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Intrathecal Bleed Following Percutaneous Spinal Cord Stimulator Trial Lead Placement

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Intrathecal Bleed Following Percutaneous Spinal Cord Stimulator Trial Lead Placement

Background

  • Biologically-associated complications with spinal cord stimulator (SCS) placement include pain at the electrode insertion or generator site, clinical infections, inadvertent dural puncture, spinal cord injury and hematoma formation 3,7
  •  Incidence of epidural hematoma formation following SCS lead placement is estimated at 0.2-0.3% 8
  •  American Society of Regional Anesthesia and Pain medicine (ASRA) guidelines help guide management of neuroaxial procedures when a patient is on anticoagulation or antiplatelet medication6
  •  ASRA guidelines currently do not make recommendations for valproic acid usage2,3,6
  •  Valproic acid can cause both an increased risk of bleeding as well as thromboembolism 1,4
  •  One proposed mechanism of valproic acid induced coagulopathy is from hepatotoxicity 1
  • Other studies associate valproic acid with decreased factor levels (VII, VIII, XIII, IX), protein C and S levels, fibrinogen, platelet count, antithrombin III levels; decreased von Willebrand factor antigen and ristocetin cofactor; increased lipoprotein levels; qualitative and functional platelet defects 1
  • Case reports discuss the incidence of arachnoiditis causing tethering of the spinal cord 5

Case Description

  • A 34 year old male with the chief complaint of failed back surgery syndrome underwent percutaneous spinal cord stimulator lead placement 
  •  A 14G introducer was inserted at the inferior portion of the pedicle shadow at L2, and the epidural space was entered at the T12-L1 interspace.  The left lead was advanced to the T8 vertebral body
  •  Another 14G introducer was placed on the right in the same location.  The right lead was advanced until the patient experienced a paresthesia at T11-12
  •  The right introducer was removed and replaced, entering the epidural space at the L1-2 interspace.  The right lead was advanced to the T8 vertebral body.  No paresthesia was elicited during this placement
  •  No CSF or blood return was noted at any time during the procedure
  •  In the PACU, the patient reported right calf pain that resolved with intravenous hydromorphone 
  •  One day following discharge, the patient experienced edema of the right calf with dysesthesia.  Lower extremity ultrasound was negative for a deep vein thrombosis
  •  One week from the trial, the edema progressed more proximal with L5 and S1 dysesthesia, 4/5 strength of the right lower extremity and 5/5 strength of left lower extremity
  •  Lumbar MRI revealed linear T1 hyperintense, T2 hypointense signal within the lumbar portion of the thecal sac.  A dural tear was not noted
  •  Conservative management was undertaken including a multimodal pain regimen, physical therapy, and occupational therapy
  •  The patient was discharged on day four of hospitalization.  One month after discharge, the patient reported improving pain with intact sensation and 5/5 strength

Discussion and Conclusion

  • A dural tear may have occurred despite lack of CSF appearance during the trial and lack of evidence of dural tear on MRI
  • The patient’s arachnoiditis may have caused some tethering of the spinal cord leading to a tighter interspace at the T12-L1 level
    • The patient’s paresthesia during right lead placement may indicate a defect at the T12-L1 level
    • The spinal cord stimulator leads may have contributed to trauma of the dural sac
  • The patient’s use of valproic acid may have contributed to an increased risk for bleeding despite normal PT,  INR, PTT, liver enzymes and platelet count

References

  1. Abdallah C. Considerations in perioperative assessment of valproic acid coagulopathy. J Anaesthesiol Clin Pharmacol. 2014;30:7-9.
  2. Banerjea MC, Diener W, Kutschke G, Schneble HJ, Korinthenberg R, Sutor AH. Pro- and anticoagulatory factors under sodium valproate-therapy in children. Neuropediatrics. 2002;33:215-220
  3. Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: a 20-year literature review. J Neurosurg. 2004 Mar;100(3 Suppl Spine):254-67.
  4. Cannizzaro E, Albisetti M, Wohlrab G, Schmugge M. Severe bleeding complications during antiepileptic treatment with valproic acid in children. Neuropediatrics. 2007;38:42-45
  5. Rajpal S, Chanbusarakum K, Deshmukh PR. Upper cervical myelopathy due to arachnoiditis and spinal cord tethering from adjacent C-2 osteomyelitis. Case report and review of the literature. J Neurosurg Spine. 2007 Jan;6(1):64-7
  6. Horlocker TT, Wedel DJ, Rowlingson JC, Enneking FK, Kopp SL, Benzon HT, Brown DL, Heit JA, Mulroy MF, Rosenquist RW, Tryba M, Yuan C. Regional Anesthesia in the Patient Receiving Antithrombotic or Thrombolytic Therapy: American Society of Regional Anesthesia and Pain Medicine Evidence-Based Guidelines. Regional Anesthesia & Pain Medicine. 2010; 35(1 ): 64-101
  7. Turner JA, Loeser JD, Bell KG. Spinal cord stimulation for chronic low back pain: a systematic literature synthesis. Neurosurgery. 1995 Dec;37(6):1088-95; discussion 1095-6.
  8. Zan E, Kurt KN, Yousem DM, Christo PJ. Spinal cord stimulators: typical positioning and postsurgical complications. AJR Am J Roentgenol.2011 Feb;196(2):437-45. doi: 10.2214/AJR.10.4789. 
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