**3. Background**

### **3.1 History**

The contemporary understanding of "neurogenic shock" was born with Alfred Blalock's "classification of peripheral circulatory failure," which he described in articles between 1927 and 1942. His "pure" types of shock included cardiogenic, hematogenic (better known as hypovolemic), neurogenic, and vasogenic (anaphylactic and septic) [1]. In descriptions of the neurogenic type, Blalock wrote: "the primary alteration is vasodilatation dependent on diminished constrictor tone as a result of influences acting through the nervous system," a description that has persisted [2]. At the time, Blalock associated neurogenic shock with spinal cord injury, spinal anesthesia, and vasovagal syncope [2]. Though our definition of neurogenic shock has evolved since Blalock's time, his classification system remains, and so do the challenges of defining, identifying, and managing neurogenic shock.

#### **3.2 Neurogenic shock vs. spinal shock**

Neurogenic shock is considered distributive in nature and refers to the loss of vasomotor tone and the instability that subsequently follows due to an imbalance in the autonomic nervous system (ANS) [3, 4]. Loss of sympathetic tone leads to unopposed parasympathetic control, manifested by refractory hypotension and bradycardia [3]. Other aspects of neurogenic shock include temperature dysregulation, autonomic dysreflexia, and orthostatic hypotension [5]. Aside from bradycardia and hypotension, many patients develop autonomic dysreflexia defined as a profound autonomic response to what would typically be a mild stimulus such as bladder or bowel distension [6]. The presence of a focal neurological deficit is not required for diagnosis, and although this is most often encountered in the setting of an acute SCI, theoretically any damage resulting in the loss of cerebral control of the autonomic nervous system may place a patient at risk for neurogenic shock. Neurogenic and spinal shocks are distinct consequences of spinal cord injury and the terms should not be used interchangeably.

Neurogenic shock most often occurs after an acute injury above T6, with a possible incidence of 29% in the cervical SCI population and 19% in the thoracic SCI population [4]. The onset may be variable in relation to the timing of the injury, but in SCI patients it most commonly manifests within 2 h of the trauma [7]. In most patients it is transient and may last for 1–6 weeks after injury [5, 8].

Conversely, spinal shock is the transient loss of reflexes and sensorimotor function that manifests acutely after injury to the spinal cord. It is a symptom of underlying spinal cord injury and the term "shock" in this situation does not refer to cardiovascular instability. Spinal shock is characterized by flaccid paralysis, anesthesia, and areflexia or hyporeflexia [3, 7]. Note that often enough the two may be present in the same patient but their natural course and treatment are distinct; furthermore there are often other potential causes for shock in the trauma patient (e.g. hypovolemic secondary to acute blood loss) clouding the diagnosis. It has been proposed that there are four phases of complete spinal shock resolution: hyporeflexia or areflexia (0–24 h), initial return of reflexes (1–3), early hyperreflexia (day 4 – 1 month) and spasticity (1–12 months) [7]. The total duration of spinal shock depends on the definition of its resolution. Resolution has been defined as the appearance of any reflex, the appearance of the bulbocavernosus reflex, return of reflex detrusor functions, or the return of deep tendon reflexes [7, 9]. Depending on which definition you use, spinal shock can last anywhere from days to months.

**99**

*Neurogenic Shock*

Associated autonomic symptoms

**Table 1.**

more accurately assessed.

well as the adrenal gland [10].

**4. Anatomic and epidemiologic considerations**

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

Definition Transient loss of reflexes and

of injury

Reflexes Areflexia or hyporeflexia in early

Treatment Stabilization and treatment of underlying injury

of resolution

*Comparison between spinal shock and neurogenic shock [3–5, 7–9].*

Spinal shock and neurogenic shock may occur at the same time in a patient, complicating management, but they are not synonymous (see **Table 1**). Perhaps the most significant distinction is the difference in their management. The mainstay of treatment of neurogenic shock is fluids and vasopressors. As a transient symptom of spinal cord injury, spinal shock is expected to resolve on its own, in a predictable manner. Once spinal shock resolves, the underlying injury may be

**Spinal shock Neurogenic shock**

Loss of sympathetic tone with unopposed parasympathetic control, leading to cardiovascular instability

Autonomic dysreflexia, orthostatic hypotension, temperature dysregulation

Fluids and vasopressors with appropriate

Varies with injury

temperature monitoring

sensorimotor function below level

Blood pressure Hypotension Hypotension Heart rate Bradycardia Bradycardia

> Difficulty breathing, bowel and bladder dysfunction, priapism

Motor Flaccid paralysis Varies with injury

stage, hyperreflexia in later stage

Duration Days to months Most often 1–6 weeks

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

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


#### **Table 1.**

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

the challenges of defining, identifying, and managing neurogenic shock.

Neurogenic shock is considered distributive in nature and refers to the loss of vasomotor tone and the instability that subsequently follows due to an imbalance in the autonomic nervous system (ANS) [3, 4]. Loss of sympathetic tone leads to unopposed parasympathetic control, manifested by refractory hypotension and bradycardia [3]. Other aspects of neurogenic shock include temperature dysregulation, autonomic dysreflexia, and orthostatic hypotension [5]. Aside from bradycardia and hypotension, many patients develop autonomic dysreflexia defined as a profound autonomic response to what would typically be a mild stimulus such as bladder or bowel distension [6]. The presence of a focal neurological deficit is not required for diagnosis, and although this is most often encountered in the setting of an acute SCI, theoretically any damage resulting in the loss of cerebral control of the autonomic nervous system may place a patient at risk for neurogenic shock. Neurogenic and spinal shocks are distinct consequences of spinal cord injury and

Neurogenic shock most often occurs after an acute injury above T6, with a possible incidence of 29% in the cervical SCI population and 19% in the thoracic SCI population [4]. The onset may be variable in relation to the timing of the injury, but in SCI patients it most commonly manifests within 2 h of the trauma [7]. In most

Conversely, spinal shock is the transient loss of reflexes and sensorimotor function that manifests acutely after injury to the spinal cord. It is a symptom of underlying spinal cord injury and the term "shock" in this situation does not refer to cardiovascular instability. Spinal shock is characterized by flaccid paralysis, anesthesia, and areflexia or hyporeflexia [3, 7]. Note that often enough the two may be present in the same patient but their natural course and treatment are distinct; furthermore there are often other potential causes for shock in the trauma patient (e.g. hypovolemic secondary to acute blood loss) clouding the diagnosis. It has been proposed that there are four phases of complete spinal shock resolution: hyporeflexia or areflexia (0–24 h), initial return of reflexes (1–3), early hyperreflexia (day 4 – 1 month) and spasticity (1–12 months) [7]. The total duration of spinal shock depends on the definition of its resolution. Resolution has been defined as the appearance of any reflex, the appearance of the bulbocavernosus reflex, return of reflex detrusor functions, or the return of deep tendon reflexes [7, 9]. Depending on which definition you use, spinal shock can last anywhere from days to months.

patients it is transient and may last for 1–6 weeks after injury [5, 8].

**3.2 Neurogenic shock vs. spinal shock**

the terms should not be used interchangeably.

The contemporary understanding of "neurogenic shock" was born with Alfred Blalock's "classification of peripheral circulatory failure," which he described in articles between 1927 and 1942. His "pure" types of shock included cardiogenic, hematogenic (better known as hypovolemic), neurogenic, and vasogenic (anaphylactic and septic) [1]. In descriptions of the neurogenic type, Blalock wrote: "the primary alteration is vasodilatation dependent on diminished constrictor tone as a result of influences acting through the nervous system," a description that has persisted [2]. At the time, Blalock associated neurogenic shock with spinal cord injury, spinal anesthesia, and vasovagal syncope [2]. Though our definition of neurogenic shock has evolved since Blalock's time, his classification system remains, and so do

**3. Background**

**3.1 History**

**98**

*Comparison between spinal shock and neurogenic shock [3–5, 7–9].*

Spinal shock and neurogenic shock may occur at the same time in a patient, complicating management, but they are not synonymous (see **Table 1**). Perhaps the most significant distinction is the difference in their management. The mainstay of treatment of neurogenic shock is fluids and vasopressors. As a transient symptom of spinal cord injury, spinal shock is expected to resolve on its own, in a predictable manner. Once spinal shock resolves, the underlying injury may be more accurately assessed.
