Cervical spine MRI of a patient with SCI: C4 fracture and dislocation, spinal cord compression
|Classification and external resources|
Neurogenic shock is a distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate, that is attributed to the disruption of the autonomic pathways within the spinal cord. It can occur after damage to the central nervous system such as spinal cord injury. Low blood pressure occurs due to decreased systemic vascular resistance resulting in pooling of blood within the extremities lacking sympathetic tone. The slowed heart rate results from unopposed vagal activity and has been found to be exacerbated by hypoxia and endobronchial suction. Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death if not promptly recognized and treated. It is not to be confused with spinal shock, which is not circulatory in nature.
Neurogenic shock can result from severe central nervous system damage (brain injury, cervical or high thoracic spinal cord). In more simple terms: the trauma causes a sudden loss of background sympathetic stimulation to the blood vessels. This causes them to relax (vasodilation) resulting in a sudden decrease in blood pressure (secondary to a decrease in peripheral vascular resistance).
Neurogenic shock results from damage to the spinal cord above the level of the 6th thoracic vertebra. It is found in about half of people who suffer spinal cord injury within the first 24 hours, and the usually does not go away for one to three weeks.
Signs and symptoms
Because it causes a loss of sympathetic tone, which plays a major role in other forms of shock, neurogenic shock causes a unique and atypical presentation.
Typically, in other forms of shock, the sympathetic nervous system triggers various compensatory mechanisms by releasing epinephrine and norepinephrine, its major chemical mediators. These neurotransmitters trigger an increased heart rate, faster breathing, and sweating. They also trigger vasoconstriction, to shunt blood away from the extremities and to the vital organs. This causes increased blood pressure and pale, cool skin. In end-stage shock, the patient generally exhibits very low blood pressure; a weak, fast pulse; and rapid, shallow breathing.
In neurogenic shock, the body loses its ability to activate the sympathetic nervous system and cannot trigger these compensatory mechanisms. Only parasympathetic tone remains. Consequently, neurogenic shock's unique presentation includes:
- Instantaneous hypotension due to sudden, massive vasodilation
- Warm, flushed skin due to vasodilation and inability to vasoconstrict
- Priapism, also due to vasodilation
- The patient will be unable to get tachycardic, and may become bradycardic
- If the injury is below the 5th cervical vertebra, the patient will exhibit diaphragmatic breathing due to loss of nervous control of the intercostal muscles (which are required for abdominal breathing).
- If the injury is above the 3rd cervical vertebra, the patient will go into respiratory arrest immediately following the injury, due to loss of nervous control of the diaphragm.
- Dopamine (Intropin) is often used either alone or in combination with other inotropic agents.
- Vasopressin (antidiuretic hormone [ADH])
- Certain vasopressors (ephedrine, norepinephrine). Phenylephrine may be used as a first line treatment, or secondarily in people who do not respond adequately to dopamine.
- Atropine is administered for slowed heart rate.
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