Chapter 56 - Intracranial Pressure
Skull has three essential components
 Brain tissue
 Blood
 Cerebrospinal fluid (CSF)
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
 The Monro-Kellie doctrine states that the three components must remain at a relatively
constant volume within the closed skull structure. If the volume of any one of the three
components increases within the cranial vault and the volume from another component
is displaced, the total intracranial volume will not change.
 This hypothesis is only applicable in situations in which the skull is closed.
 The hypothesis is not valid in persons with displaced skull fractures or
hemicranectomy.
 Normal ICP 5 to 15 mm Hg
o Elevated if > 20 mm Hg sustained
 Normal compensatory adaptions
o Changes in CSF volume
 The CSF volume can be changed by altering CSF absorption or production and by
displacement of CSF into the spinal subarachnoid space.
o Changes in intracranial blood volume
 occur through the collapse of cerebral veins and dural sinuses, regional cerebral
vasoconstriction or dilation, and changes in venous outflow.
o Changes in tissue brain volume
 compensates through distention of the dura or compression of brain tissue
 Ability to compensate is limited
o If volume increase continues, ICP rises → decompensation = compression and ischemia
Cerebral Blood Flow
 Amount of blood in mL passing through 100 g of brain tissue in 1 minute
 About 50 mL/min per 100 g of brain tissue
 The maintenance of blood flow to the brain is critical because the brain requires a constant supply of
oxygen and glucose. The brain uses 20% of the body’s oxygen and 25% of its glucose.
o The maintenance of blood flow to the brain is critical because the brain requires a constant supply
of oxygen and glucose. The brain uses 20% of the body’s oxygen and 25% of its glucose.
 Autoregulation
o Adjusts diameter of blood vessels (to maintain constant BF during changes in arterial BP)
o Ensures consistent CBF
 To meet metabolic needs of brain tissue and to maintain cerebral perfusion pressure
o Only effective if mean arterial pressure (MAP) 70 to 150 mm Hg
 < 70 = CBF decreases; symptoms of cerebral ischemia (syncope & blurred vision)
 > 150 = vessels maximally constricted & further vasoconstrictor response is lost
 Cerebral perfusion pressure (CPP) – pressure needed to ensure BF to the brain
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o CPP = MAP – ICP
o Normal is 60 to 100 mm Hg
o <50 mm Hg is associated with ischemia and neuronal death
o < 30 mm Hg results in ischemia and is incompatible with life
Effect of cerebral vascular resistance
o CPP = Flow x Resistance
 High = BF to brain tissue is impaired
 Transcranial doppler used to monitor resistance
Pressure changes
o Compliance is the expandability of brain
o Impacts effect of volume change on pressure
 It is represented as the volume increase for each unit increase in pressure.
 With low compliance, small changes in volume result in greater increases in pressure.
o Compliance = Volume/Pressure
o Intracranial volume pressure curve – used to represent the
stages of increased ICP
 At stage 1 on the curve, there is high compliance. An
increase in volume (in brain tissue, blood, or CSF)
does not increase the ICP.
 At stage 2, the compliance is beginning to decrease,
and an increase in volume places the patient at risk of
increased ICP and secondary injury.
 At stage 3, there is significant reduction in
compliance. Any small addition of volume causes a
great increase in ICP.
 As the patient enters stage 4, the ICP rises to lethal
levels with little increase in volume.
Stages of increased ICP
o Stage 1: Total compensation (accommodation and autoregulation intact)
o Stage 2: ↓ Compensation; risk for ↑ICP
o Stage 3: Failing compensation; clinical manifestations of ↑ ICP (Cushing’s triad)
 Cushing’s triad = by systolic hypertension with a widening pulse pressure, bradycardia
with a full and bounding pulse, and altered respirations = neuro emergency
o Stage 4: Herniation imminent → death
Factors affecting cerebral blood vessel tone
o CO2
o O2
o Hydrogen ion concentration
 Carbon dioxide, oxygen, and hydrogen ion concentration affect cerebral blood vessel
tone.
 An increase in the partial pressure of carbon dioxide in arterial blood (PaCO2) relaxes
smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance, and
increases CBF. A decrease in PaCO2 constricts cerebral vessels, increases cerebrovascular
resistance, and decreases CBF.
 Cerebral O2 tension less than 50 mm Hg results in cerebrovascular dilation. This dilation
decreases cerebral vascular resistance, increases CBF, and increases O2 tension.
However, if O2 tension is not increased, anaerobic metabolism begins, resulting in an
accumulation of lactic acid.
 As lactic acid increases and hydrogen ions accumulate, the environment becomes more
acidic. Within this acidic environment, further vasodilation occurs in a continued attempt
to increase blood flow.
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The combination of a severely low partial pressure of oxygen in arterial blood (PaO2)
and an elevated hydrogen ion concentration (acidosis), which are both potent cerebral
vasodilators, may produce a state where autoregulation is lost and compensatory
mechanisms fail to meet tissue metabolic demands.
Increased ICP
 Life-threatening
 Increase in any of three components
o Brain tissue
o Blood
o CSF
 ↑ Cerebral edema
 Common causes: a mass (e.g., hematoma, contusion, abscess, tumor) and cerebral edema (associated
with brain tumors, hydrocephalus, head injury, or brain inflammation)
Progression of Increased Intracranial Pressure
 Cerebral edema distorts brain tissue, further increasing the ICP, and leads to even
more tissue hypoxia and acidosis. This figure illustrates the progression of
increased ICP.
 It is critical to maintain CBF to preserve tissue and thus minimize secondary
injury. 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.
Herniation
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A, Normal relationships of intracranial structures. B, Shift of intracranial structures.
Compression of the brainstem and cranial nerves may be fatal.
Herniation forces the cerebellum and brainstem downward through the foramen magnum.
If compression of the brainstem is unrelieved, respiratory arrest will occur due to compression of the
respiratory control center in the medulla
Cerebral Edema
 ↑ Extravascular fluid in brain
 Variety of causes
o Mass lesions, head injuries, cerebral infection, vascular insult & toxic or met. Encephalopathy
 Three types of cerebral edema
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Vasogenic
 Most common type
 Occurs mainly in white matter
 Fluid leaks from intravascular to extravascular space
 Variety of causes
• brain tumors, abscesses, and ingested toxins, may cause an increase in the
permeability of the blood-brain barrier and produce an increase in the
extracellular fluid volume
 Continuum of symptoms HA → coma
Cytotoxic
 Disruption of cell membrane integrity
 Secondary to destructive lesions or trauma to brain tissue
  cerebral hypoxia or anoxia & SIADH
 Fluid shift from extracellular to intracellular
Interstitial
 Usually result of hydrocephalus
 Hydrocephalus is a build-up of fluid in the brain and is manifested by ventricular
enlargement.
 Excess CSP production, obstruction of flow, or inability to reabsorb CSF
 Treat with ventriculostomy or shunt
Clinical Manifestations
 Change in level of consciousness (*most sensitive and reliable factor)
 Change in vital signs
o Cushing’s triad
 Ocular signs (compression of CN III)
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Change in level of consciousness
o Flattening of affect → coma
Change in vital signs
o Cushing’s triad (widened pulse pressure, bradycardia, irregular respirations)
 Sign of brainstem compression and impending death
o Change in body temperature
 Increased ICP affects hypothalamus
Compression of oculomotor nerve
o Unilateral pupil dilation (ipsilateral to mass lesion)
o Sluggish or no response to light
o Inability to move eye upward
o Eyelid ptosis
 a fixed, unilateral, dilated pupil = neurologic emergency; indicates herniation
Other cranial nerves (optic II, tochlear IV, abducens VI)
o Diploplia, blurred vision, EOM changes
↓ In motor function
o Hemiparesis/hemiplegia (contralateral – opp. Side of mass lesion)
o Decerebrate posturing (extensor)
 Indicates more serious damage
o Decorticate posturing (flexor)
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A, Decorticate response. Flexion of arms, wrists, and fingers with
adduction in upper extremities. Extension, internal rotation, and plantar
flexion in lower extremities.
B, Decerebrate response. All four extremities in rigid extension, with
hyperpronation of forearms and plantar flexion of feet.
C, Decorticate response on right side of body and decerebrate response
on left side of body.
D, Opisthotonic posturing.
Headache
o Often continuous
o Worse in the morning
 Vomiting
o Not preceded by nausea
o Projectile
Complications
 Inadequate cerebral perfusion
 Cerebral herniation
o Tentorial herniation
 (central herniation) occurs when a mass lesion in the cerebrum forces the brain to
herniate downward through the opening created by the brainstem.
 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 Uncal herniation
 occurs with lateral and downward herniation
o Cingulate herniation
 occurs with lateral displacement of brain tissue beneath the falx cerebri
Diagnostic Studies
 CT scan / MRI / PET
 EEG
 Cerebral angiography
 ICP and brain tissue oxygenation measurement (LICOX catheter)
 Doppler and evoked potential studies
 NO lumbar puncture
• Reasoning: cerebral herniation could occur from the sudden release of the pressure in the skull
from the area above the lumbar puncture.
 Infrascanner – used to detect life threatening intracranial bleeding
• Scanner directs a wavelength of light that can penetrate tissue and bone
• Blood from intracranial hematomas absorbs the light differently than other areas of brain
Measurement of ICP
 Guides clinical care
 Indications – neuro insults (hemorrhage, stroke, tumor, infection, injury)
 Monitored in patients with:
o Glasgow Coma Scale of ≤8
o Abnormal CT scans or MRI (hematoma, contusion, edema)
 Ventriculostomy = GOLD STANDARD
o Catheter inserted into lateral ventricle
o Coupled with an external transducer
• This technique directly measures the pressure within the ventricles, facilitates removal
and/or sampling of CSF, and allows for intraventricular drug administration.
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CSF can be drained via a ventriculostomy when ICP exceeds the
upper pressure parameter set by the physician. Intermittent
drainage involves opening the three-way stopcock to allow CSF
to flow into the drainage bag for brief periods (30 to 120
seconds) until the pressure is below the upper pressure
parameters. ICP, Intracranial pressure.
Potential Placements of ICP Monitoring Devices
o Patients with conditions known to
elevate ICP usually undergo ICP
monitoring in an ICU, except those with
irreversible problems or advanced
neurologic disease.
o Multiple methods and devices are
available to monitor ICP in various sites.
o This graphic shows a coronal section of
brain showing potential sites for
placement of ICP monitoring devices
Measurement of ICP cont.
 Fiberoptic catheter
o Sensor transducer located within catheter tip
o The sensor tip is placed within the ventricle or the brain tissue and provides a direct measurement
of brain pressure.
 Air pouch/pneumatic technology
o Air-filled pouch at catheter tip that maintains constant volume
o The pressure changes within the cranium are transmitted through the changes exerted on this
pouch to the monitor.
 Prevent and monitor for infection
o Factors that contribute to infection: ICP monitoring > 5 days, use of ventriculostomy, CSF leak,
concurrent systemic infection
 Measure as mean pressure
o If a CSF drainage device is in place, the drain must be closed for at least 6 minutes to ensure an
accurate reading.
 Waveform should be recorded
o Normal, elevated, and plateau waves
 ICP Monitoring
o The normal ICP waveform has three phases.
o 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 (shown in visual).
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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
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o Bubbles/air in tubing
Can control ICP by removing CSF (with ventricular catheter)
Intermittent (x2-3min) or continuous drainage
Careful monitoring of volume of CSF drained is essential
o Normal CSF production is about 20 to 30 mL/hr, with a total CSF volume of about 150 mL within
the ventricles and subarachnoid space.
Prevent infection and other complications
Measurement of Cerebral Oxygenation and Perfusion
• LICOX catheter
• Measures brain oxygenation (PbtO2) and temperature
• The normal range for PbtO2 is 20 to 40 mm Hg
• A cooler brain temp (96.8F/ 36C) may produce better outcomes
• Placed in healthy white brain matter
• Jugular venous bulb catheter
• Measures jugular venous oxygen saturation (SjvO2) (measures global oxygen extraction)
• Places in internal jugular vein and positioned so that the catheter tip is located in the jug bulb
• Placement verified by X-Ray
• Normal SjvO2 range is 55% to 75%.
• < 50% demonstrate impaired cerebral oxygenation.
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Visual of the LICOX brain tissue oxygen system.
Catheter inserted through an intracranial bolt (A).
The system measures oxygen in the brain (PbtO2), brain tissue temperature, and intracranial pressure
(ICP) (B).
Interprofessional Care
 Treat underlying cause
o Increased blood (hemorrhage), brain tissue (tumor or edema), or CSF (hydrocephalus)
 Adequate oxygenation
o PaO2 > 100 mm Hg
o PaCO2 35-45 mm Hg
o Intubation
o Mechanical ventilation
 Surgery (tumor or hematoma)
o In aggressive situations, a craniectomy (removal of part of skull) may be performed to reduce ICP
and prevent herniation
 Drug Therapy
o Mannitol (Osmitrol) (25%) – osmotic diuretic given IV
 Plasma expansion
• reduces the hematocrit and blood viscosity, thereby increasing CBF and cerebral
oxygen delivery
 Osmotic effect
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fluid moves from the tissues into the blood vessels. Therefore the ICP is reduced
by a decrease in the total brain fluid content.
 Monitor fluid and electrolyte status
o Hypertonic saline
 Moves water out of cells and into blood
 Monitor BP and serum sodium levels
o Corticosteroids (dexamethasone [Decadron])
 Tx: Vasogenic edema
• NOT rec. for traumatic brain injury
• Corticosteroids stabilize the cell membrane and inhibit the synthesis of
prostaglandins, thus preventing the formation of proinflammatory mediators.
Corticosteroids also improve neuronal function by improving CBF and restoring
autoregulation.
• Complications: hyperglycemia, increase risk infection, GI bleed
 Monitor fluid intake, serum sodium and glucose levels
 Concurrent antacids, H2 receptor blockers, proton pump inhibitors – to prevent GI
ulcers/ bleeds
o Antiseizure medications
o Antipyretics
o Sedatives
o Analgesics
o Barbiturates
 Metabolic demands such as fever (greater than 38°C), agitation/shivering, pain, and
seizures can also increase ICP. The health care team should plan to reduce these
metabolic demands in order to lower the ICP in the at-risk patient. Monitor patients for
seizure activity. They may need to be placed on prophylactic antiseizure medication.
 Fever should be well-controlled in order to maintain a temperature of 36° to 37°C by
using antipyretics (e.g., acetaminophen), cool baths, cooling blankets, ice packs, or
intravascular cooling devices as necessary without causing the patient to shiver or
shake. Shivering should be avoided as this increases the metabolic workload on the
brain, and sedatives may be needed or a different type of cooling method selected.
 Manage pain while being careful not to oversedate or medicate. Finally, the patient
should remain in a quiet and calm environment with minimal noise and interruptions.
Observe the patient for signs of agitation, irritation, or frustration. Also teach the
caregiver and family about decreasing stimulation. Coordinate with the
interprofessional team to minimize procedures that may produce agitation.
 Drug therapy for reducing cerebral metabolism may be an effective strategy to control
ICP. Reducing the metabolic rate decreases the CBF and therefore the ICP. High doses of
barbiturates (e.g., pentobarbital [Nembutal], thiopental [Pentothal]) are used in patients
with increased ICP refractory to other treatments. Barbiturates decrease cerebral
metabolism, causing a decrease in ICP as well as a reduction in cerebral edema.
Nutritional Therapy (malnutrition promotes continued cerebral edema)
o Hypermetabolic and hypercatabolic state ↑ need for glucose
o Enteral or parenteral nutrition
o Early feeding (within 3 days of injury)
o Keep patient normovolemic fluid state
o IV 0.9% NaCl preferred over D5W or 0.45% NaCl
Nursing Assessment
 Subjective data
 Level of consciousness (LOC)
o Glasgow Coma Scale
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Eye opening
Best verbal response (speak)
Best motor response (obey commands)
• Highests score = 15 (fully alert person)
• Lowest score = 3
• </= 8 – indicative of coma (mech. Vent. Should be considered)
Pupillary Check for Size and Response
o Compare the pupils with one another for size,
shape, movement, and reactivity.
o If the oculomotor nerve (CN III) is compressed, the
pupil on the affected side (ipsilateral) becomes
larger until it fully dilates. If ICP continues to
increase, both pupils dilate.
o Test pupillary reaction with a penlight. The normal
reaction is brisk constriction when the light is shone
directly into the eye. Also note a consensual
response (a slight constriction in the opposite pupil)
at the same time. A sluggish reaction can indicate
early pressure on CN III (oculomotor nerve).
o A fixed pupil unresponsive to light stimulus usually
indicates increased ICP.
Cranial nerves
o Eye movements (CN 3,4,6)
o Corneal reflex (CN 5,7)
o Oculovestibular (caloric stimulation)
o Oculocephalic reflex (doll’s eye reflex)
 To test the oculocephalic reflex (doll’s-eye reflex), turn the patient’s head briskly to the
left or right while holding the eyelids open. A normal response is movement of the eyes
across the midline in the direction opposite that of the turning. Next, quickly flex and
then extend the neck. Eye movement should be opposite to the direction of head
movement—up when the neck is flexed and down when it is extended. Abnormal
responses can help locate the intracranial lesion. This test should not be attempted if a
cervical spine problem is suspected.
Motor strength
o Squeeze hands
o Pronator drift test
o Raise foot off bed or bend knees
Motor response
o Spontaneous or to pain
Vital signs
Abnormal Respiratory Patterns of Coma 
Overall Planning
 Maintain a patent airway
 ICP within normal limits
 Normal fluid and electrolyte balance
 Prevent complications secondary to immobility and
decreased LOC
Acute Care
 Respiratory function
o Maintain patent airway
o Elevate head of bed 30 degrees
o Suctioning needs
• Suctioning and coughing will cause transient decreases in the PaO 2 and increases in the
ICP.
• Keep suctioning to a minimum and less than 10 seconds in duration, with administration
of 100% oxygen before and after to prevent decreases in the PaO 2.
• To avoid cumulative increases in the ICP with suctioning, limit suctioning to two passes
per suction procedure, if possible.
o Minimize abdominal distention
• Insertion of a nasogastric tube to aspirate the stomach contents can prevent distention,
vomiting, and possible aspiration. However, in patients with facial and skull fractures, a
nasogastric tube is contraindicated unless a basal skull fracture has been ruled out, and
oral insertion of a gastric tube is preferred.
o Monitor ABGs
o Maintain ventilatory support
 Pain and anxiety management (can increase ICP and BP, further complicating mgmt.)
o Opioids
o Propofol (Diprivan)
o Dexmedetomidine (Precedex)
o Neuromuscular blocking agents
o Benzodiazepines
 Fluid and electrolyte balance
o Monitor IV fluids
o Daily electrolytes
o Monitor for DI or SIADH
• DI (Diabetes insipidus) is caused by a decrease in antidiuretic hormone (ADH); results in
increased urinary output and hypernatremia. The usual treatment of diabetes insipidus is
fluid replacement, vasopressin (Pitressin), or desmopressin acetate (DDAVP). If not
treated, severe dehydration will occur
• SIADH caused by excess ADH; results in decreased urinary output and dilutional
hyponatremia. It may result in cerebral edema, changes in LOC, seizures, and coma
 Monitor and minimize increases in ICP
o Valsalva maneuver, coughing, sneezing, suctioning, hypoxemia, and arousal from sleep are
factors that can increase ICP
 Interventions to optimize ICP and CPP
o HOB elevated appropriately- 30 (promotes drainage and decreases vascular congestion)
o Prevent extreme neck flexion ( venous obstruction)
o Turn slowly (rapid changes, pain, aggitation increase ICP)
o Avoid coughing, straining, Valsalva (increased intrathoracic pressure increases ICP)
o Avoid hip flexion (to decrease intrabdominal pressure)
 Minimize complications of immobility
 Protection from self-injury
o Judicious use of restraints; sedatives (Versed, Ativan)
o Seizure precautions
o Quiet, nonstimulating environment
 Psychologic considerations
Expected Outcomes
 Maintain ICP and CPP within normal parameters
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No serious increases in ICP during or following care activities
No complications of immobility
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.
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.