The relative contribution of edema and hemorrhage to raised intrathecal pressure following traumatic spinal cord injury

Abstract

Raised intrathecal pressure (ITP) following traumatic spinal cord injury (SCI) is a critically important aspect of injury development that may result in significantly greater tissue damage and worsened functional outcome. Raised ITP is caused by the accumulation of blood and/or water (edema), and while their occurrence following traumatic SCI has been well established, the relative contribution of both processes to the development of ITP following SCI has not yet been determined. Accordingly, the current study investigates the temporal profile of raised ITP following traumatic SCI in relation to both haemorrhage and edema development. A closed balloon compression injury was induced at T10 in New Zealand White rabbits. Animals were thereafter assessed for spinal water content (edema), intrathecal pressure (ITP), lesion and hemorrhage volume, and albumin immunoreactivity from 5 hours to 1 week post-SCI. Early increases in ITP at 5 hours post-injury were associated with significant increases in blood volume. However, ITP was maximal at 3 days post-SCI, at which time there was an associated significant increase in edema that persisted for 1 week. We conclude that raised ITP following traumatic SCI is initially driven by volumetric increases in hemorrahge, whilst edema becomes the primary driver of ITP at 3 days post-injury.