This document discusses increased intracranial pressure (ICP) including its causes, effects, and management. It begins by describing the components within the rigid skull and how an increase in any component can raise ICP. Increased ICP decreases cerebral blood flow and can cause brain herniation, a fatal event. Management aims to reduce cerebral edema, lower CSF volume, and maintain cerebral perfusion through interventions like osmotic diuretics, corticosteroids, fluid restriction, and CSF drainage. ICP is monitored invasively to identify pressure elevations and guide treatment effectiveness.

2. Increased Intracranial Pressure
 The rigid cranial vault contains brain tissue (1,400 g), blood (75 mL),
and CSF (75 mL).
 The volume and pressure of these three components are usually in a
state of equilibrium and produce the ICP.
 ICP is usually measured in the lateral ventricles; normal ICP is 10 to 20
mm Hg.
 Because of the limited space for expansion within the skull, an increase
in any one of the components causes a change in the volume of the
others.

3.  Because brain tissue has limited space to change, compensation
typically is accomplished by displacing or shifting CSF, increasing the
absorption of CSF, or decreasing cerebral blood volume.
 Without such changes, ICP will begin to rise.
 Under normal circumstances, minor changes in blood volume and CSF
volume occur constantly due to alterations in intra thoracic pressure
(coughing, sneezing, straining), posture, blood pressure, and systemic
oxygen and carbon dioxide levels.

4. Pathophysiology
 Increased ICP is a syndrome that affects many patients with acute
neurologic conditions.
 This is because pathologic conditions alter the relationship between
intracranial volume and pressure.
 Although an elevated ICP is most commonly associated with head
injury, it also may be seen as a secondary effect in other conditions,
such as brain tumors, subarachnoid hemorrhage, and toxic and viral
encephalopathies.

5.  Increased ICP from any cause decreases cerebral perfusion, stimulates
further swelling (edema), and shifts brain tissue through openings in
the rigid dura, resulting in herniation, frequently fatal event.
DECREASED CEREBRAL BLOOD FLOW
 Increased ICP may significantly reduce cerebral blood flow, resulting
in ischemia and cell death.
 In the early stages of cerebral ischemia, the vasomotor centers are
stimulated and the systemic pressure rises to maintain cerebral blood
flow.

6.  Usually a slow bounding pulse and respiratory irregularities
accompany this.
 These changes in blood pressure, pulse, and respiration are important
clinically because they suggest increased ICP.
 The concentration of carbon dioxide in the blood and in the brain
tissue also has a role in the regulation of cerebral blood flow.
 A rise in carbon dioxide partial pressure (PaCO2) causes cerebral
vasodilatation, leading to increased cerebral blood flow and increased
ICP; a fall in PaCO2 has a vasoconstrictive effect.
 Decreased venous outflow may also increase cerebral blood volume,
thus raising ICP.

7. CEREBRAL EDEMA
 Cerebral edema or swelling is defined as an abnormal accumulation of
water or fluid in the intracellular space, extracellular space, or both,
associated with an increase in brain tissue volume.
 Edema can occur in the gray, white, or interstitial matter.
 As brain tissue swells within the rigid skull, several mechanisms
attempt to compensate for the increasing ICP.
 These mechanisms include autoregulation and decreasing the
production and flow of CSF.

8.  Autoregulation refers to the brain’s ability to change the diameter of its
blood vessels automatically to maintain a constant cerebral blood flow
during alterations in systemic blood pressure.

9. CEREBRAL RESPONSE TO INCREASED ICP
 As ICP rises, compensatory mechanisms in the brain work to maintain
blood flow and prevent tissue damage.
 The brain can maintain a steady perfusion pressure when the arterial
systolic blood pressure is 50 to 150 mm Hg and ICP is less than 40 mm
Hg.
 The cerebral perfusion pressure is calculated by subtracting the ICP
from the mean arterial pressure.
 For example, if the mean arterial pressure is 100 and the ICP is 15, then
the cerebral perfusion pressure is 85 mm Hg.

10.  The normal cerebral perfusion pressure is 70 to 100 mm Hg.
 As ICP rises, however, and the auto regulatory mechanism of the brain
is overwhelmed, cerebral perfusion pressure can rise to greater than
100 mm Hg or fall to less than 50 mm Hg.
 Patients with a cerebral perfusion pressure less than 50 mm Hg
experience irreversible neurologic damage.
 If ICP equals mean arterial pressure, cerebral circulation ceases .

11.  A clinical phenomenon known as the Cushing’s response (or
Cushing’s reflex) is seen when cerebral blood flow decreases
significantly.
 When ischemic, the vasomotor center triggers a rise in arterial pressure
in an effort to overcome the increased ICP.
 A sympathetically mediated response causes a rise in the systolic
blood pressure with a widening of the pulse pressure and cardiac
slowing.

12.  This response, which is mediated by the sympathetic nervous system,
is seen clinically as a rise in systolic blood pressure, widening of the
pulse pressure, and reflex slowing of the heart rate.
 This is a sign requiring immediate intervention; however, perfusion
may be recoverable if treated rapidly.

13.  At a certain volume or pressure, the brain’s ability to autoregulate
becomes ineffective and decompensation (ischemia and infarction)
begins.
 When this occurs, the patient exhibits significant changes in mental
status and vital signs.
 The bradycardia, hypertension, and bradypnea associated with this
deterioration are known as Cushing’s triad, a grave sign.
 At this point, herniation of the brain stem and occlusion of the cerebral
blood flow occur if therapeutic intervention is not initiated.
 Herniation refers to the shifting of brain tissue from an area of high
pressure to an area of lower pressure.

14. Cross section of normal brain (left) and brain
with intracranial shifts from supratentorial lesions (right). (1) Herniation
of the cingulated gyrus. (2) Herniation of the temporal
lobe into the tentorial notch. (3) Downward displacement of the
brainstem through the notch.

15.  The herniated tissue exerts pressure on the brain area to which it has
herniated or shifted, interfering with the blood supply in that area.
 Cessation of cerebral blood flow results in cerebral ischemia and
infarction and brain death.
Clinical Manifestations
 When ICP increases to the point at which the brain’s ability to adjust
has reached its limits, neural function is impaired; this may be
manifested by clinical changes first in LOC and later by abnormal
respiratory and vasomotor responses.

16.  Any sudden change in the patient’s condition, such as restlessness
(without apparent cause), confusion, or increasing drowsiness, has
neurologic significance.
 These signs may result from compression of the brain due to swelling
from hemorrhage or edema, an expanding intracranial lesion
(hematoma or tumor), or a combination of both.

17.  As ICP increases, the patient becomes stuporous, reacting only to loud
auditory or painful stimuli.
 At this stage, serious impairment of brain circulation is probably
taking place, and immediate intervention is required.
 As neurologic function deteriorates further, the patient becomes
comatose and exhibits abnormal motor responses in the form of
decortication, decerebration, or flaccidity.
 When the coma is profound, with the pupils dilated and fixed and
respirations impaired, death is usually inevitable.

18. Assessment and Diagnostic Findings
 The patient may undergo cerebral angiography, computed
tomography (CT) scanning, magnetic resonance imaging (MRI), or
positron emission tomography (PET).
 Trans cranial Doppler studies provide information about cerebral
blood flow.
 The patient with increased ICP may also undergo electrophysiologic
monitoring to monitor cerebral blood flow indirectly.

19.  Lumbar puncture is avoided in patients with increased ICP because
the sudden release of pressure can cause the brain to herniate.

20. Complications
 Complications of increased ICP include brain stem herniation, diabetes
insipidus, and syndrome of inappropriate antidiuretic hormone
(SIADH).
 Brain stem herniation results from an excessive increase in ICP, when
the pressure builds in the cranial vault and the brain tissue presses
down on the brain stem.
 This increasing pressure on the brain stem results in the cessation of
blood flow to the brain, causing irreversible brain anoxia and brain
death.

21.  Diabetes insipidus is the result of decreased secretion of antidiuretic
hormone.
 The patient has excessive urine output, and hyperosmolarity results.
Therapy consists of administration of fluid volume, electrolyte
replacement, and vasopressin (desmopressin, DDAVP) therapy.

22.  Syndrome of inappropriate antidiuretic hormone (SIADH) is the result
of increased secretion of antidiuretic hormone.
 The patient becomes volume-overloaded, urine output diminishes, and
serum sodium concentration becomes dilute.
 Treatment of SIADH includes fluid restriction, which is usually
sufficient to correct the hyponatremia; severe cases call for judicious
administration of a 3% hypertonic saline solution.
 Patients with chronic SIADH may respond to lithium carbonate or
demeclocycline, which reduces renal tubule responsiveness to
antidiuretic hormone.

23. Management
 Increased ICP is a true emergency and must be treated promptly.
 Invasive monitoring of ICP is an important component of management, but
immediate management to relieve increased ICP involves decreasing cerebral
edema, lowering the volume of CSF, or decreasing cerebral blood volume
while maintaining cerebral perfusion.
 These goals are accomplished by administering osmotic diuretics and
corticosteroids, restricting fluids, draining CSF, controlling fever, maintaining
systemic blood pressure and oxygenation, and reducing cellular metabolic
demands.
 Judicious use of hyperventilation is recommended only if the ICP is
refractory to other measures.

24. MONITORING ICP
 The purposes of ICP monitoring are to identify increased pressure
early in its course (before cerebral damage occurs), to quantify the
degree of elevation, to initiate appropriate treatment, to provide access
to CSF for sampling and drainage, and to evaluate the effectiveness of
treatment.
 An intraventricular catheter (ventriculostomy), a subarachnoid bolt, an
epidural or subdural catheter, or a fiberoptic transducer-tipped
catheter placed in the subdural space or the ventricle can be used to
monitor ICP.

25.  When a ventriculostomy or ventricular catheter monitoring device is
used for monitoring ICP, a fine-bore catheter is inserted into a lateral
ventricle, usually in the nondominant hemisphere of the brain.
 The catheter is connected by a fluidfilled system to a transducer, which
records the pressure in the form of an electrical impulse.
 In addition to obtaining continuous ICP recordings, the ventricular
catheter allows CSF to drain, particularly during acute rises in
pressure.

26.  The ventriculostomy also can be used to drain the ventricle of blood.
 Also, continuous drainage of ventricular fluid under pressure control
is an effective method of treating intracranial hypertension.
 Another advantage of an indwelling ventricular catheter is the access it
provides for the intraventricular administration of medications and the
instillation of air or a contrast agent for ventriculography.
 Complications include ventricular infection, meningitis, ventricular
collapse, occlusion of the catheter by brain tissue or blood, and
problems with the monitoring system.

27.  The subarachnoid bolt (or screw) is a hollow device inserted through
the skull and dura mater into the cranial subarachnoid space.
 It has the advantage of not requiring a ventricular puncture.
 The subarachnoid screw is attached to a pressure transducer, and the
output is recorded on an oscilloscope.
 The hollow screw technique has the advantage of avoiding
complications from brain shift and small ventricle size.
 Complications include blockage of the screw by clot or brain tissue,
which leads to a loss of pressure tracing and a decrease in accuracy at
high ICP readings.

28.  An epidural monitor uses a pneumatic flow sensor that functions on a
nonelectrical basis.
 his pneumatic epidural ICP monitoring system has a low incidence of
infection and complications and appears to read pressures accurately.
 Calibration of the system is maintained automatically, and abnormal
pressure waves trigger an alarm system.
 One disadvantage of the epidural catheter is the inability to withdraw
CSF for analysis.

29.  A fiberoptic monitor, or transducer-tipped catheter, is becoming a
widely used alternative to standard intraventricular, subarachnoid,
and subdural systems.
 The miniature transducer reflects pressure changes, which are
converted to electrical signals in an amplifier and displayed on a
digital monitor.
 The catheter can be inserted into the ventricle, subarachnoid space,
subdural space, or brain parenchyma or under a bone flap.
 If inserted into the ventricle, it can also be used in conjunction with a
CSF drainage device.

30.  Waves of high pressure and troughs of relatively normal pressure
indicate changes in ICP.
 Waveforms are captured and recorded on an oscilloscope.
 These waves have been classified as A waves (plateau waves), B
waves, and C waves.
 The plateau waves (A waves) are transient, paroxysmal, recurring
elevations of ICP that may last 5 to 20 minutes and range in amplitude
from 50 to 100 mm Hg.

31.  Plateau waves have clinical significance and indicate changes in
vascular volume within the intracranial compartment that are
beginning to compromise cerebral perfusion.
 A waves may increase in amplitude and frequency, reflecting cerebral
ischemia and brain damage that can occur before overt signs and
symptoms of raised ICP are seen clinically.

32.  B waves are shorter (30 seconds to 2 minutes), with smaller amplitude
(up to 50 mm Hg).
 They have less clinical significance, but if seen in runs in a patient with
depressed consciousness, they may precede the appearance of A
waves.
 B waves may be seen in patients with intracranial hypertension and
decreased intracranial compliance.
 C waves are small, rhythmic oscillations with frequencies of
approximately six per minute.

33.  They appear to be related to rhythmic variations of the systemic
arterial blood pressure and respirations.
 DECREASING CEREBRAL EDEMA
 Osmotic diuretics (mannitol) may be given to dehydrate the brain
tissue and reduce cerebral edema.
 They act by drawing water across intact membranes, thereby reducing
the volume of brain and extracellular fluid.
 An indwelling urinary catheter is usually inserted to monitor urinary
output and to manage the resulting diuresis.

34.  When a patient is receiving osmotic diuretics, serum osmolality should
be determined to assess hydration status.
 Corticosteroids (eg, dexamethasone) help reduce the edema
surrounding brain tumors when a brain tumor is the cause of
increased ICP.
 Another method for decreasing cerebral edema is fluid restriction.
 Limiting overall fluid intake leads to dehydration and
hemoconcentration, drawing fluid across the osmotic gradient and
decreasing cerebral edema.
 Conversely, overhydration of the patient with increased ICP is
avoided, as this will increase cerebral edema.

35.  It has been hypothesized that lowering body temperature will decrease
cerebral edema, reduce the oxygen and metabolic requirements of the
brain, and protect the brain from continued ischemia.
 If body metabolism can be reduced by lowering body temperature, the
collateral circulation in the brain may be able to provide an adequate
blood supply to the brain.

36.  The effect of hypothermia on ICP requires more study, but as yet
induced hypothermia has not been proven to be beneficial in the brain-
injured patient.
 Inducing and maintaining hypothermia is a major clinical procedure
and requires knowledge and skilled nursing observation and
management.

37. MAINTAINING CEREBRAL PERFUSION
 The cardiac output may be manipulated to provide adequate perfusion
to the brain.
 Improvements in cardiac output are made using fluid volume and
inotropic agents such as dobutamine hydrochloride.
 The effectiveness of the cardiac output is reflected in the cerebral
perfusion pressure, which is maintained at greater than 70 mm Hg.
 A lower cerebral perfusion pressure indicates that the cardiac output is
insufficient to maintain adequate cerebral perfusion.

38. REDUCING CSF AND INTRACRANIAL BLOOD
VOLUME
 CSF drainage is frequently performed because the removal of CSF with
a ventriculostomy drain may dramatically reduce ICP and restore
cerebral perfusion pressure.
 Caution should be used in draining CSF because excessive drainage
may result in collapse of the ventricles.
 Hyperventilation, which results in vasoconstriction, has been used for
many years in patients with increased ICP.

39.  Recent research has demonstrated that hyperventilation may not be as
beneficial as once thought .
 The reduction in the PaCO2 may result in hypoxia, ischemia, and an
increase in cerebral lactate levels.
 Maintaining the PaCO2 at 30 to 35 mm Hg may prove beneficial.
 Hyperventilation is indicated in patients whose ICP is unresponsive to
conventional therapies, but it should be used judiciously.

40. CONTROLLING FEVER
 Preventing a temperature elevation is critical because fever increases
cerebral metabolism and the rate at which cerebral edema forms.
 Strategies to reduce temperature include administration of antipyretic
medications, as prescribed, and use of a cooling blanket.
 Additional strategies for reducing fever are included in the Nursing
Process: The Patient With an Altered Level of Consciousness section of
this chapter.
 The patient’s temperature is monitored closely, and the patient is
observed for shivering, which should be avoided because it increases
ICP.

41. MAINTAINING OXYGENATION
 Arterial blood gases must be monitored to ensure that systemic
oxygenation remains optimal.
 Hemoglobin saturation can also be optimized to provide oxygen more
efficiently at the cellular level.

42. REDUCING METABOLIC DEMANDS
 Cellular metabolic demands may be reduced through the
administration of high doses of barbiturates when the patient is
unresponsive to conventional treatment.
 The mechanism by which barbiturates decrease ICP and protect the
brain is uncertain, but the resultant comatose state is thought to reduce
the metabolic requirements of the brain, thus providing some
protection.

43.  Another method of reducing cellular metabolic demand and
improving oxygenation is the administration of pharmacologic
paralyzing agents.
 The patient who receives these agents cannot move, decreasing the
metabolic demands and resulting in a decrease in cerebral oxygen
demand.
 Because the patient cannot respond or report pain, sedation and
analgesia must be provided because the paralyzing agents do not
provide either.

44.  Patients receiving high doses of barbiturates or pharmacologic
paralyzing agents require continuous cardiac monitoring, endotracheal
intubation, mechanical ventilation, ICP monitoring, and arterial
pressure monitoring.
 Pentobarbital (Nembutal), thiopental (Pentothal), and propofol
(Diprivan) are the most common agents used for high-dose barbiturate
therapy.
 Serum barbiturate levels must be monitored.
 The ability to perform serial neurologic assessments on the patient is
lost with the use of barbiturates or paralyzing agents.

45.  Therefore, other monitoring tools are needed to assess the patient’s
status and response to therapy.
 Important parameters that must be assessed include ICP, blood
pressure, heart rate, respiratory rate, and response to ventilator
therapy.
 The level of pharmacologic paralysis is adjusted based on serum levels
and the assessed parameters.
 Potential complications include hypotension due to decreased
sympathetic tone and myocardial depression.

46. TRENDS IN NEUROLOGIC MONITORING
 One controversial trend in cerebral monitoring is the ongoing
measurement of venous oxygen saturation in the jugular bulb (SjO2).
 Readings taken from a catheter residing in the jugular outflow tract
theoretically allow for a comparison of arterial and venous oxygen
saturation, and the balance of cerebral oxygen supply and demand is
demonstrated.
 Venous jugular desaturations can reflect early cerebral ischemia,
alerting the clinician prior to a rise in ICP.

47.  Minimizing elevations in ICP can potentially improve outcome.
 This type of monitoring appears beneficial in the management of
patients at risk for cerebral ischemia; however, the invasive nature of
this type of monitoring and current limitations in technology mandate
caution in its use.
 More study is needed before SjO2 monitoring can be considered a
valid and reliable tool for the management of cerebral ischemia.

48. ICP monitoring. A fiber-optic, transducer-tipped device
placed in (A) the ventricle or (B) the subarachnoid
space. These devices connect to a pressure transducer and a
display system.

49. Location of the foramen of Monro for calibration of
intracranial pressure monitoring system.