Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms

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✓ In patients with spinal cord injury, the primary or mechanical trauma seldom causes total transection, even though the functional loss may be complete. In addition, biochemical and pathological changes in the cord may worsen after injury. To explain these phenomena, the concept of the secondary injury has evolved for which numerous pathophysiological mechanisms have been postulated. This paper reviews the concept of secondary injury with special emphasis on vascular mechanisms. Evidence is presented to support the theory of secondary injury and the hypothesis that a key mechanism is posttraumatic ischemia with resultant infarction of the spinal cord. Evidence for the role of vascular mechanisms has been obtained from a variety of models of acute spinal cord injury in several species. Many different angiographic methods have been used for assessing microcirculation of the cord and for measuring spinal cord blood flow after trauma. With these techniques, the major systemic and local vascular effects of acute spinal cord injury have been identified and implicated in the etiology of secondary injury.

The systemic effects of acute spinal cord injury include hypotension and reduced cardiac output. The local effects include loss of autoregulation in the injured segment of the spinal cord and a marked reduction of the microcirculation in both gray and white matter, especially in hemorrhagic regions and in adjacent zones. The microcirculatory loss extends for a considerable distance proximal and distal to the site of injury. Many studies have shown a dose-dependent reduction of spinal cord blood flow varying with the severity of injury, and a reduction of spinal cord blood flow which worsens with time after injury. The functional deficits due to acute spinal cord injury have been measured electrophysiologically with techniques such as motor and somatosensory evoked potentials and have been found proportional to the degree of posttraumatic ischemia. The histological effects include early hemorrhagic necrosis leading to major infarction at the injury site.

These posttraumatic vascular effects can be treated. Systemic normotension can be restored with volume expansion or vasopressors, and spinal cord blood flow can be improved with dopamine, steroids, nimodipine, or volume expansion. The combination of nimodipine and volume expansion improves posttraumatic spinal cord blood flow and spinal cord function measured by evoked potentials. These results provide strong evidence that posttraumatic ischemia is an important secondary mechanism of injury, and that it can be counteracted.

Article Information

Address reprint requests to: Charles H. Tator, M.D., Toronto Western Division, Toronto Hospital, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada.

© AANS, except where prohibited by US copyright law.

Headings

Figures

  • View in gallery

    Colloidal carbon angiogram 1 hour after severe clip compression injury of the spinal cord at the T-1 vertebral level in the rat. There is considerable hemorrhage in the gray matter and adjacent white matter. Much of the microcirculation in both the gray and white matter has not filled, although the anterior spinal artery and the anterior sulcal artery have filled.

  • View in gallery

    Left: Colloidal carbon angiogram of a cross-section of the normal rat cord at the T-1 level. Note the extensive microcirculation, especially in the gray matter. Right: Colloidal carbon angiogram 2 hours after a moderately severe clip compression injury at T-1 in the rat. There is extensive hemorrhage in the gray matter. Large areas of white and gray matter show loss of the microcirculation.

  • View in gallery

    Left: Colloidal carbon angiogram of a longitudinal section of the normal rat cord at the C7—T2 level. Note extensive microcirculation, especially in the gray matter. Right: Colloidal carbon angiogram 2 hours after a moderately severe clip compression injury at the T-1 level in the rat. There are scattered hemorrhages centrally with large ischemic zones in both the white and gray matter.

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