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Saving Lives By Strengthening Our Region’s Trauma Care System December 5, 2013 KELLI CASPER, APNP CASE STUDIES IN NEURO TRAUMA.

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Presentation on theme: "Saving Lives By Strengthening Our Region’s Trauma Care System December 5, 2013 KELLI CASPER, APNP CASE STUDIES IN NEURO TRAUMA."— Presentation transcript:

1 Saving Lives By Strengthening Our Region’s Trauma Care System December 5, 2013 KELLI CASPER, APNP CASE STUDIES IN NEURO TRAUMA

2 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





7 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)

8 MANY “FLAVORS” OF BLUNT TBI Skull fractures Brain contusions Hematomas/Intracerebral hemorrhages Epidural Hematoma Subdural Hematoma Traumatic SAH Diffuse axonal injury

9 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)

10 TBI PATHOGENESIS Primary injury: immediate impact injury Secondary injury: ensuing neuropathologic processes after initial injury Our job in the hospital is to intervene and disrupt these processes and secondary mechanisms

11 SECONDARY BRAIN INJURY Amino acid and cytokine release F ree radicals formed Mitochondrial damage BBB damage Altered CBF Increased ICP Brain damage/cell death Functional deficits

12 INTERVENING FACTORS IN TBI Hypoxia Hypotension Cerebral edema Increased ICP Reduced cerebral blood flow Electrolyte imbalance

13 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 when circumstances 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-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)

14 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.

15 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)

16 Epidural: Usually produces more “mass effect” Subudural: Usually more diffuse and concave appearance



19 Small epidural hematoma (< 1 cm maximum thickness)

20 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

21 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.

22 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)


24 TREATMENT COURSE Surgical evacuation via Craniotomy with evacuation of EDH He eventually regained consciousness and able to ambulate and use right hand

25 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


27 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

28 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 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

29 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


31 CEREBRAL PERFUSION PRESSURE Importance of Cerebral Perfusion Pressure CPP = Mean arterial pressure (-) Intracranial pressure Goal > 60 mm Hg, prefer > 70 mm HG

32 MANNITOL (LEVEL II RECOMMENDATION FOR INTRACRANIAL HTN AFTER SEVERE TBI) Pro’s Increases cerebral blood flow by it’s plasma expansion and osmotic effect Reduces ICP within minutes Possible free radical scavenging (Greenberg, 2010) 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

33 HYPERTONIC SALINE Pro’s Effective at reducing ICP through osmotic effects similar to Mannitol Less risk of hypovolemic hypotension (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

34 SUPPORTIVE CARE Sedation / Pain management Nutrition Stress Ulcer prophylaxis DVT prophylaxis Skin care Oral hygiene

35 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 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

36 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 (Chittiboina, et al. 2012)

37 CAUSES OF SCI (Chittiboina, et al. 2012)

38 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.



41 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

42 DISCUSSION “Level of Injury” “Complete Injury vs Incomplete Injury Spinal shock

43 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

44 MAJOR SPINAL NERVE ROOT MOTOR DISTRIBUTIONS SegmentMuscleAction to Test C1 – C4Neck muscles C3, C4, C5DiaphragmInspiration/FEV1 C5, C6Deltoid, BicepsAbduct arm, Elbow flexion C6, C7Extensor carpi radialisWrist extension C7, C8Triceps, Extensor digitorum, hand intrinsics Elbow Extension, Finger Extension L2, L3IliopsoasHip flexion L3, L4QuadricepsKnee extension L4, L5Medial hamstrings, tibialis anterior Ankle dorsiflexion L5, S1Lateral hamstrings, posterior tibialis, extensor hallucis longis Foot inversion, great toe extension, ankle plantarflexion

45 MUSCLE STRENGTH GradeStrength 0No contraction 1Flicker or trace contraction 2Movement with gravity eliminated 3Movement against gravity 4Movement against resistance 4 – slight resistance 4 moderate resistance 4+ strong resistance 5Normal strength


47 DISCUSSING SPECIAL REFLEXES IN SCI Priapism Cremasteric reflex Anal cutaneous reflex (“anal wink”) Bulbocavernous reflex

48 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

49 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

50 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 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

51 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


53 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

54 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 (Greenberg, 2010)

55 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)

56 DVT PROPHYLAXIS IN SCI Level 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 12 hours to a PTT of 1.5 x control *Heparin 5000 units q 12 hours (Greenberg, 2010)




60 REFERENCES Blumenfeld, H. Neuroanatomy through Clinical Cases. Sinauer Associates, Inc., Sunderland, Massachusetts; 2002. Fix, J.D. Neuroanatomy. Lippincott Williams & Wilkins, 3 rd edition, 2002. Greenberg, M.S. Handbook of Neurosurgery. Thieme Publishing, 7 th 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, 4 th 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.

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