Hypotension and Bradycardia After a C6 Diving Injury
Ms. T, 28, dove into shallow water and sustained a C6 ASIA A tetraplegia. She also has a stable pelvic ring fracture from the same injury. In the trauma bay 2 hours after the injury: BP 76/42, HR 46, SpO2 95% on 15 L nonrebreather, skin warm and dry, capillary refill 2 seconds, urine output 20 mL/hr, Hb 10.4 g/dL, lactate 2.0 mmol/L. There is no external bleeding and the abdomen is soft. She is awake, talking, and says she feels "fine." The monitor shows sinus bradycardia. A colleague wants to give a 1 L crystalloid bolus and start vasopressors.
1. Is this neurogenic shock or hemorrhagic shock? Which findings support each, and why can you not exclude hemorrhage?
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The hypotension with bradycardia and warm, dry skin strongly suggests neurogenic shock from loss of sympathetic tone above the level of the injury (cervical cord injury interrupts the sympathetic outflow from T1–L2). In hemorrhagic shock you would expect tachycardia, cool clammy skin, delayed capillary refill, and narrowed pulse pressure; here the heart rate is 46 and the skin is warm.
You cannot exclude hemorrhage, however, because:
- She has a pelvic ring fracture, which can bleed heavily into the retroperitoneum.
- Hemoglobin measured 2 hours after injury is unreliable; it has not had time to equilibrate.
- Bradycardia from a high cervical injury can mask the usual tachycardic response to blood loss. The two causes can coexist, and neurogenic shock is a diagnosis of exclusion in trauma.
Lactate 2.0 is mildly elevated and urine output is low, so she needs volume assessment, FAST or CT, and serial hemoglobin and lactate. The decision is to resuscitate and simultaneously look for bleeding.
2. What are your first interventions, and what blood pressure target will you aim for?
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Interventions:
- Airway and breathing first - cervical injuries impair ventilation; keep the collar and spine precautions, monitor respiratory effort, and prepare for intubation if vital capacity falls.
- Cautious fluids - a modest bolus, then reassess. Aggressive crystalloid in a cord-injured patient can cause pulmonary edema without fixing the pressure.
- Vasopressor - norepinephrine is typical once volume is addressed; it is the preferred agent for the MAP target.
- Atropine - give 0.5 mg IV for symptomatic bradycardia (some give up to 1 mg) and repeat as needed; be ready for pacing if bradycardia is refractory.
- Keep warm, place a urinary catheter, and log-roll with spinal precautions.
MAP target: the American Association of Neurological Surgeons and Congress of Neurological Surgeons guidelines recommend maintaining MAP 85–90 mmHg for 5–7 days after acute spinal cord injury to preserve cord perfusion. Document pressures and push back gently against accepting the low baseline as adequate.
3. What complications would you anticipate in the first 72 hours, and how does your care reflect them?
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High cervical injury affects nearly every system in the first days:
- Bradycardia and cardiac arrest with vagal stimuli - suctioning, turning, and inserting a nasogastric tube can trigger profound bradycardia. Pre-oxygenate, limit suction passes to 10 seconds, have atropine at the bedside, and monitor continuously.
- Respiratory failure - diaphragmatic weakness and inability to cough. Encourage incentive spirometry, reposition, and monitor vital capacity and oxygen saturation.
- Pressure injuries - immobility plus a hard trauma board or backboard. Remove the board as soon as possible, turn every 2 hours, inspect the sacrum and heels, and use a pressure-redistribution surface.
- Deep vein thrombosis and ileus - mechanical prophylaxis and ordered pharmacologic prophylaxis; monitor bowel sounds and abdomen.
- Autonomic dysreflexia is a later risk once spinal shock resolves; teach staff to recognize headache and severe hypertension with a full bladder.
- Hyponatremia and aspiration - track electrolytes and keep the head of the bed elevated as tolerated.