STROKE

A stroke is a disruption of blood ow to a region of the brain that is sudden in

onset and results in permanent damage. Approximately 75% of strokes in the
United States are due to vascular obstruction (thrombi or emboli). As in
myocardial infarction, a stroke-inducing thrombosis is frequently caused by an
atherosclerotic plaque rupture. An embolus may be a result of blood clots
(frequently seen in association with atrial brillation), fragments of
atheromatous plaques, lipids, or air. The remain- ing 25% of strokes are
hemorrhagic, resulting from hypertensive vascular disease (which causes an
intracerebral hemorrhage), a ruptured aneurysm, or an AVM.
RED FLAG! Early recognition and prompt entry into the emergency medical
system are essential to reduce death and disability from stroke. Delay in seeking
medical care may eliminate the potential for tissue-saving thrombolytic therapy.
The time to needlethe time from symptom onset (ie, the time the patient
was last seen well) to administration of thrombolytic therapyis 3 to 4.5
hours.16
Risk Factors for Stroke
Modiable Risk

Nonmodiable Factors

Risk Factors High blood pressure Smoking Diabetes mellitus

Atherosclerosis Atrial brillation Other heart disease TIAs Sickle cell
anemia High cholesterol Obesity Excessive alcohol intake Certain illegal
drugs
TIAs
transient ischemic attacks.
Older age Sex (more common in men) Heredity Prior stroke or heart
attack

Prevention of Stroke
1. Incidence of stroke can be lessened by reduction of risk factors (above).
2. Keeping hypertension, cholesterol level, weight, and diabetes controlled
can go a long way in pre- venting strokes.
3. Smoking cessation is essential.
4. Emboli may be prevented with warfarin in individuals at high risk from
atrial brillation.
5. Aspirin or other antiplatelet agents help prevent abnormal clotting.
6. Carotid endarterectomy can be done in patients with carotid stenosis.
7. It is important to educate all patients about new treatments for stroke and
the potential for reversal of symptoms with the use of the thrombolytic
agent t-PA.
8. Patients must be educated about symptoms of stroke and the importance
of receiving emergency treatment within 3 hours to maximize the
potential for prevention of neurological decits. Too often patients ignore
early symptoms or delay calling for help. This delay can mean the
difference between leading a normal life and permanent disability.
Pathophysiology
When blood ow to any part of the brain is impeded as a result of a thrombus or
embolus, oxygen deprivation can lead to ischemia and eventually to infarction
(necrosis) of the cerebral tissue. If the neurons are ischemic only and have not
yet infarcted, the injury may be reversible. However, necrosis is irreversible. The
necrotic zone is surrounded by an ischemic zone called the penumbra.
The goal of acute stroke management is to salvage the ischemic penumbra.
Without prompt intervention, the entire ischemic penumbra can eventually
become an infarcted region.17 Damage to the brain tissue may also result from
localized vasogenic cerebral edema, which forms around the penumbra.

Ischemic Stroke
An ischemic stroke can be caused by embolism or thrombosis, with resulting
decreased perfusion Although any vessel may be involved, the bifurcation of the
common carotid artery into the internal and external branches is the most
common location for cerebral atherosclerosis and sub- sequent occlusion from an
embolism or thrombosis.
When arteries are narrowed due to atherosclerotic plaque, they can become
occluded (thrombotic stroke). If emboli break away from plaque, they can travel
and lodge in narrowed cerebral vessels (embolic stroke). Either case results in
ischemia or infarct of the brain cells that are per- fused by the affected vessel.
Emboli in the brain may be arterial or cardiac in origin. Patients in atrial
brillation can have small clots develop in the atria because the blood is not
ejected normally, and as a result pools. These clots can be ejected into the
circulation and become emboli.
Other commonly recognized cardiac sources for embolism include sinoatrial
disorder, recent acute myocardial infarction (AMI), subacute bacterial
endocarditis, cardiac tumors, and valve disorders. Most strokes of cardiac origin
occur in the rst weeks after AMI, but some risk for stroke remains for an
indenite time. Stroke due to decreased perfusion occurs with severe stenosis of

the carotid or basilar arteries, or with stenosis of the small deep arteries of the
brain. The smallest, most dis- tal vessels are affected rst, before the larger
proximal vessels, a process termed watershed infarction. People with diabetes
and hypertension have an increased risk for atherosclerosis and thrombosis.
Decreased perfusion may also occur from vasculitis, an inammatory condition
involving the cerebral blood vessels. Common causes of vasculitis are systemic
lupus erythematosus, bacterial or tuberculous meningitis, fungal infection, and
herpes zoster arteritis (arterial inammation).
Hemorrhagic Stroke
Hemorrhagic stroke is caused by the rupture of a cerebral blood vessel.
When a cerebral blood vessel ruptures, the brain tissue beyond the vessel does
not receive oxygen and nutrients and can die. Additional damage can occur to
the brain tissue surrounding the rupture from blood being released in the brain
outside of the vascular system.
The most common cause of an intracerebral hemorrhage (ICH) is poorly
controlled hypertension. Another cause is a ruptured aneurysm. Hemorrhages
tend to occur deep within the brain tissue.
Subarachnoid hemorrhage (SAH) is caused by rupture of blood vessels on the
surface of the brain. This type of infarct has the slowest rate of recovery and the
highest probability of leaving the patient with extensive neurological decits.
The most common etiology of brain attack in younger patients is illicit drug
usage. PCP (phencyclidine), crack, cocaine, amphetamines, and heroin have all
been associated with cerebrovascular accident from subarachnoid or intracerebral hemorrhage because these drugs raise the blood pressure and increase
pressure within the cerebral vessels.

Risk Factors

Risk factors for ischemic stroke are classied as modiable or nonmodiable.

Nonmodiable risk factors are those things that cannot be altered, such as age,
gender, race, prior stroke history, and heredity.
Modiable risk factors are those risks which can be changed by treatment, such
as treating high blood pressure, or by lifestyle modication, such as stopping
smoking (Box 49.1). Following physician recommendations and medication
orders for modiable risk factors will help individuals reduce stroke risk.
Warning Signs
All patients should be taught to recognize warning signs of a stroke, and to call
911 immediately if they occur. Warning signs include:
Sudden numbness or weakness of face, arm, or leg, especially on one side of
the body Sudden confusion, trouble speaking, or understand
ing
Sudden trouble seeing in one or both eyes Sudden trouble walking, dizziness,
loss of balance, or coordination
Sudden severe headache with no known cause

Assessment
A stroke is usually characterized by the sudden onset of focal neurological
impairment. Speci c manifestations depend on the anatomical location of the
lesion.
Common signs and symptoms include

weakness,
numbness,

visual changes,
dysarthria,
dysphagia, or
aphasia

It is important to obtain a description of the neurological event;

the onset and progression of symptoms; and whether the symptoms are the
same as at the time of onset, worsening, resolving, or completely gone.
The pattern of symptoms can help determine the diagnosis and identify possible
vascular involvement.
The National Institutes of Health Stroke Scale (NIHSS) may be used in
conjunction with the neurologic assessment to assign a score indicating the
severity of the stroke (Table 23-8).17

National Institutes of Health Stroke Scale (NIHSS)

Instructions

Scale Denition

1a. Level of Consciousness: The investigator must choose a response if a full

evaluation is prevented by such obstacles as an endotracheal tube, language
barrier, orotracheal trauma/bandages.
0 = Alert; keenly responsive.
1 = Not alert; but arousable by minor stimulation.
2 = Not alert; requires repeated stimulation to attend.
3 = Responds only with re ex motor or autonomic effects or totally
unresponsive,
accid, and areexic.
1b. LOC Questions: The patient is asked the month and his/her age. The answer
must be correct - there is no partial credit for being close.
0 = Answers both questions correctly.
1 = Answers one question correctly.
2 = Answers neither question correctly.
1c. LOC Commands: The patient is asked to open and close the eyes and then to
grip and release the non-paretic hand. Substitute another one-step command if
the hands cannot be used.
0 = Performs both tasks correctly.
1 = Performs one task correctly.
2 = Performs neither task correctly.
2. Best Gaze: Only horizontal eye movements will be tested. Voluntary or
reexive (oculocephalic) eye movements will be scored, but caloric testing is not
done.

0 = Normal.
1 = Partial gaze palsy; gaze is abnormal in one or both eyes.
2 = Forced deviation, or total gaze paresis not overcome by the
oculocephalic maneuver.
3. Visual: Visual elds (upper and lower quadrants) are tested by confrontation,
using nger counting or visual threat, as appropriate.
0 = No visual loss.
1 = Partial hemianopia.
2 = Complete hemianopia.
3 = Bilateral hemianopia (blind including cortical blindness).
4. Facial Palsy: Ask or use pantomime to encourage the patient to show teeth
or raise eyebrows and close eyes.
0 = Normal symmetrical movements.
1 = Minor paralysis ( attened nasolabial fold, asymmetry on smiling).
2 = Partial paralysis (total or near-total paralysis of lower face).
3 = Complete paralysis of one or both sides (absence of facial movement
in the upper and lower face).
5. Motor Arm: The limb is placed in the appropriate position: extend the arms
(palms down) 90 degrees (if sitting) or 45 degrees (if supine). Drift is scored if
the arm falls before 10 seconds. 5a. Left Arm 5b. Right Arm
0 = No drift; limb holds position for full 10 seconds.
1 = Drift; limb holds position, but drifts down before full 10 seconds; does
not hit bed or other support.
2 = Some effort against gravity; limb cannot get to or maintain (if cued)
position, drifts down to bed, but has some effort against gravity.
3 = No effort against gravity; limb falls.
4 = No movement. UN = Amputation or joint fusion.
6. Motor Leg: The limb is placed in the appropriate position: hold the leg at 30
degrees (always tested supine). Drift is scored if the leg falls before 5 seconds
. 6a. Left Leg
6b. Right Leg
0 = No drift; leg holds position for full 5 seconds.
1 = Drift; leg falls by the end of the 5-second period but does not hit bed.
2 = Some effort against gravity; leg falls to bed by 5 seconds, but has
some effort against gravity.
3 = No effort against gravity; leg falls to bed immediately.

4 = No movement. UN = Amputation or joint fusion.

7. Limb Ataxia: The nger-nose-nger and heel-shin tests are performed on both
sides with the eyes open.
0 = Absent.
1 = Present in one limb.
2 = Present in two limbs. UN = Amputation or joint fusion.
8. Sensory: Sensation or grimace to pinprick when tested, or withdrawal from
noxious stimulus in the obtunded or aphasic patient.
0 = Normal; no sensory loss.
1 = Mild-to-moderate sensory loss; patient feels pinprick is less sharp or is
dull on the affected side; or there is a loss of super cial pain with pinprick,
but patient is aware of being touched.
2 = Severe to total sensory loss; patient is not aware of being touched in
the face, arm, and leg.
9. Best Language: The patient is asked to describe what is happening in a
picture, to name the items on a naming sheet, and to read from a list of
sentences.
0 = No aphasia; normal.
1 = Mild-to-moderate aphasia; some obvious loss of uency or facility of
comprehension, without signi cant limitation on ideas expressed or form
of expression.
2 = Severe aphasia; all communication is through fragmentary
expression; great need for inference, questioning, and guessing by the
listener.
3 = Mute, global aphasia; no usable speech or auditory comprehension.

10. Dysarthria: An adequate sample of speech is obtained by asking patient to

read or repeat words from a list.
0 = Normal.
1 = Mild-to-moderate dysarthria; patient slurs some words and can be
understood with some difculty.
2 = Severe dysarthria; patients speech is so slurred as to be unintelligible
in the absence of or out of proportion to any dysphasia, or is
mute/anarthric. UN = Intubated or other physical barrier.
11. Extinction and Inattention (formerly Neglect): Sufcient information to
identify neglect may be obtained during the prior testing.
0 = No abnormality.

1 = Visual, tactile, auditory, spatial, or personal inattention or extinction

to bilateral simultaneous stimulation in one of the sensory modalities.
2 = Profound hemi-inattention or extinction to more than one modality;
does not recognize own hand or orients to only one side of space.
Although an area of infarction may not show on the CT scan for 12 to 24 hours,
an urgent noncontrast CT scan (obtained within 1 hour of arrival in the
emergency department) is performed to rule out intracerebral hemorrhage and
facilitate treatment decisions.
Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are also
frequently used to evaluate the patient with acute ischemic stroke. DWI and PWI
are MRI-based techniques that help identify the infarct core and penumbra,
which is important because the presence of viable tissue directs interventions
such as reperfusion. DWI can reveal changes associated with infarcted tissue a
few hours after the onset of symptoms (hours before a CT scan or conventional
MRI can detect any abnormality). PWI shows the regional abnormalities of
cerebral blood ow
Cerebral angiography, traditionally the gold standard for evaluating cerebral
vasculature, can demonstrate an arterial occlusion or embolus, but because of
the time that it takes to perform cerebral angiography, the window of
opportunity to treat a patient with IV thrombolytics may be missed. Alternative
studies, such as MRA and CTA, are used to view vasculature and are faster and
less invasive. An electrocardiogram (ECG) is obtained to assess for evidence of
dysrhythmia (eg, atrial brillation).

Management
The management of an ischemic stroke has four primary goals:

restoration of cerebral blood ow (reperfusion),

prevention of recurrent thrombosis,
neuroprotection,
and supportive care.

If the patient is a candidate for IV thrombolytic therapy, treatment with tissue

plasminogen activator (t-PA) begins in the emergency department, and the
patient is then moved to the critical care unit for further monitoring. If the
patient is not a candidate for thrombolytic therapy, the complexity of the
patients problems determines whether the patient is transferred to the critical
care unit, a medical unit, or a stroke specialty unit for ongoing care.

Early Management
The focus of initial treatment is to save as much of the ischemic area as
possible.

Thrombolytic Therapy
Thrombolytic agents (eg, t-PA) dissolve clots and permit reperfusion of the brain
tissue. The history, neurological examination, NIHSS score, and results of
neuroimaging studies assist the physician with the decision to offer thrombolytic
therapy. Eligibility criteria for thrombolytic therapy are given in Box 23-4.
A major risk of this therapy is intracerebral hemorrhage. If the patient is a
candidate for thrombolytic therapy, the systolic blood pressure is maintained at
less than 185 mm Hg to the lower risk of hemorrhage. When t-PA is given, 10% of
the total dose (0.9 mg/kg, not to exceed 90 mg) is administered as an IV bolus
over 1 to 2 minutes, with the remainder infused over 60 minutes. No other
antithrombotic or antiplatelet therapy is given for the next 24 hours.
Interventional Radiology
Interventional radiology techniques include intra- arterial thrombolysis (ie, the
direct administration of t-PA to the site of the clot via the femoral artery) and the
use of mechanical clot removal devices (eg, the mechanical embolus removal for
cerebral ischemia, or MERCI retriever).
Intra-arterial thrombolysis can be given up to 6 hours after the onset of
symptoms
. Angiography is required, and the patient must be admitted or transferred to a
specialty center equipped to per- form the procedure.
Mechanical clot removal entails the use of a device that typically works like a
corkscrew to snare and remove the embolus.
Mechanical clot removal can be performed up to 8 hours after symptom onset
and even longer if obstruction involves the basilar artery. Eligibility criteria for
mechanical clot removal are given in Box 23-5. Potential complications include
bleeding and vascular dissection or perforation; close monitoring is required for
24 hours following the procedure to detect adverse effects.

Ongoing Management
A collaborative care guide for the patient who has had a stroke is given in Box
23-6. Supportive care measures include the following:
Anticoagulation therapy.
Antithrombotic and antiplatelet agents (eg, warfarin) may be administered to
prevent future thrombotic or embolic events.
Control of hypertension.
Patients with moderate hypertension usually are not treated acutely. If the
patient is not a candidate for thrombolytic therapy, the blood pressure is not
treated unless it exceeds 220 mm Hg systolic or 120 mm Hg diastolic because
reducing blood pressure reduces the CPP and can cause infarction of the penumbra. When necessary, blood pressure is lowered gradually using short-acting IV
antihypertensive agents.
Control of ICP.

Elevation of the ICP in a patient who has had a stroke, when it occurs, usually
occurs after the rst day. Measures to lower ICP are described in Chapter 22.
Control of blood glucose level.
Hyperglycemia and hypoglycemia can have potentially deleterious effects in
patients who have had a stroke.
Glycemic control may be achieved with a continuous insulin infusion or a slidingscale regimen.

Eligibility Criteria for Mechanical Clot Removal

Inclusion Criteria
Clinical diagnosis of ischemic stroke with aNational Institutes of Health Stroke
Scale (NIHSS) score greater than 8
Occlusion of the internal carotid artery, basilar artery, or vertebral artery on
angiography
Exclusion Criteria
Excessive vessel tortuosity
Hemorrhagic tendency
Blood glucose less than 50 mg/dL, elevated international normalized ratio
(INR), decreased platelets
Sustained hypertension

Large areas of hypodensity on computed tomography (CT)

Arterial stenosis proximal to the embolus on angiography C O L L A B O R AT I
V E C A R E G U I D E for the Patient with a Stroke
OUTCOMES

INTERVENTIONS

Oxygenation/Ventilation
Adequate airway is maintained. SpO2 is maintained within normal
limits. Atelectasis is prevented.
Monitor breath sounds every shift.
Check oxygen saturation every shift.
Instruct patient to cough and deep breathe and use incentive spirometry
q2h while awake.
Assist with removal of airway secretions as needed.
Circulation/Perfusion Patient is free of dysrhythmias.
Monitor vital signs closely.

 Manage blood pressure carefully; avoid sharp drops in blood pressure

that could result in hypotension and cause an ischemic event secondary to
hypotension.
During cardiac monitoring, identify dysrhythmias.
Treat dysrhythmias to maintain adequate perfusion pressure and reduce
chance of neurological impairment.
Neurological
Adequate CPP is maintained.
Obtain vital signs and perform a neurological assessment to establish a
baseline and to monitor for the development of additional decits.
Use the NIHSS for detection of early changes suggesting cerebral edema
or extension of stroke.
Position head of bed at 30 degrees to promote venous drainage.
Effective communication is established.
Assess patients ability to speak and to follow simple commands.
Arrange for consultation with speechlanguage pathologist to
differentiate language disturbances.
Use communication aids to enhance communication
. Provide a calm, unrushed environment. Listen attentively to the
patient. Speak in a normal tone.
Fluids/Electrolytes
Electrolytes are within normal limits.
Monitor laboratory results, especially glucose.
Monitor intake and output.
Mobility/Safety
Safety is maintained.
Complications of immobility are avoided.
Initiate DVT precautions (eg, compression stockings, sequential
compressive devices, subcutaneous heparin) as ordered.
Perform fall risk assessment.
Consult with physical therapy.
Provide active or passive range-of-motion exercises to all extremities
every shift.
Establish splinting routine for affected limbs.
Instruct patient in use of mobility aids and fall prevention strategies.
For visual eld cuts, teach scanning techniques.

Skin Integrity

Patient is without evidence of skin breakdown.

Perform skin assessment using the Braden scale.

Provide pressure relief mattress as indicated by Braden scale.
Turn and reposition q2h
. Consult with wound nurse specialist for skin issues and concerns.
Nutrition

Patient has adequate caloric intake and does not experience decrease in
weight from baseline.
Patient is free from aspiration.
Obtain admission weight.

Perform cranial nerve assessment (including ability to swallow) to

identify decits.
Obtain consultation from speechlanguage pathologist to determine
whether oral intake of food and liquids is safe.
Provide proper diet and assist with feeding as needed.
Monitor calorie intake; implement calorie count, if necessary.
Obtain dietary consultation to obtain recommendation for nutritional
supplements.
Psychosocial Support

network is established.

Assess for family support systems.

Screen for poststroke depression.
Teaching/Discharge Planning

Risk factors are modied. Secondary preventive measures are

taken.

Provide education about blood pressure management.

Provide information regarding modi able risk factors and lifestyle
changes to reduce the incidence of a secondary stroke.