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Traumatic Brain Injury

A Case Study

Lisa Randall, RN, MSN, ACNS-BC

RNSG 2432



Demographics/CC

23 y.o. AAM

Auto vs. ped

8/10/08



HPI

Dancing on I-35 under the influence ofcrack cocaine and ETOH.

Hit by 2 cars > 50mph

GCS 12 on arrival, but declined to 4

Eyes 4>1

Verbal 3>1

Motor 5>2



History

PMH Denies, but GSW (metallic pellets CXR)

PSH Denies

Social Hx Single, no children, unemployed, unfunded +ETOH, +amphetamines, +cannibis

Recently released from jail for drug possession Meds

Denies



Diagnostics

Normal CT



Subdural Hematoma



Diagnostics



Focused A/P

R frontotemporoparietal SDH Craniectomy

EVD

Monitor/treat ICP

Paraplegia/paresis

L2 burst fracture c subluxation L2-L3

T11 lamina/TP fracture T10-L3 posterior fusion when stable

PT/OT/STrehab


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A/P cont

10th & 11th rib fractures

R femur fracture

Acetabular fracture

Mediastinal hematoma



Post-Op



Nursing Concerns

Neuro checks/VS q1h ICP monitoring

Mannitol CSF drainage

CPP monitoring IVF Vasopressors

MAP monitoring Sedation/analgesia

Seizure prophylaxis Infection prophylaxis Skin care



Interdisciplinary

Collaboration Trauma

Pulmonary/CC

Orthopedics ID

SW/CM

Nursing

PT/OT/ST/RT

WOCN Dietary



Evaluation

Rehabilitation

Assessment Decreased short

term memory

Paraparesis

DF 2/5, PF 2/5, HF4-/5

Cranioplasty



Epidemiology of Head

Trauma Occurs every 15

seconds 500,000 annual ED

visits Most common causes:

MVAs, falls, assaults Males 15-24, elderly

> 75 Accounts for 40% of

traumatic deaths



Pathophysiology of TBI

1st

Primary Injury: initial insult i.e. from bleed



Second

Secondary Injury: delayed injury from hypoxia,ischemia, and release of neurotoxins

Excitatory amino acids can cause swelling and

neuronal death Endogenous opioids cause increased metabolism,

using glucose supplies

Increased ICP, especially > 40 leads to brain

hypoxia, ischemia, hydrocephalus, herniation Hydrocephalus: clotted blood obstructs CSF outflow

tracts and absorption of CSF, disrupts blood-brainbarrier



Head Trauma

Concussion

Contusion

Epidural hematoma (EDH)

Subdural hematoma (SDH)

Basilar skull fracture Diffuse axonal injury (DAI)



Epidural

Basilar skull

fractureDepressed skull

Fracture

Contusions



Types of Injuries

Mild Traumatic Brain Injury: Concussion: brief change in mental

status with axonal swelling Moderate to Severe Brain Injury:

Contusion:bruising

Fractures: linear,comminuted,depressed, basalar

Bleeds: epidural, subdural,intracerebral



Mild Traumatic Brain

Injury1. Period of LOC < 30 mins with a GCS

of 13-15 after this LOC

2. Amnesia to the event3. Alteration in mental status at the

time of the event (dazed and

confused)



Types of Concussion

Grade I (confusion, no amnesia, no LOC) Remove from activity (may return when asymptomatic) 3 concussions in 3 months: no activity that risks head

trauma for 3 months

Grade II (confusion and amnesia) Remove from activity for day Recheck in 24 hours No activity for 1 week Two grade II concussions in 3 months, no activity for 3

months Grade III (LOC)

To ED for CT Symptom free for 2 weeks, then another 30 days Two grade III concussions, no activity for 3 months



Post-Concussive

Syndrome Somatic symptoms: headache, sleep

disturbance, dizziness, vertigo,

nausea, fatigue, sensitivity to light ornoise

Cognitive: attention, concentration,

memory problemsAffective: irritability, depression,

anxiety, emotional lability



Moderate andSevere Brain Injury



Contusion

Small bleeds

Cerebral Edema

Deficits are basedon lobe involved



Fractures

Linear

Comminuted



Depressed Skull Fracture

95% go to surgery

Antibitoics for

infection Brain tissue is

involved



Treatment for CSF leak



Epidural Hematoma

Laceration of duralarteries or veins

Classically laceration ofmiddle meningeal artery

Temporal bone fractures

Lucid interval followedby rapid deterioration

Acute bleed



Subdural Hematoma

60-80% mortality

Tearing of bridging

veins, pial artery, orcortical veins

Acute vs chronic



Traumatic Subarachnoid

Hemorrhage Lacerations of vessels

in subarachnoid space

TSAH SAH



Intraventricular and

Intraparenchymal Hemorrhage Intraventricular

hemorrhage

Very severe TBI

Poor prognosis

Intracerebral hemorrhage

Parenchymal injuries from

lacerations or contusions Large deep cerebral vessel

injury



Coup and Contrecoup

Injuries Coup: direct skull

impact

Contrecoup:opposite side ofimpact

Due to negative

pressure forcescausing bothvascular and tissuedamage



DAIDiffuse Axonal

Injury



Neurologic Exam

Decreasedneurologic function

is best predictor ofbrain injury

Pay attention tocranial nerves



Management of Acute BrainTrauma

Labs: CBC, electrolytes, type andscreen, tox and ETOH screen

CT Brain

CT angiography or cerebralangiography (penetrating)

MRI contraindicated if metallicfragments



Management Continued.

. . Intubate GCS 8 or less or airway

protection issue (Cricothyroidotomy if

necessary) Maintain BP 90 mmHg systolic

C-spine precautions

Tetanus prophylaxis Sterile dressing to wounds

Antibiotics in penetrating injury



ICP Management is the

Key ICP monitor in patients with GCS < 8 Hyperventilation not routinely recommended Elevate head of bed to 30 degrees Sedation

Propofol Barbiturate Induced Coma

Contraindicated in hypotension

Mannitol Reduces ICP by reducing blood viscosity, improves cerebral blood

flow Serum osmolality should not be > 320 Bolus dosing



To Image or Not to

Image? GCS < 15

Intoxicated

Age > 55 or < 2

Amnesia to events

Witnessed LOC (> 15 minutes)

Repeated vomiting

Evidence of basilar skull fracture

Inability to recall 3 of 5 objects

Coagulopathy

Penetrating head injury



Ventriculostomy



Evidenced Based MedicalGuidelines for TBI Management

BP and oxygenation

Hyperosmolar

therapy ICP monitoring

CPP

Infectionprophylaxis

DVT prophylaxis http://youtu.be/YQ609Tk-qQI

PbtO2

Analgesic/sedatives

Nutrition Antiseizure

prophylaxis

Hyperventilation Steroids

Hypothermia
http://youtu.be/YQ609Tk-qQIhttp://youtu.be/YQ609Tk-qQIhttp://youtu.be/YQ609Tk-qQIhttp://youtu.be/YQ609Tk-qQI



New Therapy

Stem Cell Therapy

Neural/Glial differentiation

Neurogenesis Neuroplasticity

Improve motor function

Improve cognitive function



AANN Core Curriculum for Neuroscience Louis, MO.Nursing, 4th Ed. 2004. Saunders. St.

Davis, F.A. (2001). Tabers Cyclopedic MedicalDictionary. F.A. Davis, Philadelphia.

Greenberg, Mark. (2006). Handbook of Neurosurgery.Greenberg Graphics, Tampa, Florida.

Lewis, S., Heitkemper, M., OBrien, P., Bucher, L.(2007). Medical-Surgical Nursign. Assessment of

Management of Medical Problems. Mosby

Elsevier, St. Louis, Missouri Silvestri, Linda. (2008). Comprehensive review for theNCLEX-RN Examination. Saunders Elsevier, St.Louis, Missouri.

References



Introduction

YouTube - Brain Plasticity
http://www.youtube.com/watch?v=TSu9HGnlMV0http://www.youtube.com/watch?v=TSu9HGnlMV0http://www.youtube.com/watch?v=TSu9HGnlMV0http://www.youtube.com/watch?v=TSu9HGnlMV0http://www.youtube.com/watch?v=TSu9HGnlMV0



Neuroplasticity

Organizational changes caused by experience



Neurogenesis

Formation of new nerve cells



Nature vs. Nurture

Genetics

2500 connections

major highways

Environment

15000avenues & side roads



Future

Directed Neuroplasticity
http://www.newsweek.com/id/163924http://www.newsweek.com/id/163924



Brain Fitness Program

YouTube - The Brain Fitness Program(1/8)
http://www.youtube.com/watch?v=CRldD_Z9l2s&feature=emailhttp://www.youtube.com/watch?v=CRldD_Z9l2s&feature=emailhttp://www.youtube.com/watch?v=CRldD_Z9l2s&feature=emailhttp://www.youtube.com/watch?v=CRldD_Z9l2s&feature=emailhttp://www.youtube.com/watch?v=CRldD_Z9l2s&feature=emailhttp://www.youtube.com/watch?v=CRldD_Z9l2s&feature=emailhttp://www.youtube.com/watch?v=CRldD_Z9l2s&feature=email

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