**4. Treatment**

A detailed history is imperative for accurate diagnosis and treatment of spinal shock. As mentioned previously, prior patient life experiences (i.e., athletes, ballerinas, etc.) may play a role in the rate of hyperreflexia appearance [3]. Thus, a thorough history will help guide appropriate expectations of the clinical evolution of reflexes. The history will also help direct the clinician to what developments could be expected as these can depend on the type, severity, and timing of the incident. Certain substances and chemical mediators for reducing inflammatory processes, protecting neurons, and regenerating neural capacities have been investigated for efficacy in the management of SCI [6, 81–88]. Corticosteroids, specifically methylprednisolone, have been postulated to be part of a generalized recommendation to help alleviate inflammatory processes mediated by neutrophils and macrophages; however, clinical trials and non-randomized studies point to not having this as a general recommendation [81–85]. It has been recommended that a young patient, free of any underlying disease which could be influenced by corticosteroids, could be started on a short trial of methylprednisolone with a loading dose of 30 mg/kg with a maintenance dose of 5/mg/kg/h for the next 24 hours [6]. Symptomatic medications for autonomic dysfunction can include treatments for headaches, flushing, elevated blood pressure, orthostasis, and bladder and abdominal distension. Prompt attention to bowel and bladder hygiene, bladder catheterization, cautious use of bowel preparations, and anticholinergic medications may help with any associated hemodynamic instability. There are ongoing investigations into G-CSF and FGF-2, among others, as possessing neuroprotective qualities as well as stem cells of varying stages, olfactory ensheathing cells, and mesenchymal

**115**

*Spinal Shock: Differentiation from Neurogenic Shock and Key Management Approaches*

chapter for the diagnosis and management of that phenomenon.

1.Immediate immobilization through traction and alignment.

a.Above C3: Immediate mechanical ventilation.

c.Maintain supportive care and ensure SBP > 90.

2.Unstable fractures: Surgical decompression [90].

a.Reduction with brace for up to 4 months.

**5. Considerations for incomplete SCI**

stromal cells that are possible candidates for regenerating neural capacities [86–88]. Consequently, the clinician should remain up to date on the current literature for therapeutic developments. Providers should also keep in mind that lesions above T6 can be accompanied by neurogenic shock, and we refer you to the neurogenic shock

Current guidelines and recommendation can be split up based on the loca-

b.C3–C5: Monitor closely for respiratory decompensation and ventilate if

While it has been a standard practice to give high-dose methylprednisolone after spinal cord injury, recent studies have found that there is no advantage of steroids when considering neurological recovery [91, 92]. Given that SCI can result in long periods of immobility, it is important to consider antithrombotic prophylactic treatment. If patient is on bed rest, gastric and skin ulcer precautions must also be in place.

Incomplete SCI can be classified using the American Spinal Injury Association (ASIA) into three broad categories. Grade A, B, and C injury designations are based

3.Neurosurgery consult to determine if neurosurgery is necessary [89].

1.Stable fractures: Stabilization with brace from 6 to 12 weeks.

*DOI: http://dx.doi.org/10.5772/intechopen.92026*

2.Identify if injury is above c5.

tion of SCI.

Cervical SCI:

necessary.

Thoracolumbar SCI:

1.Unstable sacral fractures:

b.Immediate reduction.

2.Stable sacral fracture:

b.Limit activity.

a.Identify any active bleeds.

Sacral SCI:

*Spinal Shock: Differentiation from Neurogenic Shock and Key Management Approaches DOI: http://dx.doi.org/10.5772/intechopen.92026*

stromal cells that are possible candidates for regenerating neural capacities [86–88]. Consequently, the clinician should remain up to date on the current literature for therapeutic developments. Providers should also keep in mind that lesions above T6 can be accompanied by neurogenic shock, and we refer you to the neurogenic shock chapter for the diagnosis and management of that phenomenon.

Current guidelines and recommendation can be split up based on the location of SCI.

Cervical SCI:

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

been seen as low as T10 [80].

ing its emergence can become chronic/protracted.

**3.4 Phase IV**

**4. Treatment**

during this period [3, 68]. The return of these reflexes is as follows: Babinski sign recovery will follow AJ recovery closely, with the AJ preceding the return of the KJ [3, 68, 74]. The clinician should expect to see most DTRs resolve during this phase with only 10% persisting beyond **Phase III** [3]. Ditunno discussed the variability of reflex return regarding the timing trend. There have been studies showing reduced tendon reflex excitability in certain trained populations, such as ballet dancers and power-trained athletes, relative to untrained or even endurance athletes [75–77]. There has also been evidence that pre-SCI experiences could influence the reflex excitability below an SCI [78, 79]. During this time the clinician will have to be aware of the developing autonomic functions. There is expected improvement in the bradyarrhythmia and hypotension described before; however, around this time autonomic dysreflexia can arise and is most commonly due to a distended bladder or bowel causing a massive sympathetic outflow below the neurologic level of injury [3]. Autonomic dysreflexia can lead to difficult-to-control hypertension and bradycardia and is most commonly seen in patients with SCI at or above T6 but has

One to 12 months post-injury, spasticity and hyperreflexia usually set in, characteristic of **Phase IV**. The remaining DTRs not extinguished during **Phase III** of SS should become absent during this period [3]. Minimal stimuli will elicit cutaneous reflexes, Babinski sign, and DTRs. It has been estimated that there will be detrusor paralysis recovery by 4–6 weeks [3]. The autonomic dysreflexia described in Phase III can also develop during Phase IV, including malignant hypertension, and follow-

A detailed history is imperative for accurate diagnosis and treatment of spinal

shock. As mentioned previously, prior patient life experiences (i.e., athletes, ballerinas, etc.) may play a role in the rate of hyperreflexia appearance [3]. Thus, a thorough history will help guide appropriate expectations of the clinical evolution of reflexes. The history will also help direct the clinician to what developments could be expected as these can depend on the type, severity, and timing of the incident. Certain substances and chemical mediators for reducing inflammatory processes, protecting neurons, and regenerating neural capacities have been investigated for efficacy in the management of SCI [6, 81–88]. Corticosteroids, specifically methylprednisolone, have been postulated to be part of a generalized recommendation to help alleviate inflammatory processes mediated by neutrophils and macrophages; however, clinical trials and non-randomized studies point to not having this as a general recommendation [81–85]. It has been recommended that a young patient, free of any underlying disease which could be influenced by corticosteroids, could be started on a short trial of methylprednisolone with a loading dose of 30 mg/kg with a maintenance dose of 5/mg/kg/h for the next 24 hours [6]. Symptomatic medications for autonomic dysfunction can include treatments for headaches, flushing, elevated blood pressure, orthostasis, and bladder and abdominal distension. Prompt attention to bowel and bladder hygiene, bladder catheterization, cautious use of bowel preparations, and anticholinergic medications may help with any associated hemodynamic instability. There are ongoing investigations into G-CSF and FGF-2, among others, as possessing neuroprotective qualities as well as stem cells of varying stages, olfactory ensheathing cells, and mesenchymal

**114**

1.Immediate immobilization through traction and alignment.

2.Identify if injury is above c5.


Thoracolumbar SCI:


Sacral SCI:

	- a.Identify any active bleeds.
	- b.Immediate reduction.
	- a.Reduction with brace for up to 4 months.

b.Limit activity.

While it has been a standard practice to give high-dose methylprednisolone after spinal cord injury, recent studies have found that there is no advantage of steroids when considering neurological recovery [91, 92]. Given that SCI can result in long periods of immobility, it is important to consider antithrombotic prophylactic treatment. If patient is on bed rest, gastric and skin ulcer precautions must also be in place.

#### **5. Considerations for incomplete SCI**

Incomplete SCI can be classified using the American Spinal Injury Association (ASIA) into three broad categories. Grade A, B, and C injury designations are based on functions that are preserved. **Table 2** describes the preserved functions in all grades. Incomplete spinal cord injuries can be categorized into four types: central cord syndrome, anterior cord syndrome, posterior cord syndrome, and Brown-Sequard syndrome.

The incidence of incomplete SCI has reported range from 40 to 50% of all spinal injuries [93–95]. Central cord syndrome tends to be the most common injury with posterior cord being the rarest of the incomplete spinal injuries. We will start by exploring the central cord syndrome. Most cases of incomplete SCI are caused by motor vehicle accidents (MVA), falls, and swimming injuries [96, 97].
