NEUROGENIC SHOCK

NEUROGENIC SHOCK

Primarily due to blockade of sympathetic nervous system

Leading to loss of arterial and venous tone with pooling of
blood in the dilated peripheral venous system
Loss of vasoconstrictor impulses results in increased
vascular capacitance, decreased venous return and
decreased cardiac output.
PATHOPHYSIOLOGY
 ETIOLOGY

Spinal cord trauma :

spinal cord injuries from
vertebral body fractures of the cervical or high thoracic
region , disrupting sympathetic tone.
Spinal cord neoplasm :
epidural hematoma impinging
on the spinal cord can produce neurogenic shock
Spinal/Epidural anesthesia
Acute spinal cord injury results in activation of
multiple secondary injury mechanisms :
Vascular compromise to the spinal cord with loss of
autoregulation, vasospasm and thrombosis.
Loss of cellular membrane integrity and impaired energy
metabolism
Neurotransmitter accumulation and release of free
radicals
Importantly, hypotension leads to further
reduction in blood flow to spinal cord worsening
acute spinal cord injury
 The classic description of neurogenic shock consists
of
Decreased blood pressure associated with
bradycardia (absence of reflexive tachycardia due to
disrupted sympathetic discharge)
Warm extremities (loss of peripheral
vasoconstriction)
Motor and sensory deficits indicative of a spinal
cord injury
Radigraphic evidence of a vertebral column fracture
 TREATMENT
Airway is secured and ventilation is made adequate
Fluid resuscitation and restoration of intravascular
volume( improves perfusion)
Vasoconstrictor administration :
increase peripheral vascular tone
decrease vascular capacitance
increase venous return
If blood pressure has not responded to adequate fluid
resuscitation, initially dopamine and later
phenylephrine