Metastatic Spine disease

Abstract

A 56 year old lady presented with a low back ache associated with other constitutional symptoms. Radiographic examination revealed a metastatic lesion at T12, L4 and S2 vertebras. Further investigation with biopsy and CT scan of abdomen, thorax and pelvis showed a metastatic adenocarcinoma with primary from the lung.

Keywords: Metastatic spine disease, vertebrectomy, low back ache.

Case Report

This is a case of a 56 year old female patient who was complaining of backache for 3 months duration prior to consultation. She has been treated by general practitioner prior to the visit to orthopaedic surgeon but the pain was not resolved. The pain was severe at times. The analgesics temporarily give some respite. The pain was localized to the upper lumbar region. There was no leg pain. Numbness or weaknesses of both lower limbs were not noted. Passing motion and urine were not problematic. She was also complaining of loss of appetite and loss of weight.

She was a thin lady and signs of dehydration were evidenced by decreased skin turgor and dried mucosal surface. Her vital signs were normal. Examination of the spine revealed tenderness over the thoracolumbar junction. Neurologic examinations were normal. Other physical examinations were normal. Laboratory investigations showed raised erythrocyte sedimentation rate (40mm/hr), C-reactive protein (68 mg/l), alkaline phosphatase (121 U/L), and gamma GT (97 U/L). Tumour markers were normal except for a slightly elevated CA 15-3 (32.3 U/ml). Plain radiograph showed a compression fracture of T12. Magnetic resonance imaging showed a metastatic lesion at T12 vertebra. A bone scan revealed spinal metastases at T12, L4 and S2 levels. A subsequent CT scan of the thorax, abdomen and pelvis revealed a large heterogamous mass measuring 2.7 mm x 4.5 mm x 5.8 mm in the subpleural space of cardiophrenic angle. A biopsy was taken and histopathological examination showed a metastatic adenocarcinoma with possible primaries from lung and pancreas.

She was referred to oncology unit for further treatment with radiotherapy. Vertebroplasty and kyphoplasty were not done because of advanced collapse of the vertebra.

Discussion

Forty percent of patients with advanced cancer develop visceral or bony metastases during the course of their illness.¹ Patients older than 40 years are particularly vulnerable, as this age group corresponds to the peak incidence of carcinomas, myelomas, and lymphoma. The spinal column is the most common site of skeletal or osseous metastases.² Overall, 5 to 10% of cancer patients develop spine metastases during the course of their disease. Rates of metastatic spread to the spine vary widely according to the primary tumor of origin. Among women, breast cancer metastases account for nearly 54% of all spine metastases.³ The most frequent locations of tumors, in descending order, are the vertebrae (85%), the paravertebral spaces (10–15%), the epidural space (<5%), and intradural/intramedullary.⁴ Brihaye et al reported that 70.3% of metastases were located in the thoracic and thoracolumbar spine, 21.6% in the lumbosacral spine, and 8.1% in the cervical spine.⁵. Metastases are detected in multiple noncontiguous spine sites in 10 to 38% of patients.⁶

Spinal metastases precede lung and liver lesions in many cancer patients.⁷ The most common target is a lumbar vertebra.⁸

Each vertebra behaves as a separate compartment surrounded by anatomic barriers (i.e., intervertebral disc, periosteum, cortex) to neoplastic cells. The posterior one-half of the vertebral body generally is seeded first, whereas the anterior one-half, the pedicles, and the lateral masses are involved later in the disease process as cortical bone destruction advances. Minimum biologic requirements for metastasis are a competent cell, a patent anatomic route for spread, and a receptive microenvironment.⁹ The capacity to metastasize appears to arise spontaneously among tumor cells, and its genetic basis remains unknown.

Tumors can spread by direct extension, via lymphatic channels, or through hematogenous routes. Although bone lymphangiography has detected lymphatic channels in bone, most vertebral metastases appear to arise from hematogenous spread.¹⁰ Cancellous bone is attractive to many types of tumors. A typical vertebra contains 34% cancellous bone, whereas peripheral bones average 20%. Bone marrow–derived endothelial cells express adhesion ligands for prostatic cancer cells that are not expressed on hepatic endothelial cells or nonendothelial cells of the marrow.¹¹ Batson proposed that prostate carcinoma cells seed the lumbar vertebrae via the vertebral venous plexus'a network of longitudinal, valveless veins running parallel to the vertebral column that form innumerable anastomoses to the sinusoids of the vertebral marrow and the epidural venous channels.¹² Breast tumors drain via the azygous system into the Batson's plexus of the upper thoracic region, which may explain the relatively high frequency of breast lesions in the cervical spine.

Once a tumor has metastasized to a vertebra, it may locally spread to adjacent vertebrae. The pathways include (a) the subspaces beneath the anterior or posterior longitudinal ligaments (PLLs) (via direct or hematogenous routes), (b) direct extension through the anterior or posterior vertebral body rims (areas frequently uncovered by cartilage), and/or (c) migration through the paravertebral muscles. Local spread of metastatic vertebral tumors into the epidural space is most probable through the PLL because the anterior longitudinal ligament and the intervertebral disc are relatively resistant to cellular invasion.¹³ The anterior longitudinal ligament is biomechanically stronger than the PLL, and its integrity is less compromised because of a smaller number of perforating vessels.¹⁴. The highly durable intervertebral disc is resistant to tumor-related proteolysis and angiogenesis.¹⁵ The dura, which undergoes considerable thickening in the presence of tumor, also appears to be an effective barrier to local tumor spread.¹⁶

Clinical Presentation

Pain is the most common presenting complaint for patients with metastatic disease of the spine.¹⁷ The pain is gradual in onset, but progressive. It often is unrelenting, nonmechanical pain that worsens at night. Early in the disease course, the pain usually is axial. However, as the disease progresses, neural compression can lead to complaints of radicular pain. The symptoms can be reproduced by localised pressure or percussion. Patients with thoracic lesions may occasionally experience bilateral radicular pain in a corset-like distribution.³ The cause of pain is multifatorial. Several authors have suggested that the primary and most clinically relevant source of discomfort is spinal instability.¹⁸ Other causes of pain include periosteal stretching due to expansion of the cortex of the vertebral body by tumor mass, compression or invasion of adjacent nerve roots (radicular pain/paresthesias), pathologic fractures (macro- and microscopic), spinal cord and/or dura compression, and bony destruction or invasion of paraspinous tissues, such as muscles and ligaments.¹⁹. The periosteum is highly innervated by nociceptors and has the lowest pain threshold of deep somatic structures. Some metastases, such as lung, lymphoma, and renal cancer, may present as painless neurologic deficits.

Although neurologic symptoms usually occur late in the disease process, they frequently lead patients to seek medical attention. Weakness, usually in the lower extremities, may become apparent months or even years after the onset of pain and is rarely the first symptom.

Gilbert et al reported that motor weakness was a presenting symptom in 76% of patients, including 17% who were paralyzed. Fifty percent of the patients reported numbness or paresthesias. Radicular pain often accurately localized the tumor to within one or two vertebral levels.³

Light-touch fibers, running in the dorsal columns, are usually the last sensory component encroached on by a vertebral body tumor.Isolated bowel and bladder dysfunction are uncommon presenting complaints, but when present, must be assessed fully with MRI scanning, CT scanning, or myelography to determine whether neurologic compression is the cause.²⁰

Patients who present with progressive neurologic signs or symptoms must have urgent evaluation. Patients who present with severe deficits or rapidly progressive deficits have a much poorer prognosis.

Spinal cord syndromes such as Brown-Séquard or autonomic dysfunction may occur depending on the tracts affected. Orthostatic hypotension, Horner's syndrome, and ventilatory compromise may arise from lesions in the midthoracic, cervical, and high cervical spine, respectively. Respiratory distress may also arise from direct compression of the medulla oblongata or of intercostal nerves. Symptomatic compression of the cauda equina is much less common than the spinal cord or conus. Ampil et reported that only 16 (0.7%) patients presented with cauda equina compression.²¹

Other important symptoms include unintentional weight loss, anorexia, fatigue, hemoptysis, hematuria, hematochezia, hematemesis, and tobacco use. The presence of a mass in the neck, axilla, breast, abdomen, or groin and a previous personal or family history of malignancy should be evaluated.

A general physical examination, including a rectal examination, should be done on all patients suspected of having metastatic disease of the spine. The examination should focus on areas in which most primary tumors occur, including the breasts, chest, prostate, abdomen, and lymphatic system. A detailed neurologic examination also must be done and documented so that future comparison for possible neurologic deterioration can be done. Localized spinal tenderness often is present over the area involved with tumor. Multilevel tenderness may represent multilevel disease.²²

The imaging modalities most useful in the assessment of metastatic disease of the spine include plain radiographs, bone scans, CT scans, CT myelographs, and MRI scans. Anteroposterior and lateral views of the plain radiographs can reveal fractures, detect abnormal bone, and confirm disruption of spine alignment. However, small metastatic lesions may be missed because 30% to 50% of the trabecular bone must be destroyed before radiographic evidence of bone destruction is apparent.²³ In up to 60% of spine patients with neoplastic cord compression, plain radiographs are normal.²⁴ The first clue to vertebral compromise is often the “winking owl” sign seen on the anteroposterior radiograph (Figure 1). The unilateral loss of the pedicle ring corresponds to the destruction of the cortex of the pedicle, usually by tumor invading from the vertebral body proper.²⁵

Lytic lesions on radiograph are usually features of primary tumours from lung, kidneys, thyroid, adrenal and uterus. Primaries from prostate, bladder and bronchial carcinoids usually show blastic lesions.

A technetium-99 bone scan is a useful test for identifying metastatic lesions with an osteoblastic response. It is less reliable when evaluating purely lytic lesions. The overall sensitivity of technetium-99m scans (>70%) can be further improved (>90%) by adding single-photon emission tomography.²⁶

CT scan is important for the evaluation of cortical erosion, fracture, overall bone quality, and surgical planning. It is however not as accurate as MRI in determining the extent of tumor soft-tissue and bone marrow involvement. Axial images can demonstrate whether canal compromise is due to bone or soft tissue and can assess the structural integrity of contiguous vertebral elements. CT of the lungs is an essential staging tool for patients who have musculoskeletal malignancies. CT-myelography can be used to diagnose and evaluate spinal cord compression. Myelography, however, is invasive, uncomfortable for the patient, and prone to complications. MRI has largely replaced myelography, particularly when surgical planning requires defining the cranial and caudal boundaries of the lesion. However, patients with implanted pacemakers, aneurysm clips, intraocular devices, and cochlear implants may not be suitable for MRI, and myelography may be the only alternative.

Magnetic resonance imaging is the imaging modality of choice for evaluation of metastatic disease of the spine. Bony involvement, soft tissue extension, and neural element compression can be assessed in the same study. MRI can detect lesions as small as 3 mm in diameter.²⁷ Imaging of the entire spine in patients with a single known metastasis reveals multiple, clinically unsuspected foci in 25% of cases.²⁸ Li and Poon reported a 93% sensitivity and 97% specificity for MRI in the assessment of metastatic disease.²⁹ Gadolinium-enhanced MRI is not helpful in most cases of vertebral metastases.³⁰

Tumor infiltration of bone marrow decreases the signal on T1-weighted images and increases the signal on T2-weighted images. A normal T1 marrow signal within a collapsed vertebral body effectively rules out a neoplastic etiology. Pedicle involvement and an associated soft-tissue mass are both fairly specific for tumor. The T1-weighted and T2 short tau inversion recovery sequences are very sensitive in detecting tumor-infiltrated bone.³¹ Although MRI is useful for estimating tumor dimensions in the extremities, MRI consistently overestimates the dimensions of spine tumors. MRI is useful in avaluating spinal cord compression, however, the clinically defined sensory levels correlate poorly with MRI abnormalities.^28,32

Recently, positron emission tomography (PET) has been shown to be a sensitive and specific instrument for detecting and monitoring metastases.³³ As a screening modality, [¹⁸F]fluorodeoxyglucose (FDG)-PET has been shown to be superior to skeletal scintigraphy and [¹⁸F]fluoride-PET in detecting bone metastases.³⁴

Evaluation

A thorough and complete evaluation must be performed in order to exclude other pathologic conditions. Differential diagnoses for spine tumors include infection, metabolic disorders, congenital abnormalities, trauma and pseudotumors (e.g., spinal tuberculosis, hydatid cysts, the SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, osteitis), fibrous dysplasia, brown tumors, osteoporotic collapses, and bone islands).

A complete evaluation includes routine laboratory serology, plain radiographs of the lesion and of the chest, a bone scan, appropriate CT scans (chest/abdomen/pelvis), and a biopsy.

The tissue diagnosis of a new lesion may be necessary to guide treatment, even in patients with known metastatic disease. The biopsy should be performed by the definitive treating surgeon. Biopsies can be incisional, excisional or performed by fine-needle aspiration. A biopsy with a Craig needle should be performed under local anesthesia with mild sedation so the patient can warn the clinician if nerve root irritation is occurring. The overall diagnostic accuracy of fine-needle aspiration varies between 67 to 97%, with a definitive result in 65% of osteolytic and 20 to 25% of osteoblastic lesions.^35,36 The incisional (open) biopsy should be the last step in staging the patient, performed just before the definitive surgical resection. Laminectomies should be avoided in patients with suspected tumors, due to the inevitable contamination of the epidural space. Transpedicular biopsy is preferred, and the empty pedicle may be plugged with acrylic cement. A transpedicular approach is safe at any level within the entire thoracolumbar spine.

Carcinomas that frequently metastases to the spine include lung, prostate, breast, thyroid, renal, and gastrointestinal tract cancers. The biology of the primary cancer dictates the presentation, treatment, and prognosis. Paraplegia may often evolve acutely (within 48 hours) from metastatic bronchogenic carcinoma, lymphoma, and renal cell cancers. Breast cancers however, tend to follow slower course. The overall prognosis for patients with metastases from lung and gastrointestinal source is poor.

Classification and Scoring System

Treatment of patients with metastatic disease of the spine is palliative, not curative. The goal of treatment is to maximize the patient’s quality of life by providing pain relief and maintaining or restoring neurologic function. In the majority of patients, this goal is reached through nonoperative means by chemotherapy and radiation. For patients who are appropriate candidates, surgical intervention offers an opportunity to maintain or restore quality of life.

Few classification schemes have been proposed as a guide to treatment. Harrington divided patients with spinal metastases into five categories based on the extent of neurologic compromise and bone destruction. Patients in Class I have no significant neurologic involvement. Patients in Class II have involvement of bone without collapse or instability and minimal neurologic involvement. Patients in Class III have major neurologic impairment without significant involvement of bone. Patients in Class IV have vertebral collapse with pain attributable to mechanical causes or instability but without significant neurologic compromise. Finally, patients with vertebral collapse or instability with major neurologic impairment are designated as being in Class V.³⁷ Patients in Class I and II generally obtain pain relief with chemotherapy or hormonal manipulation. If these are unsuccessful, then local radiation is recommended. Patients in Class III usually respond to radiotherapy alone. If neurologic compromise is acute, then the addition of steroid treatment should be considered. Surgical treatment is considered for patients in Class IV and Class V.

Tokuhashi et al developed a prognostic scoring system based on six parameters. The parameters are general health condition, number of extraspinal bone metastases, number of vertebral metastases, metastases to the major internal organs, and primary site of cancer and level of spinal cord palsy (Table 1). Tokuhashi et al applied this system to 183 patients and reported that patients with a total score of 12 to 15 survived an average of 12 months or more, those with 9 to 11 survived 6 months or more; and those with 8 points or less survived 6 months or less.³⁸ Based on this information, they recommended that patients with a score of 12 points or greater have an excisional procedure, whereas a palliative operation is indicated for patients scoring 8 points or less. In patients with a total score of 9 to 11, excisional procedures were rarely indicated in a single lesion without metastases to the major internal organs.

Walker et al has proposed an algorithm for evaluation and treatment of patients with metastatic disease of the spine.³⁹ For patients with an acceptable prognosis for survival (> 3–6 months) and medical status, surgical indications include progressive neurologic deficit secondary to neurologic compression from a radioresistent tumor; spinal instability; severe intractable pain unrelieved by nonoperative measures; radioresistant tumor that is enlarging, causing intractable pain, or impending instability; and the need for a definitive histologic diagnosis.^40,41 Patients with inadequate bone stock, multiple areas of epidural compression, or life expectancy less than 3 months, generally are not considered for operative treatment.

Spinal instability is important in metastatic spine disease. A proper assessment must be carried out before making an appropriate treatment decisions. White et al defined stability as the ability of the spine, under physiologic loads, to prevent initial or additional neurologic damage, severe intractable pain, and gross deformity.⁴² There are several classification systems for the assessment of spinal instability as it relates to spinal trauma. For thoraculumbar spine trauma, the most widely used classification scheme is the three-column system of Denis.⁴³ The anterior column includes the anterior longitudinal ligament and the anterior half of the vertebral body, disk, and annulus. The middle column includes the posterior half of the vertebral body, disc, and annulus and the posterior longitudinal ligament. The posterior column includes the posterior elements and their associated ligaments, and the facet capsules (Figure 3). The spine is considered unstable if two of the three columns are disrupted. However, its usefulness in patients with metastatic disease of the spine has been questioned. A six-column system has been proposed by Kostuik and Erico in an attempt to design a set of criteria specific for instability in spinal tumors.⁴⁴. Their system was based on Denis three-column system with the spine is subdivided into right and left halves. The spine is considered unstable if at least three columns are destroyed or there is more than 20° of angulation.

A classification system for primary neoplasm proposed by Weinstein et al described the anatomic location and provided information for surgical planning and communication. It is also applicable to metastatic disease.⁴⁵

Management

Treatment options can be non-surgical or surgical options. Radiation, chemotherapy, and surgery complement each other in optimizing local and distant tumour control. Non-surgical treatments include physical therapy and orthoses, radiation therapy, embolisation, vertebroplasty and kyphoplasty, and chemotherapy.

Cancer patients must be carefully monitored for tumor-related complications. Malnutrition, depression, venous thromboembolism (particularly in primary central nervous system tumors and mucinous adenocarcinomas), hypercalcemia (multiple myeloma, metastatic breast, lung, kidney), anemia, and pleural effusions (metastatic breast, lung, and gastrointestinal tumors) are often overlooked in advanced-stage cancer.

Although more than 90% of patients with advanced disease report adequate pain control, analgesia is inadequate in 30 to 50% of ambulators.⁴⁶ A three-step model for analgesia is generally accepted. Step 1 is nonsteroidal antiinflammatory drugs, step 2 is short-acting opioids and step 3 is pure opioid agonists with relatively linear dose-response curves.

Prophylactic use of bisphosphonates in breast cancer and multiple myeloma decreases the incidence of new bone metastases, orthopedic events, and malignant hypercalcemia.⁴⁷ Second generation agent pamidronate decreases tumor burden, induces remission, and promotes healing in patients with metastatic breast cancer or myeloma.⁴⁸

Physical therapy sessions should include instruction in back-sparing transfers, training in the use of assistive devices, and evaluation for bracing. Orthoses may be helpful in restricting motion and alleviating symptoms in patients whose pain is exacerbated by spinal flexion or rotation. Bracing also may help prevent kyphotic collapse while the bone heals after local therapy. Although spinal movement is limited between the endpoints of the orthosis, spinal motion may actually be increased at either end of the brace.⁴⁹ The braces should be extended several segments above and below the involved spine segments. In general, 10 to 12 weeks of bracing from the onset of radiation therapy is adequate.⁵⁰ General indications for radiation therapy include pain without instability, neurologic compromise, or deformity. Sensitivity to radiation is variable. Metastases from prostate is highly radiosensitive while metastases from renal, thyroid, colon and sarcomas are relatively insensitive.

The efficacy of radiation is dependent on active cell division occurring in the target tissue. Radiation therapy reduces pain in more than 70% of patients, improves motor function in 45 to 60%, and reverses paraplegia in 11 to 16%.⁵¹ The radiation affects the skin healings and the survival of the graft. It should be avoided preoperatively. The radiation therapy also should be delayed until after 4 or more weeks postoperatively. Side effects of skeletal radiation therapy are divided into acute (i.e., mild to moderate fatigue, skin irritation, nausea, bone marrow suppression) and late (i.e., fractures, nonunions). Radiation-related osteitic bone necrosis most commonly occurs after doses greater than 3,500 cGy and may result in progressive kyphosis.⁵² Marrow is uniformly depressed after the first week, but hematopoietic regeneration begins in 7 to 10 days. Neoplasia is associated with dosages greater than 3,000 cGy and becomes clinically evident only after a lag period of several years (e.g., 3 to 4 years for leukemia, 11 years for sarcomas). Radiotherapy does not prevent progressive collapse after the onset of vertebral deformity.⁵³ Six to twelve months is required for the maturation of irradiated lesions to normal bone.

Percutaneous injection of polymethylmethacrylate (PMMA) cement into a pathologically collapsed vertebral body (vertebroplasty) has been shown to be effective for the treatment of pain (Figure 4).⁵⁴ Symptom relief in vertebroplasty is often immediate. Significant initial pain relief was reported in 95% of patients treated by vertebroplasty for osteoporotic fractures or for neoplastic lesions.⁵⁵ Although it is assumed that such techniques minimize mechanical pain via cement-augmented structural support, it is possible that the cement itself possesses analgesic properties within the vertebral body.⁵⁶ Main complication of vertebroplasty is leakage of PMMA through cortical defect with epidural compression of the neural elements.⁵⁷ Vertebroplasty, however, fails to restore vertebral height and correct deformity particularly in patients with multiple compromised adjacent segments. Kyphoplasty, on the other hand, is a modification of vertebroplasty designed to reduce deformity and spinal malalignment (Figure 5). During kyphoplasty, a balloon-equipped bone tamp is passed into the vertebral body and inflated to restore lost vertebral height. Once inflated, the balloon creates a cavity for the subsequent injection of PMMA, stabilizing the reconstruction. Lieberman et al⁵⁸ reported that symptoms and function were improved in 90% of patients, the average postprocedure anterior vertebral height was 99 ± 13% of that predicted for prefracture, and major complications were rare.

Surgical treatment

The goals of surgery are to decrease pain, to preserve or to improve neurologic function, and to mobilize the patient without lifelong external orthosis. Indications for surgery include the need to access the spine to obtain a diagnosis, to decompress neural elements, or to stabilize and/or reconstruct the spine. The approach depends on the location of the tumor and the surgical goal. Currently, technical advances allow resection of tumors at all levels of the spinal column.

Restoration of the stability of the spine is the major goal of surgery. A 3-column an 6-column concepts proposed by Denis⁴³ and Kostuik⁴⁴ are widely used. However, determination of stability is not always straight forward. There is no consensus regarding what constitutes instability except in obvious cases of fracture-dislocations, translational instability, or notable kyphosis.

The spine is a load-sharing system with 80% to 90% of the axial load bearing absorbed by the vertebral bodies and approximately 10% to 20% through the posterior joints. Although most tumors involve the middle and anterior columns, anterior reconstruction alone may be insufficient for restoring torsional stability or tensile strength because the pedicles and joint may be involved. However, an extensive anteroposterior fixation is often unnecessary. The rationale for surgery should be based not only on biomechanical considerations but also on the expected goals of therapy and the longevity of the patient.

Several clinical prognosticators have been proposed in cases of spinal metastatic disease. Yamashita et al⁵⁹ reported longer survival in patients with spinal or pelvic lesions compared with those with appendicular lesions or both. Tokuhashi et al³⁸ proposed a scoring system which predicts patient’s survival period and gives guide on treatment option.

Decompressive laminectomy and posterior instrumentations is performed easily to relieve compression of the spinal cord, cauda equine and nerve roots of the cervical, thoracic and lumbar spine. However, this approach is beneficial in 405 of patients.^60,61 Other authors found no significant difference in outcome in studies comparing combined radiotherapy and laminectomy with laminectomy alone.^622,63

The mediocre outcomes of laminectomy are not surprising because pure posterior lesions are uncommon and the procedure does not adequately decompress the ventral spinal cord. Major limitations of laminectomy are inadequate access to the anterior aspect of the spinal cord and loss of stability.

Posterolateral approaches combine the simplicity of laminectomy with the ability to decompress the ventral aspect of the dural tube. These approaches are useful in patients with ventral disease and comorbidity that prevent transthoracic, transabdominal, or retroperitoneal approaches. It provides adequate access to the posterolateral spine while allowing concurrent posterior access.

Most metastatic tumours arise from the vertebral body. An anterior excision and reconstruction is preferable.⁶⁴ The anterior approach is technically more challenging but is associated with an 85% success rate, moderate blood loss, and few neurologic complications. Anterior instrumentation with strut grafting (e.g., allograft, cage, PMMA) provides excellent stability after corpectomy.^65,66 After vertebrectomy, anterior plate fixation combined with anterior column reconstruction restores sagittal, coronal, and torsional rigidity, often eliminating the need for posterior fixation in selected patients.⁶⁷ Anterior instrumentation also minimizes the chance for strut graft, cage, or PMMA spacer displacement. Although the operative mortality rates were identical for both surgical methods, the complication rate was higher in the posterior group because of the poor healing of irradiated wounds.⁶⁸

Patients with advanced-stage cancers are generally in poor medical condition. Patients undergoing palliative resection of spine metastases are prone to further neurologic deterioration, wound breakdown, and increased rates of infection. Reported surgical complication rates of 20 to 25% are common.^69,70

Inadequate wound healing is a very common postoperative complication in spinal surgery, particularly in cancer patients. Factors contributing to poor wound healing include concurrent use of corticosteroids for vasogenic cord edema, local radiation, bone marrow suppression, and poor nutritional status.

Complications of surgery include damage to the great vessels, ureters and intra-abdominal contents. Also, urogenital complications, such as retrograde ejaculation, due to sympathetic injury are well described.⁷¹ As with thoracoabdominal exposure, damage to the anterior spinal artery can occur with anterior approaches. There are areas of limited blood supply to the anterior spinal cord at the upper and lower cervical and throughout the thoracic spine. The artery of Adamkiewicz, the largest radiculomedullary artery supplying the inferior thoracic cord, generally branches from the left side between T8 and L2.

Conclusion

The vertebral column is the most common site for bony metastases. Pain is the most common presentation followed by progressive neurological deficits. Treatment of patients with metastatic disease of the spine is a challenging problem. The goal should be clearly defined. The treatment should be a multidisciplinary effort that follows a logical orderly protocol. Patients with advanced-stage cancer are almost uniformly debilitated and may have other visceral or osseous sites of involvement. Medical and physical condition of these patients should be maximised before undertaking surgical intervention to improve their chances of positive short and long term outcomes. The patient's preoperative functional status and level of activity correlate directly with postoperative outcome.⁷² Multimodality therapy with vertebroplasty/kyphoplasty, stereotactic radiosurgery, bisphosphonates, and other pharmacological therapies and a team approach to the operative and nonoperative care of patients with spinal metastases will lead to better outcomes.

Parameters	Points
	0	1	2
General health condition		Poor	Moderate	Good
No. Of extraspinal bone metastases		≥3	1-2	0
No. Of vertebral metastases		≥3	2	1
Metastases to the major internal organ		Unremovable	Removable	No mets
Primary site of cancer		Lung, stomach	Kidney, liver, uterus, others, unidentified	Thyroid, breast, prostate, rectum
Spinal cord palsy		Complete	Incomplete	None

Table and Figures

Table 1: Prognostic scoring scheme by Tokuhashi et al.

Figure 1: Winking Owl sign (Black arrow).

Figure 2: Algorithm for evaluation and treatment of patients with metastatic disease of the spine. (Walker et al. Clinical Orthopaedics and Related Research October 2003)

Figure 3: Three column concept. (Denis F Clinical Orthopaedic 1984)

Figure 4: Vertebroplasty. A biopsy needle is guided into the fractured vertebra through a small incision in the skin.

Figure 5: Kyphoplasty

Reference

1. Asdourian PL. Metastatic disease of the spine. In: Bridwell KH, DeWald RL, eds. The textbook of spinal surgery, 2nd ed., vol. 2. Philadelphia: Lippincott–Raven, 1997:2007–2050.

2. Aaron AD. The management of cancer metastatic to bone. JAMA. 1994;15:1206–1209.

3. Gilbert H, Apuzzo M, Marshall L, et al. Neoplastic epidural spinal cord compression. A current perspective. JAMA. 1978;240:2771–2773.

4. Byrne TN. Spinal cord compression from epidural metastases. N Engl J Med 1992;327:614–619.

5. Brihaye J, Ectors P, Lemort M, et al. The management of spinal epidural metastases. Adv Tech Stand Neurosurg 1988;16:121.

6. Gilbert et al. Ruff RL, Lanska DJ. Epidural metastases in prospectively evaluated veterans with cancer and back pain. Cancer. 1989;63:2234–2241.

7. Bubendorf L, Schopfer A, Wagner U, et al. Metastatic patterns of prostate cancer: an autopsy study of 1,589 patients. Hum Pathol. 2000;31:578–583.

8. Galasko CSB. Incidence and distribution of skeletal metastases. In: Skeletal metastases. Stoneham, MA: Butterworth, 1986:14–22.

9. Mollabashy A, Scarborough MT. The mechanism of metastasis. Orthop Clin North Am. 2000;31:529–535.

10. Spjut HJ, Dorfman HD, Fechner RE, et al. Tumors and cartilage. Washington, DC: 1971.

11. Haq M, Goltzman, D, Tremblay G, et al. Rat prostate adenocarcinoma cells disseminate to bone and adhere preferentially to bone-marrow derived endothelial cells. Cancer Res. 1992;52:4613–4619.

12. Batson OV. The function of the vertebral veins and their role in the spread of metastases Arch Surg. 1940;112:138-149.

13. Fujita T, Ueda Y, Kawahara N, et al. Local spread of metastatic vertebral tumors. Spine 1997;22:1905–1912.

14. Mykleburst JB, Pinter F, Yoganandan N, et al. Tensile strength of spinal ligaments. Spine 1988;13:526–531.

15. Eisenstein R, Kuettner KE, Neapolitan C, et al. The resistance of certain tissues to invasion, III. Cartilage extracts inhibit the growth of fibroblasts and endothelial cells in culture. Am J Pathol 1975;81:337–347.

16. Harrington KD. Metastatic disease of the spine. J Bone Joint Surg Am 1986;68:1110–1115.

17. Gilbert RW, Kim JH, Posner JB: Epidural spinal cord compression from metastatic tumor: Diagnosis and treatment. Ann Neurol 3:40–51, 1978.

18. Galasko CSB, Norris HE, Crank S. Spinal instability secondary to metastatic cancer. J Bone Joint Surg Am 2000;82:570–576.

19. Boriani S, Weinstein JN. Differential diagnosis and surgical treatment of primary benign and malignant neoplasms. In: Frymoyer JW, ed. The adult spine. Philadelphia: Lippincott–Raven, 1997: 951–987.

20. Riley LH, Frassica, DA, Kostuik JP, Frassica FJ: Metastatic disease to the spine: Diagnosis and treatment. Instr Course Lect 49:471–477, 2000.

21. Ampil FL, Mills GM, Burton GV. A retrospective study of metastatic lung cancer compression of the cauda equina. Chest 2001;120:1754–1755.

22. O’Connor MI, Currier BL: Metastatic disease of the spine. Orthopedics 15:611–620, 1992.

23. Edelstyn GA, Gillespie PJ, Grebbell ES: The radiologic demonstration of osseous metastases: Experimental observations. Clin Radiol 18:158–162, 1967.

24. Silverberg E, Lubera J. Cancer statistics. Cancer 1988;381:5–22.

25. Brice J, McKissock W. Surgical treatment of malignant extradural spinal tumors. BMJ 1965;1:1341–1344. Jacobson JG, Poppel MH, Shapiro JH, et al. The vertebral pedicle sign. AJR Am J Roentgenol 1958;80:817.

26. Han LJ, Au-Yong TK, Tong WC, et al. Comparison of bone single-photon emission tomography and planar imaging in the detection of vertebral metastases in patients with back pain. Eur J Nucl Med 1998;25:635–638.

27. Petren-Mallmin M, Nordstrom B, Andreasson I, et al. MR imaging with histopathological correlation in vertebral metastases of breast cancer. Acta Radiol 1992;33:213–220.

28. Husband DJ, Grant KA, Romaniuk CS. MRI in the diagnosis and treatment of suspected malignant spinal cord compression. Br J Radiol 2001;74:15–23.

29. Li KC, Poon PY: Sensitivity and specificity of MRI in detecting malignant spinal cord compression and in distinguishing malignant from benign compression fractures of vertebrae. Magn Reson Imaging. 1988;6:547–556.

30. O’Connor MI, Currier BL: Metastatic disease of the spine. Orthopedics. 1992;15:611–620.

31. Baker LL, Goodman SB, Peckash I. Benign versus pathological compression fracture of vertebral bodies: assessment with conventional spin-echo, chemical shift, and STIR MR imaging. Radiology. 1990;174:495–502.

32. Lau TN, Tomlinson MJ, et al. Magnetic resonance imaging of the whole spine in suspected malignant spinal cord compression: impact on management. Clin Oncol (R Coll Radiol). 1998;10:39–43.

33. Cook GJ, Fogelman I: The role of positron emission tomography in the management of bone metastases. Cancer. 2000;88:2927–2933.

34. Fogelman I, Cook G, Israel O, Van der Wall H: Positron emission tomography and bone metastases. Semin Nucl Med. 2005;35:135–142.

35. Ayala AG, Zornosa J. Primary bone tumors: percutaneous needle biopsy. Radiologic-pathologic study of 222 biopsies. Radiology. 1983;149:675–679.

36. Boland PJ, Lane JM, Sundaresan N. Metastatic disease of the spine. Clin Orthop. 1982;169:95.

37. Harrington KD: Metastatic disease of the spine. J Bone Joint Surg. 1986;68A:1110–1115.

38. Tokuhashi, Yasuaki MD; Ajiro, Yasumitsu MD; Umezawa, Natsuki MD. Outcome of Treatment for Spinal Metastases Using Scoring System for Preoperative Evaluation of Prognosis. Spine. 2009:34(1);69-73.

39. Walker, Matthew P., Yaszemski, Michael J, Kim, Choll W, Talac, Robert, Currier, Bradford L. Metastatic Disease of the Spine: Evaluation and Treatment. Clinical Orthopaedics and Related Research. 2003:415;165-175.

40. Kostuik JP, Errico TJ, Gleason TF, et al: Spinal stabilization of vertebral column tumors. Spine.1988;13:250–256

41. McLain RF, Weinstein JN: Tumors of the spine. Semin Spine Surg. 1990:2:157–180.

42. White III AA, Panjabi MM, Posner I, Edwards WT, Hayes WC: Spinal stability: Evaluation and treatment. Instr Course Lect. 1981:30:457–483.

43. Denis F: Spinal instability as defined by the three-column spine concept in acute spinal trauma. Clin Orthop. 1984:189:65–76.

44. Kostuik JP, Errico JN: Differential Diagnosis and Surgical Treatment of Metastastic Spine Tumors. In Frymoyer JW (ed). The Adult Spine: Principles and Practice. Vol 1. New York, Raven Press 861–888, 1991.

45. Abdu WA, Provencher MT, Weinstein JN: Classification of Spinal Metastases. In Heiner JP, Kinsella TJ, Zdeblick TA (eds). Management of Metastatic Disease to the Musculoskeletal System. St Louis, Quality Medical Publishing. 2002:370–372.

46. Savage PD, Ward WG. Medical management of metastatic skeletal disease. Orthop Clin North Am. 2000;31:545–555.

47. Lipton A. Bisphosphonates and breast carcinoma. Cancer 1997; 80:1668–1673.

48. Diel IJ, Solomayer E-F, Costa SD, et al. Reduction in new metastases in breast cancer with adjuvant clodronate treatment. N Engl J Med 1998;339:357–363.

49. Abeloff MD, Armitage JO, Lichter AS, eds. Clinical oncology. New York: Churchill Livingstone, 1995:2207.

50. Zdeblick TA. Metastases to the lumbar spine. In: Heiner JP, Kinsella TJ, Zdeblick TA, eds. Management of metastatic disease to the musculoskeletal system. St. Louis: Quality Medical Publishing, Inc., 2002.

51. Maranzano E, Latini P. Effectiveness of radiation therapy without surgery in metastatic spinal cord compression: final results from a prospective trial. Int J Radiat Oncol Biol Phys 1995;32:959–967.

52. Howland WJ, Loeffler JS, Starchman DE, et al. Postirradiation atrophic changes of bone and related complications. Radiology. 1975;117:677.

53. Asdourian PL, Weidenbaum M, DeWald RL, et al. The pattern of vertebral involvement in metastatic vertebral breast cancer. Clin Orthop Rel Res. 1990;164–170.

54. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg. 2003;98:21–30.

55. Barr JD, Barr MS, Lemley TJ, et al. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine 2000;25:923–928.

56. Aebli N, Goss BG, Thorpe P, et al. In vivo temperature profile of intervertebral discs and vertebral endplates during vertebroplasty: an experimental study in sheep. Spine. 2006;31:1674–1678.

57. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg 2003;98:21–30.

58. Lieberman IH, Dudeney S, Rheinhardt M-K, et al. Initial outcome and efficacy of kyphoplasty in the treatment of painful osteoporotic vertebral compression fractures. Spine 2001;26:1631–1639.

59. Yamashita K, Denno K, Ueda T, et al. Prognostic significance of bone metastases in patients with metastatic prostate cancer. Cancer. 1993;71:1297-1302.

60. Constans JP, de Divitiis E, Donzelli R, Spaziante R, Meder JF, Haye C. Spinal metastases with neurological manifestations: review of 600 cases. J Neurosurg. 1983;59:111-118.

61. Sorensen S, Borgesen SE, Rohde K, et al. Metastatic epidural spinal cord compression: results of treatment and survival. Cancer. 1990;65:1502-1508.

62. Byrne TN. Spinal cord compression from epidural metastases. N Engl J Med. 1992;327:614-619.

63. Young RF, Post EM, King GA. Treatment of spinal epidural metastases: randomized prospective comparison of laminectomy and radiotherapy. J Neurosurg. 1980;53:741-748.

64. Simmons ED Jr. Anterior reconstruction for metastatic thoracic and lumbar spine disease. In: Bridwell KH, DeWald RL, eds. The textbook of spinal surgery. Philadelphia: Lippincott–Raven, 1997:2057–2070.

65. Walsh GL, Gokaslan ZL, McCutcheon IE, et al. Anterior approaches to the thoracic spine in patients with cancer: indications and results. Ann Thorac Surg. 1997;64:1611–1618.

66. Harrington KD. Anterior cord decompression and spinal stabilization for patients with metastatic lesions of the spine. J Neurosurg. 1984;61:107–117.

67. Hall DJ, Webb JK. Anterior plate fixation in spine tumor surgery. Indications, technique, and results. Spine. 1991;16:S80–S83.

68. Siegal T, Tiqva P. Vertebral body resection for epidural compression by malignant tumors. Results of forty-seven consecutive operative procedures. J Bone Joint Surg Am. 1985;67:375–382.

69. Wise JJ, Fischgrund JS, Herkowitz HN, et al. Complication, survival rates, and risk factors of surgery for metastatic disease of the spine. Spine. 1999;24:1943–1951.

70. McPhee IB, Williams RP, Swanson CE. Factors influencing wound healing after surgery for metastatic disease of the spine. Spine 1998;23:726–732.

71. Johnson RM, McGuire EJ. Urogenital complications of anterior approaches to the lumbar spine. Clin Orthop Relat Res. 1981;154:114-118.

72. Bednar DA, Brox WT, Viviani GR. Surgical palliation of spinal oncologic disease: a review and analysis of current approaches. Can J Surg. 1991;34:129-131.