Exam 3

 Stroke is a episode of neurologic dysfunction caused by a blockage or rupture of vessel to the

brain
 Risk factors for a stroke: pt should exercise 30 min. a day; begin evaluating risk factors at 20yrs
age; Risk factors: prehypertension 120-140/80-90; hypertension over 140/90; contraceptives;
antiphospholi pid antibodies; DM; stress; sleep apnea; cardiac disease; smoking; polycythemia;
sickle cell; cholesterol want ldl below 100 Hdl above 50; triglycerides; homocysteine; obesity;
family hx; age; gender; race; drug abuse; previous stroke/tia; c reactive protein; chagas disease;
migraine aura; alcoholism; pregnancy
 Triggers to stroke: anger, stress
 Thrombotic (ischemic stroke) – due to atherosclerosis (elderly, usually not fatal); usually occurs
at rest; may be TIA’s before; wake up with symptoms; s/s peak at 72hrs
 Anterior thrombotic ischemic stroke – decreased strength; decreased movement; aphasia,
mental confusion; paralysis
 Posterior thrombotic ischemic stroke – dizziness, visual problems; dysarthria; numbness;
headache
 Brain stem thrombotic ischemic stroke – effects vital signs
 Thrombotic stroke had increased edema in area once resolved s/s decrease; there is necrotic
tissue and penumbra surrounds it. The penumbra still gets little blood flow. The goal is to
increase the blood flow to the penumbra.
 Embolic ischemic stroke – bp normally stays normal; occlusion of vessels due to traveling emboli
(usually from the heart, carotids, aortic arch) due to post mi, l ventrical thrombus, decreased
c.o., endocarditis, orthopedic surgery (fat embolism)
 AF (embolic ischemic stroke)- atria contracts irregularly; potential for thrombus; therapy is
Coumadin, or dibigatran (predaxa)
 Embolic ischemic stroke – s/s – effects many ages; sudden onset; unrelated to activity; no
prodromal symptoms; consciousness preserved; h/a where embolus is lodged; usuall effects
MCA ( mca supplies 2/3 of the anterior cerebral hemisphere including lateral portion, frontal,
parietal, and upper half of the temporal regions) s/s may be temporary if clot breaks up; PLAATO
prevents clots therefore prevents emboli from forming
 Intracerebral Hemorrhage - occurs during activity, ruptured cerebral vessel directly to brain;
increased mortality rate; due to elevated bp, brain tumor, trauma, vascular malformation,
coagulation disorder, ruptured aneurysm, oral anticoagulation
 Intracerebral hemorrhage – usually after age 50; during activity; severity depends on amount of
bleeding; thalamus and cerebellar hemispheres are common sites but pons area is the most life
threatening location; severe h/a; n/v; hypertension; impaired LOC; 70 % mortality rate;
 Subarachnoid hemorrhage (thunderclap) – known as the worst h/a ever; hemorrhage w/I the
subarachnoid space; due to ruptured aneurysm, av malformation, trauma, cocaine abuse; may
show prodromal signs/symptoms if an aneurysm; an unruptured anyrism can be treated; if a
rupture occurs rapid neuro changes will progress to parylsis, coma, and death; 85% are in the
circle of willis;
 Subarachnoic hemorrhage (thunderclap) post complications and treatments – vasospasm is a
common and serious complication that occurs in 3-5 days past hemorrhage and causes
narrowing of the vessel; Utilize the triple H therapy , Hypertension, high fluids (500 to 1000),
Hemodilution. This can cause n/v, quickly decreased deteriorates and death.
 TIA’s – transient episode of neuro dysfunction caused by focal brain or retinal ischemia without
acute infarct, caused by micro emboli due to atrial fib or carotid artery stenosis
 Carotid system TIA – loss of motor function, hemiparalysis, difficulty speaking
 Vertebrobasilar system TIA – posterior, darkened blurred vision, dysphagia
 Limb shaking TIA – looks like a seizure activity, stops when they back down
 Hemiplegia – paralysis of one side of the body, shoulder can freeze, luction of joints, everything
adducts
 Aphasia – deficit understanding and using language usually left hemisphere stroke
 Sensory receptive aphasia – pt. not aware of mistakes, temporal lobe damage, they cannot read
or understand words, repeat words and are easily flustered
 Motor Expressive Aphasia – effects speech, pt forgets little words and are aware of errors
 Global anaphasia – combination of both usually with MCA
 Apraxia – can move the affected extremity but cannot use it for purposeful learned movements
 Visual Changes – occur due to lesions in the parietal temporal lobes
 Homonymous Hemianopsia – loss of vision in the same half of the eye, corresponds with the
paralyzed side.
 Amaurosis Fagux – produced by micro-emboli to the retina (monocular blindness) like a window
shade, temporary
 Agnosia – disturbance in the interpretation of visual, tactile, or other sensory info, cannot tell
arm is part of their body
 Dysarthria – slurred speech, trouble chewing and swallowing
 Hemianesthesia – loss of sensation on one side
 Paresthesia – c/o heaviness, numbness, tingling
 Horners syndrome – eye sympather nerve paralysis, sinking of eyeball and droopy eye, pupils
constrict, no tears form.
 Unilateral/left sided neglect – neglect the left side of body, pt with right sided stroke, don’t
recognize the left side of body
 Other s/s of strokes – elimination is altered if infarct is in frontal lobe or bons and bladder
training is needed; central post stroke pain occurs on the affected side of the stroke; should
hand syndrome the hand swells
 Brain stem stroke effects the vitals
 Left sided stroke – right sided weakness; slow cautious behavior; speech language
deficit/aphasia; emotional lability; aware of deficit (left knows they left their speech behind);
memory deficit; lack of automatic and functional speech; short attention span; impaired
comprehension related to language and math; hard to learn; impaired right/left discrimination;
need lots of feedback
 Right sided stroke – lft sided weakness; left sided neglect; quick and impulsive behavioral style;
misjudge distances; spatial perceptual deficits; impaired judgment; impaired time concepts; not
aware of deficits (right always thinks they are right); tends to deny problems; no clutter; good
lighting
 Cerebellar stroke – Balance; coordination; dizzy; posture
 Brain stem stroke – life supporting functions
 Silent stroke – whispering stroke; can be seen on mri; r/t hypertension; no symptoms
 Luncunar – r/t small vessel occlusions; caused by hypertension, smoking and diabetes
 Treatment – admit anyone having Tia symptom; consider using tissue plasma activator; IVs,
blood work, glucometer; cbd, electrolytes, pt, ptt, chem prof, lipids; keep npo; keep NPO;
dysphagia screening/speech consult, swallow study, tongue lip coordination, ekg; NIH stroke
scale; CT scan; mra; mri, dwi, pwi; pet scan; Doppler flow studiens of the carotids; meds,
Thrombolytic therapy;
 NIH stroke scale – measures neuro deficits higher number is worse prognosis
 Ct scan – r/o bleeding
 MRA – see better, dwi detects acute infarcts earlier, pwi is better
 PET scan – chemical activity
 Doppler flow studies of the carotid – greater than 50% blockage surgery is discussed
 Anti platelet agents – given w/I 24-48 hrs, first class, give aspirin, agronox, Plavix
 Anticoagulants – if immobile give sub q heparin to prevent dvt’s
 Steroids
 Dilantin – if there is seizure activity
 Antihypertensives – normally pt is on them before stroke. If it is over 220/120 they will give it
during a stroke
 Ace inhibitors – Ramaqual
 Thrombolytic therapy for acute ischemic stroke – Alteplase – (TPA) bp must be under 185/110 to
give Alteplase. Give 0.9 mg/kg (max 90mg), give 10%as IV bolous; remainder over 1 hour
through iv, pt must be 18 or older, must be less than 3 to 4.5 hrs from the onset of s/s. Ideally
w/I 60 minutes; cannot be a bleed,
 Post tpa care – close neuro assessments q 15 min first 2 hrs then q 30 minutes for the next 6 hrs
look for signs of cereberal hemorrhage, frequent vitals; watch for bleeding, no anticoagulants or
antiplatelet drugs for 24 hrs following TPA
 Intra-arterial thrombolysis with prourokinase or urokinase – direct thrombolytic delivered into
the clot by catheter, good results in the internal carotid, mca, and basilar artery
 Tumor cell research – turning cancerous cells into non cnacerous cells
 Stem cell research – prompts cells to correct damage
 Trans cranial laser therapy – non invasive procedure 2 monutes per site, it can cuase retinal
damage
 Merci retriever – contraindicated w/ contourous vessels, hemorrhage conditions, platelets
below 30,000, hypoglycemic
 Carotid endarterectomy – surgically excise the artery, remove plaque, place a drain in incision,
can only do one side at a time
 Carotid enderectomy post op care – vitals; keep head straight; raise hob after vitals are stable;
maintain systolic bp w/I 20 mmhg of normal; good neuro exam q 2 hr.; check edema; check
resp. compromise; especiall 7,10, 11, 12…7 facial 10 vagus
 Stents are contraindicated with previous endarectomy
 Angioplasty with stent – used in stenosis of vertebrobasilar or carotid arteries, insertion of a
balloon to open up the artery. (risk for emboli)
 Surgery for intracerebral Hemorrhage – evacuation of hematoma, poor survival rate
 Surgery for subarachnoid hemorrhage – interventional neuroradiology combines angiography
with neurosurgery, leaking aneurysm is a clipping (subarachnoid anyrism) or coil procedure
(better outcome than clipping)
 Nursing DX for stroke – alteration in cerebral tissue perfusion r/t decreased cerebral blood flow
aeb decrease in NIH assessment data (pt will have decrease in loc); implementation – monitor
icp, monitor neuro, elevate hob, monitor temp and vitals, maintain head and neck alignment,
avoid hypervolemia (csf drainage, diuretics)
 Impaired physical mobility r/t right side hemiplegia (due to left sided stroke); implementation –
improve gait, posture, strength, hob 30 degree or flat, position to unaffected side, don’t flex
upper thigh at acute angle during side lying position, upright sitting for short periods of time, no
pillow under affected knee (do put pillows between legs), pillow in axillary area, sling on
 affected side, trochanter roll (blanket from ileum to thigh affected to arm), prone position if
tolerable, prevent foot drop (chair with feet flat, Oscar boots, high tops), trochanter roll (rolled
blanket illieum to thigh, arms neutral with hands in a functional position, ROM (first day post
stroke), spasticity (uncontrollable muscle tightness), up with good down with pad, bilateral
repetitive rhythmic training intervention, constraint induced movement therapy,
 Self care deficit r/t right sided weakness or paralysis; will be complete care at first, encourage
them to do as much as possible, encourage self care with unaffected hand
 Potential for falls r/t weakness – keep side rails up, visual disturbances will increase risks, bed in
low position
 Risk for ineffective airway clearance, r/t inability to expectorate secretions = assess congestion,
assess cough, check lung sounds, observe amount color consistency of sputum
 Potential for aspiration r/t loss of swallowing reflex – pt is npo till gag reflex is checked
 Checking gag reflex – longer time to eat, speech therapy evaluates, cookie swallow, high fowlers
position to eat, small bites on unaffected side, chen down, head flexed forward stroke throat,
double swallow, check mouth for food, thicket use, avoid milk
 Communication problems – impaired verbal communication, decrease background noise, talk
slow, clear secretions, identify objects, anticipate needs, repeat directions slow and clear
 Disorientation – keep oriented, environmental cues, residual deficit adjustment
 Residual disabilities – need to be treated, give family good education
 Stroke in a newborn – before 28 days, caused by prom, birthing process, seizures, perinatal
cuases
 Stroke in a child – 30 days to 18 yrs ischemic or hemorrhagic
 Stroke in children, neonates – disabilities, posture/movement abnormalities, confusion,
agitation, Infarct sites (basal ganglia, thalamus), problems solving deficit, memory problems,
epilepsy; language problems;
 Considerations with strokes in minors – moya moya (cva base brain arteries don’t develop and
become stinosed and are replaced with collateral circulation), arteriovenous malformation,
sickle cell disease, heart defects, patent foramen ovale (shunting), atrial septal defect,
coagulation defect