6845-2
Terms
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- * Southern states: “stroke belt”
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- High fat diet
- Smoking
- More elderly individuals - Stroke (CVA)
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* Disruption in the normal blood supply to the brain
* Cerebral vascular accident (CVA) "brain attack"
* Medical emergency that strikes suddenly
* Should be treated immediately
* Third most common cause of death in U.S.
* Primary cause of adult disability - Stroke, “Brain Attack”
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* National Stroke Association
* Medical emergency
* Requires prompt/immediate intervention - Pathophysiology of Stroke
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* Brain unable to store O2, glucose
* Unable to remove toxins, byproducts
* Damage within few minutes
* Cerebral autoregulation
* 1000ml/min blood flow
* Dilation/constriction prn
* Lack of perfusion
* Involved area/contralateral hemisphere involvement with stroke
* Small strokes “lacunar infarcts” - Types of Strokes
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* Ischemic (occlusive)
* Caused by occlusion of cerebral artery by thrombus or embolus
* Thrombolic stroke - Thrombolic stroke
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1. Accounts for more than one half of all strokes
2. Associated with atherosclerosis
3. Lacunar stroke - Embolic stroke
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* Middle cerebral artery (MCA) most commonly involved
* Emboli occlude the vessel, ischemia develops
* Occlusion often temporary, ª fragments
* Become lodged in smaller bifurcations or where lumen narrows
Transient Ischemic Attack TIA
* gSilenth stroke
* precedes other strokes -
Transient ischemic attack (TIA)
Reversible ischemic neurologic deficit (RIND) - *
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Ischemic Brain Attacks
Etiology: occlusion (thrombus/embolus) -
* Thrombolytic – more than half
* Associated with plaques
* May affect any blood vessel
* Deposits continue to build up
* May occur over many years
* Collateral circulation develops
* Transient ischemia to affected area
* Complete ischemia and infarction
* Total occusion = 72 hours severe s/sx such as necrosis, edema, cavity devel
* Most common sites: bifurcation of the common carotid artery, vertebral arteries at juncture with basilar artery
* SLOW onset, TIAs often precede these
Embolic stroke (~1/3 of all)
* Embolism/emboli travel to cerebral arteries via carotids
* UsuallyÂ…CARDIAC origination
* A fib
* Ischemic heart disease
* RHD
* Mural thrombi p MI
* Prosthetic valve/other structures
* Plaque that breaks free from other vessels - Reversible Ischemic Neurologic Deficit (RIND)
- * Transient focal dysfunction d/t brief interruption of blood flow, e.g., spasms
- TIA and RIND differ in
- duration
- TIA duration?
- = few minutes, <24 hours
- TIA -
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* Blurred/double/blindness/tunneling
* Weakness/gait disturbance
* Numbness (transient)
* Vertigo
* Aphasia/dysarthria (slurred speech)
* RIND = > 24 hours <week
* Brain tissue is damaged in both types - Hemorrhagic Stroke
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* Interruption of vessel integrity
* Bleeding occurs into tissue/spaces
* Ventricular, subdural, subarachnoid
* Hemorrhage from rupture of
* saccular (berry) aneurysm
* Arteriovenous malformation
* Cerebral aneurysm
* Hypertension
* Speculation: elevated systolic/diastolic pressure rupture vessel walls
* Cerebral aneurysm = abnormal distension (may be congenital, traumatic)
* Weakening of the vessel wall
* Continued pressure stretches/thins
* Rupture usually during ACTIVITY
* Aneurysm rupture
* Intracerebral hematoma
* Ventricular bleeding
* Subarachnoid bleeding
* Vasospasms (sudden, transient constriction) may occur p hemorrhage
* Distal blood flow « leading to ischemia - Arteriovenous Malformation (AVM)
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* Embryonic development
* Entangled mass
* Thin-walled, dilated vessels
* Abnormal communication with arterial and venous systems
* Ruptures may cause bleeding - Risk Factors - stroke
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* HTN
* Diabetes mellitus
* Heart disease
* Nonvalvular atrial fibrillation
* Smoking/substance abuse
* Sedentary lifestyle
* Women: ªHgb (>14 g) « bone density, migraines - Stroke-Clinical Manifestations
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* Cognitive changes
* Motor changes
* Sensory changes
* Cranial nerve intactness
* Cardiovascular assessment
* Psychosocial assessment - History
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* Accurate history
* Important to affected area
* s/sx?
* When did it start? (ischemic = sleep; hemorrhagic = activityÂ…usually)
* How the s/sx progressed?
* Onset important (embolic/hemo = abrupt; thrombolytic = gradualÂ…usually)
* S/Sx come and go? (TIA, RIND) - Hx
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* Observe LOC during interview
* Monitor speech pattern/body posture, etc
* Medical hx?
* Family hx?
* Diet?
* Other risk factors?
* Medications? - Physical Assessment - neuro
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* Cognitive Changes
* LOC may vary
* Denial
* Hemiparesis
* Spatial/proprioceptive dysfunction
* Memory impairment
* Problem-solving/decision-making -
Left v Right Sided Hemispheres
(Table 45-4)
Terms -
* Aphasia = inability to use/comprehend
* Alexia = reading difficulty
* Agraphia = writing difficulty
* Hemiplegia = paralysis, one side
* Hemiparesis = weakness, one side - Aphasia =
- inability to use/comprehend
- Alexia =
- reading difficulty
- Agraphia =
- writing difficulty
- Hemiplegia =
- paralysis, one side
- Hemiparesis =
- weakness, one side
- Motor ∆s
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* Provides info about which hemisphere
* Nurse must assess for hypotonia (flaccidity) = tends to fall to one side
* Extremities may feel heavy
* Inadequate balance, equilibrium
* Hypertonia (spastic paralysis) → fixed
* contractures - Sensory ∆s
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* Assess response to stimuli, touch
* May be unable to write, comprehend, use an object correctly, or be purposful
* Neglect syndrome (esp RIGHT sided)
* e.g. resident/patient in wheelchair leaning
* Perceives he/she is upright
* May wash/dress only one side of body - Visual changes:
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* Ptosis (eyelid drooping)
* Visual field deficits
* Pallor/petechiae of conjunctiva
* Amaurosis fugax = brief blindness
* Hemianopsis = blindness, half field (damage to optic tract/occipital lobe); most often bilat - Cardiovascular Assessment
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* Embolic strokes– murmur, dysrhythmia, HTN
* Psychosocial
* Finances, ADLs, care at home
* Emotional lability (esp with frontal lobe)
* Labs, radiographs (CT), MRI - Interventions - stroke
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* Stabilize patient, reduce further injury
* Determined by type/extent of injury
* Nonsurgical management
* Patient may be at risk for ª ICP
* Neurological Nursing Assessment
* Glasgow Coma Scale (GCS) - ICP monitoring
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* Key Features:
* «LOC sensorimotor ∆
* Behavioral ∆s pupillary ∆
* HA cranial nerve involve
* N/V ataxia
* Speech ∆ sz
* Aphasia CushingsÂf Triad
* Slurred speech Posturing - Nursing Interventions - ICP
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* Frequent nursing assessments
* First 72 hours critical
* Elevate HOB
* Maintain head position ¨ drainage
* Avoid extreme flexion (ª ITP)
* Avoid clustering of activities - Drug therapy - stroke
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* Thrombolytic therapy – dissolves occlusion
* Rt-PA (recomb tissue plasminogen act)
* Anticoagulants
* PT
* PTT
* INR (International Normalized Ratio)
* Target 2-3; 3-4.5 (cardiac-related strokes)
* Other medications, e.g., anti-seizures - Surgical Management stroke
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* Endarterectomy
* Extracranial-intracranial bypass
* AVM management
* Craniotomy
* Remove clots - Nursing interventions stroke
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* Self-Care Deficit
* Facilitate increased muscle strength/function
* Positioning important
* Splinting Avoid contractures
* DVTs are a risk to develop
* Antiembolism stockings
* Compression boots
* Frequent position changes
* Mobilization of the client
Disturbed Sensory Perception
* Assist patient to adapt to ∆s
* Interventions:
* R ¨ visual/perceptual or spatial impairments depth perception/discrimination (up/down) thus ADLs
* Provide frequent cues
* Break down tasks into simple steps
* Approach from UNAFFECTED side
* UNAFFECTED side: should FACE the door
* Teach patient to turn head/scan environment
* Diplopia: use patch
* Remove cluter - L sided repercussions:
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* Memory deficits, simple tasks difficult
* Reorient to month, day, year
* Establish routine schedule
* Structured environment
* Familiar objects
* Step by step teaching - Unilateral Neglect
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* Goal: compensate for affected side
* Most common with R-sided stroke
* ª risk for injury (« proprioception)
* Teach patient to touch/use both sides
* Affected side first
* Turn head for full vision fields
* gscanningh technique - Impaired Verbal Communication
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* Goal: effective communication
* Language/speech (dominant hemisphere) - Aphasia:
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* Expressive (BrocaÂ’s; motor) frontal
* Receptive (WernickeÂ’s; sensory) T-P area may talk but language is meaningless
* Global (mixed) - Stroke-Impaired Verbal Communication
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* Occurs in dominant hemisphere/majority in left hemisphere
* Dysarthria due to loss of motor function
* Aphasia caused by cerebral hemisphere damage
* Expressive (Broca's or motor) aphasia - Expressive (Broca's or motor) aphasia
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1. Motor speech problem
2. Understands but unable to communicate
3. Difficulty with writing
4. Frustration and anger - Receptive (Wernicke's or sensory) aphasia
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1. Unable to understand spoken and written word
2. Neologisms
3. Global or mixed aphasia
4. Reading and writing equally affected - Impaired swallowing
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* Goal: ingestion without aspiration
* Interventions:
* Assess swallowing ac
* Facial drooping, drooling, weak/hoarse voice
* Gag/cough reflex
* Positioning
* Monitor weight/diet
* Avoid foods that ª salivary production
- Beef broth
- Sweet, sour, salty
- Place food in back of mouth, UNAFFECTED side
* Distractions may cause aspiration
* Reduce sensory stimulation
* Observe for s/sx fatique -
Incontinence
Goal: regain continence -
* From ∆LOC, innervation, « communication
* Etiology must be established
* Patients may re-learn
* Bladder training program
* Place on bedpan/commode q 2 hr
* Encourage fluid intake 2000 cc/d
* Check residual urines - Bowel retraining program
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* Establish normal BM for patient
* Identify any routines
* Place patient on bedpan/commode during this time
* High fiber/bulk diet
* Fluids
* Suppositories
* Digital stimulation may assist - Health Teaching
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* Medication schedule
* Mobility
* Communication
* Safety
* Dietary
* Activity/self-care skills
* Psychosocial intervention
* Families encouraged to permit individual to do as much as possible
* Families – take and plan for extra time to do things
* Care givers may need respite/time to relax
* Counseling
* Social worker - Traumatic Brain Injury (TBI)
- * 18-34 years – #1 cause of death
- Traumatic Brain Injury (TBI)Pathophysiology
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consciousness ∆
* Direct/Indirect
* Reversible/irreversible
* Temporary ¨ permanent
* Primary Brain Injury - TBI Incidence/Prevalence
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* MVA, most common cause
* 7 million Americans/year
* 500,000 hospitalized
* 100,000 with permanent damage
* 2000 vegetative state
* Summer, spring, pm, noc, weekends
* 3X ª in males - Pathophysiology TBI
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* TBI: Mild with GCS 13-15 gait altered
* Mod: « LOC GCS 9-12¨ 24 h observation
* Severe: GCS <9 ¨ critical care
* Open: unique fracture, CSF leakage
* Most: gunshot, knife
* Risk for infection
* Closed: blunt trauma
* Concussions, contusions, lacerations - Concussion =
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brief loss of consciousness
* Damage is functional, not structural (thus, not “permanent”) - Contusion =
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bruising of brain at coup or contracoup site
* laceration - Traumatic Brain Injury-Types of Forces
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* Acceleration injury
* Deceleration injury
* Shearing
* Straining
* Distortion of brain tissue
* Destruction of adjacent brain tissue - Types of Forces
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* Acceleration injury – velocity
* Deceleration injury – e.g., whiplash - 2˚ injuries
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* Increase mortality/morbidity
* Most common: ª ICP
* Edema
* Hemorrhage
* Impaired cerebral autoregulation
* Hydrocephalus
* Hypoxemia
* Hypercapnia
* Systemic hypotension - Increased Intracranial Pressure
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* Monro-Kellie hypothesis
* Normal ICP 10 to 15 mm Hg
* Leading cause of death from head trauma -
Increased Intracranial Pressure
Monro-Kellie hypothesis -
* Normal ICP 10 to 15 mm Hg
* Leading cause of death from head trauma
* ICP = cerebral blood flow = tissue hypoxia = serum pH and CO2 = cerebral vasodilation = edema = ICP = brain hernation = irreversible brain damage = death (uncal herniation) -
* Edema
* Vasogenic
* Cytotoxic
* Interstitial - *
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ICP
Monro-Kelli hypothesis -
* ª in volume « volume elsewhere
* CSF shunted/displaced from cranial compartment ¨ subarachnoid space
* OR, rate of CSF reabsorption ªª
* Compensation protects structures
* LEADING CAUSE OF DEATH
* ª ICP = cerebral blood flow decreases
* Tissue hypoxia
* Decrease in pH
* Increase in CO2 levels
* causes cerebral vasodilation, edema, ª ICP
* Cycle continues
* Brain may herniate into brainstem
* Irreversible damage
* UNCAL HERNIATION -
ICP
Two types edema cause ª ICP -
* Vasogenic
* Cytoxic - * One type edema exacerbates:
- interstitial
- Vasogenic: adults
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* Abnormal permeability of cerebral vessels
* Protein-rich plasma leaks
* Fluid collection: white matter -
ICP
Cytotoxic, cellular edema -
* From hypoxia
* Disturbance in cellular metabolism
* Sodium pump
* Active ion transport
* Brain depleted of O2, CHO, glycogen
* Na+ pump fails
* Na+ enters the cells and pulls H2O
* Simultaneous « Na+ serum (<120 mEq/L) -
ICP
Abnormal accumulation of cellular fluids -
* Decrease in ECF space
* Cytotoxic edema ensues
* Interstitial edema:
* Acute brain swelling
* Assoc with HTN, ª ICP -
Cerebral Hemorrhage
Life-threatening
Three primary types: -
* Epidural
* Subdural
* Intracerebral - Epidural
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* Arterial bleeding
* Space: skull and dura mater - Hemorrhage
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* Intracerebral Hemorrhage
* Accumulation of blood within tissue
* Loss of Autoregulation
* Usually, remains constant
* Loss of regulation ¨ ∆ in blood flow
* Systemic HTN ¨ ª ICP - Subdural Hematoma (SDH)
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* venous
* Space: dura mater and arachnoid
* Common: laceration of brain tissue
* Bleed is slower
* Acute, subacute, chronic - TBI
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* Hydrocephalus
* Abnormal ª CSF volume
* Caused dilation of ventricles
* May lead to ª ICP
* Herniation
* Uncal: life threatening
* Shift of one/both temporal lobes (uncus)
* Pressure on 3rd cranial nerve
* S/Sx: dilated/fixed pupils
* Ptosis
* Rapid ∆ in conciousness
* CENTRAL HERNIATION
* Downward shift of brainstem
* Diencephalon
* S/Sx: Cheyne-Stokes respirations
* Pinpoint, fixed, nonreactive pupils - Traumatic Brain Injury-Interventions
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* Nonsurgical management
* Prevention of ICP
* Fluid and electrolyte balance
* Positioning/hyperventilation
* Induction of barbiturate coma/drug therapy - Strategies for sensory/perceptual alterations
- * Pulmonary management/behavioral management
- Strategies for preventing complications of immobility
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* Nutrition management
* Surgical management
* Intracranial pressure monitoring
* Craniotomy - Brain Tumors
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* Primary tumors
* Secondary tumors - s/s brain tumors
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* Increased ICP
* Focal neurologic deficits
* Obstruction of flow of cerebrospinal fluid (CSF - Brain Tumors-Complications
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* Cerebral (vasogenic) edema/ ICP
* Herniation of brain tissue/ischemia of affected area
* Rupture/hemorrhage into brain tissue
* Seizure activity/hydrocephalus
* Pituitary dysfunction/SIADH/diabetes insipidus
* Fluid and electrolyte imbalances - Brain Tumors-Classification
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* Malignant/benign
* Location:
* Gliomas
* Meningiomas
* Pituitary gland
* Acoustic neuromas - Brain Tumors-Symptoms
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* Headache (severe on awakening in the AM)
* Nausea and vomiting
* Visual symptoms
* Seizures
* Changes in mentation or personality
* Papilledema (swelling of the optic disk) - Brain Tumors-Interventions
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* Nonsurgical management
* Radiation/chemotherapy
* Blood brain barrier disruption
* Recombinant DNA
* Monoclonal antibodies
* Antineoplastic drugs
* Immunotherapy/hyperthermia
* Surgical management
* Biopsy
* Craniotomy - Brain Tumors-Postoperative Complications
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* Increased ICP
* Hematomas
* Hydrocephalus
* Respiratory problems
* Neurogenic pulmonary edema
* Wound infection
* Meningitis
* Fluid/electrolyte imbalance