Perspective/Short Review: Diagnosis and Treatment of Aggressive Vertebral Hemangiomas and Review of 2 Cases

Abstract

Background:

Although vertebral hemangiomas (VH) are relatively common, aggressive symptomatic VH are rarely reported (i.e. in up to 11% of cases). Multiple other benign and malignant primary bone tumors must be considered in the differential diagnosis. Here, we review the clinical diagnosis and surgical management for aggressive hemangiomas, while also presenting 2 patients with thoracic lesions requiring posterior surgical decompression/fusion, with/without vertebroplasty, embolization, and/or CyberKnife radiosurgery.

Methods:

The classification system for these tumors ranges from Types I-IV; I Occupy < 50% of a vertebral body (VB), II-Occupy > 50% VB (IIb Thoracolumbar - Symptomatic), III-Occupy 100% VB, and IV-Occupy 100% VB involved plus extension into the pedicles, laminae, spinous process, and epidural space.

Results:

Radiographically (i.e. X-rays, MR, CT) these lesions originate in the vertebral bodies, but aggressive VH extend into the pedicles, laminae, spinous processes, and epidural space causing both spinal cord/root (i.e., myelopathy/radiculopathy)) compression. Surgical options include anterior, posterior, or circumferential decompressions with/without fusions, percutaneous vertebroplasty, embolization, radiation, and/or chemotherapy. Early treatment maximizes neurological recovery and limits/avoids permanent injury.

Conclusion:

Aggressive VH are rare lesions that most frequently occur in the thoracic spine. Notably, the subset of Type IV lesions that extend into the pedicles, laminae, spinous processes, and epidural space may cause symptomatic myelopathy/radiculopathy warranting early surgical intervention to optimize neurological outcomes.

INTRODUCTION

Although vertebral hemangiomas (VH) are relatively common, aggressive lesions are rare; reportedly only 11% become symptomatic.[1,4,6,7,9,10,12] Several authors have offered classification systems ranging from Types I-IV.[1,12] Multiple other both benign and malignant primary bone tumors enter the differential diagnosis.[5-7] These benign lesions typically radiographically (i.e. X-rays, MR, CT) originate in the vertebral bodies, but aggressive Type IV VH extend into the pedicles, laminae, spinous processes, and/or epidural space where the latter may cause spinal cord/root (i.e., myelopathy/radiculopathy) compression.[1,3-7,9,12] Early treatment is critical to maximize postoperative recovery and avoid permanent injury. Anterior and/or posterior decompressions with/without fusions and/or vertebroplasty may be warranted along with adjuvant therapies (i.e., embolization, radiation and/or chemotherapy).[2-11] Here, 2 patients with aggressive hemangiomas originating in thoracic vertebrae T6 and T2 respectively caused severe dorsolateral vs. ventrolateral cord compression warranting decompressive surgery/fusion with/without adjunctive percutaneous vertebroplasty (VP) and CyberKnife radiosurgery.

CASE STUDIES

Case 1

Clinical History and Radiological Studies

A geriatric patient presented with a chronic back pain increased at night and several months of increasing bilateral lower extremity weakness (4-/5). EMG’s of the upper and lower extremities were negative. The cervical X-rays/MR demonstrated mild C45/C56 spondylosis, while the lumbar X-rays/MR revealed L5S1 spondylolisthesis/bilateral L5 lysis without significant stenosis. However, thoracic X-rays, MR with/without contrast, and CT studies revealed a T6 vertebral body hemangioma [Figures 1-3]. MR T1 hyperintensity of the intraosseous tumor was consistent with the diagnosis of an aggressive hemangioma. Further the MR T6 vertebral mass extended bilaterally into the posterior elements with extraosseous/epidural extension into the right greater than left ventral, lateral, and dorsal epidural space (i.e., 3 cm cranial/caudal 9 x 8 mm) causing marked T5/T6-T6/T7 cord compression and a high cord signal. Additional hemangiomas were seen at several other levels but without aggressive features or neurological compromise.

Figure 1:

(a-b): Case 1: AP (a: facing double arrows), and Lateral (b: facing double arrows): thoracic X-rays demonstrated a T6 vertebral hemangioma.

Figure 3:

Case 1: Axial T2 weighted image showing T5/T6 disc space level of marked bilateral, lateral, and dorsal epidural cord compression from aggressive hemangioma (large single arrow).

Figure 2:

Case 1: Sagittal T2 weighted image demonstrating vertebral hemangioma (single arrow) ventrally and marked dorsal cord compression from extension of hemangioma into the epidural space (upper double arrows). Also note that the hemangioma additionally extended into the entire T6 spinous process (lower double arrows)

Surgery

The patient underwent a T5-T7 laminectomy and a bilateral T6 transpedicular approach for resection of extensive bilateral and dorsal/lateral intracanalicular resection of epidural hemangioma causing marked cord compression. A cement T6 kyphoplasty, and a T5-T8 posterior pedicle/screw fusion was performed under Neuro-Navigation (autograft/allograft) along with utilizing intraoperative neural monitoring. Under fluoroscopic guidance, T6 tumor resection was successfully accomplished utilizing the “eggshell type procedure”. The intraoperative blood loss was 700 cc. Postoperatively, the patient remained neurologically intact, and has since continued to recover months later. The patient is now being considered for postoperative follow-up CyberKnife Radiosurgery to address residual tumor in the T6 vertebral body.

Case 2

Clinical History and Radiological Studies

A geriatric patient presented with several months of increasing upper thoracic pain and gait imbalance following a motor vehicle accident. After chiropractic evaluation, they were referred to the emergency room where the neurological exam was normal. However, the MR (holospinal with/without contrast) and CT studies documented a T2 lytic lesion and a pathological fracture, with tumor extending into the posterior elements [Figures 4-8]. The MR further demonstrated marked right-sided ventral-right/lateral T1/T2 – T2/T3 epidural tumor extension markedly compressing the cord to the left (i.e., AO Bilsky Spinal Cord Compression (ESCC) Grade 3). There were other incidental typical hemangioma lesions involving the T4, T5, T9 levels; a T9 biopsy was diagnostic for hemangioma, thus ruling out lymphoma, myeloma, or metastatic carcinoma.

Figure 4:

Case 2: Axial T2 weighted image of epidural hemangioma compressing the spinal cord (single right arrow) from right to left at the T1/T2 disc space level. Note that the double left arrows show the cord compressed to the left side of the spinal canal.

Figure 8:

Case 2: Non contrast sagittal CT Scan demonstrating T2 vertebral body hemangioma (single arrow).

Figure 5:

Case 2: Right parasagittal T2 Weighted Image of ventral T2 hemangioma (large single arrow) and marked T1/T2 to T2/T3 right antero-lateral epidural cord compression from hemangioma (long horizontal and vertical single arrows).

Figure 6:

Case 2: Central sagittal T2 weighted image of ventral T2 hemangioma (large single arrow) and marked T1/T2 to T2/T3 ventral epidural cord compression from hemangioma (two single vertical and horizontal arrows).

Figure 7:

Right parasagittal T2 STIR image demonstrating both the ventral T6 vertebral body hemangioma (large single arrow) and marked extradural dorsal/right-lateral epidural extension from T1/T2 to T2/T3 causing severe cord compression (2 single long arrows).

Surgery

Utilizing the Jackson table, neural monitoring, fluoroscopy, ultrasound, and CT Neuronavigation, of a T1-T3 right-sided laminectomy with T2 transpedicular resection of T1-3 right-sided ventral/lateral epidural tumor was accomplished. Confirmation of the T2 pathological fracture was followed by a C7-T4 (C7, T1, T3, T4) posterolateral pedicle/screw fusion (Allograft/Demineralized Bone Matrix). Ultrasound was used to confirm the adequacy of intraoperative tumor resection. The final CT Neuronavigation spin further confirmed accurate pedicle/screw placement. The pathological diagnosis was atypical hemangioma. Postoperatively, the patient remained neurologically intact. Several months later the postoperative MR documented full resection of the right-sided ventral/lateral epidural T1-T3 tumor, and the cord was clearly decompressed [Figure 9]. The patient subsequently underwent CyberKnife Radiosurgery to address the residual T2 vertebral body hemangioma, and continues to do well.

Figure 9:

Case 2: Postoperative midline sagittal T2 weighted MR image demonstrating the remaining ventral T2 vertebral body hemangioma (single large arrow). Note resolution of the previously seen ventral epidural T1/T2 to T2/T3 right-anterolateral cord compression (2 single long arrows). There is also a hint of slight dilatation and an intramedullary high signal within the spinal cord at this level.

DISCUSSION

Incidence of and Differential Diagnoses for Aggressive Hemangiomas

Vertebral hemangiomas (VH) are relatively common while aggressive hemangiomas are quite rare, with only up to 11% becoming symptomatic (i.e. myelopathy/radiculopathy) aggressive lesions [Table 1].[1,4,6,7,9,10,12] Multiple primary and secondary tumors must be considered amongst the differential diagnoses. These typically include; Eosinophilic Granulomas, Osteoid Osteomas, Osteoblastomas, Osteosarcomas, Chondrosarcomas, Synovial Sarcomas, Chordomas, Giant Cell Tumors, Aneurysmal Bone Cysts, and Multiple Myeloma [Table 1].[5-7]

Table 1:

Perspective/short review of literature on hemangiomas.

Types I-IV Classification of Common vs. Aggressive VH

Several studies identified 4 types of common vs. aggressive VH [Table 1].[1,12] Yucesoy et al. (2024) defined these types as follows: Type I occupied < 50% of the vertebral body, Type II occupied > 50% (IIb Symptomatic in the thoracolumbar spine), Type III occupied 100% of the vertebral body, while Type IV occupied 100% of the vertebral body and extended into the pedicles, laminae, spinous processes, and/or epidural space (i.e., the latter likely causing symptomatic myelopathy/radiculopathy).[12] When Abul-Kasim et al. (2023) reviewed 1000 MR scans in patients with aggressive VH followed over a 3 month duration, 43% Type I fat rich lesions predominated at the L1 level. Interestingly, 7-year follow-ups revealed all Type I-IV lesions had comparable 26% growth rates.[1]

Early Diagnosis and Surgery (Decompressions with/without Fusions) for Aggressive VH

Multiple studies focused on the benefits of early diagnosis and surgical treatment of aggressive VH to maximize neurological recovery [Table 1].[3,4,6,7,12] In 2009, Jerome et al. emphasized the need for prompt diagnosis and timely surgery to limit/avoid permanent neurological deficits.[6] Kaloostian et al. (2014) stated that early total En Bloc resections of VH correlated with better long-term progression free survival rates.[7] The 14-year-old in Ayhan et al. (2015) with a C7 lytic/pathological VH fracture and C5-C6 intramedullary arteriovenous malformation (AVM) acutely deteriorated following embolization of the AVM; he required an emergent C5-C7 laminectomy/C5-T2 posterior fusion, followed 2 weeks later by a C7 anterior corpectomy/fusion [Table 1].[3] In 2021, Chopra et al. review of 154 studies involving 535 patients with aggressive VH, 80.6% required thoracic surgery that resulted in an 81.7% incidence of excellent outcomes (Odom’s Criteria).[4] Yucesoy et al. (2024) recommended timely/extensive posterior decompressions/fusions for patients with aggressive Type IV VH lesions (i.e., reported incidence of 11%).[12] Our 2 cases of aggressive thoracic T6 and T2 Type IV VH warranted both laminectomy with posterior fusions.

Varied Vertebroplasty/Kyphoplasty Techniques to Treat Aggressive Vertebral Hemangiomas

Several studies utilized varying techniques to perform kyphoplasty, vertebroplasty, or percutaneous vertebroplasty (PV) in patients with aggressive VH [Table 1].[5,8-11] Rather than performing classical surgery with radiation therapy, Guo et al. (2012) utilized a Translateral Approach (i.e., working between the carotid sheath and vertebral artery) in 15 patients with upper cervical C1-C3 hemangiomas or osteolytic spinal metastases; patients markedly improved postoperatively on Visual Analog Scale, and exhibited minimal increased postoperative morbidity [Table 1].[5] Kordecki et al. (2015) offered new Anterolateral Approaches for 10 high cervical VH as an alternative to routine transoral procedures (i.e., requiring needle placement through the bony palate/oral cavity associated with high surgical site infection rates); pain improved in 100% of patients.[8] For the 10 patients with aggressive VH treated by Qui et al. (2020: 8 thoracic lesions), 7 required laminectomies, 4 were fused, and 2 underwent intraoperative percutaneous vertebroplasty (PV).[9] In 2024, Wu et al. performed 14 (9 cervical VH/5 spinal metastases) anterolateral cervical vertebroplasties that also resulted in uniformly good postoperative outcomes.[11] For Wang et al. (2026) all 85 patients with aggressive VH (i.e., 1 cervical, 67 thoracic, 17 lumbar), all underwent both decompressions with intraoperative percutaneous vertebroplasty (PV); preoperative embolization minimized intraoperative blood loss (i.e. 670.1 cc/range 50-2500 cc), and reduced operative times (mean 168 minutes).[10] Our case 1 patient with a T6 Type IV VH successfully underwent decompression/fusion accompanied by an intraoperative T6 kyphoplasty.

Efficacy of Primary vs. Adjuvant Radiation Therapy for Treating Aggressive VH with/without Prior Decompressions/Fusions

Radiation therapy can be utilized as an effective primary or secondary treatment for aggressive VH [Table 1].[2,9,10] Aksoy et al. (2022) primarily treated 80 patients with aggressive symptomatic VH (i.e., 45 lumbar, 28 thoracic, 7 cervical) with a daily radiation dose of 2 GY for a total of 40 Gy; 3 months later, 58.8% of patients had total, and 26.2% had partial pain resolution, while 15% showed no improvement in pain.[2] Of Qui et al. (2020) 10 patients with aggressive VH (i.e. 8 thoracic), following decompressions/fusions and 2 intraoperative VP, 3 additionally received postoperative radiation; notably, no lesions recurred.[9] Out of Wang et al. (2026) 85 patients undergoing decompressions for aggressive VH with PV, 8 had recurrences; one patient required additional surgery/radiation vs. while the remaining 7 required radiation alone.[10] In our case 2 with a T2 aggressive Type IV VH, posterior decompression/fusion was followed by postoperative CyberKnife radiosurgery. Our Case 1 patient with a T6 Type IV lesion is presently being considered for postoperative CyberKnife radiosurgery.

CONCLUSION

Eleven percent of VH are symptomatic aggressive Type IV lesions that are most commonly found in the thoracic spine. With variable extension into the pedicles, laminae, spinous processes, and/or epidural space, aggressive VH most often warrant early diagnosis (i.e., MR’s) and surgery with/without additional adjunctive therapies (i.e., embolization, kyphoplasty, vertebroplasty/PV, and/or radiation) to optimize neurological recovery.

Ethical approval:

Institutional Review Board approval is not required.

Declaration of patient consent:

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given consent for their images and other clinical information to be reported in the journal. The patient understands that the patient’s names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

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