Evidence of spinal infection exists in Egyptian mummies (c.3000 BC) and Neolithic remains from earlier. The earliest scientific descriptions came from Hippocrates, but it was enunciated in more detail by Percival Pott (1779), Nelaton (1854) and Rodet (1884)1. Mortality before antibiotics was upto 70%. Even today, diagnostic delay is three months on average and recovery averages 12 months or more. Its incidence may be increasing due to greater numbers of immunocompromised patients and an increase in spinal invasive procedures.

Involvement of the disc alone is commonly referred to as discitis. Infection of the vertebral body is termed vertebral osteomyelitis. Spondylodiscitis best describes the condition where the infection involves both, the vertebral body and the disc, after having crossed the end-plate from the former to the latter. Each of these may be associated with epidural or paravertebral abscesses.

Biologic Anatomy
Spinal infection may be acquired by hematogenous spread through bacteremia from distant sites or by direct spread secondary to trauma, surgery or adjacent infections. Urologic procedures and indwelling catheters are frequently responsible for bacteremia and seeding in spinal tissue.

Arterially spread infection originates in the end plate and involves the disc secondarily. The microscopic and macroscopic anatomy of the disc plate and its relation to the contiguous end plates has been well described by Coventry2, Inou3, Wiley & Trueta4 & Whalen5. Batson6 expanded Breschet's description of pelvic venous drainage and its relation to the spine while Crock & Yoshizawa described the microvascular circulation of the end plate7.

Ratcliffe8, described changes in the end plate vasculature with age. Intraosseous arteries tend to be end arteries in adults, causing greater involvement of bone due to a septic embolus, thus leading to a greater incidence of vertebral osteomyelitis. The Nucleus Pulposus has a much greater blood flow through the adjacent end plates and the annulus in children, thus resulting more in discitis.

Natural History
Blood borne infection probably begins in the capillary loops or post capillary venous channels in the end plate. Sludging here leads to suppurative inflammation, tissue necrosis, bony collapse and spread into adjacent disc spaces.

Anterior or posterior extension can cause paravertebral or epidural abscesses. Infected bone softens and may collapse. Neurologic deficit may occur due to epidural abscess or neural compression due to pathological fracture.

Eismont9 described an increased incidence of paralysis with increasing age, higher level of involvement, co existing debility (diabetes, rheumatoid arthritis, steroid use etc.) and staphylococcus aureus infection.

Causative Organisms
A variety of organisms are implicated in pyogenic spondylodiscitis. Staphyococcus aureus is by far the most common, being isolated in 50 - 60% cases. Table 1 summarises the rest11.

In addition to Table 1, there are case reports describing spondylodiscitis due to Gardnerella vaginalis12, Eikenella corrodens13, Propionibacterium acnes14, Scedosporium prolificans15, Hemophilus aphrophilus16 and Blastoschizomyces capitatus17.

Well known associations exist between Pseudomonas and IV drug abuse, Gram-negative organisms such as Escherechia, Klebsiella and proteus with genitourinary disease, Salmonella and Sickle cell disorders. Infections secondary to Spinal instrumentation can involve staphylococcus epidermidis.

Figure 1: Indications for surgery in spondylodiscitis:

Causative Organisms in Pyogenic spondylodiscitis:

Staphylococcus aureus
Strptococcus species
Staphylococcus epidermidis
Escherechia coli
Klebsiella pneumoniae
Proteus species
Pseudomonas aeruginosa
Enterobacter species
Salmonella species
Serratia marcescens
Brucella species
Acinetobacter species

Figure 1: Radiological changes in Spondylodiscitis: Sclerosis, Vertebral body destruction and reduction in disc height Figure 2a: Spondylodiscitis changes on T1 weighted images in MRI
Figure 2b: Spondylodiscitis changes on T2 weighted images in MRI Figure 3: Posterior fusion in Spondylodiscitis

Clinical Features and Diagnosis
Ross and Fleming18 reported pain as the primary symptom in 85% patients with Spondylodiscitis. Constitutional symptoms such as fever, night sweats, weight loss etc may be present. Puig-Guri19 described four possible clinical syndromes in Spine infections: Hip Joint syndrome, Abdominal syndrome, Meningeal syndrome and Back Pain syndrome. Neurological deficit can be early if due to epidural abscess or late if secondary to deformity. Neurology due to arterial thrombosis is rare20. Infants may show irritability; toddlers may exhibit difficulty walking or eventually, refusal to walk. Muscle spasm can be pronounced. Post-operative spondylodiscitis may present with a discharging wound, commonly one - two weeks post surgery.

Xue & Guan21 found an elevated CRP and ESR in all 23 patients in their series. White cell counts were less reliable. Very elevated white cell counts may however suggest epidural abscess development. Low platelet counts (< 100 x 10(9)/L), extremely high ESR (> or = 110 mm/h) and cervical spine epidural abscess may be predictors of a poor outcome22.

X-Ray findings of Spondylodiscitis include disc space narrowing, end plate irregularity, subchondral defects and sclerosis. These may appear two weeks to three months after onset of infection23. Paravertebral masses indicate abscess formation. Vertebral collapse, segmental kyphosis and bony ankylosis are late findings.

CT scans offer a qualitative improvement over plain X rays. They also have an application in guided biopsies and para-vertebral abscess aspiration.

MRI scanning is the diagnostic modality of choice. Modic reported MRI sensitivity of 96%, specificity 92% and accuracy of 94% in disc space infections24. Ring enhancement of epidural abscesses on Gadolinium scanning may be an indication for surgery25. MRI is contraindicated in the presence of metallic heart valves or pace makers. Presence of metallic joint prostheses or claustrophobia are relative contraindications for MRI scanning.

Where MRI scanning is not feasible, Radionuclide scanning may be of use. Combined Tc99 and Ga 67 scanning is reported to be 90% sensitive, 100% specific and 94% accurate for infection. Indium 111 labelled leucocyte scanning is highly specific but not sensitive enough.

A Diagnostic biopsy is most often undertaken under CT guidance to isolate the offending pathogen and rationalise choice of antibiotics. A recent level 3 study has reported identification of causative bacteria in 47% CT guided biopsies as against 90% endoscopic biopsies26. Other studies have however reported success rates for percutaneous needle biopsies ranging from 71% to 90%27.

Differential Diagnosis
Spondylodiscitis should be differentiated from primary or metastatic malignancies of the spine, metabolic bone diseases with pathologic fractures and infections in the vicinity including the psoas, abdominal cavity and hip. Charcots arthropathy of the spine should be kept in mind.

Non operative management with antibiotics and bracing continues to be first line management in adult spondylodiscitis. Elimination of spinal pain and spontaneous fusion are the expected end points.

Bettini and Girardo28 have recently reported on their series of 56 adult patients with spondylodiscitis. They were able to treat all their patients with iv antibiotics for an average of 8.5 weeks followed by oral antibiotics and supportive spinal bracing. They monitored CRP response, ESR and WCC count as a guide for duration of antibiotic therapy.

Indications for surgery in spondylodiscitis are enumerated in Table 2 (11):

In addition to Table 2, advanced age (> 60 yrs) and immunocompromise are regarded as bad prognostic factors and are relative indications for surgery.

The principles of surgical treatment are adequate debridement, decompression of neurological structures and rigid fixation. Surgical options include anterior or posterior approaches, with decompression, debridement and fusion. Although autogenous structural bone graft has been used traditionally, there are studies reporting the use of titanium29 and PEEK30 cages being used successfully. Posterior fusion as a second stage after an anterior procedure is indicated when treating a severe kyphotic deformity or where multilevel corpectomy has been performed.

Lee and Suh31 have reported on their series of 18 patients with spondylodiscitis treated with posterior lumbar interbody fusion. All patients fused well, though one took 18 months to do so. Linhard and Kruger32 in a randomised trial comparing isolated anterior and posterior fusion for spondylodiscitis found no statistical differences in fusion rates and results at one year. The anterior fusion group mobilised earlier while the posterior group had lesser blood loss intra-op.

Results of posterior decompression without fusion in spondylodiscitis have historically been poor.

Pyogenic Spondylodiscitis most often presents with back pain and muscle spasm. Primary hematogenous infection is more common than external seeding. MRI scans are the best imaging modality, while serial CRP helps monitor response to treatment. Antibiotics are the mainstay of non-operative management. Surgery in the form of decompression and fusion may be required.


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