Neurogenic bladder and dysfunctional voiding: Viva

Branch 1: The neural control of micturition

The candidate should explain that the bladder has two jobs, to store urine at a low pressure and to empty completely on command, and that both depend on a coordinated nerve pathway. The sacral micturition centre at S2 to S4 carries the basic reflex: stretch of the bladder wall fires the pelvic nerve, the sacral centre sends the detrusor its contract command, and it relaxes the sphincter through the pudendal nerve. The pontine micturition centre coordinates that reflex so the detrusor and the sphincter act in concert, and the cerebral cortex sits on top and provides inhibition. [1]

If the examiner presses on the lesion, the candidate should explain how a cord lesion above the sacral centre, as in a thoracic or lumbar myelomeningocele, releases the detrusor from cortical inhibition and disrupts the pontine coordination. The result is detrusor overactivity during filling, detrusor-sphincter dyssynergia during voiding, and over time impaired compliance as the bladder wall stiffens against a closed outlet. A strong candidate states that impaired compliance, with a steep pressure rise as the bladder fills, is the pattern most dangerous to the upper tracts. [2]

Branch 2: Classification and assessment

If asked how to classify the bladder, the candidate should describe the urodynamic patterns that drive treatment: detrusor overactivity, impaired compliance, and detrusor-sphincter dyssynergia, and the detrusor leak point pressure as the key number. The candidate should state that a detrusor leak point pressure above 40 cm of water predicts upper-tract deterioration, and that the urodynamics rather than the symptoms decide whether the bladder is safe, because a bladder can be hostile and the child dry, or compliant and the child wet. [2]

If asked about the assessment of this infant, the candidate should describe the video-urodynamics as the gold standard, performed in infancy in spina bifida, and the upper-tract surveillance by renal ultrasound. The candidate should also distinguish the neurogenic bladder from the functional disorders, explaining that dysfunctional voiding and overactive bladder have no cord lesion and are assessed with non-invasive urodynamics such as uroflowmetry, a bladder diary, and a post-void residual. A strong candidate names the cutaneous stigmata and the lower-limb signs that should prompt an MRI to exclude an occult dysraphism in a child labelled as dysfunctional voiding. [1]

Branch 3: Management and long-term implications

If the examiner moves to the management, the candidate should state the goal up front: a low-pressure, continent, completely emptied bladder that protects the kidneys. The first-line treatment is clean intermittent catheterisation every 3 to 4 hours combined with an anticholinergic such as oxybutynin, which lowers the storage pressure while the catheterisation empties the bladder. The candidate should give the dose, oxybutynin at 0.2 mg per kg per dose twice daily titrated to a maximum of 5 mg per dose, and mention the central side effects in young children from penetration of an immature blood-brain barrier. [1]

If asked about escalation, the candidate should describe the second-line intravesical onabotulinumtoxinA, injected into the detrusor at a typical dose of 200 units and sparing the trigone, with the effect lasting 6 to 9 months. Austin and colleagues showed the efficacy in children with neurogenic detrusor overactivity, and Franco and colleagues confirmed the long-term safety of repeated treatments. The candidate should reserve bladder augmentation and a continent catheterisable channel such as a Mitrofanoff or a Monti for the end-stage hostile bladder. [9]

If asked about the long-term implications, the candidate should discuss the progressive renal damage from the high storage pressures — the hydronephrosis, the reflux, the recurrent pyelonephritis, the renal scarring, the hypertension, and the chronic kidney disease — and the lifelong surveillance of the blood pressure, the creatinine, and the renal ultrasound. A strong candidate mentions the bladder cancer risk in adulthood in the chronically managed or augmented bladder, and the planned transition to adult continence and nephrology care. [9]