Dural injury is an avoidable complication of spine surgery. A serious sequela associated with dural injury is remote cerebellar hemorrhage (RCH), which causes intracranial hemorrhage. Although there are reports of RCH due to intended or unintended dural tears [1, 2], such as from surgery for intradural tumors, we found no reports of RCH after spinal surgery in which dural injury was absent. In this report, we describe a rare case of a patient who developed a consciousness disorder immediately after lumbar spine surgery. Even though there was no apparent dural injury, an intracranial hematoma was found. Further, we discuss the reasons for the intracranial hematoma.

An 80-year-old man came to our hospital with chief complaints of low back pain and leg pain. He had no muscle weakness in his lower extremities. He was diagnosed with lumbar spinal canal stenosis after various examinations including magnetic resonance imaging (MRI) (Fig. 1). One month after the initial visit, he was admitted for an examination and underwent myelography and root block. As the pain improvement was temporary, the patient requested surgery for the improvement of symptoms. He had a history of a right capsular hemorrhage treated conservatively 9 years earlier; however, there were no sequelae. There was no subsequent episode of falls. In addition, there was no history of heavy alcohol consumption. Before lumbar spine surgery, the patient was in a normal state of consciousness and was able to communicate normally. Lumbar posterior slow pressure fusion (L4/5 transforaminal lumbar interbody fusion) was performed 2.5 months after the initial diagnosis (Fig. 2). The procedure was performed under general anesthesia in a prone position with an anesthesia time of 4 h 18 min and an operation time lasting 2 h 50 min. The associated blood loss was 34 mL and the operation was completed without complications such as an intraoperative dural tear. There were no significant changes in vital signs perioperatively. After surgery, he was unable to move his limbs according to the instructions, although he was able to open his eyes due to pain stimulation. However, there were no abnormalities in his respiration or vital signs, and he was extubated. He was considered to be poorly awake due to anesthesia, and he was shifted to the ward. However, several hours post-surgery, his state of consciousness did not improve from the very low Glasgow coma scale (GCS) (E4V1M1). Computed tomography (CT) scan of the head taken to identify the cause of prolonged loss of consciousness showed a chronic subdural hematoma with some fresh hemorrhage (Fig. 3a). The patient developed generalized tonic chronic convulsions and anticonvulsant drugs were administered and the seizures stopped. The patient consulted a neurosurgeon and underwent emergency perforator drainage under local anesthesia on the same day. The drained blood also contained fresh hemorrhage (Fig. 3b). The day after surgery, he was still unconscious with GCS 6 (E4V1M1), therefore, head MRI and an electroencephalogram (EEG) were performed. MRI showed a small hemorrhage on the surface of the brain, but there was no evidence of a cerebral aneurysm or cerebral infarction (Fig. 4). The EEG revealed that he was in a state of epileptic agglutination, which was the likely cause of unconsciousness. No cerebrospinal fluid (CSF) drainage was observed from the lumbar spine surgical drain; hence, it was removed 2-day postoperatively. Despite the adjustment of anticonvulsant medications, the patient continued to suffer from prolonged loss of consciousness. A multifocal subdural hematoma that could not be removed during initial surgery was considered the cause of prolonged epileptic convulsions. A craniotomy was performed 14 days after the initial surgery to remove the hematoma (Fig. 5a). The day after the craniotomy, he was able to speak. His consciousness gradually improved, and 3 months after the surgery, his speech improved. In addition, he was able to walk on parallel bars and was transferred to a rehabilitation hospital (Fig. 5b).

A typical complication of spine surgery is intraoperative dural injury. Leakage of CSF due to dural injury may lead to the appearance of hypomyelination syndrome, wound infection, respiratory complications, ileus, deep vein thrombosis, meningitis, epidural hematoma, prolonged hospital stay, and rehospitalization [3, 4, 5, 6, 7, 8]. In addition, a serious complication resulting from a dural injury is RCH [1, 2]. It has been reported that the cause of RCH is the flexion and occlusion of subdural veins due to downward traction of the brain caused by leakage of spinal fluid. This may be attributed to dural injury, and vascular disruption caused by an increased difference in pressure gradient between intracranial vessels and intrathecal pressure [9, 10, 11]. Even though, there was no intraoperative dural injury and no obvious post-operative CSF leakage, we discuss the reasons for the intracranial hemorrhage in our case. We believe that intracranial vascular fragility was the cause of acute subdural hematoma. The fragility of the blood vessels is suggested by the chronic subdural hematoma that occurred despite the absence of major trauma, and by the history of the conservative treatment of capsular hemorrhage. The fluctuating difference between intracranial vascular pressure and intrathecal pressure in the vulnerable vessels was the direct cause of the acute subdural hematoma. It is believed to be a combination of both intrathecal pressure changes due to spinal decompression surgery ^[12] and intracranial intravascular pressure changes caused by blood pressure fluctuations during intubation, intraoperative, and extubation. Surve et al. have shown that blood pressure fluctuation is greater under general anesthesia than under local anesthesia in surgery for chronic subdural hematoma ^[13]. Another possible cause of subdural hemorrhage is CSF leakage due to an undetected dural tear. However, the absence of CSF leakage from the post-operative drain and the lack of obvious fluid retention in the surgical site on the post-operative lumbar CT scan suggest that this was not the cause. In addition, the coagulation system was examined for the cause, and no abnormality was found in the blood sample.

This case report describes a post-operative intracranial hemorrhage resulting in impaired consciousness in a spinal surgery without dural injury. The fragility of intracranial blood vessels can cause new intracranial hemorrhage even under the influence of decompression surgery or general anesthesia. In this case, no pre-operative findings suggested intracranial disease; therefore, the presence of a chronic subdural hematoma could not be suspected beforehand. However, in the future, imaging studies such as a head CT scan may be required before spinal surgery if there is a history of intracranial hemorrhage or if an intracranial lesion is suspected on pre-operative assessment. Depending on the results, neurosurgical consultation and intervention may be required.

RCH is a rare but serious complication in spine surgery. RCH can occur even in surgeries without dural injury and pre-operative CT imaging of the head is useful in assessing intracranial vascular fragility.