|Year : 2021 | Volume
| Issue : 3 | Page : 103-106
Lumbar spinal epidural hematoma without vertebral fracture causing cauda equina syndrome
Tsung-Mu Wu1, Tien-Yu Chiang2, Po-Chang Huang1, Kin-Weng Wong1
1 Department of Orthopedic, Chi-Mei Medical Center, Taichung, Taiwan
2 Department of Orthopedic, Chi-Mei Medical Center; Department of Orthopedic, An-Nan Hospital, China Medical University, Taichung, Taiwan
|Date of Submission||03-Sep-2020|
|Date of Decision||16-Oct-2020|
|Date of Acceptance||21-Dec-2020|
|Date of Web Publication||12-Jun-2021|
Department of Orthopedic, Chi-Mei Medical Center, No. 901, Zhonghua Road, Yongkang District, Tainan
Source of Support: None, Conflict of Interest: None
Spinal epidural hematoma (SEH) is a rare disease and may lead to spinal cord compression. It could be caused by trauma, including iatrogenic procedures such as spinal surgery or spinal anesthesia or by spontaneous events related to coagulopathy or arteriovenous malformation. Once SEH is suspected clinically and confirmed by image modalities, it should be emergently decompressed by surgical intervention. Prognosis depends on the rate of symptoms development, interval from symptom onset to surgery, level of spinal involvement, and degree of neurological deficits. Here, we report the case of a 79-year-old female who sustained a fall months before admission, presented with a 3-day history of back and bilateral lower limbs weakness. Radiography and magnetic resonance imaging demonstrated epidural hematomas at the level of T12 to L2 without associated vertebral fracture. An urgent decompressive laminectomy with blood clot removal was performed immediately. Postoperatively, her neurologic deficits improved significantly except for residual numbness.
Keywords: Cauda equina syndrome, laminectomy, spinal epidural hematoma, spinal fracture
|How to cite this article:|
Wu TM, Chiang TY, Huang PC, Wong KW. Lumbar spinal epidural hematoma without vertebral fracture causing cauda equina syndrome. Formos J Surg 2021;54:103-6
|How to cite this URL:|
Wu TM, Chiang TY, Huang PC, Wong KW. Lumbar spinal epidural hematoma without vertebral fracture causing cauda equina syndrome. Formos J Surg [serial online] 2021 [cited 2021 Jul 24];54:103-6. Available from: https://www.e-fjs.org/text.asp?2021/54/3/103/318212
| Introduction|| |
Spinal epidural hematoma (SEH) is a relatively rare disease that was first described by Jackson in 1869. The first case successfully treated surgically was reported by Jonas, who performed a laminectomy to remove the epidural blood clot. SEH usually presents with sudden onset of back pain, followed by neurologic deficits due to the spinal cord or nerve root compression. Early diagnosis and prompt management correlate with good outcomes, but the disease still remains a challenge for physicians. Here, we report a case of SEH several months after an episode of minor trauma over thoracolumbar segments causing cauda equina syndrome.
| Case Report|| |
A 79-year-old Taiwanese female was brought to our emergency department with the complaint of sudden onset of low back pain and lower limb weakness for 3 days; in addition, she also complained of numbness over both of her thighs. The symptoms progressively worsened over time. She had been on various medications for hypertension but denied taking anticoagulants. She recalled that she had an accidental fall from standing height and landed on her back about several months ago. After the fall, she was able to ambulate and noted only mild low back pain, so she did not seek medical advice. However, days before this admission, she gradually developed bilateral lower extremity weakness and numbness. A physical examination was significant for weakness in bilateral lower limbs with muscle power scored as 2/5 (move with gravity eliminated). Digital rectal examination showed normal anal sphincter squeeze tone. The bowel sound was normoactive and urination was smooth and without incontinence after Foley catheter removal. Laboratory data showed no leukocytosis and no coagulopathy (normal prothrombin time, activated partial thromboplastin time, and international normalized ratio). There was no vertebral fracture or dislocation on the radiographs. Due to the severe neurological compromise, emergent magnetic resonance imaging (MRI) of the thoracolumbar spine was taken the day of admission and revealed an epidural fusiform mass at the right posterolateral aspect of the spinal canal, extending from T12 to L2 levels. The mass had a mixed intensity on T1- and T2-weighted images, consistent with blood clots at different stages of organization. The size of the lesion was more than 75% of the cross-sectional area of the cord on axial imaging [Figure 1] and [Figure 2]. SEH was highly suspected. Emergency operation with laminectomy and evacuation of the epidural hematoma was performed to relieve the cauda equina syndrome. During the surgery, the blood clot appeared organized and could not be suctioned easily because of firm adherence to the spinal cord. Therefore, we removed the hematoma piece by piece gently with dissector instruments [Figure 3]. Pathologic report confirmed hematoma without tumor cell or abnormal blood vessels. Three days after the operation, her motor symptom improved significantly (muscle power: 2/5–5/5) with residual numbness, and the back pain was also relieved. At 1-month outpatient follow-up, she could ambulate without assistance. The final diagnosis is posttraumatic SEH because of the history of significant injury event and the similar back pain symptoms before cauda equina syndrome developed, as well as the pathological proof of hematoma.
|Figure 1: T1-weighted axial and sagittal magnetic resonance image of the thoracolumbar spine|
Click here to view
|Figure 2: T2-weighted axial and sagittal magnetic resonance image of the thoracolumbar spine|
Click here to view
| Discussion|| |
SEH is a collection of blood in the potential space between the dura and the bone. Significant bleeding can lead to spinal cord damage, causing neurological deficits, which requires emergency management.
However, the overall incidence is unclear. According to the literature reviewed, SEH was more prevalent in males than female patients, and the distribution of cases according to age showed that SEH was more prevalent in the second and sixth decades of life. SEH could occur in any segment of the spinal column, but the most common sites affected were the cervicothoracic vertebrae, with rare involvement of the sacral canal. It mainly extended over consecutive vertebrae and cases involving either a single vertebra or the entire length of the spine were extremely rare. In addition, posttraumatic SEHs that occur in the thoracic spine could be symptomatic with smaller hematomas because of the anatomically narrower canal of the thoracic spine compared to that of the cervical or lumbar spine.
The etiology of SEH is generally divided into spontaneous and traumatic causes. Vascular malformation accounts for 14% of spontaneous SEH, and the most frequently reported type of vascular malformation is arteriovenous malformation. Other causes of spontaneous SEH include coagulopathies, anticoagulant therapy-related causes, and prolonged Valsalva maneuvers. The traumatic cause is less common than spontaneous lesion. Traumatic causes include vertebral fractures related event and iatrogenic procedures such as obstetrical birth trauma, lumbar punctures, postsurgical bleeding, and epidural anesthesia. Iatrogenic procedures related event was relatively rare and contribute only 0.1%–1% to the SEH.
The pathophysiologic mechanism of SEH remains obscure. The current literature supports both venous and arterial origins as the source of epidural hematomas. The most widely accepted hypothesis for the source of bleeding is venous owing to the fact that spinal epidural veins have no valves and are thus unprotected from changes in abdominal and thoracic pressure. According to the hypothesis proposed by Bruyn and Brosma, increased intrathoracic and intra-abdominal pressure leads to brief increase in intravenous pressure in valve-less and thin-walled epidural veins subsequently leading to their rupture. However, others assumed that bleeding is from arterial rupture, especially in the cervical region, owing to low epidural venous pressure. In our case, due to the relatively large-sized hematoma and the mixed intensity on T1- and T2-weighted images, we think it is likely from arterial source.
The clinical picture of posttraumatic SEH is a sudden onset of severe back pain or radicular pain, exacerbated by percussion of the spine or by movements that increase intraspinal pressure. The duration between onset of symptoms and inciting event varies from minutes to months. Progressive spinal cord compromise can lead to paraplegia, quadriplegia, cauda equina syndrome, or even death.
A plain film can detect the associated compression or burst fracture and computed tomography myelography is the classic diagnostic study. However, MRI is the gold standard imaging modality and is superior to CT as it helps define the extent, volume, and precise location of the hematoma. In the first 24 h, the hematoma is usually isointense or slightly hyperintense on T1-weighted image and hyperintense on T2-weighted image. After 24 h, the hematoma becomes mostly hyperintense on both T1- and T2-weighted images.
The differential diagnosis of patients with intense neck or back pain and progressive neurological deficits is extensive and includes spontaneous SEH, other intradural hemorrhages, pathologic fracture, spinal tumor, prolapsed intervertebral disk, dissecting aortic aneurysm, anterior spinal artery syndrome, transverse myelitis, spinal vascular malformation, spinal epidural abscess, and spondylitis.
Although SEH in some patients with mild neurologic symptoms could be successfully managed with conservative treatment, early surgical decompression is still the treatment of choice for SEH. The postoperative neurologic function is related to preoperative neurologic function and the time interval to decompression. Delay in surgical management can lead to permanent neurologic sequelae.
In conclusion, posttraumatic SEH is a rare entity and remains a challenge for clinical physicians. MRI is the best imaging modality choice for early diagnosis. Urgent surgical decompression with the evacuation of hematoma could improve some neurologic deficits, especially vital cord functions.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initial will not be published and due efforts will be made to conceal the identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Jackson R. Case of spinal apoplexy. Lancet 1869;2:5-6.
Jonas AF. Spinal fractures, opinions based on observations of sixteen operations. JAMA 1911;9:859-63.
Domenicucci M, Mancarella C, Santoro G. Spinal epidural hematoma: Personal experience and literature review of more than 1000 cases. J Neurosurg Spine 2017;27:198-208.
Riaz S, Jiang H, Fox R, Lavoie M, Mahood JK. Spontaneous spinal epidural hematoma causing brown-sequard syndrome: Case report and review of the literature. J Emerg Med 2007;33:241-4.
Foo D, Rossier AB. Post-traumatic spinal epidural hematoma. Neurosurgery 1982;11:25-32.
Awada A, Russell N, al Fayez N, Naufal R, al Kohlani H. Spontaneous cervical epidural hematoma: Case report. Spinal Cord 1998;36:71-2.
Bruyn GW, Bosma NJ. Spinal extradural hematoma. In: Vinken PJ, Bruyn GW, editors. Handbook of Clinical Neurology. Amsterdam: North-Holland Publishing; 1976. vol 26, p. 1-30.
Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: A literature survey with meta-analysis of 613 patients. Neurosurg Rev 2003;26:1-49.
Dinsmore AJ, Leonard RB, Manthey D. Spontaneous spinal epidural hematoma: A case report. J Emerg Med 2005;28:423-6.
Yi S, Yoon DH, Kim KN, Kim SH, Shin HC. Postoperative spinal epidural hematoma: Risk factor and clinical outcome. Yonsei Med J 2006;47:326-32.
[Figure 1], [Figure 2], [Figure 3]