Kaiser Diagnostic and
Treatment
Documents
Kaiser
Permanente Clinical Practice Guidelines for Acute Stroke Quartet
III Inpatient Management
Admission
Criteria for Acute Ischemic Stroke/Acute
Stoke/Anticoagulation
in Acute
Ischemic Stroke (Spelling errors from the original text have
not been corrected)
This
page consists of three booklets printed as one.
Also Included is CME-Pre-Test and
Post-Test
Clinical
Practice Guidelines for Acute Stroke Quartet III
Inpatient
Management Admission Criteria for Acute Ischemic Stroke
Inpatient
Management of Acute Stroke
Management
of Blood Pressure in Acute Stroke
Anticoagulation
in Acute Ischemic Stroke endorsed
by Chiefs of Neurology, Chiefs of
Medicine, Chiefs
of Emergency Medicine - April 1998
The
Permanente Medical Group Clinical Practice
Guidelines
have been developed to assist clinicians by providing an analytical framework for the
evaluation and treatment
of selected common problems encountered in patients.
These guidelines are not
intended to establish a protocol
for all patients with a particular condition.
While
the guidelines provide
one approach to evaluating
a problem, clinical conditions may vary significantly from individual to
individual. Therefore, the clinician
must exercise independent judgment and make decisions based
upon the
situation
presented. While great care has been
taken to assure the accuracy of the information presented, the
reader is
advised that TPMG cannot be
responsible for continuedcurrency
of the information, for any errors or omissions in this
guidelines, or
for any consequenses
arising from its use.
CLINICAL
PRACTICE GUIDELINES FOR ACUTE STROKE
QUARTET
III - INPATIENT MANAGEMENT
CLINICAL
LEADER
Jerry
Schlegel, MD; Neurology, San Rafael
WORK
GROUP
Jai Cho,
MD; Neurology, Santa
Teresa
John
David, MD; Emergency
Medicine, San Rafael
Philip
Eulie, MD; Medicine,
San Francisco
Ron
Gaines, MD; Physical
Medicine, San Rafael
Dale
Grahn, MD; Medicine, Park
Shadelands
Jeff
Klingman, MD; Neurology,
Park Shadelands
Steven
Okuhn, MD; Vascular
Surgery, San Francisco
Howard
Slyter, MD; Neurology,
Sacramento
Bettiane
Wiessler, RN; ICU
Nursing, San Rafael
LarryYeager,
MD; Radiology,
Redwood City
Howard
Barkan,MA,DrPH
Stephen
Sidney, MD, MPH;
Division of Research
Philip
Bellman, MPH; TPMG
Department of Quality and Utilization
TOPIC LEADERS
Admission Criteria
for Acute Ischemic Stroke
Howard Slyter, MD; Neurology,
Sacramento
Inpatient
Management
of Acute Stroke
Dale
Grahn, MD; Medicine, Park
Shadelands
Management
of Blood
Pressure in Acute Stroke
Jeff Klingman, MD; Neurology,
Park Shadelands
Anticoagulation
in
Acute Ischemic Stroke
Howard Slyter, MD; Neurology,
Sacramento
CLINICAL REVIEW GROUP
The following individuals
reviewed these guidelines and
contributed to its final content.
Neurology
Scott Abramson, MD, Hayward;
Garrick Amgott-Kwan, MD,
Oakland; Everett Austin, MD, San
Francisco; Allan L. Bernstein,
MD, Santa Rosa; Raj Bhandari,
MD, Santa Teresa; Robert Elmore, MD,
Santa Clara; Robin Fross, MD,
Hayward; Barbara Gardner,
MD, Sacramento; Michael Gibbs, MD,
Roseville; Browne Goode, MD,
San Francisco; James Laster,
MD, Santa Clara; Garter Mosher, MD,
Sacramento; George Palma, MD,
Roseville; Joel Richmon,
MD, Oakland; Sidney Rosenberg, MD,
South San Francisco; Antoine
Samman, MD, Vallejo; R.
Jay Whaley, MD, Redwood City
Medicine
Tadios Amare, MD, Vacaville;
Henry Brodkin, MD, Redwood
City; Paul Feigenbaum, MD, San
Francisco; Pansy Kwong, MD,
Oakland; David Langkammer,
MD, Antioch; James Martin, MD,
San Rafael;Joan Pont, MD, San
Rafael; Michael Weaver,
MD, Martinez; David B Williams, MD, Vallejo
Emergency Medicine
George Bulloch, MD, Redwood
City; Uli Chettipally, MD,
South San Francisco;
Gary Hashimoto, MD, Walnut
Creek; Pankaj Patel, MD, Sacramento;
Christina Shih, MD, San Francisco
Hospital Based Specialists
Mark Clark, MD, HBS, Vallejo;
Lewis Lehman, MD, HBS,
San Francisco
Pharmacy
Cathlene Richmond, PharmD,
Regional Pharmacy Operations
PROJECT MANAGEMENT
Philip Bellman, MPH; TPMG
Department of Quality and Utilization
DESIGN AND PRODUCTION
Wendy Jung, MA, TPMG
Department of Quality and Utilization
Linda Rogers, MPA; TPMG
Department of Quality and Utilization
Copyright
1998
The
Permanente Medical Group,
Inc. All rights reserved.
Please contact TPMG Department of Quality and Utilization at
510-987-2309 or tie-line
8-427-2309 for permission to
reprint any portion of this publication. For additional copies of the
guidelines, please call
510-987-2950 or tie-line 8-427-2950.
CLINICAL
PRACTICE GLIIDELINES
Summary of Guidelines
Classification and Grading of
Recommendations
ADMISSION
CRITERIA FOR ACUTE ISCHEMIC STROKE
Purpose
Background
Recommendations
References
INPATIENT
MANAGEMENT OF ACUTE STROKE
Purpose
Background
Recommendations
References
Appendices
MANAGEMENT
OF
BLOOD PRESSURE IN ACUTE STROKE
Purpose
Background
Recommendations
References
ANTICOAGULATION
IN ACUTE ISCHEMIC STROKE
Purpose
Background
Recommendations
References
Previously
Published Clinical Practice Guidelines for Acute Stroke
QUARTET I - ACUTE EVALUATION and TREATMENT (NOVEMBER 1996)
*INITIAL BRAIN
IMAGING for TIA and STROKE
*TISSUE
PLASMINOGEN AcnVATOR/or ACUTE ISCHEMIC
STROKE
*ACUTE
EVALUATION and MANAGEMENT of INTRACEREBRAL
HEMORRHAGE
*INITIAL
EVALUATION of SUSPECTED SUBARACHNOID
HEMORRHAGE
QUARTET II - TIA and MINOR ISCHEMIC STROKE (OCTOBER 1997)
*INITIAL EVALUATION
and TREATMENT of TIA
and MINOR ISCHEMIC STROKE
*HOSPITAL
ADMISSION CRITERIA/orTRANSIENT
ISCHEMIC ATTACK
*INITIAL
VASCULAR IMAGING for SUSPECTED
CAROTID ARTERY STENOSIS
*CAROTID
ENDARTERECTOMY for SYMPTOMATIC
CAROTID STENOSIS
CLINICAL
PRACTICE GUIDELINE for ACUTE STROKE
QUARTET III - INPATIENT MANAGEMENT - SUMMARY OF GUIDELINES
ADMISSION
CRITERIA FOR ACUTE ISCHEMIC STROKE
Not
all patients with ischemic
stroke will necessarily
benefit from hospitalization. Hospitalization is indicated when
the
clinical
deficit is
substantial and/or anticipated to
progress, or when complications have occurred or are
anticipated.
Patients
suitable for specific
interventions, such as
thrombolytic treatment, acute anticoagulation, or urgent
vascular
surgery,
should also be
hospitalized, as should patients
in whom acute evaluation may lead to these or other
interventions.
INPATIENT
MANAGEMENT OF ACUTE STROKE
Hospitalized
patients should
be managed with specific
goals in mind: evaluation and treatment,
prevention of complications,
initiation of early rehabilitation,
and initiation of education and
secondary prevention. A
multidisciplinary approach is
recommended that begins in the
Emergency Department (ED) and
includes the ED physician,
an on-call stroke consultant,
the attending physician,
nursing personnel with stroke
expertise, Physical Therapy, and
Discharge Planning. A stroke
pathway or carepath to coordinate
the multidisciplinary
care
is recommended. A
designated Stroke Unit facilitates
this multidisciplinary approach and
is recommended where feasible.
MANAGEMENT
OF
BLOOD PRESSURE IN ACUTE STROKE
Acute
treatment of elevated
blood pressure in acute ischemic
stroke is not generally recom-
mended, as this intervention
may aggravate an ischemic
stroke
syndrome and worsen the
clinical
outcome. However,
extreme elevations of blood
pressure, malignant hypertension, aortic
dissection, or myocardial
infarction may warrant specific
intervention to reduce blood pressure.
The continuation of previously
prescribed drugs with
antihypertensive effects should be based on
a consideration of the
original indication of the medication,
the current blood pressure, and the
stability of the stroke
deficit.
ANTICOAGULATION
IN ACUTE ISCHEMIC STROKE
Acute
anticoagulation with
heparin is generally not recommended
in patients with completed
thrombotic
stroke. Progressing
stroke is a situation
in which acute anticoagulation with heparin
may be reasonable. Acute
anticoagulation with heparin
is also reasonable in cardioembolic stroke
resulting from a source with
high-risk of early re-embolization
(cardiomyopathy, rheumatic or
prosthetic valvular disease,
and acute myocardial infarction)
if hypertension is controlled, CT
excludes hemorrhage, and the
infarct is not large. Stroke
resulting from non-valvular atrial fibrillation
generally should not be
treated acutely with heparin
as the risk of early re-embolization is relatively low;
initiation of warfarin
(starting dose of 5 mg/day) without
preceding heparin is recommended.
CLASSIFICATION
AND GRADING OF RECOMMENDATIONS
Each
guideline recommendation is justified in
terms of
the level of research evidence supporting
it and the degree of consensus
on it among the members
of the work group. The distinction
between support derived from
scientific studies and that
derived from expert opinion is important.
Well-performed and relevant
scientific studies provide
a higher standard of evidence when they
are available, but many
aspects of medical care have
not been addressed by such studies. Expert
judgments supplement research
evidence by factoring in
clinical experience and human
values that are not easily
captured in scientific studies,
and by extrapolating from scientific
findings that were obtained
with specific populations
under specific conditions to a broad
clinical context.
Support for recommendations is
characterized as follows:
RESEARCH
EVIDENCE
Grade A
Supported by the results of
two or more randomized clinical
trials (RCTs) that have good internal
validity, and also
specifically address the question
of interest in a group of patients comparable to
the one to which the
recommendation applies (external
validity).
Grade B
Supported by a single RCT
meeting the criteria given
above for "Grade A''-level evidence, by RCTS
that only indirectly address
the question of interest,
or by two or more non-randomized clinical
trials (case control or cohort
studies) in which the
experimental and control groups are demon-
strably similar or
multivariate analyses have effectively
controlled for group differences.
Grade
C
Supported by a
single non-RCT
meeting the criteria given
above for "Grade B''-level evidence,
by studies using historical
controls, or by studies using
quasi-experimental designs such as pre-
and post-treatment comparisons.
EXPERT
OPINION:
Strong Consensus
Agreement
among at least 90%
of the guideline work group
members and expert reviewers.
Consensus
Agreement among at least 75%
of the guideline work group
members and expert reviewers.
Classifications
adapted from U.S. Dept. of Public
Health,
Agency for Health Care Policy and Research.
ADMISSION
CRITERIA for ACUTE ISCHEMIC STROKE
PURPOSE
The purpose of this guideline
is to identify patients
with acute ischemic stroke for whom acute admission is
appropriate and to review the
primary diagnostic and
therapeutic considerations bearing on this decision.
BACKGROUND
Every year approximately
400,000 Americans suffer an
acute ischemic stroke. Current published guidelines
recommend that most, if not
all, patients with acute
ischemic stroke be admitted to a hospital, preferably to a
"facility that specializes in
the care of stroke," or
a "stroke unit." 1,2
However, the rationale for
admitting all strokes has
not been clearly established, nor is there yet persuasive
evidence that such a policy
improves outcomes.
While
there is no prospective controlled trial of
admission
vs. non-admission, an observational series of 976
patients with an acute stroke
cared for by general practitioners
in England found that 26% were never admitted.
There were no differences in
the functional, social,
or emotional outcomes of patients managed at home vs.
those admitted to hospital
when the severity of the initial
disability had been taken into account.3
A retrospective study from Harbor-UCLA Medical
Center
evaluated 168 stroke admissions from the emergency
department (ED) for medical
appropriateness using five
criteria: another diagnosis that warranted admission;
an inadequate home situation;
altered mental status;
an adverse event during hospitalization, including worsening
of the deficit; and the need
for a hospital-based treatment
that could not be provided on an outpatient basis4
Only 39% of the admissions met
these criteria. Nevertheless,
the authors concluded that admission of all stroke
patients was justified because
subsequent deterioration
could not be predicted in the ED.
Traditionally,
patients have been admitted in
order to
initiate and complete their diagnostic evaluation, to administer
therapies aimed at the
prevention of progression or recurrence,
and to prevent or treat complications. However, the
technological revolution which
allows outpatient scanning
and vascular imaging for many cases, as well as the
increased capability of
skilled nursing facilities and
home health resources to monitor patients, administer
intravenous medications
and provide acute
rehabilitation, all challenge
the rationale for routine admission of every stroke patient. At the same time, there are
now treatments for acute
stroke which may require hospitalization for drug
administration and patient
monitoring.
The
following sections discuss
each of the rationales
for admission.
Rationale
for
Admission:
Acute Therapy
Thrombolysis with t-PA has
been shown to be effective
in improving stroke outcome in carefully selected patients
when given within three hours
of stroke onset.5
Currently, the administration of this drug and the monitoring
of such patients requires
hospitalization.
The
accumulation and spread of neurotoxic
substances such
as calcium and glutamate is believed to be the proximate cause of neuronal death in
acute stroke. A variety of
drugs intended for neuroprotection are under investigation. Some
of these may require
hospitalization for administration
and/or monitoring.
The
routine administration of heparin has been
common-place
in some institutions for patients with acute stroke who
are neurologically stable. At
present there is no evidence
to support this practice. Two controlled studies, using either
intravenous heparin or "medium
dose" subcutaneous heparin
(12,500 U ql2h) have shown no benefit.6,7
Rationale
for
Admission:
Stroke Progression
Every published series
indicates that substantial numbers
of patients with acute ischernic stroke deteriorate due to
stroke progression in the
several days after onset. Combining
the data from several large series8,15 the risk
of such
deterioration
is in the
neighborhood of 30%. Unfortunately,
it is not possible to identify reliably patients whose stroke
will progress.
There
have been several uncontrolled series
reported on
the use-of intravenous heparin in patients with progressing
stroke. In these studies, the
deficit has continued to
progress in 21 to 50% of patients despite anticoagulation.16,19
Since these studies have
lacked control groups, it is
not possible to judge whether heparin-treated patients have
done any
better than they would
have without treatment.
The
Stroke Council of The American Heart
Association found
that "because data about the safety and efficacy of
heparin in patients with acute
ischemic stroke are insufficient
and conflicting, no recommendation can be offered...
Until more data are available,
the use of heparin remains
a matter of preference of the treating physician." 1
Even if heparin is of uncertain value in treating
stroke
progression, it is important to keep in mind that there
are many causes of neurologic
deterioration besides clot
propagation and embolization that need consideration and
may require intervention.
Chief among these is hypotension,
whether caused by the injudicious use of antihypertensive agents or by dehydration.
Other important causes of deterioration
include impaired cardiac output, hypoxia, seizures, intercurrent
infection, sedative drugs or the
development of cerebral edema. 20
Rationale
for Admission:
Acute Secondary
Prevention in Patients with
Embolic Stroke
Patients
who have suffered an
embolic stroke may be at
significant risk of a recurrent embolic event in the acute
period. Many series of
patients with cardiac emboli have
been published, with early recurrence rates varying anywhere
from 2% to 20%.21
Recommendations in this
setting have varied widely: some have advised immediate
heparin for
all alert patients (once
the CT has ruled out hemorrhage);22others
have counseled delay for at least
48 hours23,24
still others would not advise
heparin at all.25,26 Recently published
data from the International
Stroke Trial suggest that
in patients with acute stroke and atrial fibrillation, heparin
can accomplish a small
reduction in stroke recurrence
only at the cost of as many or more hemorrhagic complications.7
Again, in 1994 the American
Heart Association felt that
insufficient data prevented any firm recommendation for acute heparinization in this
setting.1
Rationale
for Admission:
Acute Vascular
Interventions
There
are patients with acute
minor or fluctuating deficits
in whom urgent carotid imaging and surgery might be
considered. While such an
approach is reported from some
centers,27,28 the benefit of such
aggressive
therapy
has not been
systematically studied.1
Rationale
for Admission:
Acute Supportive Care
There are patients who require
acute supportive care
for their new deficits or for acute complications of infarction,
such as seizures, aspiration,
or malignant arrhythmias.
Patients especially at risk of neurologic deterioration from
mass effect are those with
large middle cerebral artery
infarcts or large cerebellar infarcts. Close neurologic
monitoring, intensive medical
support, or the anticipation
of possible neurosurgical intervention may all necessitate
hospitalization.
Rationale
for Admission:
Additional Considerations
There are many patients who do
not meet any of the criteria
above who still may warrant admission to an acute
hospital, an observation unit,
or a closely-monitored
skilled nursing facility. Admission may be required by co-morbid
medical conditions, unstable
vital signs, a need to further
clarify the mechanism of the stroke, the prevention or
treatment of stroke
complications, or the initiation
of a stroke treatment plan, including secondary prevention and
rehabilitation.
RECOMMENDATIONS
1. Admission is
required for patients receiving
t-PA or other acute therapies requiring in-patient administration
and/or monitoring.
(Expert Opinion: Strong Consensus)
2. Admission is required if
urgent vascular surgery
is indicated.
(Expert Opinion:
Strong Consensus)
3- Admission is
recommended for patients
with infarcts where clinical deficit is substantial and/or deterioration
is anticipated.
(Expert Opinion: Strong Consensus)
4. Admission is
recommended when needed to
treat acute complications of stroke, such as seizures, aspiration
pneumonia, deep vein
thrombosis (DVT), or arrhythmia.
(Expert
Opinion: Strong Consensus)
5. For other
patients, admission may be indicated
based on an evaluation of specific diagnostic or therapeutic
needs of the patient and the
availability of appropriate
monitoring, care and follow-up in a non-hospital setting.
(Expert Opinion: Strong Consensus)
6. Patients not
admitted require an appropriate
and timely diagnostic evaluation, the initiation of necessary therapy,
and the initiation of an
appropriate secondary prevention
plan. Discussion with a stroke consultant (usually a
neurologist) and appropriate
follow-up with neurology
and/or primary care is generally recommended.
(Expert
Opinion: Strong Consensus)
REFERENCES
1.
Adams HP Jr, et al. Guidelines for
the management of patients with acute ischemic stroke. A statement for
healthcare professionals
from a special
writing group of the Stroke
Council, American Heart Association. Stroke 1994; 9: 1901 -14.
2.
Lanska DJ. Review criteria for hospital
utilization for patients with cerebrovascular disease. Task Force on
Hospital Utilization
for Stroke of the
American Academy of Neurology.
Neurology 1994; 44:1531-2.
3.
Wade
DT, Langton Hewer R. Hospital admission
for acute stroke: who, for how long, and to what effect? J Epidmiol
Community
Health 1985; 39:347
-52.
4.
Henneman PL, Lewis RJ. Is admission
medically justified for all patients with acute stroke or transient
ischemic attack?
Ann
Emerg Med 1995;25:458-63.
5.
The National Institute of Neurological
Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen
activator
for
acute
ischemic
stroke. NEnglJMed
1995; 333: 1581 - 7.
6.
Duke RJ, et al. Intravenous heparin
for the prevention of stroke progression in acute partial stable
stroke.
Ann Mem Med
1986;105:825-8.
7.
The International Stroke Trial Collaborative
Group. The International Stroke Trial (1ST): a randomized trial of
aspirin, subcutaneous
heparin, both, or
neither among 19435 patients
with acute ischemic stroke. Lancet 1997;349: 1569 - 81.
8. Jones
HJ, Millikan CH. Temporal profile
(clinical course) of acute carotid system cerebral infarctlon. Stroke
1976;
7:64-71.
9.
Jones HR Jr, et al. Temporal profile
(clinical course) of acute vertebrobasilar system cerebral infarction.
Stroke 1980;
11:73-7.
10.
Patrick BK, et al. Temporal profile
of vertebrobasilar territory infarction. Prognostic implications.
Stroke
1980; 11: 643 - 8.
11.
Irino T, et al. Angiographical
analysis of acute cerebral infarction followed by "cascade''-like
deterioration
of minor neurological deficits.
What is progressing
stroke? Stroke 1983; 14:363-8.
12.
Britton M, Roden A. Progression
of stroke after arrival at hospital. Stroke 1985; 16:629 -32.
13.
Davalos A, et al. Deteriorating
ischemic stroke: risk factors and prognosis. Neurology 1990; 40: 1865 -
9.
14.
Wityk RJ, et al. Serial assessment
of acute stroke using the NIH Stroke Scale. Stroke 1994; 25:362 - 5.
15.
Toni D, et al. Progressing neurological
deficit secondary to acute ischemic stroke. A study on predictability,
pathogenesis, and prognosis.
Arch Neurol 1995;
52:670 - 5.
16.
Dobkin BH. Heparin for lacunar
stroke in progression. Stroke 1983; 14:421-3.
17.
Haley EC Jr, et al. Failure of
heparin to prevent progression in progressing ischemic infarction.
Stroke
1988; 19: 10 -14.
18.
Slivka A, Levy D. Natural history
of progressive ischemic stroke in a population treated with heparin.
Stroke
1990;
21: 1657 - 62.
19.
Dahl T, et al. Heparin treatment
in 52 patients with progressive ischemic stroke. CerebrovascDis 1994;
4:
101 - 5.
20.
Caplan LR. Treatment of "progressive"
stroke. Stroke 1991; 22: 694-5.
21.
Safety of heparin in acute ischemic
stroke [letters]. Neurology 1996;46:589-91.
22.
Chamorro A, et al. Early anticoagulation
after large cerebral embolic infarction: a safety study. Neurology
1995;
45:
861 - 5.
23.
Cerebral Embolism Task Force. Cardiogenic
brain embolism.The second report of the Cerebral Embolism Task Force.
Arch Neurol 1989; 46:727 - 43.
24.
Hart RG. Cardiogenic embolism to
the brain. Lancet 1992;339:589-94.
25.
Scheinberg P. Heparin anticoagulation
[editorial]. Stroke 1989;20:173-4.
26.
Phillips SJ. An alternative view of heparin
anti- coagulation in acute focal brain ischemia. Stroke 1989; 20:295 -
8.
27.
Walters BB, et al. Emergency carotid
endarterectomy. / Neurosurg 1987:66:817-23.
28. Meyer
FB, et al. Emergency carotid endarterectomy
for patients with acute carotid occlusion and profound neurological
deficit. Ann Surg 1986; 203:82
- 9.
INPATIENT MANAGEMENT OF ACUTE STROKE
PURPOSE
The purpose of this guideline
is to provide a framework
for the inpatient management of acute stroke.
BACKGROUND
Recent years have witnessed
many developments in the
overall management of patients with cerebrovascular disease.
Risk factor modification has
improved stroke prevention.
Medical and surgical interventions after transient ischemic
attack (TIA) and minor
ischemic stroke reduce incidence
of major stroke in selected patients. Acute medical and surgical
treatment is beneficial for
identifiable subsets of stroke
patients. In addition, prevention of acute complications, along with early
rehabilitation, improve clinical outcome
after stroke.1-3
The acute management of patients with
TIA and stroke
has traditionally been in the setting of an acute care hospital,
The benefit of routine
hospitalization for all of these
patients, however, is in question.4-6 After
initial evaluation
in
the
emergency department (ED),
a patient with TIA or
stroke may be hospitalized for further evaluation and treatment,
transferred to a skilled
nursing facility (SNF) for nursing
care, or managed as an outpatient. Which of these settings is
appropriate depends on the
need for clinical observation,
the specific medical or surgical treatment considered, and the intensity of nursing care
anticipated. The patient's
stroke syndrome, the severity of neurologic deficit, and the
medical condition
and social
circumstances of the patient, all
help determine the appropriate acute management setting.
An acute care hospital is the most intense
management
setting, and care should be directed toward accomplishing
specific goals which improve
clinical outcome. For patients
admitted to a SNF for acute management, the intensity of
medical treatment and nursing
care will be less, but
the goals of management should be the same. The general principles
of inpatient management for
acute stroke outlined here
should apply as well to the management of patients with stroke in a SNF, and to the
outpatient management of
patients with acute cerebrovascular disease.
GOALS
OF ACUTE MANAGEMENT OF PATIENTS WITH STROKE
There are four goals in the
acute management of patients
with stroke. These are:
Evaluation and treatment
Prevention of acute complications
Initiation of early rehabilitation
Initiation of education and secondary prevention
Evaluation
and Treatment
The
goal of the initial
evaluation of a patient with
acute stroke is to characterize the stroke syndrome sufficiently to
initiate appropriate
treatment. This usually occurs in
the ED. Clinical assessment and CT brain imaging are generally
required to identify the
stroke syndrome as either an
ischemic stroke, an intracerebral hemorrhage, a subarachnoid hemorrhage, or a cerebral venous
thrombosis. The cerebrovascular
anatomy of the stroke syndrome, and the severity of the neurologic deficit, should
also be assessed during the
initial evaluation. Accurate initial evaluation is pivotal in directing
appropriate initial
management, and often requires discussion
or consultation with a stroke consultant.
Further
evaluation and treatment may require
repeated
assessment of neurologic status. With or without treatment,
the severity of neurologic
deficit may progress, fluctuate,
or improve. Additional brain imaging, as well as vascular or
cardiac imaging, may be
necessary to establish the stroke
mechanism and specific stroke pathophysiology. These
determinations may direct
appropriate specific treatment.
Inpatient management of acute stroke thus involves evalua-
tion and treatment that
proceed simultaneously.
Prevention
of Acute Complications
Prevention
of stroke complications improves
clinical outcome
to a degree similar to that accomplished with
specific stroke treatment.7
The major complications
to be anticipated and prevented are: adverse effects of medications;
aspiration pneumonia;
dehydration and malnutrition; skin
breakdown; urinary tract infection; deep venous thrombosis
(DVT); and falls.
Medical treatment should avoid unnecessary use of
drugs
which depress central nervous system function. The use of
such drugs in patients with
acute stroke has been associated
with worsened clinical outcome.8 Similarly, the
use of anti-hypertensives
in acute stroke
should generally be avoided,
as lowered blood pressure in this setting may aggravate the
stroke syndrome.
The
routine assessment of aspiration risk and the
use
of a routine swallow evaluation reduce the incidence of aspiration
pneumonia complicating stroke.9-11
Stroke
patients are at risk of acute dehydration and malnutrition. Swallow
evaluation aids
in establishing need for
parenteral fluids, nasogastric
feeding tube, or percutaneous endoscopic gastrostomy." Early enteral intake is
desirable to facilitate discontinuation
of otherwise unnecessary intravenous catheters.
Attention
to skin integrity and the prevention of
pressure
ulcers is important. Avoidance or rapid discontinuation of
urinary catheters reduces the
incidence of urinary tract
infections. DVT and pulmonary emboli are preventable
complications of stroke, and
their occurrence is reduced
by mobilization, pressure stockings, and/or low dose anticoagulation.13,14
Early mobilization reduces the risk of many of the
acute
complications of stroke, and improves clinical outcome.13,15
With ambulation, however, the
risk of falling increases.
Thus progressive mobilization needs to proceed along with
assessment of falling risk and
preventative measures.
Prevention
of acute complications of stroke
requires an
expertly trained nursing staff working with an attending
physician familiar with
inpatient stroke management.
Physical therapy, nutritional services, and pharmacy are also
involved. Speech therapy and
occupational therapy may
be involved when necessary. A predetermined inpatient plan,
such as a stroke carepath,
coordinates inpatient management
and reduces the incidence of acute complications.16,17
The acute care of patients in
a geographically designated
nursing stroke unit has also been associated with a lower incidence of acute
complications.18
Initiation
of Early Rehabilitation
The
Agency for Health Care
Policy and Research Post-Stroke
Rehabilitation Clinical Practice Guidelines emphasize
that rehabilitation should
begin in the acute care setting.3
Initiation of early rehabilitation aids in preventing acute
complications and improves
long-term functional outcome.
Early mobilization and the initiation of rehabilitation in the
inpatient setting will require
input from physical therapy.
Determining
the appropriate rehabilitation plan
and setting
requires early assessment. The transition from the
acute inpatient setting to the
rehabilitation setting
needs to be accomplished smoothly so that all relevant clinical information is reliably transferred
to the physician accepting
the patient, and so that continuity of ongoing care is assured.
Initiation of early
rehabilitation will rely on the discharge
planner to coordinate the transition from the acute inpatient
setting to the appropriate
rehabilitation setting.
Initiation
of Education and Secondary Prevention
The management of patients
with acute stroke and TIA
includes addressing education and secondary prevention.
Identification of the stroke
mechanism and specific patho-physiology
provides the basis for subsequent interventions.
In part these interventions
will involve patient education
and life style modification. This aspect of patient education will
be the beginning of a life
long process.
Stroke
also affects the patient's entire family.
Educational
efforts during acute management therefore should address
family needs. The family's
understanding of the course
and prognosis allows the development of realistic expectations.
Education of the family
members may need to focus on
prevention of complications as well as on rehabilitation.
Alternatively, end-of-life
issues may need to be addressed,
and psychological support of the family is often necessary.
Advance Directives may require family members to
make
critical decisions. If Advance Directives have not been completed,
family education and
involvement is even more crucial.
MULTIDISCIPLINARY
APPROACH TO ACUTE MANAGEMENT
The
acute management of patients with stroke has
evolved
into a multidisciplinary effort. A coordinated team approach
to inpatient management
improves clinical outcome of
hospitalized patients. Specific approaches include clinical
pathways or carepaths,
multidisciplinary stroke programs,
and dedicated stroke units.
It
is often difficult to generalize from studies
which
claim benefit with particular approaches. Many were done in diverse
health care systems, and it is
problematic to apply results
to other populations and settings. In many studies which demonstrate benefit with a
coordinated approach to acute
management, it is unclear whether the benefit arises from the use of a predetermined
stroke pathway, available
special expertise in stroke treatment, specific interventions such as
DVT prophylaxis, or the
multidisciplinary approach to
patient care.
A
formalized approach using a stroke pathway or
care-path
does appear to be of benefit.16,17,18Stroke
pathways and
carepaths
coordinate a
multidisciplinary clinical team
and generally include nursing protocols to prevent complications,
document clinical course, and
address early rehabilitation
issues. The role of expert nursing is an important element of
this formalized approach. A
multidisciplinary stroke
team also appears to be beneficial.6 The
benefits of such an
approach include
improved accuracy in
the diagnosis of stroke
and better resource utilization, as evidenced by shortened hospital
length of stay and fewer
unnecessary tests. 6,16,17,19
Studies
suggest that the care of patients in a
geographically
designated stroke nursing unit favorably impacts the outcome
of acute stroke.6,18,20-24
The benefits of
stroke units include reduced long-term mortality and improved
functional
outcome. Much
of the value of a
coordinated approach to inpatient
management appears to result from specialized nursing care.
This is facilitated in a
designated stroke nursing unit.
Other advantages of such designated units include a commitment of
team members to education and
early attention to rehabilitation
issues.
Fundamental to the coordinated approach to acute
management
is the involvement of the multidisciplinary
stroke team. Team members
roles may be identified as
follows:
ED Physician
The
ED physician is generally the first physician
to evaluate
the acute stroke patient. In the course of initiating acute
evaluation and treatment, the
ED physician will usually
communicate with the stroke consultant and/or attending
physician while the patient is
in the ED.
Stroke Consultant
The
stroke consultant is usually a neurologist,
neurosurgeon,
or vascular surgeon. The role of the stroke consultant is to
direct evaluation identifying
the stroke syndrome, mechanism,
anatomy, and pathophysiology, and to recommend appropriate
therapy. The stroke consultant
is also involved in directing
further evaluation, specific therapy, and approaches toward
secondary prevention.
Attending Physician
The
role of the attending physician is to
coordinate all
aspects of the patient's inpatient care. This requires close involvement
with the nursing staff in
addition to the other members
of the stroke team. The attending physician has the ultimate
responsibility for inpatient
management. The attending
physician may also be the stroke consultant.
Nursing
Nursing assesses and monitors the patient,
provides the
specific treatment ordered, and implements specific nursing
practices to prevent acute
complications. The nursing
staff needs to communicate routinely with the stroke consultant
and/or attending physician,
and needs to notify the attending
physician of any significant change in the patient's condition.
Physical Therapy
Physical
Therapy, and Rehabilitation Medicine
where available,
directs progressive mobilization and early rehabilitation.
Safety regarding ambulation
and fall risk, as well as
the long-term rehabilitation plan, is addressed by physical therapy. The
physical therapist will
therefore need to communicate
with nursing, the stroke consultant, and the attending physician.
Discharge Planning
Discharge
Planning, along with Rehabilitation
Medicine
where available, addresses continuity with long-term
rehabilitation and secondary
prevention, assuring smooth
transition to the next setting and level of care. The discharge
planner will need to work with
the attending physician,
stroke consultant, nursing, and physical therapy.
Acute
management, particularly inpatient
management, of
patients with TIA and stroke can be framed in terms of
defined goals and roles of a
multidisciplinary team.
Many inpatient carepaths have been developed and are used
successfully to coordinate the
multidisciplinary approach.
Examples of a general acute stroke pathway and a stroke unit
nursing care plan are given in
the appendices (pages
13 -14).
RECOMMENDATIONS
1. Whenever
possible,
acute management of
patients with stroke should be provided by a multidisciplinary stroke
team. The stroke team should
include an ED physician,
stroke consultant, attending physician familiar with
inpatient management, nursing
staff trained in stroke
care, physical therapy, and discharge planning. The
physician and nursing members
of the stroke team should
be available and accessible at all times.
(Expert Opinion: Strong
Consensus)
2. Inpatient
management of patients with
stroke should be programmatic and formalized with a pathway or
carepath which coordinates the
multidisciplinary care
of the stroke team.
(Expert
Opinion: Strong
Consensus)
3.
To
facilitate nursing expertise for the inpatient
management of patients with stroke, the designation
of a geographically distinct
inpatient stroke unit is
recommended where feasible.
(Expert
Opinion: Strong
Consensus)
4.
Acute evaluation and treatment
should
generally
involve a stroke consultant.
Expert Opinion: Strong
Consensus)
5.
Measures to prevent complications
should
be
incorporated
into the care of patients hospitalized with stroke. These
include:
bedside swallow
evaluation assessing risk of aspiration;
maintenance of
hydration and nutrition;
prevention
of deep
venous thrombosis (DVT) when
prolonged immobility is likely;
promotion of early
progressive mobilization and
prevention of falls;
maintenance
of skin
integrity;
avoidance
and
discontinuation of urinary catheters.
Documentation
of these measures and the patient's
neurologic
status and clinical course should be part of the
inpatient nursing record.
(Expert Opinion: Strong
Consensus)
6.
A rehabilitation plan should be
formulated
prior
to discharge from acute management.
(Expert Opinion: Strong
Consensus)
7.
Patient and family education should
be
comprehensive
and address course of illness, rationale for treatment,
prognosis, psychosocial and
safety issues, secondary
prevention, and, when appropriate, end-of-life issues.
Whenever possible, Advanced
Directives should be completed
and preferences for intensity of care documented.
(Expert Opinion: Strong
Consensus)
8.
Stroke team members should
participate in
continuing
education in the management of stroke.
(Expert Opinion: Strong
Consensus)
REFERENCES
1.
Cooper R, et al. Slowdown
in the decline of stroke mortality in
the United States, 1978-1986.
Stroke 1990; 21: 1274 -
9.
2.
Thorn TJ. Stroke mortality trends:
an international perspective.
Ann Epidemiol 1993; 3:509 -18.
3.
Gresham GE, et al. Post-stroke rehabilitation.
Clinical Practice
Guideline,
No. 16. Rockville,
MD: U.S. Department of
Health
and Human
Services. Public
Health Service, Agency for
Health
Care
Policy and Research.
AHCPR Publication No. 95-0662.
May 1995.
4 Wade DT,
Langton Hewer R. Hospital admission
for acute stroke:
who,
for how long, and to what
effect?JEpidemiol Community
Health
1985; 39:347 - 52.
5.
Henneman PL, Lewis RJ. Is admission
medically justified for all
patients
with acute stroke or
transient ischemic attack?
Ann
Emerg Med
1995; 25:458 -63.
6.
Kaste M, et al. Where and how should
elderly stroke patients be
treated?
A randomized trial.
Stroke 1995; 26:249 - 53.
7.
Davenport RJ, et al. Complications
after acute stroke. Stroke
1996;
27:415-20.
8.
Goldstein LB. Common drugs may influence
motor recovery
after
stroke. The Sygen in
Acute Stroke Study Investigators.
Neurology 1995; 45:865 -70.
9.DePippo KL, et al. Dysphasia
therapy following stroke:
a controlled
trial.
Neurology 1994 Sept;
44: 1655 - 8.
10.Holas
MA, et al. Aspiration
and relative risk of medical
complica-
tions
following stroke.Arch
Neurol 1994; 51:1051 - 3.
11.HomerJ,
et al. Aspiration
following stroke: clinical
correlates and
outcome.
Neurology 1988; 38:
1359 - 62.
12.Davalos
A, et al. Effect of
malnutrition after acute
stroke on clinical
outcome.
Stroke 1996; 27: 1028
- 32.
13.Sandset
PM, et al. A
double-blind and randomized placebo-
controlled trial of low
molecular weight heparin once
daily
to prevent
deep-vein
thrombosis in acute ischemic stroke.
Semin Thromb Hemost 1990; 16
Suppi: 25 - 33.
14.Brandstater
ME, et al.
Venous thromboembolism in stroke:
literature review and
implications for clinical practice.
ArchPhysMedRehaW 1992; 73
Suppi: 379-91.
15.Hayes
SH, Carroll SR. Early
intervention care in the
acute stroke
pnW.Ard}Pl]ysMedRehabil
1986;
67 319-21.
16.
Wentworth DA, Atkinson RP. Implementation
of an acute stroke
program
decreases
hospitalization costs and length of
stay.
Stroke
1996; 27: 1040 -3.
17.
Odderson IR, McKenna BS. A model
for management of patients
with
stroke during the acute
phase. Outcome and economic
implications.
Stroke 1993; 24:
1823 - 7.
18.
Stroke Unit Trialists' Collaboration.
Collaborative systematic
review
of the randomized
trials of organized inpatient
(stroke
unit)
care after stroke.
BrMedj 1997; 314: 1151-9.
19.Alberts
MJ, et al. Hospital
charges for stroke patients.
Stroke
1996;
27:1825-8.
20.Langhome
P, et al. Do
stroke units save lives? Lancet
1993;
342:395-8.
21.Garraway WM, et al.
Management of acute stroke in
the elderly:
preliminaiy
results of a
controlled trial. BrMedJ 1980;
280:
1040-3.
22.Strand T, et al. A
non-intensive stroke unit reduces
functional
disability
and the need for
long-term hospitalization.
Stroke
1985;16:29-34.
23.Indredavik B, et al.
Benefit of a stroke unit: a randomized
controlled trial. Stroke 1991;
22: 1026 - 31.
24.Ronning
OM, Guldvog B.
Stroke units versus general
medical
wards,
1: twelve- and
eighteen-month survival. Stroke
1998;
29:58-62.
APPENDICES
The
appendices present examples of an Acute Stroke Pathway
and a Stroke Unit Nursing Care Plan developed for
use
at the Kaiser Permanente Medical Center, San Rafael,
California. They are provided as models that can be adapted for
use in other acute stroke management care programs.
*Copyright
1998 The Permanente Medical Group, Inc.
MANAGEMENT
of
BLOOD PRESSURE in ACUTE STROKE
PURPOSE
The purpose of this guideline
is to address the management
of blood pressure in acute stroke.
BACKGROUND
Blood Pressure in Acute Ischemic Stroke
Hypertension has been
recognized for decades as one of
the most important risk factors for ischemic and hemor-
rhagic stroke. There is little
doubt that long-term control
of elevated blood pressure is beneficial in reducing the risk
of both of these types of
stroke.1,2However,
the treatment of elevated blood pressure in acute stroke involves
different
considerations,
and there are
a number of reasons for
a cautious and expectant approach rather than attempting
to reduce or normalize blood
pressure in this setting:
Elevated
blood pressure is relatively
common in
acute stroke, both in patients with pre-existing hypertension and
in those without a history of
hypertension. A number
of studies have demonstrated a tendency for elevated blood
pressure to fall without any
intervention in the first
hours or days after stroke onset.3-6
The threshold for autoregulation of cerebral
circulation
(the ability of the brain to maintain a constant blood flow
over a wide range of blood
pressures by constricting
vessels as blood pressure rises and relaxing them as blood pressure
falls) is raised in
chronically hypertensive patients.
Optimal blood flow may not be maintained if blood pressure falls
below a certain critical
level, and this level is substantially
higher in hypertensive than in normotensive individuals7-9
Tissues surrounding the area of infarction, the
"ischemic
penumbra," are tenuously perfused and at risk of perma-
nent injury if there is even a
minor reduction of local
blood supply. In the area of acute ischemic injury, autoregulation
is lost and blood flow becomes
directly proportional
to systemic blood pressure.10-16
There
are a number of published cases where acute
stroke
patients clinically worsened as their blood pressure
was aggressively treated, and
cases where clinical deficits
fluctuated directly with fluctuations of blood 14,17-19
Cerebral perfusion has been demonstrated to be
impaired
in acute stroke patients with rather mild blood pressure
reduction (13 to 16% mean
arterial pressure). When this
occurs there may be no outward sign that a harmful
process is taking place.20
There is at least one report of a possible
beneficial
effect from using pressors to raise blood pressure in acute
stroke patients.21
Treatment
of
Acute Hypertension in the Setting of Ischemic Stroke
Treatment
of hypertension in acute stroke may be
indicated
in certain very specific circumstances.
There may be an increased risk
of intracerebral hemorrhage
in severely hypertensive patients undergoing t-PA
infusion for acute stroke.22
Cautious blood
pressure control has been suggested if blood pressure rises after
institution of
treatment with t-PA.23
Elevated blood pressure
has also been suggested to be a risk factor for hemorrhage in anti-coagulated patients24
Acute vascular damage and extension of ischemia
may occur
in the setting of malignant hypertension with hyperten-
sive encephalopathy. Malignant
hypertension is characterized
by papilledema, nephropathy, encephalopathy, microangio-pathic hemolytic anemia, and
cardiac failure. In this
setting rapid treatment of hypertension is generally recommended.25,26
Other life threatening
emergencies, such as acute myocardial
infarction or aortic dissection, may also necessitate rapid
reductions in blood pressure.26,27
There are no studies showing that urgent reduction
of
blood pressure in the absence of these specific situations has
any beneficial effect. There
is also no evidence to support
the hypothesis that there is substantial risk of immediate organ
damage in leaving elevated
blood pressure untreated in
the absence of these unusual complications.26-29
Choice of Medications to Manage Blood Pressure in
Stroke
In the uncommon situation where it is necessary to
reduce
blood pressure in acute stroke, there are no controlled studies
to indicate the most
appropriate medication. However,
consideration of the mechanism of action of the various medications used to treat
hypertension may provide some
guidance.26,30 Alpha- and beta-blockers,
ganglionic blockers, and
ACE inhibitors have little
effect on cerebral vascular
tone. Short acting beta-blockers have not been specifically studied
in the setting of ischemic
cerebrovascular disease and
acute hypertension, but offer several theoretical advantages such
as ability to titrate blood
pressure response, short
duration of action, and relative lack of effect on cerebral vascular
tone.
Labetolol
was used in the
National Institute of Neurological
Disorders and Stroke (NINDS) t-PA study for blood pressure
treatnent.23
In the case of blood pressure
treatment because of acute cardiac ischemia or aortic dissection, the
reduction in
cardiac output caused by
beta-blockers also offers
potential cardiovascular benefits.
Nitroprusside
offers the advantage of close
titration
of blood pressure response, but it causes cerebral vasodilatation
that may increase intracranial
pressure. Since cerebral
perfusion pressure is related to the difference between mean
arterial pressure and
intracerebral pressure, an increase
in intracranial pressure may reduce cerebral perfusion pressure.
In the case of malignant
hypertension or intracerebral
hemorrhage (IGH), a further increase in intracranial
pressure is probably not
desirable. Calcium channel blockers
and hydralazine also cause cerebral vasodilatation and have
the added disadvantage of a
sometimes unpredictable response.
Inadvertent overaggressive blood pressure reduction may cause iatrogenic worsening
of the ischemic stroke
deficit and must be avoided.
There
is no rationale for the use of diuretics for
acute
blood pressure treatment in the setting of acute ischemic
stroke. This class of drugs
lacks an immediate effect
on blood pressure and promotes dehydration, already present in many
stroke patients.
Should
Blood
Pressure Be Raised by Pressors in the Setting of Acute
Ischemic Stroke?
There has been one report investigating induced
hypertension
in the treatment of acute ischemic stroke.21This
study demonstrated improvement
in some patients whose
blood pressure was raised by the use of phenylepherine.
There are several anecdotal
reports of worsening of ischemic
stroke deficit concomitant with blood pressure reduction.14,16-19
Pathophysiologically, one
might expect that blood pressure
reduction could impair cerebral perfusion, thus worsening
the clinical deficit.
Therefore, there is some rationale
for an induction of a higher blood pressure in the setting of relative
hypotension and acute ischemic
stroke.
Should
Outpatient Antihypertensives Be Continued or Discontinued in
the Setting of Acute Ischemic Stroke?
Unfortunately,
there are few clinical data and
little
discussion in review articles to help answer this important
question. One recent report
studied this question by
discontinuing antihypertensive agents in half of a randomized group
of patients with hypertension
and acute stroke. No difference
in outcome between the groups of patients in whom
anti-hypertensives were
continued or discontinued
was observed.31
Vasoactive
drugs are often given for reasons other
than
for reducing blood pressure. For example, beta-blockers and calcium channel blockers may be
used for treatment of ischemic
heart disease as well as hypertension. In this setting, the need
to maintain the therapeutic
effects of these drugs must
be considered in light of possible adverse blood pressure effects.
Since prior studies of blood
pressure in acute ischemic
stroke have sometimes correlated clinical fluctuations with blood
pressure fluctuations, the
stability of the clinical
deficit may also be useful in guiding the decision regarding the
continuation of vasoactive
drugs.
Management
of
Blood Pressure in the Setting of Intracerebral Hemorrhage
Marked
elevations in blood pressure are common
immediately
after intracerebral hemorrhage (ICH). Enlargement of
the area of hemorrhage has
been observed in some patients
with ICH.32 Whether
control of acute hypertension reduces the
risk of enlargement of
hemorrhage is unknown. As
in the case with ischemic stroke, altered autoregulatory thresholds in chronically
hypertensive patients, and
impaired autoregulation in ischemic brain adjacent to the hemorrhage,
are a concern.10
One
prospective study evaluated the role of
antihypertensive
therapy in ICH.33
A
positive outcome was reported for treated patients compared to those in
whom blood pressure was
left untreated. However, the study was unblinded, performed in the
pre-CT era, and patients
allocated to the treatment arm
were clinically far less impaired at onset than those left untreated.
Another study retrospectively
reviewed the outcome of
patients with ICH treated with antihypertensive agents and concluded
that those with blood
pressures of greater than 145 mean
arterial pressure (MAP) had worse outcomes than those with
lower blood pressures.
However, since attempts were made
to control blood pressure in all patients, it is uncertain whether
there was a positive effect of
treatment. It is possible
that uncontrollable blood pressure, even in the face of attempted
aggressive therapy, is a
marker for a worse prognosis.
At
this time, the issue of hypotensive therapy for
acute
ICH is unresolved. The value of early hypotensive therapy in
preventing rebleeding or edema
is unknown. As in ischemic
stroke, there are concerns of possible ischemic damage with
acute blood pressure
reductions.
RECOMMENDATIONS
1. In
general, urgent
treatment of elevated
blood pressure in acute ischemic stroke is not recommended. There
is no evidence that such
treatment is beneficial. There
is evidence that such treatment may be harmful.
(Research Evidence: Grade C)
2.
Several authorities have
suggested that
treatment of
"sustained,
extreme"
(>220 systolic or >130 MAP) blood
pressure elevation is advisable.34 38
Based upon
these
recommendations,
treatment of such sustained, extreme
elevated blood pressure may be considered.
However, the treating
physician should be aware that
there are no prospective or retrospective data to support
this therapeutic intervention.
(Expert Opinion: Strong
Consensus)
3.
There are specific cases where
acute reduction
of elevated blood pressure is, or maybe, indicated:
t-PA treatment of
acute ischemic stroke
Anticoagulation
Malignant
hypertension
Aortic
dissection
Acute
myocardial
ischemia
In
these conditions, the
anticipated benefit of acute
blood pressure reduction must be carefully weighed against the
risk of potentially worsening
the stroke deficit.
(Expert
Opinion: Strong
Consensus)
4.
If acute reduction of blood
pressure is
needed, pathophysiologic considerations should guide management.
In general, there is no
evidence that one antihypertensive
is safer than another in this setting, although a titratable
and predictable response is
desirable. Therefore, consideration
should be given to choosing a medication that
has the most desirable
mechanism of action in the setting
in which it is being used.
(Expert
Opinion: Strong
Consensus)
5.
In a patient who is taking
chronic antihypertensive
medications, it is uncertain whether such medications
should be continued in the
setting of acute stroke. If
vasoactive medications are being used for a purpose
other than hypertension
treatment, their continuation
should be evaluated in light of the original indication,
current blood pressure, and
the stability of the stroke
deficit.
(Expert
Opinion: Strong
Consensus)
6.
If there is a suspicion of
stroke progression
due to relative hypotension, measures to elevate the blood
pressure may be considered.
Such measures could include
discontinuing antihypertensives, fluid resuscitation,
supine or Trendelenburg
position, or the use of pressors.
(Research Evidence: Grade C)
7.
Routine treatment of
hypertension in ICH
is not recommended. Treatment of cases with extremely
elevated blood pressure should
be considered on a case
by case basis with the understanding that the benefits
of such treatment are unproven.
(Expert Opinion: Strong
Consensus)
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335:765 - 74.
2.
Collins
R, et al. Blood pressure, stroke
and coronary heart diseases.
Part 2, Short-term reductions
in blood pressure: overview
of
randomized
drug trails in
their epidemiological context.
Lancet 1990; 335:827 -38.
3.
Britton M, et al. Blood pressure
course in patients with acute stroke
and matched controls. Stroke
1986; 17:861- 4.
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focal
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Neurology 1990; Suppl 40:145.
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WJ. Cerebral hemodynamics in ischemic
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Ann Neurol 1991;
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Paulson
OB, et al. Cerebral autoregulation.
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10.
Powers WJ. Acute hypertension after
stroke: the scientific basis for
treatment decisions. Neurology
1993; 43:461 - 7.
11.
Diragi
U, Pulsinelli W. Autoregulation
of cerebral blood flow in
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1990:10:327-36.
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Heiss WD, Rosner G. Functional
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related to degree and duration
of ischemia. Ann Neurol
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Siesjo BK. Cerebral circulation
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in
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Neurology 1968; 18:1166 -
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Britton M, et al. Hazards of therapy
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Farhat SM, Schneider RC. Observations
on the effect of systemic
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Evidente V,
Yagnik P. Blood pressure management
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Neurology
1996; 46: A256.
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Lisk DR, et al.
Should hypertension be treated
after acute stroke?
A
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using single photon emission
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G, et al.
Pharmacological elevation of blood
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acute
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Levy DE, et al.
Factors related to intracranial
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23.
The National
Institute of Neurological Disorders
and Stroke rt-PA
Stroke
Study Group. Tissue
plasminogen activator for
acute
ischemic
stroke.
EnglJMed 1995; 333: 1581 - 7.
24. Shields RWJr, et
al. Anticoagulant-related
hemorrhage in acute
cerebral
embolism. Stroke
1984; 15:426 - 37.
25.
Calhoun DA,
Oparil S. Treatment of hypertensive
crisis. NEngl
J
Med 1990; 323: 1177 -8.
26.
Gifford RWJr.
Management of hypertensive crises.JAMA
1991;
266:829-35.
27. Ferguson RK,
Vlasses PH. How urgent is 'urgent'
hypertension?
Arch
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Ferguson RK,
Vlasses PH. Hypertensive emergencies
and urgencies.
JAMA
1986; 255: 1607 -13.
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Fagan TC. Acute
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in asymptomatic
patients
with severe
hypertension. An idea whose time
has come
and
gone Arch Intern Med 1989;
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Tietjen CS, et
al. Treatment modalities for
hypertensive patients
with
intracranial pathology:
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1996:24:311-22.
31. Popa G, et al.
Stroke and hypertension. Antihypertensive
therapy
withdrawal.
RomJ Neural
Psychiatry 1995; 33:29 - 35.
32. Bae HG, et al.
Rapid expansion of hypertensive
intracerebral
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31:35-41.
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Dandapani BK, at
el. Relation between blood
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in
intracerebral hemorrhage.
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Adams HPJr, et
al. Guidelines for the management
of patients with
acute
ischemic stroke. A
statement for healthcare professionals
from a special writing group
of the Stroke Council, American
Heart Association. Stroke
1994; 9: 1901 -14.
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SpenceJD, Del
Maestro RF. Hypertension in acute
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Lavin P.
Management of hypertension in patients
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BillerJ. Medical
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Oppenheimer
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Complications of acute stroke.
Lancet 1992; 339:721-4.
ANTICOAGULATION
in ACUTE ISCHEMIC STROKE
PURPOSE
The purpose of this guideline
is to identify those situations
where acute anticoagulation may be appropriate
in the management of patients
with acute ischemic stroke.
BACKGROUND
Anticoagulation
with heparin
has long been common management
in patients with acute ischemic stroke. Even
though convincing clinical
trials supporting the value
of this treatment have been lacking, this practice has continued
in an attempt to forestall
clot propagation and to prevent
re-embolization. Reviewing existing evidence for the use
of heparin, the American Heart
Association's (AHA) Stroke
Council
stated in 1994:
.
Because
data about the safety and efficacy of
heparin in patients with acute ischemic stroke are insufficient
and conflicting, no
recommendation can be offered...
Data about the safety and
efficacy of heparin in patients
with recent cardioembolic stroke are also too sparse to
support a recommendation...
There are no data concerning
any effects of the vascular distribution of the
ischemic symptoms or the
underlying vascular disease
on the response to heparin... Until more data are avail-
able, the use of heparin
remains a matter of preference
of the treating physician.'
Since
this AHA Guideline was written, further
studies
have cast doubt on the benefit of heparin. What follows
includes a brief review of the
evidence of heparin's
role in three common clinical situations - completed thrombotic stroke,
completed cardioembolic
stroke, and progressing stroke,
or "stroke in evolution."
Anticoagulationfor
Completed Presumed Thrombotic Stroke
In
1986, Duke et al. published the first large
randomized
study of intravenous heparin vs. placebo in 225 patients with
acute thrombotic stroked
Excluded were patients with
suspected cardiac embolism, uncontrolled hypertension, or stroke
progression. Treatment was
initiated within 48 hours
of stroke onset with a target partial thromboplastin time (PIT) between
50 and 70 seconds. Primary
outcome measures included
progression of neurologic deficit or death within 7 days. There
was no statistically
significant difference in primary
outcomes,and the only significant difference found was an increased
death rate at one year in the
heparin-treated group.
In
1995 a group from Hong Kong reported a trial
involving
just over 300 patients with acute ischemic stroke assigned to
one of three groups - placebo,
high-dose low molecular
weight (LMW) heparin given subcutaneously (SQ), or low-
dose LMW heparin SQ for 10
days.3 Patients
with cardioembolic strokes were not excluded. Primary outcomes were
death
at 10 days and
dependency for
activities of daily living
at 6 months. By this measure, 45% of high-dose patients had a
"poor outcome" compared with
52% of the low-dose patients
and 65% of the placebo group.
The
International Stroke Trial (IST) randomized
nearly
20,000 patients with acute ischemic stroke (with no clear
indications for, or
contraindications to, heparin or
aspirin), to one of six groups: half of the patients received aspirin
300 mg, while
half received no
aspirin.4 Patients
in each of these two groups were assigned one of three heparin
regimens:
no heparin,
5,000 IU SQ bid, and
12,500 IU SQ bid. Primary
endpoints were death from any cause at 14 days and death or disability at 6 months. The
higher dose of heparin
was associated with a higher rate of serious extracranial bleeding,
more hemorrhagic strokes, no
reduction in other strokes
and hence a significantly higher risk of death or non-fatal stroke
within 14 days. Whether
patients with atrial fibrillation
were included or were separately analyzed, there was no advantage
of heparin.5
Preliminary reports from the Trial of Org 10172 in
Acute
Stroke Treatment (TOAST) have been disappointing as well.
In this study high-dose
intravenous heparinoid or placebo
were begun within 24 hours of stroke onset. "No difference
was found between the
treatments at 7 days and at 3 months in
the number of patients with
a favorable outcome (Glasgow
Outcome score I or II and Barthel index of 12 or greater)."6
Anticoagulation
for Completed Presumed Cardioembolic Stroke
Many
studies of patients with presumed
cardioembolic stroke
have been published over the past two decades, producing widely-varying estimates
of the risk of recurrent
embolism in the acute period. At the low end, some studies have found
the risk to be 2 to 4%, while
others have estimated it
to be as high as 20%7
The
recently-published 1ST trial found the risk of recurrent stroke to be 4,9%
at 14 days in patients
with atrial fibrillation who were not assigned to heparin therapy.4
(Note - patients were excluded
from the study if the
treating physician felt that heparin was clearly indicated.) While
there are data indicating that
there is a higher risk
with some embolic sources than with others (mechanical valves,
rheumatic disease, and acute
myocardial infarction being
more risky than atrial fibrillation),8,9
there seems to be no
consensus
on the risk of
recurrent embolism as compared
with the risks and benefits of immediate or early use of
heparin in the setting of
acute embolic stroke.
The
Cerebral Embolism Study Group performed a
small randomized
controlled study comparing immediate
heparinization (bolus and
adjusted infusion) with no
anti-coagulation or aspirin for 10 days in patients with acute
(presumed) cardioembolic
strokes.'" Among 24 patients
receiving heparin there were no embolic recurrences and
no significant hemorrhagic
complications. Among the 21
patients receiving no specific therapy there were 2 recurrent
strokes - in one patient one
week after acute myocardial
infarction and in another patient with a known ventricular
aneurysm, mural thrombus, and
sick sinus syndrome.
The
1ST trial found that patients in atrial
fibrillation
assigned to heparin had a 2.1% lower incidence of recurrent
ischemic stroke at 14 days
than those not receiving heparin
(2.8% vs. 4.9%), but this was offset by an increased risk of
hemorrhagic stroke (2.1% vs.
0.4%). Aspirin appeared
more beneficial in decreasing the risk of recurrent or hemorrhagic
stroke (1% decrease) than did
heparin (0.4% decrease).
There
are no controlled studies, nor any
consensus, on
the appropriate timing of heparin when it is used:
Placing
emphasis on the studies finding a high
risk
of re-embolization, there are advocates of immediate
heparinization, once a CT scan
has ruled out a cerebral
hemorrhage.11
The Consensus Conference on Antithrombotic Therapy
of the American College of Chest Physicians recommends
waiting 2 or 3 days, repeating
the CT scan to rule out
hemorrhagic transformation, and then administering
heparin, followed by warfarin,
to non-hypertensive patients
with small to moderate-sized infarcts.11When
atrial fibrillation is the
presumed embolic source, warfarin
without initial heparin is recommended.
The
Cerebral Embolism Study Group has made similar
recommendations and further advises the avoidance of
either heparin bolus or
over-anticoagulation." Clinical
experience suggests that these practices, uncontrolled
hypertension, and large-size
infarcts are important risk
factors for hemorrhagic transformation.
Anticoagulation
for Other Stroke Mechanisms
There
are certain clinical
situations, such as arterial
dissection, acute large vessel occlusion, or well-defined
hypercoagulable states, where
many experts favor the
use of acute anticoagulation for a stable completed stroke. While
there are plausible
pathophysiologic reasons to consider
this option, in none of these clinical situations has this treatment
been tested in a controlled
trial.
Anticoagulation
for Progressing Stroke or "Stroke in Evolution"
Among patients presenting with
an acute ischemic stroke,
many will show progression of their deficit over the next
several days. Aggregate
results from several studies
indicate that approximately 30% of patients will progress, and there
are no reliable clinical
predictors of which will do
so. 14-17 In an unknown
number of patients, progression may be due to factors other than clot
propagation or distal embolism,
e.g. relative hypotension, local edema, the release of neurotoxins,
etc. Heparin has been the
traditional therapy in patients
with progressive stroke, but there are no controlled studies of its
benefit. In uncontrolled
experience, heparin failed to
stop progression in 21 to 50% of cases where it was given, and was
associated with a risk of
serious hemorrhage. 18-21
Whether this is better than the natural course in such patients is
unknown.
Heparin
as Deep
Vein Thrombosis (DVT) Prophylaxis
Pulmonary
embolism accounts
for 10% of deaths
following
stroke' and both leg
paralysis and immobility
increase
the risk for DVT. Low
intensity anticoagulation
using
subcutaneous
heparin or LMW
heparin is effective in prevent-
ing DVT in stroke patients and
decreases the risk of
death from
pulmonary
embolism.22,23 Early
mobilization and alternating
pressure stockings are other
strategies to reduce DVT.
Initiation
of
Oral Anticoagulation
When
warfarin is initiated,
there is a progressive fall
in vitamin K-dependent clotting factors, most importantly factors
II, VII, X and protein G. The
decline of protein C tends
to produce a procoagulant effect, while the rapid decrease of
factor VII causes a
prolongation of prothrombin time
days before clinically-significant anticoagulation is accomplished.
A recent study has found that
initiation of anticoagulation
with 5 mg/day of warfarin achieves therapeutic anticoagula-
tion at 5 days as well as
"loading doses" of 10 mg/day
without risking a transitional hypercoagulable state." Furthermore a
"stable" dose is achieved much
more quickly if one initiates
therapy with 5 mg rather than 10mg. 24,25
RECOMMENDATIONS
1. In general,
heparin is not recommended
in patients with completed thrombotic stroke. There is no persuasive
evidence that either
therapeutic heparin or LMW heparin is
useful in this setting.
(Research Evidence: Grade A)
2. In patients with
embolic stroke, there
is no consensus on the use of heparin:
A. Patients with
non-valvular atrial fibrillation
are at lower risk of a second early embolism than other
patients with cardioembolic
stroke. The initiation of
warfarin, without preceding heparin, is suggested
for these patients.
(Expert Opinion: Strong
Consensus)
B. Other patients with
high-risk cardiac embolic
sources (cardiomyopathy, rheumatic or prosthetic
valvular disease, acute
myocardial infarction) appear
to be at greater risk and may be candidates
for heparin, provided
hypertension is controlled, there
is no hemorrhage on CT, and the infarct is
not "large." Because of many
clinical variables, and
the lack of controlled data, no recommenda-
tion can be made regarding
immediate heparin vs. a delay
of 2 to 3 days.
(Expert
Opinion: Strong
Consensus)
3. In
patients with progressing
stroke, heparin
is a reasonable treatment option, but in the absence of controlled
data,
no firm recommendation can be made. In such patients,
consideration should always be given to the
possible
role of hypotension or other factors in causing
the clinical worsening.
(Expert
Opinion: Strong Consensus)
4.
In patients with acute
arterial dissection,
acute large vessel occlusion, occlusion or high-grade stenosis of
large vessels, or
hypercoagulable states, anticoagulation
with heparin and/or coumadin is a reasonable treatment
option. However, in the
absence of controlled data, no
firm recommendation can be made.
(Expert Opinion: Strong
Consensus)
5.
In patients with acute
ischemic stroke
and either prolonged immobility or significant leg paralysis, early
subcutaneous heparin or LMW
heparin, and early mobilization,
are recommended to reduce the risk of
DVT and pulmonary embolism.
(Research Evidence: Grade A)
6.
When oral anticoagulation is
to be initiated,
a starting dose of 5 mg/day of warfarin is preferred to larger
"loading" doses,
(Expert
Opinion: Strong Consensus)
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