A case report of multiple aggressive vertebral hemangiomas: a rare mimic of metastatic malignancy

Introduction

Background

Spinal haemangiomas are benign vascular lesions that represent the most common primary tumour of the spine (1), found in 10–26% of individuals (2). They appear to be sex-independent, present in a patient’s 50s, and have equivocal prevalence among the vertebral levels (3), although cases of spinal cord compression preferentially affect the thoracic level (4). Haemangiomas at multiple vertebral levels are rare but have been described in the literature (5-8). While the exact pathogenesis of vertebral haemangiomas is poorly understood, they are of dysembryogenetic origin (2). Vascular proliferation can result in osseous displacement into neuraxial foramina or the spinal cord canal, resulting in neurological symptoms.

Rational and knowledge gap

There is only a handful of cases in the literature documenting cases of multiple aggressive vertebral haemangiomas (6,9-11), and only one associated with an underling systemic disorder (12). The rationale of this paper is to document a rare case and emphasize the need for considering cystic angiomatosis when encountering multiple vertebral lesions.

Objective

We present an extremely unique case of a patient with multiple aggressive vertebral haemangiomas manifesting as a neurological deficit with a particularly expansile lesion requiring surgical decompression. This was associated with multiple extra-axial skeletal lesions that we purport may represent the uncommon entity of cystic angiomatosis. We present this case in accordance with the CARE reporting checklist (available at https://amj.amegroups.com/article/view/10.21037/amj-24-99/rc).

Case presentation

A 55-year-old female was referred to the neurosurgery service from the primary care setting with a 4-month history of lower back pain radiating to her bilateral lower limbs.

She denied lower limb weakness nor sphincter or bladder dysfunction. She denied constitutional symptoms. She had a past medical history of hypertension, hypercholesterolemia, and type 2 diabetes but not malignancy. She had a maternal family history of multiple myeloma. Her regular medications included perindopril and semaglutide.

On examination, she had a normal gait, intact limb power and strength without, normal reflexes throughout, no clonus, and down-going plantar reflexes. She had reduced sensation in her anterior thighs bilaterally.

A computed tomography (CT) of the lumbar spine demonstrated multi-level vertebral body lytic lesions with evidence of cord compression at the T12 vertebral level (Figure 1). She then underwent magnetic resonance imaging (MRI) of the spine which demonstrated expansile compressive T1 and T2 weighted hypointense lesions within the T12, L5 and S1 vertebral bodies. The T12 lesion caused canal stenosis and cord compression without cord signal change (Figure 2). At this stage, a metastatic malignant process was suspected. CT of the chest, abdomen and pelvis did not identify a primary malignancy, but revealed additional mixed lytic and sclerotic lesions found within the left ninth rib, right first and ninth rib, the manubrium, and in bilateral pelvic bones and femurs (Figure 3). A positron emission tomography (PET) scan demonstrated minimal fludeoxyglucose (FDG) uptake in the spinal T12 lesion, without FDG abnormality elsewhere. Her serum haematological profile, electrolytes and tumour markers, carcinoembryonic antigen, cancer antigen (CA) 125, CA 15-3 and CA19-9 were all within normal limits.

Figure 1 CT of the lumbar spine: sagittal and axial views. (A) Sagittal CT of lumbar spine partially capturing the T12 and L5 vertebra (arrows) showing lytic lesions involving the T12 and L5 vertebra. Note the absence of the typical trabecular “Polka dot or Corduroy” lesions. (B) Axial CT of lumbar spine at the level of T12 vertebra showing bony lesion involving the vertebral body and lamina encroaching into the canal (arrow), likely causing cord compression. CT, computed tomography.

Figure 2 MRI of the thoracic and lumbar spine: sagittal and axial views. (A) Sagittal MRI of thoracic spine showing T12 vertebral lesion extending circumferentially and causing focal cord compression (arrow). (B) Axial MRI at level of T12 vertebra (see white line on sagittal MRI) showing T12 vertebral and lamina lesion extending into the canal causing complete CSF effacement and cord compression (arrow). (C) Sagittal MRI T1 weighted of lumbar spine showing hypointense L5 and S1 vertebral body lesions (arrows). MRI, magnetic resonance imaging; CSF, cerebrospinal fluid.

Figure 3 Axial view of a CT of the chest, abdomen and pelvis showing lesions in the (A) bilateral femurs (arrows), (B) left posterior rib (arrow), (C) left pelvis (arrow), and (D) manubrium (arrow). CT, computed tomography.

Management

Following a multidisciplinary consensus, the patient was counselled on surgery to decompress the T12 lesion and to obtain a histological diagnosis. She proceeded for a T11 to L1 posterior decompression and instrumented fixation. After intraoperative imaging to confirm the operative level, a subperiosteal dissection was performed. The pedicles of T11 and L1 were cannulated bilaterally using a navigated pedicle probe, feeler, tap and screw technique, all with 5.5 mm screws. The screw positions were confirmed with imaging (Figure 4). The T12 vertebral level was decompressed with a drill and Kerrison rongeurs. A soft tissue tumour was visualised dorsally at the T12 level which appeared macroscopically abnormal and indented the compressed spinal cord. This tumour was excised en bloc. Normal cord was visualized cranially and caudally to this lesion. The patient did not suffer adverse events, underwent an uncomplicated postoperative recovery and discharged home 2 days later. Histopathology of the T12 vertebral lesion was consistent with that of a benign intraosseous hemangioma (Figure 5).

Figure 4 Postoperative lateral (A) and anterior-posterior (B) plain X-rays of thoracic spine showing 5.5 mm pedicle screws and rod fixation of T11–L1 spine.

Figure 5 Histopathology images of the T12 vertebral lesion. (A) Haematoxylin and eosin, ×12.5 magnification. Low-power view of intraosseous haemangioma demonstrates encapsulation of tumour. (B) Haematoxylin and eosin, ×40 magnification. Cavernous-type blood vessels congested with blood, dissecting between bony trabeculae. (C) Haematoxylin and eosin, ×100 magnification. Remodelling of bone demonstrated with osteoblastic activity. There were multiple thin walled, dilated cavernous vascular channels congested with blood, lined by a single layer of flattened unremarkable endothelial cells. The stroma between the vascular channels comprised of loose connective tissue, containing giant cells and including multiple foci of intramedullary haematopoiesis. Extensive new bone formation with osteoblastic activity were identified and no atypical or epithelioid cells were present.

After 1 week, the patient’s back pain had improved, and her lower limb numbness had resolved; However, she had developed a right L5 distribution radiculopathy. An MRI performed at 2 months demonstrated good hardware positioning and an adequate thoracic decompression, but slight progression of the L5 vertebral body disease, with epidural extension causing mild spinal canal stenosis and bilateral lateral recess stenosis (Figure 6). To treat the presumably aggressive haemangioma, the patient proceeded for an endovascular angioembolisation of the L5 haemangioma 5 months after the first operation, followed by a cement vertebroplasty. There was extensive onyx embolization of the lesion with a good angiographic result (Figure 7), and her pain following this was tolerable.

Figure 6 MRI of the thoracolumbar spine performed 2 months post-operatively: sagittal and axial views. (A) T2 weighted sagittal MRI of the thoracolumbar spine showing decompressed T12 spinal cord (obscured by instrument artefact) and progressively expansile L5 vertebral lesion (arrow). (B) T2 weight axial MRI at L5 level [see white line in sagittal in (A)] showing expansile L5 vertebral body lesion causing bilateral lateral recess stenosis (arrows). MRI, magnetic resonance imaging.

Figure 7 Anterior-posterior radiograph of L5 lesion following onyx radioembolization of L5 vertebral body lesion and sclerosant cement injection (arrow).

On further 1-month follow-up, the patient’s pain had reduced to a tingling sensation in the same distribution. Considering the reassuring histopathological diagnosis, a subsequent medical decision making (MDM) review decided for continued radiological surveillance, with an early MRI to ensure stability of her L5 lesion, followed by a 12-month interval MRI of her spine. She is satisfied with her symptom relief. The entire treatment timeline including follow up is summarized in Figure 8.

Figure 8 Timeline of presentation and treatment course. Radiological findings described in corresponding figures. MRI, magnetic resonance imaging.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

This case report describes a rare instance of a 55-year-old female with multiple aggressive vertebral haemangiomas requiring surgical decompression and fusion followed by angioembolization of another lesion with an uncomplicated recovery course. There may be an underling disorder given the presence of disseminated skeletal lesions.

Strengths and limitations

This study’s strengths include its unique presentation and exemplifies the array of approaches to the vertebral haemangioma—spanning from surgical stabilization in the compressive lesion, radiological surveillance, then endovascular embolization and percutaneous vertebroplasty for a symptomatic lesion with radiological progression. Limitations of the study includes the relatively short follow-up time available at the time of reporting, the reliance upon a histology of a single lesion without biopsy of other lesions, and the uncertainty in the diagnosis given the lack of visceral organ involvement.

Comparison with similar research

It is exceedingly rare for multiple discrete vertebral haemangiomas to be aggressive. We found 5 cases in our literature review of patients with multiple aggressive vertebral haemangiomas (Table 1). One patient had an underlying systemic hamartoma tumour syndrome predisposing them to haemangiomatous formation (12).

Explanation of findings

The vast majority of vertebral haemangiomas are asymptomatic and quiescent; 0.9–1.2% become symptomatic, with 55% presenting as back pain (13). They may become symptomatic with time; 50% of those who do have pain and 18% manifest radiological spinal cord compression within 10 years. Lesions may be classified based on the Enneking classification into latent (Stage 1), active (Stage 2) featuring pain due to bony destruction, and aggressive (Stage 3) due to bony destruction and epidural soft tissue extension (14). The aggressive spinal haemangioma represents approximately 1% of spinal haemangiomas, characterized by significant osseous expansion and extraosseous extension (15). Seventy-five percent of these originate from the thoracic vertebrae. Due to the relatively narrow canal dimensions, lesions here are predisposed to developing symptoms (16). Therefore, a lower threshold for treatment may be warranted for such lesions. Lesions are classified as compressive if accompanied by neurological symptoms due to compression of the spinal cord, nerve roots, or both (17). Haemangiomas may be classified histologically into either cavernous or capillary angiomas. These microscopic types frequently coexist (2).

Radiological characteristics can assist to differentiate haemangiomas from differentials such as metastatic deposits and primary bone tumours. On axial CT, appearances of “polka dotted” or “salt and pepper” and on sagittal, the “corduroy” sign due to thicker or denser vertical trabeculae can help to delineate a lesion as a haemangioma (2). MRI can determine extension into the spinal canal or neuroforamina, and therefore patients at risk of developing pain, radiculopathy, or myelopathy (17).

As vertebral haemangiomas are often asymptomatic and remain so, uncomplicated lesions are not routinely monitored. Sharma et al. (18) described the appearances for its variations and the suggested management. Lesions with typical appearances of hypointensity on CT with “polka dot” or “corduroy” signs, hypointense on T1 and hyperintense on T2, and variable contrast enhancement require no further imaging and no treatment unless symptomatic (in which case medical therapy is suggested). Atypical lesions appear isointense to hypointense on T1, hyperintense on T2, and have variable postcontrast enhancement; CT is suggested to look for typical features and management is the same as typical vertebral haemangiomas. Aggressive vertebral haemangiomas appear hypointense on CT with variable involvement of the vertebral body and posterior elements, and may feature cortical expansion/infiltration, soft-tissue extension, spinal cord/nerve root compression. On magnetic resonance (MR), they appear T1 hypointense, have variable intensity on T2, and have variable contrast enhancement. Further investigation with MR, CT, angiography, and biopsy may be of utility. Vertebroplasty and/or surgical management is suggested for lesions causing compressive myelopathy or radiculopathy. This patient’s vertebral body lesions lacked the typical trabecular pattern and MRI appearances favoured an aggressive haemangioma based on the T1 and T2 weighted hypointensity. In fact, the initial working diagnosis was a metastatic malignancy.

As a caveat, Wang et al. describe over a third of aggressive vertebral haemangiomas with at least 1 atypical feature (19). Such lesions can mimic metastatic deposits and further investigation with MRI may be warranted. Dynamic contrast MRI, diffusion weighted MRI, and ratio of signal intensity between T1 and fat suppression T1 MRI can help clinicians to differentiate them from metastases (20). Adjuncts to further differentiate lesions from metastatic deposits include FDG PET, on which haemangiomas demonstrate reduced uptake (21), and 99m technetium (Tc-99m) red blood cell labelled single-photon emission computer tomography (SPECT) showing increased Tc-99m labelled red blood cells (22). CT guided biopsy, featuring 89% diagnostic accuracy, is recommended to rule out alternative suspected tumours for patients who do not exhibit the typical features or location of vertebral haemangioma (20).

Subramaniam et al. (20) proposed an algorithm for the management of aggressive vertebral haemangiomas, suggesting percutaneous vertebroplasty, CT guided ethanol sclerosis, or external beam radiation for lesions that only present as back pain refractory to medical therapy, or those with radicular symptoms. For back pain with neurological symptoms, they recommended posterior decompression with vertebroplasty. There is a consensus that lesions causing progressive neurological deficit necessitate surgical treatment (20).

Radiotherapy is effective for treating symptomatic vertebral haemangioma, preventing or halting the development of neurological deficits, and in preventing recurrence post-resection (23). In cases of cord compression resulting from bony displacement or hypertrophy however, it is considered unlikely to be effective as it has no demonstrable effect on bone tissue (24). We decided against radiotherapy, as the dorsal tumour was excised en-bloc and the vertebral body component was unlikely to have responded.

Operative management in the aggressive vertebral haemangioma ranges from posterior decompression laminectomy with vertebroplasty, direct alcohol injection, to anterior corpectomy with reconstruction (20). Anterior corpectomy and reconstruction preceded by endovascular embolization is specifically indicated for ventrally located lesions causing primary bony compression over the cord, or in recurrent lesions (20). The extent of resection can vary from decompression alone, to gross-total resection, to en bloc resection. When combined with vertebroplasty or adjuvant radiotherapy, the aforementioned surgical approaches have similar oncological outcomes in preventing recurrence, although en bloc vertebrectomy has greater postoperative morbidity (25), and is deemed by some authors to be an overly aggressive approach for a benign lesion with low rates of recurrence if postoperative radiotherapy is administered (26).

For symptomatic vertebral haemangiomas, cement vertebroplasty is an effective and less invasive alternative to surgical vertebroplasty for medication-refractory pain (27), and may be combined with ethanol injection.

Preoperative lesion angioembolization can be useful given the vascular nature of haemangiomas (28). However, aggressive lesions often occur in the midthoracic spine, where there is a potential watershed area for spinal cord supply. Embolization should be deferred in the presence of only one dominant feeder to the spinal arteries (29) due to the risk of infarction. As it is the epidural soft tissue component of a haemangioma that causes cord compression and neurological symptoms, a posterior compression combined with vertebroplasty can produce good outcomes without requiring pre operative feeding vessel embolization (20). Given the risk of watershed infarct in the thoracic spine, an endovascular approach was not undertaken.

The recommended follow-up period for aggressive vertebral haemangiomas is not well defined. Subramaniam et al.’s systematic review of 88 cases in the literature found the mean follow up period to be 26 months (20). There is similarly sparse literature for cystic angiomatosis, with Aumann et al. conducting 6 monthly surveillance for 3 years in an asymptomatic patient (30). We would undertake similarly close surveillance.

Implications and actions needed

The broad range of aetiologies for vertebral lesions must be considered. Primary osseous lesions include benign differentials such as lipoma, sclerosis, aneurysmal bone cyst, osteoid osteoma, and osteoblastomas, and the malignant, including chondrosarcoma, chordoma, Ewing’s sarcoma, neuroblastoma, and osteosarcoma (31). Other common malignancies include multiple myeloma and lymphoma. Other vascular lesions that rarely occur in the spine include paraganglioma, haemangioblastoma, haemangiosarcoma, and haemangiopericytoma. Infective causes such as bacterial osteomyelitis and echinococcal infection should be considered (32).

An underlying systemic disorder or syndrome should be considered in the case of disseminated lesions. Cystic angiomatosis, an extremely rare condition characterized multifocal dissemination of haemangiomatous or lymphangiomatous skeletal lesions affecting the axial and appendicular skeleton with possible visceral organ involvement (33), was considered in this case. Vigorita defined cases with lesions restricted to the skeleton as cystic angiomatosis of the bone, and those involving both bone and extraosseous tissue as skeletal-extraskeletal angiomatosis (34). Visceral involvement is optional. However, cystic angiomatosis is histologically indistinguishable from typical haemangiomas or lymphangiomas. Langerhans histiocytosis is another systemic disorder known for causing multiple osseous lesions (32).

Ching et al. faced a similar diagnostic dilemma (35)—cystic angiomatosis is more common in men and in ages 10–30 years, so similarly to ours, their case’s demographic was atypical. Spinal cord compression tends to be less common than with primary vertebral haemangioma (11). Finally, given the lack of visceral organ involvement or confirmed lymphangiomatous lesions, there was equipoise in securing this diagnosis. However, this remains a diagnostic consideration for this patient given the uncertain prognosis and optimal management for this condition. We note that reassuringly, cases with only skeletal lesions have a comparatively favourable prognosis to those with visceral involvement, and that lesions may regress without treatment (30).

As cystic angiomatosis is not diagnosable by histology alone, we purport that cases may be underrecognized and suggest greater awareness of this syndrome. The presence of multiple osseous vertebral lesions should raise this suspicion, and the possibility of associated visceral lesions should be considered due to the prognostic implications.

Conclusions

It is extremely rare for multiple haemangiomas to present aggressively. Every effort should be made to exclude malignancy if radiological investigations are indecisive, but aggressive expansile lesions are not necessarily neoplastic. There should be a consideration for alternative causes for disseminated lesions such as cystic angiomatosis, or a genetic hamartoma tumour syndrome. It is similarly crucial to exclude visceral organ involvement due to the substantial difference in mortality to cases limited to the skeletal system. It is beneficial to characterize lesions with MRI, CT, and PET imaging preoperatively, as haemangiomas may benefit from preoperative embolization to reduce intraoperative blood loss.

Acknowledgments

This abstract was presented as an e-poster in 2024 at the Royal Australasian College of Surgeons Annual Scientific Meeting.

Funding: None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://amj.amegroups.com/article/view/10.21037/amj-24-99/rc

Peer Review File: Available at https://amj.amegroups.com/article/view/10.21037/amj-24-99/prf

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://amj.amegroups.com/article/view/10.21037/amj-24-99/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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