Diskitis

An infection does not ordinarily originate in the vertebra or disk space; rather, it typically spreads there from other sites via the bloodstream. Spinal arteries form two lateral anastomotic chains and one median anastomotic chain along the posterior surface of the vertebral bodies. The spinal arteries are the origins of the periosteal arteries, which in turn give rise to metaphyseal arteries.

In children, anastomoses between metaphyseal arteries are made by the intermetaphyseal arteries; however, in adults, the intermetaphyseal arteries degenerate, causing direct diffusion from the adjacent endplate to be the only source of nutrients for the disk. Septic emboli travelling through this arterial system enter the metaphyseal arteries, which have become end arteries in the adult, causing a large area of infarction. Infarction of the vertebral endplates is followed by localized infection that subsequently spreads through the vertebral body and into the poorly vascularized disk space. Infection can then spread to the epidural space or paraspinal soft tissues.

The other anastomotic vascular system of the spine is the venous system. The venous system of the spine, like the arterial system, forms an anastomotic plexus (Batson plexus) in the epidural space. This plexus drains each segmental level and is continuous with the pelvic veins. Retrograde flow through this plexus during periods of high intra-abdominal pressure has been postulated to allow the spread of infection from the pelvic organs.

Support for this hypothesis comes from the observation that pelvic disease is one of the most common primary sites of infection in patients with diskitis. Other authors take issue with this hypothesis, citing animal studies that show retrograde flow through the epidural venous plexus only at extremely high intra-abdominal pressures that are not physiologic.

Diskitis is thought to spread to the involved intervertebral disk via hematogenous spread of a systemic infection (eg, urinary tract infection [UTI]). Many sites of origin have been implicated, but UTI, pneumonia, and soft-tissue infection seem to be the most common. Direct trauma has not been conclusively shown to be related to diskitis. Intravenous (IV) drug use with contaminated syringes offers direct access to the bloodstream for a variety of organisms. Often, no other site of infection is discovered.

Staphylococcus aureus is the organism most commonly found; however, Escherichia coli and Proteus species are more common in patients with UTIs. Pseudomonas aeruginosa and Klebsiella species are other gram-negative organisms observed in IV drug abusers, although they are not seen as commonly as S aureus. Not surprisingly, medical conditions that predispose patients to infections elsewhere in the body are associated with diskitis. Diabetes, AIDS, steroid use, cancer, and chronic renal insufficiency are common comorbidities. ^[1]

Although rare, infection of the disk space can also occur following surgical intervention at the site. The infection rate after anterior cervical diskectomy has been quoted at 0.5% of cases; the infection rate for lumbar diskectomy is half that. In such cases, infection is transmitted through direct inoculation of the operative site. As in spontaneous diskitis, the most common organism is S aureus, but Staphylococcus epidermidis and Streptococcus species also should be considered.

Childhood diskitis has not been consistently associated with an initial causative infection elsewhere in the body. S aureus is the most common organism found.

In the United States, the incidence of diskitis ranges from 1 in 100,000 population to 1 in 250,000 population. In other developed nations, the incidence of diskitis is similar; however, in less developed nations, infectious diskitis is much more common. In some areas of Africa, it has been reported that 11% of all patients seen for back pain were diagnosed with diskitis.

A bimodal distribution of ages occurs with diskitis. Childhood diskitis affects patients with a mean age of 7 years. The incidence of diskitis then decreases until middle age, when a second peak in incidence is observed at approximately 50 years of age. Some authors argue that childhood diskitis is a separate disease entity and should be considered independently.

The predominance of diskitis in males is more pronounced in adults, with male-to-female ratios ranging from 2:1 to as high as 5:1. Childhood diskitis has a slight male prevalence, with a male-to-female ratio of 1.4:1.

No specific racial predilection has been noted.

Most patients are cured by a treatment protocol of antibiotics, either alone or in combination with surgery. Only 15% of patients experience permanent neurologic deficits. Recrudescence of infection occurs in 2-8% of patients.

Mortality associated with diskitis occurs from the spread of infection, either through the nervous system or through other organs. Mortality has been reported to be 2-12%.

Karadimas et al retrospectively analyzed the outcomes of a large series of patients treated for spondylodiskitis. Patients were divided into three groups: 70 who received nonoperative treatment (group A), 56 who underwent posterior decompression alone (group B), and 37 who underwent decompression and stabilization (group C). ^[6] At 12-month follow-up, treatment had failed in eight of the group A patients. Reoperation was necessary in 24 of the group B patients and in six of the group C patients. None of the group A patients had neurologic symptoms; 11 of the group B patients had neurologic deficits, five of whom benefited from surgery; and 11 of the group C patients had altered neurologic deficits.

The significance of antibiotic regimen compliance is the single most important factor in patient education. Incomplete treatment can lead to resistance with devastating results.

The importance of orthotic brace compliance must also be stressed.

Educate patients on early neurologic signs, and instruct patients to return for medical attention on detection of the slightest deficit.