Against All OddsMaximizing Outcomes in SCI

Mary Kay Bader RN, MSN, CCNS, FAHA, FNCS, CCRN, CNRN

Neuro Critical Care CNSMission Hospital

Badermk@aol.com

Disclosures

• American Association of Neuroscience Nurses– Immediate Past President

• Medical Advisory Board– Brain Trauma Foundation– Neuroptics

• Honorarium– Bard– Neuroptics– The Medicines Company

Epidemiology

• Causes– MVAs 42%– Interpersonal violence

24%– Falls 27%– Acts of violence (15%)– Sports 8%

• (diving=cervical vs parachuting = thoracolumbar)

– Industrial (crush) 2%• Location

– majority c-spine– thoracic-lumbar 20-

30%

Epidemiology• Incidence: 12,000/year

– 50% age 16-30 mean (age 40)– 81% male– Alcohol intoxication present 17-19%

• Prevalence– 259,000 survivors in US– Average life expectancy

• High tetraplegics 36 years after injury• Low tetraplegics 40 years after injury• Paraplegics 45 years after injury

Factors that Impact Outcome

• Age at time of SCI

• Level of injury

• Grading of Injury (ASIA)

• Increased mortality– Higher lesions– Advanced age

Description

• Primary Injury– A temporary or permanent loss of

function as a result of injury produced from compression, tearing, lacerations or ischemia

• Secondary Injury– Further compromise to cord function

• spinal cord edema• hemorrhage

– Results in a decrease in perfusion to cord

Vertebral Column

Spinal Cord

Meninges

Vertebral Column

• Ligaments– Anterior support

• ant. long lig• post. long. lig

– Posterior support• interspinous• supraspinal• cruciform

SCI: Degree of Stability

• Stable

• Unstable - ligamentous injury

Intervertebral Discs

•Ruptured discs can manifest motor/sensory or both

Blood Supply to SC• Anterior and posterior spinal arteries• Radicular arteries

Spinal Cord

• C1-L2– max movement

C5-6– greatest flexion

L4-5

• Gray matter: cell bodies/dendrites

• White matter: myelinated axons

Etiology• Causes

– MVAs 44%– Interpersonal violence 24%– Falls 22%– Sports 8%

• Location– majority c-spine– thoracic-lumbar 20-30%

Mechanism of Injury

• Hyperflexion• Hyperextension

• Compression• Rotation• Penetrating

Characteristics of Injury• Rotational Injuries

– caused by extreme lateral flexion or twisting of neck

– tears posterior ligamental structures causing dislocation and instability

Soft Tissue Injury

Vertebral Trauma

• Simple-single break– Usually spinous/transverse

processes, pedicles or facets

• Compression: cause flattening/wedging of VB– wedge, burst or teardrop

(hyperextension)– Amenable to orthosis

• Dislocation– ligaments damage

Crush injury

Atlas and Axis InjuriesC1 burst: disruption of ant and post arch of C1. Results from force to vertex of head/rarely causes neuro injury. Usually managed with external orthosis.

http://www.google.com/url?sa=i&rct=j&q=spinal+cord+hangmans+fracture&source=images&cd=&cad=rja&docid=t1ZbAjMq9m0oEM&tbnid=Itidkkw8ILzSyM:&ved=0CAQQjB0&url=http%3A%2F%2Fdermatologic.com.ar%2F4.htm&ei=8cBYUeDZNJGu8QTurICoCg&bvm=bv.44442042,d.dmQ&psig=AFQjCNFQbyZny2YNQztNSvOlBeULzzAAvg&ust=1364857224911192

Types of C2 Fractures

2. Transverse or oblique fX thru dens: Unstable

Often displaced anteriorly or posteriorly. Associated with high nonunion rate when managed conservatively

3. Base of Dens: May require light traction for initial reduction with Halo

1: usually stable

Usually involves ligament. Stable. May be ass. with antlanto-occipital dislocation

Atlas and Axis InjuriesHangman’s Fracture

Fx through bilateral pedicles

Separates C2-C3 and posterior elements

CT SpineFloating Dens (C2)

Posterior C1

Anterior C1

Chance Fractures

• Mechanism– a flexion-distraction injury (seatbelt injury)

• may be a bony injury• may be ligamentous injury (flexion-distraction injury)

– more difficult to heal

• middle and posterior columns fail under tension  • anterior column fails under compression

• Associated injuries  – high rate of gastrointestinal injuries (50%)

Chance Fractures

• Result from hyperfexion of the spine around an anterior fulcrum in combo with a posterior vertical distraction force

• Horizontal fractures of the pedicles with extension through vertebral body

• Associated with visceral injuries

Fracture-Dislocations

Subluxation

Rotary sublux: caused by abnormal rotation at C1-C2; Seen on CT; exhibit torticollis

Sublux: facet malignment; may be no bony fx, only ligament –unstable; aka locked, perched, jumped facets.

Spinal Cord Injury

• Concussion – Transient loss of SC function

• Contusion– Intramedullary hemorrhage &

edema

• Laceration– Cut in the cord

Spinal Cord Injury

• Transection– Complete cut through SC; very

rare

• Hemorrhage– Parenchyma of SC or within one

of meninges (can lead to SC compression)

• Vascular– Damage to vessels perfusing the

cord lead to ischemia

• Cellular Dynamics

Complete Injury: Anatomical Levels

http://www.google.com/url?sa=i&rct=j&q=spinal+cord+injury+assessment&source=images&cd=&cad=rja&docid=Jacvj9YwLVXwTM&tbnid=rgb8iZ7PUkifCM:&ved=0CAQQjB0&url=http%3A%2F%2Fwww.yourshealthy.com%2F&ei=IbpYUeOvGIuA9QSyo4CoCA&bvm=bv.44442042,d.dmg&psig=AFQjCNEy75p04w3B9O-NUeu-HR2uRK82Yg&ust=1364855704791603

Cord Injury

• Level of lesion and functional impairment– C 1-4 tetraplegia with loss of respiratory – C 4-5 tetraplegia with possible phrenic nerve– C 5-6 tetraplegia with gross arm/diaphragm– C6-7 tetraplegia with biceps intact– C7-8 tetraplegia with triceps, biceps, & w.e.– T1-L2 paraplegia with loss of intercostals and

abdominal muscle function– Below L2: Cauda equina vs. conus medullaris

Cord Injury• Level of lesion and functional impairment

– Below L2: Cauda equina–Compression of lumbosacral nerve roots

below L1 vertebrae

–Variable motor loss

–Absent Achilles reflex

–Radicular pain

–Variable sensory loss

–Areflexive bowel and bladder

–No upper motor neuron findings

Cord Injury

• Below L2: conus medullaris• Compression of conical termination

of cord with damage to lower lumbar/sacral gray matter and nerve roots

• Causes –Fractures –Disc herniation in the T12/Lumbar

region of vertebral column

Cord Injury• Below L2: conus medullaris

• Urinary retention• Impotence• Constipation• Lax anal sphincter• Saddle anesthesia (variable)• Loss of anal/bulbocavernosus reflex• Minimal to no motor weakness – varies

may have lower motor neuron impairment

Cord Injury

• Horner’s syndrome– Ptosis– Miosis– Anhidrosis on affected side– Associated with spine lesions above

T1 that disrupts the cervical sympathetic chain or it central pathways

Incomplete Injury

• Central cord

• Anterior cord syndrome

• Brown Sequard• ipsilateral loss of motor

and position/vibratory sense

• contralateral loss of pain and temperature

Cord Injury

• Pathophysiology– decreased blood supply to cord– progressive edema– decrease tissue oxygenation

Cord Injury• Spinal shock –primary injury to

cord– Areflexia

– flaccid paralysis

– loss of sensation

– Loss of autonomic function

– Loss of bowel/bladder function

Cord Injury• Neurogenic shock –secondary to autonomic

dysfunction especially injuries above T6

• Interrupts normal sympathetic outflow from T1-12 region of SC– Peripheral dilatation & unopposed vagal tone– S/S

• hypotension/bradycardia

• Hypothermia

• lose ability to sweat below level of lesion

Assessment• History

– How did injury occur?

• Remember your P’s– Pain– Paralysis– Paresthesias– Position– Ptosis– Points– Priapism

Assessment Principles

• Upon arrival–Rapid, thorough evaluation

–Airway patency, ventilation, and circulation

–Gross neurologic assessment• Repeat at regular intervals

Assessment Principles

• Why do patients deteriorate?– Early clinical deterioration (<24 hours)

• Usually due to treatment • Application or removal of traction• Inadequate immobilization

– Delayed deterioration (24 hours-7days)• Often associated with hypotension in

patients with fracture dislocations

– Late deterioration (> 7 days)• Associated with vertebral artery injuries

• Maintain neck in neutral position– Immobilization

• ABC– Airway-Intubation and airway support– BP and Heart rate

• Disability – GCS and pupils– Motor 0-5 scale– Sensory– Reflex

Assessing Motor Function

• Upper extremities– C5 Deltoids: Raise arms– C5-6 Biceps: Flexion of elbow– C6-7 wrist extensors: Extension of wrist– C7 Triceps: Extension of elbow– C8-T1 Hand intrinsics:

• Finger flexion• Hand squeeze• Finger abduction

Assessing Motor Function

• Lower extremities– L2 Iliopsoas: Hip flexion– L2-4 Hip adductors: Adduct hips– L4-S1 Hip abductors: Abduct hips– L3-4 Quadriceps: Knee extension– L4-5 S1-2 Hamstrings: Dorsiflex foot– L5 EHL: Extend great toe– S1 Gastrocnemius: Plantar flex foot

Assessing Sensory Function

• Sensation: Sharp vs dull distinction in each dermatome– Lateral spinothalamic tract mediates pain

and temperature– Tongue depressor (dull) and pin (sharp)– Compare side to side

• Porprioceptioin (position sense)– Dorsal column– Toe and Thumb positions

Sensory Dermatomes

AANS Guidelines 2013

• Published 2013 by AANS/CNS

Hospital Based Protocol

• Collaboration• Protocol

– ED• Maintain spine stabilization• Assess/intervene:

–Airway protection and stabilization• Assess/intervene:

–Hemodynamic assessment– Interventions: VS/2 large bore IVs

Hospital Based Protocol

• ED

– Maintain Systolic BP• Infuse NS• Start vasopressors: Dopamine #1

– Secondary Survey

– Radiographic evaluation

Medical Surgical Recommendations

Consult Neurosurgery

or OrthoSpine

stabilization

Hospital Based Protocol: ICU Care

• Respiratory– Cervical lesion: loss of C3-4-5 and

diaphragm• loss of intercostals with thoracic level

dysfunction• abdominals assist with expiration and blow off

CO2• cough reflex is diminished

– Acceptable parameters for quad• VC 1 - 1.2 liters/ NIF -25/ CO2 45-50

– Aggressive pulmonary toilet

Hospital Based Protocol: ICU Care -Ongoing Care Respiratory

• Airway maintenance– Intubated, trached, non-intubated– Ventilator dependent vs independent– Secretion control

• Assisted cough: cough reflex intact but loss of respiratory muscles impact cough

• Manually assisted quad cough• In-exsufflator cough machine: helps clear secretions

by delivering a positive pressure deep breath and shifting rapidly to a negative pressure high expiratory flow (via a mask or trache)

• Electrical stimulation of abdominal wall

Hospital Based Protocol: ICU Care -Ongoing Care Respiratory

• Airway maintenance– Chest PT– Bronchoscopy– Glossopharyngeal breathing (gulping several

breaths then exhale for bigger tidal volumes)– Mucolytics– Hydrating agents– Positioning and mobilization – 5% of all SCI patients are ventilator dependent

at 1 year

Hospital Based Protocol• Optimize Spinal Cord Perfusion

– MAP > 85-90• Crystalloid/colloid IV• Packed RBCs• Dopamine and/or Dobutamine

• Administer Methylprednisilone???– Absolutely NOT!

Hospital Based Protocol ICU Care

• Maintain OG tube • Assess nutritional

needs through indirect calorimetry– Begin feedings– H2 blockers– Bowel program

Hospital Based Protocol ICU Care

• Maintain foley until spinal shock resolves– D/C foley– In/Out catheterization

schedule

Hospital Based Protocol ICU Care

• Musculoskeletal– Spasticity– Contractures– Osteoporosis– Heterotrophic

ossification– Interventions: ROM,

positioning important with PRAFO or splints, and turn frequently

Hospital Based Protocol: ICU Care

• Skin– Frequent inspection– Frequent turning

• Psychological

• Rehab

Effects of Injury on systemic function

• Motor– Upper motor neuron: motor strip to sc

• loss of voluntary function• increase in muscle tone and hyperreflexia• reflex arc is intact• spasticity

– Lower motor neuron: spinal nerve roots/reflex

• loss of voluntary function• decrease in resting voluntary function• wasting of muscle and loss of reflexes

Effects of Injury on systemic functionAutonomic Dysreflexia

– Lesions above T6– Triggered by #1 bladder distention, #2bowel

distention, skin breakdown, stimulation of pain receptor

– Signs and Symptoms of Autonomic Dysreflexia

Effects of Injury on systemic functionAutonomic Hyperreflexia TX:

1. Sit the patient upright

2. Loosen any tight clothing

3. Search for the cause!

4. If SBP > 150 mm Hg, start pharmacologic treatment

NO

Pre-Hospital

• 51 year old male backseat passenger in auto– TC hit from behind– Paramedics arrived

• GCS 1-1-1

• BP 170

• Agonal respirations

• Pt intubated

• IV initiated

Emergency Department 0921

• ABC– Intubated– HR 92 BP 129/53 RR assisted– BP decreased to systolic 80s within 30

minutes of arrival• IV fluids• Vasopressor: Dopamine started

• Neuro: No motor movement• To Radiology

Neurosurgical Consultation

• Pt intubated on ventilator– No spontaneous respirations– No motor movement on arrival– No sensation– Diagnostics

• C1-C2 fractures• C5-6 dislocation• T2-3 fracture• Ankylosing spondylitis with extensive fusion

of entire spine

Dens of C2

C2 type 2 fracture

C1 anterior

C1 posterior

Diagnostics

C5 fracture

Cord Contusion C1-2

CT SpineFloating Dens (C2)

Posterior C1

Anterior C1

CT Spine

Space between C5-6

T2 Fracture

Odontoid Screw

Neurosurgical plan Postop

SICU Nursing Care• Implement the hypothermia

protocol– Stabilize Airway and

breathing– Assure MAP adequate for

spine perfusion– Assess neurologic status

prior to induction– Stabilize spine for further

operative interventions

Close Tabs on Vital Info

Hospital Course

Day 8

Spinal Cord Injury Flowsheet

Ongoing SCI Assess

Outcome• On PCSU

– Moving arms/legs

• Transferred to ARU and Discharged – Ambulating– Weakness in arms 4/5

Emerging Treatment/Research

• Early decompression surgery

• Use of lumbar drains to reduce spine pressure

• Augmenting Spinal perfusion– Lumbar drains– Combination studies (drug + drain +

MAP enhancement)

Emerging Treatment/Research

• Neuroprotection– Targeting decreasing ionic deranangements,

limiting excitatory neurotransmittors, stabilizing blood brain barrier, lessening immune response and inhibiting apoptosis

• Pharmacologic– Minocycline: decreases inflammation and

inhibits apoptosis– Riluzole (used in ALS) blocks activation of

sodium channels and reduces glutamate

• Hypothermia• Regeneration of nerves• Stem cell

Questions