Tuberculosis of the Spine

Spinal tuberculosis is an age-old disease and occurs most commonly in children and young adults. It causes bone destruction, spinal deformity and neural complications. The treatment of spinal tuberculosis has evolved during the last 60 years. In the preantibiotic era healing of the lesion was expected to occur from the body's natural immunity, and the usual outcome was death, draining sinus, deformity and/or paralysis. The development of antitubercular treatment (ATT) has changed the picture dramatically. Now we know that tubercular lesions can heal under the influence of ATT and inflamed, ischemic and even infarcted bone can reconstitute.1 Imaging, surgical facilities and instrumentations have evolved. The understanding of pathophysiology of the disease is better. Spinal tuberculosis can be diagnosed in the early stages when bone is inflamed but has not lost its height, ie, the “predestructive stage,” to achieve healing of the lesion with minimal or no deformity. Skeletal tuberculosis constitutes 3% to 5% of all tuberculosis cases in the HIV negative population while 60% of HIV positive patients have skeletal tuberculosis. The emergence of multidrug resistance is described as “a tragedy in the making” and “the end of the beginning.”2,4 The situation in developing countries where two-thirds of the world's population lives is grave because of malnutrition, poor sanitation, and lack of universal health facilities. Large numbers of patients report to the hospital for the first time with already developed kyphotic deformity with or without paraplegia. Some of these patients have poor general health, comorbidities and are HIV-positive. In most places, the hospital infrastructure is grossly inadequate. As a result, large numbers of spinal TB patients heal with significant kyphosis. The kyphosis in children progresses with growth.5 The life expectancy in developing countries has increased to 50 to 60 years, thus we are likely to have patients who could live 30 to 40 years with healed severe kyphosis. As a result, the spinal cord may develop intrinsic changes to produce neural deficit with healed disease (late onset paraplegia). It is observed mostly in cases of long-standing healed kyphosis of 60° or more.6 Late onset paraplegia is difficult to treat as cardiopulmonary compromise makes these patients poor candidates for surgery.3,6 The physiological reserves of the spinal cord are exhausted, therefore the chances of neural recovery are remote with increased risk of neural deterioration during surgical decompression. Orthopaedic surgeons must be educated and trained to look for spinal tuberculosis during the most elementary examination, ie plain radiographs, and use modern imaging judiciously to diagnose and treat TB spine in a “predestructive stage” to achieve healed status with no or minimal deformity, while at the same time treating advanced cases of varying severity. Strategies must evolve to prevent the development and promote the correction of severe kyphosis and the treatment of late onset paraplegia. Unfortunately the description of spinal TB is disappearing from text books written by Western authors and most do not give a holistic description of spinal TB. Today we have patients with the most severe clinical presentations treated in unequipped hospitals while those with early presentation are treated at the most well-equipped centers. Various clinical problems observed include: (1) TB spine with active disease with severe kyphosis with or without paraplegia; (2) TB spine with healed disease with severe kyphosis with or without late onset paraplegia; (3) a case of suspected TB spine; (4) TB spine presenting with atypical clinical presentation or location of lesion, thus more liable to present with neural complications; (5) TB spine caused by a multidrug resistant organism; and (6) dual disease, ie, TB spine in an HIV-positive patient. In spinal TB patients with paraplegia with little or no kyphosis, treatment consists of surgical decompression to achieve neural recovery. The goal of surgery is not only decompression, but also kyphosis correction when severe kyphosis is associated with paraplegia. Criteria for establishing instability in spine injuries cannot be equated with criteria for spines infected with tuberculosis. In spinal trauma the tissues are disrupted at the point of impact, thus the spine is most unstable on the day of trauma. In chronic infections like TB of the vertebral body, the tissue begins healing even when in an early stage of inflammation. Eventually, there is a race between inflammatory destruction and healing. The outcome in TB depends on virulence of the organism and immunity of the patient. Not all TB spine cases have unstable spine. The number of vertebral bodies (VB) and the column of VB affection determines the instability present. The spine is unstable when the anterior, middle and posterior columns are destroyed even if one vertebral body is affected. The problem is a long segment disease cannot be compared with a short segment disease. During surgical decompression part of the diseased vertebral body is resected to decompress the spinal cord, thus a gap is created to be bridged by bone graft. The graft is structurally weakest on the day of surgery and therefore needs to be protected from graft-related complications if too much time elapses before incorporation. The kyphosis in TB spine is acute (significant at short segment) and neural tissue may also be inflamed. It usually takes 6 months or more to develop severe kyphosis, therefore closed correction of kyphosis will render the patient more vulnerable to neural deterioration. The final outcome in TB spine depends on no vertebral body affection (short segment or long segment), pan vertebral affection, presence of neural deficit, kyphosis and age of the patient. TB spine is a medical disease. Surgery is indicated for neural complications, deformity correction, instability and diagnostic dilemma. Any patient who has a typical paradiscal lesion presenting with radiological findings such as regional osteoporosis with fuzziness of disc margin or obliteration of disc space, destruction of bone, loss of anterior height of vertebra with eventual kyphosis, or paravertebral shadow in an endemic zone for TB can be treated nonoperatively. However, despite the most sophisticated imaging, 5% to 10% of the cases which look like TB may not be. Thus, if the patient does not fit into the classic picture, an attempt should be made to establish the tissue diagnosis. We need to establish the pretreatment variables in TB spine which are associated with progression of kyphosis in adults, and which forewarn us about the behavior and eventual progression of kyphosis in children so the kyphosis may be corrected in active disease. We need to define indication of instrumented stabilization, whether anterior or posterior. Anterior instrumentation has limitations in long segment disease, while posterior instrumentation, along with anterior decompression, needs two approaches, hence a severe morbidity. We lack objective parameters which indicate the healing of tubercular lesions in bone. How can we clinically predict multidrug resistance in TB spine? The chances of in vitro growth of the organism to recognize drug sensitivity are remote in a partially treated paucibacillary disease such as TB spine. Short intermittent and 12 to 18 months daily dose regimens are in vogue to treat skeletal tuberculosis. MRC failed to resolve the duration of ATT, therefore prospective studies are needed to define the optimum duration of chemotherapy. Many of these issues are addressed in this Symposium. Kyphosis in spinal TB is addressed in three articles in which progression of kyphosis in children, the principles of kyphosis correction and decompression in healed kyphosis are discussed. The usefulness of anterior instrumentation and video-assisted surgery in spinal TB are each represented in separate articles. I would like to thank CORR (Clinical Orthopaedics and Related Research) for publishing this Symposium, which is of interest to a large international community and will help educate surgeons and redefine future goals to treat spinal TB. Anil K.