Infections of the Cervical Spine

Demographics, Etiology, and Epidemiology

Hadjipavlou and colleagues described pyogenic spine infection as a spectrum of disease comprising spondylitis, diskitis, spondylodiskitis, pyogenic facet arthropathy, and epidural abscess. Of these disorders, more than 95% manifest as spondylodiskitis. Hematogenous pyogenic vertebral osteomyelitis in the cervical spine represents 6% of all cases of vertebral osteomyelitis. Vertebral pyogenic osteomyelitis is two to three times more common in male patients than in female patients. The rising numbers of patients with immunosuppression, whether from human immunodeficiency virus infection, chronic disease, or steroid use, along with intravenous drug abuse and an aging population, are increasing the prevalence of pyogenic infections. Multiple studies evaluating potential risk factors concluded that a current active infection at any site in the body is the leading risk factor for the development of pyogenic vertebral osteomyelitis. Recent urinary tract infection was the most common concurrent infection (28%), followed by soft tissue infection and respiratory tract infection, respectively. Box 25-1 contains a list of risk factors.

Staphylococcus species has been isolated as the causative pathogen in 50% to 80% of cases. Methicillin-sensitive Staphylococcus aureus (MSSA) accounts for greater than 36% of the Staphylococcus species isolated, but the incidence of methicillin-resistant S. aureus (MRSA) is on the rise (6.8%). Streptococcus species were isolated from 19% of culture specimens, whereas gram-negative bacteria were found in approximately 14%. Pseudomonas and Escherichia coli are the most commonly isolated gram-negative bacteria at 3.9% and 2.9%, respectively. Investigators found that 24% to 40% of cultures were unable to isolate a causative organism.

Pathogenesis

Vertebral osteomyelitis and diskitis were once viewed and treated as two distinct pathologic entities. More recent studies suggested, however, that these two infectious processes comprise a spectrum of disease, with one rarely existing without the other. The vascular supply to the intervertebral disk is robust at birth. This hypervascular blood supply allows pathogens direct access to the nucleus pulposus in children, as manifested in the increased incidence of isolated diskitis seen in the pediatric population. Pediatric diskitis occurs most commonly in the lumbar spine but is seldom seen in the cervical spine. With age, the vascularity of the intervertebral disk is obliterated, and isolated diskitis is rarely seen in the adult population (only 1% of all cases of spinal infection). In adults, the pathogenesis of spondylodiskitis begins with seeding of the vertebral metaphysis near the vertebral end plate.

The inflammatory cascade instigated by the infectious process upregulates osteoclastic destruction of bone and enzymatic degeneration of the intervertebral disk. Pain and neurologic deficits develop as the destruction of the spine leads to instability, protrusion of intervertebral disks, and development of kyphosis across the affected segment. Invasion of the epidural space by pus or granulation tissue may cause direct compression of neurologic elements. Ischemic damage to neural tissue may also result from septic thrombosis or inflammatory infiltration of the dura.

Hematogenous seeding of the cervical spine also occurs in the pathogenesis of postinfectious cervical osteomyelitis of the atlantoaxial articulation or upper subaxial spine. This condition, known as Grisel syndrome, is most common in patients less than 30 years old who have had a recent or active upper respiratory infection. It may also result from otolaryngologic procedures. The atlantoaxial articulation is directly seeded by the pharyngovertebral venous plexus that allows upper respiratory pathogens direct access to the upper cervical spine. Periodontoid inflammation of the C1-C2 articulation leads to attenuation of the transverse ligament, pain, rotatory subluxation, torticollis, and atlantoaxial instability. Most patients recover with immobilization and treatment of the underlying infection.

Diagnosis