Spinal tuberculosis (spinal TB, Pott’s Disease) comprises up to 50% of all patients afflicted with musculoskeletal tuberculosis. The anterior column (vertebral body) is affected in 98% of these cases. These patients develop varying degrees of kyphotic deformity, and 10% to 47% develop neural complications.
Eradication of infection is the primary aim of treatment in spinal tuberculosis, in addition to the correction or prevention of an increase in angular deformity and recovery from any neurological deficits. Treatment of tuberculosis of the spine has evolved in the last 50 years from healing of the lesion with residual deformity to healing of the lesion with minimal or no spinal deformity due to developments in imaging, surgical facilities, and implants.
Surgery in spinal tuberculosis is indicated for diagnostic dilemma, neural complications, and prevention of kyphosis progression. Up to 76% canal encroachment is compatible with a normal neurologic state as the spinal cord can tolerate gradually developing compression. Patients with relatively preserved cord size, but with edema/myelitis and predominantly fluid compression on MRI respond well to nonoperative treatment. Literature believes patients with extradural compression by granulation tissue with little fluid component compressing or constricting the cord circumferentially with cord oedema/myelitis or myelomalacia need early surgical decompression. Transthoracic transpleural anterior decompression and extrapleural anterolateral decompression have similar results in the dorsal spine. Instrumented stabilisation helps prevent graft-related complications when post debridement defects exceed two disc spaces (4-5 cm). Progression of kyphosis may occur in a short-segment disease despite instrumented stabilisation. Its outcome in a long-segment disease needs observation. The correction of healed kyphosis requires multistage surgery and is fraught with complications. Prospective studies are needed to define surgical approach, steps, stages, problems, and obstacles to correct severe kyphosis in spinal TB.
General Treatment of Spinal TB
The objectives of treatment are to confirm the diagnosis, achieve a bacteriological cure of the lesion, treat compression on the spinal cord and its sequelae, and treat spinal deformity and its sequelae such as late onset paraplegia. Spinal tuberculosis can be confidently diagnosed with clinical history, examination and with radiological studies including x rays, CT scan and MRI. If any case does not fit into classical clinical or radiological findings suggestive of spinal tuberculosis, surgical decompression should be performed and adequate tissue should be obtained for histopathological examination and final diagnosis.
The compromise of host immunity in the large number of patients with HIV infection and the causative organism‘s resistance to many drugs have added a new dimension to the treatment of spinal tuberculosis. The recent technical revolution in spinal reconstruction and instrumentation has added a variety of new treatment options for patients with Pott’s disease. Radical resection of the tuberculosis-infected focus and bone grafting were developed before the advent of modern imaging modalities when patients presented with severe neurological deficits with or without kyphosis and antituberculosis chemotherapy was new. Even now in developing countries, large numbers of patients still present with advanced spinal TB. With the advent of CT scanning and MRI, early diagnosis has become possible. More effective regimens of antituberculosis therapy have made nonoperative treatment possible and successful.
When a patient with TB of the spine who receives non-operative treatment develops a new lesion or does not show an adequate clinical radiographic healing response, the patient should be considered a nonresponder and surgery should be strongly considered. The surgery is indicated to ascertain the diagnosis as well as to reduce the disease load and to procure adequate tissue for culture and sensitivity.
Two management philosophies existed for surgery in spinal tuberculosis over the last 50 years. One philosophy included universal extirpation surgery for all spinal tuberculosis cases to excise the diseased tissues. A second philosophy considered surgery with defined and limited indications. Current antitubercular drugs reach pus, granulation tissue, caseous tissue, bone and cavities in concentration well above the minimum inhibitory concentration and the lesion can be sterilised. The differences between divergent philosophies of management from radical surgery to ambulant chemotherapy were resolved by a multicenter trial by the British Medical Research Council (BMRC).
The comparison of nonoperative treatment (two and three antitubercular drugs, bed rest, and ambulant chemotherapy) versus the Hong Kong method (anterior radical resection and debridement with fusion) suggested both approaches achieved favourable results. While fusion has improved overall results and prevents further progression of deformity, infrastructure and resources for such treatment are limited in developing countries with large numbers of cases. Further, the patients included in the BMRC study were limited to two-vertebra disease with or without mild neural deficit. The patients seen in developing countries often have a large number of vertebrae involved. These patients treated nonoperatively have a slight progression of kyphosis until the lesion heals and require brace support.
The spine is considered unstable if two columns are disrupted as in spinal trauma. In vertebral fracture, the force of trauma disrupts both columns acutely and the spine is maximally unstable on the day of trauma. However, chronic inflammation of the two columns as in tuberculosis may not always render a spine unstable because the tissues are showing a concomitant healing response despite the infectious destruction. Along with the infection process, if mechanical insult in the form of a pathological fracture has also taken place, then the spine becomes unstable.
The spine with tuberculosis is also unstable when facets and posterior complexes are destroyed along with vertebral bodies (paravertebral lesion). The proximal vertebral column in such cases can translate at the destroyed vertebra causing neural deficit. Such lesions should be identified on AP radiographs of the spine, which show loss of shadows of pedicles with or without minimal scoliosis. If CT/MRI shows destruction of the anterior and posterior column of the vertebral bodies, the spine should be stabilised. Long-segment disease (more than three-vertebral-body affection) with severe kyphosis or an increasing kyphosis in active disease may also be considered an unstable spine. At what degree one labels a severe kyphosis is unclear.
The causative factors for neurologic complications can be categorised as cord compression, instability, intrinsic causes, and infective thrombosis/endarteritis. The spinal cord may be compressed by pus, granulation tissue, caseous tissue, discs, or bony sequestra. The cord compression as observed on MRI is not always correlated with neural deficit. Up to 76% canal encroachment has been reported as compatible with intact neural state. Instability occurs with pathological subluxation, or dislocation as a result of pan vertebral disease. Some intrinsic causes of neural complications are cord edema, myelomalacia, direct affection of meninges and spinal cord. Infective thrombosis or endarteritis may also cause neural complications. However, combination factors may produce neural complications with lesser canal compromise.
The objective of treatment is to decompress the spinal cord with nonoperative treatment or surgery and to stabilise the spine if needed and respond appropriately for direct affection of the spinal cord and the meninges.
Neurologic deficit in tuberculosis of the spine has been classified by Frankel and in few articles by Tuli. The ASIA scale and Frankel‘s classification do not classify all types of neural deficit associated with spinal tuberculosis, such as very early neural deficit where only spasticity is detected with exaggerated deep tendon reflexes and no motor and sensory deficit, paraplegia with bladder and bowel involvement, paraplegia in flexion/flaccidity, and paraplegia with flexor spasm. In the ASIA scale, severity of impairment reflected by the score depends upon the level of involvement in addition to the severity of compression at the involved level.
In tuberculosis of the spine, the development of neurological deficit is a gradual process and follows a pattern. Hence it should be classified in 5 stages. An ideal classification system should assess the functional status of the tetraplegic/paraplegic patient and should reflect the severity of cord compression. Each stage should have numeric sensory/motor scoring to show early deterioration or improvement of neurologic status. The motor scoring should be performed as for the ASIA score, while sensory deficit should be recorded as: grade 0, complete loss of sensation; grade 1, impairment of lateral as well as posterior column sensation; grade 2, impairment of lateral column sensation only; and grade 3, normal sensory appreciation.
In stage one, the patient is unaware of the neurological deficit, but the clinician detects signs of upper motor neuron lesion. In stage two, the patient has spasticity with motor deficit but with paraplegia is able to walk or in the case of tetraplegia can raise upper limbs against gravity. The motor score in a case of tetraplegia may be between 60 and 100 and in paraplegia between 80 and 100, with impairment of lateral column sensation. In stage three, the patient is bedridden and spastic. Anticipated motor score is 0 to 30 for quadriplegic, and 50 to 80 for paraplegic with impairment of lateral column sensation. The patient is bedridden with severe sensory loss in stage four. The anticipated motor score is 0 for quadriplegic and 50 for paraplegic with impairment of both lateral and posterior column sensation. Stage five is the same as stage four with bladder and bowel involvement, and/or flexor spasms/flaccid tetraplegia or paraplegia.
If diagnosed, confirmed, and effectively treated in the early stages, paralysis in these cases can be averted or reversed, or the potentially devastating effect of paraplegia can be minimised. Universal surgical extirpation is practised worldwide by most of the authors for these cases. Even loss of a few degrees of motor power is graded as severe neural deficit and surgery is recommended. Tuli suggested a “middle path regime” and reported 30% to 40% neural recovery with nonoperative treatment while preparing and waiting for surgery. Thus, universal surgical extirpation in all cases of Pott‘s paraplegia seems overstated. A judicious combination of nonoperative treatment and operative decompression when needed should form a comprehensive integrated course of treatment in tuberculosis of the spine with neurologic complication. Jain reported the changes in spinal cord as observed on MRI in spinal tuberculosis with paraplegia. The patients with relatively preserved spinal cords with evidence of oedema or myelitis with a predominantly fluid collection in the extradural space respond well to nonoperative treatment if compression is the only offending cause of neural deficit.
Early surgical decompression should be performed in cases where the neurological deficit is developing, remaining stationary or getting worse with nonoperative treatment (bed rest and antitubercular drugs). Patients with acute onset paraplegia in which severe neural complication has developed in a short span of time and patients with paraplegia with neural arch affection are also candidates for early surgical decompression. Paraplegia with pan vertebral disease producing pathological subluxation and/or dislocation or spinal tumour syndrome as a diagnostic dilemma is indicated for surgery as well. Patients with extradural compression whose MRIs reveal granulation or caseous tissue with little fluid component compressing the spinal cord circumferentially and constricting the cord with features of cord edema, myelitis, or myelomalacia should also undergo early surgical decompression.
Surgery is performed to decompress the spinal cord and reconstruct the resulting gap to achieve healing of the lesion. Radical resection is defined as excision of the disease focus to uncover the dura mater as completely as possible until healthy bleeding bone is reached, leaving a wide gap to be reconstructed by autograft. Debridement is defined as removal of pus, granulation tissue, caseous tissue, and loose sequestrated bone from the lesions and the part of viable bone needed to decompress the spinal cord, leaving a relatively stable spine. The inflamed, infiltrated, infracted, and demineralized bone typical of tuberculosis reconstitutes under the influence of antitubercular drugs.
Only sequestrated bone should be removed; removal of the non-offending bone, even of questionable viability, is not required. Radical resection was advocated in an era when antitubercular drugs were relatively new and their effectiveness in spinal tuberculosis unknown. Surgeons therefore recommended radical excision of the disease focus. With the advent of effective antitubercular therapy, radical resection in infective cases is neither necessary nor desirable, and we believe the term radical should be reserved for surgery of tumours. Radical resections and debridement provided comparable neurological recovery and healing of disease focus in one long follow up study where the radical resection group had marginally better correction of kyphosis. However, most of these cases were a short-segment disease (two- to three-vertebral body affection). In another series with long-segment disease, marked deterioration of kyphosis has been reported.
In an anterior vertebral lesion surgical decompression should be anterior. Literature believes laminectomy in an anterior vertebral lesion is disastrous because it removes the only healthy segment of vertebral column and renders the spine unstable. The dorsal spine can be approached through a transthoracic transpleural approach in which the chest cavity is opened in a single lung ventilation anaesthesia.
When patients are anaemic, have extensive disease, and have compromised pulmonary function because of concomitant pulmonary tuberculosis and/or paralyzed intercostals, the risk of transthoracic surgery greatly increases. Extrapleural anterolateral decompression allows adequate exposure of the spinal cord in a severely kyphotic spine.
The determining factors for a particular approach are the preference and technical skill of the surgeon, availability of surgical and intensive care facilities, and the general and pulmonary reserve of the patient. If all conditions are ideal, one can choose any approach; however, if anything is lacking, extrapleural anterolateral decompression provides adequate surgical decompression with lower risk than the transthoracic transpleural approach for thoracic spine. For the cervical and lumbar spine, all authors have used similar anterior approaches.
Video-assisted thoracoscopic decompression and biopsy was reported (n = 26) in mid thoracic tubercular lesions as less morbid with less blood requirement and a shorter hospital stay. The complications reported were atelectasis (one), and pleural adhesions (six).
The procedure could not be completed in two patients due to severe pleural adhesions. This seems to be the method for mid-thoracic lesions in short segment disease when there is no associated lung/pleural tuberculosis, particularly for biopsy, and the surgeon should be ready to convert it into open thoracotomy.
Instrumented stabilisation has been performed in the last 20 years to improve the kyphosis or prevent deterioration of kyphosis on treatment. The surgical decompression by laminectomy in an anterior vertebral body disease renders the spine grossly unstable because the only healthy component of bone and soft tissue is disrupted by surgery. Spinal instability is likely to increase after surgical decompression in the immediate postoperative period. The bone graft does not give initial stability when inserted. Until the bone graft incorporates and adds to the structural strength, patients may experience graft breakage or slippage. Graft-related complications occur more often when the span of the graft exceeds a two-disc space.
Stabilisation of the spine was reported initially with Harrington distraction rods or with sublaminar segmental wiring in a case of circumferential spine involvement in dorsal spine or in a spine where laminectomy is performed in an anterior disease. In later series posterior stabilisation by Harrington rod or Luque segmental wiring was reported to prevent the graft-related complications and eventual progression of kyphosis where preoperative vertebral body loss is more or the graft length after surgical decompression exceeded two discs in height. Most of the series in the past decade reported the use of anterior or posterior instrumentation in an attempt either to correct kyphosis or prevent postoperative progression of kyphosis. Anterior instrumentation such as plate and screws or rod and screws are used. Various types of plates are used in cervical spine cases. For the dorsal and lumbar spine in short segment disease, plate-and-screw or rod-and-screw constructs were used.
The outcome of anterior instrumentation in long segment disease needs observation. Posterior instrumentation such as sublaminar wire with Luque rods or Hartshill rectangles were in use; however, later pedicle instrumentation was used. In long segment disease Hartshill instrumentation is still a reasonable option because it takes purchase against the posterior healthy segment of vertebra, and one healthy vertebra on either side could give adequate stabilisation. In a patient with short segment anterior disease without concomitant posterior column involvement, internal fixation may not be needed as the graft-related complications are few and the patient is already bedridden due to paraplegia.
In such patients kyphus progression can be noted despite anterior instrumentation. Posterior instrumentation with anterior decompression and fusion can be performed in one or two stages. If performed in one stage, the procedure has enormous morbidity. If performed in two stages, correction of kyphosis will not be effectively achieved. When anterior decompression and bone grafting is performed as a first stage procedure, there is a risk of graft slippage and neural deterioration while waiting for second stage stabilisation. In the second stage, only in situ stabilisation will be performed. When the posterior procedure is performed first, it will be only in situ stabilisation followed by second-stage decompression, so kyphosis correction will be minimal.
After debridement, various anterior structural grafting techniques have been used such as autogenous iliac crest graft or rib graft, femoral, humeral, or fibular allograft, autogenous/allogenic cancellous graft in a cage as a filler. The titanium cage filled with autogenous graft along with anterior screw-and-rod construct has been used in two vertebral diseases with a minimal kyphosis mean of 24.6° (range, 15°-32°) and corrected to a mean of 10° (range, 4°-18°) in dorsal and lumbar spinal tuberculosis. The suggested advantages were good short segment fusion, early mobilisation in comparison to no instrumentation, and less kyphosis progression as a result of graft subsidence.
Similar results have been reported where only autogenous graft is used without anterior or posterior instrumentation. Fibular, femoral, or humeral cortical allograft has been used in children. Autogenous corticocancellous bone grafts are osteoinductive, immune compatible with no risk of disease transfer. The disadvantages of their use include limited bone availability, inadequate structural support, and donor site morbidity. The incorporation of allograft is frequently slow and unpredictable, resulting in nonunion and fatigue fracture. The measurable humoral response to donor tissue antigen is 5% to 14%. The risk of infection with allograft is 4% to 5%.
The fibular allograft in combination with rib autograft is reported to combat the shortcomings of both. The allograft provides structural support in the initial stages and the autograft provides osteoconductivity.
Spinal TB causes destruction, deformity and paralysis. It is not only prevalent in much of the world, but there is a trend towards an increase in incidence in developed as well as developing countries in parallel with the growing number of immunocompromised patients, either from HIV infection or medical immunosuppression. Insight to the pathology of tuberculosis of the spine, ease of diagnosis, major advances in chemotherapy for TB, and the efficacy of spinal canal decompression in patients with neurological involvement allow us to expect excellent outcomes. The incidence of paraplegia together with residual spinal deformity is approximately 20% and has not changed even with current medical knowledge once the spine is involved with tuberculosis.
Gross kyphosis, especially in the thoracic spine, causes progressive loss of pulmonary function, may lead to respiratory and secondary cardiac failure, and is cosmetically unacceptable. Chemotherapy may inactivate the disease, but vertebral collapse may continue until granulation tissue and anteriorly diseased bone matures into a bone block, which is regarded as the surest evidence of healing.
The lack of uniformity of terms and descriptions makes the comparison of studies by different authors difficult. Evolution of standardised descriptions of the procedures and of follow-up observations may make comparison more meaningful. Furthermore, the data presented in the various studies is nonuniform, limiting any descriptions or comparisons to a relatively small percentage of all cases. Literature cannot ensure our descriptions in these limited cases represent the whole, although the relatively large number and relative uniformity of the results available suggest they are reproducible and might be generalizable.
Surgery for late onset paraplegia is fraught with the risk of neural deterioration. Any adult patient with initial vertebral body loss of 1.5 VB height would heal with kyphosis of 50° ± 10°.In children, vertebral destruction is more severe because most of the bone is cartilaginous and growth adds to the angulation due to growth retardation of the anterior column and unrestricted growth of the posterior column. Rajasekaran has suggested “spine at risk” signs to predict which patients are going to heal with severe kyphosis. These cases should be singled out for correction of kyphosis in active disease, since correction is easier when performed in active disease as opposed to healed disease.
Theoretically, one should achieve as near normal a kyphosis as possible, but in the dorsal spine, which has a natural kyphosis, the correction may not be needed for 10° to 20° kyphosis. Dorsolumbar kyphosis is cosmetically unacceptable, results in severe compensatory lumbar lordosis, and may need to be corrected for a lesser degree.
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