Running head: QUALITY IMPROVEMENT AND PERFORMANCE INDICATORS FOR 1 Quality Improvement and Performance Indicators for Primary Stroke Center Certification at St. Francis Health Center Jill Collins Washburn University NU 670 Dr. Monica Scheibmeir December 5th, 2012
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Running head: QUALITY IMPROVEMENT AND PERFORMANCE INDICATORS FOR 1
Quality Improvement and Performance Indicators for Primary Stroke Center Certification at St.
Francis Health Center
Jill Collins
Washburn University
NU 670
Dr. Monica Scheibmeir
December 5th, 2012
Quality Improvement and Performance Indicators for Primary Stroke Center Certification at St.
Francis Health Center
Introduction
Cerebrovascular accident (CVA), also referred to as a “stroke” in the lay literature, is the
third-leading cause of death and the leading cause of disability annually in the United States
(Leifer, et al., 2011). An estimated 795,000 people in the United States are diagnosed with a
CVA each year. For more than 600,000 of these Americans, this will be their first CVA but
almost 200,000 of the yearly CVAs are recurrences (George, Tong, & Yoon, 2011).
Approximately 140,000 CVA deaths occur annually and in addition, it is listed as a contributing
factor in another 100,000 deaths (Katz, 2010). With the steady incline in medical conditions
putting people at risk for a CVA including obesity, hypertension, dyslipidemia and diabetes,
these numbers will likely continue to rise. The resulting effects will cost consumers millions of
dollars in both direct healthcare costs as well as loss of productivity and income secondary to the
profound and devistating disabilities resulting from a CVA. In 2010, an estimated $73.7 billion
was spent on CVA-related medical costs and disability alone (Otwell, Phillippe, & Dixon, 2010).
This project will assist St. Francis Health Center in collecting data on their current management
of stroke care. The data can then be used to improve the care provided by St. Francis Health
Center to victims of cerebrovascular accidents.
Pathophysiology
Before discussing the evaluation of stroke care, it is important to review and understand
the anatomy and pathophysiology of the underlying disease. This makes it easier to understand
why certain criteria are chosen to evaluate appropriate care. The brain is a relatively small part
in the human body occupying only 2% of the body’s mass. However, it receives 17% of the
heart’s output and consumes 20% of the body’s oxygen supply. The brain receives it’s vital
blood supply through four arteries. The two largest arteries are the right and left internal carotids
which branch off the left and right common carotids respectively and travel up the anterior
portion of the neck. The common carotids arise from the aorta. These internal carotids give rise
to the middle and anterior cerebral arteries which supply blood to the anterior portion of the brain
including most of the frontal, parietal and temporal hemispheres as well as the basal ganglia.
There are also two smaller arteries that travel up the posterior portion of the neck and are the
right and left vertebral arteries. These arteries arise from a single basilar artery. The basilar
artery arises from a branch off the subclavian artery which in turn branches off the aorta. These
arteries supply blood to the posterior portion of the brain including the brainstem, cerebellum
and most of the posterior cerebral hemispheres. The anterior and posterior circulations connect
through a circular anastamosis of arteries called the Circle of Willis. The brain receives about
80% of it’s blood supply from the carotid arteries and the remaining 20% from the vertebral
arteries (Katz, 2010).
One characteristic of the brain is many of it’s functions are not diffusely spread meaning
specific neurologic functions are dependent on certain brain regions. In the cerebral vasculature,
each artery supplies a particular brain region. Because most of these regions are associated with
a characteristic neurological function, damage to a particular cerebral artery tends to cause
characteristic losses of neurological functions which are often referred to as “focal neurological
deficits” (Appendix A) (Katz, 2010).
Cerebrovascular accidents can be broadly defined as an interruption in blood supply to
the cells which compose brain tissue and are classified as either ischemic or hemorrhagic. This
can sometimes be confusing though because both actually cause ischemic damage. In the case of
an ischemic stroke, resulting injury to brain tissue is caused by a reduced blood flow to a specific
region without initially causing significant cerebral bleeding. This reduction in blood flow is
most often secondary to a blocked artery but can also occur as a result of hypoprofusion as in the
case of sustained cardiac arrest. Hemorrhagic strokes result from injuries that cause bleeding
into the brain or cerebral spinal fluid from the outset. This bleeding is generally due to a tear in
an artery or the rupture of an aneurysm. These conditions are often secondary complications
from conditions such as hypertension, tumors or drugs. They can also be the result of trauma or
physical activity. The majority of strokes (87%) are ischemic from the outset and as mentioned
above, are primarily caused by the blockage of an artery. This blockage is predominantly due to
a thrombus or blood clot (Katz, 2010).
Ischemic strokes, as the name implies, cause ischemic damage which is either complete
or incomplete. If the blood supply to the brain is cut off completely, as is the case with cardiac
arrest, there is widespread cell damage and neurons begin to die quickly. The brain uses energy
quickly but only has a small back-up supply. When complete ischemia occurs, there is an
immediate decrease in available oxygen and glucose that brain cells need to survive. Local
neurons will begin to run short on their internal ATP (the back-up intracelluar energy stores)
within a matter of seconds. As ATP is depleted, the cell membranes depolarize and extracellular
ions rush in. This leads in water accumulation in the cells and eventually causes the cell to self-
destruct, burst and die. This process is also known as apoptosis. As cells die in this manner, the
toxic substances released from them can have a detrimental domino effect on surrounding cells
which will continue until the blood supply is re-established (Katz, 2010).
Most ischemic strokes are not a result of complete ischemia. They are primarily caused
by incomplete ischemia as a result of a partially or completely blocked artery. These blockages
are generally caused by a blood clot or thrombus. The thrombus itself is usually the result of
other conditions including but not limited to coagulopathies, atrial fibrillation and
atherosclerosis. Even when an artery is competely occluded, the cerebral circulation has many
overlaps and interconnections. Some blood will usually reach the affected brain regions via
collateral circulation. The remaining perfusion will vary throughout the affected region. A
common pattern is severely reduced perfusion in the center with gradually increasing profusion
toward the edges. The area of minimally profused cells is referred to as the pneumbra. Neurons
will become functionally silent when arterial profusion drops by even a small amount. In the
case of a stroke, as soon as the cerebral blood flow is reduced, electrical activity in the region
will stop and neurological deficits begin to appear. For a short time, silent neurons remain alive
but no longer have the energy to generate membrane potentials sufficient enough to respond to
stimuli or transmit signals. To remain alive, these neurons need some arterial profusion and if
cerebral blood flow falls below 13% of normal in the affected region, silent neurons begin to die
in the same fashion as complete ischemia.
The amount of irreversible damage increases steadily as long as regions are without
sufficient blood supply. If the affected areas have no blood flow, neurons begin to die in less
than 10 minutes. In areas with <30% of normal blood flow, neurons begin to die within an hour.
In areas with 30-40% of normal blood flow, some neurons will die within an hour but others can
be revived after many hours. In has been found that collateral and residual blood flow can
preserve neurons in the pneumbra and border areas for as long as six hours after an ischemic
stroke. If treatments are given within this time period to destroy the thrombus, there may be a
reduction in the amount of irreversible brain damage.
Fortunately, in most ischemic strokes, patients lose neurologic functions early in the
course before all the neurons in the affected area are irreversibly damaged. Typically, most
strokes leave enough arterial perfusion that many neurons can maintain a low level of energy
production sufficient enough to slow the onset of their death. This is why early recognition of
stroke symptoms and early initiation of thrombotic administration in the appropriate candidate is
crucial (Katz, 2010).
Hemorrhagic strokes result in a release of blood into the brain parenchyma or
cerebrospinal fluid (CSF) and produce damage by three mechanisms: ischemia, physical
destruction and pressure. Hemorrhagic strokes produce ischemia by diverting blood from
cerebral arteries and by pressure from a hematoma or edema also causing contstriction. Bleeding
into the CSF raises intracranial pressure which will also reduce cerebral blood flow. Physical
destruction is a result of blood flowing extracellularly in the brain parenchyma which pushes
hippocampus underside of temporal lobe medial surface of occipital
lobe motor areas of the midbrain
sensory loss of the entire contralateral body
third nerve palsy with hemiparesis, hemiplegia, ataxia or decreased LOC
movement disorders of one side of the body
visual loss, specifically homonymous hemianopia
APPENDIX B
Stroke Core Measurements1. Venous thromboembolism (VTE) prophylaxis within 48 hours of admission2. Discharged home on antithrombotic therapy if no contraindications3. Anticoagulation therapy provided for patients with atrial fibrillation/flutter unless
contraindicated4. Thrombolytic therapy within appropriate time frame if patient meets criteria5. Antithrombotic therapy by the end of hospital day 2 if no contraindications6. Patient receives education about stroke including their personal modifiable risk factors, how
to activate EMS for stroke symptoms, prescribed medications, stroke warning signs and symptoms and the need for follow-up after discharge
7. Patient discharged on a statin medication if there are no contraindications8. Patient is assessed for rehabilitation needs
APPENDIX C
Disease-Specific Care Certification Manual Standards Clinically Specific Requirements and Expectations for Primary Stroke Center Certification
Program management Delivering or facilitating clinical care Supporting self-management Clinical information management Performance improvement and
measurement
Use a standardized method of delivering care based on the Brain Attack Coalition’s “Recommendations for Establishment of Primary Stroke Centers”
Support patient self-management activities
Tailor treatment and intervention to individual needs
Promote the flow of patient information across settings and providers, while protecting patient rights, security and privacy
Analyze and use standardized performance measure data to continually improve treatment plans
Demonstrate their application of and compliance with clinical practice guidelines published by the AHA/ASA or equivalent evidence-based guidelines
APPENDIX D
Data Entry Items for “Get With the Guidelines-Stroke” database Final clinical diagnosis related to stroke ICD-9 principal diagnosis code Earliest documentation of comfort measures only if applicable Discharge disposition If not discharged home, where was the person discharged Patient location when stroke symptoms started How patient arrived to hospital Where did patient first receive care in the hospital Was there advanced notification by EMS Arrival date and time Admit date If patient was not admitted, reason for not admitting Where was the patient admitted to in the hospital, by who, was there a stroke consult Initial physician seeing the patient Demographics: age, gender, ethnicity, health insurance status Medical history pertaining to stroke risk factors Ambulatory status prior to current event, at admission and at discharge Symptom duration if presenting with TIA Resolution of stroke symptoms at time of presentation? NIH stroke scale: was it done and what was the score Initial exam findings related to stroke symptoms Current medication class if antiplatelet/anticoagulant, antihypertensive, diabetic medication, and
cholesterol-reducer Date and time patient last known to be well Date and time of discovery of stroke symptoms Date and time of brain imaging if done for this episode of care with results Date and time IV tPA given if qualified Documentation of contraindications if tPA not given Was tPA given at another facility prior to transfer with date and time Complications of tPA therapy Was dysphagia screen done prior to giving the patient anything by mouth and results Was the patient treated for hospital acquired pneumonia or DVT Was DVT prophylaxis initiated by the end of day 2 and what type and when Was the patient ambulating by the end of day 2 If DVT prophylaxis not initiated, is there proper documentation of the reason Was antithrombotic therapy administered by the end of hospital day 2 Labs including lipid levels, PT/INR, creatinine, Hgb A1c and blood glucose Vitals including admit and discharge BP and pulse, height, weight, waist circumference and BMI Discharge date Discharge medications including antithrombotics, antihypertensives, anticoagulants, diabetic
meds and cholesterol reducing medications Lifestyle interventions Stroke education Assessment for rehab services
APPENDIX E
Inclusion/Exclusion Criteria for IV tPA from www.strokecarenow.com
Patient Inclusion Criteria (must be YES to all) Age 18 years or older Clinical diagnosis of Ischemic Stroke Measureable neurological deficit Clearly defined time of stroke onset (within 180 minutes of stroke onset) Informed consent (if possible) May extend treatment window to 4.5 hours if patient does not meet additional exclusion
criteria (see below)
Patient Exclusion Criteria (all must be NO before treatement) Evidence of intracranial hemorrhage on pretreatment CT scan Minor or rapidly improving symptoms Symptoms of subarachnoid hemorrhage, even with normal head CT Active internal bleeding: Gastrointestinal or urinary bleeding within last 21 days or
known bleeding risk, including but not limited to: a. Platelet count less than 100,000/mm3 b. Heparin during the preceding 48 hours associated with elevated aPTT g. Currently taking oral anticoagulants (e.g.
Warfarin sodium) or recent use with an elevated prothrombin time (PT) greater than 15 seconds or INR greater than 1.7 d. Major surgery or other serious trauma during preceding 14 days e. Stroke, serious head trauma or intracranial surgery during preceding 3 months f. Recent arterial puncture at a non-compressible site g. Recent lumbar puncture during preceding 7 days
Systolic BP greater than 185 mm of Hg or diastolic BP greater than 110 mm of Hg at the time of t-PA infusion and/or patient requires aggressive treatment to reduce blood pressure to within these limits
History of intracranial hemorrhage, neoplasm, arteriovenous malformation, or aneurysm Recent Acute Myocardial Infarction Observed seizure at stroke onset
Relative Contraindications Early signs of a large cerebral infarction: edema, hypodensity, mass effect, and
obliteration of sulci in more than 1/3 of middle cerebral artery territory on CT scan. NIHSS greater than 22 Glucose less than 50 mg/dL or greater than 400 mg/dL. Pregnant female Difficult to control hypertension Age greater than 75
Additional Exclusion Criteria for 4.5 hour window Patient older than 80 years of age Patient with a history of both diabetes AND stroke Coumadin (warfarin) use regardless of INR NIHSS greater than 25
APPENDIX F
Diagnosis: _________________ Date of Assessment: _________________ Time: _________Respiratory status: □ TRACH □ VENT □ Abnormal Lung Sounds □ Abnormal Chest x-rayDiet Prior to Admission: □ Regular □ Pureed □ Thickened Liquids □ Tube FeedingCognitive Status: Alert- □Yes □No Follows Commands: □Yes □NoThe following items are important warning signs for patients with possible dysphagia. Please indicate by placing a check markbedside the appropriate warning sign if they are observed. The patient should be elevated to a 90 degree hip flexion angle prior tocompleting the screen. Ensure the patient can maintain alertness for at least 10 minutes prior to completing this screen.IF ONE OR MORE WARNING SIGNS ARE OBSERVED THE PATIENT WILL BE MADE NPO. OBTAIN A PHYSICIANS ORDER TO CONSULT SPEECH THERAPY. PAGE SPEECH THERAPIST ON CALL MONDAY THROUGH FRIDAY 0900-1700 SATURDAY 0800-1630, AND SUNDAY 0800-1200□ Control of Secretions- drooling, difficulty swallowing saliva or coughing, difficulty expelling secretions□ Facial Symmetry- facial/lip droop on one side of the face, inability to move one side of face/lips, tremor inmuscle when patient asked to smile or pucker lips.□ Tongue Mobility- tongue deviates to right or left side when protruding, unable to touch corners of mouth□ Inadequate Oral Hygiene- dried, encrusted secretions on tongue or elsewhere in mouth□ Lip Seal- decreased lip closure□ Cough- absent or weak cough□ Wet Vocal Quality- wet/gurgly voice when saying “AHH”□ Aspiration- history of aspiration pneumonia□ Dry Swallow- delayed (5 seconds or more)IF ANY OF THE FOLLOWING ARE PRESENT, OBTAIN A PHYSICIANS ORDER TO CONSULT SPEECH THERAPY.THIS DOES NOT WARRANT AN NPO STATUS□ Slurred Speech□ Aphasia□ Disorientation/Confusion (Person, Place and Time)Date/Time Speech Pathology notified: ________________________Nurse Completing Screen: ____________________________