Basal Cell Carcinoma With Metastasis to the Thoracic Spine: An Uncommon Case Report and Review of the Literature

Basal cell carcinoma (BCC) is the most common malignancy within the US population and is particularly common among White peoples with excess UV exposure.1,2 Clinical sequelae of BCC are largely benign if timely diagnosis, surveillance, and appropriate treatment are initiated. Surgical excision and topical therapy (imiquimod, 5-fluorouracil) are mainstays of treatment for noninvasive tumors, while more advanced tumors may necessitate micrographically oriented histographic surgery excision, systemic therapy, or radiation therapy.2,3 Distant BCC metastasis is exceedingly rare and requires more complex surgical excision with adjunctive oncologic care. Few previous reports of spinal metastatic BCC exist in the literature. Although there is no standard treatment algorithm, managing spinal metastatic disease necessitates tailored and individualized approaches to prevent neurologic injury and spinal deformity, treat pain, preserve function, and improve oncologic prognosis, when feasible. This report presents the diagnosis and unique treatment of a patient with metastatic BCC to the spine, and review of the available literature.

Case Presentation History and Injury

A 66-year-old man presented to our Emergency Department with complaints of acute on chronic low back pain, progressive bilateral lower extremity weakness, and paresthesia 1 week after a ground-level fall due to gait instability. Imaging demonstrated a thoracic burst fracture at the T8 level with retropulsion, myelomalacia, and disruption of the posterior vertebral elements, in addition to a mass spanning T7-T9 concerning for pathologic lesion (Figure 1). His medical history is significant for tobacco use and BCC diagnosed 8 years prior which demonstrated continued growth after diagnosis (Figure 2). He had no continued dermatologic care after diagnosis, and the patient noted prolonged ongoing feelings of depression, likely contributing to his failure to seek treatment.

F1Figure 1:

T1 precontrast (left) and postcontrast (right) sagittal thoracic spine MRI demonstrating metastatic disease spanning T7-T9, with a pathologic T8 burst fracture. Thoracic cord deformity and myelomalacia are evident on postcontrast imaging.

F2Figure 2:

Photo demonstrating basal cell carcinoma. Left: Large central facial erosion with loss of nasal architecture, secondary to untreated basal cell carcinoma. Right: Appearance of facial lesion after treatment with vismodegib therapy.

At the time of presentation, the patient was ambulatory with assistance of a walker and neurologic examination demonstrated subtle left lower extremity weakness, diminished sensation across the lower abdomen and bilateral lower extremities, and urinary retention, representing an American Spinal Injury Association C thoracic myelopathy. He was indicated for surgical fixation to stabilize the three-column vertebral injury and decompress the spinal canal. Completion MRI demonstrated no evidence of skip lesions throughout the spine.

Surgical Treatment and Hospital Course

The patient was placed under general anesthesia, and prepositional baseline neuromonitoring was obtained demonstrating intact somatosensory-evoked potentials bilaterally, reduced motor-evoked potential (MEP) of the right lower extremity, and nondiagnostic left lower extremity MEP signals. He was positioned prone in Mayfield tongs, and posterior exposure from T5-T11 was completed. Pedicle screws from T5-T7 and T9-T11 were placed under fluoroscopic guidance, and a right-sided rod was secured with the intended level of kyphosis. Wide laminectomies were then done from T7-T9, and the tumor was debulked to the extent possible. Removal of tumor in entirety was not feasible because of diffuse adherence to the adjacent dura and surrounding anatomic constraints. Posterior arthrodesis was then done (Figure 3A). An intraoperative frozen section was consistent with carcinoma. Permanent histology demonstrated a poorly differentiated carcinoma with basaloid features. Immunohistochemical stains demonstrated tumor cell positivity for AE1/AE3, P63, BCL-2, and androgen receptor, and focal positivity for CD10, BER-EP4, and GATA3, supporting a diagnosis of metastatic BCC (Figure 4).

F3Figure 3:

Radiograph demonstrating surgical intervention. A, Initial surgical intervention consisting of tumor debulking with laminectomies and posterior thoracic fusion from T5-T11. B, Subsequent T8 anterior corpectomy and interbody cage placement.

F4Figure 4:

Sections demonstrating a poorly differentiated carcinoma with basaloid features and focal squamous differentiation. Tumor cells demonstrate expression of keratin AE1/AE3, p63, and BCL2, focal expression of BerEP4, CD10, and GATA3, and lack expression of NKX2.2, supporting a diagnosis of metastatic metatypical basal cell carcinoma.

He was evaluated by dermatology postoperatively and agreed to initiate oncologic care after consultation with the palliative care service. Staging imaging demonstrated no evidence of intracranial spread or other distant metastatic disease. He was discharged on hospital day 15 and initiated vismodegib therapy with good clinical response (Figure 2). He additionally underwent adjuvant radiation therapy to the thoracic spine (25 Gy in five fractions) to control pain and prevent additional disease progression.

Postoperative course was complicated by persistent back pain, and updated imaging at 7 months post procedure demonstrated lack of bony fusion and vacuolation on CT imaging consistent with persistent motion (Figure 5). He was offered a T8 corpectomy to address his spinal instability and persistent pain, and he elected to proceed with this procedure. Anterior corpectomy was done through a right-sided thoracotomy, and an interbody cage (Globus Fortify, globus inc.) was placed spanning levels T7-T9 (Figure 3B). At 1 year after posterior spinal fusion (3 months after corpectomy), the patient was doing well with near complete pain relief and full return of neurologic function.

F5Figure 5:

CT scan demonstrating lack of bony fusion at 7 months post procedure with evidence of vacuolation and persistent motion.

Discussion

Basal cell carcinoma is locally invasive and can lead to aggressive local destruction if neglected,4,5 and although the propensity for metastatic spread is exceedingly low, distant metastasis can occur in the absence of appropriate clinical surveillance. Metastatic BCC often requires multimodal treatment and carries a poor prognosis with mean survival of approximately 1 year.5 The rate of overall BCC metastasis is estimated at <0.1%,5–8 and reports of spinal metastatic BCC are infrequently encountered in the literature. The facial lesion on this patient measured approximately 5.5 × 5.8 cm, and the metastasis rate does increase with increasing tumor size—tumors >3 cm in diameter are estimated to metastasize at a rate of 2%, while tumors >10 cm demonstrate >50% metastasis.9 Many of the existing spinal metastatic BCC reports were published in the 1960s-1990s,10–13 possibly representing a period of more limited access to regular dermatologic care. Although more advanced care is now accessible and tumors are often treated earlier, comorbid depression and untreated mental health conditions in this patient likely precluded his pursual of timely care.

The treatment of spinal metastasis necessitates a multimodal approach that is often primarily palliative. Patient symptoms, functional status, and prognosis should be carefully considered to determine the most suitable management strategy. Goodwin et al.14 conducted a review outlining the treatment options for spinal metastatic BCC including radiation therapy, chemotherapy, and combination chemoradiation. Interestingly, surgical management is not frequently pursued, with only 13% of patients with spinal metastatic BCC undergoing surgical treatment. Platinum-based chemotherapy is available for BCC but yields poor response rates.3 Other pharmacologic adjuncts for metastatic BCC include medications, such as vismodegib and sonidegib, targeting the sonic hedgehog pathway. Vismodegib, a small-molecule inhibitor of the sonic hedgehog pathway, has shown favorable outcomes in patients with locally advanced or metastatic BCC15 and did elicit a positive response in this patient (Figure 2).

Surgical management for spinal metastatic disease is considered in instances involving neural element compression, instability, and progressive deformity. Alternatively, radiation therapy can address metastasis-related pain and prevent local recurrence.16 In the present case, neurologic deficits warranted urgent surgical intervention to prevent additional neurologic deterioration and our initial surgical strategy involved a posterior decompression and fusion. Although anterior reconstruction was not initially pursued, a subsequent anterior cage was placed because of persistent pain and insufficient bony fusion. Previous reports cite improved outcomes with anterior or combined anterior/posterior reconstructive strategies compared with posterior alone.16,17 In this case, corpectomy and cage placement restored anterior column integrity and addressed kyphosis, which reduces stress on the posterior elements and enhances overall stability. Surgical strategy and decisions regarding tumor debulking versus en bloc resection, anterior versus posterior approach, and decompression/fusion versus reconstruction should be tailored individually and based on factors including neurological compromise, deformity, and prevention of oncologic progression.

In conclusion, BCC is a rare cause of spinal metastatic disease requiring tailored surgical, dermatologic, and oncologic care. Tumor excision and spinal stabilization prevent neurologic insult and address deformity, while radiation therapy and pharmacologic therapy manage disease progression. Comprehensive primary care and improved mental health access can minimize advanced disease and late-stage metastasis.

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