Transient ventriculoperitoneal shunt dysfunction in children with myelodysplasia and urinary bladder infection. Report of three cases
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Published on: August 5, 2010
R Shane Tubbs1, John C Wellons, Jeffrey P Blount
1Department of Cell Biology, University of Alabama at Birmingham, USA. richard.tubbs@uab.edu
Insights
Urinary bladder infections in children with myelomeningocele and hydrocephalus can mimic shunt malfunction. Treating these infections may resolve shunt dysfunction, avoiding surgery in select cases.
Area of Science:
- Pediatric Neurosurgery
- Urology
- Infectious Diseases
Background:
- Myelomeningocele and hydrocephalus often necessitate ventriculoperitoneal shunts.
- Shunt malfunction is a common complication requiring surgical intervention.
- Urinary tract infections are prevalent in patients with myelodysplasia.
Observation:
- Three pediatric patients with myelomeningocele and hydrocephalus presented with symptoms suggestive of ventriculoperitoneal shunt malfunction.
- All patients had significant urinary bladder infections, which were treated.
- No underlying shunt infection was identified.
Findings:
- Resolution of shunt dysfunction symptoms occurred after treatment of urinary bladder infections in observed patients.
- Urinary bladder infections may precipitate or exacerbate subclinical shunt malfunction or temporary malabsorption.
- The exact mechanism linking bladder infection to shunt dysfunction remains unclear.
Implications:
- Urinary bladder infection treatment may resolve shunt dysfunction symptoms, potentially avoiding surgery.
- Careful observation is crucial for patients with mild symptoms to assess shunt function post-infection treatment.
- This highlights the importance of considering and treating urinary infections in shunt-dependent patients with myelodysplasia.
Abstract:
The authors present three children born with myelomeningocele and hydrocephalus. Each presented with symptoms/signs of ventriculoperitoneal shunt malfunction. All patients at the time of presentation exhibited significant urinary bladder infections and were appropriately treated for their infection. No patient was found to have an underlying shunt infection. All patients without medically threatening symptoms were carefully observed and noted to have resolution of their shunt dysfunction symptoms/signs following treatment of their urinary bladder infections and thus did not undergo a shunt operation. Based on the courses of these patients, we believe that significant urinary bladder infection in patients with myelodysplasia in whom a shunt has been placed may often be enough to bring a subclinical shunt malfunction to clinical attention or even to be the cause of temporary distal peritoneal shunt malabsorption. Although the exact mechanism for this dysfunction is unclear, treatment of the bladder infection may address the symptomatic shunt dysfunction in some patients so as to avoid operative intervention. We emphasize, however, that careful observation of these patients should be performed during hospitalization because they often rely on adequate cerebrospinal fluid diversion. Only patients with mild symptomatology should be observed first as the initial line of treatment.
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