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Published on : Aug 27, 2020 | Views : 1851 | Downloads : 9

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THE SPECTRUM OF TUBERCULOSIS OF THE SPINE IN PEDIATRIC AGE GROUP: A REVIEW Sandip Chatterjee & Aditya Banta
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Abstract INTRODUCTION Pediatric spinal tuberculosis is characterized by rapid bone destruction and carries the risk of rapid onset neurological deficits and severe deformity of the spine  affected by growth of spine  presents with challenges which are quite different from adults with caries spine. DISCUSSION This is based on the senior author’s experience of dealing with tuberculosis of the spine in children over the last two decades. Recent advances in field of rapid diagnosis of tuberculosis based on nuclear material-related diagnostic tests have further improved the management of tuberculosis. CONCLUSION Tuberculosis in the spine in children needs early attention. Prompting to diagnostic and medical therapy measures can avoid neurological sequellae and delayed deformity. KEYWORDS: Pediatric spinal tuberculosis . Caries spine . Skeletal system
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Introduction The spine is the most common site of tuberculosis in the skeletal system = spinal tuberculosis is further complicated by the presence of neural structures in the vicinity Pediatric spinal tuberculosis is further complicated by additional factors: more cartilaginous nature of bones relative rapid destruction the effect of growth modulation on the ultimate fate of deformity. WHO (2017) report: “estimated pediatrics population (< 14 years) suffering from tuberculosis in India is 227 (range 99–355) thousand worldwide; this number rises to 1050 (Range 646–1450) thousand” The proportion of the pediatric population having extrapulmonary tuberculosis is typically 20–25% (which is higher than the overall incidence of extrapulmonary tuberculosis) In children, the incidence of spinal tuberculosis is variable.
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Anatomic and Pathological Consideration The vertebrae develop from 3 primary ossification centers (one for the vertebral body and two for the posterior spinal elements)  These centers have a central site of bone formation with the surrounding scaffold of cartilage Secondary ossification centers for the spinous process, transverse process, facets, and an apophyseal ring at superior and inferior endplate of the vertebral body. The Initial phase of accelerated growth in an infant is  relatively slower rate of growth during 2–10 years of age following by another phase of accelerated growth during the pubertal surge caused by Mycobacterium tuberculosis and is always a secondary infection, while the primary may be in the lung, genitourinary, or gastrointestinal system  spread invariably by hematogenous: following a bacillaemia or through the Batson’s venous plexus. SPINAL TUBERCULOSIS
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Soft tissue spread is typically seen in the form of a psoas abscess  may further present as discharging sinuses at atypical locations  The extension of abscess into the epidural region  lead to neurological deficits* Tubercular lesion which heals in kyphosis may progress over time owing to the growth of spine  lead to late-onset paraplegias in healed tuberculosis cases. Four types of spinal bony tuberculosis: THE PARADISCAL LESION starts at the vertebral metaphysis and destroys the cartilage and then the disc. THE CENTRAL TYPE is marked by initial infection in the midsection of the vertebral body, and then the infection spreads centrifugally leading to hyperemia and osteoporosis. THE ANTERIOR LESION has involvement of the body beneath the anterior longitudinal ligament. THE APPENDICEAL TYPE is characterized by involvement of the pedicle, lamina, the articular process, or the spinous process. Mycobacterium is deposited in the anterior aspect of vertebral endplates via the end arterioles = most common form of childhood tuberculosis* (cont) Spinal Tuberculosis..
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Presentation Delay in the diagnosis of pediatric spinal tuberculosis is very common Pain  associated with muscle spasms, night cries, and sometimes deformity. Cold abscess and discharging sinus  the presenting symptoms in a subset of cases. Neurological deficit  associated with delayed presentation SYSTEMIC DISEASE Malaise, anorexia, night sweats, and weight loss THE BONY LESION Localized pain in the spine with limitation of movement occurs due to the bony involvement. Severe spasm of the paraspinal muscles  most common with atlantoaxial or upper cervical caries who can present with torticollis (even down to gluteus region) Paraspinal abscess (maybe a retropharyngeal abscess in the neck or in the paraspinal area of the dorsal or lumbar spine) Night cries  The pain is often worse at night Abscesses is a sign of active disease  spread in area that low resistancy*
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Fig. 2 Tuberculous fistula in the neck following subaxial cervical spine caries Fig. 1 Cold abscess in the gluteal region
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NEUROLOGICAL MANIFESTATIONS Two types of the neurological deficit : Paraplegia of early onset with active disease usually occurring within the first 2 years Early-onset paraplegia have been postulated to be mechanical compression and/or pathological subluxation/dislocation of involved vertebrae Paraplegia of late-onset which occurs years after the healing of the disease Late-onset paraplegia is thought to occur secondary to pressure symptoms from internal gibbus formed after progression of deformity. Slow-progression lesion causing gradual compression. The neurological deficits in tuberculosis spine have been classified by Tuli and modified by Jain into 5 stages: Stage I: patient unaware of the neural deficit, clinician detects plantar extensor, and/or ankle clonus Stage II: the patient has spasticity with a motor deficit but is a walker. The sensory impairment is the lateral column Stage III: bedridden spastic patient. Stage IV: bedridden patient with a severe sensory loss and/or pressure sores. There is impairment of both lateral and posterior column sensations. Stage V: same as stage IV and/or bladder and bowel involvement, and/or flexor spasms/flaccid tetraplegia/ paraplegia.
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DEVELOPMENT OF KYPHOSIS Kyphosis occurs in active disease due to the destruction of vertebral bodies and resultant collapse of the anterior column  3 or more vertebral bodies loose anterior height and lead to an angular kyphosis, nearby vertebral bodies may show inflammatory changes A truly symmetric destruction would lead to the development of a kyphotic spine. Asymmetry in this destruction process is responsible for deformity in the coronal plane leading to kyphoscoliotic deformities. Cartilaginous nature of vertebral bodies in children predisposes children to relatively rapid destruction of vertebral bodies  that’s why deformities in children are severe  causing an increase in the size of internal gibbus causing more neural deficits. KYPHOTIC DEFORMITIES affected by: differential destruction of growth plates by disease process or by surgical debridement, differential loading of spine, and altered vascularity. “Spine at risk”  can be used to predict the possibility of progression in a particular child with spinal tuberculosis (Rajshekheran et al) Progressive kyphosis and severe spinal deformity in very young children  growth of thoracic cavity  ecreased pulmonary functions.
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Fig. 3 Kyphotic deformity in cervicodorsal caries spine Fig. 4 Stretching of the cord over a kyphotic deformity in late stage of
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Investigating a Child with Tuberculosis of the Spine CRP  to monitor response to treatment. LFT  to detect adverse reactions to tubercular treatment TESTS FOR LATENT TUBERCULAR INFECTION (LTBI) are considered diagnostic of tuberculous infection in pediatric population. Patients with LTBI have a 4–6% lifetime risk of developing TB disease.* Tuberculin skin test (Mantoux test) detects delayed hypersensitivity to Mycobacterial TB antigens Interferon-Gamma Release Assays (IGRA) have the advantage that there is no cross-reactivity with BCG minimal cross-reactivity with nontuberculous mycobacteria. Tissue diagnosis is the most conclusive way of establishing a diagnosis of spinal tuberculosis in any form  Conventional way (results in 4- to 6-week duration) and Nucleic acid amplification test (shorter period). Genotyping of Mycobacterium tuberculosis has epidemiological use in tracing contacts, elucidating sites and patterns of transmission within communities. Plain radiographs are usually the initial investigation for suspected cases of spinal TB  radiolucent lesion to be at least 30% of bone mineral loss. Computed tomographic (CT) helps detail of irregular lytic lesions, sclerosis, disc collapse, and disruption of bone circumference than plain radiograph.
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Magnetic resonance imaging (MRI) is the best diagnostic modality for tuberculosis of the spine. MRI frequently demonstrates disc collapse/destruction, cold abscess, vertebral wedging/collapse, marrow edema, and spinal deformities. The spinal cord may show edema, myelomalacia, syringomyelia, cord atrophy, thickening of meninges, and/or arachnoiditis with clumping of roots Fig. 5 plain radiography. C1-C2 instability in a case of caries of atlantoaxial joint
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Fig. 6 MRI. Extradural compression in caries of upper cervical spine demonstrating prevertebral cold abscess Compression could be due to extradural fluid collection, caseous material, or granulation tissue. Early surgical decompression may improve patients with extradural granulomatous compression on a near normal size cord BUT, Patients with significant cord compression with evidence of myelomalacia have the least chances of recovery with any sort of treatment
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Treatment Drug regimens used in treatment of tuberculosis in adults and children inherently are the same DRUG Four weight groups are used to decide drug dosage: < 10, 10–17, 18–25, and > 25 kg. Isoniazide and rifampicin 75 mg each, pyrazinamide 250 mg along with ethambutol 200 mg/day are prescribed for a child weighing < 10 kg. Then after that adjust with the weights. Weight must be measured at regular interval and dosage of drug given as per appropriate weight band. The duration varies between 6, 9, 12, and 18 months. Bracing is an important component of treatment of pediatric spinal tuberculosis as it helps in enforcing movement restriction in otherwise noncomprehending patients. BRACING
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Surgical treatment is typically reserved for rapid onset dense neurological deficit  which is progressive or which is not improving with conservative treatment. This treatment is for significant deformity at presentation, and in case of panvertebral involvement (disease of both anterior and posterior column), and for significant mechanical instability/potential. Presence of large paraspinal abscesses causing mass effect, persistent pain not improving with chemotherapy, and need for definitive diagnosis are also indications for surgical intervention SURGICAL SPINAL TUBERCULOSIS WITH NEURODEFICIT 30 to 40% of patients showed improvement in neurology during these 4 to 6 weeks after being on antitubercular treatment and rest therapy (Tuli et.al). Consider early surgical decompression (when MRI shows granulomatous or caseous extradural compression with edema/myelitis of the cord) The aims of surgical treatment: disease control along with maintenance of stability, normal spinal growth, sagittal alignment of the spine, and ensuring protection of neurological function including providing an environment conducive for neurological recovery.
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DEBRIDEMENT should be limited to excision of pus, caseous tissue, and sequestra. Inflamed/ischemic and infracted bone tends to recover on starting medical therapy as blood supply to the area improves. Access to cervicodorsal junction using a U-shaped manubriotomy is used, thus preserving the sternoclavicular articulation Fig. 7 Transmanubrial approach to cervicodorsal caries
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ACTIVE DISEASE WITH KYPHOSIS Surgical treatment is typically reserved for: rapid onset dense neurological deficit neurological deficit which is progressive or which is not improving with conservative treatment, for significant deformity at presentation, and in case of panvertebral involvement* Significant mechanical instability/potential for future deformity Presence of large paraspinal abscesses causing mass effect, persistent pain not improving with chemotherapy, and need for definitive diagnosis All kyphotic tubercular spines** with moderate to severe kyphosis (> 50°)  treated with kyphosis correction surgery because of the inherent potential for neurological deficits in acute and healed stages  correction which an acceptable option is mild shortening of cord (balance). Any attempt at deformity correction should be accompanied by neural decompression from the anterior compressing elements  because the compression is caused by retropulsion of material into the spinal canal  risk of neural deficit. Spinal cord should be visualized throughout the procedure.***
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Fig. 8 Anterior corpectomy and posterior fixation in a cervical caries It is recommended routine use of intra-operative neuromonitoring for correction of delayed deformity due to cervical spinal tuberculosis. The use of somatosensory evoked potential (SSEP) in addition to monitoring of Trans Cranial MEP (TcMEP) acts as a guide to help dictate the extent of the correction.
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The various methods of kyphosis correction secondary to spinal tuberculosis are: Transpedicular approach can be achieved by using a transpedicular decancellation osteotomy or a costotransversectomy and pedicular excision at the apex of kyphosis Anterior decompression followed by posterior instrumentation or vice versa. Anterior decompression is done using transthoracic/retroperitoneal approach, the anterior column may be reconstructed by a bone graft or a mesh cage, and this is augmented by a posterior instrumentation Extrapleural anterolateral approach It provides exposure to both anterior and posterior elements at the same time  stability is maintained during the procedure (no need for temporary stabilization). Fig. 9 Pedicle substraction osteotomy in a tuberculous kyphotic deformity
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KYPHOSIS CORRECTION IN HEALED LESION Correction of kyphosis in healed lesion is a technically demanding surgery and has been associated with higher risk of neural injury  not for cosmetic purpose. The aim of surgery in patients with neurodeficit = decompression and acceptable sagittal and coronal balance. Paraplegia of late-onset  anterior decompression and fusion are recommended. Here internal gibbus needs to be removed by approaches similar to those used in active disease. When it comes to healed disease, these procedures are technically more challenging and recovery is less predictable FOLLOW-UP PERIOD Regular monitoring = blood counts, ESR CRP, and liver function Radiological investigations in form of MRI should be repeated earliest at 6 months as repeating imaging before caries the risk of misinterpretation of drug lysis as nonresponsiveness of disease Recent practice is to have a repeat MRI at 12-month duration and stop AKT when the disease shows near complete healing. Persistence of small abscesses is not considered an indication for the continuation of therapy
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TERIMA KASIH