Chp 45- Iggy- care critical ill neuro

Increased Intracranial pressure

decreased LOC behavior changes, restlessness, irritability, and confusion headache n/v which can be projectile change in speech pattern-aphasia, slurred change in sensorimotor status-pupillary changes like dilated and nonreactive or contrricted and nonreactive, cranial nerve dysfunction, ataxia seizures usually within first 24 hrs of stroke cushings triad- severe HTN, widened pulse pressure, bradycardia abnormal posturing-decerebrate and decorticate

Stroke

brain attack caused by an interruption of perfusion to any part of the brain MEDICAL EMERGENCY, TIME MATTERS leading cause of death in US infarction and edema can occur causing more brain damage and increased ICP TYPES 1. Ischemic: caused by occlusion of a cerebral artery by either a thrombus or embolus -thrombotic stroke common assoc with atheroscerosis bifurcation (point of division) of common carotid artery and vertebral arteries are most common sites SLOW ONSET (min-hrs) -embolic stroke thrombus/thrombi that break off and travel to cerebral arteries wia carotid or vertebrobasilar system usual source is from the heart (A-fib, valve disease, mural thrombi after MI) plaque or clot from carotid sinus or internal carotid artery emboli lodge in smaller cerebral vessels at point of bifurcation or narrowing MCA is most common artery with embolic stroke SUDDEN DEVELOPMENT AND RAPID OCCURRENCE OF NEURO DEFICITS resolve over several hours-daysmay bevome hemorrhagic stroke r/t hemodynamic stress that causes vessels to rupture 2. Hemorrhagic Stroke: vessel integrity is interrupted and bleeding occurs into the brain tissue or subarachnoid space -intracerebral hemorrhage is bleeding into the brain tissue from severe/unsustained HTN damage to brain from bleeding, edema, distortion, and displacement to brain tissue COCAINE IS A TRIGGER FOR DRAMATIC B/P elevation that leads to hemorrhagic stroke -subarachnoid hemorrhage MORE COMMON from bleeding into subarachnoid space of the meninges caused by ruptured aneurysm (abnormal balloning/blister along a normal artery/weak spot develops) or arteriovenous malformation (develops during embryonic-tangled collection of malformed thin walled dilated vessels without a capillary network-dont handle pressure well) or trauma vasospasm follows SAH or bleeding decreased blood flow and reduced perfgusion cause ischemia and infarct and neuro dysfunction RISK FACTORS genetic and environmental MODIFIABLE smoking substance use obesity sedentary lifestyle oral contraceptive use heavy alcohol use use of PPA (antihistamines) NONMODIFIABLE family history of: HTN atherosclerosis aneurysm HIGHER PREVELANCE IN AMERICAN INDIAN/ALASKAN, BLACK MEN AND WOMEN, HISPANIC MEN ASSESS History transport to stroke center TIME MATTERS, FAST ACTION BETTER OUTCOME determine if recent bleeding event or anticoags fibrinolytic therapy if ordered what were they doing when stroke began? (hemorrhagic accur with activity) how did they progress? (hemorrhagic are abrupt, thrombotic are gradual) how severe are symptoms monitor LOC assess for cognition/memory impairments assess speech and hearing if decreased LOC check glucose and O2 assess for motor changes assess for visual problems assess gait assess reading/writing abilities any trauma diabetes? HTN? heart disease? anemia? obesity? what meds are they on (including herbs and supplements) smoking, diet, exercise, drug/alcohol use? if hemorrhage from aneurysm will report sudden severe headache SAH, aneurysm, and AVM are bleeding, n/v, photophobia, cranial neuropathy, stiff neck, and change in mental status PHYSICAL neuro NIHSS ASSESS WITHIN 10 MINUTES ABCs glasgow coma scale to monitor LOC SYMPTOMS CAN APPEAR ANY TIME suden confusion trouble speaking or understanding others sudden numbness or weakness of face, arm, leg sudden trouble seeing in one or both eyes sudden dizziness trouble walking loss of balance or coordination sudden severe headache with no cause assess for denial of illnes spatial and prprioceptive dysfunction impairment of memory, judgment, problem solving, decision making decreased ability to concentrate Right cerebrum is more relative to visual/spatial/personality/judgment Left cerebral is more relative to language/math/analytical skills Right hemiplegia/hemiparesis indicates stroke in left cerebrum and vice versa if brainstem/cerebellum may be hemiparesis/quadriparesis and ataxia (gait disturbance) assess muscle tone assess sensory responses assess ability to chew assess all cranial nerves elevated b/p, heart murmur, dysrhthmias assess psychosocial status DEPEND ON AREA AFFECTED -MIDDLE CEREBRAL ARTERY contralateral hemiparesis:arm>leg contralateral sensory perception deficit homonymoushemianopsia unilateral neglect or inattention aphasia, anomia, alexia, agraphia, acalculia impaired vertical sensation spatial deficit perceptual deficit visual field deficit altered loc, drowsy to comotose -POSTERIOR CEREBRAL ARTERY perseveration aphasia, amnesia, alexia, agraphia, visual agnosia, ataxia loss of dep sensation decreased touch sensation stupor, coma -INTERNAL CAROTID ARTERY contralateral hemiparesis sensory perception deficit hemianopsia, blurred vision, blindness aphasia (dominent side) headache bruit -ANTERIOR CEREBRAL ARTERY STROKE contralteral hemiparesis:leg>arm bladder incontinence personality and behavior changes aphasia and manesia postive grasp and sucking reflex perseeveration sensory perception deficit (lower extremety) memory impairment apraxic gait -VERTEBROBASILAR ARTERY headache and vertigo coma memory loss and confusion flaccid paralysis areflexia, ataxia, and vertigo cranial nerve dysfunction disconjugate gaze visual deficits (uniorbital) and homonymous hemianopsia sensory loss numbness DIAGNOSE clinical history and presentation no definitive labs to confirm elevated H/H assoc with severe/major elevated WBCs for infection (endocarditis or stress inflammation) cardiac enzymes if cardiac related PT/INR and PTT for baseline brain imaging CT without contrast for diagnose MRI shows ischemic earlier than CT Ultrasound and echo 12 lead ECG may show inverted T wave, ST depression, and prolonged QT interval INTERVENTIONS start two IV lines with non dextrose isotonic saline supine position with low HOB to improve cerebral perfusion continuous monitoring for ICP systemic fibroinolytic therapy is standard practice TIME IS IMPORTANT IN INITIATION must administer within 3-4.5 hours unless they are older than 80, anticoags with INR of 1.7, stroke scale >25, hx of stroke and DM explain procedure and obtain consent frequent monitoring of vitals OBSERVE FOR HEMORRHAGE DURING ADMIN OF FIBRINOLYTIC THERAPY intra arterial thrombolysis (used if come in after time window for tpa) mechanical embolectomy carotid stent placement carotid artery angioplasty with stenting to prevent and manage TEACH PATIENT AFTER CAROTID STENT TO REPORT SEVERE HEADACHE, CHANGE IN LOC/COGNITION, MUSCLE WEAKNESS, MOTOR DYSFUCTION, SEVERE NECK PAIN, NECK SWELLING, HOARSENESS OR DIFFICUTLY SWALLOWING if hemorrhagic procedure to stop the bleeding prevent bleeding in AVM or aneurysm prior to onset or SAH following endovascular procedures may result in hyperfusion syndrome (high morbidity)-symptoms of severe temporal headache, HTN, seizures, and focal neuro deficits-assoc with hemorrhage and may occur withing 1 hr to 24 hrs postprocedure monitor increasing ICP-from edema during the stroke assess every 1-4 hours FIRST SING OF INCREASED ICP IS DECREASED LOC AND NEEDS TO BE IMMEDIATELY REPORTED slightly elevate HOB for perfusion and decreased aspiration risk keep flat as best as possible to stop ICP from elevating DO NOT DO CLUSTER CARE stimulates increased DO NOT HYPEROXYGENATE BEFORE SUCTION wuiet environment close monitoring of blood pressure, R and rythm, o2 sats, glucose, and body temp to prevent further brain injury vitals every 1-2 hrs if SBP is more than 180 notify IMMEDIATELY AND ANTICIPATE IV ANTIHYPERTENSIVE MEDS. MONITOR MAP EVERY 5 MIN UNTIL 140-150 AVOID A SUDDEN DROP monitor for signs of hydrocephalus-change of loc, headache, gait disturbance, pupil changes, seizures, poor coordination, and behavior changes monitor for vasospasm if SAH-decreased loc, motor and reglex changes, and increased neuro deficits-CAN RESULT IN PERMANENT BRAIN DAMAGE monitor for rebleeding or rupture of aneurysm or AVM especially within 24 hours and up to 7-10 days later assess for severe headache, n/v, decreased loc, and neuro deficits observe for cardiac dysrhythmias via ECG-special attention for afib or murmurs monitor blood sugars drug therapy to prevent thrombotic episodes (anticoagulants) ASA within 24-48hrs (unless tPA) CCB to treat or prevent cerebral vasospasm stool softeners analgesics for pain antianxiety decompresive craniectomy for massive stroke extracranial intracranial bypass to improve cerebral circulation craniotomy to remove AVM aspiration precautions-SLP eval NPO until swallowing is evaled dietition to avoid malnurishment support affected flaccid arm, avoid pulling on it, prevent it from hanging freely PT and OT evals and support devices at risk for VTE and DVT and PE intermittent sequential pneumatic devices promote effective communication remind to practice exercises for facial and oral muscles promote continence toilet Q 2 hours total fluid intake to dilute urine and and monitor I/Os bedside bladder ultrasound for residual bladder training program-risk for uti high fiber to promote bowel function manage changes in sensory perception break down tasks into steps ALWAYS APPROACH ON UNAFFECTED PLACE WITH UNAFFECTED SIDE TOWARDS THE DOOR place objects within field of vision for double vision place patch over affected eye FALL RISK-keep safe environment re-orient r/t memory loss teach patient to touch and use both sides of their body to prevent unilateral neglect remind to turn head side to side to increase visual field may be discharged to home, rehab, or skilled nursing home teach regarding post stroke depression educate on disease prevention, disease specific info, and self management-to family also Teach lifestyle changes, drug therapy, ambulation/transfer skills, communication skills, safety precautions, nutritional management, activity level, self management provide written and verbal instruction RETURN DEMONSTRATIONS FOR COMPETENCY

Acquired Hypoxic Anoxic Brain injury

brain damage caused by a reduced/absent supply of oxygen CAUSES: cardiac arrest asphyxiation from suicide attempt near drowning drug use/overdose accidntal electrocution severe asthma ISCHEMIA INJURY AND CELL DEATH IN 4 MINUTES SYMPTOMS global decrease in cognition, mobility, sensation that occur with event and persist in unpredicatble manner following resuscitation DIAGNOSE MRI most sensitive test INTERVENTIONS initially supportive with focus on ABCs to restore oxygen hypothermia when related to witnessed cardiac arrest neuro assess to detect and prevent secondary injury increased. ICP from edema in following days-management same as tbi emotional support for u ncertainty neuro rehab, early physical to promote outcomes of functionality

Traumatic Brain Injury

damage to the brain from an external mechanical force and not caused by neurodegenerative or congenital conditions temporary and permanent impairment of cognitive, physical, and psychosocial functions blow to the head=DIRECT INJURY force applied to another body part with a rebound effect to the brain = INDIRECT INJURY ACCELERATION=external force contacts head and puts head in motion DECELERATION=head is moving and is suddenly stopped by object PRIMARY BRAIN INJURY occurs at the time of injury and results from the physical stress within the tissue caused by blunt force Focal-confined to specific area and causes localized damage-can be detected by CT or MRI Diffuse-damage throught many areas of the brain-may not be detectable on CT but MRI may but not until necrosis occurs Open-skull is fractured or peirced by a penetrating object -linear fracture-simple clean break where impacted area of bone bends inward and area around it bends outward-most common -depressed fracture-bone is pressed inward into the brain tissue to at least the thickness of the skull -open fracture-scalp and dura are lacerated creating direct opening to the brain tissue -comminuted fracture-involves fragmented bone with depression into the brain tissue -basilar fracture-at the base of the skull extending into the anterior, middle, or posterior fossa and can result in CSF leakage from the nose or ears-increased risk for infection and hemorrhage which can damage carotid artery or cranial nerves Closed-integrity of the skull is not violated -caused by blunt force or shock wave -contusion-bruising of the brain tissue and is most commonly found at the site of impact or in a line opposite the site -lacerations-actual tearing of the cortical surface vessels that can lead to hemorrhage and edema/inflammation -diffuse axonal injury-related to high speed acceleration/deceleration (motor vehicle crash)-shearing of large nerve fibers and stretching of blood vessels-may be seen on CT or MRI-symptoms are impaired cognitive function, impaired memory, inattentiveness, coma, and require long term care Mild traumatic-aka concussion -blow to the head -transient confusion -feeling of dazed or disoriented -loss of consciousness (not necessarily) -loss of memory immediately before or after accident -focal neuro deficits -n/v fatigue -photophobia -sensitive to noise -more emotional -no evidence of brain damage on CT/MRI -headache, dizziness, changes in behavior-symptoms usually resolve in 72 hours but can last months Moderate traumatic-period of loss of consciousness for 30min-6 hours --GSC of 9-12 -amnesia up to 24 hours -seen on CT or MRI possibly -short acute/critical care for monitoring and secondary injury -secondary unjury from edema, bleeding, or inadequate perfusion Severe traumatic-GCS of 3-8 and loss of consciousness >6 hours -focal/diffuse damage to brain, vessels, and/or ventricles -open and closed can cause -CT and MRI to capture tissue damage early -critical care -monitoring of hemodynamics, neuro, ICP -high risk for secondary brain injury from cerebral edema, hemorrhage, reduced perfusion, biomolecular cascade SECONDARY INJURY any processes that occur AFTER the initial injury and worsen or negatively influence patient outcomes -result from physiologic, vascular, and biochemical events that are an extension of the primary injury -result from hypotension(MAP of <70) , hypoxia(PaO2 <80), intracranial HTN (>15mmHg-leading cause of death from head trauma-decreases cerebral perfusion causing ischemia and edema that can cause brain herniation syndromes), and cerebral edema (vasogenic, cytotoxic, interstitial) -delivery of O2 and glucose is interrupted -hemorrhage-vascular damage-LIFE THREATENING Epidural hematoma-arterial bleeding into the space between the dura and the inner skull-caused by fracture of temporal bone-lucid moments followed by unconsciousness Subdural hematoma-venous bleeding into the space beneath the dura and above the arachnoid-tearing of the bridging veins within the cerebral hemispheres or laceration of brain tissue-MORE SLOW BLEED-acute within 48 hrs, subacute between 48hr-2wks, Intracerebral hemorrhage-accumulation of blood within the brain tissue caused by the tearing of small arteries and veins in the subcortical white matter -space occupying lesion like a tumor -brain edema and ICP elevations Hydrocephalus-abnormal increase in CSF volume -caused by impaired reabsorption of CSF at the arachnoid villi -caused by interference/blockage with CSF outflow from the ventricles -if untreated leads to increased ICP Brain Herniation-brain tissue shifts or herniates downward in the presence of increased ICP -uncal herniation IS LIFE THREATENING -uncal is caused by a shift of one or both areas of the temporal lobe (uncas) -creates pressure on the the third cranial nerve(occulomotor) -LATE findings-dilated/nonreactive pupils, pstosis, and rapidly deteriorating LOC -Central herniation is caused by downward shift of the brainstem and diencephalon from a supratentorial lesion -manifested by Cheyne-strokes, pinpoint/nonreactive pupils, can be life threatening, NOTIFY PHYSICIAN IMMEDIATELY IF SUSPECTED RISK FACTORS -falls (most common in older adults) -motor vehicle crashes -colliding with a stationary or moving object -alcohol and drugs significant contributing factors -wartime blast injuries -associated with summer, spring, evening, nights, and weekends -young males more likely -sports -risks while driving ASSESSMENT History -may have amnesia -may be unconscious or confused -may be combative -if above then ask first responders or witnesses -ask where when and how -did they lose consciousness and how long -change in LOC? -if drugs/alcohol may be hard to differientiate neuro from TBI -hx of seizures? especially if they are having fluctuated consciousness or seizures -hand dominance -disease/injuries to eyes -any allergies to drugs/food -assess hx of drug/alcohol use -victim of violence? -are they in residential care? -HAS TO BE SCREENED FOR ABUSE/NEGLECT Physical -no two are alike -depends on severity and ICP -assess for signs of increased ICP =hypotension -hypoxemia -hypercarbia (>40-45 paco2, can cause cerebral vasodilation and increase further ICP) MONITOR DURING INTUBATION WITH END TIDALCARBOD DIAXIDE MONITOR =earlier detected the better to treat complications -assess b/p, consciousness, and pupils for neuro deterioration -PRIORITY IS ABCS =can assoc with spinal cord injuries TREATED AS SUCH UNTIL RULED OUT -assess for above by loss of motor function and sensory, tenderness along the spine, and abnormal head tilt -injury to brainstem can cause cheyne-stokes, central neuro hyperventilation, apnea -artificial airway if unconscious -rigid cervical collar and long spine board in place -IF DAMAGE TO UPPER CERVICAL SPINAL NERVES THEN WILL HAVE TROUBLE BREATHING BECAUSE IT INNERVATES THE DIAPHRAGM=SO MONITOR FOR RESPIRATORY AND DIAPHRAGMATIC BREATHING AS WELL AS DIMINISHED REFLEXES IN AIRWAY -hypotension or hypertension r/t increased ICP -cushings triad-late sign of increased ICP, severe HTN, widened pulse pressure, bradycardia -hypotension and tachycardia suggest hypovolemic shock, decreased CPP with secondary brain ischemia/injury (usually from bleeding with traumatic injuries to abdomen or chest) -cardiac dysrhythmias from chest trauma, bruising of heart, or interference with atonomic nervous system from brain/spinal injuries -glascow coma scale-change in 2 points is clinically important and URGENT TO CONTACT PROVIDER -DECREASE IN LOC NEEDS IMMEDIATE ATTENTION - change in behavior, disorientation -report ANY CHANGES IN PUPIL SIZE, SHAPE, AND REACTIVITY IMMEDIATELY-sign of increased Icp -pinpoint-nonresponsive = brainstem/pons -ovoid pupils -asymmetric pupils, loss of light reaction, unilateral/bilateral dilated = herniation of brain from increased ICP -fixed nonreactive upils and dialted-POOR PROGNOSIS *BLOWN PUPILS* -visual loss-from direct injury to eyes or occipital lobe-can be permanent or temporary -diminished extraoccular movements d/t increased ICP -diplopia-damage to optic chiasm or optic tract -late signs of increased ICP=severe headache, n/v, seizures -papilledema=edema and hyperemia of optic disc-sign of increased ICP -motor loss/dysfunction contralateral of site of lesion -deceberate/decorticate poturing-indicates progressive brain injury -ataxia, decreased/increased muscle tone, weakness-brainstem/cerebellar injury -CSF leaks from eary/nose-basilary skull fracture -battle sign/mastoid ecchymosis-bruising behind the ears and lower jaw DIAGNOSE -no labs to diagnose a primary brain injury -protein s-100B indicates brain injury -ABG, CBC, slucose, osmolarity, electrolyte toxicology screen and ECG -CT to brain 0radiography and CT scanning of spine and skull to r/o frac tures -MRI to dtect subtle changes detail of injury -ultrasound to measure integrity of vessels -Evoked potentials to look at cerebral function INTERVENTIONS -Admitted to critical care or trauma center -maintain patent airway, breathing and circulation -prevent and detect secondary brain injury -vital signs Q 1-2 hours -IV fluids or drug therapy to prevent severe htn/hypotension -document and report cardiac dysrhythmias, hypotension, and htn -obtain target range for b/p and HR -cooling for fever=therapeutic hypothermia even if no fever 24-48 hours after injury (to reduce brain metabolism and prevent cascade) -ABG, SaO2, and end tidal CO2 to eval resp status and guide mechanical vent -hyperventilation for first 24 hours IS AVOIDED - may cause ischemia -prevent hypoxemia by monitoring sao2 -PaO2 maintained at 80-100 -if intubated provide 100% o2 before suction -lidocaine IV or endotracheally to suppress cough -humidified air and chest physiotherapy -STOP SUCTIONING IF SIGNS OF INCREASED ICP -POSITION TO AVOID EXTREME FLEXION/EXTENSION OF NECK TO MAINTAIN IN MIDLINE NEUTRAL POSITION -LOG ROLL DURING TURNING TO AVOID EXTREME HIP FLEXION -KEEP HOB ELEVATED AT LEAST 30 DEGREES TO PREVENT ASPIRATION -above is contraindicated if b/p is lowered, so adjust hob to maintain CPP >70 -avoid sudden vertical changes of head -check to see if organ donor-severe brain njury often die, so do this before they die -osmotic diuretic to treat crebral edema -loop diuretic to reduce incidence of rebound from osmotic diuretics ADMIN MANNITOL (OSMOTIC DIURETIC) THROUGH A FILTERED TUBING -monitor I/Os -monitor for dehydration, renal failure, weakness, edema and any changes in output -serum electrolytes -sedatives to manage agitation and ventilator asychrony -opiods to decrease agitation and control restlessness if caused by pain -NARCAN IS ANTAGONIST -antiepileptic drugs to prevent seizure activity -barbiturate coma for intracranial hypertension that cant be controlled by other means -at risk for diabetes insipidus and SIADH so monitor fluid and electrolytes closely-monitor urine osmolarity -manage nutrition-NG tube or nasoduodenal tube or peg tube -parenteral if not met r/t to GI disfunction -if able to take in orally, use aspiration precautions and SLP eval -manage sensory perception -manage ognitive changes -manage behavioral changes -seizure precautions -ICP monitoring -STRICT STERILE TECHNIQUE WITH PLACEMENT OF ICP MONITORING DEVICES AND WITH CARE -decompressive craniectomy if ICP cannot be controlled or craniotomy -MUST NOT LAY ON THE SIDE WHERE SKULL WAS REMOVED -MUST WEAR A PROTECTIVE HELMET WHEN OUT OF BED -educate on neuros until at baseline -educate tylenol Q 4 hours for headache -avoid sedatives, sleeping pills, or alcohol for 24 hours -educate do not allow strenuous activity for 48 hours -fall precautions -RETURN TO ER IF SEVERE HEADACHE, PERSISTENT N/V, BLURRED VISION, DRAINAGE FROM EAR/NOSE, WEAKNESS, SLURRED SPEECH, PROGRESSIVE SLEEPINESS, WORSENING HEADACHE, UNEQUAL PUPIL SIZE -EDUCATE TO KEEP FOLLOW UP APPTS

Brain Tumors

named according to the cell.tissue they are located crebral are most common PRIMARY-originate within CNS and rarely spread outside .SECONDARY-.metastasis from other areas of the body CLASSIFICATIONS Benign-noncancerous Malignant-cancerous need aggressive intervention Supratentorial-located within cerebral hemispheres-USUALLY CAUSE PARALYSIS, SEIZURES, MEMORY LOSS, COGNITIVE IMPAIRMENT, LANGUAGE IMPAIRMENT, OR VISION PROBLEMS Infratentorial-beneath the tentorium where brainstem structures cerebellum are-PRODUCE ATAZIA, AUTONOMIC NERVOUS SYSTEM IMPAIRMENT, INCREASED ICP AND BECOMES MORE SEVERE AS TUMOR GROWS Gliomas are malignant tumors Meningiomas-benign from covering of the brain-meninges-capsular, globular, and welll outlined-causes compression and displacement of nearby brain tissue-can remove but tend to recur Pituitary-in anterior lobe cause endocrine dysfunction-Adenoma-benign-MOST OCCUR IN YOUNG/MIDDLE AGED ADULTS-visual disturbances and hypotiuitary signs-body hair, DI, infertility, visual field defects, and headaches Acoustic Neuromas-sheath of Schwann cells in peripheral portion of cranial nerve VIII-AKA CPA tumors-compress brain tissue and surround nearby cranial nerves-difficult to remove without nerve dysfuntion- WOMEN TWICE AS LIKELY TO HAVE-hearing loss, tinnitus, and dizziness/vertigo Metastatic/secondary-cancer from lung, breast, colon, pancreas, and kidney travel to brain via blood and lymph-multiples are common Grade I-benign-cells look nearly normal and slow growing Grade II-malignant, cells look less normal then 1st grade Grade III-malignant tissue has cells that look very different and are actively growing Grade IV- malignant tissue has cells that look most abnormal and grow quickly RISK FACTORS unknown Investigating: genetic mutations environmental factors cell phones age 40-70 low survival rate ASSESS/NURSING history from patient and family: s/s neuro for basline and deficits Assess: headache that is more severe on awakening in am n/v visual symptoms seizures/convulsion facial numbness/tingling loss of balance/dizziness weakness/paralysis in one part/side of body difficulty thinking, speaking, or articulating changes in mentation or personality papilledema indicating increased ICP DIAGNOSE history, neuro assess, clinical exam, and results of neurodiagnostic testing: CT MRI skull films Cerebral angiography not indicated but may be used to provide additional info about blood supply to tumor EEG, lumbar puncture (unless showing signs of increased ICP to prevent brain herniation), brain scan, and PET to provide further info about size, location, and characteristics Labs to eval endocrine function, renal, and electrolyte balance INTERVENTIONS Decrease size, improve quality of life, and improve survival time DEPENDS ON TUMOR SIZE AND LOCATION, SYMPTOMS, AND GENERAL CONDITION AND RECURRANCE Experimental treatments like blood brain barrier disruption, recombinant DNA, monoclonal antibodies, new chemo drugs, immunotherapy Radiation thereapy may be used alone, after surgery, or in combo with chemo and surgery Drugs to treat tumor, manage symptoms, and prevent complications Chemo (if given systemically must be lipid soluble to cross BBB) lomustine, temozolomide, procarbazine, methotrexate, vincristine MONITOR FOR SIDE OF EFFECTS - SIMILAR TO CHEMO Disk shaped drug wafers placed directly into cavity created during surgical tumor removal-carmustine analgesics like codeine and tylenol for headache dexamethasone for edema phytoin to prevent seizures PPI to decrease gastric acid secretion and prevent stress ulcers Sterotactic radiosurgery-gamma knife single dose of ionized radiation to focus multiple beams of gamma radiation to destroy lesions without damageing surrounding healthy tissues-used with imaging to precise localization-NONINVASIVE, LOWER RISK THAN CRANIOTOMY, SURGICAL PRECISION, DECREASED COST, DECREASED MORBIDITY, DECREASED LENGTH OF HOSPITAL STAY, RAPID RECOVERY TIME but requires uncomfortable rigid head frame-may yse cyberknife without frame Craniotomy to remove tumor, improve symptoms, or decrease tumor size-post op criticual care/neurosurgical unit PREOP-reassurance, teaching about immediate post op and recovery, NO ALCOHOL, TOBACCO, ANTICOAGS, NSAIDS FOR 5 DAYS BEFORE NPO for 8 hours OPERATION-local or general anesthesia/sedationbone flap removed to expose tumor bone flap replaced after tumor removed or whatever soft dressing to keep clean POSTOP-monitor to detect changes in status, minimize complications, ESPECIALLY INCREASED ICP assess neuo/vitals Q 15-30 minutes for first 4-6 hours then every hour REPORT AND DOCUMENT NEURO DEFICITSLIKE LOC MOTOR WEAKNESS/PARALYSIS, PUPIL REACTION PERSONALITY CHANGES May have periporbital edema INTERVENTIONS cold compresses to decrease periorbital edema irrigate affected eye with warm saline solution cardiac monitoring if in critical care unit record I/Os first 24 hours fluid restriction to 1500ml daily if pituitary involved reposition but not on operative side delegate/deep breathing Q 2 hours ISPDs to prevent VTE until ambulating supratentorial surgery elevate hob 30 degrees as tolerated to promote drainage avoid extremehip or neck flexion and keep in midline neutral to prevent increased ICP turning to prevent ulcers and pneumonia Infratentorial keep flat and positioned sidelying, alternating sides every 2 hours for 24-48 hours NPO for 24 hours because edema around medulla and lower cranial nerves cause vomitting and aspiration Check head dressing Q 1-2 hours for drainage-mark drainage once a shift for baseline small/moderate is expected may a hemovac, jackson pratt or other drain for 24 hours measure drainage Q 8 hours and record amount and color 30-50ml every 8 hours is normal REPORT DRAINAGE GREATER THAN 50 ASAP OBSERVE FOR MANIFESTATION OF HYPOVOLEMIC SHOCK AND KEEP FLAT TO MAINTAIN B/P IF NEEDED POST OP labs CBC, electrolyte levels, osmolarity and coags H&H may be low from blood loss during surgery or elevated if blood replaced hyponatremia may occur from fluid overload, SIADH, or steroid admin Hypokalemia may cause cardiac irritation, weakness, change in loc, and confusion hypernatremia caused by meningitis, dehydration, DI-muscle weakness, restlessness, extreme thirst, dry mouth dehydration-decreased output, thick secretions, hypotension mech vent for 24 hours-48 hours postop to manage airway and O@ demedetomidine propofol and fentanyl to treat pain and anxiety and promote rest and comfort suction as needed - hyperoxygenate CARFULLY BEFORE DURING AND AFTER antiepileptic, histamine blockers, PPIs for prohpylaxis, glucocorticoids to reduce edema tylenol for fever/pain ABT to prevent infections COMPLICATIONS increased ICP hydrocephalus-IV cath to drain, shunt for long term subdural/epidural hematomas/intracranial hemorrhage-severe headache, rapid decrease in loc, neuro deficits, herniation syndromes, bleeding into posterior fossa may lead to sudden cardiovascular and respiratory arrest-SURGICAL REMOVAL OF HEMATOMA-AGGRESSIVE MANAGEMENT FOR HEMORRHAGE respiratory complications such as atelectasis, pneumonia, and neuro pulmonary edema (life threatening and usually dont survive with this-cardio effects) Wound infections-ABTs menigitis DI, SIADH, cerebral salt wasting INTERVENTIONS (TUMOR) managed at home if possible quality of life rehab follow up health drug therapy teaching- no OTC unless approved maintain physical exercise within limits dietition seizure precautions American Brain Tumor Assoc or National Brain Tumor Foundation, Amercian Cancer Scoiety hospic if terminal prevention is key for all above

Brain Abcess

purulent infection of brain in which pus forms in the extradural, subdural,, or intracerebral area or the brain CAUSE usually bacteria directly or indirectly complication of meningitis organisms from ear, sinus, mastoid travel through cerebral veins lung infection ear infection/sinus infection bullet, knife wound, neurosurgery abscess from a distant organ break off and enters circulation penetrating trauma, open head injuries, neurosurgy strep most common E coli, yest toxoplasma gondii AIDS SYMPTOMS local infection acute inflammation that surrounds involved area necrosis of tissue, pus, and tissue liquefies cerebral edema from vascular congestion and swelling area becomes encapsulated usually deep within cerebral hemisphere manifestation begin slow and similar to menigitis headache fever neuro deficits/nonspecific s/s may be mildly lethargic or confused PERLA in early stages increased ICP pupils become sluggish, unequal, dilated, and nonreactive loc declines airway/respir function altered pain motor deficits-hemiplegia ataxia senosry impairment-varies aphasia seizure activity visual field changes-temporal field blindness, nystagmus, SEVERE WILL HAVE DECREASED LOC, SEVERE HA, BRADY CARDIA, WIDENED PULSE PRESSURE DIAGNOSE WBC & ESR elevated if encapsulated WBCs may be normal obtain cultures of blood, ear, nose, and throat to determine source of infection CT to determine if cerebritis, hydrocephalus, or midline shift MRI to detect early or late EEG can localize lesion, electrosilence where abscess is Radiography of sinuses and mastoid lumbar puncture if menigitis is suspected and no ICP elevation INTERVENTIONS Drug thereapy if several abscessesor small one, or deep in brain, meningitis, shunt in placy for hydrocephalus (may need to be removed/replaced), toxoplasma gondii with HIV ABT to ensure CNS penetration-very useful in early stages combo of ABT if from septic emboli Antiepileptic to prevent seizures Strict drug regimen and therepeutic blood levels analgesics for headache surgically drain abscess via burr hole craniotomy may be performed to remove abscess surgery is based on patients condition, stage, and site of abscess routine preop and postop care

Transient Ischemic Attack

temporary dysfunction resulting from a brief interruption in cerebral blood flow, symptoms may resolve before get to the ER (usually resolve 30-60 min) Single are high risk for stroke multiple are increase risk for permanent brain damage ASSESS complete neuro assess blurred vision diplopia blindness in one eye tunnel vision weakness facial dropp arm/leg drift hand grasp weakened ataxia numbness in face, hand, arm, leg vertigo aphasia dysarthia (slurred speech) DIAGNOSE ECG CT labs always admitted for observation and further tests MRI of carotid and cerebral blood vessels and brain tissue TREATMENT focus on preventing another TIa or stroke reduce high blood pressure (most common risk) ASA or antiplatelet control diabetes (bs between 100-180) promote lifestyle changes (no smoking, heart healthy, active) make sure aware of precautions and actions of antiplatelets and risk for bleeding educate on follow up care