Nur 265 Exam 3 Study Guide
Increased ICP (939-940, chart 941)
• 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 survive
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)
1
,Traumatic Brain Injury (946-957)
• 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 (contercoup)
▪ 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 stay 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
2
, ▪ 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
▪ Uncus- dilated non-reactive pupils, ptosis, decreased LOC
▪ Central – Down shift brain stem – Cheyne-Stokes, Pinpoint & nonreactive pupils,
hemodynamic instability. NOTIFY PHYSICIAL IMMEDIATELY
• Etiology
o Young males, play more sports, take more risks when driving (MVC), consume more alcohol
o Falls most common in older adults.
• Assessment/Interventions
o Hx – Did pt lose consciousness? Drug or alcohol consumption? All screened for abuse/neglect
o Physical
▪ First priority is assessment of ABCs - Report any sign of respiratory problems immediately!
▪ Suspect neck injury until proven otherwise, stabilize w/ C-Collar and backboard
• Skin breakdown & pressure ulcer formation are concern with spine board & c-collar
• Once board removed, spinal precautions maintained until HCP indicates it is safe
o (1) Bedrest; (2) No neck flexion with a pillow or roll; (3)No thoracic or lumbar
flexion w/HOB elevation (reverse T acceptable); (4) Manual control of C spine
anytime collar removed; (5) Log roll
▪ Prevent secondary brain injury – O2 & lowering ICP, Vent if needed, do not want CO2 to rise
as it causes vasodilation & IICP.
o Vital Signs
▪ Monitor VS Q 1-2 hrs – May be hypotensive or hypertensive (IV fluids to maintain above 90)
▪ Central fever caused by hypothalamic damage – no sweating, high, last days-weeks
• Responds better to cooling (sponge bath, cool air)
• Fever from any cause is associated w/higher mortality rates
▪ Cushing’s Triad – HTN, Wide PP, & Bradycardia – late sign of IICP and indicates imminent
death
▪ Hypotension and tachycardia indicate hypovolemic shock
o Neuro
▪ GCS
▪ Most important variable to assess w/any brain injury is LOC
▪ Dec or change in LOC is first sign of deterioration (behavior changes, restlessness,
disorientation)
▪ Assess pupils
• Pinpoint - & nonresponsive – Brainstem dysfunction @ level of ponds
• Asymmetric, loss of light reaction, unilateral or bilateral dialed – herniation
o Late signs of IICP – severe HA, N/V, seizures, papilledema - always sign of IICP
▪ Motor response - Decorticate or Decerebrate posturing
o Psychosocial
▪ Personality changes – temper outbursts, depression, risk-taking, denial, talkative, outgoing
o Therapeutic Hypothermia
▪ Rapidly cool pt to 89.6 – 93.2 for 24-48 hrs after primary injury to reduce brain metabolism
and reduce secondary brain injury.
o Mechanical ventilation
▪ Maintain PaCO2 at 35 to 38 to prevent IICP from vasodilation from CO2
▪ Maintain PaO2 between 80-100 to prevent secondary injury
▪ Lidocaine given IV or endotracheally to suppress cough reflex; coughing increases ICP
3
Increased ICP (939-940, chart 941)
• 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 survive
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)
1
,Traumatic Brain Injury (946-957)
• 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 (contercoup)
▪ 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 stay 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
2
, ▪ 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
▪ Uncus- dilated non-reactive pupils, ptosis, decreased LOC
▪ Central – Down shift brain stem – Cheyne-Stokes, Pinpoint & nonreactive pupils,
hemodynamic instability. NOTIFY PHYSICIAL IMMEDIATELY
• Etiology
o Young males, play more sports, take more risks when driving (MVC), consume more alcohol
o Falls most common in older adults.
• Assessment/Interventions
o Hx – Did pt lose consciousness? Drug or alcohol consumption? All screened for abuse/neglect
o Physical
▪ First priority is assessment of ABCs - Report any sign of respiratory problems immediately!
▪ Suspect neck injury until proven otherwise, stabilize w/ C-Collar and backboard
• Skin breakdown & pressure ulcer formation are concern with spine board & c-collar
• Once board removed, spinal precautions maintained until HCP indicates it is safe
o (1) Bedrest; (2) No neck flexion with a pillow or roll; (3)No thoracic or lumbar
flexion w/HOB elevation (reverse T acceptable); (4) Manual control of C spine
anytime collar removed; (5) Log roll
▪ Prevent secondary brain injury – O2 & lowering ICP, Vent if needed, do not want CO2 to rise
as it causes vasodilation & IICP.
o Vital Signs
▪ Monitor VS Q 1-2 hrs – May be hypotensive or hypertensive (IV fluids to maintain above 90)
▪ Central fever caused by hypothalamic damage – no sweating, high, last days-weeks
• Responds better to cooling (sponge bath, cool air)
• Fever from any cause is associated w/higher mortality rates
▪ Cushing’s Triad – HTN, Wide PP, & Bradycardia – late sign of IICP and indicates imminent
death
▪ Hypotension and tachycardia indicate hypovolemic shock
o Neuro
▪ GCS
▪ Most important variable to assess w/any brain injury is LOC
▪ Dec or change in LOC is first sign of deterioration (behavior changes, restlessness,
disorientation)
▪ Assess pupils
• Pinpoint - & nonresponsive – Brainstem dysfunction @ level of ponds
• Asymmetric, loss of light reaction, unilateral or bilateral dialed – herniation
o Late signs of IICP – severe HA, N/V, seizures, papilledema - always sign of IICP
▪ Motor response - Decorticate or Decerebrate posturing
o Psychosocial
▪ Personality changes – temper outbursts, depression, risk-taking, denial, talkative, outgoing
o Therapeutic Hypothermia
▪ Rapidly cool pt to 89.6 – 93.2 for 24-48 hrs after primary injury to reduce brain metabolism
and reduce secondary brain injury.
o Mechanical ventilation
▪ Maintain PaCO2 at 35 to 38 to prevent IICP from vasodilation from CO2
▪ Maintain PaO2 between 80-100 to prevent secondary injury
▪ Lidocaine given IV or endotracheally to suppress cough reflex; coughing increases ICP
3
