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Chapter IV
 ICP is the pressure exerted by the contents
inside the cranial vault the brain tissue ,CSF,
and the blood volume. Increased ICP is
defined as CSF pressure greater than 15 mm
Hg.
 ICP is comprised of the following components
and volume ratio: brain tissue, 80%; CSF,
10%; blood volume, 10%.
 The brain 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.
Change in LOC
 Caused by increased cerebral pressure. Assess
for:
 Change in LOC (awareness): drowsiness, lethargy
 Early behavioral changes: restlessness,
irritability, contusion,
 Falling score on the GCS
 Change in orientation: disorientation to time, place,
or person
 Difficulty or inability to follow commands
 Difficulty or inability in verbalization or in
responsiveness to auditory stimuli
 Change in response to painful stimuli (eg, purposeful
to inappropriate or absent responses)
 Posturing (abnormal flexion or extension)
Changes in Vital Signs
Caused by pressure on brain stem. Assess for:
 hypertension.
 Pulse changes with bradycardia changing to
tachycardia as ICP rises.
 Respiratory irregularities: tachypnea (early
sign of increased ICP);
 Hyperthermia followed by hypothermia.
NURSING ALERT
 Respiratory irregularities may not be
apparent if patient is mechanically
ventilated.
Pupillary Changes
 Caused by increased pressure on optic and
oculomotor nerves.
 Inspect the pupils with a flashlight to
evaluate size, configuration, and reaction to
light.
 Compare both eyes for similarities or
differences, particularly pupillary changes
related to location and progression of brain
stem herniation.
 Midbrain involvement: fixed and dilated
 Pontine involvement: pinpoint pupils
 Uncal herniation
 Unilaterally dilating pupil ipsilateral to lesion.
 Anisocoria (unequal) with sluggish light reaction in dilated pupil.
 If treatment is delayed or unsuccessful, contralateral pupil
becomes dilated and fixed to light.
 When herniation of brainstem occurs, both pupils assume
midposition and remain fixed to light.
 Central transtentorial herniation
 Pupils are small bilaterally (1 to 3 mm).
 Reaction to light is brisk but with small range of constriction.
 Treatment is delayed or unsuccessful; small pupils dilate
moderately (3 to 5 mm) to fix irregularly at midposition.
 When herniation of brainstem occurs, both pupils dilate widely
and remain fixed to light.
 Perform fundoscopic examination to inspect the retina
and optic nerve for hemorrhage and papilledema.
Extraocular Movements
 Evaluate gaze to determine if it is conjugate
(paired, working together) or dysconjugate
(eye deviates or movement is asymmetrical).
 Evaluate movement of eyes.
 Inability to abduct or adduct: deviation of one or
both eyes.
 Alteration in vision (eg, blurred vision, diplopia,
field cut)
 Spontaneous roving, random eye movements
 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.
Other Changes
Be alert for:
 Headache increasing in intensity and aggravated
by movement and straining
 Vomiting recurrent with little or no nausea;
especially in early morning; may be projectile
 Papill edema from optic nerve compression
 Subtle changes, such as restlessness, headache,
forced breathing, purposeless movements, and
mental cloudiness
 Motor and sensory dysfunctions (proximal muscle
weakness, presence of pronator drift)
 Contralateral hemiparesis progressing to
complete hemiplegia
 Speech impairment (expressive, receptive, or
global aphasia) when dominant hemisphere
involved
 Seizure activity: focal or generalized
 Decreased brain stem reflexes (cranial nerve
deficits; eg, corneal, gag, and swallow)
 Pathologic reflexes: Babinski, grasp,
chewing, sucking.
 Decreased Intracranial Adaptive Capacity
Decreasing Intracranial Pressure
NURSING ALERT
 Increased ICP is a true life-threatening medical emergency
that requires immediate recognition and prompt
therapeutic intervention.
 Establish and maintain airway, breathing, and circulation.
 Promote normal PCO2. Hyperventilation is not
recommended for prophylactic treatment of increased ICP
as cerebral circulation is reduced by 50% the first 24 hours
after injury. Hyperventilation causes cerebral
vasoconstriction and decreases cerebral blood volume and
results in decreased ICP; this can potentiate secondary
injury to the brain. Hyperventilation should be used only
after all other treatment options have been exhausted or
in an acute crisis.
 Avoid hypoxia. Decreased PO2 (less than 60) also causes
cerebral vasodilation, thus increasing ICP.
 Maintain adequate cerebral perfusion pressure (CPP).
CPP is determined by subtracting the ICP from the
mean arterial pressure (MAP): CPP = MAP ICP
 Administer mannitol (Osmitrol), an osmotic diuretic,
if ordered. 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.
The mannitol will be ineffective if the blood-brain
barrier is not intact.
 Administer hypertonic saline, as ordered. It creates
an osmotic gradient that pulls extra fluid from the
brain with an intact blood-brain barrier, lowers ICP,
improves cerebral blow flow, and delivers oxygen.
Use of hypertonic saline/dextran is currently under
investigation.
 Insert an indwelling urinary catheter for management of
diuresis.
 Administer corticosteroids, such as dexamethasone
(Decadron), as ordered, to reduce edema surrounding
brain tumor, if present. Corticosteroids are used to reduce
inflammation and decrease vasogenic (extracellular)
cerebral edema. Corticosteroids are useful in the
treatment of vasogenic edema associated with brain
tumors but are not recommended in the treatment of
cytoxic (intracellular) cerebral edema related to trauma.
 Maintain balanced fluids and electrolytes. Diabetes
insipidus (DI) results from the absence of antidiuretic
hormone (ADH); this is reflected by increased urine output
with elevation of serum osmolarity and sodium. 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. Either extreme may occur with ICP.
 Monitor effects of neuromuscular paralyzing agents, such as
pancuronium (Pavulon), anesthetic agents, such as propofol (Diprivan),
and sedatives, such as midazolam (Versed) or lorazepam (Ativan), which
may be given along with mechanical ventilation to prevent sudden
changes in ICP due to coughing, straining, or fighting the ventilator.
Neuromuscular paralyzing agents, such as pancuronium (Pavulon) or
vecuronium (Norcuron), or high-dose barbiturates, may be used in cases
that are difficult to manage.
 High-dose barbiturates induce a comatose state and suppress brain metabolism,
which, in turn, reduces cerebral blood flow and ICP (not recommended unless all
other treatments failed).
 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.
 Cough or gag reflex will be absent and the patient will be unable to protect the
airway, increasing susceptibility to pneumonia.
 Monitor ICP
, arterial pressure, and serum barbiturate levels as indicated. Perform
continuous EEG monitoring to document burst suppression (suppression of
cortical activity) and ensure adequate dosing of barbiturates, if used.
 Monitor temperature because barbiturate coma causes hypothermia.
 Treat fever aggressively because 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. Also, infection is a common
complication of ICP.
 Avoid positions or activities that may increase ICP. Keep head in
alignment with shoulders; neck flexion or rotation increases ICP
by impeding venous return. Keep head of bed elevated 30
degrees to reduce jugular venous pressure and decrease ICP.
 Minimize suctioning, keep procedure less than 15 seconds, and, if
ordered, instill lidocaine via endotracheal (ET) tube before suctioning.
Coughing and suctioning are associated with increased intrathoracic
pressure, which is associated with ICP spikes. Lidocaine 5 to 10 ml
injected into ET tube before suctioning dampens the cough response.
 Minimize other stimuli, such as alarms, television, radio, and bedside
conversations, that may precipitously increase ICP (stimuli are patient
dependent).
 Avoid hyperglycemia. Treat with sliding scale
insulin or insulin drip as ordered.
 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).
 Avoid taking pressure readings immediately
after a procedure. Allow patient to rest for
approximately 5 minutes.
 Record ICP readings every hour, and correlate
with significant clinical events or treatments
(suctioning, turning).
 ICP and vital signs stable; alert and
responsive

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3. Intra Cranial Pressure and nursing interventions.pptx

  • 2.  ICP is the pressure exerted by the contents inside the cranial vault the brain tissue ,CSF, and the blood volume. Increased ICP is defined as CSF pressure greater than 15 mm Hg.
  • 3.  ICP is comprised of the following components and volume ratio: brain tissue, 80%; CSF, 10%; blood volume, 10%.  The brain 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.
  • 4. Change in LOC  Caused by increased cerebral pressure. Assess for:  Change in LOC (awareness): drowsiness, lethargy  Early behavioral changes: restlessness, irritability, contusion,  Falling score on the GCS  Change in orientation: disorientation to time, place, or person  Difficulty or inability to follow commands  Difficulty or inability in verbalization or in responsiveness to auditory stimuli  Change in response to painful stimuli (eg, purposeful to inappropriate or absent responses)  Posturing (abnormal flexion or extension)
  • 5. Changes in Vital Signs Caused by pressure on brain stem. Assess for:  hypertension.  Pulse changes with bradycardia changing to tachycardia as ICP rises.  Respiratory irregularities: tachypnea (early sign of increased ICP);  Hyperthermia followed by hypothermia. NURSING ALERT  Respiratory irregularities may not be apparent if patient is mechanically ventilated.
  • 6. Pupillary Changes  Caused by increased pressure on optic and oculomotor nerves.  Inspect the pupils with a flashlight to evaluate size, configuration, and reaction to light.  Compare both eyes for similarities or differences, particularly pupillary changes related to location and progression of brain stem herniation.  Midbrain involvement: fixed and dilated  Pontine involvement: pinpoint pupils
  • 7.  Uncal herniation  Unilaterally dilating pupil ipsilateral to lesion.  Anisocoria (unequal) with sluggish light reaction in dilated pupil.  If treatment is delayed or unsuccessful, contralateral pupil becomes dilated and fixed to light.  When herniation of brainstem occurs, both pupils assume midposition and remain fixed to light.  Central transtentorial herniation  Pupils are small bilaterally (1 to 3 mm).  Reaction to light is brisk but with small range of constriction.  Treatment is delayed or unsuccessful; small pupils dilate moderately (3 to 5 mm) to fix irregularly at midposition.  When herniation of brainstem occurs, both pupils dilate widely and remain fixed to light.  Perform fundoscopic examination to inspect the retina and optic nerve for hemorrhage and papilledema.
  • 8. Extraocular Movements  Evaluate gaze to determine if it is conjugate (paired, working together) or dysconjugate (eye deviates or movement is asymmetrical).  Evaluate movement of eyes.  Inability to abduct or adduct: deviation of one or both eyes.  Alteration in vision (eg, blurred vision, diplopia, field cut)  Spontaneous roving, random eye movements
  • 9.  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.
  • 10. Other Changes Be alert for:  Headache increasing in intensity and aggravated by movement and straining  Vomiting recurrent with little or no nausea; especially in early morning; may be projectile  Papill edema from optic nerve compression  Subtle changes, such as restlessness, headache, forced breathing, purposeless movements, and mental cloudiness  Motor and sensory dysfunctions (proximal muscle weakness, presence of pronator drift)
  • 11.  Contralateral hemiparesis progressing to complete hemiplegia  Speech impairment (expressive, receptive, or global aphasia) when dominant hemisphere involved  Seizure activity: focal or generalized  Decreased brain stem reflexes (cranial nerve deficits; eg, corneal, gag, and swallow)  Pathologic reflexes: Babinski, grasp, chewing, sucking.
  • 12.
  • 13.  Decreased Intracranial Adaptive Capacity
  • 14. Decreasing Intracranial Pressure NURSING ALERT  Increased ICP is a true life-threatening medical emergency that requires immediate recognition and prompt therapeutic intervention.  Establish and maintain airway, breathing, and circulation.  Promote normal PCO2. Hyperventilation is not recommended for prophylactic treatment of increased ICP as cerebral circulation is reduced by 50% the first 24 hours after injury. Hyperventilation causes cerebral vasoconstriction and decreases cerebral blood volume and results in decreased ICP; this can potentiate secondary injury to the brain. Hyperventilation should be used only after all other treatment options have been exhausted or in an acute crisis.  Avoid hypoxia. Decreased PO2 (less than 60) also causes cerebral vasodilation, thus increasing ICP.
  • 15.  Maintain adequate cerebral perfusion pressure (CPP). CPP is determined by subtracting the ICP from the mean arterial pressure (MAP): CPP = MAP ICP  Administer mannitol (Osmitrol), an osmotic diuretic, if ordered. 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. The mannitol will be ineffective if the blood-brain barrier is not intact.  Administer hypertonic saline, as ordered. It creates an osmotic gradient that pulls extra fluid from the brain with an intact blood-brain barrier, lowers ICP, improves cerebral blow flow, and delivers oxygen. Use of hypertonic saline/dextran is currently under investigation.
  • 16.  Insert an indwelling urinary catheter for management of diuresis.  Administer corticosteroids, such as dexamethasone (Decadron), as ordered, to reduce edema surrounding brain tumor, if present. Corticosteroids are used to reduce inflammation and decrease vasogenic (extracellular) cerebral edema. Corticosteroids are useful in the treatment of vasogenic edema associated with brain tumors but are not recommended in the treatment of cytoxic (intracellular) cerebral edema related to trauma.  Maintain balanced fluids and electrolytes. Diabetes insipidus (DI) results from the absence of antidiuretic hormone (ADH); this is reflected by increased urine output with elevation of serum osmolarity and sodium. 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. Either extreme may occur with ICP.
  • 17.  Monitor effects of neuromuscular paralyzing agents, such as pancuronium (Pavulon), anesthetic agents, such as propofol (Diprivan), and sedatives, such as midazolam (Versed) or lorazepam (Ativan), which may be given along with mechanical ventilation to prevent sudden changes in ICP due to coughing, straining, or fighting the ventilator. Neuromuscular paralyzing agents, such as pancuronium (Pavulon) or vecuronium (Norcuron), or high-dose barbiturates, may be used in cases that are difficult to manage.  High-dose barbiturates induce a comatose state and suppress brain metabolism, which, in turn, reduces cerebral blood flow and ICP (not recommended unless all other treatments failed).  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.  Cough or gag reflex will be absent and the patient will be unable to protect the airway, increasing susceptibility to pneumonia.  Monitor ICP , arterial pressure, and serum barbiturate levels as indicated. Perform continuous EEG monitoring to document burst suppression (suppression of cortical activity) and ensure adequate dosing of barbiturates, if used.  Monitor temperature because barbiturate coma causes hypothermia.
  • 18.  Treat fever aggressively because 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. Also, infection is a common complication of ICP.  Avoid positions or activities that may increase ICP. Keep head in alignment with shoulders; neck flexion or rotation increases ICP by impeding venous return. Keep head of bed elevated 30 degrees to reduce jugular venous pressure and decrease ICP.  Minimize suctioning, keep procedure less than 15 seconds, and, if ordered, instill lidocaine via endotracheal (ET) tube before suctioning. Coughing and suctioning are associated with increased intrathoracic pressure, which is associated with ICP spikes. Lidocaine 5 to 10 ml injected into ET tube before suctioning dampens the cough response.  Minimize other stimuli, such as alarms, television, radio, and bedside conversations, that may precipitously increase ICP (stimuli are patient dependent).
  • 19.  Avoid hyperglycemia. Treat with sliding scale insulin or insulin drip as ordered.  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).  Avoid taking pressure readings immediately after a procedure. Allow patient to rest for approximately 5 minutes.  Record ICP readings every hour, and correlate with significant clinical events or treatments (suctioning, turning).
  • 20.  ICP and vital signs stable; alert and responsive