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Cancer has consistently been a leading cause of death in the developed world and, by most predictions, has now become the leading cause of death worldwide. Carcinomas arising from lung, breast, prostate, and thyroid are by far the most common types of cancer, with more than 1.5 million new cases in the United States annually. Ten to thirty percent of those patients present with symptomatic metastases to bone. Sarcomas involving bone are less common and comprise approximately 2000 new cases per year.
The spine is the most common site of metastatic disease involving bone. Most spine metastases occur in the thoracic and lumbar spine. The cervical spine is less often affected by metastatic disease, yet metastasis still occurs with a greater frequency per year than do primary bone sarcomas.
Metastatic cervical spine disease presents unique challenges to both the patients fighting their malignant diseases and the medical professionals involved in their care. Optimal care of the patient with metastatic disease of the cervical spine requires a multidisciplinary team that includes physicians specializing in both spinal surgery and oncology, medical oncologists, radiation oncologists, interventional radiologists, pathologists, therapists, nutritionists, and skilled nursing staff. All these individuals are critical in (1) identifying the unique challenges metastatic spine disease presents and (2) developing a comprehensive treatment plan that addresses all the necessary issues to give the patient the best possible functional outcome.
The approach to the patient with a pathologic lesion in the cervical spine should be systematic, with three basic points in mind: (1) prevent irreversible damage in the acute setting, (2) confirm the diagnosis of metastatic disease, (3) and develop an individualized treatment plan based on the personality of the patient and the specific features of the disease ( Fig. 24-1 ).
First, the clinician must determine the acuity of the patient’s symptoms and the possibility for rapid decline. This determination helps the clinician determine whether prompt care is warranted, thereby superseding other basic principles that guide care in the oncologic patient. When an emergency arises, prompt medical and surgical treatment should be initiated to stabilize the patient while at the same time minimizing future complications that may affect the definitive management of the patient.
Second, the clinician must determine whether the lesion is a metastatic lesion. Imaging should be obtained to localize all areas of disease. Does the patient have a known primary tumor? Are multiple lesions present, or is this a solitary lesion? Is the lesion anatomically and radiologically consistent with metastatic disease? The imaging results can often help the clinician make a radiologic diagnosis of metastatic disease; occasionally however, radiologic findings are equivocal, and further steps must be taken. If the lesion cannot be firmly attributed to metastatic disease, then the clinician is obligated to obtain tissue to make the diagnosis.
The biopsy should adhere to firm principles that limit contamination of vital structures anatomically associated with the lesion. A core needle biopsy usually provides diagnostic tissue without the potential destabilizing consequences of an open biopsy requiring laminectomy or corpectomy. A needle biopsy also minimizes contamination of surrounding tissue when compared with an open biopsy. If the results of a needle biopsy are nondiagnostic, then an open biopsy should be performed. The open biopsy must be well planned and coordinated with a pathologist so that a firm pathologic decision can be made and the appropriate intraoperative procedures can be performed.
Third, the definitive management plan must consider the patient’s overall health, prognosis, ability to withstand invasive procedures, and personal goals and expectations. Clear and realistic expectations must be defined and related to the patient. Counseling regarding planned treatments and possible complications should be comprehensive and involve as many members of the family and health care team as possible, under the direction of a team leader.
The term metastasis was first introduced in 1829 by Joseph Récamier when he differentiated primary bone and soft tissue “sarcomas” from lesions that arose in bone secondarily from another site, “metastasis.” His description of metastasis was preceded by Astley Cooper’s reporting in 1818 of several cases of “tumors of a similar kind forming other parts of the body . . . and in organs of the greatest importance to life.” Such early observations have inspired years of investigation by brilliant, dedicated people, yet the exact mechanism by which tumors spread from one organ to another is, frankly, not well understood.
Similarly, the reason that the spine is the most common site of metastatic disease is unknown. Bidirectional blood flow through Batson valveless venous channels may explain to some degree the tendency for metastasis to occur with such frequency in the spine. Several such theories exist; however, none of them can fully explain the observed phenomena. The most reasonable explanation for metastatic deposits in the spine is likely multifactorial, involving both mechanical and biologic factors.
Once the tumor has metastasized to bone, the effects of the tumor on bone can vary. The subsequent progression of disease is related to the aggressiveness of the tumor, the level of the lesion within the cervical spine, the location of the lesion within the vertebral body, and the association of the lesion with anatomic structures. Tumor growth cannot occur within the vertebral body without displacing or destroying that which previously exists. The tumor cells accomplish this by activating osteoclasts, which then resorb bone, thereby allowing further growth of the tumor while undermining the structural integrity of the spine.
The loss of the structural integrity of the cervical spine has serious ramifications. Locally, the collapse of the vertebral body may lead to significant kyphotic deformity. The deformity can cause, alone or in the presence of extruded tumor, compression on the neural structures resulting in progressive and permanent neurologic dysfunction. Tumor can also compress the vertebral or spinal arteries and lead to ischemic complications.
The cervical spine is composed of seven vertebrae, three biomechanically distinct regions, and two junctions. The posterior half of the vertebral body is most likely affected early, and disease in this location may be related to vascular transmission of tumor from the primary site. As tumor progresses and cortical bone is destroyed, the anterior half of the vertebral body, as well as areas dense in cortical bone such as the pedicles, lateral masses, and transverse processes, is affected.
The upper cervical region (C1 and C2) functions as a distinct unit and, when considered with its occipital articulation, forms the basis of the occipitocervical junction. The middle cervical region (C3 to C6) is the most common region affected by metastatic disease. It is responsible for the lordotic sagittal alignment and does not contain a transitional zone. The last cervical segment (C7), together with the upper thoracic vertebrae (T1 and T2), forms the cervicothoracic junction.
The location and the level of the lesion affect not only the patient’s symptoms, but also the indication for invasive treatments and their approaches. The spacious spinal canal and thick ligaments in the upper cervical region make spinal cord compression and neurologic deficits uncommon; mechanical instability and pain predominate. Recalcitrant pain and instability are indications for surgical treatment.
In the midcervical region, spinal cord compromise is more common, and patients often present with pain and myelopathy. Sagittal imbalance may occur, leading to a disabling kyphotic posture.
The normal transition from lordosis of the midcervical spine to kyphosis of the thoracic spine occurs at the cervicothoracic junction. This region is normally under high stress. When the structural support is disrupted by tumoral progression, it results in a high rate of myelopathy secondary to exacerbation of the kyphotic stresses and a relative small spinal canal size.
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