Plancarte et al. 
Bilateral paramedian extradiscal approach (fluoroscopy)
Avoids risks associated with intervertebral disc and spinal canal penetration
• Technical difficulties due to anatomical variability (tall iliac crests, large L5 transverse process, L5 nerve root)
• Two separate injections
• Unpredictable spread in the presence of retroperitoneal adenopathy/tumor
Waldman and Wilson 
CT-guided paramedian single needle approach
• Avoids risk of vascular, intervertebral disc, and spinal canal penetration
• Accurate needle placement
• Increased radiation exposure
• Access to CT scan
• Unpredictable and limited spread in the presence of retroperitoneal adenopathy/tumor
Kanazi and Frederick 
Single needle anterior approach (fluoroscopy, CT, or ultrasound guidance)
• Easy, simple technique
• Supine position
Risk for bowel and bladder perforation or vascular injury
Single needle paramedian, transdiscal approach (fluoroscopy)
• Accurate needle placement
• Risk for disc infection, rupture, herniation
• Can be painful
• Unnecessary discogram
Single needle posteromedian approach (fluoroscopy)
• Easy, simple
• Avoids anatomical barriers
• Lateral or prone position
• Accurate needle placement
• Risk for infection (discitis, meningitis, epidural abscess), neural injury, postdural puncture headache
A single needle posteromedian transdiscal approach can be used to achieve bilateral blockade with less technical difficulties. This technique, described by Turker et al. , is simple and can be performed with patient positioned in prone or lateral decubitus. Compared to the classic two-needle posterior approach, the transdiscal technique is easier and has less potential for complications while having the same efficacy . Although no significant complications have been reported so far with any of these techniques, potential problems should always be considered.
Retroperitoneal bleeding, nerve root injury, or atherosclerotic plaque embolization from iliac arteries can occur with the posterior extradiscal needle placement. Bowel or bladder perforation can complicate the anterior approach, while discitis and disc trauma are of particular concern when transdiscal techniques are used.
26.2.2 The Intervertebral Disc: Age-Related Structural Changes
The two main components of the disc—nucleus pulposus and annulus fibrosus—are confined in the intervertebral space by the end-plate cartilage, a hyaline structure adherent to the vertebral metaphysis, and by the anterior and posterior longitudinal ligaments. With aging all these entities undergo multiple structural changes. At birth the disc is well vascularized and contains 80–90% water. The collagen and elastin fibers are organized in very complex networks. Proteoglycans are responsible for maintaining the osmotic pressure and disc hydration, which further allows the disc to maintain height when loaded. With time the fibers become less organized and lose their strength. Proteoglycans are degraded and subsequently the osmotic pressure and water content decrease .
At birth, branches of the segmental arteries penetrate the annulus and provide blood supply to the entire disc. Progressively the intradiscal vascular bed contracts. In the third decade of life, the disc becomes almost avascular, maintaining only limited blood supply to the outer margin of the annulus fibrosus. The adult disc receives nutrients by diffusion through the cartilaginous end plates and from its own poor peripheral vasculature. The innervation also regresses to the disc periphery. Nociceptive and mechanosensitive fibers accompanying the blood vessels or branching from the sinuvertebral nerves are found only in the outer third of the adult annulus. Cartilaginous end plates become more frail, prone to fissures, allowing disc material to herniate into adjacent vertebrae to form Schmorl’s nodes.
The disc starts to lose height and becomes more susceptible to degenerative, traumatic, and infectious processes.
26.2.3 Discitis Etiology and Pathogenesis
In adults, the infection of the intervertebral disc is most frequently the result of hematogenous spread, from a distant source (genitourinary, endocardial, respiratory, gastrointestinal, cutaneous ulcers, etc.). Infected emboli reach the well-vascularized vertebral metaphysis via arterial or retrograde venous (Batson’s veins) blood flow, subsequently producing bone infarction, destruction, and osteomyelitis. From the subchondral area, the infection diffuses then into the intervertebral disc space to the avascular nucleus pulposus.
Direct hematogenous colonization of the disc occurs mostly in children, as their discs are still vascularized. Infection is often limited to the disc space . The rich vascular supply allows good antibiotic penetration. Overall, in these very young patients, discitis has a better prognosis . Less frequently, discitis is caused by direct iatrogenic or traumatic disc contamination. Spine surgery and intradiscal procedures are the most common iatrogenic causes of discitis. The incidence of post-discography infection varies from 1 to 4% .
Because discitis can be either preceded or complicated by vertebral osteomyelitis, the two conditions are frequently described as spondylodiscitis . Most disc infections are bacterial, but mycobacterial and fungal etiology should be considered in specific circumstances.
Staphylococcus aureus, Staphylococcus epidermidis, and gram-negative Escherichia coli are some of the pathogens commonly isolated in the spinal infections involving the disc. Many predisposing comorbidities have been described, among them diabetes, immunocompromised states, malignancies, intravenous drug use, chronic alcoholism, previous spine surgery, infective endocarditis, etc.
26.2.4 Discitis Clinical Presentation, Diagnosis, and Treatment
22.214.171.124 Clinical Presentation
Most of the patients with discitis experience severe back pain, stiffness, muscle spasm, and tenderness to palpation. Often the onset is insidious with the pain intensifying progressively. The incidence of fever varies in different reports from 37 to 70% of patients with bacterial spondylodiscitis [15–17]. Fatigue, anorexia, and malaise can occur as the disease progresses. Sepsis is rare.
When the infection occurs as a complication of an intradiscal procedure, the symptoms become evident at 2–4 weeks after the intervention .
Delays in diagnosis and treatment allow infection to diffuse to the adjacent vertebral bodies, epidural space, and paraspinal muscles. Paravertebral contamination, psoas abscesses, compression fractures, and spine instability may complicate advanced stages. Depending on the site and size of the infection, different degrees of neurologic symptoms can develop. Isolated radicular pain, sensory-motor deficits, cord or cauda equina compression, or even paraplegia can complicate the course of spondylodiscitis.
Although spondylodiscitis presents with non-specific symptoms, centered on progressive back or neck pain, the diagnosis should be suspected whenever fever and elevated inflammatory markers accompany the axial symptoms. Other painful spine conditions should be taken into account as part of the differential diagnosis: painful intervertebral disc disease, fractures, or vertebral metastases.
A complete clinical examination, with emphasis on neurologic and musculoskeletal aspects, can reveal axial tenderness, muscle spasms, sensory/motor deficits, or, in advances stages, spine deformities and even instability. The exam should also address the existence of a potential source of bacteremia.