A 31-year-old female patient presented with back pain and left leg radiating pain. Physical examination showed decreased motor power in the left big toe (big toe dorsiflexion motor grade IV). The patient’s symptoms had persisted despite 5 months of conservative treatment including medication, physical therapy, and transforaminal epidural steroid injection. The patient underwent 4 transforaminal epidural steroid injections, with the last injection administered 2 weeks before surgery. Because the patient’s symptoms persisted despite these interventions, we decided to perform the operation. Plain radiographs showed no significant disc height loss or segmental instability. Computed tomography revealed no vacuum phenomenon or calcification within the intervertebral disc. Magnetic resonance imaging (MRI) demonstrated severe central canal stenosis (Schizas grade D) with coexisting central disc herniation at the L4–5 level (Figure 1) [12]. Therefore, we decided to perform UBE ULBD via the left approach with lumbar discectomy to address these lesions.

The patient was positioned in the prone position with routine aseptic drape under general anesthesia. Two portals were made with C-arm guidance. On the anteroposterior image of the C-arm, 2 portals were located on the left pedicle medial line of L4 and L5. On the lateral image, the working portal for instruments was located at upper endplate of L5, and the endoscopic portal was located at lower border of L4 pedicle. After establishment of the 2 portals, ipsilateral partial hemilaminectomy with medial facetectomy, and contralateral sublaminar decompression were performed. After completing bony decompression, the ligamentum flavum was removed. Before removal, we meticulously dissected between the ligamentum flavum and thecal sac to avoid inadvertent dural tear due to adhesion. Additionally, we checked for the presence of the posterior epidural ligament to prevent pulling of the dura and subsequent dural tear during ligamentum flavum removal. The ligamentum flavum was removed in 2 pieces. Bony decompression was completed before removing the ligamentum flavum. The ipsilateral (left) half of the ligamentum flavum was first removed en bloc as the initial piece. Additionally, a discectomy was performed on the ipsilateral side. With extra caution not to damage the dura, the herniated disc fragment was identified and removed (Figure 2A). Then, the contralateral (right) half of the ligamentum flavum was removed en bloc. During removal of the ligamentum flavum, there was no significant adhesion between the ligamentum flavum and the dura. Instead, adhesion was noted between the epidural fat and the dura. Although there was no dural tear after meticulous dissection, the dorsal dura was extremely thinned and translucent, such that the roots within the thecal sac were faintly visible (Figure 2B). Nevertheless, the dura and arachnoid remained intact (Supplementary Video Clip 1). After complete removal of the herniated disc fragment and decompression of thecal sac and L5 traversing nerve root, a Jackson-Pratt drainage catheter was inserted under endoscopic guidance to avoid pushing against the fragile dura. The operation was then completed.

After the initial operation, the patient’s symptoms resolved. Postoperative MRI demonstrated adequate decompression, complete removal of disc herniation, and no evidence of complications (Figure 2C and D). The patient was discharged on postoperative day 2 without complications.

One week later, the patient presented again with severe back pain and left leg radiating pain. Follow-up MRI was obtained to identify any cause of pain such as recurrent disc herniation, hematoma, or others. Follow-up MRI revealed cerebrospinal fluid (CSF) collection and low signal intensity extending from the inner to the outer aspect of the thecal sac on T2-weighted imaging, suspicious for nerve root herniation (Figure 3).

We decided to perform revision surgery to reduce the herniated nerve root and repair the dural tear. Among open surgery and UBE, we used UBE to minimize dead space, which would be larger in open surgery. Supplementary Video Clip 2 shows revision surgical procedure. Two portals established in the initial surgery were used again. After endoscope were inserted, accumulated CSF and epidural hematoma gushed out. Then, herniated nerve root and dural tear were exposed (Figure 4A). The nerve root was reduced using blunt-end instrument such as freer elevator or Penfield No. 4 dissector (Figure 4B). Although the herniated nerve root was reduced, it fluctuated through the dural tear due to the hydrostatic pressure of continuous saline irrigation. TachoSil was applied immediately after spontaneous reduction of the nerve root following cessation of irrigation. However, the repair with TachoSil seemed insufficient, as the previously thinned dura had progressed to a definite defect and had completely ruptured (Figure 4C). Furthermore, because the thinned dura was fragile and already ruptured in nature, primary suturing was deemed infeasible as it would likely tear further. Therefore, only TachoSil was applied. Although we repaired dura with TachoSil, there would be high risk of re-ruptured of dura defect and subsequent root re-herniation (Figure 4D). Therefore, we decided to convert to open surgery. Before conversion, Gelfoam was additionally placed in the epidural space to reinforce the dural repair, and the epidural space was subsequently covered with cottonoid patties for protection (Figure 4E and F). After removal of the endoscope and instruments from the 2 portals, a linear incision was made extending between the 2 portals. During subperiosteal dissection, extra caution was taken to avoid injuring the dura. The blue thread of the cottonoid patty served as a guide to the epidural space during subperiosteal dissection. When previous laminectomy site and dura were exposed, dural tear were approximated with prolene 6-0 and an additional fat graft and fibrin sealant glue was applied. After surgery, the patient’s symptoms resolved, and postoperative MRI performed on 1 week showed no evidence of CSF leakage (Figure 5). During 6 months of follow-up, no further complications were observed.

This case report was approved by the Institutional Review Board (IRB) of the Leon Wiltse Memorial Hospital (IRB No. 2025-W03). Written informed consent was obtained from the patient.

Töppich et al. first reported 2 cases of nerve root herniation through a dural tear following lumbar discectomy [13]. Subsequent literature has described nerve root herniation through a dural tear after open lumbar discectomy or decompression [14,15]. Recently, endoscopic spine surgery, including full-endoscopic and UBE surgery, has gained popularity in response to the growing demand for minimally invasive spine surgery. With the increasing adoption of endoscopic spine surgery for discectomy or decompression, nerve root herniation through dural tear has also been reported following endoscopic spine surgery [10,11,16]. Park et al. [16] reported this complication following endoscopic lumbar ULBD for spinal canal stenosis, but they did not clarify that surgery was performed by full-endoscopy or UBE. To date, only 2 cases of nerve root herniation secondary to dural tear has been described after UBE decompression for lumbar spinal stenosis [10,11]. Chun et al. [10] reported a case of UBE decompression performed for L4–5 lateral recess stenosis caused by a juxtafacet cyst. An intraoperative dural tear occurred and was repaired with TachoComb. Three weeks postoperatively, the patient presented with severe radicular pain due to nerve root herniation. Instead of revision surgery, they performed an epidural blood patch, which successfully resolved the patient’s symptoms. Matsukawa et al. [11] performed L3–4 and L4–5 UBE ULBD for lumbar spinal canal stenosis. Three weeks after the operation, the patient developed severe radicular pain that necessitated open revision surgery. Intraoperatively, they identified nerve root herniation through a dural tear, with the arachnoid membrane remaining intact and without CSF leakage. The uniqueness of our case lies in the fact that an initially intact dura subsequently was torn in a delayed fashion, leading to nerve root herniation. Although the dura was markedly thinned and translucent at the time of the index surgery, both the dura and the arachnoid membrane remained intact. However, at revision surgery, we found that the previously thinned dura had ruptured, resulting in herniation of the nerve root through the defect. Our case suggests that nerve root herniation can occur even in the setting of a delayed dural tear.

The incidence of delayed dural tear following spinal surgery has been reported to range from 0.2 to 0.8% [17,18]. A delayed dural tear may occur even when no tear is recognized during the index procedure. Such cases may result from an unrecognized intraoperative dural tear or from a dural defect that develops postoperatively. Khazim et al. [17] proposed possible mechanisms for delayed dural tear: (1) an unrecognized intraoperative dural tear, and (2) erosion of the dura caused by contact with a bony spicule or the edge of the laminectomy site, which may be exacerbated by Valsalva maneuvers or physical activity. Durand et al. [18] analyzed the American College of Surgeons National Surgical Quality Improvement Program data set, and reported that 174 of 86,212 patients underwent reoperation or readmission due to delayed dural tear. The independent risk factors for delayed dural tear were lumbar procedures (odds ratio [OR], 2.79; p<0.0001, vs. cervical), decompression only (OR, 1.72; p=0.0017, vs. fusion and decompression), and operative duration ≥250 minutes (OR, 1.70; p=0.0058, vs. <250 minutes). They suggested that prolonged operative time may increase the likelihood of an unrecognized durotomy or reduce the chance of detecting a durotomy intraoperatively. Kalidindi et al. [19] reported 6 cases of late-presenting dural tear among 1,929 patients who underwent surgery for degenerative spinal disease. The anatomical location was lumbar in 5 patients and cervical in 1 patient, which is consistent with the findings of Durand et al. [18], who noted that delayed dural tears are more prevalent in the lumbar region. Kalidindi et al. [19] proposed several possible mechanisms for delayed dural tear: (1) an unrecognized dural tear occurring at the time of the initial operation, (2) delayed development of a dural tear due to the expanded dura rubbing against a bony spur or the edge of the laminectomy site, and (3) an initial dural injury with an intact arachnoid membrane, followed by delayed arachnoid rupture due to physical activity.

In our case, the most plausible mechanism for the delayed rupture of the translucent dura may be attributable to elevations in CSF pressure. Episodes of increased intraabdominal pressure, such as those associated with Valsalva maneuvers or physical activity, may cause repeated elevations in CSF pressure, exerting focal stress on the thinned dura and ultimately resulting in its delayed rupture.

Our experience suggests that translucent or markedly thinned dura encountered during endoscopic decompression should be regarded as high risk for delayed rupture. Prophylactic reinforcement with a dural sealant, such as TachoSil, may therefore be advisable even in the absence of a dural tear to prevent delayed dural tear.

Management strategies for intraoperative dural tears during endoscopic spine surgery have been described in the literature, ranging from simple dural sealant application to primary repair or conversion to open surgery, depending on tear size and configuration [20-23]. Although no clear consensus exists for the management of delayed dural tears following endoscopic spine surgery, several treatment algorithms for dural repair have been proposed for UBE [22,23]. For small dural tears (< 10–12 mm), application of a dural sealant has been recommended. Nam et al. [24] introduced a double-layer TachoSil packing method for the management of incidental durotomy. This technique involves applying 2 layers of TachoSil (an intradural inner layer and an epidural outer layer). However, in cases of large dural tears (>10–12 mm), clip suturing or open conversion with primary repair may be required. Hong et al. introduced a novel suturing technique using a knot pusher [25]. This technique enables direct dural suturing with silk without necessitating open conversion. Regarding clip suturing, Heo et al. [21] reported successful repair of a dural tear using sutureless, nonpenetrating clips by UBE. In our case, we initially re-entered via the UBE approach, as immediate open revision would have required subperiosteal dissection of the paraspinal muscles, potentially risking further injury to the already herniated root. Using UBE, the herniated root was reduced, and the dural defect was temporarily reinforced with TachoSil. While small, linear tears may be adequately managed with TachoSil alone, ruptured or large dural tears often require conversion to open surgery. In such cases, direct dural repair with fat grafting would be the most reliable treatment option.