Introduction

Spinal infections may be classified as mycobacterial, fungal, or pyogenic. ¹ Tuberculous spondylitis was once the most common form of spinal infection, but its incidence has fallen for the past 50 years due to successful diagnosis and treatment of pulmonary tuberculosis. Fungal infections are rare conditions and mainly affect immunocompromised patients. Nowadays, most cases are monomicrobial, and Staphylococcus aureus is the dominant organism (30–80%). Understanding the vascular anatomy of the spine, the anatomic differences between the child and adult, and the clinical presentation of pyogenic infections should assist accurate diagnosis and early treatment, avoiding serious complications. ¹ , ²

Pathogenesis

Spinal infections account for 2 to 7% of orthopedic infections. ³ There are three main routes for pathogen dissemination in pyogenic spondylodiskitis: hematogenous spread, contiguous spread, and direct inoculation. The hematogenous spread of bacteria is responsible for most cases of spinal infections, frequently affecting the lumbar spine in up to 58% of cases, followed by the thoracic spine in 30% of patients and the cervical spine in 11% of patients. ⁴ Contiguous spread occurs when bacteria spread from a contiguous focus of infection (e.g., retropharyngeal abscess and aortic implant infections). Direct inoculation often occurs as postoperative infections (e.g., after diskectomy or instrumented fusions). ⁵ , ⁶

Vascular Anatomy of the Spine

In an attempt to elucidate the pathogenic pathways of vertebral infection, Batson ⁷ in 1940 and Wiley and Trueta ⁸ in 1959 described a paravertebral plexus of veins and arterial anastomoses in the vertebral body, respectively. In 1926, while studying the diploic veins in the cranial bone, Batson turned to Breschet’s ⁹ 1828 work on the paravertebral venous plexus and its communication with the intracranial venous system. Breschet identified a longitudinal large-capacitance vertebral venous plexus, which connected to the venae cave and extended to the cranial venous sinuses. According to Breschet’s study and the reports of pathologists on metastatic spread through veins, Batson believed in a connection between the vertebral venous plexus and pelvic venous system that justified bone metastases from prostate cancer. Finally, Batson reported a paravertebral plexus of veins that extended from the skull to the sacrum, which connected veins to the pelvic venous system. Changes in intra-abdominal pressure resulted in retrograde flow between these systems during physiological processes, such as coughing or straining. Therefore, it has been suggested that there is a relationship between Batson’s plexus and dissemination of tumoral emboli and infections. ⁷ , ¹⁰

Wiley and Trueta highlighted a rich arterial anastomotic system that supplied the vertebral metaphysis with terminal arterioles. Spinal arteries enter the spinal canal through the intervertebral foramen at the disk level. Ascending and descending branches supply the vertebral bodies above and below through the posterior nutrient foramina. The authors reported that the metaphyseal arterioles were more easily filled by contrast than was the venous system described by Batson. They suggested that there are two different routes of hematogenous spread: the nutrient arteries, which are easier to access by contrast injection, and the paravertebral plexus of veins, which is more difficult to fill with contrast and, therefore, is a less common dissemination route. ⁸

The vascular anatomy of the spine and the anatomic differences between the child and adult explain the findings on imaging studies and clinical evaluation. In the child, the blood supply of the intervertebral disk comes from the vessels crossing the vertebral end plates and reaching the disk space. Thus, a septic embolus should cause not a bone infarction but rather an infection of the disk. ⁴ After 8 years of age, these vessels obliterate and the adult disk becomes avascular. At this point, disk cells depend on diffusion from the richly vascularized vertebral end plate for nutrition. ¹ , ¹¹ As septic emboli reach the end arterioles of the vertebral metaphysis, a suppurative inflammation begins. Initially, vascular dilatation and fluid extravasation from fenestrated vessels cause edema in the bone marrow. The pressure in the intertrabecular space increases, diminishing the local blood flow and initiating an ischemic cascade. As a result of ischemia and local suppurative process, bone necrosis occurs. ¹² The disk is damaged after involvement of the vertebral end plate by enzymes, in a similar fashion to the destruction of the articular cartilage in septic arthritis. This leads to the classic spondylodiskitis diagnostic imaging: erosion of the vertebral end plate, osteolytic lesions, abscesses, and compression fractures that may cause spinal instability, deformity, and compression of neural elements. ⁴

Occasionally, an abscess may exude through the larger sciatic notch and appear in the gluteal region, below the piriform fascia, in the perirectal region, or even in the popliteal fossa. More virulent organisms may not follow a fascial plane and may extend into the visceral structures. ¹¹ Neurologic findings may be due to direct compression by epidural abscesses, granulation tissue, bone, or disk as spinal deformity and instability develop. In addition, the neural elements may suffer ischemic injury from septic thrombosis or inflammatory cell infiltration. ¹³

Microbiology

A single organism is usually the cause of pyogenic spondylodiskitis (68%). ¹⁴ , ¹⁵ Staphylococcus aureus and Streptococcus species (over 50%) are the most common causative organisms, followed by gram-negative aerobic bacilli (4–30%). ¹⁶ , ¹⁷ Streptococci are often associated with endocarditis, Pseudomonas species with intravenous drug use, and Escherichia coli and Proteus species with infections of the gastrointestinal and genitourinary tract. ¹⁶ , ¹⁷ Anaerobic infections (3%) are frequently related to diabetes, and organisms of low virulence (coagulase negative staphylococci and streptococci viridans) to immune deficiency. ¹⁶ , ¹⁷ Methicillin-resistant S. aureus (MRSA) should be considered in endemic regions and in patients with prior infection. A polymicrobial cause is uncommon (two organisms, 21%; more than two organisms, 11%) and may be seen as a contiguous spread of infection from decubitus ulcers. ¹⁴ – ¹⁶