Spinal Cord Injury

Pathophysiology Normal Spinal Cord Spinal cord begins at the foramen magnum in the cranium Cord ends at the L1-L2 vertebra level Spinal nerves continue to the last sacral vertebra The Human Spine

Spinal Cord Gray matter- cell bodies of voluntary and autonomic motor neurons White matter axons of ascending and descending motor fibers

Upper Motor Neurons UMN Originate in cerebral cortex Project downward Result in skeletal muscle movement Injury = SPASTIC paralysis Lower Motor Neurons LMN Originate at each vertebral level Project to specific parts of the body Result in movement /sensation Injury = FLACCID paralysis

Normal Spinal Cord Dermatones Skin innervated by sensory spinal nerves Myotome- muscle group innervated by motor neurons

Nervous System and the Spinal Cord ANS can be affected by SCI Sympathetic chains on both sides of the spinal column (T1-L2) Parasympathetic nervous system is the cranial-sacral branch (brainstem, S2-4)

Spinal Cord Protection Bones- vertebral column 7 Cervical 12 Thoracic 5- Lumbar 5- Sacral Discs- between vertebra

Spinal Cord Protection Internal and external ligaments Dura Meninges CSF in subarachnoid space allow for movement within spinal canal

Etiology of Traumatic SCI MVA- most common cause Other: falls, violence, sport injuries SCI typically occurs from indirect injury from vertebral bones compressing cord SCI frequently occur with head injuries Cord injury may be caused by direct trauma from knives, bullets, etc

Etiology of Traumatic SCI 78% people with SCI are male Typically young men – 16-30 Number of older adults rising (>61 yr) Greater complications

Spinal Cord Injury- SCI Compression Interruption of blood supply Traction Penetrating Trauma

Spinal Cord Injury Primary Initial mechanism of injury Secondary Ongoing progressive damage Ischemia Hypoxia Microhemorrhage Edema

Spinal and Neurogenic Shock Spinal Shock Decreased reflexes and loss of sensation below the level of injury Motor loss- flaccid paralysis below level injury Sensory loss- loss touch, pressure, temperature pain and proprioception perception below injury Lasts days to months

Spinal and Neurogenic Shock Due to loss of vasomotor tone peripheral pooling and decreased cardiac output Hypotension and Bradycardia Orthostatic hypotension and poor temperature control (poikilothermic)

How do you know spinal shock is over? Clonus is one of the first signs Hyperreflexia of foot Test by flexing leg at knee & quickly dorsiflex the foot Rhythmic oscillations of foot against hand clonus

Classifications of SCI Mechanism of Injury Skeletal and Neurologic Level Completeness (degree) of Injury Flexion Hyperextension Compression Flexion /Rotation

Classifications of SCI Mechanism of Injury Flexion (hyperflexion) Most common because of natural protection position. Generally cause neck to be unstable because stretching of ligaments

Classifications of SCI Mechanism of Injury Hyperextention Caused by chin hitting a surface area, such as dashboard or bathtub Usually causes central cord syndrome symptoms

Classifications of SCI Mechanism of Injury Compression Caused by force from above, as hit on head Or from below as landing on butt Usually affects the lumbar region

Classifications of SCI Mechanism of Injury Flexion/Roatation Most unstable Results in tearing of ligamentous structures that normally stabilize the spine Usually results in serious neurologic deficits

Levels of Function in Spinal Cord Injury Skeletal level Vertebral level where the most damage to the bones Neurologic level The lowest segment of the spinal cord with normal sensory and motor function on both sides of the body Levels of Function in Spinal Cord Injury

Classification of SCI- Level of Injury Spinal cord level When referring to spinal cord injury, it is the reflex arc level (neurologic)not the vertebral or bone level. the thoracic, lumbar & sacral reflex arcs are higher than where the spinal nerves actually leave through the opening of vertebral bone

Classifications of SCI Completeness (Degree) of Injury Incomplete Central cord syndrome Anterior Cord syndrome Brown-Sequard Syndrome Posterior Cord Syndrome Cauda Equina and Conus Medullaris

Classification of SCI Completeness (degree) of Injury Complete (transection) After spinal shock: Motor deficits- spastic paralysis below level of injury Sensory- loss of all sensation perception Autonomic deficits- vasomotor failure and spastic bladder

Classification of SCI Completeness (degree) of Injury Incomplete Central Cord Syndrome Injury to the center of the cord by edema and hemorrhage Motor weakness and sensory loss in all extremities Upper extremities affected more

Classification of SCI Completeness (degree) of Injury Incomplete Brown-Séquard Syndrome Hemisection of cord Ipsilateral paralysis Ipsilateral superficial sensation, vibration and proprioception loss Contralateral loss of pain and temperature perception

Classification of SCI Completeness (degree) of Injury incomplete Anterior Cord Syndrome Injury to anterior cord Loss of voluntary motor, pain and temperature perception below injury Retains posterior column function (sensations of touch, position, vibration, motion)

Classification of SCI Completeness (degree) of Injury incomplete Posterior Cord Syndrome Least frequent syndrome Injury to the posterior (dorsal) columns Loss of proprioception Pain, temperature, sensation and motor function below the level of the lesion remain intact

Classification of SCI Completeness (degree) of Injury incomplete Conus Medullaris Injury to the sacral cord (conus) and lumbar nerve roots Cauda Equina Injury to the lumbosacral nerve roots Result- areflexic (flaccid)bladder and bowel, flaccid lower limbs

Clinical Manifestations of SCI Skin: pressure ulcers Neuro: pain sensory loss upper/lower motor deficits autonomic dysreflexia Cardio: dysrhythmias spinal shock orthostatic hypotension,

Respiratory- GI GU Musculoskeletal decrease chest expansion, cough reflex & vital capacity diaphragm function-phrenic nerve GI stress ulcers paralytic ileus bowel- impaction & incontinence GU upper/lower motor bladder sexual dysfunction Musculoskeletal joint contractures bone demineralization osteoporosis muscle spasms muscle atrophy pathologic fractures para/tetraplegia

Common Manifestation/Complications Upper and Lower Motor Deficits Upper motor deficits result in spastic paralysis Lower motor deficits result in flaccid paralysis and muscle atrophy

Common Manifestations/Complications Spinal cord injuries are described by the level of the injury– the cord segment or dermatome level Such as C6; L4 spinal cord injury Terms used to describe motor deficits Prefix: para- meaning two extremities tetra- or quadra- all four extremities Suffix : -paresis meaning weakness -plegia meaning paralysis Quadraparesis means what?

Immediate Care Emergency Care at Scene, ER & ICU Transport with cervical collar Assess ABC’s; O2; tracheotomy/vent IV for life line NG to suction

Diagnostic Studies for SCI X-ray of spinal column CT/MRI Blood gases

Therapeutic Interventions Medications IV methylprednisolone (Solu-Medrol) within 8 hrs to decrease cord edema

Therapeutic Interventions Stabilization/ Immobilization Traction- Gardner-wells tongs Halo Casts Splints Collars Braces

Therapeutic Interventions Surgery for SCI Manipulation to correct dislocation or to unlock vertebrae Decompression laminectomy Spinal fusion Wiring or rods to hold vertebrae together

Nursing Management Assessment HEALTH HISTOY Description of how and when injury occurred Other illnesses or disease processes Ability to move, breathe, and associated injury such as a head injury, fractures

Nursing Management Assessment PHYSICAL EXAM LOC and pupils- may have indirect SCI from head injury Respiratory status- phrenic nerve (diaphragm) and intercostals; lung sounds Vital signs Motor Sensory Bowel and bladder function

Nursing Management Assessment Motor Assessment Upper Extremity Movement, strength and symmetry Hand grips Flex and extend arm at elbow- with and without resistance

Nursing Management Assessment Motor Assessment Lower Extremity Flex and extend leg at knee with and without resistance Planter and dorsi flexion of foot Assess for Clonus

Nursing Management Assessment Sensory assessment With the sharp and dull ends of a paperclip have the individual, with their eyes closed identify Use the dermatome as reference to identify level C6 thumb; T4 nipple; T10 naval

Nursing Problems/Interventions 1.Impaired mobility 2.Impaired gas exchange 3. Impaired skin integrity 4. Constipation 5. Impaired urinary elimination 6. Risk for autonomic dysreflexia 7. Ineffective coping

1. Impaired Physical Mobility provide assistance as needed to keep alignment; teach patient Care traction, collars, splints, braces, assistive devices for ADL’s Flaccid paralysis- use high top tennis shoes or splints to prevent contractures. Remove at least every 2 hrs for ROM (active ROM best)

1. Impaired Physical Mobility Spastic Paralysis Prevent spasms by avoiding; sudden movements or jarring of the bed; internal stimulus (full bladder/skin breakdown; use of footboard; staying in one position too long; fatigue Treat spasms by decreasing causes; hot or cold packs; passive stretching; antispasmodic medications Assess skin break down thrombophlebitis; remove TED hose(compression stockings) at least every shift

1. Impaired Physical Mobility Prevent/treat orthostatic hypotension Abdominal binder, calf compressors, TED hose when individual gets up Assess BP, especially when rising Teach use of transfer board Assist Physical Therapy with tilt table as individual gradually gets use to being in an upright position

2. Impaired Gas Exchange Phrenic nerve (C3-5) controls the diaphragm bilaterally. If nerve is nonfunctioning then individual is ventilator dependent. Thoracic nerves control the intercostals muscles for breathing and abdominal muscles aide in breathing and coughing

2. Impaired Gas Exchange Respiratory rate, rhythm, depth, breath sounds, respiratory effort, ABG’s, O2 saturation Need for ventilatory assistance tracheotomy, ventilator Quad cough (assistive cough) as needed

3. Impaired Skin Integrity Change position frequently Protection from extremes in temperature Inspect skin at least 2x/day especially over boney prominences Avoid shearing and friction to soft tissue with transfers Removal of TED hose every 8 hours Nutritional status

4. Constipation Bowels rely more on bulk than on nerves Stimulate bowels at the same time each day. Best after a meal when normal peristalsis occurs Individual may progress from Dulcolax suppository to glycerin then to gloved finger for digital stimulation Assess bowel sounds prior to giving food for the first time– paralytic ileus!

5. Impaired Urinary Elimination Flaccid bladder (lower motor neuron lesion) No reflex from S2,3,4 Automatic empting of bladder Urine fills the bladder and dribbles out Need Foley or freq intermittent self catheterization Spastic bladder (upper motor neuron lesion) Reflex arc but no connection to or from brain Bladder training- trigger points to stimulate empting; self catheterization

5. Impaired Urinary Elimination Use bladder scan to see amount of urine in bladder Goal- residual <100ml/20% bladder capacity Some individuals may need suprapubic catheter Assess effectiveness of medication Urecholine to stimulate bladder contraction Urinary antiseptic

6. Risk for Autonomic Dysreflexia Elevate head of bed- causes orthostatic hypotension Identify cause/alleviate- if full bladder- cath; if skin- remove pressure, if full bowel- empty, etc Remove support hose/abdominal binder Monitor blood pressure- can get > 300 S Give PRN medication to lower BP If above not effective– call physician

7. Ineffective Coping/ Grief and Depression Assess thoughts on ‘quality of life’; body image; role changes Physical and psychological support Most common SCI is 15-30 yeas old and generally a risk taker– this greatly affects their perception of life and rehabilitation

THANK YOU