Nur 265 Exam 3 Study Guide
Increased ICP (907, 913
● Normal ICP 10-15 mmHg, pressures >20 mmHg impair cerebral circulation
● IICP is leading cause of death from head trauma in pts who reach the hospital alive.
● Cerebral Perfusion Pressure (CPP)
o Blood flow required to provide adequate oxygenation & glucose for brain metabolism
o Maintenance above 70 mmHg
o CPP= MAP-ICP
MAP= (2xD) + S MAP NEEDS TO BE ATLEAST 80
3
● Compensation
o First Response – CSF is shunted or displaced into the spine (compliance)
o Next – Reduction of blood volume in the brain (autoregulation)
o As ICP continues to increase cerebral perfusion decreases leading to brain tissue ischemia, edema,
vasodilation then acidosis which causes further increases ICP
o In edema remains untreated the brain may herniate into spinal canal – death from brain stem compression
● Assessment Findings
o Changes in LOC – First sign of IICP is declining LOC & includes restlessness or confusion to Stuporous
W/o glucose & 02, brain shuts down. Ex. Pt knew who you were in am & now don’t remember
o Headache – Quite environment may have photophobia so keep room lights very low.
o Change in speech pattern – Aphasia, Slurred Speech
o Changes in pupil size – 2 cm change in either direction is significant, dilated or constricted, Notify Dr
Normal is 6 mm. Getting better if going back toward normal from dilated or constricted
Uneven pupils tx as IICP until proven otherwise; pinpoint - brain stem (pons) dysfunction
o Abnormal Posturing – Decorticate (flexion) or Decerebrate (extensor)
Decorticate – arms drawn to core, legs straight
Decerebrate – arms straight and stiff, pts rarely survives
o Hyperthermia – followed later by hypothermia
When hypothermic – BE CONCERNED, pressure on hypothalamus located next to brain stem
o Cardiac & respiratory rate/rhythm changes
Tachy first – Increased HR & RR before brady HR & RR
o N/V – Common in IICP
o Cushing’s Triad – Severe HTN, Widened Pulse Pressure, Bradycardia
Late response & indicates severe IICP w/loss of autoregulation, Imminent death
Systolic BP increases bc decreased blood flow to brain
Pressure on Vagus nerve and brainstem = bradycardia
● Managing IICP
o Elevate HOB 30-45 degrees (unless contraindicated)
If hypotension, elevate HOB where CPP >70
o Maintain head in a midline neutral position
, o Avoid sudden and acute hip or neck flexion during positioning – Log roll pt
o Avoid clustering of care (bath followed by linen change)
o Coughing and suctioning increase ICP
o Decrease cerebral edema – osmotic diuretics (mannitol) & fluid restriction
Mannitol is hypertonic- pulling fluid into vascular space- will inc. fluid output & monitor BP for HTN
Furosemide used in adjunct to reduce incidence of rebound from mannitol. Helps reduce edema &
blood volume, decrease Na uptake by the brain, & decrease production of CSF at choroid plexus.
o LOW CSF using intraventricular drain system
o Control fever w/antipyretics or cooling blanket – do not allow pt to shiver as will increase ICP
When febrile every cell in body needs more 02 and glucose
o Oxygenation – Hyperventilate on a vent to decrease CO2 which causes vasodilation
o Reduce cellular metabolic demands – barbiturates (-bital, -barbital) and/or sedation (coma)
Traumatic Brain Injury (912-922)
● Primary Brain Injury
o Occurs at time of injury
o Open – Head fractured or penetrated; Closed – Blunt trauma, shaken baby
o Open Head Injuries
Skull Fractures
● Linear Fx – thin line on x-ray, no tx unless underlying brain tissue damaged
● Depressed Fx – Brain damage from bruising (contusion), laceration from bone fragments
● Basilar skull Fx – Fx of bones of the base of skull & results in CSF leak from nose & ears.
o May not be seen on plain x-ray, R/F Infection w/ CSF leak
o Manifested by bruises around eyes (raccoon eyes) or behind ears (Battle’s sign)
o Has potential for hemorrhage if it damages the internal carotid
o Closed Head Injuries
Caused by blunt force trauma
Contusion – Bruising to brain tissue @ site of impact (coup) or opposite (contrecoup)
Laceration – tearing of the cortical surface vessels, lead to secondary hemorrhage, cerebral
edema and inflammation
Diffuse Axonal Injury (DAI) – Tissue of entire brain from high speed acel/decel MVC
● Impaired cognitive functioning, results in disorganization, impaired memory
● Severe will present with immediate coma, survivors require lone-term care
o Classified as
Mild – GCS 13-15 (concussion)
● Blow to head, transient confusion, or feeling dazed or disoriented
● Loss of consciousness for up to 30 min, loss of memory before and after accident
● No evidence of brain damage, sx resolve w/i 72 hrs
● Sx: HA, N/V, Fatigue, Foggy, Balance off, Irritable, Sad, Nervous, Emotional, Visual probs
, Moderate – GCS 9-12
● Loss of consciousness 30 min – 6 hrs w/ memory loss up to 24 hrs.
● Short hospital stays to prevent secondary injury
● Memory loss up to 24 hrs.
Severe – GCS 3-8
● Loss of consciousness >6 hrs
● High risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion
● Pupil changes, Bradycardia, Papilledema, HTN w/wide PP, Nuchal rigidity if CSF leak
o Glasgow Coma Scale
Score from 3-15; score 3-8 in a coma
A change of 2 points requires immediate notification to HCP
● Secondary Brain Injury
o Any process that occurs after the initial injury and worsen or negatively influences patient outcomes.
While trying to recover from initial event, something else happens (ex: meningitis)
o Most common result from hypotension, hypoxia, IICP, & cerebral edema
Damage to brain tissue due to delivery of O2 and glucose to brain is interrupted
Low blood flow and hypoxemia contribute to cerebral edema
o Hypotension & Hypoxia
hypotension (MAP <70), hypoxia (PaO2 <80)
Hypotension may be from shock & hypoxia from resp. failure, loss of airway, or impaired ventilation
o Increased Intracranial Pressure (IICP)
See Increased ICP section above
o Hemorrhage
Begins at moment of impact & potentially life threatening
Epidural Hematoma – Arterial bleeding between dura and inner skull, from fx of temporal bone
● Have “lucid intervals” – Pt awake & talking then momentary unconsciousness
Subdural Hematoma – Venous bleeding into space beneath dura & above arachnoid
● From laceration of brain tissue, bleeding is slower than epidural, Highest mortality rate
● Acute SDH – w/i 48 hrs after impact
● Subacute SDH – 48 hrs – 2 weeks
● Chronic SDH – 2 weeks to several months
A loss of consciousness from an epidural or subdural hematoma is a neurological emergency!
o Hydrocephalus – abnormal increase in CSF volume
Caused by impaired reabsorption or blockage with outflow of CSF, leads to IICP
o Brain Herniation
Increased ICP (907, 913
● Normal ICP 10-15 mmHg, pressures >20 mmHg impair cerebral circulation
● IICP is leading cause of death from head trauma in pts who reach the hospital alive.
● Cerebral Perfusion Pressure (CPP)
o Blood flow required to provide adequate oxygenation & glucose for brain metabolism
o Maintenance above 70 mmHg
o CPP= MAP-ICP
MAP= (2xD) + S MAP NEEDS TO BE ATLEAST 80
3
● Compensation
o First Response – CSF is shunted or displaced into the spine (compliance)
o Next – Reduction of blood volume in the brain (autoregulation)
o As ICP continues to increase cerebral perfusion decreases leading to brain tissue ischemia, edema,
vasodilation then acidosis which causes further increases ICP
o In edema remains untreated the brain may herniate into spinal canal – death from brain stem compression
● Assessment Findings
o Changes in LOC – First sign of IICP is declining LOC & includes restlessness or confusion to Stuporous
W/o glucose & 02, brain shuts down. Ex. Pt knew who you were in am & now don’t remember
o Headache – Quite environment may have photophobia so keep room lights very low.
o Change in speech pattern – Aphasia, Slurred Speech
o Changes in pupil size – 2 cm change in either direction is significant, dilated or constricted, Notify Dr
Normal is 6 mm. Getting better if going back toward normal from dilated or constricted
Uneven pupils tx as IICP until proven otherwise; pinpoint - brain stem (pons) dysfunction
o Abnormal Posturing – Decorticate (flexion) or Decerebrate (extensor)
Decorticate – arms drawn to core, legs straight
Decerebrate – arms straight and stiff, pts rarely survives
o Hyperthermia – followed later by hypothermia
When hypothermic – BE CONCERNED, pressure on hypothalamus located next to brain stem
o Cardiac & respiratory rate/rhythm changes
Tachy first – Increased HR & RR before brady HR & RR
o N/V – Common in IICP
o Cushing’s Triad – Severe HTN, Widened Pulse Pressure, Bradycardia
Late response & indicates severe IICP w/loss of autoregulation, Imminent death
Systolic BP increases bc decreased blood flow to brain
Pressure on Vagus nerve and brainstem = bradycardia
● Managing IICP
o Elevate HOB 30-45 degrees (unless contraindicated)
If hypotension, elevate HOB where CPP >70
o Maintain head in a midline neutral position
, o Avoid sudden and acute hip or neck flexion during positioning – Log roll pt
o Avoid clustering of care (bath followed by linen change)
o Coughing and suctioning increase ICP
o Decrease cerebral edema – osmotic diuretics (mannitol) & fluid restriction
Mannitol is hypertonic- pulling fluid into vascular space- will inc. fluid output & monitor BP for HTN
Furosemide used in adjunct to reduce incidence of rebound from mannitol. Helps reduce edema &
blood volume, decrease Na uptake by the brain, & decrease production of CSF at choroid plexus.
o LOW CSF using intraventricular drain system
o Control fever w/antipyretics or cooling blanket – do not allow pt to shiver as will increase ICP
When febrile every cell in body needs more 02 and glucose
o Oxygenation – Hyperventilate on a vent to decrease CO2 which causes vasodilation
o Reduce cellular metabolic demands – barbiturates (-bital, -barbital) and/or sedation (coma)
Traumatic Brain Injury (912-922)
● Primary Brain Injury
o Occurs at time of injury
o Open – Head fractured or penetrated; Closed – Blunt trauma, shaken baby
o Open Head Injuries
Skull Fractures
● Linear Fx – thin line on x-ray, no tx unless underlying brain tissue damaged
● Depressed Fx – Brain damage from bruising (contusion), laceration from bone fragments
● Basilar skull Fx – Fx of bones of the base of skull & results in CSF leak from nose & ears.
o May not be seen on plain x-ray, R/F Infection w/ CSF leak
o Manifested by bruises around eyes (raccoon eyes) or behind ears (Battle’s sign)
o Has potential for hemorrhage if it damages the internal carotid
o Closed Head Injuries
Caused by blunt force trauma
Contusion – Bruising to brain tissue @ site of impact (coup) or opposite (contrecoup)
Laceration – tearing of the cortical surface vessels, lead to secondary hemorrhage, cerebral
edema and inflammation
Diffuse Axonal Injury (DAI) – Tissue of entire brain from high speed acel/decel MVC
● Impaired cognitive functioning, results in disorganization, impaired memory
● Severe will present with immediate coma, survivors require lone-term care
o Classified as
Mild – GCS 13-15 (concussion)
● Blow to head, transient confusion, or feeling dazed or disoriented
● Loss of consciousness for up to 30 min, loss of memory before and after accident
● No evidence of brain damage, sx resolve w/i 72 hrs
● Sx: HA, N/V, Fatigue, Foggy, Balance off, Irritable, Sad, Nervous, Emotional, Visual probs
, Moderate – GCS 9-12
● Loss of consciousness 30 min – 6 hrs w/ memory loss up to 24 hrs.
● Short hospital stays to prevent secondary injury
● Memory loss up to 24 hrs.
Severe – GCS 3-8
● Loss of consciousness >6 hrs
● High risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion
● Pupil changes, Bradycardia, Papilledema, HTN w/wide PP, Nuchal rigidity if CSF leak
o Glasgow Coma Scale
Score from 3-15; score 3-8 in a coma
A change of 2 points requires immediate notification to HCP
● Secondary Brain Injury
o Any process that occurs after the initial injury and worsen or negatively influences patient outcomes.
While trying to recover from initial event, something else happens (ex: meningitis)
o Most common result from hypotension, hypoxia, IICP, & cerebral edema
Damage to brain tissue due to delivery of O2 and glucose to brain is interrupted
Low blood flow and hypoxemia contribute to cerebral edema
o Hypotension & Hypoxia
hypotension (MAP <70), hypoxia (PaO2 <80)
Hypotension may be from shock & hypoxia from resp. failure, loss of airway, or impaired ventilation
o Increased Intracranial Pressure (IICP)
See Increased ICP section above
o Hemorrhage
Begins at moment of impact & potentially life threatening
Epidural Hematoma – Arterial bleeding between dura and inner skull, from fx of temporal bone
● Have “lucid intervals” – Pt awake & talking then momentary unconsciousness
Subdural Hematoma – Venous bleeding into space beneath dura & above arachnoid
● From laceration of brain tissue, bleeding is slower than epidural, Highest mortality rate
● Acute SDH – w/i 48 hrs after impact
● Subacute SDH – 48 hrs – 2 weeks
● Chronic SDH – 2 weeks to several months
A loss of consciousness from an epidural or subdural hematoma is a neurological emergency!
o Hydrocephalus – abnormal increase in CSF volume
Caused by impaired reabsorption or blockage with outflow of CSF, leads to IICP
o Brain Herniation
