The Clinical Rules for the Management of Neurogenic Shock

Dear Editor,

Traumatic spinal cord injury (SCI) can be a highly disabling disease associated with permanent neurologic deficits and systemic complications, the representation of which is that of neurogenic shock (NS).[1] All forms of neurotrauma, spinal and brain, are public health problems. It is important to mention that around 60% of spinal injuries occur in young males aged between 15 and 35 years, with cervical spine injuries being the most prevalent.[2] [3] NS is an acute, life-threatening form of distributive shock caused by interruption of sympathetic input to the cardiovascular system, leading to severe hypotension, bradycardia, and, in the most extreme circumstances, multi-organ dysfunction. The rapid progression of NS underscores the need for its early recognition and intervention to promote better patient outcomes.

The cardiovascular impact of SCI has been recognized and studied for over two centuries. NS, a pathological state, arises when tissue perfusion is severely compromised, falling short of the metabolic demands required by the tissues.[4] [5] This condition is particularly associated with SCIs at or above the T6 level, where the disruption of cardioaccelerator fibers in the upper thoracic segments plays a critical role.

These fibers, originating from preganglionic neurons located in the hypothalamus, pons, and medulla oblongata, are organized in intermediolateral columns (lateral horns) extending through the spinal cord from T1 to L2. Damage to these pathways disrupts the excitatory sympathetic control, leading to diminished opposition to parasympathetic vagal activity. As a result, vascular tone and peripheral vascular resistance are significantly reduced, creating the conditions for the onset of NS. We propose a new rule that is easy to learn and can help improve the management of patients with NS (see [Fig. 1]).

Fig. 1 The clinical rules for the management of neurogenic shock.

• Rule of primary site identification: NS is produced by dysfunction of the autonomic mechanisms, typically due to injury to the spinal cord or central nervous system. We must always evaluate the integrity of key spinal cord segments (T1–L2) while considering the involvement of the brainstem to properly recognize the source of dysfunction.

• Rule of hemodynamic dissociation: NS uniquely presents hypotension and bradycardia, both of which distinguish it from other forms of shock like septic or hypovolemic. We must monitor the heart rate and blood pressure continuously, initiating therapies that enhance perfusion without producing compensatory tachycardia.

• Rule of perfusion preservation: Systemic vasodilation due to NS endangers perfusion to vital organs, particularly the brain and kidneys. We must optimize intravascular volume through fluid resuscitation and use direct-acting vasopressors, such as norepinephrine, to reestablish organ perfusion, all while avoiding cardiovascular overload.

• Rule of autonomic reflex control: Autonomic dysfunction may provoke abnormal reflexes, such as autonomic dysreflexia or ablated sympathetic tone. We must monitor autonomic reflex responses cautiously and steer away from management tactics that might trigger dangerous hypertensive or hypotensive episodes.

• Rule of neurological protection: Patients with NS face high chances of secondary neurological injury emerging from ischemia or hypoxia. We must establish neuroprotective strategies by assuring adequate mean arterial pressures (MAP >85 mm Hg) to facilitate perfusion of the spinal cord for spinal areas released to oxygen demands.

• Rule of secondary factors: Consider systemic complications secondary to NS, such as neurogenic pulmonary edema, tissue hypoxia, and infections associated with critical illness. We must enforce a broad-spectrum management plan, including ventilatory support, radical measures toward infective complications, and appropriate nutritional paradigms.

The clinical rules for the management of NS can have a significant impact on practice, considering that they would provide direction in the effective identification of this potentially fatal condition. The proposed clinical rules aimed at the management of NS should be appropriate for standardization of treatment, early identification, guiding practitioners on time, and using evidence-based treatment to maximize the outcomes for the life-threatening condition of patients.

Conflict of Interest

None declared.

• References

• 1 Ahuja CS, Wilson JR, Nori S. et al. Traumatic spinal cord injury. Nat Rev Dis Primers 2017; 3: 17018
• 2 van Den Hauwe L, Sundgren PC, Flanders AE. Spinal trauma and spinal cord injury (SCI). In: Hodler J, Kubik-Huch RA, von Schulthess GK. eds. Diseases of the Brain, Head and Neck, Spine 2020–2023: Diagnostic Imaging. Cham:: Springer;; 2020
• 3 Moscote-Salazar LR, Duarte Misol D, Rubiano A. Neurogenic shock: pathophysiology, diagnosis and treatment. Rev Traum Amér 2016; 6: 27-30
• 4 Florez-Perdomo WA, Guillermo ACC, García-Ballestas E. et al. Pathobiology of traumatic spinal cord injury: an overview. Egypt J Neurosurg 2024; 39: 27
• 5 Padilla-Zambrano H, Ramos-Villegas Y, Raphael Alvis-Miranda H, Joaquin AF, Rafael Moscote-Salazar L, Rafael Moscote L. Fisiopatología del trauma raquimedular [Pathophysiology of spinal trauma.]. Rev Mex Neurosci 2017; 18: 46-53

Publikationsverlauf

Artikel online veröffentlicht:
13. Februar 2025