Emergency Medicine · Shock Syndromes
The facts most likely to be tested
Neurogenic shock results from loss of sympathetic vascular tone due to spinal cord injury typically at or above the T6 level.
The classic hemodynamic profile is hypotension accompanied by bradycardia or an inappropriate lack of tachycardia in response to low blood pressure.
Physical examination reveals warm, dry skin due to peripheral vasodilation and the inability to mount a sympathetic vasoconstrictive response.
Initial management requires aggressive fluid resuscitation to maintain adequate mean arterial pressure and spinal cord perfusion.
Vasopressors, specifically norepinephrine or phenylephrine, are indicated if the patient remains hypotensive despite adequate fluid resuscitation.
Atropine or cardiac pacing is indicated for patients with symptomatic bradycardia resulting from unopposed vagal tone.
Neurogenic shock is a distributive shock state that must be distinguished from hypovolemic shock, which presents with tachycardia and cool, clammy skin.
Vignette unlocked
A 24-year-old male is brought to the emergency department after a high-speed motorcycle collision. He is alert but complains of inability to move his legs. Physical examination reveals a blood pressure of 82/50 mmHg, a heart rate of 52 bpm, and a respiratory rate of 16/min. His skin is noted to be warm and dry to the touch. Neurological exam shows absent sensation and motor function below the level of the umbilicus.
What is the most likely diagnosis and the underlying pathophysiology?
Neurogenic shock due to loss of sympathetic tone.
The patient presents with the classic triad of hypotension, bradycardia, and warm skin following a spinal cord injury, which is pathognomonic for neurogenic shock (a form of distributive shock).
Full handout
High yield triage
Etiology / Epidemiology
Occurs following acute spinal cord injury (SCI) above T6, causing loss of sympathetic tone.
Clinical Manifestations
Characterized by hypotension with paradoxical bradycardia and warm, dry skin.
Diagnosis
A diagnosis of exclusion; requires ruling out hemorrhagic shock via FAST exam or CT.
Treatment
First-line is IV fluids followed by norepinephrine; avoid aggressive fluid resuscitation.
Prognosis
High risk of autonomic dysreflexia; requires strict hemodynamic monitoring in ICU.
Full handout
Epidemiology & Etiology
Typically follows high-energy trauma resulting in cervical or high thoracic spinal cord injury. It is a form of distributive shock caused by the disruption of descending sympathetic pathways. Non-traumatic causes include spinal anesthesia or high-level spinal cord tumors.
Pertinent Anatomy
The sympathetic outflow originates from the T1-L2 segments of the spinal cord. Injury above T6 disrupts the sympathetic chain, leaving the vagus nerve (parasympathetic) unopposed.
Pathophysiology
Loss of sympathetic tone leads to systemic vasodilation and decreased systemic vascular resistance. The loss of sympathetic innervation to the heart prevents the expected compensatory tachycardia in response to hypotension. This results in the classic triad of hypotension, bradycardia, and peripheral vasodilation.
Clinical Manifestations
Patients present with hypotension and bradycardia, distinguishing this from other shock states. Skin is typically warm and dry due to peripheral vasodilation, unlike the cool, clammy skin of hypovolemic shock. Red flag: Any patient with a suspected SCI and hypotension must be treated for hemorrhage until proven otherwise.
Diagnosis
Diagnosis is clinical and requires the exclusion of hemorrhage. The FAST exam or CT trauma series is the gold standard to rule out internal bleeding. A MAP of 85-90 mmHg is the target threshold for the first 7 days to ensure adequate spinal cord perfusion.
Treatment
Initial management involves isotonic crystalloids to optimize preload, but avoid fluid overload which can lead to pulmonary edema. If hypotension persists, norepinephrine is the vasopressor of choice due to its alpha and beta-adrenergic effects. Atropine may be used for symptomatic, severe bradycardia.
Prognosis
Patients are at high risk for venous thromboembolism and require prophylactic anticoagulation. Long-term complications include autonomic dysreflexia, a life-threatening hypertensive emergency triggered by noxious stimuli below the level of injury.
Differential Diagnosis
Hypovolemic shock: Tachycardia and cool, clammy skin
Cardiogenic shock: Elevated JVP and pulmonary edema
Septic shock: Fever and elevated white blood cell count
Spinal shock: Temporary loss of all reflex activity below injury
Anaphylactic shock: Presence of urticaria, wheezing, or angioedema