Taylor Kimberly, Stefan Schwab, Eric E. Smith, Rafael J. Tamargo and Max Wintermark
Eelco F. M. Wijdicks, Kevin N. Sheth, Bob S. Carter, David M. Greer, Scott E. Kasner, W.
Association/American Stroke Association
Swelling: A Statement for Healthcare Professionals From the American Heart
Recommendations for the Management of Cerebral and Cerebellar Infarction With
Print ISSN: 0039-2499. Online ISSN: 1524-4628
Copyright © 2014 American Heart Association, Inc. All rights reserved.
is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke
published online January 30, 2014;Stroke.
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1
Background and Purpose—There are uncertainties surrounding the optimal management of patients with brain swelling
after an ischemic stroke. Guidelines are needed on how to manage this major complication, how to provide the best
comprehensive neurological and medical care, and how to best inform families facing complex decisions on surgical
intervention in deteriorating patients. This scientific statement addresses the early approach to the patient with a swollen
ischemic stroke in a cerebral or cerebellar hemisphere.
Methods—The writing group used systematic literature reviews, references to published clinical and epidemiology studies,
morbidity and mortality reports, clinical and public health guidelines, authoritative statements, personal files, and expert
opinion to summarize existing evidence and to indicate gaps in current knowledge. The panel reviewed the most relevant
articles on adults through computerized searches of the medical literature using MEDLINE, EMBASE, and Web of
Science through March 2013. The evidence is organized within the context of the American Heart Association framework
and is classified according to the joint American Heart Association/American College of Cardiology Foundation and
supplementary American Heart Association Stroke Council methods of classifying the level of certainty and the class and
level of evidence. The document underwent extensive American Heart Association internal peer review.
Results—Clinical criteria are available for hemispheric (involving the entire middle cerebral artery territory or more) and
cerebellar (involving the posterior inferior cerebellar artery or superior cerebellar artery) swelling caused by ischemic
infarction. Clinical signs that signify deterioration in swollen supratentorial hemispheric ischemic stroke include new
or further impairment of consciousness, cerebral ptosis, and changes in pupillary size. In swollen cerebellar infarction,
a decrease in level of consciousness occurs as a result of brainstem compression and therefore may include early loss of
corneal reflexes and the development of miosis. Standardized definitions should be established to facilitate multicenter
and population-based studies of incidence, prevalence, risk factors, and outcomes. Identification of patients at high risk
for brain swelling should include clinical and neuroimaging data. If a full resuscitative status is warranted in a patient
with a large territorial stroke, admission to a unit with neurological monitoring capabilities is needed. These patients are
Recommendations for the Management of Cerebral and
Cerebellar Infarction With Swelling
A Statement for Healthcare Professionals From the American Heart
Association/American Stroke Association
The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists.
Endorsed by the American Association of Neurological Surgeons and Congress of Neurological Surgeons
Endorsed by the Neurocritical Care Society
Eelco F. M. Wijdicks, MD, PhD, FAHA, Chair; Kevin N. Sheth, MD, FAHA, Co-Chair;
Bob S. Carter, MD, PhD; David M. Greer, MD, MA, FAHA;
Scott E. Kasner, MD, FAHA; W. Taylor Kimberly, MD, PhD; Stefan Schwab, MD;
Eric E. Smith, MD, MPH, FAHA; Rafael J. Tamargo, MD, FAANS;
Max Wintermark, MD, MAS; on behalf of the American Heart Association Stroke Council
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship
or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete
and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee October 15, 2013. A copy of the
document is available at http://my.americanheart.org/statements by selecting either the “By Topic” link or the “By Publication Date” link. To purchase
additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com.
The American Heart Association requests that this document be cited as follows: Wijdicks EFM, Sheth KN, Carter BS, Greer DM, Kasner SE,
Kimberly WT, Schwab S, Smith EE, Tamargo RJ, Wintermark M; on behalf of the American Heart Association Stroke Council. Recommendations for the
management of cerebral and cerebellar infarction with swelling: a statement for healthcare professionals from the American Heart Association/American
Stroke Association. Stroke. 2014;45:XXX–XXX.
Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines
development, visit http://my.americanheart.org/statements and select the “Policies and Development” link.
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express
permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/Copyright-
Permission-Guidelines_UCM_300404_Article.jsp. A link to the “Copyright Permissions Request Form” appears on the right side of the page.
© 2014 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/01.str.0000441965.15164.d6
AHA/ASA Scientific Statement
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2 Stroke April 2014
The emergence of brain swelling is the most troublesome and even life-threatening consequence of a large-territory isch-
emic stroke. Brain swelling occurs as a result of loss of func-
tion of membrane transporters, causing sodium and water influx
into the necrotic or ischemic cell, leading to cytotoxic edema.
Unrelenting swelling disrupts the blood- brain barrier (BBB);
therefore, a component of vasogenic edema may coexist.1
The development of clinically significant cerebral edema
is expected only in large-territory cerebral infarcts and can
be observed by the clinician in 3 ways: a rapid and fulminant
course (within 24–36 hours), a gradually progressive course
(over several days), or an initially worsening course followed
by a plateau and resolution (about a week).2–5 Currently, no
methods are available to predict the course of brain swelling
reliably. There is a clinical perception that when brain swell-
ing occurs in the cerebral or cerebellar hemisphere, medical
management to reduce brain swelling is not successful in
changing outcome.4,6 Therefore, a decompressive craniectomy
is offered to relieve the mass effect of the swollen hemisphere
on the thalamus, brainstem, and network projections to the
cortex, manifested mainly by a decreased level of arousal.
Decompressive craniectomy for cerebral edema after ischemic
hemispheric stroke has significantly increased in US hospitals.7
Clinical experience has matured over the years, but there
are uncertainties about how to approach a patient with neuro-
imaging and clinical evidence of emerging brain swelling after
an ischemic stroke. These include recognition of key warning
neurological signs, comprehensive evaluation of changing neu-
roimaging patterns, prevention of clinically significant swelling,
options for reducing cerebral edema by pharmacological means,
and selection of patients for decompressive craniectomy and
methods to measure the degree of postoperative morbidity. This
scientific statement addresses the early approach to the patient
with a swollen ischemic stroke in the cerebellum and cerebral
hemisphere. It provides a guideline on how to provide the best
comprehensive care and how to manage this complication.
Communicating prognosis with family members is also dis-
cussed. The level of evidence is rated for all recommendations.
Methods
Writing group members were nominated by the committee chair
and co-chair because of their previous work in relevant topic areas
and were approved by the American Heart Association (AHA)
Stroke Council’s Scientific Statement Oversight Committee and
the AHA’s Manuscript Oversight Committee. The writers used
systematic literature reviews, references to published clinical and
epidemiological studies, morbidity and mortality reports, clinical
and public health guidelines, authoritative statements, personal
files, and expert opinion to summarize existing evidence and to
indicate gaps in current knowledge. The panel reviewed the most
relevant articles on adults through computerized searches of the
medical literature using MEDLINE, EMBASE, and Web of
Science through March 2013. The evidence is organized within
the context of the AHA framework and is classified according
to the joint AHA/American College of Cardiology and supple-
mentary AHA Stroke Council methods of classifying the level
of certainty and the class and level of evidence (Tables 1 and
2). All members of the writing group approved the final ver-
sion of this document. The document underwent extensive
AHA internal peer review, Stroke Council Leadership review,
and Scientific Statements Oversight Committee review before
consideration and approval by the AHA Science Advisory and
Coordinating Committee.
Epidemiology
Variation in terminology complicates the accurate estimation
of the incidence of severe brain edema caused by massive
infarction. The estimated prevalence of severe stroke may be
affected by referral patterns because most data come from sin-
gle tertiary care hospitals and thus may not be representative of
the population as a whole. The term malignant middle cerebral
artery (MCA) infarction, introduced in 1996, was originally
defined as infarction of the entire MCA territory appearing on
computed tomography (CT) within 48 hours, with or without
infarction in other vascular territories.4 This term has been
used frequently in the subsequent literature, along with closely
related terms such as large hemispheric infarction, but almost
best admitted to intensive care or stroke units attended by skilled and experienced physicians such as neurointensivists or
vascular neurologists. Complex medical care includes airway management and mechanical ventilation, blood pressure
control, fluid management, and glucose and temperature control. In swollen supratentorial hemispheric ischemic stroke,
routine intracranial pressure monitoring or cerebrospinal fluid diversion is not indicated, but decompressive craniectomy
with dural expansion should be considered in patients who continue to deteriorate neurologically. There is uncertainty
about the efficacy of decompressive craniectomy in patients ≥60 years of age. In swollen cerebellar stroke, suboccipital
craniectomy with dural expansion should be performed in patients who deteriorate neurologically. Ventriculostomy to relieve
obstructive hydrocephalus after a cerebellar infarct should be accompanied by decompressive suboccipital craniectomy to
avoid deterioration from upward cerebellar displacement. In swollen hemispheric supratentorial infarcts, outcome can be
satisfactory, but one should anticipate that one third of patients will be severely disabled and fully dependent on care even
after decompressive craniectomy. Surgery after a cerebellar infarct leads to acceptable functional outcome in most patients.
Conclusions—Swollen cerebral and cerebellar infarcts are critical conditions that warrant immediate, specialized
neurointensive care and often neurosurgical intervention. Decompressive craniectomy is a necessary option in many
patients. Selected patients may benefit greatly from such an approach, and although disabled, they may be functionally
independent. (Stroke. 2014;45:00-00.)
Key Words: AHA Scientific Statements ◼ brain edema ◼ decompressive craniectomy ◼ infarction
◼ patient care management ◼ prognosis ◼ stroke
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liu Jian
高亮
Wijdicks et al Management of Cerebral and Cerebellar Infarction 3
always with a study-specific definition that deviated from the
original. These variable definitions were based on some com-
bination of neurological symptoms or signs,8–13 MCA occlu-
sion,10 involvement of some or all of the MCA-perfused brain
territory based on either CT or magnetic resonance imaging
(MRI) diffusion-weighted imaging (DWI),4,8,13–16 radiographic
evidence of brain edema,10,12,17 postadmission neurological
deterioration,17,18 or use of decompressive craniectomy.9,11,19
The prevalence of hemispheric MCA infarction by these
variable definitions has been reported to be 2% to 8% of all hos-
pitalized ischemic stroke,4,10,11,14,17,18 10% to 15% of all MCA
territory ischemic stroke,13,20 and 18% to 31% of all ischemic
stroke caused by MCA occlusion.9,16,21 The risk of subsequent
neurological deterioration and death is high, 40% to 80%.4,22
A population-based study estimated that 0.3% of all ischemic
stroke patients may be eligible for decompressive craniec-
tomy on the basis of criteria used in randomized, controlled
trials.23 The actual frequency of decompressive craniectomy
for malignant MCA infarction is estimated to have increased
from 0.04% of all ischemic stroke admissions in 1999 to 2000
to 0.14% of all ischemic stroke admissions in 2007 to 2008.7
Data on the incidence of severe brain edema complicating cer-
ebellar infarction and the frequency of decompressive craniec-
tomy for cerebellar edema are sparse. Studies suggest that ~20%
of patients will develop radiographic signs of mass effect accom-
panied by neurological deterioration.24,25 One series of 84 patients
Table 1 . Applying Classification of Recommendation and Level of Evidence
A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do
not lend themselves to clinical trials. Although randomized trials are unavailable, there may be a very clear clinical consensus that a particular test or therapy is useful
or effective.
*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as sex, age, history of diabetes, history of prior myocardial
infarction, history of heart failure, and prior aspirin use.
†For comparative effectiveness recommendations (Class I and IIa; Level of Evidence A and B only), studies that support the use of comparator verbs should involve direct
comparisons of the treatments or strategies being evaluated.
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4 Stroke April 2014
included 34 patients with craniectomies and 14 with ventriculos-
tomies,26 but selection criteria for surgery remain arbitrary, with
many neurosurgeons operating on comatose patients.27
Epidemiology: Recommendations
1. Standardized terms and definitions for severe hemi-
spheric and cerebellar edema resulting from infarc-
tion should be established to facilitate multicenter and
population-based studies of incidence, prevalence, risk
factors, and outcomes (Class I; Level of Evidence C).
2. Additional data should be collected to determine the
use of decompressive craniectomy in current clinical
practice, including whether there is variation by phy-
sician, hospital, health system, or patient character-
istics and preferences (Class I; Level of Evidence C).
Definition and Clinical Presentation
The target population is defined as patients who are at high
risk for or who ultimately suffer neurological deterioration
attributable to cerebral swelling after ischemia.
Hemispheric Stroke
Patients with significant swelling typically have occlusions of
the internal carotid artery, MCA, or both. The natural history
of a large infarction after internal carotid artery versus MCA
infarction is not clear, especially when independent of ante-
rior cerebral artery territory infarction. Infarctions from MCA
branch occlusions typically do not result in swelling with
clinically significant mass effect.4 Additional vascular territo-
ries, incomplete circle of Willis, and marginal leptomeningeal
collateral supply are also risk factors for the development of
cerebral edema after ischemia.28
Although baseline follow-up neuroimaging parameters
have been described that identify stroke patients who experi-
ence swelling with high specificity,16,29,30 a number of clinical
features are commonly seen in this syndrome. The most com-
mon findings are hemiplegia, global or expressive aphasia,
severe dysarthria, neglect, gaze preference, and a visual field
defect.4 Pupillary abnormalities are a reflection of significant
brainstem shift, typically not expected on initial presenta-
tion, and develop within the first 3 to 5 days. An early Horner
syndrome may point to an acute carotid artery occlusion or
dissection.4 The initial National Institutes of Health Stroke
Scale score is often >20 with dominant hemispheric infarction
and >15 with nondominant hemispheric infarction, although
this clinical predictor has not undergone rigorous prospective
validation.31–33 The initial score is a reflection of stroke sever-
ity and infarct volume, not a marker of tissue swelling, and
although sensitive, it is not highly specific.
The most specific sign of significant cerebral swelling
after stroke is a decline in the level of consciousness attrib-
utable to brain edema shifting the thalamus and brainstem,
where major components of the ascending arousal system are
situated.34 Although right hemisphere infarction may result
in a flattened affect, complete infarction of either hemi-
sphere itself is rarely associated with diminished arousal.35
Responsiveness, however, is diminished early in combined
MCA and anterior cerebral artery infarctions. Cerebral pto-
sis (apraxia of eyelid opening) may be present and falsely
suggest a decreased level of consciousness. It may appear de
no
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