Exam 3: ICP And Head Injury Flashcards
1
Q
The skull has three essential components:
A
- Brain tissue
- Blood
- CSF
2
Q
Intracranial Pressure
A
The hydrostatic force measured in the brain CSF compartment
3
Q
What maintains the ICP?
A
Balance among the brain tissue, blood and CSF.
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))
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.
6
Q
Normal ICP
A
5-15 mm Hg
7
Q
Elevated ICP
A
If ICP >20 mm Hg sustained
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
- Changes in CSF volume
- Changes in intracranial blood volume
- Changes in tissue brain volume
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.
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.
11
Q
Changes in tissue brain volume compensates through
A
Distention of the dura or compression of brain tissue
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.
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
14
Q
What is the normal cerebral blood flow?
A
About 50 mL/min per 100 g of brain tissue
15
Q
Why is maintenance of blood flow important?
A
Critical because the brain requires a constant supply of oxygen and glucose
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
17
Q
Cerebral Perfusion Pressure (What is the formula, normal)
A
- CPP = MAP – ICP
- Normal is 60 to 100 mm Hg
18
Q
Effect of cerebral vascular resistance is links CPP and blood flow as follows:
A
CPP = Flow x Resistance
19
Q
What is cerebral perfusion pressure?
A
The pressure needed to ensure blood flow to the brain.
20
Q
As CPP decreases, what happens?
A
Autoregulation fails, and CBF decreases
21
Q
A CPP less than 50 mm Hg is associated with what?
A
Ischemia and neuronal death
22
Q
A CPP less than 30 mm Hg results in what?
A
Ischemia and dis incompatible with life
23
Q
What is cerebral vascular resistance?
A
Generated by the Arteriosus within the cranium, links CPP and blood flow.
24
Q
If ICP is up, what is going to happen to blood flow?
A
It’s going to go down
25
Cerebral Blood Flow: Pressure Changes
- Compliance is the expandability of brain
- Impacts effect of volume change on pressure
- Compliance = Volume/Pressure
*read notes
26
What are stages of increased ICP?
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
27
What are factors that affect cerebral blood vessel tone?
1. CO2
2. O2
3. Hydrogen ion concentration
28
Factors affecting cerebral blood vessel tone: An increase in CO2 can lead to
- Relaxation of smooth muscle
- Dilation of cerebral vessels
- Decreased cerebrovascular resistance
- Increased CBF
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Factors affecting cerebral blood vessel tone: A decrease in PaCO2 can lead to
- Constricted cerebral vessels
- Increased cerebrovascular Resistance
- Decreased CBF
30
Factors affecting cerebral blood vessel tone: Cerebral O2 tension less than 50 mm Hg results in
- Cerebrovascular dilation
- Dilation decreases CVR
- Increases CBF
- Increases O2 tension
31
Factors affecting cerebral blood vessel tone: If O2 tension is not increased
- 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.
32
Increased ICP
- Life-threatening
- Results from an increase in any of three components (Brain tissue, blood and CSF)
- ↑ Cerebral edema
*Read notes!!
33
Progression of Increased Intracranial Pressure
- 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.
34
Effects of Herniation
- 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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Cerebral Edema
- ↑ Extravascular fluid in brain
| - Variety of causes
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What are the three types of cerebral edema?
1. Vasogenic
2. Cytotoxic
3. Interstitial
*Read notes
37
Vasogenic Cerebral Edema
- Most common type
- Occurs mainly in white matter
- Fluid leaks from intravascular to extravascular space
- Continuum of symptoms → coma
38
What can cause vasogenic cerebral edema?
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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Cytotoxic Cerebral Edema
- Disruption of cell membrane integrity
- Secondary to destructive lesions or trauma to brain tissue
- Fluid shift from extracellular to intracellular
*READ NOTES!
40
Interstitial Cerebral Edema
- Usually result of hydrocephalus
| - Excess CSP production, obstruction of flow, or inability to reabsorb
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How do you treat interstitial cerebral edema?
Treat with ventriculostomy or shunt
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Clinical Manifestations of Cerebral Edema
-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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Clinical Manifestations of Cerebral Edema: Compression of oculomotor nerve
- 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!
44
Clinical Manifestations of Cerebral Edema: Decreased motor function
- Hemiparesis/hemiplegia
- Decerebrate posturing (extensor): Indicates more serious damage
- Decorticate posturing (flexor)
*READ NOTES!
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What are complications of cerebral edema?
- Inadequate cerebral perfusion
- Cerebral herniation:
- Territorial herniation
- Uncalled herniation
- Cingulate herniation
*Read notes!!
46
Tentorial herniation
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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Uncalled herniation occurs with
Lateral and downward herniation
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Cingulate herniation
Occurs with lateral displacement of brain tissue beneath he falx cerebri
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Diagnostic Studies
- 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
50
What are indications for measurement of ICP?
- Glasgow Coma Scale of < or = 8
| - Abnormal CT scans or MRI
51
Potential Placements of ICP Monitoring Devices
- #1 is in the ventricle
- Subarachnoid
- Intraparenchymal
- Epidural
- Subdural
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Measurement of ICP include
- Ventriculostomy (Gold standard)
- Fiberoptic Catheter
- Air pouch/pneumatic technology
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Measurement of ICP: Ventriculostomy
- Catheter inserted into lateral ventricle
| - Coupled with an external transducer
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Leveling a Ventriculostomy
- 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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Measurement of ICP: Fiberoptic Catheter
- 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.
56
Measurement of ICP: What is Air pouch/pneumatic technology?
- 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.
57
What is important when measuring ICP?
- Prevent and monitor for infection
- Measure as mean pressure
- Waveform should be recorded (shows normal, elevated, and plateau waves)
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What factors can contribute to the development of infection during CIP monitoring?
1. ICP monitoring >5 days
2. Use of ventriculostomy
3. A CSF leak
4. Concurrent systemic infection
59
When an ICP waveform is normal, P1, P2 and P3 will resemble
A staircase
60
As ICP increases, what happens to the waveform and what does it indicate?
P2 will rise above P1, indicating poor ventricular compliance
61
Measurement of ICP: Inaccurate readings can be caused by
- 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
Measurement of ICP can control ICP by
- 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!
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Measurement of Cerebral Oxygenation and Perfusion include
1. LICOX Catheter
| 2. Jugular venous bulb catheter
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LICOX Catheter
- Measures brain oxygenation (PbtO2) and temperature
- Placed in healthy white brain matter
*Read notes
65
Jugular Venous Bulb Catheter
Measures jugular venous oxygen saturation (SjvO2)
*Read notes!!
66
Interprofessional Care of ICP
- Treat underlying cause
- Adequate oxygenation:
- PaO2 > 100 mm Hg
- PaCO2 35-45 mm Hg
- Intubation
- Mechanical ventilation
- Surgery
*Read notes!
67
Drug Therapy for ICP
- Mannitol (Osmitrol)
- Hypertonic Saline
- Corticosteroids
- Antiseizure meds
- Antipyretics
- Sedatives (propifol)
- Analgesics (morphine)
- Barbiturates (phenobarbital, dilantin)
*READ NOTES
68
Drug Therapy for ICP: Mannitol
- 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!
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Drug Therapy for ICP: Hypertonic Saline
- Moves water out of cells and into blood
| - Monitor BP and serum sodium levels (intravascular fluid volume excess can occur)
70
Drug Therapy for ICP: Corticosteroids
- 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
Intraprofessional Care of ICP: Nutritional Therapy
- 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
Nursing Assessment of ICP
- 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
ICP Potential Nursing Diagnoses include
* 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
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Overall Goals of Nursing Care for ICP
-Maintain a patent airway
ICP within normal limits
-Normal fluid and electrolyte balance
-Prevent complications secondary to immobility and decreased LOC
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Acute Care for ICP: Maintaining respiratory function includes
- Maintain patent airway
- Elevate head of bed 30 degrees
- Suctioning needs
- Minimize abdominal distention
- Monitor ABGs
- Maintain ventilatory support
*read notes
76
Acute Care for ICP: Pain and anxiety management include
(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
Know how to do Glasgow Coma Scale!!!
Page
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Acute Care for ICP: Maintaining fluid and electrolyte balance includes
- Monitor IV fluids
- Daily electrolytes
- Monitor for DI or SIADH (need to know how this relates to ICP!!)
*Read notes!
79
Acute Care for ICP: Interventions to optimize ICP and CPP include
- HOB elevated appropriately
- Prevent extreme neck flexion
- Turn slowly
- Avoid coughing, straining, Valsalva
- Avoid hip flexion
*Read notes!
80
Acute Care for ICP includes
- 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
Pupillary check for size and response:
Check slide! Might need to know!
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Acute Care for ICP: Protecting from self injury
- Judicious use of restraints; sedatives
- Seizure precautions
- Quiet, nonstimulating environment
*Read notes
83
ICP Expected Outcomes of Care
- Maintain ICP and CPP within normal parameters
- No serious increases in ICP during or following care activities
- No complications of immobility
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Head injury
- Any trauma to skull, scalp or brain
- Traumatic brain injury (TBI)
- High incidence
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What are the most common causes of head injury?
- Falls
| - Motor vehicle accidents
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What are other causes of head injury?
- Firearm related injuries
- Assaults
- Sports-related trauma
87
Head Injury: Death occurs at three points in time after injury including
1. Immediately after the injury
2. Within 2 hours after the injury
3. 3 weeks after the injury
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Types of Head Injuries
1. Scalp Lacerations
2. Skull Fractures
3. Diffuse (generalized)
4. Focal (localized)
5. Postconcussion syndrome
6. Diffuse Axonal Injury
7. Lacerations
8. Contusion
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Scalp Lacerations
- External head trauma (most minor type)
- Scalp is highly vascular → Profuse bleeding
- Major complications – blood loss and infection
90
Skull Fractures can be classified as
- 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
Complications of Skull Fractures
- Infections
- Hematoma
- Tissue damage
92
Raccoon Eyes
- Periorbital edema and ecchymosis to that area
| - Facial fracture
93
Battle’s Sign
Postauricular ecchymosis caused by tear in capillaries
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Diffuse Head Injury: Concussion
- Brief disruption in LOC
- Retrograde amnesia
- Headache
- Short duration
- May result in postconcussion syndrome
*READ NOTES
95
Focal Head Injuries can be classified as
- Minor (GCS 13-15)
- Moderate (GCS 9-12)
- Severe (GCS 3-8)
(Based on Glasgow coma scale)
96
Rhinorrhea or otorrhea
- 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
Two Methods for Testing can be used to determine whether fluid leaking from nose or ear is CSF: (not sure if need to know)
- 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
Postconcussion Syndrome can cause
- Persistent headache
- Lethargy
- Personality and behavior changes
- Shortened attention span, decreased short-term memory
- Changes in intellectual ability
*Read notes!
99
Diffuse Axonal Injury: What is it and what are clinical signs of diffuse axonal injury?
-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
Focal Injury
- Can be minor to severe and can be localized to area of injury.
- Consists of lacerations, contusions, hematomas and cranial nerve injuries.
101
Lacerations
-Tearing of brain tissue
-With depressed and open fractures and penetrating injuries
Includes:
-Intracerebral hemorrhage
-Subarachnoid hemorrhage
-Intraventricular hemorrhage
102
Intracerebral Hemorrhage
- 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
Contusion
- Bruising of brain tissue
- Associated with closed head injury
- Can cause hemorrhage, infarction, necrosis, edema
104
Intraventricular Hemorrhage Coup-Conrecoup Injury
- 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
Contusion: Clinical Manifestations
- Can rebleed
- Focal and generalized manifestations
- Potential for increased hemorrhage if on anticoagulants
106
What should you monitor for in patients with contusions?
Monitor for seizures!
107
Epidural Hematoma
- Bleeding between the dura and the inner surface of the skull
- Neurologic emergency
- Can be venous or an arterial origin.
108
Venous Epidural Hematomas
Associated with a tear of the dural venous sinus and develops slowly.
109
Arterial Epidural Hematomas
- 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
Epidural Hematomas: Clinical Manifestations
- Initial period of unconsciousness
- Brief lucid interval followed by decrease in LOC
- Headache, nausea, vomiting
- Focal findings
- Requires rapid evacuation
111
What are complications of head injuries?
1. Subdural Hematoma
| 2. Epidural Hematoma
112
Subdural Hematoma
Bleeding between the dura matter and arachnoid
113
Subdural Hematoma: Most common source is
- Veins that drain brain surface into sagittal sinus
- Can also be arterial
*read notes!!
114
Acute Subdural Hematoma
- Within 24 to 48 hours of injury
- Symptoms related to increased ICP
- ↓ LOC, headache
- Ipsilateral pupil dilated and fixed if severe
*Read notes!
115
Subacute Subdural Hematoma
- Within 2 to 14 days of the injury
| - May appear to enlarge over time
116
Chronic Subdural Hematoma
- Weeks or months after injury
- More common in older adults
- Presents as focal symptoms
- ↑ Risk for misdiagnosis
*Read notes!
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Intracerebral Hematoma
- Bleeding within brain tissue
- Usually within frontal and temporal lobes
- Size and locations of hematoma determine patient outcome.
118
Head Injury: Diagnostic Studies include
- 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
Emergency treatment for head injuries include
- 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
Treatment Principles for Head Injuries
- Prevent secondary injury
- Timely diagnosis
- Surgery if necessary
121
Intraprofessional Care for Concussions and contusions
Observation and management of ICP
122
Intraprofessional Care for Skull Fractures include
- Conservative treatment
- Surgery if depressed
*Read notes
123
Intraprofessional Care for Subdural and epidural hematomas
- Surgical evacuation: craniotomy, burr-holes; craniotomy if extreme swelling
* Read notes
124
Nursing Assessment of Head Injuries: Subjective Data includes
- 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
Nursing Assessment of Head Injuries: General Objective Data includes
- Altered mental status
- Lacerations, contusions, abrasions
- Hematoma
- Battle’s sign
- Periorbital edema and ecchymosis
- Otorrhea
- Exposed brain
126
Nursing Assessment of Head Injuries: Respiratory Objective Data includes
- Rhinorrhea
- Impaired gag reflex
- Altered/irregular respirations
127
Nursing Assessment of Head Injuries: Cardiovascular Objective Data includes
Cushing’s triad
128
Nursing Assessment of Head Injuries: GI/GU/Reproductive Objective Data includes
- Vomiting
- Bowel and bladder incontinence
- Uninhibited sexual expression
129
Nursing Assessment of Head Injuries: Neurologic Objective Data includes
- Altered LOC
- Seizures
- Pupil dysfunction
- Cranial nerve deficit(s)
130
Nursing Assessment of Head Injuries: Musculoskeletal Objective Data includes
- Motor deficit
- Palmar drift
- Paralysis
- Spasticity
- Posturing
- Rigidity or flaccidity
- Ataxia
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Craniotomy
- Surgical opening into the skull.
- Go in and evacuate the hematoma.
*Get more info!!
132
Craniectomy
- Removal of the bone
- Sew the skin over that portion
*Get more info!
133
Cranioplasty
Surgical repair, steel plate
*Get more info!
134
Nursing Assessment for Head Injuries: Possible diagnostic findings include
- Abnormal CT scan or MRI
- Abnormal EEG
- Positive toxicology screen or alcohol level
- ↑ or ↓Blood glucose level
- ↑ ICP
135
Potential Nursing Diagnoses for Head Injuries
* 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
Overall goals for patients with head injuries include
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
Acute Care for Head Injuries include
- Maintaining cerebral perfusion
- Preventing secondary cerebral ischemia
- Monitoring for changes in neurologic status
- Patient and family teaching
138
Acute Care for Head Injuries: Major focus of nursing care relates to
Increased ICP
139
Acute Care of Head Injuries: Eye Problems
Eye drops, compresses and patch
140
Acute Care of Head Injuries: Hyperthermia
- Goal 36°to 37° C
- Prevent shivering!!
*Read notes!!
141
Acute Care of Head Injuries: Measures for patients leaking CSF include
- 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
Acute Care of Head Injuries: Measures for immobilized patients include
- Antiemetics (for nausea and vomiting)
- Analgesics (for headache)
- Preop preparation, if needed
*Read notes
143
Acute Rehabilitation for Head Injuries include
- Motor and sensory deficits
- Communication issues
- Memory and intellectual functioning
- Nutrition
- Bowel and bladder management
*READ NOTES!!
144
Other ambulatory care includes
- Seizure disorders
- Mental and emotional difficulties
- Progressive recovery
- Family participation and education
*READ NOTES!!
145
Expected Outcomes of Treatment for Head Injuries
- Maintain normal cerebral perfusion pressure
- Achieve maximal cognitive, motor, and sensory function
- Experience no infection or hyperthermia
