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Saving Lives By Strengthening Our Regions Trauma Care System
December 5, 2013 KELLI CASPER, APNP
CASE STUDIESIN NEURO
TRAUMA
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GOALS
Brief anatomy review Discuss important exam findings in brain and
spine trauma
Discuss key management principles in brainand spine trauma
Case study of Epidural Hematoma
Case study of Diffuse Axonal Injury
Case study of Cervical Spinal Cord Injury
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ANATOMY REVIEW
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TRAUMATIC BRAIN INJURY
A traumatic brain injury occurs every 7seconds and results in death every 5minutes in the US
TBI accounts for 1/3 of all trauma relateddeaths in the US
Annual cost of TBI medical care in the US
approximately $56 billion (Heegaard & Biros, 2007)
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MANY FLAVORS OF BLUNT TBI
Skull fractures
Brain contusions
Hematomas/Intracerebral hemorrhages Epidural Hematoma
Subdural Hematoma
Traumatic SAH Diffuse axonal injury
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CATEGORIZING HEAD INJURY
Minimal: GCS= 15, No loss of consciousness, No amnesia
Mild: GCS= 14 OR GCS= 15 plus EITHER: Brief LOC < 5 min OR impaired alertness
or memory
Moderate: GCS 9-13 OR LOC > 5 min OR Focal neurologic deficit
Severe: GCS 5-8
Critical: GCS 3-4
(Greenberg, 2010)
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TBI PATHOGENESIS
Primary injury: immediate impact injury
Secondary injury: ensuing neuropathologic processes afterinitial injury
Our job in the hospital is to
intervene and disrupt these
processes and secondary
mechanisms
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SECONDARY BRAIN INJURY
Amino acid andcytokinerelease
Free radicalsformed
Mitochondrialdamage
BBB damageAltered CBF
Increased ICP
Brain damage/cell death
Functional deficits
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INTERVENING FACTORS IN TBI
Hypoxia
Hypotension
Cerebral edema
Increased ICP
Reduced cerebral blood flow
Electrolyte imbalance
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PRACTICE GUIDELINE DEFINITIONS
Level I: High degree of clinical certainty Level A: Based on consistent Class I evidence (well-designed,
prospective randomized controlled studies)
Level B: Single Class I study or consistent class II evidence whencircumstances preclude clinical trials
Level II: Moderate degree of clinical certainty
Level C: Usually derived from Class II evidence (one or more well-designed comparative clinical studies or less well-designedrandomized studies) or a preponderance of Class III evidence
Level III: Unclear clinical certainty
Level D: Generally based on Class III evidence (case series,historical controls, case reports and expert opinion). Useful foreducational purposes and to guide future research
(Greenberg, 2010)
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CASE STUDY #1
51 y/o male fell down a flight of cement stairsafter domestic altercation striking the lefttemporal area. Lost consciousness for about 10minutes.
By the time EMS arrived, the patient was fullyawake. He was brought to the ED forevaluation. GCS 15 in ED. CT scan without
contrast of head showed a small left temporalepidural hematoma and left temporal bonefracture.
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EPIDURAL VS SUBDURAL HEMATOMAS
Epidural 1% of head trauma
admissions
Arterial source (MMA)
(85% of cases)
Can expand rapidly
More often requires
surgical evacuation
Mortality 20-55%
Classic presentation
Subdural Seen in 10-20% of head
trauma cases
Usually venous source of
bleeding (bridging veins)
Usually expand less rapidly
than EDH
More often has associated
underlying brain injury
(contusions, SAH)
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Epidural: Usually produces more mass effect
Subudural: Usually more diffuse and concave
appearance
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Small epidural hematoma (< 1 cm maximum thickness)
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CASE STUDY #1
Patient was admitted to ICU for observation EDH can rapidly expand
Moderate head injury
Neuro checks every hour
HOB elevated 40 degrees NPO status
Seizure prophylaxis started
Temporal region associated w/higher seizure risk Minimize sedation!
Avoid hypertension
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UNFOLDING EVENTS
Overnight becoming increasingly agitated followed byincreasing somnolence and difficulty arousing
Thrashing of left extremities only
No longer following commands and not speaking
Left pupil 5mm and fixed, Right pupil 2mm, responsive tolight
Neurosurgeon being called
Patient declined rapidly, developing respiratory distress
Rapid response called and patient emergently intubated OR was called for emergent craniotomy and evacuation of
hematoma.
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DISCUSSION OF EVENTS
Agitation/Restlessness is often first sign of increasing
ICP
Somnolence and hemiparesis will follow as ICPcontinues to rise
Pupil dilates (late sign)
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TREATMENT COURSE
Surgical evacuation via Craniotomy withevacuation of EDH
He eventually regained consciousness andable to ambulate and use right hand
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CASE STUDY #2
47 y/o male in MCA on highway, lost control,no helmet, thrown from motorcycle.
Unresponsive at scene, CPR initiated
Intubated at scene, arrived to ED GCS 3,chemically paralyzed and sedated.
Neuro exam very limited
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DIFFUSE AXONAL INJURY
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INITIAL PERTINENT CLINICAL INFORMATION
SBP on admit to ICU 140s. MAP 80s.
Pupils unequal, R= 4mm, reactive to 2mm,L= 8mm, non-reactive to light.
Sodium: 141
H/H: 13.3/38.8
Platelet: 227,000
PCO2 = 37, PO2 = 129
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INITIAL TREATMENT COURSE
Arterial line inserted. Central line inserted. HOB elevated 40 degrees
Sedated with propofol / fentanyl drips
Loaded with Cerebyx (Fosphenytoin) 20 mg PE/kg, then
TID ICP bolt placed by Neurosurgeon. Initial ICPs 7-9mm Hg.
CPP 60s
Mannitol 25 gm IV every 6 hours started
Stress ulcer prophylaxis, Protonix 40 mg IV daily Bilateral SCDs placed for DVT prophylaxis
Serum electrolytes / osmolality q 6 hrs
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DISCUSSION OF TREATMENT
ICP monitoring & goals CPP monitoring & goals
Sedation goals
Mannitol treatment
3% saline treatment DVT prophylaxis
Stress ulcer prophylaxis (SUP)
Nutrition goals
Refractory increased ICP
Barbituate coma
Decompressive Craniectomy
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TYPES OF ICP MONITORING DEVICES
Goal ICP < 20
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CEREBRAL PERFUSION PRESSURE
Importance of Cerebral Perfusion Pressure
CPP = Mean arterial pressure (-) Intracranialpressure
Goal > 60 mm Hg, prefer > 70 mm HG
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MANNITOL(LEVEL II RECOMMENDATION FOR INTRACRANIAL HTN AFTER SEVERE TBI)
Pros Increases cerebral
blood flow by itsplasma expansion andosmotic effect
Reduces ICP withinminutes
Possible free radicalscavenging
(Greenberg, 2010)
Cons Risk of acute renal
failure
Risk of hypotension
May draw more fluidinto CNS causingworsening cerebraledema
Electrolytedisturbances due toexcessive urinaryoutput
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HYPERTONIC SALINE
Pros Effective at reducing
ICP through osmoticeffects similar toMannitol
Less risk ofhypovolemichypotension
(Greenberg, 2010)
Cons May cause severe
hypernatremia
Electrolyte
disturbances Not enough convincing
evidence to supportuse over Mannitol
No changes inneurologic outcomeover Mannitol
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SUPPORTIVE CARE
Sedation / Pain management Nutrition
Stress Ulcer prophylaxis
DVT prophylaxis
Skin care
Oral hygiene
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CONTINUED HOSPITAL COURSE
IVC filter placed (DVT risk with ICH) Percutaneous bedside tracheostomy placed, dobbhoff placed for
nutrition
Required a few days of Levophed for goal CPP > 60
ICPs remained relatively normal
Gradually began to open eyes, and although not commanding,localized purposefully to stimulus
~ 12 days post-injury, nodding to questions, trying to mouthwords, began sitting on edge of bed
~ 18 days post-injury, speaking more sense, less agitation,progressing in PT/OT/Speech, trach removed
Discharge to a brain rehab facility ~ 3 weeks post-injury
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SPINAL CORD INJURY
12,000 new cases each year
Average age at time of injury ~ 40 years
77% of these are males
$4 Billion spent annually on acute andchronic care of spinal cord injured patients
(Chittiboina, et al. 2012)
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CAUSES OF SCI
Cause%
MVC's
Falls
Violence
Other/unknown
Sports
(Chittiboina, et al. 2012)
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CASE STUDY #3
22 y/o male dove into shallow lake. Friendspulled him out of water, patient unable to
move arms or legs. In ED, cervical CT scanshowed at C7 burst fracture.
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CT CERVICAL SPINE
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MRI CERVICAL SPINE
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INITIAL NEUROLOGICAL EXAM
Alert and oriented with normal speech CN IIXII grossly intact
Motor exam showed preserved biceps 3+/5,triceps 2/5 bilaterally, Hand intrinsics absenton right side, subtle finger movement on leftside
No motor or sensory perception below C7
+ priapism
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DISCUSSION
Level of Injury
Complete Injury vs Incomplete Injury
Spinal shock
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LEVEL OF INJURY
Some use level of completely normalfunction
Some use most caudal segment with motor
function at least 3/5
Know the major spinal nerve root motordistribution
Know the major spinal nerve root sensorydermatomes
MAJOR SPINAL NERVE ROOT MOTOR
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MAJOR SPINAL NERVE ROOT MOTOR
DISTRIBUTIONSSegment Muscle Action to Test
C1C4 Neck muscles
C3, C4, C5 Diaphragm Inspiration/FEV1
C5, C6 Deltoid, Biceps Abduct arm, Elbow flexion
C6, C7 Extensor carpi radialis Wrist extension
C7, C8 Triceps, Extensor digitorum,hand intrinsics Elbow Extension, FingerExtension
L2, L3 Iliopsoas Hip flexion
L3, L4 Quadriceps Knee extension
L4, L5 Medial hamstrings, tibialis
anterior
Ankle dorsiflexion
L5, S1 Lateral hamstrings, posterior
tibialis, extensor hallucis
longis
Foot inversion, great toe
extension, ankle
plantarflexion
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MUSCLE STRENGTH
Grade Strength
0 No contraction
1 Flicker or trace contraction
2 Movement with gravity eliminated
3 Movement against gravity
4 Movement against resistance
4 slight resistance
4 moderate resistance
4+ strong resistance
5 Normal strength
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SENSORY DERMATOMES
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DISCUSSING SPECIAL REFLEXES IN SCI
Priapism
Cremasteric reflex
Anal cutaneous reflex (anal wink)
Bulbocavernous reflex
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COMPLETE VS INCOMPLETE SCI
Incomplete lesionAny residual motor or
sensory function more
than 3 segments below the
level of injury Sensation or voluntary
movements in LEs
Preserved sensation
around anus, voluntary
rectal sphinctercontraction
Complete lesion No preservation of any
motor and/or sensory
function more than 3
segments below the levelof injury
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SPINAL SHOCK
Hypotension following spinal cord injury Interruption of the sympathetics (implies
injury above T1)
Loss of vascular tone below level of injury Leaves parasympathetics relatively unopposed causing a
relative bradycardia
Loss of muscle tone results in venous
pooling Blood loss from other associated wounds
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TREATMENT COURSE
Cervical immobilization with rigid collar initially
Methylprednisolone drip started per protocol
Placed in cervical tongs by Neurosurgeon in ICU
Central/Arterial lines placed
Levophed drip used in ICU for maintaining SBP > 90 SCDs for DVT prophylaxis
Foley catheter insertion
NPO
SUP: Protonix 40 mg IV daily Anxiety & Pain control with small doses Ativan/Fentanyl as
needed
Pre-operative readiness for surgical stabilization
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CERVICAL TRACTION
Level III recommendation Purpose: to restore anatomic alignment
Complications:
Skull penetration of pins
Reduction of cervical dislocations may cause neurologic
deterioration (i.e. retropulsed disc)
Higher level injuries (C1-C3) need caution (fragmentspulled toward canal)
Infection (Osteomyelitis)good pin care is essential
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HOSPITAL COURSE / OUTCOME
Early physical and occupational therapies
Improving left hand intrinsics by POD 2
Transferred to a Spinal Cord Rehab facilityby POD 3
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STEROID PROTOCOL IN SCI
Still highly controversial Considered Level III Recommendation
Asserted that beneficial (sensory & motor)effects at 6 weeks, 6 months and 1 year areseen for both complete and incompleteinjuries only if given within 8 hour of injury
(Greenberg, 2010)
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STEROID PROTOCOL
Administration: 16 Gm/256 ml bacteriostatic water
30 mg/kg initial IV bolus over 15 minutes, followed by 45
minute pause, then maintenance drip at 5.4 mg/kg/hour x
23 or 47 hours**
(Greenberg, 2010)
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DVT PROPHYLAXIS IN SCILevel I
Recommendation
Level II
Recommendations
Level III
Recommendations* LMW heparin, rotating bed,
adjusted dose heparin or
some combination of these
measures
* Low dose heparin +
pneumatic compression
stockings or electrical
stimulation
Not recommended: low-
dose heparin used alone
Not recommended: oral
anticoagulation alone
Duplex doppler
ultrasound, venography
are recommended as
diagnostic tests for DVT
in patients with SCI
Vena Cava interruption
filters for patients who do
not respond to or are not
candidates for
anticoagulation
*Titrate dose of SQ heparin q 12hours to a PTT of 1.5 x control
*Heparin 5000 units q 12 hours
(Greenberg, 2010)
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EVALUATING STABILITY
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TYPES OF VERTEBRAL FRACTURES
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BRACING OPTIONS
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REFERENCES
Blumenfeld, H. Neuroanatomy through Clinical Cases. SinauerAssociates, Inc., Sunderland, Massachusetts; 2002.
Fix, J.D. Neuroanatomy. Lippincott Williams & Wilkins, 3rdedition, 2002.
Greenberg, M.S. Handbook of Neurosurgery. Thieme Publishing,7thedition, 2010.
Heegard, W. & Biros, M. (2007). Traumatic Brain Injury.Emergency Medicine Clinics of North America, 25, 655-678.
Lindsay, K.W., Bone, I. & Callander, R. Neurology andNeurosurgery Illustrated. Churchill Livingstone, 4thedition, 2004.
Ling, G. & Marshall, S. A. (2008). Management of Traumatic BrainInjury in the Intensive Care Unit, Neurologic Clinics, 26, 409-426.
Chittibonia et al. (2012). Head and Spinal Cord Injury. NeurologyClinics, 30 (1), 241-276.
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