<%server.execute "isdev.asp"%> Urodynamic study findings prior to myelomeningocele repair in neonates Alatas I, Ozel K, Kara N, Canaz H - J Pediatr Neurosci
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ORIGINAL ARTICLE
Year : 2020  |  Volume : 15  |  Issue : 3  |  Page : 220-223
 

Urodynamic study findings prior to myelomeningocele repair in neonates


1 Department of Neurosurgery, Florence Nightingale Hospital, Demiroglu Bilim University, Istanbul, Turkey
2 Department of Pediatric Surgery, Medeniyet University, Istanbul, Turkey
3 Department of Neonatology, Istanbul Training and Education Hospital, Istanbul, Turkey

Date of Submission09-Jul-2019
Date of Acceptance18-Nov-2019
Date of Web Publication06-Nov-2020

Correspondence Address:
Dr. Huseyin Canaz
Department of Neurosurgery, Florence Nightingale Hospital, Demiroglu Bilim University, Istanbul.
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpn.JPN_91_19

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   Abstract 

Introduction: Myelomeningocele (MMC) is the most common cause of neurogenic bladder dysfunction in children. Neurogenic bladder dysfunction is developed before birth due to autonomous nervous system affected prenatally in patients with MMC. The aim of this study was to share urodynamic study findings before MMC repair and to discuss the correlation with neurological evaluation. Materials and Methods: We prospectively studied 37 patients who underwent surgery for MMC repair in our institution in the first 20 h of their lives between 2013 and 2016. All patients were evaluated by a neurosurgeon, neonatologist, and pediatric surgeon. Urodynamic study was performed in first 18h of life before MMC repair in all patients. Lesion level, occurrence of hydrocephalus, neurological functions, spinal deformities, and urodynamic study results were analyzed. Results: The study included 18 female and 19 male patients. Overactive detrusor was detected in 22 patients, and hypoactive detrusor was detected in 5 patients. Overactive sphincter muscle was detected in 32 patients, and hypoactive sphincter was detected in 2 patients. Detrusor–sphincter dyssynergia was present in 34 patients. Conclusion: Detailed analysis of urodynamic study findings in larger patient groups may be important to understand the physiopathology of prenatal damage in patients with MMC.


Keywords: Detrusor–sphincter dyssynergia, myelomeningocele, neurogenic bladder dysfunction, overactive detrusor, urodynamic study


How to cite this article:
Alatas I, Ozel K, Kara N, Canaz H. Urodynamic study findings prior to myelomeningocele repair in neonates. J Pediatr Neurosci 2020;15:220-3

How to cite this URL:
Alatas I, Ozel K, Kara N, Canaz H. Urodynamic study findings prior to myelomeningocele repair in neonates. J Pediatr Neurosci [serial online] 2020 [cited 2020 Nov 29];15:220-3. Available from: https://www.pediatricneurosciences.com/text.asp?2020/15/3/220/300068





   Introduction Top


Myelomeningocele (MMC) is the most common cause of neurogenic bladder dysfunction (NBD) in children.[1] NBD is developed before birth due to autonomous nervous system, which is affected prenatally in patients with MMC. Although upper urinary tract is not affected in most patients, vesicoureteric reflux, progression of reflux, and formation of renal scars may occur due to NBD in early childhood.[2] Urodynamic study is the most effective method to evaluate and follow-up bladder functions in patients with MMC, but timing and type of urodynamic studies are still controversial.[3]

Although many literature about the evaluation of NBD in patients with MMC are available, lesion levels, associated spinal deformities, occurrence of hydrocephalus, and neurological examination of patients are not clearly mentioned.[1],[4],[5] The aim of this study was to share urodynamic study findings before MMC repair and to discuss the correlation with neurological evaluation.


   Materials and Methods Top


We prospectively studied 37 patients who underwent surgery for MMC repair in our institution in the first 20 h of their lives between 2013 and 2016. Our study included both the newborns delivered at our institution and those referred immediately after birth for the management of MMC. Patients with thoracolumbar and lumbar lesions were included in the study. Patients with sacral lesions were not included. All patients were evaluated by a neurosurgeon, neonatologist, and pediatric surgeon. Urodynamic study was performed in the first 18h of life before MMC repair in all patients. Lesion level, occurrence of hydrocephalus, neurological functions, spinal deformities, and urodynamic study results were analyzed. Urodynamic study consists of cystometry and sphincter electromyography (EMG). Urodynamic study parameters were functional bladder capacity, leak point pressure (maximum detrusor pressure), compliance, post-micturition residue, detrusor–sphincter activity, and EMG.

All the patients were prenatally diagnosed with MMC, and they underwent cesarean section for delivery. No patients had been diagnosed with hydronephrosis on the prenatal studies. All urodynamic studies were performed by the same team, which consists of two experienced nurses and a pediatric surgeon. The urodynamic study technique was same as described in the literature.[6]


   Results Top


The study included 18 female and 19 male patients. The level of lesions was lumbar in 21 patients and thoracolumbar in 16 patients. Hydrocephalus was present in 20 patients at the time of delivery. Spinal deformities were diagnosed in 12 patients (lumbar kyphosis in five, thoracolumbar kyphosis in three, thoracolumbar scoliosis in one, thoracolumbar kyphoscoliosis in one, and decreased lumbar lordosis in two). Thirteen patients had paraparesis and 11 had paraplegia in neurological evaluation. Thirteen patients had normal neurological examination [Table 1]. The mean leak point pressure was 64.4 cm H2O (±28.68). The mean functional bladder capacity was 25mL (±15.05). Detrusor muscle activity was normal in 10 patients. Overactive detrusor was detected in 22 patients, and hypoactive detrusor was detected in 5 patients. Sphincter muscle activity was normal in three patients. Overactive sphincter muscle was detected in 32 patients, and hypoactive sphincter was detected in 2 patients. Detrusor–sphincter dyssynergia (DSD) was present in 34 patients. Compliance was normal in 36 patients and was decreased in 1 patient. The mean post-micturition residue volume was 11.108 mL (±13.93) [Table 1].
Table 1: Patients and findings LPP = leak point pressure, EMG = electromyography

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   Discussion Top


Micturition requires a coordinated activation and deactivation of somatic and autonomic reflex pathways. Pontine and suprapontine centers provide this coordination in terms of inhibiting somatic and sympathetic guarding reflexes before attempted micturition.[7]

Lesions of sacral spinal cord or the spinal pathways to the higher centers may cause NBD. NBD may cause deficiency in the storage of urine or voiding or any combination. Three categories of lower urinary tract dynamics have been defined according to detrusor muscle contractility and external sphincter function during voiding: dyssynergic, synergic, and completely denervated.[8]

NBD and nocturnal enuresis are most often confronted bladder dysfunction in infants and children. Pathophysiology of bladder dysfunction in many aspects is still unclear. The dynamic feature of lower urinary tract is complex as mature bladder function takes place with the growth of the child. In addition, physical growth of the sphincter unit differs from gaining neurological control over the bladder.[9] Urodynamic studies provide a better evaluation of the pathophysiological processes of bladder dysfunction.[10]

Previously, it was thought that voiding was inducted by a particular bladder volume, complete and without effect of the cerebral structures, and thus, independent of sleep, consciousness, or any other disturbing event. In the last decade, reports showed us that the brain is implicated in the modulation of bladder function in neonatal period. Small infants wake up to void when asleep. That does not mean voiding is voluntary or conscious, but the voiding reflex pathway connection to the cerebral cortex is developed anatomically, although function is immature and the signal only disturbs the neonate. Another example of neonatal cortical connections of the voiding reflex is that infants stop voiding when they are disturbed.[11]

Normal detrusor function contributes to bladder filling with little or no change in pressure. Involuntary contractions do not appear despite provocation. Detrusor overactivity is characterized by involuntary detrusor contractions during the filling phase, which may be spontaneous or provoked.[12] Isolated detrusor overactivity may be a result of suprapontine lesions. Detrusor overactivity was present in 22 patients (59.4%), and it was associated with DSD in 21 patients. Detrusor function was normal in 10 patients (27%), and 9 of them also had DSD. Detrusor hypoactivity was diagnosed in five patients (13.5%). Although hypoactive detrusor is expected to be seen with the injury of sacral levels, lesions of our patients with hypoactive detrusor were in thoracolumbar levels. In addition, hypoactive detrusor was associated with overactive sphincter muscle in three patients. Spina bifida causes abnormal development of corticospinal tracts.[13] There are some hypothesis about neurophysiological pathways that coordinate contractions of detrusor muscle and external sphincter. But the influence of these pathways is unclear in patients with MMC.[3] These findings show that pathophysiology of spinal injury in patients with MMC is more complex because of abnormal embryology and unpredictable intensity of intrauterine damage.

DSD is defined as the presence of an involuntary contraction of the external urethral sphincter during an involuntary detrusor contraction. DSD has been originally understood as a result of unconditional execution and coordination of the somatic guarding reflex by the external urethral sphincter, resulting from a loss of input from the pontine micturition center. DSD leads to several complications, which increase morbidity in patients with MMC. Poor bladder emptying and high bladder pressures can cause recurrent urinary tract infections, structural bladder damage, and vesicoureteric reflux, which finally causes hydronephrosis and renal failure.[5],[14] DSD was present in 34 patients (92%) at the time of birth in our series. Damage of spinal cord in affected levels may vary in patients with MMC.[5] In addition, several supratentorial abnormalities, including hydrocephalus, exist in this group of patients. Spine deformities are another important condition, which deteriorates the clinical outcome. Hydrocephalus was detected in 20 patients (54%), and spine deformities were defined in 25 patients (67.5%) in our series. Occurrence of many abnormalities makes the pathophysiology and management of NBD more sophisticated in patients with MMC. Although impairment of bladder compliance is a component of NBD in the following years, it was detected in only one patient (2.7%) in our series.


   Conclusion Top


Urodynamic study findings are important in patients with MMC because of not only their predictive value for kidney diseases in following years but also changes in them can be an early sign for tethered cord, which is a real challenge in both prenatally and postnatally operated patients with MMC. Underlying pathological processes of NBD in patients with MMC are still unclear. Detailed analysis of urodynamic study findings in larger patient groups may be important to understand the physiopathology of prenatal damage in patients with MMC.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Stoneking BJ, Brock JW, Pope JC, Adams MC Early evolution of bladder emptying after myelomeningocele closure. Urology 2001;58:767-71.  Back to cited text no. 1
    
2.
Thorup J, Biering-Sorensen F, Cortes D Urological outcome after myelomeningocele: 20 years of follow-up. BJU Int 2011;107:994-9.  Back to cited text no. 2
    
3.
Madersbacher H Neurogenic bladder dysfunction in patients with myelomeningocele. Curr Opin Urol 2002;12:469-72.  Back to cited text no. 3
    
4.
Kroovand RL, Bell W, Hart LJ, Benfield KY The effect of back closure on detrusor function in neonates with myelomeningocele. J Urol 1990;144:423-5.  Back to cited text no. 4
    
5.
Van Gool JD, Dik P, De Jong TP Bladder-sphincter dysfunction in myelomeningocele. Eur J Pediatr 2001;160:414-20.  Back to cited text no. 5
    
6.
Meyrat BJ, Tercier S, Lutz N, Rilliet B, Forcada-Guex M, Vernet O Introduction of a urodynamic score to detect pre- and postoperative neurological deficits in children with a primary tethered cord. Childs Nerv Syst 2003;19:716-21.  Back to cited text no. 6
    
7.
Park JM, Bloom DA, McGuire EJ The guarding reflex revisited. Br J Urol 1997;80:940-5.  Back to cited text no. 7
    
8.
Snodgrass WT, Adams R Initial urologic management of myelomeningocele. Urol Clin North Am 2004;31:427-34.  Back to cited text no. 8
    
9.
Sillen U Bladder function in infants. Scand J Urol Nephrol Suppl 2004;215:69-74.  Back to cited text no. 9
    
10.
Wen JG, Yeung CK, Djurhuus JC Cystometry techniques in female infants and children. Int Urogynecol J Pelvic Floor Dysfunct 2000;11:103-12.  Back to cited text no. 10
    
11.
Sillén U Bladder function in healthy neonates and its development during infancy. J Urol 2001;166:2376-81.  Back to cited text no. 11
    
12.
Nevéus T, von Gontard A, Hoebeke P, Hjälmås K, Bauer S, Bower W, et al. The standardization of terminology of lower urinary tract function in children and adolescents: report from the Standardisation Committee of the International Children’s Continence Society. J Urol 2006;176:314-24.  Back to cited text no. 12
    
13.
Geerdink N, Cuppen I, Rotteveel J, Mullaart R, Roeleveld N, Pasman J Contribution of the corticospinal tract to motor impairment in spina bifida. Pediatr Neurol 2012;47:270-8.  Back to cited text no. 13
    
14.
Stoffel JT Detrusor sphincter dyssynergia: a review of physiology, diagnosis, and treatment strategies. Transl Androl Urol 2016;5:127-35.  Back to cited text no. 14
    


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