~**~ Omentum Transposition ~**~

Spinal cord injury (SCI) resulting in permanent paralysis is one of humankind's most devastating injuries. Over the years, wide-ranging experimental effort has focused on improving the treatment for these injuries, but in spite of these efforts, there has been small clinical improvement in this group of patients.

Forceful impact on a spinal cord triggers many biological factors that can subsequently influence neurological function. As the hours and days pass after injury, vasogenic edema accumulates within the spinal cord, which begins to swell from the edema almost immediately after. As the volume of edema increases within the cord, which is encased by the unyielding dura mater, there is an associated rise in spinal cord interstitial tissue pressure, which can lead to complete cessation of capillary perfusion at the site of injury. High-dose steroids are given commonly as an early treatment for this condition, but one has to question whether a significant amount of this material can perfuse into a spinal cord whose vascular supply is compromised severely.

A very high spinal cord tissue pressure that causes an inversely proportional fall in capillary perfusion at the site of the cord injury would be expected to severely restrict administered steroids from entering the major area of spinal cord impaction. Conversely, a minimal or moderately injured spinal cord would be expected to produce less vasogenic edema, thus allowing a still-maintained capillary perfusion pressure to allow the circulating steroids to enter the area of spinal cord injury. The opportunity for steroid perfusion would, therefore, be greater in minor spinal cord injury, but markedly decreased in the presence of a severe cord injury.

The disappearance of spinal shock after spinal cord trauma is awaited to see of there is some return of neurologic improvement. In the overwhelming majority of patients who experience complete motor and sensory loss immediately after SCI , there is no return of neurologic function. Many patients in the United States with SCI are commonly treated by some form of vertebral column stabilization and, when necessary, decompression of the spinal canal and removal of matter the might be impinging on the spinal cord. If surgery is performed nothing is done specifically to decrease the vasogenic edema that is already present and will continue to develop within the spinal cord. This may well be a golden period in which to achieve subsequent functional improvement.

Significant vasogenic edema within the human spinal cord can be observed weeks after trauma in association with loculation of edema fluid in the area surrounding the cord (personal observation.) The vasogenic edema that develops after SCI is a plasma transudate in which fibrinogen, a normal component of blood, is activated at the injury site to form fibrin in and around the injury site. Traumatized, but still viable, spinal cord tissue has the potential to heal, but may be prevented from doing so by subsequent scar development caused by the fibrotic reaction initiated by the fibrinogen in the edema fluid. The progressive scar formation that develops in the area of cord injury results in progressive ischemia to damaged nerve tissue that needs increased blood flow and oxygenation for healing purposes. Basically, it is the vasogenic edema caused by the SCI, which becomes a, if not the, major problem after injury because of its initial compressing effect on spinal cord capillaries shortly after injury and its later potential for the edema fluid to form constricting scar tissue within and surrounding the spinal cord.

The enormous absorptive capacity of the omentum is generally unappreciated. This fact can be easily demonstrated by simply placing an intact piece of the omentum in a beaker filled with dye (Indian ink) and saline. The dye will be absorbed within minutes by the omentum. Additional evidence is shown by a study that reported that one-third of the entire cerebrospinal fluid reservoir can be absorbed by the intact omentum. This absorptive capability explains why placing the omentum on an acutely injured spinal card can markedly decrease edema formation. Such absorption subsequently limits the post-injury fibrotic reaction the arises for the vasogenic edema, which is the substrate for scar formation. Even though the mechanism of omental absorption of edema fluid presently remains unknown, the omentum probably decreases scar formation around an injured spinal cord by absorbing fluid with its associated fibrinogen component by way of a dynamic equilibrium that develops between production of fluid within the injured cord and its absorption by the omentum.

Operative treatment for spinal cord injuries frequently involves a vertebral body fusion and, when indicated, laminectomy without opening the dura mater. A traumatized spinal cord that is expanding laterally because of edema and is encased in a nonexpansile dura mater covering cannot be expected to have its high spinal cord tissue pressure lowered simply by performing a decompressive laminectomy. To preserve a critical level of spinal cord capillary perfusion pressure at the site of injury, it seems reasonable to believe that the dura mater should be opened as early after a severe SCI as is reasonable. This can be accomplished by opening the dura through two separate incisions made in the same line well above and below the mail area of spinal cord impaction. The two longitudinal dural incisions are slowly made toward each other over a period of 5-10 minutes until they finally connect directly over the major spinal cord injury site. By opening the dura in this manner, there is longitudinal dissipation of edema fluid up and down the spinal cord which limit the opportunity for edematous spinal cord tissue to extrude when the dura directly overlying the cord impaction site is opened.

Many SCI specialists are unaware that placing an intact pedicled omental flap directly on an injured spinal cord improves neuroelectrical and functional activity in the experimental animal. Performing a decompressive laminectiomy and opening up the dura mater may prove important in treating an acute SCI, but based on experimental observations, additional surgical measures may be necessary if improved functional results are to be achieved. Specifically, a decrease of vasogenic edema after cord injury seems critical. A recent publication from Japan showed that a standard injury to a cat's spinal cord caused hemorrhagic necrosis and scattered small and large vacuoles within the injured cord I association with cessation of nueroelectrical activity as measured by somatosensory-evoked potentials (SEP). In contrast, experimental animals whose omentum was placed on their spinal cord shortly after a standard injury showed the morphology of their injured cord to be significantly spared in association with the post-surgery return of somatosensory-evoked potentials. These results led the investigators to conclude that "omental transposition helps to accelerate the healing process after crush injury to the spinal cord." Based on this and other laboratory findings, it would now seem appropriate to evaluate the effect of early application of the omentum on severely injured human spinal cords performed in a controlled clinical study.

Extensive basic research has continued over many years involving axonal regeneration within the spinal cord for the purpose of understanding and eventually manipulating the reconnection of neural circuitry. But such laboratory research has no significance for the patient who sustains a spinal cord injury, today; a child who is injured in a swimming pool, the equestrian who falls from his horse, or the hockey player who crashes into the boards and breaks his neck. Why shouldn't surgeons in the operating room, today, be evaluating reasonable forms of surgical treatment that have been studied carefully in the laboratory in the hope that new research techniques might be successfully transferred to the operating table? Improvement in the disheartening functional results that are routinely expected after a serious SCI might result.

Laboratory research is carried out in the hope that encouraging results might become the basis for subsequent human testing that could lead to improved clinical achievements. If clinicians fail to evaluate promising results of bench research the might have a beneficial effect on a spinal cord injury ,much may be being lost. Theroretical considerations and laboratory data have indicated that the pedicled omentum can improve electrical and functional results after SCI and that the best time to apply the omentum is as early after the injury as practical. Omental transposition for chronic SCI is already being done in an increasing number of patients, but this is a problem that deals with scar formation not edema. As far as omental placement an acute SCI is concerned, a patient with multiple trauma would not be a candidate for this, But a healthy patient with an isolated spinal cord injury might be suitable for evaluating the combined effects of decompressive laminectomy, dura mater opening, vertebral column stabilization, and omental transposition to the spinal cord. Treating a severe spinal cord injury as an acute surgical emergency seems deserving of a clinical trial in view of information that is presently available. A controlled study performed by motivated people with the necessary surgical experience and skills seems reasonable at this time.

Harry S. Goldsmith
Glenbrook, Nevada