**6. Rehabilitation and recovery**

Rehabilitation in patients with spinal cord injuries should be comprehensive, interdisciplinary, and patient-centered, with goals that are individualized and realistic. Interventions should not be delayed and complications need to be anticipated and promptly identified.

Neurogenic shock can persist for 1–6 weeks after the initial injury, certainly long enough to interfere with rehab in some cases [8, 22]. In additional to that, patients with spinal cord injuries are vulnerable to a number of cardiovascular complications which should be anticipated in the course of rehabilitation, and some with prolonged or severe bradycardia may require permanent pacemakers [16]. Cardiovascular complications are the leading causes of morbidity and mortality in patients in both the acute and chronic stages of spinal cord injury [17]. Common complications include autonomic dysreflexia, orthostatic hypotension, reduced cardiovascular reflexes and absence of cardiac pain during ischemia [18].

Independent of neurogenic shock, autonomic dysreflexia (AD) is a potentially fatal complication that occurs in 48–90% of patients with injuries above T6 [17]. It is caused by the loss of supraspinal sympathetic modulation and is characterized by sudden episodes of hypertension, headache, and tachycardia with prevailing reflex bradycardia [23, 24]. Additional sympathetic features include piloerection and cool extremities

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

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

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 fludrocortisone [23, 27].

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 may have atypical presentations of cardiac ischemia including referred pain.

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 achieving optimal functional recovery.

#### **7. Conclusion**

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

**105**

*Neurogenic Shock*

patient outcomes.

**Author details**

Bethlehem, PA, USA

Network, Bethlehem, PA, USA

provided the original work is properly cited.

Anna Volski1

**Conflict of interest**

*DOI: http://dx.doi.org/10.5772/intechopen.89915*

The authors report no conflict of interest.

and Daniel J. Ackerman2

\*

2 Department of Neurology, St. Luke's University Health Network,

\*Address all correspondence to: daniel.ackerman@sluhn.org

1 Lewis Katz School of Medicine at Temple University, St. Luke's University Health

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

dangerous for the patient, and may lead to cerebral anoxia, cardiac arrest, and more. Although there is no single accepted blood pressure and heart rate cutoff to define neurogenic shock, the signs are reasonably well established and definitive treatment is in line with current critical care management standards. Beyond the short term, neurogenic shock as well as autonomic dysreflexia, which may commonly accompany spinal injuries at the same level, can complicate the rehabilitation process. Hopefully future prospective studies will adopt standard ways of isolating and confirming neurogenic shock and establish treatment paradigms that improve
