Neurogenic Shock

Description

Neurogenic shock is a type of distributive shock resulting from the loss of sympathetic outflow and unopposed parasympathetic (vagal) nerve activity.
Usually due to a relatively high spinal cord injury (SCI), such as the cervical spine or high thoracic (usually above level T6) vertebrae. It may also result from regional anesthesia (high block).
There is no universally accepted definition of neurogenic shock. Some define it as an SBP <100 mm Hg with an HR <60 bpm, whereas others define it as an SBP <90 mm Hg (1,2). Overall, it is a significantly decreased MAP from baseline value, and is usually symptomatic.
Neurogenic shock differs from spinal shock in that spinal shock is defined as the temporary loss of spinal reflex activity occurring below a total or near-total SCI. The term "shock" is not a description of the circulatory system, but of reflex activity.

Epidemiology

15–52.5 cases per million in the population. 80% males between 15 and 35 years, 5% children (3)
In a recent study of 490 patients presenting with isolated SCI, neurogenic shock occurred with:
- Cervical cord injuries: 19.3% (4)
- Thoracic injuries: 7%
- Lumbar injuries: 3%

Severe hypotension may result in significant end organ damage to the brain, kidneys, and heart.
Further nerve injury can result from an unstable spine, particularly during intubation.

Untreated neurogenic shock may result in death due to organ hypoperfusion.

Etiology/Risk Factors

Severe injury to the CNS:
- Brain
- Cervical spinal cord
- High thoracic spinal cord
Other causes include:
- Spinal anesthesia
- Drugs
- Emotional stress
- Pain
- CNS dysfunction

Physiology/Pathophysiology

Autonomic nervous system
- Parasympathetic nerves have a craniosacral outflow and their preganglionic and postganglionic connections are close to the target organs.
  - Cranial nerves: CN 3, 7, 9, 10
  - Sacral nerves: S2, S3, S4
- Sympathetic preganglionic neurons have a thoracolumbar outflow. T2-L2 nerves exit the cord via ventral roots and synapse with postganglionic neurons in the paravertebral chain. Cardiac sympathetic neurons are carried from T1 to T4.
Neurogenic shock occurs due to interruption of spinal sympathetic outflow causing loss of vasomotor tone to peripheral arterial beds as well as the loss of compensatory reflex tachycardia. This results in:
- Increased venous capacitance
- Decreased venous return
- Decreased cardiac output
- Hypothermia
- Warm/dry skin due to the loss of the ability to sweat
- Bradycardia (unopposed parasympathetic tone results via the vagal nerve).

Prevantative Measures

Prevention of primary injury

Diagnosis ⬆ ⬇

Neurogenic shock is a diagnosis of exclusion.
Classic findings are:
- Hypotension
- Bradycardia
- Motor and sensory deficits (corresponding to the level of cord injury)
- Warm extremities
- Radiologic evidence of vertebral injury
- However, only 20% of patients present with classic neurogenic shock symptoms (4).
Diagnosis may be difficult due to associated injuries. A head injury may make motor/sensory assessment impossible, or hypotension may be due to concomitant injury such as bleeding. Thus, prior to making the diagnosis of neurogenic shock, other causes must be sought out.

Differential Diagnosis

Concomitant hypovolemic shock from occult bleeding origin in the abdomen, chest, etc.
Isolated head injury causes Cushing's triad (hypertension, bradycardia, abnormal respiration) as opposed to shock.
Spinal shock is due to the loss of spinal reflex activity below the level of SCI and is not of a circulatory etiology; typically resolves in 3–6 weeks. The term "shock" is a misnomer.

Treatment ⬆ ⬇

Adequate IV access and a secure airway are mandatory. Techniques to maintain cervical immobility will likely be necessary if intubation is required.
Monitors. In addition to standard monitors, invasive monitors are usually necessary to aid with management and assess response to therapy (arterial line, central line, pulmonary artery catheter, transesophageal echocardiogram).
Fluid resuscitation is performed to increase the effective circulating blood volume. Transfusion with blood products may be required depending on blood loss. A Foley catheter is placed for loss of bladder function and assessment of volume resuscitation.
Vasopressor support is often required if volume fails to treat hypotension.
- Inotropic agents, such as dopamine, dobutamine, and epinephrine, may be added to improve cardiac output and perfusion pressure.
- Infusion of an alpha-adrenergic agent (phenylephrine or norepinephrine) or vasopressin may be indicated to provide direct vasoconstriction and thus increase blood pressure. Isolated vasoconstrictive activity has the potential for worsening bradycardia.
- In the presence of severe bradycardia, atropine or a temporary pacemaker may be required.
Surgery may be needed to stabilize the spinal cord especially in cases of complete transection or removal of a foreign body.
High-dose steroid administration for SCI is usually center-dependent and discussed with emergency, neurosurgery, or orthopedic personnel.

Follow-Up ⬆ ⬇

References ⬆ ⬇

Zipnick RI , Scalea TM , Trooskin SZ , et al. Hemodynamic responses to penetrating spinal cord injuries. J Trauma. 1993;35:578–583.
Levi L , Wolf A , Belzberg H. Hemodynamic parameters in patients with acute cervical cord trauma: Description, intervention, and prediction of outcome. Neurosurgery. 1993;33:1007–1017.
Grigorean VT , Sandu AM , Popescu M , et al. Cardiac dysfunction following spinal cord injury. J Med Life. 2009;2(2):133–145.
Guly HR , Bouamra O , Lecky FE. The incidence of neurogenic shock in patients with isolated spinal cord injury in the emergency department. Resuscitation. 2008;76:57–62.
Piepmeyer JM , Lehmann KB , Lane JG. Cardiovascular instability following acute cervical spine trauma. Cent Nerv Syst Trauma. 1985;2:153–159.