CASE STUDIES
IN NEURO
TRAUMA
December 5, 2013
KELLI CASPER, APNP
Saving Lives By Strengthening Our Region’s Trauma Care System
GOALS
• Brief anatomy review
• Discuss important exam findings in brain and
spine trauma
• Discuss key management principles in brain
and spine trauma
• Case study of Epidural Hematoma
• Case study of Diffuse Axonal Injury
• Case study of Cervical Spinal Cord Injury
ANATOMY REVIEW
TRAUMATIC BRAIN INJURY
• A traumatic brain injury occurs every 7
seconds and results in death every 5
minutes in the US
• TBI accounts for 1/3 of all trauma related
deaths in the US
• Annual cost of TBI medical care in the US –
approximately $56 billion
• (Heegaard & Biros, 2007)
MANY “FLAVORS” OF BLUNT TBI
• Skull fractures
• Brain contusions
• Hematomas/Intracerebral hemorrhages
• Epidural Hematoma
• Subdural Hematoma
• Traumatic SAH
• Diffuse axonal injury
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)
TBI PATHOGENESIS
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Primary injury: immediate impact injury
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Secondary injury: ensuing neuropathologic processes after
initial injury
Our job in the hospital is to
intervene and disrupt these
processes and secondary
mechanisms
SECONDARY BRAIN INJURY
Amino acid and
cytokine
release
Free radicals
formed
BBB damage
Altered CBF
Increased ICP
Brain damage/cell death
Functional deficits
Mitochondrial
damage
INTERVENING FACTORS IN TBI
• Hypoxia
• Hypotension
• Cerebral edema
• Increased ICP
• Reduced cerebral blood flow
• Electrolyte imbalance
PRACTICE GUIDELINE DEFINITIONS
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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 when
circumstances preclude clinical trials
Level II: Moderate degree of clinical certainty
Level C: Usually derived from Class II evidence (one or more welldesigned comparative clinical studies or less well-designed
randomized 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 for
educational purposes and to guide future research
(Greenberg, 2010)
CASE STUDY #1
• 51 y/o male fell down a flight of cement stairs
after domestic altercation striking the left
temporal area. Lost consciousness for about 10
minutes.
• By the time EMS arrived, the patient was fully
awake. He was brought to the ED for
evaluation. GCS 15 in ED. CT scan without
contrast of head showed a small left temporal
epidural hematoma and left temporal bone
fracture.
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)
• Epidural: Usually produces more “mass effect”
• Subudural: Usually more diffuse and concave
appearance
Small epidural hematoma (< 1 cm maximum thickness)
CASE STUDY #1
• Patient was admitted to ICU for observation
• EDH can rapidly expand
• Moderate head injury
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Neuro checks every hour
HOB elevated 40 degrees
NPO status
Seizure prophylaxis started
• Temporal region associated w/higher seizure risk
• Minimize sedation!
• Avoid hypertension
UNFOLDING EVENTS
• Overnight becoming increasingly agitated followed by
increasing 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 to
light
• 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.
DISCUSSION OF EVENTS
• Agitation/Restlessness is often first sign of increasing
ICP
• Somnolence and hemiparesis will follow as ICP
continues to rise
• Pupil dilates (late sign)
TREATMENT COURSE
• Surgical evacuation via Craniotomy with
evacuation of EDH
• He eventually regained consciousness and
able to ambulate and use right hand
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
DIFFUSE AXONAL INJURY
INITIAL PERTINENT CLINICAL INFORMATION
• SBP on admit to ICU 140’s. MAP 80’s.
• 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
INITIAL TREATMENT COURSE
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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 ICP’s 7-9mm Hg.
CPP 60’s
Mannitol 25 gm IV every 6 hours started
Stress ulcer prophylaxis, Protonix 40 mg IV daily
Bilateral SCD’s placed for DVT prophylaxis
Serum electrolytes / osmolality q 6 hrs
DISCUSSION OF TREATMENT
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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
TYPES OF ICP MONITORING DEVICES
Goal ICP < 20
CEREBRAL PERFUSION PRESSURE
• Importance of Cerebral Perfusion Pressure
• CPP = Mean arterial pressure (-) Intracranial
pressure
• Goal > 60 mm Hg, prefer > 70 mm HG
MANNITOL
(LEVEL II RECOMMENDATION FOR INTRACRANIAL HTN AFTER SEVERE TBI)
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Pro’s
Increases cerebral
blood flow by it’s
plasma expansion and
osmotic effect
Reduces ICP within
minutes
Possible free radical
scavenging
(Greenberg, 2010)
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Con’s
Risk of acute renal
failure
Risk of hypotension
May draw more fluid
into CNS causing
worsening cerebral
edema
Electrolyte
disturbances due to
excessive urinary
output
HYPERTONIC SALINE
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Pro’s
Effective at reducing
ICP through osmotic
effects similar to
Mannitol
Less risk of
hypovolemic
hypotension
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(Greenberg, 2010)
Con’s
May cause severe
hypernatremia
Electrolyte
disturbances
Not enough convincing
evidence to support
use over Mannitol
No changes in
neurologic outcome
over Mannitol
SUPPORTIVE CARE
• Sedation / Pain management
• Nutrition
• Stress Ulcer prophylaxis
• DVT prophylaxis
• Skin care
• Oral hygiene
CONTINUED HOSPITAL COURSE
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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
ICP’s 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 mouth
words, 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
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 and
chronic care of spinal cord injured patients
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(Chittiboina, et al. 2012)
CAUSES OF SCI
Cause%
MVC's
Falls
Violence
Other/unknown
Sports
(Chittiboina, et al. 2012)
CASE STUDY #3
• 22 y/o male dove into shallow lake. Friends
pulled him out of water, patient unable to
move arms or legs. In ED, cervical CT scan
showed at C7 burst fracture.
CT CERVICAL SPINE
MRI CERVICAL SPINE
INITIAL NEUROLOGICAL EXAM
• Alert and oriented with normal speech
• CN II – XII grossly intact
• Motor exam showed preserved biceps 3+/5,
triceps 2/5 bilaterally, Hand intrinsics absent
on right side, subtle finger movement on left
side
• No motor or sensory perception below C7
• + priapism
DISCUSSION
• “Level of Injury”
• “Complete Injury vs Incomplete Injury
• Spinal shock
LEVEL OF INJURY
• Some use level of completely normal
function
• Some use most caudal segment with motor
function at least 3/5
• Know the major spinal nerve root motor
distribution
• Know the major spinal nerve root sensory
dermatomes
MAJOR SPINAL NERVE ROOT MOTOR
DISTRIBUTIONS
Segment
Muscle
Action to Test
C1 – C4
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, Finger
Extension
L2, L3
Iliopsoas
Hip flexion
L3, L4
Quadriceps
Knee extension
L4, L5
Medial hamstrings, tibialis
anterior
Ankle dorsiflexion
L5, S1
Lateral hamstrings, posterior Foot inversion, great toe
tibialis, extensor hallucis
extension, ankle
longis
plantarflexion
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
SENSORY DERMATOMES
DISCUSSING SPECIAL REFLEXES IN SCI
• Priapism
• Cremasteric reflex
• Anal cutaneous reflex (“anal wink”)
• Bulbocavernous reflex
COMPLETE VS INCOMPLETE SCI
Incomplete lesion
• Any residual motor or
sensory function more
than 3 segments below the
level of injury
• Sensation or voluntary
movements in LE’s
• Preserved sensation
around anus, voluntary
rectal sphincter
contraction
Complete lesion
• No preservation of any
motor and/or sensory
function more than 3
segments below the level
of injury
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
TREATMENT COURSE
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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
SCD’s 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
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 (fragments
pulled toward canal)
• Infection (Osteomyelitis) – good pin care is essential
SURGICAL STABILIZATION
HOSPITAL COURSE / OUTCOME
• Early physical and occupational therapies
• Improving left hand intrinsics by POD 2
• Transferred to a Spinal Cord Rehab facility
by POD 3
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 are
seen for both complete and incomplete
injuries only if given within 8 hour of injury
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(Greenberg, 2010)
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**
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(Greenberg, 2010)
DVT PROPHYLAXIS IN SCI
Level I
Recommendation
Level II
Recommendations
* LMW heparin, rotating bed, • Not recommended: lowadjusted dose heparin or
dose heparin used alone
some combination of these
• Not recommended: oral
measures
anticoagulation alone
* Low dose heparin +
pneumatic compression
stockings or electrical
stimulation
*Titrate dose of SQ heparin q 12
hours to a PTT of 1.5 x control
*Heparin 5000 units q 12 hours
(Greenberg, 2010)
Level III
Recommendations
• 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
EVALUATING STABILITY
TYPES OF VERTEBRAL FRACTURES
BRACING OPTIONS
REFERENCES
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Blumenfeld, H. Neuroanatomy through Clinical Cases. Sinauer
Associates, Inc., Sunderland, Massachusetts; 2002.
Fix, J.D. Neuroanatomy. Lippincott Williams & Wilkins, 3rd
edition, 2002.
Greenberg, M.S. Handbook of Neurosurgery. Thieme Publishing,
7th edition, 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 and
Neurosurgery Illustrated. Churchill Livingstone, 4th edition, 2004.
Ling, G. & Marshall, S. A. (2008). Management of Traumatic Brain
Injury in the Intensive Care Unit, Neurologic Clinics, 26, 409-426.
Chittibonia et al. (2012). Head and Spinal Cord Injury. Neurology
Clinics, 30 (1), 241-276.