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)
,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
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
o Drug Therapy
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)
,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
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
o Drug Therapy
