Spinal Cord Injury

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Spinal Cord Injury:

Spinal Cord Injury Background, Clinical Syndromes, Acute Medical Management University of St. Augustine

Objectives:

Objectives Upon completion of this lecture, you should be able to: Describe the most common etiologies and mechanisms of injury for spinal cord injury (SCI) Identify the six clinical syndromes with SCI and discuss the most common symptoms and clinical findings associated with each Discuss the medical management (surgical and non surgical interventions) of an acute SCI Discuss patient positioning and pressure relieving techniques to prevent skin breakdown Identify common complications associated with SCI and how to manage them Discuss mobility precautions for cervical, thoracic, and lumbar levels of SCI Discuss pharmacological and therapeutic interventions for managing spasticity University of St. Augustine

Section I: Background to Spinal Cord Injury:

Section I: Background to Spinal Cord Injury Demographics Etiology Mechanism of Injury Pathological Changes University of St. Augustine

Demographics:

Demographics Prevalence 270,000 individuals in the United States with SCI Incidence Approximately 12,000 individuals sustain SCI’s annually (does not include people who die at the scene of the accident) 40 cases per million in U.S. population University of St. Augustine

Demographics:

Demographics Age of Injury SCI primarily affects young adults 55% occurs in persons 16-30 years of age Gender Male: 80.6% (slight decrease since 1980 when it was at 81.8%) Female: 19.4% University of St. Augustine

Demographics :

Demographics Trends are consistent with general population trends University of St. Augustine 1970’s 2000’s Mean age (years) 28 35 Individuals >60 years old (% of SCI population) 4.7% 11.5%

Demographics:

Demographics Race University of St. Augustine 1973-9 2005 White 76.8% 66% African American 14.2% 26.2% Hispanic 6% 8.3% Asian 0.9% 2.1% Native American 0.09% 0.9%

Etiology:

Etiology University of St. Augustine www.fscip.org/facts.htm

Etiology- Direct:

Etiology- Direct Penetrating wound from bullet or knife Fracture-dislocation resulting in transection of the cord University of St. Augustine

Etiology- Indirect:

Etiology- Indirect Herniated disc tumor University of St. Augustine

Etiology- Indirect:

Etiology- Indirect VASCULAR MALFORMATIONS OF THE SPINAL CORD Thrombosis of the cord vessels Embolus Hemorrhage Arteriovenous Malformation (AVM) University of St. Augustine

Etiology- Indirect:

Etiology- Indirect OTHER CAUSES Congenital: Spina bifida Infection: Transverse myelitis Disease: Multiple Sclerosis Hysterical paralysis- SCI may occur without detectable vertebral injury University of St. Augustine

Mechanism of Injury:

Mechanism of Injury Most SCI’s are a result of indirect trauma to the vertebral column Violent motion of the head and/or trunk Magnitude and direction determine the type, extent, and severity of injury University of St. Augustine

Cervical Injury:

Cervical Injury More vulnerable than any other area of the vertebral column due to poor mechanical stability 52% of SCI occur in the cervical region Types: Flexion Flexion with rotation Vertical compression Extension Lateral flexion University of St. Augustine

Cervical Injury:

Cervical Injury FLEXION Head on collision or rapid deceleration Compression force anteriorly Distraction force posteriorly Results in a Wedge Fracture (often does not result in neurological injury) University of St. Augustine

Cervical Injury:

Cervical Injury FLEXION Tear Drop Fracture Result of extreme flexion with axial loading Unstable and associated with high incidence of cord damage May lead to disruption of ligaments and instability May cause facet joints to lock University of St. Augustine

Cervical Injury:

Cervical Injury FLEXION WITH ROTATION Locking of single facet joint Brown- Sequard Syndrome due to instability University of St. Augustine

Cervical Injury :

Cervical Injury VERTICAL COMPRESSION C4 or C5 W ith a burst fracture- crushing of vertebral body Bony fragments Associated with diving in shallow water accidents University of St. Augustine

Cervical Injuries:

Cervical Injuries EXTENSION Most commonly occurs during falls where head/chin is struck from below or during a MVA when struck from behind causing cervical hyperextension Elderly population, hyperextension injuries can occur with only mild trauma Results in anterior distraction and posterior compression Posterior compression can lead to vertebral arch fractures Hangman’s Fracture University of St. Augustine

Cervical Injury:

Cervical Injury LATERAL FLEXION Compression on one side may lead to a wedge fracture Distraction on the other side may lead to ligamentous disruption University of St. Augustine

Vertebral Fractures :

Vertebral Fractures Flexion Extension Flexion with rotation Compression University of St. Augustine

Thoracic Injury:

Thoracic Injury Less common due to stability of the rib cage, but more likely to be complete injuries Most common injury site is T12-L1 Often caused by GSW, MVA, falls Usually accompanied by other injuries such as rib and transverse process fractures Neural damage may occur when fragments enter the neural canal. University of St. Augustine

Thoracic Injury:

Thoracic Injury FLEXION May result in a wedge fracture due to compression of the vertebral body anteriorly In severe cases, may get disruption of the posterior elements University of St. Augustine

Thoracic Injury:

Thoracic Injury FLEXION WITH ROTATION When adding rotation, secondary shearing forces occur in addition to anterior compression and posterior distraction Usually does not affect stability University of St. Augustine

Thoracic Injury:

Thoracic Injury VERTICAL COMPRESSION Often results in a burst fracture at T10, T11, or T12 May lead to bony fragments in the spinal canal University of St. Augustine

Thoracic Injury :

Thoracic Injury EXTENSION WITH LATERAL FLEXION Thoracic spine is rarely injured in this isolated motion University of St. Augustine

Lumbar Injury :

Lumbar Injury Thoracolumbar junction is the most common site for lumbar spine injury Neural damage is frequently incomplete due to good blood supply and large vertebral canal University of St. Augustine

Lumbar Injury:

Lumbar Injury FLEXION Wedge fracture are often seen anteriorly Not often associated with neural damage FLEXION WITH ROTATION Dislocations are rare with this movement due to vertical orientation of the facets which allows for better anterior/posterior stability However, can occur with violent flexion with rotation University of St. Augustine

Lumbar Injury:

Lumbar Injury FLEXION WITH DISTRACTION Seen with seatbelt injuries Horizontally oriented fracture and dislocation May get distraction of the posterior aspect and compression anteriorly University of St. Augustine

Lumbar Injury :

Lumbar Injury SHEAR Horizontally directed force- as in being struck from behind or falling on an uneven surface Due to disruption of ligaments and dislocation, severe neurological damage can occur along with fractures of the vertebral bodies and posterior arches University of St. Augustine

Lumbar Injury:

Lumbar Injury VERTICAL COMPRESSION May be due to falls Often results in burst fractures 50% sustain neurological damage, usually incomplete University of St. Augustine

Pathological Changes after SCI:

Pathological Changes after SCI ASSOCIATED INJURIES Fractures, brain injury, peripheral nerve injury PATHOLOGICAL CHANGES Trauma to the spinal cord may lead to destruction of the damaged neurons as well as secondary tissue damage Secondary reactions include ischemia, edema, demyelination, and necrosis of the spinal cord Secondary tissue destruction may progress superiorly and inferiorly along the spinal cord spreading over 1-3 segments and gross edema may also further damage the cord University of St. Augustine

Mechanisms of Secondary Tissue Destruction:

Mechanisms of Secondary Tissue Destruction ISCHEMIA Decreased blood supply to the cord due to rupture or compression of blood vessels and intravascular thromboses Decreased blood flow to the spinal cord due to injury to arteries and arterioles supplying the spinal cord Vasoconstriction occurs due to norepinephrine, serotonin, histamine, and prostaglandins being released University of St. Augustine

Mechanisms of Secondary Tissue Destruction:

Mechanisms of Secondary Tissue Destruction INFLAMMATION Contributes to expansion of the lesion beyond its initial site of injury Inflammatory cells can attack cells of the damaged area disrupting cell function and contributing to necrosis Although inflammation can contribute to the process of tissue destruction it can also protect existing neurons and promote tissue repair University of St. Augustine

Mechanisms of Secondary Tissue Destruction:

Mechanisms of Secondary Tissue Destruction ION DERANGEMENT Abnormal concentrations of K+, Na+, and Ca2+ in neurons after injury lead to decreased neuronal excitement and ability to reach an action potential This leads to demyelination, destruction of the cell membrane, and axon, and cell death University of St. Augustine

Mechanisms of Secondary Tissue Destruction:

Mechanisms of Secondary Tissue Destruction APOPTOSIS Programmed cell death Active pathological process performed by individual cells after central nervous system damage Occurs 4-6 hours after initial injury and can spread to adjacent levels for up to 3 weeks University of St. Augustine

Section II: Clinical Syndromes:

Section II: Clinical Syndromes University of St. Augustine

Central Cord Syndrome:

Central Cord Syndrome Central damage to the spinal cord with sparing along the periphery Most common in the cervical region Mechanism of Injury (MOI): central hemorrhage and necrosis that does not progress outward, usually extension injuries in the elderly, but can also occur with flexion injuries University of St. Augustine

Central Cord Syndrome:

Central Cord Syndrome SYMPTOMS Paralysis and sensory loss of the upper extremities Varying involvement of the trunk and LE’s University of St. Augustine

Brown Sequard Syndrome:

Brown Sequard Syndrome Trauma or damage to side of the spinal cord MOI: gun shot or stab wounds, flexion with rotation, burst fractures University of St. Augustine

Brown Sequard Syndrome:

Brown Sequard Syndrome Symptoms Severe loss of motor, proprioceptive, vibratory sense, and discriminative touch ipsilateral to the lesion Severe loss of sensitivity to pin prick, pain and temperature on the contralateral side University of St. Augustine

Anterior Cord Syndrome:

Anterior Cord Syndrome Trauma or damage to the anterior and anterolateral aspect of the cord with preservation of posterior columns MOI: trauma to cord itself, damage to anterior spinal artery, damage from a tear drop or burst fracture University of St. Augustine

Anterior Cord Syndrome:

Anterior Cord Syndrome SYMPTOMS Bilateral loss of motor function below the level of lesion Loss of pain and temperature sensation Preservation of proprioception University of St. Augustine

Posterior Cord Syndrome:

Posterior Cord Syndrome Trauma or damage to the posterior aspect of the spinal cord with preservation of the anterior aspect MOI: cervical hyperextension injuries University of St. Augustine

Posterior Cord Syndrome:

Posterior Cord Syndrome SYMPTOMS Loss of proprioception below the level of lesion resulting in tingling, sensory ataxia, and hypotonia Preservation of motor function, and sensation of pain and temperature University of St. Augustine

Conus Medullaris Syndrome:

Conus Medullaris Syndrome Damage to the sacral cord ( conus ) and lumbar nerve roots within the spinal canal Usually results in an areflexic bowel & bladder Flaccid paralysis of lower extremities University of St. Augustine

Cauda Equina Syndrome:

Cauda Equina Syndrome Injury to the lumbar and sacral nerve roots that arises from the conus medullaris Usually results in an areflexic bowel & bladder Flaccid paralysis of lower extremities University of St. Augustine

Section III: Acute Medical Management :

Section III: Acute Medical Management Hospital Care Orthoses Spasticity Precautions University of St. Augustine

Pre-hospital Care:

Pre-hospital Care Immobilization and movement procedures Ventilation and respiration University of St. Augustine

Hospital Care:

Hospital Care Airway Respiration Circulation/Cardiac Neuro Fractures Integumentary Systems University of St. Augustine

Pharmacological Management:

Pharmacological Management No clinical evidence exists to definitively recommend the use of any neuroprotective pharmacologic agent, including steroids, in the treatment of acute spinal cord injury in order to improve functional recovery. However, commonly used drugs: Methylprednisone GM-1 Gacyclidine Tirilazad Naloxone Prevention and Treatment of Venous Thromboembolism Mechanical compression devices Heparin IVC filter University of St. Augustine

Fracture Management:

Fracture Management Patient is initially immobilized in traction followed by use of an orthosis for a period of weeks or months Length of time a patient spends immobilized varies with the nature of the injury and the philosophy of the physician University of St. Augustine

Nonsurgical Management:

Nonsurgical Management Skeletal Traction University of St. Augustine

Cervical Spinal Orthoses:

Cervical Spinal Orthoses HALO Minerva University of St. Augustine

Cervical Spinal Orthoses:

Cervical Spinal Orthoses SOMI PHILADElphia collar University of St. Augustine

Thoracolumbar Spinal Orthoses:

Thoracolumbar Spinal Orthoses TLSO Jewett Hyperextension brace University of St. Augustine

Thoracolumbar Spinal Orthoses:

Thoracolumbar Spinal Orthoses Knight- Taylor brace LSO University of St. Augustine

Surgical Management:

Surgical Management Indications: unstable fracture, fracture that will not reduce without surgery, gross spinal malalignment , evidence of cord compression, deteriorating neuro status Open reduction and internal fixation Decompression University of St. Augustine

Beds:

Beds Stryker Frame bed Kinetic Frame bed University of St. Augustine

Bed Positioning:

Bed Positioning Prevent respiratory infections Prevent skin breakdown Staff rolls patient every 2 hours University of St. Augustine

Wheelchair Positioning:

Wheelchair Positioning Select an appropriate wheelchair (power vs. manual) Select an appropriate cushion Pressure relief every 10-15 minutes University of St. Augustine

Precautions:

Precautions Cervical Collar and Halos No proning unless permission from MD, no lifting >5 lbs unilaterally, but can do more bilaterally TLSO (T10 and below) No hip flexion past 90° (sitting in W/C, transfers, or dressing) Logrolling LSO (lumbar fractures) No hip flexion past 90° or SLR past 60° (this will affect HS length) University of St. Augustine

Precautions:

Precautions Scapular Precautions ( tetraplegia or high paraplegia with surgical incision through trapezius musculature) No pulling with arms to roll No excessive shoulder protraction/retraction, UE bike, reaching beyond base of support, push-up pressure relief, self ROM or dressing tasks No independent transfer with or without slideboard No resistive scapular exercises (lat pulls, rows, shoulder ext/flex/ABD) No high level W/C skills No long push strokes in W/C University of St. Augustine

Complications:

Complications Compromised respiratory function Orthostatic hypotension Thermoregulation problems Autonomic dysreflexia Spasticity and clonus Sexuality issues University of St. Augustine

Orthostatic Hypotension:

Orthostatic Hypotension Also known as postural hypotension Monitor vitals especially BP with position changes Levels of injury T6 and above: bradyarrhythmias , hypotension and orthostatic hypotension University of St. Augustine

Orthostatic Hypotension:

Orthostatic Hypotension SYMPTOMS: Loss of vision Dizziness Ringing in the ears Nausea Lightheadedness University of St. Augustine

Orthostatic Hypotension:

Orthostatic Hypotension What should you do? RECLINE THEM! MONITOR BP. University of St. Augustine

Orthostatic Hypotension:

Orthostatic Hypotension To work on sitting tolerance… Abdominal binders Ace wrap Ted hose/compression stockings Gradual upright posture University of St. Augustine

Thermoregulation:

Thermoregulation In patients with SCI, the ability to get the information from the skin UP to the brain (hypothalamus) is lost Patients with SCI will lose the ability to shiver or sweat BELOW the level of lesion because of the loss of sympathetic and somatic systems The higher the lesion the greater the impairment University of St. Augustine

Autonomic Dysreflexia:

Autonomic Dysreflexia Due to a disconnection between the brain and sympathetic neurons in the thoracolumbar spine Occurs usually in injuries above T6 Occurs when a noxious stimulus below the level of lesion triggers an excessive sympathetic response University of St. Augustine

Autonomic Dysreflexia:

Autonomic Dysreflexia SIGNS AND SYMPTOMS: Nasal obstruction Slow pulse ( bradycardia ) Pounding headache Increased blood pressure Red blotching of the skin Feeling anxious Flushing or paling Chills without fever Goosebumps Sweating (above the level of lesion) University of St. Augustine

Autonomic Dysreflexia:

Autonomic Dysreflexia COMMON CAUSES: Irritation of the bladder: spasms, infection or stones A plugged or kinked catheter Distension of the bowel Contraction of spasm of the uterus Pressure sores Ingrown toenail Range of motion exercises or other cutaneous stimulation Muscle spasms University of St. Augustine

Autonomic Dysreflexia:

Autonomic Dysreflexia What should you do? SIT the patient UP or keep them UP (remember BP is lower in sitting than supine so do NOT lay them down) Search for the source of the irritation : Check catheter Nursing may need to check for bowel impaction Inspect skin REMEMBER this is a life threatening situation so getting assistance is necessary! University of St. Augustine

Spasticity:

Spasticity Velocity dependent increase in muscle tone in response to passive stretch More prevalent in cervical and upper thoracic injuries and with incomplete lesions (ASIA B &C) University of St. Augustine

Spasticity :

Spasticity Mechanism of spasticity and hyperreflexive responses are unknown, but possible causes include: Motor neurons below the lesion are released from supraspinal descending inhibitory influences Loss of the brain’s ability to moderate the reflexes therefore they become exaggerated Loss of afferent input from limb loading Sprouting of new synaptic terminals within the spinal cord caudal to the lesion University of St. Augustine

UMN vs. LMN Spasticity:

UMN vs. LMN Spasticity UMN: damage to descending tracts  spastic paralysis, clonus , increased deep tendon reflexes, muscle spasms, abnormal reflex to cutaneous stimuli LMN: conus medullaris , cauda equina injuries, or damage to higher lesion that occur at or peripheral to anterior horn cells  flaccid paralysis, decreased or absent deep tendon reflexes Most SCI’s are a combination of both UMN and LMN because both white and grey matter are disrupted at the level of lesion University of St. Augustine

Spasms:

Spasms Manifest as muscle jerking which occurs involuntarily May indicate irritation below the level of lesion Tight clothing A quick stretch a muscle Ingrown toenail Urinary tract infection Bowel impaction Oncoming cold or some other irritant University of St. Augustine

The Good, The Bad, The Ugly:

The Good, The Bad, The Ugly Spasticity is not necessarily a bad thing. Spasticity can actually have some positive effects. University of St. Augustine

The Good:

The Good Can prevent loss of muscle and tone Can assist in preventing muscle edema and thrombus formation Can assist in circulation by constricting the venous walls and raising blood pressure, thereby reducing hypotension May assist in bowel and bladder program May assist with transfers and walking so that patient can weight bear Can aid in ADL activities (patient can trigger to assist with dressing) Can serve as a warning to an irritant University of St. Augustine

The Bad:

The Bad Can decrease ROM and lead to contractures Painful Disturb sleep Violent spasms can interfere with ADL’s and ambulation Severe spasticity can make bowel, bladder, and sexual activities difficult Constant clonus can be a nuisance (having to keep changing positions) May require costly pharmacological interventions or need for attendant care University of St. Augustine

Spasticity Treatment:

Spasticity Treatment Consider if the spasticity is impeding function or independence and if it is painful to the person Think about side effects of your treatment intervention Daily range of motion and stretching can be helpful Avoid stressful situations Use relaxation and stress management techniques Warm bath University of St. Augustine

Spasticity Treatment:

Spasticity Treatment Splinting Bracing Adaptive seating Inhibitive casting University of St. Augustine

Pharmacological Management of Spasticity:

Pharmacological Management of Spasticity Baclofen : can be given orally or via infusion pump which is surgically implanted in the abdomen, programmed to release the medication at specific times Clonidine : can be given orally or via a patch Dantrolene sodium: given orally Diazepam: given orally Tizandine : given orally Botulinum Toxin (Botox): injected into the spastic muscle University of St. Augustine

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