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Spinal Cord Injury

SCI High-yield Verified · Oct 2026

Spinal cord injury is a neurologic condition, from trauma or nontraumatic causes, that disrupts the motor, sensory, and autonomic pathways carrying signals between the brain and the body.

The highest-yield neuro-trauma topic: the level→function map, spinal shock vs neurogenic shock, and autonomic dysreflexia — the emergency where the first intervention is sitting the patient up.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 A cable cut — and a second injury that keeps cutting

The spinal cord is the cable that carries every signal between brain and body; injury disrupts those signals below the level of the damage. Most traumatic SCIs do not sever the cord: the trauma fractures or dislocates vertebrae, and the damage happens when bone fragments tear into cord tissue or press on the nerve pathways.

The mechanical insult is only the beginning. That primary injury triggers a secondary injury that begins within minutes and continues for weeks to months: vascular damage, ionic imbalances, free-radical formation, inflammation, and neurotransmitter accumulation (excitotoxicity) keep destroying cord tissue the trauma never touched. This ongoing cascade is why acute SCI care is time-critical — perfusion targets, early decompression, and every neuroprotective decision are aimed at limiting the injury that is still happening.

Whether an injury is complete or incomplete matters as much as where it is. Complete injury = total bilateral loss of motor function and of pain, temperature, proprioceptive, vibratory, and tactile perception below the level — the cord can’t send signals below the injury. Incomplete injury = some movement and/or sensation preserved below it. The dividing line is tested at the very bottom of the cord: sacral sparing at S4–S5 (deep anal pressure, voluntary anal contraction). The ASIA Impairment Scale grades the result: A complete · B incomplete, sensory preserved but motor lost · C motor preserved with less than half of key muscles at grade ≥ 3 · D at least half of key muscles ≥ grade 3 · E normal exam.

02 Level determines everything

Read the cord like a floor plan: everything wired below the injury is affected. A cervical injury involves some degree of both upper and lower body — tetraplegia (quadriplegia); a thoracic, lumbar, or sacral injury involves the lower body — paraplegia.

The respiratory stakes sit at the top. The phrenic nerve arises from C3, C4, and C5 and drives the diaphragm, the main muscle of inhalation — a cord cut above C3 makes spontaneous breathing impossible, and a complete injury at or above C5 can weaken or eliminate diaphragm function, so tracheostomy and/or mechanical ventilation may be needed (some patients injured below C5 need a ventilator early and are later weaned). Even a purely thoracic injury steals breathing power: abdominal muscles provide most of the force behind a cough, and thoracic nerves drive the intercostals — so secretions stay put even when the diaphragm works. Thoracic injury also disturbs blood-pressure and temperature regulation (the sympathetic chain), and lumbar/sacral injury takes the legs plus bowel and bladder control.

Not every incomplete injury looks alike. Central cord syndrome — the most common incomplete SCI — classically follows a low-energy fall or hyperextension injury (a forward fall striking the chin) in an older adult with cervical spondylosis: because fibers to the arms run near the center of the cord and fibers to the legs run farther out, the arms are weaker than the legs, worst in the hands. Anterior cord syndrome takes pain and temperature bilaterally but spares vibration and position sense; Brown-Séquard (hemisection) takes motor, proprioception, and touch on the same side but pain and temperature on the opposite side; posterior cord syndrome impairs touch, vibration, and proprioception with motor spared.

The level→function ladder: each level down preserves one more key motion — and one more piece of independence.

03 Spinal shock vs neurogenic shock — two different problems

These two are the classic exam conflation, and they are not the same thing. Spinal shock is a neurologic event: a sudden, temporary loss of cord function below the injury — flaccid paralysis, areflexia, lost sensation, absent bowel/bladder control and anal sphincter tone (priapism may occur in males) — lasting days to weeks. It resolves in a recognizable sequence (Ditunno phases): the delayed plantar reflex returns first within 24 hours, cutaneous reflexes over days 1–3, deep tendon reflexes around day 4 to 1 month, then hyperreflexia over months 1–12 — the window in which autonomic dysreflexia may first appear. Deficit that persists after spinal shock resolves is the anatomic injury declaring itself.

Neurogenic shock is a hemodynamic event, seen with cervical and upper-thoracic injuries — especially above T6. Losing sympathetic outflow while vagal (parasympathetic) tone runs unopposed dilates the capacitance vessels, dropping venous return: hypotension. The unopposed vagal influence on the heart adds bradycardia, and cutaneous vasodilation makes the skin warm and pink. That skin-and-rate combination is the discriminator from hypovolemia: hypovolemic shock = hypotension + tachycardia + cool, pale skin; neurogenic shock = hypotension + bradycardia + warm, pink skin. Working parameters: SBP below 90 mm Hg with HR below 80 bpm, persisting up to 4–5 weeks. The two shocks can coincide — spinal shock is the reflex/motor/sensory picture, neurogenic shock the blood-pressure one.

Treatment defends cord perfusion. IV fluids come first; norepinephrine is the preferred vasopressor (α plus β activity), with atropine or glycopyrrolate for bradycardia. The MAP target has two generations: 2024 guidance (per StatPearls) says augment MAP to a minimum of 75–80 mm Hg, avoid actively pushing beyond 90–95 mm Hg, and maintain for 3–7 days — while the long-standing convention of MAP 85–90 mm Hg for the first ~7 days is still widely taught and still appears in the shock references.

Neurogenic shock: lost sympathetic tone vasodilates and slows the heart at the same time — hypotension with bradycardia and warm skin.

04 Autonomic dysreflexia — the reflex with no off switch

After spinal shock resolves — typically within the first year, rarely in the first month — patients with injuries at or above T6 become susceptible to autonomic dysreflexia (AD); up to 90% of people with cervical or high-thoracic SCI are. A noxious stimulus below the injury (a full bladder, above all) fires an intense sympathetic discharge that clamps down the splanchnic vasculature: blood pressure soars. The brain notices and sends the corrective parasympathetic response — but those signals cannot cross the lesion. The result is a body split in two at the injury level: above it, compensatory vagal outflow produces bradycardia, flushing, and profuse sweating; below it, unrelenting vasoconstriction keeps the skin cold and pale — and the hypertension continues until someone finds and removes the trigger.

The trigger list is ranked, and the ranking is the treatment algorithm: a urologic source in ~85% of cases — a distended bladder is the number-one cause, plus UTI and clogged or kinked catheters — then bowel (fecal impaction, constipation), then skin (pressure injury, tight clothing), fracture, sexual activity, menstruation. An episode is a rise in SBP ≥ 20 mm Hg above the patient’s baseline; a significant episode typically shows SBP ≥ 150 mm Hg, and pressures can reach 300 mm Hg. The catch: baseline BP in high SCI runs low — so a "normal-looking" reading can already be dysreflexia.

The AD loop: the brain’s corrective signal can’t cross the lesion, so hypertension persists until the trigger below is found and removed.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Motor vehicle collisions (~38% of new cases — the leading cause) modifiable Falls (~30% of new cases) modifiable Older age with cervical spondylosis/stenosis — low-energy falls and hyperextension injuries (central cord syndrome) Historically younger men, but a growing proportion of people with SCI are older than 65 Nontraumatic etiologies also disrupt motor, sensory, and autonomic pathways

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Loss of movement and sensation below the injury level Expected
Why: The cord can’t carry signals past the damage: complete injury = total bilateral loss of motor function and of pain, temperature, position, vibration, and touch perception below the level; incomplete = some function preserved.
Flaccid paralysis with absent reflexes (early) early Expected
Why: Spinal shock — a temporary shutdown of all cord function below the injury: areflexia, lost sensation, absent bowel/bladder control and anal tone; priapism may occur in males. Lasts days to weeks.
Hypotension + bradycardia with warm, pink skin (injury above T6) early Report immediately
Why: Neurogenic shock: lost sympathetic tone vasodilates the capacitance vessels (dropping venous return) while unopposed vagal tone slows the heart. Contrast hypovolemia: hypotension with tachycardia and cool, pale skin.
Weak, ineffective cough — even in thoracic-level injury Hold & notify
Why: Abdominal muscles provide most of the force of a cough and thoracic nerves drive the intercostals; losing them means retained secretions and pneumonia risk even when the diaphragm is intact.
Declining respiratory effort or falling lung volumes in cervical injury Report immediately
Why: The phrenic nerve (C3–C5) drives the diaphragm; injury at or above C5 can weaken or eliminate it. Early-intubation indications: level above C5, total paralysis, low lung volumes, concomitant chest injuries.
Pounding headache with flushing and sweating above the injury, cold pale skin below Report immediately
Why: Autonomic dysreflexia: unopposed sympathetic discharge below the lesion drives severe hypertension; the brain’s corrective signals can’t cross, so vagal effects (flushing, sweating, bradycardia) appear only above the level.
Bradycardia during a hypertensive episode (rarely tachycardia) · nasal congestion · blurred vision · goosebumps Report immediately
Why: The rest of the AD picture — baroreceptor-driven vagal outflow above the lesion against ongoing vasoconstriction below it.
Urinary retention or uncontrolled bladder emptying Expected
Why: Neurogenic bladder follows the level: injury above the sacral micturition center → reflex ("spastic") bladder that empties without control; injury at or below it → flaccid bladder with retention.
Absent bowel control · constipation Expected
Why: The same disrupted autonomic wiring produces neurogenic bowel dysfunction — and fecal impaction is the second most common AD trigger, which is why the bowel program is prophylaxis, not comfort care.
Arms weaker than legs, worst in the hands Expected
Why: Central cord syndrome — fibers to the arms run near the center of the cord where a hyperextension injury does its damage; classic in an older adult after a forward fall striking the chin. Bladder retention is typical; sacral sensation is preserved.
Returning reflexes, then spasticity and hyperreflexia late Expected
Why: Spinal shock resolves in sequence (plantar reflex → cutaneous reflexes → deep tendon reflexes → hyperreflexia over months 1–12). Velocity-dependent tone from lost descending inhibition follows in ~40% of patients — and AD becomes possible in this window.
Impaired temperature regulation Expected
Why: Impaired thermoregulation is frequent, especially after cervical and high-thoracic injury, leaving the patient vulnerable to both hyperthermia and hypothermia — it stays impaired chronically.

Diagnostics

Test In this disorder Normal
Noncontrast CT Fast and first; it finds the fractures and dislocations The primary imaging modality — sensitivity > 98% for cervical spine injuries StatPearls —
MRI The follow-on study when the deficit needs explaining beyond the bones More reliable than CT for soft-tissue and cord pathology — what the cord itself looks like —
ASIA (ISNCSCI) examination Serial exams are the point — they track ascent or improvement shift by shift Sensory + motor levels and sacral sparing at S4–S5 (deep anal pressure, voluntary anal contraction) → grade A (complete) through E (normal) ASIA —
MAP (arterial pressure monitoring) Perfusion defense against the ongoing secondary injury; fluids first, then norepinephrine as the preferred pressor Augment to a minimum 75–80 mm Hg, avoid actively pushing beyond 90–95 mm Hg, maintain 3–7 days 2024 guideline (per StatPearls) Classic convention: MAP 85–90 mm Hg × ~7 days — still widely taught
Neurogenic shock parameters Can persist up to 4–5 weeks; warm pink skin separates it from hypovolemia SBP < 90 mm Hg with HR < 80 bpm — hypotension that cannot mount a tachycardia StatPearls —
AD episode (BP against baseline) Know the patient’s baseline — a "normal-looking" BP can already be dysreflexia. Check BP every 5 minutes during an episode SBP ≥ 20 mm Hg above the patient’s baseline; a significant episode typically SBP ≥ 150; pressures can reach 300 mm Hg StatPearls / MSKTC Baseline BP in high SCI runs low

Complications

Warning: Autonomic dysreflexia Report immediately
Pounding headache, SBP ≥ 20 mm Hg over baseline, flushing/sweating above the lesion, pale cold skin below — uncontrolled, it can cause seizures, hemorrhagic stroke, MI, heart failure, kidney failure, or death.
The response is a fixed sequence: 1) sit the patient upright, legs dangling, and loosen everything tight (clothing, shoes, belts, binders); 2) bladder first — the trigger in ~85% of cases (kinked or clogged catheter, distention); 3) bowel — check for impaction, lidocaine gel before the digital exam; BP every 5 minutes throughout; 4) if SBP stays > 150 mm Hg, rapid-onset/short-duration antihypertensive — most easily 1 to 2 inches of 2% nitroglycerin paste on the skin above the injury level, or nifedipine 10 mg bite-and-swallow. Escalate/call 911 if the cause can’t be found or the BP won’t come down.
Warning: Respiratory failure & pneumonia Report immediately
Respiratory complications are the most common cause of morbidity and mortality in SCI; pneumonia and sepsis remain the leading causes of death.
Serial respiratory assessment is the watch: know the early-intubation indications (injury above C5, total paralysis, low lung volumes, chest injuries) and expect tracheostomy if ventilation runs past 2 weeks. Report fever and chills, cough, chest tightness, or shortness of breath — and screen for obstructive sleep apnea (loud snoring, waking choking or gasping, unrefreshing sleep).
Warning: DVT / pulmonary embolism Hold & notify
Immobile, vasodilated limbs pool blood; VTE is on the standard SCI complication list.
Start DVT prophylaxis as soon as possible, no later than 72 hours after the injury (Neurocritical Care Society, per StatPearls); enoxaparin beats unfractionated heparin for preventing PE in SCI, typically continued at least 8 weeks.
Caution: Pressure injuries Hold & notify
Insensate, immobile skin over bony prominences breaks down silently — and a pressure injury is itself an AD trigger.
The prevention numbers are teachable: seated weight shifts every 15–30 minutes for at least 30–90 seconds, repositioning in bed every 2–6 hours, skin inspection at least twice a day with a mirror, lift — don’t slide (shear), wash and dry immediately after any leakage, and stay off any discolored area until it returns to normal color.
Caution: Untreated spasticity → contractures
Unmanaged tone causes pain, impaired hygiene, contractures, pressure ulcers, subluxation, heterotopic ossification, and functional decline.
But some spasticity is useful — standing, weight-bearing, transfers, circulation, bone density — so the goal is function, not zero tone. Physical measures come first: stretching, splinting, serial casting, heat/cold, functional electrical stimulation.

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Corticosteroids
Endocrine · prednisone

Methylprednisolone (MPSS) is an option, not a standard of care — and the timing rules are exam gold. The 2017 AOSpine guideline suggests a 24-hour infusion of high-dose MPSS be offered within 8 hours of injury as a treatment option (weak recommendation, moderate evidence; pooled motor-score gain 3.88 points at 6–12 months) — and suggests not offering it after 8 hours, and never as a 48-hour infusion (NASCIS III showed significantly more severe pneumonia at 48 h). The history matters: the 2013 AANS/CNS guideline made a Level I recommendation against MPSS (not FDA-approved for SCI; harms including death outweighed unproven benefit), and 2017 bridged the conflict by splitting on timing and duration.
Skeletal Muscle Relaxants First-line
Musculoskeletal · cyclobenzaprine

Spasticity — velocity-dependent tone from lost descending inhibition — develops in ~40% of SCI patients once spinal shock resolves. Baclofen is the drug of choice for spinal forms of spasticity (a GABA-B agonist acting at the cord level), FDA-approved for flexor spasms, clonus, and associated pain in spinal cord lesions. Physical modalities come first; intrathecal baclofen is reserved for severe spinal spasticity unresponsive to maximal oral baclofen, tizanidine, or dantrolene — and abrupt intrathecal withdrawal after > 2 months can cause a hypermetabolic emergency (hyperpyrexia, rigidity, severe rebound spasticity).

Beyond medications

  • Spinal motion restriction (SMR) from the scene: limit undesired spine movement during transfer with devices such as backboards or scoop stretchers. SCI is a medical emergency — call 911 for loss of movement or feeling after trauma.
  • Early surgical decompression — ideally within 24 hours when indicated and feasible — may improve neurologic outcomes; braces or traction stabilize the spine, and surgery can decompress, realign, or fuse.
  • Bladder program — acute retention gets an indwelling catheter (16–18 Fr, or suprapubic); long-term, clean intermittent catheterization is preferred (fewer problems, more spontaneous voiding, fewer UTIs): usually 4–6 times/day, keeping volumes < 500 mL.
  • Bowel program — dietary adjustment, stool softeners, scheduled evacuation/digital stimulation and suppositories. A consistent program is itself AD prevention (impaction is the #2 trigger).
  • Pressure-relief schedule — seated weight shifts every 15–30 minutes (30–90 seconds), repositioning every 2–6 hours, twice-daily mirror skin checks.
  • Airway clearance & rehab — mechanical cough-assist or trained manual assisted cough, hydration to thin secretions, vaccinations (influenza yearly, pneumococcal, COVID-19, and RSV for adults 75 and older or 50–74 at increased risk, per CDC); then rehabilitation therapy, mobility aids, and assistive devices.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Run serial neuro exams (ASIA framework: motor, sensory, sacral sparing) and compare against the last one, shift by shift.
Why: Secondary injury evolves for weeks — serial exams are how ascent or improvement is caught, and persistent deficit after spinal shock resolves is the anatomic injury declaring itself.
In cervical injury, treat respiratory status as the headline: rate, effort, lung volumes, cough strength — trend them.
Why: The phrenic nerve lives at C3–C5, and early-intubation indications (level above C5, total paralysis, low lung volumes, chest injuries) are recognized at the bedside. Respiratory complications are SCI’s leading killer.
Defend the MAP target (minimum 75–80 mm Hg per the 2024 guidance; classic 85–90 × 7 days) with fluids first, norepinephrine as ordered.
Why: Hypotension starves a cord already fighting secondary injury; MAP augmentation for 3–7 days is the perfusion defense.
Know the patient’s baseline BP and check BP every 5 minutes during any suspected AD episode.
Why: Baseline runs low in high SCI, so AD is defined against baseline (SBP ≥ 20 mm Hg above it) — a "normal" number can be a significant episode in progress.
Inspect skin at least twice daily, bony prominences especially, and verify the pressure-relief schedule is actually happening.
Why: Insensate skin can’t report damage — and a pressure injury is both a morbidity in itself and an AD trigger.
Confirm DVT prophylaxis is started within 72 hours of injury and continued as ordered.
Why: The Neurocritical Care Society window is 72 hours; enoxaparin outperforms unfractionated heparin for preventing PE in SCI and typically runs at least 8 weeks.
When autonomic dysreflexia hits
Sit the patient upright, legs dangling — first, before anything else — and loosen or remove everything tight: clothing, shoes, belts, binders.
Why: Position is the fastest pressure reduction available and needs no order; constrictive items are themselves potential triggers.
Hunt the trigger bladder-first: check the catheter for kinks and clogs, check for distention, restore drainage.
Why: A urologic source drives ~85% of episodes — the distended bladder is the number-one cause, so restoring drainage is the most likely cure.
Bladder clear? Check the bowel for impaction — apply lidocaine gel before the digital exam.
Why: Impaction is the second most common trigger, and the exam itself is a noxious stimulus that can worsen the episode unless the mucosa is numbed.
If SBP stays > 150 mm Hg, give the ordered rapid-onset antihypertensive — nitroglycerin 2% paste, 1–2 inches, above the injury level (alternative: nifedipine 10 mg bite-and-swallow) — and escalate/call 911 if the trigger can’t be found or the BP won’t break.
Why: The vessels below the lesion are clamped shut and won’t absorb or respond predictably; short-acting agents above the level drop the pressure without overshooting once the trigger is removed. Uncontrolled AD ends in stroke, MI, or death.
For neurogenic shock: fluids first, then anticipate norepinephrine; atropine or glycopyrrolate for symptomatic bradycardia.
Why: The problem is lost vascular tone plus unopposed vagal slowing — norepinephrine’s dual α/β activity addresses both, which is why it is the preferred pressor.
Patient teaching
Teach the AD drill until it’s automatic: sit up, loosen clothing, check the bladder, check the bowel, check the skin — and get help if the headache and BP don’t break.
Why: Up to 90% of people with cervical or high-thoracic SCI are susceptible, typically within the first year — the patient and family are the first responders.
Keep the bladder and bowel programs on schedule: catheterize 4–6 times/day keeping volumes under 500 mL; follow the scheduled bowel routine.
Why: Bladder distention is AD trigger #1 and impaction is #2 — the programs are emergency prevention, not just convenience. Chronic indwelling catheters cause bladder stones in ~3 of 10 users, which can present as leaking, pain, UTI, blood in urine, or an AD episode.
Do pressure reliefs every 15–30 minutes when seated (hold 30–90 seconds), reposition every 2–6 hours in bed, and inspect skin twice daily with a mirror; lift rather than slide; stay off any discolored area until it returns to normal.
Why: Pressure damage happens where the patient can’t feel it; shear from sliding and moisture from leakage accelerate it.
Report respiratory infection warning signs — fever and chills, cough, chest tightness, shortness of breath — and keep vaccinations current (influenza yearly, pneumococcal, COVID-19, and RSV for adults 75 and older or 50–74 at increased risk, per CDC).
Why: A weak cough retains secretions; pneumonia and sepsis remain the leading causes of death after SCI.
Mention sleep: loud snoring, waking up choking or gasping, unrefreshing sleep are worth reporting.
Why: Obstructive sleep apnea screening is part of the SCI respiratory watch.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The cues that matter: SBP 112 mm Hg above her baseline with bradycardia, a pounding headache, and a body split at the lesion — flushed and sweating above T4, pale and cool below — plus blurred vision and goosebumps. The empty drainage bag with tubing pinned under her thigh is not a plumbing note; it may be the whole story. The normal temperature and SpO₂ are background.

  2. 2
    Analyze cues

    A T4 injury is above T6, spinal shock resolved months ago, and the presentation is the textbook split: this is autonomic dysreflexia. A noxious stimulus below the lesion — most likely the bladder distending behind a kinked catheter — is driving unopposed sympathetic vasoconstriction; the brain’s corrective signals can’t cross the lesion, so vagal effects (bradycardia, flushing, sweating) appear only above it. It is not neurogenic shock — that is the acute-phase problem and runs in the opposite direction: hypotension with bradycardia.

  3. 3
    Prioritize

    The BP is the threat: uncontrolled AD can cause seizures, hemorrhagic stroke, MI, or death, so this outranks everything else on the unit right now. Sequence: sit her upright and loosen constrictive items → find and remove the trigger, bladder first → BP every 5 minutes → antihypertensive only if SBP stays above 150 after the trigger hunt. Nothing on that list waits for a provider callback.

  4. 4
    Generate solutions

    Keep her upright with legs dangling; loosen the abdominal binder and any tight clothing; straighten the catheter tubing and check for clogs and distention; if the bladder is flowing and BP holds, check for fecal impaction with lidocaine gel; have the rapid-acting antihypertensive ready — 2% nitroglycerin paste above the injury level or nifedipine 10 mg bite-and-swallow; escalate or call the rapid response if no trigger surfaces or the pressure won’t break.

  5. 5
    Take action

    She is already sitting — keep her fully upright, legs dependent, and loosen the binder now. Free the catheter tubing from under her thigh: urine floods the bag. Recheck BP in 5 minutes and every 5 minutes after. Report: "T4 SCI with autonomic dysreflexia — BP peaked 210/110 against a baseline of 98/60, trigger was a kinked catheter, drainage restored, BP trending down, monitoring q5min; will request nitroglycerin paste if SBP holds above 150."

  6. 6
    Evaluate

    Success looks like: BP stepping back toward her baseline over minutes, headache easing, flushing fading, drainage continuing. Keep the q5-minute checks until she is at baseline. If SBP sits above 150 despite a flowing catheter and clear bowel check — or no trigger is ever found — that is the antihypertensive-and-escalate branch, not a watch-and-wait. Afterward: document the episode, and close the loop with teaching, because the next episode will start at home.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Inpatient rehabilitation unit · 1030, mid-morning therapy break

A 26-year-old woman with a complete T4 spinal cord injury (ASIA A) from a motor vehicle collision 6 months ago. Indwelling urinary catheter. Baseline BP runs 98/60. She calls out from her wheelchair: "My head is pounding — something is wrong."

1030 vitals — BP 210/110 (baseline 98/60) · HR 52 · RR 18 · T 37.0 °C · SpO₂ 98% RA
Assessment — face and neck flushed and diaphoretic; arms sweaty; legs pale and cool; goosebumps below the chest; vision "a little blurry"
Lines — indwelling catheter; drainage bag empty × 3 hours; tubing runs under her thigh
Also noted — abdominal binder in place, snug; alert and oriented ×4
Q1 Select all that apply
The nurse answers the call light. Which findings support autonomic dysreflexia? Select all that apply.
  1. A. BP 210/110 against a baseline of 98/60
  2. B. Pounding headache with flushed, sweaty face and neck
  3. C. Pale, cool legs with goosebumps below the chest
  4. D. Temperature 37.0 °C
  5. E. Heart rate 52
  6. F. SpO₂ 98% on room air
Reveal answer & rationale
Answer: A, B, C, E
AD is defined against baseline — an SBP ≥ 20 mm Hg above it; 210/110 over 98/60 is a severe episode (A). The split presentation is the signature: flushing and sweating above the lesion (B) from compensatory vagal outflow that can’t cross, with pale, cold, vasoconstricted skin below it (C). Bradycardia (E) is the baroreceptor response — AD is hypertension with a slow heart. Temperature (D) and oxygenation (F) are normal here and don’t discriminate.
Q2 Multiple choice
What should the nurse do first?
  1. A. Sit her fully upright with legs dangling and loosen the abdominal binder
  2. B. Administer the PRN antihypertensive immediately
  3. C. Call the provider and wait for orders
  4. D. Recheck the blood pressure in 15 minutes
Reveal answer & rationale
Answer: A
The response sequence is fixed and starts with position + loosening: fully upright, legs dependent, everything constrictive off (A) — it lowers pressure immediately, needs no order, and the binder itself may be contributing. Antihypertensives (B) come fourth, only if SBP stays > 150 after the trigger hunt — dropping the BP first can mask an ongoing trigger. Waiting for orders (C) or 15 minutes (D) leaves her at stroke-level pressures; AD checks are every 5 minutes, and the first interventions are nursing-independent.
Q3 Put in order
Put the nurse’s actions in priority order:
  1. A. Check the catheter: straighten the kinked tubing and confirm drainage
  2. B. Sit her fully upright, legs dangling; loosen the binder and tight clothing
  3. C. If BP remains elevated, check for fecal impaction using lidocaine gel
  4. D. If SBP stays > 150 mm Hg, apply nitroglycerin 2% paste above the injury level as ordered
Reveal answer & rationale
Correct order: B → A → C → D
Both sources give the same order: 1) upright + loosen (immediate, order-free pressure relief), 2) bladder — the trigger in ~85% of cases, so restoring drainage is the most likely cure, 3) bowel — impaction is trigger #2, numbed with lidocaine so the exam doesn’t worsen the surge, 4) antihypertensive only for persistent SBP > 150, short-acting and above the level. Jumping to the bowel or the drug before the bladder skips the most probable fix; skipping the lidocaine turns an exam into a new trigger.
Q4 Multiple choice
The nurse straightens the tubing, urine flows freely, and 10 minutes later BP is 132/84 with the headache easing. The best next action is:
  1. A. Continue BP checks every 5 minutes until she returns to baseline, then document and reinforce prevention teaching
  2. B. Lay her flat to rest now that the episode has resolved
  3. C. Apply the nitroglycerin paste to prevent a rebound episode
  4. D. Discontinue monitoring — the trigger is gone
Reveal answer & rationale
Answer: A
The episode is breaking, not over: her baseline is 98/60, so monitoring continues q5min until she’s back there, then documentation and teaching — bladder and bowel programs are the prevention (A). Lying her flat (B) reverses the positional intervention that is helping. Nitroglycerin (C) is indicated only for SBP persisting > 150 — medicating a falling pressure invites hypotension in a patient whose baseline is low. Stopping monitoring (D) misses a recurrence or an unresolved second trigger.
Q5 Multiple choice
During discharge teaching, which statement shows the patient understood AD prevention?
  1. A. "If I get the pounding headache, I should lie down flat and rest until it passes."
  2. B. "I only needed to worry about this during the first month after my injury."
  3. C. "I’ll keep my bladder and bowel programs on schedule — a full bladder is the most common trigger, and constipation is next."
  4. D. "As long as my blood pressure reads normal, I know I’m not having an episode."
Reveal answer & rationale
Answer: C
Prevention is the programs: bladder distention drives ~85% of episodes and impaction is #2, so a consistent bladder and bowel routine — plus daily skin checks and avoiding tight clothing — is the shield (C). Lying flat (A) is the opposite of the response — sit up first. AD is uncommon in the first month and typically appears within the first year after spinal shock resolves, with susceptibility persisting (B). And because baseline BP in high SCI runs low, a "normal-looking" reading can already be dysreflexia (D) — the definition is relative to baseline.

Common questions

What causes spinal cord injury?
Common causes and risk factors include motor vehicle collisions (~38% of new cases — the leading cause), falls (~30% of new cases), older age with cervical spondylosis/stenosis — low-energy falls and hyperextension injuries (central cord syndrome), historically younger men, but a growing proportion of people with sci are older than 65, nontraumatic etiologies also disrupt motor, sensory, and autonomic pathways.
What are the early signs of spinal cord injury?
Early findings include Flaccid paralysis with absent reflexes (early), Hypotension + bradycardia with warm, pink skin (injury above T6).
Which findings should a nurse report immediately in spinal cord injury?
Report immediately: Hypotension + bradycardia with warm, pink skin (injury above T6), Declining respiratory effort or falling lung volumes in cervical injury, Pounding headache with flushing and sweating above the injury, cold pale skin below, Bradycardia during a hypertensive episode (rarely tachycardia) · nasal congestion · blurred vision · goosebumps, Autonomic dysreflexia, and others. These signal deterioration that needs rapid intervention.
What is the difference between spinal shock and neurogenic shock?
Spinal shock is neurologic: a temporary loss of all cord function below the injury — flaccid paralysis, absent reflexes, lost sensation and bowel/bladder control — resolving over days to weeks as reflexes return in sequence. Neurogenic shock is hemodynamic: with injuries above T6, lost sympathetic tone plus unopposed vagal tone produces hypotension with bradycardia and warm, pink skin. They are distinct entities that can occur at the same time.
Why is sitting the patient upright the first action in autonomic dysreflexia?
It is the fastest blood-pressure reduction available and requires no order. The full sequence is: sit upright with legs dangling and loosen tight clothing → check the bladder first (the trigger in ~85% of cases) → check the bowel → antihypertensive only if SBP stays above 150 mm Hg — with BP checks every 5 minutes throughout. Giving a drug first can mask an ongoing trigger.
Is methylprednisolone still given for acute spinal cord injury?
It is an option, not a standard of care. The 2017 AOSpine guideline suggests a 24-hour high-dose MPSS infusion may be offered within 8 hours of injury as a treatment option (weak recommendation) — and suggests not offering it after 8 hours, and never as a 48-hour infusion (more severe pneumonia in trials). The 2013 AANS/CNS guideline had recommended against it entirely, which is why the question stem’s timing details matter.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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