WKU Med Surg Exam 4

when it comes to neurological problems, early recognition and aggressive management may prevent what

permanent neurologic dysfunction or death

what is a transient ischemic attack/ silent stroke

brief interruption in cerebral blood flow

when do s/s of a transient ischemic attack/ silent stroke appear

w/in 30-60 mins

how long do s/s of a transient ischemic attack/ silent stroke last

<24 hrs

when does damage from a transient ischemic attack/ silent stroke occur

w/ repeated insults: use ABCD assessment tool to determine seriousness/ risk of CVA (age, BP, clinical s/s, duration)

what is the tx for a transient ischemic attack/ silent stroke

- antiplatelets (aspirin, clopidogrel)

- BP control

- glycemic control

- lifestyle changes

what causes a CVA/ brain attack

change in normal blood supply to the brain

what does a CVA/ brain attack cause

- affects brain metabolism and blood flow around the infarction and contralateral hemisphere (s/s appear on the opposite side of the body/ brain of where the damage actually is)

- possible brain swelling leads to increased ICP: potentially life threatening

what are the 2 different types of CVA/ brain attack

- ischemic: occlusion (blockage) of cerebral artery

- hemorrhagic: bleeding in brain tissue or surrounding space

what are the 2 different types of ischemic strokes

thrombotic and embolic

what is a thrombotic ischemic stroke r/t

- atherosclerosis in intra/ extracranial arteries

- HTN

what is the onset of thrombotic ischemic strokes

slow

what is an embolic ischemic stroke r/t

- thrombi that break off and travel to cerebral arteries

- almost always due to heart problem: afib (stationary blood), ischemic heart disease, rheumatic heart disease, MI, valve replacement sx

what are the characteristics of s/s of an embolic ischemic stroke

develop suddenly and cause rapid neuro deficits that may resolve on their own

what are the complications of an embolic ischemic stroke

possible conversion to hemorrhagic stroke due to rupture

what are the different types of hemorrhagic strokes

intracerebral and subarachnoid

what is an intracerebral hemorrhagic stroke

bleeding into the brain tissue

what causes intracerebral hemorrhagic stroke

- severe HTN: sudden, dramatic elevation

- cocaine: constricts blood vessels

- vessels rupture, bleed out into brain, constricts other vessels around it, and then can worsen condition

what is a subarachnoid hemorrhagic stroke

bleeding into the subarachnoid space

what causes a subarachnoid hemorrhagic stroke

ruptured aneurysm or AV malformation

what does an aneurysm cause in a subarachnoid hemorrhagic stroke

vasospasms

how does an aneurysm cause a stroke

blood flow to distal areas of brain diminished which leads to cerebral ischemia/ infarction

what is an AV malformation

congenital absence of capillary networks forms abnormal communication between arterial and venous systems

what occurs in an AV malformation and how can it cause a subarachnoid hemorrhagic stroke

pressure builds up in the capillary bed r/t arterial pressure which can rupture and bleed into the subarachnoid space

what is the classic s/s of a subarachnoid hemorrhagic stroke

worst h/a of their life

what is a pnumbra

area of ischemia/ damage that occurs when someone has a stroke (this is the part of the brain you try and save)

what are the nonmodifiable risk factors for a stroke

- genetics

- age

- gender (males are at more risk before 75, then changes to women (they are also more prone to death and hemorrhagic))

- race: AA, Alaskan Native, American Indian

- hx of MI

- sickle cell disease

- berry aneurysms

what are the modifiable risk factors for a stroke

- smoking/ substance abuse

- obesity/ sedentary lifestyle

- oral contraceptive use (high levels or estrogen/ progesterone)

- heavy alcohol use

what are the modifiable w/ tx risk factors for a stroke

- HTN and/ or CV disease

- hyperlipidemia

- DM

- blood clotting disorders

- sleep apnea

what is the Cincinnati prehospital stroke scale mnemonic to help you remember how to assess for CVAs

BEFAST

what are "the suddens" to look out for when assessing someone for CVA

- sudden confusion, trouble speaking, or understanding others

- sudden numbness or weakness of the face, arm, or leg

- sudden trouble seeing in 1 or both eyes

- sudden dizziness, trouble walking, or loss of balance or coordination

- sudden severe h/a w/ no known cause

what pt hx do you need to obtain when assessing someone for a CVA

- activity when stroke began

- how s/s progressed: come and go? worsen? improve?

- LOC/ neuro changes

- medical/ social/ family hx

what is the most important thing to establish about someones s/s if they are having a CVA

establish time of s/s onset (aka last seen normal or last known well): most critical factor especially w/ ischemic stroke

if someone comes in w/ a suspected CVA, how long do you have to complete a physical exam and focused neuro exam starting from the time they walked in the door

10 min

what does a CT help identify w/ a CVA

determines what type: ischemic does not show up on a scan until 24 hrs after occurring but hemorrhagic shows up immediately

what things are a part of the NIHSS assessment

- assesses LOC, gaze, vision, facial palsy, motor (arm & leg), limb ataxia, sensation, language, dysarthria, and neglect

- assesses cranial nerves and determines where damage is

- score from 0 to 42 (higher the number indicates more damage (>25=severe))

once someone comes in and you suspect stroke, what is the first thing you need to do besides assess them

initiate stroke protocol and/ or activate stroke team

what is the first thing you want to get for someone suspected of having a CVA

emergent CT/ MRI (CT is better)

how do you manage the ABCs in someone w/ a CVA

- give O2 if needed to maintain SpO2 94% or greater

- BP control: pts often have HTN crisis (<185/ <110)

- frequently associated w/ a fib

what other things need to be done when someone comes in for a CVA

- obtain IV access

- EKG: determine if they are in afib

- draw labs

what labs need to be drawn when someone has a CVA

- glucose: critical to know if they are hypo (D50 if low) or hyper (do not tx until it is > 180 mg/dL): rules out CVA because hypo/ hyper has CVA s/s

- PT/ INR

- WBC for inflammation, platelet

if the CT scan shows it is a hemorrhagic stroke, what needs to happen

initiate intracranial hemorrhage protocol: stabilize and send to neuro ICU, high risk for seizures, possible sx

if the CT scan shows it is an ischemic stroke, what needs to happen

consider fibrinolytic therapy (alteplase): review candidacy and if not a candidate, consider endovascular therapy; still no, go to neuro ICU

what is fibrinolytic/ thrombolytic/ alteplase (tPA) used for

ischemic strokes only

what is the door to needle time of alteplase

45-60 min

what is fibrinolytic/ thrombolytic/ alteplase (tPA) contraindicated in

- hemorrhagic strokes

- bleeding problems or active bleeding

- VAs

how do fibrinolytics/ thrombolytics/ alteplase (tPA) work

dissolves cerebral artery occlusion to restore blood flow (puts them at risk for bleeding)

when should you give fibrinolytics/ thrombolytics/ alteplase (tPA)

w/in 3 hrs for any at risk or age or for any who has mild but disabling s/s

how long can you extend giving fibrinolytics/ thrombolytics/ alteplase (tPA)

4.5 hrs if someone has less risk, <80 yrs old, no anticoagulant prescriptions, imaging shows less than 1/3 of brain tissue involved, NIHSS <25, no hx of CVA or DM

what are the administration considerations for fibrinolytics/ thrombolytics/ alteplase (tPA)

- must be in a critical care or specialized stroke unit

- frequent monitoring of VS

- observe for signs of intracranial hemorrhage, bleeding (minimal bleeding is normal)

- frequent neurological assessments

- tx HTN (before >185/110; during/ after >180/105)

- DC if pt reports severe h/a, severe HTN that is uncontrolled, bleeding, n/v: notify HCP immediately!

- follow up CT after tx

- start on antiplatelet 24 hrs after starting tPA

what is another tx option for stroke if someone is not a candidate for fibrinolytics

endovascular therapy

what is the window of time for beginning endovascular therapy for a stroke

6-24 hrs: based on what the CT shows

what are the different endovascular therapies for ischemic strokes

- mechanical embolectomy w/ stent retrievers: sx clot removal

- intra arterial thrombolysis (rtPA): fibrinolytic agent directly into thrombus

- carotid artery angioplasty w/ stenting: prevent/ manage ischemic stroke; cleans arteries out and puts a stent in; action alert (hyperperfusion syndrome (rush of blood back to brain: severe h/a, changes in LOC, CVA s/s, actual CVA, neck pain/ swelling)

what is the endovascular therapy for ischemic strokes

may require sx such as AVM removal or aneurysm repair

what tx can be done for uncontrollable ICP

craniotomy

when is the greatest risk for increased ICP after the onset of a CVA

w/in 72 hrs

what is normal ICP

7-15 mmHg

what is the earliest sign of increased ICP

change in LOC

what are some other s/s of increased ICP

- n/v

- vision changes

- h/a

- motor problems

what is a complication of increased ICP

brain cannot compensate or accommodate volume changes so it may cause brain herniation which can lead to death

how do you monitor ICP

- internal ICP monitoring device placed through a burr hole

- monitor cerebral perfusion pressure (CPP: pressure gradient in which brain is perfused) and maintain >70 mmHg)

how do you calculate CPP

MAP-ICP

what are some causes of increased ICP

- cerebral edema s/t ischemia

- hydrocephalus: abnormal increase in CSF w/in ventricular and subarachnoid spaces

- vasospasm

- rebleeding/ rupture

hydrocephalus is most common w/ what

aneurysm or AVM

what are the causes of hydrocephalus

impaired reabsorption or CSF outflow

what can vasospasms cause

- decreased LOC

- motor/ reflex changes

- increased neuro deficits

what can cause the medical emergency rebleeding/ ruptures

aneurysms/ AVM pts

when can rebleeding/ ruptures occur

24 hrs to 7-10 days later

what are the s/s of rebleeding/ rupture

- severe h/a

- n/v

- decreased LOC

- neuro deficits

how do you tx/ prevent increased ICP

- monitor for s/s

- HOB to 30 degrees or per protocol

- keep O2 sat >94%, manage airway

- maintain head in midline, neutral position

- avoid extreme hip/ neck flexion

- space procedures

- low lighting, quiet environment

- monitor VS especially temp

- maintain SBP 140 to 150 for optimal CPP

- avoid sudden changes

what are the s/s of right hemisphere stroke

- problems w/ visual/ spatial awareness

- proprioception

- impulsivity

- judgment

- denial

what are the s/s of left hemisphere stroke

problems w/ speech, language, math skills, analytic thinking

what are some other drug therapies for a CVA

- antiplatelet/ anticoagulant: initial dose of aspirin w/in 24 to 48 hrs after onset (do NOT give w/in 24 hrs of admin of tPA)

- antihypertensives: labetalol (cautiously maintain BP 150/100) and calcium channel blockers (prevent/ tx cerebral vasospasms (ex: nimodipine))

- stool softeners

- antianxiety drugs

- analgesics

what motor changes occur from a CVA

- apraxia

- ataxia

- hypertonia

- hypotonia

- hemiplegia

- hemiparesis

- loss of neurologic control like incontinence

what is apraxia

cannot carry out purposeful movements

what is ataxia

gait disturbance

what is hypertonia

spastic paralysis

what is hypotonia

flaccid paralysis

what is hemiplegia

one sided paralysis

what is hemiparesis

one sided weakness

what are the interventions for motor changes due to CVAs

- collaborate w/ occupational/ physical therapist

- evaluate ability to perform mobility skills, ADLs, and household tasks

- begin rehab ASAP

- prevent shoulder subluxation!

- VTE prophylaxis

- provide mobility assistance and use gait belt

- determine cause

- consider bladder training

what are the cognitive changes that occur due to CVAs

- changes in LOC

- denial of illness

- impaired memory, judgment, problem solving, and/ or decision making

- aphasia

- dysarthria

what is expressive aphasia

the pt can comprehend what you are saying but they cannot use language to say it back

what is receptive aphasia

the pt does not understand what you say and but they can respond to you

what is mixed/ global aphasia

mix between expressive and receptive aphasia

what is dyarthria

difficulty speaking

what are the interventions for cognitive changes due to CVAs

- frequent neuro checks

- reorient pt, encourage family to bring familiar objects

- establish repetitive, structured, and consistent routine

- step by step approach

- collaborate w/ SLP

- encourage practice

- provide reassurance and support

- present 1 idea at a time

- speak slowly w/ gestures as needed

- avoid yes/ no questions for expressive aphasia

- use alternative forms of communication

what are the sensory changes due to CVAs

- spatial or proprioceptive dysfunction (r/t to right hemisphere)

- unilateral neglect (inattention)

- visual changes: can either be just 1 eye, opposite hemispheres, or the same hemispheres

- homonymous hemianopsia (HH): lose vision in same part of both eyes

what are the interventions for sensory changes due to CVA

- teach to touch objects

- balance training

- dual task training

- risk for injury leads to falls

- teach to touch/ use both sides of body

- dress the affected side first

- frequent verbal/ tactile cues

- breakdown tasks into discrete steps

- always approach pt from unaffected side

- place objects w/in pts field of vision

- if HH present, turn head side to side to expand visual field, especially when eating/ ambulating

- if diplopia, use an eye patch

- remove clutter

how are the cranial nerves impaired from a CVA

- chewing impaired (CN V)

- dysphagia (CN IX, X)

- facial paralysis (CN VII)

- absent gag reflex (CN IX)

- impaired tongue movement (CN XII)

what are the interventions for cranial nerve impariment due to a CVA

- aspiration precautions

- NPO until dysphagia screening and/ or swallow study

- implement nutritional interventions

what are the psychosocial changes due to CVAs

- personality changes

- coping issues

- emotional lability

- family coping

what are the interventions for psychosocial changes due to CVAs

- be patient

- observe for impulse and/ or easily distracted behaviors

- collaborate w/ interdisciplinary team to determine placement and continued care

- maximize pts abilities in all aspects of life when possible

- if going home, assess environment

- keep follow up appointments

- poststroke depression (PSD) education

- education regarding disease prevention, disease specific info, self management: teach warning signs

- supportive behaviors

- respite care

what are the expected outcomes for tx CVAs

- adequate cerebral perfusion

- BP and blood sugar maintenance

- performs max self care and mobility

- adapts to sensory perception changes

- communicates effectively

- adequate nutrition w/ no aspiration

where do primary brain tumors come from

originate w/in the CNS/ brain

where do secondary brain tumors come from

metastasis from somewhere else (lungs, breast, kidney, GI tract, etc)

how do you classify brain tumors

- benign (ex: meningioma) vs malignant (ex: astrocytoma)

- location (supratentorial vs infratentorial)

how do you diagnose brain tumors

- MRI, CT

- LP (lumbar puncture assessing CSF; never do this if you suspect ICP)

- biopsy

- EEG

- PET scan

what are the s/s of brain tumors

- h/a (more severe upon waking)

- n/v

- visual changes

- loss of balance, dizziness

- weakness, paralysis

- difficulty speaking

- seizures

- changes in mentation/ personality

what are the complications of brain tumors

- cerebral edema/ brain tissue inflammation

- increased ICP

- neuro deficits

- hydrocephalus

- pituitary dysfunction which leads to endocrine problems