Week 3 Acute Care CVA Flashcards
Infarction: tissue death (necrosis) due to inadequate blood supply to the affected area
Typically evident, but not always, on neuroimaging
(Not all/All) strokes are symptomatic
Why so important; why a whole pres. On this? (>50% statistic). If you work in or have a clinical in AC, you will almost certainly see some pts with acute stroke. Good news, treatable!
Not all
~ 80% suffer (ischemic/hemorrhagic), ~20% (ischemic/hemorrhagic) stroke
(Ischemic/Hemorrhagic) stroke – weakening of the blood vessel wall, and with high BP it will burst that weakened part of the wall and blood will distribute wherever it goes. These don’t follow a typical arterial presentation. The blood will travel in a way of where the path of least resistance is. It only represents 15-20% of the stroke population.
(Ischemic/Hemorrhagic) stroke – The more classic form of a stroke where some sort of clot forms within the brain and then the blood can’t physically get through and the tissues where the blood should be going start to die fairly quickly. This is about 80-90% of the stroke population.
Every minute counts post stroke because as time passes the more the tissue dies and the less opportunity that tissue has to recover.
ischemic; hemorrhagic; Hemorrhagic; Ischemic
Even before we consider stroke ——- can we prevent one from ever happening????
80% of stroke (can be/can’t be) prevented – National Stroke Association
Atrial Fibrillation (irregular heartbeat) - ↑ stroke risk 5 x’s
Decreasing (SBP/DBP) by 5-6 mmHg has been shown to decrease stroke risk by up to 40%
The incidence of stroke (halves/doubles) with every decade of life after age 55
There are hypothesized to be many alleles with small effect sizes associated with multifactorial strokes (Goodman and Fuller)
Heart disease and patent foramen ovale are both risk factors for stroke. Numerous other pathologies of the cardiovascular system would also qualify, but these two are more prominent so worth mentioning. They don’t neatly fit into either category.
Causes of CHF are multi-factorial and can be related to lifestyle, or more idiopathic.
http: //www.lifelinescreening.com/Partners/BD-Landing-Pages/Business-Partners/partner-pages/Health-Insurance/Carotid-Artery-Disease (last accessed 1/13/2018)
High blood pressure (decreases/increases) risk of stroke!!
Sickle cell – blood properties themselves are sick and maintain its integrity and carry oxygen where it needs to go to.
Whether inpatient or outpatient, can potentially save a life by discussing modifiable risk factors with pts.
can be; DBP; doubles; increases;
MANY FACTORS ARE SILENT!
- CAD often no warning signs or symptoms of carotid artery disease (plaque)
- A-fib not everybody with atrial fibrillation experiences symptoms, these warning signs may indicate heart issues: Heart palpitations (sudden pounding, fluttering, or a racing feeling in the chest), Lack of energy, Lightheadedness, Confusion, Chest discomfort, Shortness of breath, even at rest
[Post acute a-fib monitoring via CardioKey, CardioNet, LINQ, holter]
- High cholesterol and CRP Warning signs - none
- DM – may live for years w/o symptoms
Total Cholesterol (Source: American Heart Association)
Less than 200 mg/dL - Desirable level that puts you at lower risk for coronary heart disease. A cholesterol level of 200 mg/dL or higher raises your risk.
200 to 239 mg/dL - Borderline high.
240 mg/dL and above - High blood cholesterol. A person with this level has more than twice the risk of coronary heart disease as someone whose cholesterol is below 200 mg/dL.
LDL (Bad) Cholesterol Level - Less than 100mg/dL is optimal (Source: National Heart, Lung, and Blood Institute )
HDL (Good) Cholesterol Level - 60 mg/dL and higher is considered protective against heart disease (Source: NHLBI)
C-reactive Protein Screening
- It’s now believed that high CRP levels are associated with cardiovascular disease, stroke, coronary heart disease, peripheral arterial disease, and type 2 diabetes. CRP is part of the immune system and is released into the blood when the body responds to injury or infection. Within 24 to 48 hours of an infection or trauma, CRP levels can increase 1000-fold. The high-sensitivity C-reactive Protein (hs-CRP) screening measures CRP levels in the blood. In 2003, the American Heart Association and the Centers for Disease Control and Prevention announced that CRP >3 mg/L indicates a high risk for cardiovascular disease, even if cholesterol levels are low.
Have to take BP as PTs especially on an initial visit.
Got it
Prevention (education):
—Only about 60% of Americans can recognize even one warning sign, and only 55% can identify one stroke symptom.
- **This was updated a few years back to be BE-FAST Balance, Eyes, Face, Arm, Speech, Time
https: //www.ahajournals.org/doi/10.1161/STROKEAHA.116.015169
FAST turned into BEFAST. BEFAST can be used as a pt education tool to teach pts the signs and symptoms of a stroke.
What is the individual words for the acronym BEFAST?
If you feel something is funny, try to get to the hospital ASAP.
B - Balance E - Eyes F - Face A - Arms S - Speech T - Time
Got it
Got it
General Clinical Presentation of a stroke – Hyperacute stage
(Chronic/Sudden) weakness or numbness of the face, arm, or leg
(Chronic/Sudden) loss of vision, particularly in one eye
(Chronic/Sudden) difficulty speaking or understanding speech
(Chronic/Sudden) severe headache with no known cause
Unexplained dizziness, unsteadiness, or falls
What do all these features have in common?
Acute/sudden change – usually indicates (neurological/vascular) problem compared to gradual/slower progression of symptoms
Not a comprehensive list nor do all these features need to be present
When you have an acute sudden attack that happens within seconds/minutes it is typically suggestive of a vascular problem.
In strokes the blood vessel has either infarcted or there is a clot within the blood and the blood can’t get through or the weakening of the blood vessel has become too much and the blood is bursting out. That happens in seconds/minutes.
In strokes, it doesn’t build up over weeks, rather it takes place relatively quickly.
Sudden; sudden; sudden; sudden; vascular
If you are experiencing these symptoms you have to get to the hospital ASAP because every second, minute, hour is important to save as much (heart/brain) tissue as possible. Once that brain tissue dies, we are under the impression that it is gone forever.
brain
FIRST, vital signs and serum glucose. Establish LKN (last known normal). Examine patient (NIHSS). Then HCT without contrast is always first imaging test.
-why CT shows hemorrhage vs infarct (cellular level)? CT more sensitive to fluid/water changes compared to tissue death
CT scan is 1) fastest, 2) most convenient, and 3) most widely available test to use for diagnosis of stroke
the primary reason to use CT is related to the point listed above. If the HCT shows a hemorrhage, then IV tPA is not appropriate and we begin (usually) aggressive BP management.
If it shows an infarct, then the stroke is likely > 4.5 hours old and the patient is outside the window for IV tPA, however may be appropriate for thrombectomy.
If there is no stroke and the patient is medically appropriate for tPA, then we look at the NIHSS -> generally, scores that indicate moderate deficits (5-15 ish) on the NIHSS are considered candidate for tPA.
MRI is then used to confirm presence of an occlusion and the patient is evaluated for appropriateness of thrombectomy
LATER: all the others. Angiogram: uses x-ray techniques such as fluoroscopy
All patients with suspected acute ischemic stroke who arrive within 6 hours and are potentially eligible for endovascular thrombectomy should undergo immediate brain imaging with non-contrast CT and CT angiography (CTA) without delay, from arch-to-vertex including the extra- and intra-cranial circulation, to identify large vessel occlusions eligible for endovascular thrombectomy [Evidence Level A].
Angio-”related to blood vessels”
HCT scan – a bunch of xrays taken all at once to create a 3D representation of the brain.
CTA – Look at the blood flow of the brain
Carotid US – Picture on this slide. Done to look for clots.
TTE/TEE – Looking for clot like formations in the heart itself.
To determine if this person did have a stroke, imaging is going to help with that.
Got it
Imaging: Head CT
CT scans may appear normal with acute embolic (ischemic) stroke
However, hemorrhagic strokes (will be/will not be) seen - Can be seen up to 5 days following insult
Displacement of brain structures such as ventricles can sometimes be seen early in a large infarct
CT scans of ischemic stroke will eventually reveal area of decreased density and loss of grey/white matter differentiation associated with cerebral edema
60% of infarcts are seen within 3-6 hrs and virtually all are seen in 24 hours.
If someone gets a CT scan and it is normal and there’s no evidence of abnormality it is likely an (death/infarct).
will be; infarct
Differentiation of Stroke Type
(Hemorrhagic/Ischemic) strokes do not follow an artery distribution, and as such, symptoms may not follow typical (artery) pattern
Vomiting, a severe headache, seizures, and/or impaired consciousness are symptoms that may differentiate hemorrhagic from ischemic strokes
Important to determine hemorrhagic vs ischemic for medical management (HCT!)
With a hemorrhagic stroke you will see displacement of certain structures
The fluid in (hemorrhagic/ischemic) strokes may have impacted structures responsible for autonomic regulation of the brainstem which is why you will get vomiting, headaches, etc.
In (hemorrhagic/ischemic) strokes you will feel the facial droop, arm weakness, etc.
Hemorrhagic; hemorrhagic; ischemic;
The less amount of bleeding, the (worse/better)
Hemorrhages tend to do functionally a little bit (worse/better) than ischemic strokes because the tissues don’t necessarily die. The blood gets reabsorbed into the body versus causing true ischemia to brain tissue.
Hemorrhages on a macroscale are more severe early on, but they tend to do (worse/better), while infarcts are less severe early on but they tend to do (worse/better)
better; better; better; worse
If you draw a line through the middle of the skull you can see it is not directly straight up and down, it is shifted over. There is (less/more) volume of fluid than the brain is used to so tissue has to move to accommodate it and it will eventually end up disrupting function. The white stuff is blood.
more
Subarachnoid Hemorrhage (SAH)
(Chronic/Abrupt) onset usually from burst aneurysm/AVM
Occurs typically in (younger/older) adults
(Posterior/Anterior) communicating artery is common site
Severe headache, loss of consciousness (LOC)
High fatality rate (50%)
(Decreased/Increased) risk of vasospasm
With SAH, we worry about risk of vasospasm 7-10 days following symptom onset > risk of hypoperfusion, you may see acute fluctuations in a person’s exam (facial droop, language deficits) which could indicate acute spasm, and would necessitate need to return to (prone/supine) position.
Abrupt; younger; Anterior; Increased; supine
The volume of fluid is so small by the arrow that you don’t see a ton of displacement by the ventricles. This might be a smaller hemorrhage and if that person can survive the first 7-10 days so to speak, they’ll likely do very well.
Got it
Hemorrhagic Conversion
Ischemic infarct may convert into a hemorrhagic lesion
Thrombi (clot in the brain) can migrate, lyse and reperfuse into an ischemic area, leading to small hemorrhages
Damaged capillaries and small blood vessels no longer maintain their integrity
Conversions more common in (small/large) infarcts such as an occluded MCA – there’s so much pressure in the vessel that the smaller capillaries and blood vessels can’t maintain it.
A risk of tPA - tPA is a clot buster and it is medication that dissolves the clot. But when that happens the blood is on the thinner side and can give you a hemorrhagic conversion
The blood itself is not being managed enough to the point where it can hold the integrity and you get these microhemorrhages. The stroke team want to make sure once the clot is there that they do everything to get rid of it to prevent secondary complications.
large;
Aneurysm vs. AVM
Aneurysm:
Congenital or d/t long standing HTN (Strengthened/Weakened) area of vessel Balloons out Risk of embolic clot formation Risk of rupture/bleed
Arterial-Venous Malformation:
Congenital malformation of an arterial/venous bed
(Low/High) risk of bleed
Surgical management either pre/post bleed
12% cause CNS signs, others are benign
Imaging: cerebral angiography
Aneurysm & AVMs can both lead to hemorrhages.
An (aneurysm/AVM) is dilation of the blood vessels. It hasn’t ruptured yet, think of it as a little pimple on the blood vessel that increases the risk of it rupturing.
(Aneurysm/AVM) - the blood isn’t getting to and from where it should and the disturbance of the architecture of the plumbing of the brain can increase risks for hemorrhages.
Weakened; High; aneurysm; AVM
Won’t be tested on this
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SAH Outcome
May have (worse/better) functional outcome than ischemic CVA - Greater functional gains
(Low/High) degree of cognitive impairments - Usually end up physically independent
(Low/High) fatiguability
Physically they do well, but cognitively they won’t do so well.
better; high; high
Look at how the hemorrhage has evolved, that is not a good sign. Need to physically (increase/reduce) the BP so they don’t have as much blood pumping through the brain making this worse.
reduce
Acute Phase Management
Special consideration - MAP (Mean Arterial Pressure)
Definition: average arterial pressure throughout one cardiac cycle, systole, and diastole
MAP= (2(DBP) + SBP)/3
Ischemic typical MAP goal <140 (UPHS)
BP “should not be lowered unless it is as high as 230/120 mmHg. The goal is not to try to normalize the pressure, but to bring it down from dangerously high levels…cerebral perfusion is the main concern” (Goodman & Fuller 2009)
Medical management of cardiac function may include permissive HTN for ~10 days post stroke - Blood pressure will be resting (low/high). If there is a physical block within the blood vessel. If you have higher pressure it is going to keep all that blood moving to allow blood to get to those parts that are dying as best as they can.
Chart review: check orders! (and ask RN)
Mean arterial pressure is significant because it measures the pressure necessary for adequate perfusion of the organs of the body. It is considered by many to be a better indication of perfusion than systolic blood pressure.
Too high: (>100) - too much stress on organs
Too low – risk of organ death
Good – emphasis of BP parameters for stroke patients – discuss both goal BP’s and cutoff BP’s. May be in POC and not necessarily in an order. There may be variation from MD to MD (or between facilities), so it’s important for therapists to independently consider them. Neurologist may be providing the order in your setting. What is the evidence for the SBP/DBP and duration limit? (Unclear?)
BP goals fluctuate a lot. The general rule is < 220/110 or MAP <140 for ischemia, <180/105 for ischemic stroke with HT, and < 160/90 for hemorrhage. Most of the time, it’s more about big changes in the moment (i.e. if a person starts at 200/100, and then upon sitting up is light-headed and BP is 160/80, then the significant drop in BP is more concerning than the high starting BP
The goal is to manage pressure in and out of the brain so that way you don’t worsen someone’s function or their tissue integrity. Want just enough blood to the brain so the organs can have enough oxygen to survive.
high;
Monitor warnings of (increased/decreased) ICP.
GOAL of NICU IS PREVENT (PRIMARY/SECONDARY) BRAIN DAMAGE.
Goal of most of these: manage cerebral perfusion pressure and ICP
AC can be reversed quickly with fresh frozen plasma; vitamin K takes 12-24hrs
Preventing seizure: done with medication
EVD = External Ventricular Drain - can both monitor ICP and remove fluid device placed by neurosurgerythatrelieves elevated intracranial pressure(blood or CSF) andhydrocephaluswhen thenormal flowofcerebrospinal fluid aroundthebrainisobstructed (or there’s blood in the ventricles)
Ventriculostomy: the surgery itself > EVD is usually placed on the R side of the brain to avoid language centers (occasionally will be placed on L for various extenuating circumstances, or confirmed that the patient is L handed and language center is more likely on the right)
Monitor and manage ICP: Thenormal ICPis 7-15 mmHg. There is no defined set point at which treatment for intracranial hypertension should be initiated, but levels above 20 mmHg are usually treated. However it is more important to maintain an adequate cerebral perfusion pressure.
Avoid Vasospasm > risk for vasospasm is highest days 7-10 post bleed. Look for elevated velocities on TCDs or vessel narrowing on CTA or MRA of brain. With TCDs, the Lindegaard ratio (aka LR is a ratio of MCA velocity to terminal ICA velocity) helps to 1) minimalize interrater reliability, and 2) indicate true vasospasm. Scores ~1.5-3 indicate minimal spasm, 3-6 is moderate spasm, and >6 is severe spasm with risk for ischemia and hypoperfusion
Medical/Surgical: Ventilate, HOB position, 3% NaCl (hypertonic sodium chloride – pulls out fluid, monitor HTN), Mannitol (diuretic), Ventriculostomy, CSF diversion, Phenobarbital Coma, &/or decompression.
Intracranial Pressure Monitoring @ http://emedicine.medscape.com/article/1829950-overview?src=emailthis#a5 (last accessed 1/13/2018)
Communication with Megan Moyer at megan.moyer@uphs.upenn.edu on 12/17/2015
If someone has a hemorrhage there is too much pressure in the brain so need to reduce the pressure, but make sure it isn’t too low.
increased; SECONDARY;
Intracranial Pressure (ICP)
Intracranial pressure (ICP) is a resultant of the pressure applied by the components within an inflexible and rigid skull (Kawoos et. al, 2015)
Signs of increased ICP? Headache. Blurred vision. Feeling (more/less) alert than usual. Vomiting. Changes in your behavior. Weakness or problems with moving or talking. Lack of energy or sleepiness.
If someone has a hemorrhage there is too much fluid volume in a fixed rigid skull and then what happens is all of the signs of the increased ICP.
Greater than 20 mmHG is considered too high for ICP .
less;
Perfusion Goals
Cerebral Perfusion Pressure (CPP) = MAP – ICP
CPP 50-70 mmHg to avoid cerebral ischemia and hyperaemia -
Important with driving oxygen to brain tissue!
Too (low/high)? Too much blood flow and edema can worsen
Too (low/high)? Risk for ischemia
ICP less than 20 mmHg to maintain CPP, avoid brain herniation
- ↑ ICP, ↓ outcomes
↑ ICP, carries a mortality rate of 20%
CPP is the pressure gradient acting across the cerebrovascular bed and, therefore, a major factor in determining cerebral blood flow (CBF).
Normal ICP 7-15mmHg
CPP (Cerebral Perfusion Pressure) = mean arterial blood pressure (MAP) - mean intracranial pressure (MIC)
CBF is kept constant in spite of wide variation in CPP and MAP by autoregulation.
CBF normal = 50 ml/100g/min (remember: below 20 = neuronal functioning impaired. <10, neuronal death (infarction) occurs
CVR = Cerebral Vascular Resistance
Hyperaemia: shunting of blood to other tissues
Intracranial Pressure Monitoring @ http://emedicine.medscape.com/article/1829950-overview?src=emailthis#a5 (last accessed 1/13/2018)
Communication with Megan Moyer at megan.moyer@uphs.upenn.edu on 12/17/2015
The goal with stroke management is to keep enough pressure in the brain to provide oxygen but not too little where you get ischemia.
high; low; less than
You can mobilize someone who has an EVD. You should nave a nurse with you to clamp the EVD so the pressure is stable. Don’t want pressure to change because they could pass out.
Want the HOB (down/elevated) because you don’t want more pressure getting into the brain so you use gravity to your advantage by keeping it upright.
elevated
NIH stroke scale is used to determine the severity of the stroke. The more severe the stroke the (better/worse) the prognosis.
worse
https://www.ahajournals.org/doi/epub/10.1161/01.STR.0000048217.44714.02
The lower the number (less than 5), the more they are likely (not going to/going to) be discharged home.
going to
Concern to distinguish between ischemic versus hemorrhagic [Will discuss hemorrhagic shortly]
”time is brain” each minute since the start of the stroke results in 1.9 million lost neurons, and about 14 billions synapses (roughly the same as 3.6 years of aging)
Lack of oxygen due to decreased blood flow causes cell death in 3-4 minutes.
Parenchyma: tissue of the brain
“when cerebral blood flow falls below 20mL/100mg of tissue per minute, neuronal functioning is impaired. Neuronal death does not occur until a lower threshold (10mL/100mg/min). In an acute infarct, a portion of the brain receives no blood, while a surrounding area receives sufficient blood from collateral circulation to maintain viability BUT NOT sustain function. This area is called the ISCHEMIC PENUMBRA.
Diaschisis: loss or change of function of a portion of the brain connected to a distant, but damaged, brain area. This is due to alterations in metabolism caused by deafferentation with altered oxygen and glucose consumption.
Cerebral edema: swelling within the enclosed cranial vault causes inc. ICP: global brain damage possible – more on this in hem. Section
TIA: transient ischemic attack, usually impairments last <2 hours and it is NOT visible on imaging (no visible bleed) therefore, early mgmt with AC. 35% of people with TIA have stroke within 5 years (that’s 1 in 3!); w/u essential to prevent future stroke – the same thing that caused the TIA is likely to cause the CVA
1 in 3
Goal in ischemic stroke is reperfusion.
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He skipped the slide
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Ok so what else is on the table besides tPA?
Can get both thrombectomy then tPA
Current ASA guidelines: recommend acute stroke patients lie flat but should have their head elevated if they are at risk of aspiration, have difficulty breathing or have brain swelling. This is typically for 24 hours AFTER the STROKE, not necessarily from admission. Minimal evidence supporting this; nowhere near as valuable/important as tPA/thrombectomy
Specialty stroke units: staff with specific training, needed equipment is already on hand. Higher volumes often associated with better outcomes (if you practice something, you get better at it. If you see something often, you recognize it quicker)
https://www.heart.org/en/news/2018/05/01/head-position-after-stroke-up-or-down
People who’ve had an infarct might qualify for a tPA – head CT doesn’t show evidence of a hemorrhage so the assumption is that they had an infarct.
How do you know when the stroke happened? – Trace back to when the pt started feeling weird (Last known normal LKM). If stroke happened (within/after) the past 4.5 hours they qualify for a tPA. If they don’t qualify for the Tpa they might qualify for the thrombectomy (physically removing the clot with a wire).
Individuals who have had a stroke sometimes have the HOB (flat/elevated) especially in the first 24 hours especially if they’ve had a tpa and part of the reason for that is to allow for the body to reacclimate to what is going on and not over stress the body.
within; flat
Historically, tPA referred to the medication Alteplase. It now also refers to the medication Tenecteplase (abbreviated TNK) both meds are forms of tPA. In the US, we’ve always used alteplase, but TNK has been used in Europe for years. The US is now moving towards universal administration of TNK. TNK and tPA have similar outcomes regarding mortality and morbidity data, and risk for hemorrhagic transformation with both is similar, however TNK has two distinct advantages: 1) improved long term outcomes, and 2) the ability to “drip and ship” to a comprehensive stroke center for consideration of mechanical thrombectomy in a quicker manner (TPA is delivered with a 10% bolus, followed by a 1 hr drip to deliver the remaining 90%, vs TNK which is entirely delivered via bolus) – with all of this said, tPA currently remains the standard of care, TNK is probably worth mentioning
For a smaller infarct the TPA might suffice, for the larger infarcts you may need both.
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If blood flow to this ischemic area is restored (before/after) irreversible damage occurs, then the tissue will likely recover and resume normal function – Goodman & Fuller
Additional contraindications to tPA (not present in Al)
- INR >1.7 or use of Warfarin/coumadin therapy - Rapidly improving or minor symptoms (suggest possible TIA) - bacterial endocarditis - Platelets < 100,000mm3 (Want normal PT/PTT) - want normal glucose *** checking BG right away, remember?
Comprehensive Stroke Center IV rt-PA door-to-needle times ≤ 60 minutes in 50% or more of applicable acute ischemic stroke patients (minimum of 6) during one calendar quarter. How long to get to CT Scan? Comprehensive Stroke Center targets are 6-8 minutes for ischemic strokes to get to CT Scan
This matters – if you go to a CSC, you can be confident their door to needle times are quick, facilitating optimal outcomes.
Complete or near complete recovery (38% in tPA vs. 21%) Absolute increase of 13% in number of people with minimal/no disability in tPA group
Intra-arterial tPA directly to clot via angiography (also up to 4.5 hours) Intra-arterial (IA) treatment is effective for emergency revascularization of proximal intracranial arterial occlusions
CLOTBUST (Combined Lysis Of Thrombus in Brain ischemia Using transcranial ultrasound and Systemic t-PA): not standard of care; research phase (unproven)
‘nothing is free:’ - intracerebral hemorrhage conversion (6.4% in TPA vs. 0.6%) 10-fold increased risk of ICH with tPA treatment - ‘nothing is free’
So, why didn’t tPA put therapists like me out of business?
General Info:
tPA first approved by FDA in 1996
Platelets (PT): Anormal plateletcountrangesfrom 150,000 to 450,000plateletsper microliter of blood. Having more than 450,000plateletsis a condition called thrombocytosis; having less than 150,000 is known as thrombocytopenia. You get yourplateletnumber from a routine blood test called a complete blood count (CBC).
Partial Thromboplastin Time (PTT):In general, clotting should occur within 25 to 35 seconds. If the person is taking blood thinners, clotting takes up to two-and-a-half times longer. Normalvalueranges may vary slightly among different labs. Some lab use different measurements or may test different specimens.
http: //www.heart.org/HEARTORG/Professional/GetWithTheGuidelines/GetWithTheGuidelines-Stroke/Get-With-The-Guidelines-Stroke-Overview_UCM_308021_Article.jsp#.WHqLRvkrK70 (last accessed 1/13/2018)
https: //www.pennmedicine.org/for-patients-and-visitors/find-a-program-or-service/neurology/stroke/penn-stroke-center (Last accessed 1/13/2018)
Saver JL, Fonarow GC, Smith EE, Reeves MJ, Grau-Sepulveda MV, Pan W, Olson DM, Hernandez AF, Peterson E, Schwamm LH. Time to Treatment With Intravenous Tissue Plasminogen Activator and Outcome From Acute Ischemic Stroke. JAMA. 2013;309(23):2480-2488
before;
Vascular imaging, blood tests, cardiac workup
Patients suspected of having a stroke based on clinical presentation will often undergo extensive imaging workups to determine:
Location, extent of the stroke (brain MRI, MRA),
potential sources of the stroke, including occlusion of cerebral blood flow (carotid ultrasound, CTA(?), angiogram) cardiac sources of emboli that may have traveled to the brain via the circulation and caused the stroke (TTE/TEE, angiogram (?)).
The findings of these latter studies may determine the need for cardiac or neurosurgical interventions which may affect a patient’s acute care stay.
Embolic most common (blood clot at another location & travels to brain); 80% cardiac emboli that occlude MCA; vascular typically plaques from carotid a. or aorta; paradoxical such as PFO or DVT.
Lacunar: ischemia in one distal, smaller a. branching off one of larger, higher pressure a. in circle of Willis, deep sub-cortical stroke; typically assoc w/ chronic HTN & DM microvasc dz.; 2mm-3cm in size; account for 20% of all strokes.
http://www.lifelinescreening.com and search Carotid Ultrasound Image
Image: http://www.lifelinescreening.com/~/media/Images/Marketing/What%20To%20Expect/whattoexpectstep9revised.ashx (last accessed 1/13/2018)
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Cerebral Cortex Blood Supply
Where does each artery go to and what do those lobes do in terms of their function?
The (frontal/parietal) lobe is responsible for cognition, motor control, and personality.
The (frontal/parietal) lobe is responsible for cognition and sensory perception.
The (parietal/occipital) lobe is responsible for cognition and vision.
The (occipital/temporal) lobe is responsible for hearing, language recognition, and memory processing
The (limbic system/occipital lobe) is responsible for emotions and memory processing.
Anterior Cerebral Artery: (Frontal & parietal/temporal & occipital) lobes (Medial/Lateral) surface Small part of (medial/lateral) surface (Minority/Majority) of cingulate gyrus
Middle Cerebral Artery
(Frontal, parietal, & temporal lobes/frontal, parietal, & occipital lobes)
Posterior Cerebral Artery
(Frontal/Occipital) lobe
(Parietal/Temporal) lobe - Inferior medial surface
frontal; parietal; occipital; temporal; limbic system; frontal and parietal; Medial; lateral; Majority; Frontal, parietal, & temporal lobes; Occipital; Temporal
The anterior cerebral artery impacts the legs (less/more) than the arm and face.
The middle cerebral artery impacts the legs (less/more) than the arm and face.
MCA strokes are 85% of all strokes because the first path of the internal carotid is the MCA.
more; less
It’s like a bell curve where people get worse and then they get better. Also shows the potential progression in recovery – someone might be flaccid and then move to becoming spastic, then they may or may not improve from that point on.
This is an observation based study.
“Brunnstrom, a physical therapist, was particularly concerned with the problems of patients with hemiplegia. The basic premises of this approach are: In normal persons, spinal cord and brain stem reflexes become modified during development and their components rearranged into purposeful movement by the influence of higher centers. Since reflexes represent normal stages of development, they can be used when the CNS has reverted to an earlier developmental stage as in hemiplegia.” (https://www.kau.edu.sa/Files/0053607/Files/60661_Brunnstrom.pdf)
(1) Reflexes should be used to elicit movement when none exists (normal
developmental sequence).(2) Proprioceptive and extroceptive stimuli also can be used
therapeutically to evoke desired motion or tonal changes.
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Midline shift – so much fluid seen in the CT scan that there is a midline shift which is a negative prognostic indicator. The ventricles should be straight up and down through the middle of the picture, but they are pushed so far to the left that they’ll start to compromise function.
Large mass and hydrocephalous –note only one ventricle visible, compression of healthy tissue
Got it
The better function (FIM status) the (worse/better) prognosis.
better
What do you feel the primary goal of physical therapy in acute care?
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Hospitals typically divided into specialized ‘floors’ or ’wings’. Where a patient is, especially within a large and/or specialized hospital, may tell you a lot about them! You need to understand the workflows of the floor/wing you are working within as a PT.
Patients start in ED. Then, to OR with neurosurgery, or to Neuro ICU, or to Neuro floor, depending on type and severity of stroke
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Acute stroke patient’s typically on bed rest first 24 to 48 hours FROM THE ONSET OF STROKE NOT ADMISSION … But as soon bed rest period over, the team wants the patient aggressively mobilized (assuming there are no other issues)
Discuss “head of bed flat” meant to increase perfusion in ischemic stroke. In hemorrhagic stroke, HOHB is maintained > 30 degrees to help decrease blood flow to help manage BP.
BP goals in ischemic stroke: acutely < 220/110 or MAP < 140, long term goals usually < 140/90 (once pt is in subacute to chronic phase of healing)
- Swallow Assessment
- Consider fall risk with anticoagulation
- Vital signs often monitored by the mean arterial pressure (MAP) as mentioned earlier
Acute care PT – focus on aggressive mobilization and DC planning, less so on normalization of movement patterns, neuromuscular reeducation, etc. – different roles for different levels of care.
https: //www.nlm.nih.gov/medlineplus/ency/article/000793.htm (last accessed 1/13/2018)http://emedicine.medscape.com/article/1829950-overview#a1 (last accessed 1/13/2018)
* ***
Front Neurol.2019 Feb 19;10:113. doi: 10.3389/fneur.2019.00113. eCollection 2019.
High Intensity PhysicalRehabilitationLater Than 24 h PostStrokeIs Beneficial in Patients: A Pilot Randomized ControlledTrial(RCT) Study in Mild to Moderate IschemicStroke.
Tong Y1,2,Cheng Z1,2,Rajah GB1,3,Duan H1,2,Cai L1,2,Zhang N1,2,Du H1,2,Geng X1,2,3,Ding Y1,3.
Cumming TB, Thrift AG, Collier JM, Churilov L, Dewey HM, Donnan GA, Bernhardt J. Very early mobilization after stroke fast-tracks return to walking. Further results from the Phase II AVERT randomized controlled trial. Stroke. 2011;42:153-158.
N= 71; Hosp setting; mean age 74.7; RCT; < 24 hr s/p CVA; VEM vs SC
1⁰ outcome = 50 m gait 2⁰ outcome = B.I. and RMA @ 3 & 12 mos
**VEM returned to sig faster than SC [P = 0.032, 3.5 vs 7.0 dys]
VEM independently assoc w/ good functional outcome on B.I @ 3 mos (P=0.008) & RMA @ 3 (P=0.050) and 12 (p=0.024) mos.
Adler J and Malone D. Early mobilization in the intensive care unit: A systematic review. Cardiopulmonary Physical Therapy Journal. 2012; 23(1):5-13.
- *Safe to mobilize (≤ 4% adverse effect, mostly ↓ SaO2)
- *Impact function (↑FIM, ↑ B.I., sooner milestones, longer distances, quad strength) (Gen. not increase strength in unit)
- QoL – only 2 studies
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DON’T NEED TO MEMORIZE!
Hemedex: connects to intracranial probe; monitors tissue (parenchyma) perfusion
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Is it safe to mobilization these individuals w/i 24 hours of a stroke ? > generally, (no/yes) assuming there are no contraindications
The big takeaway - Mobilization is going to be based on hospital procedure and pt’s chart
Benefit: prevent secondary complications, promote recovery
Cons: medical ”harm:
No impact on QOL at 3 or 12 months (Cumming 2019) I think this study is most telling, there isn’t much benefit o be gained from mobilizing OOB within < 24 hours (in ischemic strokes).
yes
Craniectomy Precautions (maintained as long as bone flap is absent): “A craniotomy is a surgical operation in which a bone flap is temporarily removed from the skull to access the brain.” Craniotomy precautions PLUS helmet must be worn at all times when out of bed
Craniotomy Precautions (maintained for two to four weeks following surgery or until cleared by neurosurgeon):
Avoid bending so that head is in a dependent position during functional activities
Head of bed elevated 30 degrees, use pillows at home
No vigorous exercise until cleared by physician
No driving until cleared by physician
No lifting of objects weighing greater than ten pounds
Transphenoidal Craniotomy (“Nasal”) Precautions:
Head of bed should be elevated 30 degrees, use pillows at home
Avoid sneezing if at all possible
Do not blow nose
Notify physician if fluid is dripping or draining from nose or ears
Avoid bearing down (Valsalva maneuver)
Do not use straws
BRIGHAM & WOMEN’S HOSPITAL
Department of Rehabilitation Services
Occupational Therapy
Standards of Care
Copyright © 2011 The Brigham and Women’s Hospital, Inc., Department of Rehabilitation Services. All rights reserved
http://www.brighamandwomens.org/Patients_Visitors/pcs/RehabilitationServices/Occupational%20Therapy%20Standards%20of%20Care-Protocols/Neuro%20-%20Craniotomy.doc (last accessed 1/3/2016, access as of 1/14/2017 no longer available)
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https: //www.youtube.com/watch?v=D53gygWRhLM
(last accessed 1/13/2018) Uploaded by JHU 2009
3 minutes
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https://www.ted.com/talks/jill_bolte_taylor_my_stroke_of_insight?language=en
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Stroke is the example for the respiratory cares in this lecture
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Structures are more stable at rest than when they are working
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Posture effects breathing – better posture = more efficient breathing.
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