Tuberculosis of spine or TB spine or spinal TB was first described by Percivall Pott. He noted this as a painful kyphotic deformity of the spine associated with paraplegia. Since then condition is also referred to as Pott’s disease or Pott’s spine. It is also called vertebral tuberculosis. Because tuberculosis is also called Koch’s lesion, the term spinal Koch’s is also used. Another term used is caries spine or spinal caries.
Spine tuberculosis is the commonest form of skeletal tuberculosis. It constitutes about 50 percent of all cases of bone and joint TB.
Spine TB is mostly commonly found in first three decades of life but can occur in any age group.
There is no gender predilection.
Tuberculosis of spine occurs most commonly in lower thoracic region. It is followed by lumbar, upper dorsal, cervical and sacral regions in decreasing order of frequency.
Tuberculosis of spine is also referred as tuberculous spondylitis. Tuberculosis of the spine used to be a disease of early childhood in the past. But with improved public health measures, this age incidence has changed, and adults are more frequently affected.
Before the availability of modern antitubercular drugs the mortality rate of the patients was about 30 percent. With the use of modern antitubercular drugs, the outcomes of the treatment have been changed.
Anatomy of Spine
Detailed anatomy of spine is discussed separately. Here A general overview with terms is presented.
Human spine or vertebral column is a structure made of multiple small units called vertebra and extends from just below the base of skull to a point jut below the beginning of gluteal cleft.
A vertebra is smallest unit of vertebral column. Plural term is vertebrae. Vertebrae have been modified according to the function they are expected to serve in different parts of spine.
These curves are called kyphotic if they are concave in anterior(front) and convex on posterior (back) and lordotic if they are convex in anterior and concave on posterior.
Spine is divided into five regions
This part of the spine is present in the neck and consists of first seven vertebrae. Thus first vertebra is called C1 and last vertebra is called C7. Cervical spine has a normal lordotic curve.
Also called dorsal spine, it is below cervical spine and spans upper trunk or thorax or area corresponding to chest. It contains total of 12 vertebrae and are designated as T1 to T12
Thoracic spine has a normal kyphotic curve.
It follows thoracic spine and consists of 5 vertebrae, L1 to L5. Anatomical variations in which 4 or 6 vertebrae might be present in lumbar spine are known.
Sacral spine is composed of five sacral vertebrae S1 to S5. Vertebrae in sacral spine are fused to each other. This part of spine follows lumbar spine and is present in pelvic area.
Coccyx or Coccygeal Spine: This is also known as tail bone. It consists of four fused vertebrae (the coccygeal vertebrae) below the sacrum.
Vertebrae, the structural units of spine are stacked together to form entire vertebral column. Discs are cushion like structures acting as shock absorbers between two vertebrae.
They also permit some movement between the vertebral bodies and transmission of weight.
Each vertebra consist of an anterior body which is attached to a posterior ring called posterior neural arch [pedicle and laminae together].
Two struts of bones called pedicles arise from body and join two converging struts called laminae. Pedicles, laminae and posterior surface of body forms boundaries of spinal canal, which is the space for passage of spinal canal.
This spinal canal is the space where spinal cord passes. There is a transverse process on either side of the arch which serves as attachment to various muscles and ligaments. Posteriorly is the posterior spinous process that also serve as attachment to ligaments and muscles of spine.
The neural foramen is the opening where the nerve roots exit the spine and travel to the rest of the body. There are two neural foramen located between each pair of vertebrae, one on each side.
Muscles and Ligaments
Various muscles and ligaments attach to spine. They help the spine to stabilize and allow it to carry various movements.
Pathology of Tuberculosis of Spine
The bacteriae reaches the site of infection via blood stream. The focus of infection usually begins in the cancellous bone of the vertebral body. Occasionally, it is in the posterior neural arch, transverse process, or subperiosteally deep to the anterior longitudinal ligament in front of the vertebral body. Up to 5% of spinal tuberculosis has been reported in posterior elements.
As the disease progresses, the area of infection gradually enlarges and spreads to involve two or more adjacent vertebrae by extension beneath the anterior longitudinal ligament or directly across the intervertebral disc.
Sometimes there may be multiple vertebrae may be involved which are separated by normal vertebrae termed as skip lesions. The infection may be disseminated to distant vertebrae via the paravertebral abscess.
As the tuberculosis of spine progresses, vertebral bodies lose their mechanical strength due to progressive destruction under the force of body weight. Extreme weakening leads to angular kyphotic deformity.
The severity of the deformity depends upon the extent of destruction, the level of the lesion, and the number of vertebrae involved.
Kyphosis is most marked in thoracic area because of the normal dorsal curvature. In the lumbar area it is less because of the normal lumbar lordosis becasue of which the body weight is transmitted posteriorly and collapse is partial.
The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes.
Healing takes place by gradual fibrosis and calcification of the granulmatous tuberculous tissue. Eventually the fibrous tissue is ossified, with resulting bony ankylosis of the collapsed vertebrae.
Paravertebral abscess [abscess around vertebra – literal meaning], formation occurs in almost every case. With collapse of the vertebral body, tuberculous granulation tissue, caseous matter, and necrotic bone and bone marrow are extruded through the bony cortex and accumulate beneath the anterior longitudinal ligament.
These cold abscesses gravitate along the fascial planes andpresent externally at some distance from the site of the original lesion.
- In the lumbar region the abscess gravitates along the psoas fascial sheath and usually points into the groin just below the inguinal ligament.
- In the thoracic region, the longitudinal ligaments limit the abscess, which is seen in the radiogram as a fusiform radiopaque shadow at or just below the level of the involved vertebra.
- Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels.
Neural Deficit in Spine Tuberculosis
Neurological complications may arise due to compression of the cord by the abscess, caseating or granulating mass, intervertebral disc or edge of bone c. Other contributory factors may be thrombosis of the local vessels and edema of the cord.
Neural deficit can be paraparesis to begin with and eventually lead to paraplegia. It occurs most often in the mid-or upper-thoracic region, where the kyphosis is most acute, the spinal canal is narrow, and the spinal cord is relatively large.
Neural deficit in TB spine occurs due to pressure on the tissues of the cord, as follows. Other factors are cord edema and inflammation.
Following can contribute to the pressure on spinal cord.
- Extradural Mass formed by tubercular abscess [fluid pus, granulation tissue or caseous material.
- Extradural Granuloma and Tuberculoma
- Sequestra [dead bone] from avascular diseased vertebral bodies or intervertebral disc
- Granulation tissue on the with paridural fibrosis [cicatrization or scar formation]
- Infarction of the cord by thrombosis or artertitis.
- Cord atrophy
Paraplegia due to tuberculosis of the spine can be early onset or late onset.
Early onset paraplegia occurs during the active phase of the vertebral disease usually within first 2 years of the onset.
Late onset paraplegia occurs many more than 2 years after the disease has persisted and could be due to recrudescence of the disease or mechanical pressure on the cord.
It is also called paraplegia associated with healed disease.
Types of Lesions in Spinal Tuberculosis
Four types of lesion are known in spinal tuberculosis
- Paradiscal type – On the either side of disc
- Central type – central part of the vertebral body
- Anterior type – anterior surface of the vertebral body
- Appendicial type (involving pedicles, laminae, spinous process or transverse processes).
In this type, the infection is on the either side of the disc, involving two vertebrae. This is most common type of presentation. The narrowing of the disc space is often the earliest radiological finding, often associated with a fuzziness of The narrowing of the disc space may either be due to either atrophy of the disc tissue or prolapsed.
Central Type of Lesion
The infection starts from the centre of the vertebral body, where it reaches through Batson’s venous plexus or through the branches of the posterior vertebral artery.
On xray, the diseased vertebral body loses the normal bony trabeculae and many show areas of destruction or the body may be expanded or ballooned out like a tumor and finally collapse like vertebra plana.
Loss of disc space is minimal.
The infection starts beneath the anterior longitudinal ligament and the periosteum.
On xray, the peripheral portion of the vertebral body shows erosion as shallow excavations. Vertebral collapse and decrease in the disc space is usually minimal and occurs late.
This involves isolated infection of the pedicles, transverse processes, laminae and spinous process does occur.
These lesions are not generally visible on routine xrays.
CT or MRI are better at detecting these lesions.
Presentation of Tuberculosis of Spine
The onset of is usually insidious. Initial symptoms are vague, consisting of generalized malaise, easy fatiguability, loss of appetite and weight, and loss of desire to play outdoors in children. There may be an afternoon or evening fever.
However, acute presentation of tuberculosis is known.
Backache is usually minimal and may be referred segmentally.
Muscle spasm makes the back rigid. Motion of the spine is limited in all direction. The patient may complain of inability to flex spine when picking an object up from the floor. For doing this, the patient flexes his hips and knees, keeping the spine in extension.
On examination, the spine is stiff and painful on movement. Stiffness of the spine is noticed by increase of depth of spinal midline gutter as paraspinal muscle spasm makes them prominent.
There may be a localized kyphotic deformity which would be tender on palpation.
A cold abscess may be noticed. The abscesses may be palpated as fluctuant swellings in the groin, iliac fossa, retropharynx, or on the side of the neck, depending upon the level of the lesion.
In spite of vast spectrum of the disease, the early cases may not have any clinical finding except for tenderness in the region of the complaint. Several of these symptoms and sign may be absent even in cases of active vertebral disease.
A history of contact with known case of tuberculosis or recent visit to endemic area should be asked.
A kyphus in the thoracic region may be the first noticeable sign. As the kyphosis increases, the ribs will crowd together and a barrel chest deformity may develop.
When the lesion is situated in the cervical or lumbar spine, a flattening of the normal lordosis is the initial finding.
The gait of the person with Pott’s disease is peculiar, reflecting the protective rigidity of the spine. His steps are short, as he is trying to avoid any jarring of his back. In tuberculosis of the cervical spine, he holds his neck is extension and supports his head with one hand under the chin and the other over the occiput.
The compression of neural structures leads to signs of neural deficit. The compression of neural structures is indicated by
- Spasticity of the limbs [uper and lower limbs in case of cervical spine and lower limbs in case of dorsal and lumbar spines]
- Hyperactive deep tendon reflexes
- Spastic gait
- Motor weakness
- Disturbances of bladder and anorectal function.
Neural deficit in tuberculosis could be caused by following factors
- Inflamatory edema – recovers by rest and drug therapy
- Tuberculous granulation tissue – mostly recovers by rest and drug therapy
- Tuberculous abscess – recovers by conservative therapy, rarely requires evacuation and decompression
- Tuberculous caseous tissue – May subside by conservative therapy, sometimes requires evacuation and decompression
- Tubercular debris- Solid debris requires removal and decompression
- Sequestra from vertebral body and disc – Require operative removal and decompression
- Constriction of cord due to stenosis of vertebral canal- Requires operative decompression
- Localized pressure due to internal gibbus along anterior wall of vertebral canal – Requires operative decompression
- Prolonged stretching of the cord over a sever deformity – Decompression, release of cord, and anterior transposition may lead to recovery
- Atrophy of cord – Does not recover completely
- Infective thrombosis/endarteritis of spinal vessels – Does not recover appreciably
- Pathological dislocation of spine – Rare complication, causes irreparable severance of cord
- Tuberculous meningomyelitis – Does not recover completely
- Syringomyelic changes – poor recovery
- Spinal Tumor syndorme – Poor recovery
- Diffuse extradural granuloma or tuberculoma or peridural fibrosis -Present as spinal tumor syndrome
Neural deficit in spine TB is classified as follows
- Patient walks normally and is not aware of any deficit
- Extensor plantar response
- Ankle clonus
- May be accompanied by brisk tendon reflexes
- Clumsy gait
- Incoordinated jumpy gait
- Weakness, walks with support
- Severe weakness
- Patient bedridden and cannot walk because
- <50% sensory deficit
- The patient has paraplegia with flexor spasms or paraplegia in flexion.
- Paraplegia in extension with spontaneous flexor spasms
- Sphincter disturbances
- Flaccid paralysis [ occurs due to very severe cord compression]
Neural deficit in tuberculosis is of slow onset.
Earliest symptom may be twitching of muscles in the lower limbs and clumsiness while walking.
Motor functions are almost always affected before and to a greater extent than the sensory functions due to anterior site because the disease is mostly in the anterior part [motor tracts are anterior too] and probably the motor tracts are more sensitive to compression of the cord.
In severe compression of the cord, flexor spasms may occur which refers to involuntary flexions of the lower limb. This indicates complete loss of conductivity in the pyramidal and extrapyramidal neural tracts.
Bladder and anal sphincters may be involved.
There may be sensory deficit. Sense of position and vibration are the last to disappear.
In severe cases all spasticity disappears and the paralysis becomes flaccid (areflexic paraplegia) with anesthesia and loss of sphincter control.
Sometimes, the insult to cord is sudden [such as ischaemia] and patient may present with flaccid paralysis ”spinal shock” and later gradually change into spasticity.
Rarely, the disease may present like a ”spinal tumor syndrome” due to a localized tuberculoma or a diffuse granuloma or due to peridural fibrosis.
Differential Diagnosis of Tuberculosis of Spine
Mostly the diagnosis of tuberculosis can be made by clinical and radiological examination by its characteristic findings.
Doubtful cases need to be confirmed by biposy and/or culture.
The differential diagnoses vary with age of presentation. Congenital defects of spine, Calve’s disease are common d/ds in young patients. Schmorl’s disease and Scheuermann’s disease may sometimes cause confusion in adolescent patients.
Tuberculosis is suggested by presence of constitutional symptoms [fever, malaise etc], characteristic radiological appearance and disc space is well maintained. Local signs like pain, spasm and tenderness are less pronounced in other diseases than TB spine.
In adults, malignancy is major d/d.
Following is list of main differentials of tuberculous spine.
This may follow infection or surgery of urogenital tract, or postabortal or postpartum infections . Also called pyogenic osteomyelitis, it presents as sudden onset diesase with severe localized pain, spasm and high grade fever with chills and rigors.
Bone destruction is eventually followed by sclerosis and new bone formation and even bony ankylosis.
This is a rare complication of enteric fever. Most of the cases present at the time intervals of 4 weeks to a few months after the episode of typhoid fever.
Excruciating pain and muscle spasm. Radiological picture resembles that of tuberculosis and low grade pyogenic spondylitis. Confirmation can be obtained by agglutination tests, thereapeutic trial or by biopsy.
This can produce changes in the spine which can be very similar to those seen in tuberculosis of the spine. The diagnosis is best established by identification of the causative organisms, agglutination tests or by biopsy.
Actinomyces group or blastomycosis group can be responsible for infection of vertebrae.
Collapse of the vertebral is rare, sometimes the involved vertebrae may produce an appearance described as ”honeycomb” or ”lattice-like” and the condition is usually accompanied by multiple sinus formation and involvement of the subcutaneous tissues.
Diagnosis can be confirmed by demonstration on mycotic organism from the discharging sinuses, pus or from the diseased bone.
It is quite rare.
The commonest site of involvement is thoracolumbar and lumbar spine though it is of rare occurrence after modren antibiotics which cure syphilis much earlier.
Three types are known
- Arthralgic type of syphilitic spondylitis
- Gummatous type of syphilitic spondylitis
- Charcot’s disease of the spine.
Xrays show gross disorganization and destruction of the involved vertebrae along with proliferative new bone formation extending into the adjacent paraspinal tissues. It is extremely difficult to differentiate this condition on x-rays alone.
Diagnosis is confirmed by serological tests, tissue biopsy or by response to antisyphilitic treatment.
Hydatid disease of the spine is a very rare condition
Following benign tumorous conditions may clinically and radiologically have some resemblance with spinal tuberculosis.
- aneurysmal bone cyst
- Osteogenic sarcoma
- Multiple Mycloma
- eosinophilic granuloma (spine-Calve’s disease)
- Hand-Suhuller-Christan disease
- Letterer-Siwe disease
- Block Vertebrae [Fusion of two or more vertebral bodies]
- Neural arch defects
The absence of any constitutional reaction, spasm or any radiological paravertebral shadows and bony destruction, together with minimal local symptoms distinguishes this condition from infective lesions of the spine.
It is a forward displacement of one vertebra on another. The commonest sites are between L5 and S1, and L4 and L5.
Destruction of posterior articular elements or destruction of pars interarticularies with or without involvement of paradiscal regions due to tuberculous process or other infective lesions may result in sponylolisthesis.
Imaging in Tuberculosis of Spine
In addition to the lesion specific appearance of the disease [ radiolucent lesion, fuzzy vertebral margins, reduced disc space, vertebral collapse – refer to types of the lesions], following findings may be noted.
Findings are suggestive, but not pathognomonic. Routine views are anteroposterior and lateral views of the spine. Chest radiograms are taken to rule out outer foci of systemic disease in case of a suspected person.
In the cervical region, this presents as increased prevertebral space.
Prevertebral space is soft tissue shadow between the vertebral bodies and pharynx and trachea. On an average, the normal space between the pharynx and spine above the level of cricoid cartilage is 0.5 cm and below this it is 1.5 cm.
An increased space suggests collection in the prevertebral space.
In upper thoracic spine, abscess appears V-shaped shadow stripping the lung apices laterally and downwards.
It may also show as squaring of borders of superior mediastinum.
Shifting of tracheal shadow to one side may be present on AP view.
Normal tracheal shadow is concave anteriorly in lateral view of thoracic spine. Any change in the contour should raise the suspicion of the disease from C7 to D4 vertebrae.
Below that region [D4 vertebra is watershed], a typical fusiform-shape (bird nest appearance) shadow suggests paravertebral abscess.
Abscesses below the diaphragm tend to extend along the course of psoas muscle which may be noted as bilateral widening of the psoas shadow, but is less common.
This occurs in typical para discal lesion due to collpase of two vertebral bodies.
Lateral Shift and Scoliosis
A lateral curvature and deviation has been recognized as one of the rare deformities of Pott’s disease.
CT and MRI
CT and MRI provide cross-sectional imaging which describes the extent of involvement better and are good at showing the presence of an epidural component and cord compression. MRI is the investigation of choice for this, with CT with contrast being a distant second.
In addition to this, MRI also reveals the status of the spinal cord health.
These show vertebral destruction and paraspinal collections.
Most of the times, especially in endemic regions, the diagnosis of tuberculosis is clinicoradiological but lab tests are called for help when a clear diagnosis cannot be reached out at.
Routine lab investigations done in Pott’s spine are complete blood count, ESR and CRP. Liver and kidney functions should also be assessed during treatment.
CBC might show lymphocytosis but could be normal as well.
ESR and CRP are generally elevated but in some cases the increase is not seen.
ESR is deemed to be inflammation marker and some authors recommend serial ESR levels to assess the decrease in activity of the tubercular disease.
Tuberculin skin test is found positive in most of the patients with spine TB who are not infected with HIV
The tissue for microbiological studies can be obtained through CT guided biopsy. This is more useful in cases with equivocal diagnosis.
- AFB staining of the tissue
- Culture and sensitivity.
Treatment of Tuberculosis of Spine
The treatment of spinal tuberculosis is mainly by chemotherapy. Presence of neurological deficit complicates the matters and for sake of simplicity, I have divided the treatment into two groups
Treatment of Spine Tuberculosis Without Neural Deficit
The prevention of neural deficit in tuberculous disease of the spine is of paramount importance, it can be largely achieved by early diagnosis of spinal caries and its prompt and suitable treatment.
These patients are treated with antitubercular chemotherapy which consists of isoniazid, rifampicin, pyrazinamide and ethambutol as first line of drugs. However, depending upon the patient profile, drugs may be added or replaced.
Gradual mobilization of the patient is encouraged in the absence of neural deficit with the help of suitable spinal braces. After 3 to 9 weeks of starting of treatment the patient is put on back extension exercises . Spinal brace is continued for about 18 months to 2 years.
Surface cold abscesses may be aspirated, deeper collections may not be required to drain.
Open drainage of the abscess is performed if aspiration fails to clear the collection.
Sinuses in a large majority of cases heal within 6 weeks to 12 weeks from the onset of the treatment
Periodic evaluation of patient with X-rays and ESR is done to assess the activity of the disease and decreasing ESR is deemed to be sign of reducing bacterial activity.
Treatment of Spine Tuberculosis With Neural Deficit
Patients with neural deficit require more aggressive approach. Classical approach was to put all the patients on chemotherapy and strict bed rest.
Some authors in recent past suggested radical approach which advocated operating almost every tubercular lesion with [or even without] neural deficit to debride the tissue and relieve the pressure on neural structures.
While first approach produced less than desirable results, second one is associated with increased surgical burden and associated mortality.
Middle path regime solves this problem to a great extent by taking best of both approaches.
It puts the patient on chemotherapy and rest and observes for response. The premise of the treatment is that, as the drugs act on the bacteriae, the reduced destruction and pus production leads to lesser pressure on the neural structures which tend to recover once mileu gets better by use of medicine.
This regime advocates surgery for the patients of TB of the spine who do not get better with the initial treatment or are not candidates for conservative treatment.
The surgery is indicated in following situations
Every patient with neural complications will not be cured by antitubercular drugs and rest alone, however, all patients do not need surgical decompression.
An absoultely conservative approach to Pott’s paraplegia is considered unjustifiable as one might be losing very valuable time. Irreparable damage of the cord may take place if the deterioration progresses to complete loss of motor and sensory function.
Indications for surgery in presence of neural deficit are
- Neurological complications which do not start showing signs of progressive recovery to a satisfactory level after a fair trial of conservative therapy (3 to 4weeks).
- Patients with spinal caries in whom neurological complications develop during the conservative treatment
- Patients with neurological complications which become worse while they are undergoing therapy with antituberculous drugs and bedrest
- Patients who have a recurrence of neurological complication
- Patients with prevertebral cervical abscesses, neurological signs and difficulty in deglutition and respiration
- Advanced cases of neurological involvement such as marked sensory and sphincter [bladder/bowel] disturbances, flaccid paralysis or severe flexor spasms.
In the cases who started showing progressive recovery complications on triple drug therapy between 3 to 4 weeks and progressed to complete recovery surgical decompression was considered unnecessary.
Surgery in Spinal Tuberculosis
Surgery in the spinal tuberculosis is required mostly for decompression of the neural structures or drainage of abscesses.
Surgery is also done for deformity correction in severe kyphus.
In children, posterior spinal fusion is done so as to correct the deformity with growth.
Operative Procedures for Decompression of Neural Tissues
- Decompression and debridement with or without bone grafting
- Crvical spine and cervicodorsal junction- anterior approach
- Dorsal spine and dorsolumbar junction – anterolateral approach or transpleural approach
- Lumbar spine and lumbosacral junction – extrapeitoneal approach.
- Laminectomy for posterior spinal disease, extradural granuloma or tuberculoma
- Anterior transpostiton of the cord through the anterolateral in severe kyphotic deformity causing paraplegia.
Recovery after surgery has been observed after 24 hours to 12 weeks after the decompression. Most of the patients showed the first evidence of objective recovery within 3 weeks of the decompression, however, others took a longer time to recover. The time taken for near complete recovery varied between 3 to 6 months, and in few cases more than a year.
Extensor plantar response, a sign of pyramidal tract involvement, lasts for a very long time.
Patients who recover are able to return to their full activity within 6 to 12 months of the treatment. Brace is recommeded for about 2 years.
The prognosis of the disease is determined by the severity and duration of the disease.
If diagnosed and treated in very early stages, before bony destruction and deformity has occurred, the patient usually recovers completely without any residual problem.
After, vertebral collapse, the deformity occurs. This deformity would persist after the treatment as well when tubercular activity has finished.
If this deformity is severe, it could cause mechanical back pain in later years.
With neural deficit, the prognosis is better if there is
- partial cord involvement
- Neural complications are of short duration
- Early onset neural deficit
- Slow progression of neural complications
- Young patient
- Good general condition of the patient
The prognosis is relatively poor if there is
- Complete cord involvement
- Severe flexor spasms
- Flaccid paralysis
- Gross sensory loss
- Long standing neural complication
- Late onset neural deficit
- Rapid development of neural complications
- Patient is of older age
- Poor general condition of the patient. Irrespective of the mode of treatment the patients who show neural recovery various modalities generally recover in the following order. Vibration and joint sensation; temperature, touch, pain, voluntary motor activity, sphincter functions and wasting of muscles.
Recurrence or relapse of a tuberculous lesion [ Also called recrudescence of the Disease] poses a special problem. The commonest cause is grumbling activity of infection caused by resistance strain of acid fast bacilli.
Surgery may be required in these cases.
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