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NURS 425 > Exam 3: ICP And Head Injury > Flashcards

Exam 3: ICP And Head Injury Flashcards

1
Q

The skull has three essential components:

A
  1. Brain tissue
  2. Blood
  3. CSF
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2
Q

Intracranial Pressure

A

The hydrostatic force measured in the brain CSF compartment

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3
Q

What maintains the ICP?

A

Balance among the brain tissue, blood and CSF.

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4
Q

What are factors that influence ICP?

A
  • Arterial pressure
  • Venous pressure
  • Intraabdominal and intrathoracic pressure
  • Posture (i.e lying down increases pressure)
  • Temperature (i.e when cold = vasoconstriction = decreased blood flow to brain)
  • Blood gases (CO2 levels) (high CO2 levels = vasodilation, however with high CO2 = low O2; want PaO2 as close to 100 as possible))
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5
Q

What is the Monro-Kellie Doctrine?

A
  • If one component increases, another must decrease to maintain ICP.
  • Only applicable in situations in which the skull is closed.
  • Not valid in persons with displaced skull fractures or hemicranectomy.
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6
Q

Normal ICP

A

5-15 mm Hg

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7
Q

Elevated ICP

A

If ICP >20 mm Hg sustained

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8
Q

The body can adapt to volume changes within the skull in what three different ways in order to maintain a normal ICP?

A
  1. Changes in CSF volume
  2. Changes in intracranial blood volume
  3. Changes in tissue brain volume
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9
Q

Changes in CSF volume

A

Can be changed by altering CSSF absorption or production and by displacement of CSF into the spinal subarachnoid space.

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10
Q

Changes in intracranial blood volume can occur through

A
  • The collapse of cerebral veins and dural sinuses
  • Regional cerebral vasoconstriction or dilation
  • Changes in venous outflow.
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11
Q

Changes in tissue brain volume compensates through

A

Distention of the dura or compression of brain tissue

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12
Q

Initially, an increase in volume produces no increase in ICP as a result of the compensatory mechanisms. However

A
  • The ability to compensate for changes in volume is limited.
  • As the volume increase continues, the ICP rises, and decompensation ultimately occurs, resulting in compression and ischemia.
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13
Q

What is the definition of cerebral blood volume?

A

Amount of blood in mL passing through 100 g of brain tissue in 1 minute

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14
Q

What is the normal cerebral blood flow?

A

About 50 mL/min per 100 g of brain tissue

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15
Q

Why is maintenance of blood flow important?

A

Critical because the brain requires a constant supply of oxygen and glucose

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16
Q

What is autoregulation?

A
  • Is the automatic adjustment in the diameter of the cerebral blood vessels by the brain to maintain a constant blood flow during changes in arterial blood pressure.
  • Purpose is to ensures consistent CBF
  • Only effective if mean arterial pressure (MAP) 70 to 150 mm Hg
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17
Q

Cerebral Perfusion Pressure (What is the formula, normal)

A
  • CPP = MAP – ICP

- Normal is 60 to 100 mm Hg

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18
Q

Effect of cerebral vascular resistance is links CPP and blood flow as follows:

A

CPP = Flow x Resistance

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19
Q

What is cerebral perfusion pressure?

A

The pressure needed to ensure blood flow to the brain.

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20
Q

As CPP decreases, what happens?

A

Autoregulation fails, and CBF decreases

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21
Q

A CPP less than 50 mm Hg is associated with what?

A

Ischemia and neuronal death

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22
Q

A CPP less than 30 mm Hg results in what?

A

Ischemia and dis incompatible with life

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23
Q

What is cerebral vascular resistance?

A

Generated by the Arteriosus within the cranium, links CPP and blood flow.

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24
Q

If ICP is up, what is going to happen to blood flow?

A

It’s going to go down

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25
Q

Cerebral Blood Flow: Pressure Changes

A
  • Compliance is the expandability of brain
  • Impacts effect of volume change on pressure
  • Compliance = Volume/Pressure

*read notes

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26
Q

What are stages of increased ICP?

A

Stage 1: Total compensation
Stage 2: ↓ Compensation; risk for ↑ICP
Stage 3: Failing compensation; clinical manifestations of ↑ ICP (Cushing’s triad)
Stage 4: Herniation imminent → death

*Read notes

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27
Q

What are factors that affect cerebral blood vessel tone?

A
  1. CO2
  2. O2
  3. Hydrogen ion concentration
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28
Q

Factors affecting cerebral blood vessel tone: An increase in CO2 can lead to

A
  • Relaxation of smooth muscle
  • Dilation of cerebral vessels
  • Decreased cerebrovascular resistance
  • Increased CBF
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29
Q

Factors affecting cerebral blood vessel tone: A decrease in PaCO2 can lead to

A
  • Constricted cerebral vessels
  • Increased cerebrovascular Resistance
  • Decreased CBF
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30
Q

Factors affecting cerebral blood vessel tone: Cerebral O2 tension less than 50 mm Hg results in

A
  • Cerebrovascular dilation
  • Dilation decreases CVR
  • Increases CBF
  • Increases O2 tension
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31
Q

Factors affecting cerebral blood vessel tone: If O2 tension is not increased

A
  • Anaerobic metabolism begins. This results in accumulation of lactic acid.
  • Accumulation of lactic acid increases and hydrogen ions accumulate = acidic environment.
  • Acidic environment = further vasodilation in an attempt to increase BF.
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32
Q

Increased ICP

A
  • Life-threatening
  • Results from an increase in any of three components (Brain tissue, blood and CSF)
  • ↑ Cerebral edema

*Read notes!!

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33
Q

Progression of Increased Intracranial Pressure

A
  • Cerebral edema distorts brain tissue, further increasing the ICP, and leads to even more tissue hypoxia and acidosis.
  • Sustained increases in ICP result in brainstem compression and herniation of the brain from one compartment to another.
  • Displacement and herniation of brain tissue can cause a potentially reversible process to become irreversible.
  • Ischemia and edema are further increased, compounding the preexisting problem.
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34
Q

Effects of Herniation

A
  • Compression of the brainstem and cranial nerves which may be fatal.
  • Forces the cerebellum and brainstem downward through the Foramen magnum.
  • If compression is unrelieved, respiratory arrest will occur due to compression of the respiratory control center in the medulla.
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35
Q

Cerebral Edema

A
  • ↑ Extravascular fluid in brain

- Variety of causes

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36
Q

What are the three types of cerebral edema?

A
  1. Vasogenic
  2. Cytotoxic
  3. Interstitial

*Read notes

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37
Q

Vasogenic Cerebral Edema

A
  • Most common type
  • Occurs mainly in white matter
  • Fluid leaks from intravascular to extravascular space
  • Continuum of symptoms → coma
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38
Q

What can cause vasogenic cerebral edema?

A

Variety of insults such as brain tumors, abscesses and ingested toxins, may cause an increase in the permeability of the BBB and produce an increase in the extracellular volume.

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39
Q

Cytotoxic Cerebral Edema

A
  • Disruption of cell membrane integrity
  • Secondary to destructive lesions or trauma to brain tissue
  • Fluid shift from extracellular to intracellular

*READ NOTES!

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40
Q

Interstitial Cerebral Edema

A
  • Usually result of hydrocephalus

- Excess CSP production, obstruction of flow, or inability to reabsorb

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41
Q

How do you treat interstitial cerebral edema?

A

Treat with ventriculostomy or shunt

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42
Q

Clinical Manifestations of Cerebral Edema

A

-Change in level of consciousness: Flattening of affect → coma
-Change in vital signs: Cushing’s triad (widened pulse pressure, bradycardia, irregular respirations)
-Change in body temperature (tend to be hypothermic - can’t regulate body temp)
-Compression of oculomotor nerve
-Other cranial nerves (Diplopia, blurred vision and EOM changes)
-Decrease in motor function
-Headache (often continuous and worse in morning)
-Vomiting (not proceeded by nausea and projectile)
-

*READ NOTES

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43
Q

Clinical Manifestations of Cerebral Edema: Compression of oculomotor nerve

A
  • Unilateral pupil dilation (i.e right sided dilation can indicate problems on the left side)
  • Sluggish or no response to light
  • Inability to move eye upward
  • Eyelid ptosis

*Read notes!

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44
Q

Clinical Manifestations of Cerebral Edema: Decreased motor function

A
  • Hemiparesis/hemiplegia
  • Decerebrate posturing (extensor): Indicates more serious damage
  • Decorticate posturing (flexor)

*READ NOTES!

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45
Q

What are complications of cerebral edema?

A
  • Inadequate cerebral perfusion
  • Cerebral herniation:
    • Territorial herniation
    • Uncalled herniation
    • Cingulate herniation

*Read notes!!

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46
Q

Tentorial herniation

A

Central herniation that occurs when a mass lesion in the cerebrum forces the brain to herniate downward through the opening created by the brainstem

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47
Q

Uncalled herniation occurs with

A

Lateral and downward herniation

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48
Q

Cingulate herniation

A

Occurs with lateral displacement of brain tissue beneath he falx cerebri

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49
Q

Diagnostic Studies

A
  • CT scan / MRI / PET
  • EEG (measuring brain activity is it normal, is there no brain activity?)
  • Cerebral angiography
  • ICP and brain tissue oxygenation measurement (LICOX catheter)
  • Doppler and evoked potential studies (need to suction, can’t be sedated)
  • NO lumbar puncture (increases ICP!!)

*READ NOTES

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50
Q

What are indications for measurement of ICP?

A
  • Glasgow Coma Scale of < or = 8

- Abnormal CT scans or MRI

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51
Q

Potential Placements of ICP Monitoring Devices

A
  • # 1 is in the ventricle
  • Subarachnoid
  • Intraparenchymal
  • Epidural
  • Subdural
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52
Q

Measurement of ICP include

A
  • Ventriculostomy (Gold standard)
  • Fiberoptic Catheter
  • Air pouch/pneumatic technology
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53
Q

Measurement of ICP: Ventriculostomy

A
  • Catheter inserted into lateral ventricle

- Coupled with an external transducer

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54
Q

Leveling a Ventriculostomy

A
  • It is important to make sure that the transducer of the ventriculostomy is level to the foramen of Monro (interventricular foramen) and that the ventriculostomy system is at the ideal height.
  • A reference point for this foramen is the tragus of the ear.
  • When the patient is repositioned, the system needs to be re-zeroed.
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55
Q

Measurement of ICP: Fiberoptic Catheter

A
  • Uses a sensor transducer located within the catheter tip.

- The sensor tip is placed within the ventricle or the brain tissue and provides a direct measurement of brain pressure.

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56
Q

Measurement of ICP: What is Air pouch/pneumatic technology?

A
  • Another system for monitoring ICP, has an air-filled pouch at the tip of the catheter that maintains a constant volume.
  • The pressure changes within the cranium are transmitted through the changes exerted on this pouch to the monitor.
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57
Q

What is important when measuring ICP?

A
  • Prevent and monitor for infection
  • Measure as mean pressure
  • Waveform should be recorded (shows normal, elevated, and plateau waves)
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58
Q

What factors can contribute to the development of infection during CIP monitoring?

A
  1. ICP monitoring >5 days
  2. Use of ventriculostomy
  3. A CSF leak
  4. Concurrent systemic infection
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59
Q

When an ICP waveform is normal, P1, P2 and P3 will resemble

A

A staircase

60
Q

As ICP increases, what happens to the waveform and what does it indicate?

A

P2 will rise above P1, indicating poor ventricular compliance

61
Q

Measurement of ICP: Inaccurate readings can be caused by

A
  • CSF leaks (can decrease ICP)
  • Obstruction in catheter/ kinks in tubing
  • Differences in height of bolt/transducer
  • Incorrect height of drainage system
  • Bubbles/air in tubing

*Read notes

62
Q

Measurement of ICP can control ICP by

A
  • Removing CSF (with ventricular catheter)
  • Intermittent or continuous drainage
  • Careful monitoring of volume of CSF drained is essential (can cause fluid shifts!)
  • READ NOTES! A lot of info!
63
Q

Measurement of Cerebral Oxygenation and Perfusion include

A
  1. LICOX Catheter

2. Jugular venous bulb catheter

64
Q

LICOX Catheter

A
  • Measures brain oxygenation (PbtO2) and temperature
  • Placed in healthy white brain matter

*Read notes

65
Q

Jugular Venous Bulb Catheter

A

Measures jugular venous oxygen saturation (SjvO2)

*Read notes!!

66
Q

Interprofessional Care of ICP

A
  • Treat underlying cause
  • Adequate oxygenation:
    • PaO2 > 100 mm Hg
    • PaCO2 35-45 mm Hg
    • Intubation
    • Mechanical ventilation
  • Surgery

*Read notes!

67
Q

Drug Therapy for ICP

A
  • Mannitol (Osmitrol)
  • Hypertonic Saline
  • Corticosteroids
  • Antiseizure meds
  • Antipyretics
  • Sedatives (propifol)
  • Analgesics (morphine)
  • Barbiturates (phenobarbital, dilantin)

*READ NOTES

68
Q

Drug Therapy for ICP: Mannitol

A
  • Mannitol acts to decrease the ICP in two ways: plasma expansion and osmotic effect.
  • Need to monitor fluid and electrolyte status!

*Read notes!! A lot of info!

69
Q

Drug Therapy for ICP: Hypertonic Saline

A
  • Moves water out of cells and into blood

- Monitor BP and serum sodium levels (intravascular fluid volume excess can occur)

70
Q

Drug Therapy for ICP: Corticosteroids

A
  • Used to treat vasogenic edema
  • Not recommended for traumatic brain injury!
  • Monitor fluid intake, serum sodium and glucose levels (can cause hyperglycemia, increased incidence of infections and GI bleeding)
  • Should be given concurrently with antacids, H2 receptor blockers, proton pump inhibitors

*READ NOTES!!

71
Q

Intraprofessional Care of ICP: Nutritional Therapy

A
  • Hypermetabolic and hypercatabolic state ↑ need for glucose
  • Enteral or parenteral nutrition
  • Early feeding (within 3 days of injury)
  • Keep patient normovolemic
  • IV 0.9% NaCl preferred over D5W or 0.45% NaCl

*Read notes

72
Q

Nursing Assessment of ICP

A
  • Subjective Data
  • LOC
  • Glasgow Coma Scale
  • Cranial nerves: eye movements, corneal reflex, oculocephalic reflex (doll’s eye reflex), oculovestibular (caloric stimulation)
  • Motor strength (i.e squeeze hands)
  • Motor response (spontaneous or to pain)
  • Vitals

*Read notes!

73
Q

ICP Potential Nursing Diagnoses include

A
  • Decreased intracranial adaptive capacity related to decreased cerebral perfusion or increased ICP
  • Risk for ineffective cerebral tissue perfusion related to reduction of venous and/or arterial blood flow and cerebral edema
  • Risk for disuse syndrome related to altered level of consciousness, immobility, and altered nutritional intake
74
Q

Overall Goals of Nursing Care for ICP

A

-Maintain a patent airway
ICP within normal limits
-Normal fluid and electrolyte balance
-Prevent complications secondary to immobility and decreased LOC

75
Q

Acute Care for ICP: Maintaining respiratory function includes

A
  • Maintain patent airway
  • Elevate head of bed 30 degrees
  • Suctioning needs
  • Minimize abdominal distention
  • Monitor ABGs
  • Maintain ventilatory support

*read notes

76
Q

Acute Care for ICP: Pain and anxiety management include

A

(Increases O2 demand = increase metabolism = increased risk for seizure activity)

  • Opioids
  • Propofol (Diprivan)
  • Dexmedetomidine (Precedex)
  • Neuromuscular blocking agents (need to make sure you’re breathing for patient!)
  • Benzodiazepines

*Read notes!

77
Q

Know how to do Glasgow Coma Scale!!!

A

Page

78
Q

Acute Care for ICP: Maintaining fluid and electrolyte balance includes

A
  • Monitor IV fluids
  • Daily electrolytes
  • Monitor for DI or SIADH (need to know how this relates to ICP!!)

*Read notes!

79
Q

Acute Care for ICP: Interventions to optimize ICP and CPP include

A
  • HOB elevated appropriately
  • Prevent extreme neck flexion
  • Turn slowly
  • Avoid coughing, straining, Valsalva
  • Avoid hip flexion

*Read notes!

80
Q

Acute Care for ICP includes

A
  • Respiratory function
  • Pain and anxiety management
  • Fluid and electrolyte imbalances
  • Monitor and minimize increases in ICP
  • Interventions to optimize ICP and CPP
  • Minimize complications of immobility
  • Protect form self injury
  • Psychologic considerations
81
Q

Pupillary check for size and response:

A

Check slide! Might need to know!

82
Q

Acute Care for ICP: Protecting from self injury

A
  • Judicious use of restraints; sedatives
  • Seizure precautions
  • Quiet, nonstimulating environment

*Read notes

83
Q

ICP Expected Outcomes of Care

A
  • Maintain ICP and CPP within normal parameters
  • No serious increases in ICP during or following care activities
  • No complications of immobility
84
Q

Head injury

A
  • Any trauma to skull, scalp or brain
  • Traumatic brain injury (TBI)
  • High incidence
85
Q

What are the most common causes of head injury?

A
  • Falls

- Motor vehicle accidents

86
Q

What are other causes of head injury?

A
  • Firearm related injuries
  • Assaults
  • Sports-related trauma
87
Q

Head Injury: Death occurs at three points in time after injury including

A
  1. Immediately after the injury
  2. Within 2 hours after the injury
  3. 3 weeks after the injury
88
Q

Types of Head Injuries

A
  1. Scalp Lacerations
  2. Skull Fractures
  3. Diffuse (generalized)
  4. Focal (localized)
  5. Postconcussion syndrome
  6. Diffuse Axonal Injury
  7. Lacerations
  8. Contusion
89
Q

Scalp Lacerations

A
  • External head trauma (most minor type)
  • Scalp is highly vascular → Profuse bleeding
  • Major complications – blood loss and infection
90
Q

Skull Fractures can be classified as

A
  • Linear or depressed (inward indentation)
  • Simple (without fragmentation or communicating lacerations), comminuted (shattered, pieces), or compound (overlapping or pushed into the other)
  • Closed or open
  • Location determines manifestations
91
Q

Complications of Skull Fractures

A
  • Infections
  • Hematoma
  • Tissue damage
92
Q

Raccoon Eyes

A
  • Periorbital edema and ecchymosis to that area

- Facial fracture

93
Q

Battle’s Sign

A

Postauricular ecchymosis caused by tear in capillaries

94
Q

Diffuse Head Injury: Concussion

A
  • Brief disruption in LOC
  • Retrograde amnesia
  • Headache
  • Short duration
  • May result in postconcussion syndrome

*READ NOTES

95
Q

Focal Head Injuries can be classified as

A
  • Minor (GCS 13-15)
  • Moderate (GCS 9-12)
  • Severe (GCS 3-8)

(Based on Glasgow coma scale)

96
Q

Rhinorrhea or otorrhea

A
  • Rhinorrhea (CSF leakage from the nose) or otorrhea (CSF leakage from the ear) generally confirms that the fracture has traversed the dura.
  • Rhinorrhea may also manifest as postnasal sinus drainage.
97
Q

Two Methods for Testing can be used to determine whether fluid leaking from nose or ear is CSF: (not sure if need to know)

A
  • The first method is to test the leaking fluid with a Dextrostix or Tes-Tape strip to determine whether glucose is present.
  • CSF gives a positive reading for glucose.
  • If blood is present in the fluid, testing for the presence of glucose is unreliable because blood also contains glucose.
  • In this event, look for the halo or ring sign.
  • To perform this test, allow the leaking fluid to drip onto a white gauze pad (4 × 4) or towel, and then observe the drainage. Within a few minutes, the blood coalesces into the center, and a yellowish ring encircles the blood if CSF is present.
  • Note the color, appearance, and amount of leaking fluid because both tests can give false-positive results.
98
Q

Postconcussion Syndrome can cause

A
  • Persistent headache
  • Lethargy
  • Personality and behavior changes
  • Shortened attention span, decreased short-term memory
  • Changes in intellectual ability

*Read notes!

99
Q

Diffuse Axonal Injury: What is it and what are clinical signs of diffuse axonal injury?

A

-Is a widespread axonal damage
-Decreased LOC
-Increased ICP
-Decortication, decerebration
-Global cerebral edema
(I.e its like shaken baby syndrome except in adults)

100
Q

Focal Injury

A
  • Can be minor to severe and can be localized to area of injury.
  • Consists of lacerations, contusions, hematomas and cranial nerve injuries.
101
Q

Lacerations

A

-Tearing of brain tissue
-With depressed and open fractures and penetrating injuries
Includes:
-Intracerebral hemorrhage
-Subarachnoid hemorrhage
-Intraventricular hemorrhage

102
Q

Intracerebral Hemorrhage

A
  • Generally associated with cerebral laceration.
  • This hemorrhage manifests as a space-occupying lesion accompanied by unconsciousness, hemiplegia on the contralateral side, and a dilated pupil on the ipsilateral side.
  • As the hematoma expands, signs of increased ICP become more severe.
103
Q

Contusion

A
  • Bruising of brain tissue
  • Associated with closed head injury
  • Can cause hemorrhage, infarction, necrosis, edema
104
Q

Intraventricular Hemorrhage Coup-Conrecoup Injury

A
  • Damage from coup-contrecoup injury occurs when the brain moves inside the skull due to high-energy or high-impact injury mechanisms.
  • Contusions or lacerations occur both at the site of the direct impact of the brain on the skull (coup) and at a secondary area of damage on the opposite side away from injury (contrecoup), leading to multiple contused areas.
  • Contrecoup injuries tend to be more severe, and overall patient prognosis depends on the amount of bleeding around the contusion site.
105
Q

Contusion: Clinical Manifestations

A
  • Can rebleed
  • Focal and generalized manifestations
  • Potential for increased hemorrhage if on anticoagulants
106
Q

What should you monitor for in patients with contusions?

A

Monitor for seizures!

107
Q

Epidural Hematoma

A
  • Bleeding between the dura and the inner surface of the skull
  • Neurologic emergency
  • Can be venous or an arterial origin.
108
Q

Venous Epidural Hematomas

A

Associated with a tear of the dural venous sinus and develops slowly.

109
Q

Arterial Epidural Hematomas

A
  • The middle meningeal artery lying under the temporal bone is often torn.
  • Hemorrhage occurs into the epidural space, which lies between the dura and the inner surface of the skull.
  • Because this is an arterial hemorrhage, the hematoma develops rapidly.*
110
Q

Epidural Hematomas: Clinical Manifestations

A
  • Initial period of unconsciousness
  • Brief lucid interval followed by decrease in LOC
  • Headache, nausea, vomiting
  • Focal findings
  • Requires rapid evacuation
111
Q

What are complications of head injuries?

A
  1. Subdural Hematoma

2. Epidural Hematoma

112
Q

Subdural Hematoma

A

Bleeding between the dura matter and arachnoid

113
Q

Subdural Hematoma: Most common source is

A
  • Veins that drain brain surface into sagittal sinus
  • Can also be arterial

*read notes!!

114
Q

Acute Subdural Hematoma

A
  • Within 24 to 48 hours of injury
  • Symptoms related to increased ICP
  • ↓ LOC, headache
  • Ipsilateral pupil dilated and fixed if severe

*Read notes!

115
Q

Subacute Subdural Hematoma

A
  • Within 2 to 14 days of the injury

- May appear to enlarge over time

116
Q

Chronic Subdural Hematoma

A
  • Weeks or months after injury
  • More common in older adults
  • Presents as focal symptoms
  • ↑ Risk for misdiagnosis

*Read notes!

117
Q

Intracerebral Hematoma

A
  • Bleeding within brain tissue
  • Usually within frontal and temporal lobes
  • Size and locations of hematoma determine patient outcome.
118
Q

Head Injury: Diagnostic Studies include

A
  • CT scan: Best diagnostic test to determine craniocerebral trauma
  • MRI, PET, evoked potential studies
  • Transcranial Doppler studies
  • Cervical spine x-ray
  • Glasgow Coma Scale (GCS)

*Read notes

119
Q

Emergency treatment for head injuries include

A
  • Patent airway
  • Stabilize cervical spine
  • Oxygen
  • IV access
  • Intubate if GCS <8
  • Control external bleeding
  • Remove patient’s clothing
  • Maintain patient warmth
  • Ongoing monitoring
  • Anticipate possible intubation
  • Assume neck injury
  • Administer fluids cautiously
120
Q

Treatment Principles for Head Injuries

A
  • Prevent secondary injury
  • Timely diagnosis
  • Surgery if necessary
121
Q

Intraprofessional Care for Concussions and contusions

A

Observation and management of ICP

122
Q

Intraprofessional Care for Skull Fractures include

A
  • Conservative treatment
  • Surgery if depressed

*Read notes

123
Q

Intraprofessional Care for Subdural and epidural hematomas

A
  • Surgical evacuation: craniotomy, burr-holes; craniotomy if extreme swelling
  • Read notes
124
Q

Nursing Assessment of Head Injuries: Subjective Data includes

A
  • Past medical history: Mechanism of injury**
  • Medications: Anticoagulants**
  • Alcohol/drug use; risk-taking behaviors
  • Headache
  • Mood or behavioral changes
  • Mentation changes; impaired judgment
  • Aphasia, dysphasia
  • Fear, denial, anger, aggression, depression
125
Q

Nursing Assessment of Head Injuries: General Objective Data includes

A
  • Altered mental status
  • Lacerations, contusions, abrasions
  • Hematoma
  • Battle’s sign
  • Periorbital edema and ecchymosis
  • Otorrhea
  • Exposed brain
126
Q

Nursing Assessment of Head Injuries: Respiratory Objective Data includes

A
  • Rhinorrhea
  • Impaired gag reflex
  • Altered/irregular respirations
127
Q

Nursing Assessment of Head Injuries: Cardiovascular Objective Data includes

A

Cushing’s triad

128
Q

Nursing Assessment of Head Injuries: GI/GU/Reproductive Objective Data includes

A
  • Vomiting
  • Bowel and bladder incontinence
  • Uninhibited sexual expression
129
Q

Nursing Assessment of Head Injuries: Neurologic Objective Data includes

A
  • Altered LOC
  • Seizures
  • Pupil dysfunction
  • Cranial nerve deficit(s)
130
Q

Nursing Assessment of Head Injuries: Musculoskeletal Objective Data includes

A
  • Motor deficit
  • Palmar drift
  • Paralysis
  • Spasticity
  • Posturing
  • Rigidity or flaccidity
  • Ataxia
131
Q

Craniotomy

A
  • Surgical opening into the skull.
  • Go in and evacuate the hematoma.

*Get more info!!

132
Q

Craniectomy

A
  • Removal of the bone
  • Sew the skin over that portion

*Get more info!

133
Q

Cranioplasty

A

Surgical repair, steel plate

*Get more info!

134
Q

Nursing Assessment for Head Injuries: Possible diagnostic findings include

A
  • Abnormal CT scan or MRI
  • Abnormal EEG
  • Positive toxicology screen or alcohol level
  • ↑ or ↓Blood glucose level
  • ↑ ICP
135
Q

Potential Nursing Diagnoses for Head Injuries

A
  • Risk for ineffective cerebral tissue perfusion related to interruption of CBF associated with cerebral hemorrhage, hematoma, and edema
  • Hyperthermia related to increased metabolism, infection, and hypothalamic injury
  • Impaired physical mobility related to decreased LOC
  • Anxiety related to abrupt change in health status, hospital environment, and uncertain future
  • Potential complication: increased ICP related to cerebral edema and hemorrhage
136
Q

Overall goals for patients with head injuries include

A
  1. Maintain adequate cerebral oxygenation and perfusion (MAP 70-150; CPP >60; ICP <20 (15 ideally))
  2. Remain normothermic
  3. Achieve control of pain and discomfort
  4. Be free from infection
  5. Have adequate nutrition
  6. Atain maximal cognitive, motor, and sensory function.
137
Q

Acute Care for Head Injuries include

A
  • Maintaining cerebral perfusion
  • Preventing secondary cerebral ischemia
  • Monitoring for changes in neurologic status
  • Patient and family teaching
138
Q

Acute Care for Head Injuries: Major focus of nursing care relates to

A

Increased ICP

139
Q

Acute Care of Head Injuries: Eye Problems

A

Eye drops, compresses and patch

140
Q

Acute Care of Head Injuries: Hyperthermia

A
  • Goal 36°to 37° C
  • Prevent shivering!!

*Read notes!!

141
Q

Acute Care of Head Injuries: Measures for patients leaking CSF include

A
  • Head of bed elevated
  • Loose collection pad under nose/over ear
  • No sneezing or blowing nose
  • No NG tube
  • No nasotracheal suctioning

*Read notes

142
Q

Acute Care of Head Injuries: Measures for immobilized patients include

A
  • Antiemetics (for nausea and vomiting)
  • Analgesics (for headache)
  • Preop preparation, if needed

*Read notes

143
Q

Acute Rehabilitation for Head Injuries include

A
  • Motor and sensory deficits
  • Communication issues
  • Memory and intellectual functioning
  • Nutrition
  • Bowel and bladder management

*READ NOTES!!

144
Q

Other ambulatory care includes

A
  • Seizure disorders
  • Mental and emotional difficulties
  • Progressive recovery
  • Family participation and education

*READ NOTES!!

145
Q

Expected Outcomes of Treatment for Head Injuries

A
  • Maintain normal cerebral perfusion pressure
  • Achieve maximal cognitive, motor, and sensory function
  • Experience no infection or hyperthermia

NURS 425 (19 decks)

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