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Bladder dysfunction is a common problem in children, though underdiagnosed and constitutes up to 40 percent of pediatric urology clinic visits. It results from disruptions of the normal voiding process by neurogenic, anatomic, or functional causes. Congenital defects of the neural tube (CDNT) are common abnormalities that lead to a neurogenic bladder in children. Spinal dysraphism is responsible for up to 93% of cases (open myelodysplasia: 85%, closed/occult dysraphism: 8%), sacral agenesis, imperforate anus and lesion of the spinal cord represent 1% each, and cerebral palsy, 3%. Other less frequent causes are cerebral/spinal tumours and pelvic surgery. We present a rare case of neurogenic bladder in a 20-month-old male.
A 20-month-old previously well toddler with a three-month history of recurrent fever, vomiting, and straining at micturition was referred to the renal unit of a teaching hospital after being managed for urinary tract infection twice in a peripheral facility. The child cried during urination and produced cloudy urine sometimes. The mother had an antenatal scan done but was unaware of any abnormality. She delivered at term and the baby had an uneventful neonatal period. His immunization is complete for his age, and his development is normal. There is no consanguinity; the child is the last of three staying with both parents. No sibling or family member has been diagnosed with kidney disease or abnormality.
He was ill-looking, afebrile (T-36.20), not pale, and well-hydrated on examination. Respiratory rate was 44 breaths/minute with mild flaring of the alae nasae and lower chest wall indrawing. However, air entry was adequate, and breath sounds were vesicular with no added sounds. His abdomen was mildly distended with no palpable bladder or tenderness. No spinal deformity was seen. No tuff of hair, dimple of lipomas seen in the sacral area, and no deformity in the feet. The cardiovascular system was unremarkable. Bedside urine dipstick showed; Leucocyte- ++, Nitrite- +, pH-6.0.
His urine cultured klebsiella pneumonia, sensitive to Amikacin and Gentamicin. Complete blood count (CBC) showed: WBC-10.57, Neut-70.2% (high), Lymph-21.9%, Hb-10.3g/dl, Platelet-110. Urea-10.2mmol/L, Cr-89µmol/L, bicarbonate-21mmol/L and electrolytes normal.
An abdominal ultrasound showed the following kidney sizes: RT: 9.7x4.8cm LT: 10.2x5.5cm. Severe dilatation of the pelvicalyceal systems and ureters bilaterally. Urinary bladder distended with wall trabeculations and internal debris. Dilatation of the posterior urethra gives the keyhole appearance. A micturating cystourethrogram (MCUG) showed a characteristic Christmas-tree tower bladder (urinary bladder that appears elongated with a conical shape, hypertrophied and well-demarcated bladder neck). The posterior urethra is not dilated, and the anterior urethra appears normally outlined. Lumbosacral x-ray done was normal.
A non-enhanced MRI scan of the lumbar spine showed no posterior vertebral scalloping, no defect in the posterior elements, no evidence of spina bifida or tethered cord but an increase in the anterior-posterior diameter of the dural sac, suggestive of Dural Ectasia.
Conclusions
Not all voiding difficulties in male children are due to urethral pathology like the posterior urethral valve. Dural ectasia, a rare condition marked by abnormal dural sac enlargement, could cause abnormal bladder innervation in children.