• Global incidence: approximately 250,000–500,000 new SCI cases per year worldwide (WHO estimate). Traumatic SCI incidence is roughly 10–80 per million population per year depending on region.
• Hong Kong: SCI incidence is approximately 20–30 per million per year. Queen Mary Hospital and Princess Margaret Hospital are the major SCI referral centres.
• Prevalence: due to improved survival, the global prevalence of SCI is rising; estimated 2–3 million people living with SCI worldwide.

• Bimodal distribution ^[2]:
  • Young adults (15–35 years): predominantly high-energy trauma (road traffic accidents, falls from height, sports injuries, assaults) ^[2]
  • Older adults (≥ 65 years): predominantly low-energy trauma in the setting of osteoporotic bone and pre-existing spinal stenosis (meaning a minor fall can cause cord injury in an already narrow canal) ^[2]
• Male:Female ratio ≈ 3–4:1 (young males are overrepresented due to high-risk behaviours and occupational hazards)

• Falls (most common overall, especially in children and the elderly) ^[3]
• Road traffic accidents (RTA) (most common cause of death < 40) ^[4][3]
• Assaults (knife/bullet injuries — these produce specific injury patterns such as Brown-Séquard syndrome) ^[1][5]
• Sports/recreation-related injuries (diving into shallow water, rugby, equestrian)
• In Hong Kong, falls from height (especially construction-related) and RTAs are the leading causes.

• 50% cervical ^[6] — this is the most mobile segment of the spine and has the least bony protection relative to the range of movement
• 15% associated with non-adjacent level injuries ^[6] — meaning if you find one spinal fracture, you must image the entire spine because there may be another fracture elsewhere
• 25% associated with other organ injuries ^[6] — polytrauma is the norm, not the exception

Polytrauma involves injuries to the spine in up to 30% of cases. Multiple spinal fractures occur in 3 to 5% — examine and XR the whole spine. ^[2]

• 33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused), 4 coccygeal (fused)
• The spinal cord ends at approximately L1-L2 (conus medullaris) in adults. Below this, the cauda equina (Latin: "horse's tail") — a bundle of nerve roots, not spinal cord — occupies the vertebral canal.
• Critical clinical implication: injuries above L1 cause spinal cord syndromes (UMN); injuries below L2 cause cauda equina syndrome (pure LMN) ^[7][8].

This is used for assessing stability of the lower cervical spine and thoracolumbar spine ^[3]:

Unstable fracture if 2/3 segments are disrupted ^[3]. This is the key principle — if two or more columns are broken, the spine cannot hold itself together and the cord is at risk of further damage from instability.

The cross-section of the spinal cord contains:

• Anterior spinal artery (ASA): supplies the anterior 2/3 of the cord (corticospinal tracts, spinothalamic tracts, anterior horns). This is a single vessel — a "watershed" area vulnerable to ischaemia.
• Paired posterior spinal arteries (PSA): supply the posterior 1/3 (dorsal columns).
• Segmental radicular arteries: feed into the ASA and PSA. The most important is the artery of Adamkiewicz (usually arises T9–T12 on the left) — occlusion causes devastating anterior cord syndrome.
• Venous drainage: internal vertebral venous plexus (Batson's plexus) — valveless, which is why metastases from prostate, breast, lung, kidney, and thyroid spread to the spine so readily.

The diaphragm is innervated by the phrenic nerve (C3-C5). This is clinically critical:

• Respiratory arrest if injury above C3 (loss of control of diaphragm → cannot breathe at all) ^[8]
• Diaphragmatic breathing if C5 or below (loss of control of intercostal muscles, but diaphragm preserved) ^[8]
• Paradoxical ventilation ^[6]: when intercostal muscles are paralysed, diaphragmatic contraction during inspiration draws the rib cage inward instead of expanding it — the chest and abdomen move out of phase.

Trauma is the commonest cause of acute paraplegia ^[1][7].

Common causes of paraplegia: Spinal trauma, Spinal tumours, Degenerative conditions, Infection, Spinal dysraphism ^[1]

These are the immediate mechanical forces applied to the cord at the moment of injury:

1. Compression: most common — fractured vertebral body or disc material pushes into the cord. Think of a burst fracture where bone fragments retropulse into the canal.
2. Contusion: cord is bruised by transient compression/impact. The cord bounces back to normal position but the internal damage is done — central haemorrhagic necrosis of grey matter with relative white matter sparing (explains central cord syndrome).
3. Laceration/transection: complete or partial cutting of the cord (e.g., knife or bullet wound — produces Brown-Séquard).
4. Distraction: the cord is stretched longitudinally beyond tolerance (e.g., seatbelt injuries, hangings).
5. Vascular disruption: tearing of vessels supplying the cord → ischaemia.

After the primary insult, a devastating cascade unfolds over hours to weeks:

Key points:

• Ischaemia is the main driver of secondary injury — the cord's blood supply is disrupted and autoregulation fails
• Excitotoxicity: damaged neurons release excessive glutamate → overactivation of NMDA receptors → massive calcium influx → cell death
• Inflammation: neutrophils infiltrate within hours, followed by macrophages — this initially worsens damage but is also necessary for debris clearance
• Oedema: vasogenic and cytotoxic oedema expand the zone of injury cranially and caudally
• Glial scar: astrocytes form a barrier (the "glial scar") that prevents axonal regeneration — this is why spinal cord injuries are so permanent

Secondary neurological injury occurs from instability due to bony and ligamentous injuries, and haematoma → this leads to delayed neurological deterioration ^[1]

Spinal shock has TWO meanings ^[1]:

Treatment of neurogenic shock: IV fluids and vasopressors/inotropes ^[1]

The bulbocavernosus reflex (squeeze glans penis or tug on Foley catheter → anal sphincter contraction) is the first reflex to return after spinal shock resolves. Its return signals the end of spinal shock — at that point, whatever deficits remain are likely permanent.

This is a chronic complication but worth understanding the pathophysiology now ^[8]:

• Lesion at or above T6 disrupts descending sympathetic regulation
• A noxious stimulus below the lesion (full bladder, constipation, skin pressure) generates a massive afferent signal
• This triggers a reflex sympathetic discharge below the lesion → vasoconstriction → severe hypertension (the brain cannot send inhibitory signals down through the damaged cord)
• The brain detects the hypertension via baroreceptors → sends vagal reflex → bradycardia + vasodilation above the lesion only (because the sympathetic inhibition cannot pass through the cord lesion)
• Result: paroxysmal HTN, throbbing headache, excessive sweating and flushing above the lesion, bradycardia, anxiety ^[8]

The American Spinal Injury Association (ASIA) Impairment Scale classifies the severity of SCI:

Sensory: test pinprick and touch in each dermatome Motor: test the 10 key motor functions ^[1][6]

Complete injury — prognosis is generally poor. Incomplete injury — prognosis highly variable. ^[1]

• Stable injury: ligaments not damaged ^[6]
• Unstable injury: ligaments disrupted ^[6]
• Mechanism of injury helps determine degree of stability ^[6]

Clinical signs of instability:

• "Step over spinous processes" for any tenderness, swelling or gap between spinous processes ^[6] — a gap indicates rupture of the interspinous ligament (i.e., unstable injury)

A 28-year-old man sustained a fall from height. On admission, he was fully conscious. He was unable to move his lower limbs. His upper limbs were normal. ^[1]

What other symptoms and signs should you look for? UMN/LMN signs; sensory level & segmental loss; saddle anaesthesia; AROU; lax anal tone; spinal shock ^[1]

What was the likely level of spinal cord injury? Likely below T1; see sensory level ^[1]

What was the extent of injury? Determined by ASIA classification — need to assess motor and sensory function systematically.

Detrusor sphincter dyssynergia (DSD) ^[8][9]:

• Cause: spinal cord injury, pontine stroke
• Mechanism: interruption of descending control by pontine micturition centre → failure of detrusor-sphincter coordination → synchronous contraction of both detrusor and sphincters
• Consequence: ↑↑urinary tract pressure → upper tract damage

This is different from the initial areflexic bladder during spinal shock (where the detrusor is flaccid). After spinal shock resolves:

• Suprasacral lesion → spastic (reflex) bladder with DSD
• Sacral lesion / cauda equina → flaccid (paralytic) bladder → overflow incontinence

Patients with long-term indwelling catheters have a 16–20x risk of developing SCC (squamous cell carcinoma) in the bladder (NOT UCC, because of chronic irritation by catheter in bladder) ^[10].

Spinal cord injury: sensory level, motor deficits, anal tone should be assessed as part of head injury evaluation ^[3]. In polytrauma, always assume a spinal injury until proven otherwise.

Long-term issues include: dysreflexia, neurogenic bladder, spasticity, contracture, and skin problems ^[1]

Differential diagnosis of back pain: Degeneration (spondylosis), Prolapsed intervertebral disc, Spinal stenosis, Cauda equina syndrome, Muscle/ligamentous injury (muscle strain), Fractures/injuries, Infection (TB spine, epidural abscess), Tumour (primary, metastases e.g. lung, breast, prostate), Inflammation (AS, PSA, RA), Extra-spinal causes/Referred pain (pancreatitis, AAA, uro/gynae causes, zoster) ^[3]

The main differential is:

• Traumatic SCI (obvious mechanism) — but you must also consider:
  • Delay in diagnosis due to: unconscious patient, head injury, alcohol intoxication, multiple distracting injuries ^[2]
  • Pre-existing pathology unmasked by minor trauma: cervical spondylotic myelopathy + hyperextension → central cord syndrome (elderly)
  • Pathological fracture: metastasis or osteoporosis → low-energy mechanism causing fracture → cord compression
  • Chronic condition with acute deterioration ^[1] — e.g., patient with ankylosing spondylitis whose rigid "bamboo spine" fractures like a long bone from a minor fall

The key differentiation is:

• Compressive (tumour, abscess, disc, haematoma) — requires urgent surgical decompression → MRI is the modality of choice; plain XR cannot make or exclude diagnosis of cord compression ^[16]
• Non-compressive (transverse myelitis, vascular, inflammatory, metabolic) — managed medically

D/dx of transverse myelitis includes: Non-inflammatory myelopathy by MRI spine (mechanical: disc herniation, vertebral body compression fractures...) ^[14]. The first step is always MRI to exclude compression.

The ASIA classification (IMPORTANT!) ^[3] is the internationally accepted system for classifying spinal cord injury severity. ASIA stands for American Spinal Injury Association; ISNCSCI stands for International Standards for Neurological Classification of Spinal Cord Injury.

Sensory: test pinprick and touch in each dermatome ^[6] Motor: in the 10 key motor functions listed ^[6]

The ASIA Examination systematically assesses:

Sensory examination — 28 dermatomes on each side (C2–S4/5), tested for:

• Light touch (tests dorsal column-medial lemniscal pathway)
• Pinprick (tests spinothalamic pathway)
• Each scored 0 (absent), 1 (impaired), 2 (normal) → maximum sensory score = 112 per side per modality

Motor examination — 10 key muscles on each side (5 upper limb, 5 lower limb):

Each scored 0–5 (MRC scale) → maximum motor score = 50 per side

Key definitions:

• Neurological level of injury (NLI): the most caudal segment with both normal sensory AND motor function (grade ≥ 3 motor + grade 2 sensory on both modalities)
• Sensory level: most caudal dermatome with normal sensation
• Motor level: most caudal myotome with ≥ 3/5 power, provided the segment above is 5/5

Sacral sparing — the critical determinant of complete vs incomplete:

• Test: voluntary anal contraction (motor) + S4-S5 light touch/pinprick (sensory) + deep anal pressure (sensation)
• If ANY of these are present → incomplete (ASIA B–D)
• If ALL absent → complete (ASIA A)

ASIA Impairment Scale ^[3]:

Grade	Type	Definition
A	Complete	No motor, No sensory, No sacral sparing
B	Incomplete	No motor, sensory only (preserved below level including S4-5)
C	Incomplete	> 50% of key muscles below the level have muscle grade < 3 (cannot raise arms or legs off bed)
D	Incomplete	≥ 50% of key muscles below the level have muscle grade ≥ 3 (can raise arms or legs off bed)
E	Normal	Motor and sensory function are normal

Mechanism of injury helps determine degree of stability ^[6]:

• Stable: ligament not damaged ^[6]
• Unstable: ligament disrupted ^[6]

On physical examination:

• "Step over spinous processes" for any tenderness, swelling or gap between spinous processes ^[6] — a palpable gap indicates rupture of interspinous ligament (i.e. unstable injury) ^[6]

Three-column theory (Denis) for thoracolumbar spine ^[3]:

• Unstable fracture if 2/3 segments disrupted ^[3]
• Anterior column: anterior 2/3 of vertebral body + disc + ALL
• Middle column: posterior 1/3 of vertebral body + disc + PLL
• Posterior column: posterior arch

You cannot definitively classify a patient as ASIA A (complete) during the spinal shock phase, because areflexia from spinal shock mimics complete injury. You must wait for the bulbocavernosus reflex to return (signalling end of spinal shock) before declaring an injury "complete" ^[3]:

The bulbocavernosus reflex (squeeze glans penis or tug Foley catheter → look for anal wink) is the first sacral reflex to return. Once it returns, if there is still no sacral sparing, the injury is truly complete.

CSF analysis: only if suspect transverse myelitis ^[8] May cause deterioration for cord compression! ^[8] — this is critically important. If there is any possibility of a compressive lesion, lumbar puncture is DANGEROUS because removing CSF below a block can cause the cord to herniate downward.

Send: R/M, cell count, C/ST, biochemistry, TB workup, viral studies, cytology ± VDRL, oligoclonal bands ^[8]

• Assess neurogenic bladder function (detrusor pressure, sphincter coordination)
• Important for long-term management of bladder in established SCI
• Shows detrusor sphincter dyssynergia (DSD) in suprasacral lesions

Collar & log roll to protect spine ^[1]

Extreme caution in transportation of patient in those likely to have spinal cord injury ^[6]

Why immobilise? An unstable fracture means the vertebral column cannot hold its alignment. Any movement (even routine nursing care) can cause further displacement → further cord compression → secondary neurological injury ^[1]. Immobilisation buys time until definitive imaging and treatment.

As detailed above: IV fluids + vasopressors, target MAP ≥ 85 mmHg × 5-7 days.

SCI patients have one of the highest rates of DVT/PE of any patient population (prevalence up to 80% without prophylaxis). Why? Loss of lower limb muscle pump + immobility + hypercoagulable state from trauma.

SCI patients are at high risk of stress-related mucosal disease (Curling-type ulceration) due to unopposed vagal stimulation to the stomach (particularly in high thoracic/cervical injuries where sympathetic innervation to the gut is lost).

Prophylaxis for AROU (urinary catheter) ^[6]

Neurogenic bladder is universal in acute SCI — the patient cannot sense bladder fullness (loss of afferent sensation) and cannot voluntarily initiate micturition (loss of descending control to sacral micturition centre). An over-distended bladder risks:

• Detrusor muscle damage (myogenic stretch injury)
• Vesicoureteric reflux → hydronephrosis → renal damage
• UTI

Contraindications to urethral catheterisation ^[21]:

• Absolute: urethral injury (blood at urethral meatus, high-riding prostate on DRE — typically associated with pelvic trauma)
• Relative: urethral stricture, recent urological surgery

If urethral catheterisation fails or is contraindicated → suprapubic catheterisation (SPC) ^[21].

• Neurogenic bowel → ileus initially, then constipation
• Regular bowel programme: scheduled glycerine suppositories, digital stimulation, stool softeners (docusate), adequate fibre intake
• Prevent faecal impaction (a common trigger for autonomic dysreflexia in chronic SCI)

Analgesics ^[6] — SCI pain is multifactorial:

High SCI (C3-C5) patients require:

• Early intubation if respiratory compromise
• Assisted cough techniques (quad cough — manual abdominal thrust synchronised with cough effort)
• Incentive spirometry and chest physiotherapy
• Tracheostomy if prolonged mechanical ventilation expected (facilitates weaning, bronchial toileting)
• Monitor vital capacity serially — a declining VC in a cervical SCI patient may indicate ascending oedema or deterioration

• Impaired thermoregulation ^[8] — patients become poikilothermic below the lesion
• Active warming/cooling measures as needed
• Avoid hypothermia (worsens coagulopathy in polytrauma) and hyperthermia (worsens secondary injury)

Methylprednisolone is associated with higher risk of morbidity and complications and should NOT be used. ^[6]

Methylprednisolone(?) ^[1] — the question mark in the lecture slides is deliberate.

The story: The NASCIS-II trial (1990) suggested that high-dose methylprednisolone (30 mg/kg bolus then 5.4 mg/kg/hr for 23 hours) within 8 hours of non-penetrating SCI improved motor recovery. This led to widespread use for decades ^[21].

The problem: Subsequent analysis and further trials (NASCIS-III, multiple Cochrane reviews) showed:

• The original NASCIS-II benefit was a post-hoc subgroup analysis (not pre-specified), making it statistically questionable
• Increased complications: wound infections, pneumonia, sepsis, GI haemorrhage, hyperglycaemia, avascular necrosis
• No mortality benefit
• No improvement in long-term neurological outcomes in well-designed replications

Current guideline (AO Spine 2017, AANS/CNS 2013, updated 2024): Routine use of methylprednisolone in acute SCI is NOT recommended. It may be considered as an option (not a standard) within 8 hours for non-penetrating SCI, but the risks likely outweigh the benefits.

Note the critical distinction: steroids are not recommended for traumatic SCI but are indicated for inflammatory myelopathy and metastatic cord compression — these are different diseases with different pathophysiology.

Surgical treatment in unstable injuries ^[6]:

Principles of Management — Surgical treatment if: Progressive neurological deficit; Myelopathy / Radiculopathy; Intractable pain ^[1]

Three goals of surgery ^[6]:

1. Decompression of spinal cord — relieve external pressure on the cord
2. Reduction of fractures or dislocation — restore normal alignment
3. Fixation of unstable spinal elements — prevent future displacement

Timing of surgery — The Debate:

Current evidence (STASCIS trial, 2012; AO Spine guidelines) supports early surgery (within 24 hours) for acute traumatic SCI with ongoing compression:

• Earlier decompression → better neurological outcomes in incomplete SCI (ASIA B, C, D)
• Reduced duration of ICU stay and complications
• For complete SCI (ASIA A), the benefit is less clear but early stabilisation still prevents complications and facilitates rehabilitation

The latest AO Spine consensus (2024) recommends decompression within 24 hours whenever safely feasible, particularly for incomplete injuries.

Non-surgical immobilisation only in stable injuries ^[6]:

Use: 2-3 months after injury to facilitate healing ^[6] Problems: pressure sores, weakening of muscles, soft tissue contractures, ↓pulmonary function, chronic pain syndrome ^[6]

Principles of Management — Spinal Tumours ^[1]:

• Steroids to reduce oedema
• Surgical resection within safety limit
• Intraoperative monitoring with motor evoked potential (MEP) and somatosensory evoked potential (SSEP)
• Adjuvant radiotherapy for some

For Metastasis ^[1]:

• Primarily ERT (external beam radiotherapy)
• Surgery for pain, instability, or lesions resistant to RT
• Palliative in nature

Conservative management: Physiotherapy, Analgesia ^[1] Surgical treatment if: Progressive neurological deficit; Myelopathy / Radiculopathy; Intractable pain ^[1]

• TB spine: anti-TB treatment (2HRZE / 9HR±E) ± surgery if neurological deficit or significant deformity ^[15]
• Epidural abscess: urgent surgical drainage + IV antibiotics (empiric: flucloxacillin + third-gen cephalosporin; adjust based on C/ST)

• IV methylprednisolone 1 g IV over 1 hour daily × 3-5 days ^[8]
• If refractory → plasma exchange (PLEX)
• Treat underlying cause (NMO → rituximab; MS → disease-modifying therapy; SLE → immunosuppression)

Neurogenic (spinal) shock in SCI down to T1 ^[8]:

• Cause: sympathetic signal disruption ^[8]
• Presentation: vasodilatation → hypotension, bradycardia, warm, flushed skin ^[8]
• Diaphragmatic breathing if C5 or below (loss of control of intercostal muscles) ^[8]
• Respiratory arrest if above C3 (loss of control of diaphragm) ^[8]

Why it happens: The sympathetic chain exits the cord from T1–L2. Any cervical or upper thoracic SCI disrupts this entire outflow → the body cannot constrict its blood vessels or increase heart rate → profound vasodilatory hypotension with paradoxical bradycardia (because the vagus nerve, which exits the brainstem and is NOT affected by the spinal injury, is now unopposed).

Why it's dangerous: Hypotension reduces cord perfusion → worsens secondary ischaemic injury. Bradycardia can progress to cardiac arrest in high cervical lesions.

Management: IV fluids and vasopressors/inotropes ^[1]. Target MAP ≥ 85 mmHg.

The most common cause of death in acute SCI, particularly for cervical injuries.

Specific respiratory complications:

• Atelectasis and pneumonia: the combination of poor cough, retained secretions, and immobility creates a perfect environment for lung collapse and lower respiratory tract infections. Pneumonia is the leading cause of death in both acute and chronic SCI.
• Pulmonary embolism: from DVT (see below) — a massive PE is a sudden, catastrophic complication.
• Ventilator dependence: high cervical SCI patients may require lifelong mechanical ventilation or diaphragmatic pacing.

Prevention: chest physiotherapy, assisted cough techniques (quad cough), incentive spirometry, early mobilisation where possible, suctioning of secretions, VTE prophylaxis.

SCI patients have the highest rate of DVT of any hospitalised population — up to 80% without prophylaxis.

Why? Virchow's triad is perfectly fulfilled:

1. Stasis: paralysed lower limbs → no calf muscle pump → blood pools in deep veins
2. Endothelial injury: trauma, surgery, catheterisation
3. Hypercoagulability: trauma-induced coagulopathy with elevated tissue factor and reduced fibrinolysis

Clinical problem: the patient cannot feel leg swelling or pain (sensory loss below the level) → DVT is often clinically silent until it presents as massive PE.

Prevention: LMWH + intermittent pneumatic compression + compression stockings from day 1. Continue for 2-3 months.

Spinal injury and operation are recognised causes of paralytic ileus ^[22].

Why? Acute SCI disrupts the autonomic innervation of the gut. The sympathetic (T5-L2) and parasympathetic (vagus for proximal gut, S2-4 for distal gut) inputs are both affected to varying degrees. In the acute phase, there is a generalised loss of coordinated peristalsis → the gut becomes atonic.

Clinical features: abdominal distension, absent bowel sounds, vomiting, inability to tolerate oral feeds.

Management: NPO, nasogastric tube drainage, IV fluids, correction of electrolytes (especially K⁺ and Mg²⁺). Usually resolves within days as autonomic reflexes partially recover.

Risk: a distended gut elevates the diaphragm → further compromises the already-limited respiratory function in a cervical SCI patient. This is a vicious cycle.

Anogenital issues: spastic or paralytic bladder, incontinence ± constipation and sexual dysfunction ^[8]

In the acute phase (during spinal shock), the detrusor muscle is areflexic — it cannot contract. The patient cannot sense bladder fullness (loss of afferent S2-4 pathways) and cannot voluntarily initiate voiding (loss of descending control). The result is painless AROU.

Why painless? Because the afferent sensory fibres from the bladder (travelling via S2-4) are also disrupted → the patient has no urge to void and no suprapubic discomfort. This contrasts with mechanical obstruction (e.g., BPH) where the patient is in significant pain because the sensory pathways are intact.

Management: indwelling urethral catheter in the acute phase → transition to intermittent clean catheterisation (ICC) once stable.

High SCI causes unopposed vagal (parasympathetic) stimulation to the stomach → excessive gastric acid secretion → stress-related mucosal damage.

Prevention: PPI (omeprazole) or H₂-blocker from day 1.

Others: pressure sores ^[8]

One of the most devastating and costly complications of SCI. Prevalence: 25–60% of SCI patients will develop a pressure ulcer at some point.

Why? Three factors converge:

1. Loss of sensation: the patient cannot feel the pain of prolonged pressure on a bony prominence → no reflexive repositioning
2. Immobility: cannot shift weight, roll, or adjust position
3. Autonomic dysfunction: impaired vasomotor control below the lesion → poor microcirculation → tissue is more vulnerable to ischaemic damage from external pressure

Common sites: sacrum, ischial tuberosities (sitting), greater trochanters, heels, occiput (lying on hard spinal board).

Pathophysiology: sustained pressure > capillary closing pressure (~32 mmHg) → local tissue ischaemia → necrosis → ulceration → secondary infection → osteomyelitis → sepsis → death.

Grading (NPUAP/EPUAP):

Prevention (far easier than treatment):

• 2-hourly turning/repositioning
• Pressure-relieving mattress (alternating air pressure)
• Regular skin inspection (especially over bony prominences)
• Adequate nutrition (protein, vitamin C, zinc for wound healing)
• Weight shifts every 15–30 minutes when seated in wheelchair

Treatment: offloading, wound debridement, moist wound dressings, VAC therapy, flap surgery for Grade III-IV ulcers, antibiotics if infected.

Spasticity ^[1] — this is a hallmark late complication of UMN-type SCI.

Pathophysiology: After spinal shock resolves (1-2 weeks), the loss of descending inhibitory input from the cortex and brainstem (reticulospinal, vestibulospinal pathways) results in anterior horn cells becoming hyperexcitable → exaggerated stretch reflexes → velocity-dependent increase in muscle tone.

Think of it this way: normally, the brain sends "calm down" signals to spinal motor neurons. When those signals are cut off, the motor neurons fire excessively in response to even minimal stretch stimuli.

Clinical features: increased muscle tone (clasp-knife pattern), hyperreflexia, clonus, flexor or extensor spasms (often painful), muscle contractures if left untreated.

Double-edged sword: some degree of spasticity can be useful — it maintains muscle bulk (preventing atrophy), aids venous return (reducing DVT risk), and can be used functionally for standing/transfers. But excessive spasticity causes pain, interferes with function, causes contractures, and triggers autonomic dysreflexia.

Management:

• Physiotherapy: stretching, range-of-motion exercises, standing programmes
• Oral medications: baclofen (GABA-B agonist — reduces presynaptic excitatory neurotransmitter release), tizanidine (α₂-agonist — reduces spinal excitatory interneuron activity), diazepam (GABA-A agonist — general CNS depression)
• Focal: botulinum toxin injections for localised problematic spasticity
• Intrathecal baclofen pump: for severe, diffuse, refractory spasticity — delivers baclofen directly to the CSF around the spinal cord at much lower doses than oral (avoids systemic side effects like sedation)
• Surgical: tendon lengthening, neurectomy (rarely needed)

Contracture ^[1] — fixed shortening of muscles, tendons, or joint capsules.

Why? Immobility + spasticity → muscles held in shortened position for prolonged periods → fibrosis and permanent shortening of soft tissues → the joint becomes fixed in one position.

Common patterns: hip flexion, knee flexion, ankle equinus (plantarflexion), wrist flexion.

Prevention: daily range-of-motion exercises, proper positioning, splinting, stretching programmes.

Treatment: serial casting, dynamic splinting, surgical release if fixed.

Autonomic dysreflexia (if lesion at or above T6) due to episodic autonomic fluctuation ^[8]

This is a medical emergency unique to SCI patients with lesions at or above T6.

Mechanism (from first principles) ^[8]:

1. A noxious stimulus below the level of injury (most commonly a full bladder, constipation, skin pressure, UTI, ingrown toenail)
2. Afferent signals travel to the spinal cord and trigger a massive reflex sympathetic discharge below the lesion → widespread vasoconstriction below the injury level → ↑↑BP
3. The brain detects the hypertension via intact carotid/aortic baroreceptors → sends strong vagal reflex → bradycardia and attempted vasodilation above the lesion
4. But the inhibitory sympathetic signals from the brain CANNOT pass through the damaged cord → the vasoconstriction below the lesion continues unchecked → BP keeps rising

S/S: paroxysmal HTN, throbbing headache, excessive sweating, flushing of skin, bradycardia, anxiety etc ^[8]

Why is it dangerous? Systolic BP can exceed 250–300 mmHg → risk of seizures, intracranial haemorrhage, retinal detachment, cardiac arrhythmia, myocardial infarction, death.

Why ≥ T6? Because the major splanchnic vascular bed (supplied by the greater splanchnic nerve from T5-T9) is the largest capacitance vessel system in the body. If the lesion is above T6, this entire bed participates in the unopposed sympathetic vasoconstriction → massive rise in BP. Lesions below T6 do not produce enough vasoconstriction to overwhelm the compensatory vasodilation above.

Emergency management:

1. Sit the patient upright (uses gravity to lower BP)
2. Loosen any tight clothing or constrictive devices
3. Identify and remove the trigger:
   • Check the bladder (blocked catheter? → flush or replace; no catheter? → catheterise)
   • Check the bowels (faecal impaction? → digital disimpaction with anaesthetic gel)
   • Check the skin (pressure ulcer, ingrown toenail, tight clothing)
4. Pharmacological BP control if trigger cannot be immediately identified or BP remains dangerously high:
   • Sublingual nifedipine (10 mg) — calcium channel blocker → rapid vasodilation
   • GTN paste (2% topical) — direct smooth muscle relaxant
   • IV hydralazine or labetalol for refractory cases

Anogenital issues: spastic or paralytic bladder ^[8]

This is one of the most functionally significant and dangerous long-term complications.

The two patterns (depending on level of lesion):

Detrusor sphincter dyssynergia (DSD) is the most dangerous pattern ^[8]:

• Cause: spinal cord injury, pontine stroke
• Mechanism: interruption of descending control by pontine micturition centre → failure of detrusor-sphincter coordination → synchronous contraction of both detrusor and sphincters
• Consequence: ↑↑urinary tract pressure → upper tract damage

Long-term complications of neurogenic bladder:

• Recurrent UTIs (the most common complication of SCI overall): stagnant urine + instrumentation + impaired immune responses below the lesion
• Bladder stones (stagnant, alkaline urine + catheter as nidus)
• Hydronephrosis and renal failure (from high-pressure DSD or chronic reflux)
• Squamous cell carcinoma of the bladder: chronic irritation from indwelling catheter → squamous metaplasia → SCC (16-20× risk) ^[10]

Management: intermittent clean catheterisation (gold standard), anticholinergics (oxybutynin) for overactive detrusor, alpha-blockers for sphincter relaxation in DSD, botulinum toxin injection into detrusor, augmentation cystoplasty for refractory cases, regular surveillance for bladder cancer in long-term catheter users.

Patients with spinal cord injuries who have long-term indwelling catheters have a 16-20× risk of developing SCC in the bladder (NOT UCC because of chronic irritation by catheter in bladder) ^[10]

Loss of autonomic and voluntary control of defecation. Two patterns mirror the bladder:

• Suprasacral (reflex) bowel: intact reflex arc → stool held by spastic sphincter → responds to rectal stimulation (suppositories, digital stimulation)
• Sacral (areflexic) bowel: flaccid sphincter → faecal incontinence, no reflex defecation

Complications: constipation (commonest), faecal impaction (trigger for autonomic dysreflexia), bowel obstruction, megacolon, haemorrhoids.

Management: scheduled bowel programme (same time every day/every other day), digital stimulation or glycerine suppositories, adequate fluid/fibre, stool softeners (docusate), prokinetics (metoclopramide if needed).

Sexual dysfunction ^[8]

Management: PDE5 inhibitors (sildenafil — "Viagra") for erectile dysfunction; electroejaculation or vibratory stimulation for fertility; psychological support and counselling.

Impaired thermoregulation ^[8]

Why? Thermoregulation depends on:

• Cutaneous vasodilation/vasoconstriction (sympathetic T1-L2 control)
• Sweating (sympathetic cholinergic fibres)
• Shivering (motor — requires functioning skeletal muscles)

All three are disrupted below the lesion → the patient becomes poikilothermic below the injury level (body temperature drifts with environmental temperature).

Clinical significance: patients are at risk of both hypothermia (in cold environments — cannot shiver or vasoconstrict) and hyperthermia (in hot environments — cannot sweat or vasodilate). Hyperthermia can worsen secondary cord injury in the acute phase.

Present in 60-80% of SCI patients. Two major types:

Management: pregabalin/gabapentin (first-line for neuropathic), amitriptyline/duloxetine, TENS, intrathecal drug delivery, psychological approaches (CBT), exercise.

Formation of mature lamellar bone in soft tissues (usually around paralysed joints — hip, knee, elbow).

Why? The exact mechanism is unclear, but involves aberrant mesenchymal stem cell differentiation in response to local inflammation + neurogenic signalling disruption. Incidence: 10-53% of SCI patients.

Clinical features: joint swelling, reduced ROM, warmth (can mimic DVT); if severe, complete ankylosis of the joint.

Diagnosis: elevated serum ALP (early), triple-phase bone scan (sensitive early), plain XR (once mature).

Prevention: NSAIDs (indomethacin), early mobilisation, low-dose radiation in high-risk patients.

Treatment: physiotherapy to maintain ROM; surgical excision once the bone is mature (wait ≥ 12-18 months — premature surgery leads to recurrence).

Why? Wolff's law — bone remodels in response to mechanical load. Paralysed limbs bear no weight → osteoclastic resorption exceeds osteoblastic formation → rapid bone loss below the level of injury (up to 40% bone mineral density loss in the first 2 years).

Consequence: fragility fractures from minimal trauma (transfers, physiotherapy). These fractures may go unrecognised because the patient cannot feel pain.

Prevention: standing programmes (standing frame), bisphosphonates (limited evidence in SCI), calcium and vitamin D supplementation, denosumab.

A late complication in 3-4% of SCI patients. A fluid-filled cavity (syrinx) develops within the injured cord, usually at or above the level of injury, and gradually expands.

Clinical features: progressive ascending neurological deficit (pain, weakness, sensory loss) months to years after the original injury — often presenting as a new "central cord syndrome" pattern.

Why? Altered CSF dynamics from arachnoid adhesions at the injury site → fluid is driven into the central canal → progressive cavitation.

Diagnosis: MRI — shows an intramedullary cystic cavity.

Management: observation for small/stable syrinx; surgical drainage (syringoperitoneal or syringopleural shunt) or untethering of scar tissue for progressive symptomatic syrinx.