Neurogenic shock occurs after an injury to the spinal cord. Sympathetic outflow is disrupted resulting in unopposed vagal tone. The major clinical signs are hypotension and bradycardia. Acute spinal cord injury is most commonly seen with blunt trauma accounting for approximately 85 to 90 percent of cases. The most commonly affected area is the cervical region, followed by the thoracolumbar junction, the thoracic region, and the lumbar region. Neurogenic shock must be differentiated from “spinal” shock. Spinal shock is defined as temporary loss of spinal reflex activity occurring below a total or near-total spinal cord injury.
Patients are generally hypotensive with warm, dry skin. The loss of sympathetic tone may impair the ability to redirect blood flow from the periphery to the core circulation leading to excessive heat loss and hypothermia. Bradycardia is a characteristic finding of neurogenic shock; however, it is not universally present. These symptoms can be expected to last from one to three weeks.
The anatomic level of the injury to the spinal cord impacts the likelihood and severity of neurogenic shock. Injuries above the T1 level have the capability of disrupting the spinal cord tracts that control the entire sympathetic system. Injuries occurring in the levels from T1 to L3 may only partially interrupt the sympathetic outflow. The higher the level of injury the more likely it is for the patient to exhibit severe symptoms.
Neurogenic shock may be present with both complete and incomplete spinal cord lesions. The initial presentation represents the acute traumatic injury to the cord. However, a secondary cord injury may evolve over the first few days to weeks following the initial injury. The secondary cord injury is thought to be a result of ischemia to the spinal cord and may lead to a higher level of dysfunction than originally present or to an incomplete injury becoming a complete lesion.
DIAGNOSIS AND DIFFERENTIAL
The diagnosis of neurogenic shock should be one of exclusion. Neurogenic shock must be differentiated from other types of shock, particularly hypovolemic. When dealing with a trauma patient, one must always assume that any hypotension is a result of ongoing blood loss. A patient suffering from neurogenic shock may also have concomitant injuries which may contribute to hemodynamic instability. Clinical clues such as hypotension, bradycardia, neurologic dysfunction, and warm, dry skin may lead the clinician to suspect neurogenic shock; however, only after other injuries have been identified and treated can the diagnosis of neurogenic shock safely be made.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
The initial evaluation and care of the patient with potential neurogenic shock is the same as for all trauma patients, that is, rapid identification and stabilization of life-threatening injuries.
- Airway control should be insured with spinal immobilization and protection.
- Crystalloid IV fluids should be infused to maintain a mean arterial blood pressure above 70 torr. To prevent excessive fluid administration, a pulmonary artery catheter may be placed to monitor hemodynamic response. If fluid resuscitation is inadequate to insure organ perfusion, inotropic agents such as dopamine 2.5 to 20.0 µg/kg per min and dobutamine 2.0 to 20.0 µg/kg per min may be added to improve cardiac output and perfusion pressure. The doses should be titrated to the appropriate clinical response.
- If necessary, severe bradycardia may need to be treated with atropine 0.5 to 1.0 mg IV (every 5 min for a total dose of 3.0 mg) or with a pacemaker.
- In the presence of neurologic deficits, high-dose methylprednisolone therapy should be instituted within 8 h of injury. A 30 mg/kg bolus should be administered over 15 min followed by a continuous infusion of 5.4 mg/kg per h for the next 23 h.
- Trauma surgery, neurosurgery, and orthopedic consultation should be obtained and arrangement made for transfer if necessary.