Intracranial Pressure and Acute Head Injury
Intracranial Pressure: Physiology and Principles
Intracranial Pressure:
 Skull has three essential components:
o brain tissue
o blood
o cerebrospinal fluid (CSF)
 The skull can be thought of as a box
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Review Components of the brain: FILL IN THE REST OF THE PARTS
 Brain stem: responsible for basic functioning like heart rate, breathing, and sleep/wake
 Cerebellum: controls gait and balance
 Cerebrum: impulsivity, judgment, sense of humor, memory
o Contains the Left and Right brain
 Diencephalon: contains both the hypothalamus and thalamus and controls higher level functioning
o Hypothalamus: hunger, thirst, blood temperature
o Thalamus: senses pain
 Pituitary gland:
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Midbrain:
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Medulla:
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Pons:
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Corpus collosum:
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Intracranial Pressure:
Factors that influence ICP:
 Arterial pressure
 Venous pressure
 Intraabdominal and intrathoracic pressure
 Posture
 Temperature
 Blood gases (CO2 levels)
Regulation and Maintenance:
 Monro-Kellie doctrine
o If one component increases, another must decrease to maintain ICP
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Normal ICP= 5-10 mmHg
o Elevated= > 20 mmHg is sustained
 Above 20- this is when damage starts to occur
Normal compensatory adaptations:
o Changes in CSF volume
o Changed in intracranial blood volume
o Changes in tissue brain volume
Ability to compensate is limited
o If volume increase continues, ICP rises decompensation
 if a mass or something is growing slow= ↑ in brain mass, ↓CSF or IC blood volume to accommodate so
there is no ↑ ICP
 if it is growing fast or there is another insult (fall or car accident) and there is a bleed in the head- body
can’t compensate for quick changes
 Can’t handle rapid or extensive change
 decompensation- changes in mental status, effects whole body (VS) due to pressure on the midbrain
o how many cc’s of CSF are usually in the brain?
 ??? in CNS estimated to be 125 cc of which 15-25 cc is in the ventricular system
o
Cerebral Blood Flow:
 Definition: The amount of blood in milliliters passing through 100 g of brain tissue in 1 minute
o About 50 mL/min per 100 g of brain tissue
o How much glucose and O2 does the brain use?
 20% O2 and 25% glucose
o The Circle of Willis: the arteries combine to share blood in case something happens to the external carotid arteries
 Autoregulation:
o Independent of systemic regulation that occurs
o Adjusts diameter of blood vessels
o Ensures consistent CBF
o Only effective if mean arterial pressure (MAP) 70 to 150 mm Hg
 Normal MAP = 70-90
 Arteries can’t get any tighter at 70 or looser at 150
o If BP ↓, arterioles in the brain dilate to get the last bit of blood and if there is too much it will constrict flow
 Cerebral Perfusion Pressure (CPP):
o CPP = MAP – ICP
o Normal CPP is 60 to 100 mm Hg
o Goal in treatment is 70-80
o <50 mm Hg is associated with ischemia and neuronal death
 Less than 30% = death
 Effect of cerebral vascular resistance
o CPP = Flow x Resistance
 Pressure changes:
o Cerebral blood flow is directly tied to compliance
o Compliance is the expandability of the brain (wiggle room)
 A bit more fluid or mass volume is okay only because of compliance
o Impacts effect of volume change on pressure
 When you exceed compliance and ↑ pressure or volume = ↑ pressure
o Compliance = Volume/Pressure
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Stages of Increased ICP:
o Stage 1: total compensation
o Stage 2: ↓compensation; risk for ↑ICP
o Stage 3: failing compensation; clinical manifestations of ↑ICP (Cushing’s triad)
o Stage 4: Herniation imminent → death
Factors affecting cerebral blood vessel tone (these all make the vessels dilate):
o ↑ CO2
o ↓ O2
o ↑ Hydrogen ion concentration or acidosis (↓ pH)
ICP and Cerebral Oxygenation:
 If there is an ↑ in SBP, cerebral arterioles will constrict
 If there is an ↓ in SBP, cerebral arterioles will dilate
 This is why with hypertensive emergency’s you can’t drop the BP too low to give arterioles time to accommodate
Increased ICP:
 Life- threatening
 Increase in any of the three components:
o Brain tissue
o Blood
o CSF
 ↑ cerebral edema- brain tissue ↑
o Due to electrolyte imbalances (decreases Na or fluid overload)
o ↑ extravascular fluid in the brain
o Variety of causes:
 Mass lesions
 Head injuries- bleeding
 Cerebral infections
 Vascular insult
 Toxic or metabolic encephalopathy (liver failure)
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Compression of the ventricles- holds CSF so decrease in CSF out
Herniation:
 A: normal relationships of intracranial structures
 B: shift of intracranial structures
o Compression of the brainstem and cranial nerves may be fatal.
o Herniation forces the cerebellum and brainstem downward through the foramen magnum.
o If compression of the brainstem is unrelieved, respiratory arrest will occur due to compression of the respiratory
control center in the medulla.
 There is limited space for the brain to go down so it herniates into midbrain and this is fatal because it controls the
respiratory center and HR so it may cause respiratory arrest
 L or R herniation is recoverable
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Intracranial Pressure: Manifestations and Measurement
Clinical Manifestations:
 Change in level of consciousness IS THE FIRST SIGN anytime ICP ↑
o Flattening of affect  coma
 Change in vital signs
o Cushing’s triad
 Widened pulse pressure (systolic BP ↑)
 Bradycardia
 Irregular respirations (Cheyne- stokes)
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o Change in body temperature- presses on hypothalamus that controls this
Ocular signs RELEARN CRANIAL NERVES
o Compression of oculomotor nerve (III)
 Unilateral pupil dilation
 Ipsilateral side- side with pupil dilation is seen on the side of lesion or injury
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 Sluggish or no response to light
 Inability to move eye upward
 Eyelid ptosis
Other cranial nerves:
 Diplopia, blurred vision, EOM changes
 Optic:
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Trochlear:
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Abducen: can they see well, blurred vision, move eyes???
 KNOW CRANIAL NERVES AND NEURO ASSESSMENT
Decrease in motor function:
o Hemiparesis/hemiplegia- more specific to spinal cord injury
o Decerebrate posturing (extensor)
 Indicates more serious damage
 More associated with injury of brainstem or midbrain
 Arms straight and feet dorsiflexed down
o Decorticate posturing (flexor)
 Arms to core and dorsiflex and abducted feet
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Headache
o Often continuous
o Worse in the morning
o It is not the brain tissue causing the pain it is the arterioles in the cranial nerves that cause the headache
Vomiting
o Not preceded by nausea
o Projectile
Complications of uncontrolled increased ICP:
 Inadequate cerebral perfusion
 Cerebral herniation
 To better understand cerebral herniation, two important structures in the brain must be described
 The falx cerebri is a thin wall of dura that folds down between the cortex, separating the two
cerebral hemispheres
 The tentorium cerebelli is a rigid fold of dura that separates the cerebral hemispheres from the
cerebellum. It is called the tentorium (meaning tent) because it forms a tentlike cover over the
cerebellum
o Tentorial/ Tonsillar herniation
 (Central herniation) occurs when a mass lesion in the cerebrum forces the brain to herniate downward
through the opening created by the brainstem- more deadly
o Uncal herniation
 Occurs with lateral and downward herniation
o Cingulate herniation
 Occurs with lateral displacement of brain tissue beneath the falx cerebri
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Diagnostic Studies:
 CT scan / MRI / PET
o CT- more quickly available but doesn’t show ischemia
o MRI- more difficult, can’t have any metal on or in them
 EEG- helpful because it shows sub cranial seizures
 Cerebral angiography - rare
 ICP and brain tissue oxygenation measurement (LICOX catheter)
 Doppler and evoked potential studies
 NO LUMBAR PUNCTURE: pressure drops to see????** CSF, brainstem may herniate
 There is also a new handheld device
Measurement of ICP and EVD Requirement:
 Guides clinical care
 Indications: ICP should be monitored in:
o In persons with
 Glasgow Coma Scale of ≤8 &
 Abnormal CT scans or MRI
 OR
o Patients with evidence of altered cerebral tissue perfusion, have a normal CT but have 2 of the following
(increase in ICP but no change in CT):
 Age> 40
 Unilateral or bilateral motor posturing
 SBP < 90 mm hg
Glasgow Coma Scale:
 may be available to us on test?
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Moves to localized pain- push someone off that is inflicting pain
o If you press on their eyes and they can move their hand to eye
Flexion withdrawal- barely pulling back from pain
o If press on their eyes and they can’t move their hand past their chin
Potential Placements of ICP Monitoring Devices:
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Subarachnoid- bolts
Ventricular- ventriculostomy- best because it tells us pressure and can drain fluid
Measurement of ICP:
 GOLD STANDARD: Ventriculostomy
o Catheter inserted into lateral ventricle
 Use a drill to get through the skull to place this catheter- many risks
o Coupled with an external transducer to translate pressure
o Leveling a Ventriculostomy:
 It is important to make sure that the transducer of the ventriculostomy is level to the Foramen of Monroe
(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.
 Drain is placed about 10-20 cm above tragus to drain so when ICP ↑ above 20 it drains
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Fiberoptic catheter:
o Sensor transducer located within the catheter tip
Subarachnoid bolt or screw
o Between arachnoid membrane and cerebral cortex
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Prevent and monitor for infection
Measure as mean pressure
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Waveform should be recorded- normal, elevated, and plateau waves
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Normal ICP waveform has three phases:
It is important to monitor the ICP waveform, as well as the mean CPP.
 When ICP is normal, P1, P2, and P3 will resemble a staircase.
 As ICP increases, P2 will rise above P1, indicating poor ventricular compliance
o My notes:
 It looks at mean pressure
 Want to keep ICP below 20 and calculate CPP (mainly) because if:
 Ex: ICP is 50 and MAP is 80  CPP= 30 – DEATH
o Either have to ↓ ICP or ↑ BP
 Ex: maybe BP is 160/80 so MAP =110 ICP=50  CPP= 60 (right at the bottom of cusp)
Evaluate changes with patient condition
Inaccurate readings caused by:
o CSF leaks
o Obstruction in catheter/ kinks in tubing
o Differences in height of bolt/transducer
o Incorrect height of drainage system
o Bubbles/air in tubing
Can control ICP by removing CSF (with ventricular catheter)
o The physician will typically order a specific level to initiate drainage (e.g., if ICP is greater than 20 mm Hg) as well as
the frequency of drainage (intermittent or continuously)
o When the ICP is above the indicated level, the ventriculostomy system is opened by turning a stopcock and
allowing the drainage of CSF, thus relieving the pressure inside the cranial vault
Intermitted or continuous drainage
o There are two options for CSF drainage: intermittent and continuous
 If intermittent drainage is ordered: open the ventriculostomy system at the indicated ICP and allow CSF to
drain for 2 to 3 minutes. Then the stopcock is closed to return the ventriculostomy to a closed system
 If continuous ICP drainage is ordered: careful monitoring of the volume of CSF drained is essential,
keeping in mind that normal CSF production is about 20 to 30 mL/hr, with a total CSF volume of 90 to 150
mL within the ventricles and subarachnoid space
Careful monitoring of the volume of CSF drained is essential
o It is also recommended that a sign be posted above the patient’s bed to notify anyone before turning, moving, or
suctioning the patient to prevent the removal of too much CSF, which can result in other complications.
Prevent infection and other complications
o Strict aseptic technique during dressing changes or sampling of CSF is imperative to prevent infection. The system
must remain intact to ensure that the ICP readings are accurate because treatment is initiated based on the
pressures
 Maintain dressings, hand hygiene
o Complications of this type of drainage system include: ventricular collapse, infection, and herniation or subdural
hematoma formation from rapid decompression
Measurement of Cerebral Oxygenation and Perfusion:
 LICOX catheter
o Measures brain oxygenation (PbtO2) and temperature and is placed in healthy white brain matter
 The LICOX system provides continuous monitoring of the pressure of oxygen in brain tissue (PbtO 2). The
normal range for PbtO2 is 20 to 40 mm Hg. A lower-than-normal PbtO2 level is indicative of ischemia.
 Another advantage of the LICOX catheter is the ability to measure brain temperature. A cooler brain
temperature (96.8°F [36°C]) may produce better outcomes
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Visual of the LICOX brain tissue oxygen system:
 A: Catheter inserted through an intracranial bolt
 B: The system measures oxygen in the brain (Pbt02), brain tissue temperature, and intracranial
pressure (ICP)
Jugular venous bulb catheter- not used as often
o Measures jugular venous oxygen saturation (SjvO2) and is placed in the internal jugular vein and positioned so that
the catheter tip is located in the jugular bulb
 Placement is verified by an x-ray.
 This catheter provides a measurement of jugular venous oxygen saturation (SjvO 2), which indicates total
venous brain tissue extraction of oxygen.
 This is a measure of cerebral oxygen supply and demand. The normal SjvO2 range is 55% to 75%. Values
less than 50% demonstrate impaired cerebral oxygenation.
Intracranial Pressure: ICP Assessment and Collaborative Care:
READ THE ARTICLES AND VIDEOS
Nursing Assessment:
 Subjective data
o Because they have a head injury or increased ICP, they probably are intubated so get this information from family
or caregivers
 Level of consciousness (LOC)
o Measure this immediately so you can assess and then observe for any changes
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 Understand these terms and where they fall as they move up and down
Glasgow Coma Scale
o Eye opening
o Best verbal response
o Best motor response
My notes:
o You will FREQUENTLY perform:
 LOC
 Glasgow Coma Scale
 Neuro cranial assessment
Pupillary check for Size and Response:
 Looking at oculomotor nerve III
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Cranial nerves: KNOW CRANIAL NERVES AND ASSESSMENT
o Eye movements
 3,4,6- need to be awake and follow commands to test these
o Corneal reflex
 5,7 – can assess in an unconscious patient
o Oculocephalic reflex (doll’s eye reflex)
 Signs of involvement with midbrain- indicates higher level of damage- done by neurologist
 Eyes dramatically turn to one side or the other- stay fixed with movement
o Oculovestibular (caloric stimulation)
 Signs of involvement with midbrain- indicates higher level of damage- done by neurologist
 Instill water into ear canal and eyes dramatically move to this stimulation
Motor Strength:
o Squeeze hands- equal strength
o Palmar drift test- palms up and with eyes closed do they drop one arm
o Raise foot off bed or bend knees
Motor response
o Spontaneous or to pain
Vital signs
Abnormal Respiratory Patterns of Coma:
 Cheyne- stokes= cushing’s triad
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Collaborative Care:
 Treat underlying cause then supportive care
 Adequate oxygenation- ABC – maintain airway- probably intubate and mechanical ventilation
o Goals:
 PaO2 > 100 mm Hg
 PaCO2: 35-45 mm Hg
o Intubation
o Mechanical ventilation
 Surgery – if there is a mass, lesion, or bleed
 When do we intubate? GCS score less than 8- they can’t maintain or protect their airway
 Drug Therapy:
 Most treatments are treating cerebral edema
o Mannitol (Osmitrol):
 Goal: provide osmotic effect- high concentration fluid to pull fluid with it into the vasculature to relieve
cerebral edema
 Plasma expansion
 Osmotic effect
 Monitor fluid and electrolyte status
 Equally as efficient as hypertonic saline
 Often give mannitol first then hypertonic saline
Hypertonic saline: (3% saline)
 Goal: provide osmotic effect- high concentration fluid to pull fluid with it into the vasculature to relieve
cerebral edema
 Moves water out of cells and into blood
 Monitor BP and serum sodium levels
 Equally as efficient as mannitol
o Corticosteroids
 Vasogenic edema- edema that surrounds tumors or abscesses
 Monitor fluid intake, serum sodium and glucose levels.
 Concurrent antacids, H2 receptor blockers, proton pump inhibitors
 Concerned with development of a stress ulcer so provide these
o Antiseizure medications
 Many new ones that are effective and we now want to monitor for sub clinical seizures
 You can’t drive until you have been on seizure medications for at least 6 months or haven’t had a
seizure in 6 months
 Increased ICP causes seizures
o Antipyretics
 With increased ICP increases temperature which increases oxygen and metabolic demand
 Also provide: cooling blankets, cold rags on forehead
o Sedatives, Analgesics, or Barbiturates
 All go hand in hand
 May be having pain and we don’t know, may be anxious, fighting ventilator, confused and all increase
metabolic demand
 Can’t lower ICP with increased demand, anxious or in pain
Nutritional Therapy:
o Hypermetabolic and hypercatabolic state increased need for glucose
o Enteral or parenteral nutrition
o Early feeding (within 3 days of injury)
 Dolloff tube into jejunum to provide feedings and also keeps the gut working to not develop an ileus or
diarrhea
o Keep patient normovolemic
o IV 0.9% NaCl preferred over D5W or 0.45% NaCl
 Want to give concentrated fluids because we want osmosis to pull fluid out of the brain
 Even piggy backs need to be infused with NS, ½ NS or D5W
o My notes:
 We have a good record of keeping these patients from going into ARDS
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Nursing Planning:
 Overall Goals:
o Maintain a patent airway
o ICP within normal limits
o Normal fluid and electrolyte balance
o Prevent complications secondary to immobility and decreased LOC
Nursing Implementation:
 Respiratory function:
o Maintain patent airway
o Elevate head of bed 30 degrees or more
o Suctioning needs
o Minimize abdominal distention
 So that they do not develop reflux and aspirate
o Monitor ABGs
o Maintain ventilatory support
 Pain and Anxiety management:
o Opioids
o Propofol (Diprivan)- sedated
o Dexmedetomidine (Precedex)- sedated
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Neuromuscular blocking agents
Benzodiazepines
My notes:
 Want to keep them as comfortable as possible
 Watch for nonverbal clues
 Sedation holidays- asses where they are and neurological status
 Maybe had to completely paralyze them to reduce metabolic demands (only for a bit) barbiturate comas
with benzos, Diprivan and neuromuscular blocking agents
Fluid and Electrolyte balance:
o Monitor IV fluids
o Daily electrolytes
o Monitor for DI or SIADH
Monitor and minimize increases in ICP
Interventions to optimize ICP and CPP:
o HOB elevated appropriately
o Prevent extreme neck flexion (want to promote drainage)
o Turn slowly
o Avoid coughing, straining, Valsalva
 They are put on a lot of stool softeners
o Avoid hip flexion
 Because intraabdominal pressure can increase ICP
Minimize complications of immobility
Protection from self-injury:
o Judicious use of restraints; sedatives
o Seizure precautions
o Quiet, nonstimulating environment
Psychologic considerations
o How they will recover after this
Evaluation:
 Expected Outcomes:
o Maintain ICP and CPP within normal parameters
o No serious increases in ICP during or following care activities
o No complications of immobility
Questions:
1. A patient with a head injury has an arterial BP of 92/50 mm Hg and ICP of 18 mm Hg. The nurse uses the assessments to
calculate the cerebral perfusion pressure (CPP). How should the nurse interpret the results?
a. The CPP is so low that brain death is imminent.
b. The CPP is low, and the BP should be increased.
c. The CPP is high, and the ICP should be reduced.
d. The CPP is adequate for normal cerebral blood flow.
Rationale:
The cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. CPP is equal to the MAP minus the
ICP (CPP = MAP – ICP).
MAP = DBP + 1/3 (SBP-DBP) = 50 + 1/3 (92-50) = 64 mm Hg
CPP = MAP – ICP = 46 mm Hg
Normal CPP is 60 to 100 mm Hg. CPP <50 mm Hg is associated with ischemia and neuronal death. A CPP <30 mm Hg results in
ischemia and is incompatible with life. It is critical to maintain MAP when ICP is elevated. A patient with a head injury may require a
higher blood pressure, increasing MAP and CPP, to increase perfusion to the brain and prevent further tissue damage.
2.
A patient with increased ICP is positioned in a lateral position with the head of the bed elevated 30 degrees. The nurse
evaluates a need for lowering the head of the bed when the patient experiences
a. ptosis of the eyelid.
b. unexpected vomiting.
c. a decrease in motor functions.
d. decreasing level of consciousness.
Rationale:
Decreasing level of consciousness indicates increased intracranial pressure. Maintain the patient with increased ICP in the head-up
position and prevent extreme neck flexion, which can cause venous obstruction and contribute to elevated ICP. Adjust the body
position to decrease the ICP maximally and to improve the CPP. Elevation of the head of the bed reduces sagittal sinus pressure,
promotes drainage from the head via the valveless venous system through the jugular veins, and decreases the vascular congestion
that can produce cerebral edema. However, raising the head of the bed above 30 degrees may decrease the CPP by lowering
systemic BP. Careful evaluation of the effects of elevation of the head of the bed on both the ICP and the CPP is required. Position
the bed so that it lowers the ICP while optimizing the CPP and other indices of cerebral oxygenation.
Intracranial Pressure: Head Injuries
SIADH vs. DI:
 Very clear video to watch: https://www.youtube.com/watch?v=pThRKktJXL0
 Pro-tip: what will the urine osmolality be in each condition? How do we measure this?
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My notes:
o SIADH: pituitary gland- no release of ADH- huge shifts in volume- one of the shifts with a head injury patienthypervolemic- too much ADH – retain fluid and low UO so dilute blood
o DI: hypovolemic- increased UO, high NA
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Seizures after brain injury:
 Complete list found here: https://www.epilepsy.com/learn/treating-seizures-and-epilepsy/seizure-medication-list
 Often patients must be started on 2-3 medications to control the seizures
 New ones of note: Zonisamide & Lacosamide
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My notes:
o Subclinical seizures- monitor for them
o 60-70% of people with penetrating head injury- develop seizures
o Blood clot- 35%
o Trauma no penetration- 20%
Head Injury:
 Any trauma to the:
o Skull
o Scalp
o Brain
 Traumatic brain injury (TBI)
 High incidence
o In young people
o 50,00 people die
o 275,000 hospitalized with traumatic brain injury
o 5.3 million Americans live with disabilities following traumatic brain injury
 Causes:
o Motor vehicle collisions
o Falls
o Firearm-related injuries
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o Assaults
o Sports-related injuries
o Recreational accidents
o War-related injuries
High potential for poor outcome
Deaths occur at three points in time after injury:
o Immediately after the injury
o Within 2 hours after the injury
o 3 weeks after the injury
 With this most of the time it is due to multi-system failure
Types of Head Injuries:
o Scalp Lacerations
 External head trauma
 Scalp is highly vascular → Profuse bleeding
 Major complications – blood loss and infection
 Vitamin E oil is not good for scars as it traps the infection
o Skull Fractures
 Linear or depressed
 Simple, comminuted, or compound
 Closed or open
 Location determines manifestations
 Complications:
 Infections
 Hematoma
 Tissue damage
 Classic signs of skull fractures:
 Battle’s sign
o Bruising around eye and behind the ear
 What about that leakage from his ears and nose???
 Raccoon eyes
 My notes:
o May be leaking CSF fluid- huge hit and now shakes head
o Rhinorrhea or otorrhea- clear blue or yellowish
o Measure for glucose- if has blood- may have halo sign
o If CSF- surgery
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 What about that leakage from his ears and nose? **
Types of Head Injuries: good to know!
o Diffuse injury (generalized)
 Concussion
 Brief disruption in LOC
 Retrograde amnesia
 Headache
 Short duration
 May result in Post-concussion syndrome
o 87% of football players had this- personality changes, amnesia, early onset dementia
 Post-concussion syndrome:
o Persistent headache
o Lethargy
o Personality and behavior changes
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Focal injury (localized)
 Lacerations
 Tearing of brain tissue
 With depressed and open fractures and penetrating injuries
 Intracerebral hemorrhage
 Subarachnoid hemorrhage
 Intraventricular hemorrhage
 Contusions
 Bruising of brain tissue
 Associated with closed head injury
 Can cause hemorrhage, infarction, necrosis, edema
 Contusion is worse than a concussion
 Can rebleed- if injured again
 Focal and generalized manifestations
 Monitor for seizures
 Potential for increased hemorrhage if on anticoagulants
o Children are not on anticoagulants
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Shortened attention span, decreased short-term memory
Changes in intellectual ability
2 weeks- 2 months
 If they have a second injury the likelihood of permanent head injury disability is
huge- without time to heal develop bleed, need surgery, or death
o Inability to recall is a huge sign of injury- ask what they had for breakfast?
 Hematomas
 Cranial nerve injuries
Minor (GCS 13-15)
Moderate (GCS 9-12)
Severe (GCS 3-8)
 8 or below intubate and ICP monitoring
Diffuse Axonal Injury:
 Widespread axonal damage
 Widespread injury in brain- mild, moderate or severe brain injury
 May take 12-24 hours
 Decreased LOC
 Increased ICP
 Decortication, decerebration
 Global cerebral edema
 These patients are in a persistent vegetative state- never wake up
Coup- Contrecoup Injury:
 With contusion, the phenomenon of coup-contrecoup injury is often noted and can range from minor to
severe.
 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.
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Note: Sports head injuries in children: **
 In April 2013, at Scottish Rite hospital, the governor signed the Return to Play Act of 2013 into law.
 The law includes developing return to play policies for young athletes who get a concussion and educating parents on the
risks of concussions.
 You have to pledge that if your child has any head injury they have to seek care
Epidural and Subdural Hematomas:
 Type by location:
 Dura is normally attached to skull
o Epidural:
 Bleeding between the dura and the inner surface of the skull
 Neurologic emergency
 More likely arterial origin
 Initial period of unconsciousness
 Brief lucid interval followed by decrease in LOC
 Headache, nausea, vomiting
 Focal findings
 Requires rapid evacuation
 My notes:
 Bleed quickly, symptoms soon- neurologic emergency, after initial period of unconsciousness
they come around then drop LOC
 Need to get a CT
o Subdural:
 Bleeding between the dura mater and the arachnoid
 Most common source is the veins that drain the brain surface into the sagittal sinus:
 Acute (2-24 hours)
 Subacute: 2-24 days
 Chronic: weeks or months
o Weeks or months after injury
o More common in older adults
o Presents as focal symptoms
o ↑ Risk for misdiagnosis
 My notes:
 May be more slow, harder with older patients and decreased LOC because may think they are
developing Alzheimer’s
 Need to get a CT
o Subarachnoid:
 Bleeding in the space between brain and the surrounding membrane (subarachnoid space)
 The primary symptom is a sudden, severe headache; nausea, vomiting and a brief loss of consciousness.
 Often arteriole
o Intracerebral:
 Bleeding within the brain tissue- aneurysm bleed
 Usually within frontal and temporal lobes
 Size and location of hematoma determine patient outcome.
 May clip aneurysm and they are fine

Diagnostic Studies:
 CT SCAN IS #1
o Best diagnostic test to determine craniocerebral trauma
 MRI, PET, evoked potential studies
 Transcranial Doppler studies
 Cervical spine x-ray
o C spine them- collar and neck stabilized because you may damage the C spine
 Glasgow Coma Scale (GCS)
Collaborative Care: Emergency Treatment:
 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
 Treatment Principles:
o Prevent secondary injury
o Timely diagnosis
o Surgery if necessary- want to always go to a trauma center in case of emergent surgery
 Concussion and contusion
o Observation and management of ICP
 Skull fractures:
o Conservative treatment
o Surgery if depressed
 Hematomas/ Bleeds
o Surgical evacuation, ICP monitoring
 Craniotomy, burr-holes
 Craniectomy if extreme swelling
Question:
1. The nurse is caring for a patient after a head injury. How should the nurse position the patient in bed?
a. Prone with the head turned to the right side
b. High-Fowlers position with the legs elevated
c. Supine position with the head on two pillows
d. Side-lying with the head elevated 30 degrees
Rationale:
To prevent increased intracranial pressure, the nurse should maintain the patient in the head-up position (no more than 30
degrees). Head elevation over 30 degrees may decrease cerebral perfusion pressure. Extreme neck flexion (head on two pillows) and
hip flexion (high-Fowler’s position) should be avoided. Head should remain midline.
Spinal Cord Injury
SCI Etiology & Epidemiology
 260,000 American’s living with a SCI
 12,000 annually
 Males between 16-30 have the greatest risk- 81%
 Motor vehicle accidents: 47%
 Falls: 23%
 Violence (especially gunshot wounds) 14%
 Sports accidents 9%
 Other 7%

Patho



Primary = the traumatic injury- actual insult at the moment of impact
Secondary = damage post-injury- damage to tissue from event
When spinal cord is injured it can’t send and receive messages below the level of injury
Classification - Mode & Degree
 Mode of injury
o Flexion
 Head is flexed forward
o Hyperextension
o Flexion-rotation
o Hyperextension-rotation
o Compression
 Spinal cord gets compressed- diving or sports
o My notes: tearing of ligaments is rotation
 Degree of injury
o Complete
 Total loss of sensory or motor function below the level of injury
 Quadriplegia (C1) /tetrapelegia (T2)
 Paraplegia
o Incomplete
 Loss of motor and sensory changes below level of injury vary
Central Cord Syndrome
 Etiology
o From an incomplete spinal cord injury
o Often in cervical region- middle of spinal cord most effected
o Hyperextension/flexion injuries
 Symptoms
o Motor Weakness and sensory loss
o Disproportionately greater motor impairment in upper > lower extremities
Anterior Cord Syndrome
 Etiology
o From an Incomplete spinal cord injury
o Disruption of blood flow to the anterior 2/3rd of the cord
 Related to vascular insufficiency
o Flexion injuries, herniation of disc, or injury to cord from bony fragments
 Symptoms
o Complete loss of movement, pain, and temp (legs > arms)
o Deep pressure and proprioception are retained in trunk and lower extremities
o Can’t feel light touch
 Worst prognosis: good if recovery is in first 24 hours, if no sense or feel or temp after 24 hours prognosis is poor
 10%-15% patients have recovery
Posterior Cord Syndrome
 Etiology
o From an incomplete spinal cord injury
o Acute posterior cord compression
o Hyperextension injuries
 Symptoms
o Loss of deep touch sensation
o Preserved motor, however difficult to rehab secondary to loss of proprioception
Brown-Sequard Cord Syndrome
 Etiology
o From an incomplete spinal cord injury
o Damage to only one side of the cord
o Common result to knife or bullet wound
 Symptoms
o Contralateral loss of pain
o Ipsilateral weakness, loss of vibration, and loss of proprioception
o Loss of pain on opposite side of injury
o No bladder symptoms
 Classification - Level of Injury

Dermatomes
Dermatome: area of skin that is supplied by a single spinal nerve
 7 Cervical
o C 3-4 Respiratory function
o C5 - top of the shoulder
 12 thoracic
o T4 - nipple line
o T10 - umbilicus
 5 Lumbar
o L4 - Big toe
 5 sacral
 4 coccyx fused together as 1
SCI - Dermatome Innervation- know these, limitations and interventions
 C3 through C5 innervate the diaphragm,
The chief muscle of inspiration, via the
Phrenic nerve
 C4 through C7 innervate the shoulder and
Arm musculature
 C6 through C8 innervate the forearm extensors and flexors
 C8 through T1 innervate the hand and musculature
 C6 - T11 innervate intracoastal and abdominal muscles
 L2 and L3 mediate hip flexion
 L3 and L4 mediate knee extension
 L4 and L5 mediate ankle dorsiflexion and hip extension
 L5 and S1 mediate knee flexion
 S1 and S2 mediate ankle plantar flexion
SCI - Impact on respiratory system
 Signs/Symptoms
o C4 or higher (phrenic nerve)
 Total loss of respiratory muscle function - mechanical ventilation
o Lower C and Thoracic
 Diaphragmatic breathing - respiratory insufficiency
 Paralysis of abd and intercostal muscles - ineffective cough
 Nursing care/ Intervention
o ABCS- protect airway
o Breath sounds and pattern
o Chest movement
o Care of ETT/Trach
o Increased risk for infection
o Risk of neurogenic pulmonary edema
 Secondary to SNS overactivity post-injury that shunts blood to lungs
SCI - Impact on Cardiovascular System
 Signs/Symptoms
o Above T6 -> decrease in influence of SNS
 Bradycardia
 Peripheral vasodilation - hypotension
 Relative hypovolemia because of increase in dilation of the veins and low venous return (venous
capacitance)
 Manifest as decreased CO
 Nursing care/ intervention
o Monitor VS
o No bowel movements- no vagal stimulation
o Atropine to increase HR
o IV fluids and Vasopressors to increase BP
o MAP GOALS!
 85-90 in acute phase
 > 65 once stable to maintain perfusion
 Give IV fluids or pressor
SCI - Impact on GI and GU Systems
 Signs/Symptoms
o Above T5 -> Hypomotility
 Paralytic ileus
 Gastric distention
o Stress ulcers- excess acid
o Intra-abdominal bleeding
o Urinary retention/constipation
o Neurogenic bladder/ bowel (loss of neuro control over bowel)

Nursing care / Intervention
o NG tube to intermittent suctioning to relieve gastric distention
o Medications (most common is Reglan) to improve GI motility
o H2 blockers and PPIs
o Bowel regimen (Stool softener, enema, etc)
o Foley and intermittent catheter
SCI - Impact on Integumentary System
 Signs/Symptoms
o Potential for skin breakdown
 Especially over bony prominences or in areas with decreased or absent sensation
 Avoid excess moisture
 Any blanching or erythema
o Thermoregulation
 Interruption of SNS provides peripheral temperature sensation from reaching hypothalamus
 Inability to sweat/shiver
 Loss of regulation below SCI
 Higher cervical have a loss of ability to regulate temperature than thoracic or lumbar injuries
 Nursing care/ intervention
o Assess skin at least once per shift
o Turn your patient
o Check patient’s temperature
o Control temp of environment
Additional Nursing Care
 Metabolic needs
o NG suction - metabolic alkalosis
o Get labs- Na and K with suctioning
 Nutritional Support
o High protein diet
o NG, G tube or TPN feedings
 Pain control
o Visceral and neuropathic
 Peripheral Vascular Problems
o DVT prevention
o PE’s are one of the leading causes of death of patients with spinal cord injuries
Immobilization Devices & Techniques
 Halo
o Reduces movement of the neck
 Traction
o Reduces movement of the neck
 Log-roll
 C-collar
o Back board used for log rolling
 Clam
o Controls trunk for lower injuries
 Backboard
SCI Complications - Spinal Shock
 Complete but TEMPORARY syndrome
 Occurs immediately post-injury
 Lasts days or months
o My mask neuro function for as long as it lasts
 Absence of all voluntary and reflex neurologic activity below level of injury
o Communication between brain and body is cut off below level of injury
o See: loss of reflexes, sensation and flaccid paralysis
 ABC, monitor BP
SCI Complications - Neurogenic Shock
 Subtype of distributive shock
 Occurs within 30 minutes of injury to T6 or above
 Can last up to 6 weeks
 Loss of vasomotor tone and loss of sympathetic nervous system tone - massive vasodilation - tissue hypoperfusion impaired cellular metabolism - cell death
 Critical features
o Hypotension
o Bradycardia - due to unopposed parasympathetic stimulation
o Peripheral vasodilation
o Venous pooling
o Issues regulating temperature
 Fluids, pressors, atroping, airway, monitoring support
SCI Complications - Autonomic Dysreflexia
 Medical emergency, life-threatening
 With injuries at or above T6
 Unopposed SNS stimulation
 Most common causes
o Distended bladder/bowel
o Skin stimulus
 Baroreceptors can stimulate PNS to decrease HR, but can’t cause vasodilation because of SCI- HIGH BP and low HR
 S/SX:
o Hypertension
o Diaphoresis above SCI
o Bradycardia
 Nursing interventions
o BP q2-3 min
 Headache or blurred vision check BP
o Raise HOB to > 45 degrees
 Distended bladder from a kinked foley catheter
o Get BP down
o Find the cause!!!

Acute SCI Priorities
 Remember your ABC’s -> Think about where the patient’s SCI is located and its effect on pulmonary status
 C3,4,5 keep you ALIVE. Complete injuries above C5 require intubation
 MAP goals 85-90
Dermatomes: