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Strokes: Understanding the Different Types

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Contact Hours: 3

This online independent study activity is credited for 3 contact hours at completion.

Course Purpose   

The purpose of this course is to provide healthcare providers with an overview of the types of strokes and their presentations, treatment options, and how to differentiate between transient ischemic attack, strokes, and Bell’s palsy.

Continuing Education Credit Designation   

This educational activity is credited for 3 contact hours at completion of the activity.

Overview

Stroke is a heterogeneous syndrome, and determining risk factors and treatment depends on the specific pathogenesis.In comparison, transient ischemic attacks and Bell’s palsy symptoms can mimic a stroke, however there are key identifiers that can help the healthcare professional differentiate between the diagnoses. This course provides an overview of the different types of strokes and their interventions and treatments, transient ischemic attacks, and Bell’s palsy.

Objectives

By the end of this learning activity, the learner will be able to: 

  • Differentiate between ischemic stroke and hemorrhagic stroke.
  • Identify key factors of a transient ischemic attack.
  • Recognize the difference between stroke and Bell’s palsy.
  • Understand the use of FAST in identifying stroke symptoms.
  • Review treatment options as recommended by the American Stroke Association guidelines.

Policy Statement   

This activity has been planned and implemented in accordance with the policies of FastCEforless.com.

Disclosures  

Fast CE For Less, Inc. and its authors have no disclosures. There is no commercial support.

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Definitions
AneurysmA dilatation in the wall of an artery supplying blood to a specific area. 
Arteriovenous MalformationAn abnormal tangle of blood vessels where the arterial blood bypasses capillaries and reaches the veins.
Blood-Brain Barrier (BBB)A layer of cells keeps your brain safe from pathogens and other toxins. 
Brudzinski SignA symptom of meningitis that occurs when the neck is flexed forward and the knees and hips bend involuntarily.
Carotid EndarterectomyA procedure to treat carotid artery disease.
Computerized Tomography (CT)A scan that combines a series of X-ray images taken from different angles around the body and uses computer processing to create cross-sectional images (slices) of the bones, blood vessels and soft tissues inside the body. 
HematomaA solid swelling of clotted blood within the tissues.
Hemorrhagic StrokeCaused by bleeding in the brain from a ruptured blood vessel.
Intracerebral Hemorrhage (ICH)A blood vessel in the brain ruptures and causes bleeding inside the brain. 
Intracranial Pressure (ICP)A measurement of the pressure of brain tissue and the cerebrospinal fluid that cushions and surrounds the brain and spinal cord.
IsodenseEvenly or uniformly dense.
Kernig SignA physical maneuver used to evaluate an individual for a suspected case of meningitis, a condition characterized by inflammation of the membranes that surround the brain and spinal cord. 
Level Of Consciousness (LOC)A medical term used to describe how awake, alert, and aware a person is.
Magnetic Resonance Imaging  (MRI)Provides precise details of your body parts, especially soft tissues, with the help of magnetic fields and radio waves.
MeningismusA state of meningeal irritation with symptoms suggesting meningitis, such as stiff neck, headache, photophobia, and sometimes visual blurring, tinnitus, and vertigo.
Moya-Moya DiseaseA progressive blood vessel disorder where the carotid artery in the skull is blocked or narrowed reducing blood flow to the brain. 
Patent Foramen Ovale (PFO)A small hole between the left and right atria (upper chambers) of the heart remains open after birth
Reactive Oxygen Species (ROS)Molecules capable of independent existence, containing at least one oxygen atom and one or more unpaired electrons.
Stroke A disease process that affects the arteries leading to and within the brain.
Subarachnoid Hemorrhage (SAH)Bleeding within the subarachnoid space, which is the area between the brain and the tissue covering the brain. 
Transesophageal Echocardiogram (TEE)A type of ultrasound test that produces pictures of your heart and its internal structures
Introduction

Stroke is a heterogeneous syndrome, and determining risk factors and treatment depends on the specific pathogenesis.It is characterized by either a blockage of blood vessels, where clots form in the brain and interrupt blood flow, or a rupture of blood vessels causing them to break, which leads to intracerebral bleeding.1 Rupture of the brains blood vessels during stroke results in a lack of oxygen to the brain and death of brain cells.1 Stroke can also lead to depression and dementia.1

Although stroke mortality has decreased in the United States during the past 2 decades, recent trends indicate that these decreases may have leveled off and that stroke mortality may be rising again.3 The morbidity associated with stroke remains high, with costs estimated at $34 billion per year for healthcare services, medications, and missed workdays.3 The prevalence, danger, and severity of the disease make it crucial for patients, nurses, and other healthcare professionals to be aware of the pathophysiology of the disease, its different types, and treatment options. This course will cover the risk factors, different types, signs and symptoms, diagnosis, and management options for nurses and primary healthcare professionals. 

Stroke Types

There are two major types of strokes:

  • Hemorrhagic stroke
  • Ischemic stroke

Hemorrhagic Stroke 

Hemorrhagic stroke is caused by bleeding in the brain from a ruptured blood vessel.6 It accounts for approximately 10–15% of all strokes and has a high mortality rate.1 In this condition, the stress in the brain tissue and internal injury cause blood vessels to rupture. It produces toxic effects in the vascular system, resulting in infarction.1

Hemorrhagic stroke may be further subdivided into intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH).6 

  • ICH is bleeding into the brain parenchyma6
  • SAH is bleeding into the subarachnoid space6

The common sites of the bleed are the basal ganglia (50%), cerebral lobes (10% to 20%), the thalamus (15%), pons and the brain stem (10% to 20%), and the cerebellum (10%).6 The hematoma disrupts the neurons and glia. This results in oligemia, neurotransmitter release, mitochondrial dysfunction, and cellular swelling. Thrombin activates microglia and causes inflammation and edema.6 The primary injury is caused by compression of the brain tissue by a hematoma, resulting in an increase in intracranial pressure (ICP).6 The secondary injury is caused by inflammation, disruption of the blood-brain barrier (BBB), edema, overproduction of free radicals such as reactive oxygen species (ROS), glutamate-induced excitotoxicity, and release of hemoglobin and iron from the clot.6

Ischemic Stroke

Most strokes are ischemic strokes.4 An ischemic stroke occurs when blood clots or other particles block the blood vessels to the brain.4 They contribute to around 85% of casualties in stroke patients, with the remainder caused by intracerebral bleeding.1

 It is caused by either a thrombotic or embolic event that reduces blood flow to the brain.5

In a thrombotic event, the blood flow to the brain is obstructed within the blood vessel because of dysfunction within the vessel itself, usually secondary to atherosclerotic disease, arterial dissection, fibromuscular dysplasia, or inflammatory condition.5 In an embolic event, debris from elsewhere in the body blocks blood flow through the affected vessel.5 The etiology of stroke affects both prognosis and outcomes.5

Other key events contributing to stroke pathology are inflammation, energy failure, loss of homeostasis, acidosis, increased intracellular calcium levels, excitotoxicity, free radical-mediated toxicity, cytokine-mediated cytotoxicity, complement activation, impairment of the blood-brain barrier, activation of glial cells, oxidative stress, and infiltration of leukocytes.1

Transient Ischemic Attack

A transient ischemic attack (TIA) differs from other types of major strokes and is referred to as a “mini-stroke” because blood flow to the brain is blocked for only a short time, usually no more than an hour.4 It is a medical emergency and a transient episode of neurologic dysfunction from focal brain, spinal cord, or retinal ischemia without acute infarction or tissue injury.7 An evaluation of a TIA should be done urgently with imaging and laboratory studies to decrease the risk of subsequent strokes.7

As stated above, a TIA typically lasts less than an hour, more often minutes and can be considered a serious warning of an impending ischemic stroke as the risk is highest in the first 48 hours following a transient ischemic attack.7

Transient ischemic attack subtypes, classified according to pathophysiological mechanisms, are similar to ischemic stroke subtypes.7 They include: 

  • Cardiac embolism
  • Large artery atherothrombosis
  • Small vessel (lacunar)
  • Uncommon subtypes such as vascular dissection, vasculitis, etc. 
  • Unknown cause

Signs and Symptoms

During a stroke, every minute counts, and faster reaction time can help lessen the brain damage that a stroke can cause.8 Thus, it is important to be aware of the common signs and symptoms so that any individual can take quick action.8

Signs and symptoms of stroke include:8,9,10

  • Difficulty swallowing (dysphagia)
  • Dizziness and confusion
  • Loss of consciousness
  • Problems with balance and coordination
  • Sudden confusion or trouble speaking or understanding speech
  • Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.
  • Sudden severe headache with no known cause
  • Sudden trouble in seeing in one or both eyes
  • Sudden trouble walking, dizziness, loss of balance, or lack of coordination.

The best stroke treatments are available only if the stroke is recognized and diagnosed within 3 hours of the first symptoms.8 Stroke patients may not be eligible for treatments if the diagnosis is not made within the timeframe.8 

There is a F.A.S.T test that can help you remember what look for in a person experiencing a suspected stroke.8,9,10

F – Face: Ask the person to smile. Does one side of the face droop?

A – Arms: Ask the person to raise both arms. Does one arm drift downward?

S – Speech: Ask the person to repeat a simple phrase. Is the speech slurred or strange?

T – Time: If you see any of these signs, call 9-1-1 right away

If stroke symptoms disappear after a few minutes, a TIA may have occurred8 Because TIAs resolve, many people ignore them. But paying attention to a TIA can save a person’s life.8 It’s a serious warning sign of a problem with the blood supply to the brain and means there is an increased risk of having a stroke in the near future.10

Stroke Risk Factors

The risk of stroke increases with age and doubles over the age of 55 years in both men and women.1 The risk is further increased when an individual has an existing medical condition like hypertension, coronary artery disease, or hyperlipidemia.Nearly 60% of strokes are in patients with a history of transient ischemic attack (TIA).1 

Risk factors for stroke are categorized by modifiable and non-modifiable factors.1,3

Non-Modifiable Risk Factors

Nonmodifiable risk factors (also called risk markers) for stroke include age, sex, race, and genetics.3 In general, stroke is a disease of the aging population.3

Age

Recent research has indicated that people aged 20–54 years are at increased risk of stroke when pre-existing secondary factors are present.1

Sex

The relationship between sex and stroke risk depends on age. Women have a higher risk of stroke at young ages than men, however, with the progression of age, the relative risk is slightly higher for men.3

Race

There are well-documented racial disparities in stroke.3 Research shows that Hispanic and Black populations are at higher risk of stroke than White population and the  incidence of hemorrhagic stroke is significantly higher in African Americans than in age-matched White populations.1

Genetics

Genetic factors are known to be both modifiable and nonmodifiable risk factors for stroke, with parental history and family history increasing the risk.1,3 The following are some of the mechanisms that increase the risk of stroke.1,3

  • A parental or family history of stroke increases an individual’s chance of developing this neurological disorder. 
  • A rare single gene mutation can contribute to pathophysiology in which stroke is the primary clinical manifestation, such as cerebral autosomal dominant arteriopathy. 
  • Stroke can be one of many after-effects of multiple syndromes caused by a genetic mutation, such as sickle cell anemia. 
  • Some common genetic variants are associated with increased stroke risk, such as genetic polymorphism in 9p21.

Modifiable Risk Factors 

The modifiable risk factors are of utmost importance, as intervention strategies to reduce these factors can subsequently reduce the risk of stroke. Early identification and modification of risk factors are imperative.3 

The major modifiable risk factors for stroke are hypertension, diabetes, lack of physical exercise, alcohol and drug abuse, high cholesterol, diet management, and genetics.1,3

Hypertension

Hypertension is the most important modifiable risk factor for stroke, with a strong, direct, linear, and continuous relationship between blood pressure and stroke risk.3 In one study, a blood pressure (BP) of at least 160/90 mmHg and a history of hypertension were considered equally essential predispositions for stroke, with 54% of the stroke-affected population having these characteristics.1

Regardless of hypertension status, blood pressure rises with age, thereby increasing the lifetime risk of developing hypertension.3

Treatment of hypertension through medication or lifestyle changes remains one of the most effective strategies in reducing stroke risk.3

Diabetes

Diabetes mellitus is an independent risk factor for stroke, with a 2-fold increased risk of stroke for diabetic patients. Diabetes accounts for ≈20% of stroke related deaths.3 Prediabetics are also at increased risk of stroke.3 

Moreover, the prognosis for diabetic individuals after a stroke is worse than for non-diabetic patients, including higher rates of severe disability and slower recovery.1 Tight regulation of glycemic levels alone is ineffective; medical intervention plus behavioral modifications could help decrease the severity of stroke for diabetic individuals.1

Atrial Fibrillation 

Atrial fibrillation (AF) has long been recognized as a major risk factor for stroke, which has only increased with the aging of the US population.3 The incidence of strokes related to AF has nearly tripled in the past  three decades.3 Atrial fibrillation contributes to 15% of all strokes and produces more severe disability and higher mortality than non-atrial fibrillation related strokes.1 Atrial fibrillation strokes are often caused by decreased blood flow in the left atrium, which results in a collection a blood and thrombosis, resulting in an embolism that travels to the brain. 1

Alcohol and Drug Abuse

The relationship between stroke risk and alcohol intake follows a curvilinear pattern, with the risk related to the amount of alcohol consumed daily.1 

  • Low to moderate consumption of alcohol (≤2 standard drinks daily for men and ≤1 for women) reduces stroke risk, whereas high consumption of alcohol increases it. In contrast, even low consumption of alcohol escalates the risk of hemorrhagic stroke.1
  • Regular use of illegitimate substances such as cocaine, heroin, phencyclidine (PCP), lysergic acid diethylamide (LSD), cannabis/marijuana, or amphetamines is related to an increased risk of all subtypes of strokes.1 

Hyperlipidemia 

Hyperlipidemia is a major contributor to coronary heart disease, but its relationship to stroke is complicated.1 Total cholesterol is associated with the increased risk of stroke, whereas high-density lipoprotein (HDL) decreases stroke incidence.1 Therefore, evaluation of lipid profile enables estimation of the risk of stroke.1

Smoking

Cigarette smoking remains a significant risk factor for stroke, nearly doubling the risk with a dose-response relationship between pack-years and stroke risk.3 Smoking is estimated to contribute to ≈15% of all stroke deaths annually.3

Research suggests that an individual who stops smoking reduces the relative risk of stroke, while prolonged second-hand smoking results in a 30% increase in the risk of stroke.1

Poor Diet 

Insufficient physical activity and poor diet are associated with an increased risk for stroke.1 Insufficient physical activity is also linked to other health issues like elevated blood pressure, obesity, and diabetes, all related to high stroke incidence.Likewise, certain dietary components are well known to heighten risk, such as excessive salt intake, which is also linked to hypertension.1 

A diet high in fruit and vegetables is recommended and has been shown to decrease the risk of stroke.1

How Strokes are Diagnosed

Stroke diagnosis is based on symptoms, medical history, physical exam, and test results.11

Ischemic Stroke History and Physical 

Ischemic strokes present acutely, and establishing the time of symptom onset is critical.5 If the time of symptom onset is unknown, the time the patient was last known to be without new neurological symptoms is used. The established time is then utilized to decide whether giving intravenous thrombolytics is indicated.5

Moreover, a neurological exam should be performed for all patients suspected of stroke.5 The National Institutes of Health Stroke Scale (NIHSS) is most commonly used to measure the severity of the stroke and has 11 categories and a score that ranges from 0 to 42.5 The 11 categories include the level of consciousness (LOC), which incorporates LOC questions evaluating the following:5

  • Best gaze
  • Visual
  • Facial palsy
  • Motor arm
  • Motor leg
  • Limb ataxia
  • Sensory
  • Best language
  • Dysarthria
  • Extinction
  • Inattention

The stroke scale should be performed in the order listed. Each score is based on the patient’s action on the exam, and it is not a prediction of what the patient’s prognosis.5

Evaluation 

An organized stroke protocol is highly recommended to expedite evaluation.5

The initial evaluation of any patient is airway, breathing, circulation, and vital signs.5 Patients may present with respiratory abnormalities from elevated intracranial pressure and are at risk of aspiration and asphyxiation.5 In such cases, endotracheal intubation may be necessary to ensure adequate oxygenation and ventilation.The Following should also be performed when a stroke is suspected:

  • A fingerstick glucose check should be performed, as it is an easy way of ruling out hypoglycemia as a cause of neurological abnormalities.5
  • A plain Computerized tomography (CT) head or brain magnetic resonance imaging (MRI) is recommended for patients within 20 minutes of acute care presentation to rule out hemorrhage.5
  • Acute ischemic stroke can be seen on diffusion-weighted MR sequence. The FLAIR sequence helps predict the time since the onset of the stroke, which is of paramount importance in planning thrombolytic therapy in the patient.5
  • Other diagnostic tests include an electrocardiogram (ECG), troponin, complete blood count, electrolytes, blood urea nitrogen (BUN), creatinine (Cr), and coagulation factors.5

Hemorrhagic Stroke History and Physical 

The common presentations of stroke are headache, aphasia, hemiparesis, and facial palsy.6 The presentation of hemorrhagic stroke is usually acute and progressive.6 

Acute onset headache, vomiting, neck stiffness, increases in blood pressure, and rapidly developing neurological signs are the common clinical manifestations of hemorrhagic stroke.6

Symptoms of hemorrhagic stroke can lead to the extent and location of hemorrhage.6 For instance, vomiting indicates raised intracranial pressure and is common with cerebellar hematoma. Seizures, aphasia, and hemianopia are seen in lobar hemorrhage, and headache is more common in a large hematoma.6

Cerebellar Hemorrhage

Cerebellar hemorrhage produces symptoms of raised ICP, such as lethargy, vomiting, and bradycardia.6 Progressive neurological deterioration indicates the enlargement of hematoma or increased edema.6

Subarachnoid Hemorrhage

The clinical features of subarachnoid hemorrhage are severe headaches described as a thunderclap, vomiting, syncope, photophobia, nuchal rigidity, seizures, and decreased level of consciousness.6 Signs of meningismus, such as the Kernig sign (pain on straightening the knee when the thigh is flexed to 90 degrees) and Brudzinski sign (involuntary hip flexion on flexing the neck of the patient), may be positive.6

Evaluation 

Computerized tomography (CT) is usually the initial investigative tool and is considered the “gold standard” in detecting acute hemorrhage due to its sensitivity.6 However, gradient echo and T2* susceptibility-weighted magnetic resonance imaging (MRI) has the same sensitivity as CT to detect acute hemorrhage. These sequences are more sensitive than CT for the identification of prior hemorrhage.6

In the subacute phase, the hematoma may be isodense to brain tissue, and MRI may be necessary.6 An MRI can distinguish between the hemorrhagic transformation of infarct and primary hemorrhage and can detect underlying causes of secondary hemorrhages, such as vascular malformations, including cavernomas, tumors, and cerebral vein thrombosis.6

Other diagnostic tools include:6

  • Extravasation of contrast in CT angiogram (CTA) indicates ongoing bleeding associated with fatality. 
  • Multidetector CT angiography (MDCTA) helps rule out the causes of secondary hemorrhagic stroke such as arteriovenous malformation (AVM), ruptured aneurysm, dural venous sinus (or cerebral vein) thrombosis (DVST/CVT), vasculitis, and Moya-Moya disease.
  • Four-vessel digital subtraction angiography (DSA) is necessary in the case of SAH.

Blood investigations such as bleeding time, clotting time, platelet count, peripheral smear, prothrombin time (PT), and activated partial thromboplastin time(aPTT) will detect any abnormality of bleeding or coagulation and any hematological disorder which can cause hemorrhage.6 Moreover, liver function tests and renal function tests are also needed to exclude any hepatic or renal dysfunction as a cause.6

Transient Ischemic Attack History and Physical 

Transient ischemic attack symptoms often resolve by the time the patient presents to the hospital.7 The history of the present illness should include onset, duration, timing, complete neurological symptoms, associated symptoms, and any aggravating or relieving factors.7

The history should include etiological clues such as a history of atrial fibrillation, recent myocardial infarction to suggest a cardioembolic source, and transient loss of vision like a curtain rising or descending will suggest an internal carotid artery problem.7 Moreover, the presence of any cortical symptoms, such as language disturbance or visual field loss, will point to a cortical TIA rather than a lacunar syndrome.7

The physical examination should focus on identifying focal neurological deficits and speech disturbances which are the most common presenting symptoms in patients with TIA.7 Other evaluation areas include:7

  • Cranial nerve examination to yield findings of monocular blindness, disconjugate gaze, facial droop, hemianopia, diplopia, abnormal tongue movement, difficulty swallowing, and auditory dysfunction. 
  • Some of the motor findings include unilateral weakness in the upper or lower extremities, face, and tongue, increased tone, clonus, rigidity, and abnormal reflexes that could occur with TIA. 
  • Cardiac examination and carotid auscultation for a carotid bruit are very important. 
  • Fundoscopy is important to look for any fundoscopic evidence of vascular changes resulting from hypertension or diabetes.

Evaluation 

The 2022 AHA/ASA guidelines include “neuroimaging within 24 hours of symptom onset and further recommend MRI and diffusion-weighted MRI imaging as preferred modalities.”7

A head CT, preferably with a CT angiogram, is recommended if an MRI cannot be performed.7 However, brain MRI with diffusion-weighted imaging has a greater sensitivity than CT for detecting small infarcts in patients with TIA.7 

In candidates for a carotid endarterectomy procedure, carotid imaging should be performed within 1 week of the onset of symptoms.7 Cardiac assessment should be done with ECG, Transesophageal echocardiogram (TEE) to find a cardioembolic source and the presence of patent foramen ovale (PFO), valvular disease, cardiac thrombus, and atherosclerosis.7

Routine blood tests, including complete blood count (CBC), PT/INR, CMP, FBS, lipid panel, urine drug screen, and ESR, should be considered.7

ABCD2 Score

The ABCD2 score is very important for predicting subsequent risks of TIA or stroke.7 The ABCD2 score was derived from providing a more robust prediction standard. The ABCD2 score includes factors including age, blood pressure, clinical symptoms, duration, and diabetes, such as:7

  • Age: older than 60 years (1 point)
  • Blood pressure greater than or equal to 140/90 mmHg on first evaluation (1 point)
  • Clinical symptoms: a focal weakness with the spell (2 points) or speech impairment without weakness (1 point)
  • Duration greater than 60 min (2 points), or 10 min to 59 min (1 point)
  • Diabetes mellitus (1 point)

Results of the ABCD2 score are evaluated as:7

  • The 2-day risk of stroke was 0% for scores of 0 or 1, 1.3% for 2 or 3, 4.1% for 4 or 5, and 8.1% for 6 or 7. 
  • Most stroke centers will admit patients with TIA to the hospital for expedited management and observation if the score is 4 or 5, or higher. 
  • For patients with a lower score, expedited evaluation and management are still warranted. This expedited approach has been proven to improve the outcome.
Difference Between Stroke and Bell’s Palsy

Bell’s palsy (BP) is the most frequent diagnosis linked to facial nerve palsy/paralysis as well as the most frequent acute mono-neuropathy.12 It affects individuals across multiple ages and both sexes, with an annual incidence ranging from 11.5 to 53.3 per 100,000 persons.12 

The diagnosis of Bell’s palsy can be challenging, especially as there are many differential diagnoses, including trauma, neoplasm, and infection.13 This is due to the facial nerve’s both complex and convoluted journey from its origin in the pons through the cranium until it branches superficially to supply motor function to the 18 muscles of facial expression.13

For many clinicians, acute stroke remains a concerning diagnosis in patients presenting with facial palsy, but there are key characteristics that facilitate the differentiation of the two conditions, often without the need for further investigations.13

For instance, understanding the origin and route of cranial nerve CN VII through the nervous system, its adjacent anatomical structures, and a detailed history helps narrow down the differentials and pinpoint a diagnosis.13

Table 1: Typical presentation of Bell’s palsy compared to acute stroke

Characteristics Bell’s palsyAcute stroke
Age, years30–50Usually >60
Symptom time courseProgressive; over hours or daysSudden; over seconds or minutes
Unilateral facial paralysisYesYes
Upper faceAlways affectedUsually not affected
Lower faceAlways affectedAffected
Ability to close eye on asymptomatic sideNot likelyLikely
Ear or TMJ area painLikelyNot likely
HyperacusisLikelyNot likely
Decreased lacrimation, salivation or change in tasteLikelyNot likely
Pupils affectedNot likelySometimes
Arm or leg weaknessNot likelyLikely
Speech or vision affectedNot likelyLikely

Initial assessment of any patient must involve establishing the onset characteristics and duration of the facial palsy.13 Here, the timing and progression of Bell’s palsy help distinguish it from an acute cause such as stroke.13 

A key feature is the progressive nature of Bell’s palsy, which can be elucidated by detailed history taking. The nurse must also check for recent trauma, surgery, or infection.13

Determining whether the facial nerve paralysis is central or peripheral is also key to diagnosis.13 A full cranial nerve examination, as well as ocular, otologic and oral examinations, must be carried out in all patients presenting with facial palsy.13 Moreover, neuroimaging should only be reserved for those patients with other associated physical findings suggestive of a central lesion (such as paralysis of other cranial nerves, associated limb weakness, or ataxia) or those whose symptoms have not resolved despite appropriate treatment.13

Treatment Interventions for Strokes

Ischemic Stroke

The goal of therapy in acute ischemic stroke is to preserve tissue in areas where perfusion is decreased but sufficient to avoid infarction.5

Levels of Care

Hospitals have differing capabilities in terms of treatment of acute ischemic stroke, and an international consensus exists on levels of care 1 through 3.14

  • Level 1 stroke centers have the full spectrum of endovascular care, do a minimum number of mechanical thrombectomies, have dedicated neurointensive care and stroke units, and have full neurosurgical services.14 
  • Level 2 requires at least 100 stroke patients a year, a stroke unit, and a minimum of 50 mechanical thrombectomies, but neurointensive and neurosurgical services are not required.14
  • Level 3 requires only a minimum of 50 patients a year and a stroke unit.14

The following treatment options are considered for ischemic stroke:

Alteplase

The American Heart Association/American Stroke Association (AHA/ASA) recommends intravenous (IV) alteplase for patients who satisfy inclusion criteria and have symptom onset or last known baseline within 3 hours.5 Inclusion criteria include diagnosis of ischemic stroke with “measurable neurological deficit,” symptom onset within 3 hours before treatment, and age 18 years or older.5

Intravenous alteplase dose is 0.9 mg/kg, with a maximum dose of 90 mg.5 The first 10% of the dose is given over the first minute as a bolus, and the remainder of the dose is given over the next 60 minutes. The time has been extended to 4.5 hours for selected candidates.5

Tenecteplase

Tenecteplase is another tissue plasminogen activator, which has been shown to have a higher affinity for fibrin and a longer half-life than alteplase.14 It is widely used for acute coronary events and has a lower rate of systemic hemorrhage than alteplase in that setting.14 

The 2019 AHA/ASA acute stroke management guidelines gave the following guidance for tenecteplase: “Tenecteplase administered as a 0.4-mg/kg single IV bolus has not been proven to be superior or non-inferior to alteplase but might be considered as an alternative to alteplase in patients with minor neurological impairment and no major intracranial occlusion.”14 

Mechanical Thrombectomy 

In recent years, there has been significant advancements in acute stroke care.5 Multiple stroke trials in 2015 showed that endovascular thrombectomy in the first six hours is much better than standard medical care in patients with large vessel occlusion in the arteries of the proximal anterior circulation.5 These benefits are sustained irrespective of geographical location and patient characteristics.5

In 2018, the DAWN trial showed significant benefits of endovascular thrombectomy in patients with large vessel occlusion in the arteries of the proximal anterior circulation.5,14 This trial extended the stroke window up to 24 hours in selected patients using perfusion imaging. Subsequently, now more patients can be treated, even up to 24 hours.5

The current recommendation in selected patients with large vessel occlusion with acute ischemic stroke in the anterior circulation and who also meet other DAWN and DEFUSE 3 criteria, mechanical thrombectomy is recommended within the time frame of 6 to 16 hours of last known normal.5 In selected patients who meet the DAWN criteria, mechanical thrombectomy is reasonable within 24 hours of the last known normal.5 

Blood Pressure

Management of blood pressure in acute ischemic stroke must balance multiple factors, including elevated pressures to improve tissue perfusion, with the consideration of the increased the risk of hemorrhage or secondary damage to already infarcted areas of the brain.14 It is recommended to lower the BP initially by 15% in patients with comorbid conditions such as acute heart failure or aortic dissection.5

Oxygen Management

The AHA/ASA guidelines recommend supplemental oxygen to maintain O2 saturation above 94%.14 Some debate has taken place about whether all patients should be treated with supplemental oxygen in the acute stroke setting.14

Temperature

  • Hyperthermia of greater than 38oC should be avoided and treated appropriately.5 
  • Antipyretics such as acetaminophen may be used.5 
  • Common sources of infection should be ruled out, such as pneumonia and urinary tract infections.5 

A retrospective study recently demonstrated an association between a peak temperature in the first 24 hours of greater than 38oC (100.4 F) and an increased risk of in-hospital mortality.5

Nutrition 

  • Early enteral feeding should be encouraged. For patients with dysphagia, use a nasogastric tube to promote enteral feeding.5 
  • If there is concern that the patient may have swallowing difficulties for a prolonged period (more than 2 to 3 weeks), placing a percutaneous gastrostomy tube is recommended.5
  • Early feeding has been demonstrated to have an absolute reduction in the risk of death.5

Hemorrhagic Stroke 

Following are the different treatment options for hemorrhagic stroke:

Hemostatic Therapy

Hemostatic therapy is given to reduce the progression of hematoma. This is especially important to reverse coagulopathy in patients taking anticoagulants.6 Vitamin K, prothrombin complex concentrates (PCCs), recombinant activated factor VII (rFVIIa), fresh frozen plasma (FFP), etc., should be considered.6

The American Stroke Association (ASA) recommends that patients with thrombocytopenia receive platelet concentrate, and patients with elevated prothrombin time INR receive intravenous vitamin K and FFP or PCCs.6 

  • FFP has the risk of allergic transfusion reactions.6 
  • PCCs are plasma-derived factor concentrates containing factors II, VII, IX, and X. PCCs can be reconstituted and administered rapidly.6

Management of Raised Intracranial Pressure

The initial treatment for raised intracranial pressure (ICP) is elevating the head of the bed to 30 degrees and using osmotic agents (mannitol, hypertonic saline). Mannitol 20% is given at a dose of 1.0 to 1.5 g/kg.6

The ASA recommends monitoring ICP with a parenchymal or ventricular catheter for all patients with Glasgow coma scale (GCS) <8 or those with evidence of transtentorial herniation or hydrocephalus.6

Antiepileptic Therapy

Approximately 3-17% of patients will have a seizure in the first two weeks following a stroke, and 30% of patients will show electrical seizure activity on EEG monitoring.6 Those with clinical seizures or electrographic seizures should be treated with antiepileptic drugs.6 

Lobar hematoma and the enlargement of hematoma produce seizures associated with worsening neurological status. Subclinical seizures and nonconvulsive status epilepticus can also occur. Continuous EEG monitoring is indicated in patients with a decreased level of consciousness. Otherwise, according to ASA guidelines, prophylactic anticonvulsant medication is not recommended.6 

Blood Pressure

Blood pressure should be reduced gradually to a minimum of 150/90 mmHg using beta-blockers (labetalol, esmolol), ACE inhibitor (enalapril), calcium channel blockers (nicardipine), or hydralazine.6 During treatment, the blood pressure should be checked every 10-15 minutes.6

The ASA recommendation for patients presenting with a systolic blood pressure (SBP) between 150 and 220 mmHg is to have the SBP lowered to 140 mmHg, as it is safe and can improve functional outcomes.6 For patients presenting with a SBP greater than 220 mmHg, an aggressive reduction of blood pressure with a continuous intravenous infusion is recommended.6

Surgery

The different types of surgical interventions for hemorrhagic stroke include craniotomy, decompressive craniectomy, stereotactic aspiration, endoscopic aspiration, and catheter aspiration.6

  • Emergency surgical evacuation is indicated in cerebellar hemorrhage with hydrocephalus or brainstem compression.6
  • Patients with cerebellar hemorrhages of >3 cm in diameter will have better outcomes with surgery.6
  • Cerebellar hematoma is evacuated by suboccipital craniectomy.6
  • Decompressive hemicraniectomy with hematoma evacuation is performed in patients with GCS scores of 8 or less and large hematomas with a volume greater than 60 ml (fig.5).6 It reduces mortality and may improve functional outcomes.6

Cerebroprotection

The secondary injury of hemorrhagic stroke comprises inflammation, oxidative stress, and toxicity of erythrocyte lysates and thrombin.6 Strategies to reduce secondary injuries are being tried, such as:6

  • Pioglitazone, misoprostol, and celecoxib are to reduce inflammatory damage. 
  • Edaravone, flavonoid, and nicotinamide mononucleotide to reduce oxidative stress. 
  • The iron chelator deferoxamine is also in the experimental phase.
  • The calcium channel blocker nimodipine to improve outcomes in SAH by a neuroprotective effect.

Transient Ischemic Attack 

The main aim of treatment of TIA is to decrease the risk of subsequent stroke or TIA.7 Early treatment after a TIA can significantly reduce the risk of early stroke.7 

Post TIA, the risk of stroke within 3 months has been reported to be around 20%, with approximately 50% of these strokes occurring within the first 2 days after the initial presentation.7 It is extremely important to evaluate the vessel status and look for atrial fibrillation when a patient experiences a transient ischemic attack. This will significantly reduce future strokes.7

Studies have shown that a combination of diet, exercise, antiplatelet, statin, and antihypertensive therapy may reduce the subsequent risk of stroke after a TIA by 80-90%.7

Post-Stroke Complications

For many stroke survivors and their families, an acute stroke is the beginning of an ongoing struggle with physical impairment and subsequent disability.15 Over time, the immediate clinical consequences of the stroke may be complicated by a variety of unanticipated medical, musculoskeletal, and psychosocial difficulties.15 

Thus, early screening and appropriate management are key, and the healthcare professional is best positioned to optimize chronic disease control, reduce risk, and manage complications of a stroke.15

Table 2: long-term complications post-stroke15

Medical ComplicationsCharacteristics 
Post-stroke seizuresTreat with conventional anticonvulsants. Seizure advice: general safety advisory, driving, and operating machinery.
Urinary Incontinence Exclude exacerbating/precipitating risk factors. Consider oxybutynin in selected patients and indwelling catheters as a last resort.
Bowel IncontinenceReview of medications, improving diet/fluid intake, using drugs such as codeine phosphate with a twice weekly enema or loperamide to reduce the frequency of incontinence. 
Cognitive Impairment Control of risk factors to prevent a recurrence. Physical and cognitive stimulation.
Spasticity And Hypertonicity Physiotherapy, splinting, positioning of limbs. Systemic drugs include baclofen, dantrolene, diazepam, tizanidine, and botulinum toxin in selected cases.
Hemiplegic Shoulder PainProper handling and positioning. Refer to physiotherapy and simple analgesic, transcutaneous electrical nerve stimulation in selected patients.
Wrist And Hand FlexionActive and passive physiotherapy. Ready-made or custom-made splints.
Post-Stroke DepressionSelective serotonin reuptake inhibitors (SSRIs) are commonly used. Psychological counseling is helpful but often underused.
Emotional Lability Therapeutic trial of antidepressants, especially SSRIs.
Mood/Emotional ChangesStroke and caregivers support groups may be helpful.

Late medical complications of stroke occur weeks to months after discharge from the hospital.15 Some stroke survivors go on to develop these complications years after the acute stroke.15

Post-Stroke Rehabilitation

Rehabilitation helps someone who has had a stroke relearn skills that are suddenly lost when part of the brain is damaged.16 Equally important in rehabilitation is to protect the individual from developing new medical problems, including pneumonia, urinary tract infections, injury due to falls, or a clot formation in large veins.16

As stated above, many medical complications and disabilities can arise post-stroke depending on the degree of the stroke and the part of the brain that was affected, such as paralysis, sensory disturbances, problems with thinking and memory, problems with understanding language, and emotional disturbances.16  

Rehabilitative therapy typically begins in the acute-care setting once the condition has stabilized, often within 48 hours after the stroke.16

The first steps often involve promoting the independent movement to overcome any paralysis or weakness. A therapist will help with assisted or self-performed range of motion exercises to strengthen and increase mobility in stroke-impaired limbs.16 A stroke victim may need to learn how to sit up, move between the bed and a chair, and to stand and walk, with or without assistance. Beginning to reacquire the ability to carry out basic activities of daily living, such as bathing, dressing, and using a toilet, represents the first stage in return to independence.16

With the surge in technological advances over the past 10 years, the number of stroke rehabilitation randomized control trials has increased, which plays a significant role in stroke management.16 Some examples include:

  • Telerehabilitation: A
  •  home-based telehealth system designed to improve motor recovery and patient education post-stroke.16
  • Sleep-SMART (Sleep for Stroke Management and Recovery Trial) will determine whether treatment of sleep-disordered breathing with positive airway pressure after acute ischemic stroke or high-risk transient ischemic attack prevents recurrent stroke.16
  • The multi-site I-ACQUIRE trial in infants with perinatal arterial stroke will determine the effectiveness of intensive infant rehabilitation to increase upper extremity skills.16
Nursing Considerations

Nurses often have difficulties with using interdisciplinary stroke guidelines for patients with stroke as they do not focus sufficiently on nursing. Therefore, the Stroke Nursing Guideline (SNG) was developed and implemented.17

The Stroke Nursing Guideline (SNG) aims to provide an overview of evidence-based recommendations for the daily nursing care and rehabilitation of patients with stroke.17 The SNG was developed based on systematic reviews and studies focusing on the following areas: 

  • Depressive symptoms
  • Education
  • Falls
  • Mobility and activities of daily living 
  • Pain

The SNG was critically reviewed by a group of 20 interdisciplinary professional experts on the guideline’s readability, layout, and usability.17 The final SNG includes a total of 23 recommendations focusing on assessment and therapeutic interventions categorized in the following areas:17

  • Activities of daily living and mobility and falls (14 recommendations)
  • Pain/shoulder pain (3 recommendations)
  • Depression (3 recommendations)
  • Patient education (2 recommendations)
  • Discharge planning (1 recommendation)

The SNG guidelines were created to improve the care provided by a nurse to the patient who has experienced a stroke.17 The guidelines include patient and family teaching, and ancillary staff education, which significantly contributes to the rehabilitation of patients with stroke.17

Conclusion

Stroke is the second leading cause of death and a significant contributor to disability worldwide 1

The last 25 years of stroke research has brought considerable progress with respect to therapeutic drugs, clinical trials, and post-stroke rehabilitation studies, and as a result, survivability and rehabilitation from strokes has improved.

There are many modifiers that increase the risk of stroke, including diet, exercise, history of TIA, genetics, etc., and as such, a nurse must be prepared to quickly identify the signs of stroke (most notably through using FAST), and the treatment options and common interventions implemented to improve patient outcomes.

References
  1. Kuriakose D, Xiao Z. Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. International Journal of Molecular Sciences. 2020;21(20):7609. doi:10.3390/ijms21207609
  2. Feigin VL, Norrving B, Mensah GA. Global Burden of Stroke. Circulation Research. 2017;120(3):439-448. doi:10.1161/circresaha.116.308413
  3. Boehme AK, Esenwa C, Elkind MSV. Stroke Risk Factors, Genetics, and Prevention. Circulation research. 2017;120(3):472-495. doi:10.1161/CIRCRESAHA.116.308398
  4. CDC. About Stroke | cdc.gov. Centers for Disease Control and Prevention. Published May 4, 2022. https://www.cdc.gov/stroke/about.htm#:~:text=There%20are%20two%20types%20of
  5. Hui C, Tadi P, Patti L. Ischemic Stroke. Nih.gov. Published 2019. https://www.ncbi.nlm.nih.gov/books/NBK499997/
  6. Unnithan AKA, Mehta P. Hemorrhagic Stroke. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK559173/
  7. Panuganti KK, Tadi P, Lui F. Transient Ischemic Attack. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK459143/
  8. CDC. Stroke Signs and Symptoms | cdc.gov. www.cdc.gov. Published August 28, 2020. https://www.cdc.gov/stroke/signs_symptoms.htm#:~:text=Sudden%20numbness%20or%20weakness%20in
  9. Stroke – Symptoms | NHLBI, NIH. www.nhlbi.nih.gov. https://www.nhlbi.nih.gov/health/stroke/symptoms
  10. NHS. Symptoms – Stroke. NHS. Published 2019. https://www.nhs.uk/conditions/stroke/symptoms/
  11. Stroke – Diagnosis | NHLBI, NIH. www.nhlbi.nih.gov. Published March 24, 2022. https://www.nhlbi.nih.gov/health/stroke/diagnosis
  12. Zhang W, Xu L, Luo T, Wu F, Zhao B, Li X. The etiology of Bell’s palsy: a review. Journal of Neurology. Published online March 28, 2019. doi:10.1007/s00415-019-09282-4
  13. Induruwa I, Holland N, Gregory R, Khadjooi K. The impact of misdiagnosing Bell’s palsy as acute stroke. Clinical Medicine. 2019;19(6):494-498. doi:10.7861/clinmed.2019-0123
  14. Phipps MS, Cronin CA. Management of acute ischemic stroke. BMJ. 2020;368:l6983. doi:10.1136/bmj.l6983
  15. Chohan S, Venkatesh P, How C. Long-term complications of stroke and secondary prevention: an overview for primary care physicians. Singapore Medical Journal. 2019;60(12):616-620. doi:10.11622/smedj.2019158
  16. Post-Stroke Rehabilitation Fact Sheet | National Institute of Neurological Disorders and Stroke. www.ninds.nih.gov. Published July 25, 2022. https://www.ninds.nih.gov/post-stroke-rehabilitation-fact-sheet
  17. Bjartmarz I, Jónsdóttir H, Hafsteinsdóttir TB. Implementation and feasibility of the stroke nursing guideline in the care of patients with stroke: a mixed methods study. BMC Nursing. 2017;16(1). doi:10.1186/s12912-017-0262-y
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