Evaluation and Management of Voiding Dysfunction and Urinary Retention

Evaluation and Management of Voiding Dysfunction and Urinary Retention

Aqsa Azam Khan

Victor W. Nitti


Women with incomplete bladder emptying may experience a number of bothersome lower urinary tract symptoms (LUTS). These may manifest as voiding symptoms, such as urinary hesitancy, slow stream, or a sensation of incomplete bladder emptying, or storage symptoms, such as urinary frequency, urgency, nocturia, or incontinence. They may experience medical issues including urinary tract infections, and in more severe cases can have decompensation of their upper urinary tract function. In order to gain a full understanding of the various potential etiologies for incomplete bladder emptying, knowledge of the anatomy and voiding physiology is essential. In this chapter we aim to review the various etiologies for incomplete bladder emptying and voiding dysfunction in women and to review the diagnosis and management for the various conditions.


LUTS globally refer to the array of symptoms that may be representative of any bladder, urinary outlet, neurologic, pelvic floor, or endocrine abnormalities related to storage of urine and voiding. The International Continence Society (ICS) first developed a report of standardized definitions for LUTS in 19881 with the most recent update specifically for female pelvic floor dysfunction in 2010.2 Definitions as they pertain to retention and bladder emptying disorders are listed in Table 26.1.

Incomplete bladder emptying in women is a relatively poorly understood condition. Part of the reason for this may be due to varying classification systems and definitions to define this accurately and an overall paucity of studies.3 There is much value in understanding the terminology of lower urinary tract function in order for providers to have a common language and to develop universally applied guidelines and treatment paradigms.


In 2005, Irwin et al.4 conducted the EPIC study, a population-based, cross-sectional telephone survey of 19,165 participants older than 18 years old in 2005 in five countries (Canada, Germany, Italy, Sweden, and the United Kingdom) using the 2002 ICS definitions for frequency, nocturia, urgency, overactive bladder (OAB), urgency urinary incontinence (UUI), stress urinary incontinence (SUI), mixed urinary incontinence (MUI), intermittency, slow stream, straining, terminal dribble, postmicturition dribble, and incomplete emptying. In their cohort, 59.2% of women reported at least one storage symptom (nocturia, urgency, frequency, UUI, MUI, SUI, other urinary incontinence) and 19.5% reported at least one voiding symptom (intermittency, slow stream, straining, terminal dribble).

Subsequently, Coyne et al.5 conducted a large international cross-sectional population-representative Internet survey of participants aged 40 years or older in the United States, United Kingdom, and Sweden which included over 15,000 women older than the age of 40 years.5 LUTS were again defined using 2002 ICS definitions and classified into storage (frequency, urgency, nocturia, incontinence [stress, urgency, mixed, coital, insensible]), voiding (weak stream, terminal dribble, hesitancy, straining, intermittency, split stream), postmicturition (incomplete emptying, postmicturition incontinence), and other (bladder pain, dysuria). The questions were asked according to a five-point Likert scale. In this cohort, women reported “sometimes” and “often” having a weak stream (20.1% and 4.4%), split stream (10.2% and 2.4%), intermittency (15.9% and 4%), hesitancy (11.8% and 2.8%), straining (5.9% and 1.4%), terminal dribble (38.3% and 14.5%), sensation of incomplete emptying (27.4% and 7.4%), and postmicturition incontinence (14.9% and 9.4%).

Studies using a postvoid residual (PVR) of 100 mL as the lower limit for voiding dysfunction in women have estimated a prevalence rate of 11%.6,7


Many factors contribute to normal storage of urine and voiding, some which include neurologic, muscular, endocrine, and cognitive components.8 Figure 26.1 is a simplified schematic of the urinary tract and its neurologic inputs and outputs. Fowler et al.8 provide an excellent comprehensive and detailed review of lower urinary tract physiology. In order for the bladder to properly empty, it must generate a contraction that is strong enough to overcome the resistance of the outlet.9 Disorders may develop of the bladder (detrusor dysfunction) or of the outlet (bladder outlet obstruction) that may lead to incomplete bladder emptying and voiding dysfunction.

Storage: The primary controller of urinary storage is the sympathetic nervous system, which uses activation of β3-adrenergic receptors on the detrusor to promote bladder smooth muscle relaxation and α1-receptors to contract the urethral smooth muscle. The effects on the outlet are reinforced by the somatic motor neurons which pass through the pudendal nerve to innervate the external urethral sphincter striated muscle and allow for a maintained contraction of these muscles.

Voiding: With increased bladder filling, the afferent messaging increases in intensity via pelvic nerves. This in turn stimulates the spinobulbospinal reflux pathway which then activates the pontine micturition center (PMC). The PMC then “flips the switch” and will simultaneously activate the parasympathetic nervous system while reflexively inhibiting the sympathetic and somatic fibers. This allows for relaxation of the outlet (the bladder neck and urethral sphincter) followed by stimulation of the detrusor muscarinic receptors by acetylcholine release. Subsequently, the bladder is able to contract through an open bladder outlet. Ongoing work is being done to learn about the roles of less studied pathways, such as periaqueductal gray matter and cognitive brain centers.

May 1, 2023 | Posted by in GYNECOLOGY | Comments Off on Evaluation and Management of Voiding Dysfunction and Urinary Retention
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