NEO Stroke Network’s
Acute Nursing Certification
Program
Level ONE
NEO Stroke Network’s
Acute Nursing Certification Program
Launched at Hôpital régional de Sudbury Regional Hospital in the summer and fall of 2010, this program is a regional initiative made available to medical nursing units in the North East for use as a nursing certification Self Learning Program.The program is currently available as a paper copy in a binder that includes all text, pictures, diagrams, tests, references and appendices.
In the future, a paperless, online copy will be available for those nurses who choose to complete this program on a work or personal computer.
The program consists of eight Stroke Care Topics that can be completed in any order and are arranged as separate modules, each with its own quiz. Each module should take 45 minutes to 75 minutes to complete depending on the module and the nurse’s
background/experience. A score of 80% is considered a passing score. Although the answer key will not be posted, it is acceptable that the quizzes be done with an “open book”.
Once initiated, the nurse will be given a set amount of time as determined by the manager to complete all eight modules.
The Nurse Clinician of the unit or a designate will be the official monitor and tracker of the certification program, accepting and marking all the quizzes and issuing Certificates of Completion to each nurse.
The Nursing Certification Program consists of three distinct levels of certification.
Level one is includes eight modules, which are:
1) Neuroanatomy, Pathophysiology and Classification of Stroke 2) Pre-hospital and Emergency Management
3) Diagnostics and Assessments 4) Acute Stroke Management 5) NIHSS Training
6) Swallowing, Feeding and Oral Care
7) Mobility and Positioning for the Stroke Patient (incl the DVD) 8) Secondary Stroke Prevention
Level two ishighly desired for all nurses working in acute stroke care as it is consistent with best practice. It includes training for and certification in an evidenced-based
Swallowing Screen Tool. An example of one is TOR-BSST©. Your centre may not have implemented a tool at this time. At Sudbury Regional Hospital, TOR-BSST training is currently organized by the Speech Language Pathologist whereby the nurse participates in a four hour training session and is observed completing two skilled
TOR-BSST © screens on stroke patients.
Level three is completion of Apex Innovation’s Hemisphere’s Stroke Competency e-learning series. This is a new multi-level; interactive; comprehensive; web based
educational series from pre-hospital stroke management to emergency care to acute care. It has been designed to train all levels of users, from students to physicians.
It has a very comprehensive module on neuroanatomy and pathophysiology of stroke.
Registered users receive a “key” which acts as a one year license to participate in the online series. Users can take as much time as desired to complete each module as long as all modules are successfully completed at the one year mark. The fee for this “key” will be reimbursed to the nurse once he/she has shown their Certificate of Completion for the series to the Nurse Clinician or designate.
Staying current
Each nurse is required to re-certify every two years by completing Level one again and demonstrating a score of 80% or better on each of the module’s quizzes.
The content in the binder (and electronic version) will be reviewed annually and updated according to current Canadian Best Practice Recommendations for Stroke Care and other evidence-based guidelines relevant to the content.
NEO Stroke Network’s
Acute Nursing Certification Program
TABLE OF CONTENTS
1. Acute Nursing Certification Program Description and Process
2. Table of Contents 3. MODULE ONE
Pathophysiology of Stroke, Neuroanatomy, Stroke Syndromes
i) Classification of Stroke ii) Etiology
iii) Brain Anatomy iv) Blood Supply v) Stroke Syndromes vi) References
vii) Module One Quiz 4. MODULE TWO
Pre-Hospital Care and Emergency Management
i) Warning Signs of Stroke ii) Emergency Medical Services iii) Acute Thrombolytic Therapy iv) Adverse Effects of t-PA (Alteplase) v) Stroke Mimics
vi) Acute ASA Therapy
vii) Reducing Ischemic Damage from Hypertension, Hyperglycemia, Hyperthermia, O2 de-saturation
viii) References
ix) Module Two Quiz 5. MODULE THREE
Diagnostics and Assessments
i) Acute Nursing Assessment
ii) Standardized Neurological Assessments (CNS, NIHSS, GCS) iii) Other Assessments
iv) Investigations v) References
vi) Module Three Quiz 6. MODULE FOUR
Acute Stroke Management
i) Stroke Unit
ii) The Team of Professionals iii) Post – Stroke Complications iv) Other Effects of Stroke v) Discharge Planning vi) References
vii) Module Four Quiz
7. MODULE FIVE
NIHSS Training OR CNS Training
8. MODULE SIX
Swallowing, Feeding and Oral Care i) Dysphagia Facts
ii) Normal Swallow iii) Aspiration
iv) Dysphagia Screening v) Dysphagia Diets vi) Feeding Strategies
vii) Indications for Enteral Nutrition viii) Oral Care
ix) References x) Module Six Quiz 9. MODULE SEVEN
Mobility and Positioning
Educational DVD (to be available soon)
i) Considerations
ii) General Principles When Assisting a Stroke Survivor iii) Preventing Injury to the Stroke Survivor and You iv) Hemiplegic Shoulder
v) Aids and Equipment vi) Positioning Techniques
vii) Mobilizing Techniques Including Transfers
viii) DVD: Mobilizing and Positioning a Stroke Survivor ix) References
10. MODULE EIGHT
Secondary Stroke Prevention i) Primary Prevention ii) Lifestyle Modification iii) Medication Management iv) Carotid Intervention
v) Transient Ischemic Attack (TIA) vi) Secondary Prevention Clinic vii) Patient Teaching re: Medications
v) References
v) Module Eight Quiz
11. Hospital - Specific Chart Forms (content will vary for each centre) 12. Other Resources
i) Northeastern Ontario Stroke Network (NEOSN) Info sheet
ii) EVERYTHING STROKE…at your fingertips: an Electronic Toolkit for Health Care Providers (announcement)
iii) Stroke Organizations: Lists and Websites iv) NEOSN Professional Education Fund
13. APPENDICES
i) How to Obtain Level Two Certification
ii) How to Obtain Level Three Certification with Apex Innovations’ Hemisphere’s Stroke Competency Series
14. Acknowledgements
15. Certificate of Completion of LEVEL ONE and
NEO Stroke Network’s
Acute Nursing Certification Program
LEARNING OBJECTIVES
MODULE ONE
Pathophysiology of Stroke
Neuroanatomy
Stroke Syndromes
Upon completion of this module, nurses will be able to define
and/or describe:
Types of Stroke
Etiology of Stroke
General Brain Anatomy
Major Blood Vessels of Cerebral Circulation
Common Stroke Syndromes
Right Sided Clinical Deficits
MODULE ONE
The following content is from the Acute Stroke
Management Resource,
Heart and Stroke
Foundation of Ontario
, Anatomy and Physiology
workshop package.
It has been edited and formatted for the NEO
Stroke Network Self Learning Package
1
Pathophysiology and Anatomy of Stroke
Ischemic stroke
• 80% of all strokes are caused by blockage of an artery resulting in diminished blood flow
• Usually the result of a blood clot, either thrombotic or embolic in nature
• Blockage may also occur because of progressive blood vessel occlusion, due to atherosclerosis, or because of local high pressure collapse of small blood vessels
http://www.strokecenter.org/education
• Approximately 50% of ischemic strokes are due to a thrombosis
Of that 50%, 30% are related to large-vessel disease, especially of the carotid, middle cerebral, or basilar arteries
20% are related to small vessel disease of the deep penetrating arteries, such as the lenticulostriate, basilar penetrating, and medullary arteries (these are known as lacunar infarcts)
2 Medical Illustration © 2010 Nucleus Medical Media, Inc. www.nucleusinc.com
Etiology of Ischemic Stroke
The cause of ischemic stroke can be further classified as one of the
following:
1. Large vessel disease may be classified as:
a) Cardioembolism - often a result of atrial fibrillation or left ventricular damage after myocardial infarction
b) Atherosclerosis - causes a progressive narrowing of the blood vessel through deposit of plaque on the arterial wall.
2. Small vessel disease, known as lacunar infarct, is thought to be the result of occlusion of single, small perforating arteries, located deep in the subcortical areas of the brain.
Hypertension is thought to be a major risk factor associated with lacunar infarcts.
Clot stops blood supply to an area of the brain
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3. Cryptogenic strokes are strokes with no identified cause or etiology.
Cryptogenic strokes are more commonly found in younger population, <45years. (Ionita et al., 2005)
The classic risk factors for stroke are usually absent in cryptogenic stroke patients.
However, Ionita et al (2005) reported that echocardiography studies in these stroke patients showed an increase incidence of Patent Foramen Ovale (PFO) in up to 45% of cases.
Hemorrhagic stroke
• Caused by arterial rupture
• Can damage other brain tissue as a result of increased intracranial pressure and compression of brain tissue
• 20% of all strokes
10% of are due to intracerebral hemorrhage
10% are due to subarachnoid hemorrhage or bleeding from AVM (arteriovenous malformation)
Medical Illustration © 2010 Nucleus Medical Media, Inc. www.nucleusinc.com
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Etiology of Intracerebral Hemorrhage:
1.
PRIMARY hemorrhage
• Hypertension is responsible for approximately 75% of all cases
of primary Intracerebral Hemorrhage (ICH).
• Cerebral amyloid angiopathy (a disease of small blood vessels in the brain with deposits of amyloid protein which may lead to
stroke, brain hemorrhage or dementia) is also a common cause.
• The use of fibrinolytics and anticoagulants make up approximately 10% of all ICH. (Manno et al, 2005)
• Drug abuse may cause sudden and severe elevations in blood pressure resulting in ICH.
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2.
SECONDARY hemorrhage
• Underlying vascular abnormalitiessuch as aneurysm,
arteriovenous malformation are causes of secondary ICH, which makes up approximately 5 % of all ICH.
• Hemorrhagic transformation, secondary bleeding into the infarcted site, is considered by some to be a natural evolution of a stroke and some studies suggest that almost all infarcts have some element of petechial hemorrhage. Hemorrhagic transformation may be influenced by the size, location and cause of the stroke. • The use of antithrombotics including anticoagulants and
thrombolytics increases the likelihood of hemorrhagic transformation.
Cerebrum
The cerebrum is the largest portion of the brain and contains 2 hemispheres.
Theleft hemisphere controls the right side of the body and the right hemisphere controls the left side of the body.
The two hemispheres are joined by the corpus callosum.
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In 97% of the population, the left hemisphere is the dominant hemisphere.
Cerebral Cortex
is
divided into
4 lobes
: Frontal
Parietal
Temporal
Occipital
http://www.strokecenter.org/education
Two important structures are found in the frontal and parietal lobes.
In the posterior portion of the frontal lobe, the primary motor cortex
can be found. This is also referred to as the motor strip and is involved in the ability of the body to move various body parts. Damage to parts of the motor strip may result in symptoms such as paralysis of the face, arm or leg or difficulty speaking.
In the anterior part of the parietal lobe is the primary sensory cortex or sensory strip. It corresponds directly to the body part locations of the motor strip and is involved in the ability to feel or recognize textures.
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Blood Supply to the Brain
Arterial supply is from carotid and vertebral arteries which begin extracranially
http://www.strokecenter.org/education
Internal carotid arteries supply anterior 2/3 of hemispheres
Vertebral and basilar arteries supply posterior and medial regions of hemispheres, brainstem, diencephalon, cerebellum; cervical spinal cord Both the carotid (anterior) and vertebral(posterior) blood supply originates
outside of the cranium from the internal carotid arteries.
The carotid and vertebral arteries enter the cranial cavity via the internal carotid, which come off the common carotids and vertebral arteries which originate from the subclavian arteries.
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The internal carotid arteries and its branches supply 2/3 of the cerebral hemispheres.
The anterior circulation’s major blood vessels are the anterior cerebral and the middle cerebral arteries.
The posterior circulation’s major vessels are the vertebral, basilar and posterior cerebral arteries and supply the medial and posterior sections of the
hemispheres, the brainstem, deep brain structures such as the diencephalon, the cerebellum and the cervical section of the spinal cord.
Circle of Willis
An important structure within the cerebral circulation is the Circle of Willis. It is located at the base of the brain.
The primary purpose of the Circle of Willis is to provide multiple paths of oxygenated blood to the brain.
If any of the major vessels become occluded, the various paths of the Circle of Willis attempt to ensure circulation is maintained.
9
The Circle of Willis is comprised of the following vessels:
Anterior Cerebral Artery
Middle Cerebral Artery
Anterior Communicating Artery
Posterior Cerebral Artery
Posterior Communicating Artery
The Posterior and Anterior Communicating Arteries are responsible for connecting the right and left side blood vessels so that circulation is seamless.
Anterior Circulation
Posterior Circulation
Image courtesy of Communications, Alberta Health Services
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The Anterior Cerebral Artery (ACA) originates from the internal carotid artery and supplies the anterior portion of the basal ganglia, the corpus callosum, the medial and superior portions of the frontal lobe and the anterior part of the parietal lobe.
Permission granted to use image www.cnsforum.com
Legend for picture:
Anterior Cerebral Artery-blue
Middle Cerebral Artery- pink
Posterior Cerebral Artery- green
The key functional areas that receive blood supply from the anterior cerebral artery are:
Primary motor cortex involving the leg and foot areas
The centre for micturation found in the frontal lobe
The motor planning centre found in the frontal lobe
The anterior and middle portions of the corpus callosum
A patient who has a stroke involving the anterior cerebral artery may experience weakness in the leg and foot,difficulties with micturation, difficulties with the ability to plan and carry out tasks such as dressing.
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TheMiddle Cerebral Artery(MCA)arises from the internal carotid artery.
Permission granted to use image www.cnsforum.com
Legend for picture:
Anterior cerebral artery-blue
Middle cerebral artery- pink
Posterior cerebral artery- green
The middle cerebral artery is the largest of the major vessels and supplies blood to over 2/3 of the cerebrum. The MCA has 3 branches and passes laterally under the frontal lobe and between the temporal and frontal lobes. The M1 segment is also referred to as
lentriculostriate arteries and are located in the deeper sections of the brain called the basal ganglia and most of the internal capsule.
http://www.strokecenter.org/education
12
These lentriculostriate vessels are small vessels located deep in the brain and are also a common site for small vessel or lacunar strokes.
The superior branch of the MCA supplies the lateral and inferior frontal lobe and anterior parts of the parietal lobe.
The inferior branch of the MCA supplies the lateral temporal lobe, the posterior parietal lobe and the lateral occipital lobe.
ThePosterior Cerebral Artery(PCA) is responsible for the blood supply for midbrain, hypothalamus and thalamus, posterior medial parietal lobe, corpus callosum, inferior and medial temporal lobe and inferior occipital lobe.
Key Functional Areas
that receive blood supply from the PCA are: Primary visual cortex in the occipital lobe
3rd cranial nerve in the midbrain
Sensory control
Hypothalamus-body temperature control, hunger, thirst, hormone release (Antidiuretic hormone)
Thalamus-relaying messages to cortex, level of arousal, awareness, pain
Communication between the hemispheres
Permission granted to use image www.cnsforum.com Region of Posterior Cerebral Artery
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Legend for picture:
Anterior Cerebral Artery- blue
Middle Cerebral Artery- pink
Posterior Cerebral Artery- green
Patients who experience a stroke in the Posterior Cerebral Artery may present with symptoms such as problems with recognizing objects, visual disturbances, drooping eyelid, inability to move the eye in, up & out, down & out, difficulty maintaining body temperature, abnormal hormone
responses, coma, hyperesthesia
Cerebellum
The cerebellum has its own major blood vessels which originate from the vertebrobasilar vessels. The 3 cerebellar vessels are:
Superior Cerebellar
Anterior Inferior Cerebellar
Posterior Inferior Cerebellar
The major functions of the cerebellum are control of fine motor movement,
coordination of muscle groups and maintaining balance and equilibrium.
Permission granted to use image www.cnsforum.com
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There are 2 syndromes often seen with cerebellar strokes
:
1. Lateral pontine syndrome
Involves basilar and anterior inferior cerebellar artery
Symptoms: ipsilateral ataxia of arm and leg, contralateral weakness of upper and lower extremities, contralateral hemisensory loss - pain and temperature
2. Lateral Medullary Syndrome (Wallenberg Syndrome)
Involves distal and superior medullary artery branches of vertebral artery and the posterior inferior cerebellar artery
Symptoms: Ipsilateral sensory loss-face-pain and temperature, ipsilateral ataxia of arm and leg, gait ataxia, nystagmus, nausea and vomiting, vertigo, hoarseness, dysphagia, contrateral hemisensory loss-pain and temperature, horner syndrome (constricted pupil, partial ptosis, loss of hemifacial
sweating), hiccoughs
Brain Stem
The brain stem receives its blood supply from the posterior cerebral artery and the vertebrobasilar vessels.
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The brain stem is divided into 3 major sections:
Midbrain: major functions include involvement in vision, hearing, eye movement and body movement
Pons: involved in motor control and sensory analysis, level of consciousness, sleep
Medulla: responsible for maintaining vital body functions such as breathing and heart rate
One of the major structures housed in the brain stem are the cranial nerves. While there are 12 cranial nerves, Cranial nerves 1& ll originate in the frontal lobe and will not be discussed in this section.
Cranial nerves lll-Xll originate in the brain stem. Patients that experience a stroke in the brain stem will present with symptoms that involve cranial nerve functions such as swallowing, eye movements, facial expression and tongue movements.
The brain stem serves animportant role as a pathway between the spinal cord and the brain. The afferent and efferent pathways run through the spinal cord and connect with brain centres for interpretation and response to stimuli.
The Reticular Activating System originates in the brain stem and is responsible for our wakefulness and attention. It is a very sensitive system that spans the brain and reacts to interruptions in its ability to work. An expanding stroke will interrupt its ability to keep the patient awake, resulting in the patient presenting with a decreased level of consciousness.
Patients who experience a brain stem stroke may present with any of the following:
Decreased level of consciousness
Ipsilateral lower motor neuron facial weakness or sensory loss
Contralateral hemiparesis
Pupillary changes
Hiccoughs, vertigo
Bilateral motor findings
Diplopia, gaze palsies, intranuclear opthalmoplegia
16 Dysarthria
Ataxia
Collateral Circulation
Collateral circulation is an important feature of the brain and for stroke patients.
Not all blood vessels have the capability to be able to create collateral circulation. Vessels such as the lenticulostriate vessels are terminal vessels
which do not connect with other vessels. Therefore, vessels associated with the lenticulostriate vessels that become occluded will become ischemic.
However, there are vessels that can connect or anastomose with other vessels, creating a redundancy that can permit collateral circulation when one vessel is blocked.
These vessels include:
External and internal carotid via branches of the opthalmic artery
Major intracranial vessels via the Circle of Willis
Small cortical branches of the anterior cerebral, middle cerebral and posterior cerebral and cerebellar arteries
Some stroke may go unnoticed as the collateral circulation has taken over the function of supplying an area of the brain
Thanks to the Circle of Willis, by design, the anterior circulation is connected to the posterior circulation
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Ischemic Stroke: Carotid Syndromes
The carotid arteries and their branches, the anterior and middle cerebral arteries, form the anterior circulation and the vertebral, basilar, posterior cerebral arteries and their branches form the posterior circulation.
Clinical stroke syndromes depend on the area of the cerebral circulation disrupted.
Typically, the anterior or carotid circulation stroke syndromes present with
symptoms that include
sensory or motor deficits
aphasia
cortical sensory loss
apraxia or neglect
visual field deficits or retinal ischemia
Ischemic Stroke: Vertebrobasilar Syndrome
Strokes affecting the posterior circulation or vertebrobasilar system, present with symptoms such as
Diplopia
Vertigo
Coma at onset
Crossed sensory loss
Bilateral motor signs
Isolated field defect
Pure motor and sensory deficit
Dysarthria
Dysphagia
Ischemic Stroke: Lacunar Syndromes
Makes up 25% of all ischemic strokes Presumed to be occlusion of single small perforating artery
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Blood vessel: lenticulostriate branches of the Anterior Cerebral and Middle Cerebral Arteries
http://www.strokecenter.org/education
Lacunar infarction results from infarction of one of the lenticulostriate vessels, the penetrating branches of the circle of Willis, the MCA stem, or vertebral or basilar arteries.
Type of Syndrome
Patient Presentation
Pure motor hemiparesis
Results from an infarct in the internal capsule or pons
Contralateral Hemiparesis of face, arm and leg, dysarthria
Contralateral motor hemiparesis with motor aphasia
Results from an infarct of the left frontal area with cortical involvement
Hemiparesis of face, arm and leg with inability to speak
Ataxic hemiparesis
Results from an infarct in the pons
Paresis of the contralateral leg and side of the face, ataxia of the contralateral leg and arm
19 Dysarthria and clumsy hand syndrome
Results from an infarct in the pons or internal capsule
Dysarthria, dysphagia, contralateral facial and tongue weakness, paresis and
clumsiness of the contralateral arm and hand
Pure sensory stroke
Results from an infarct in the thalamus
Contralateral sensory loss to all modalities that usually affect the face, upper and lower extremities
May be painful
Kistler JP, Ropper AH, Martin JB. Cerebrovascular diseases. In: Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL, eds. Harrison’s Principles of Internal Medicine. 13th ed. New York: McGraw Hill; 1994: 2233-2256. Fisher,CM. (1991). Lacunar Syndromes, 1, 311-320.
Ischemic Stroke: Left (dominant) Hemisphere Stroke
The CT scan shows a large area of infarction in the territory of the left middle cerebral artery. The MCA is the artery most often occluded in ischemic stroke.
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The associated neurological signs and symptoms form a common pattern of stroke presentation involving the left, or dominant, hemisphere.
Aphasia
Right field defect
Left gaze preference
Right upper motor neuron facial weakness
Right hemiparesis
Right hemisensory loss
Ischemic Stroke: Right (non-dominant) Hemisphere Stroke
The CT scan shows a large area of infarction in the territory of the right middle cerebral artery.
21
The associated neurological signs and symptoms form a common pattern of stroke presentation involving the right, or non-dominant, hemisphere.
Left neglect, inattention
Left field defect
Right gaze preference
Left upper motor neuron facial weakness
Left hemiparesis
Left hemisensory loss, sensory extinction
Ischemic Stroke: Cerebellar Infarct
The MRI scan shows an area of ischemia in the left cerebellum.
This stroke presentation should be considered a neurological emergency
because of the possible risk of raised intracranial pressure due to compression of the fourth ventricle.
22
The following associated signs and symptoms form a common pattern of stroke presentation involving the cerebellum.
Headache, nausea/vomiting
Vertigo, imbalance
Normal tone, power, reflexes
Inability to sit or stand
Ataxia or loss of normal coordination
Late signs:
Decreasing level of consciousness
Diplopia, gaze palsy
Ipsilateral V, Vll impairment
Ischemic Stroke: Brainstem Stroke
This MRI scan shows an area of ischemia in the right pons, in the brainstem
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The following associated neurological signs and symptoms form a common pattern of stroke presentation involving the brainstem.
Decreased LOC
Crossed findings
Ipsilateral lower motor neuron facial weakness or sensory loss AND contralateral hemiparesis
Pupillary changes
Hiccoughs, vertigo
Bilateral motor findings
Diplopia, gaze palsies, intranuclear opthalmoplegia
Dysphagia
Dysarthria
Ataxia
The Brain and Function
Frontal lobe Temporal lobe Parietal lobe Occipital lobe Cerebellum BrainstemAnterior Cerebral Artery Middle Cerebral Artery Posterior Cerebral Artery
Cerebellar Arteries
Basilar Artery Vertebral Artery Opthalmic Artery
Internal Carotid Artery
Blood Supply and the Brain
The Anterior Cerebral Artery supplies blood to the medial (central) parts of the Frontal and Parietal Lobes. The Middle Cerebral Artery supplies blood to the lateral (outer) parts of the Frontal and Parietal Lobes and the
Temporal Lobe. The Middle Cerebral Artery is the most common site of stroke.
The Posterior Cerebral Artery and Vertebro-Basilar Artery systems supply blood to the Cerebellum, Brain Stem, Occipital Lobe, and the posterior (back) part of the Temporal Lobe.
How Stroke Affects Function
A stroke is a loss of function that results from the blood supply to the brain being cut off. The following describe how a stroke affects the function of different areas of the brain:
Parietal Lobe
• Arm, opposite side of stroke • Leg, opposite side of stroke • Sensation of touch • Visual and sensory
perception, if stroke is on the non-dominant side
Frontal Lobe
• Arm, opposite side of stroke • Leg, opposite side of stroke • Judgment, personality,
attention
• Speaking and writing if stroke is on the dominant side Occipital Lobe • Vision Cerebellum • Coordination • Balance Brain Stem • Breathing • Modulation of temperature and blood pressure • Swallowing Temporal Lobe
• Sense of smell • Memory
• Understanding spoken and written language and math skills if stroke is on the dominant side (part of the Parietal lobe as well)
Module One
Pathophysiology of Stroke, Neuroanatomy, Stroke
Syndromes
REFERENCES
The main source for this module was:
Acute Stroke Management Resource. (2007).Heart and Stroke Foundation of Ontario, Anatomy and Physiology of Acute Stroke power point presentation. Retrieved from
http://www.heartandstroke.on.ca/site/c.pvI3IeNWJwE/b.5346923/k.8D25/HCP__Eng lish.htm
That presentation listed the following sources for the content:
American Association of Neuroscience Nurses
www.aann.org
American Stroke Association
www.strokeassociation.org
Brain Attack Coalition
www.stroke-site.org
Canadian Hypertension Education Program
www.hypertension.ca/chep/en/default.asp
Canadian Stroke Strategy
www.canadianstrokestrategy.ca
European Stroke Initiative
www.eusi-stroke.com
Heart and Stroke Foundation Prof Ed
www.heartandstroke.ca/profed
Heart and Stroke Foundation of Canada
www.heartandstroke.ca
Internet Stroke Centre
www.strokecenter.org
www.stroke.org/site/PageServer?pagename=HOME
Scottish Intercollegiate Guidelines Network
www.sign.ac.uk
StrokeEngine
www.medicine.mcgill.ca/strokengine www.cnsforum.com
NEO Stroke Network’s
Nursing Certification Program
MODULE ONE
Pathophysiology of Stroke
Neuroanatomy
Stroke Syndromes
Quiz
You may use your binder as a reference to answer these questions
Submit your completed quiz to the Nurse Clinician or designate for marking
Your test will be returned to you to keep in your binder
NEO Stroke Network
DATE: ____________________ NAME: ___________________
1. The etiology of ischemic stroke can be classified as
a. Large vessel b. Small vessel c. Cryptogenic d. all of the above
2. The Cerebrum is made up of all but one of the following structures. Select the structure not part of the cerebrum.
a. Temporal lobes b. Occipital lobes c. Parietal lobes
d. Superior and inferior cerebellar lobes
3. Hemorrhagic transformation, or secondary bleeding into an infarcted lesion, is often considered to be a natural evolution of an ischemic stroke. It can be serious clinically if there is bleeding beyond the original territory or if mass effect occurs. It is influenced by the
a. Size of the stroke b. Location of the stroke c. Etiology of the stroke d. All of the above
4. The three main branches of the Internal Carotid Artery: the Anterior Cerebral Artery (ACA), Middle Cerebral Artery (MCA) and Anterior Communicating Artery together form the
a. Posterior circulation b. Circle of Willis c. Anterior circulation d. Cerebellar circulation
5. Collateral Circulation can occur because of the:
a. Redundancy in our cerebral vasculature b. The Circle of Willis
c. Terminal vessels d. Both Answer A and B
6. Small vessel disease causing stroke is thought to be the result of
occlusion of single, small penetrating arteries deep in the brain. These strokes are called:
a. Cerebellar strokes b. Lacunar strokes c. Cryptogenic strokes
d. Arteriovenous malformations
7. Cerebellar infarct may present with all but one of these signs: (Choose the exception)
a. Impaired executive functioning; decision making b. Vertigo ,imbalance
c. Ataxia or loss of normal coordination d. Diplopia
8. The brainstem is responsible for
a. Understanding written language
b. Perception of the surrounding environment
c. Autonomic functions ie. respiration, blood pressure, heart rate d. Thoughts and behaviour
TRUE/FALSE Questions
(CIRCLE the correct letter)T F 1. The left hemisphere controls the right side of the body AND is most often where the language center is located.
T F 2. The cerebellum is responsible for sensation, vision and memory.
T F 3. The middle cerebral artery has a large territory and is most often the artery occluded in stroke.
T F 4. Lacunar syndrome is commonly referred to as a pure motor stroke presenting with contralateral hemiparesis.
T F 5. Tumour or a brain abscess may present like a stroke and is considered to be one of the so-called Stroke Mimics.
SCORE:
_____ / 13
Stroke Unit/Medical Unit Nurse Clinician/Designate ____________________ (
signature)
NEO Stroke Network’s
Acute Nursing Certification Program
LEARNING OBJECTIVES
MODULE TWO
Pre-Hospital and Emergency Management
Upon completion of this module, nurses will be able to:
State the Warning Signs of Stroke
Understand the Role of EMS in Hyperacute Stroke
Explain Thrombolytic Therapy - and the importance of quick
assessment and administration within the time window
Identify Stroke Mimics
Understand Acute ASA Therapy
NEO Stroke Network’s
Acute Nursing Certification Program
MODULE TWO
Pre-hospital Care and Emergency Management
Self Learning Program
NEO Stroke Network Developed April 2010
2
Pre-hospital Care and Emergency Management
Warning Signs of Stroke
Sudden onset of:
Weakness or numbness Speech disturbances Unexplained dizziness Visual changes
Sudden severe headache of unknown cause
Emergency Medical Services
Hyperacute Stroke is defined as the health care activities that take place from the time of first contact between a potential stroke patient and medical care. This period ceases once the patient is either admitted to hospital or discharged back into the community.
Patients who show signs and symptoms of hyperacute stroke in the community must be treated as time-sensitive emergency cases and
should be transported without delay to the
closest institution that provides emergency stroke care. Immediate contact with emergency services by
patients or members of the public is strongly recommended because it reduces time to treatment for acute stroke.
EMS service dispatchers must triage patients showing signs of hyperacute stroke as a priority dispatch. EMS providers should be using a standardized screening tool.
EMS implemented a newly revised“Paramedic Prompt Card”. The prompt card assists EMS providers in, first, recognizing the signs and symptoms of stroke and second, in decision making around the most appropriate hospital to which to transport the patient.
3 Paramedic Bypass Protocols exist in each region whereby the EMS providers will bypass the local community hospital and transport the patient, up to 2 hours in the ambulance, to access a centre equipped to provide optimal acute stroke treatment, and arrive within 3.5 hours from the time of stroke onset.
The 2008 Canadian Best Practice Recommendations for Stroke Care also emphasize the need for rapid transport of acute stroke patients to appropriate facilities but unfortunately lack of public awareness of stroke signs and symptoms AND lack of knowledge that stroke is an emergency still exists.
PARAMEDIC PROMPT CARD FOR
ACUTE STROKE PROTOCOL
Indications for Patient Redirect or Transport to a Designated Stroke Centre
Exclusions for Patient Redirect to a Designated Stroke Centre
CACC will authorize the transport once notified of the patient's need for redirect under the Stroke Protocol.
Redirect or transport to a Designated Stroke Centre will be considered for patients who: Present with a new onset of at least one of the following symptoms suggestive of the onset of an acute ischemic stroke:
unilateral arm/leg weakness or drift
slurred speech or inappropriate words or mute
unilateral facial droop
AND
Can be transported to arrive at a Designated Stroke Centre within 3.5 hours of a clearly determined time of symptom onset or the time the patient was “last seen in a usual state of health”.
NOTES:
1. A Designated Stroke Centre is a Regional Stroke Centre, District Stroke Centre or Telestroke Centre.
2. Patients will be redirected or transported to the closest Designated Stroke Centre.
3. Patients whose symptoms improve significantly or resolve during transport will continue to a Designated Stroke Centre
4. Out-of-hospital transport will not exceed two hours.
Any of the following conditions exclude a patient from being redirected to a Designated Stroke Centre:
CTAS Level 1 and/or uncorrected Airway, Breathing or Circulation problem
Patients whose symptoms have resolved prior to paramedic assessment
Blood sugar < 3.0mmol/l
Seizure at onset of symptoms or observed by paramedic
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Acute Thrombolytic Therapy
All patients with disabling acute ischemic stroke who can be treated within 4.5 hours after symptom onset should be evaluated without delay to determine their eligibility for treatment with t-PA (Alteplase).
Eligible patients are those who can receive t-PA within 4.5 hours of the onset of stroke symptoms in accordance with criteria adapted from the National Institute of Neurological Disorders and Stroke tPA Stroke Study and Third European Cooperative Acute Stroke Study (ECASS III).
The introduction of thrombolytic therapy has provided a proven treatment for acute ischemic stroke patients if given as soon as possible and within the time window. However, it is a high risk treatment that should only be given by personnel trained in its use, in a centre equipped to investigate and monitor patients appropriately.
Goal of thrombolytic therapy isto limit irreversible ischemic damage caused by an arterial occlusion. Thrombolysis will promote reperfusion of the viable tissue of the penumbra, improving stroke prognosis and outcome. It is important to note that “time is brain” and the closer to the time of stroke onset that
reperfusion occurs, the better the patient prognosis.
What is Tissue Plasminogen Activator (t-PA or Alteplase) ?
As excerpted from Faaast FAQs for Nurses, page 7, Heart and Stroke Foundation of Ontario (2007)……..
…..t-PA (Alteplase) is athrombotic agent (clot-busting drug) that can destroy an existing blood clot that is approved for use in select patients having an ischemic stroke.
It is to be given within the time window of 4.5 hours from “last seen normal”. Prior to administration of the drug, the patient must undergo specific diagnostic procedures to determine if there is any hemorrhage. This requires immediate access to CT scan imaging and blood work.
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Administration is most often administered intravenously or sometimes
intra-arterially directly to the site of the clot via catheter, allowing for a greater dose of the drug with fewer potential side effects.
What is the usual process prior to a patient receiving t-PA (Alteplase) ?
Ascertain time of onset (<than 4.5 hours)
History and physical symptoms consistent with acute ischemic stroke
CT to rule out hemorrhage stroke [or other etiology]
CBC, platelets, lytes, glucose, INR, PTT etc
Assessment by a Stroke Physician
What are the major inclusion criteria for t-PA (Alteplase) ?
Ischemic stroke
Clearly definable time of onset
t-PA can be administered within 4.5 hours of symptom onset
Symptoms present more than 1 hour without signs of resolution
What are some absolute contraindications for t-PA (Alteplase) ?
TIA or stroke with rapidly improving deficit
Hemorrhagic stroke
BP>185/110 that does not respond to treatment
Major surgery or trauma within 14 days
Active internal bleeding or history of hematological abnormality or
anticoagulation [this is dependent on INR value – which may vary at across centres]
Why work quickly to determine if t-PA (Alteplase) is the appropriate treatment?
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Below you will see the infarcted tissue (ischemic core), the tissue that is still viable but lacking perfusion, therefore, at risk (ischemic penumbra), and the normal brain tissue.
NOTE:Our brain requires a constant uninterrupted supply of glucose and oxygen as the brain does not store glucose or oxygen. An interruption in either of these
substances can lead to dysfunction.
A complete interruption of blood supply to part of the brain for only 30 seconds can alter brain metabolism, for example, neuronal function may cease after 1 minute. After 5 minutes anoxia initiates a chain of events that may lead to death of brain tissue. Penumbra tissue remains viable for several hours after stroke. Penumbra cells are supplied by collateral arteries which contribute to reperfusion and thrombolytic therapy also works to perfuse the penumbra.
http://www.strokecenter.org/education/ais_pathogenesis/22_ischemic_penumbra.htm
A stroke patient should receive thrombolytic therapy as soon as possible but within a maximum of 60 minutes of arrival. A rapid and coordinated emergency department response to the arrival of a stroke patient facilitates early diagnosis and treatment.
Normal brain tissue
Brain tissue that is lacking perfusion, at risk of death
Infarcted brain tissue
7 The following maximum target times for emergency management of ischemic stroke have been established.
Door-to-triage 1 minute Door-to-stroke team notification 5 minutes Door-to-CT scan 25 minutes Door-to-needle 60 minutes
(The absolute and relative exclusion criteria for administration of t-PA and the t-PA
Order Set are included in the Hospital-Specific Chart Forms section of those packages that are available at District Stroke Centres and Telestroke sites)
There are adverse effects of t-PA to be aware of:
Hemorrhage
a) Superficial Bleeding
Observe potential bleeding sites: venous & arterial puncture, lacerations, etc.
Avoid invasive procedures during t-PA (Alteplase) and for 24 hours after (incl. N/G and foley catheter)
Monitor all secretions for bleeding b) Intracranial hemorrhage
Observe for deterioration of neuro status If suspected, stop t-PA (Alteplase) and
notify M.D.
Obtain CT scan and coagulation workup
Angiodema
a)Risk assessment
Inquire if patient has had angioedema in past
Take ACE inhibitor history Although angiotensin II (ATII)
receptor antagonists have not been implicated in the angioedema reaction, caution is advised in patients reporting a history of ATII antagonist use
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b)Monitoring
Observe for facial, tongue, and/or pharyngeal angioedema 30 minutes, 45 minutes, 60 minutes and 75 minutes after initiation of IV t-PA infusion and periodically for 24 hours afterwards
Stroke Mimics
Not all cases that appear as a stroke are in fact a stroke.
Be aware of the many other conditions that would be part of the differential diagnoses as they can present much like a stroke.
Seizure
Infection
Hypoglycemia
Syncope
Brain abscess or tumour
Drug overdose
Head trauma
Migraine
Bell’s palsy
Hypertensive encephalopathy
Acute ASA Therapy
All acute stroke patients should be given at least 160mg of ASA immediately as a one time loading dose after brain imaging has excluded intracranial hemorrhage. [Evidence Level A] (ESO, NZ, RCP, SIGN 13). (Canadian Best practice Recommendations -2008)
• In patients treated with t-PA (Alteplase), ASA should be delayed until after the 24 hour post-thrombolysis scan has excluded intracranial hemorrhage.
• ASA (80-325 mg daily) should then be continued
indefinitely or until an alternative antithrombotic regime is started.
• In dysphagic patients, ASA may be given by enteral tube or by rectal suppository
The administration of ASA in the hyperacute phase of stroke comes as a result of research that concluded that the administration of ASA within 48 hours of onset of presumed ischemic stroke reduces the risk of early recurrent ischemic stroke without a major risk of early hemorrhagic complications and improves long term outcomes.
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Goals of Acute Ischemic Stroke Management
• Reduce or minimize ischemic damage
• Reduce cerebral edema
• Prevent secondary complications • Determine etiology of stroke • Prevent recurrent stroke
• Facilitate access to rehabilitation and community reintegration
Contributing Factors to Ischemic Damage
While restoring blood flow to the penumbra is the goal of acute stroke management, there are multiple factors that should be considered and addressed as part of the management plan.
Factors that play a role in contributing to potential increase in size of the infarct include:
a) Blood pressure b) Blood glucose c) Body temperature d) Oxygen saturation
It is important to assess and monitor vital signs to keep this goal at the forefront.
from Heart & Stroke: Best Practice Guidelines for Stroke Care
Acute Ischemic Stroke receiving t-PA
Vital signs (including temperature) should be assessed as follows after beginning t-PA infusion:
• q 15 minutes for 2 hours • q 30 minutes for 2 hours • q 1hour for 6 hours • q 4 hours for 14 hours
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Acute Ischemic Stroke Non t-PA
Vital signs (including temperature) should be assessed as follows: • q 1 hour for 24 hours
• q 4 hours for 24 hours
• Or as indicated by hospital protocol
a) Hypertension (HTN)
Acute stroke patients often experience hypertension in the
immediate hours after stroke onset. Elevated blood pressure may act as a compensatory mechanism to maintain cerebral perfusion.
Normally, cerebral auto regulation maintains cerebral blood flow. However, as cerebral perfusion pressure decreases in the presence of stroke, normal auto regulation is lost and blood flow is dependant on the blood pressure
There are many factors that cause hypertensionsecondary to stroke: full bladder, nausea, pain, pre existing hypertension, anxiety, a physiological response to hypoxia or increased intracranial pressure.
The reason for lowering blood pressure is because HTN can increase cerebral edema, increase risk of hemorrhagic
transformation, cause further vascular damage and stroke recurrence.
There is a concern that reducing blood pressure too quickly and too low may cause neurological damage as a result of reduced perfusion pressure to the ischemic areas. Lowering of the blood pressure can result in serious consequences. Both hypertension and hypotension have been associated with poor patient outcomes.
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For some stroke patients, blood pressure may decline spontaneously within the first few hours as a result of interventions such as moving the patient to a quieter area, emptying the bladder, allowing the patient to rest or controlling pain. Also, the treatment of increased intracranial pressure may result in a lowering of blood pressure.
Blood Pressure Reduction
• BP reduction should be addressed cautiously • Measure BP accurately, continuously monitor • Clear data is lacking but:
2007 AHA/ASA Guidelines recommend: Initiate treatment if SBP>220mmHg or
DBP>120mmHg
t-PA candidates: Initiate treatment if SBP>185mmHG or DBP>110mmHG Lower blood pressure by 15-25% within 24
hours
Medication selection on case by case basis but consider ability to lower blood pressure quickly but ability for rapid reversal
NOTE The HRSRH non-t-PA Order Set adopted these guidelines:
“Hold antihypertensives x 24 hours unless SBP>220mmHg or
DBP>120mmHg
*Caution* - avoid rapid lowering of BP.If necessary treat with goal of reduction by ~ 15% within the first 24 hours”
NOTE Use of sublingual Nifedipine is contraindicated due to its prolonged effect and rapid decline in BP.
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b)
Blood Glucose - Hyperglycemia
All patients with suspected acute stroke should have their blood glucose concentration checked immediately
Blood glucose measurement should be repeated if the first value is abnormal or if the patient is known to have diabetes
Markedly elevated blood glucose concentrations should be treated with glucose lowering agents immediately.
(CSQCS, Australia)
Hyperglycemia is associated with worse stroke outcomes and is also a risk factor for hemorrhagic transformation. It can also have a serious effect on aphasia, hemiparesis, and changes in mental status.
It is unclear as to what extent post-stroke hyperglycemia is a normal physiological response or whether hyperglycemia increases cerebral damage.
But studies have also shown that hyperglycemia is
• linked to an increased risk for in-hospital mortality in non-diabetic patients
• linked to an increased risk of a poor functional recovery Many stroke patients may not have known that they have diabetes (a modifiable risk factor) until admission to hospital.
c)
Body Temperature - Hyperthermia
Increased body temperature (fever) in the setting of acute ischemic stroke is associated with poor neurological outcome (increased risk of morbidity and mortality), possibly secondary to increased
metabolic demand, enhanced release of neurotransmitters, and increased free radical production. The source of any fever should be ascertained. The fever may be secondary to a cause of stroke, such as infective endocarditis, or may represent a complication such as pneumonia.
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d)
Oxygen Saturation - Desaturation
Ensuring adequate oxygenation of tissues is important in acute stroke management. Oxygen desaturation may exacerbate and
worsen ischemic damage.
Oxygen saturation should be monitored with the use of pulse oximetry and oxygen applied if oxygen saturation is <92%. (American Heart Association, 2007).
Supplemental oxygen given to patients who are not hypoxic may result in the production of oxygen free radicals and contribute to worse outcome.
Consideration and assessment of other causes of hypoxia should also be reviewed. These include pneumonia, partial airway
obstruction, hypoventilation and atelectasis. Patients who have brain stem infarcts have the greatest risk of airway compromise due to impaired oropharyngeal mobility and loss of reflexes.
NEO Stroke Network’s
Acute Nursing Certification Program
MODULE TWO
Pre-Hospital and Emergency Management
QUIZ
You may use your binder as a reference to answer these questions
Submit your completed quiz to the Nurse Clinician or designate for marking
Your test will be returned to you to keep in your binder
NEO Stroke Network
DATE: ____________________ NAME: ___________________
1. List the five warning signs of stroke:
5 points
2. The accepted time window to deliver the drug t-PA to a new stroke patient in our region is:
a. 1.5 hours since last seen normal b. 4.5 hours since last seen normal c. 3.5 hours since last seen normal d. Within 24 hours of symptom onset
3. Adverse effects of t-PA to be aware of include:
a. Bleeding b. Memory loss c. Angiodema d. Answer A and C
4. List three Stroke Mimics:
3 points
5. The following are contributing factors to ischemic damage
except:
(Choose the exception)
a. blood pressure b. weakness
c. oxygen saturation d. body temperature
6. All acute stroke patients should be given at least ____ of ASA immediately as a one time loading dose:
(fill in the blank)
a. 160 mg b. 80 mg c. 325 mg d. 125 mg
TRUE/FALSE Questions
(CIRCLE the correct letter)T F 1. There are serious inclusion and exclusion criteria the physician MUST consider before determining if an acute stroke patient qualifies for thrombolytic therapy.
T F 2. Blood Pressure reduction in the acute phase should be addressed cautiously and follow the guidelines of “Hold antihypertensives x
24 hoursunless SBP>220mmHg or DBP>120mmHg and avoid rapid lowering of BP”.
T F 3. Reduction of fever can wait till it has reached 38.5º C or beyond.
SCORE:
_____ / 15
Stroke Unit/Medical Unit Nurse Clinician/Designate ___________________
NEO Stroke Network’s
Acute Nursing Certification Program
LEARNING OBJECTIVES
MODULE THREE
Assessment and Diagnostics
Upon completion of this module, nurses will be able to:
Describe the Acute Stroke Nursing Assessment
Understand why Neurological Assessments are important
State the Standardized Neurological Assessments
Explain the Relevant Stroke Investigations and why they are
NEO Stroke Network’s
Acute Nursing Certification Program
MODULE THREE
Assessment and Diagnostics
Self Learning Program
NEO Stroke Network
Developed April 2010
Acute Care Nursing Assessment
Acute stroke patients require skilled and knowledgeable professionals attending to their care.
Organized stroke units create the opportunity to develop a critical mass that
facilitates the development of expertise of clinicians. Expertise in stroke assessment by clinicians ensures that stroke patients are offered appropriate investigations and receive appropriate and timely care.
“The nurse is often the first to see changes and early warning signs that may predict a neurological crisis. Familiarity with a stroke nurse assessment promotes the nurse’s ability to gather accurate patient information, identify stroke emergencies and
promote timely referrals to appropriate specialists and time-dependent investigations” (Faaast FAQs, Heart and Stroke Foundation, page 9, 2007)
A stroke assessment includes
:(Faaast FAQs, page 10, 2007)
1. ABC
2. Health History
The purpose of the health history is to collect subjective data and combine it with objective data from the physical examination. The combined data base is then used to make a judgment or diagnosis about the health status of the individual (Jarvis, 2000).
3. Vital Signs
Temperature, heart rate, blood pressure, respiration rate, pain assessment and oxygen saturation are all measured/monitored according to Standards of Care for the unit. See frequency as outlined in Module TWO.
Begin a general assessment the moment you first encounter the person. Take note any signs of acute distress that are present and assess ABC (airway-breathing-circulation).
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4. Pupils
Record size of the pupils in mm using the pupil scale prior to the application of the light stimulus. Indicate the reaction of pupils as either:
+
=
Brisk ReactionS =
Sluggish-
=
No ReactionIf the eyes are closed due to swelling, record “C”
5. Standardized Neurological Assessment
Why do a neuro assessment?Provides a standardized method to rapidly identify “emerging”
stroke complications.
Early identification of “emerging” stroke complications may:
lead to early intervention
limit the extension of neurological damage
impact patient outcomes
provide a better patient prognosis (Hachinski & Norris, 1980)
The use of standardized and validated stroke assessment tools in both the acute and rehabilitation settings enables sound decision making and care planning.
What are you looking for?
Symptoms of Change in Neurological Status
Restlessness
Combativeness
Confusion
Severe headache
Lethargy
Decline in motor strength
Decrease in coordination
Change in balance
Change in speech/language
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There are three neurological assessment tools that are available for nurses to use: Canadian Neurological Scale, the National Institutes of Health Stroke Scale and the Glasgow Coma Scale (HSFO and RNAO, 2005).
Canadian Neurological Scale (CNS):
The Canadian Neurological Scale is an assessment tool for evaluating and monitoring the neurological status of acute stoke patients. It has been found to be brief, valid and reliable, and can be administered in approximately 5 minutes.
The CNS assesses:
level of consciousness
orientation
speech
motor function of the face, arm and legs
A limitation of the scale may be that some useful measures are omitted as it does not include assessment of cerebellar or brainstem function. (HSFO and RNAO, 2004)
National Institute of Health Stroke Scale (NIHSS):
The National Institute of Health Stroke Scale was designed for use in clinical trials and practice to assess stroke severity and degree of recovery. The NIHSS has demonstrated reliability and validity for patients with stroke. It can take up to 20 minutes to administer until you are quite comfortable with each item, then it may be completed in 5-10 minutes.
The NIH Stroke Scale (NIHSS) assesses:
level of consciousness visual fields motor response sensation language neglect
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It is an 11 item scale that measures various physiological deficits associated with stroke:
• LOC • Best gaze
• Visual field testing • Facial paresis
• Arm & leg motor function
• Limb ataxia • Sensory
• Best language • Dysarthria
• Extinction & inattention
The NIHSS allows us to:
– objectively quantify our clinical exam (give it a score)
– determine if the patients’ neurological status is improving or deteriorating;
– provide standardization in assessment (from one nurse to the next – the same exam is performed)
– communicate patient status to staff (nurses and MDs talking the same language)
– aid in decision making re: t-PA(Alteplase) treatment, acute care needs, needs at discharge
A limitation of the scale is that it has a low sensitivity to small changes (HSFO and RNAO, 2004).
Glascow Coma Scale (GCS):
The Glasgow Coma Scale is a standardized and valid neurological assessment tool for assessing level of consciousness or coma.
It is a neurological assessment that is widely used by the neurological and neurosurgery community and is found in the curriculum of most undergraduate nursing programs.
It lacks specificity and applicability when applied to stroke patients as most do not have impaired LOC.
Other Assessments
There are many more assessments that are relevant to the stroke inpatient. Some of these assessments are administered by other members of the team.
Consult with your Nurse Clinician or Stroke Nurse to learn more about any one of the assessments listed below.
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AlphaFIM® (an abbreviated version of the FIM® Instrument to assess function and disability in the acute care setting)
Pain (Visual Analog Scale)
Skin Breakdown (Braden Risk Assessment)
Balance (Berg Balance Scale)
Cognition (Mini Mental; MoCA)
Depression (Beck Depression Inventory)
Investigations
The following investigations are part of the Acute Ischemic Stroke
non t-PA Order Set at Hôpital régional de Sudbury Regional Hospital.
Your centre may use a variation of these tests. Check with your Stroke
Program’s Stroke RN or District Stroke Coordinator.
Descriptors for each test were obtained from American Stroke Association’s “Stroke Tests”http://www.strokeassociation.org and www.labtestsonline.org
Blood tests
confirm (or refute) suspicions of specific clinical conditions Levels of cardiac enzymes (including troponin and creatine kinase) can confirm heart muscle damage and extent of damage.
Creatinine findings can show reduced renal blood flow, atherosclerosis.
GlucoseRandom Testing indicates blood glucose levels in the blood.
PTT/INRPartial Thromboplastin Time indicates the function of all coagulation factors. International Normalized Ratio is a ratio used to monitor the effectiveness of blood thinning drugs such as warfarin (Coumadin).
Lipid Profile is a complete fasting lipoprotein profile that will show total blood cholesterol level, HDL, LDL and triglyceride levels.
HbA1cis a test that measures the amount of glycated hemoglobin in your blood. Glycated hemoglobin is a substance in red blood cells that is formed when glucose attaches to hemoglobin. It indicates how well blood sugar has been controlled over the previous 2-3 months. HbA1c results can contribute to a diagnosis of diabetes.