STROKE, PART 2

36 l Nursing2011 l March

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Respond aggressively to

hemorrhagic
stroke
By Janice Mink, BSN, RN, CCRN, CNRN, and
Julie Miller, BSN, RN, CCRN

2.5

CHRIS BJORNBERG /P HOTO R ESEARCHERS, INC.

ANCC
CONTACT HOURS

PATIENTS MAY ARRIVE at the hospital any

time from minutes to days after a hemorrhagic
stroke, and nurses need to be prepared for the
unique challenges associated with their care.
Performing serial neurologic assessments is the
single most important nursing action for every
patient diagnosed with a stroke. As the direct
caregiver, youll constantly monitor these patients,
communicating your findings to other members
of the healthcare team so that any deterioration
in neurologic functioning can receive immediate
attention.
Initial emergency stroke care is identical for
all patients with stroke regardless of the type.
Assessing and supporting the ABCs is extremely
important in patients with hemorrhagic stroke
because these patients more often experience
decreased levels of consciousness and inability to
protect their airway.
The first article in this series, Opening the
Window of Opportunity for Treating Acute
Ischemic Stroke (January 2011),* detailed

initial assessment and emergency care for both

ischemic and hemorrhagic strokes. This second
article focuses on the two types of hemorrhagic
stroke, their risk factors, and how to care for
patients experiencing hemorrhagic strokes.
Primary stroke centers are key
At the moment a stroke is identified as
hemorrhagic based on a noncontrast computed
tomography (CT) scan, patient care changes
dramatically from a focus on eligibility for
fibrinolytic therapy (which is indicated for
acute ischemic stroke only) to a focus on
preventing or decreasing further bleeding.
Research demonstrates that hospitals providing care for more than 35 patients with subarachnoid hemorrhage each year have lower 30day mortality rates than hospitals that care for
fewer of these patients.1 Primary stroke centers
have the resources and systems to either treat
patients with a hemorrhagic stroke or transfer
them to an appropriate treatment facility.2

*Individual subscribers can access this article free online at http://ww.nursing2011.com.

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Two categories of
hemorrhagic stroke
Intracerebral hemorrhage (ICH),
also known as intraparenchymal
hemorrhage, describes bleeding into
the brain tissue, frequently as a result
of rupture of a deep, penetrating
artery.3 Approximately 10% of
all strokes are due to ICH, which
affects about 70,000 Americans
annually.4 Typically, patients present
with sudden-onset focal neurologic
deficits that progress rapidly over
time (1-24 hours).3 Focal neurologic
deficits may include unilateral or
bilateral weakness or sensory loss,
visual deficits, speech deficits, gait
disturbances, and dizziness.3 Some
patients experience headache and
vomiting, though these symptoms
arent specific for ICH.5
Subarachnoid hemorrhage (SAH) is
the result of bleeding into the subarachnoid space (the space between
the pial and arachnoid membranes),

most often as a result of a ruptured aneurysm or brain arteriovenous malformation (BAVM). Relative to aneurysmal subarachnoid hemorrhage (aSAH),
BAVM is rare, with an incidence of
3 per 100,000 people each year or 1
patient with a BAVM for every 10 with
aSAH. Emergency treatment focuses
on immediate amelioration of significant signs and symptoms. Definitive
treatment is elective with many options
and is beyond the scope of this article.
Please refer to the BAVM recommendations published in 2001.6
aSAH affects about 30,000 people
each year.1 About 80% of patients
experience sudden onset of headache
described as the worst headache of
their life. Nausea, vomiting, and nuchal rigidity may also occur. About
half of patients lose consciousness.
Interestingly, about 20% of patients
have a sentinel or warning headache,
which is sudden in onset and milder,
2 to 8 weeks prior to the aSAH.1

Zeroing in on the circle of Willis

Cerebral aneurysms occur most often in the circle of Willis where its believed that
a combination of physical forces and unknown pathology causes artery walls to
weaken and expand.3
Cerebrum (frontal lobe)
Cerebrum
(temporal lobe)

Arteries of the circle of Willis:

Anterior communicating
Anterior cerebral
Middle cerebral
Internal carotid
Posterior communicating
Posterior cerebral

Basilar artery

Vertebral arteries
Pons
Medulla
oblongata
Cerebellum
Spinal cord

38 l Nursing2011 l March

Unique risk factors

The list of risk factors for ICH is
shorter than the list for acute ischemic
stroke. Male gender, older age,
poorly controlled hypertension, and
excessive alcohol use are specific risk
factors for ICH.7 Individualize patient
and family teaching based on the risk
factors that apply to your patient.
The primary risk factors for aSAH
include smoking, hypertension, and
excessive alcohol use.8 Because most
aneurysms are found after they hemorrhage, youll provide much of the
patient and family teaching while the
patient is struggling with the stress
of an acute condition. But if your patient has an aneurysm that was found
incidentally before rupture, you can
focus your efforts on modifiable risk
factors, such as smoking. How to
treat aneurysms that havent ruptured
continues to be controversial because
the risks of treatment may be greater
than the risk of rupture.9 See Zeroing
in on the circle of Willis.
Why some aneurysms rupture
and others dont is under investigation. The annual risk of rupture of
untreated aneurysms when found
incidentally and not treated is 0.4%
to 0.5%.9
Approximately 12% to 14% of
patients are receiving therapeutic
anticoagulation with warfarin at the
time of the ICH because of other
health problems, such as atrial fibrillation or venous thromboembolism
(VTE). Although anticoagulation by
itself isnt a risk factor, it complicates
patient care by introducing the need
for emergent warfarin reversal.5
Determining the time
If the stroke is hemorrhagic, determine
the time your patient was last seen
normal (LSN). The first few hours
are critical in hemorrhagic strokes
because of the risk of increased
intracranial pressure (ICP) and
decreased level of consciousness.4,5
Changes in level of consciousness are common in all hemorrhagic
strokes. Closely monitor the Glasgow
Coma Scale score, pupillary assessment findings, and the National Inwww.Nursing2011.com

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stitutes of Health Stroke Scale in the

early hours of care.
If your patient had a hemorrhagic
stroke with symptom onset less than
1 hour from time LSN, assess the
patients neurologic status and BP
frequently because this is the period
in which the size of an ICH is most
likely to increase.5 Also, the risk of
rebleeding in aSAH is highest in the
first 24 hours.1
Patients with either type of hemorrhagic stroke who seek medical attention after their signs and symptoms
have stabilized will be treated based
on the underlying cause of the hemorrhage and their condition at the
time they present for care. However,
if the patient arrives 5 days from time
LSN, most likely the hemorrhage has
become stable. If the patients BP and
neurologic exam are stable, you may
need to monitor this patient only
every 4 hours and as needed.
Need for neuroimaging
In the setting of suspected stroke
signs and symptoms, the standard
initial diagnostic imaging study is an
emergency CT scan without contrast
to differentiate acute ischemic
stroke from hemorrhagic stroke,
because stroke due to hemorrhage
will generally be clearly visible.3
Additional neuroimaging studies
may be ordered for special reasons
later in the course of the patients
hospitalization. 3 For example, in the
setting of an aSAH, further imaging
is required to locate the aneurysm.
Spiral computed tomography
angiography can provide detail
of the anatomy of the aneurysm
and its location for the surgeon or
interventional radiologist.3
BP may be extremely high
When patients arrive early after
the onset of signs and symptoms,
prepare them to be treated in the
CCU because of the early risk of
rebleeding and the need for frequent
monitoring. (See Considering surgical
and endovascular interventions.)
Currently, we dont have evidence
to define when and how much to
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Considering surgical and endovascular interventions

Surgery is recommended only in specific instances of ICH, such as cerebellar hemorrhages that compress the brainstem or cause rapid neurologic deterioration.
Surgery may also be considered for large lobar hemorrhages (> 30 mL) near the
surface of the brain (< 1 cm).5
In aSAH, two options are available for treating an aneurysm. Clipping a cerebral
aneurysm requires a craniotomy. Endovascular treatment with coil embolization of
ruptured aneurysms is another option, especially for those patients not eligible for
surgical clipping.3 The approach used to occlude an aneurysm depends on individual patient and aneurysm factors. The goal for any treatment is to completely occlude
circulation to and within the aneurysm so it can no longer bleed or expand.1

control BP in ICH. Although studies

have demonstrated an area of ischemia around the infarct (penumbra) in
patients whove had acute ischemic
stroke, this isnt the case in patients
whove had ICH. The absence of an
ischemic penumbra in ICH indicates
that permissive hypertension is unlikely to help preserve brain tissue.5
One study of patients with ICH
indicated that poor outcomes are
associated with systolic BPs (SBPs)
that rise above 150 mm Hg. 5 The
same study found that SBPs of 180
or higher are associated with greater
hematoma expansion in the first 24
hours than when SBPs are decreased
to a range of 140 to 150 mm Hg.5
For effective BP management of
patients with ICH, monitor not
only the systolic and diastolic BP,
but also mean arterial pressure
(MAP). Automated BP monitors
will calculate MAP, which can be
recorded with the patients vital
signs. If you take manual BP measurements, calculate MAP using the
following formula (SBP = systolic
blood pressure and DBP = diastolic
blood pressure). DBP counts twice
as much as SBP because two-thirds
of the cardiac cycle is spent in
diastole.
MAP =

[SBP + (2 DBP)]
3

Because of the lack of evidence,

ICH guidelines are not prescriptive.
If your patients SBP is 200 mm Hg
or higher or MAP is higher than 150
mm Hg, expect the healthcare provider to prescribe a continuous I.V.
infusion to reduce the BP while the

patients BP and MAP are monitored

every 5 minutes. The critical care
nurse implementing this prescription may increase the antihypertensive medication as often as every 5
minutes to reach the target SBP. The
target range for SBP in ICH is 140
to 150 mm Hg to maintain brain
perfusion while limiting the risk of
hematoma expansion. For SBP of
180 mm Hg or higher or MAP higher
than 130 mm Hg with evidence of
increased ICP, the recommendation
is to administer intermittent or continuous I.V. medication and perhaps
use ICP monitoring to maintain
cerebral perfusion pressure (CPP)
at 60 mm Hg or higher. If theres no
evidence of increased ICP, then the
target BP may be slightly higher at
160/90 or a MAP of 110.5 See Watch
for these signs of increased ICP.
CPP is an indirect measure of the
blood flow to the brain. The normal
range for CPP in the average adult is
70 to 100 mm Hg.3 If the patient has
an ICP monitor, you calculate CPP
using the following formula:
MAP ICP = CPP
For example, if the BP is lowered
to 120/60 mm Hg, MAP is 80 mm
Hg. Normal adult ICP is 15 mm
Hg or less.10 If the ICP is in the upper limit of normal, the CPP is 65
(80 15 = 65). If MAP falls or ICP
rises even slightly, blood flow to the
brain (CPP) will soon fall below 60
mm Hg, the lowest desired level for
CPP in ICH.5
If the patient doesnt have an ICP
monitor, perform neurologic assessments routinely and when needed.
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Assess level of consciousness, vital

signs, pupils, eye movements, motor strength, and speech to identify
deterioration.
BP control in aSAH
In aSAH, BP is controlled to prevent
hypertension-related rebleeding and
maintain CPP. aSAH also causes an
early, sudden increase in ICP due to
blood rushing into the subarachnoid
space, which is usually occupied
by cerebrospinal fluid (CSF). If this
blood obstructs CSF flow out of the
subarachnoid space through the
arachnoid villi, ICP will continue
to increase as the choroid plexus in
the portions of the lateral, third, and
fourth ventricles continue to secrete
CSF.3 These patients may require
an external ventricular device or
ventriculostomy to drain CSF and
reduce intracranial hypertension.3
Reducing BP and maintaining CPP is
also essential for these patients.
Rebleeding is the greatest risk
prior to definitive treatment of the
aneurysm. As long as the lesion
remains untreated, the target SBP
range is 120 to 150 mm Hg.10 Although the 2009 aSAH guidelines
dont make specific recommendations, the two studies reviewed in
the guidelines indicate that a 17%
rehemorrhage rate is associated with
SBP above 150 mm Hg, and a 13.6%
rehemorrhage rate is associated with
SBP above 160 mm Hg.1 Medications used to reach the target BP are
short acting, can be administered I.V.
continuously, have reliable effect on
BP, and are relatively safe. Labetalol,
nicardipine, and esmolol meet these
criteria for treatment of hypertension
in aSAH.1
Beware of vasospasm and
hyponatremia
Once treatment for aSAH is under
way, turn your attention to the risk
of vasospasm. The blood circulating
in the subarachnoid space is believed
to cause chemical irritation and
vasospasm of cerebral arteries.
Studies indicate that 30% to 70% of
patients with aSAH will experience
40 l Nursing2011 l March

Watch for these signs of

increased ICP
headache
decreased level of consciousness
motor dysfunction (hemiparesis or
hemiplegia)
aphasia
visual disturbances
pupillary abnormalities
changes in respiratory patterns
changes in vital signs.
Source: Hickey JV. The Clinical Practice of
Neurological and Neurosurgical Nursing. 6th ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2009.

vasospasm, which usually occurs

3 to 5 days after the hemorrhage.
Vasospasm can occur over the next
1 to 2 weeks and may not resolve for
up to 4 weeks.1
Vasospasm is an emergency. It
results in ischemia involving a specific arterial distribution in the brain
and creates focal neurologic deficits
like those you might see in ischemic
stroke, such as hemiparesis. Your serial neurologic nursing assessments,
the primary method of identifying
symptomatic vasospasm, are crucial
because the signs may be subtle.
They may occur suddenly or develop
over time. Your nursing assessments
not only indicate when treatment
is needed, but they also indicate if
treatment is effective.
Transcranial Doppler flow velocities in major cerebral arteries may be
measured daily or every other day to
identify a trend toward vasospasm.
Absolute values of blood flow velocity may be elevated by any number of
factors. The Lindegaard ratio, which
has been used to evaluate trends in
cranial artery flows, is the ratio of the
mean velocity of the chosen cerebral
artery divided by the mean velocity
of the ipsilateral extracranial internal
carotid artery. Ratios of 5 or 6 may be
a sign of severe spasm, which will be
treated based on the patients clinical
status.
In addition, almost all aSAH patients receive the calcium channel
blocker nimodipine either orally or
through a nasogastric tube for 21
consecutive days initiated within

96 hours.1 Nimodipine is associated with decreased morbidity and

improved functional outcome. This
medication has been shown to decrease BP significantly, so monitor
vital signs closely when initiating this
therapy.3
If cerebral vasospasm occurs,
be prepared to start hypervolemia,
hypertension, and hemodilution
(triple H) therapy to maintain cerebral blood flow. In this therapy, the
patients central venous pressure is
maintained at 8 to 10 mm Hg using
0.9% sodium chloride and colloids.
Monitor the patients response to
treatment to elevate SBP to about
160 mm Hg, or as prescribed. If
therapy is started before the aneurysm is definitively treated, the target
BP may be lower. Vasopressors may
be added to reach this level and SBP
may be taken as high as 200 mm
Hg after treatment of the aneurysm.
Hematocrit is permitted to fall to
approximately 30% during this
therapy.10
Pulmonary edema and myocardial
stress are risks of this therapy, so
frequently monitor cardiac rate and
rhythm, fluid balance, oxygenation,
and breath sounds. If vasospasm isnt
relieved by triple H therapy, the patient may need endovascular therapy
such as balloon angioplasty and
intra-arterial transcatheter infusion
of a potent vasodilator, such as the
calcium channel blocker, verapamil.3
Hyponatremia is a documented
complication of aSAH in up to 30%
of patients.1 Studies indicate that
hyponatremia may occur due to
physiologic loss of fluid volume and
release of alpha natriuretic peptide
that causes excess excretion of both
fluid and sodium.1 The initial step to
prevent this complication is to ensure that the patient doesnt receive
hypotonic solutions such as D5W.1
Monitor fluid volume status by monitoring serum sodium levels, daily
body weights, and accurate intake
and output. If the serum sodium
level begins to fall, the patient may
need more frequent invasive monitoring of central venous pressure or
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pulmonary artery wedge pressure.3

Hypertonic saline and fludrocortisone acetate may also be prescribed.1
Seizures a risk
Seizure risk in ICH is from 2.7%
to 17%.5 Seizure prophylaxis isnt
recommended in ICH, unless the
patient experiences clinical seizure
activity.5
In aSAH, the risk of seizures is between 6% and 18%. Patients may be
treated for seizures prophylactically
for a brief period in the immediate
posthemorrhagic period and then
the antiepileptic drug (AED) will be
tapered off if no seizures occur.1
When an AED is added to the
treatment plan, provide patient and
family education, and provide information about seizure precautions.
What to do about VTE
In all patients diagnosed with
hemorrhagic stroke, perform a
VTE risk assessment and institute
mechanical thromboprophylaxis with
intermittent pneumatic compression
(IPC), unless contraindicated.11 For
patients with ICH, low-molecularweight heparin (LMWH) may
begin after intracranial bleeding has
stopped, usually 3 to 4 days after the
stroke.5 If the patient develops VTE,
a vena cava filter may be placed.
The patient with aSAH will have
IPC, unless contraindicated, initiated
immediately. Because of the rebleeding risk, this patient isnt likely to
receive routine LMWH therapy, even
after definitive treatment of an aneurysm.10
Outcome depends on
rehabilitation
Because of the high morbidity
associated with hemorrhagic stroke,
enlisting rehabilitation professionals
is critical to achieving the best
functional patient outcomes.12
Interventions should begin within
24 to 48 hours of admission, starting
with range of motion exercises and
anatomically correct positioning.3
Collaborate with other members
of the healthcare team, including
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duces rebleeding risk and mortality

in aSAH.1

Patient care for hemorrhagic

stroke will focus on
preventing or decreasing
further bleeding.
physical therapists, to develop a
plan of care to progress patients to
increased active range of motion and
mobilization.
Secondary prevention
If patients survive a first ICH, their
risk of recurrent ICH is 2.1% to
3.7% per year.5 Risk factors for
recurrent ICH include lobar location,
older age, anticoagulation, certain
apolipoprotein alleles, and the
presence of cerebral microbleeds.5
Base your patient teaching on each
patients unique risk profile.
Hypertension is a risk factor in all
strokes. Treatment goals include a BP
less than 149/90 mm Hg. If the patient has diabetes mellitus or chronic
kidney disease, the goal is less than
130/80 mm Hg.5
In aSAH, secondary prevention
focuses on reducing the risk of
rebleeding. Complete occlusion of
the aneurysm is the most effective
method of reaching this goal. Here,
experience and teamwork are key
to the best patient outcomes. The
characteristics of each aneurysm
and patient are unique. The neurosurgeon and the endovascular
practitioner will identify the best
treatment for each individual. Early
treatment of the aneurysm also re-

Anticoagulation: What to
do after ICH
Because many patients with ICH
were taking oral anticoagulants
before the ICH, these patients pose
a challenge after the acute stage of
stroke treatment. Whether or not
to restart anticoagulation will be
based on various patient-dependent
factors, including the location of
the hemorrhage and the original
indication for anticoagulation.5
For example, if the patient has
atrial fibrillation thats not due to
valvular disease and the hemorrhage
was lobar, the patient may not receive anticoagulation because study
models show a longer quality-of-life
expectancy when anticoagulation is
avoided. But if the hemorrhage was
in the deep brain, anticoagulation
might be considered as the study
model showed no difference in quality-of-life expectancy with or without
anticoagulation.13
Poorer patient outcomes
ICH is associated with high morbidity
and mortality. The 30-day mortality
rate is between 35% and 52%. Half
of deaths occur within 2 days of
the ICH. Approximately 70,000
Americans will experience ICH this
year, but only about 14,000 will be
able to care for themselves 6 months
later.4 Although the prognosis is often
grim, the guidelines recommend
giving aggressive full care early
on and delaying any new do-notresuscitate orders until day 2.5 This
recommendation is based in part on
the fact that clinicians dont have a full
picture of the patients hemorrhage,
response to treatment, and deficits
until that time. aSAH mortality is as
high as 45% and functional outcomes
have remained poor.1
These patients are more likely to
require more professional nursing
care and for longer periods, from the
acute care phase through to residential
or home care. They also require continued neurologic care over their life
March l Nursing2011 l 41

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span because they have a higher risk

of stroke than the general population.
The beginning of great
stroke care
Like acute ischemic stroke, hemorrhagic stroke requires prompt identification of signs and symptoms
followed by emergent transport and
treatment. All sudden onset neurologic change is considered a potential
stroke until proven otherwise. This
approach is working: Deaths from
stroke declined during the years
1999 to 2007.14
You can help reduce death and
disability from all types of stroke.
Your readiness to assess and manage
sudden onset neurologic changes
within your practice setting provides
your patients with the opportunity
for the best possible outcome. Your
passionate, effective teaching and
psychosocial support helps patients
and caregivers prevent stroke. By
reinforcing and encouraging patients
undergoing rehabilitation therapy,
you promote increased physical ability and self-care.

REFERENCES
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Guidelines for the management of aneurysmal
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2. Alberts MJ, Latchaw RE, Selman WR, et al.
Recommendations for comprehensive stroke
centers: a consensus statement from the Brain
Attack Coalition. Stroke. 2005;36(7):1597-1616.
3. Hickey JV. The Clinical Practice of Neurological and
Neurosurgical Nursing. 6th ed. Philadelphia,
PA: Wolters Kluwer/Lippincott Williams &
Wilkins; 2009.
4. Broderick J, Connolly S, Feldmann E, et al.
Guidelines for the management of spontaneous
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American Stroke Association Stroke Council, High
Blood Pressure Research Council, and the Quality
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Working Group. Stroke. 2007;38(6):2001-2023.
5. Morgenstern LB, Hemphill JC 3rd, Anderson
C, et al. Guidelines for the management of
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for healthcare professionals from the American
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Stroke. 2010;41(9):2108-2129.
6. Ogilvy CS, Stieg PE, Awad I, et al. AHA
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Stroke. 2001;32(6):1458-1471.
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Risk factors for intracerebral hemorrhage in the
general population: a systematic review. Stroke.
2003;34(8):2060-2065.

8. Feigin VL, Rinkel GJ, Lawes CM, et al. Risk

factors for subarachnoid hemorrhage: an updated
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Stroke. 2005;36(12):2773-2780.
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International Study of Unruptured Intracranial
Aneurysms Investigators. N Engl J Med. 1998;
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10. Greenberg MS. Handbook of Neurosurgery. 7th ed.
New York, NY: Thieme Medical Publishers; 2010.
11. Geerts WH, Bergqvist D, Pineo GF, et al.
American College of Chest Physicians. Prevention
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Chest Physicians Evidence-Based Clinical Practice
Guidelines (8th ed). Chest. 2008;133(6 suppl):
381S-453S.
12. Andersen KK, Olsen TS, Dehlendorff C,
Kammersgaard LP. Hemorrhagic and ischemic
strokes compared: stroke severity, mortality, and
risk factors. Stroke. 2009. 40(6):2068-2072.
13. Eckman MH, Rosand J, Knudsen KA, Singer
DE, Greenberg SM. Can patients be anticoagulated
after intracerebral hemorrhage? A decision analysis.
Stroke. 2003;34(7):1710-1716.
14. Schwamm L, Fayad P, Acker JE 3rd, et al.
Translating evidence into practice: a decade
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Stroke Association. Stroke. 2010;41(5):1051-1065.
At Trinity Mother Frances Hospitals and Clinics in
Tyler, Tex., Janice Mink is staff development educator
for neuroscience, and Julie Miller is staff development
educator for critical care.
The authors have disclosed that they have no financial relationships pertaining to this article.
DOI-10.1097/01.NURSE.0000394077.52606.9b

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