(Circulation. 2000;102:I-204.)
© 2000 American Heart Association, Inc.
ECC Guidelines |
Part 7: The Era of Reperfusion
Section 2: Acute Stroke
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Major Guidelines Changes |
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- Intravenous administration of tissue-type
plasminogen activator (tPA) for patients with
acute ischemic stroke and no contraindications is
recommended: —Within 3 hours of onset of stroke symptoms
(Class I) —Between 3 and 6 hours of onset of stroke
symptoms (Class Indeterminate)
- Intra-arterial fibrinolysis within 3 to 6
hours after the onset of symptoms may be beneficial in patients with
occlusion of the middle cerebral artery (Class IIb).
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Introduction |
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A stroke is a disruption in blood supply to a region of the brain that causes neurological impairment. Stroke is ranked among the top 3 leading causes of death in most countries and is the leading cause of brain injury in adults. Internationally millions of people have a new or recurrent stroke each year, and nearly a quarter of these people die.1 The stroke rate is declining in most western and northern European countries, but there is a large and increasing rate in Russia, possibly attributable to a higher prevalence of hypertension.2 Although stroke mortality and attack rates are falling in many countries, the gain achieved by prevention has been counterbalanced by a growth in the aging population (more people at risk).3 4
Strokes can be classified into 2 major categories, ischemic and hemorrhagic. Approximately 85% of all strokes are ischemic.5 Ischemic strokes occur primarily because a blood vessel supplying the brain is occluded, usually by a thrombus or embolism. Hemorrhagic strokes are the result of rupture of a cerebral artery. Associated spasm of the artery and various degrees of bleeding occur. Until recently, care of the stroke patient was largely supportive, focusing on prevention and treatment of respiratory and cardiovascular complications. No specific therapy was available to alter the course and extent of the evolving stroke. Therefore, little emphasis or need was placed on rapid transport or intervention.
Fibrinolytic therapy now offers healthcare providers an opportunity to possibly limit the extent of neurological damage and to improve outcome in stroke patients. A time-dependent benefit similar to that observed in patients with acute myocardial infarction (AMI) is possible. The time available for treatment, however, is limited.6 Early recognition of stroke and rapid triage, evaluation in the Emergency Department (ED), and definitive management are essential.7 8 9
Early Recognition
Early treatment of stroke depends strongly on recognition of the
event by the patient, family members, or bystanders.10
Common symptoms of transient ischemic attack (TIA) and stroke
are described in Table 1
.
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Role of EMS in Stroke Care
Rapid activation of the EMS system is essential to optimize care
of the patient with stroke. Stroke patients who use the EMS system
arrive at the hospital faster than those who do not, a major advantage
for time-critical treatment.11 12 13 14 15 16 17 18 Furthermore, emergency
dispatchers can send the appropriate emergency team with a
priority dispatch response and provide instructions for care of the
patient until arrival of EMS personnel.19 20 21 EMS
personnel can then quickly transport the patient to a stroke center and
notify the facility before arrival to ensure rapid hospital-based
evaluation and treatment. Initial contact of the family physician and
transport of the patient by car have been shown to delay patient
arrival and initial evaluation at the hospital. Such delays may render
the patient ineligible for fibrinolytic
therapy.11 15 19
Only half of stroke patients currently use the EMS system for transport to the hospital.11 22 Strokes that occur when the patient is alone or sleeping may further delay prompt recognition and action.23 Eighty-five percent of strokes occur at home.22 As a result, public education programs have appropriately focused their efforts on persons at risk for stroke and their friends and family members. Public education has reduced the time to arrival at the ED.8 12
The 7 "D’s" of Stroke Management
Key points in the management of stroke can be remembered by
using the mnemonic of the 7 D’s: Detection,
Dispatch, Delivery, Door,
Data, Decision, and Drug
(see algorithm for suspected stroke).24 Delay
may occur at any point, so the response at each point must be skilled
and efficient. The first 3 D’s (detection, dispatch, and delivery) are
the responsibility of BLS providers in the community, including the lay
public and EMS responders. Detection occurs when a patient,
family member, or bystander recognizes the signs and symptoms of a
stroke or TIA and activates the EMS system (by phoning 911 or
other emergency response number). EMS dispatchers must prioritize the
call for a suspected stroke patient as they would for a victim of AMI
or serious trauma and dispatch the appropriate EMS team with
high transport priority. EMS providers must respond rapidly, confirm
the signs and symptoms of stroke, and transport the patient
(delivery) to a stroke center (a hospital that can provide
fibrinolytic therapy within 1 hour after arrival at the ED
door). The remaining 3 D’s are performed in the hospital:
data includes obtaining a computed tomography (CT) scan,
decision is made in identifying candidates eligible for
fibrinolytic therapy, and drug includes treating eligible
patients with fibrinolytic therapy.
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Airway and Ventilation
Airway obstruction may be a major problem in acute stroke,
particularly if the patient loses consciousness. Hypoxia and
hypercarbia can occur as the result of inadequate ventilation,
contributing to cardiac and respiratory instability. Aspiration of
secretions or gastric contents is a serious complication associated
with considerable morbidity and mortality. EMS providers must ensure
that the patient has an adequate airway. Assisted ventilation or
tracheal intubation may be required.
Vital Signs
Check vital signs (pulse, respirations, blood pressure, and
temperature) frequently to detect abnormalities and changes. Abnormal
respirations are particularly prevalent in comatose stroke patients and
usually reflect serious brain dysfunction. Hypertension often occurs
after a stroke and may be caused by underlying hypertension, a stress
reaction to the neurological event, or a
physiological response to decreased brain
perfusion. Blood pressure often returns to normal without
antihypertensive treatment.25
A variety of cardiovascular problems may be present in the patient with stroke. Cardiac arrhythmias may contribute to the cerebral thromboembolism, or they may be the consequence of brain injury. In particular, episodes of paroxysmal atrial fibrillation, severe symptomatic bradycardia, or high-degree atrioventricular block may point to cardiac rhythm disturbances as causative or contributory. In the elderly and in patients with diabetes, AMI with atypical or undetectable symptoms can occur.26 27 Obtain a 12-lead ECG and attempt to rule out left ventricular mural emboli if an acute or recent MI is suspected. Life-threatening cardiac arrhythmias are a potential early complication of stroke, particularly of intracranial hemorrhages.28 29 30 Continuous monitoring of cardiac rhythm and systemic perfusion is part of the early management of a stroke patient.
General Medical Assessment
Examine the patient for evidence of injury to the head or neck,
because trauma is an important consideration in the differential
diagnosis of stroke. Blood pressure in both upper extremities should be
measured. A difference of >10 mm Hg should raise consideration
of aortic dissection and compromise of brain blood supply. Perform
diagnostic studies such as CT or angiography if indicated
by history or clinical findings. Cardiac murmur, arterial
bruit, absent pulse, or other abnormalities should be sought during the
cardiovascular examination. The presence of an ocular
hemorrhage may allow early identification of intracranial
bleeding.
Brief Emergency Neurological Evaluation
The emergency neurological evaluation for stroke should include 6
key elements:
- Stroke screen or scale
- Time of onset of stroke signs
- Level of consciousness
- Type of stroke (hemorrhagic versus nonhemorrhagic)
- Location of stroke (carotid versus vertebrobasilar)
- Severity of stroke
Stroke Screen or Scale
Performing an extensive neurological examination outside the
hospital is impractical because it delays transport of the patient to
the ED. To conduct an out-of-hospital neurological evaluation, use a
validated tool such as the Cincinnati Prehospital Stroke Scale (Table 2) or the Los Angeles Prehospital Stroke Screen (LAPSS)16
(Table 3).31 32 The
Cincinnati scale is used to elicit any of the 3 major physical findings
suggestive of stroke: facial droop, arm drift, and abnormal
speech.31 LAPSS requires the examiner to rule out other
causes of altered level of consciousness (eg, history of seizures or
severe hyperglycemia or hypoglycemia) and then identify asymmetry
(right versus left) in facial smile/grimace, grip, or arm strength.
Asymmetry in any category indicates a possible
stroke18 32 These two scales
are sensitive and specific in identifying stroke
patients.18 31 32 Either evaluation can be performed
quickly.
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Ambulance personnel can identify stroke patients with reasonable sensitivity and specificity. Once a stroke is suspected, minimize time in the field and immediately transport the patient to a stroke center.
Clinical signs and symptoms of acute stroke often fluctuate. Deterioration or improvement can be detected by frequent and repeated focal neurological examinations. Repeated examinations need not be exhaustive. The Glasgow Coma Scale tests eye opening, verbal response, and motor response.33 It is useful for assessing the initial severity of neurological injury in patients with altered consciousness, especially in cases of injury caused by intracerebral hemorrhage.
Obtain the following information en route to or at the hospital. (Do not delay transport to complete a more detailed evaluation. Rapid transport is essential.)
Time of Onset of Symptoms
If stroke symptoms started within 6 hours of the arrival of EMS
personnel, immediately notify the receiving hospital. Prearrival
notification of the receiving hospital shortens the time to definitive
hospital-based evaluation and intervention. Provide results of
the stroke scale or screen, the Glasgow Coma Scale score,
and the estimated time of symptom onset in addition to standard
information. This allows the ED or Casualty Service time to prepare and
coordinate the patient’s time-sensitive therapy. The receiving
hospital should have a written plan to begin therapy as quickly as
possible.
Level of Consciousness
Determining the stroke patient’s level of consciousness is
crucial. Depressed consciousness within hours of the onset of symptoms
implies severe brain injury with increased intracranial pressure (ICP),
usually due to an intracerebral or subarachnoid
hemorrhage. Coma, the lack of any purposeful response to
external stimuli, is the result of damage to both cerebral hemispheres
or the brain stem. Coma usually implies massive hemorrhage,
occlusion of the basilar artery, or cardiac arrest with global brain
ischemia. Massive ischemic stroke with cerebral edema
may cause coma but is rare. Do not overlook concurrent
metabolic problems. Consider drug overdose, sepsis, or
severe metabolic abnormalities.
Type of Stroke (Ischemic Versus Hemorrhagic)
The history and physical findings of hemorrhagic and
ischemic stroke overlap (see Table 4). Do not depend solely on clinical
presentation for diagnosis. In most cases,
noncontrast CT is the definitive test for differentiating
ischemic and hemorrhagic stroke. (CT is discussed in
"Emergency Diagnostic Studies.")
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Location of Stroke
Higher cortical, language, visual, cranial nerve, motor, and
sensory functions should be assessed in alert patients with brain
infarction. Neurological signs help distinguish infarction of the
carotid territory from infarction with a vertebrobasilar distribution.
Crossed (cranial nerve palsy with contralateral motor or sensory
deficit) or bilateral neurological signs suggest that the infarct is
located in the brain stem. Specific patterns of
deficit, such as pure sensory stroke or dysarthria with a clumsy hand,
may be present. Such deficits suggest a subcortical or lacunar
infarct caused by small-vessel disease. The specificity of clinical
signs such as pure motor deficit, however, is low. Distinguishing
between lacunar and nonlacunar infarcts on the basis of clinical
features is often difficult, especially within hours of the onset of
stroke.
Severity of Stroke
The National Institutes of Health Stroke Scale (NIHSS)
measures neurological function, and scores on this scale are correlated
with the severity of stroke and long-term outcome in patients with
ischemic stroke.25 34 35 The scale provides a
reliable, valid, and easy-to-perform alternative to the standard
neurological evaluation for patients with ischemic stroke, and
it has been used for triage of patients to different treatment
protocols.36 37 The NIHSS total score ranges from 0
(normal) to 42 points, evaluating 5 major areas of
functioning:
- Level of consciousness
- Visual function
- Motor function
- Sensation and neglect
- Cerebellar function
- The NIHSS is not a comprehensive neurological examination (eg,
it does not record gait or all cranial nerve deficits), and more
detailed neurological assessment may be required in certain cases.
- The Scandinavian Stroke Scale was used in the European Cooperative
Acute Stroke Study and has been shown to identify predictors of early
and late progression in stroke
patients.38 39
- The Hunt and Hess Scale (see Table 5) is
often used to grade the severity of stroke in patients with
subarachnoid hemorrhage.40 The Hunt and
Hess grade is correlated with survival after subarachnoid
hemorrhage and the risk of complications such as vasospasm. The
scale may be used to guide the timing of aneurysm clipping or
coiling.
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Differential Diagnosis
Very few nonvascular neurological diseases will cause sudden
onset of focal brain dysfunction, the hallmark of stroke. The list
of potential diagnoses (see Table 6) is
longer if the patient is comatose and the medical history is
unavailable. If the patient’s condition gradually worsens over several
days, a nonvascular neurological disease may be present.
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Prehospital Transport
EMS systems should develop protocols that provide for priority
dispatch, treatment, and transport of patients with signs and symptoms
of acute ischemic stroke. These protocols should convey the
same urgency as those for patients with signs and symptoms of AMI or
major trauma (Class IIb). Give highest priority to patients with a
suspected stroke and airway compromise or an altered level of
consciousness.
In addition, triage and transport patients with acute onset of stroke symptoms to a facility that can begin fibrinolytic therapy within 1 hour of arrival, unless that facility is >30 minutes away by ground ambulance (Class IIb).
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ED Triage and Treatment |
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The ED must be prepared for the arrival of the stroke patient so that triage and therapy can begin immediately. Maximum time intervals for completion of diagnostic studies of candidates for fibrinolytic therapy are listed in Table 7
.
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Emergency Diagnostic Studies
Emergency diagnostic studies are used to establish
stroke as the cause of the patient’s symptoms, to differentiate
between brain infarction and brain hemorrhage, and to determine
the most likely cause of the stroke. Protocols may prioritize and
streamline the order of these tests.
CT is the most important diagnostic test for differentiating between infarction and hemorrhage or other intracranial masses.41 To avoid confusing blood and contrast medium, perform CT without contrast enhancement. Withhold anticoagulants and fibrinolytics until brain hemorrhage is ruled out.
The CT scan of almost all patients with a recent intracerebral hemorrhage will show increased density at the site of bleeding.42 Findings in patients with subarachnoid hemorrhage, however, may be subtle (eg, the scan may show only a thin, white layer adjacent to the brain). Approximately 5% of patients with subarachnoid hemorrhage will have normal findings on the CT scan.43 44 Such patients usually have a small subarachnoid hemorrhage and are alert with no focal neurological deficits (Hunt and Hess grade 1). If clinical suspicion of subarachnoid hemorrhage remains despite negative findings on the CT scan, perform lumbar puncture.
Magnetic resonance imaging (MRI) is not part of the routine evaluation of acute stroke. MRI is very sensitive and will detect some lesions missed by CT. Although MRI can detect early hemorrhage,45 46 it is not superior to CT. MRI is also time consuming and may hamper continuous observation of acutely ill patients. New MRI techniques such as magnetic resonance angiography and diffusion- and perfusion-weighted MRI may help delineate the site of occlusion or the region of the brain at risk for infarction.47 48 These techniques are being evaluated for use in clinical practice. Diffusion-weighted MRI has been approved for use in stroke patients by the US Food and Drug Administration (Class Indeterminate).
Emergency cerebral angiography is performed in many patients with subarachnoid hemorrhage in anticipation of aneurysm clipping. Neurointerventional procedures such as aneurysm coiling, angioplasty, and intra-arterial thrombolysis also require emergency angiography in certain patients. Many other studies, including echocardiography, ultrasonography of the carotid artery, and transcranial Doppler, can be performed electively.
Emergency Management
Rapidly identify, evaluate, and treat all patients with signs and
symptoms of acute stroke. Stroke protocols and pathways may assist in
the rapid assessment of these patients. Clinicians may find the use of
a checklist helpful to identify contraindications to tPA
therapy.49 Target times for in-hospital evaluation and
treatment are given in Table 7
.50
General Emergency Therapy
Establish intravenous access en route to the hospital
or in the ED (see Table 8). Administer
normal saline or lactated Ringer’s solution at a rate of 50 mL/h.
Unless the patient is hypotensive, avoid rapid infusions, which
increase the risk of cerebral edema. Do not administer dextrose in
water unless hypoglycemia is strongly suspected; this solution is
hypotonic and may increase cerebral edema.51 52 53 54 55 56 57 Correct
hyperglycemia and hyperthermia (Class IIa). Do not routinely administer
supplemental oxygen to nonhypoxic (oxygen saturation >90%)
stroke victims with minor or moderate strokes. Oxygen may be
beneficial, however, to patients with severe strokes, but additional
research is needed.58
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Management of Elevated Blood Pressure
Management of blood pressure after acute ischemic or
hemorrhagic stroke is controversial. Many patients have hypertension
after an ischemic or hemorrhagic stroke, but few require
emergency treatment. Elevated blood pressure after a stroke is not a
hypertensive emergency unless there are other medical problems (eg, AMI
or aortic dissection).59 In most patients, blood pressure
will spontaneously decline as pain, agitation, vomiting, and increased
ICP are controlled.25
Antihypertensive treatment is reserved for patients with markedly
elevated blood pressures or specific medical indications. Current
recommendations are based on the type of stroke (hemorrhagic or
ischemic) and whether the patient with ischemic stroke
is a candidate for fibrinolytic therapy. In response to requests for
general guidance regarding the management of hypertension in stroke
patients, a table of suggested antihypertensive therapy approaches is
provided (see Table 9). It is important
to note, however, that these suggestions were based on consensus
opinion and are not evidence-based.
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Antihypertensive therapy can be harmful. Antihypertensive therapy can lower the cerebral perfusion pressure and lead to worsening of the stroke.59 In addition, the response of stroke patients to antihypertensive therapy can be exaggerated. Use of short-acting nifedipine is contraindicated.59 For patients with an arterial occlusion, maintenance of adequate collateral flow is of paramount importance.
In candidates for fibrinolytic therapy, however, strict control
of blood pressure is required to reduce the potential for
bleeding. Fibrinolytic therapy is not recommended for patients who
have a systolic blood pressure >185 mm Hg or a
diastolic blood pressure >110 mm Hg at the time of
treatment (see Table 9).60 61 Simple measures
often can lower blood pressure below this level. If more aggressive
measures are required, do not use fibrinolytics.
Management of Seizures
Recurrent seizures are a potentially life-threatening complication
of stroke. They can worsen the stroke and should be controlled.
Administration of anticonvulsant medications to prevent recurrent
seizures is strongly recommended, but prophylactic
administration is not indicated.59 Protection of the
airway, administration of supplementary oxygen, and maintenance
of normothermia are part of supportive care.
Benzodiazepines are first-line agents for treating seizures. Intravenous diazepam (5 mg over 2 minutes to a maximum of 10 mg) or lorazepam (1 to 4 mg over 2 to 10 minutes) usually will stop seizures but may produce respiratory depression. Lorazepam, which has a short half-life, may be the superior agent. Administration of these agents can be repeated, but they should be followed by a longer-acting anticonvulsant such as phenytoin, fosphenytoin, or phenobarbital.
Management of Increased ICP
Death during the first week after stroke commonly is caused
by brain edema and increased ICP. Fortunately only 10% to 20% of
stroke patients develop brain edema sufficient to cause clinical
deterioration. When brain edema is clinically suspect, modest fluid
restriction, elevation of the head of the bed (20° to 30°), support
of oxygenation and ventilation (avoidance of hypoxemia
and hypoventilation), and control of agitation and pain will help lower
increased ICP. Goals of therapy are (1) reduction of increased ICP, (2)
maintenance of cerebral perfusion to prevent worsening of
ischemia, and (3) prevention of brain herniation.
Reduction of the partial pressure of CO2 in
arterial gas (PaCO2)
through intubation and hyperventilation is the most rapid means of
lowering ICP in cases of impending brain herniation. Optimal
PaCO2 is 30 to 35
mm Hg.62 PaCO2 values
25 mm Hg are occasionally acceptable in rapidly deteriorating
patients, but if such values are sustained, ischemia of the
brain may occur.62 Aggressive tracheal suctioning
increases ICP and should be avoided, with suctioning reduced in
frequency and duration to that necessary to maintain tracheal tube
patency.
Hyperosmolar therapy with mannitol is used to reduce the mass effect on diencephalic structures or to maximize cerebral perfusion pressure. Mannitol can be given as a bolus (0.25 to 0.5 g/kg per dose given over 20 minutes rapidly) and repeated every 6 hours to a maximum dose of 2 g/kg daily.59 High initial doses are given in emergencies. The effect on ICP usually occurs about 20 minutes after administration. Lower doses (25 to 50 g every 4 hours) given as intermittent boluses are used to manage ICP over longer periods. Furosemide, hypertonic saline, and acetazolamide may also help lower ICP.
High doses of barbiturates (eg, thiopental 1 to 5 mg/kg) rapidly lower ICP and suppress electrical brain activity. Because high doses of barbiturates suppress respiratory activity and may produce vasodilation and myocardial depression, they should be administered in conjunction with mechanical ventilatory support and careful blood pressure monitoring. ICP must be monitored when a barbiturate coma is induced, because the barbiturates obliterate the clinical response. The ICP is used to evaluate response to therapy.
Routine measurement of ICP is not indicated, and the value of ICP measurement has not been shown. ICP measurement, however, may be helpful in deteriorating patients, can guide therapy, and can serve as an indicator of prognosis and outcome.59
Neurosurgical decompression can be lifesaving in some patients with high ICP and intracranial hemorrhage, edema after stroke, or other mass effects on brain tissue. Surgery for cerebellar hemorrhage or edema after stroke can produce remarkable improvement. Pharmacological and ventilatory measures for controlling ICP are much less effective than surgery in patients with cerebellar lesions. Corticosteroids are not effective and should not be used.63 Cerebellar edema or hemorrhage frequently causes obstructive hydrocephalus, necessitating ventricular drainage. Closely monitor patients with cerebellar lesions for neurological deterioration.
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Pharmacological and Interventional Therapies |
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Ischemic Stroke
Fibrinolytic Therapy
Use of intra-arterial and intravenous fibrinolytic agents such as tPA, streptokinase, ancrod, urokinase, and prourokinase in stroke patients has been evaluated in several clinical trials.39 64 65 66 67 68 69 70 71 72 The Cochrane Stroke Review group73 evaluated 17 trials with >5000 patients in which >50% of patients received tPA. Fibrinolytic therapy significantly increased the odds ratio of death within the first 10 days and at follow-up, mainly because of fatal intracerebral hemorrhage. Patients treated within 3 hours, however, had reduced death and dependency compared with patients treated within 3 to 6 hours. Overall, the proportion of patients with death or disability was reduced. It is difficult to draw conclusions from this review because there was significant heterogeneity among the comparison trials.73 In the clinical trials reviewed, many different agents were administered, with many different time intervals between onset of stroke symptoms and drug administration.
The National Institute of Neurological Disorders and Stroke rtPA Stroke Trial64 evaluated a single agent administered within 3 hours of symptom onset in a prospective, blinded, randomized, controlled clinical trial. Intravenous tPA was administered in a dose of 0.9 mg given as a 10% bolus over 1 minute, followed by a 1-hour infusion versus a placebo. In this trial, patients treated with tPA within 3 hours of onset of symptoms were at least 30% more likely to have minimal or no disability at 3 months compared with those treated with placebo. The risk of fatal intracranial hemorrhage, however, was 10 times greater in the tPA-treated group (3% versus 0.3%). A similar increase in the frequency of all symptomatic hemorrhages (6.4% versus 0.6%) was also observed in this group. This increase in symptomatic hemorrhage did not lead to an overall increase in mortality in the treated group.
Based on the results of parts I and II of the National Institute
of Neurological Disorders and Stroke study, intravenous
administration of tPA is recommended for carefully selected patients
with acute ischemic stroke if they have no contraindications to
fibrinolytic therapy and if the drug can be administered within 3 hours
of the onset of stroke symptoms (Class I). Contraindications to tPA are
listed in Table 10.
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Investigators have tried to extend the time for treatment beyond 3 hours by using various fibrinolytic agents and new approaches to administration (eg, intra-arterial therapy).39 65 66 67 69 70 71 72 Evidence suggested that use of intravenous tPA 3 to 6 hours after the onset of symptoms may be beneficial in certain patients,73 but recent studies have been discouraging. The ATLANTIS Trial found no significant differences in 90-day efficacy end points in patients treated between 3 and 5 hours.65 The Thrombolytic Therapy in Acute Ischemic Stroke Study enrolled 142 patients at 42 sites in North America and found a small but significant benefit of tPA in patients treated after 3 hours when assessed at 1 day; this benefit was not maintained at 30 days.74 In both of these trials, the rate of symptomatic intracerebral hemorrhage was increased. At this time routine use of intravenous tPA >3 hours after the onset of symptoms is not recommended (Class Indeterminate).
Results of a recent, randomized trial of intra-arterial prourokinase suggest that use of intra-arterial fibrinolytic agents 3 to 6 hours after the onset of symptoms may be beneficial in patients with occlusion of the middle cerebral artery (Class IIb).71
Three large, randomized trials of streptokinase in patients with stroke have been reported.69 70 75 All 3 studies were suspended because of increased hemorrhage and mortality in the group treated with streptokinase. Do not use streptokinase in patients who have had a stroke except in clinical studies approved by the appropriate institutional review board.
Anticoagulant Therapy
The efficacy of anticoagulants in acute stroke has not been
established. Heparin is frequently administered to patients with acute
ischemic stroke, but its value is unproved.76 77
Heparin may help prevent recurrent embolism or propagation of a
thrombus, but it may lead to bleeding complications, including brain
hemorrhage. There is no consensus on when heparin therapy
should be started or on the dose and duration of therapy. Emergency
physicians should consult the attending neurologist about the use of
heparin in specific patients (Class IIb). Low-molecular-weight
anticoagulants have several advantages not provided by unfractionated
heparin.71 Use of low-molecular-weight anticoagulants in
the management of stroke is being evaluated.
Aspirin, warfarin, and ticlopidine reduce the risk of subsequent stroke in patients with TIA.78 79 80 81 These antiplatelet agents should be started within the first few days after a TIA. When started within 48 hours of the onset of ischemic stroke, aspirin produces a small but definite net benefit in patients who are ineligible for fibrinolytic therapy.82 83 Antiplatelet therapy with aspirin 160 to 300 mg daily within 48 hours of onset of presumed ischemic stroke reduces the risk of early recurrent ischemic stroke without a major risk of early hemorrhagic complications and improves long-term outcome.84
The Cochrane Stroke Group completed a comprehensive review of anticoagulants in 21 trials involving 23 427 patients. A number of anticoagulants were used in clinical trials: standard unfractionated heparin, low-molecular-weight heparins, heparinoids, oral anticoagulants, and thrombin inhibitors. The conclusion of the Cochrane group was that immediate anticoagulant therapy in patients with acute ischemic stroke is not associated with net gain for either short- or long-term benefit. Routine use of any type of anticoagulant in acute ischemic stroke is not recommended.85
Other Treatments
Calcium channel–blocking drugs, volume expansion,
hemodilution, and low-molecular-weight dextran have not been shown to
improve clinical outcome after ischemic stroke. A number of
cytoprotective agents are being investigated for use in patients with
acute ischemic or hemorrhagic stroke. Many of these agents have
been shown to provide no benefit in humans, even though benefit was
shown in animal models.86
Hemorrhagic Stroke
Subarachnoid Hemorrhage
Patients with subarachnoid hemorrhage often
require emergency arteriography. If a saccular aneurysm is
detected, early intracranial surgery with clipping (or coiling) of the
aneurysm is usually advised.87 The calcium
channel–blocking drug nimodipine (60 mg orally every 4 hours, 0.35
mg/kg) improves outcome after subarachnoid
hemorrhage.88 89 90 91 92 Correction of
hyponatremia and water loss is also important. Avoid
strict fluid restriction, however, which may stimulate inappropriate
secretion of antidiuretic hormone.
Intracerebral Hemorrhage
Hemorrhage into the brain can be devastating. Death
may occur because of compression or distortion of vital deep-brain
structures or increased ICP. Mortality is a function of the volume and
location of the intracerebral bleeding. Optimal
management requires prevention of continued bleeding, appropriate
management of ICP, and timely neurosurgical decompression when
warranted. Large intracerebral or cerebellar hematomas
often require surgical intervention. A CT scan is required for
differential diagnosis. Placement of a ventriculostomy tube through a
burr hole can be lifesaving if hydrocephalus is the cause of
coma.
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Footnotes |
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Circulation. 2000;102(suppl I):I-204–I-216.
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References |
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