary incontinence are significantly more likely to report bowel symptoms (constipation, faecal incontinence).[17] Constipation, with chronic repeated, prolonged defecatory straining efforts, is thought to contribute to progressive neuropathy and dysfunction, resulting in lower urinary tract symptoms.[18] Concomitant urinary incontinence and chronic constipation in young women with long-standing history of urinary incontinence may indicate occult spina bifida. Conversely, faecal incontinence commonly coexists with urinary incontinence, particularly in older people and in nursing home residents.[17][19][20]
High-impact activity (e.g., long-distance running) increases stress on pelvic support structures, which leads to stretching and weakening of the muscles, nerves, and other pelvic structures, and results in urinary incontinence.[21][22]

Urgency incontinence

Several theories regarding the aetiology of urgency incontinence have been published.[23] Traditionally, the aetiology of urgency incontinence was believed to be either myogenic or neurogenic. Myogenic refers to changes in the detrusor muscle itself and neurogenic refers to any disruption in the autonomic nervous system or supraspinal nervous system.[23]

In some patients, laxity of the peri-urethral tissues that support the bladder neck may not only cause stress incontinence but may also induce urgency incontinence.[24] As valsalva is experienced in the patient, the urine begins to enter the proximal portion of the urethral which causes a reflex signal to the brain to contract the bladder in preparation for voiding, which will lead to an incontinence event if the patient is not ready to void.[24]
Other aetiologies of urgency incontinence include sensory changes in the urothelium that cause the bladder to become more sensitive to bladder irritants. This may be influenced by hormonal changes such as lack of oestrogen. Both metabolic syndromes and disorders of affect (e.g., anxiety and depression) have been associated with urgency incontinence.[23] The urinary microbiome has also been implicated as a cause of urgency in patients who lack Lactobacillus species colonisation of the bladder.[25]

In women with a cerebrovascular accident, interruption of central nervous system inhibitory pathways is associated with lower urinary tract dysfunction.[26] Detrusor overactivity and less commonly detrusor underactivity with urinary retention resulting from upper motor neuron lesions after stroke may present as urinary urgency and urgency incontinence.[27][28]

Upper motor neuron lesions, as seen in traumatic injuries to the brain or spinal cord, Parkinson’s disease, and multiple sclerosis, which affect descending pathways from the central nervous system, may lead to delayed bladder sensation, urinary retention, and resultant overflow incontinence, though detrusor overactivity is the most common presentation.[27][29]
Dementia is associated with increased incidence of urinary incontinence in older women and can be observed in dementia with Lewy body disease, vascular dementia, normal pressure hydrocephalus, frontotemporal dementia, and Alzheimer's disease.[27] Incontinence may be due to neurological problems, behavioural problems, or myogenic changes, but also from the cognitive impairment and impaired mobility often seen in dementia.[27]

Indirect effects of a stroke and other neurological conditions such as Parkinson's disease, multisystem atrophy, and multiple sclerosis may include motor, visual, or speech problems that make the task of accessing toilet facilities a challenge and result in functional urinary incontinence.[27][28]

Drugs that cause incontinence include (but are not limited to) alpha-blockers, calcium-channel blockers, diuretics, lithium, opioids, anticholinergics, ACE inhibitors, selective serotonin-reuptake inhibitors (SSRIs), gabapentin, thiazolidinediones, and non-steroidal anti-inflammatory drugs (NSAIDs).[11] In addition, caffeine and artificial sweetener consumption may cause frequency and urgency.[30]

Other risk factors for urinary incontinence include a family history of incontinence, childhood enuresis, post-menopausal status, and functional impairment (e.g., arthritis, impaired vision). In addition, chronic medical conditions may be associated with incontinence (e.g., chronic cough, obstructive sleep apnoea, diabetes mellitus, cardiopulmonary disease, and recurrent bladder infections).[11] Genitourinary and pelvic surgery may play a role in the aetiology of urinary incontinence, including radiation exposure.

Micturition is a voluntary act controlled by the central nervous system.[11] The signals are coordinated by the pontine micturition centre. Urine storage requires contraction of the internal and external urethral sphincters and relaxation of the bladder.[1] Somatic nerves mediate external urethral sphincter contraction, whereas sympathetic nerves trigger internal urethral sphincter contraction. The pudendal nerve stimulates the external urethral sphincter, which is supported by the lateral vaginal wall on either side, specifically the levator ani muscle, fascia, and ligamentous attachments. Involuntary and voluntary input to these structures results in an increase in outlet resistance, which helps to maintain urinary continence. In addition, the submucosal vascular plexus contributes to maintenance of urethral turgor, and therefore is involved in sustaining closure of the urethral sphincter.

Voiding requires coordinated urethral sphincter relaxation and bladder contraction. Initiation of these processes is under the control of the parasympathetic nervous system, and is triggered by signals that originate from S2-S4 of the spinal cord and travel through the hypogastric nerves. Once stimulated, these nerve endings release the neurotransmitter acetylcholine, which in turn binds to muscarinic receptors located in the bladder. The receptor subtypes present are primarily M2 and M3. Contraction of the smooth muscle of the bladder - the detrusor muscle - occurs, resulting in urinary flow through the relaxed urethra.

Inhibition of voiding is controlled by the pontine storage centre, which receives afferent signals from the distended bladder. These signals are then mediated through a branch of the sympathetic nervous system that originates in T11-L2 of the spinal cord. These nerves release noradrenaline, which binds to beta receptors on the bladder wall and alpha receptors at the bladder neck and urethra. Binding of noradrenaline triggers smooth muscle relaxation at the level of the bladder, inhibiting detrusor contraction. Meanwhile, sympathetic stimulation at the alpha receptors causes muscle contraction. This coordinated event inhibits micturition. Both types of autonomic nervous system contain afferent input that recognises bladder fullness, which are A-delta and C fibres contained in both parasympathetic and sympathetic pathways.

Injury to the sympathetic and parasympathetic nerves can result in a range of voiding-dysfunction symptoms including urgency urinary incontinence, retention of urine, and/or stress urinary incontinence.[31] As one example, compression by the fetal head during prolonged labour can injure the parasympathetic nerves in the pelvic plexus (resulting in postnatal retention of urine and urgency incontinence) and the pudendal nerves (resulting in loss of tone of the external sphincter and stress urinary incontinence).[31]

Urgency incontinence in women is caused by any disruption to the well-coordinated process of micturition and remains poorly understood. Abnormal central nervous system signaling is an important factor.[31] Most theories propose either a neurogenic or a myogenic origin.[11] A commonly used treatment regimen targets the muscarinic receptors of the bladder.

By contrast, stress urinary incontinence tends to be caused by pelvic floor dysfunction and resulting anatomical abnormality, such as urethral hyper-mobility. The support structures of the bladder and/or urethra may alter the system in such a way that urethral closure pressure is no longer maintained, or no longer exceeds intra-abdominal pressure during strenuous activity, which creates a pressure gradient favouring loss of urine, albeit involuntarily.[32] Alternatively, the support structures may be intact but the urethra may be weak. This occurrence is referred to as intrinsic sphincter deficiency.

Standardised terminology of lower urinary tract function[2]

Clinical classification of the different types of incontinence is as follows:

Stress incontinence - involuntary leakage on effort, exertion, sneezing, or coughing
Urgency incontinence - involuntary leakage accompanied by or immediately preceded by urgency
Overactive bladder (detrusor overactivity) - urgency, usually with frequency, with or without urgency incontinence; usually with frequency and nocturia in the absence of an underlying metabolic or pathological condition
Mixed incontinence - combination of stress and urgency incontinence symptoms
Nocturia - sleep interruption to urinate one or more times
Nocturnal enuresis - involuntary loss of urine occurring during sleep
Continuous incontinence - continuous loss of urine
Overflow incontinence - urinary leakage from an over-distended bladder; terminology is no longer widely used
Other - involuntary leakage during situations not encompassed by other classifications (i.e., during sexual activity or change in body position).

Pathophysiology

Classification

Standardised terminology of lower urinary tract function[2]