INTRODUCTION
Unilateral biportal endoscopic (UBE) spine surgery has gained increasing popularity due to its advantages such as reduced postoperative pain, minimal intraoperative bleeding, and shortened hospital stay [5].
To date, the most reported complications associated with UBE include dural tear (2-5%) and epidural hematoma (1-4%) [6,8]. Although intracranial subdural hygroma has been previously reported following endoscopic spinal surgery [9], there have been no published cases of spinal subdural hematoma (SSH), even at the index surgical level [13]. Here, we present two rare cases of remote SSH that occurred after UBE procedures, aiming to share our clinical experience and highlight this uncommon but potentially significant complication.
CASE REPORT
Case 1 : 76-year-old female
A 76-year-old female presented to our hospital with chronic neurogenic claudication (NIC), having received multiple nerve blocks and conservative treatments over several years. She had a medical history of hypertension and dyslipidemia and was on medication for these conditions. Notably, she was not taking any antiplatelet agents, and her preoperative prothrombin time (PT)/activated partial thromboplastin time (aPTT) and platelet count were within normal limits.
Preoperative lumbar spine magnetic resonance imaging (MRI) revealed L5/S1 foraminal stenosis, L4/5 spondylolisthesis, and L3/4 central stenosis (Fig. 1). The patient underwent anterior lumbar interbody fusion (ALIF) at L4/5 and S1, along with left-sided biportal endoscopic unilateral laminotomy for bilateral decompression (ULBD) at L3/4. During surgery, no dural tear or cerebrospinal fluid (CSF) leakage was observed. However, severe flavum adhesion due to chronic stenosis was noted at L3/4, which is commonly seen in elderly patients. The operation lasted 4 hours and 55 minutes, and estimated blood loss was 200 mL.
Immediately postoperatively, the patient exhibited left leg monoplegia, specifically grade 0 hip flexion, which was absent preoperatively. Emergent MRI revealed a left-dominant, severe SSH extending from L1 to the posterior aspect of the L2 vertebral body, with compression of the nerve rootlets. No abnormalities were found at the surgical level L3/4 (Fig. 2). Radiological evaluation, interpreted by a board-certified radiologist, indicated a subdural hematoma or subdural fluid collection extending dorsally from T12 to L3, centered at the L2-3 level, with moderate central canal compromise at this level. The patient was status post ALIF with posterior pedicle fixation at L4-S1 and left-sided unilateral biportal decompression at L3/4, and the surgical site appeared relatively well decompressed.
The patient was treated with intravenous steroids. Four hours later, her hip flexion improved to grade IV- and gradually recovered to grade IV+. There was no evidence of CSF leakage on postoperative days 1 and 2. Mild paresthesia persisted for several weeks but was manageable with medication. Follow-up MRI at 3 months demonstrated a resolving hematoma, and the patient showed no residual neurological deficits (Fig. 3).
Case 2 : 88-year-old male
An 88-year-old male presented with NIC and low back pain, which was refractory to conservative management. He had a history of anemia, glaucoma, and benign prostatic hyperplasia, and was on medication for these conditions. He was not on any antiplatelet therapy, and his preoperative PT/aPTT and platelet count were normal.
MRI showed L4/5 spondylolisthesis with central canal stenosis (Fig. 4). The patient underwent a left-sided ULBD using biportal endoscopic technique at the L4/5 level. No intraoperative complications or dural injury were observed. The surgery lasted 2 hours and 25 minutes with an estimated blood loss of 80 mL.
On postoperative day 1, routine MRI revealed a subdural hematoma extending from L2 to L4 (Fig. 5). Interpretation by a board-certified radiologist indicated a subdural hematoma or subdural fluid collection at the dorsal aspect from L1 to L4, with moderate to severe central canal compromise. Postsurgical changes were also noted, including bilateral partial hemilaminectomy of L4 via a left unilateral approach, bilateral flavectomy and foraminotomy at L4-5, and an epidural hematoma at the laminectomy site with moderate central canal compromise. The patient remained asymptomatic, with no evidence of CSF leakage, and was discharged on postoperative day 2. At the 4-week outpatient follow-up, he reported improvement of his preoperative symptoms, including NIC, and no clinical signs attributable to the subdural hematoma were observed. Thereafter, the patient was lost to follow-up, and a 3-month postoperative MRI could not be obtained.
Both cases underwent surgery under general anesthesia in the prone position.
DISCUSSION
Remote spinal subdural hemorrhage is a rare complication. Case reports have been published in association with full-endoscopic surgery [2] and microscopic surgery [3,11], but no such cases have been previously reported following UBE procedures.
In the full-endoscopic case, a 68-year-old female underwent L4/5 decompression for stenosis. No intraoperative dural tears occurred, but on postoperative day 2, she developed right leg numbness and urinary retention. MRI revealed a subdural hematoma at the L5/S1 level. Intraoperative findings during revision surgery showed xanthochromic fluid gushing out at high pressure following durotomy, with the arachnoid found intact. The patient recovered completely after evacuation.
In the microscopic surgery case, an 80-year-old male developed bilateral leg numbness immediately after L4/5 microscopic discectomy. MRI showed an extensive subdural hematoma from L1 to S1. As there was no neurological deficit, conservative treatment was pursued, and the hematoma resolved over 2 months. Another case involved a 76-year-old male who developed a subdural hematoma from T11 to L2 following L3/4 and L4/5 laminectomy and discectomy. Hematoma evacuation via durotomy led to full recovery. Table 1 summarizes the previously reported cases of remote SSH following various spine surgeries, including our current cases.
Several hypotheses may explain the pathogenesis of these remote subdural hematomas, as outlined below. First, CSF pressure shift and venous traction : sudden decompression may alter CSF dynamics, causing traction on bridging veins and resulting in bleeding. This mechanism is supported by the presence of severe chronic stenosis in all reported cases, absence of CSF leakage, and intraoperative confirmation of intact dura. Second, subclinical dural tear with intact arachnoid : water used during UBE may enter the epi-arachnoid space through a tiny dural defect, generating a subdural hygroma. In elderly patients with adhesions, this could evolve into hematoma. Clinical features such as rapid symptom improvement in one case and absence of symptoms in another support this theory. Third, direct mechanical or hydrostatic injury : manipulation or irrigation pressure may rupture vessels in the subdural space, or ALIF-related mechanical impact may contribute. However, no intraoperative bleeding or dural contact was noted, and no similar events have been observed in other ULBD cases, making this mechanism less likely. And fourth, positional or unrelated traumatic factors : though theoretically possible, there is no clinical evidence or history of antiplatelet use or coagulopathy in our patients, making this an unlikely cause. Because remote SSH is extremely rare and its pathogenesis remains poorly understood, the proposed hypotheses are partly extrapolated from mechanisms described in cranial subdural hematoma. These analogies should be interpreted with caution, and we have supplemented the discussion with additional references to clearly distinguish cranial subdural hematoma from reported spinal/remote subdural hematoma pathways [10].
At present, the precise etiology of remote SSH remains uncertain. However, this phenomenon has been reported not only in the two cases described herein, but also in previously published literature, suggesting that although rare, it is a genuine complication.
In addition, it should be acknowledged that case 1 involved a combined procedure of ALIF and UBE decompression. Therefore, it is difficult to attribute the occurrence of the remote subdural hematoma solely to the UBE procedure. Mechanical impact during cage insertion or even patient repositioning could have contributed to the development of the hematoma. This represents a clear limitation of our report and should be considered when interpreting the present findings.
Furthermore, all five patients, including our two cases and three previously reported cases, were elderly (ages 68, 76, 76, 80, and 88 years). Elderly individuals generally show reduced CSF compliance, more extensive spinal canal adhesions, and increased vascular fragility [1,4,7,12,14]. These age-related changes make the aged spine more susceptible to intraoperative pressure shifts and shear forces, thereby predisposing such patients to the development of remote subdural hematoma. It is therefore reasonable to assume that advanced age played a substantial role in precipitating hemorrhage in the present cases.
Interestingly, one of our cases (case 2) demonstrated an incidental subdural hematoma detected on routine postoperative day 1 MRI, despite the absence of new neurological symptoms. This finding suggests that remote SSHs may occasionally remain clinically silent. Because postoperative MRI is not universally performed in asymptomatic UBE patients, some cases might go undetected, and the true incidence of this complication could be higher than currently appreciated. At our institution, postoperative MRI is routinely obtained on postoperative day 1 for UBE patients. Despite our large surgical volume, only the two cases presented here have been identified to date, suggesting that while the incidence is extremely low, additional asymptomatic cases cannot be entirely excluded. Fortunately, both of our cases showed favorable outcomes with conservative management and did not require surgical intervention. However, in previously reported cases where neurological deficits persisted, durotomy and hematoma evacuation were necessary. Delayed recognition and management in such cases may lead to permanent sequelae. Therefore, clinicians should remain vigilant for the possibility of remote subdural hematoma when unexplained postoperative neurological deficits occur, particularly in elderly patients undergoing UBE procedures. Because of its rarity, the diagnosis may be easily overlooked unless a systematic stepwise evaluation is actively pursued. We recommend the following sequence : 1) emergent spinal MRI to evaluate the operative site, 2) brain work-up to exclude intracranial pathology, 3) assessment for pathology at the level of the neurological deficit itself (e.g., hip or peripheral joint problems), and 4) careful consideration of remote spinal lesions beyond the operative site. We hope that the two cases presented in this study will raise awareness, provide a practical diagnostic framework, and ultimately facilitate earlier recognition and management of this rare but significant complication.
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