Spinal cord injury and autonomic hyperreflexia
Why examiners ask this
Spinal cord injury gives the examiner two patients in one topic: the acute injury with spinal shock and an unstable neck, and the chronic paraplegic coming for a cystoscopy who develops a blood pressure of 230/130 on the table. It tests application of knowledge (why succinylcholine kills after day two, why the pressure rises), judgment (does a patient with no sensation still need an anesthetic?), and adaptability when the hypertension appears. The chronic patient is the more common stem because the physiology is so clean.
The 60-second answer
For the chronic injury above T6 I plan around autonomic hyperreflexia: any stimulus below the lesion, usually bladder or bowel, triggers unopposed sympathetic discharge with severe hypertension, reflex bradycardia and flushing above the lesion.1 I prevent it with an anesthetic that blocks the afferent limb, so I give a spinal anesthetic for lower-body procedures whenever I can, or a general anesthetic deep enough to suppress the reflex; sedation alone is not enough. I avoid succinylcholine because of hyperkalemia, I place an arterial line for lesions above T6 with any history of dysreflexia, and I have nitroglycerin or nicardipine drawn up. For the acute injury I keep the mean pressure at least 75–80 mmHg and no higher than 90–95 mmHg for 3–7 days to perfuse the cord,2 stabilize the neck during a video or fiberoptic intubation, and treat spinal shock with volume, vasopressors and atropine for the bradycardia of a high lesion.
Decision points and the "why"
- Neuraxial over general for the chronic patient — a spinal anesthetic blocks the afferent arm of the reflex completely and is my first choice for urologic and perineal surgery; an epidural is less reliable because sacral roots can be spared. I accept the technical difficulty of a scarred back and the unpredictable level, and I test the block by the pressure response rather than by sensation.
- No succinylcholine from about 48 hours after injury through at least a year, and I avoid it indefinitely — denervation spreads extrajunctional acetylcholine receptors across the muscle membrane, and depolarization releases enough potassium to arrest the heart; the label contraindicates it after the acute phase, with risk peaking at 7–10 days and no defined end.3 Rocuronium with sugammadex covers every indication.
- Arterial line for any lesion above T6 — hyperreflexia occurs in most patients with high lesions and the pressure surge takes seconds; I want beat-to-beat data and quick access to gases in a patient who already has poor respiratory reserve.
- Mean arterial pressure goal in the acute injury — cord perfusion depends on it and hypotension worsens secondary injury; the 2013 AANS/CNS target was 85–90 mmHg for 7 days, and the 2024 AO Spine guideline suggests at least 75–80 mmHg, not above 90–95, for 3–7 days, leaving the vasopressor choice to the clinician.2 I use norepinephrine, because the high lesion has lost cardiac sympathetic tone and phenylephrine alone worsens the bradycardia.
- Airway in the acute injury — manual in-line stabilization with the collar front removed, video laryngoscopy or awake fiberoptic if the patient cooperates, and succinylcholine is still acceptable in the first 24–48 hours. I prepare for bradycardia on laryngoscopy in a cervical lesion.
- Temperature — poikilothermia below the lesion means I warm actively and measure core temperature.
- Positioning and pressure areas — insensate skin and contractures; I pad everything and I own the positioning because the patient cannot report pain.
The complication they will inject
During cystoscopy under sedation, the pressure climbs to 220/120 with a heart rate of 45, a pounding headache and a flushed face. I tell the surgeon to stop the stimulus and drain the bladder, sit the patient up to pool blood, and deepen the anesthetic, because removing the trigger is the definitive treatment.1 If the pressure stays high I give nitroglycerin 50–100 mcg or nicardipine 0.5–1 mg IV in increments, or immediate-release nifedipine or nitrate paste if I have no line, and I treat any systolic above 150.4 I do not treat the bradycardia; it is a baroreceptor reflex and resolves as the pressure falls. I check for the consequences: a 12-lead for ischemia, a neurologic exam for hemorrhage, a chest exam for pulmonary edema. I then convert to a spinal or a general anesthetic before the surgeon continues, and I keep the patient monitored postoperatively, because dysreflexia can first appear as the anesthetic wears off and recurs with bladder distension on the ward.1
Pitfalls that cost points
- Giving a chronic paraplegic no anesthetic for a procedure below the lesion because "they cannot feel it".
- Treating the bradycardia with atropine, which removes the only brake on the pressure.
- Choosing labetalol as first-line; beta-blockade worsens the bradycardia and the alpha effect is weak.
- Stating a succinylcholine window without the mechanism of extrajunctional receptors.
- Forgetting that the acute patient is vasodilated and bradycardic, not hypovolemic, and drowning them in crystalloid.
Rapid-why
Q: Why do lesions above T6 produce dysreflexia and lower lesions rarely do? A: The splanchnic bed, the largest vascular reservoir, is innervated from T5–T9; a lesion above it leaves that vasoconstriction unopposed by descending inhibitory pathways.
Q: Why flushing above the lesion and pallor below? A: Baroreceptors trigger compensatory parasympathetic output and vasodilation that can only act above the level of injury.
Q: Why is pulmonary function tested before an anesthetic in a cervical lesion? A: Vital capacity falls with loss of intercostals, cough is weak, and a C3–C5 lesion compromises the diaphragm; postoperative ventilation is a real possibility.
Q: How long does spinal shock last? A: Flaccidity, areflexia and hypotension for days to weeks, usually 1–3 weeks; spasticity and hyperreflexia follow as the cord recovers reflex activity.
Numbers to know
| Item | Value |
|---|---|
| Lesion level at risk for dysreflexia | T6 and above; about 85% of these patients1 |
| Succinylcholine | Avoid after 48 hours post-injury; I avoid it permanently |
| Acute injury MAP goal | At least 75–80, not above 90–95 mmHg, for 3–7 days2 |
| Nitroglycerin | 50–100 mcg IV increments or infusion |
| Nicardipine | 0.5–1 mg IV bolus, 5–15 mg/h infusion |
| Treatment threshold | Systolic above 150 mmHg or symptoms4 |
Links
- succinylcholine, hyperkalemia, Airway management with cervical spine injury (coming), Trauma: initial management and damage control, Perioperative hypertension, Spinal anesthesia: dosing, spread, hypotension
- AANS/CNS Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries (2013) and the AO Spine acute spinal cord injury guideline (2024); Consortium for Spinal Cord Medicine clinical practice guideline on autonomic dysreflexia
Sources
- 1.Autonomic Dysreflexia · OpenAnesthesia (IARS), 2025 · openanesthesia.org
- 2.A Clinical Practice Guideline on the Timing of Surgical Decompression and Hemodynamic Management of Acute Spinal Cord Injury: Introduction, Rationale, and Scope · AO Spine / Praxis (Global Spine Journal), 2024 · ebi.ac.ukFull text via Europe PMC (PMC10964894); summarizes the 2013 AANS/CNS 85-90 mmHg for 7 days and the 2024 MAP recommendations.
- 3.QUELICIN (succinylcholine chloride) injection prescribing information · FDA / DailyMed · dailymed.nlm.nih.govContraindicated after the acute phase of upper motor neuron injury; risk peaks at 7-10 days, duration undetermined.
- 4.Autonomic Dysreflexia wallet card (adult) · Christopher & Dana Reeve Foundation · christopherreeve.orgSit upright; treat systolic above 150 mmHg with a rapid-onset, short-acting agent (nitrate paste, immediate-release nifedipine).
Facts on this page were checked against these sources on Oct 14, 2026. Guidelines change; confirm doses against current institutional protocols.