A 52-year-old man is brought to the emergency department after a high-speed motor vehicle collision. When the patient was extracted from the damaged car, he was responsive and had a blood pressure of 180/90 mm Hg and a pulse of 120/min. The emergency medical team applied a cervical collar, placed him on a back board, and began intravenous fluid resuscitation. On arrival to the emergency department, the patient is awake, alert, anxious, and reporting neck pain. Temperature is 35.5 C (95.9 F), blood pressure is 84/52 mm Hg, pulse is 50/min, and respirations are 20/min. There are small facial abrasions and bruising over the chest and abdominal wall, but no other obvious external injuries or signs of active bleeding. Pupils are equal and reactive to light. Neck veins are flat. Bilateral breath sounds are equal, and heart sounds are normal. Abdominal examination reveals a palpable mass in the suprapubic region. The patient is unable to move any of his extremities, and deep tendon reflexes are diffusely absent. Sensation to pinprick is absent below the neck. Which of the following best explains this patient's current cardiovascular status?
This patient's complete loss of spinal cord function (eg, areflexia, anesthesia, paralysis, distended bladder) is associated with bradycardia, hypotension, and hypothermia, raising strong suspicion for neurogenic shock due to a traumatic spinal cord injury (in the cervical spine). Acute spinal cord injury is generally associated with an initial period (several minutes) of massive sympathetic stimulation (leading to hypertension and tachycardia) due to release of norepinephrine from the adrenal glands.
Quickly thereafter, sympathetic tone plummets due to injury to the descending spinal tracts that carry signals from the brainstem to the preganglionic sympathetic neurons in the lateral horn of the spinal cord (at levels T1-L2). This results in unopposed parasympathetic stimulation (carried by the intact vagus nerve), leading to hypotension and hypothermia from peripheral vasodilation and bradycardia.
Neurogenic shock often lasts 1-5 weeks before improving, but patients with spinal cord injury are at increased risk for hypotension, bradycardia, and hypothermia due to long-standing reduced sympathetic tone.
(Choice A) Elevated intracranial pressure due to a traumatic brain injury often causes CN VI palsy, papilledema, and Cushing triad (bradycardia, respiratory depression, and hypertension). This patient's hypotension, bradycardia, and hypothermia are more consistent with neurogenic shock.
(Choice B) A massive adrenal stress response causes hypertension and tachycardia for the first few minutes after spinal injury. Sympathetic tone then drops precipitously due to injury to the descending sympathetic pathways, not due to an inadequate adrenal response.
(Choice D) Large intraperitoneal hemorrhage could result in hemorrhagic shock, which is generally characterized by hypotension and tachycardia (not bradycardia). This patient's suprapubic mass is most consistent with a distended bladder from bladder paralysis (rather than abdominal hemorrhage).
(Choice E) Cardiac tamponade can cause hypotension but is generally associated with tachycardia, distended neck veins, and muffled heart sounds.
Educational objective:
Acute spinal cord injury often manifests with loss of spinal cord function (eg, areflexia, anesthesia, paralysis, distended bladder) below the level of the lesion. Lesions that arise above T1 also often cause neurogenic shock due to interruption of the descending sympathetic fibers, which results in unopposed parasympathetic stimulation of the vessels (hypotension) and heart (bradycardia). Hypothermia is also common due to a lack of peripheral vasoconstriction.