INCREASED INTRACRANIAL PRESSURE

Introduction
Any patient who becomes unconscious acutely, regardless of the cause, should be suspected of
having increased ICP.

What is ICP?
● Increased ICP is a potentially life-threatening situation that results from an increase in
any or all of the three components (brain tissue, blood, CSF) within the skull.
● Elevated ICP is clinically significant because it diminishes CPP (cerebral perfusion
pressure).
○ increases risks of brain ischemia and infarction

Common Causes

Mass Cerebral edema

● Hematoma ● Brain tumor
● Abscess ● Hydrocephalus
● Tumor ● Head injury
● Contusion ● Brain inflammation
> These cerebral insults, which may result in hypercapnia, cerebral acidosis, impaired
autoregulation, and systemic hyper- tension, increase the formation and spread of cerebral
edema. This edema distorts brain tissue, further increasing the ICP, and leads to even more
tissue hypoxia and acidosis.

● The Monroe-Kellie doctrine states that the intracranial vault is a closed structure with a
fixed intracranial volume. The intracranial contents must be kept in equilibrium, and the
ratio between volume and pressure must remain constant. Any increase in the volume of
one component must be accompanied by a reciprocal decrease in one of the other
components. When this volume-pressure relationship becomes unbalanced, ICP
increases.

Pathophysiology
● The brain attempts to compensate for rises in ICP by:
○ Displacement/shunting of CSF from the intracranial compartment to the lumbar
subarachnoid space (SAS).
○ Increased CSF absorption.
○ Decreased cerebral blood volume by displacement of cerebral venous blood
into the venous sinuses.
● Intracranial compliance is “tightness” of the brain. Compliance is the relationship
between intracranial volume and ICP. It is a nonlinear relationship; as ICP increases,
compliance decreases.
● Factors that influence the ability of the body to achieve this steady state include:
○ Systemic BP.
○ Ventilation and oxygenation.
 ○ Metabolic rate and oxygen consumption (fever, shivering, physical activity).
○ Regional cerebral vasospasm.
○ Oxygensaturationandhematocrit.
● Increased ICP constitutes an emergency and requires prompt treatment. ICP can be
monitored by means of an intraventricular catheter, a subarachnoid screw or bolt, or
an epidural pressure-recording device.
● Alterations or compromise in cerebral blood flow can be measured noninvasively by a
transcranial Doppler (TCD). Increased velocities indicate vasospasm, diminished
velocities indicate low blood flow, and absent velocities are consistent with no flow, or
brain death.

Risk Factors
> Sustained increases in ICP
● Brainstem compression
● Herniation of the brain from one compartment to another.

Laboratory Findings
Laboratory findings to consider in the workup for elevated ICP:
1. Complete Blood Count (CBC)
● Leukocytosis: Elevated white blood cell count could suggest infection, such as
meningitis or encephalitis, which can lead to increased ICP.
● Anemia or thrombocytopenia: May be seen in systemic infections or conditions
like leukemia, which could lead to altered mental status and elevated ICP if
associated with space-occupying lesions or disseminated infection.
2. Serum Electrolytes (especially sodium)
● Hyponatremia: Low sodium can occur in conditions like Syndrome of
Inappropriate Antidiuretic Hormone Secretion (SIADH), which can cause cerebral
edema, and may increase ICP.
● Hypernatremia: Can indicate dehydration or an impaired thirst mechanism, which
may affect cerebral perfusion and intracranial pressure.
3. Serum Osmolality and Osmolal Gap
● Elevated osmolality: Can indicate dehydration or hyperglycemia, which might
worsen cerebral edema in some cases.
● Osmolal gap: A large gap can point to poisoning (e.g., methanol, ethylene glycol),
which might lead to encephalopathy and ICP changes.
4. Blood Cultures and CSF Analysis (if infection suspected)
● Infectious causes (e.g., meningitis, encephalitis): CSF analysis can reveal an
elevated white blood cell count, low glucose, and/or elevated protein. Cultures
from blood or CSF can help identify bacterial or viral pathogens that might cause
increased ICP.
5. Coagulation Profile (PT, aPTT, INR)
● Coagulopathy: Can be associated with hemorrhagic events like intracranial
hemorrhage or brain tumors, which might result in elevated ICP. A prolonged
PT/INR or aPTT could suggest bleeding, which needs further neuroimaging for
confirmation.
 6. Liver Function Tests (LFTs)
● Elevated liver enzymes (AST, ALT) and bilirubin could suggest liver failure, which
in turn might cause hepatic encephalopathy, leading to altered mental status and
possible changes in ICP.
7. Blood Glucose
● Hypoglycemia or hyperglycemia: Can cause altered mental status. Severe
changes in glucose levels may present similarly to conditions causing elevated
ICP (e.g., diabetic ketoacidosis with altered consciousness).
8. Renal Function Tests (BUN, Creatinine)
● Renal failure: Can lead to uremic encephalopathy, which might mimic signs of
elevated ICP due to altered mental status.
9. Thyroid Function Tests
● Hypothyroidism or hyperthyroidism: These can present with altered mental
status, though they would not directly cause elevated ICP. Hypothyroidism may
cause myxedema coma, leading to confusion and coma.
10. Arterial Blood Gases (ABG)
● Hypoxia or Hypercapnia: Respiratory failure with hypoxia or hypercapnia can
increase cerebral blood flow and exacerbate ICP. Metabolic acidosis may also
lead to changes in the brain’s compensatory mechanisms.

Imaging and Other Tests:

While laboratory findings are critical, neuroimaging (CT or MRI) is essential for directly
diagnosing elevated ICP, identifying masses (e.g., tumors or abscesses), hemorrhage, or
hydrocephalus. Additional tests include:
● Fundoscopy: Can reveal papilledema, a classic sign of increased ICP.
● CT or MRI of the Brain: For identifying space-occupying lesions, hemorrhage, or
hydrocephalus.
● Brain EEG: If seizures are suspected.

Nursing Assessment
Change in LOC
Caused by increased cerebral pressure. Assess for:
1. Change in LOC (awareness): drowsiness, lethargy
2. Early behavioral changes: restlessness, irritability, contusion, and apathy
3. Falling score on the GCS (see page 488)
a. Change in orientation: disorientation to time, place, or person
b. Difficulty or inability to follow commands
c. Difficulty or inability in verbalization or in responsiveness to auditory stimuli
d. Change in response to painful stimuli (eg, purposeful to inappropriate or absent
responses)
e. Posturing (abnormal flexion or extension)

Changes in Vital Signs

Caused by pressure on brain stem. Assess for:
1. Rising BP or widening pulse pressure (the difference between systolic and diastolic BP).
This may be followed by hypotension and labile vital signs, indicating further brain stem
compromise.
2. Pulse changes with bradycardia changing to tachycardia as ICP rises.
3. Respiratory irregularities: tachypnea (early sign of increased ICP); slowing of rate with
lengthening periods of apnea; Cheyne-Stokes (rhythmic pattern of increasing and
decreasing depth of respirations with periods of apnea) or Kussmaul (paroxysms of
difficult breathing) breathing; central neurogenic hyperventilation (prolonged, deep
breathing); apneuistic (sustained inspiratory effort) breath- ing; and ataxic (incoordinated
and spasmodic) breathing.
4. Hyperthermia followed by hypothermia.

Pupillary Changes
1. Caused by increased pressure on optic and oculomotor nerves.
2. Inspect the pupils with a penlight to evaluate size, config- uration, and reaction to light.
3. Compare both eyes for similarities or differences, particu- larly pupillary changes related
to location and progression of brain stem herniation.
a. Midbrain involvement—fixed and dilated
b. Pontine involvement—pinpoint pupils
c. Uncal herniation
i. Unilaterally dilating pupil ipsilateral to lesion.
ii. Anisocoria (unequal) with sluggish light reaction in dilated pupils.
iii. If treatment is delayed or unsuccessful, contralateral pupil becomes
dilated and fixed to light.
iv. When herniation of the brainstem occurs, both pupils assume midposition
and remain fixed to light.
d. Central transtentorial herniation
i. Pupils are small bilaterally (1 to 3 mm).
ii. Reaction to light is brisk but with a small range of constriction.
iii. Treatment is delayed or unsuccessful; small pupils dilate moderately (3 to
5 mm) and fix irregularly at midposition.
iv. When herniation of the brainstem occurs, both pupils dilate widely and
remain fixed to light.
4. Perform fundoscopic examination to inspect the retina and optic nerve for hemorrhage
and papilledema.

Extraocular Movements
1. Evaluate gaze to determine if it is conjugate (paired, working together) or dysconjugate
(eye deviates or move- ment is asymmetrical).
2. Evaluate movement of eyes.
a. Inability to abduct or adduct: deviation of one or both eyes.
b. Alteration in vision (eg, blurred vision, diplopia, field cut)
c. Spontaneous roving, random eye movements
 d. Nystagmus on horizontal/vertical gaze
3. Oculocephalic reflex (doll’s eyes): brisk turning of the head left, right, up, or down with
observation of eye movements in response to the stimulus. Tests brain stem pathways
between cranial nerves III, IV, VI, and VIII. This should not be performed on patients with
suspected cervical spine injury, patients in a cervical collar, or patients with known
cervical spine injuries unless part of the brain death exam.
4. Oculovestibular reflex (cold calorics): 30 to 60 mL of ice water instilled into the ear with
the head of the bed ele- vated to 30 degrees. Tests brain stem pathways between
cranial nerves III, IV, VI, and VIII. Response preserved longer than the doll’s eyes
maneuver. Performed by physi- cian as part of brain death examination.

Other Changes
Be alert for:
1. Headache increasing in intensity and aggravated by movement and straining
2. Vomiting recurrent with little or no nausea; especially in early morning; may be projectile
3. Papilledema from optic nerve compression
4. Subtle changes, such as restlessness, headache, forced breathing, purposeless
movements, and mental cloudiness
5. Motor and sensory dysfunctions (proximal muscle weakness, presence of pronator drift)
6. Contralateral hemiparesis progressing to complete hemi- plegia
7. Speech impairment (nonfluent, fluent, or global aphasia) when dominant hemisphere
involved
8. Seizure activity: focal or generalized
9. Decreased brain stem function (cranial nerve deficits, such as loss of corneal reflex, gag
reflex, and ability to swallow)
10. Pathologic reflexes: Babinski, grasp, chewing, sucking.

Nursing Diagnosis
● Decreased Intracranial Adaptive Capacity

1. Ineffective Cerebral Tissue Perfusion

● Rationale: Increased ICP can lead to compromised blood flow to the brain, which
may result in hypoxia, ischemia, and neuronal damage.
● Related Factors: Increased intracranial pressure, cerebral edema, brain injury,
tumors, or hemorrhage.
● Defining Characteristics: Decreased level of consciousness, altered mental
status, motor deficits, and changes in vital signs (e.g., bradycardia, hypertension,
irregular respirations).
● Expected Outcomes:
○ Maintain adequate cerebral perfusion pressure (CPP).
○ Show no signs of ischemic injury on neurological assessment.
○ Maintain stable vital signs.
2. Risk for Ineffective Breathing Pattern
 ● Rationale: Increased ICP can impair the brain's ability to regulate breathing,
leading to respiratory distress, irregular breathing, or hypoventilation.
● Related Factors: Increased intracranial pressure affecting the brainstem,
decreased respiratory drive, and neurological changes.
● Defining Characteristics: Abnormal respiratory rate, rhythm, and depth (e.g.,
Cheyne-Stokes respirations), or labored breathing.
● Expected Outcomes:
○ Demonstrate normal breathing patterns.
○ Oxygen saturation levels within normal range.
○ Report ease of breathing and no signs of respiratory distress.
3. Risk for Imbalanced Fluid Volume
● Rationale: Increased ICP often results in cerebral edema, and the management
of fluid balance is crucial. Administering fluids too rapidly or incorrectly can
worsen ICP.
● Related Factors: Cerebral edema, changes in antidiuretic hormone (ADH)
secretion, osmotic imbalances, or excessive intravenous fluids.
● Defining Characteristics: Fluid retention or dehydration signs, changes in urine
output, changes in weight, electrolyte imbalances.
● Expected Outcomes:
○ Maintain optimal fluid balance.
○ Stable vital signs (e.g., blood pressure, heart rate).
○ Normal electrolyte values and urine output.
4. Decreased Intracranial Adaptive Capacity
● Rationale: The brain’s ability to adapt to increases in ICP is limited. If ICP rises
beyond a compensatory threshold, it can lead to herniation and severe brain
damage.
● Related Factors: Rapid or severe increase in ICP, lack of compensatory
mechanisms, brain injury, or mass effect (tumor, hemorrhage).
● Defining Characteristics: Decreased level of consciousness, dilated pupils, motor
deficits, changes in vital signs (Cushing’s triad: hypertension, bradycardia, and
irregular respirations).
● Expected Outcomes:
○ Demonstrate stable neurological function (e.g., alert, oriented).
○ Normal or stable vital signs.
○ Absence of signs of brain herniation.
5. Acute Pain
● Rationale: Increased ICP can lead to significant headaches, discomfort from
pressure on the brain and surrounding tissues, and pain from underlying causes
(e.g., trauma or tumors).
● Related Factors: Increased intracranial pressure, swelling, ischemia, or trauma.
● Defining Characteristics: Complaints of severe headache, facial grimacing,
increased heart rate, and blood pressure with pain.
● Expected Outcomes:
○ Verbalize relief or a decrease in pain intensity.
 ○ Demonstrate relaxation techniques or other comfort measures.
○ Stable vital signs.
6. Risk for Injury
● Rationale: Elevated ICP can lead to decreased consciousness, seizures, or
motor deficits, all of which increase the risk for injury.
● Related Factors: Altered level of consciousness, motor impairment, risk of
seizures, and environmental hazards.
● Defining Characteristics: Confusion, impaired mobility, or risk of falls.
● Expected Outcomes:
○ Remain free from injury.
○ Maintain safety through appropriate monitoring and environmental
modification.
○ Participate in the prevention of falls (e.g., use of bed rails, side rails, and
appropriate support).
7. Impaired Skin Integrity
● Rationale: Decreased mobility, poor circulation, and prolonged bed rest can
contribute to the development of pressure ulcers, particularly in patients with
severe neurological deficits.
● Related Factors: Altered level of consciousness, immobility, or poor nutrition.
● Defining Characteristics: Redness, pressure sores, or breakdown of skin integrity,
especially in bony prominence areas.
● Expected Outcomes:
○ Skin remains intact without signs of breakdown.
○ No pressure ulcers develop during hospitalization.
8. Disturbed Thought Processes
● Rationale: Increased ICP can lead to confusion, disorientation, and difficulty with
concentration, thought processing, or memory.
● Related Factors: Cerebral edema, ischemia, hypoxia, brain injury, or pressure on
brain structures.
● Defining Characteristics: Disorientation, inability to follow commands, altered
speech, and confusion.
● Expected Outcomes:
○ Demonstrate improved orientation and cognitive function.
○ Show consistent ability to follow simple commands and communicate.
9. Deficient Knowledge
● Rationale: Patients and their families may lack understanding about increased
ICP, its causes, and the importance of treatment.
● Related Factors: New diagnosis of increased ICP, lack of prior education about
neurological conditions.
● Defining Characteristics: Patient/family verbalizing confusion or
misunderstanding about the condition and its management.
● Expected Outcomes:
○ Verbalize understanding of ICP, its causes, and treatment.
○ Demonstrate adherence to prescribed care regimens.
 10. Anxiety
● Rationale: The diagnosis of increased ICP can lead to anxiety for both the patient
and their family due to uncertainty about the outcome and the severity of the
condition.
● Related Factors: Fear of brain injury, worsening condition, or impending surgery.
● Defining Characteristics: Restlessness, elevated heart rate, increased respiratory
rate, and verbal expressions of worry.
● Expected Outcomes:
○ Demonstrate reduced anxiety, as evidenced by relaxed body language
and calm communication.
○ Report a sense of control or understanding of their condition.

Management
Nursing Interventions
1. Establish and maintain airway, breathing, and circula- tion.
2. Promote normal PCO2. Hyperventilation is not recom- mended for prophylactic
treatment of increased ICP as cerebral circulation is reduced by 50% the first 24 hours
after injury. Hyperventilation causes cerebral vasocon- striction and decreases cerebral
blood flow to decrease ICP; this can potentiate secondary injury to the brain.
Hyperventilation should be used only after all other treat- ment options have been
exhausted or in an acute crisis.
3. Avoid hypoxia. Decreased PO2 (less than 60) causes cerebral vasodilation, thus
increasing ICP.
4. Maintain cerebral perfusion pressure (CPP) greater than 60. CPP is determined by
subtracting the ICP from the mean arterial pressure (MAP): CPP MAP ICP.
5. Administer mannitol (Osmitrol), an osmotic diuretic, if ordered. Dosing: 0.25 to 1 gm/kg.
Osmotic diuretics act by establishing an osmotic gradient across the blood-brain barrier
that depletes the intracellular and extracellular fluid volume within the brain and
throughout the body. Mannitol will be ineffective if the blood-brain barrier is not intact.
6. Administer hypertonic saline (2% or 3%), if ordered. It creates an osmotic gradient that
pulls extra fluid from the brain with an intact blood-brain barrier, lowers ICP, improves
cerebral blood flow by reducing viscosity, and improves oxygen carrying capacity. Saline
(23.4%) is used as a bolus to treat acute increases in ICP in conjunc- tion with or in
place of mannitol.
7. Insert an indwelling urinary catheter for management of diuresis.
8. Administer corticosteroids, such as dexamethasone (Decadron), as ordered, to reduce
vasogenic edema associated with brain tumors. Corticosteroids are not recom- mended
in the treatment of cytotoxic (intracellular) cerebral edema related to trauma or stroke.
9. Maintain balanced fluids and electrolytes. Watch for increased or decreased serum
sodium due to the following conditions that may occur with increased ICP.
 a. Diabetes insipidus (DI) results from the absence of antidiuretic hormone (ADH);
this is reflected by increased urine output with elevation of serum osmo- larity
and sodium.
b. The syndrome of inappropriate antidiuretic hormone (SIADH) results from the
secretion of ADH in the absence of changes in serum osmolality. This is reflected
by decreased urine output with decreased serum sodium and increased free
water.
c. Cerebral salt wasting is associated with abnormal release of aldosterone
resulting in increased elimina- tion of sodum and decreased interstitial volume.
(See Table 15-4).
10. Monitor effects of neuromuscular paralyzing agents, such as pancuronium (Pavulon);
anesthetic agents, such as propofol (Diprivan); and sedatives, such as midazolam
(Versed), which may be given along with mechanical ventilation to prevent sudden
changes in ICP due to coughing, straining, or “fighting” the ventilator. Short- acting
medications are preferred to allow for intermittent neurological assessment.
11. High-dose barbiturates, such as pentobarbital (Nembutal), may be used in patients with
intractable increased ICP. (Note: not recommended unless all other treatments failed.
a. High-dose barbiturates induce a comatose state and suppress brain metabolism,
which, in turn, reduces cerebral blood flow and ICP. Only pupillary response is
assessed.
b. Be alert to the high level of nursing support required. All responses to
environmental and noxious stimuli (suctioning, turning) are abolished as well as
all protective reflexes.
c. Cough or gag reflex will be absent and the patient will be unable to protect the
airway, increasing susceptibility to pneumonia.
d. Monitor ICP, arterial pressure, and serum barbiturate levels as indicated. Perform
continuous EEG monitor- ing to document burst suppression (suppression of cor-
tical activity) and ensure adequate dosing of barbitu- rates, if used.
e. Monitor temperature because barbiturate coma causes hypothermia.
f. Diminished GI motility and high risk for ileus.
12. Maintain normothermia and treat fever aggressively. Fever increases cerebral blood flow
and cerebral blood volume; acute increases in ICP occur with fever spikes. Cerebral
temperature is 4 to 5 degrees higher then body core temperature; therefore, small
increases in body core temperature can create drastic increases in the core temperature
of the brain. Induced mild hypothermia (32 to 35 C) is currently being utilized in some
facilities; how- ever, results of research are inconclusive. Hypothermia is felt to be
neuroprotective because it lowers metabolic needs, reduces intracellular acidosis,
decreases the influx of intracellular calcium, and reduces the production of oxygen free
radicals. Infection is a common complication of ICP and in the presence of fever, an
infectious work-up should be completed.
13. Avoid positions or activities that may increase ICP. Keep head in alignment with
shoulders; neck flexion or rota- tion increases ICP by impeding venous return. Keep the
head of the bed elevated 30 degrees to reduce jugular venous pres- sure and decrease
ICP.
 a. Minimize suctioning, keep procedure less than 15 seconds, and, if ordered, instill
lidocaine via endo- tracheal (ET) tube before suctioning. Coughing and
suctioning are associated with increased intrathoracic pressure, which is
associated with ICP spikes. Inject 5 to 10 mL of lidocaine into the ET tube before
suctioning to dampen the cough response.
b. Minimize other stimuli, such as alarms, television, radio, and bedside
conversations, which may precipitously increase ICP (stimuli that create elevation
in ICP are patient dependent).
14. Avoid hyperglycemia. Treat with sliding scale insulin or insulin drip as ordered.
15. Initiate treatment modalities, as ordered, for sustained increased ICP (above 20 mm Hg
persisting 15 minutes or more or if there is a significant shift in pressure).
16. Pretreat prior to known activities that raise ICP, and avoid taking pressure readings
immediately after a proce- dure. Allow the patient to rest for approximately 5 minutes.
17. RecordICPreadingseveryhour,andcorrelatewithsignificant clinical events or treatments
(suctioning, turning).