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Case Studies in Neuro Trauma SCRTAC

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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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