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Traumatic Brain Injury A Case Study
Lisa Randall, RN, MSN, ACNS-BC RNSG 2432
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Demographics/CC 23 y.o. AAM Auto vs. ped 8/10/08
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HPI Dancing on I-35 under the influence of crack 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
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History PMH PSH Social Hx Meds Denies, but GSW (metallic pellets CXR)
Single, no children, unemployed, unfunded +ETOH, +amphetamines, +cannibis Recently released from jail for drug possession Meds
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Diagnostics Normal CT
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Subdural Hematoma
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Diagnostics
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Diagnostics
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Focused A/P R frontotemporoparietal SDH Paraplegia/paresis
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/ST…rehab
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A/P con’t 10th & 11th rib fractures R femur fracture
Acetabular fracture Mediastinal hematoma
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Post-Op
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Post-Op
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Nursing Concerns Neuro checks/VS q1h ICP monitoring CPP monitoring
Mannitol CSF drainage CPP monitoring IVF Vasopressors MAP monitoring Sedation/analgesia Seizure prophylaxis Infection prophylaxis Skin care
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Interdisciplinary Collaboration
Trauma Pulmonary/CC Orthopedics ID SW/CM Nursing PT/OT/ST/RT WOCN Dietary
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Evaluation Rehabilitation Assessment Cranioplasty
Decreased short term memory Paraparesis DF 2/5, PF 2/5, HF 4-/5 Cranioplasty
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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
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Pathophysiology of TBI
1st Primary Injury: initial insult … i.e. from bleed
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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-brain barrier
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Head Trauma Concussion Contusion Epidural hematoma (EDH)
Subdural hematoma (SDH) Basilar skull fracture Diffuse axonal injury (DAI)
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Epidural Contusions Basilar skull fracture Depressed skull Fracture
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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
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Mild Traumatic Brain Injury
Period of LOC < 30 mins with a GCS of after this LOC Amnesia to the event Alteration in mental status at the time of the event (dazed and confused)
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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
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Post-Concussive Syndrome
Somatic symptoms: headache, sleep disturbance, dizziness, vertigo, nausea, fatigue, sensitivity to light or noise Cognitive: attention, concentration, memory problems Affective: irritability, depression, anxiety, emotional lability
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Moderate and Severe Brain Injury
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Contusion Small bleeds Cerebral Edema
Deficits are based on lobe involved
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Fractures Linear Comminuted
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Depressed Skull Fracture
95% go to surgery Antibitoics for infection Brain tissue is involved
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Treatment for CSF leak
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Epidural Hematoma Laceration of dural arteries or veins
Classically laceration of middle meningeal artery Temporal bone fractures “Lucid interval” followed by rapid deterioration Acute bleed
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Subdural Hematoma 60-80% mortality
Tearing of bridging veins, pial artery, or cortical veins Acute vs chronic
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Traumatic Subarachnoid Hemorrhage
Lacerations of vessels in subarachnoid space TSAH SAH
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Intraventricular and Intraparenchymal Hemorrhage
Intraventricular hemorrhage Very severe TBI Poor prognosis Intracerebral hemorrhage Parenchymal injuries from lacerations or contusions Large deep cerebral vessel injury
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Coup and Contrecoup Injuries
Coup: direct skull impact Contrecoup: opposite side of impact Due to negative pressure forces causing both vascular and tissue damage
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DAI Diffuse Axonal Injury
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Neurologic Exam Decreased neurologic function is best predictor of brain injury Pay attention to cranial nerves
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Management of Acute Brain Trauma
Labs: CBC, electrolytes, type and screen, tox and ETOH screen CT Brain CT angiography or cerebral angiography (penetrating) MRI contraindicated if metallic fragments
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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
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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
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To Image or Not to Image? GCS < 15 Intoxicated
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
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Ventriculostomy
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Evidenced Based Medical Guidelines for TBI Management
BP and oxygenation Hyperosmolar therapy ICP monitoring CPP Infection prophylaxis DVT prophylaxis PbtO2 Analgesic/sedatives Nutrition Antiseizure prophylaxis Hyperventilation Steroids Hypothermia
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New Therapy Stem Cell Therapy Neural/Glial differentiation
Neurogenesis Neuroplasticity Improve motor function Improve cognitive function
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References AANN Core Curriculum for Neuroscience Louis, MO. Nursing, 4th Ed Saunders. St. Davis, F.A. (2001). Taber’s Cyclopedic Medical Dictionary. F.A. Davis, Philadelphia. Greenberg, Mark. (2006). Handbook of Neurosurgery. Greenberg Graphics, Tampa, Florida. Lewis, S., Heitkemper, M., O’Brien, P., Bucher, L. (2007). Medical-Surgical Nursign. Assessment of Management of Medical Problems. Mosby Elsevier, St. Louis, Missouri Silvestri, Linda. (2008). Comprehensive review for the NCLEX-RN Examination. Saunders Elsevier, St. Louis, Missouri.
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Introduction YouTube - Brain Plasticity
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Neuroplasticity Organizational changes caused by experience
Neurons constantly lay down new pathways for neural communication and to rearrange existing ones throughout life—hence learning, memory, etc. Example—eyelids of a cat sutured—they perform better with sound localization tasks—neurons expand into cortical areas normally used for visual processing. There was also an increase in the cortical area devoted to whiskers.
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Neurogenesis Formation of new nerve cells
1980’s—song birds—increased neurons during seasons when engaged in singing. During other times when not singing, the number of neurons decreased—no neurogenesis. However, not thought to occur in primates—neurogenesis was thought to be restricted throughout evolution as brain becomes more complex.
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Nature vs. Nurture Genetics Environment 2500 connections 15000
“major highways” Environment 15000 “avenues & side roads” The avenues and side roads form a dense, complex network that is always under construction.
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Future “Directed Neuroplasticity”
Stem cells stimulated to migrate to areas and differentiate into specific types of neurons—replace cells lost to stroke, etc. New tx for brain damage/injury and/or cog. Disabilities (ADHD, dyslexia, down syndrome). With directed neuroplasticity, scientists and clinicians can deliver calculated sequences of input, and/or specific repititive patterns of stimulation, to cause desirable and specific changes in the brain. Skills lost can be relearned, the decline of abilities can be staved off or reversed and entirely new fxns can be gained.
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Brain Fitness Program YouTube - The Brain Fitness Program (1/8)
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