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The initial cardiovascular response after spinal cord injury may include hypertension, widened pulse pressure, and tachycardia. 1 This acute response has been shown experimentally to last from 2 to 3 min.9 In animal experiments, the hypotension that is characteristic of neurogenic shock generally begins within 5 min of the acute spinal cord injury.9

Patients with neurogenic shock are hypotensive and usually have warm, dry skin.10 Bradycardia is characteristic but not universal. The patient may lose the ability to redirect blood from the periphery to the core because of the loss of sympathetic tone.10 This can result in excessive loss of heat from the skin, with subsequent hypothermia.10

These symptoms of neurogenic shock can be expected to last from 1 to 3 weeks.10 In some cases, significant rehabilitation using elastic stockings, an abdominal binder, and a tilt table may be required to prevent an orthostatic drop in blood pressure when the patient is placed upright. 11

The anatomic level of the spinal cord injury influences the likelihood and severity of neurogenic shock. Any injury above T1 should be capable of disrupting the spinal tracts that control the entire sympathetic system. Any injury from T1 to L3 has the potential to partially disrupt the sympathetic outflow; intuitively, the higher the injury in this zone, the more likely or more severe the resulting neurogenic shock.1 In one of the few studies to quantify this relationship, Zipnick and colleagues described this relationship in five patients with true neurogenic shock resulting from penetrating injuries: two in the cervical region, one in the lumbar region, and one each in the upper and lower thoracic regions.1

The question of an incomplete versus a complete spinal cord lesion causing neurogenic shock has also been considered. In a large study of 408 patients with cervical cord/column injuries, Soderstrom and Ducker reported a near equal incidence of neurogenic shock in patients with incomplete versus complete lesions. 12 The explanation for this is not entirely clear. Guha and Tator, working with an acute spinal cord injury model in rats, have suggested that the decline in cardiac output following acute cord injury is not due to decreased sympathetic tone alone but may also be caused by direct myocardial injury, similar to that seen after head injury or subarachnoid hemorrhage.9

An interesting difference has been found with regard to incidence of neurogenic shock between patients with blunt versus penetrating spinal cord injuries. 1 In a study of patients with blunt cervical spine/cord injury, neurogenic shock alone was believed to be responsible in 69 percent of all patients in shock. 5 In Zipnick's study of patients with penetrating spinal injury at various anatomic levels, neurogenic shock was thought to be responsible in only 22 percent of patients in shock. 1 The reason for the difference is unclear but probably related to the fact that the two groups were not equivalent: blunt trauma patients had only cervical injuries, while the penetrating injury patients had injuries at all levels of the spinal cord. Also, part of the difference may stem from the fact that patients with penetrating trauma are more likely to have associated injuries.

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