Treatment of Acute Injury of the Cervical Spine
Incidence
Aetiology
Anatomical Location
Pathophysiology
Cervical Instability - White & Panjabi
Spinal Cord Injury
Neurological Classification
Anterior Cord Syndrome
Central Cord Syndrome
Brown-Sequard Syndrome
Posterior Cord Syndrome
Cervical Root Syndrome
Immediate Patient Care Accident Scene Management
Hospital Management
Spinal Shock
Radiographic Examination
Immobilization and Realignment
Pharmacological Treatment
Physical Approaches
Acute Operative Treatment (Decompression)
TREATMENT OF ACUTE INJURY OF THE CERVICAL SPINE
Incidence
Aetiology
Anatomical Location
Pathophysiology
Cervical Instability - White & Panjabi
Spinal Cord Injury
Neurological Classification
Anterior Cord Syndrome
Central Cord Syndrome
Brown-Sequard Syndrome
Posterior Cord Syndrome
Cervical Root Syndrome
Immediate Patient Care Accident Scene Management
Hospital Management
Spinal Shock
Radiographic Examination
Immobilization and Realignment
Pharmacological Treatment
Physical Approaches
Acute Operative Treatment (Decompression)
Successful long-term treatment
- early recognition of injury
- prompt resuscitation
- stabilization of injury
- prevention of additional neurological injury
- avoidance of complications - improvement of emergency care
- ATLS -> better survival
- huge cost on society
Incidence
- 3.2 - 5.3 new spinal-cord injuries per 100,000 persons in USA
- late spring / summer
- highest prevalence between 15 – 24 yrs old
- second, smaller peak > 55 yrs old
- more frequent in boys & men
Aetiology
- MVA - 40 - 55%
- falls from a height 20 - 30%
- gunshots 10 - 20%
- sports-related activities 6% (primarily diving)
- varies with age
Anatomical location
- 60% cervical spine
- diving -> 97% involved C-spine (C5-6-7)
- MVA -> 65% (C1 & C5-6-7)
- fall from height -> 55% (C5-6-7)
- GSW -> 35% random distribution
Pathophysiology
Injury Mechanism
- Allen classified fracture-dislocations into six groups
- compressive flexion
- distractive flexion
- vertical compression
- compressive extension
- distractive extension
- lateral flexion
Cervical instability - White & Panjabi
- > 11° of angular rotation compared with adjacent levels
- 3,5 mm sagittal translation
- clinical signs of injury of medulla or nerve root
Spinal Cord Injury
- energy of impact -> micro-haemorrhage in cord -> biochemical cascade (inflammatory response) -> neurolysis
- spinal cord lesion progresses
- vascular theory (endothelial damage & thrombus formation -> ischemia)
- neuronal theory (injury of neurological membrane of axon -> cascade -> neurolysis)
Neurological Classification Complete
- no sensory or motor function caudad to level of injury
- spinal shock must be over (bulbocavernosus reflex returns)
Incomplete
- voluntary muscle power or sensation distal to level of injury
- check for sacral sparing!!!
- recovery possible
Anterior Cord Syndrome
- loss of neurological function in anterior 2/3 of spinal cord
- lost pain & temperature (spinothalamic) & motor function (corticospinal)
- retain proprioception, sense vibration & deep pressure
- usually flexion injury, fracture-dislocation or burst fracture
- prognosis poor
Central Cord Syndrome
- most common incomplete sy.
- hyperextension injury -> pinching of cord between ligamentum flavum & intervertebral disc or posterior vertebral body bone spurs
- mixed upper & lower-motor-neuron lesion
- flaccid paralysis of upper extremities (LMN lesion)
- spastic paralysis of lower extremities (UMN)
- sacral sparing
- recovery fair -> lower extremities better function than hand
Brown-Sequard syndrome
- unilateral damage to spinothalamic & corticospinal tracts
- ipsilateral motor paralysis
- loss of contralateral pain & temperature sensation
- penetrating trauma or unilateral facet fracture or dislocation
- good prognosis for walking & bladder/bowel control
Posterior Cord Syndrome
- rare syndrome
- loss of dorsal column function (deep pressure and proprioception)
- prognosis good - motor function preserved, but slapping gait
Cervical root syndrome
- isolated deficit in a specific nerve root
- with acute disc protrusion or facet dislocation
- expected to recover
- except if root avulsion (brachial plexus injury)
Immediate Patient Care Accident Scene Management
- recognition or suspicion of cervical injury -> immobilise
- delayed or missed diagnosis common
- concurrent head injury, unconsciousness
- ABC’s of resuscitation
- loss of sympathetic tone (bradycardia, hypotension) -> avoid overload
- patient in Trendelenburg position
- increases central venous return & reduces aspiration
- IV atropine (0.4 mg) to block vagal effects
Hospital Management
Resuscitation
- re-evaluate respiratory & circulatory status
- placement of IV lines, nasogastric tube & Foley catheter
- blood gases, electrolytes & Hb
Physical Examination
- accident history
- neurological examination
- cranial nerve function
- sensory & motor function
- rectal tone, reflexes (also bulbocavernosus reflex)
Spinal shock
- condition of altered spinal-cord conduction with transient loss of all motor, sensory & reflex function caudad to the injury
- persist for forty-eight hours and occasionally longer
- definitive neurological status cannot be assessed
- return of bulbocavernosus or anal wink reflex signals end
Radiographic Examination
- for all alert patients who have neck pain or tenderness
- if neurological deficit, polytrauma, or craniofacial injuries
- all intoxicated or unconscious patients
Standard Radiographic Study
- lateral radiograph (first), AP, odontoid
- swimmer’s view for cervicothoracic junction
- non-contiguous vertebral injuries
- associated thoracic, pelvic, or long-bone
Computerized Tomography
Magnetic Resonance Imaging
- excellent visualization of soft-tissue
- clear definition of canal compromise
- spinal cord signal
- inadequate cervical radiographic findings
- standard cuts 5 mm
- suspect areas 3mm cuts -> allows for sagittal reconstruction
Indicated
- patients with complete or incomplete neurological deficit
- neurological status deteriorated
- suspicion of disc retropulsion
Contraindicated
- pacemaker, aneurysm clips, metallic fragments in the eye or spinal cord
- severe claustrophobia
Tomograms
- fracture of the odontoid process
- extent of a facet or a lateral mass injury
Dynamic Radiographs
- strong suspicion of ligamentous instability -> “stretch test”
- moderate suspicion -> flexion test (Nash)
- low suspicion -> flexion-extension views
Immobilization and Realignment
- if instability -> skeletal traction (Gardner-Wells tongs, Cone’s callipers or halo ring)
- ten pounds (4.5 kilograms) of weight applied to the tongs
- monitored for any change in neurological condition
- post-traction alignment must be confirmed by a lateral radiograph
Closed reduction – if malalignment
- under the supervision of a physician
- patient awake & alert
- skeletal traction
- 10 pounds (4.5 kgs) for occiput
- additional 5 pounds (2.3 kilograms) for each vertebra
Attempts Discontinued
- when reduction achieved
- > 1 cm distraction occurs at site of injury or at any level
- neurological status deteriorates
- evident that reduction cannot be achieved
- once reduction achieved -> traction weight reduced
Pharmacological Treatment
High-dose methylprednisolone
- reduction of edema, anti-inflammatory effect & protection of neuronal membranes
- within 8 hrs
- 30 mg/kg IV bolus over 15 minutes
- followed by 5,4 mg/kg/hour infusion for 23 hrs
- complications included wound infection, GIT haemorrhage
GM-1 Ganglioside
- major component of cell membrane
- enhance neurological motor function at a one-year follow-up
- 100 mg IV daily for eighteen to thirty-two days
- must start within seventy-two hours after injury
- all patients also received a bolus of 250 mg of methylprednisolone followed by 125 mg IV every 6 hrs for 72 hours
- facilitation of neurite growth, modulation endotoxicity
21-Aminosteroids (Tirilizad Mesylate-U74006F)
- lack the drawbacks of the glucocorticoid-modulated systemic effects
- neuroprotective effect
Naloxone & Thyrotropin-Releasing Hormone
- opiate-receptor antagonists
- blockade of release of endogenous spinal-cord opioids
- reversal of systemic hypotension
- decreased spinal cord blood flow
- controversial
Vitamin E
- anti-oxidation effect & phospholipid membrane stabilization
- need for pre-injury treatment
Calcium-channel blockers
- stabilization of postinjury calcium influx -> minimizing injury cascade
- decreased post-traumatic spinal-cord ischemia in some models
Osmotic diuretics
- mannitol, glycerol & low-molecular weight dextran
- no evidence of clinical effectiveness
Physical Approaches
Hypothermia
- cooling of traumatized spinal-cord segments
- local decrease of spinal cord metabolism and oxygen consumption
- reduction of edema
- blockade of injury biochemical cascade
- controversy with regard to degree & duration of cooling
- experimental
Acute Operative Treatment (Decompression)
Benefits
- removal of mechanical compression
- correction of malalignment
- improved neurological circulation
Opponents
- maximum damage to spinal cord occurs at time of injury
- neurological deterioration if within five days after spinal cord injury
Absolute indication
- progressive neurological deterioration
- presence of irreducible canal compromise
- grossly unstable osseous or ligamentous injury patterns
Contraindication
- deteriorating neurological status w/out evidence of canal compromise
- suggests irreversible ascending necrosis of cord