It is impossible to separate the initial evaluation and management of the patient with neurogenic shock from that of the general trauma patient. In essence, the diagnosis of neurogenic shock should be one of exclusion. Certain clues—such as bradycardia and warm, dry skin—may be evident, but hypotension in the trauma patient can never be presumed to be due to neurogenic shock until all other possible sources of hypotension have been eliminated. 1 Again, a difference has been noted between blunt and penetrating spinal injuries, but a large percentage of these patients will have significant concomitant injuries, causing blood loss, which will explain their hypotension.15 It is only after these other injuries have been excluded that neurogenic shock can be said to be present.
Once the ABCDEs have been attended to and all other possible sources of hypotension have been investigated and treated, the treatment will focus on the hypotension and bradycardia of neurogenic shock.
Hypotension is treated by rapid infusion of crystalloid; this is usually effective in treating neurogenic shock. 14 During neurogenic shock, blood pools in the distal circulation because of the loss of sympathetic innervation. Infusion of intravenous crystalloid will correct this relative hypovolemia. Adequate fluid resuscitation should be undertaken with the aim of keeping the mean arterial blood pressure above 70 mmHg.14 This level of blood pressure is a bit arbitrary and has been arrived at by clinical experience. It is thought that this level of pressure provides adequate perfusion and minimizes the effects of secondary cord injury.
The use of fluids in neurogenic shock must, however, be judicious. There is a danger of excessive fluid replacement, with resultant heart failure and pulmonary edema.15 The placement of a pulmonary artery catheter and its resultant pressure measurements can be of tremendous benefit and help prevent excess fluid administration.16 If intravenous fluids are not adequate to maintain organ perfusion, the use of positive inotropic pressor agents such as dopamine or dobutamine may be beneficial.10 These agents will improve cardiac output and raise perfusion pressure.10 The doses required are variable and should be titrated to the patient's hemodynamic response.
Bradycardia, when present, usually occurs within the first few hours or days of spinal cord injury 9 because of a predominance of vagal tone to the heart. In severe cases and when the patient's hemodynamics warrant, atropine can be used for treatment. In some patients who may present with heart block or asystole, a pacemaker may be required.9
One topic that deserves discussion is the physiologic significance of the hypotension associated with neurogenic shock. For most patients treated in the ED, an adequate blood pressure is important to ensure perfusion and normal functioning of end organs. This can be especially important in the patient with a spinal cord injury, in whom optimal perfusion and oxygenation of the spinal cord may maximize nervous system recovery.15 On the other hand, the authors' clinical experience has shown that moderate hypotension may be tolerated by some of these patients without any evident sequelae. In these patients, more harm than good may be done by trying to normalize the blood pressure, as evidenced by the pulmonary edema that can result from overvigorous fluid resuscitation. Perhaps, in these patients, careful monitoring and the tincture of time, allowing the sympathetic nervous system to recover its function, might be the best course of action. This group of patients might more accurately be labeled as having "neurogenic hypotension" rather than "neurogenic shock." This is because these patients, though hypotensive, have no problems with peripheral perfusion. They maintain clear mentation and adequate urine output, and do not develop the typical laboratory abnormalities of patients that are in shock.
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