Pathophysiology of Spinal Cord Injury

One of the most important factors associated with an SCI is the production of vasogenic edema and extravasated blood that occurs rapidly at the site of the injury. A traumatized SC decreases the amount of localized edema that accumulates at the site of the injured SC by the dynamic movement of the fluid up and down the SC.¹ This compensatory action within the SC, however, usually is inadequate to decrease the high interstitial pressure that is caused by fluid accumulation at the site of the SCI. The swelling of the SC caused by this fluid accumulation continues within the confines of the nonyielding dura mater and the rigid spinal canal. When the interstitial pressure within the SC becomes excessive due to swelling, venous compression results. This action results in an elevated upstream venous pressure, which further enhances the capillary extrusion of blood from the porous blood vessels at the injury site. This situation causes an increase in focal osmotic pressure, which leads to a further increase in fluid accumulation. The high interstitial pressure within the SC also compresses small capillaries in the region of the SCI, which can lead to the progressive loss of capillary perfusion. This eventually can lead to complete blockage of vascular flow, causing the destruction of viable neural tissue in the area of the SC impaction.

Over the years, surgeons dealing with SCIs have appreciated the dangers of a high interstitial pressure occurring in an injured SC. This concern prompted the development of two surgical procedures—laminectomy and myelotomy—to lower the high interstitial pressure at the site of an SCI. Because the results of these attempts were unpredictable, however, they were not often used. A probable cause of these surgical failures was the inability of either operation to absorb the edema and blood accumulation that routinely develop at the site of an SCI.

The inability of edema fluid and blood to be absorbed at the site of an SCI is due to the absence of a lymphatic system in the SC. Without the absorbing mechanisms of a lymphatic system, edema fluid and blood remain at the SCI site, and the fluids eventually result in fibrosis scarring. This scarring is thought to be caused by the fibrinogen that is present in the blood that leaks from injured SC blood vessels. The fibrinogen apparently becomes activated at the SC injury site to make fibrin scar, which causes compression on blood vessels, a decrease in SC blood flow, and the blockage of axons from penetrating through the tissue (Fig. 121-1).

FIGURE 121-1 Spinal cord injury (450 g/cm weight injury) 1 month postoperatively. Note surface and circumferential scarring. Persistence of edema fluid also present.

If healing of an acute SCI is to take place, it would appear that action should be undertaken as early as possible after injury to limit edema and blood accumulation resulting from the SCI. It has been shown that if an intact omentum pedicle is placed directly on an SC shortly after injury, absorption of edema and blood can be accomplished with little, if any, fluid accumulation or scar formation (Fig. 121-2), due to the enormous ability of the omentum to absorb fluids.^2,3 Placing the omentum directly on an injured SC apparently establishes a dynamic equilibrium between the production of blood and edema by the traumatized SC and the absorption of these fluids by the overlying omentum. Such absorption by the omentum not only decreases interstitial pressure in the area of the SCI, but, most importantly, its absorptive capability decreases the amount of blood (fibrinogen) in the injured area, thereby lessening the potential for scar formation at the injury site.

FIGURE 121-2 Omentum placed on injured spinal cord (SC; 450 g/cm weight injury) 3 weeks following injury. Note the complete adherence of the omentum to the SC with no presence of fibrosis or fluid accumulation.

To apply the omentum directly onto an SCI location, a laminectomy is required, followed by opening of the dura mater. These maneuvers alone have a beneficial effect on an SCI, because they allow the injured SC to expand, thereby lowering the high interstitial pressure in the SC, which promotes capillary perfusion to increase in the area of the SC injury. It cannot be overemphasized that in an acute SC it is not sufficient to simply surgically stabilize the vertebral column. It appears to be necessary to open the dura mater and treat the SC directly by applying the omentum onto the injured SC, thus allowing edema absorption. This procedure must be done shortly after injury (within a few days), because a fibrotic process begins within a week of injury.

Spinal Cord Revascularization

As with any type of wound, adequate blood supply to the involved area is essential to optimize healing. Research has shown that when the omentum is laid directly on an injured SC, vascular connections penetrate from the omentum into the SC within hours.⁴ This ability to revascularize the SC by the omentum was clearly proven by injecting India ink into an artery located within an intact omental pedicle that had been placed directly on a normal SC. The injected dye marker was subsequently observed on the surface of the SC, as well as in the deepest positioned capillaries that are located within the SC. It subsequently was observed in laboratory animals that omental blood vessels revascularize the SC rapidly and that a sizeable amount of blood was delivered to an uninjured SC through these omental vessels. The revascularization process was found to be even more rapid when the omentum was placed directly on an injured SC (Fig. 121-3). It is important, however, that the omentum be placed on the SCI as early following the injury as clinically possible.⁵

FIGURE 121-3

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