Vaidyanathan Subramanian, Soni Bakul M, Oo Tun, Hughes Peter L, Singh Gurpreet, Watt John W H, Sett Pradipkumar
Regional Spinal Injuries Centre, District General Hospital, Southport, PR8 6PN, UK.
BMC Urol. 2003 Mar 25;3:3. doi: 10.1186/1471-2490-3-3.
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.
脊髓损伤(SCI)患者痉挛加剧,其痉挛之前通过鞘内注射巴氯芬治疗得到良好控制,原因(按频率排序)依次为药物耐受性、刺激增加、储液器容量低、导管故障、疾病进展、人为失误和泵机械故障。我们报告一名SCI患者,膀胱结石成为痉挛加剧的干扰因素,而真正原因是导管从鞘内空间自发脱出。
一名44岁男性C5/6骨折,C8水平不完全性四肢瘫。13个月后植入美敦力Synchromed泵进行鞘内注射巴氯芬治疗以控制严重痉挛。导管尖端置于T10水平。初始巴氯芬剂量为300微克/天,通过简单持续输注给药。在九个月期间,他需要增加巴氯芬剂量(875微克/天)来控制痉挛。腹部X线显示膀胱区域有多个不透X线阴影。未检测到泵故障。因此,痉挛加剧归因于膀胱结石。成功进行了膀胱结石的电液压碎石术。即使在膀胱结石去除后,该患者仍需要进一步增加鞘内巴氯芬剂量(950、1050、1200然后1300微克/天)。对泵 - 导管系统的仔细评估发现导管已自发脱出,位于L4的椎旁间隙,导管在进入蛛网膜下腔之前在此处固定。一根新导管插入蛛网膜下腔,导管尖端位于T8水平。鞘内巴氯芬剂量降至300微克/天。
膀胱结石成为痉挛复发的干扰因素。痉挛加剧的真正原因是导管从蛛网膜下腔全长自发脱出。为缓解压力以及从轮椅转移时反复向前弯曲和伸直躯干可能导致该患者导管从椎管自发脱出。