30 Infections of the Cervical Spine
KEY POINTS
Basic Science
There are several potential routes for the dissemination of infections to the cervical spine, including direct extension from contiguous structures, open spinal trauma or surgery, hematogenous, or lymphatic. Both venous and arterial mechanisms have been implicated in hematogenous spread. The Batson venous plexus was proposed as a valveless conduit through which infections of the pelvis, such as urinary tract infections, may spread to the spine. This venous mechanism has been largely refuted, and an alternative arterial route postulated.1 In the case of vertebral pyogenic osteomyelitis, infection is thought to seed the metaphyseal (subchondral) bone near to the anterior longitudinal ligament via a rich arterial network. The posterior spinal arteries that branch off the dorsal artery entering the intervertebral foramen are probably responsible for cervical epidural abscesses. Infections of the retropharyngeal space can enter the lymphatics and spread along the spinal nerves to communicate with the spinal subarachnoid space and Virchow-Robin space, thus leading to cervical subdural empyemas or cervical intramedullary abscesses.
Interestingly, discitis is seen in two distinct patient populations: pediatric and adult. While discitis in the pediatric population is usually caused by a hematogenous source, adult discitis occurs in patients who have undergone prior surgery involving the disc space. The reason for this clear distinction is that, as the spine ages, there are changes that take place in its vascularity. Histologic studies have shown that an end-arteriolar supply of the disc is present during infancy and childhood, and these end arteries are obliterated by the third decade of life.2
Clinical Practice Guidelines
Clinical Presentation
The most common chief complaint for all cervical spine infections is vague, nonspecific neck pain of a progressive nature. With pyogenic osteomyelitis and discitis, this pain is exacerbated by neck motion, and eventually becomes extremely debilitating. Radicular pain is frequently present in epidural abscesses, and results from either direct nerve root compression or inflammation.3 If a cervical epidural abscess spreads to the retropharyngeal space, then dysphagia or even airway compromise may result.
The time course to presentation for cervical spine infections varies from acute (less than 1 week), to subacute (1 to 6 weeks), to chronic (more than 6 weeks). In the case of pediatric discitis, this pain is usually so severe at an early stage that a diagnosis is made before the infection spreads to the adjacent vertebral bodies.4 For pyogenic vertebral osteomyelitis, the presentation tends to be subacute to chronic in 90% of cases, partly because of its more insidious onset. A definitive diagnosis of pyogenic vertebral osteomyelitis is made, on average, 8 weeks to 3 months after disease onset.5 Patients who present acutely (less than 1 week) are more likely to be febrile, and to have other constitutional signs and symptoms.
Infections that result in the formation of a mass-occupying abscess have a greater chance of presenting with neurological deficit. This may be seen in vertebral osteomyelitis that extends into the epidural space, or with a primary spinal epidural abscess. Likewise, subdural empyemas and intramedullary abscesses cause neurological deficit at an early stage. In some instances of vertebral osteomyelitis, the bony quality is compromised to the extent that bony collapse may occur, leading to spinal instability and secondary neurological deficit. Sometimes, spinal epidural abscesses and subdural empyemas may cause neurological compromise that is out of proportion with the degree of compression. This is thought to be secondary to vascular compromise from venous compression, thrombosis, or thrombophlebitis.6