Acute Stroke

Part 1: Intro to Stroke

Quick overview of brain perfusion
Types of stroke and the risk factors for each
Introduction to infective endocarditis (IE)
Part 2: Acute Stroke Care
Manifestations of stroke
Immediate bedside actions
Diagnosis and immediate treatments
Part 3: Nursing Care After an Acute Stroke
Preventing and identifying acute and subacute complications
1

The focus of these notes is on the nursing responsibilities related to caring for a patient
in the acute stroke period in a hospital setting. We will not be exploring rehabilitation
and maintenance care in the post-acute period.

American Heart Association. (2021). Infective Endocarditis. AHA.

https://www.heart.org/en/health-topics/infective-endocarditis

Canadian Stroke Best Practices (2018; 2022). Recommendations.

https://www.strokebestpractices.ca/en/recommendations/

Chu, V. (2023). Prevention of endocarditis: Antibiotic prophylaxis and other measures—

UpToDate.

Rizza, S. (2023). Inflammatory and structural heart disorders In J. Kwong, C. Reinisch, J.

Tyerman, S. Cobbett, D. Hagler, M. Harding, & R. Dottie (Eds.), Medical surgical nursing
in Canada: Assessment and management of clinical problems (5th Canadian ed., pp.
872-897). Elsevier Canada.

Paulin, M. (2023). Nursing Management: Stroke. In J. Kwong, C. Reinisch, J. Tyerman, S.

Cobbett, D. Hagler, M. Harding, & R. Dottie (Eds.), Medical surgical nursing in Canada:
Assessment and management of clinical problems (5th Canadian ed., pp. 1485-1510).
Elsevier Canada.

McCarron, M., Goldstein, L. & Matchar, D. (2023). Screening for asymptomatic carotid
artery stenosis. UpToDate

1
 Part 1: Basics of Brain Perfusion
• The brain needs constant supply of blood to deliver glucose and oxygen
to maintain normal function (20% of CO)
• During times of ischemia, the brain can switch to anaerobic metabolism
(but it is VERY ineffective)
• The brain is protected by cerebral autoregulation to maintain cerebral
perfusion pressure (CPP)
• Vessels within the brain can vasodilate/vasoconstrict in order to
maintain constant blood flow (in response to blood gas changes)
• Collateral circulation can also develop to compensate for decreased
cerebral blood flow

Cerebral blood flow autoregulation becomes important when trying to understand how the brain
responds during acute stroke, so let’s briefly review these concepts.

The brain requires a constant supply of oxygen, glucose, and nutrients (via cerebral arteries,
arterioles, and capillaries). Remember what happens when myocardial cells doesn’t get oxygen?
Anaerobic metabolism kicks in to provide the cells energy in times of ischemia. The brain doesn’t do
this very effectively, so brain cells begin to die within 4 minutes of not getting oxygen (you’ll learn
more about this process in Patho 2)

Because of this poor ability to use anaerobic metabolism, the brain is protected by cerebral
autoregulation defined as “the maintenance of constant cerebral blood flow despite changes in
cerebral perfusion pressure” (International Anesthesia Research Society, 2017). This local control of
BP in the brain is done via vasodilation and vasoconstriction in response to changes in carbon
dioxide levels in the blood (these levels may be affected locally as in local ischemia/infarct or
systemically). For example: If hypoxia or hypercapnia develops, the cerebral arteries/arterioles will
vasodilate (in an attempt to increase blood flow).

Cerebral perfusion pressure is the difference between intracranial pressure and mean arterial
pressure (MAP). This means that the higher the ICP, the higher the MAP has to be to create enough
CPP to maintain cerebral perfusion. We need to ensure the difference between ICP and MAP does
not drop below 60 mmHg. There is an optional video posted describing this process on Learn.

2
 2 Types of Stroke
1) Ischemic
2) Hemorrhagic
A. Thrombotic
B. Embolic

By far, the most common type of stroke is an ischemic stroke- which may be either thrombotic
or embolic. Today, we will focus on ischemic strokes, which make up over 80% of all strokes.
Lucky for you, it is also covered in Patho 2 this term!

Because a central part of acute stroke care is differentiating between hemorrhagic and ischemic
causes, we will be touching on a few key things related to hemorrhagic strokes including the
different risk factors and initial presentation that can help inform which type of stroke may be
happening. Some basic facts about hemorrhagic strokes:
• 15% of strokes
• Bleeding into brain tissue or subarachnoid space
• Results in ↑ICPs
• Discussed in more detail in Acute Conditions in Adults (surgery) and Patho

Stroke can also be caused by a tumor- a primary malignant tumor or metastases. The growing
tumor will press on surrounding vessels and brain cells, resulting in increase ICP, but this is very
rare.

3
 Ischemic Stroke –A. Thrombotic
Partial or total obstruction of a cerebral artery

• Atherosclerotic plaque ruptures and a thrombus forms which

occludes the artery
• Risk factors are basically the same as for coronary artery
disease- this patho is essentially the same.

Temporary obstructions = transient ischemic attacks

(TIAs). Common warning sign for thrombotic stroke.

Ischemia results from either a partial or total obstruction of a cerebral artery due to formation
of a thrombus within the artery/arteriole.

TIA:
• temporary occlusions of cerebral blood flow that results narrowed cerebral arteries due to
atherosclerosis (similar to how angina happens in CAD).
• important warning sign that the pt may imminently experience a thrombotic stroke
• can also be from an embolus that only temporarily occludes an artery
• recurrent, milder TIAs are associated with thrombotic disease as these patients are more
likely to have developed collateral circulation due to chronically decreased blood flow.
• embolic TIAs tend to be singular events with more pronounced symptoms.
• By definition, TIA symptoms resolve within one hour.

NOTE: We cannot know whether neurological symptoms will persist and become a true stroke
or resolve and be labeled a TIA. Because of this, and because stroke risk following TIA is
greatest immediately after the event, it is urgent that individuals seek medical attention
immediately upon symptom onset.

After experiencing a TIA patients should be referred to a Stroke Prevention Clinics (there are
several located in Manitoba).

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 Carotid stenosis

• Important risk factor for both

thrombotic and embolic
stroke
• Commonly associated with
TIAs
• Stenosis may promote
collateral circulation
formation
• May produce a carotid
“bruit” that can be heard on
auscultation
5

Atherosclerosis at the bifurcation of the carotid artery is a risk factor for TIA or stroke. There
can be decreased blood flow due to narrowing of the artery (thrombosis) or a plaque
fragment/clot can dislodge causing an embolus.

Carotid ultrasound (US) is part of standard TIA/stroke assessment, but it is not typically done
during the acute stroke period. Instead, it is part of follow up testing for risk factors.

Part of screening pts at risk for carotid stenosis is auscultating the carotid artery for the
presence of a ‘bruit”. This warning sign can prompt an US and if significant stenosis is present,
the pt can have surgery to remove the plaque (carotid enterectomy) or may undergo
angioplasty and stent placement similar to coronary angioplasty.

If cerebral vascular disease develops slowly through atherosclerosis, this will promote
collateral circulation formation. Collateral circulation provides alternate pathways for
cerebral blood flow. Therefore, these pts often do not experience as significant an infarction
area if they have an acute stroke (i.e., they will have milder neurological impairment)
compared to a patient with healthy cerebral arteries who has a sudden embolic stroke.

5
 Ischemic Stroke –B. Embolic stroke
Partial or total obstruction of a cerebral artery

Cause- Embolus (moving thrombus or other debris) becomes

lodged in a cerebral artery.

May be from carotid plaques as discussed on previous slide,

but most embolic strokes are cardioembolic secondary to:
A. Atrial fibrillation
B. Valvular disease/artificial valves
C. Endocarditis
6

It is important you understand that ALL ischemic strokes are from clots in the ARTERIAL system
and that the end point of any artery is a capillary bed. Therefore, you should recognize the
following principles by “following the clot” as discussed in the Core Concepts notes.

6
 How does AF lead to stroke?
• Thrombus forms in in the left atria
• Moves into LV and into circulation
• Moves into cerebral circulation and
gets stuck in a cerebral artery

As you’ve already learned, atrial fibrillation is the most common cause of cardioembolic stroke.
The reason stroke is far more likely to result from a fib compared to pulmonary embolism is
because the left atrium has a “pocket” or “appendage” where stasis of blood (and therefore
clot formation) is more likely.

The high risk for stroke in patients with sustained/chronic AF is why they need to be
anticoagulated.
As a reminder:
• the oral anticoagulants of choice in pts with good renal function and who do not have
artificial heart valves are the direct oral anticoagulants (DOACs), such as dabigatran,
rivaroxaban, and apixaban.
• these medications are more expensive than warfarin but do not require blood
monitoring for a therapeutic value and have far fewer medication and food
interactions, making them easier to manage for most pts.
• if the pt has significantly impaired renal function (eGFR <30ml/min) or an artificial heart
valve, warfarin is the oral anticoagulant of choice.

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 Endocarditis
• Inflammation of the endocardium and valves

• Can be infective (IE) or non-infective

• In IE, pathogens (bacteria) infect valves

resulting in vegetations to develop

• These vegetations can become emboli

Endocarditis is another risk factor for cardioembolic stroke. It is inflammation of the endocardium and
heart valves that is often categorized as being infective (most common) or non-infective. Any infective
organism (bacteria, virus, or fungi) can lead to IE, but since bacterial is by far the most common, that
will be the focus of the notes.
• Once bacteria is introduced into the blood they can be trapped in the rough, damaged
endocardium where they multiply creating “vegetations”.
• Vegetations consist of fibrin, leukocytes, platelets, and microbes that adhere to the valve surface or
the endocardium. The loss of portions of these friable vegetations into the circulation results
in emboli.
Common reasons for damage to the endocardium/valves:
• Rheumatic heart disease- is a complication of rheumatic fever. Rheumatic fever is an inflammatory
disease that affects connective tissues of the body and commonly affects the endocardium
including heart valves, with the mitral valve being most affected.
• Rheumatic fever most often is the result of an abnormal immune response following a
streptococcal infection (e.g., strep throat). (Heart & Stroke Foundation, n.d.).
Types of “native” valve disorders that predispose patients to IE
• Prolapse and regurgitation- can occur in any valve, but are most common in the mitral valve
• Mitral valve prolapse (MVP)- a structural abnormality of the mitral valve leaflets and the
papillary muscles or chordae that allows the leaflets to prolapse, or buckle, back into the
left atrium during ventricular systole
• Mitral regurgitation (MR) – usually associated with prolapse. Regurgitation is when blood
flows backward from the left ventricle to the left atrium because of incomplete mitral valve
closure during systole. This leads to higher hydrostatic pressure in the LA promoting
pulmonary edema and dilation that contributes to a fib. There can also be decreased CO
from left ventricle=L HF.
• Stenosis- most common in the aortic valve but also common in mitral valve
• Aortic or mitral stenosis= (AS or MS) stiffness and non-compliance of the valve. Most often
age related due to build up of calcifications or rheumatic heart disease. Causes increased
afterload on the chamber where the valve is moving the blood from (so LA for MS, LV for
AS). These conditions can contribute to LV hypertrophy and HF.
• Pulmonic or tricuspid stenosis= most often related to rheumatic fever this can lead to RV
hypertrophy and HF.
Prosthetic valves- just like injured valves, prosthetic valves can also attract pathogens, increasing the
risk of IE. Since native valves (and prosthetic valves) do not have a direct blood supply, it is difficult for
the body to have an immediate and strong inflammatory response, therefore infection can easily
develop.

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 Risk factors for developing IE
• Invasive procedures cause about 25% of all cases ofIE
• Guidelines for prophylactic antibx before high-risk procedures
• highest risk for IE is from invasive dental procedures involving such as tooth
extractions or drainage of a dental abscess
• non-dental procedures that involve incision of known/suspected infectious
tissues may also qualify for prophylactic antibiotics
• IV drug use- bacteria introduced into the venous system so the R side
of the heart (tricuspid and pulmonary valves) primarily affected.

Remember, first, the pt is usually at increased risk for IE because there has been damage to the
endocardium/valves THEN there is the introduction of bacteria into the blood stream as the
second step in the patho. So, on this slide, we are just listing common ways the bacteria gets
into the blood.

Guidelines recommend against routine use of prophylactic antibiotics during respiratory tract,
gastrointestinal, genitourinary, dermatological, or musculoskeletal procedures unless
performed at a known, or suspected infected or colonized site (Chu, 2023).
Older sources will likely have a broader list of recommendations, but these notes are based on
current recommendations. The reason for decreasing the use of prophylactic antibiotics for
these pts is based on research findings related to risk of developing IE vs developing antibiotic
resistant organisms.

Approximately 90 percent of patients with right-sided IE are people who inject drugs due to the
introduction of bacteria and other particulate matter into the venous system. This leads to
depositing of these materials/organisms on the R-side of the heart and the development
endocardial damage- most often affecting the tricuspid valve.

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 Table 39-3
Etiology of IE p.891

10

As you can see, the side of the heart where the vegetations exist will determine where the embolized
vegetations will end up. These emboli arise from left-sided heart vegetations and progress to various
organs (particularly the brain, the kidneys, and the spleen), or leading to arterial infarction of a limb.
Right-sided heart lesions embolize to the lungs. The risk of embolization is greatest within the first few
days of commencing antimicrobial therapy.

10
 Diagnosis of IE
• Clinical history
• Presenting symptoms
• Fever and chills, fatigue, night sweats, abdominal
discomfort
• Heart murmur
• Micro-emboli can lead to
• Petechiae
• Splinter hemorrhage
• Blood cultures
• ECG
• Echocardiogram
11

Obtaining the patient's recent health history is important in assessing IE. Inquiry should be
made regarding any recent (within the past 3–6 months) dental, urological, surgical, or
gynecological procedures. Previous history of use of illicit IV drugs, valvular or congenital heart
disease, intracardiac prosthetic device, recent cardiac catheterization, and skin, respiratory, or
urinary tract infections should be documented.

• Persistently positive blood cultures are the major diagnostic criteria. This means more than
one sample has to be drawn at different times and all samples over time are positive
(meaning there is bacterial in the blood). The most common organism associated with L-
sided IE is Staphylococcus aureus.
• Baseline ECG and subsequent telemetry or serial electrocardiograms- pt’s are at risk for
heart block. An electrocardiogram (ECG) may show first- or second-degree atrioventricular
(AV) block because the cardiac valves lie in proximity to cardiac conductive tissue, especially
the AV node. Cardiac catheterization may be used to evaluate coronary artery patency and
valvular function when surgical intervention is being considered for patients with IE.
• Echocardiography should also be done (may be transthoracic or transesophageal).

The most common manifestations of IE are flu-like symptoms (fever and chills, fatigue, night
sweats), abdominal discomfort, petechiae, and a heart murmur. In untreated cases, HF can
develop (right or left side) and therefore the patient can present with dyspnea and peripheral
edema.

11
 Collaborative Interventions for IE Anticoagulants are
not recommended
Acute IE:
• IV antibiotics (type and duration of tx depends on the organism
identified)
• Antipyretics for fever PRN
• Valve repair/replacement
• Assess for/treat complications -(stroke, HF, PE, sepsis)

Prevention:
• Antibiotics before certain procedures (see previous slide).

12

Acute IE is treated with IV antibiotics (empiric until blood cultures results are known). Surgical
intervention is sometimes required to repair or replace the infected valve. A surgical consult is
recommended for all pts diagnosed with IE. Unless the patient has other reasons to be on
anticoagulants (like atrial fibrillation or a mechanical valve), anticoagulants are not
recommended for patients with IE.

Prophylactic antibiotics before certain procedures as listed on the previous slide.

American Heart Association. (2021). Infective Endocarditis. AHA.

https://www.heart.org/en/health-topics/infective-endocarditis

12
 Part 2: Acute Stroke Care
General Manifestations of Stroke

13

You should be familiar with basic assessments that indicate possible stroke as outlined
on the slide which are those taught to the public from Heart and Stroke.

For the most part, manifestations are similar in hemorrhagic and ischemic stroke, and
variations are more related to which cerebral artery that is affected, the area of brain
that becomes ischemic, and the amount of collateral circulation.
• Manifestations have a sudden onset and are usually unilateral (occur on one side of
the body), with motor deficits being the most obvious. The last point on these
public education messages is to call 911. Calling 911 must be stressed as better for
outcomes compared to being driven to the hospital by a family member. First
responders can initiate “acute stroke protocol” immediately to improve outcomes.

At first detecting signs of stroke, complete an immediate baseline bedside neuro

assessment and NOTE THE TIME OF ONSET-
• Although there are special stroke neuro scales such as the National Institutes of
Health Stroke Scale and Canadian Neurological Scale, in local hospitals we are using
the standard GCS and neuro assessment for pupil size/reactivity, limb strength, and
VS.

Note that pain is NOT a typical manifestation of ischemic stroke. If a severe headache
is present this greatly increases the chance this is hemorrhagic in nature, but this
cannot be known without brain imaging.

13
 Immediate Assessment & Interventions

Ax2
B
C
D
(& Neuro assessment per previous page)

14

Our focus here is on what your actions would be should you find a patient in the hospital environment
with evidence of acute stroke. The importance of having an established stroke protocol for hospitalized
pt is highlighted by the fact that “patients with in-hospital stroke onset underwent intravenous
thrombolysis and endovascular therapies at significantly slower rates with worse functional outcomes
than those with out-of-hospital onset” (Akbik et al., 2020, p. 1486). In Winnipeg hospitals, we generally
call a “code 25” and ideally, a neurologist is included in the initial assessment/guidance of treatment.

ABCDs of Acute Stroke:

Activate Acute Stroke Team/Code or call Code Blue or Code “25” Call for help immediately if you
suspect the pt is having signs of acute stroke.
Airway- Position so airway is patent (elevate HOB- usually 30 degrees) and remove dentures. A head-
tilt/chin-lift or jaw-thrust or an oral airway may be required (if LOC is significantly decreased- not
common in most ischemic strokes). Have suction available and keep NPO. During the acute phase of
stroke, the position of the patient (head and body alignment) is important as a twisted neck or bending
at the waist can impair venous flow from the brain and increase ICP.

Breathing- Assess RR and O2sat. Although gas exchange is not impaired in a stroke (unless airway is not
patent), you should apply oxygen to maintain Sat >94% to prevent vasodilation of cerebral arteries
since vasodilation increases ICP (and remember an increase in ICP= a DECREASE in CPP). NOTE: Even if
the pt has COPD and has an O2 titration order less than 95%- you should increase the O2 when suspecting
acute stroke. You can always ask the MD to clarify how much O2 to give once the stroke code is being
carried out.

Circulation- If conscious, there is no need to palpate a pulse! “Circulation” should mean assessing BP,
HR/rhythm (this means attaching pt to telemetry if available, you can call ECG, but this should not delay
CT scan), temperature, and establishing an IV (2 lines if possible). This is also the time to send blood work
(specific tests discussed later).
Blood pressure control is crucial during the acute phase of stroke. The goal is to keep blood pressure
below 180/105 mmHg but maintain SBP >140s. This is because we need an adequate MAP to ensure
adequate CPP and prevent further ischemia. Also, the blood pressure cannot be moved to the target too
aggressively. We should not lower BP by more than 25 percent, over the first 24 hours with further
gradual reduction thereafter.
Dextrose- Check the patient’s blood sugar at the bedside to rule out hypoglycemia (since it can mimic a
stroke) Treat hypoglycemia using hypoglycemia protocol with parenteral glucose and assess for resolving
symptoms. Hyperglycemia must also be prevented as outcomes worsen in pts with poor glycemic
control.

14
 Diagnosis of a stroke- CT/CTA scan or MRI

• Hemorrhagic stroke- easily diagnosed with CT scan

• Ischemic stroke- may not be seen on CT for 1-2 days
CTA

CT is usually repeated
24-48h post ischemic
stroke

15

Choice of imaging modality should be based on most immediate availability and local resources.
Primary stroke centres should make all efforts to perform combined CT and CTA on patient
arrival.
• The CT and CTA should be done at same time and not in separate visits to the imaging suite.
Stroke centres that cannot do CTA should have pre-planned arrangements for rapid transfer of
appropriate patients.
• They should complete non-contrast CT and offer intravenous thrombolysis as appropriate and
then rapidly transfer the patient to a comprehensive stroke centre for more advanced imaging
and consideration for EVT (Canadian Stroke Best Practices, 2022).

CT-angio or CTA: Though this involves injecting radiocontrast to visualize arteries similar to a
cardiac angiogram, there is a key difference!
In CTA we are ONLY injecting the contrast into a vein and then the scan is timed based on
whether we want to look at arteries or veins. So, unlike coronary angio, there is no
catheter being inserted into an artery, the pt just has a venipuncture. However, in the
procedure called endovascular therapy (ETV-discussed later) a catheter is being threaded
into the femoral artery.

If we do not use contrast, this is referred to as un-infused or non-contrast CT.

• Often, a repeat CT is done 24-48 hours post stroke.

• This is done to identify possible hemorrhagic transformation of ischemic stroke (discussed later
under complications) but this repeat CT can also identify the area of infarct of the ischemic
stroke. When the first CT is done, there will not be any edema present yet and so, the area of
infarct may not be visible. After 24-48 hours edema will have set in at the area and will be more
visible on the CT.

15
Other Diagnostics
AND 12 lead ECG
for everyone
possible telemetry when indicated

Other tests:
Carotid Ultrasound- to check for carotid artery stenosis in setting of TIAs or ischemic CVA
Echocardiogram- may be indicated if cardioembolic stroke suspected (e.g., endocarditis)

None of these tests should delay brain imaging! 16

The tests in white should be done for everyone. Many of these initial tests are related to
ensuring it is safe for the patient to receive thrombolytic therapy
• CBC- baseline hgb, assess PLT
• PTT & INR- required to r/o coagulopathy which may cause hemorrhage & check if INR in
clients on warfarin (AF).
• Electrolytes, Cr/Ur- acute electrolyte abnormalities that would require intervention and
check renal function
• 12-lead ECG to assess cardiac rhythm (telemetry only for those who meet criteria)

Those in green are done based on the situation and are not needed to guide immediate
treatment. Remember, you have already done a bedside BG check, so the lab is just for
follow-up related to DM as a risk factor.

Brain imaging to r/o hemorrhage is the most critical for guiding treatment so any of these
other diagnostics can wait if they will delay imaging. This includes not waiting for renal
function tests if the patient is to get an infused CT- we have to prioritize “neurons over
nephrons”. If the patient has known CKD, then the physician will weigh risks and benefits of
waiting.

16
 Treatment of Ischemic Stroke
Goal: Re-establish Blood Flow=
“Reperfusion Techniques”

IV Thrombolytics (tPA) Endovascular therapy (EVT)

Within 4.5 hours Within 6 hours 17

The priority is to re-establish blood flow by removing the clot. This can be done using
thrombolytic medications or by physically removing the clot using EVT.

17
 Thrombolytics-”clot busters”
Alteplase (tPA) and Tenecteplase (TNK)

Inclusion criteria for tPA for all pts:

✓Diagnosis of ischemic stroke (hemorrhagic and TIA ruled out)
✓Clearly definable time of onset- within 4.5 hours
✓ At least 18 years old

See table for variation in timing based on risk vs benefit. 18

Thrombolytic treatment can reduce the risk of disability and death, despite the risk of
serious bleeding (CSBP, 2022).
• most common thrombolytic: alteplase, a tissue plasminogen activator (tPA)
• tenecteplase (TNK) was recently approved for use in stroke; also commonly used in MI.
• thrombolytics “lyse” any thrombus in the body, placing the patient at a high risk of
bleeding.
• inclusion and exclusion criteria can vary between facilities- below are the guidelines from
Canadian Stroke Best Practices.

This table is just to illustrate the various considerations taken related to time frames- you do not
need to memorize the details...just get the general idea.

18
Thrombolytics- Exclusion criteria
Absolute Exclusion Criteria
Active hemorrhage or risk of major hemorrhage
Relative Exclusion Criteria (requires clinical judgement)
Historical
History of intracranial hemorrhage.
Stroke or serious head or spinal trauma in the preceding three months.
Major surgery, in the preceding 14 days
Arterial puncture at a non-compressible site in the previous seven days.
Clinical - *Treatable and pt may still get tPA
Symptoms suggestive of subarachnoid hemorrhage
PLTs < 100 (N=150-450)
*Stroke symptoms likely due to another condition such as seizure or hypoglycemia
*Hypertension >180/105
*Patient taking anticoagulants
*INR>1.7, or elevated PTT
*BG<2.7 or > 22.2 19

First, the patient must meet the INCLUSION criteria on the previous slide. From there, we look
at possible reasons thrombolytics may pose more risk than harm.
These are guidelines and there is clinical judgement also applied by the MD/team in
determining the risk vs benefit balance. Some of the exclusion criteria are temporary and
reversible. For example, we can treat the BP, reverse the INR, treat hypoglycemia and monitor
response and the pt could still get tPA if these parameters resolve. If the INR can be reversed
to less than <1.7 (with vit K for example) a pt may be able to get tPA. The use of DOAC makes
things a bit more complicated as described below.

Intravenous thrombolytic administration for patients on DOACs: Intravenous thrombolytics

should not routinely be administered to patients on DOACs who present with acute ischemic
stroke. In comprehensive stroke centres with access to specialized tests of DOAC levels and
reversal agents, thrombolysis could be considered, and decisions should be based on individual
patient characteristics, in consultation with thrombosis specialists, patients, and their families.
a. Anticoagulation is not a contraindication for EVT, and the decision to treat should be based
on individual patient factors and assessment of benefit and risk.
b. Patients who present with stroke who are taking a DOAC may be considered for rapid
reversal if otherwise eligible for IV thrombolysis and if a reversal agent is readily available.
Consultation with an expert in stroke care in strongly advised for these cases.

19
 Endovascular therapy
Inclusion criteria:
• >18 years old
• therapy should initiated within 6 hours of onset of symptoms
• neurovascular imaging to determine eligibility (CTA)
Procedure:
• procedural sedation similar to coronary angio in most cases
• cerebral artery is accessed via radial or femoral artery
• clot is removed
• the patient can still receive thrombolytics in addition to EVT

20

HSC is designated as the stroke center for Manitoba and EMTs are directed to transport pts
with suspected acute stroke to HSC. There is an endovascular interventional program and
specialists available. An officially dedicated acute stroke unit is supposed to be in the works
(Manitoba is the only province currently without one ).

Risks associated with this therapy:

• Intracranial hemorrhage due to vessel perforation (ripping the blood vessel) or stent
retriever device perforating a vessel while attempting to remove the blood clot from the
artery.
• Systemic bleeding related to thrombolytics (which can also be administered to the clot with
the catheter during EVT)
• Bleeding at the arterial site of catheter introduction

20
 Post therapy care…
• Although tPA lessens disability and decreases mortality r/t stroke, it greatly
increases the risk of bleeding, including intracranial hemorrhage=
“hemorrhagic transformation”

Post tPA & EVT care:

Monitoring is dictated by protocols and focuses on neurological and
hemodynamic assessments
• Pt needs remain on bedrest for a period post cannulation for EVT
• No invasive procedures for 12 hours post tPA
• No antiplatelets or anticoagulants for 24 hours post tPA

21

Potential complication connection: Risk for acute bleeding!

• Are you familiar with the signs of both intracranial and systemic (usually GI) bleeding?

Pts who are on anticoagulants for atrial fibrillation and experience acute ischemic stroke:
• If on warfarin, look at INR trends
• If on a DOAC, assess medication adherence or possible interactions affecting therapeutic levels
of anticoagulation

When anticoagulation is restarted post-stroke depends on the size and severity of the stroke.
- TIA: anticoagulation can be started right away
- Small ischemic stroke: restart within 3 days
- Larger ischemic stroke: restart in about one week
- Severe ischemic stroke: wait up to two weeks

21
Part 3: Nursing care in the immediate post-stroke period
• Maintaining cerebral perfusion
• positioning
• fever, pain
• fluid balance, constipation
• acute causes of altered perfusion: hemorrhagic transformation and cerebral edema

Prevention or early identification of other complications:

• Acute systemic bleeding
• DVT & PE
• Aspiration pneumonia
• UTI/other acute infection
• Seizures
22

Maintaining cerebral perfusion:

Positioning: position to promote venous drainage, such as elevating the head of the
bed, maintaining head and neck in alignment, and avoiding hip flexion.
Fever: contributes to increased cerebral metabolism and increase O2 demand,
worsening ischemia. Administer antipyretic such as acetaminophen (rectally if NPO).
Aggressive management of temperature during the first 24 hours after a stroke
improves outcomes. Other conditions that increase SNS activity and cerebral cell
activity should be treated (pain, agitation).
Manage other conditions that increase ICP or cerebral edema like constipation and
hypervolemia
Hemorrhagic transformation and cerebral edema- discussed on next slide

Bleeding- GI bleeding risk will vary from pt to pt. Obviously tPA and anticoagulants increase the
risk but consider the pt’s other risk factors such as history of previous gastrointestinal bleeding
or risk for GI ulcers.
Deep vein thrombosis & pulmonary embolism: The risk of DVT (and therefore PE) is elevated
in the first one to three months after stroke, due in part to stroke-related immobility. PE
accounts for up to 25% of all deaths post-stroke. Prophylaxis should include thigh-length
intermittent pneumatic compression (IPC) or sub-cut heparin (if pt got tPA, wait at least 24
hours).
Aspiration pneumonia- covered on next few slides
UTI: incontinence common. Indwelling urinary catheters should be avoided
Seizures- occur in less than 10% of stroke patients and is most prevalent in the first 24 hours.
Acute management with IV benzodiazepines is most common.

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 “Early neurologic deterioration” in ischemic stroke
• Hemorrhagic Transformation: fragile/weak arteries
distal to occlusion are re-perfused and may “rupture”
resulting in a hemorrhagic stroke. Risk factors include:
• tPA recipient
• Large infarct
• Age >70
• Anticoagulant use
• Cerebral edema: cytotoxic edema at infarct as part of
the inflammatory response to injury
• Can cause subtle to severe neurological decline depending on
size of original infarct. Usually peaks at 72h.

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Early neurologic deterioration (END) after acute stroke occurs in 2 to 38 percent of patients and is
associated with poor outcomes. Because it cannot be known what is causing a sudden and significant
decline in neurological status after stroke, we should start the acute stroke protocol all over again
from the beginning when there is evidence of neurological deterioration. If changes are more subtle,
there may be no need for intervention and a “wait and see” approach may be used. However, ANY
decline in neurological status in the acute stroke period should be brought to the attention of the MD
as we want to catch complications early.
Hemorrhagic transformation: Cerebral arteries at the site of infarction and distal to it become weak
and frail, making them prone to hemorrhage once blood flow is restored. Hemorrhagic transformation
(HT) is more likely in elderly pts, those who experienced large ischemic infarcts and received tPA, and
in pts who were started on anticoagulants post-stroke. Sometimes called hemorrhagic “conversion” as
well, this is essentially a hemorrhagic stroke and if significant, can cause sudden and rapid
neurological decline. However, most cases of hemorrhagic transformation are small and do not cause
any symptoms. Often asymptomatic HTs are found on the 24-48h post-infarct CT and if present, it may
complicate post-stroke anticoagulation.
For significant intracranial bleeding, cryoprecipitate, fresh frozen plasma, or tranexamic may be
considered case-by-case basis. Prothrombin complex concentrate and platelet transfusions are not
currently recommended.
Cerebral edema- Is common post stroke and most often is not serious. It is cytotoxic in nature and the
amount of edema is primarily influenced by the size of the original infarct. Increased ICP from cerebral
edema usually peaks in 72 hours and can be severe enough to cause brain herniation in very large
infarcts. When severe, it is referred to as “malignant cerebral edema”.
If ICP continues to rise (ICP becomes very high), a characteristic set of manifestations arise called
Cushing’s Triad:
1. Increased systolic blood pressure to increase blood flow to ischemic brain, which further increases
ICP and compresses brainstem leading to
2. Bradycardia
3. Irregular respiratory rate
Note that is these signs are present, the prognosis is very poor.

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Aspiration Pneumonia - p.602 Lewis
• Prevention is key
• Identifying those at risk (dysphagia, on tube feed, etc.)
• NPO until screened for dysphagia
• Reducing oral bacterial load of oral cavity
Pneumonia Manifestations:
• Preventing GI reflux
• Possible history of
• Positioning
aspiration (in past 48-72 h)
• If we cannot prevent, then detect early • Dyspnea/tachypnea
• Decreased oxygen sat
• Fever
Breath sounds?
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Potential complication connection: Aspiration pneumonia can interfere with oxygenation

and also lead to sepsis. Because aspiration pneumonia can occur within 48-hours of the initial
stroke, it is included under the acute complications here, but we also discuss specifics related
to tube feeding later in the context of ongoing risk for complications in the recovery period.

• Even while NPO, there is the risk for aspiration if the pt has dysphagia.
• Aspirating one’s own saliva or gastric reflux contents are common causes of
aspiration pneumonia.
• Therefore, mouth care, positioning, etc. are essential even while NPO.

Note, it usually takes 48-72 hours for aspiration pneumonia to develop after aspiration
occurs.
• if a pt has a choking episode, we cannot know if this will develop into pneumonia and
doing an x-ray or sputum culture at this time will not be of any use.
• Although the pt may have some immediate respiratory distress related to the
aspiration event, they will not have adventitia consistent with pneumonia
(evidence of consolidation), fever, etc. until the inflammatory response has kicked
in, which takes time.
• Your priority in the immediate post-aspiration period is to:
• monitor the pt more closely in the 72 hour period after the incident for early
evidence of pneumonia
• Assessing why the pt aspirated and if there needs to be any alteration in the plan
of care to prevent it from happening again

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 Subacute complications
1. Orthopedic/mobility related complications
• risks vary depending on stage of hemiparesis (flaccid→spastic)
• shoulder subluxation**
• skin breakdown
2. Malnutrition
3. Communication disorders (aphasia)
4. Specific Sensory–Perceptual Alterations (unilateral neglect)
5. Depression, anxiety, emotionalism and coping
6. Incontinence
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Most of these complications are prevented or addressed by basic supportive nursing care. We will
not be going into each in detail. For example, principles for prevention of skin breakdown should
already be familiar to you, so will not be reviewed here.
• Early in acute stroke, the affected side may be paralyzed (hemiplegia) and will usually be
flaccid (no muscle tone). Milder strokes and for those who underwent reperfusion therapy, the
affected side may just be weak (hemiparesis).
• Later in the recovery period (timeframe varies from person to person), muscle spasticity sets
in. Interventions differ depending on the stage the person is in.

Primary prevention of complications related to impaired mobility is to mobilize as early and often
as possible as directed by PT/OT.
• ROM, proper positioning, and use/application of supportive devices may be delegated to HCAs,
but the nurse should ensure the proper technique is being used.
• Signage at the beside with reminders may be helpful.

Specific to shoulder subluxation:

Joint protection strategies should be applied when flaccid muscle paralysis/weakness is present.
Without muscle tone, the shoulder joint can be partially pulled out of the socket (subluxation) due
to the weight of the pt’s arm.
To prevent subluxation:
• Position and support the arm during rest in a neutral position- may use a hemi-tray, arm
trough, or pillow to support arm
• Do not move shoulder beyond 90 degrees of flexion or abduction
• Avoid pulling on the affected arm
• Support arm during transfers- sling may be recommended by OT
• Note: Although the use of slings is recommended during the flaccid stage, they are
discouraged beyond this stage as long-term use may discourage arm use, inhibit arm swing,
and contribute to contracture formation

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 2. Malnutrition post-stroke
and Clinical implications of TFs
• rapid infusion of feeds can cause diarrhea,
leading to dehydration
• dehydration can also be r/t ↓free H20
• BG management & drugs that are taken with
meals may need adjustment
• tube feed volume should be considered when
calculating I/O

Tube feeds (and dysphagia)

increase the risk of aspiration
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Swallowing assessment to determine which type of feeding is needed should be done within 24 hours for
stable patients.
• early tube feeding (within 3 days of stroke) is associated with reduced mortality
• risk for aspiration has been found to be similar for NG and percutaneous feeding tubes (e.g., PEG/GT)
• PEGs are less likely to have issues with occlusion and dislodgement and reduce exposure to radiation from
x-ray compared to NG feeding.
• if needing enteral feeding for more than a couple of weeks, a PEG may be recommended.
Remember some key points:
• TFing requires MD or RD order
• Most pts will begin with continuous tube feeding (via pump) at slow rate while tolerance is assessed (helps
reduce issues like diarrhea and reflux). Rate is gradually increased per order
• If the tube ends in the stomach (gastric)- continuous OR bolus feeds may be delivered by pump or gravity.
*Bolus gastric feeds via a PEG are the goal for long-term tube feeding maintenance for most patients.
• If the tube ends in the small bowel (jejunum, duodenum)- SBFT- these can ONLY be done as continuous
feeds and must be to a pump.
Reducing complications related to tube feeding:
Positioning: minimum 30 degrees, sitting upright preferred for bolus feeding. If needing to lie pt flat, or other
changes in position that could increase the risk for aspiration in a pt with a continuous TF running, flushing and
disconnecting the tube is a reasonable precaution- just know that doing this frequently/for long periods
could increase the risk for malnutrition.
Monitoring for gastric residual volume (GRV): remember this is only relevant if the pt is getting GASTRIC
feeding, there is no residual volume measured in SBFTs. The risk for aspiration from high GRV has to be
weighed against malnutrition. Follow hospital policy related to re-feeding and holding the TF based on GRV.
“Free water” flushes: It is essential that pts receive enough free water to prevent hypernatremia/dehydration,
but we also need to ensure we are not putting pts at risk for FVE into overload. Monitoring fluid and
electrolyte balance is important during the early stages especially as sodium imbalances can also influence
cerebral edema. If pt was on an IV for hydration before TF prescribed, this can usually be discontinued once
TF started.
Medication and BG management: Pts may require changes to medications, but most can be given in the tube.
Some will need to be crushed, others only dissolved. If in doubt, check unit resources/pharmacy.
Pts who have a continuous TF and are prescribed SUBCUT insulin: only basal and correction insulins should
be prescribed. Remember, being on a TF is not a reason to have IV insulin!
• Risk for hypoglycemia if TF becomes interrupted. Apply your principles of glucose management.

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 2. Malnutrition
Decreasing the risk of aspiration for a patient who
is eating
• Sitting up (90 degrees) chin down is the ideal position for feeding
• A quiet, calm environment with few distractions
• Ensure the patent is well rested and alert
• Offer/encourage small bites, chew on the unaffected side (if
paralysis is an issue), don’t mix textures, don’t “wash down” food
with fluid
• Post-meal- provide mouth care, remain upright
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Not all patients with dysphagia will require TFs obviously. Some are prescribed an oral diet in
the immediate post stoke period while many will start on TFs and the transition to an oral diet.

The first few oral meals in a pt with dysphagia should always be administered by the RN and not
delegated to the HCA. This is because the nurse should assess tolerance and safety, which is out
of scope for a HCA.
• have suction available
• ensure the pt is alert
• position at >90 (leaning forward- chin tucked) to stop gravity from pulling food down airway

Misconception alert! Often students will say we position a patient upright to eat to allow
gravity to help with swallowing. This is actually the OPPOSITE of what we want! We put the
person upright and leaning forward slightly with chin tucked down to PREVENT gravity from
moving the food/fluid. The idea is we want the pt’s muscles to be in control of when swallowing
takes place. So having the food/fluid placed more forward with chin down allows the pt time to
initiate the muscles needed for the voluntary phase of swallowing. After the bolus has been
swallowed, then having the pt upright can help reduce the incidence of reflux into the
esophagus, so this is when gravity is “our friend” in preventing aspiration, but NOT during the
swallowing phase.

If the patient begins coughing/gagging during feeding:

• Stop feeding, lean pt forward
• Allow pt to try to clear own airway
• Inspect mouth for pocketed food and suction if necessary
• Check VS (especially oxygen saturation) and auscultate chest
• Notify the physician and document incident with a plan for increasing related assessments

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 3. Communication Disorders: Aphasia
• May be expressive, receptive or global (affecting both)
• Approaches will be individualized by SLP. Some basics are for expressive
aphasia are:
• Minimize distraction and ensure eye contact before speaking
• Speak in normal tone and volume
• Use simple questions that can be answered with “yes” or “no.”
• Pt will need extra time to process and respond, avoid repeating
questions
• Use alternate forms of communication such as gestures or picture
boards as appropriate
• The patient should be given time to process information and generate
a response before a question or statement is repeated
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Like other manifestations, the location of the infarct will dictate the type of severity of
communication disorders. Overt communication issues, such as aphasia (difficulty
understanding and expressing language) are more common in pts who had infarcts in the left
side of the brain.

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 4. Specific Sensory–Perceptual Alterations

• Unilateral neglect is the most common

• Initially safety is key- ensure pt has items
on unaffected side
• Rehab involves teaching client how to
overcome neglect

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The most common type of visual perception disorder following stroke is visual neglect or
inattention which affects an average of 32% of patients following stroke. Homonymous
hemianopia refers blindness in the same half of each visual field which contributes to
“unilateral neglect”. Often this perceptual deficit will improve over time, so as the pt
recovers/is rehabilitated, the interventions will change. Basic therapeutic approaches to treat
neglect include remedial approaches (e.g., visual scanning, feedback or cueing, virtual reality,
and mental practice), and compensatory approaches (e.g., prisms, half-field, eye-patching, limb
activation).

Basics to include in the plan of care per Nursing Care Plan 60-1 from Lewis:
Immediate acute period: priority is safety
• Position bed in room so that individuals approach and care for patient on unaffected side.
• Rearrange the environment so pt can see essential items easily (call bell, etc.)
• Touch unaffected shoulder when initiating conversation to attract patient's attention.

As pt recovers, focus is on rehabilitation and adjusting to deficits:

• Instruct patient to scan from left to right to visualize the entire environment.
• Gradually move personal items and activity to affected side as patient demonstrates an
ability to compensate for neglect.
• Include caregiver(s), family member(s), or both in rehabilitation process to support the
patient's efforts and assist with care to promote reintegration with the whole body.

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 5. Depression, Anxiety, Emotionalism and Coping
• All patients should be screened for depression and anxiety
• Often a “watchful-waiting” approach will be used at first rather than
starting medications. Nurse should assess mood and document as part
of tx plan.
• Emotional and behavioural changes may occur. Education of pt and
family about neurological basis important.
• Excellent discharge planning is essential for ensuring adequate supports
and ability for pt and family to cope in the recovery period.
• Stroke recovery planning requires most members of the multidisciplinary
team. The nurse has essential role in coordination and integration of
care plan.
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Pseudobulbar affect causes pt to display emotional responses that do not align with current
emotional state (e.g., laughing when upset, crying when happy). This condition is more common
in neurodegenerative disorders such as ALS and MS but can be seen is some pt’s post stroke.

Interventions for atypical emotional responses are to

a) Explain to the patient and family that emotional outbursts may occur after a stroke
b) Encourage family and pt to share this with others to avoid misunderstandings
c) Avoid shaming or scolding the patient during emotional outbursts (e.g., tell family to avoid
saying things like, “Why are you laughing? This is not funny.”)
d) Distract the patient by using touch, or encouraging the pt to change position when having
an emotional episode

Coping: Proper discharge planning can increase the ability for pt and family to cope with self-
management. This will be a team approach with the nurse acting as a coordinator of overall
patient care plan which will include input from the MD, PT, OT, HC, SLP, and SW.

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 6. Incontinence
• In the acute stroke period, close to 75% of pts will experience urinary
incontinence
• Indwelling catheters should be avoided
• Post-void residual volumes help diagnose type of incontinence and
treatment (intermittent catheterization may be needed)
• Most recover continence by one year time, but about 30% will have
some degree of incontinence
• Bowel incontinence is rare but is associated with poor bowel
management in the acute period (chronic constipation/impaction)
• Inability to self manage will affect discharge planning
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All individuals who have had a stroke should be screened for urinary incontinence and retention
(with or without overflow), fecal incontinence, and constipation. If urinary incontinence is
present, the cause should try to be narrowed down and an individualized plan developed.

Things for the RN to incorporate into the plan of care

• Incorporating pt’s elimination plan consistently, reinforcing with other staff (bladder
routines, etc.)
• Prevention of skin breakdown and pressure injury
• Frequent assessment for signs of urinary tract infection (UTI)
• Fall risk for pts mobilizing to BR (urgency/frequency combined with fear of incontinence
increases risk for those with mobility or sensory limitations). However, we should encourage
use of a commode or toilet rather than a bedpan, if safe to do so as this promotes better
bladder emptying and is better for pt’s overall rehab.

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In Summary
• All test questions will be taken from these notes pages
• There is a Learning Activity posted which combines applying your
knowledge related to stroke in addition to DM and ESKD. Feedback is
embedded.
• Let me know if you have any questions related to the content or the
learning activity.

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