Spinal Shock

Overview

Spinal shock is a complex neurophysiological phenomenon characterized by temporary loss of all neurological function below the level of a spinal cord injury (SCI), including flaccid paralysis, areflexia, and autonomic dysfunction. This state represents complete suppression of spinal cord activity caudal to the injury level, typically lasting days to months before gradual return of reflex activity. [1,2]

The condition is clinically critical because it masks the true extent of neurological injury during the acute phase, making accurate prognostication difficult. Approximately 50-60% of patients with acute traumatic SCI experience spinal shock, with higher incidence in complete injuries and cervical lesions. [3] Early recognition is essential to differentiate spinal shock from permanent spinal cord damage and to distinguish it from neurogenic shock, a distinct circulatory phenomenon that frequently coexists. [4]

Understanding spinal shock is fundamental to emergency medicine, neurology, neurosurgery, and critical care practice. The American Spinal Injury Association (ASIA) Impairment Scale, introduced in its current form in 1992 and revised most recently in 2019, provides the standardized framework for assessment during and after resolution of spinal shock. [5] The resolution of spinal shock marks a critical transition point where definitive prognostication becomes more reliable and rehabilitation strategies can be tailored appropriately.

Exam Detail: Pathophysiological Mechanisms

The precise mechanisms underlying spinal shock remain incompletely understood, but current evidence suggests multiple concurrent processes:

1. Neuronal Hyperpolarization: Loss of descending facilitatory input from supraspinal centers leads to hyperpolarization of spinal neurons below the lesion level. The sudden withdrawal of tonic excitatory input causes membrane potentials to fall below threshold for action potential generation. [6]

2. Neurotransmitter Depletion: Acute disruption of descending pathways results in depletion of excitatory neurotransmitters (particularly glutamate and substance P) at the spinal level, while inhibitory neurotransmitters (GABA, glycine) remain relatively preserved, creating an inhibitory-dominant environment. [7]

3. Loss of Descending Facilitation: The reticulospinal, vestibulospinal, and corticospinal tracts normally provide continuous excitatory drive to spinal motor circuits. Their sudden interruption removes this facilitation, rendering spinal reflex arcs temporarily non-functional despite intact segmental anatomy. [8]

4. Axonal Conduction Block: Primary mechanical injury creates a zone of axonal damage with demyelination and ionic dysregulation, producing conduction block that extends beyond the zone of anatomical transection. This functional block gradually resolves as ionic homeostasis is restored. [9]

5. Inflammatory Mediator Effects: The acute injury triggers massive release of inflammatory cytokines (IL-1β, IL-6, TNF-α) and excitotoxic substances that create a biochemical environment suppressing neuronal excitability in the peri-lesional zone. [10]

6. Microvascular Changes: Immediate post-injury hypoperfusion of spinal cord tissue below the lesion level, combined with loss of autoregulatory mechanisms, contributes to reversible ischemic dysfunction of otherwise intact neurons. [11]

Phases of Spinal Shock

Modern understanding recognizes four distinct phases, originally described by Ditunno et al. in 2004 based on longitudinal studies of reflex return: [12]

Phase 1 (0-24 hours): Areflexia/Hyporeflexia

• Complete loss of all reflexes below injury level
• Flaccid paralysis with absent muscle tone
• Absent bulbocavernosus reflex (BCR) - the key clinical marker
• Profound autonomic dysfunction
• May see transient minimal reflex activity in first 30-60 minutes post-injury (not true spinal shock)

Phase 2 (1-3 days): Initial Reflex Return

• Return of deep tendon reflexes begins, typically starting with delayed minimal responses
• BCR remains absent or becomes weakly present
• Cutaneous reflexes begin to emerge
• Continued autonomic instability

Phase 3 (1-4 weeks): Early Hyperreflexia

• Progressive increase in reflex responses
• Development of flexor spasms
• Emergence of Babinski sign
• Early autonomic dysreflexia may begin (in cervical/high thoracic injuries)

Phase 4 (1-12 months): Spasticity

• Full development of hyperreflexia and spasticity
• Established upper motor neuron syndrome pattern
• Return of mass reflex responses
• Bladder and bowel reflex activity established

The transition between phases is gradual and individual variation is substantial, influenced by injury level, completeness, age, and associated injuries.

Epidemiology

Spinal shock occurs as a consequence of acute spinal cord injury, affecting approximately 17,000 new patients annually in the United States, with global incidence estimated at 40-80 cases per million population. [13]

Risk Factors for Prolonged Spinal Shock:

• Complete anatomical transection (ASIA A)
• Cervical level injuries
• Older age (> 60 years)
• Severe associated polytrauma
• Hemodynamic instability requiring vasopressor support
• Delayed surgical decompression (> 24 hours post-injury) [16]

Mechanism of Spinal Injury (causing spinal shock):

• Motor vehicle accidents: 38%
• Falls: 30%
• Violence (predominantly gunshot wounds): 14%
• Sports/recreation: 9%
• Other: 9% [13]

Aetiology & Pathophysiology

Primary Causes

Spinal shock develops following acute disruption of spinal cord function. The most common etiologies include:

Traumatic (85% of cases):

• Vertebral fracture-dislocation with cord contusion/transection
• Hyperflexion, hyperextension, or axial loading injuries
• Penetrating trauma (gunshot, stab wounds)
• Severe ligamentous disruption without fracture (SCIWORA - Spinal Cord Injury Without Radiographic Abnormality, more common in children)

Non-Traumatic (15% of cases):

• Acute epidural hematoma (spontaneous or post-procedural)
• Spinal cord infarction (anterior spinal artery syndrome)
• Acute transverse myelitis (inflammatory, infectious, autoimmune)
• Acute epidural abscess with rapid cord compression
• Massive acute disc herniation with cord compression
• Iatrogenic (complication of spinal surgery or epidural anesthesia)
• Radiation myelopathy (acute onset rare, usually delayed) [17]

Pathophysiological Cascade

The development of spinal shock follows a predictable sequence:

1. Primary Injury (t=0): Mechanical disruption of axonal tracts and vascular injury at lesion level
2. Immediate Neural Suppression (minutes): Loss of descending excitatory drive causes hyperpolarization of spinal neurons
3. Secondary Injury (hours-days): Inflammatory cascade, excitotoxicity, free radical formation, and microvascular thrombosis extend damage
4. Functional Silence (days-weeks): Maximal suppression of spinal cord function below lesion
5. Gradual Recovery (weeks-months): Progressive return of reflex activity as spinal circuits reorganize

Exam Detail: Molecular Mechanisms of Reflex Suppression

Research utilizing animal models and human studies has elucidated several key molecular events:

Glutamate Receptor Downregulation: Following spinal cord transection, expression of NMDA and AMPA glutamate receptors on motor neurons below the lesion decreases by 40-60% within 72 hours, reducing excitatory responsiveness. [18]

GABA-ergic Disinhibition Paradox: While inhibitory GABAergic interneurons initially maintain function, the loss of descending noradrenergic and serotonergic modulation alters their firing patterns, contributing to motor neuron suppression. [7]

Potassium Channel Upregulation: Studies demonstrate increased expression of calcium-activated potassium channels (SK and BK types) in motor neurons during spinal shock, enhancing hyperpolarization and reducing excitability. [19]

Growth Factor Dynamics: Brain-derived neurotrophic factor (BDNF) levels decrease acutely below the lesion, reducing support for neuronal excitability. Recovery of BDNF expression correlates temporally with reflex return. [20]

Dendritic Retraction and Synapse Loss: Electron microscopy studies show acute dendritic retraction and synaptic stripping on motor neurons during spinal shock, with gradual re-establishment of synaptic contacts during recovery phases. [21]

Clinical Presentation

Cardinal Features

The clinical hallmark of spinal shock is the triad of flaccid paralysis, areflexia, and autonomic dysfunction below the level of injury. This presentation can mask the true neurological deficit and complicate initial assessment.

Neurological Features

Motor Findings:

• Flaccid paralysis of all muscles below the injury level
• Complete loss of voluntary movement
• Absent muscle tone (hypotonia)
• No response to painful stimuli below lesion
• Preservation of function at and above the injury level (unless multiple levels injured)

Reflex Findings:

• Absent deep tendon reflexes (knee jerk, ankle jerk, biceps, triceps) below lesion
• Absent bulbocavernosus reflex (BCR) - pathognomonic feature
  • Tested by squeezing glans penis/clitoris and palpating anal sphincter contraction
  • Absence indicates ongoing spinal shock
  • Return marks resolution of spinal shock (typically 24-72 hours, can be delayed)
• Absent cremasteric reflex
• Absent superficial abdominal reflexes
• Absent plantar responses (neither flexor nor extensor)

Sensory Findings:

• Loss of all sensory modalities below the injury level
• Loss of pain, temperature, touch, vibration, and proprioception
• Sensory level corresponds to injury level (may be 1-2 segments lower than motor level initially)
• May report bizarre sensations at the level of injury

Autonomic Dysfunction

Cardiovascular:

• Hypotension (particularly in cervical/high thoracic injuries T1-T6)
• Bradycardia (loss of sympathetic tone, unopposed vagal activity)
• Hypothermia (poikilothermia - inability to thermoregulate)
• Loss of compensatory tachycardia and vasoconstriction

Bladder and Bowel:

• Urinary retention with bladder atony (requires catheterization)
• Absent bladder sensation and voluntary control
• Fecal retention, absent rectal tone
• Paralytic ileus (in high thoracic/cervical injuries)

Sexual Function:

• Loss of erectile function
• Loss of genital sensation
• Absent ejaculation

Respiratory (in cervical injuries C3-C5):

• Diaphragmatic paralysis (if C3-C5 injured, phrenic nerve involvement)
• Loss of intercostal muscle function (T1-T12)
• Paradoxical breathing pattern
• Ineffective cough

Temporal Evolution

Clinical Pearl: Distinguishing Spinal Shock from Neurogenic Shock

These terms are frequently confused but represent distinct pathophysiological entities that often coexist:

Critical Clinical Point: A patient with cervical SCI will typically have BOTH spinal shock (neurological) AND neurogenic shock (cardiovascular). Neurogenic shock requires active treatment to maintain spinal cord perfusion pressure, while spinal shock is monitored for resolution to enable accurate prognostication.

Differential Diagnosis

The presentation of acute flaccid paralysis with areflexia requires systematic evaluation of multiple etiologies:

Must-Not-Miss Diagnoses

1. Neurogenic Shock (distinct from spinal shock)

   • Distinguishing features: Primarily hemodynamic (hypotension, bradycardia)
   • Requires T6 or higher lesion
   • Treated with vasopressors and fluids
   • Often coexists with spinal shock

2. Complete Spinal Cord Transection (permanent state vs. reversible spinal shock)

   • Cannot be definitively distinguished during spinal shock phase
   • Requires resolution of spinal shock (BCR return) for accurate ASIA grading
   • MRI may show cord transection or severe contusion

3. Epidural Hematoma (potentially reversible with urgent decompression)

   • May present identically to traumatic SCI
   • Requires urgent MRI
   • Surgical emergency if causing cord compression

Other Important Differentials

Distinguishing Spinal Shock from Permanent Cord Injury

A critical clinical challenge is determining whether neurological deficits represent reversible spinal shock or permanent cord damage during the acute phase. This distinction profoundly impacts family counseling and prognostication.

Features Suggesting Spinal Shock (Potentially Reversible):

• Presentation within hours of injury
• Complete areflexia (absent BCR, DTRs, plantar responses)
• Flaccid paralysis with no muscle tone whatsoever
• Lack of any reflex activity below lesion
• Autonomic dysfunction out of proportion to injury level
• Early phase (less than 72 hours) since injury

Features Suggesting Permanent Complete Injury (ASIA A After Spinal Shock Resolution):

• BCR has returned but no motor/sensory recovery
• Time elapsed > 72 hours with persistent complete paralysis after BCR return
• MRI shows complete anatomical transection or extensive hemorrhage > 4mm
• No sacral sparing despite resolution of spinal shock
• Absence of any voluntary movement or sensation below level after BCR return

Intermediate Features (Incomplete Injury - Better Prognosis):

• Any sacral sparing (S4-S5 sensation, voluntary anal contraction)
• Asymmetric motor or sensory findings
• Partial preservation of any modality below injury level
• MRI shows focal contusion without complete transection
• Specific incomplete cord syndrome patterns (see below)

Exam Detail: Anatomical Localization of Spinal Cord Syndromes

Understanding incomplete cord syndromes is essential for exam scenarios and clinical practice:

Central Cord Syndrome

• Mechanism: Hyperextension injury in elderly with cervical spondylosis
• Pattern: Arms > legs weakness (due to lamination of corticospinal tract)
• Sensory: Variable, often cape-like suspended sensory loss
• Prognosis: Best of incomplete syndromes, lower limbs recover first
• Spinal shock: Usually mild or absent

Anterior Cord Syndrome

• Mechanism: Flexion injury, anterior spinal artery occlusion
• Pattern: Complete motor loss, pain and temperature loss
• Preserved: Dorsal column (proprioception, vibration)
• Prognosis: Poor, less than 10% significant motor recovery
• Spinal shock: Common and may be profound

Brown-Séquard Syndrome (Hemicord Lesion)

• Mechanism: Penetrating trauma, lateral cord injury
• Pattern: Ipsilateral motor and proprioception loss, contralateral pain/temperature loss
• Classic presentation: Rare in pure form
• Prognosis: Best prognosis, > 90% regain ambulatory function
• Spinal shock: Typically mild, affecting ipsilateral side more

Posterior Cord Syndrome

• Mechanism: Rare, extension injury, vertebral artery compromise
• Pattern: Bilateral loss of proprioception and vibration
• Preserved: Motor function, pain and temperature
• Prognosis: Good motor recovery
• Spinal shock: Rare

Conus Medullaris Syndrome

• Level: T12-L2
• Pattern: Sudden onset, bladder/bowel dysfunction, saddle anesthesia, symmetric
• Reflexes: Mixed UMN/LMN, BCR absent or diminished
• Prognosis: Poor for bladder/bowel recovery

Cauda Equina Syndrome

• Level: Below L2 (nerve roots, not cord)
• Pattern: Asymmetric, radicular pain, areflexic bladder/bowel
• Reflexes: LMN pattern (areflexia is permanent, not spinal shock)
• Prognosis: Variable, depends on duration and severity of compression

ASIA Impairment Scale

The American Spinal Injury Association (ASIA) Impairment Scale is the gold standard for classification of spinal cord injury severity. [5] However, accurate grading cannot be performed during spinal shock due to areflexia and uncertain recovery potential.

ASIA Grades (Applied After Spinal Shock Resolution)

Key Examination Points

Motor Level:

• Defined as the lowest segment with normal strength (5/5) with segment above also 5/5
• 10 key muscles tested bilaterally (C5-T1, L2-S1)
• Scored 0-5 using standard MRC grading (total 100 points)

Sensory Level:

• Defined as most caudal dermatome with normal sensation
• 28 dermatomes tested bilaterally (C2-S4/5)
• Light touch and pinprick scored 0-2 (total 224 points)

Neurological Level of Injury (NLI):

• Most caudal segment with normal motor AND sensory function bilaterally
• May differ on right and left sides

Sacral Sparing (Critical for Incomplete Classification):

• Presence of any of the following indicates incomplete injury:
  1. Sensation at S4-S5 (perianal sensation)
  2. Voluntary anal sphincter contraction (deep anal pressure)
  3. Sparing of motor function more than 3 levels below motor level

Zone of Partial Preservation (ZPP):

• Only applies to ASIA A injuries
• Dermatomes and myotomes caudal to neurological level with some preservation

Clinical Pearl: Critical Timing of ASIA Assessment

The ASIA examination cannot be accurately graded during spinal shock because:

• Areflexia prevents assessment of true lower motor neuron vs upper motor neuron patterns
• Edema and inflammatory changes may suppress function in partially injured segments
• Cannot definitively determine completeness of injury

Standard Practice:

• Perform initial ASIA examination to establish baseline
• Document that patient is in spinal shock (BCR absent)
• Grade as ASIA A provisionally if no sacral sparing, but note "examination during spinal shock, final grade pending resolution"
• Repeat ASIA examination at 72 hours (when most spinal shock resolves)
• Definitive ASIA grading at time of BCR return
• Further assessment at discharge and 6 months post-injury

The 72-hour examination is prognostically important: patients with ASIA B or better at 72 hours have > 80% probability of significant motor recovery, while those with ASIA A at 72 hours (post-spinal shock resolution) have less than 5% probability of conversion to incomplete status. [22]

Investigations

Immediate Assessment (Emergency Department)

The initial evaluation prioritizes identification of injury, assessment of stability, and exclusion of surgically correctable lesions.

Primary Survey (ATLS Protocol):

• Airway: Cervical spine immobilization, assess for airway compromise
• Breathing: Respiratory rate, paradoxical breathing (cervical injury), oxygen saturation
• Circulation: Blood pressure, heart rate (expect bradycardia with hypotension in neurogenic shock)
• Disability: GCS, pupillary response, gross motor/sensory assessment
• Exposure: Complete examination with log-roll, rectal examination (tone, BCR)

First-Line Investigations

Advanced/Specialized Investigations

MRI Spine - Detailed Findings:

• T2-weighted: Hyperintensity indicates edema, contusion (poor prognostic sign if extensive)
• T1-weighted: Hemorrhage appears hyperintense
• STIR sequences: Sensitive for edema and ligamentous injury
• Gradient echo: Detects microhemorrhage and hemosiderin deposition
• Prognostic significance:
  • "Hemorrhage > 4mm in length on T2*: very poor prognosis (ASIA A likely permanent) [23]"
  • "Complete loss of signal at injury level: suggests complete transection"
  • "Focal contusion with surrounding edema: incomplete injury pattern, better prognosis"

CT Angiography:

• Indicated if vertebral artery injury suspected (cervical fracture through foramen transversarium)
• Identifies vascular injury requiring anticoagulation or intervention

Somatosensory Evoked Potentials (SSEPs):

• Limited utility in acute phase during spinal shock
• Absence of cortical response indicates complete sensory pathway disruption
• May be useful for intraoperative monitoring during decompression

Motor Evoked Potentials (MEPs):

• Not typically performed acutely
• Used in research settings to assess motor pathway integrity
• May predict motor recovery potential after spinal shock resolution

Monitoring During Spinal Shock

Continuous Parameters:

• Mean arterial pressure (MAP) - target ≥85-90 mmHg for 7 days post-injury [24]
• Heart rate - monitor for bradycardia
• Oxygen saturation - especially in cervical injuries
• Urine output - guide for adequate perfusion
• Temperature - poikilothermia common

Daily Assessments:

• Neurological examination (ASIA-based)
• Bulbocavernosus reflex - daily testing to detect resolution of spinal shock
• Bladder volumes (via ultrasound or catheter)
• Bowel function
• Skin integrity (pressure area prevention)

Weekly/Serial Assessments:

• Repeat MRI if neurological deterioration
• Pulmonary function tests (FVC, FEV1) in cervical injuries
• DVT surveillance ultrasound

Exam Detail: Mean Arterial Pressure Management in Acute SCI

The maintenance of spinal cord perfusion pressure is critical during the acute phase to prevent secondary ischemic injury. Current guidelines are based on prospective observational data:

Evidence Base:

• Hawryluk et al. (2015) demonstrated improved neurological outcomes with MAP 85-90 mmHg maintained for 7 days post-injury in a prospective cohort of 100 patients. [24]
• Retrospective studies show that hypotensive episodes (MAP less than 70 mmHg) correlate with worse ASIA grade outcomes
• Animal models demonstrate critical perfusion thresholds below which secondary injury propagates

AOSpine/CNS Guidelines (2017):

• Recommendation: Maintain MAP 85-90 mmHg for 7 days following acute SCI
• Level of Evidence: Level III (observational studies)
• Grade of Recommendation: Conditional recommendation (based on moderate-quality evidence)

Practical Implementation:

• Invasive arterial line for continuous MAP monitoring
• Adequate volume resuscitation (avoid over-resuscitation causing pulmonary edema)
• Vasopressor support (norepinephrine first-line) if volume alone insufficient
• Balance risk of cardiovascular complications vs. benefit to spinal cord perfusion
• Higher MAP targets may be harmful (cardiac strain, pulmonary edema)

Controversies:

• Optimal duration (7 days is consensus, but some advocate 5 days)
• Benefit in ASIA A injuries (where recovery unlikely) vs. incomplete injuries
• Risk-benefit in elderly patients with cardiovascular comorbidities

Management

Management of spinal shock is primarily supportive, focusing on spinal cord protection, prevention of secondary injury, monitoring for resolution, and complication prevention. Treatment of the underlying spinal cord injury (surgical decompression, stabilization) proceeds in parallel.

Acute Management (First 24 Hours)

Immobilization and Spinal Protection:

• Rigid cervical collar for cervical injuries
• Spinal board initially, then transition to bed with log-roll precautions
• Avoid excessive manipulation before imaging
• Maintain neutral spinal alignment

Hemodynamic Optimization:

• Target MAP 85-90 mmHg for 7 days [24]
• Large-bore IV access
• Volume resuscitation: Crystalloid (avoid excessive volumes)
• Vasopressor support if needed:
  • "Norepinephrine (first-line): 0.05-0.5 μg/kg/min"
  • "Dopamine (alternative): 5-20 μg/kg/min"
  • Phenylephrine (if tachycardia problematic)
• Invasive arterial line for continuous MAP monitoring
• Central venous access if large vasopressor requirements

Respiratory Management (Cervical/High Thoracic Injuries):

• Supplemental oxygen to maintain SpO2 > 95%
• Monitor for respiratory fatigue (decreased vital capacity, rising PaCO2)
• Early intubation if:
  • C5 or above injury (likely phrenic nerve involvement)
  • Vital capacity less than 15 mL/kg
  • Progressive respiratory acidosis (PaCO2 > 50 mmHg rising)
  • Inability to clear secretions
• Non-invasive ventilation may bridge some patients
• Tracheostomy consideration if prolonged ventilation anticipated (usually after 7-14 days)

Bladder Management:

• Indwelling urethral catheter initially
• Strict intake/output monitoring
• Prevent overdistension (bladder atony is universal during spinal shock)
• Transition to intermittent catheterization when stable if possible

Bowel Management:

• Nil by mouth if paralytic ileus present (check bowel sounds, abdominal X-ray)
• Nasogastric tube if gastric distension or vomiting
• Early enteral nutrition via feeding tube when ileus resolves (typically 48-72 hours)
• Bowel regimen to prevent fecal impaction (suppositories, digital evacuation initially)

Temperature Regulation:

• Expect poikilothermia (inability to thermoregulate)
• Monitor core temperature
• Warming blankets if hypothermic (less than 36°C)
• Cooling measures if hyperthermic (> 38°C)

Bradycardia Management:

• Asymptomatic bradycardia (HR 40-60): Monitor, no treatment required
• Symptomatic bradycardia (HR less than 40, or HR 40-60 with hypotension):
  • Atropine 0.5-1 mg IV (may be ineffective due to loss of sympathetic tone)
  • Temporary pacing if refractory and symptomatic
  • Aminophylline 2.5-5 mg/kg IV (off-label use, some evidence of benefit)

Surgical Management

Indications for Urgent Surgery (less than 24 hours):

• Acute epidural hematoma with cord compression
• Progressive neurological deterioration
• Unstable fracture requiring stabilization
• Gross malalignment requiring reduction

Indications for Early Surgery (24-72 hours):

• Incomplete injury with canal compromise > 50%
• Facet dislocation requiring reduction
• Fracture with instability

Evidence for Timing:

• Meta-analysis data suggest early decompression (less than 24 hours) may improve neurological outcomes in incomplete injuries, but no clear benefit in complete injuries (ASIA A) [16]
• STASCIS trial (2012): Early surgery (less than 24 hours) associated with improved ASIA grade conversion in cervical injuries [25]
• Optimal timing remains controversial; individualized decision-making required

Surgical Options:

• Anterior decompression and fusion (ACDF, corpectomy)
• Posterior decompression and instrumented fusion
• Combined anterior-posterior approach for highly unstable injuries

Evidence Debate: Methylprednisolone in Acute Spinal Cord Injury: Controversy and Current Practice

High-dose methylprednisolone (MP) for acute SCI is one of the most controversial topics in spinal trauma management.

Historical Background:

• NASCIS II (1990) suggested benefit of MP if started within 8 hours of injury: 30 mg/kg bolus, then 5.4 mg/kg/hr for 23 hours [26]
• NASCIS III (1997) suggested extended 48-hour infusion if started 3-8 hours post-injury
• These trials formed basis for widespread adoption in 1990s-2000s

Criticisms of NASCIS Trials:

• Post-hoc subgroup analysis (not pre-specified endpoints)
• Marginal clinical benefit (2-3 motor points on ASIA scale)
• Statistical methodological concerns
• High complication rates (pneumonia, sepsis, GI bleeding)
• Not placebo-controlled (comparison to naloxone, tirilazad)

Subsequent Evidence:

• Cochrane Review (2012): "The effectiveness of methylprednisolone remains unclear"
• concluded evidence does not support routine use [27]
• Systematic reviews show increased complications (infection, GI bleeding, death) outweigh marginal neurological benefits
• No neuroprotective benefit demonstrated in complete injuries (ASIA A)

Current Guidelines:

AOSpine/CNS 2017 Guidelines:

• "We suggest a treatment option of 24-hour infusion of high-dose methylprednisolone to be undertaken with the knowledge that evidence suggesting harmful side effects is more consistent than evidence suggesting clinical benefit."
• Level of Evidence: Level I (good quality RCT data exists, but results controversial)
• Grade of Recommendation: Weak recommendation AGAINST routine use

AO Spine 2022 Position Statement:

• Routine use NOT recommended
• May be considered in highly selected cases (incomplete injury, less than 8 hours, informed consent about risks)
• Use has declined dramatically since 2010s

Practical Current Practice:

• Most major trauma centers in UK, US, Australia: Do NOT use routinely
• If used, strictly within 8 hours of injury, informed consent, close monitoring for complications
• Never delay surgical decompression to administer MP
• Increased infection risk requires enhanced vigilance

Mechanisms (Theoretical):

• Lipid peroxidation inhibition
• Anti-inflammatory effects
• Preservation of blood-spinal cord barrier
• Reduction of edema

Bottom Line for Exams:

• Understand the controversy thoroughly
• Know that current practice is NOT to use routinely
• If examiner asks "Would you give methylprednisolone?", appropriate answer: "Current guidelines do not recommend routine use due to lack of clear benefit and increased complications. I would not administer it routinely, but would discuss with neurosurgical colleagues and family in context of specific case if incomplete injury presenting within 8 hours."

Monitoring for Spinal Shock Resolution

Daily Assessment:

• Bulbocavernosus reflex (BCR) testing
  • "Method: Squeeze glans penis/clitoris or pull Foley catheter, palpate anal sphincter contraction"
  • Return indicates resolution of spinal shock (typically 24-72 hours, range up to months)
  • Enables accurate ASIA grading
• Deep tendon reflexes (knee, ankle, biceps, triceps)
  • Initial absence, then gradual return
  • May become hyperactive as spasticity develops
• Muscle tone assessment
  • Flaccid initially
  • Progressive increase in tone (spasticity) after spinal shock resolves

Definitive ASIA Examination:

• Performed after BCR returns
• Repeated at 72 hours, discharge, 6 months, and 12 months
• Provides prognostic information

Complication Prevention

DVT Prophylaxis Timing:

• Controversy regarding timing due to bleeding risk
• Most protocols: Start enoxaparin after 72 hours if no contraindications
• If high bleeding risk (neurosurgery, active hemorrhage): Mechanical prophylaxis only initially (compression devices)
• IVC filter indicated if contraindication to anticoagulation and high risk (complete motor paralysis)

Respiratory Complications:

• Leading cause of death in acute cervical SCI
• Aggressive pulmonary hygiene essential
• Assisted coughing techniques (quad cough, mechanical insufflation-exsufflation)
• Early tracheostomy facilitates weaning and secretion clearance

Autonomic Dysfunction Management

Autonomic dysfunction is a cardinal feature of spinal shock and persists in varying degrees after resolution, particularly in injuries at T6 and above where sympathetic outflow is disrupted.

Cardiovascular Instability

Neurogenic Shock (Distinct from but Often Coexisting with Spinal Shock):

Neurogenic shock results from loss of sympathetic tone and unopposed parasympathetic (vagal) activity, manifesting as:

• Hypotension (systolic BP less than 90 mmHg, MAP less than 70 mmHg)
• Relative or absolute bradycardia (HR 40-60 bpm)
• Warm, dry skin below injury level (loss of sympathetic vasoconstriction)
• Poikilothermia (core temperature matches ambient temperature)

Management Protocol:

1. Volume Resuscitation:

   • Crystalloid 500-1000 mL bolus
   • Avoid excessive volumes (risk of pulmonary edema in setting of capillary leak)
   • Monitor urine output (target 0.5-1 mL/kg/hr)
   • Central venous pressure monitoring if large volumes required

2. Vasopressor Support:

   • First-line: Norepinephrine 0.05-0.5 μg/kg/min
     • Mixed α and β agonist
     • Addresses both peripheral vasodilation and cardiac inotropy
     • Titrate to MAP target 85-90 mmHg
   • Alternative: Dopamine 5-20 μg/kg/min
     • May worsen tachycardia
     • Risk of cardiac arrhythmias
   • Phenylephrine (pure α-agonist)
     • If significant tachycardia present
     • May worsen bradycardia (reflex)

3. Bradycardia Management:

   • Asymptomatic bradycardia (HR 40-60, adequate perfusion): Observe only
   • Symptomatic bradycardia:
     • Atropine 0.5-1 mg IV (often ineffective in high SCI)
     • Glycopyrrolate 0.2-0.4 mg IV
     • Aminophylline 2.5-5 mg/kg IV over 20 minutes (increases HR via adenosine antagonism)
     • Temporary pacing if refractory and hemodynamically unstable
   • Consider isoprenaline infusion (0.5-10 μg/min) for persistent symptomatic bradycardia

4. Duration of Support:

   • Neurogenic shock typically improves over 2-5 weeks
   • Vasopressor weaning as autonomic recovery occurs
   • Some patients require prolonged low-dose support

Orthostatic Hypotension

After acute phase resolution, orthostatic hypotension becomes a major rehabilitation barrier:

Clinical Features:

• Drop in systolic BP > 20 mmHg or diastolic > 10 mmHg on sitting/standing
• Symptoms: Dizziness, lightheadedness, syncope, fatigue, visual blurring
• Severely limits sitting tolerance and wheelchair mobilization
• May persist for months to years

Management Strategies:

• Compression garments: Abdominal binder, compression stockings (thigh-high)
• Graduated mobilization: Tilt table training, progressive sitting time
• Adequate hydration: 2-3 L/day fluid intake
• Salt supplementation: 6-9 g/day (increases intravascular volume)
• Pharmacological:
  • Fludrocortisone 0.1-0.4 mg daily (mineralocorticoid, increases Na+ retention)
  • Midodrine 2.5-10 mg TDS (α-agonist, increases peripheral vascular resistance)
  • Pyridostigmine 60 mg TDS (acetylcholinesterase inhibitor, improves ganglionic transmission)
• Avoid: Dehydration, prolonged recumbency, excessive heat

Temperature Dysregulation (Poikilothermia)

Loss of hypothalamic-spinal reflex pathways controlling thermoregulation:

Pathophysiology:

• Loss of sympathetically-mediated cutaneous vasoconstriction
• Loss of shivering thermogenesis below lesion level
• Inability to sweat below lesion level
• Core temperature passively follows ambient temperature

Clinical Implications:

• Hypothermia in cold environments (less than 20°C)
• Hyperthermia in warm environments (> 25°C) or with infection
• No fever response to infection below lesion level (may mask sepsis)

Management:

• Monitor core temperature regularly (rectal or esophageal)
• Environmental temperature control (thermoneutral zone 25-27°C)
• Warming blankets for hypothermia (less than 36°C)
• Cooling measures for hyperthermia (> 38°C): Fans, cool fluids, ice packs
• Educate patient/carers about seasonal clothing adjustments
• High index of suspicion for infection even without fever

Autonomic Dysreflexia (Typically Post-Spinal Shock, Chronic Phase)

While uncommon during acute spinal shock, autonomic dysreflexia (AD) may begin to emerge during late spinal shock phases (weeks 3-4) in injuries T6 and above. Recognition is critical as it represents a medical emergency.

Pathophysiology:

• Noxious stimulus below injury level triggers massive sympathetic discharge
• Intact spinal reflex arc causes unopposed vasoconstriction
• Baroreceptor response via intact vagus causes bradycardia
• But descending inhibitory pathways cannot modulate sympathetic outflow

Clinical Features:

• Sudden severe hypertension (SBP > 200 mmHg, may exceed 300 mmHg)
• Pounding headache (cardinal symptom)
• Bradycardia or tachycardia
• Flushing and sweating above lesion level
• Pallor and piloerection below lesion level
• Anxiety, apprehension, sense of impending doom
• Vision changes, nasal congestion
• Complications if untreated: Seizure, intracerebral hemorrhage, myocardial infarction, retinal hemorrhage, death

Common Triggers:

1. Bladder distension (most common 75-85%): Blocked catheter, UTI, bladder stones
2. Bowel distension: Fecal impaction, constipation, hemorrhoids, anal fissure
3. Cutaneous stimuli: Pressure ulcers, tight clothing, ingrown toenail, fractures
4. Iatrogenic: Cystoscopy, colonoscopy, sexual activity, labor and delivery

Emergency Management (Step-by-Step Protocol):

1. Sit patient upright (lowers BP via orthostatic effect)
2. Loosen tight clothing, remove constricting devices
3. Monitor BP every 2-5 minutes
4. Identify and remove trigger:
   • Check bladder: Flush catheter or catheterize if not catheterized
   • Check bowel: Digital rectal examination AFTER topical anesthetic (lidocaine gel), remove impaction gently
   • Inspect skin: Check for pressure areas, wounds, ingrown toenails
5. Pharmacological intervention if BP remains > 150 mmHg systolic:
   • Nifedipine 10 mg PO/SL (bite and swallow capsule) - onset 5-10 minutes
   • Glyceryl trinitrate 2% paste 1-2 inches topically - onset 5-15 minutes (easily removable)
   • Captopril 25 mg SL - onset 15-30 minutes
   • Hydralazine 10-20 mg IV - for refractory cases
6. Monitor for hypotension after trigger removal (risk of overshoot)
7. If initial measures fail: ICU admission, arterial line, continuous antihypertensive infusion

Prevention:

• Regular bowel program to prevent constipation
• Scheduled bladder emptying (intermittent catheterization Q4-6H)
• Prompt treatment of UTI
• Pressure area prevention
• Patient/carer education on recognition and triggers
• Medical alert bracelet
• AD action plan card carried by patient

Rehabilitation

Early Mobilization (After Stabilization):

• Begin passive range of motion within 24-48 hours
• Sitting tolerance in wheelchair as soon as hemodynamically stable
• Prevents contractures and pressure ulcers
• Tilt table for graduated orthostatic challenge in cervical/high thoracic injuries

Multidisciplinary Team:

• Spinal cord injury specialist/rehabilitation physician (coordinates care)
• Physiotherapy: Mobility, transfers, strengthening, respiratory care
• Occupational therapy: ADLs, adaptive equipment, home modifications assessment
• Speech and language therapy (if tracheostomy/swallowing issues)
• Psychology/psychiatry: Adjustment, depression (affects 20-30%), suicide risk assessment
• Dietitian: Optimize nutrition for wound healing, prevent obesity
• Social work: Discharge planning, equipment provision, benefits, housing
• Specialist nurses: Bowel/bladder management, skin care, equipment training
• Seating clinic: Wheelchair prescription, pressure mapping, cushion selection
• Orthotist: Bracing, splints, orthoses for functional positioning

Timing of Rehabilitation Milestones:

Functional Goals (Depend on Injury Level):

Respiratory Rehabilitation (Cervical Injuries):

• C1-C4 (Phrenic nerve involvement):
  • Mechanical ventilation via tracheostomy initially
  • Phrenic nerve pacing consideration (if nerve intact, stimulates diaphragm)
  • Non-invasive ventilation (NIV) weaning protocols
• C5-C8 (Intercostal paralysis):
  • "Assisted coughing techniques (quad cough: manual thrust on abdomen during cough)"
  • Mechanical insufflation-exsufflation devices (cough assist)
  • Incentive spirometry to prevent atelectasis
  • Glossopharyngeal breathing (frog breathing) technique for supplemental ventilation
• Monitoring:
  • Serial pulmonary function tests (FVC, FEV1)
  • Oxygen saturation monitoring
  • Annual influenza vaccination, pneumococcal vaccination
  • Early treatment of respiratory infections

Bladder and Bowel Programs:

Neurogenic Bladder Management:

• During spinal shock: Indwelling catheter (bladder areflexic, large capacity, overflow incontinence risk)
• After spinal shock resolution:
  • "Suprasacral injuries (above S2-S4): Reflex bladder develops"
    • Intermittent catheterization every 4-6 hours (target less than 400 mL volumes)
    • Alpha-blockers (tamsulosin 0.4 mg daily) to reduce sphincter tone
    • Anticholinergics (oxybutynin, solifenacin) if detrusor overactivity
    • Botulinum toxin injection into detrusor if refractory incontinence
  • "Sacral injuries (S2-S4): Areflexic bladder persists"
    • Intermittent catheterization every 4-6 hours
    • Valsalva/Credé maneuver (controversial, risk of reflux)
    • Indwelling catheter or suprapubic catheter if unable to self-catheterize
• Long-term monitoring:
  • Annual renal ultrasound (detect hydronephrosis)
  • Urodynamic studies (assess detrusor-sphincter dyssynergia)
  • Serum creatinine (renal function)
  • Treat UTI only if symptomatic (asymptomatic bacteriuria is universal)

Neurogenic Bowel Management:

• Goal: Predictable, controlled evacuation on schedule (prevent incontinence and autonomic dysreflexia)
• Upper motor neuron bowel (suprasacral injury):
  • Reflex defecation can be triggered
  • "Program: Every 1-2 days, 30 minutes after meal (gastrocolic reflex)"
  • Suppository (glycerin or bisacodyl) or mini-enema
  • Digital rectal stimulation to trigger reflex
  • Sitting position on commode (if safe transfers)
• Lower motor neuron bowel (sacral injury):
  • No reflex, requires manual evacuation
  • "Program: Every 1-2 days"
  • Manual disimpaction required
  • Stool softeners, adequate fluids, dietary fiber
• Pharmacological adjuncts:
  • Stool softeners (docusate)
  • Osmotic laxatives (macrogol/PEG)
  • Stimulant laxatives (senna, bisacodyl) - use sparingly
  • Avoid opiates (worsen constipation)

Sexual Function and Fertility:

Male Sexual Function:

• Erectile Function:
  • Psychogenic erections (lost in complete injuries)
  • Reflex erections (preserved if S2-S4 intact, absent in cauda equina)
  • "Management options:"
    • PDE5 inhibitors (sildenafil 50-100 mg, tadalafil 10-20 mg) - first-line, effective in 60-80%
    • Intracavernosal injection (alprostadil 5-20 μg) - if PDE5i fails
    • Vacuum erection devices
    • Penile prosthesis (inflatable or semi-rigid) - last resort
• Ejaculation:
  • Impaired in 90% of SCI men
  • Fertility reduced (abnormal sperm parameters)
  • "Assisted ejaculation techniques:"
    • Penile vibratory stimulation (PVS) - 60% success in injuries T6+
    • Electroejaculation (under sedation) - if PVS fails
    • Testicular sperm extraction (TESE) - if above methods fail
  • Sperm quality often impaired, may require IVF/ICSI for conception

Female Sexual Function:

• Fertility: Preserved (menstruation returns 3-6 months post-injury)
• Pregnancy possible but high-risk:
  • Autonomic dysreflexia during labor (T6+ injuries) - requires careful monitoring, epidural anesthesia protective
  • UTI risk increased
  • Pressure ulcer risk
  • Respiratory compromise if high cervical injury
  • Antenatal care in specialist center
  • Cesarean section rates higher (difficulty assessing labor)
• Sexual sensation: Variable depending on completeness and level
• Vaginal lubrication: May be impaired, water-based lubricants recommended
• Contraception: Consider carefully (hormonal contraception may increase DVT risk)

Psychological Adjustment:

• Predictable stages: Shock → denial → anger/depression → adjustment → acceptance (not linear)
• Depression: 20-30% at 1 year, higher suicide risk than general population
• Anxiety disorders: Common, particularly regarding health complications
• Body image issues: Profound impact on self-esteem and relationships
• Interventions:
  • Peer support (meeting others with SCI invaluable)
  • Cognitive behavioral therapy (CBT)
  • Antidepressants (SSRIs first-line) if clinical depression
  • Couple/family therapy
  • Goal-setting and achievement of milestones

Vocational Rehabilitation:

• Assessment of previous occupation and transferable skills
• Workplace adaptations assessment
• Phased return to work planning
• Retraining programs if previous job not feasible
• Disability employment support services
• Success rates: 30-40% return to paid employment by 5 years (higher in incomplete injuries, younger age, higher education level)

Prognosis

Prognosis in spinal cord injury depends critically on injury completeness, level, and ASIA grade after resolution of spinal shock. Assessment during spinal shock is unreliable.

Natural History

Spinal Shock Resolution:

• 50% resolve by 72 hours (BCR returns)
• 80% resolve by 4 weeks
• 95% resolve by 3 months
• Rare cases persist up to 12 months [12]

Neurological Recovery:

• Most recovery occurs within first 6 months
• Continued improvement possible up to 18-24 months
• Minimal further recovery beyond 2 years

Outcome by ASIA Grade (at 72 hours post-injury, after spinal shock resolution)

Predictors of Good Recovery:

• ASIA B, C, or D at 72 hours (after spinal shock resolution)
• Sacral sparing present
• Young age (less than 50 years)
• Incomplete injury on MRI (no complete cord transection)
• Early surgical decompression (less than 24 hours)
• Absence of significant medical comorbidities

Predictors of Poor Recovery:

• ASIA A at 72 hours after spinal shock resolution
• No sacral sparing
• Complete anatomical transection on MRI
• Hemorrhage > 4mm length on T2-weighted MRI [23]
• Older age (> 65 years)
• Delayed decompression (> 72 hours)
• Significant polytrauma

Long-Term Outcomes

Life Expectancy:

• High cervical (C1-C4, ventilator-dependent): 10-15 year reduction
• Other cervical injuries: 15-20 year reduction
• Thoracic injuries: 10-15 year reduction
• Incomplete injuries: Near-normal life expectancy

Leading Causes of Death:

• Pneumonia (acute phase and long-term)
• Sepsis (particularly from pressure ulcers, UTI)
• Pulmonary embolism (acute phase)
• Cardiovascular disease (long-term)
• Suicide (psychological burden)

Quality of Life:

• Highly variable, depends on social support, resources, complications
• Depression affects 20-30% at 1 year
• Employment rates: 30-40% return to work by 5 years post-injury
• Relationship strain common, divorce rates elevated
• Pain (neuropathic and musculoskeletal) affects > 60%

Functional Independence:

• Complete high cervical (C1-C5): Complete care dependence
• Mid-cervical (C6-C7): Partial independence with modifications
• Low cervical/thoracic (C8-T9): Full ADL independence, wheelchair mobility
• Below T10: Potential for ambulation with aids

Special Considerations

Pediatric Spinal Cord Injury:

• Better neurological recovery potential than adults
• SCIWORA (Spinal Cord Injury Without Radiographic Abnormality) more common
• Growth-related complications (scoliosis, hip dislocation)
• Neurogenic bladder management critical to preserve renal function
• Lifelong impact on development, education, socialization

Elderly (> 65 years):

• Poorer recovery potential
• Higher complication rates (pneumonia, pressure ulcers, cardiac events)
• Pre-existing cervical spondylosis increases injury severity
• Difficult rehabilitation due to comorbidities
• Lower functional independence rates

Key Guidelines

AOSpine and Congress of Neurological Surgeons (2017): Guidelines for acute SCI management

• Early surgical decompression (less than 24 hours) suggested for cervical SCI with cord compression
• MAP maintenance 85-90 mmHg for 7 days recommended
• Methylprednisolone NOT routinely recommended [24]

International Standards for Neurological Classification of SCI (ASIA, 2019 Revision):

• Standardized examination and grading system
• Defines motor level, sensory level, neurological level of injury, ASIA Impairment Scale
• Requires resolution of spinal shock for accurate grading [5]

UK NICE Guideline NG41 (2016): Spinal Injury: Assessment and Initial Management

• Imaging protocols for suspected SCI
• Spinal immobilization recommendations
• Transfer to specialist spinal injury center within 4 hours

Consortium for Spinal Cord Medicine (2008): Early Acute Management

• Respiratory management in cervical SCI
• Hemodynamic management protocols
• DVT prophylaxis timing and methods

Common Exam Questions

Viva Questions

1. "What is spinal shock and how does it differ from neurogenic shock?"

2. "How would you assess and manage a patient with acute C6 spinal cord injury in the emergency department?"

3. "When can you accurately determine the ASIA grade after spinal cord injury, and why?"

4. "Describe the phases of recovery from spinal shock and their clinical features."

5. "What are the indications for and controversies surrounding methylprednisolone use in acute SCI?"

6. "A patient with T6 spinal cord injury has HR 45 bpm and BP 85/50 mmHg. Explain the pathophysiology and your management approach."

7. "What is the significance of the bulbocavernosus reflex in spinal cord injury assessment?"

8. "Explain the difference between complete cord transection and spinal shock."

Viva Point: Opening Statement for Spinal Shock:

"Spinal shock is a temporary neurophysiological phenomenon characterized by complete loss of neurological function below the level of an acute spinal cord injury, manifesting as flaccid paralysis, areflexia, and autonomic dysfunction. It represents suppression of spinal cord activity due to sudden loss of descending input from supraspinal centers, typically lasting from days to weeks before gradual reflex return."

Key Facts to Mention:

• Affects 50-60% of acute SCI cases, more common in complete injuries [3]
• Distinguished from neurogenic shock (hemodynamic vs. neurological phenomenon)
• Hallmark sign: Absent bulbocavernosus reflex; return marks resolution
• Four phases of recovery (Ditunno): areflexia → initial reflex return → hyperreflexia → spasticity [12]
• Accurate ASIA grading only possible after resolution
• ASIA A at 72 hours post-spinal shock resolution: less than 5% conversion to incomplete [22]
• Management: Supportive, MAP 85-90 mmHg for 7 days, monitor for complications [24]
• Methylprednisolone NOT routinely recommended (AOSpine 2017) due to lack of clear benefit and increased complications [27]

Structured Approach to Acute SCI Patient:

1. Immobilization: Cervical collar, spinal precautions, neutral alignment
2. Imaging: CT spine (fracture/subluxation), urgent MRI (cord compression, hematoma)
3. Hemodynamics: Target MAP 85-90 mmHg (volume, vasopressors if needed)
4. Respiratory: Monitor for failure (C5+), early intubation if vital capacity less than 15 mL/kg
5. Neurological: Full ASIA examination, document spinal shock (BCR absent), repeat at 72 hours
6. Surgery: Early decompression (less than 24 hours) if incomplete injury with compression
7. Complications: DVT prophylaxis (enoxaparin after 72 hours), pressure area care, bladder catheterization
8. Rehabilitation: Early MDT involvement, goal setting based on injury level

Common Pitfalls:

• Confusing spinal shock with neurogenic shock
• Attempting definitive ASIA grading during spinal shock (areflexia makes this inaccurate)
• Failing to differentiate complete injury from ongoing spinal shock
• Administering methylprednisolone routinely (outdated practice)
• Not monitoring MAP targets adequately in acute phase
• Delayed DVT prophylaxis leading to PE

Common Mistakes

❌ Failing to distinguish spinal shock from neurogenic shock - These commonly coexist but are distinct entities requiring different management approaches

❌ Definitive ASIA grading during spinal shock - Areflexia makes accurate assessment impossible; must wait for BCR return

❌ Assuming ASIA A during spinal shock is permanent - Cannot confirm complete injury until spinal shock resolves

❌ Routine use of methylprednisolone - Current evidence does not support routine use due to increased complications without clear benefit

❌ Inadequate MAP maintenance - Target 85-90 mmHg for 7 days is evidence-based for reducing secondary injury

❌ Missing sacral sparing - Even minimal S4-S5 sensation or voluntary anal contraction changes classification from complete to incomplete

❌ Delayed DVT prophylaxis - SCI patients have 50-100% DVT risk without prophylaxis; must balance bleeding risk vs. thrombotic risk

❌ Neglecting respiratory monitoring in cervical injuries - Delayed respiratory failure is common; early intubation is safer than emergency intubation

Model Answers

Q: A 25-year-old man presents 2 hours after a motorcycle accident with complete motor and sensory loss below T6. BP 80/45, HR 50 bpm. Describe your management approach.

A: "This patient has acute spinal cord injury with features of both spinal shock (neurological) and neurogenic shock (hemodynamic). My immediate priorities are spinal protection, hemodynamic stabilization, definitive imaging, and preventing secondary injury.

Immediate Actions:

• Maintain spinal immobilization with cervical collar (until entire spine cleared)
• Establish large-bore IV access and commence volume resuscitation with crystalloid
• Insert arterial line for continuous MAP monitoring
• Target MAP 85-90 mmHg for spinal cord perfusion - if volume alone insufficient, commence norepinephrine infusion
• Urgent CT spine entire (confirm level, assess for fracture/subluxation, canal compromise)
• Urgent MRI spine (assess cord injury severity, exclude surgically correctable hematoma)

Neurological Assessment:

• Complete ASIA examination documenting motor level, sensory level, and test bulbocavernosus reflex
• Likely BCR absent indicating spinal shock - document this as examination cannot be definitively graded until resolution
• Test for sacral sparing (S4-S5 sensation, voluntary anal contraction) - critical for complete vs. incomplete classification

Definitive Management:

• Neurosurgical consultation for surgical planning (early decompression less than 24 hours if unstable fracture or cord compression)
• ICU admission for MAP monitoring, vasopressor management, neurological observations
• Indwelling catheter for bladder atony
• DVT prophylaxis planning (enoxaparin after 72 hours if no bleeding contraindications, mechanical compression initially)
• Pressure area care (turn every 2 hours, pressure-relieving mattress)
• NOT administering methylprednisolone as current evidence shows increased complications without clear benefit

Ongoing:

• Daily BCR testing to detect spinal shock resolution
• Repeat ASIA examination at 72 hours for prognostication
• Early MDT rehabilitation involvement (physio, OT, psychology)
• Complications surveillance (pneumonia, pressure ulcers, DVT)"

---

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