Traumatic Brain Injury
Brain
Cerebrum
Largest part of the brain, composed of 2 hemispheres and 4 lobes.
Frontal
Parietal
Temporal
Occipital
Cerebrum
Frontal – Conceptualization, motor ability and judgment, thought process, emotions.
Parietal – Interpretation of sensory information, ability to recognize body parts.
Temporal – memory storage, integration of auditory stimuli.
Occipital – Visual Center
Cerebellum
Keeps person oriented in space, balance.
Doesn’t initiate movement but coordinates it.
Controls skeletal muscles.
Controls voluntary movements.
Brain Stem
Brain stem
Central core of the brain
Contains midbrain, pons, and medulla
Midbrain
Contains many neurons and tracts
Pons
Controls rhythmicity of respiration
Contains motor and sensory pathways
Medulla
Cardiac, respiratory, vasomotor control
Swallow, gag, and cough reflex
Motor and sensory fibers cross here
Spinal Cord
Continues with the brain stem
Coverings of the Brain & Spinal Cord
Meninges
3 layers tissue
Dura mater
Arachnoid layer
Pia mater
Spaces
Epidural
Subdural
Subarachnoid
Prevalence and Incidence of TBI
Leading cause of disability and death in the US
1.7 million people sustain a traumatic brain injury (TBI) annually
Males > Females
Mechanisms of Injury
Acceleration/Deceleration Injury
Acceleration
Something hits the skull
Weapon
Deceleration
The skull hits something
Wall
Coup-Contrecoup
Something hits the skull
Then the skull bounces off
Rotational
Force of impact pushes the head in a twisting motion
Twists and tears axons
Penetrating Injury
Foreign object enters the brain
Straight-through
Bounce around
Shock waves
TBI Classification
Mild
GCS 13 – 15
Loss of consciousness or amnesia 5 – 60 min
No abnormality on CT and Length of Stay greater than 48 hours
Moderate
GCS 9 – 12
Loss of consciousness or amnesia for 1 – 24 hours
May have abnormality on CT
Severe
GCS 3 – 8
Loss of consciousness or amnesia > 24 hours
May have a cerebral contusion, laceration, or intracranial hematoma
Primary and Secondary Brain Injuries
Primary Injury
Impact
Immediate neuron damage
Irreversible damage
Secondary Injury
Response to primary injury
Inflammation
Cerebral swelling
Ischemia
Can be reversible
Skull Fractures
Linear
Crack in skull without bone fragmentation
Usually not apparent without head CT
Treatment
Allow to close
Depressed
Skull fragments are pushed into cranial vault
Obvious indentation deformity
Scalp is intact
Severe brain damage
Treatment
Craniectomy with cranioplasty
Removal of hematoma
Open
Skull fragments protrude through scalp
High risk for infection
Treatment
Craniectomy with cranioplasty
Debridement of wound
Antibiotics
Basilar
Fracture of base of skull (behind the face)
Usually is not apparent
Results in CSF leak through nose and ears
Racoon eyes and Battle’s sign
Treatment
Allow it to close
Allow CSF to drain
Sterile cotton gauze to absorb CSF
Antibiotics
Basilar Fracture Signs
Nursing Care of Skull Fractures
Frequent focused neurological assessment
Increasing ICP
Seizures
Focal deficits
Monitor for CSF leak
Halo Sign – CSF on white gauze will be yellow with blood in center
Nose and ears are most common
Dressing changes with strict aseptic technique
Manage pain
Use acetaminophen
Avoid NSAID’s and opioids
Decreased Intracranial Adaptive Capacity
Cranial vault cannot expand
Increase in any component can impair cerebral perfusion:
Brain volume
Blood volume
Cerebrospinal fluid volume
Focal Brain Injuries
Subdural Hematoma
Epidural Hematoma
Intracerebral Hematoma
Subdural Hematoma (Focal Brain Injury)
Between arachnoid layer and dura
Typically, venous
Slow progression
Acute – < 48 hours
Subacute – 2 – 14 days
Chronic – >2 weeks
Common with:
Falls in elderly
Falls from substance abuse
Use of anticoagulants
Subdural Hematoma Manifestations and Treatment
Manifestations:
Ipsilateral headache
Mild ipsilateral hemiparesis
Ipsilateral pupil dilation
Vision changes
Confusion
Drowsiness
Treatment:
Burr holes or craniotomy
Subdural drain
Epidural Hematoma (Focal Brain Injury)
Between dura and skull
Usually, arterial
Fast progression
Initial loss of consciousness
Able to arouse
Loses consciousness again
Fixed and dilated ipsilateral pupil
Common with high impact injury
Epidural Hematoma Treatment:
Craniotomy with cauterization
Continuous ICP monitoring
Diffuse Brain Injuries
Concussion
Subarachnoid Hemorrhage
Diffuse Axonal Injuries
Concussion (Diffuse Brain Injury)
Caused by blunt trauma
Damage is microscopic
Signs & Symptoms:
Loss of consciousness <20 minutes
Confused
Stunned / Dazed
Headache
Dizziness
Slurred speech
Nausea & vomiting
Usually, no pupil changes
Treatment:
Avoid further injury
Monitor for neurological changes for 24 – 48 hours
Acetaminophen or ice for pain
Management of Concussion
E R observation 1-2 hours
Discharge instructions:
Signs of increasing I C P
Signs of neurological problems
Post-concussion syndrome can last for several weeks
Headache
Dizziness
Irritability
Insomnia
Impaired memory/concentration
Learning problems
If L O C >15 minutes, may admit to hospital
Subarachnoid Hemorrhage (Diffuse Brain Injury)
Type of hemorrhagic stroke
Results from ruptured aneurysm
Direct damage to neurons
Enters CSF
Common symptoms:
“Thunderclap headache”
Altered LOC
Double vision
Nuchal rigidity
Photophobia
Seizures
Diffuse Axonal Injuries (Diffuse Brain Injury)
Axons and nearby vessels are torn
High-speed acceleration/deceleration injury
Rotational injury
Results in coma
Can be mild (hours/days)
Can result in death or persistent vegetative state
Treatment:
ABC’s
Reduce ICP
Increase BP
Plan for rehab
Assessment
Mechanism of injury
Pre-hospital care
ABC’s (Airway, Breathing, & Circulation) and Vital Signs
Cushing’s Triad:
Bradycardia
Severe Systolic BP hypertension with wide Pulse Pressure
Irregular breathing pattern
Fever can increase I C P
Focused Neuro Assessment:
Glasgow Coma Scale
Motor movements
Pupil responses
Respiratory pattern
Signs & Symptoms of increased I C P:
Vomiting
Headache
Change in L O C from baseline
Restlessness
Breathing Pattern
Rate
Depth
Rhythm
Effort
Lung sounds
Accessory muscle use
Cyanosis
Pulse oximetry
ABG’s
Neurologic Nursing Assessment
Level of consciousness
Glasgow Coma Scale-ranges from 3-15
<8=INTUBATE-Coma
Ranchos Los Amigos Cognitive Function
Galveston Orientation/Amnesia
Diagnostic Tests
CT scan is essential
MRI if CT is inconclusive
ABG’s
Hemoglobin
Platelets
PT/INR
PTT
Urine toxicity
Blood alcohol level
Lumbar Puncture
Goals of Acute TBI Care
Limit ischemic tissue injury
Prevent and treat hypoxia
Minimize cerebral oxygen demand
Maximize cerebral oxygen delivery
Optimize cerebral perfusion pressure (C P P = M A P – I C P)
Minimize I C P
Brain swelling
Vasodilation
CSF blockage
Increase M A P > 90 mm Hg
Increase cardiac output
Increase systemic vascular resistance
Normal C P P is 60 – 160 mm Hg, but goal for T B I is 70 – 80 mm Hg
Leveled Approach to I C P Management
Level One
Pain and sedation
Avoid fever
Acetaminophen
Ice bags
Cool washcloth to forehead
H O B 30 degrees
Midline neck alignment
Level Two
Intraventricular C S F drain
Hyperosmolar therapy
Mannitol
Hypertonic saline
Mechanical ventilation to maintain
P a O 2 is >60
P a C O 2 = 35 – 45
Level Three
Neuromuscular blockade
Mild hyperventilation
Therapeutic hypothermia (33-35C)
Level Four
Barbiturate coma
Decompression craniotomy
Review in ATI…
Drug Class
Examples
Osmotic diuretic
Mannitol (Osmitrol)
Hypertonic saline
3% or 5% sodium chloride
Synthetic ADH
Desmopressin (DDAVP)
Sedatives
Propofol (Diprivan)
Midazolam (Versed)
Lorazepam (Ativan)
Opioid analgesic
Morphine
Fentanyl
Barbiturates
Pentobarbital
Thiopental
Neuromuscular blocking agents
Pancuronium (Pavulon)
Vecuronium
Anticonvulsants
Phenytoin (Dilantin)
Fosphenytoin (Cerebyx)
Nursing Care Plan: Ineffective Cerebral Tissue Perfusion
Monitoring:
Focused neurological assessment
Vital signs
Respiratory pattern
Oxygen saturation
I&O
Intracranial pressure
PaCO2
Nursing Actions
H O B at 30 degrees
Midline neck alignment
Control seizure activity
Prevent overstimulation
Space out activities
Dark, quiet environment
Avoid strong odors
Tepid baths and ice packs
Know when to implement level 1 – 4 interventions
Contact provider if neurological status worsens
Nursing Care Plan: Ineffective Breathing Pattern
Monitor
Changes in respiratory character
Rate
Pattern
Depth
ABG
Hemoglobin
Nursing Actions
Give oxygen
May need mechanical ventilation
Decrease oxygen demand
Prevent pneumonia
Reposition
Excellent oral care
H O B 30 degrees
Limit suctioning
10 seconds per pass
Sedate/paralyze if needed
Complications
Diabetes Insipidus (Complication)
NOT ENOUGH ADH
Excessive water loss
Polyuria (up to 20 L/day)
Low urine specific gravity
Hypotension
Hypernatremia
High serum osmolality
Treatment
Aggressive IV fluid replacement
Vasopressin IV
Desmopressin intranasal
Evaluation
Syndrome of Inappropriate ADH (Complication)
TOO MUCH ADH
Very low urine output (<400mL/day)
High urine specific gravity
Hyponatremia
Low serum osmolality
Can worsen cerebral edema
Treatment
Fluid restriction
Manage elevated ICP
Will resolve as ICP decreases
Cerebral Salt Wasting
TOO MUCH NATRIURETIC PEPTIDE
High urine output
Low urine specific gravity (but high Salty Sodium)
Hyponatremia
Low serum osmolality
Can worsen cerebral edema
Can also decrease MAP
Treatment
I V saline
P O salt tablets
Fludrocortisone (Florinef)
Early Onset Seizures (Complications)
Caused by irritation of neurons
May be a good sign…
Can increase I C P
Monitoring
Continuous EEG
Duration of seizures
Oxygenation
Treatment
Benzodiazepines
Anticonvulsants
Sedatives
Barbiturate coma
Mechanical ventilation
Prevent further injury
Late-Onset Seizures (Complication)
Caused by scarring
Results in epilepsy
Monitoring
Duration of seizures
Oxygenation
Anticonvulsant levels
Support system
Treatment
Anticonvulsants
Patient education
Medication compliance
Activity/driving restrictions
Medic-Alert bracelet
Herniation (Complications)
Catastrophic complication of T B I
Brain tissue becomes displaced due to cerebral edema
A – Cingulate
B – Central
C – Uncal
D – Infratentorial
Cushing’s Triad
Pattern of pupil changes
Unequal and sluggish/unresponsive
Bilateral fixed and fully dilated
Requires craniotomy
Brain Death
Criteria for brain death in Indiana:
Brain death must have been caused by an acute CNS catastrophe
Absence of severe metabolic causes
Absence of drug intoxication or poisoning
Core temperature >32 C (90 F)
Coma must be present
No response to nail-bed or supraorbital pressure
Brainstem reflexes are absent
Pupils fixed and dilated
Oculocephalic reflex absent
Oculovestibular reflex absent
Corneal reflex absent
Gag reflex absent
Apnea persists despite PaCO2 > 60 mmHg after 8 minutes off mechanical ventilator
Bacterial Meningitis-Bacterial/BAD
Medical emergency!
Acute inflammation of meningeal tissues
Infection of arachnoid mater and CSF
Causes:
Streptococcus pneumoniae and Neisseria meningitidis
High risk populations:
Older adults and those debilitated
College students living in dorms, prisoners
Bacterial Meningitis-Clinical Signs & Symptoms
Look for these key signs:
Fever
SEVERE headache
Nuchal rigidity
Nausea and vomiting
Petechial rash
Seizures
Coma
Bacterial Meningitis-D x & T x
Diagnostics:
CBC, Blood cultures
CT scan
Lumbar puncture (LP)
Sometimes purulent, ↑ WBC, ↑ protein, ↓ glucose
Culture and sensitivity of CSF, sputum
Treatment:
I V F’s
I V antibiotics
Control headache &/or fever
phenytoin (Dilantin), mannitol (Osmitrol)
Acute Spinal Cord Injury
Overview
Relay between brain and body
Cervical
Vital Signs
Neck
Shoulders, arms, wrists, fingers
Thoracic
Chest
Abdomen
Lumbar
Pelvis
Anterior legs and feet
Sacral
Bowel
Bladder
Posterior legs and feet
Overview cont.…
Body
↓
Spinal cord
↓
Brain
↓
Spinal cord
↓
Body
Upper Motor Neurons = BRAIN
Purposeful
Able to override reflexes
Lower Motor Neurons = SPINAL CORD
Uncontrollable
“Tense” and ready to fire
SCI Etiologies
Trauma-related
MVA-38%
Falls 31%
Acts of violence 14% (GSW)
Sports/recreation 9%
Main causes of death after insult:
Pneumonia and septicemia (sepsis)
Non-trauma-related
Conditions producing narrowing of the spinal canal
Osteoarthritis (hyperextension injuries)
Ankylosing spondylitis (calcification of ligaments and soft tissue)
Rheumatoid arthritis (inflammation causing osteoporosis and decreased mobility)
Space Occupying lesions
Acute Spinal Cord Infarction-rare
Spinal Cord Injuries
Average age of occurrence is 41
Tetraplegia 56.6%
Paraplegia 21.6%
Usually trauma-related
Dual nature of injury
Primary – Mechanical disruption
Secondary – Effects on neurons
Inflammation
Ischemia
Cellular Calcium Influx
Differentiating Types of SCI
Mechanism of Injury
ASIA Classification System
Sensory Level
Motor Level
Complete vs Incomplete
Autonomic Involvement
PAGE 544 Will not have to classify according to ASIA – but need to know what is being done
to determine
Mechanisms of Injury
Flexion
Hyperextension
Flexion-Rotation
Compression
Distraction
Mechanisms of Injury
Hyperflexion
Head-on collision
Hyperextension
Rear-end collisions/Whiplash
Flexion-Rotation
Sports or MVA hit broadside
Compression
Diving into shallow water
Jumping from tall heights
Landing on feet or buttocks
Distraction
Hanging
American Spinal Injury Association (ASIA) Classification System
Determine sensory levels for right/left sides
Determine motor levels for right/left sides
Determine lowest segment where motor and sensory function is normal on both sides
Determine whether complete or incomplete
Determine ASIA Impairment Scale Grade
Tetraplegia – Cervical to T 1
Paraplegia – T 2 and below
ASIA Complete vs Incomplete
Complete – Transection of spinal cord
Sacral function (rectal tone) is always lost
Total loss of sensory and motor control below level of injury
Incomplete – Section of spinal cord is damaged
Sacral function remains intact
Partial losses of sensory and/or motor control below level of injury
May have an incomplete SCI syndrome (Table 19-1)
ASIA Impairment Scale Grades
Grade
Type of Injury
Findings
All sensorimotor lost
Rectal reflexes lost
A
Complete
B
Incomplete
All motor lost
Sensory intact below LOI
Rectal reflexes intact
C
Incomplete
Motor and sensory intact below LOI
Strength < 3/5 in most muscles below LOI
D
Incomplete
Motor and sensory intact below LOI
Strength > 3/5 in most muscles below LOI
E
Normal
All sensorimotor intact
Assessment and Diagnosis of SCI
Secure ABC’s
Determine mechanism of injury
Possibility of other injuries
ALWAYS suspect SCI when TBI is present
Imaging studies must be done STAT!
Spine X-ray
CT scan with contrast
MRI of known SCI region
Somatosensory evoked potentials (E P’s) after spinal cord edema is treated
Determine MOTOR function
No movement (0/5)
Against gravity (3/5)
Against resistance (5/5)
Determine SENSORY function
Line where normal sensation ends
Assess from toes to head
Patient reports where they start to “feel something”
Light touch
Pain
Proprioception
Somatosensory-Evoked Potentials
Test for intact sensory pathway from body to cerebral cortex
Assessment and Diagnosis of SCI
Assessing Shock States- Spinal Shock
Occurs within 30-60 minutes
Absences of all reflex activity, flaccidity and loss of sensation below level of injury
Syndrome generally subsides within 24 hour (could last 7-20 days)
Resolved when return of deep tendon reflexes, spasticity, and increased muscle tone
Treatment is symptomatic
Assessing Shock States- Neurogenic Shock
Occurs in patients with injury above T6
Classified as a form of hypovolemic shock due to massive vasodilation & peripheral pooling
of blood
Loss of sympathetic control from the brainstem = inability to maintain perfusion
Patient experiences hypotension, bradycardia, decreased CO, and hypothermia with loss of
the ability to sweat below the level of the lesion!!!!
Treatment = O 2, fluid resuscitation, & vasopressor medications!!!!!
Assessment and Diagnosis of SCI
Determine autonomic function
Cervical = Poor autonomic control
Spinal Shock
Almost immediate loss below injury:
Muscle tone
Sensation
Reflexes
Lasts 1 – 20 days
Hard to classify SCI until resolved
Neurogenic Shock
Injury above T6
Profound hypotension
Bradycardia
Hypothermia
Treatment:
Oxygen
I V fluids
Vasopressors
Assessment and Diagnosis of S C I SUMMARY
ABC’s
Mechanism of Injury
Diagnostic Evidence of Spinal Cord Damage
Motor Function
Sensory Function
Spinal Reflex Function
Autonomic Function
Emergency Care for S C I
Ensure patent airway
Immobilize neck
Administer oxygen
IV access x2
Start I V fluids
Give atropine if H R <60
Start dopamine or norepinephrine if M A P < 90 (This was changed from the original
slide but Bump said we will not be asked about this on the exam.
First aid for other injuries
Obtain cervical spine X-ray or CT scan
Manual Stabilization of SCI
Soft Cervical Collar
For whiplash or cervical strain
Worn for symptom management
Use only while sleeping or driving
Miami-J Collar
Used for stable cervical SCI
Worn for 8-12 weeks
Precautions:
Skin care under collar
Provide 2nd collar for washing
Hard Cervical Collar
Prehospital phase
Uncleared c-spine
Used for <48 hours
Precautions:
Skin care
Pressure ulcers
Gardner-Wells Tongs
Unstable c-spine fracture
Used as bridge until surgery
Precautions:
Pin site care
Maintain traction
Muscle relaxants and analgesics
Gardner-Wells Tongs
Manual Stabilization of S C I
Halo Vest
Unstable c-spine fracture
No surgery is needed
Allows for mobility
8 – 12 weeks
Precautions:
Tape a halo vest wrench to vest
Pin site care per hospital policy
Never pull-on struts!
Focused neuro assessment q 2–4 hours
Keep skin clean and dry
A D L assistance
Physical Therapy consult
Thoraco-Lumbar Support Orthotic (TLSO)
Stable thoracic or lumbar fractures
Can be used after surgical repair
Worn 8-12 weeks
Precautions:
Requires custom fit
Skin care with soap and water
Dry thoroughly
These are used after spinal surgery.
Surgical Stabilization of SCI
Open Spinal Fracture Reduction
Realignment
Decompression of canal
Fixation with spinal rods
Should occur within 24 hours
Postoperative Care:
Log roll
Pain management
Frequent focused neuro assessment
Jewett orthosis, TLSO, or Philadelphia collar
Promote mobility
Jewett Orthosis
Steroid Therapy for SCI
Use is controversial
Decreases risk for secondary S C I
No clear benefit, but many risks
Methylprednisolone on day of S C I
I V bolus after injury
I V infusion x 23 hours
THERE IS NO CLEAR EVIDENCE OF STEROIDS HELPING ANYTHING. IT
DEPENDS ON THE PATIENT AND THE COST VS. BENEFIT.
Ineffective Airway Clearance
Intubate for cervical SCI
Discuss tracheostomy
Monitor:
Respiratory effort
Lung sounds and chest rise
Ability to cough
Pulse oximetry and ABG’s
Humidify oxygen
Prevent atelectasis
Incentive spirometer
Quad cough with Heimlich assist
Frequent repositioning or CLRT
Bronchodilators
Mucolytics
Suction only as needed
Decreased Cardiac Output
Neurogenic Shock Management
Bradycardia + Low BP
Cardiac monitoring for all >T6
Avoid touching E T T and suctioning unless absolutely necessary
Atropine at bedside
Maintain M A P 85 – 90 mm Hg
Cardiac pacemaker
Fluid Management
Avoid fluid overload
May require CVP monitor
Inotropes
Vasopressors
Bladder and Bowel Problems
Impaired Urinary Elimination
Above T12 causes hyperreflexic bladder
Bladder is easily triggered
Use suprapubic triggers
T12 or below causes flaccid bladder
Bladder cannot be triggered
Use suprapubic catheter
Use intermittent catheterization
Constipation
Above L2 causes reflexic bowel
Responds to bowel training
Bisacodyl (Dulcolax) suppository
Digital stimulation
Gastrocolic reflex
L2 or below causes flaccid bowel
Does not respond to bowel training
Stool softener
Bisacodyl (Dulcolax) suppository
Manual stool removal
Spasms and Spasticity
Muscle spasms
Exaggeration of normal reflexes
Triggered by range of motion and stretching
Early warning sign
May be useful
Use a lot of body energy
Baclofen
Autonomic Dysreflexia
SCI occurs at or above T6 level
Life-threatening increase in BP caused by SNS stimulation below the level of injury
Bladder distention
Bowel impaction
Temperature changes
Ingrown toenails
Tight, irritating clothes
Urinary tract infection
Below level of injury, SNS is unopposed, causing:
Vasoconstriction = Pallor
Sweating
Piloerection (goosebumps)
Sudden headache
Blurred vision
Anxiety
Above level of injury, PNS will try to oppose the SNS, causing:
Vasodilation = Flushed appearance
Pupil constriction
Stuffy nose
Bradycardia
Autonomic Dysreflexia
Autonomic Dysreflexia Management:
Elevate H O B
Notify provider
Determine and treat cause:
Insert catheter if bladder distended
Relieve kink in catheter
Remove fecal impaction
Dis-impact the bowel
Loosen clothing
Adjust room temperature
Block drafts
Assess for injury below nipple line
What really needs to happen is we need to remove the offending agent.
Monitor Vital Signs
Administer hydralazine or nitrates
I V to reduce severe HTN
Pain
Anticonvulsant
Gabapentin (Neurontin)
Pregabalin (Lyrica)
Spasticity-related pain
Cannabinoids
Intrathecal baclofen
Diazepam
Botulinum toxin
Tricyclic Antidepressants
Amitriptyline
SSRIs
Lexapro
Zoloft
Prozac
Neuropathic
Unrelated to movement
Worsens with infections
“Pins and needles”
Allodynia
Type of pain that makes one extremely sensitive to touch.
Anticonvulsants or Antidepressants
Musculoskeletal
Overuse of tissues (bones, joints, and muscle)
NSAID’s
Narcotics
Psychosocial Issues
Sexual dysfunction
Arousal and orgasm are possible
Men
Reflexic erections
Unlikely to ejaculate
Vibratory stimulation
Electrical stimulation of prostate
Sperm harvesting
Women
Lubricant
Fertility is unaffected
Menses may pause after S C I
Labor can cause autonomic dysreflexia
Hopelessness
Hope for improvement
Management:
Rehabilitation
Focus on abilities (not disabilities)
Promote independence
Preserve ego integrity
Use faith
Maintain social network
Encourage acceptance
Monitor for depression
Functional Issues