NUR 265 EXAM 3 STUDY GUIDE (100% Correct)

NUR 265 EXAM 3 STUDY GUIDE (100% Correct) 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