**5.1 Identification of patients**

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

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

*as the celiac and mesenteric ganglia) [10, 11]. Created with Biorender.com.*

*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* 

**100**

**Figure 1.**

even at centers of reasonably high volume [13].

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

#### **Figure 2.**

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

#### **Figure 3.**

*Sagittal STIR c-spine MRI (left pane) with noted intra-axial edema and hemorrhage at the base of the odontoid (red triangle and top axial slice), more inferior cord edema (yellow triangle and bottom axial slice), and significant posterior compartment paravertebral edema (yellow star). Created with Biorender.com.*

injuries at higher risk (**Figure 1**). The authors suggest that the American Spinal Injury Association Autonomic Standards Assessment Form [14] is a reasonable place to start and takes into account blood pressure, heart rate, sweating, temperature regulation, the bronchopulmonary system, and the lower urinary tract and bowel. Even with this tool, however, no specific definition of bradycardia/hypotension is forthcoming; thus it will need to be set by individuals and institutions. As there is no single accepted treatment cutoff for the bradycardia and hypotension, it may be important for systems to consider their patient population in relation to prior studies and establish parameters for automatic physician notification during hemodynamic monitoring with reasonable case reviews to establish the best local standard.

It is agreed, however, that the profound systemic hypotension that characterizes neurogenic shock may lead to hypoperfusion of the spinal cord with subsequent ischemia and secondary injury [15]. To improve outcomes, prompt and aggressive treatment of hypotension should be undertaken in a monitored intensive care unit, with adequate cardiopulmonary and ventilatory support [8]. Medical treatment consists of sufficient fluid administration as well as vasopressor therapy for sustaining blood pressure and maintaining perfusion [4]. That being said, it should be noted that the data regarding pressor use in SCI may be conflicting in this regard, as a distinction needs to be made between pressor use in an attempt to stabilize or improve the motor and sensory loss related to SCI, and that to preclude hypotension and bradycardia related to neurogenic shock from causing complications such as systemic hypoperfusion and cardiac arrest among others. According to one author, up to 100% of patients suffering from neurogenic shock may also have bradycardia, with 71% reported as having severe bradycardia (HR < 46 BPM) and 16% progressing to cardiac arrest [16].

#### **5.2 Patient management**

Fluid resuscitation is the first line therapy for hypotension in the setting of neurogenic shock [17]. Maintenance of blood volume influences both blood pressure

**103**

*Neurogenic Shock*

therapy [16].

stabilization.

**6. Rehabilitation and recovery**

and promptly identified.

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

anticipated and prevented as much as possible.

and blood flow around the site of injury [8]. If there is an inadequate response to fluid resuscitation, agents with α1 and β1 adrenergic receptor activity should ideally be used to increase sympathetic activation [15]. What is otherwise considered routine care such as suctioning, as well as abdominal changes such as elevated bladder and bowel pressures, are known to produce wide swings in heart rate and blood pressure that may be refractory to treatment [18]. These changes should be

Blood pressure can be further augmented through the administration of intravenous vasopressor agents. These include norepinephrine, epinephrine, dopamine, phenylephrine, as well as concurrent atropine in patients with significant bradycardia [15]. There are some prior reports of transitioning individuals that need extended treatment with a non-intravenous agent to propantheline, aminophylline, theophylline, and ephedrine although the evidence is extremely limited [16]. Enteral pseudoephedrine has also been used successfully as an adjunctive

Current management guidelines dictate that mean arterial pressure (MAP) should be maintained above 85–90 mmHg for the first 5–7 days of therapy [19]. This resuscitation target has been questioned due to the lack of quality evidence showing a positive effect on outcomes [8]. Additionally, maintenance for 5–7 days may be insufficient because certain individuals benefit from longer management [4]. One study has shown that vasopressor therapy achieving the MAP goal is more likely to cause complications than to improve neurological outcomes, with dopamine leading in complications [20]. As such, the risk of vasopressors should be balanced against their benefits in each individual patient, and there should be clear goals for use in regard to improvement of the sensory and motor deficits vs. cardiovascular

A recent study suggests that maintenance of a spinal cord perfusion pressure (mean arterial pressure – cerebral spinal fluid pressure) above 50 mmHg is a stronger predictor of neurologic recovery than systemic MAP and may also be useful in guiding management [21]. More studies with high quality evidence are needed to establish reasonable treatment goals that are linked to improved patient outcome.

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

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

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

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

injuries at higher risk (**Figure 1**). The authors suggest that the American Spinal Injury Association Autonomic Standards Assessment Form [14] is a reasonable place to start and takes into account blood pressure, heart rate, sweating, temperature regulation, the bronchopulmonary system, and the lower urinary tract and bowel. Even with this tool, however, no specific definition of bradycardia/hypotension is forthcoming; thus it will need to be set by individuals and institutions. As there is no single accepted treatment cutoff for the bradycardia and hypotension, it may be important for systems to consider their patient population in relation to prior studies and establish parameters for automatic physician notification during hemodynamic

*Sagittal STIR c-spine MRI (left pane) with noted intra-axial edema and hemorrhage at the base of the odontoid (red triangle and top axial slice), more inferior cord edema (yellow triangle and bottom axial slice), and significant posterior compartment paravertebral edema (yellow star). Created with Biorender.com.*

monitoring with reasonable case reviews to establish the best local standard.

It is agreed, however, that the profound systemic hypotension that characterizes neurogenic shock may lead to hypoperfusion of the spinal cord with subsequent ischemia and secondary injury [15]. To improve outcomes, prompt and aggressive treatment of hypotension should be undertaken in a monitored intensive care unit, with adequate cardiopulmonary and ventilatory support [8]. Medical treatment consists of sufficient fluid administration as well as vasopressor therapy for sustaining blood pressure and maintaining perfusion [4]. That being said, it should be noted that the data regarding pressor use in SCI may be conflicting in this regard, as a distinction needs to be made between pressor use in an attempt to stabilize or improve the motor and sensory loss related to SCI, and that to preclude hypotension and bradycardia related to neurogenic shock from causing complications such as systemic hypoperfusion and cardiac arrest among others. According to one author, up to 100% of patients suffering from neurogenic shock may also have bradycardia, with 71% reported as having severe bradycardia (HR < 46 BPM) and 16% progressing to cardiac arrest [16].

Fluid resuscitation is the first line therapy for hypotension in the setting of neurogenic shock [17]. Maintenance of blood volume influences both blood pressure

**102**

**Figure 3.**

**5.2 Patient management**

and blood flow around the site of injury [8]. If there is an inadequate response to fluid resuscitation, agents with α1 and β1 adrenergic receptor activity should ideally be used to increase sympathetic activation [15]. What is otherwise considered routine care such as suctioning, as well as abdominal changes such as elevated bladder and bowel pressures, are known to produce wide swings in heart rate and blood pressure that may be refractory to treatment [18]. These changes should be anticipated and prevented as much as possible.

Blood pressure can be further augmented through the administration of intravenous vasopressor agents. These include norepinephrine, epinephrine, dopamine, phenylephrine, as well as concurrent atropine in patients with significant bradycardia [15]. There are some prior reports of transitioning individuals that need extended treatment with a non-intravenous agent to propantheline, aminophylline, theophylline, and ephedrine although the evidence is extremely limited [16]. Enteral pseudoephedrine has also been used successfully as an adjunctive therapy [16].

Current management guidelines dictate that mean arterial pressure (MAP) should be maintained above 85–90 mmHg for the first 5–7 days of therapy [19]. This resuscitation target has been questioned due to the lack of quality evidence showing a positive effect on outcomes [8]. Additionally, maintenance for 5–7 days may be insufficient because certain individuals benefit from longer management [4]. One study has shown that vasopressor therapy achieving the MAP goal is more likely to cause complications than to improve neurological outcomes, with dopamine leading in complications [20]. As such, the risk of vasopressors should be balanced against their benefits in each individual patient, and there should be clear goals for use in regard to improvement of the sensory and motor deficits vs. cardiovascular stabilization.

A recent study suggests that maintenance of a spinal cord perfusion pressure (mean arterial pressure – cerebral spinal fluid pressure) above 50 mmHg is a stronger predictor of neurologic recovery than systemic MAP and may also be useful in guiding management [21]. More studies with high quality evidence are needed to establish reasonable treatment goals that are linked to improved patient outcome.
