What is the pathophysiology of diskitis?

Updated: May 13, 2020
  • Author: Alvin Marcovici, MD; Chief Editor: Jeffrey A Goldstein, MD  more...
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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.

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