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Traumatic Brain Injury (TBI)
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Adult Health II
Traumatic Brain Injury—Part 2
Jerry Carley RN, MA, MSN, CNE
Summer 2010
Concept Map: Selected Topics in Neurological Nursing
ASSESSMENT
Physical Assessment
Inspection
Palpation
Percussion
Auscultation
ICP Monitoring
“Neuro Checks”
Lab Monitoring
PATHOPHYSIOLOGY
PHARMACOLOGY
Traumatic Brain Injury
Spinal Cord Injury
Specific Disease Entities:
Amyotropic Lateral Sclerosis
Multiple Sclerosis
Huntington’s Disease
Alzheimer’s Disease
Huntington’s Disease
Myasthenia Gravis
Guillian-Barre’ Syndrome
Meningitis
Parkinson’s Disease
Care Planning
Plan for client adl’s,
Monitoring, med admin.,
Patient education, more…based
On Nursing Process:
A_D_P_I_E
--Decrease ICP
--Disease Specific
Meds
Nursing Interventions & Evaluation
Execute the care plan, evaluate for
Efficacy, revise as necessary
Objectives
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 Recall anatomy and physiology of the brain &
cranial nerves
 Explain pathophysiology of various brain (head)
injuries
 Detail signs, symptoms and prevention of
Increased Intracranial Pressure (ICP)
 Demonstrate effective use of Glasgow Coma Scale
 Discuss medical & nursing management of brain
injuries
Prevent Secondary Injury !!!
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Meaningful recovery of function after
head injury is possible IF secondary
injuries are prevented or minimized
Secondary Brain Injury
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 Any physiological event that can occur within
minutes, hours, or days after the initial injury and
leads to further damage of nervous tissue
 Secondary Injury is mostly due to Increased ICP
caused by hypotension, hypoxia, intracranial
bleeding, seizures
Brain Injury Management
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Frequent
Re-assessments
+
Rapid Response
Be Vigilant for Increased ICP !
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To understand intracranial
pressure, think of the skull as a
rigid box. After brain injury, the
skull may become overfilled with
swollen brain tissue, blood, or CSF.
The skull will not stretch like skin
to deal with these changes. The
skull may become too full and
increase the pressure on the brain
tissue. This is called increased
intracranial pressure.
ICP Peaks 48 – 72 hours after injury
Foramen
Magnum
Monitor: Neuro Checks q 15 minutes
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 Vital Signs Q15 minutes
 Glasgow Coma Score Q15 minutes
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Expanded
Neuro
Assessment
Tool
EARLY
Signs of
↑ ICP
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1. Slight LOC changes ***MOST IMPORTANT****
2. Pupils sluggish / Impaired eye movement
3. Limb strength changes
4. Headache
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Change in
Level Of Consciousness (LOC)
***MOST IMPORTANT****
+
EARLIEST
Indicator of neurological deterioration
Cushing’s Triad: Signs of ↑ ICP
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 Blood Pressure



Systolic BP Increases
Diastolic BP Decreases
Pulse Decreases
Widening
Pulse
Pressure
Bradycardia
*** You will also see listed in some resources:
--Irregular Respirations (Cheyne-Stokes)
--Elevated Temperature (Hyperpyrexia)
TREND
Re-Assessment Data
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+
COMPARE
to Baseline Assessment Data
Temp
Pulse
BP
LATE(R) Signs of ↑ ICP
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1. Further decreased LOC
2. Cushing’s Triad / Reflex
3. Abnormal respiration patterns
4. Pupils asymmetrical / Dilated
5. Projectile vomiting
6. Hemiplegia / decorticate or decerebrate posturing
Decerebrate Rigidity
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Brain Herniation
occurs when a part
of the brain16pushes
downward inside
the skull through
the opening that
leads into the neck
(Foramen Magnum)
Too Late Now!
Tentorial (Brain) Herniation)
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Tentorial (Brain) Herniation
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Normal
ABI Nursing Interventions
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1) Continuous monitoring of Vitals, PERL and
Glasgow Coma Score
2) Report client condition changes ASAP
3) Maintain airway patency (eg positioning,
suctioning, etc)
4) Minimize cerebral edema
5) Maximize cerebral perfusion
6) Implement seizure precautions / Siderails
7) Provide emotional support
8) Address all self-care deficits
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ICP Monitoring
IntraCranial Pressure
Neurosurgeon drilling prior to placing an
intracranial pressure monitor
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Normal ICP for adults:
10 to 15 mm Hg
ABI Priority Nursing GOALS
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* Minimize cerebral edema
* Maximize cerebral perfusion
ABI Nursing Interventions
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
Continuous monitoring of Vitals, PERL and
Glasgow Coma Score

Report client condition changes ASAP

Maintain airway patency BUT…

Avoid suctioning or Hyperventilate
with 100% O2 FIRST
ABI Nursing Interventions
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
Implement seizure precautions / Siderails

Phenytoin (Dilantin) (prevent / treat Sz)

Maintain head midline (neutral position)

HOB > 30 degrees
ABI Nursing Interventions
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
Address all self-care deficits…BUT

Avoid clustering activities

Provide emotional support
ABI Nursing Interventions
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 High dose barbituates > induced coma
*decreases metabolic demands*
 Pharmacological paralysis
 Avoid overstimulation:
-
Dark quiet room
Limit visitors appropriately
Speak softly
Limit dialogue – keep topics light hearted
Minimize Cerebral Edema
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 Mannitol (Osmitrol) + Urinary catheter
 Fluid restriction (I & O)…?
 Dexamethasone / Decadron (Know side effects!)
 Prevent / Treat fever
 Prevent Infections (closed STERILE monitoring system)
Burr Holes
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Minimize Cerebral Edema
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Maintain
Cerebral perfusion pressure
MAP of 50 – 70 mm Hg
Prevents Hypoxia (Hypercarbia)
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If BP too low…then O2 perfusion is poor…and
Brain Can’t Function
Optimize Cerebral Perfusion
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 Keep head position midline
 HOB elevated ( 30 - 60 degrees )
 Oxygen ****
 Sedate prior to activity
 Minimal ADL movement of client
Teach Client / Family
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• Minimal stimulation environment
• No coughing, no straining, no hard laughing
• Head midline + Bedrest + HOB elevated
• S & S to report to nurse ASAP (Headache, drainage, etc)
• Purpose + frequency of neuro checks
• Medication regime (Narcotics, diuretics, stool softeners, etc)
• Medical interventions (Tests, traction, logrolling, surgery,
etc)
Cerebral Concussion
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 A ‘concussion’ is a relatively mild form of traumatic brain
injury that results in temporary neurological changes
 No apparent structural damage
 Usually involves unconsciousness for a few seconds or
minutes
 Frontal lobe = bizarre irrational behavior
 Temporal lobe = amnesia or disorientation
Discharge ….
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 Mild concussion & neurological stability =
usually will not require hospital admission
 However !!! Must be observed by a reliable
companion for at least 12 hours
 No alcohol for several days
 No pain medications stronger than Tylenol
Cerebral Contusion
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 More severe
 Brain bruised
 Possible surface hemorrhage
 Initially appears like shock
 Can have B & B incontinence
 Can be aroused…briefly
IntraCerebral
Hemorrhage
Bleeding within the tissue of
the brain
IntraCranial
Hemorrhage
Bleeding within
the cranial vault
IntraCranial38Hemorrhage
Bleeding within the cranial vault
Intracranial
Epidural / Extradural Hematoma
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- Between skull and dura
- Extreme emergency
- Mostly arterial
Epidural / Extradural Hematoma
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Subdural Hematoma
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Between dura and brain
Mostly venous
Subdural Hematoma
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3 Types:
Acute
Sx in 24 – 48 hours
Subacute
Sx in 48 hours – 2 weeks
Chronic
Sx in 3 weeks – months
Common in elderly after even minor injury
Often misdiagnosed as stroke
Subdural Hematoma
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Head trauma leading to subdural hematoma
and intracranial hypertension
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Subarachnoid Hemorrhage
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
Subarachnoid space is brain surface where blood vessels that supply
the brain are located

Common causes of subarachnoid hemorrhage are trauma to “Circle
of Willis” aneurysms and congenital arteriovenous malformations
(AVM)

Unique S & Ss:
- Sudden & unusually severe headache & loss of consciousness
- Neck pain & ridigity (nuchal rigidity) d/t meningeal irritation

Untreated, the blood supply to a given area of the brain may fall so
low that the brain tissue dies resulting in a stroke
Subarachnoid Hemorrhage
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IntraCerebral Hemorrhage
Bleeding within the tissue of the brain
Intracerebral
Hemorrhage / Hematoma
Causes:
area
- Force is exerted to the head over a small
(missile injuries, bullet wounds, etc)
- Systemic hypertension causes
degeneration and rupture of blood vessels
- Tumors
- Bleeding disorders
Gunshot Wounds (GSW)
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 Suicides, homicides or accidental shootings
 GSWs to the head are the most lethal of all firearm injuries
 Estimated that greater than 90% fatality rate and at least two
thirds of the victims die before ever reaching a hospital
 Because of the high mortality associated with gunshot wounds
to the head, they account for only approximately 10% of all
traumatic brain injury patients who survive
GSW to the Head
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Visualization of a gunshot wound through the
cerebellum by showing the bony details using
CT. Clearly visible is the typically funnel
shaped exit wound.
Comparative visualization of the soft tissue
damage along the bullet track within the
cerebellum using MRI.
Outcomes
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 The predictors of poor neurological outcome or death after a gunshot
wound to the head include:
- Initial Glasgow Coma Scale score
- Older age
- Presence of low blood pressure or inadequate oxygenation early
after injury
- Dilated non-reactive pupils
 Bullet trajectory through the brain has major significance. Bullets that
traverse the brainstem, multiple lobes of the brain, or the ventricular
system (chambers where cerebrospinal fluid is located) are particularly
lethal
 Many initial survivors develop uncontrollable intracranial pressure and
subsequently succumb
ALL Cranial Injury Tx
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
ATLS evaluation & intervention
(ABCs / Foley / NG / oxygen / Maintain traction)

Constant Monitoring

Diagnosis:
- CT scan (FAST!)
- MRI
- PET Scan (brain function assessment)

Medical interventions depend on severity:
- Endotracheal intubation / hyperventilation
- Sedation
- Diuresis
- Rapid surgical evacuation
Surgical Outcomes
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
Normal pupil reactivity prior to surgery is associated with a
favorable outcome in 84 -100% of patients

When both pupils are dilated a poor outcome or death occurs in
the great majority of individuals

Postoperative seizures are relatively common in these patients

In general, a favorable (functional) outcome is more likely in those
patients who are treated very soon after injury, those who are
younger adults, those with a higher GCS (above GCS of 6 or 7),
those with reactive pupils, those without multiple cerebral
contusions and those who do not develop difficult to control raised
intracranial pressure
Head Injury Recovery
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
Despite very severe initial injuries, some patients make dramatic recoveries
within several months to a year after injury

Despite intensive intervention, long-term disability occurs in a large
portion of the survivors

Patients with significant neuro-cognitive impairment are best managed at a
comprehensive rehabilitation unit for several weeks or months after they
leave the hospital

Recovery of function from the time of discharge to 6 months post-injury
can be dramatic, even in some deeply comatose individuals

Improvement generally begins to plateau at 6 months post-injury and is
typically maximal by one year to 18 months
Continued….
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
Every brain injury is unique. Severity and types of impairments depend on
the area and extent of the damage to the brain

Rehabilitation and support provided to a person who has received an injury
has a major impact on the person’s recovery
 ABI is known as an Invisible Disability due to the invisible nature of
changes that may occur following an injury to the brain, such as memory
loss, cognitive impairments, challenging behaviours and personality
changes
 People with ABI usually retain previous IQ, past memories, skills and
interests. Their ability to use this knowledge can be lost to varying degrees
 ABI is not an Intellectual or Psychiatric disability and therefore the needs of
a person with an ABI are different from the needs of people with an
intellectual or psychiatric disability
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Recovery can be a long process…
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