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KINI MEMORIAL ORATION Table of Contents   
Year : 2005  |  Volume : 39  |  Issue : 2  |  Page : 81-89
Tuberculosis of lumbar spine


Ahmedabad, India

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How to cite this article:
Kanabar P. Tuberculosis of lumbar spine. Indian J Orthop 2005;39:81-9

How to cite this URL:
Kanabar P. Tuberculosis of lumbar spine. Indian J Orthop [serial online] 2005 [cited 2017 Sep 26];39:81-9. Available from: http://www.ijoonline.com/text.asp?2005/39/2/81/36779
Introduction

Tuberculosis is as old as mankind. Neolithic skeleton found in Arene Candide cave (Liguria, Italy) represent one of the earliest cases of this disease lesions localized to the lower thoracic and upper lumbar vertebral bodies [1] .

One fifth of TB population is in India. Three percent are suffering from skeletal TB, 50% of these suffer from spinal lesion and almost 50% are from pediatric group. An estimated 2 million or more patients have active spinal tuberculosis, and the global incidence of the disease is increasing [2] . Every day 1000 die of tuberculosis in India.

There is rebirth of tuberculosis and that too of resistant type in developed and developing countries due to non­adherence and invasion by HIV.

Treatment failure is due to non-adherence and can be avoided by directly observed therapy, life and family circumstances, motivation, education, incentives and combination strategies. Till there is poverty, tuberculosis will always affect mankind.

Between 1950 -1976 three schools developed. 1. Essentially non operative. 2. Radical surgery, 3. Middle path [3] . The results have shown that posterior instrumentation surgery was not a hazard to spinal tuberculosis infection when combined with radical debridement and intensive anti­tuberculosis chemotherapy [4] . With the advent in modern pharmacotherapy, advance in theater set up, availability of implants and improved surgical skills; there is a revival of primary surgical management.

Pathology and pathogenesis

The vascular supply is derived from branches of the vertebral and lumbar arteries. The vertebral venous plexus communicates directly with the veins of the pelvic viscera, thoraco-abdominal wall and the retroperitoneal space. The anastomosis allows direct extension of infected material within the abdominal cavity or from lower limbs to the vertebral column. In addition, it has been shown that the vascular channels traverse the vertebral end plate connecting the vertebral body with the disc. Blood and lymph vessels were found in connective tissue outside the annulus. They were detected in specimen from patients up to the age of 20 years. In the cartilage end plate, blood vessels were seen in the specimens up to 7 years of age (cartilage canal). In the nucleus pulposus, neither blood nor lymphatic vessels could be seen at any age. This suggests that childhood disc infection can occur without simultaneous affection of vertebral body. The presence of perforating vascular channels connecting the disc and the vertebral end plate, however may allow, early direct extension of infection from disc to the adjacent vertebral body and vice versa.

Usually it is haematogenous infection but lymphatic and direct inoculation is possible. Cartilaginous tissue is resistant to tuberculous destruction.

The lesion could be:

  1. Florid - invasive and destructive lesion.
  2. Non destructive - lesion suspected clinically but identifiable by modern investigations like CT scan or M.R.I.
  3. Encysted disease
  4. Carries sicca
  5. Hypertrophied
  6. Periosteal lesion.


Recently, two distinct patterns of spinal TB can be identified, the classic form, called spondylodiscitis (SPD) and an increasingly common atypical form characterized by spondylitis without disk involvement (SPwD). SPwD seems to be the most common pattern of spinal TB. The reasons for this remain to be elucidated [5] .

Anatomically the lesion could be

  1. Central [Figure - 1],
  2. Paradiscal or Anterior type.


HIV and tuberculosis spine

The clinical presentations of spinal tuberculosis are similar in HIV-positive and -negative patients, and good outcomes can be expected with regard to mycobacterial disease. Patient may present with atypical features. This suggests those traditional diagnostic criteria for spinal tuberculosis may be inadequate. Major orthopaedic surgery in HIV-positive patients has increased risks of sepsis. The risk of transmission of HIV between patient and surgeon is small; especially if recommended precautions are universally applied [6] .

Antitubercular drugs

Chemotherapy of tuberculosis has evolved in last 50 years to present status, With the advent of newer drugs the whole scenario has changed. The results after the chemotherapy are so good that the surgery for spinal tuberculosis is less resorted to. Earlier myth that the drug may not reach the bacteria is forgotten. In uncomplicated lesion, at present, the chemotherapy is the main stay in under privileged patient.

The Fourteenth report of the Medical Research Council Working Party on Tuberculosis of the Spine presently recommends Isoniazid + Rifampicin for 6 to 9 months. In Madras study results were same with both ambulatory and after surgery. Only important suggestion was that the appropriate treatment be given under supervision [2] .

There is a consensus that the first phase of antitubercu­lous chemotherapy should consist of three drugs (Isoniazid, Rifampicin, and Pyrazinamide) or four drugs (plus Ethambutol) given for two to three months. When neither resistance nor side effects occur, Isoniazid and Rifampicin should be continued as maintenance therapy. The large sample size and long follow-up are needed to obtain conclusive data and would probably require a multicenter international study [7].

Present day chemotherapy is with primary or secondary drugs.

Primary drugs

Isoniazid

Ethambutol

Rifampicin

Pyrizinamide

Alternative drugs

They are instituted, only after drug sensitivity reports or on clinical resistance after side effects. They are Streptomycin, Ethionamide, Cycloserine, Viomycin, and Kanamycin. They are fairly toxic.

INH must be always there. Avoid more than one hepatotoxic drug. Multi drug resistance is now recognized. Now in our country, the anti tuberculous drugs are easily available.

Prevention & prophylaxis

It is aimed to prevent new cases of infection. Exposed subjects should be protected by B.C.G. vaccination. Exposed subjects like children and immuno-depressed must be separated. Chemoprophylaxis is by Isoniazid 5 mg./kg for three months. In MDR other protocols with Ethambutol, Pyrazinamide and Ofloxacine can be prescribed. In children and immuno-depressed patients, isonizid can be given for 6 months.

B.C.G. vaccination protects 80%. After B.C.G. complications like osteitis, generalized B.C.G. infection can occur.

Symptoms and signs

Up to the age of 10 years the involvement is florid and associated with large abscesses without neurological involvement. After the age of 10 the lesions are more like adult, and associated with dryer lesions and more often with neurological deficits. Commonly thoracic and thoraco lumbar areas are more involved. The lumbar spines are next to get involved. Pure neural arch and sacral TB is rare [8],[9] .

Erroneous initial diagnoses [Figure - 2] & [Figure - 3] are common - 41% [10] , when patient presents for the first time. This calls for a good detailed clinical examination.

General



  1. Insidious onset.
  2. Loss of Feeling of Well being
  3. Loss of Appetite
  4. Loss of Weight
  5. Evening Fever


Local

Pain and stiffness

Local tenderness

Deformity

Limitation of extension to start with. Scoliosis occasionally.

As the disease advances, the involved level shows prominence of spinous process. This is knuckle deformity due to anterior destruction of one vertebra. Gibbus [Figure - 4] occurs when more than one vertebra is destroyed. Occasionally generalized kyphosis is seen when minimal involvement anteriorly of more than two vertebrae.

Abscess

Children, most often present with the abscess [10] may be paraspinal, Petit's triangle, psoas, below inguinal ligament, in the thigh or in course of femoral or sciatic nerve. If abscess bursts, a sinus [Figure - 5] may be formed.

Vertebral Lesion

  1. Paradiscal [Figure - 6] - destruction of adjacent end plates and diminution of disc space.
  2. Appendeceal (Posterior) - involvement of pedicles, laminae, spinous process.
  3. Central - Cystic or lytic, concertina collapse.


X Ray appearances

Discovertebral lesions, detected in 93% of patients, are the most frequent radiological presentation [11] . In the early stage, plane X Rays are normal or show loss of lumbar lordosis. Occasionally oblique views are required. Localized fluffy osseous destruction with surrounding osteoporosis is the earliest signs. Paravertebral abscess may be the only evidence. As the disease advances, the destruction becomes more evident. In the central lesion now the collapse is seen. The appearance may be concentric collapse and may look like A.V.N. Local lytic lesion may cause problem of diagnosis from neoplasic lesion. With destruction of adjacent vertebrae Konstram (K) angle appears and shows the progress on follow up. If the lesion is peripheral in the body in A P view, lateral bending may be seen. The destruction of only transverse process [Figure - 7] is very evident in A P view. A good quality lateral image taken for spinous process may show affection. Single pedicular destruction or facetal lesion shall be evident in oblique image. Skipped lesion (10% cases) can be diagnosed on suspicion and in correct size film. In presence of evident congenital malformation, the lesion is many times missed.

Healing process takes two to three months to show the changes in X-Ray. In fact, the disease may be seen, as advanced, in the images. For the response to the treatment, other parameters must be taken in to consideration. Earliest effect is arrest of progress of the lesion. The osteoporosis starts decreasing. The sclerosis appears and the lesion seems to be getting localized. Further collapse stops and the K angle become stationary. Abscess shadow takes a very long time to go. Calcification appears and the fusion [Figure - 8] process may be seen. If the natural fusion does not occur, end plates will show sclerosis. Anterior new bone formation in form of osteophytes may appear. The trabecular pattern will start appearing and the bones will look normal.

While on treatment, soft-tissue masses may increase in size for up to 1.5 months and take about 12 months to resolve. Bone destruction may progress in 70% of patients. The loss of vertebral body height may progress for up to 14 months; any recovery of height is a very late feature. Sclerosis is seen at presentation in 52% and develops in most of the patients within 5 months of treatment. It progresses for up to 14 months and takes, on average, 31 months to return to normal. Reduction in disc height [Figure - 9] is commonly seen and the vertebrae fuse in three-quarters of those affected, the time of onset of fusion being very variable [12] .

CT Scan

Prior clinical localization is a must. It is very easy to see minimal destructive lesion. The soft tissues can be enhanced by I.V. contrast. The abscess can be easily seen. The appendeceal lesions are well diagnosed. When the differentiation from other neoplasic lesions is difficult, a CT guided F.N.A. C (minimum 2-mm.-diameter trephine) [Figure - 10] can be very useful.

M.R.I.

T1 and T2 images give good soft tissue differentiation and even the earliest inflammation can be picked up. The soft tissue extension can be well demonstrated. The effect of the disease on soft tissues like disc can be pin pointed. Involvement of the spinal and [Figure - 11] root canal can be diagnosed and the cause of neural compression can be established.

Patient may present as spinal stenosis above a healed tuberculous kyphosis [13] . One must remember that inflammatory spinal pain is typical of the spondylarthropathies and can be treated as tuberculosis without image evidence [14] .

Differential Diagnosis

In our country, we have to think of tuberculous etiology first. There may be atypical presentations of tuberculosis of the spine as a herniated lumbar intervertebral disc [15] . Detailed history taking, thorough clinical examination, and good quality X-Ray images are primary requirement. Routine laboratory investigations and the immunological assays are partly helpful. The modern imaging can give a very high probability. Radiologically guided FNAC with AFB culture is a simple, reliable and practical approach to diagnosing spinal TB lesion [16] . CT guided aspiration, biopsy, culture, histological examination only can be most speculative but final word can be given after Guinea Pig inoculation and getting a tubercle at the inculcation site. ATT can be started and if need be, can be stopped and case can be reviewed.

An attempt must be made to think of the etiology all through out the process of coming to a diagnosis. This will never allow one to lose the bull eye i.e. diagnosis.

Following is a summary attempt of differentiation:

Pyogenic spinal osteomyelitis - -
It starts with acute onset of severe pain, muscle spasm, and high fever. Spine goes in to hyperextension. At early stage bone destruction is replaced by new bone formation. Disc is destroyed very early with early bone fusion. TB is more difficult to be ruled out and the biopsy helps.

Typhoid Spine - Usually follows enteric fever. Laboratory investigations and biopsy only can help.

 Brucellosis More Details - Undulant fever. Agglutination tests, culture, and biopsy confirm.

Mycotic Infection - - is very rare. Usually comes with sinuses and typical discharge. Plane images show variegated appearance. Microscopy of the discharge helps.

Tumorous condition -

A. Benign -
Usually symptoms in months. Haemangioma - coarse vertical trabeculae with negative serology. Giant cell tumor & ABC - - It is usually difficult to differentiate by clinical and plane images. C.T can help. Histological examination proves.

B. Primary malignant - Rare. Ewing's sarcoma, osteosarcoma, lymphoma, chordoma, chondo sarcoma, fibrosacoma must be considered in aatypical case. Biopsy confirms. Multiple myeloma and lymphomas can be diagnosed by presence of multi focal and the M.R. can give a good differentiation.

C. Secondaries - They create more confusion and have to be differentiated more often. [Figure - 12]

Others like, osteoid osteoma, histiocytosis, hydatid, osteoporosis, etc. can cause diagnostic riddle and the final word can be given by histological examination.

In developed countries clinical presentation of the condition was often similar to that of malignant disease within the spine, with the commonest presenting features being back pain (95%), an evaluated erythrocyte sedimentation rate (ESR) (100%) and neurological deficits (47%). The radiological appearances were diagnostic of spinal tuberculosis in less than 50% of cases [17] .

Progression

As the disease advance, the lesion will spread to the adjoining part of the spinal anatomy. A paradiscal lesion will gradually affect the adjoining part of the body of the vertebra and the vertebral height decreases (79%). The disease can spread to the disc and disc will get destroyed and the vertebrae will get collapsed on each other. Kyphosis appears. In course of time, the K angle will increase. The destruction on one side leads to lateral bending - scoliosis. From the front, the lesion can spread to pedicle and then to laminae and the facetal joint. The involvement of body can lead to destruction of the transverse process. The appendeceal lesion may be the starting point and the lesion can spread elsewhere. The lesion may remain dry without formation of abscess. Commonly there are paravertebral abscesses and the pus may form even in the central canal. Pus can go along the muscle or the nerve root and can become superficial. The burst open abscess can lead to a sinus formation and can get secondarily infected by pyogenic organisms. The sequestration of the body can also occur. The pus, granulation tissue and the sequestration can lead to compression of the neural tissue leading to neurological deficit. By treatment or by body defense mechanism the lesion can come under control and the disease can stop the progress and show healing.

At the end, patient will end up with kyphotic or kyphoscoliotic deformity. If the neurological deficit does not recover, patient will end up with permanent weakness and also loss of bowel and bladder control. The kyphotic deformity can lead to internal gibbous. This in itself can lead to late onset complications.

If the K angle is more, the prognosis regarding the end result kyphosis is poor. If it is more, there can be severe kyphotic deformity. The average kyphosis angle per lumbar vertebral body loss is far less than in the dorsolumbar spine. Kyphosis is minimal in older than 17 years. Children younger than 10 years old have more severe involvement with increased tendency toward greater kyphosis. Surgery is indicated in this group to prevent greater deformity. In children with small kyphosis, there is possibility of future correction [18] .

Treatment

In spinal tuberculosis without unsightly kyphosis and neurologic symptoms, the treatment is medical. The arguments that surgery is necessary for biopsy and to allow for removal of infection and its byproducts have been usurped by advanced biopsy techniques and trials demonstrating resolution of infection and most abscesses using chemotherapy [19] . The pharmacotherapy is according to the age and weight of the patient.

The results of chemotherapy on an outpatient basis were not improved by bed rest or a plaster jacket [20] . Occasionally, when there is a highly unstable situation one can resort to POP Cast. There is no role of routine use of Plaster beds or jacket.

Corsets and braces are also given up. Occasionally, still after extirpative surgeries, many resort to them. They may be used after surgery, if one is not too confident of the achieved stability. However, how much they are of help, is doubtful. Patient is given rest, preferably bed rest to start with. As the patient gives favorable response in few weeks in uncomplicated case, the patient can be made ambulatory [20] . Patient compliance is a must. The patient is followed up monthly to monitor progress. Symptomatic relief is noted. Anemia and liver functions are monitored. Ocular functions are inquired into. The plane X-Ray images are repeated every three months to record the recovery in osseous lesion.

If the patient does not show positive response in three to four week's time, the patient is reviewed for the diagnosis. If the diagnosis remains same, one can consider that the bacteria are not sensitive and second line of pharmacotherapy is considered. The patient is again continued on this expectant line of treatment. If the patient remains irresponsive, surgical extirpation is considered.

With the pharmacotherapy, most of the patients respond favorably, even with abscess, sinus or neurological deficit[21] . Solid bony union was found in 75% of patients. The kyphotic deformity occurred in the lumbar spine with a mean angle 12 degrees (range, 5-26 degrees) [22] . If the neurological deficit increase or not recover the disease extirpation and decompression is called for. Only aspiration or drainage of abscess and instillation of drugs or only debridement or only sinus excision have gone out of use.

Surgery is reserved for those patients who have advanced tuberculosis with unacceptable complications such as paraplegia and/or deformity [21] . Correction of deformity and bone grafting is considered together. A larger gap should not be treated with rib grafting, as the failure rate is fairly high. A fibular graft or cortico-cancellous [Figure - 13] graft from iliac crest/tibia is considered. A vascularized iliac bone graft, based on the upper (first or second) lumbar vessels can be used [23] .

There is no evidence of disproportionate posterior spinal growth, after anterior debridement surgery for spinal tuberculosis[18] . If there is late recurrence, one can give an expectant line of treatment. A patient may come for deformity; the patient can be offered corrective surgery and fusion.

Common surgical procedures:

The curettage of a central lesion can be done if indicated to conserve the anatomy. Most of the time the extirpation is the answer, supported by a bone graft for enhancing fusion in 96% [24] or stabilizing the lesion or maintaining the correction of deformity. The lesion is approached directly by retroperitoneal and transperitoneal approaches according to the involvement. Impotency and incision hernia [Figure - 14] can be complications after transperitoneal approach. Retroperitoneal extra pleural approach can be used for thoraco-lumbar junction.

In older children nearing maturity or in adults, severe spinal instability can be stabilized further by adding metallic implants support. For large corpectomies or gaps, cages can be used. The cage is implanted filled with cancellous bone and can give excellent support. Posterior implant can give added support. Varieties of anterior and posterior implants are available. The surgeries are real major one, need very good expertise and very good theater infrastructure. Various complications, including deaths, are reported [15] . Preferably, they must be carried out only in specialized centers.

Neural deficit in lumbar spine tuberculosis

Neurological complication in a patient of tuberculosis of lumbar spine is fairly uncommon. Patient may come with paraplegia or nerve root lesion. Lesion at or above L1 can cause cord compression, and below that cauda equina gets compressed.

Classification:

Early onset - This comes up in active stage of the disease within first 2 years.

Compressive Agents are inflammatory edema, granulation, abscess, casseous material, sequestra and rarely ischaemic lesion.

Late onset- Usually after 2 years of onset of the disease. May be due to recurrence or by mechanical pressure. This can be better divided into paraplegia with active disease and with healed disease.

Active disease - Caseous material, debris, sequestrated disc or bone, internal gibbus, stenosis and deformity can cause compression.

Healed disease - Usually internal gibbus and acute kyphotic deformity can also give late onset paraplegia. Usually there is a continuous traction, compression leading to paraplegia. The progress is very gradual and when the patient reports, it is already too late and the changes are irreversible and the surgery does not cure. It may prevent further deterioration.

It is uncommon to get a patient with neural deficit after patient is on proper chemotherapy. The history is of slow onset of weakness in the lower limbs. The patient gives symptoms due to flaccidity. Usually the patient has changed gait. The walking becomes clumsy and needs support. Usually sensations, bowel and the bladder functions are not affected, if the patient comes early. When the paraplegia lasts longer and leads to changes in cord or if there is cord ischaemia, patient may have lost all these functions.

Rarely patient may come as spinal tumor syndrome due to localized tuberculoma, diffuse granuloma, or peridural fibrosis and is diagnosed by lumbar puncture.

Treatment

Early diagnosis of tuberculosis of spine and proper chemotherapy is very important. We must prevent dropouts. This will also decrease resistant cases. H I V is going to be a menace. Management may differ from those without HIV infection [25] . In an established case the treatment is of tuberculosis. Non operative management with chemotherapy can be tied and on failure, after 3 to 4 weeks, surgery is offered.

Surgery is that of decompression. Posterior decompression by laminectomy is never resorted to except when the disease is of only posterior element and anteriorly every thing is normal by CT or MR. The compressive agent is usually anterior and in the canal anteriorly. Anterior decompression is required. Complete debridement of the disease is done. The compressive and diseased corpus is excised till the normal and bone grafting stabilizes the spine. Fresh-frozen allografts can be used to help to stabilize the spine after anterior decompression for tuberculosis [26] .

Anterior instrumentation is more effective than posterior instrumentation for reducing the deformity and stabilizing the vertebral column in patients who have kyphosis related to tuberculosis of the spine [27] . Transpedicular decompression is offered in selected localized lesions with bone grafting.

Transpedicular instrumentation provides rapid relief of instability catch and prevents late angular deformity in patients with thoracolumbar and lumbar spinal tuberculosis in whom limited (< 50%) bone destruction of the involved vertebral bodies has been shown and whose main symptom is instability catch [28] .

Posterior instrumental stabilization and anterior interbody fusion were found helpful in arresting the disease early, providing early fusion, preventing progression of kyphosis, and correcting the kyphosis [19] . In satisfactorily stabilized spine the patient is made ambulatory after recovery.

 
   References Top

1.Formicola V, Milanesi Q, Scarsini C. Evidence of spinal tuberculosis at the beginning of the fourth millennium BC from Arene Candide cave (Liguria, Italy). Int Orthop. 1987;11(4):315-22.  Back to cited text no. 1    
2.Rajasekaran S, Shanmugasundaram TK. Tuberculous lesions of the lumbosacral region. A 15-year follow-up of patients treated by ambulant chemotherapy. Spine. 1998;23(10):1163-7  Back to cited text no. 2    
3.Tuli SM. Tuberculosis of the Skeletal System. 2nd Edition. Bangalore; Jaypee Brothers. 1997:  Back to cited text no. 3    
4.Oga M, Arizono T, Takasita M, Sugioka Y. Evaluation of the risk of instrumentation as a foreign body in spinal tuberculosis. Clinical and biologic study. Spine. 1993; 18(13):1890-4.  Back to cited text no. 4    
5.Pertuiset E, Beaudreuil J, Liote F, et al. Spinal tuberculosis in adults. A study of 103 cases in a developed country, 1980-1994. Medicine (Baltimore). 1999;78(5):309-20.  Back to cited text no. 5    
6.Jellis JE. Orthopaedic surgery and HIV disease in Africa. Int Orthop. 1996; 20(4): 253-6  Back to cited text no. 6    
7.Pertuiset E. Medical therapy of bone and joint tuberculosis in 1998. Rev Rhum Engl Ed. 1999;66(3):152-7.  Back to cited text no. 7    
8.Raymond F, Levard G, Bataille B. Sacral bone tuberculosis in a 6 year-old child, Arch Pediatr. 1994;1(5):489-92.  Back to cited text no. 8    
9.Naim-Ur-Rahman, El-Bakry A, Jamjoom A, et al. Atypical forms of spinal tuberculosis: case report and review of the literature. Surg Neurol. 1999;51(6):602-7.  Back to cited text no. 9    
10.Pun WK, Leong JC, et al. Tuberculosis of the lumbosacral junction. Long-term follow-up of 26 cases. J Bone Joint Surg [Br] 1990 Jul;72(4):675-8.  Back to cited text no. 10    
11.Cotten A, Flipo RM, et al. Spinal tuberculosis. Study of clinical and radiological aspects from a series of 82 cases. J Radiol. 1996;77(6):419­26.  Back to cited text no. 11    
12.Boxer DI, Pratt C, Hine AL, McNicol M. Radiological features during and following treatment of spinal tuberculosis. Br J Radiol. 1992;65(774):476-9.  Back to cited text no. 12    
13.13. Luk KD, Krishna M. Spinal stenosis above a healed tuberculous ky­phosis. A case report. Spine. 1996;21(9):1098-101.  Back to cited text no. 13    
14.Cantini F, Salvarani C, Olivieri I, Niccoli L, Padula A, Bellandi F, Palchetti R Tuberculous spondylitis as a cause of inflammatory spinal pain: a report of 4 cases. Clin Exp Rheumatol. 1998;16(3):305-8.  Back to cited text no. 14    
15.15. Korkusuz F, Islam C, Korkusuz Z.. Prevention of postoperative late kyphosis in Pott's disease by anterior decompression and intervertebral grafting. World J Surg. 1997;21(5):524-8.  Back to cited text no. 15    
16.16. Francis IM, Das DK, Luthra UK, Sheikh Z, Sheikh M, Bashir M. Value of radiologically guided fine needle aspiration cytology (FNAC) in the diagnosis of spinal tuberculosis: a study of 29 cases. Cytopathol­ogy. 1999;10(6):390-401.  Back to cited text no. 16    
17.Hayes AJ et al. Spinal tuberculosis in developed countries: difficulties in diagnosis. J R Coll Surg Edinb. 1996;41(3):192-6.  Back to cited text no. 17    
18.Upadhyay SS, Saji MJ, et al. The effect of age on the change in deformity after anterior debridement surgery for tuberculosis of the spine. Spine. 1996;21(20):2356-62.  Back to cited text no. 18    
19.Moon MS, Woo YK, et al. Posterior instrumentation and anterior interbody fusion for tuberculous kyphosis of dorsal and lumbar spines. Spine. 1995;20(17):1910-6.  Back to cited text no. 19    
20.Thirteenth Report of the Medical Research Council Working Party on Tuberculosis of the Spine. A 15-year assessment of controlled trials of the management of tuberculosis of the spine in Korea and Hong Kong. J Bone Joint Surg (Br). 1998;80(3):456-62.  Back to cited text no. 20    
21.Moon MS,Spine 1997 Aug 1;22(15):1791-7.  Back to cited text no. 21    
22.Wimmer C, Ogon M, Sterzinger W, Landauer F, Stockl B. Conser­vative treatment of tuberculous spondylitis: a long-term follow-up study. J Spinal Disord. 1997;10(5):417-9.  Back to cited text no. 22    
23.Hayashi A, Maruyama Y, Okajima Y, Motegi M. Vascularized iliac bone graft based on a pedicle of upper lumbar vessels for anterior fusion of the thoraco-lumbar spine. Br J Plast Surg. 1994;47(6):425-30.  Back to cited text no. 23    
24.Usmanov IV. Possibilities of reducing the duration of the treatment of patients with tuberculous spondylitis. Ortop Travmatol Protez 1991 May;(5):20-3.  Back to cited text no. 24    
25.Risko Z. Therapeutic problems with HIV-infected tuberculous spondyli­tis patients in the South African Republic. Orv Hetil. 1999;140(13):711-3.  Back to cited text no. 25    
26.Govender S, Parbhoo AH. Support of the anterior column with al­lografts in tuberculosis of the spine. J Bone Joint Surg (Br). 1999;81(1):106­9.  Back to cited text no. 26    
27.Yilmaz C, Selek HY, Gurkan I, Erdemli B, Korkusuz Z., Anterior instrumentation for the treatment of spinal tuberculosis. J Bone Joint Surg (Am). 1999;81(9):1261-7.  Back to cited text no. 27    
28.Lee TC, Lu K, Yang LC et al. Transpedicular instrumentation as an adjunct in the treatment of thoracolumbar and lumbar spine tuberculosis with early stage bone destruction. J Neurosurg. 1999;91(2 Suppl):163-9.  Back to cited text no. 28    

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Correspondence Address:
Pravin Kanabar
Ahmedabad
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5413.36779

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