1 Introduction

A subdural hematoma complicating a spinal surgery is a rare occurrence and has only been reported in 20 cases.^1–15 Decompression surgery is occasionally performed to treat subdural hematomas; however, they are otherwise treated conservatively. Good recovery rates have been reported with conservative treatment.^3,5,8,10 However, to our knowledge, conservative treatment for a subdural hematoma case resulting in syringomyelia with neurological deficits has not been reported. Secondary acquired forms of syringomyelia due to trauma, vascular disturbances, infection, or tumor develop chronically, and in these forms, the neurological deficits develop after a while.^16,17 We present a rare case of a complication of syringomyelia after a minimally invasive spinal surgery.

2 Case report

A 43-year-old healthy man fell from a 3-m height while snowboarding. He presented with back pain and was unable to walk or sit. Because of severe back pain, his physical examination was limited, however no evidence of any neurological deficits at admission. A T12 chance fracture was diagnosed using X-ray and computed tomography (CT), showing the fracture line extending through the vertebral body and into the pedicle. Magnetic resonance imaging (MRI) revealed both the intradural sac lesion and spinal cord to be intact (Fig. 1). The patient had not been able to walk for 10 days despite conservative treatment with analgesics and a spinal brace because of the severe back pain caused by the chance fracture. Hence, we decided to operate. Percutaneous transpedicular vertebroplasty of T12 and posterior fixation with percutaneous pedicle screws of T11–L1 across T12 were performed (Fig. 2).

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Fig. 1 Computed tomography and magnetic resonance imaging at admission. The anterior column of the T12 vertebral body is compressed with horizontal fracture line extending through the pedicle (Arrows). Signals of the T12 vertebral body show low intensity on T1WI and high intensity on T2WI. The intradural sac lesion shows no signal change or mass, indicating that nothing was compressing the spinal cord. T1WI: T1-weighted images, T2WI: T2-weighted images.

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Fig. 2 X-ray immediately after surgery and Magnetic resonance imaging at a week postoperatively. X-ray front and lateral view show Percutaneous transpedicular vertebroplasty of T12 and posterior fixation with percutaneous pedicle screws of T11–L1 across T12. Sagittal T1WI and T2WI show high signal lesion in the dural sac. Axial T2-weighted image scan shows a high signal lesion ventrally compressing the spinal cord. T1WI: T1-weighted images, T2WI: T2-weighted images.

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3 Clinical findings

At 1 h postoperatively, the patient complained of bilateral thigh pain and lower extremity weakness. Medical Research Council scale for Manual muscle testing (MMT) Right/Left was Hip flexors (HF) 2/2, Knee extensors (KE) 2/2, Ankle dorsiflexors (AD) 2/2, Ankle plantar flexors (AP) 2/2. Patella tendon reflex and Achilles tendon reflex were not present. However, in the next few hours, his pain gradually improved and he was gradually able to move his ankles and toes increasing range of motion.

4 Diagnostic assessment

On MRI at a week postoperatively, T1-and T2-weighted images showed subdural high signal mass ventrally compressing the spinal cord and it was seen widely throughout the thoracolumbar region (Fig. 2). His paraparesis was diagnosed with a subdural hematoma.

5 Therapeutic intervention

Because his symptoms were in improving trend, he was treated conservatively with analgesics but without any anticoagulants. He could walk without any support at approximately two months postoperatively. MMT was HF 4/5, KE 4/5, AD 4/5, AP 4/5. Patella tendon reflex and Achilles tendon reflex were normal.

6 FOLLOW-UP and outcomes

However, at six months postoperatively, he again had paraparesis. He exhibited a spastic staggering gait and needed a cane for ambulation. He had hyperalgesia below the hypochondrium and urinary and fecal incontinence. Patella tendon reflex and Achilles tendon reflex were hyperactive. MRI at six months postoperatively revealed a cord-like structure providing traction on the thoracic spinal cord ventrally, in which a cavitary lesion extended from T5 to T11 (Fig. 3). His exacerbated paraparesis was considered to be resulted from syringomyelia via adhesive arachnoiditis. He underwent symptomatic therapy with medication, and the neurosurgeon who was also managing his condition suggested that syrinx drainage should be performed in case of neurological deterioration. There was no remarkable change in his symptoms with analgesics at two years postoperatively.

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Fig. 3 Magnetic resonance imaging at 6 months postoperatively. T2WI shows the cord-like structure providing traction on the spinal cord ventrally and a cavity extending from T5 to T11. T2WI: T2-weighted images.

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7 Discussion

This report presented a case of a T12 chance fracture, flexion distraction injury, without evidence of neurological deficits, in which posterior minimally invasive surgery fixation was performed. Immediately following the procedure, the patient complained of paraparesis due to a subdural hematoma. Because his symptoms were in improving trend, the patient was treated conservatively. At six months postoperatively, the patient developed leg weakness and urinary and fecal incontinence. MRI revealed adhesive arachnoiditis and syringomyelia.

A subdural hematoma complicating a spinal surgery is a rare occurrence. A literature review was performed to identify articles describing postoperative spinal subdural hematoma, querying PubMed using the search terms “postoperative,” “spinal subdural,” “hemorrhage,” or “hematoma,” for relevant articles up to the year 2024. References in the literature were also reviewed for additional sources. Only 20 cases having been previously reported (Table 1).^1–15 Among these cases, five cases underwent percutaneous vertebroplasty, which is similar to our case, and two cases were complicated by adhesive arachnoiditis. However, no case complicated by syringomyelia has been reported.

There are two potential mechanisms by which percutaneous vertebroplasty could cause subdural hemorrhage.¹ First, in percutaneous vertebroplasty, a hydroxyapatite block or cement is placed in the vertebrae, increasing the pressure of the vascular venous system between the internal and external vertebral venous plexus. Second, the prone position required during surgery can induce sudden episodes of increased intraabdominal or intrathoracic pressure, rupturing the venous plexus under the dura matter. Postoperative subdural hematoma can occur either immediately after surgery or several days later.¹⁵ While the reported cases present with symptoms such as sensory abnormalities, pain, and muscle weakness, there have also been a report of asymptomatic occurrences.¹⁸ The severity of symptoms and onset time of subdural hematoma could be varied depending on the degree of bleeding.

We hypothesize that a subdural hematoma causes syringomyelia in two ways: a cerebrospinal fluid (CSF) flow disorder and an ischemic change. The CSF flow is a pulsatile perfusion in the central canal, and the subarachnoid space of the spinal cord is predominately ventral, both in the longitudinal and horizontal planes.¹⁹ Therefore, a CSF flow on the ventral side diffuses subdural hemorrhage, and the hemorrhage is absorbed before forming a hematoma. However, once a massive hematoma has formed on the ventral side of the dura matter, it prevents diffusion and absorption of subdural hemorrhage and forms a larger hematoma. The retention hematoma leads to adhesive arachnoiditis between the dura and spinal cord. Adhesive arachnoiditis blocks CSF pulsatile flow perfusion from the choroid plexus of the cerebral ventricles in the subdural space, thus relatively forcing the blood to flow through the central canal of the spinal cord below the adhesion. This increases the pressure of the central canal, resulting in syringomyelia. Second, the central sulcal arteries diverging from the anterior spinal artery feed the gray matter of the spinal cord. Adhesive arachnoiditis prevents arterial circulation around the dura matter, including the sulcal arteries, inducing an ischemic change in the gray matter.²⁰ Adhesion in the ventral side of the spinal cord is a risk factor for syringomyelia because the anterior spinal artery may be potentially impaired (Fig. 4). Ben Nsir et al. reported a case of syringomyelia due to arachnoiditis caused by a spontaneous subdural hematoma, although the hematoma had been evacuated. The MRI in their case showed a hematoma on the ventral side, which caused arachnoiditis.¹⁶

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Fig. 4 Syringomyelia due to ischemic change. A: The blood supply to the gray matter is through the sulcal arteries originating from the anterior spinal arteries. B: Adhesive arachnoiditis (gray area) prevents the blood flow, resulting in ischemia of the gray matter, which causes syringomyelia. Upward is ventral side. Downward is dorsal side.

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Surgery and conservative treatment have been reported to manage a subdural hematoma after a spinal surgery with good recovery.^1–15 Conservative treatment cases showed the symptoms were in improving trend, with four out of five cases recovering without sequelae, and only one case remaining mild residual urinary dysfunction. Surgical treatment cases showed rapid and severe progression of paralysis. Seven patients had residual pain or paresthesia in the lower back or lower limbs, and only one patient had residual lower limb muscle weakness. Because the course and severity of symptoms differed between surgical and conservative treatment, the superiority of treatment methods is not clear. However, in cases of paralysis due to a subdural hematoma without improving trend, durotomy and evacuation of the hematoma may be options for decompression of the spinal cord.

In our case, the patient showed his symptoms were in improving trend, but developed syringomyelia with severe sequelae at six months. Although no preventive measures or satisfactory standard treatments for syringomyelia have been established, adhesiotomy or intravenous steroid injection for adhesive arachnoiditis and syrinx drainage for syringomyelia may be option.^16,17 Therefore, subdural hematomas should be closely followed up following treatment.

The strength of this case report is that it is the first to describe a complication of a syringomyelia after the formation of subdural hematomas following spine surgery. The syringomyelia was found at six months postoperatively during an outpatient visit. Previous reports^1–15 did not mention how long the cases were followed up. However, there is still the possibility of missing the syringomyelia owing to the short-term follow-up.

The approach to the present case is limited as the mechanism of pathogenesis is unknown. A spine fracture itself can cause adhesive arachnoiditis and syringomyelia.¹⁷ An iatrogenic injury, such as the penetration to the spinal cord, can also cause it. These injuries to the spinal cord and subarachnoid limit the CSF flow, resulting in the formation of a syringomyelia. However, in our case, the patient did not have any neurological deficit preoperatively, and MRI at admission did not show any abnormal intensity in the spinal canal and cord. In addition, postoperative CT and MRI did not show a needle trajectory to the spinal canal.

8 Conclusion

A conservatively treated case of subdural ventral hematoma after a spinal surgery complicated with adhesive arachnoiditis, resulting in syringomyelia with severe sequelae. Postoperative subdural hematoma may be considered closely followed up for appropriate and timely treatment of adhesive arachnoiditis and syringomyelia.

9 Take away lessons

Subdural hemorrhage rarely occurs after spinal surgery. Surgery and conservative treatment of the subdural hematoma have been reported with good recovery, while our case complicated with adhesive arachnoiditis leading to syringomyelia and severe sequelae. Patients may be considered followed up to avoid missed opportunities for early intervention for adhesive arachnoiditis or syringomyelia.

Informed consent

Informed consent was obtained from the patient for the publication of this case report.

Authors contribution

MA was a major contributor in supervising the manuscript. HH and HS are surgeons of the patient, and following up him. All authors read and approved the manuscript.

Ethical statement

This study was approved by the Institutional Review Board of Ibaraki Prefectural Central Hospital and was conducted according to the principles of the Declaration of Helsinki.

Funding statement

This work was not supported by any foundation.

Patient's consent

Informed consent was obtained from the patient for the publication of this case report.

CRediT authorship contribution statement

Michita Noma: is a corresponding author. Masato Anno: is a major contributor in supervising the manuscript. Hiroshi Shinbori: are surgeons of the patient, and following up him, All authors read and approved the manuscript. Hiroshi Hayashi: are surgeons of the patient, and following up him.