- Case report
- Open Access
- Open Peer Review
Bladder stones – red herring for resurgence of spasticity in a spinal cord injury patient with implantation of Medtronic Synchromed pump for intrathecal delivery of baclofen – a case report
© Vaidyanathan et al; licensee BioMed Central Ltd. 2003
- Received: 16 January 2003
- Accepted: 25 March 2003
- Published: 25 March 2003
Increased spasms in spinal cord injury (SCI) patients, whose spasticity was previously well controlled with intrathecal baclofen therapy, are due to (in order of frequency) drug tolerance, increased stimulus, low reservoir volume, catheter malfunction, disease progression, human error, and pump mechanical failure. We present a SCI patient, in whom bladder calculi acted as red herring for increased spasticity whereas the real cause was spontaneous extrusion of catheter from intrathecal space.
A 44-year-old male sustained a fracture of C5/6 and incomplete tetraplegia at C-8 level. Medtronic Synchromed pump for intrathecal baclofen therapy was implanted 13 months later to control severe spasticity. The tip of catheter was placed at T-10 level. The initial dose of baclofen was 300 micrograms/day of baclofen, administered by a simple continuous infusion. During a nine-month period, he required increasing doses of baclofen (875 micrograms/day) to control spasticity. X-ray of abdomen showed multiple radio opaque shadows in the region of urinary bladder. No malfunction of the pump was detected. Therefore, increased spasticity was attributed to bladder stones. Electrohydraulic lithotripsy of bladder stones was carried out successfully. Even after removal of bladder stones, this patient required further increases in the dose of intrathecal baclofen (950, 1050, 1200 and then 1300 micrograms/day). Careful evaluation of pump-catheter system revealed that the catheter had extruded spontaneously and was lying in the paraspinal space at L-4, where the catheter had been anchored before it entered the subarachnoid space. A new catheter was passed into the subarachnoid space and the tip of catheter was located at T-8 level. The dose of intrathecal baclofen was decreased to 300 micrograms/day.
Vesical calculi acted as red herring for resurgence of spasticity. The real cause for increased spasms was spontaneous extrusion of whole length of catheter from subarachnoid space. Repeated bending forwards and straightening of torso for pressure relief and during transfers from wheel chair probably contributed to spontaneous extrusion of catheter from spinal canal in this patient.
- Spinal Cord Injury
- Spinal Canal
- Spinal Cord Injury Patient
- Bladder Stone
A 44-year-old male sustained rupture of aorta, fracture of both tibiae, fracture of C5/6 in a traffic accident. He underwent thoracotomy and repair of transected aorta. Internal fixation and fusion of cervical spine was done at C-5/C-6 level. He had developed incomplete tetraplegia (ASIA scale D) at C-8 level. He was transferred to spinal injuries centre thirteen months later. By then he had developed severe spasticity of lower limbs.
Over the next six months, this patient required increasing amounts of baclofen ((875 micrograms/day) to control spasms. The pump had been functioning satisfactorily during this period. There was no pump stall. We did not observe any discrepancy between telemetry reading and the volume of fluid aspirated from the reservoir before refilling the pump. No noxious lesion such as kidney stones, which could account for increased spasticity, was detected in this patient. 
Chronology of clinical events, dose of intrathecal baclofen, location of tip of catheter for delivery of baclofen and presence of bladder stones
Dose of intrathecal baclofen Micro-grams/day
Location of catheter tip
Road traffic accident Spinal cord injury
Implantation of Medtronic Synchromed EL pump
X-ray of abdomen
The catheter has come out of the spinal canal. The catheter is coiled in the paraspinal space at L-4 level.*
Cystoscopy and electrohydraulic lithotripsy of vesical calculi
X-ray of abdomen
The catheter has come out of the spinal canal. The catheter is coiled in the paraspinal space at L-4 level.
MRI and CT scan of lumbar spine
No CSF collection in paravertebral soft tissue. The tip of catheter is coiled superficially within right longissimus lumborum muscle.
Exploration revealed the catheter lying under the sheath of paraspinal muscle.
A new catheter was passed into the subarachnoid space and the tip of catheter was located at T-8 level, which was confirmed by X-ray screening.
We report spontaneous extrusion of catheter from the spinal canal, which is a very unusual complication of intrathecal baclofen therapy. It is likely that repeated bending forwards and straightening of torso for pressure relief and during transfers from wheelchair, contributed to extrusion of catheter from the spinal canal in this patient. After extruding out of the spinal canal, the catheter got coiled in paravertebral space, where the catheter had been anchored firmly to intermuscular septum. Spontaneous extrusion of catheter from the spinal canal is unlikely to occur in profoundly disabled individuals, who do not actively move their trunk. For example, there may be individuals with advanced multiple sclerosis, who are confined to the chair and who do not have the ability to bend forwards and then straighten the torso for pressure relief or, perform unassisted transfers from the wheel chair to bed, toilet seat, or car. These patients are unlikely to develop extrusion of catheter from spinal canal if they undergo implantation of Medtronic pump for intrathecal baclofen therapy.
Abrupt withdrawal of intrathecal baclofen therapy can result in a life-threatening syndrome (high fever, altered mental status, profound muscular rigidity that may sometimes progress to fatal rhabdomyolysis). The intrathecal baclofen withdrawal syndrome is clinically and pathophysiologically distinct from autonomic dysreflexia, malignant hyperthermia, and neuroleptic-malignant syndrome. . This patient did not develop intrathecal baclofen withdrawal syndrome at any stage. Probably, the catheter came out of thecal space very gradually over a period. Even when the catheter was extruded completely from thecal space, it is likely that a fibrous channel existed between the tip of the catheter and thecal space, which provided an entry path to the infused drug to reach thecal space. This would explain prompt relief of spasticity when the dose of intrathecal baclofen was increased.
The tip of catheter was placed at T-8 level during the second operation. Initially, the tip of catheter was located at T-10 level. Burns and Meythaler  emphasised the importance of the level of intrathecal catheter placement to achieve satisfactory control of spasticity. Placement of the tip of the intrathecal catheter at the T-6 / T-7 level was associated with greater relief of upper-extremity spasticity without loss of effect on the lower extremities. The mean dosages of baclofen in children with spastic tetraparesis, in whom intrathecal catheter was placed at the T-6 / T-7 level with fluoroscopic guidance, were lower compared with mean dosages when the catheter tip had been placed at the T-11 / T-12 level. No morbidity related to the more rostral location of the catheter was observed in the children, in whom the catheter tip had been placed at the T-6 / T-7 level. 
It is possible that some physicians might have encountered similar mishap after implantation of baclofen pump, but have not published the adverse events for fear of recrimination. We favour voluntary reporting and dissemination of information on adverse events related to clinical procedures and medical implants [9–11]. Quite often, mishaps occur due to system errors and therefore, apportioning blame to individual health professionals should be avoided. A joint team approach by health professionals belonging to various medical disciplines, which is strengthened by frequent, informal and honest discussions of a patient's clinical condition, is likely to reduce delays in diagnosis and medical errors in spinal cord injury patients.
We thank the patient for giving consent to publication of this case report. The authors are grateful to Professor David Rushton, Departments of Neurology and Rehabilitation, Kings College Hospital, Denmark Hill, London, United Kingdom, and Dr J.M. Meythaler, Department of Physical Medicine and Rehabilitation, Division of Neurological Surgery, University of Alabama at Birmingham School of Medicine, Birmingham, USA.
Professor Rushton and Dr Meythaler made valuable comments to the original manuscript. A review of our submission by internationally renowned experts in the subject of intrathecal baclofen therapy helped the authors to revise the manuscript incorporating the useful suggestions made by Professor Rushton and Dr Meythaler.
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- The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2490/3/3/prepub
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