Spinal shock and autonomic dysreflexia

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Spinal shock begins immediately after major cord injury and describes neurological suppression below the lesion: flaccid paralysis, areflexia and loss of some autonomic activity. It is distinct from circulatory neurogenic shock. Reflexes return in a variable sequence over days or weeks, often with the bulbocavernosus reflex among early signs. The phase can obscure the eventual pattern and completeness, so neurological classification is repeated rather than finalised from one early examination.

Autonomic dysreflexia usually occurs after spinal shock has evolved in people with a lesion at or above T6. A noxious stimulus below the injury sends afferent impulses into an isolated sympathetic cord, causing widespread vasoconstriction and abrupt hypertension. Descending inhibition cannot cross the lesion. Baroreceptors provoke vagal slowing and vasodilatation above the lesion, producing the characteristic pounding headache, flushing, sweating and sometimes bradycardia.

Recognition uses change from baseline. People with tetraplegia often have low resting pressure, so a rise of twenty to forty millimetres of mercury may be important before an apparently extreme absolute value. Ask the patient: experienced individuals often recognise the syndrome and know their trigger and rescue plan. Check headache, visual disturbance, anxiety, nasal congestion, sweating, piloerection, skin colour, pulse and pressure in both the initial and upright positions.

Immediate non-drug treatment reduces pressure and afferent input. Sit the person upright and lower their legs when spinal and transfer safety permit, loosen tight clothing, binder and compression devices and call for help. Recheck pressure every two to five minutes. Inspect the urinary catheter and tubing first because bladder distension is common. Do not flush or replace beyond competence; use local anaesthetic and the individual's protocol for instrumentation because the procedure itself can worsen the episode.

If urinary drainage is restored but pressure remains high, search bowel and skin systematically. Check constipation history, rectal medication, pressure areas, ingrown nail, footwear, burns, wounds, fracture, heterotopic ossification and recent procedures. Digital rectal examination and evacuation are delayed until pressure is controlled and local anaesthetic precautions are applied. Pregnancy and labour require simultaneous obstetric and spinal expertise because dysreflexia can mimic pre-eclampsia.

Persistent severe hypertension needs a rapid, short-acting medicine that can be stopped as the trigger resolves. Follow the patient's emergency card and local spinal protocol. Glyceryl trinitrate spray or paste is used in some UK pathways; ask about sildenafil, tadalafil or another phosphodiesterase-5 inhibitor because the combination can cause profound hypotension. Avoid long-acting agents that produce prolonged hypotension after the noxious stimulus is removed.

Observe after resolution for recurrence and for complications. New focal neurology, seizure, chest pain, pulmonary oedema or persistent headache requires emergency brain and cardiac evaluation. Document the trigger, urinary or bowel intervention, maximum pressure, medicines and response. Prevention includes reliable catheter supplies, bowel programme, skin care, pressure relief, equipment fit, patient-held emergency instructions and staff training across ambulance, primary, maternity and acute settings.

Key points

Spinal shock is flaccidity and areflexia below an acute cord lesion; neurogenic shock is hypotension from sympathetic loss; autonomic dysreflexia is later episodic hypertension, usually with lesions at T6 or above.
Know the person's baseline pressure because a clinically dangerous rise can occur before an absolute threshold appears striking by general-population standards.
For suspected dysreflexia, sit upright and lower legs if safe, remove tight garments and abdominal binders, and measure pressure and pulse every 2–5 minutes.
Check the urinary system first: inspect catheter tubing for kinks, bag position, blockage and displacement; use only the patient's trained irrigation or catheter-replacement pathway.
If urinary drainage is satisfactory, assess bowel, skin, pressure areas, footwear, fractures, wounds, infection and recent sexual, reproductive or procedural triggers.
Avoid digital rectal examination or manual evacuation until pressure is controlled and the spinal protocol's topical local-anaesthetic precautions are followed, because manipulation can intensify dysreflexia.
Use a prescribed rapid short-acting antihypertensive when trigger removal is insufficient and pressure remains dangerous; check PDE5-inhibitor exposure before giving nitrate.
Continue monitoring after resolution, document the trigger and successful intervention, replace emergency medication and update the patient's portable dysreflexia plan.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Acute spinal shock

Cord injury transiently suppresses reflex arcs below the lesion, producing flaccidity and areflexia that evolves over days to weeks as reflex activity returns.

Urinary trigger

Bladder distension from a kinked, blocked or displaced catheter, infection, stones or retention is the most frequent precipitant of autonomic dysreflexia.

Bowel and skin trigger

Constipation, impaction, fissure, pressure injury, burn, tight clothing, fracture and invasive procedures create noxious afferent input below the lesion.

Reproductive trigger

Sexual activity, ejaculation, menstruation, pregnancy, labour and urological or gynaecological procedures can precipitate dysreflexia in susceptible people.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Reflex suppression
After acute cord trauma, loss of descending and segmental activity produces temporary flaccid paralysis and absent tendon and autonomic reflexes below injury.
2
Disconnected sympathetic response
After reflexes return, afferent stimulation below a high lesion activates sympathetic vasoconstriction that cannot be adequately inhibited by descending pathways.
3
Baroreceptor response
The intact brain detects hypertension and increases vagal output, causing bradycardia and vasodilatation above the lesion while vasoconstriction persists below.
4
End-organ pressure injury
Abrupt severe hypertension damages cerebral, retinal and cardiac vessels and can cause seizure, haemorrhagic stroke, myocardial ischaemia, arrhythmia and pulmonary oedema.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Spinal shock pattern

New flaccidity and absent reflexes below acute injury with gradual reflex return describes spinal shock and does not itself determine final completeness.

Classic dysreflexia

Sudden headache with rising pressure, sweating and flushing above a high lesion and pale cool skin below strongly supports autonomic dysreflexia.

Urinary precipitant

No catheter output, suprapubic discomfort, kinked tubing, overfull bag or leakage around the catheter suggests bladder distension or obstruction.

Bowel precipitant

Missed bowel routine, abdominal discomfort, rectal loading or recent anorectal procedure becomes likely after urinary drainage is confirmed.

Skin and mechanical precipitant

Pressure damage, tight straps, wrinkles, footwear, burns, fractures and sexual or procedural stimulation may be painless below the lesion yet drive hypertension.

End-organ complication

Seizure, focal deficit, visual loss, chest pain, arrhythmia, hypoxia or persistent severe headache indicates hypertensive injury requiring emergency escalation.

Red flags requiring action

Sudden pounding headache, marked rise above usual low blood pressure, flushing or sweating above the lesion, nasal congestion, visual change and piloerection after a T6-or-higher cord lesion is autonomic dysreflexia until proven otherwise.
Blocked urinary catheter, distended bladder, bowel impaction, pressure injury, tight equipment, fracture, infection, sexual activity or labour are common triggers that must be identified without delaying pressure control.
Chest pain, severe bradycardia or tachyarrhythmia, seizure, focal deficit, reduced consciousness or persistent hypertension despite trigger removal requires critical-care escalation and investigation for end-organ injury.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line repeated blood pressure and rhythmFirst stepFirst line
Why
Confirm the hypertensive change and detect dangerous bradycardia or arrhythmia.
Interpretation and limitations
Measure every 2–5 minutes during acute management and compare with the person's baseline; improvement should follow posture and trigger removal quickly.
02
Bedside catheter-system inspection
Why
Identify the most common reversible dysreflexia trigger.
Interpretation and limitations
Check tubing, clamps, bag, sediment and position before invasive manipulation; use bladder scan if drainage and distension remain uncertain.
03
Urinalysis and culture
Why
Assess infection when urinary features or recurrent episodes suggest it.
Interpretation and limitations
Treat symptomatic infection in context; asymptomatic bacteriuria is common with long-term catheters and may not explain an acute blockage.
04
Bowel and skin assessment
Why
Find hidden afferent triggers after the urinary tract is addressed.
Interpretation and limitations
Inspect all pressure areas and equipment, review bowel record and use rectal examination only after pressure control with protocol precautions.
05
CT head or neurological imaging
Why
Exclude intracranial haemorrhage or another cause when symptoms persist or focal signs occur.
Interpretation and limitations
Do not delay initial dysreflexia actions for imaging; scan after stabilisation when headache, seizure or deficit does not resolve as expected.
06
ECG and cardiac biomarkers
Why
Assess chest pain, arrhythmia or suspected myocardial injury.
Interpretation and limitations
Autonomic pressure surges can cause ischaemia and pulmonary oedema even without typical pain below a high lesion.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Neurogenic shock

This is hypotension from sympathetic loss in acute high cord injury, not the later paroxysmal hypertension of autonomic dysreflexia.

Intracranial emergency

Subarachnoid haemorrhage, stroke and raised intracranial pressure cause severe headache and hypertension and require assessment when symptoms or pressure do not resolve with trigger treatment.

Sepsis or pain crisis

Infection and untreated pain alter heart rate, pressure and sweating, but lack the characteristic lesion-linked trigger and above-below autonomic pattern.

Essential hypertension

Chronic pressure elevation is less abrupt and trigger-dependent; many people with high spinal lesions normally have low resting blood pressure.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01ImmediateLower pressure and find bladder triggerFirst stepA susceptible person develops abrupt headache, autonomic signs and blood-pressure rise.

1Sit upright, lower legs when safe, loosen restrictive garments and call spinal and emergency support while recording pressure and pulse every few minutes.
2Ask the patient about their usual trigger and rescue plan, current catheter, bowel routine and recent medicines including PDE5 inhibitors.
3Inspect urinary tubing and bag, correct simple kinks or closed clamps and use trained local protocol for blockage, irrigation or catheter replacement.
4Give the prescribed rapid short-acting antihypertensive if pressure remains dangerously raised while trigger treatment continues.

02Second searchCheck bowel, skin and proceduresUrinary drainage is working but hypertension and symptoms persist.

1Inspect skin, pressure areas, clothing, braces, footwear and wounds and remove any obvious mechanical or thermal stimulus.
2Review constipation and the bowel record; delay digital examination until pressure is safer and use topical anaesthetic and protocol preparation.
3Consider fracture, infection, heterotopic ossification, sexual activity, menstruation, pregnancy, labour and recent invasive procedures.
4AlternativeEscalationEscalate persistent pressure to critical care and investigate end-organ or alternative neurological pathology.

03PreventionStop recurrencePressure and symptoms resolve after a trigger is treated.

1Continue observation for rebound hypotension or recurrent dysreflexia and document the maximum pressure, trigger, medicine and response.
2Correct the underlying catheter, bowel, skin or equipment problem and replace emergency medicines before discharge.
3PreferredUpdate the patient-held plan with baseline pressure, lesion level, preferred medicine, nitrate contraindications and emergency contacts.
4Educate carers and receiving teams and arrange spinal review for unexplained, frequent or pregnancy-associated episodes.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Provides rapid short-lived vasodilatation while the bladder, bowel, skin or other noxious trigger is identified and removed.

Glyceryl trinitrate sublingual spray for protocol-defined dysreflexia

If the individual emergency plan specifies GTN and pressure remains dangerously high, give 1–2 metered sprays of 400 micrograms each under the tongue while seated; repeat only under the monitored local protocol, not exceeding 3 sprays in 15 minutes.

Do not give with recent sildenafil, tadalafil or another PDE5 inhibitor, marked hypotension, severe aortic stenosis or nitrate allergy; continuous pressure monitoring is essential because trigger removal can cause a sudden fall.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Intracranial haemorrhage

Extreme pressure can rupture cerebral vessels, causing seizure, focal deficit, reduced consciousness and death even when the original trigger is simple.

Cardiac injury

Sudden afterload and autonomic instability can provoke dangerous bradyarrhythmia, tachyarrhythmia, myocardial ischaemia, ventricular dysfunction and pulmonary oedema.

Recurrent dysreflexia

Uncorrected catheter, bowel, skin or equipment problems cause repeated episodes and may create increasingly unpredictable daily risk.

Injury during spinal shock

Absent pain and reflexes obscure fractures, pressure damage and bladder overdistension while flaccidity increases handling and joint-position risk.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Measure pressure and pulse every two to five minutes during the episode and until stable after the trigger and any medicine are withdrawn.
Record urinary output, catheter interventions, bowel findings, skin and equipment checks and the sequence of symptom resolution.
Monitor for rebound hypotension, syncope and nitrate adverse effects after sitting, decompression and antihypertensive treatment.
Perform neurological and cardiac reassessment for persistent headache, visual change, seizure, focal deficit, chest pain or hypoxia.
Track recurrence frequency and triggers in the spinal service so catheter, bowel, skin and pregnancy plans can be revised.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Baseline pressure is low

A clinically important dysreflexic rise may look ordinary to staff unfamiliar with the person's usual spinal physiology.

Bladder comes first

Catheter obstruction is common, rapidly reversible and should be checked before more invasive bowel manipulation.

Rectal examination can worsen it

Control pressure and use the spinal protocol's local-anaesthetic steps before provoking further afferent input.

Bradycardia is not required

Vagal response varies, and tachycardia can occur; the defining danger is abrupt hypertension with a compatible lesion and trigger.

The emergency plan travels

A patient-held card prevents delay and contraindicated treatment in services that rarely manage autonomic dysreflexia.

11Common pitfallsFrequent interpretation and management errors.

01
Confusing flaccid spinal shock, hypotensive neurogenic shock and hypertensive autonomic dysreflexia.
02
Laying the person flat while severe dysreflexic hypertension continues.
03
Starting rectal evacuation before checking catheter drainage and controlling pressure.
04
Giving a nitrate without asking about sildenafil, tadalafil or related medicines.
05
Using a long-acting antihypertensive that persists after the trigger is removed.
06
Discharging after pressure falls without correcting the cause and updating the emergency plan.