Neoplastic cord compression

By far the commonest type of neoplastic spinal cord compression is that caused by secondary tumour deposits. Up to one third of patients with malignant disease have deposits in the spine.57,58 These are most commonly found in the vertebral body and pedicles with direct spread into the spinal canal (Figure 10.9). Metastatic tumour is confined to the spinal extradural space in only about 5% of cases.59 The most common primary tumours are bronchus, breast, gastrointestinal tract, prostate, kidney, myeloma, and lymphoma. Most secondary deposits are found in the thoracic spine, and where there are multiple lesions they may not be contiguous. Secondary deposits are less common in the lumbar and cervical spine and they are uncommon or rare in the sacral spine. This distribution may be explained by the venous drainage of affected primary organs through the spinal extradural venous plexus and the relatively larger size of the thoracic spine.

As the tumour enlarges and encroaches on the spinal cord, the signs and symptoms of myelopathy develop progressively. This is associated with spinal pain in over 90% of patients and in retrospect these patients are often found to have complained of pain in the affected region for many weeks before the development of clinical myelopathy.60 In most cases the myelopathy progresses gradually, usually over a period of days or weeks. As the compression increases, the ability of the spinal canal to accommodate the extra volume is exhausted and the rate of neurological deterioration increases rapidly. The typical patient has complained of thoracic spinal pain for perhaps four to six weeks with gradual development of fatigue in the lower limbs followed by decreased gait quality and finally rapid development of weakness and loss of sensation. The apparent acute presentation is therefore usually only the final stage of a more gradual process.61 Spinal pain in a patient with a known malignancy demands investigation even in the absence of neurological symptoms and signs. Once these occur the need for imaging becomes emergent.

Acute spinal cord compression due to secondary tumour does occur when the tumour enlarges very rapidly as a result of haemorrhage or where a vertebral body suddenly collapses because of extensive neoplastic infiltration.

The clinical features of acute neoplastic cord compression are not sufficiently characteristic to permit an accurate pathological diagnosis. Other causes of acute cord compression may present in a similar clinical fashion. The diagnosis must be confirmed by appropriate spinal imaging. Initially plain radiographs of the relevant spinal region should be obtained, although the whole spine needs to be imaged as up to 17% of patients have multiple lesions.60 The typical features of metastatic involvement include loss of vertebral height, an irregular lucent appearance within the fine architecture of the bone, preservation of the intervertebral disc space, and the possibility of multiple lesions (Figure 10.10). Spinal radiographs

Figure 10.10 Plain AP thoracic film of the same patient shown in Figure 10.9.

Loss of vertebral height, irregular lucency within the vertebral body and right pedicle, and preservation of the adjacent disc spaces are shown

Figure 10.10 Plain AP thoracic film of the same patient shown in Figure 10.9.

Loss of vertebral height, irregular lucency within the vertebral body and right pedicle, and preservation of the adjacent disc spaces are shown should be taken in combination with chest radiographs and a clinical examination, either or both of which may reveal evidence of a primary lesion. Definitive spinal imaging is MRI or CT myelography.62 All the relevant information can be obtained from MRI including the number of levels affected, the extent of local extravertebral infiltration, and soft tissue involvement. CT gives a clear indication of the extent of bone involvement and makes surgical planning of the route of access and the achievable extent of excision easier.

If the primary tumour is known or can be identified, the pathological nature of the secondary tumour can be inferred. When no primary can be found a histological diagnosis is required. In the spine between about T8 and L5 this can be achieved through percutaneous vertebral body biopsy carried out under biplanar imaging intensifier control.63 CT guided needle biopsy may be performed at almost any level, although this technique does not readily provide samples of bone tissue but rather of infiltrated soft tissue immediately adjacent to the vertebra. Either technique is safe in experienced hands and yields a high rate of positive diagnosis.

The subsequent management takes account of a number of factors.64 The histopathology of the tumour must be considered primarily, with the overall tumour load, that is, the number of secondary deposits, and the best estimate of the patient's life expectancy. The severity of the neurological deficit has the major influence on neurological and functional recovery following decompressive surgery. The most severely affected patients and those who are paraplegic have the lowest chance of regaining the ability to walk independently. Levels of recovery which do not permit the patient either to transfer, stand, or walk are of little practical benefit, although return of sensation is of great importance to someone who is confined to a wheelchair.

The first surgical decision to be made is whether or not a surgical procedure is indicated. Surgery provides the most rapid method of cord decompression. By contrast, radiotherapy may take several days to have its optimum decompressive effect. Even patients with highly radiosensitive tumours such as myeloma or lymphoma occasionally require urgent surgery where the compression is due to a collapsed vertebra rather than to tumour tissue surrounding the spinal cord.

The route of access should then be decided and at all spinal levels the surgeon has a choice of posterior, lateral, or anterior routes. ln general, where the compression and major disease lie anterior to the spinal cord this should be the preferred route to decompression. This may be transoral, transcervical, transthoracic, or retroperitoneal depending on the level of the spine affected. Lateral access can be achieved through a laminectomy extended laterally to include the pedicle and facet joint, a true costotransversectomy, or a lateral extracavity approach which is the equivalent of an extended multiple level costotransversectomy. Where the spinal cord is primarily compressed posteriorly, laminectomy still has a role to play, but studies from the late 1970s and early 1980s clearly showed how ineffective a laminectomy is in the presence of vertebral body disease. In this situation about 20% of patients are made neurologically worse and a similar number are made unstable by the posterior approach. The decompression may entail removal of a considerable amount of bone from the spine and necessitate stabilisation using internal metallic fixation, bone graft, or in some cases methyl methacrylate in combination with metal fixation.

Surgical decision making in these situations is complex. The overriding aims are to provide the most effective form of decompression of the spinal cord and to leave the patient with a pain free stable spine in order to facilitate return of spinal cord function. In some situations, such as a patient with widespread metastatic bronchogenic tumour, it is inappropriate to carry out a transthoracic spinal decompression. In a patient who has multiple non-contiguous spinal lesions, major surgery on any one of these is likely to be followed by further cord compression at a different level. In selected patients, however, even relatively major surgery, to access and decompress the spinal cord and stabilise the spine, is indicated before further treatment with radiotherapy or chemotherapy.

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