CHAPTER 37

SPINAL CORD INJURY

• SCI is a catastrophic event causing loss of mobility or sensation.

• Can result from direct spinal cord injury or indirect damage to bones, tissues, or blood vessels.

• Mechanisms of injury:

  • Hyperextension

  • Hyperflexion

  • Rotation

  • Vertical compression (axial loading)

  • Penetrating injuries

  • Compression

• 12,000 new SCIs each year in US

  300,000 Americans living with SCI.

• Decrease life expectancy and increase mortality

• 30% rehospitalization rate

• Risk factors:

  • High-risk physical activities (speeding, alcohol, drug use).

  • Lack of protective gear in sports.

  • Falls in the elderly.

  • Age 16-18

  • Male

• Most common injury levels: C4, C5, C6, T12.

• Types of SCI:

  • Incomplete tetraplegia (47%)

  • Paraplegia (~20%)

  • Quadriplegia (~20%)

• Leading causes:

  • Motor vehicle accidents (38%)

  • Falls (31%)

  • Violence/gunshot wounds (15%)

  • Sports injuries (8%)

Pathophysiology

• SCI results from:

  • Concussion

  • Contusion

  • Compression

  • Tearing/laceration

  • Transection

  • Ischemia

• Spinal cord anatomy:

  • Upper motor neurons: Carry messages between brain and spinal cord.

  • Lower motor neurons: Transmit signals to the body (sensory + motor).

• Primary Injury: Direct trauma to neurons, glia, and blood vessels, or a penetrating trauma

• Mechanical injury such as shering and compression forces, Vasculature disruption, Cell death

• Disruption: Respiratory difficullties, neurogenic shock, inflammation, membrane compromise, alteration in ions and neurotransmitter levels

• Secondary Injury: Biochemical cascade causing further damage.

• Ongoing progressive damage that occurs after primary injury

• Ischemia: activation of the ischemic cascade, Excessive Ca and ROS production, Apoptosis

• Inflammation: Astrogliosis, lymphocyte infiltration of lesion, activated phagocytic monocytes

• Excitotoxicity: Excessice Ca2+ leading to ROS production and oxidative stress, Excessive glumate, Apoptosis.

Effects of SCI:

• Axonal injury: Some neurons may recover, others lead to paralysis.

• Swelling: Can cause anoxia (oxygen deprivation).

• Blood pressure drop: Interferes with neuron function.

• Inflammatory response:

  • WBCs invade damaged area.

  • Neutrophils, T cells, macrophages, monocytes contribute to scar formation.

• Excitotoxicity: Excessive glutamate release damages neurons.

• Free radicals: Contribute to cell damage and degeneration.

• Apoptosis: Leads to myelin loss and worsens function.

SCI Classification

1. Complete SCI

   • Total loss of motor & sensory function below injury level.

2. Incomplete SCI (some function preserved)

   • Central Cord Syndrome:

     Result: cervical spinal injuries, greaater motor impairement in the upper body compared to lower body. variable sensory loss below the level of injury

     • Most common incomplete cervical injury.

     • Etiology

     • Hyperextension injury leading to central cord swelling.

     • Common in elderly individuals with cervical spine degeneration.

   • Clinical Manifestations (Symptoms):

     • Motor loss:

       • Greater weakness in arms than in legs.

     • Bladder dysfunction (may include urinary retention or incontinence).

     • Variable sensory loss (extent depends on severity of injury).

   • Anterior Cord Syndrome:

   • Result: below injury level, motor paralysis and loss of pain and temperature sensation. Preprioception (position sense) touch and vibratory sensation preserved

     • Etiology

     • Acute anterior compression of the spinal cord.

     • Common causes:

       • Bony fragments from vertebral fractures.

       • Acute disk herniation.

   • Clinical Manifestations (Symptoms):

     • Loss of:

       • Motor function (paresis or paralysis) below the injury level.

       • Pain sensation.

       • Temperature sensation.

       • Crude touch and pressure.

     • Preserved (intact) functions:

       • Proprioception (position sense).

       • Fine touch and pressure.

       • Vibration sensation.

     • Additional symptoms:

       • Urinary incontinence.

   • Posterior Cord Syndrome:

   • Result: Below injury level, motor fuction preserved, loss of sensory function, pressure, strech and preprioception.

     • Etiology

       • Acute compression of the posterior spinal cord.

     • Clinical Manifestations

       • Loss of:

         • Proprioception (body position awareness).

         • Fine touch and pressure.

         • Vibration sensation.

       • Intact (preserved) functions:

         • Pain sensation.

         • Temperature sensation.

         • Crude touch and pressure

   • Brown-Séquard Syndrome:

   • Result: below injury level, motor weakness and paralysis on one side of the body(heiparaplegia), loss of sensation on the opposite side (hemianesthesia)

     • Cause: Hemisection of spinal cord (gunshot, stabbing, ischemia, infection, hemorrhage).

     • Etiology

       • Hemisection (one-sided damage) of the spinal cord.

       • Common causes:

         • Penetrating injuries (gunshot, knife wounds).

         • Other causes: Primary ischemia, infection, hemorrhage.

       Clinical manisfestation

       • Ipsilateral (same side as injury):

         • Loss of motor function (paralysis/paresis).

         • Loss of proprioception (body position awareness).

         • Loss of vibration sensation.

       • Contralateral (opposite side of injury):

         • Loss of pain sensation.

         • Loss of temperature sensation.

Clinical Manifestations

• Level of injury predicts affected body functions:

• Incomplete SCI, cause mixed manisfestation

  • Cervical (C1–C4): Can lead to quadriplegia, loss of respiratory function (C4 and above affect the phrenic nerve).

  • Above C3 total loss of respiratory function

  • C3- C5- respiratory insufficiency

  • Thoracic (T1–T12): Paraplegia, poor trunk control, variable bowel/bladder function.

  • injury above T6 leads to dysfuction of the SNS leads to neurogenic shock

  • Lumbar/Sacral (Below L1): Affects leg movement, bowel/bladder control, sexual function.

• Other effects of SCI:

  • Chronic pain- Noiceptive or neuropathic pain

  • Low blood pressure.

  • Inability to sweat below injury level.

  • Decreased temperature regulation

  • GI: neurogenic bowel and bladder

  • Integumentary: Risk for skin breakdown

  • Thermoregulation- Poikilothermia

level of Injury

Diagnostic

SCI is a medical emergency

Initial steps:

• If the patient is admitted with a suspected SCI (associated with trauma to the head or neck), the spine is immobilized (cervical collar, spine backboard)

• Transfer to a specialized spine center for expert care.

Thorough neurological exam

•CT scan

Preferred study for location and degree of injury and degree of spinal canal compromise

it determines the location, severity, and extent of injury (e.g., hematomas, cord compression)

•MRI

Soft tissue injury

Guide decisions about surgery

X-rays

Hard to see C7 and T1

Identifies vertebral fractures or misalignments.

Medical management

• SCI is irreversible once damage occurs.

• Treatment focuses on airway, breathing, circulation, and preventing further injury.

• Spinal shock monitoring is critical.

• High cervical injuries (C3-C5) require immediate ventilatory support due to phrenic nerve involvement.

• Maintain airway Patency

• Maintain blood pressure

• Spinal immobilization

Acute care

The loss of autoregulation and reduced sympathetic stimulation result in:

•Cardiac dysrhythmias

•Hypotension

•Decreased blood vessel tone

•Reduced cardiac output

Manage ABCs and vital signs

•Secure airway

•Keep SpO2 >92%

•MAP > 65mmHg

•SBP > 90mmHg

Drug therapy

•SCI disrupts autonomic regulation, leading to:

• Bradycardia, hypotension, arrhythmias (esp. in T6 and above injuries).

• Loss of vasomotor tone → blood pooling → hypotension.

Medications Used

• IV Fluids: Crystalloids, colloids, blood products.

• Vasopressors & Inotropes: Used if hypotension persists after fluids.

  • Dopamine, norepinephrine, epinephrine, vasopressin, dobutamine, phenylephrine.

• Oral Midodrine & Desmopressin: Reduce IV vasopressor use.

• Corticosteroids NOT routinely recommended due to risks (hyperglycemia, immunosuppression).

Nursing Considerations for Vasopressors

• Continuous BP monitoring (arterial line recommended).

• Large IV access (18G or central line) for administration.

• Monitor for ischemia (cold/mottled extremities, low pulses).

• Monitor fluid balance (risk of pulmonary edema).

Immobilization & Stabilization

• Early spinal reduction & immobilization prevents complications.

• Methods include:

• •Maintain neck in neutral position

  •Maintain traction at all times

  Sternal-occipital-mandibular immobilizer brace

  Halo vest

  •Stable thoracic or lumbar spine injuries

  Thoracolumbar sacral orthosis (TLSO)

  Jewett brace

  •Pin site care

  •Effects of immobility

  • Halo traction device (cervical immobilization with external fixation).

  • Gardner-Wells tongs (skull traction for spinal alignment).

  • Surgery (decompression, fusion, laminectomy) if needed.

Surgical Management

• Indications for surgery:

  • Spinal cord compression.

  • Progressive neurological deficits.

  • Penetrating injuries, fractures, or bony fragments.

• Surgical options:

  • Decompression laminectomy (relieves pressure from edema).

  • Anterior/posterior fusion (stabilizes the spine with bone grafts or rods).

• Decompression laminectomy

• Spinal fusion

Management Focus

• Early intervention, respiratory support, hemodynamic stabilization.

• Prevent secondary injury & optimize recovery.

Complication

1. Spinal Shock

• Occurs immediately after injury and can last days to week due to temporary loss of all spinal reflexes, loss of sensation, motor, and autonomic function below the injury, flaccid paralysis below level of injury.

• Clinical Signs:

  • Flaccid paralysis

  • Loss of deep tendon reflexes

  • Urinary & fecal retention

  • Absence of sweating (anhidrosis)

  • Paralytic ileus

• Duration: Can last from hours to weeks/months depending on reflex recovery.

2. Neurogenic Shock

• A form of distributive shock seen in brain, cervical, and upper thoracic injuries.

• Cause: Loss of sympathetic nervous system signals leads to vasodilation, bradycardia, and hypotension.

• Occurs in cervical or high thoracic (at or above T6) injury; can last 1 to 3 weeks

• Loss of SNS innervation causing unopposed parasympathetic response

• Pheriperal vasodilation

• venous pooling

• decreased CO

• Clinical Signs:

  • Severe hypotension less than 90mmHg

  • Bradycardia

  • Temperaturedysregulation

• Treatment:

  • IV fluids, vasopressors (norepinephrine, dopamine)

  • Atropine for bradycardia

3. Autonomic Dysreflexia (AD)

• Occurs in 48%-70% of SCI patients with injuries at or above T6.

• Triggered by noxious stimuli (e.g., bladder distension or UTI, full bowel, infection, tight clothing, pressure injuries).

• Mechanism:

  • Sympathetic surge → severe vasoconstriction → hypertension.

  • Brain attempts to lower BP but is blocked by spinal injury.

  • Parasympathetic system slows heart rate (bradycardia), but hypertension persists.

• Clinical Signs:

  • Severe headache

  • Hypertension (20-40 mmHg above baseline)

  • Bradycardia or tachycardia

  • Flushing & sweating above injury, pallor below

  • Nasal congestion, blurred vision, chest pain

• Potential Complications:

  • Seizures, MI, pulmonary edema, cerebral hemorrhage, death

• Treatment:

  • Elevate head of bed (first intervention)

  • Identify & remove trigger (e.g., empty bladder, check for pressure injuries)

  • Administer antihypertensives if needed

4. Halo Brace/Traction Complications

• Pin site infections (20% of cases)

• Skin breakdown from prolonged pressure

• Pin loosening or migration

• Swallowing difficulty

• Dural tears (potential CSF leaks)

• Nursing Care:

  • Monitor pin sites for infection (redness, drainage, pain).

  • Clean pin sites with normal saline (no hydrogen peroxide).

  • Ensure proper alignment to prevent pressure ulcers.

Respiratory Dysfunction

• Respiratory complications are the leading cause of acute and chronic morbidity and mortality in SCI

• During first 48 hours after SCI, edema may increase the level of dysfunction and cause respiratory distress

• Regular assessment

• Maintain ventilation

• Atelectasis, pneumonia, ARDS

• •Vagal response unopposed

Cardiovascular Instability

• Hypotension

• Bradycardia

• Decreased cardiac output

• Impaired tissue perfusion

• Orthostatic hypotension

• VTE prophylaxis

Gastrointestinal

• First 38 to 72 hours, GI tract may not function (paralytic ileus); requires NG tube

• Nutrition should be started within 72 hours; patient in hypermetabolic state

Bowel management

• Neurogenic bowel initially

• Start bowel program to prevent constipation; allow 30 to 60 minutes

• Daily rectal stimulant

• suppository or small-volume enema

• Adequate fluid and fiber intake

• Increased activity and exercise

Bladder management

• Immediately following SCI, urinary retention occurs from loss of autonomic and reflex control of bladder and sphincter; neurogenic bladder

• Overdistention

• Indwelling urinary catheter

• CAUTI – prevention

Skin care

• Pressure injury is the most common long-term complication

• Prevention

• Risk assessment

• Daily comprehensive visual and tactile examination

• Vulnerable areas:

• sacrum, ischia, trochanters, and heels

  check surgical incisions and skin under collars and braces

• Assess nutritional status

• Care positioning and repositioning every 2 hours

• Specialty mattresses