Spinal Cord Injury

Introduction

• The annual incidence of spinal cord injury in United States is 54 per million and almost 17,730 new cases of SCI are being reported annually.

• The traumatic spinal cord injury often results from a gunshot wound (10.4%), accidental trauma to head, neck and back region (31.5%), falling (25.3%) and spinal sports injuries (4.3%).

• Non-traumatic spinal cord injuries can have a range of etiologies like degenerative changes, infections (Staph. Aureus and Mycobacterium tuberculosis), malignancy of spine (Primary: multiple myelomas, Metastasis: prostate in male and breast in females are common etiologies), inflammation or congenital abnormalities

Pathophysiology

Acute traumatic spinal cord injury

• Primary injury (immediate) is due to trauma or and hemorrhage in the spinal cord that lead to ischemia, necrosis, and neuronal damage.

• Secondary injury (days to weeks), followed by primary injury, is due to inflammatory cascade that leads to edema, free radical formation, apoptosis, and release of neurotransmitters

Complete spinal cord transection

• Common causes include fracture of vertebrae, penetrating injury and expanding tumor.

• Bilateral at level of the lesion: Flaccid paralysis and atrophy

• Bilateral below the level of lesion:
• Spastic paralysis and absent superficial reflexes (corticospinal tract)
• Loss of the pain and temperature sensations (Lateral spinothalamic tract)
• Loss of light touch and pressure sensations two to three levels below due to different levels of decussations (anterior spinothalamic tract)
• Loss of the vibration, two-points discrimination and proprioception (posterior column).

Incomplete spinal cord syndromes

• Central Cord syndrome
• Involvement of cervical spines is the most common presentation. Elderly people are the high-risk population (hyperextension injury and fall)
• Associated with cervical spondylosis, syringomyelia and neuromyelitis optica.
• Symptoms are due to compression of spinothalamic and corticospinal tracts.
• Upper extremities are affected more than lower extremities due to the central location of nerves.
• Bladder dysfunction and some sensory loss.
• Cruciate paralysis: Rare condition involving cervico-medullary junction. Commonly due to trauma to C1 and C2 vertebrae with the involvement of upper limbs only.
• Syringomyelia: Formation of cyst within the spinal cord (syrinx) that can expand and destroy the spinal cord. Lower cervical and upper thoracic spine are commonly locations.
• Symptoms include bilateral loss of pain and temperature sensations in specific dermatomes (Cape like distribution).
• Associated with Chiari malformation.

• Brown Sequard syndrome (hemisection of spinal cord)
• Common etiologies include penetrating injury and expanding tumor of cervical spine (most common).
• Ipsilateral at the level of lesion: Hypotonic paralysis (anterior grey horn) and anesthesia (posterior grey horn)
• Ipsilateral below the level of lesion:
• Spastic paralysis and loss of superficial reflexes (corticospinal tract)
• Loss of vibration, two-point discrimination and proprioception (Posterior column)
• Contralateral below the level of lesion:
• Loss of pain and temperature sensations (Lateral spinothalamic tract)
• Loss of fine touch and pressure sensations two to three levels below due to different levels of decussations (anterior spinothalamic tract)

• Anterior cord syndrome:
• Anterior 2/3rd of spinal cord is affected due to a range of etiologies like ischemia (anterior spinal artery occlusion and severe hypotension), trauma, disc herniation and multiple sclerosis.
• Bilateral at level of lesion: Flaccid paralysis (Anterior grey horn)
• Bilateral below the level of injury:
• Spastic paralysis (corticospinal tracts)
• Loss of pain, temperature, light touch and pressure sensation (anterior and lateral spinothalamic tracts)
• Dorsal column: Sensations of two-point discrimination, vibration and proprioception are preserved bilaterally.

• Posterior cord syndrome:
• Posterior 1/3rd of spinal cord is affected
• Common causes include MS, trauma, and hyperextension injury.
• Ipsilateral loss of vibration, two points’ discrimination and proprioception.
• Pain, temperature, fine touch and pressure sensations (anterior and lateral spinothalamic tract) and motor functions (corticospinal tract) are intact.

Cauda equina syndrome

• Injury at the level of L2 or below due to various etiologies like disc herniation or compression due to tumor or abscess.

• LMN, sensory and autonomic nerves are involved.

• Common symptoms include pain radiating to legs, bladder and anal dysfunction, saddle anesthesia, impotence (male) and loss of ankle and knee reflexes.

• Conus medullaris syndrome: Injury between T12 to L2. Spontaneous pain is not common and loss of motor function and saddle anesthesia is symmetrical. Conus medullaris syndrome may be associated with cauda equina syndrome.

• Treatment: Surgical

Spinal shock syndrome

• Transient depression or loss of entire functions below level of the lesion.

• Anal sphincter reflex testing is used for diagnosis except in patient with lower spinal cord injury(S2-S4).

• Reflexes are absent

• Many patients recover in 24 hours, while others may take one to four weeks

Figure 2: Spinal Cord Transection Syndromes

Table 1: Upper Motor Neuron Lesion vs Lower Motor Neuron Lesion

Table 2: Localization of lesions (Cervical Region)

Table 3: Localization of lesions (Thoracic and Lumbosacral Region

Table 4: ASIA Impairment Scale

Physical examination

Motor system

• Bulk
• Compare both sides. Atrophy in LMN lesions.

• Tone
• Spastic paralysis (UMN lesion)
• Cog-wheel rigidity (Lesion of basal ganglia)
• Flaccid paralysis (LMN and sensory pathway lesions, cerebellar dysfunction and spinal shock)

• Power
• Common terminologies are Monoplegia (one limb involvement), Paraplegia (both lower limbs involvement), Diplegia (both upper limbs involvement), Quadriplegia (Both upper and lower limbs involvement).

• Reflexes
• Reflex arc is made up of afferent (sensory) and efferent (motor) limbs. Each reflex arc represents specific spinal nerve roots.

Sensory system

• Pain and temperature (lateral spinothalamic tract)

• Light touch and pressure (anterior spinothalamic tract)

• Sense of position and localization (spinocerebellar tract)

• Vibration and two-point discrimination (posterior column)

Table 5: Grading of Muscle Power

Table 6: Nerve Root values for reflexes

Table 7: Important points to consider during examination

Table 8: Acute Spinal Injury Management Steps

Workup

• Blood: CBC, Serum electrolytes, ABGs, LFTs, Serum amylase and lipase, Coagulation studies, blood typing and screening for alcohol

• Complete Urine and toxicology

• Chest X-ray

• ECG

• PFTs

• Imaging: CT/MRI spine

Management

ABCs

Airway

• Goals
• Prevention of atelectasis
• Removal of respiratory secretions
• Prevention of respiratory infections.
• Increased oxygen delivery to the spinal cord

• Monitor
• Respiratory rate, use of accessory muscles and paradoxical chest movements.
• Respiratory mechanics (NIF, FVC and TV)
• Oxygen saturation
• Changes in secretions
• Temperature
• Breathing adequately (15L/min oxygen) is required to maximize patient oxygenation and carbon dioxide elimination
• Monitor respiratory rate and effort.
• Atelectasis can be prevented by using higher tidal volume (10-15ml.kg).
• Use diaphragmatic pacer in quadriplegics during the weaning process.

• Ventilated patients:
• Pneumonia can be prevented by following VAP (Ventilator-associated pneumonia) protocol.
• Assist coughing every 4 hours
• Nebulized with 2.5mg Albuterol every 4 hours

• Non-ventilated patients:
• Spirometry every 1-2 hours
• Assist coughing
• EZ-PAP every 4 hours
• Nebulized with 2.5mg Albuterol every 4 hours

Circulatory collapse

• Goals
• Prevention of bradycardia
• Prevention of hypotension (MAP > 85mmHg and MAP > 65mmHg in incomplete and complete SCI, respectively.
• Stabilize hemodynamic parameters

• Hypotension
• Fluid challenge: 2L normal saline
• 0.05mcg/kg/min norepinephrine if BP doesn’t improve
• Check for serum cortisol if BP is still low. Start 100mg IV hydrocortisone every 8 hours.

• Bradycardia
• Assess airway blockage
• 0.5mg IV atropine if HR<40
• Consider albuterol, caffeine or external pacemaker for refractory bradycardia

• DVT prophylaxis
• LMW heparin (5000 units SQ)
• IV filter in high-risk patients.

Neurological management

• Evaluate both motor and sensory system.

• Localize the level of the lesion.

• Use rotorest bed for patients who need immobilization and log roll method to transfer the patients.

• Neurosurgery should be done within 72 hours for immediate support (bilateral locked facet for incomplete SCI)

• Gastrointestinal management:
• Goals:
• Prevention of paralytic ileus
• Diet management
• NPO until bowel sounds return
• Clear NG tube every 4 hours
• Peptic ulcers prophylaxis: Proton pump inhibitors (20mg omeprazole)
• Constipation:
• Irritant suppository
• Digital stimulation
• Abdominal massage
• Use of assistive devices to improve bowel evacuation.

• Continence:
• Catheterization due to neurogenic bladder
• Prevent catheter-associated infections
• Measure total fluid intake and urine volume per day

• Skincare:
• Apply the appropriate collar (cervical).
• Initiate protocol to prevent pressure ulcers

Rehabilitation

• In the cervical spine, reduction can be achieved and maintained with traction, whereas in the thoracolumbar spine recumbency and appropriately positioned bolsters are used.

• Emphasize on respiratory management such as deep breathing, assisted cough, chest physiotherapy, and abdominal support should be given.

• Patient education, functional independence training including bed mobility, transfer and wheelchair mobility.

• Preservation plus strengthening of the existing function of muscle by a range of motion exercises.

• Restoration of fine motor abilities and the learning of adaptive methods for mobility.

• Stretching of muscles with spasm plus pelvic exercise for bowel and bladder control.

• Strollers, crutches and orthoses training is considered essential for providing ambulation in later phases

Further Reading

• Bennett J, M Das J, Emmady PD. Spinal Cord Injuries. [Updated 2021 Aug 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560721/

• Zhang Y, Al Mamun A, Yuan Y, Lu Q, Xiong J, Yang S, Wu C, Wu Y, Wang J. Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review). Mol Med Rep. 2021 Jun;23(6):417. doi: 10.3892/mmr.2021.12056. Epub 2021 Apr 13. PMID: 33846780; PMCID: PMC8025476.

Bibliography

• American spinal injury association. (2019 ). International Standards for Neurological Classification of SCI (ISNCSCI) Worksheet. from https://asia-spinalinjury.org/international-standards-neurological-classification-sci-isncsci-worksheet/

• Kara Birrer, B. H., Amanda Giancarelli, Suzanne Ashworth, Rhonda Clancy, . (2018, September 10, 2018). ACUTE SPINAL CORD INJURY MANAGEMENT. Retrieved August, 22, 2019, from http://www.surgicalcriticalcare.net/Guidelines/Acute%20Spinal%20Cord%20Injury%202018.pdf

• Kristine H. O’Phelan, B. B., JW Kuluz (2017). Emergency Neurologic Life Support: Spinal Cord Compression. Neurocritical Care, 23(Suppl 2), 129-135. doi: 10.1007/s12028-015-0166-1

• Walker, J. (2009). Spinal cord injuries: acute care management and rehabilitation. Nursing Standard, 23(42), 47-56. doi: 10.7748/ns2009.06.23.42.47.c7055