Neuro Trauma

Motor vehicle collisions (MVC)
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Terms in this set (82)
Concurrent Injuries-not only the brain is injured -cervical spine and facial injuries -get a good hx of precipitating eventsThe skull contains-brain tissue(parenchyma) -CSF -Bloodparenchyma-divided into three functional areas cerebrum,cerebellum,brain stem -can be damaged by trauma or indirectly by bleeding or swellingCerebellum-Balance and coordination -surgery to area risky -offers little room for expansionCerebrum-damage here causes autoregulation issues to occur -processing for sensory info and autonomic controlbrain stemConnects the brain and spinal cord -responsible for many basic functions such as HR and breathing -recovery almost NONEXISTENTfrontal lobethinking,judgement,voluntary movementparietal lobeprocessing and interpretation of sensory infotemporal lobehearingoccipital lobevisual processingDiencephalonContains thalamus and hypothalamusCushing's triadthree classic signs‚ÄĒbradycardia, hypertension, and bradypnea indicates impending herniationCranial nervescompression is indicative of impending herniation 1st sign of compression: pupil/visual changesCSFprotects the brainprimary injuryDirect injury to the brain not much can be done by the nurse -irreversiblesecondary injurybrain damage that occurs as a response to the initial injury -alterablesecondary injury pt 2hypotension SBP <90 hypoxia PaO2 <60 increased ICPTwo most common causes of secondary injuryhypoxia PaO2 <60 and hypotension SBP <90ICPreflective of brain,blood (arterial and venous),and CSF once your body stops compensating,it will riseCerebral Perfusionpressure in the cerebral veins is assumed to be the same as ICPCPPMAP-ICP want to maintain above 60;less leads to ischemiaNormal ICP5-15 TBI up to 20;more than 20 is concerningAdequate delivery of O2 and nutrients is dependent uponCPP and cerebral autoregulationMonro-Kellie hypothesisif something is added,something must be taken away or herniation will occurIt can take up to how long for brain to show s/s of a TBI72 hoursEarly signs of increased ICP‚ó¶Headache ‚ó¶Nausea and vomiting ‚ó¶Amnesia ‚ó¶Altered level of consciousness(CONFUSION AND RESTLESSNESS ARE THE 1ST SIGNS) ‚ó¶Restlessness, drowsiness, changes in speech, loss of judgmentLate signs of increased ICP‚ó¶Dilated, non-reactive pupils ‚ó¶Unresponsiveness to verbal or painful stimuli ‚ó¶Abnormal motor posturing ‚ó¶Changes in respiratory rate and pattern -Cushing's response-attempt to increase cerebral blood flow -Elevated SBP-widening pulse -Decreased respiratory effort -Reflex bradycardiaGCS less than 8intubateMinor head traumaGCS 13-15 low or high risk for deteriorationModerate Head Traumamust go to ICU GCS 9-13 may deteriorate to severe head injurysevere head traumaGCS of 8 or lessDecorticate posturingarms flexed inward and bent in toward the body and the legs are extendedDecerebrate posturinginvolves the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backward -indicates extensive brain damagePosturing visualfocal brain injurytypically seen on CT and treated with surgical intervention includes:contusion,hematoma,and hemorrhageDiffuse injurytypically not seen on CT include concussion and diffuse axonal injurycontusion-focal area of bruised and damaged brain tissue -most common frontal and temporal lobes -closely monitor/frequent neuro checks -effects peak 18-36 hrs. after injury -delayed hemorrhage in a intracerebral hematomaCerebral contusion s/s-altered LOC -behavior,motor and speech deficits -may see abnormal motor posturing -signs on increasing ICP but WONT necessarily see a rise in ICPHematomacollection of blood can be epidural,subdural,and intracerebralepidural hematoma-ARTERIAL BLEED -Collection of blood between the skull and dura -Associated with fractures of the temporal or parietal area -Immediate surgical intervention requiredepidural hematoma classic presentationCLASSIC PRESENTATION:Transient loss of consciousness followed by a lucid period followed by rapid neurologic declineepidural other s/s-Severe headache -Sleepiness (waxing/weaning of conunciousess) -Dizziness -Contralateral hemiparesis or hemiplegia -Late signs:Abnormal motor posturing -Unilateral fixed and dilated pupil on the same side as the hematomaSudbural Hematoma-venous bleeding -associated with direct injury to brain tissue/diffuse axonal injury -takes longer to manifest - more than 5 mm shift take action -onset may be acute -typically seen in elderly,those on anticoagulants and chronic etoh usersIntracerebral hematoma-bleeding deep within brain tissue -can result in significant mass -surgery does more harm than goodintracerebral s/s-Progressive decline in level of consciousness -Signs of increasing intracranial pressure -Pupil abnormalities -Contralateral hemiplegiaSubarachanoid hemorrhage-bleeding between arachnoid and pia mater -pressure/blood directly on brain -commonly seen with aneurysmssubarachnoid hemorrhage s/s:horrific headache,nasuea,and emesisdiffuse injuries-include concussions and DAI -involve compressing or shearing of the axonsconcussiontemporary alteration in neurological functionmild concussion‚ó¶no loss of consciousness(agitation or slight confusion);most fall under this categoryclassictemporary loss of consciousness with focal neurologic dysfunction (amnesia)concussion s/s‚ó¶Transient loss of consciousness ‚ó¶Headache ‚ó¶Confusion, memory loss, concentration difficulties ‚ó¶Dizziness ‚ó¶Nausea and vomiting ‚ó¶Irritability ‚ó¶Fatigue ‚ó¶Difficulty falling asleeppost concussion syndrome-Lasts days to months -Symptoms ‚ó¶Persistent headache, dizziness ‚ó¶Attention deficits ‚ó¶Irritability ‚ó¶Insomnia ‚ó¶Impaired judgment ‚ó¶Anxiety, depressionDiffuse Axonal Injury (DAI)similar to concussion except loss of consciousness happens immediately -widespread damage to axons within brainCategories of DAIS-mild 6-24 hrs -moderate- >24 hours,long term brain injury -severe-vegetative states for weeks to months, extensive damage, posturingSevere DAI is....the most common cause of persistent vegetative stateS/s of DAI‚ó¶Immediate unconsciousness ‚ó¶Elevated intracranial pressure ‚ó¶Abnormal posturing ‚ó¶Hypertension ‚ó¶Hyperthermia ‚ó¶Excessive sweating ‚ó¶Hypothalamic storm-hypertension, ‚ó¶Neuro sweats tx cooling blanketsLinear skull fracturenon displaced s/s headache,fatigue,decreased LOCdepressed skull fracture-extends below surface of skull -can have CSF leak -s/s headache,decreased LOC,palpable skull over fracture sitebasilar skull fracture-fracture involving bones of skull base -DO NOT PLACE NGTbasilar skull fracture s/s-periorbital ecchymosis (raccoon eyes) -mastoid ecchymosis (battle sign) -CSF leakage (otorrhea /rhinorrhea) -DO NOT PLACE NGTManagement of TBI-no tx for primary -focus is prevention for secondaryThree goals of treatment in secondary injury1.restore or maintain brain function 2.prevent or treat complications 3.maintain and enhance the person's cognitive,physchosocial and emptional processesResuscitation phase (occurs when the person comes into the hospital)-airway patency (GCS < 8 intubate) -supplemental O2/adequate ventilation (PaCO2 >60) -adequate systemic and cerebral perfusion -SBP < 90 corelated with poor outcomes -establish baseline -attempt to calm and reassure ptICP monitoringappropriate in pts with severe head injury with an abnormal CT (GCS < 8)ICP monitoring...should be started ICP above 2 appropriate in severe head trauma with abnormal CTcerebral O2 monitoringPbO2 > 20 goal normal 25-50EVDdrains off CSF do it slowly no more than 3 cc at a time zero reference right above ear (Form of Monro)crainectomyallow edema to occur without herniationCritical Care Phase-prevent /treat hypoxia/hypercapnea -respiratory care -BP MAP at least 70 CPP at least 70 -HOB at least 45 degreesCC phase countinued-mannitol keep osmolality < 320 -hypertonic solutions can increase osmolality -steroids -decrease stimulation and metabolic demand -only use paralysis in very high ICPIntermediate and Rehab phase-Maintain airway patency -Effects of immobility ‚ó¶Spasticity -Bowel and bladder function -Cognitive rehabilitation