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Test 2 🏁🏁 > MANAGEMENT OF PATIENTS WITH TBI > Flashcards

MANAGEMENT OF PATIENTS WITH TBI Flashcards

1
Q

DEFINITION: TRAUMATIC BRAIN INJURY (TBI)

A
  • Damage to the brain from an external mechanical force and not caused by neurodegenerative or congenital conditions.
  • Temporary or Permanent impairment of:
    — Cognitive
    — Physical
    — or Psychosocial functions
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2
Q

HEAD INJURY

A
  • A broad classification that includes injury to the scalp, skull, or brain
  • 2.5 million people receive head injuries every year in the United States
  • The most common cause of death from trauma
  • Most common cause of brain trauma is falls, followed by car crashes
  • Groups at highest risk for brain trauma include: children 0 to 4 years old, adolescents ages 15 to 19 years, and adults 65 years and older
  • Prevention is the best approach
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3
Q

*PREVENTION OF TBI AND SCI CHART 63-1
Teach pts to

A
  • The greatest opportunity for decreasing TBI is the implementation of prevention strategies.
  • Obey traffic laws
  • Wear Seat Belts
  • Don’t ride in the back of a truck
  • Wear Helmets
  • Promote education against violence and suicide
  • Provide water safety
  • Education to prevent falls
  • Wear protective gear in sports
  • Keep firearms locked in secure area
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4
Q

PREVENTION OF HEAD INJURY

A
  • Teach patients the following:
  • Alcohol and Drugs increase risk of injury
    -Never use drugs or drink when driving
  • Home risks such as poor lighting and loose rugs
  • Safety bars in areas for the handicapped and elderly
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5
Q

PATHOPHYSIOLOGY OF BRAIN DAMAGE:
Primary injury:

A
  • consequence of direct contact to head/brain during the instant of initial injury
  • Contusions, lacerations, external hematomas, skull fractures, subdural hematomas, concussion, diffuse axonal
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6
Q

PATHOPHYSIOLOGY OF BRAIN DAMAGE:
Secondary injury:

A
  • damage evolves over ensuing days and hours after the initial injury
  • Caused by cerebral edema, ischemia, or chemical changes associated with the trauma
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7
Q

MONROE-KELLIE HYPOTHESIS

A

Key Concepts:
- The skull is a rigid compartment that contains 3 components:
— brain tissue
— arterial and venous blood
— cerebrospinal fluid (CSF)
- Any increase in the volume of one component will elevate pressure and decrease the volume of one of the other elements.

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8
Q

PATHOPHYSIOLOGY OF TRAUMATIC BRAIN INJURY
primary /secondary?

A
  • Brain suffers traumatic injury
  • Brain, swelling, or bleeding increases intracranial volume
  • Rigid cranium allows no room for expansion of contents, so intracranial pressure increases
  • Pressure on blood vessels within the brain cause blood flow to the brain to slow
  • Cerebral hypoxia and ischemia occur
  • Intracranial pressure continues to rise. Brain may herniate.
  • Cerebral blood flow ceases
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9
Q

PRIMARY VS SECONDARY

A

Primary:
- The injury is more or less complete at the time of impact
- Skull fracture
- Concussion/bruising of the brain
- Hematoma/blood clot on the brain
- Diffuse axonal injury
Secondary:
- The injury evolves over a period of hours to days after the initial trauma
- Brain swelling/edema
- Intracranial infection
- Epilepsy
- Hypoxemia (low blood oxygen)
- High or low blood pressure
- Anoxia/hypoxia (lack of oxygen to the brain)

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10
Q

CLASSIFICATIONS OF BRAIN DAMAGE

A
  • Direct – Force to Head
  • Indirect – Force to different part of body causing rebound effect of head trauma
  • Closed brain injury (blunt trauma): acceleration/ deceleration injury occurs when the head accelerates then rapidly decelerates, damaging brain tissue
  • Open brain injury: object penetrates the brain or trauma is so severe that the scalp and skull are opened, skull is fractured (Infection)
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11
Q

COUP AND CONTRECOUP INJURY

A

https://www.youtube.com/watch?v=55u5Ivx31og

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12
Q

MANIFESTATIONS OF BRAIN INJURY

A
  • Altered level of consciousness
  • Pupillary abnormalities
  • Sudden onset of neurological deficits and neurological changes; changes in sense, movement, and reflexes
  • Changes in vital signs
  • Headache
  • Seizures
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13
Q

MILD Brain injury S/S

A
  • Appears dazed and confused
  • Loss of consciousness (LOC) for up to 30 mins
  • Headache
  • Nausea
  • Vomiting
  • balance or gait problems
  • Dizziness
  • Visual problems
  • Fatigue
  • Sensitivity to light
  • Cognitive- feeling mentally foggy, slowed down, difficulty concentrating or remembering
  • Amnesia about events immediately before or after the accident
  • Sleep disturbances such as drowsiness, sleep changes (less, more, falling asleep)
  • Emotional changes such as irritability sadness, nervousness, more emotional than usual
  • GCS: 12 or higher
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14
Q

Moderate Brain injury S/S

A
  • Loss of consciousness (LOC) for up to 30 mins to 6 hours
  • *GCS score of 9 - 12 or higher
  • Abnormal CT scan findings (Most of the time)
  • Amnesia up to 24 hours
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15
Q

Severe Brain injury S/S

A
  • GCS 3 - 8
  • LOC > 6 hours
  • Abnormal CT and/or MRI
  • High Risk for secondary damage
  • GCS 8= intubate
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16
Q

GERONTOLOGIC CONSIDERATIONS

A
  • Differs in etiology of injury, higher mortality, longer lengths of hospital stay, poorer outcomes.
  • Assessment challenges
  • 61% of TBI’s over 65 years of age
  • Fifth leading cause of death in older adults.
  • *Falls and motor vehicle crashes are the most common causes of brain injury.
  • Factors that contribute to high mortality are:
    — Falls causing subdural hematomas (closed head injuries), especially chronic subdural hematomas
    — Poorly tolerated systemic stress, which is increased by admission to a high-stimuli environment
    — Medical complications, such as hypotension, hypertension, and cardiac problems
    — Decreased protective mechanisms make patients susceptible to infections (especially pna)
    — Decreased immunologic competence, which is further diminished by brain injury
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17
Q

SCALP WOUNDS AND SKULL FRACTURES

A

Symptoms depend on severity/location of injury
- Scalp wounds
— Tend to bleed heavily and are portals for infection
- Skull fractures
— Usually have localized, persistent pain
— Fractures of the base of the skull
— Bleeding from nose pharynx or ears
— *Battle sign—ecchymosis behind the ear
— Racoon eyes: bruising around eyes
— *CSF leak: halo sign—ring of fluid around the blood stain from drainage

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18
Q

BASILAR FRACTURES ALLOW CSF TO LEAK FROM NOSE AND EARS

A
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19
Q

BASILAR FRACTURES S/S

A
  • Raccoon eyes
  • Battle’s sign
  • Cerebrospinal fluid (CSF) otorrhea
  • Cerebrospinal fluid (CSF) rhinorrhea
  • Cranial nerve palsies
  • Halo sign (or ring sign).
  • Medical Management
  • Non-depressed vs depressed
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20
Q

TYPES OF HEAD INJURIES

A
  • Most important consideration is if the brain is also damaged.
    Definitions
  • Lacerations - Actual Tearing of brain tissue
  • Contusion- Bruising of brain tissue
  • Concussion -Shaky movement of brain mild or moderate, a temporary loss of consciousness with no apparent structural damage
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21
Q

CONCUSSION

A
  • Temporary loss of neurologic function with no apparent structural damage to the brain
  • Mechanism of injury is usually blunt trauma from an acceleration–deceleration force, a direct blow, or a blast injury
  • Temporal lobe involvement can produce temporary amnesia or disorientation
  • Frontal lobe involvement can produce bizarre behavior.
  • Discharged home once return to baseline
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22
Q

Concussion S/S:

A
  • Loss of consciousness
  • Disorientation
  • Incoherent speech
  • Confusion
  • Memory loss
  • Dazed or vacant stare
  • Headache/dizziness
  • Difficulty concentrating
  • Sensitivity to light
  • Ringing in the ears
  • Fatigue
  • Vomiting
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23
Q

CONTUSION

A
  • Bruised Brain
  • Caused by severe acceleration-deceleration force or blunt trauma.
  • Impact of brain against skull leads to a contusion.
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24
Q

INTRACRANIAL HEMORRHAGE (HEMATOMA)

A
  • Collections of blood in the brain
  • Symptoms arise when:
    — it causes distortion of brain
    — Increases Intracranial Pressure ICP
    — Can be fatal
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25
Q

INTRACRANIAL HEMORRHAGE (HEMATOMA) Treatment

A
  • Supportive care
  • Control of ICP
  • Administration of fluids, electrolytes, and antihypertensive medications
  • Craniotomy or craniectomy to remove clot and control hemorrhage; this may not be possible because of the location or lack of circumscribed area of hemorrhage
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26
Q

EPIDURAL HEMATOMA

A
  • Blood collection in the space between the skull and the dura
  • Patient may have a brief loss of consciousness with return of lucid state; then as hematoma expands, increased ICP will often suddenly reduce LOC
  • An emergency situation!
  • Treatment includes measures to reduce ICP, remove the clot, and stop bleeding (burr holes or craniotomy)
  • Patient will need monitoring and support of vital body functions; respiratory support
  • GCS is usually <8: intubate
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27
Q

SUBDURAL HEMATOMA

A
  • Collection of blood between the dura and above arachnoid
  • Most commonly from tearing of bridging veins within cerebral hemispheres or from laceration of brain tissue
  • Bleeding occurs more slowly, symptoms mirror those of epidural hematoma
  • Acute or subacute
    — Acute: symptoms develop over 24 to 48 hours
    — Subacute: symptoms develop over 48 hours to 2 weeks
    — Requires immediate craniotomy and control of ICP
  • Chronic
    — Develops over weeks to months
    — Causative injury may be minor and forgotten
    — Clinical signs and symptoms may fluctuate
    — Treatment is evacuation of the clot
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28
Q

INTRACEREBRAL HEMORRHAGE AND HEMATOMA

A
  • Bleeding in parenchyma of brain
  • Usually seen with force over small area
    — (eg. Bullet wound)
  • May have non trauma causes
  • Onset insidious
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29
Q

DIFFUSE AXONAL INJURY

A
  • Results from widespread shearing and rotational forces that produce damage throughout the brain—to axons in the cerebral hemispheres, corpus callosum, and brainstem.
  • Head just bounces around in skull
  • Associated with prolonged traumatic coma!
    — No lucidity
    — Decorticate and decerebrate posturing
    — Cerebral edema
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30
Q

LOCATION OF SUBDURAL, INTRACEREBRAL, AND EPIDURAL HEMORRHAGES

A
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31
Q

THE BRAIN’S RESPONSE TO INJURY

A
  • Development of edema– cytotoxic (swelling is in cell) vs. vasogenic (outside of cell)
  • Loss of autoregulation (vasospasm or hyperemia)
  • Increase in ICP evolves over hours to days – usually peaks at 24 - 96 hours post injury, but may last 3 - 10 days
  • If secondary brain injury not prevented, a vicious cycle of deterioration ensues
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32
Q

Hemorrhage – collection of blood

A
  • Hydrocephalus – abnormal increase in CSF
  • Brain Herniation – brain moves downward
  • Uncal most clinically significant
33
Q

*BRAIN DEATH

A
  • Potential Organ Donor
    — One Legacy
  • Nurse can assist in dx of brain death and organ procurement
  • ***Three cardinal signs of brain death include:
    — Coma
    — Absence of brainstem reflexes
    — Apnea
34
Q

MEDICAL MANAGEMENT

A
  • CT
  • MRI
  • All head injury’s requires cervical spine injury to be ruled out
  • Transport must include back board and c-spine precautions
  • Cervical collar until x-rays rule out no SCI (spinal cord injury)
  • All therapy directed toward brain preservation and prevention of secondary injury.
  • https://www.youtube.com/watch?v=YI66VLKCkso
  • What is ICP
35
Q

INCREASED INTRACRANIAL PRESSURE

A
  • Brain tissues may shift through the Dura and result in herniation
  • Auto regulation: refers to the brains ability to change the diameter of blood vessels to maintain cerebral blood flow
  • CO2 plays a role; decreased CO2 results in vasoconstriction, and increased CO2 results in vasodilation
36
Q

FACTORS THAT INFLUENCE ICP

A
  • Hyperthermia
  • O2 status, CO2 status – hypoxia or hypercarbia -
  • Body Position – alignment of neck and 30-35 degrees
  • Arterial and venous pressure – high pressures
  • Anything that increases intra-abdominal/thoracic pressure
    — Eg vomiting bearing down, agitation, coughing
37
Q

Chart 63-5 Controlling ICP in Patients With Severe Brain Injury

A
  • Elevate the head of the bed as prescribed.
  • Maintain the patient’s head and neck in neutral alignment (no twisting or flexing the neck).
  • Initiate measures to prevent the Valsalva maneuver (e.g., stool softeners).
  • Maintain body temperature within normal limits.
  • Administer oxygen (O2) to maintain partial pressure of arterial oxygen (PaO2) >90 mm Hg.
  • Maintain fluid balance with normal saline solution.
  • Avoid noxious stimuli (e.g., excessive suctioning, painful procedures).
  • Administer sedation to reduce agitation.
  • *Maintain cerebral perfusion pressure (CPP) of 50–70 mm Hg. Best for pt
38
Q

INCREASED INTRACRANIAL PRESSURE

A
  • Normal ICP is 0 – 10 mm Hg with 15 being the upper limit
  • Measured in the lateral ventricles
  • Changes in ICP closely linked with Cerebral Perfusion Pressure
  • Pressure greater than 20 patient needs immediate treatment.
39
Q

ICP AND CPP

A
  • CPP (cerebral perfusion pressure) is closely linked to ICP
  • CPP = MAP (mean arterial pressure) – ICP
  • Normal CPP is 70 to 100
  • A CPP of less than 50 results in permanent neurologic damage
40
Q

HOW TO COMPUTE CPP

A
  • Need to know how to compute MAP first.
  • CPP = MAP – ICP
  • Have to know the BP and ICP values
  • Map
    — Diastolic x 2 =
    — Then take that number and add to systolic number
    — Take that number and divide by 3 = MAP
41
Q

HOW TO COMPUTE CPP

A
  • BP 90/42
  • ICP 19
  • 42 x 2 = 84
  • 84 + 90 = 174
  • 174/3 = 58
  • 58-19 = 39
42
Q

MANIFESTATIONS OF INCREASED ICP—EARLY

A
  • Changes in level of consciousness
  • Any change in condition
  • Restlessness, confusion, increasing drowsiness, increased respiratory effort, and purposeless movements
  • Pupillary changes and impaired ocular movements
  • Weakness in one extremity or one side
  • Headache: constant, increasing in intensity, or aggravated by movement or straining
43
Q

MANIFESTATIONS OF INCREASED ICP—LATE

A
  • Respiratory and vasomotor changes
  • VS:
    — increase in systolic blood pressure
    — widening of pulse pressure
    and slowing of the heart rate; pulse may fluctuate rapidly from tachycardia to bradycardia and
    — temperature increase
    —- **Cushing’s triad: bradycardia, hypertension, and bradypnea; worried about herniation
  • Projectile vomiting
44
Q

*MANIFESTATIONS OF INCREASED ICP—LATE

A
  • Further deterioration of LOC; stupor to coma
  • Hemiplegia, decortication, decerebration, or flaccidity
  • Respiratory pattern alterations including
  • Cheyne- Stokes breathing and arrest
  • *Loss of brain stem reflexes: pupil, gag, corneal, and swallowing
45
Q

ASSESSMENT OF THE PATIENT WITH ICP

A
  • Conduct frequent and ongoing neurologic assessment
  • Evaluate neurologic status as completely as possible
  • Glasgow Coma Scale
  • Pupil checks
  • Assess selected cranial nerves
  • Take frequent vital signs
  • Assess intracranial pressure
46
Q

ICP MONITORING

A
47
Q

NURSING ASSESSMENT

A
  • Health history with focus upon the immediate injury, time, cause, and the direction and force of the blow
  • Baseline assessment
  • LOC: Use Glasgow Coma Scale
  • Frequent and ongoing neurologic assessment
  • Multisystem assessment
48
Q

GLASGOW COMA SCALE

A
49
Q

ASSESSMENT

A
  • Priority is ABC’s and Spine Precautions
  • Respiratory problems are considered emergent
  • Watch for Cheyne-Stokes
  • May need intubation
  • Vital signs (watch for Cushing’s Triad) – elevated ICP, severe HTN, wide Pulse Pressure
  • Neuro Assessment – LOC most important – Perrla
  • Psychosocial Assessment
50
Q

DIAGNOSTIC EVALUATION

A
  • Physical and neurologic exam
  • Skull and spinal x-rays
  • ABG’s CBC, Electrolytes, tox screen
  • CT scan – scope of injury
  • MRI
  • PET scan
  • EKG
51
Q

COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONS

A
  • Decreased cerebral perfusion
  • Cerebral edema and herniation
  • Impaired oxygenation and ventilation
  • Impaired fluid, electrolyte, and nutritional balance
    -Risk of post-traumatic seizures
52
Q

PLAN

A
  • Severe TBI admission to ICU
  • Moderate admitted to med surg for observation
  • Mild sent home with instructions for someone to observe for 24 hours
  • Assume cervical spine injury until this is ruled out
  • Therapy to preserve brain homeostasis and prevent secondary damage
  • Treat cerebral edema
  • Maintain cerebral perfusion; treat hypotension, hypovolemia, and bleeding; monitor and manage ICP - Maintain oxygenation as well as cardiovascular and respiratory function
  • Manage fluid and electrolyte balance
  • Prevent secondary brain injury
53
Q

INTERVENTIONS

A
  • Maintain airway by: Table 68-1 pg. 2040 2041
  • Positioning to facilitate promote blood flow and drainage of oral secretions with HOB usually elevated 30 degrees to decrease venous pressure
  • Suctioning with caution
  • Prevention of aspiration and respiratory insufficiency
  • Monitor for pulmonary complications, potential ARDS
  • Monitor I&O and daily weights
  • Monitor blood and urine electrolytes, osmolality and blood glucose
  • Implement measures to promote adequate nutrition
  • Implement strategies to prevent injury
  • Assess bladder and urinary output
  • Assess for constriction due to dressings and casts
  • Pad side rails
  • Use mittens to prevent self-injury; avoid restraints
54
Q

INTERVENTIONS: Strategies to prevent injury

A
  • Reduce environmental stimuli
  • Use adequate lighting to reduce visual hallucinations
  • Implement measures to minimize disruption of sleep–wake cycles
  • Provide skin care
  • Implement measures to prevent infection
  • Therapeutic Hypothermia
  • Positioning
  • Nutrition
55
Q

INTERVENTIONS: to Maintain body temperature

A
  • Maintain appropriate environmental temperature
  • Use coverings: sheets, blankets as per patient needs
  • Administer acetaminophen for fever
    -Use cooling blankets or cool baths; prevent shivering
56
Q

INTERVENTIONS: to Prevent secondary brain injury

A
  • VS Q 1-2 hours depending on acuity including temperature
  • Monitor EKG
  • Medications for hyper or hypotension
  • Maintain prescribed BP
  • If patient intubated, monitor ABGs, SPO2, end tidal CO2.
  • Seizure precautions and prevention
  • NG tube to manage reduced gastric motility and prevent aspiration
  • Fluid and electrolyte maintenance
  • Pain and anxiety management
  • Nutrition
57
Q

INTERVENTIONS: to Support cognitive, sensory perception and behavioral changes function:

A
  • Support family
  • Provide and reinforce information
  • Implement measures to promote effective coping
  • Set realistic, well-defined, short-term goals
  • Refer patient for counseling
  • Refer patient to support groups
  • Patient and family teaching:
  • Strategies to compensate for sensory and perceptual alterations
  • Measures to maintain skin integrity
  • Temporary indwelling catheterization or intermittent catheterization
  • NG tube to alleviate gastric distention
  • High-calorie, high-protein, high-fiber diet
  • Bowel program and use of stool softeners
  • Traction pin care
  • Hygiene and skin care related to traction devices
58
Q

DRUG THERAPY

A
  • Mannitol – Osmotic Diuretic – IV needs filter
  • Sedative Agents- dexmedetomidine or Propofol
  • Opioids
  • Antiepileptics
  • Furosemide
  • Barbiturate Coma – uncontrollable ICP
59
Q

Mannitol (Osmitrol):

A
  • The onset of diuretic action of mannitol is 1 to 3 hours and reduction of intracranial pressure occurs in 15 to 30 minutes.
  • Its half-life is approximately 1 to 1.6 hours.
  • Excretion is primarily as unchanged drug in the urine.
  • reduces fluid in cells
  • most effective when given as bolus
  • takes fluid out of brain and puts it in circulation; watch for fluid overload
60
Q

Mannitol (Osmitrol):
Adult:
Cerebral edema:

A
  • 0.25-1g/ kg IV as 15%-20% solution
  • administered over: at least 30 min, every 6-8 hours as needed
61
Q

Mannitol (Osmitrol):
Adult
Intracranial pressure reduction:

A
  • 1.5-2g/kg IV
  • administered over: 30-60 min 1-1.5 hours prior to surgery
62
Q

IMPORTANT NUMBERS TO REMEMBER FROM BRUNNER FOR ICP AND CPP

A
  • ICP is usually measured in the lateral ventricles, with the normal pressure being 0 to 10 mm Hg, and 15 mm Hg being the upper limit of normal.
  • As ICP rises, compensatory mechanisms in the brain work to maintain blood flow and prevent tissue damage.
  • The brain can maintain a steady perfusion pressure if the arterial systolic blood pressure is 50 to 150 mm Hg and the ICP is less than 40 mm Hg.
  • Changes in ICP are closely linked with cerebral perfusion pressure (CPP).
  • The normal CPP is 70 to 100 mm Hg.
  • Patients with a CPP of less than 50 mm Hg experience irreversible neurologic damage. Therefore, the CPP must be maintained at 70 to 80 mm Hg to ensure adequate blood flow to the brain.
  • If ICP is equal to MAP, cerebral circulation ceases.
63
Q

*autonomic dysreflexia:

A

a life-threatening emergency in patients with spinal cord injury that causes a hypertensive emergency; also called autonomic hyperreflexia

64
Q

complete spinal cord lesion:

A

a condition that involves total loss of sensation and voluntary muscle control below the lesion

65
Q

concussion

A

a temporary loss of neurologic function with no apparent structural damage to the brain

66
Q

contusion

A

bruising of the brain surface

67
Q

halo vest:

A

external traction device that encircles the head like a halo and stabilizes the cervical spine

68
Q

incomplete spinal cord lesion:

A

a condition in which there is preservation of the sensory or motor fibers, or both, below the lesion

69
Q

neurogenic bladder:

A

bladder dysfunction that results from a disorder or dysfunction of the nervous system; may result in either urinary retention or bladder overactivity

70
Q

paraplegia

A

paralysis of the lower extremities with dysfunction of the bowel and bladder from a lesion in the thoracic, lumbar, or sacral region of the spinal cord

71
Q

primary injury:

A

initial damage to the brain that results from the traumatic event

72
Q

secondary injury:

A

an insult to the brain subsequent to the original traumatic event

73
Q

spinal cord injury (SCI):

A

an injury to the spinal cord, vertebral column, supporting soft tissue, or intervertebral discs caused by trauma

74
Q

tetraplegia

A
  • varying degrees of paralysis of both arms and legs, with dysfunction of bowel and bladder from a lesion of the cervical segments of the spinal cord; formerly called quadriplegia
75
Q

transection

A
  • severing of the spinal cord itself; transection can be complete (all the way through the cord) or incomplete (partially through)
76
Q

traumatic brain injury:

A

an injury to the skull or brain that is severe enough to interfere with normal functioning

77
Q

traumatic brain injury, closed (blunt):

A

occurs when the head accelerates and then rapidly decelerates or collides with another object and brain tissue is damaged, but there is no opening through the skull and dura

78
Q

traumatic brain injury, open (penetrating):

A

occurs when an object penetrates the skull, enters the brain, and damages the soft brain tissue in its path (penetrating injury), or when blunt trauma to the head is so severe that it opens the scalp, skull, and dura to expose the brain

Test 2 🏁🏁 (12 decks)

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