The most common pattern of tubercular spinal infection in adults is the “paradiscal” type, where the bacilli lodge in the sub-chondral marrow on either side of the disc as the disc is avascular. In children, the disc retains its blood supply till approximately 9 years of age and so the bacilli affect and destroy the vertebral body and disc simultaneously (“centrum” or “complete” type) (Fig. 27.2a–f). Due to the weaker immune response of the child and cartilaginous nature of the vertebral body, extensive vertebral destruction and exuberant abscess formation is more common in children [6]. The other types of spinal tuberculosis are the anterior type (abscess formation beneath the anterior longitudinal ligament), posterior type (isolated involvement of posterior elements), and the non-osseous type (extensive abscess formation with very little bony destruction).

Neurological compromise occurs in up to 30–75 % of the patients with spinal tuberculosis [7–9]. Though children have more severe destruction, they also have a lesser incidence of neurological involvement, probably due to the relative larger canal diameter and more flexibility of the spine. Cervical tuberculous lesions manifest with quadriparesis but since the thoracic and thoracolumbar regions are commonly affected, lower limb weakness with bladder and bowel involvement is more common. Initial symptoms are in-coordination and clumsiness while walking which slowly progresses to paraplegia and loss of sphincter control.

Children can present with neurological involvement both in the active and healed phase of the disease. In active lesions, it is due to the result of direct compression of the spinal cord by an abscess, inflammatory granulation tissue, a dislodged sequestrum, or canal compromise due to instability. In the healed disease, it occurs after many years and is usually due to stretching of the cord over a bony ridge at the apex of the deformity.

The etiology and progression of kyphosis is different in the active and healed phase of the disease. Tuberculosis affects and destroys the anterior structures of the vertebral column in more than 90 % of patients. Collapse of the vertebral body is evident as a localized kyphotic deformity. Involvement of two or three adjacent vertebral bodies manifests as a sharp, angular kyphosis called the gibbus. Chemotherapy will cure the disease but vertebral collapse will continue until the healthy vertebral bodies in the region of the kyphosis meet anteriorly and consolidate. The severity of collapse during the active phase is mainly influenced by the severity of vertebral destruction, the level of the lesion, and the age of the patient [10].

During the active phase, the deformity increases in proportion to the severity ranging about 25–35° for each vertebral body loss in thoracic and thoracolumbar lesions. The kyphotic collapse is less in lumbar lesions due to the lordotic nature of the lumbar spine, large size of the intervertebral discs, and the sagittal orientation of the facet joints which allows vertical subsidence. In the thoracic and the thoracolumbar regions, the deformity tends to be more severe due to the inherent kyphotic nature of the thoracic spine and the coronal orientation of the facets which lead to subluxation and kyphosis. Deformities in children less than 10 years of age have been observed to have greater deformity than those over 10 years of age due to soft vertebral bodies, weaker posterior stabilizing structures, and the secondary increase in deformity during the adolescent growth spurt [11, 12].

In a long-term follow-up of 15 years of 63 children, Rajasekaran reported three types of collapse and healing of the anterior column with different implications for deformity progression during the period of growth [10, 13, 14] (Fig. 27.5a–c). Type A healing was seen in minimal lesions and paradiscal type of involvement, where the facet joints were intact and there was large area of contact of vertebral bodies anteriorly. These patients showed minimal deformity in the active phase and frequently an improvement during the growth period (Fig. 27.6a–c). Type B healing was seen when the vertebral body loss is equivalent to the loss of one vertebral body. Here during the process of collapse, the facet joint at the level of destruction subluxed or completely dislocated. The superior vertebra rotates during the process of descent so that its antero-inferior margin comes into point contact with the superior surface of the inferior normal vertebra. This resulted in growth depression at the point of contact and the deformity could progress by up to further 30° during the growth period (Fig. 27.7a–c). Type C restabilization occurred when the vertebral body loss increases to more than “two.” The large anterior column defect necessitates the dislocation of two or more facet joints before anterior column restabilization can occur. The superior normal vertebra rotates 90° so that the anterior surface of superior vertebra comes into contact with the superior surface of the inferior vertebra. This was seen frequently in children less than 7 years of age with thoracolumbar disease. In children with multiple vertebral body destruction, a peculiar pattern of collapse is seen which has been termed as “Buckling Collapse” [14, 15]. Dislocation of facet joints occurs sequentially at multiple levels leading to a kyphosis of more than 120° and the entire spine is converted to two large compensatory curves. Many vertebral segments become horizontally oriented with stress shielding of their growth plates. Longitudinal overgrowth of the vertebral segments is noted leading to stretching of the spinal cord at the apex of the kyphosis with possible secondary late-onset paraplegia. Risk factors for “buckling collapse” included an age of less than 7 years at the time of the disease, thoracolumbar involvement, loss of more than two vertebral bodies, and presence of radiographic spine-at-risk signs (Fig. 27.8a–c).

Unlike adults in whom the deformity is static after cure of the disease, post-tuberculous kyphosis in children is a dynamic deformity with variable progression during growth. Three different patterns of progression have been observed depending on the pattern of healing [10]. Type 1 progression, where worsening of deformity occurs during growth, is seen in 39 %. This increase can occur after a lag period of few years after the disease control. As a result, a severe increase in deformity may be missed if the child is not followed-up carefully till the completion of growth. Forty-four percent of children had a Type II progression where after an increase in deformity during the active phase, the deformity showed a progressive and spontaneous correction. This was mostly observed with Type A healing pattern and in children younger than 7 years. Type III progression, where there was no major change during growth, was seen in the remaining 17 % who either had a minimal disease or a lower lumbar lesion (Fig. 27.9a, b).

Four radiological signs which indicate spinal instability have been identified by Rajasekaran to predict the risk of late and progressive development of deformity in childhood spinal tuberculosis [10, 13]. They basically indicate the presence of facet joint dislocation and disruption of the posterior arch. These signs are easy to identify in radiographs, appear early in the course of the disease and are useful to identify children at risk for progression so that surgical stabilization can be suitably advocated. These four “spine-at-risk” signs are: (1) dislocation of one or more facet joints in the lateral view, (2) retropulsion of the diseased vertebra, (3) lateral translation seen in antero-posterior view, and (4) the “Toppling Sign” (Fig. 27.10a–d).

Anemia and elevated erythrocyte sedimentation rate (ESR) are the two common abnormalities noted in blood investigations. ESR may be markedly elevated (>70 mm/h) and serial ESR measurements are helpful in assessing the response to treatment. ESR and low hemoglobin levels however lack specificity [16]. A positive Mantoux (tuberculin skin) test merely indicates cell-mediated immune response due to a previous tuberculous infection and in endemic regions, the test can be positive even in patients without active tuberculosis. Its diagnostic value is useful only in regions where tuberculosis is rare. Polymerase chain reaction (PCR) analysis from infected tissue is considered very sensitive and specific for the diagnosis of spinal tuberculosis [17].

Bacterial culture of the infected tissue is useful to confirm the diagnosis and to acquire antibiotic sensitivities to guide therapy. Since spinal tuberculous infection is paucibacillary (less bacilli in infected tissues), it is essential to culture material from deep structures such as bone and abscess walls. Culture media such as BACTEC™ (Becton-Dickinson and Co., USA) now are the standard culture media [18]. An important advantage is that they allow drug susceptibility assessment. This helps in identifying drug resistant strains and start early alternate second-line medications.

Earliest features observed on plain radiographs are vertebral osteoporosis, narrowing of the disc space and indistinct paradiscal margin of vertebral bodies. With progress of the disease, destruction is associated with vertebral collapse, kyphosis, and sagittal or coronal instability. In the cervical spine, the prevertebral soft tissue shadow can be enlarged due to distension of the abscess in the retropharyngeal region. In the thoracic spine, the cold abscess is visible on antero-posterior plain radiographs as a fusiform or globular radiodense shadow (bird’s nest appearance) (Fig. 27.11a–e). In children, attention should be paid toward the “spine-at-risk signs” as it indicates chances of deformity progression.