|
 
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| ORIGINAL ARTICLES |
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| Year : 2022 | Volume
: 5
| Issue : 2 | Page : 222-230 |
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Surgical management of aggressive vertebral hemangioma: Case series and review of literature
Selvin V Prabhakar1, Christopher Gerber1, Anindya Basu1, Dipendra K Pradhan1, Sukalyan Purkayastha2
1 Department of Spine and Neurosurgery, I-NK, Institute of Neurosciences, Kolkata, West Bengal, India
2 Department of Interventional Radiology, I-NK, Institute of Neurosciences, Kolkata, West Bengal, India
| Date of Submission | 25-May-2021 |
| Date of Decision | 12-Aug-2021 |
| Date of Acceptance | 18-Nov-2021 |
| Date of Web Publication | 08-Jun-2022 |
Correspondence Address:
Selvin V Prabhakar
Department of Spine and Neurosurgery, I-NK, Institute of Neurosciences, Kolkata
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/isj.isj_48_21
Background: This study includes management of aggressive vertebral hemangioma (VH). VH is the most common primary tumor affecting the vertebral column. In 0.9–1.2% of patients, VH can become symptomatic and is termed as “aggressive vertebral hemangiomas.” They usually require surgery along with adjuvant modalities. Due to its relatively low incidence, there is sparse reporting in the open literature and lack of universal consensus on treatment protocol. We would like to present our institutional experience in managing aggressive VH by surgery along with adjuvant modalities and a comprehensive review of the literature. Materials and Methods: A retrospective review of records of VH cases managed surgically in the past 3 years at our institute was done. All the relevant records and imaging of the patients were retrieved. Results: Five patients were included in the study. All were male with four dorsal and one lumbar lesion. All were treated with surgery along with an adjuvant therapy. Selective arterial embolization was used in one patient, alcohol ablation in three, and vertebroplasty in one. Only one patient had gross total resection, and others had only decompression. Fixation was done in all. All showed good clinical improvement without any complications, except in one. Conclusion: Aggressive VH often requires surgery. Currently, a decompression surgery is preferred due to less morbidity with good clinical outcomes. Various adjuvant therapies have been described in literature to be used perioperatively; yet there is no universal consensus on a standard protocol. Each of them has its own advantages and limitations and thus needs to be carefully selected on an individual basis. Alcohol ablation is an established adjuvant modality, but has to be used with caution. Keywords: Aggressive vertebral hemangioma, alcohol ablation, embolization, pedicle screw fixation, radiotherapy, vertebral hemangioma, vertebroplasty
How to cite this article:
Prabhakar SV, Gerber C, Basu A, Pradhan DK, Purkayastha S. Surgical management of aggressive vertebral hemangioma: Case series and review of literature. Indian Spine J 2022;5:222-30 |
How to cite this URL:
Prabhakar SV, Gerber C, Basu A, Pradhan DK, Purkayastha S. Surgical management of aggressive vertebral hemangioma: Case series and review of literature. Indian Spine J [serial online] 2022 [cited 2023 Apr 1];5:222-30. Available from: https://www.isjonline.com/text.asp?2022/5/2/222/346969 |
| Introduction | |  |
Vertebral hemangiomas (VHs) are benign neoplasms of endothelial cells within bone marrow. Though classified as neoplasms, they have less aggressive histopathological features, hence also referred to as hamartomas or vascular malformations.[1] VHs are most common primary tumors affecting vertebral column. VHs are reported to be approximately 2–3% of all spinal tumors, but there is a cadaveric study showing an incidence rate of up to 10–12%.[2] They are usually asymptomatic and often present as an incidental finding on imaging studies.[3] Only 0.9–1.2% of patients with VH do become symptomatic. Symptoms range from pain to neurological complications.[3] These symptomatic lesions are usually classified into Enneking Stage 3 and are termed as “aggressive vertebral hemangiomas.”[4]
Due to their relatively low incidence, there is sparse reporting in the literature and lack of universal consensus on treatment protocol. We performed surgery along with adjuvant modalities such as transarterial particulate embolization, vertebroplasty, and intra-operative, intralesional alcohol ablation. We also reported our experience of an unforeseen complication in one of the patients in whom intralesional alcohol ablation was done, which has not been documented in literature to the best of our knowledge.
| Case Series | | |
A retrospective review of OT records for VH cases managed by surgery in the past three years at our institute was done. We found records of five such patients. All the relevant records were retrieved from Medical Records Department and images downloaded from PACS. Detailed clinical findings, radiological findings, methods of management, surgical steps, and prognosis were compiled for each patient. Diagnosis of VH was based on magnetic resonance imaging (MRI), and all patients were managed surgically with one or more adjuvant therapy. A PubMed search using keywords such as vertebral hemangioma, aggressive vertebral hemangioma, absolute alcohol, pedicle screw fixation, embolization, laminectomy was performed and relevant literature review is reported. The case details are summarized in [Table 1]. | Table 1: Summary of patient demographic, clinical characteristics, and management
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Case 1
A 63-year-old male presented with pain in both lower limbs, right more than left, for past 5 months. He also had associated back pain and progressive weakness of right lower limb for 4 months. On clinical examination, power in right lower limb was grade 4/5. MRI showed lesion arising from posterior part of body of L3, extending into epidural space causing canal stenosis. It was hyperintense on T2, iso-to-hyperintense on T1 and showed homogeneous contrast enhancement [Figure 1A]. | Figure 1: Case 1. (A) Sagittal and axial T2 hyperintense extradural lesion from posterior L3 body, extending into epidural space causing severe compression of thecal sac and crowding of cauda equina. Axial intense homogeneous post-contrast enhancement seen. (B) Pre-embolization angiogram—prominent vascular blush from feeding artery at L3. Reduction of blush was seen after embolization with PVA. (C) Post-operative antero-posterior and lateral X-ray of lumbar spine showing L2 and L4 pedicle screw fixation. (D) Microphotograph of intra-operative biopsy done after embolization shows fibro adipose tissue with a cluster of back-to-back arranged vascular channels. (E) Post-operative T2 sagittal and axial cuts showing small residual component of lesion with adequate decompression
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Lumbar arterial angiogram showed a tumor blush at L3; left L2 and bilateral L3 radicular artery embolization was done using PVA particles by our interventional radiologist. Reduced vascular blush was seen after embolization [Figure 1B]. Following embolization, the patient was taken up for surgery; L3 laminectomy, gross total resection of tumor, and instrumented fusion of L2–L4 was done [Figure 1C]. Intra-operative blood loss was 600 mL. Diagnosis was confirmed by histopathological examination [Figure 1D]. Postoperative MRI done showed small residual-enhancing component of lesion with adequate decompression [Figure 1E]. Physical therapy and rehabilitation were started. At the final follow-up, the patient had power of grade 5/5 in both lower limbs and no associated back or leg pain and was able to walk without any difficulty.
Case 2
A 14-year-old male presented with a history of gradual progressive weakness, intermittent pain in lower limbs for 5 years, and inability to walk with urinary retention for past 10 months. Two years ago, he was started on antitubercular treatment (ATT) based on radiological suspicion of Pott’s spine elsewhere; clinically, he continued to worsen. At presentation, he had spastic paraplegia with grade 1/5 motor power in both lower limbs and reduced sensation below D6 dermatome. MRI with contrast was done which showed hyperintense (STIR and post contrast) D4-D6 vertebral body with a paravertebral soft tissue component and cord signal changes in T2 extending from D2 to D8 [Figure 2]. Surgery was performed with a standard posterior midline approach; transpedicular Jamshidi needles were inserted into D5 and D6 body. Gush of fresh blood was seen oozing once stellate was removed. Absolute alcohol was injected into the body in small increments of 1 cc at 1-to-2-min interval until the gush of blood stopped, indicating completion of ablation. D4 and D5 laminectomy and decompression with D3 to D6 posterior instrumented fixation were done. Intra-operative blood loss was 500 mL. Rehabilitation protocol was started. In postoperative final follow-up, the power was grade 2/5–3/5 in lower limbs; there was significant improvement in sensations and complete recovery of bladder and bowel control. | Figure 2: Case 2. Sagittal STIR and post-contrast sagittal and axial images showing hyperintense signal in D4-D6 vertebra with paravertebral soft tissue component. Cord signal changes from D2 to D8 seen
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Case 3
A 23-year-old male presented with complaints of progressively worsening weakness of both lower limbs for 10 months, inability to walk and urinary incontinence for past 2 months. He had severe spasticity of both lower limbs (MAS grade 4), and gross power was grade 3/5 with reduced peri-anal sensations. MRI showed T1 and T2 hyperintense D2 vertebra with bulging of posterior cortex causing cord compression and myelopathic changes in T2 [Figure 3]A. The patient was managed surgically. D2 intralesional alcohol ablation and decompression with instrumented fixation were done. Intra-operative blood loss was 150 mL. Post-operative day 1, the patient had developed a flaccid paraplegia with a new onset weakness of both upper limbs. Clinically, he had power of grade 0/5 in both lower limbs, grade 1/5 in the left, and 3/5 in the right upper limb. He had impaired sensations below D3 dermatome. Post-operative MRI showed an increase in extent of T2 hyperintense signal involving ventral aspect of upper dorsal cord and also newly developed signal changes in adjoining cervical cord [Figure 3]B. The patient was started on rehabilitative care; on final follow-up (6 months post-op.) his power had improved to grade 4/5 power in the right upper limb, grade 2/5 in the left upper limb, but his bilateral lower limb power was grade 0/5 with persisting sensory deficit and bladder involvement. | Figure 3: Case 3. (A) Sagittal post-contrast images with hyperintense signal of D2, soft tissue tumor component causing cord compression, and signal changes suggestive of myelopathy. T2 axial image showing significant cord compression. (B) Post-operative T2 sagittal and axial images showing newly developed T2 hyperintense signal of ventral aspect of upper dorsal and adjoining cervical cord. Adequate decompression with reduced T2 hyperintensity of D2 vertebra seen
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Case 4
A 27-year-old male presented with complaints of back pain for one year, weakness of both lower limbs and difficulty in walking (Nurick 4) for 4 months. Clinical examination showed grade 3/5 to 4/5 motor power in both lower limbs without any sensory involvement. MRI showed T2 hyper-, T1 hypointense and contrast-enhancing lesion of D10 with epidural component causing cord compression and edema [Figure 4]A. The patient was managed surgically with D10 intralesional alcohol ablation and decompression; D8, D9, D11, and D12 instrumented fixation was done [Figure 4]B and C. Intra-operative blood loss was 300 mL. Standard rehabilitative protocol was started. On final follow-up, he had power of grade 5/5 in lower limbs, no pain, no sensory disturbance, and walking independently (Nurick 2). He had mild spasticity of lower limbs, which was well controlled with medications. | Figure 4: Case 4. (A) Sagittal and axial post-contrast images showing enhancing D10 lesion with cord compression and edema. (B) Intraoperative images of intralesional injection of absolute alcohol via bilateral transpedicular approach and D10 decompression and D8, D9, D11, D12 pedicular screw fixation. (C) Post-operative anteroposterior and lateral X-ray showing D8, D9, D11, D12 instrumented fixation
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Case 5
A 35-year-old male presented with complaints of low back pain and tingling of lower limbs for 3 months with associated neurogenic claudication. Three years ago, he had similar complaints when he was diagnosed to have L4 vertebral hemangioma and was managed with image guided arterial embolization and percutaneous alcohol ablation, done at another institute. On examination, the patient had no gross sensory motor deficit or local findings. MRI showed T1 and T2 hyperintense L4 vertebrae with heterogeneous enhancement in post-contrast images [Figure 5]A. There was an L4 body cortical breach posteriorly by the tumor mass causing stenosis of canal and foramina. Diagnosis of recurrent VH of L4 vertebra was made. In a staged management approach, initially a bi-pedicular vertebroplasty was done under local anesthesia and about 11 cc of bone cement was injected, almost completely filling the vertebral body [Figure 5]B. On the following day, L4 decompression and L3 and L5 fixation were done and ventral epidural soft tissue tumor component was ablated with bipolar cautery [Figure 5]C. Intra-operative blood loss was about 500 cc. During the last follow-up, his neurogenic claudication, walking distance, and walking time had significantly improved. | Figure 5: Case 5. (A) Post-contrast sagittal and axial images showing L4 with heterogeneous enhancement. Posterior cortical breach with an enhancing epidural tumor component causing secondary canal stenosis. (B) Image guided bi-pedicular vertebroplasty with almost complete filling of vertebral body. (C) Post-operative X-ray of L4 vertebroplasty with decompression and L3, L5 instrumented fixation
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| Discussion | | |
In 1863, Virchow first reported VHs, but neurological symptoms caused by VH were first described by Gerhardt in 1895. In 1927, Makrykostas had described that epidural extension of lesion resulted in neurological symptoms due to spinal canal stenosis.[5]
Incidence of VHs is higher in women. Higher incidence of symptomatic VH is seen during the last trimester of pregnancy and young adults.[6] Common site is thoracic spine followed by the lumbar spine.[7],[8] VHs involve a single vertebra in 2/3, and in 1/3 two to five vertebra are involved.[7],[8] They have varied presentation depending on the location, the degree of cord, or nerve root compression.[9]
Based on the lesion morphology and symptoms, VHs are classified into four types, type IV being most aggressive and symptomatic.[10] Type III and type IV belong to Enneking grade 3[11] and are more likely to involve the entire vertebral body, have soft tissue component, and extend into the posterior elements and spinal canal.[12] In this article, aggressive VHs refer to type IV VH. Histopathalogically, VHs can be of three types, namely, cavernous, capillary, or a mixed type.[13],[14],[15]
Aggressive VHs cause symptoms through spontaneous epidural hemorrhage, pathological fracture,[16] expansile lesion stretching the periosteum or spinal canal stenosis. Some of the radiological differential diagnosis includes aneurysmal bone cyst, bone metastases, lymphoma, multiple myeloma, osteosarcoma, and Paget’s disease.[17] Classical finding of VH in plain radiograph is “corduroy sign,” and CT scan is “polka dots”. Computed tomography best defines bony erosions and pathological fracture. MRI with contrast is gold standard, with hyperintense T1 and T2 signal and classical post-contrast enhancement and intra-osseous signal voids,[18] similar to findings of our cases. MRI helps to assess soft tissue involvement, spinal canal extension, compression of cord and nerve root (features of aggressive VH). Spinal angiography has both diagnostic and therapeutic indications.[19] It helps in determining the vascular supply of hemangioma, spinal cord, and therapeutic transarterial embolization. Imaging findings of an unstable fracture in CT or tumor extending into canal with significant cord/nerve root compression in MRI might favor a surgical intervention.
Despite our long-standing recognition and extensive knowledge about aggressive VH, controversy regarding the optimal treatment still exists. Numerous therapeutic options have been tried with varying degrees of success and complications. There is still no universally accepted protocol/management strategy for aggressive VHs. They usually require surgery along with adjuvant therapies, either alone or in a combination depending on the lesion, patient symptoms, surgeon’s preference, and response to treatment. Access to inhouse interventional radiology services and costs involved are also important factors in deciding the modality of adjuvant treatment in aggressive VH. All of our cases were of type IV VH requiring surgical management with adjuvant therapy. We did pre-operative transarterial embolization and vertebroplasty in one case each and intra-operative, intralesional absolute alcohol ablation in the other three cases. Relevant literature for each of these modalities has been further discussed.
| Endovascular Embolization | | |
One of the dreadful surgical complications of VH is uncontrollable hemorrhage as it is highly vascular.[20],[21] Transarterial embolization is an universally accepted, safe, and effective procedure to deal with this dreadful complication.
Some of the earlier studies to recommend endovascular embolization for VH reporting good outcomes were by Gross et al.[22] in 1976 and Hekster and Endtz[23] in 1987. In 1990, Raco et al.[24] advocated for embolization as isolated treatment modality in select cases, which was contradicted by Smith et al.[25] in 1993 and Kiroglu et al.[26] in 2009. A series of significant studies including Cotten et al.[27] in 1996, Acosta et al.[28] in 2006, up to recent study by Prabhuraj et al.[29] in 2019 advocate the use of transarterial embolization before surgery.
The transarterial embolizing agents used in general are broadly classified into solids and liquids. Solid agents include PVA (polyvinyl alcohol particles), coils, and gel foam. Liquid agents consist of NBCA glue (n-butyl cyanoacrylate) and EVOH copolymer (ethylene vinyl-alcohol copolymer). Most preferred and commonly used embolizing agent for aggressive VH is PVA. An interventional radiologist does the procedure under image guidance following a digital subtraction angiography to look for the feeding vessels of the tumor. Despite embolization being a safe procedure, main disadvantage is unavailability of resource in abundance and cost factor involved, thus limiting its use. One contraindication of embolization is when feeding vessels supplying the hemangioma supplies the artery of Adamkiewicz as well. During embolization, one must be very cautious of reflux of the embolic material into the intercostal or lumbar arteries.[1],[30] In our series, we had performed pre-operative transarterial embolization as an adjuvant followed by surgical intervention in one patient.
Alcohol ablation
First documented procedure of ablation using ethanol was to produce angio-infarction of kidneys for uncontrolled hypertension.[31] One major concern of ethanol is it can rapidly “run off” into systemic circulation causing systemic side effects. In addition, it can also result in toxic necrosis of normal tissues adjacent to the site of usage when it spills over.[32],[33] Due to unique histopathological architecture of VH, arteriovenous shunting is rare and they have only low flow channels,[13],[14] which makes direct injection of embolizing agents like ethanol safe. The presence of low flow fistulas in VH does not allow rapid “run off” of alcohol, thus preventing shunting into systemic circulation and retention in local tissue allowing its embolizing and sclerosing action to take place.
Heiss et al.[34] in 1994 published the first report of VH treated by percutaneous CT-guided injection of absolute alcohol that showed good clinical results, which was also supported by Doppman et al.[35] More recently, in a study by Chandra et al.[36] in 2018, symptomatic VH was treated by intra-operative ethanol embolization, decompression, and instrumented fusion. They reported excellent clinical improvement and low re-operation rates. Complications included one patient with transient deterioration of neurology, which was similar to observations of Goyal et al.[1] and Yadav et al.[33] during use of alcohol ablation technique.
Niemeyer et al.[37] reported a case of Brown–Sequard syndrome, following percutaneous injection of alcohol which was permanent. This was similar to findings in our case 3 who developed new onset quadriparesis following intra-operative alcohol ablation. This complication could have been because of rare arteriovenous shunting in the tumor tissue, which allowed rapid retrograde extravasation of alcohol into anterior spinal artery via the feeding segmental artery, causing ischemic insult to cord territory supplied by anterior spinal artery. There were no associated intra-operative hemodynamic changes to suggest systemic alcohol toxicity. Post-operative MRI scans of case 3 showed newly developed cord signal changes on upper dorsal and adjoining cervical cord specifically on ventral aspect, supporting our theory. This MRI finding also correlated with clinical findings of the patient. No such complication has been reported in literature with use of intra-operative ethanol ablation till now.
Alcohol ablation has been used with good success in reliving neurological symptoms, but numerous complications have been reported including osteonecrosis, vertebral collapse, transient neurological deterioration, spinal cord injury, hemodynamic instability, and asystole.[1],[32],[33],[34],[35],[38] In spite of these complications, intra-operative ethanol ablation still remains a highly cost-effective, easily available technique, especially when resources for interventional radiologists are unavailable and in cases of economic constraints.
Surgery
Surgical intervention is one of the well-established modality of management, especially in aggressive VH. Majority of aggressive VHs have extraosseous tumor tissue and compression on neural structures causing neuro-deficit, hence warranting surgery. With use of adjuvant therapy like embolization, alcohol ablation, and vertebroplasty, the surgical morbidity and mortality have come down greatly making them a very safe option. Thus, their usage has grown exponentially with time. Historically en bloc resection was advocated mainly to prevent recurrence, but it had associated high morbidity and even mortality in few cases. Currently, the main aim of surgery in aggressive VH is decompression. Surgical options range from laminectomy, debulking, gross total resection, and total en bloc spondylectomy.[39] The choice varies depending on the position and extent of the tumor. Earlier studies by Fox and Onofrio[3] advocated subtotal resection and they reported recurrence of tumor in those patients who did not have any adjuvant radiotherapy. Later in studies by Bremnes et al.,[40] Cotten et al.,[27] Jayakumar et al.,[41] and Fourney,[42] only laminectomy with adjuvant therapy was done and they reported good results. Acosta et al.[28] in 2006 suggested transarterial embolization with laminectomy to be effective. It was similar to the findings published by Goldstein et al.[43] and Chandra et al.,[36] in which all patients underwent only decompression of neural structures.
All our patients had surgical intervention due to extraosseous tumor component with neural compression causing significant neurodeficit. Except for one case, in whom gross total resection was performed, all others had primarily a decompression surgery. Fixation was done in all to prevent post-operative iatrogenic instability due to extensive decompression and also further collapse of vertebra following adjuvant therapy due to necrosis of tumor. Our surgical strategy was in accordance with recent literatures,[27],[28],[36],[40],[41],[42],[43] which have shown that decompression surgery has given good outcome with reduced morbidity.
Surgical management of VH has associated significant morbidity, main causes being excessive intra-operative blood loss and post-operative hematoma. Hence, these patients should be thoroughly evaluated for any bleeding tendency and adequately optimized pre-operatively. The various adjuvant methods help to an extent in this problem. Other tips to tackle intra-operative blood loss are use of intra-operative tranexamic acid infusion, judicious use of hemostatic agents such as thrombin products, fibrin sealants, oxidized cellulose, gelatin foams, and collagen sponges. Maintaining optimal intra-operative blood pressure plays an important role to reduce blood loss. Average blood loss of our patients was around 400 mL. Meticulous hemostasis and closure of surgical site and use of negative suction drain help to reduce risk of post-operative hematoma. As these patients have a tendency to form delayed epidural hematoma, a close monitoring and frequent neurological charting is advisable for the first 24–48 h.
Radiotherapy
Low dose radiation (30–40 Gy) is used in the treatment of VH.[44] Their common indication for use is VH associated with pain and historically in post-operative cases where complete tumor excision was not possible. Recent advancement in adjuvant therapy and surgery has made post-operative radiotherapy almost obsolete. Use of radiotherapy in aggressive VH with significant neurology is controversial as they cause reduction in tumor size only after a delayed time period.[45] It is also more risky to use radiation on extraosseous tumor tissue because they lie close to neural structures and thus can cause radiation injury to neural tissue. Moreover, radiation carries the risk of radionecrosis and skin ulceration. We did not use radiation therapy in any of our cases.
| Conclusion | | |
VHs are most common primary vertebral tumors. They are grossly under-reported as they are asymptomatic in most. A small proportion of VHs are aggressive type IV lesion (Enniking grade 3) and are locally aggressive with extraosseous tumor component, causing neurological involvement in majority of the patients. Most of these patients require surgical intervention. There is no standardized methodology of surgery and use of adjuvant therapy in aggressive VH. In our limited experience, we prefer posterior approach, laminectomy, decompression, and excision of epidural/soft tissue component of tumor causing compression. The aspect of tumor recurrence and intra-operative blood loss was taken care with use of adjuvant therapy of vertebroplasty, alcohol ablation, and transarterial embolization. They have shown evidence to prevent/reduce recurrence rate as they cause necrosis of tumor cells and shrinkage of tumor. Intralesional alcohol ablation in spite of being an established adjuvant modality can at times cause catastrophic complications and hence should be used with caution.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Ethical policy and institutional review board statement
The article being a retrospective study was exempted from ethical approval.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1]
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