INTRODUCTION
Acute injury to the spinal cord in humans, especially at the cervical level, results in severe hypotension and persistent bradycardia that are common components of the phenomenon known as neurogenic shock (1,2). This event is more profound and long lasting in humans after spinal cord injury (SCI) than in experimental animals (3). In addition to neurogenic shock, the acute phase of SCI is also associated with “spinal shock” (4,5). Some authors use these terms interchangeably; however, it is important to recognize that these are 2 clinically important and distinct conditions. Neurogenic shock is characterized by changes occurring in blood pressure control following SCI, whereas spinal shock is characterized by a marked reduction or abolition of sensory, motor, or reflex function of the spinal cord below the level of injury (4).
Low arterial blood pressure (BP) and the presence of neurogenic shock (BP < 90 mmHg) after SCI may result in ischemia of the spinal cord and are potential contributing factors to the cascade of the secondary mechanisms involved in further damage of fragile neuronal tissue (6,7). Hypoperfusion of the spinal cord could result both from low systolic BP (SBP) and from mechanical compression of the spinal cord (8–10). Increases in systemic blood pressure may improve perfusion to the injured, distorted spinal cord (11–13). Several contemporary series of spinal cord injured patients treated with aggressive medical management with maintenance of mean arterial blood pressure in the high normal ranges (85–90 mmHg) have suggested improved neurological outcomes with this management plan (13–15). Presently, there is no consensus as to whether it is better to achieve surgical decompression of the spinal cord early or to postpone the procedure until patients are more stable (16,17).
Many clinical and experimental studies in the area of SCI have been predominantly focused on evaluation of motor and sensory consequences of this devastating injury. The present analysis was performed to examine the association between the timing of surgery and the severity of hemodynamic instability in the acute period following cervical SCI (18). First, we evaluated whether the hemodynamic parameters varied according to the severity of the injury. Second, we examined the change in the hemodynamic parameters over time between the time of the first emergency room assessment to the time of randomization. Finally, we evaluated whether the time from injury to surgical intervention was affected by the presence or absence of neurogenic shock in patients with different severities of cervical SCI.
INTRODUCTION
Acute injury to the spinal cord in humans, especially at the cervical level, results in severe hypotension and persistent bradycardia that are common components of the phenomenon known as neurogenic shock (1,2). This event is more profound and long lasting in humans after spinal cord injury (SCI) than in experimental animals (3). In addition to neurogenic shock, the acute phase of SCI is also associated with “spinal shock” (4,5). Some authors use these terms interchangeably; however, it is important to recognize that these are 2 clinically important and distinct conditions. Neurogenic shock is characterized by changes occurring in blood pressure control following SCI, whereas spinal shock is characterized by a marked reduction or abolition of sensory, motor, or reflex function of the spinal cord below the level of injury (4).
Low arterial blood pressure (BP) and the presence of neurogenic shock (BP < 90 mmHg) after SCI may result in ischemia of the spinal cord and are potential contributing factors to the cascade of the secondary mechanisms involved in further damage of fragile neuronal tissue (6,7). Hypoperfusion of the spinal cord could result both from low systolic BP (SBP) and from mechanical compression of the spinal cord (8–10). Increases in systemic blood pressure may improve perfusion to the injured, distorted spinal cord (11–13). Several contemporary series of spinal cord injured patients treated with aggressive medical management with maintenance of mean arterial blood pressure in the high normal ranges (85–90 mmHg) have suggested improved neurological outcomes with this management plan (13–15). Presently, there is no consensus as to whether it is better to achieve surgical decompression of the spinal cord early or to postpone the procedure until patients are more stable (16,17).
Many clinical and experimental studies in the area of SCI have been predominantly focused on evaluation of motor and sensory consequences of this devastating injury. The present analysis was performed to examine the association between the timing of surgery and the severity of hemodynamic instability in the acute period following cervical SCI (18). First, we evaluated whether the hemodynamic parameters varied according to the severity of the injury. Second, we examined the change in the hemodynamic parameters over time between the time of the first emergency room assessment to the time of randomization. Finally, we evaluated whether the time from injury to surgical intervention was affected by the presence or absence of neurogenic shock in patients with different severities of cervical SCI.
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