Neurogenic shock is a haemodynamic phenomenon that can occur with lesions above T6 and is characterised by hypotension, bradycardia and vasodilation. This is caused by loss of sympathetic outflow below the level of the SCI and can last up to 6 weeks post-injury. Patients may display a fluid resistant hypotension frequently requiring vasopressor support, and are at risk of vagally induced bradyarrhythmia (including asystole) if the lesion is above the cardiac sympathetic outflow (T2-5). As a result, cervical spine injuries may necessitate the initiation of invasive monitoring and blood pressure support.
Spinal shock is a primarily neurological phenomenon resulting in immediate temporary loss of total power, reflexes and sensation (flaccid areflexia) below the level of the injury. It may last hours to weeks and can improve once the secondary injury such as swelling resolves. Hypotension and bradycardia due to suppression of spinal cord reflexes below the level of the acute injury can be present in the initial phase of spinal shock. Days to months after the initial injury, flaccidity develops into spasticity with hyperreflexia. Autonomic dysreflexia can then occur where stimulation below the level of the injury can cause hypertension, sweating, loss of bowel and bladder control, headaches and other sympathetic effects.
