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Pathological osteolytic vertebral fractures resulting from tumor metastasis or myeloma are both relatively common as well as a significant source of painful morbidity. The skeletal system bears the brunt of neoplastic dissemination, occurring in 30 to 95% of the most common cancers including breast, prostate, lung, kidney, and thyroid. Among osseous structures, vertebrae are the most common site of spread and are the third most common site of metastases overall after the liver and lung.1 Indeed, spinal metastases occur in approximately 40% of patients who die of cancer, and a staggering 5 to 10% of all cancer patients will have symptomatic spinal metastases at some point during their disease course.^1–3 The propensity for such high rates of vertebral involvement is likely due to the unique biology of the neuraxis and its relation to the most common primary cancer sites (including breast, prostate, and lung cancer). The vertebral and epidural hematogenous plexuses directly drain both breast and prostate tissue, and likely form a direct conduit with the pulmonary and genitourinary systems. Additionally, the axial skeleton contains the majority of red marrow in the human adult, and thus maintains a distinct cellular and extracellular milieu that may favor secondary tumor deposition and growth.²

Vertebral metastases occur throughout the neoplastic disease course, with events clustering around periods of primary tumor progression and with accelerating frequency during more advanced disease.² Both oncological disease burden and tumor histology play a significant prognostic role in patients with similar rates of axial skeleton disease burden. As would be expected from tumor-specific survival curves, primary lung tumors portend a significantly shorter survival than those of breast or prostate, a fact that must be taken into account when planning surgical interventions for vertebral pathological fractures. Furthermore, prognosis is typically improved with disease recurrence within the axial skeleton compared to visceral sites. For example, median survival is 24 months in women with metastatic breast cancer confined to the skeleton, whereas survival shrinks to 5 months with dual bone and liver disease.²

Although two thirds of all vertebral metastases are asymptomatic, the development of a pathological vertebral fracture significantly alters a patient’s disease course and yields both increased morbidity and mortality. Saad et al3 demonstrated this in an examination of a large group of patients with known malignant bone disease from multiple myeloma or other solid tissue tumors. Not only did they show a high rate of fracture for each tumor type in a 2-year period of observation (39% rate of fracture with breast cancer and 22% with other solid tumors), but also demonstrated that vertebral fracture was associated with a marked increase in mortality (up to 32% in patients with breast cancer compared with the nonfracture group). It is therefore critical to have a thorough understanding of the oncological disease burden when evaluating and informing patients on vertebral augmentation interventions.

The reasons for increased mortality after vertebral pathological fracture are likely multivariate, though the root causes are likely similar to those leading to elevated mortality after osteoporotic compression fractures. Tumor- and fracture-related pain is a key symptom leading to a cascade of morbid events, including impaired mobility, concomitant increased thromboembolic risk, progressive deformity with decreased pulmonary capacity and increased risk of cardiopulmonary collapse, deconditioning, loss of functional independence, social withdrawal, depression, increased narcotic analgesia intake, and associated mental status decline. Therapies designed to disrupt this cycle of decline can therefore have a profound impact on patient survival and quality of life even in the setting of metastatic disease. Vertebral augmentation with PVP and PVK in this patient population has increasingly demonstrated efficacy, technical feasibility, and low procedure morbidity. These minimally invasive procedures both involve percutaneous cannulation of the fractured vertebral body followed by injection of a liquid that polymerizes to a durable resin within the fractured body, thereby stabilizing the fracture. PVK entails the added step of insertion of a balloon tamp through the cannula followed by inflation, out-fracturing, and compaction of cancellous bone toward the cortical vertebral margin. The end plates are pushed apart, partially restoring vertebral body height and focal kyphotic deformity. Polymer is then similarly injected into the cavity to harden and stabilize the fracture.

Patient Selection

As with any surgical procedure, proper patient evaluation and selection is critical to ensure a successful outcome. The assessment must include both medical and oncological status, and due diligence within both of these realms will guide the practitioner toward optimal diagnostic and treatment selection. Vertebral augmentation is an excellent option for patients who have severe systemic morbidity that precludes open surgical intervention, and it is likewise favored for healthy patients with osteolytic fractures that do not cause neurologic sequelae. Both of these groups, however, carry increased surgical risk from their concomitant cancer than that for the patient undergoing PVP or PVK for solely osteoporotic fracture.

Patients suitable for this procedure describe a typical axial or mechanical pain pattern that is aggravated with standing or twisting and relieved with lying flat. The location of the pain should correspond to the level of the fracture, an obvious but critically important point, as patients may have other vertebral levels with tumor involvement but no fracture. The biological pain of a tumor is differentiated from mechanical fracture pain by both constancy of pain throughout the day and night as well as its dull or throbbing qualities. This type of pain may be related to tumor release of local factors and cytokines, periosteal stretch, and local tissue production of endothelins and nerve growth factors.¹ Alternatively, neurologic pain should also be considered, as the compression or infiltration of a nerve root yields shooting pain in a dermatomal pattern and requires a decompressive procedure. An exception to this dictum is mechanical instability that causes activity-related impingement of the nerve root, where fracture stabilization prevents the intermittent nerve injury.

Eliciting a neurologic history and performing a thorough examination are important steps in the patient evaluation. Any neurologic symptoms, including paresis, sensory changes, bowel/bladder dysfunction, or changes in balance and ambulation, can indicate radicular or thecal sac compression by fracture or tumor. Changes in affect, cognition, speech, or cranial nerve dysfunction should be actively investigated due to the propensity for additional tumor–central nervous system (CNS) lesions. Patients should be counseled on the likely need for additional therapies for tumor control such as radiotherapy, as well as the need for optimization of systemic bone metabolism through pharmacological interventions to decrease future fractures. All the traditional risks of osteoporosis are present in this patient population, as well as the additional factors of cancer-related immobility, altered nutritional intake, and deranged osseous metabolism from tumor and treatment processes (chemotherapy or radiation). A detailed discussion of these pharmaceuticals is beyond the scope of this chapter. But it is important to note that bisphosphonates can reduce the incidence of additional-level fracture in both multiple myeloma and metastatic disease.2,3 More recently, receptor activator of nuclear factor κ B (RANK) ligand inhibitors of osteoclast resorption have been approved for the prevention of skeleton-related events in patients with bone metastases from solid tumors such as breast and lung cancer and appear highly effective.⁴

Practitioners should attempt a reasonable trial of medical management for the mechanical fracture-related pain, and patients must understand that vertebral augmentation carries all the attendant risks of anesthesia and surgery. Active participation of other specialists adept at pain management should be sought, including anesthesia and palliative medicine, and conservative therapy should be considered, including local injections, systemic analgesia, and external orthosis. Preoperative laboratory investigations should confirm normal clotting (platelet level) and coagulation (international normalized ratio [INR]/prothrombin time [PT]/partial thromboplastin time [PTT]), as well as ensure where appropriate that there is no active or occult infection (e.g., urinalysis with reflex culture). Bacteremia leading to hematogenous seeding and infection of injected cement often requires a technically difficult corpectomy and attendant fusion, and can be easily avoided by maintaining a high index of suspicion. Antiplatelet agents should be temporarily discontinued.

Many patients with metastatic and myelomatous osseous disease suffer from hypercalcemia, most commonly seen in tumors of the lung, breast, and kidney and in myeloma and lymphoma. Tumor production of humoral and paracrine factors, including parathyroid hormone–related peptide, nurtures an osteolytic environment and deranged bone metabolism.² Early symptoms include fatigue, anorexia, and constipation, and can progress to renal and cardiovascular collapse. Patients therefore may suffer from the dual hit of metastatic vertebral fracture as well as a deranged metabolism leading to osteoporotic fracture.

Multimodal neuraxis imaging is a required step for preoperative planning to ensure a successful augmentation outcome. Complete magnetic resonance imaging (MRI) evaluation of the brain and spine should be a standard practice for patients with known CNS metastatic disease due to the propensity of multiple metastases. T2-weighted, fat-suppression, or short tau inversion recovery (STIR) sequences delineate the acuity of fracture, edema, and reparative activity. Bone scintigraphy can provide a further index of fracture-site metabolism, with increased activity correlating with a greater response to augmentation.⁵ Both modalities can assist with symptomatic fracture localization when multiple fractures are present. Computed tomography (CT) scan provides valuable characterization of fracture morphology, vertebral height, pedicle width, trabecular disruption (characterized by intravertebral gas), and violation/retropulsion of the posterior cortical wall. We routinely obtain anteroposterior (AP) and lateral X-rays to facilitate accurate counting and to provide a corresponding view of the intraoperative fluoroscopic guidance images. Dynamic radiography with supine and upright films delivers valuable information on both the degree of kyphotic deformity as well as fracture mobility. Up to 44% of patients have a radiographically relevant change in vertebral height; patients whose vertebral height does not change are considered fixed.6

Relative and absolute contraindications to vertebral augmentation for metastatic disease are listed in the Text Box.

Procedure