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Infection of the cervical spine accounts for less than 10% of all spine infections, but it is the source of 27% of all neurologic deficits associated with an infectious process. The classification of cervical infections includes diskitis and osteomyelitis and is identical to the system used in the thoracic and lumbar spine. Multiple factors can be used to classify spine infection, including the pathogen, method of inoculation, anatomic location, and duration of infection. The most common types of spinal infections are hematogenous bacterial infection, epidural abscess, and postoperative wound infection. Table 25-1 provides classification methods. This chapter discusses pyogenic, granulomatous and postoperative infections of the cervical spine.
| Region | Cervical |
| Thoracic | |
| Lumbar | |
| Pathogen | Pyogenic (bacterial) |
| Granulomatous (tuberculosis or fungal) | |
| Parasitic (echinococcosis) | |
| Location within the spinal elements (Had) | Diskitis (isolated to the intervertebral disk) |
| Spondylitis (isolated to the vertebral body) | |
| Spondylodiskitis (involving the vertebral body and intervertebral disk) | |
| Pyogenic facet arthropathy (isolated to the facet joints; very rare) | |
| Epidural abscess (infection within the spinal canal) | |
| Duration | Acute (<6 wk) |
| Subacute (6 wk-3 mo) | |
| Chronic (>3 mo) |
Pyogenic Hematogenous Cervical Spine Infection
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.
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HIV, Human immunodeficiency virus.
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
History and Physical Presentation
Neck pain and back pain are the primary symptoms in 92% of patients presenting with spondylodiskitis. The presentation may be acute, subacute, or chronic. Delayed diagnosis of cervical infection is common as a result of the nonspecific nature of the symptoms. More than 50% of patients present with a history of symptoms lasting longer than 3 months. Sapico and Montgomerie reported that 15% of patients presented with atypical symptoms such as chest and abdominal pain, dysphasia, and headaches. Patients may experience low-grade fever, chills, night sweats, fatigue, malaise, or decreased appetite. Only half of patients presenting with cervical infections experience fevers, and individuals with acute infections lasting less than 3 weeks are more likely to have fever.
Physical findings in patients with cervical spondylodiskitis are limited. The most universal findings are tenderness to palpation, muscle spasm, and decreased range of motion. When patients present with signs of radiculopathy or myelopathy, an associated epidural abscess or neurologic compression should be suspected.
Laboratory Evaluation
Laboratory workup for cervical infection should consist of a complete blood count (CBC) with differential, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). In addition, urine and blood cultures with Gram stain should be obtained. Sapico and Montgomerie reported leukocytosis in 50% of patients with cervical infections. In the same study the ESR was elevated in almost all cases (92%). CRP is sensitive and is a more specific inflammatory marker than the white blood cell count or ESR. Spine and joint replacement literature has shown CRP to be useful in the diagnosis and treatment of infection.
CRP levels increase within 6 hours of the onset of an infection or inflammatory process. The CRP doubles every 8 hours and peaks at 3 to 5 days. As the infection or inflammatory process resolves, CRP drops precipitously, having a half-life of 24 to 48 hours. With resolution of an inflammatory process or infection the CRP returns to normal within 10 days.
ESR peaks at 5 to 7 days and remains elevated for more than 3 weeks after resolution. Thelander and Larsson studied the trends of CRP and ESR after routine spinal surgical procedures. These investigators found that CRP returned to baseline levels in 5 to 14 days. Elevation in CRP after this time should raise concerns for spinal infection. With the exception of a positive culture or biopsy result, CRP is the presumably the most informative laboratory test in the diagnosis and treatment of cervical infection. Results of blood cultures are positive in 24% to 59% of cases.
Imaging Studies
Multiple imaging modalities exist, and each has advantages and disadvantages in the evaluation of spondylodiskitis. Plain radiographs are inexpensive and easily obtained in the clinical setting; however, they cannot detect infection before it has caused significant damage to the intervertebral disk and vertebral end plate. Plain radiographs are the ideal studies for assessment of cervical alignment, and they aid in the detection of cervical deformity.
Computed tomography (CT) is an excellent modality to visualize the bony integrity of the spine. The true extent of bone destruction caused by spondylodiskitis can be evaluated with a CT scan, and an operative plan can be made accordingly ( Fig. 25-1, A and B ). Paravertebral abscesses can also be visualized with CT imaging ( Fig. 25-1, C and D ). Not uncommonly, patients have medical conditions such as cardiac stents, cerebral aneurysm clips, or automated internal cardiac defibrillators (AICD) that preclude them from obtaining a magnetic resonance imaging (MRI) scan. In these patients, CT scan following myelography can be helpful in the evaluation of the spinal canal and areas of neural compression. However, myelography may be contraindicated in cases of suspected epidural abscess, and puncture should not be performed in the area of a suspected abscess.
Early detection of spondylodiskitis is possible with radionuclide studies. They also provide imaging of the entire body with localization of multiple foci of infection, which occur in 4% of cases. MRI is the modality of choice for evaluation of spondylodiskitis. The accuracy, sensitivity, and specificity of MRI are superior to those of any other imaging method. MRI provides detailed anatomic information about the disk, vertebral body, and surrounding soft tissues ( Fig. 25-2 ). Eismont noted some degree of neurologic deficit in 80% of patients with cervical osteomyelitis, and MRI can also help identify the site and extent of compression. A comparison of imaging characteristics is provided in Table 25-2 .
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