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Module 7 > UNIT 3: Head Injury (MST 2) > Flashcards

UNIT 3: Head Injury (MST 2) Flashcards

1
Q

What are the 3 essential components of the skull?

A
  1. Brain Tissue
  2. Blood
  3. Cerebrospinal fluid (CSF)
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2
Q

What is a primary injury of the skull?

A

Primary injury occurs at the inital time of an injury… like the impact of a car accident, blunt force truama which results in displacement, brusing, or damage to any of the three components.

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3
Q

What is a secondary skull injury?

A

Secondary injury is the resulting hypoxia, ischemia, hypotension, edema or increased ICP that follows a primary injury. Secondary injury, which could occur several hours to days after the inital injury, is a primary concern when managing a brain injury.

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4
Q

Nursing managment of a patient with an acute intracranial brain injury includes?

A
  1. Managment of the secondary injury and thus increased ICP.
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5
Q

What is cerebral edema?

A

Increased accumulation of fluid in teh extravascular spaces of brain tissue.

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6
Q

Regardless of the cause of cerebral edema the result is…

A

Increase in tissue volume that can cause an increase in ICP. The extent and severity of the original insult are factors that determine the degree of cerbreal edema

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7
Q

What is ICP?

A

ICP is the hydrostatic force measured in teh brain CSF compartment. Under normal conditions in which intracranial volume remains relatively constant, the balance amount the three components (brain, blood, and CSF) maintains the ICP.

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8
Q

What factors influence ICP under normal circumstances?

A
  1. Arterial pressure
  2. Venous pressure
  3. Intraabdominal and intrathoracic pressure
  4. Posture
  5. Temp
  6. Blood gases- particularly co2 levels

The degree to which these factors increase or decrease the ICP depends on the brains ability to adapt or change.

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9
Q

What is the Monro-Kellie doctrine?

A

Simply put when the volume of something in. your head goes up the volume of something else must go down. Usually starting with CSF then blood then brain.

States that the three compoenents must remain at a relatively constant voulme within the closed skull structure. If the volume of any one of the three components increases within the cranial vault and the volume from another component is displaced, the total intracranial volume will not change but this is only valid in persons in which the skull is closed. This is not valid in persons with displaced skull fractures or hemicraniectomy

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10
Q

ICP can be measured in the…

A
  1. Ventricles
  2. Subarachnoid space
  3. Subdural space
  4. Epidural space
  5. brain tissue

Using a transducer.

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11
Q

Normal ICP range

A

5-15mmHG

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12
Q

What ICP range is considered abnormal and requires treatment?

A

20mmHG

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13
Q

What are normal compensatory adaptations to head injuries?

A
  1. Applying the monro-kellie doctrine
  2. Cerebral blood flow
  3. Autoregulation of cerbral blood flow
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14
Q

What is cerebral blood flow?

A

It is the amount of blood in mL passing through 100g of brain tissue in 1 min.

The maintenance of blood flow to the brain is critical because the brain requires a constant supply of o2 and glucose.

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15
Q

What is autoregulation of cerebral blood flow?

A

The brain regulates its own blood flow in response to its metabolic needs despite wide fluctions in systemic arterial pressure. Autoregulation is the automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintaina constant blood flow during changes in arterial pressure. (BP).

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16
Q

What is the purpose of autoregulation in head injuries?

A

The purpose of autoregulation is to ensure a consistent CBF to provide for the metabolic needs of brain tissue and to maintain cerebral perfusion pressure within normal limits.

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17
Q

What is the lower limit of systemic arterial pressure at which autoregulation is effective in a normotensive person?

May need rewording after lecture

A

MAP of 70 mmHG

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18
Q

What starts happening with CBF (blood flow) when a patients map is below 70 mmHG

A

CBF decreases and symptoms of cerebral ischemia, such as syncope and blurred vision occur.

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19
Q

What is the upper limit of systemic arterial pressure at which autoregulation is effective?

may need rewording after lecture.

A

MAP of 150mmHG

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20
Q

What happens to CBF when the MAP is above 150mmHg

A

When this pressure is exceeded, the vessels are maximally constricted, and further vasoconstrictor response is lost. CBF can be affected by cardiac or resp. arrest, systemic hemorrhage and other pathophysiologic states (diabetic coma, encephalopathies, infections, toxicities.

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21
Q

What does CPP mean?

A

Cerebral perfusion pressure

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22
Q

What does CVP mean?

A

Central venous pressure

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23
Q

ICP increases by?

A
  1. Intracranial bleeding
  2. Cerebral Edema
  3. Tumor
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24
Q

Increased ICP can result in…

A
  1. Collapse veins
  2. Decreases effective CPP
  3. Reduces blood flow
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25
Q

What is cerebral perfusion pressure?

A

It is the force driving blood into the brain, providing oxygen and nutrients. The pressure needed to ensure blood flow to the brain.

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26
Q

Cerebral perfusion pressure the primary determinant of…

A

cerebral blood flow.

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27
Q

How do we calculate cerebral perfusion pressure?

A

CPP= MAP-ICP

CPP means cerebral perfusion pressure

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28
Q

What is normal CPP?

A

60 to 100 mmHg

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29
Q

What happens as CPP decreases what happens to the CBF?

A

Autoregulation fails and CBF decreases.

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30
Q

A CPP less than 50mmHg is associated with…

A

Ischemia and neuronal death

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31
Q

A CPP less than 30 mmHg results in….

A

ischemia and is incompatible w/life

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32
Q

The formula for CPP does not consider the effect of what?

A

Cerebrovascular resistence

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33
Q

What are s/s of increased intracranial pressure?

A

Depends on the cause, location and rate of increase
1. Changes in LOC
2. Eye changes
3. Posturing
4. Decreased motor function
5. Headache
6. Seizure- impaired sensory & motor function
7. Changes in vitals
8. Vomiting
9. Changes in speech
10. Infants: bulging fontanels and cranial suture seperation, high pitched cry

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34
Q

What changes in the eyes might we see in a patient with increased ICP?

A
  1. Papilledema
  2. Pupillary changes
  3. Impaired eye movement
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35
Q

What type of posturing would we see in a patient with increased ICP?

A
  1. Decerebrate
  2. Decorticate
  3. flaccid
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36
Q

What changes in motor function might we see in a patient with increased ICP?

A
  1. Change in motor ability
  2. posturing

Decreased motor function

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37
Q

What vital sign changes might we see in a patient with increased ICP?

A

Cushings TRIAD
1. increased systolic b/p
2. Decreased pulse
3. Altered resp. pattern

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38
Q

What is the major complications of uncontrolled ICP?

A
  1. Inadequate cerebral perfusion
  2. Cerebral herniation
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39
Q

Cushings triad is considered a….

A

Neurologic emergency…

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40
Q

Symptoms of ICP are opposite of shock

What happens to our vitals as a patient with Increased ICP turns into shock?

May need to reword after lecture.

A
  1. Decreased b/p
  2. Increased pulse
  3. Increased resp.

As brain compression increases, respirations become rapid, the blood pressure may decrease, and the pusle slows further. This is an omnious development as is the rapid fluctions in vitals.

41
Q

How can we monitor ICP?

A

Transducer- This technique directly measures the pressure within the ventricles, facilitates removal and/or sampling of CSF, and allows for intraventricular drug administration.

42
Q

Slide 10- might need to add tranducer placement question.. will do after lecture

A
43
Q

What is our role as the nurse in treating patients with head injuries?

A
  1. Identify and treat underlying cause
    • The earilier the better.
    • Hx is important in dx
    • Surgical removal if caused by tumor.
  2. Support brain function
    • Ensure adequate oxygenation to prevent secondary injury
    • Endotracheal tube or tracheosmy may be needed.
    • ABG analysis
  3. Drug therapy
  4. Nutritional therpay
    • From the moment of injury the metabolism speeds up because it is using calories to heal and calories for normal day to day function. We need to make sure they eat asap.
44
Q

What are common underlying causes of increased ICP?

A
  1. Increased blood
  2. brain tissue
  3. CSF
45
Q

What is our goal with our ABGs in a head injury?

A

Goal is to maintain the paO2 greater than or equal to 100mmHg and keep PacO2 in the normal range 35-45 mmHg. The patient may need to be on a mechanical vent to ensure adequate oxygenation.

46
Q

What is a head injury?

A

Any trauma to the
1. Scalp
2. Skull
3. Brain

Head trauma includes alteration in LOC no MATTER HOW BRIEF. They have a high potential for poor outcomes.

47
Q

When does death occur when a head injury occurs?

A

3 points in time after injury
1. Immediately after the injury: usually a catostrophic injury
2. Within 2 hours of the injury: Usually r/t a bleed or edema
3. 3 weeks after injury: Usually r/t infection

48
Q

Neurologic trauma affects the…

who does it affect

A
  1. Patient
  2. family
  3. health care system
  4. society as a whole because of its major sequele and the costs of acute and long term care
49
Q

What groups are at highest risk for a head injury?

A

People between the age of 15-24. Males are at most risk.

The very young before 5 or old after 75 are at increased risk

50
Q

The best approach to head injuries

A

Prevention

51
Q

What should we know about scalp lacerations?

A

Can bleed profusely- scalp contains many blood bessels with poor constrictive abilities,

52
Q

What are types of skull fractures?

A
  1. Linear or depressed
  2. Simple, comminuted, or compound
  3. Closed or open.

The type and severity of a skull fracture depends on the velocity, momentum, direction, and shape (blunt or sharp) of the injuring agent and size of impact.

53
Q

What is the major complication of scalp lacerations

A

Blood loss and infection.

54
Q

How are brain injuries categorized?

A

Diffuse (generalized) or focal (localized)

55
Q

What should we know about diffuse injuries?

A
  1. These are injuries like a concussion, diffuse axonal injury DIA.
  2. Damage to the brain cannot be localized to one particular area
56
Q

What should we know about focal brain injuries?

A
  1. These are injuries like laceratons, contusions, coup-contrecoup, hematoma
  2. Damage can be localized to a specific area of the brain.
57
Q

Brain injuries can be classified as….

A
  1. Minor (GCS 13 to 15)
  2. Moderate (GCS 9 to 12)
  3. Severe (GCS 3 to 8)
58
Q

What is a concussion?

A

A sudden transient mechanical head injury with disruption of neural activity and change in LOC. Conisdered a minor diffuse head injury. The patient may or may not lose total consciousness with this injury.

59
Q

What are typical signs of a concussion?

A
  1. Breif disruption of LOC
  2. Amnesia regarding the event (retrograde amnesia)
  3. Headache

Short lived. If the patient has not lost consiouness or if the loss of consciousness lasts less than 5 mins. The patient is normally discharged from the care facility with instructions to notify HCP if symptoms persists or behavioral changes occur

60
Q

What is a diffuse axonal injury (DAI)

A
  1. Widespread axonal damage occuring after a mild, moderate, severe TBI.
  2. The damage occurs primary around axons in the subocortical white matter of the cerebral hemispheres, basal gangila, thalmus, and brainsteam.
  3. Initally, DAI was believed to occur from the tensile forces of trauma the sheared axons, resuling in axonal disconnect.
61
Q

What are some complications of head injuries?

A
  1. Epidural Hematoma
  2. Subdural hematoma
  3. intracerebral hemorrhage
  4. Subarachnoid hemorrhage
62
Q

What is a epidurial hematoma?

A

Results from bleeding between the DURA and INNER SURFACE of the skull.

  1. Neurologic emergency
  2. Associated w/linear fracture crossing a major artery in the dura causing a tear
  3. Venous or arterial orgin
    • Venous epidual: associated with a tear of the dural venous sinus and develops SLOWLY.
    • Arterial hematomas, the middle menigeal artery lying under the temporal bone is often torn. Hemorrage occurs into the epidural space, which lies between the dura and inner surface of the skull causing the hematoma to develope rapidly.
63
Q

What are classic signs of a epidural hematoma?

Walking dead

A
  1. inital period of unconsciousness at scene
  2. brief lucid interval followed by a decrease in LOC
  3. Headache
  4. N/V
  5. Focal findings
64
Q

How are epidural hematomas treated?

A
  1. Rapid surgical intervention to evacuate the hematoma and prevent cerebral herniation
  2. Managment for increasing ICP
65
Q

What is a subdural hematoma?

A

Occurs from bleeding between the dura mater and arachnoid layer of the meninges. A subdural hematoma usually resuts from injury to the brain tissue and its blood vessels. The veins that drain from the surface of the brain into the sagittal sinus are the source of most subdural hematomas.

Usually of venous orgin so they may be SLOWER to develope.

Bridging veins

66
Q

What do we need to know about about a subdural hematoma?

A
  1. Manifests within 24-48 hours of the injury
  2. S/S are similar to increased ICP. (headache, vomitting) SLOW BLEED
  3. Size of the hematoma determines the patients clinical presentation and prognosis. The pts appearance may range from drowsy to confused to unconscious.
  4. Injury to the actual brain tissue and vessels
  5. Treatment may include sitting on the bleed to see if it will resolve itself and reaborb.
67
Q

What do we need to know about a subacute subdural hematoma?

A
  1. Usually occurs within 2 to 14 DAYS of the injury
  2. After inital bleeding, A subdural hematoma may appear to enlarge over time as the breakdown products of the blood draw fluid into the subdural space
68
Q

What do we need to know about a chronic subdural hematoma

A
  1. Develops over WEEKS TO MONTHS after a seemingly minor head injury. Chornic subdural hematomas are more common in older adults because of a potentially larger subdural space as a result of brain atrophy.
  2. With atrophy the brain remains attached to the supportive structures but tension is increased and is more subject to tearing
  3. . because the subdural space is larger, the preseing complaint is FOCAL symptoms. (specific to certain areas of the brain) rather than signs of increased ICP.
  4. Often seen in Alcoholics as well
69
Q

Chornic alcoholics are prone to what?

A

Cerebral atrophy and because of that at higher risk for subdural hematomas because of the increased incidence of fallas

70
Q

What is an intracerebral hemorrahge?

A

Bleeding into the subatance of the brain. Onset may be insidious, beginning with the development of neuro deficits followed by a headache.

  1. Occurs from bleeding within the parenchyma
  2. Ususally occurs in the frontal and temporal lobes
  3. Size and location determine patient outcome
71
Q

When is intracerebral hemorrhages commonly seen?

A
  1. Head injuries when force is exerted to the head over a small area
    • missle injuries, bullet wounds, stab injuries
72
Q

How do we manage intracerebral hemorrhages?

A
  1. Supportive care
  2. Control of ICP
  3. Careful admin of fluids, electrolytes and Antihypertensive medications.
  4. Surgical intervention by crainiotomy- craniectomy permits the removal of the blood clot and control of the hemmorrhage but may not be possible
73
Q

What is a subarachnoid hemorrhage?

A
  1. Hemorrhage into the subarachnoid space which may occur as a result of an AVM (intracranial aneurysm), trauma, HTN, the most COMMON causes are leaking aneurysm in the area of the circle of willis and a congenital AVM of the brain.
74
Q

What is a serious complication of a subarachnoid hemorrage?

A

Vasospasm (narrowing of the lumen of the involved crainal blood vessel) is a serious complication and is the leading cause of morbidity and mortality in those who survive the intial subarachnoid hemorrhage.

Monitoring for vasospasm may be performed through the use of bedside transcranial doppler ultrasonography or follow up of cerebral angiography.

Typically occurs 3-14 days after the inital hemorrhage when the clot undergoes lysis. and the chances of rebleeding is increased. It leads to increased vascular resistence which impedes flow and causes brain ischemia and infarction.

75
Q

What is our nursing managment for head injuries?

may need to add or simplfy after lecture may need to add temp…

A

Nursing assessment
1. Airway
- Maintaing adequate airway is goal in managment of head injuries. Brain is extremely sensitvie to hypoxGia and neuro deficits can worsen if patient is hypoxic
- Maintaining the unconscious pt in a postion that facilitates drainage of oral secreations with the head of bed elevated 30 degrees to decrease ICP

  1. GCS
    • used to assess LOC at regular intervals because changes in LOC precede all changes in vitals and neuro signs.
    • Vitals monitored at frequent intervals to assess intracranial status. Depicts the general assessment parameters for the patient with a head injury
  2. Neuro status
  3. Presence of a CSF leak

Collaborative provlem: increased ICP

76
Q

What are some physical signs we may see on our patient that could indicate a head injury?

slide 17– look and add to after lecture.

A
  1. Racoon eyes and rhinorrhea
  2. Battle sign (postauricular eccymosis) with otorrhea
  3. Halo or ring sign.
77
Q

What is the GSC?

A

Glasgow coma scale is a quick, practical standardized system for assessing LOC. There are three areas assessed in the GCS.
1. Ability to open eyes when a verbal or painful stimuli is applied
2. Speak
3. Obey commands

The higher the scores the higer the level of brain functioning a patient has.

78
Q

The highest GCS score is…

A

15 for a fully alert person

79
Q

The lowest GCS score is a….

A

3

80
Q

A GCS score of less than 8 usually indicates…

A

Coma and mechanical ventilation should be considred.

81
Q

REVIEW: GCS best eye response scores.

A

Open spontaneiously: 4
Open to verbal command: 3
Open to pain: 2
No eye opening: 1

82
Q

Review: GCS Best verbal responses

A

Oriented: 5
Confused: 4
Inappropriate words: 3
Incomprehensible sounds: 2
No verbal response: 1

83
Q

Review: Best Motor Response

A

Obeys Commands: 6
Localizng pain: 5
Withdrawal from pain: 4
Flexion to pain: 3
Extension to pain: 2
No motor response: 1

84
Q

What is our nursing implementation for head injuries?

A

Acute Intervention (relates to increased ICP, hyperthermia leaking CSF)
1. Maintain cerebral perfusion
2. Prevent secondary cerebral ischemia
3. Monitor for changes in neurologic status
4. Treatment of life-threatening conditions will initally take priority in nursing care
5. monitor serum electrolyte levels is important- esp if on osmostic diuretics.
6. Serial studies of blood and urine electrolytes
- esp. in patients with SIADH, postraumatic DI due to sodium imbalences

Ambulatory and home care
1. Nutrition, bowel/bladder control
2. Seizure disorders, personality changes
3. Family participation and education.

85
Q

What should we keep in mind about sodium levels in terms of head injuries?

A
  1. Hyponatremia is common after head injury due to shifts in extracellular fluid, in electrolytes and volume. Hyperglycemia for example, can cause an increase in extracellular fluid that lowers sodium.
  2. Hypernatremia may also occur as a reulst of sodium rentention that may last several days, followed by sodium diuresis. Increasing lethargy, confusion, and seizures may be the result of electrolyte imbalances.
86
Q

What metabolic changes are occuring with head injuries?

A
  1. Increase in calorie consumption & nitrogen excretion
  2. Protien demand increases

Early initition of nurtritional therapy has been shown to improve outcomes in patients with head injury. Patients with brain injury are assumed to be catabolic and nutritional support consultation should be considrered asap.

87
Q

How can we teach the public about prevention of head injuries?

A
  1. Advise all drivers and passengers to wear seat belts and shoulder harness if applicable to the vehicle
  2. Caution passengers against riding in the back of a pickup truck
  3. promote educational programs directed toward violence and suicde prevention in the community
  4. Teach patients steps to prevent falls, particularly the elderly
  5. Advice owners of firearms to keep them locked in a secure area where children cannot access them.
88
Q

Review: Cranial nerve I
Name function and how to test.

A
  1. Olfaction
  2. Alcohol pad
89
Q

Review: Cranial nerve II
Name function and how to test

A
  1. Vision
  2. Vision Chart
90
Q

Review: Cranial nerve III
Name funciton and how to test

A
  1. Most eye muscles
  2. “following the moving finger”
91
Q
A
92
Q

Out of the CSF, Brain and blood what is normally the first to shift to normalize ICP?

A
  1. CSF- can be displaced or even stop being manufactured.
  2. Blood is next- can be compressed but when this happens pt is at risk for hypoxia in the brain and ischemia
  3. Brain– can swell to the point of herniation
93
Q

What are the ways to monitor ICP (areas)

A
  1. Epidural
  2. Intraparenchymal (brain matter)
  3. Subarachnoid (space)
  4. Ventricular (into the drainage system of the brain)gold standard
  5. Subdural
94
Q

Name A,B,C,D,E

A

A. Subarachnoid
B. Intraparenchymal
C. Epidural
D. Ventricular
E. Subdural

95
Q
A
96
Q

How do we be safe when taking care of a patient with a ICP monitor

A
  1. Infection prevention
    • Watch labs, are they flushed, running fever?
    • Maintain temp control
    • Maintain sterility
  2. Tubing
    • Label tubing in several spots esp. by the port
    • Doctor is the only person who can administer meds from the port
    • maintain control of the tubing. dont want it somewhere that is at risk of getting tripped on or pulled out of the patient
  3. Montiro ICP trends
  4. Maintain good oxygenation
    • maintain good ABGs
97
Q

How might a patient with a subarachnoid hemorrhage present?

A
  1. Severe headach (thunderclap) worst theyve ever had
  2. Photophobia (sunglasses or not looking at you)
  3. N/V

NEVER ASSUME ITS “JUST A MIGRAINE”
DONT HAVE TO HAVE TRAUMA TO HAVE A SUBARACHNOID HEMMORRAGE: HTN IS A COMMON CAUSE

98
Q

What drug is used to tx vasospasms?

A

nemopidine it is a CCB

99
Q

How do we want our pressures/volume in a patient having a vasospasm?

A

Hypertensive hypervolemic

Module 7 (22 decks)

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