A 60-year-old woman presented to the spine clinic for a complaint of progressive severe pain in her lower back of approximately 2.5 years’ duration. She previously underwent an L4-S1 TLIF for mobile spondylolisthesis and radiculopathy 3 years earlier at an outside institution. The patient reported significant improvement in her preoperative symptoms at that time, to the point where she was participating in physical therapy with minimal pain. At 6 months after the index surgery, she fell and reported hearing a distinct “pop” in her back. Since the fall, she remained bedridden with shooting, “shock-like” pain down her left leg associated with a progressively worsening left-sided foot drop (muscle strength 2/5) but with intact genitourinary function and perineal sensation. She was seen in our clinic 2.5 years after the index surgery for the progression of these symptoms. Radiological workup with radiographs and magnetic resonance imaging of the lumbar spine were notable for retropulsion of the L5-S1 interbody cage into the spinal canal, otherwise excellent positioning of the L4-5 interbody, and pedicle screws with posterolateral bridging bone [Figure and ]. These findings were stable over the previous 2.5 years based on radiographic studies obtained after her fall. The patient's original surgeon suggested revision surgery with the high risk of cerebrospinal fluid (CSF) leak and neurological deficit and the patient deferred a surgical option at that time. However, because of the her progression of her symptoms, she sought a second surgical opinion.\nConsidering the prolonged interval between the index surgery and the time of presentation to our clinic and the exact central position of the retropulsed interbody [], we were concerned that significant scar tissue and osteophytic ridge formation would hinder visualization of the graft and place the surrounding neural tissue at risk due to the retraction that would be necessary if the interbody were accessed via the original surgical corridor. In addition, the patient had adjacent segment degeneration and stenosis at the L3-4 segmental level, which explained her progression of symptoms. Our recommendation was a more direct transdural approach that would represent virgin territory, obviating scar tissue while providing adequate visualization with minimal retraction of neurological tissue during retrieval of the interbody. An anterior approach via anterior lumbar interbody fusions was also considered, but a posterior-only approach was recommended because of the presence of additional pathology at L3-4 that required treatment. After risks, benefits, and alternatives to intradural and transdural approaches were explained, the patient agreed to proceed with transdural removal of the retropulsed L5-S1 interbody, along with an L3-4 laminectomy and extension of her fixation from L3 to S1.\nThe prior surgical incision was opened, and surgical dissection was carried down to the existing instrumentation at L4-5 and L5-S1. After the locking caps on all six screwswere removed, the titanium rods were removed, and each screw was inspected for pseudarthrosis. Bilateral L4 and L5 screws were notably loose and promptly replaced with screws of larger diameter. An L3-4 laminectomy was performed, and L3 pedicle screws were placed. After this, we turned our attention toward the L5-S1 interspace, where the surgical corridor for the original TLIF was unidentifiable secondary to several large osteophytic ridges and extensive scar tissue. Residual lamina at this interspace was identified and removed easily with punch Kerrison rongeurs (Integra LifeSciences, Plainsboro, NJ) until normal midline dura was identified. The surgical microscope was brought in for the transdural portion of the operation. The thecal sac was opened with a number 11 blade in a linear fashion [], and after the egress of CSF, the dura was tacked to the muscle margins. With the retraction of intradural sacral roots [], the herniated interbody was easily visible and palpable through the ventral dura; it was compressing the left-sided exiting sacral rootlets. A Penfield number 2 was used to gently retract the nerve rootlets to either side, and a number 11 blade was once again used to open the ventral dura in a linear fashion directly over the herniated interbody [Figure and ]. Once open, the ventral dura was retracted to either side of the herniated interbody, and a graft inserter was threaded into the interbody []. Using repetitive rocking motions medially/laterally to disrupt any bridging osteophytes attached to the interbody, wecarefully shimmied the cage out through the ventral dura, traversing the thecal sac, and finally out through the opening in the dorsal dura []. The intradural nerve rootlets were inspected for any damage. The dura was closed in sequential fashion, ventrally then dorsally, using 5-0 Prolene sutures (Ethicon Endo-Surgery, Inc., Blue Ash, OH) and buttressed with DuraSeal (Covidien, Mansfield, MA) sealant []. Segmental fixation was completed with titanium rods locked in place from L3 to S1, along with autograft/allograft bone placed posterolaterally []. A lumbar drain was not placed, and the patient was kept flat for 24 h. A few hours postoperatively, the patient noted immediate improvement in her pain but had no improvement in her foot drop. She was up and mobilizing on postoperative day (POD) 2 with the physical therapy team, off all narcotics on POD 3, and discharged to rehabilitation on POD 4. At her 12-month follow-up visit, she was self-ambulatory, performing her normal activities of daily living, and had a complete resolution of pain and some improvement in foot drop (to muscle strength 3/5).
A 27-year-old gentleman, presented with 3 months history of blurring of vision associated with headache. There was no history of loss of consciousness, seizures, or weakness in limbs. Visual examination showed acuity of 6/6 bilaterally with left temporal field defect.\nMRI of brain, T1W, T2 axial, contrast and multiplanar sequences were performed which showed evidence of lobulated mixed signal intensity lesion seen in the optic chiasm, measuring 18 × 11 mm. Multiple hemorrhagic foci of varying sizes were seen within the lesion. No obvious enhancement was seen after IV contrast material injection. On the right side, the lesion was extending anteriorly up to the optic canal and superiorly abutting the hypothalamus. The features were suggestive of CM of the optic chiasm [Figures and ].\nThe lesion was removed neuro-endoscopically through the trans-nasal trans-sphenoidal route. After reaching the sella, dura opened and the pituitary gland was displaced. Under-surface of chiasm was visualized. The lesion was seen on the surface with brownish discoloration. A small incision was made and the lesion could be removed. Post–operatively, there was a transient worsening left temporal field defect. The histopathological examination and features are consistent with organizing hematoma.