The puerperium
Louise C Kenny, Jenny E Myers in Obstetrics, 2017
Voiding difficulty and overdistension of the bladder are not uncommon after childbirth, especially if regional anaesthesia (epidural/spinal) has been used. It is now known that after epidural anaesthesia the bladder may take up to 8 hours to regain normal sensation. During this time, about 1 litre of urine may be produced. Therefore, if urinary retention occurs, considerable damage may be inflicted on the detrusor muscle. Overstretching of the detrusor muscle can dampen bladder sensation and make the bladder hypocontractile, particularly with fibrous replacement of smooth muscle. In this situation, overflow incontinence of small amounts of urine may erroneously be assumed to be normal voiding. Fluid loading prior to epidural analgesia, the antidiuretic effect of high concentrations of oxytocin during labour, increased postpartum diuresis (particularly in the presence of peripheral oedema) and increased fluid intake by breastfeeding mothers all contribute to the increased urine production in the puerperium. Therefore, an intake/output chart alone may not detect incomplete emptying of the bladder.
Urology
Janesh K Gupta in Core Clinical Cases in Surgery and Surgical Specialties, 2014
Urodynamic stress incontinence (USI), previously called genuine stress incontinence USI is noted during filling cystometry, and is defined as the involuntary leakage of urine during increased abdominal pressure in the absence of a detrusor contraction. This is caused by a failure to maintain the normal retropubic position of the bladder neck and posterior urethra during increases in abdominal pressure and/or impaired internal sphincter mechanism.Detrusor overactivity, previously called detrusor instability Detrusor overactivity is a urodynamic observation characterized by involuntary detrusor contractions during the filling phase which may be spontaneous or provoked.
Urogynaecology and pelvic floor problems
Helen Bickerstaff, Louise C Kenny in Gynaecology, 2017
In health the bladder stores, and then voids, urine. This is known as the micturition cycle. Most of the time, the detrusor muscle of the bladder is relaxed allowing storage of increasing urine volumes with no increase in pressure. As bladder capacity is reached, sensory signals from stretch receptors in the bladder wall send the sensation of bladder filling. The sphincter mechanism is closed. As an adult, voluntary delay of micturition until socially convenient is achieved by cortical inhibition of the spinal voiding reflex arc. Before voiding begins, this inhibition is removed and the pelvic floor and urethral sphincters relax in a coordinated fashion, to allow detrusor contraction and bladder emptying. The detrusor muscle is innervated by muscarinic cholinergic nerves of the parasympathetic nervous system (causing detrusor muscle contraction), and the urethral sphincter by noradrenergic neurons of the sympathetic nervous system (sphincter contraction) and somatic fibres (voluntary contraction and relaxation) from the pudendal nerves.
Pelvic floor dysfunction in midlife women
Published in Climacteric, 2019
SUI, UUI, and even OAB are terms that refer to symptoms reported by patients. Although a classification of incontinence by symptoms alone is imperfect, it is easy, clinically useful, and cost-effective. Symptoms alone can help determine treatment paths and define the impact on quality of life. Urodynamic testing is performed for objective diagnosis and is often used prior to surgery. Such testing defines urodynamic stress incontinence as objective urine loss with increased intraabdominal pressure in the absence of a detrusor contraction. This objective finding would be expected in most women complaining of SUI. Urodynamics additionally objectively define the condition of detrusor overactivity, a bladder dysfunction with uninhibited detrusor muscle contractions (with or without urine loss) on bladder filling in the absence of infection or the obvious bladder pathology. Detrusor overactivity is most often associated with UUI and/or OAB symptoms.
Managing autonomic dysfunction in Parkinson’s disease: a review of emerging drugs
Published in Expert Opinion on Emerging Drugs, 2020
Dinkar Kulshreshtha, Jacky Ganguly, Mandar Jog
The primary function of urinary bladder is the storage and voiding of urine. This is facilitated by a synchronization between detrusor muscle and urethral sphincter, which in turn is related to the neuronal networks in the spinal cord and brain. The detrusor muscle and the internal urethral sphincter are supplied by the sympathetic and parasympathetic nervous system and are under involuntary control while the external urethral sphincter is under voluntary control and supplied by the pudendal nerve. While sympathetic stimulation causes detrusor relaxation and urethral sphincter contraction and aids storage, parasympathetic stimulation has the opposite effect and causes voiding [13]. Fifty-five to eighty percent of PD patients complain of bladder dysfunction at some point in time. Both storage (urinary urgency, frequency, nocturia, with or without incontinence) and voiding (slow and/or interrupted stream, terminal dribble, hesitancy and straining) symptoms occur in PD [14]. Nocturia, a common symptom in PD may be due to nocturnal polyuria, characterized by increased nocturnal urine production of more than 20–33% of the entire 24-h volume [15]. Reduced bladder capacity, poor compliance and detrusor overactivity (DO) have been shown in urodynamic studies [16]. The proposed mechanism for overactive bladder (OAB) symptoms in PD is disruption of the dopamine D1-GABAergic direct pathway and its GABAergic collateral to the micturition circuit, resulting in loss of inhibition of the micturition reflex and OAB symptoms [17–19].
Pharmacological treatments available for the management of underactive bladder in neurological conditions
Published in Expert Review of Clinical Pharmacology, 2018
Seyedeh-Sanam Ladi-Seyedian, Behnam Nabavizadeh, Lida Sharifi-Rad, Abdol-Mohammad Kajbafzadeh
In the normal situation, micturition reflex initiates after maximal filling of bladder and consequent stretch in bladder wall. Afterwards, afferent nerves, brain circuits, and efferent nerves conduct the impulse, respectively, which leads to an effective and sustainable detrusor contraction. Sacral parasympathetic nucleus and pontine micturition center (PMC) facilitate this reflex [13]. PMC is normally inhibited by limbic system and in turn receives inputs from higher cortical centers. During the storage phase, afferent fibers are responsible for bladder volume monitoring. Intact bladder sensation is fundamental to initiate micturition reflex and efferent system action [21]. Magnitude of detrusor contraction during voiding is also regulated by afferent system [22]. Efferent pathway provides contraction of bladder detrusor and adjusts speed, magnitude, and duration of contraction [21]. It is intuitive that interruption of signaling in aforementioned pathways and regulatory centers could result in diminished, absent, or ineffective detrusor contractility. Therefore, a variety of neurogenic diseases and injuries could result in UAB. Among them brain strokes, multiple sclerosis, Parkinson’s disease, diabetes mellitus, and spinal cord injuries are the well-known neurogenic causes of UAB. There is also evidence that diminution of response occurs in brain regions (responsible for interpretation of sensory inputs from the bladder) as age increases [18].
Related Knowledge Centers
- Bladder
- Muscular Layer
- Smooth Muscle
- Urination
- Urine
- Urethra
- Vagina
- Urethral Sphincters
- Pubis
- Prostate