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Exploring dysfunctional voiding in girls: a comprehensive literature review of assessment and management strategies

BMC Urology volume 25, Article number: 87 (2025) Cite this article

Abstract

Dysfunctional voiding (DV) is a multifactorial functional problem that refers to dysfunction during voiding. DV is clinically important because it increases the risk of urinary tract infections, mostly due to incomplete bladder emptying, and unfavorably affects renal function. Additionally, a child with DV may experience storage symptoms such as frequency and wetting, which can significantly impact the child’s quality of life. There is also a correlation between DV with bowel dysfunction and behavioral disorders. Girls with external urethral meatus anomalies, like hypospadias and/or meatal web, are more prone to complications related to DV. Therefore, girls exhibiting DV symptoms should also be evaluated for meatus anomalies. These patients often contract their external urethral sphincter and pelvic floor musculature, leading to voiding problems. Successful treatment involves applying appropriate diagnostic approaches. In girls with DV, urotherapy and biofeedback are considered gold standard modalities for retraining pelvic floor muscle function synchronously and properly. Although new emerging techniques such as stem cell therapy could improve urinary incontinence in adults and animal models with damaged external urethral sphincters, there is currently a lack of evidence regarding its therapeutic potential for children with DV.

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Introduction

Dysfunctional voiding (DV) has a poorly understood etiology in both children and adults. According to the International Continence Society (ICS) and the International Children’s Continence Society [ICCS], DV is characterized by a fluctuating, often interrupted uroflow resulting from overactivity of the pelvic floor and/or urethral striated sphincter [1]. Additionally, ICCS defines DV as a condition in which a child paradoxically contracts the urethral sphincter or pelvic floor during voiding. Typically, repeated uroflowmetry measurements show curves with a staccato voiding pattern with or without an interrupted uroflow. At the same time, simultaneous electromyography (EMG) activity is present in a child without any neurological lesions [2].

Despite studies focusing on dysfunctional voiding, there is a significant gap in understanding how external urethral meatus anomalies contribute to the condition, particularly in clinical diagnosis and treatment. The management of DV is challenging due to its unclear etiology, natural history, and the variability in diagnostic criteria found in the literature [1]. Approximately, 7–10% of school‐aged girls and up to 29% of males are affected [3]. "The wide range of prevalence in males is due to varying diagnostic criteria and studying methodologies across different populations." Lower urinary tract dysfunction (LUTD) symptoms may occur during any phase of urination involving bladder filling, storage, or active voiding [4]. The most common signs and symptoms of DV include hesitancy, straining, extended micturition time, and intermittent urine flow, which can lead to recurrent urinary tract infections (UTI), wetting, and urge incontinence in affected children [5].

Recurrent UTIs pose significant risks, including the potential for long-term kidney dysfunction and permanent renal damage [6]. Additionally, incontinence related to DV can greatly affect children's psychosocial well-being, resulting in social isolation and a decreased quality of life [7,8,9].

In the 1960s, a combination of urethral stenosis or abnormalities in the external urethral meatus, and recurrent UTIs in girls were described [10,11,12]. These early findings highlighted the importance of anatomical variations in diagnosing and managing DV, setting the stage for a more detailed exploration of external urethral meatus anomalies. Two types of external urethral meatus anomalies were identified: female hypospadias, characterized by the external urethral meatus being dorsally dislocated and situated on the front wall of the vagina, and hidden hypospadias, which presents as a membrane on the front wall of the vagina—a mucosal fold covering the urethral meatus [13].

Remarkably, there is an association between meatal anomalies and DV symptoms [13]. Some girls with voiding dysfunction seem to have a meatal anomaly that leads to anterior deflection of the urinary stream, resulting in wetting of the toilet rim and their legs after voiding [14, 15]. Understanding these anomalies is crucial for accurate diagnosis and tailored therapeutic approaches, given the clinical challenges in managing DV and its complications.

Considering the correlation between DV and external urinary meatus anomalies, it is important to understand the normal anatomy of the female urethra and its external meatus anomalies. Exploring management options can help reduce the burden of these conditions. This review will explore external urinary meatus deformities, their clinical significance with DV, and the most commonly used meatoplasty techniques. Additionally, we aim to differentiate DV from other LUTD subtypes and provide a comprehensive overview of the diagnostic and therapeutic tools available to urologists treating these conditions."

Anatomy and innervation of the urethra

The female urethra is crucial in maintaining urinary continence, achieved through a complex interplay of anatomical structures and neuronal control [16]. Females presenting with anomalies of the external urethral meatus are more susceptible to DV [13]. A thorough understanding of urethral anatomy and its innervation is essential for developing targeted diagnostic and treatment strategies for external urethral meatus anomalies.

The female urethra is a tubular structure composed of several layers that contribute to the overall function of the urethral sphincter. The urethral wall consists of an inner longitudinal smooth muscle layer (LSM), an outer circular smooth muscle layer (CSM), a rich submucosal vasculature, and a mucosal lining. The LSM is the thickest layer, measuring approximately 1 mm, while the CSM is about one-tenth of the LSM's thickness. These smooth muscle layers are present throughout the upper four-fifths of the urethra [17]. The external urethral sphincter (EUS), composed of striated muscle fibers, surrounds the smooth muscle layers. The EUS is thickest in the middle third of the urethra, which is considered the high-pressure zone [18]. It extends from the bladder neck to the perineal membrane and covers 20–80% of the total urethral length [19]. The bladder neck, often seen as the primary location for continence properties, continues the detrusor muscle and contains a mixture of circular and longitudinal smooth muscle fibers extending into the proximal urethra. The distal part of the female urethra lacks muscle and is composed of fibrous tissue [17]. The anatomical structure of the urethral sphincter and bladder neck plays a pivotal role in maintaining continence, and any disruption caused by anomalies in the external meatus can lead to significant functional impairment.

The female urethra receives innervation from the parasympathetic, sympathetic, and somatic nervous systems. Parasympathetic fibers originate from the sacral spinal cord (S2-S4) and release acetylcholine and nitric oxide, causing relaxation of the urethra and contraction of the bladder during micturition. Sympathetic fibers arise from the thoracolumbar spinal cord [T10-L2] and release norepinephrine, leading to contraction of the urethral smooth muscle and relaxation of the bladder detrusor, promoting continence. Somatic innervation is provided by the pudendal nerve, which originates from Onuf's nucleus in the sacral spinal cord (S2-S4) and controls the EUS. Activation of the pudendal nerve results in the contraction of the EUS, further enhancing the continence [16]. Understanding these neural pathways is essential for clinicians managing DV, as it explains the pathophysiological basis of urinary incontinence and other voiding symptoms seen in patients with meatal anomalies.

Normal morphology of the meatus

The external urethral meatus is located at the top of a small eminence that directly continues with the anterior margin of the hymen. The different morphologies formed by this little eminence are as follows. Predominantly, the eminence is observed as a crescent with two horns situated only on the dorsal half of the urethral circumference. Occasionally, it exhibits two small labia, one on the right and the other on the left; more rarely, it presents four small tubercles. Sometimes, the eminence is poorly developed or absent, and the orifice is positioned at the bottom of a small depression, or it may develop into a mass-like tissue with the meatus hidden beneath it. Other meatal configurations consist of a rounded dimple, longitudinal slit, and star-shaped forms [20, 21]. Recognizing these normal morphological variations is crucial during clinical examinations to differentiate between anatomical variations and pathological anomalies that could contribute to dysfunctional voiding.

Anomalies of the meatus

DV has been found to correlate with abnormalities of the urethral meatus in females. Therefore, healthcare providers must be knowledgeable about these anomalies. Currently, three types of meatal anomalies have been identified. The first is hypospadias, where the urethral orifice is displaced dorsally and located on the anterior wall of the vagina. The second anomaly is hidden hypospadias, in which a mucosal web covers the urethral meatus on the anterior wall of the vagina, deflecting the urinary stream anteriorly [13] (Fig. 1). The third is the meatal web, where a mucosal fold is present on the dorsal side of the urethral orifice in the absence of hypospadias, resulting in an anteriorly deflected urinary stream (ADUS) [15].

Fig. 1
figure 1

Sagittal views showing the normal anatomy of the female compared to anomalies of the external urethral meatus. Hypospadias, in which the urethral orifice is displaced dorsally; Hidden Hypospadias, in which a mucosal web covers the urethral meatus on the anterior wall of the vagina. Peri-urethral skin tag covers the external urethral meatus

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Additionally, another incidentally discovered morphology of the external meatus includes skin tags around the urethral orifice (Figs. 1, 2) [22]. The origin of these tags is the remnants of the hymen, which become hypertrophied [23]. However, no correlation has been found between the simultaneous presence of skin tags around the urethral opening and their contribution to voiding dysfunction. These skin tags are mobile and do not retract the meatus, which keeps the bacteria-laden area surrounding the meatus. Therefore, retrograde infection is not facilitated by them [22]. Accurately identifying these anomalies during clinical evaluation in future studies will allow for more tailored interventions, as they may directly contribute to the functional disturbances seen in DV patients.

Fig. 2
figure 2

Female normal anatomy versus peri-urethral skin tagged, with skin tags covering external urethral meatus in the lithotomy position

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Diagnostic measurements

All patients seeking consultation for DV symptoms should undergo a standard, minimally invasive screening protocol. This protocol includes a thorough history, voiding diary, physical examination, laboratory assessment, imaging evaluation, and urodynamics [24].

The comprehensive nature of this protocol is essential as it allows for the identification of both functional and anatomical causes of DV, ensuring a thorough assessment and accurate diagnosis.

History

A comprehensive history is essential in the diagnostic assessment of DV. The history should be adapted to the patient’s age and the stage of bladder control development [24]. The history should include the following aspects [25]:

  1. (I)

    The voiding schedule should include information on the voiding frequency and the frequency of incontinence episodes [in toilet-trained children]. If possible, the voided volume should be estimated because patients with large-capacity bladders may present with large volumes of voided urine, indicating an underactive bladder or polyuria [25]. Voided volume estimation can help determine if the bladder is functioning properly or if there are issues with underactivity or polyuria, both of which are commonly associated with DV.

  2. (II)

    Bladder dysfunction symptoms such as urgency, hesitancy, painful urination, dribbling, holding maneuvers, straining, daytime incontinence, enuresis, and an intermittent or weak urinary stream should be noted. Table 1 defines these symptoms [4, 25,26,27,28]. Understanding these symptoms is critical, as they provide clues to the underlying cause of DV, helping clinicians narrow down the diagnosis.

  3. (III)

    A completed standard questionnaire assessing daytime incontinence, voiding habits, urgency, bowel habits, dysuria, quality of life, and urine stream deflection. For example, anterior deflected urinary stream [ADUS], known as wetting the toilet rim during voiding while sitting in an upright position and the upper legs are apart. Another example is vaginal voiding caused by urine remaining in the vestibule after voiding, resulting in immediate post-urination incontinence. ADUS can be a key symptom in diagnosing structural abnormalities, which may contribute to DV and post-urination incontinence.

  4. (IV)

    Family history should be screened for any renal or urological disorders, including DV, and the age at which family members achieved bladder control. This can help assess familial maturation delays, which can provide important genetic or developmental clues to the presence of dysfunctional voiding or other urological disorders within the family.

  5. (V)

    Perinatal and neonatal history should be reviewed to investigate any perinatal or neonatal insults, such as perinatal anoxia or congenital infections. These insults could potentially affect the central and peripheral nervous systems, as well as normal bladder function. Early developmental insults have the potential to impact bladder innervation or neural control, which can predispose individuals to lifelong voiding difficulties.

  6. (VI)

    Dietary intake including details on the type and amount of fluid consumed, should be noted. Excessive urine production, especially during the night, may be a sign of diabetes mellitus, polyuria due to impaired urine concentration, or primary polydipsia.

  7. (VII)

    Hydration and urine production patterns are important as they can indicate underlying conditions like diabetes mellitus or renal issues like nephrogenic diabetes insipidus, which can lead to polyuria.

  8. (VIII)

    Neurodevelopmental delays and psychological disorders, such as ADHD, depression, or anxiety, may contribute to delayed voluntary bladder control. Although children with DV may not universally present with behavioral issues, the association with psychological disorders should be explored. Children with neurodevelopmental disorders often have delayed or impaired bladder control due to difficulties in establishing voluntary bladder coordination.

  9. (IX)

    Functional causes of DV may stem from behavioral issues following toilet training or personal stress, particularly conflicts between caregivers and children, which can often be linked to stressors or negative experiences during toilet training. This connection can lead to developmental variances even when anatomical abnormalities are absent.

  10. (X)

    Toilet training history is important to consider, particularly if it was delayed, prolonged, or stressful or if there was a period of dryness following toilet training. If a period of complete dryness was never achieved after toilet training, structural abnormalities that can cause urine incontinence, such as the ectopic ureter, hypospadias with or without a meatal web [13], and meatal web alone [15], should be taken into account [25]. Identifying whether dryness was ever achieved after toilet training is critical in distinguishing between structural and functional causes of incontinence.

Table 1 Definitions of dysfunctional voiding symptoms
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Voiding diary

A detailed voiding diary and associated symptoms can provide valuable diagnostic and management insights into DV. The diary should span three days and record the time and volume of each void, fluid intake, incontinence episodes, defecation, and fecal soiling episodes [25].

Uroflowmetry can provide key insights into the dynamics of bladder emptying. It is beneficial for children who are capable of voiding on command, particularly in cases involving a weak urinary stream, difficulty voiding without straining, frequent UTIs due to incomplete bladder emptying, or incontinence that does not respond to treatment. Uroflowmetry measures urine flow rate and offers a comprehensive view of bladder function when combined with post-void residual volume assessed via ultrasound. Repeated abnormal flow patterns may indicate bladder contraction abnormalities or the presence of a functional or structural issue at the bladder outlet or along the urethra [24].

Physical examination

The physical examination should be thorough, identifying any urologic, neurologic, or anatomical abnormalities. Table 2 outlines the key components of a comprehensive physical exam for DV [25].

Table 2 Physical Examination Components [25]
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Laboratory assessment

The urinalysis and urine culture are the first laboratory assessments that should be conducted [24]. These tests are essential to rule out underlying infections, hematuria, or proteinuria, which may indicate additional urinary system abnormalities.

Imaging evaluation

Ultrasound [US], as a non-invasive and commonly used method, is employed to investigate the kidneys and bladder of children with DV. It should be performed in every child suspected of neurological or anatomical lesions, UTI, or symptoms indicating obstructive uropathy, such as a weak or interrupted urinary stream. The US is beneficial because of its safety, ease of use, and ability to detect structural anomalies early. It can provide information regarding anomalies, such as hydronephrosis, a duplicated collecting system with or without an ectopic ureter, and scarring of the kidneys. Additionally, it assesses post-void residual volume, which indicates impaired bladder emptying when a volume exceeds 20 mL after repeated measurements [or more than 15–20% of their bladder capacity]. Increased residual volumes suggest ineffective bladder emptying, which may require further urodynamic evaluation. The US also evaluates bladder wall thickness, which, if thickened, suggests an overactive bladder due to an anatomical or functional abnormality of its outlet [25].

Urodynamics

Urodynamics can distinguish between different lower urinary tract dysfunctions and contribute to an accurate assessment of bladder and sphincter function. Urodynamic studies include invasive [cystometry] and non-invasive assessments [uroflowmetry, residual urine volume measurement, and voiding observation] [29]. Urodynamics are particularly valuable when the cause of voiding dysfunction remains unclear after initial assessments like physical examinations and imaging.

By measuring the urinary flow, uroflowmetry provides information on urine flow patterns, which is often helpful for diagnosing an etiology. It is particularly useful in assessing whether bladder emptying is complete or if voiding is obstructed. It also evaluates the emptying phase of the bladder. As children void into a special vessel, a urinary flow curve is drawn that provides data on the shape of the uroflow, flow time, voided volume, maximum uroflow rate [Qmax], and average flow rate. Interpretation of these values can guide the next step, particularly if reduced flow rates suggest anatomical or functional obstruction. In addition, electromyographic [EMG] activity of the pelvic floor and urethral sphincter can be investigated during voiding. The presence of sphincter activity during voiding, which is normally inactive, indicates dysfunctional voiding [DV]. Abnormal EMG activity may indicate inappropriate contraction of the pelvic floor muscles during voiding, which warrants targeted therapeutic interventions.

Another parameter obtained during the urodynamic study is bladder capacity. The bladder capacity can be reduced in children with overactive bladders and increased in those with underactive bladders [25].

Cystometry

Cytometry involves simultaneous measurement of bladder/intra-abdominal pressure via a transurethral catheter and transrectal probe, and sphincter activity via patched perineal electrodes. While the bladder is slowly filled, pressure is continuously monitored. Several parameters are recorded, including overactive contractions [if present], bladder filling pressures, voiding pressures, post-void residual volume, and sphincter muscle relaxation. Cystometry provides a detailed view of bladder function, identifying issues during both the filling and voiding phases, which are crucial for determining the type of bladder dysfunction. It can distinguish between an overactive bladder [a more common filling phase abnormality] and dysfunctional voiding, a result of sphincter dysfunction or contraction of pelvic floor musculature during voiding [25]. Cystometry is typically reserved for complex cases where non-invasive assessments do not provide enough information.

Differentiation of DV from Other Subtypes of LUTD

In patients with overactive bladder, involuntary detrusor contractions occur during the filling phase, known as detrusor overactivity [DO]. Dysfunctional voiding [DV] is seen in children with a neurologic lesion, referred to as detrusor sphincter dyssynergia, or in children without a neurologic lesion, known as non-neurogenic dysfunctional voiding. During voiding, the last two display abnormal urethral sphincter contraction while other urodynamic parameters remain normal, as illustrated in Table 3. In children with underactive bladder, bladder capacity increases, and impaired bladder emptying is observed due to decreased detrusor contraction, while the urethral sphincter functions normally throughout both the filling and voiding phases [25]. Table 3 offers a comparative summary of urodynamic patterns in normal and abnormal bladder conditions, aiding in the differentiation between these conditions [24].

Table 3 Urodynamic Study Patterns in Normal and Abnormal Bladder Conditions [24]
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There is an overlap between DV symptoms [1, 5] and those of LUTD [4, 25, 26]. It is crucial to understand the conditions with shared symptoms and differentiate between them. Dysfunctional voiding occurs when the external urethral sphincter overcompensates to inhibit the detrusor reflex, leading to a staccato flow curve as urine flow diminishes due to urethral sphincter or pelvic floor contraction. Incomplete bladder emptying is a common consequence and may be associated with UTIs and/or enuresis. Secondary symptoms of DV, such as wetting, urge incontinence, or overflow incontinence, often prompt visits to healthcare providers. Increased incidences of UTIs should raise suspicion of underlying DV, which may warrant further diagnostic investigation [30].

Given the variety of uroflowmetry patterns in children with DV, simultaneous pelvic floor electromyography [EMG] is recommended during initial investigations [31,32,33]. Interrupted or fractionated uroflow patterns can be observed in these children, as well as plateau-shaped curves [31, 33]. A plateau-shaped uroflow may indicate non-relaxing muscles during voiding or suggest other forms of obstruction, potentially signaling pelvic floor muscle overactivity—a form of dysfunctional voiding. According to the ICCS suggestion, this diagnosis can be made in the case of repeated staccato pattern curves in uroflowmetry or invasive urodynamic investigation [26]. The dysfunctional outflow obstruction resulting from urethral sphincter overactivity may lead to compensatory detrusor hypertrophy and hyperplasia, resulting in a functionally small capacity trabeculated bladder, increased bladder pressures, and vesicoureteral reflux [30]. In some cases, patients with dysfunctional outflow obstruction may experience detrusor decompensation and hypocontractility, necessitating clean intermittent catheterization [CIC] or surgical intervention. In children with external urethral meatus abnormalities, these conditions may occur secondary to the habitual or reflexive contraction of the external urethral sphincter to correct an inappropriate urinary stream. In addition, children with DV and coexisting detrusor underactivity/overactivity most likely experience episodes of induced storage symptoms like urgency, urge incontinence and incomplete bladder emptying. The impaired detrusor contraction results in incomplete bladder emptying, post-void residual urine, and an increasing risk of UTI [5]. Therefore, recurrent UTIs in children should prompt us to seek dysfunctional voiding with or without possible anatomical abnormalities.

Table 4 presents some usual and clinically important problems due to functional voiding abnormalities, such as detrusor overactivity, dysfunctional voiding, severe bladder–bowel dysfunction [BBD], and giggle incontinence.

Table 4 Common and Clinically Important Functional Voiding Problems
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Other considerations

There is a well-established connection between bladder and bowel dysfunction that should be considered when assessing and managing DV [34]. Stool retention, with or without fecal incontinence, often coexists with DV due to pelvic floor muscle non-relaxation [35]. Treatment of constipation in children with LUTD has been shown to improve voiding symptoms [36,37,38,39]. This aspect is critical in the holistic management of children with DV and should be emphasized in treatment plans.

Lastly, all patients showing any signs of underlying bladder dysfunction [e.g., diurnal incontinence, repeated staccato uroflow patterns, post-void residual [PVR] on ultrasound exceeding 10% of expected bladder volume for age, small bladder capacity for age, recurrent UTIs, and absence of neurological signs] should undergo a urodynamic study [UDS] to confirm the diagnosis of DV [13, 15, 28].

Management options in dysfunctional voiding (DV)

Management of children with DV should begin with an assessment of the potential risk for renal damage. Patients at high risk of renal damage or those suffering from renal failure require more extensive investigations, such as invasive video urodynamics, and may benefit from the early initiation of clean intermittent catheterization [CIC] to manage bladder storage pressures. For most patients, where the risk of renal damage is low, the primary goal is to retrain the pelvic floor muscles to relax during voiding [40]. Additionally, for children whose DV is secondary to an external urethral meatus anomaly, urethral reconstruction should be prioritized before other treatment options.

Surgery

Surgical correction is recommended for patients with DV caused by external urethral meatus anomalies. In cases of hypospadias, partial hymenectomy, which involves removing the anterior part of the hymen, has been shown to resolve vaginal voiding. For meatal webs, there are two surgical approaches available: longitudinal incision of the mucosal web followed by transverse suturing with interrupted stitches [13] or a deep dorsal web incision at the 6 o’clock position [3–5 mm], to restore a normal urinary stream [15].

Urotherapy

Urotherapy is a non-pharmacological, non-surgical treatment for lower urinary tract dysfunction [5]. This therapy encompasses a multidisciplinary approach, including education of the child/family on bladder and bowel function, adequate hydration, timed voiding, toileting posture correction, and hygiene practices. For instance, children are instructed to sit securely on the toilet with adequate support for the buttocks and feet, ensuring the hips are abducted comfortably to prevent abdominal muscle contraction and pelvic floor co-activation [2, 5, 41].

Preventive strategies for constipation, hygiene maintenance [changing wet clothing, using containment products, proper skincare, and wiping techniques], as well as setting realistic treatment timelines, are all integral parts of urotherapy [2, 5]. Prophylactic antibiotics may be prescribed to prevent recurrent UTIs [40]. In cases where neuropsychiatric issues are present, collaboration with a child psychologist or psychiatrist is advised.

Biofeedback

Biofeedback therapy helps patients gain awareness and voluntary control of their pelvic floor muscles. This is facilitated through auditory or visual feedback from uroflow patterns or non-invasive electromyography [EMG] of the abdominal or perineal muscles [5]. Success rates are higher in patients who adhere to the treatment plan and when therapists are experienced and provide consistent support. Biofeedback may require multiple sessions to achieve sustained results [40].

Pharmacological therapy

According to the ICCS, there is no specific pharmacotherapy approved for treating DV [4, 5]. However, pharmacological agents can target the detrusor muscle and the bladder neck/urethra. Pharmacotherapy is typically used as an adjunct to other treatments to enhance bladder emptying in children with DV.

Anticholinergics

Anticholinergics and antimuscarinics, which act as bladder relaxants, target the detrusor muscle. By relaxing the detrusor, these agents improve bladder storage capacity and are especially useful in treating detrusor overactivity [5].

Alpha blockers

Alpha-adrenergic receptors, present in the bladder neck and throughout the urethra, play a role in bladder outlet resistance. Alpha-blockers [alpha-adrenergic antagonists] decrease resistance at the bladder outlet, thus improving bladder emptying. They have been reported to be effective in children with incomplete bladder emptying [5, 42].

Botulinum Toxin-A

Botulinum toxin-A [Botox] works by inhibiting acetylcholine release at the presynaptic neuromuscular junction, causing flaccid paralysis of the target muscles. Investigations suggest that Botox injections may be beneficial in children with detrusor sphincter dyssynergia and impaired bladder emptying [43,44,45,46]. There are also reports of successful use of intrasphincteric botulinum toxin-A injections in children with refractory DV who do not respond to biofeedback therapy [44, 47]. After the injection, children must undergo training to re-learn correct voiding techniques.

Stem cell therapy

Regenerative medicine, as an innovative treatment strategy, focuses on enhancing the body's natural ability to heal and regenerate damaged tissues and organs, as well as supporting tissue repair and functional recovery [48]. Stem cell therapy, along with tissue engineering and delivery of growth factors, is one of the strategies of regenerative medicine [49]. Endoscopic intraurethral injection of adipose-derived mesenchymal stem cells [ADSCs] is a safe and feasible procedure for treating urinary incontinence in males and females with minimal complications or side effects, with follow-up periods of more than 12 to 15 months [50]. The autologous intraurethral co-transplantation of muscle-derived cells [MDCs] and mesenchymal stem cells [MSCs] in goats with stress urinary incontinence [SUI] has been shown to improve urethral closure more effectively than cell therapy alone. Both MSCs and MDCs promoted striated muscle formation when injected directly into the external urethral sphincter [51]. The intrasphincteric injection of bone marrow-derived mesenchymal stem cells in rats with SUI restored the injured external urethral sphincter through smooth and striated muscle regeneration, resulting in improved incontinence [52].

Unfortunately, there are currently no stem cell therapy studies specifically investigating dysfunctional voiding. However, available studies with their role in the urethral/external urethral sphincter restoration may help guide the design of future studies specific to DV, particularly in cases involving external urethral sphincter hypertrophy.

Dysfunctional Voiding and External Urethral Meatus Anomalies

In children with dysfunctional voiding [DV], the external urethral sphincter habitually contracts during voiding. These patients may experience not only dysfunctional voiding but also storage symptoms like urgency, incontinence, or urinary frequency [26, 53]. Dysfunctional voiding occurs when an overcompensating external urethral sphincter responds to address an inappropriate voiding pattern, resulting in a staccato flow curve as urine flow decreases due to urethral sphincter/pelvic floor contraction. Several hypotheses explain this condition:

  1. 1.

    Bulbocavernosus Reflex: This reflex, which is normally absent during voiding, can be stimulated by genital arousal. In cases of anterior displacement of the urethra and clitoris [ADUS], the urine stream passes over the clitoris and may stimulate the bulbocavernosus reflex, leading to sphincter activity during voiding [13]. Similarly, in girls with hypospadias, extreme vaginal voiding can activate this reflex.

  2. 2.

    Postural habits: Patients with ADUS may adopt a bent posture and "deep sitting" during voiding to avoid wetting the toilet rim. This posture results in inadequate relaxation of the pelvic floor muscles and the development of a functional obstruction during voiding [41].

  3. 3.

    Vaginal Filling and Muscle Hypertrophy: In hypospadias, excessive vaginal voiding can result in post-voiding vaginal urine loss. As a compensatory mechanism, these patients may frequently contract the pelvic floor muscles throughout the day to prevent further urine loss, leading to hypertrophy of the external urethral sphincter and contributing to DV. Additionally, vaginal filling through voiding can lead to stimulation of the bulbocavernosus reflex [13].

The association between DV and external urethral meatus anomalies emphasizes that surgical correction may lead to the normalization of the urinary stream [13]. However, in addition to correcting the anomaly, retraining the pelvic floor muscles is essential to address the habitual contraction of the pelvic floor muscles during voiding [13, 15].

Surgical vs. Non-Surgical Approaches in ADUS and DUI

While surgical correction of external urethral meatus anomalies may normalize the urinary stream, it does not always lead to an improvement in dysfunctional voiding or urinary incontinence [DUI] [54]. Factors such as improper hip abduction during voiding or avoidance behaviors due to urine splashing onto inflamed skin can perpetuate UI symptoms. In such cases, urotherapy and biofeedback should be prioritized over surgical intervention, as these approaches address the underlying habitual behaviors that contribute to UI [7, 8, 27]. Surgical correction should be considered only when it is necessary to alleviate social distress or if other therapies fail to provide adequate symptom relief [54].

Conclusion

In conclusion, the management of dysfunctional voiding (DV) in children requires a comprehensive and multifaceted approach that encompasses thorough assessment, accurate diagnosis, and tailored interventions. Integrating urodynamic studies is crucial in differentiating DV from other lower urinary tract dysfunctions (LUTD), as they provide valuable insights into bladder and sphincter function. By identifying specific urodynamic patterns associated with conditions such as detrusor overactivity and underactive bladder, clinicians can effectively optimize treatment strategies to address individual patient needs.

Furthermore, recognizing the interplay between bladder and bowel dysfunction is essential for a holistic approach to managing DV. Addressing coexisting conditions like constipation is vital for improving voiding symptoms and overall health outcomes in affected children. The management spectrum includes various strategies, such as urotherapy, biofeedback, pharmacological therapies, and surgical interventions, all tailored to the patient's unique presentation and underlying causes.

Innovative treatment options, such as stem cell therapy, present exciting possibilities for addressing refractory cases of DV and warrant further investigation. While surgical correction of external urethral meatus anomalies can enhance urinary function, it is imperative to implement supportive therapies that promote proper voiding habits and retrain pelvic floor muscles.

Ultimately, the successful management of DV hinges on a collaborative effort among healthcare professionals, patients, and their families. By fostering open communication and adherence to treatment plans, we can significantly improve the quality of life for children affected by DV and mitigate the long-term complications associated with this condition. Continued research into the underlying mechanisms of DV and the efficacy of various treatment modalities will be essential in refining our approaches and enhancing patient outcomes in this complex clinical area.

Data availability

No datasets were generated or analysed during the current study.

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Authors and Affiliations

  1. Pediatric Urology and Regenerative Medicine Research Center, Gene, Cell & Tissue Research Institute, Children’s Medical Center, Tehran University of Medical Sciences, Tehran, 1419733151, Iran

    Maryam Sadeghi & Masoumeh Majidi Zolbin

  2. Urology Research Center, Tehran University of Medical Sciences, Tehran, Iran

    Iman Menbari Oskouie

  3. Student Research Committee, Shahid Beheshti University of Medical Sciences, Tehran, Iran

    Alvand Naserghandi

  4. Center for Orthopedic Trans-Disciplinary Applied Research, Tehran University of Medical Sciences, Tehran, Iran

    Alireza Arvin

Authors
  1. Maryam Sadeghi
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  2. Iman Menbari Oskouie
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  3. Alvand Naserghandi
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  4. Alireza Arvin
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  5. Masoumeh Majidi Zolbin
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Contributions

Maryam Sadeghi: writing original draft Iman Menbari Oskouie: investigation, editing the manuscript Alvand Naserghandi: editing the manuscript Alireza Arvin: Designing figures Masoumeh Majidi Zolbin: conceptualization All authors reviewed the manuscript.

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Correspondence to Masoumeh Majidi Zolbin.

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Sadeghi, M., Oskouie, I.M., Naserghandi, A. et al. Exploring dysfunctional voiding in girls: a comprehensive literature review of assessment and management strategies. BMC Urol 25, 87 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12894-025-01772-0

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BMC Urology

ISSN: 1471-2490

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