NUR 265 Exam 3 Study Guide Exam

NUR 265 Exam 3 Study Guide & Exam Questions and Answers

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)

• Blood flow required to provide adequate oxygenation & glucose for brain

metabolism

• Maintenance above 70 mmHg
• CPP= MAP-ICP

▪ MAP= (2xD) + S MAP

NEEDS TO BE

ATLEAST 803

• Compensation

• First Response – CSF is shunted or displaced into the spine (compliance)
• Next – Reduction of blood volume in the brain (autoregulation)
• As ICP continues to increase cerebral perfusion decreases leading to brain

tissue ischemia, edema, vasodilationthen acidosis which causes further increases ICP

• In edema remains untreated the brain may herniate into spinal canal –

death from brain stem compression • Assessment Findings

• 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

• Headache – Quite environment may have photophobia so keep room lights very

low.

• Change in speech pattern – Aphasia, Slurred Speech
• 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

• Abnormal Posturing – Decorticate (flexion) or Decerebrate (extensor)

▪ Decorticate – arms drawn to core, legs straight ▪ Decerebrate – arms straight and stiff, pts rarely survive

• Hyperthermia – followed later by hypothermia

▪ When hypothermic – BE CONCERNED, pressure on hypothalamus located next to brain stem

• Cardiac & respiratory rate/rhythm changes

▪ Tachy first – Increased HR & RR before brady HR & RR 1 / 4

• N/V – Common in IICP
• 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

• Elevate HOB 30-45 degrees (unless

contraindicated) ▪ If hypotension, elevate HOB where CPP >70

• Maintain head in a midline neutral position
• Avoid sudden and acute hip or neck flexion during positioning – Log roll pt
• Avoid clustering of care (bath followed by linen change)
• Coughing and suctioning increase ICP
• 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.

• LOW CSF using intraventricular drain system 2 / 4

• 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

• Oxygenation – Hyperventilate on a vent to decrease CO2 which causes vasodilation
• Reduce cellular metabolic demands – barbiturates (-bital, -barbital) and/or sedation

(coma) Traumatic Brain Injury (946-957) • Primary Brain Injury

• Occurs at time of injury
• Open – Head fractured or penetrated; Closed – Blunt trauma, shaken baby
• 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.

• May not be seen on plain x-ray, R/F Infection w/ CSF leak
• Manifested by bruises around eyes(raccoon eyes) or behind ears

(Battle’s sign)

• Has potential for hemorrhage if it damages the internal carotid
• 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, cerebraledema 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

• 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 3 / 4

• Pupil changes, Bradycardia, Papilledema, HTN w/wide PP, Nuchal rigidity if CSF leak

• 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

• 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)

• 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

• Hypotension & Hypoxia

▪ hypotension (MAP <70), hypoxia (PaO2 <80) ▪ Hypotension may be from shock & hypoxia from resp. failure, loss of airway, or impaired ventilation

• Increased Intracranial Pressure (IICP)

▪ See Increased ICP section above

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