Download Traumatic Brain Injury A Case Study

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 

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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

History 

PMH

– Denies, but GSW (metallic pellets CXR)

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PSH

– Denies

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Social Hx

– Single, no children, unemployed, unfunded – +ETOH, +amphetamines, +cannibis – Recently released from jail for drug possession

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Meds

– Denies

Diagnostics Normal CT

Subdural Hematoma

Diagnostics

Diagnostics

Focused A/P 

R frontotemporoparietal SDH – Craniectomy – EVD – Monitor/treat ICP

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Paraplegia/paresis L2 burst fracture c subluxation L2-L3 T11 lamina/TP fracture – T10-L3 posterior fusion when stable – PT/OT/ST…rehab

A/P con’t    

10th & 11th rib fractures R femur fracture Acetabular fracture Mediastinal hematoma

Post-Op

Post-Op

Nursing Concerns  

Neuro checks/VS q1h ICP monitoring – Mannitol – CSF drainage

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CPP monitoring

– IVF – Vasopressors

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MAP monitoring Sedation/analgesia Seizure prophylaxis Infection prophylaxis Skin care

Interdisciplinary Collaboration

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Trauma Pulmonary/CC Orthopedics ID

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SW/CM

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Nursing PT/OT/ST/RT WOCN Dietary

Evaluation 

Rehabilitation

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Assessment – Decreased short term memory – Paraparesis 

DF 2/5, PF 2/5, HF 4-/5

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Cranioplasty

Epidemiology of Head Trauma  

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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  

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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

Head Trauma     

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Concussion Contusion Epidural hematoma (EDH) Subdural hematoma (SDH) Basilar skull fracture Diffuse axonal injury (DAI)

Epidural

Contusions Basilar skull fracture

Depressed skull Fracture

Types of Injuries 

Mild Traumatic Brain Injury: – Concussion: brief change in mental status with axonal swelling

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Moderate to Severe Brain Injury: – Contusion: “bruising” – Fractures: linear,comminuted, depressed, basalar – Bleeds: epidural, subdural, intracerebral

Mild Traumatic Brain Injury Period of LOC < 30 mins with a GCS of 13-15 after this LOC 2. Amnesia to the event 3. Alteration in mental status at the time of the event (dazed and confused) 1.

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

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Grade II (confusion and amnesia) – – – –

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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 

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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

Moderate and Severe Brain Injury

Contusion   

Small bleeds Cerebral Edema Deficits are based on lobe involved

Fractures  

Linear Comminuted

Depressed Skull Fracture  

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95% go to surgery Antibitoics for infection Brain tissue is involved

Treatment for CSF leak

Epidural Hematoma 

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Laceration of dural arteries or veins Classically laceration of middle meningeal artery Temporal bone fractures “Lucid interval” followed by rapid deterioration Acute bleed

Subdural Hematoma  

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60-80% mortality Tearing of bridging veins, pial artery, or cortical 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

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Intracerebral hemorrhage – Parenchymal injuries from lacerations or contusions – Large deep cerebral vessel injury

Coup and Contrecoup Injuries 

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Coup: direct skull impact Contrecoup: opposite side of impact Due to negative pressure forces causing both vascular and tissue damage

DAI

Diffuse Axonal Injury

Neurologic Exam 

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Decreased neurologic function is best predictor of brain injury Pay attention to cranial nerves

Management of Acute Brain Trauma 

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Labs: CBC, electrolytes, type and screen, tox and ETOH screen CT Brain CT angiography or cerebral angiography (penetrating) MRI contraindicated if metallic fragments

Management Continued. .. 

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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 

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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 Medical Guidelines for TBI Management

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BP and oxygenation Hyperosmolar therapy ICP monitoring CPP Infection prophylaxis DVT prophylaxis

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http://youtu.be/YQ609Tk-qQI

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PbtO2 Analgesic/sedatives Nutrition Antiseizure prophylaxis Hyperventilation Steroids Hypothermia

New Therapy 

Stem Cell Therapy – Neural/Glial differentiation – Neurogenesis – Neuroplasticity – Improve motor function – Improve cognitive function

References    

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AANN Core Curriculum for Neuroscience Louis, MO. Nursing, 4th Ed. 2004. 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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Neuroplasticity 

Organizational changes caused by experience

Neurogenesis 

Formation of new nerve cells

Nature vs. Nurture 

Genetics – 2500 connections 

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“major highways”

Environment – 15000 

“avenues & side roads”

Future “Directed Neuroplasticity”

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