**Conflict of interest**

*Clinical Management of Shock - The Science and Art of Physiological Restoration*

Other features include flushing, sweating, and nasal congestion [24].

for AD, though the exact definition is not consistent across studies [25].

due to vasoconstriction below the level of injury [23]. In contrast to the sympathetic response below the level of injury, a parasympathetic response may predominate above the level of injury. A compensatory baroreceptor response leads to reflex bradycardia.

Stimuli that may induce an AD response include bladder distension, detrusor sphincter dyssynergia, kidney or bladder stones, or other painful stimuli such as ingrown toenails, pressure ulcers, infections, fecal impaction, musculoskeletal pain, and menstrual cramps [24]. Sequelae of untreated hypertension in the setting of autonomic dysreflexia include stroke, intracranial hemorrhage, seizures, cardiac arrest, hypertensive encephalopathy, and death [25]. An increase of 20–40 mmHg in systolic blood pressure in people with spinal cord injury should raise suspicion

Primary treatment of AD includes sitting patients upright and lowering their legs, as well as removing or loosening tight clothing or accessories [26]. After that it becomes necessary to identify triggering noxious stimuli and address them. A distended bladder should be emptied with a catheter, a rectal exam may identify impaction, skin should be examined for pressure ulcers and more serious causes need to be suspected because they may not be obvious [26]. Medications that can be administered to help stabilize AD include the calcium channel blocker nifedipine, nitrates, and vasodilatory agents such as hydralazine [18, 23], although hypotension needs to be anticipated and patients will require appropriate hemodynamic monitoring. Another cardiovascular consequence of spinal cord injury related both to neurogenic shock and autonomic dysreflexia is orthostatic hypotension (OH). It is defined by the American Autonomic Society as a reduction in systolic or diastolic blood pressure of ≥20/10 mmHg, within 3 min of standing upright [27]. Symptoms occur as a result of reduced cerebral perfusion pressure and include light-headedness, dizziness, syncope, pallor, nausea, fatigue, and sweating. Nevertheless, many patients do not report symptoms despite meeting the definition of OH, and some report symptoms in spite of not fully meeting that definition. Pharmacologic therapy may be used to treat OH but should be done carefully because of the already labile blood pressure in patients with spinal cord injury. The most common treatments are compression stockings, abdominal binders, midodrine, or fludrocorti-

Additional autonomic complications that occur after injury are the reduction of cardiovascular reflexes and the absence of cardiac pain. Cardiovascular reflexes regulate blood pressure, intravascular volume, and temperature [18]. The sensation of pain related to cardiac ischemia may be altered because cardiac pain fibers that travel with sympathetic afferent fibers (visceral sensory fibers) are disrupted in cervical or thoracic injuries above T4 [28]. As a consequence, spinal cord injury patients

Other major components that are critical in spinal cord injury rehabilitation are bowel and bladder training, respiratory care, mobilization, as well as physical and occupational therapy. Not only should rehabilitation address the medical aspects of patient care, but the psychological impacts of spinal cord injury as well. A comprehensive approach treating the whole individual gives patients a better chance at

Neurogenic shock is a feared and difficult to treat complication of disruption of the sympathetic nervous system which most often occurs in the setting of a spinal cord injury. The refractory hypotension and bradycardia may be extremely

may have atypical presentations of cardiac ischemia including referred pain.

**104**

**7. Conclusion**

sone [23, 27].

achieving optimal functional recovery.

The authors report no conflict of interest.
