**4. Anatomic and epidemiologic considerations**

The autonomic nervous system constitutes the involuntary control of many crucial systems of the body. Described as a system of visceral sensory inputs and motor responses, it maintains homeostasis and responds to both internal and external stimuli by manipulating the balance between its main divisions, the sympathetic and parasympathetic systems [10]. Although much of the autonomic system includes spinal reflex arcs with visceral motor neurons originating in ganglia lying peripheral to the spinal cord, there is overarching control exerted by multiple systems in the brain (**Figure 1**) [5]. It is the loss of this input from above that produces the dysfunction of the system, leading to shock [3]. The ANS maintains control of vital functions in the heart, vasculature, lungs, liver, digestive and para-digestive organs, glands, and reproductive organs. Although there are many involved neuropeptides, norepinephrine is the most common effector molecule in the sympathetic division and exerts it influence on both alpha and beta receptors, as well as the adrenal gland [10].

Estimating the true incidence of neurogenic shock is difficult for multiple reasons. The overall definition is reasonably broad, and a patient may experience multiple subtypes of shock at the same time. Furthermore, there may not be a simple direct imaging correlate that is easily elucidated (for example, one can see a significant anterior or lateral cord injury and correlate the physical symptoms to the level of the lesion, but isolating the level of injury in the intermediolateral

#### **Figure 1.**

*Overview of sympathetic outflow. Panel 1 (top left): CNS control of the sympathetic nervous system originates in multiple brainstem areas and nuclei as well as the hypothalamus, which also receives input from the cortex and amygdala. The combined input creates a sympathetic outflow tract which descends the spinal cord to the intermediolateral gray matter. Panel 2 (bottom left): At multiple levels from T1 through the rostral lumbar spine the preganglionic neurons will exit through the ventral rami and then jump to the sympathetic chain where they may ascend, descend, or synapse at that level before exiting again as part of the spinal nerves. Panel 3 (right): Zoomed out view of the sympathetic chain with multiple Para-vertebral ganglia in which the preganglionic neurons may synapse. The exiting post ganglionic noradrenergic neurons provide direct sympathetic input to the heart, lungs, glands, vascular beds, and adrenal medulla. Note that some sympathetic neurons may exit and not synapse in the sympathetic chain but travel to pre-ganglionic neurons to synapse (such as the celiac and mesenteric ganglia) [10, 11]. Created with Biorender.com.*

gray matter and ruling out other causes of shock is more challenging). Studies of incidence after SCI have been widely variable, ranging from 14 to 44% depending on the criteria used [4]. Extrapolating from a range of papers, criteria have ranged from systolic blood pressures (SBP) <70 mmHg up to <100 mmHg, and heart rates (HR) <50 beats per minute (BPM) up to ≤90 BPM in various combinations [12]. Examples include SBP <90 mmHG or HR <50 BPM as a cutoff, more recently others have used SBP <100 mmHG and HR <80 BPM, and still others simultaneous SBP <90 mmHg and HR <80 BPM with some variability in terms of whether or not lab values accounting for hypovolemia were examined as a confounder [4]. In one cohort of patients with isolated spinal cord injury (the majority of which were related to blunt trauma), defining neurogenic shock as SBP <100 mmHg, HR <80 BPM or both, out of 490 cases the incidence of hypotension was 25.8% and of classic neurogenic shock (hypotension and bradycardia) was only 19.3% [13]. What is suggested but not thoroughly quantified in the literature is that the incidence is highest in cervical spine injury and somewhat less for upper thoracic injury (above T6) while SCI lower than T6 would be considered rarely associated with neurogenic shock [3]. There is also not a single consensus in regard to penetrating vs. blunt trauma as to which is more likely to lead to neurogenic shock. Considering that SCI accounts for only about 5% of major trauma cases, a lack of experience may play a role in limiting identification and definitive management even at centers of reasonably high volume [13].

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**Figure 2.**

*blue arrow). Created with Biorender.com.*

*Neurogenic Shock*

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

**5. Initial evaluation and stabilization**

Case Presentation: 70 y/o male presents by air to a level I trauma center following a bike accident wherein he was thrown down a hill. It is unclear if he was wearing a helmet. He was initially resuscitated by bystanders as he was in cardiac arrest, and then intubated in the field prior to arrival (GCS 3-T). At the time of arrival he is found to have bradycardia with HR 53 BPM and initial BP was 112/74 with mildly low body temp 96.3 F (35.7 C). He became more bradycardia and did not respond to atropine requiring another brief round of cardiopulmonary resuscitation. Although the initial hemoglobin on his arterial blood gas (ABG) was 13.3 g/dl, he was also transfused four units of packed red blood cells (PRBC's). Computed Tomography (CT) of the head and cervical spine showed an occipital condyle fracture as well as a type III (low) dens fracture with 6 mm distraction and a c2 spinous process fracture (**Figure 2**). Pressor support with norepinephrine was initiated and preparations were made for trans-venous pacing in the event of refractory bradycardia. Magnetic resonance imaging (MRI) the following day confirmed a likely distraction injury with cord edema and hemorrhage (**Figure 3**). Interestingly, his hemoglobin by hospital day 1 had increased to 17.5 g/dl suggesting that his perceived response to transfusion may have been related to volume resuscitation and pressers rather than the PRBC's. He continued to have issues with bradycardia but did not require trans-venous pacing. Considering his severe high cervical spine injury with resultant tetraparesis and complications he was transitioned to comfort directed care on hospital day 3.

Case Discussion: The case above illustrates the complexities in early identification of neurogenic shock as a distinct entity. Because the signs of neurogenic shock are somewhat variable in terms of timeframe from injury to onset, and in light of differences between individual patients and systems in regard to fluid resuscitation in the field, a high index of suspicion is necessary from the time of initial evaluation through the early hours and days of intensive care. Any patient presenting with a spinal cord injury should be considered to be at risk with those having higher level

*Coronal (left pane) and sagittal (right pane) CT scan views of the cervical spine showing a type III odontoid fracture (yellow arrow), C1/C2 fracture distraction (long blue arrow) and C2 spinous process fracture (short* 

**5.1 Identification of patients**
