45: NEUROLOGIC PROBLEMS
MONITORING FOR INCREASED INTRACRANIAL PRESSURE
Most at risk for increased ICP resulting from edema during the first 72 hr. after onset of a
stroke
May have worsening neuro changes starting within 24-48 after their endovascular
procedure from increased ICP
Assess these pt. Q 1-4 hr.
CHART 45-6 KEY FEATURES
Decreased LOC (lethargy to coma)
Behavior changes: restlessness, irritability, and confusion
HA
N/V (may be projectile)
Change in speech pattern/slurred speech:
o Aphasia
Change in sensorimotor status:
o Pupillary changes: dilated and nonreactive (“brown pupils”) or constricted and
nonreactive
o Cranial nerve dysfunction
o Ataxia
Seizures (usually within first 24 hr. after stroke)
Cushing’s triad:
o Severe HTN
o Widened pulse pressure
o Bradycardia
Abnormal posturing:
o Decerebrate
o Decorticate
>> INTERVENTIONS
For increased ICP experiencing a stroke:
o Elevate HOB – sitting them up is very important
o O2 therapy (for O2 < 94%)
o Maintain head in midline, neutral position – promotes venous drainage from the
brain
1
, o Avoid sudden and acute hip or neck flexion during positioning
o Avoid the clustering of RN procedures – can elevate ICP even more
Not for neuro pt.
o Hyperoxygenate before and after suctioning
o Provide airway management to prevent unnecessary suctioning and coughing
that can increase ICP
o Maintain quiet environment if pt. has a HA
o Keep the room lights low to accommodate and photophobia
o MT BP, heart rhythm, O2 sat, blood glucose, and body temp to prevent secondary
brain injury and promote positive outcomes after stroke
MD usually like BP to be slightly elevated after a stroke (SBP = 140-150)
CRITICAL RESCUE!! – Be alert for S/S of increased ICP in the head injury and report any
neuro deterioration to the MD or Rapid Response Team immediately!
o The 1st sign of increased ICP is a declining LOC
2
,TRAUMATIC BRAIN INJURY (TBI)
>>> PATHO
Can lead to temporary and permanent
impairment in cognition, mobility, sensory
perception, and psychosocial function
Direct injury: blow directly to the head
Indirect injury: force applied to another
body part with a rebound effect to the brain
Sheared: rebound or rotated on the brain
stem
Bruised: contusion of the brain
Torn: laceration of the brain as it moves
across the inner surface of the cranial
Acceleration injury: caused by n external force contacting the head, suddenly placing
the head in motion
Deceleration injury: occurs when the moving head is suddenly stopped or hits a
stationary object
PRIMARY BRAIN INJURY
Occurs at the time of injury -- Dives and hits head
Can be focal or diffuse
o Focal: confined to a specific area of the brain and causes localized damage that
can often be detected with a CT scan or MRI
o Diffuse: damage throughout many areas of the brain
Usually too small to detect with CT scan at first but cn worsen to a
detectable size
MRI can see microscopic injuries
Classified as open or closed
o Open: when the skull is fractured or pierced by a penetrating object
o Closed: the integrity of the skull stays intact
Further defined as mild, moderate, or severe – usually determined by the Glasgow
coma scale immediately after resuscitation, presence of brain damage shown in CT scan
or MRI, estimation of force of the trauma, and S/S
3
, SECONDARY BRAIN INJURY
Any processes that occur after the initial injury and worsen or negatively influence pt.
outcomes.
o Increased swelling due to primary brain injury
Result form physiologic, vascular, and biochemical events that are an extension of the
primary injury.
o Most common secondary injuries result from hypotension and hypoxia,
intracranial HTN, and cerebral edema.
o Damage to the brain tissue occurs primarily because the delivery of O2 and
glucose to the brain is interrupted from cerebral edema and increasing pressure.
> HYPOTENSION AND HYPOXIA
Hypotension = MAP < 70
o r/t shock or clot formation
Hypoxemia = PaO2 < 80
o r/t resp. failure, asphyxiation, or loss of airway and impaired ventilation
o leads to decreased cognition
These restrict the flow of blood to vulnerable brain tissue
> INCREASED INTRACRANIAL PRESSURE
Normal level of ICP = 10 – 15 mm Hg
A sustained ICP of 20 is detrimental to the brain because neurons begin to die
As a result of brain injury, the increase in the volume of one component must be
compensated for by a decrease in the volume of one of the other components
o Cerebral edema
The brain can compensate for increased ICP by sending blood volume into the sinuses or
jugular veins.
Increased ICP is the leading cause of death from head trauma in pt. who reach the
hospital alive
o Happens when the brain can no longer compensate for the increased ICP
o As ICP increases, cerebral perfusion decreases, leading to brain tissue ischemia
and edema
o Brain herniation syndrome: when the brain is forced downward thru the Forman
of Monro
> HEMORRHAGE
Causes a brain hematoma (collection of blood) or clot, may occur at the primary injury
or arise later from vessel damage
4
MONITORING FOR INCREASED INTRACRANIAL PRESSURE
Most at risk for increased ICP resulting from edema during the first 72 hr. after onset of a
stroke
May have worsening neuro changes starting within 24-48 after their endovascular
procedure from increased ICP
Assess these pt. Q 1-4 hr.
CHART 45-6 KEY FEATURES
Decreased LOC (lethargy to coma)
Behavior changes: restlessness, irritability, and confusion
HA
N/V (may be projectile)
Change in speech pattern/slurred speech:
o Aphasia
Change in sensorimotor status:
o Pupillary changes: dilated and nonreactive (“brown pupils”) or constricted and
nonreactive
o Cranial nerve dysfunction
o Ataxia
Seizures (usually within first 24 hr. after stroke)
Cushing’s triad:
o Severe HTN
o Widened pulse pressure
o Bradycardia
Abnormal posturing:
o Decerebrate
o Decorticate
>> INTERVENTIONS
For increased ICP experiencing a stroke:
o Elevate HOB – sitting them up is very important
o O2 therapy (for O2 < 94%)
o Maintain head in midline, neutral position – promotes venous drainage from the
brain
1
, o Avoid sudden and acute hip or neck flexion during positioning
o Avoid the clustering of RN procedures – can elevate ICP even more
Not for neuro pt.
o Hyperoxygenate before and after suctioning
o Provide airway management to prevent unnecessary suctioning and coughing
that can increase ICP
o Maintain quiet environment if pt. has a HA
o Keep the room lights low to accommodate and photophobia
o MT BP, heart rhythm, O2 sat, blood glucose, and body temp to prevent secondary
brain injury and promote positive outcomes after stroke
MD usually like BP to be slightly elevated after a stroke (SBP = 140-150)
CRITICAL RESCUE!! – Be alert for S/S of increased ICP in the head injury and report any
neuro deterioration to the MD or Rapid Response Team immediately!
o The 1st sign of increased ICP is a declining LOC
2
,TRAUMATIC BRAIN INJURY (TBI)
>>> PATHO
Can lead to temporary and permanent
impairment in cognition, mobility, sensory
perception, and psychosocial function
Direct injury: blow directly to the head
Indirect injury: force applied to another
body part with a rebound effect to the brain
Sheared: rebound or rotated on the brain
stem
Bruised: contusion of the brain
Torn: laceration of the brain as it moves
across the inner surface of the cranial
Acceleration injury: caused by n external force contacting the head, suddenly placing
the head in motion
Deceleration injury: occurs when the moving head is suddenly stopped or hits a
stationary object
PRIMARY BRAIN INJURY
Occurs at the time of injury -- Dives and hits head
Can be focal or diffuse
o Focal: confined to a specific area of the brain and causes localized damage that
can often be detected with a CT scan or MRI
o Diffuse: damage throughout many areas of the brain
Usually too small to detect with CT scan at first but cn worsen to a
detectable size
MRI can see microscopic injuries
Classified as open or closed
o Open: when the skull is fractured or pierced by a penetrating object
o Closed: the integrity of the skull stays intact
Further defined as mild, moderate, or severe – usually determined by the Glasgow
coma scale immediately after resuscitation, presence of brain damage shown in CT scan
or MRI, estimation of force of the trauma, and S/S
3
, SECONDARY BRAIN INJURY
Any processes that occur after the initial injury and worsen or negatively influence pt.
outcomes.
o Increased swelling due to primary brain injury
Result form physiologic, vascular, and biochemical events that are an extension of the
primary injury.
o Most common secondary injuries result from hypotension and hypoxia,
intracranial HTN, and cerebral edema.
o Damage to the brain tissue occurs primarily because the delivery of O2 and
glucose to the brain is interrupted from cerebral edema and increasing pressure.
> HYPOTENSION AND HYPOXIA
Hypotension = MAP < 70
o r/t shock or clot formation
Hypoxemia = PaO2 < 80
o r/t resp. failure, asphyxiation, or loss of airway and impaired ventilation
o leads to decreased cognition
These restrict the flow of blood to vulnerable brain tissue
> INCREASED INTRACRANIAL PRESSURE
Normal level of ICP = 10 – 15 mm Hg
A sustained ICP of 20 is detrimental to the brain because neurons begin to die
As a result of brain injury, the increase in the volume of one component must be
compensated for by a decrease in the volume of one of the other components
o Cerebral edema
The brain can compensate for increased ICP by sending blood volume into the sinuses or
jugular veins.
Increased ICP is the leading cause of death from head trauma in pt. who reach the
hospital alive
o Happens when the brain can no longer compensate for the increased ICP
o As ICP increases, cerebral perfusion decreases, leading to brain tissue ischemia
and edema
o Brain herniation syndrome: when the brain is forced downward thru the Forman
of Monro
> HEMORRHAGE
Causes a brain hematoma (collection of blood) or clot, may occur at the primary injury
or arise later from vessel damage
4
