TRIPASS XR تري باس

44 Another study considered the role of aspirin for primary stroke prevention

in women.

45 Women who took one to six tablets of aspirin per week had a slightly

reduced risk of stroke and a lower risk of large-artery occlusive disease (relative

risk, 59%; 95% confidence level, 0.29–0.85; p = 0.01). An increased risk of stroke

was seen in women who took more than 7 aspirin weekly, and an excess risk of

subarachnoid hemorrhage was seen in those taking more than 15 aspirin a week. The

Women’s Health Study also investigated the use of 100 mg/day in asymptomatic

women and followed them for 10 years, monitoring for nonfatal cardiovascular

events including stroke.

46

In this study, there was a 17% reduction in the risk for all

strokes and a 24% reduction in the risk for ischemic stroke, whereas there was a

nonsignificant increase in the risk for hemorrhage. Women 65 years of age and older

at entry into the trial showed the most consistent risk reduction, but hemorrhagic

strokes negated some of the benefit. Additionally, women with a history of

hypertension, hyperlipidemia, or diabetes, or a 10-year cardiovascular risk of at

least 10% had the most benefit. There are very limited data currently available

regarding the use of other antiplatelet drugs for primary prevention of stroke except

for cilostazol in patients with peripheral artery disease.

4

Although oral anticoagulants are not generally considered safe for primary

prevention of non-cardioembolic, patients with atrial fibrillation are candidates for

primary prevention. These individuals are at risk for an embolic event arising from

clot formation in the atrium of the heart. The CHADS2 score has been a widely used

system of stratifying the risk of thromboembolism in non-valvular atrial fibrillation

for a decade. It is generally accepted that low-risk patients (CHADS2 score = 0)

should not be treated with anticoagulants but may be considered for antiplatelet

therapy, while higher-risk patients (CHADS2 score ≥2) should be anticoagulated

with oral anticoagulants such as warfarin, dabigatran, apixaban, rivaroxaban, or

edoxaban (detailed discussion is available in Chapter 15, Cardiac Arrhythmias). The

tool recommended in the new guidelines, called “CHA2DS2

-VASc,” also considers

whether a patient has had prior vascular disease, evaluates people at younger ages

(between 65–74) and factors in gender.

47 This is important because women face

higher stroke risks. CHA2DS2-VASC score of ≥2 warrant the use of anticoagulants as

first-line option. Numerous studies have clearly shown that warfarin prevents

embolic cerebrovascular events for patients with valvular and non-valvular atrial

fibrillation.

48–51

In these studies, the warfarin dose was adjusted to maintain an

international normalized ratio (INR) of 1.5 to 4.5, with most recommendations to

adjust the dose for an INR of 2 to 3. The selection of the antithrombotic agent

depends on various factors including patient factors (risk of falls and hemorrhagic

events), cost, age of the patient, tolerability, patient preference, and potential drug

interactions. The Stroke Prevention in Atrial Fibrillation (SPAF) trial included

aspirin combined with warfarin in one study arm and indicated that some benefit may

be derived by combining antiplatelet agents with anticoagulants.

52 A follow-up study

was performed and showed no difference between warfarin and aspirin in preventing

stroke in atrial fibrillation.

51

In patients with non-valvular atrial fibrillation, aspirin

can be used as an alternative to warfarin in patients with atrial fibrillation, based on

the CHADS2 score or CHA2DS2-VASC score ( Table 61-3).

5

,

47 Additionally,

warfarin may be used in primary prevention of embolic stroke because of a patent

foramen ovale.

5

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p. 1307

Table 61-3

CHADS2 and CHA2DS2—VASC Score: Primary Stroke Prevention in Atrial

Fibrillation

CHADS2 score CHAD2DS2—VASC score

Add points for the following items. If score is <2, aspirin can be considered. If score is ≥2, anticoagulants

(warfarin, apixaban, rivoraxaban, edoxaban) are recommended.

Congestive heart failure = 1 point Congestive heart failure = 1 point

Hypertension = 1 point Hypertension = 1 point

Age >75 years = 1 point Age >75 years = 2 points

Diabetes mellitus = 1 point Diabetes mellitus = 1 point

Prior stroke or TIA = 2 points Prior stroke or TIA = 2 points

Vascular disease (e.g., peripheral artery disease,

myocardial infarction, aortic plaque) = 1 point

Age 65–74 years = 1 point

Sex category (i.e., female) = 1point

TIA, transient ischemic attack.

Source: January C et al. 2014 AHA/ACC/HRS Guideline for the management of patients with atrial fibrillation: a

report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and

the Heart Rhythm Society. Circulation. 2014;130:23.e199–e267.

For R.B., primary prevention of stroke with aspirin 81 mg/day can be considered

because of her history of hypertension and diabetes. Given that she has no atrial

fibrillation, she is not a candidate for anticoagulation therapy (see Table 61-4).

TREATMENT OF ACUTE ISCHEMIC STROKE

AND TIA

Goals of Therapy

The immediate goal is to reestablish adequate blood flow in the diseased cerebral

vessels, minimize brain injury, and treat medical complications. Longer-range

objectives are to prevent reocclusion and decrease the risk of a future ischemic

stroke.

Early Management of Acute Ischemic Stroke

CLINICAL PRESENTATION AND DIAGNOSTIC TESTS

CASE 61-2

QUESTION 1: P.C., a 65-year-old man (100 kg, 5 feet 9 inches), is admitted through the emergency

department (ED) with right-sided weakness. As per report the patient was last seen well around 8:30 PM by his

wife. Around 9:15 PM, the patient’s son heard a bump and went upstairs to find his father on the floor. The

patient had a slurred speech and had a right facial droop. At this point 911 was called and patient arrived at 9:45

PM to ED. He regained consciousness by the time he arrived in the ED. Both right extremities are flaccid. He

is unable to speak but is capable of understanding instructions (i.e., expressive aphasia). Gross ophthalmologic

examination indicates right-sided neglect (inability of his eyes to track to the right or acknowledge the right side

of his body). His blood pressure is 165/95 mm Hg; other vital signs are normal. Laboratory studies are all within

normal limits. What interventions should have been initiated before arrival in the ED?

Table 61-4

Drugs for Preventing Transient Ischemic Attacks and Ischemic Stroke

Drug Action Dose Adverse Effects

Aspirin Antiplatelet 50–325 mg/day Diarrhea, gastric ulcer, GI

upset

Dipyridamole Antiplatelet (use in

combination with aspirin)

200 mg sustained-release

twice daily

With aspirin 50 mg BID

GI upset

Ticlopidine Antiplatelet 500 mg/day Diarrhea, neutropenia, rash

Clopidogrel Antiplatelet 75 mg/day Thrombocytopenia, neutropenia

Cilostazol Antiplatelet 100 mg BID Headache, peripheral edema.

Contraindicated in congestive

heart failure patients

Warfarin Anticoagulant (only in patients

with cardioembolic cause of

stroke/TIA

Titrate to goal INR 2–3 for

most patients

2.5–3.5 with mechanical valve

Bleeding, bruising, petechiae

Rivaroxaban Anticoagulant (only in patients

with cardioembolic cause of

stroke/TIA

If CrCl >15 mL/minute, 20 mg

once daily with evening meal

Bleeding

Apixaban Anticoagulant (only in patients

with cardioembolic cause of

stroke/TIA

5 mg BID

If Scr ≥1.5 mg/dL, 2.5 mg BID

(if age >80 years or weight

≤60 kg)

Bleeding

Edoxaban Anticoagulant (only in patients

with cardioembolic cause of

stroke/TIA

60 mg daily

If CrCl 15–50 mL/minute 30

mg daily

Do not use if CrCl >95

mL/minute as high risk of

ischemic stroke

Dabigatran Anticoagulant (only in patients

with cardioembolic cause of

stroke/TIA

150 mg BID

If CrCL 15–30 mL/minute: 75

mg BID

GI bleed

GI, gastrointestinal; INR, international normalized ratio; BID, 2 times daily; CrCl, creatinine clearance; TIA,

transient ischemic attack; Scr, serum creatinine.

p. 1307

p. 1308

Immediate recognition of, and response to, stroke symptoms are essential to an

optimal outcome. As soon as stroke symptoms are recognized, the emergency medical

system should be activated. Emergency medical personnel should be trained to gather

important historical information, especially when the symptoms started. This is

defined as “when the patient was at his or her previous baseline or symptom-free

state. For patients unable to provide information or who was awaken with stroke

symptoms, the time of onset is defined as when the patient was last awake and

symptom-free or known to be normal.”

53 Use of a standardized evaluation tool such

as the Cincinnati Prehospital Stroke Scale or Los Angeles Prehospital Stroke Screen

is useful in distinguishing stroke symptoms from other disorders, such as conversion

disorder, hypertensive encephalopathy, hypoglycemia, complicated migraine, or

seizures.

53

,

54

General supportive care for respiratory and cardiovascular function should be

initiated before transporting the patient to the ED. An important key to effectively

managing acute stroke patients is to have a well-designed evaluation and treatment

algorithm that addresses assessment and care of the patient from initial onset of

symptoms through rehabilitation. Patients with suspected cerebral infarction should

be transported, if possible, to the closest certified primary care center. A certified

primary care center would have a multidisciplinary team and would be activated and

notified by the emergency personnel while potential stroke patient is en route (Fig.

61-3).

53

If a primary stroke center is not locally available, patients can be stabilized

in community hospital. In these situations, local providers may use practice

arrangements with larger centers that allow the provision of advanced care under the

supervision of experts at a primary stoke center.

CASE 61-2, QUESTION 2: What diagnostic tests and evaluations will be helpful in guiding P.C.’s therapy?

Basic laboratory and diagnostic tests should be quickly performed to exclude noncerebrovascular causes of P.C.’s symptoms, such as metabolic or toxicologic

derangement or infections. These tests include a routine serum chemistry profile

(electrolytes, blood urea nitrogen, serum creatinine, hepatic enzymes, calcium,

phosphorus, magnesium, albumin), complete blood count, and toxicology screen.

Coagulation studies, including a prothrombin time with INR and partial

thromboplastin time, should be performed to provide baseline values for potential

anticoagulation or thrombolytic therapy. In addition, a thorough physical, neurologic,

cardiovascular, and mental status examination should be performed. The neurologic

examination will assist in localization of the lesion in the CNS. The physical

examination should include use of the National Institutes of Health Stroke Scale.

54

In

addition to providing important information for diagnosis of his neurologic

compromise, these tests will provide baseline data for ongoing assessment of P.C.’s

progress and recovery.

The etiology of a stroke (ischemic versus hemorrhagic) is difficult to discern

based solely on a physical and neurologic examination. As a result, CT or magnetic

resonance imaging (MRI) is valuable in the evaluation of these patients. An MRI is

preferred to a CT because of its superior tissue contrast, ability to obtain images in

multiple planes, absence of artifacts caused by bone, vascular imaging capabilities,

absence of ionizing radiation, and safer contrast media. MRI also allows for a

magnetic resonance angiogram to be performed, allowing visualization of the

cerebro-vasculature and possible identification of the precise location of the

thrombus or embolus. Within the first 24 hours of an ischemic stroke, an MRI is

clearly more sensitive than a CT. After 48 hours, the MRI and CT are equally

effective in detecting ischemic infarcts. The primary disadvantages of the MRI are

that it is more sensitive to artifacts, more difficult to perform in unstable patients, and

not always available in smaller hospitals or communities. In addition, MRI is also

not safe to be done in patients who have metallic implants, or pacemakers.

P.C. must have either a CT or an MRI before initiation of any specific therapy for

stroke. A follow-up CT or MRI in 5 to 7 days is useful to determine the extent of

neurologic damage resulting from the ischemic stroke.

Angiographic, Doppler, or sonographic examination of the cerebral vasculature

may be helpful in identifying the location of the vascular lesion. These tests usually

are performed after the patient has been stabilized, unless angioplasty with stents,

mechanical retrieval devices, or use of intra-arterial fibrinolytics is anticipated. A

lumbar puncture with collection of CSF for evaluation may be helpful in identifying

the presence of blood in the CNS. In the presence of suspected increased intracranial

pressure, a lumbar puncture must be avoided because of the potential for tentorial

herniation.

Treatment

CASE 61-2, QUESTION 3: A head CT revealed left MCA territory infarct with no cerebral hemorrhage or

edema. Is PC a candidate for intravenous thrombolysis?

The critical primary event in a thromboembolic stroke is the development of an

acute thrombus. Prospective cerebral angiography has demonstrated an arterial

occlusion corresponding to the area of acute neurologic deficit in greater than 90% of

cases.

55

Occlusion of cerebral arteries does not cause complete ischemia because

collateral circulation from other arterial sources provides unstable and incomplete

circulation to the ischemic region of the brain.

56 When blood flow is sustained in the

range of 10 to 18 mL/100 g/minute, irreversible cellular damage may occur. Blood

flow must be restored quickly after the event. Experimental studies in dogs and cats

have shown that when blood flow is restored within 2 to 3 hours, neurologic deficits

are prevented.

57

,

58 Thrombolytic agents can reestablish blood flow to ischemic

regions of the brain. The most important factor in successful thrombolytic therapy is

early treatment. The selection of appropriate candidates for thrombolysis is

extremely important and requires the correct neurologic evaluation by a specialized

team. Before the initiation of thrombolytics, patients with high blood pressure should

have their blood pressure lowered carefully to systolic BP <185 and diastolic BP

<110 mm Hg (see Table 61-5 and the discussion later on blood pressure).

Randomized, controlled-trials have shown that intravenous tissue plasminogen

activator (tPA), alteplase, to be beneficial for select patients with acute ischemic

stroke who start treatment within 4.5 hours. For eligible patients (Table 61-6), once a

CT ruled out a hemorrhage, intravenous tPA should be started within 4.5 hours of

clearly defined symptoms. There are specific criteria to select patients for alteplase

eligibility if they present within 3 hours of onset of symptoms versus if they present

up to 4.5 hours of symptoms (see Table 61-6).

Several thrombolytics (streptokinase, alteplase, tenectaplase, reteplase, urokinase)

are available. However, only alteplase trials have shown benefits and improved

outcomes.

59–62

In three studies, streptokinase was used as the thrombolytic, and all of these

studies were terminated early owing to high rates of mortality and intracranial

hemorrhage associated with streptokinase.

59

,

60

,

63 The rates of intracranial hemorrhage

ranged from 6% to 17% for patients receiving streptokinase compared with 0.6% to

3% for patients receiving placebo.

p. 1308

p. 1309

Figure 61-3 Treatment algorithm for management of patient with acute stroke-like symptoms. CT, computed

tomography; MRI, magnetic resonance imaging; NIH, National Institutes of Health; t-PA, alteplase. (Source:

Adams HP et al. Antifibrinolytic therapy in patients with aneurysmalsubarachnoid hemorrhage: a report of the

cooperative aneurysmalstudy. Arch Neurol. 1981;38:25.)

The National Institute of Neurological Disorders and Stroke (NINDS) alteplase

trial

61 and the European Cooperative Acute Stroke Study (ECASS I)

62 used different

doses, inclusion criteria, and treatment protocols. Both trials showed the benefit of

alteplase in at least some outcome parameters. In the NINDS alteplase study, patients

were enrolled within 3 hours of symptom onset using strict inclusion and exclusion

criteria. When enrolled, patients received either alteplase 0.9 mg/kg (maximal dose,

90 mg), with 10% of the dose given as a bolus for 1 minute and the remainder infused

for 60 minutes, or placebo. In this study, there were no differences at 24 hours in

responses between the placebo group and those who received alteplase. However, at

3 months, patients who received alteplase were 30% more likely to have minimal or

no disability. There was an 11% to 13% absolute increase in the number of patients

with excellent outcomes and a corresponding decrease in the number of patients with

severe neurologic impairment or death at 3 months. Intracranial hemorrhage occurred

more frequently among patients receiving alteplase (6.4%) than in patients receiving

placebo (0.6%). Despite the increased incidence of intracranial hemorrhage,

outcomes remained better for patients receiving alteplase. For the ECASS I trial,

patients were enrolled within 6 hours of the onset of symptoms.

62 The treatment

protocol consisted of intravenous alteplase 1.1 mg/kg (maximal, 100 mg) or placebo.

There was no difference in the primary outcome measures of functionality at 3

months. However, with target population analysis, there was a significant difference

favoring alteplase. Of alteplase-treated patients, 41% had minimal or no disability

compared with 29% of placebo-treated patients. A variety of secondary outcome

measures favored alteplase. There was no difference in 30-day mortality rates, but

19.8% of alteplase-treated patients had major parenchymal hemorrhages compared

with 6.5% of placebo-treated patients.

p. 1309

p. 1310

Table 61-5

Management Guideline for Blood Pressure Treatment in Acute Ischemic Stroke

Treatment Received Alteplase Did Not Receive Alteplase

No treatment recommended If BP is <185/110 mm Hg If BP <220/120 mm Hg unless

there is another specific medical

condition

Nicardipine 5 mg/hour, titrate up by

2.5 mg/hour every 5–15 minutes

(maximum 15 mg/hour)

Labetalol 10–20 mg IV over 1–2

minutes, may repeat to maximum of

300 mg total, or Labetalol 10 mg IV

followed by continuous infusion 2–8

mg/minute

If BP >185/110 mm Hg

Goal is to lower below 185/105 mm

Hg to limit risk of ICH

If systolic BP >220 mm Hg or

diastolic 120–140 mm Hg

IV sodium nitroprusside 0.5

mcg/kg/minute

If BP not controlled by above or if

diastolic BP is >140 mm Hg

If not controlled or if diastolic BP

>140 mm Hg

Source: Jauch EC et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline

for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013;

44:870–947.

Table 61-6

Criteria for Alteplase Use in Treatment of Acute Stroke

Inclusion Criteria Exclusion Criteria

18 years of age or older

Clinical diagnosis of stroke with clinically meaningful

neurologic deficit

Clearly defined onset within 180 minutes before

treatment

Baseline CT with no evidence of intracranial

hemorrhage

CT signs of intracranial hemorrhage, or multilobar

infarction, or symptoms of subarachnoid hemorrhage

Active internal bleeding

History of intracranial hemorrhage

Stroke or serious head injury within 3 months

Current use of direct thrombin inhibitors or direct factor

Xa inhibitors with elevated sensitive laboratory test

Systolic BP >185 mm Hg, diastolic BP >110 mm Hg

Current use of anticoagulant with INR >1.7

Current use if direct thrombin inhibitors with elevated

sensitive laboratory tests (such as aPTT, INR, ECT,

TT, and factor Xa activity assay)

Heparin received in last 48 hours resulting in abnormal

elevated aPTT

Glucose <50 or 400 mg/dL

Symptoms of subarachnoid hemorrhage

Platelet count <100,000/mm

3

Relative exclusion criteria

Only minor or rapidly improving stroke symptoms

Pregnancy

Seizure at onset with postictal residual neurologic

impairments

Major surgery or serious trauma within 2 weeks

GI or urinary tract hemorrhage within 3 weeks

Additional Relative Exclusion Criteria for

Alteplase Use 3–4.5 hours after Onset of

Symptoms

Age >80 years

NIHSS score >25

Taking an oral anticoagulant regardless of INR

History of both diabetes and prior ischemic stroke

BP, blood pressure; CT, computed tomography; GI, gastrointestinal; NIHSS, National Institutes of Health Stroke

Scale; ECT, ecarin clotting time; aPTT activated partial thromboplastin time; TT, thrombin time.

Since NINDS and ECASS-I, three subsequent trials, the ECASS-II and Alteplase

Thrombolysis for Acute Non-Interventional Therapy in Ischemic stroke (ATLANTIS

A and B) found largely same effects as NINDS when therapy was initiated in the

p. 1310

p. 1311

≤3-hour time period. The ECASS-II study used an alteplase dose of 0.9 mg/kg and

replicated the NINDS trial

64

; however, patients were enrolled up to 6 hours after the

onset of stroke symptoms. This study found no difference between alteplase and

placebo. Too few patients were enrolled with stroke symptoms within 3 hours to

reliably evaluate the influence of this variable on outcome.

Since NINDS, several trials have also investigated the use of intravenous alteplase

up to 6 hours after stroke onset. ECASS-I, ECASS-II, ATLANTIS A and B, all

enrolled patients with extended window use of alteplase. None of these trials found

individually a benefit; however, a pooled analysis suggested improved outcomes.

65

Hence, the ECASS-III study was conducted to evaluate the efficacy and safety of

alteplase administered used the NINDS alteplase dose (0.9mg/kg maximum of 90mg),

but it focused on the efficacy and safety of alteplase administered 3 to 4.5 hours after

the onset of symptoms.

66 A significantly greater number of patients receiving

alteplase had favorable outcomes on the mRS global disability scale compared with

placebo (odds ratio, 1.34; 95% confidence interval, 1.02–1.76). Although the rate of

intracranial hemorrhage was greater with alteplase, mortality and reports of adverse

events were similar between the two groups. When considering the use of alteplase

in the 3- to 4.5-hour window, the ECASS-III criteria should be followed (Table 61-

6). A second large randomized placebo-controlled trial was recently published. In

this third International Stroke Trial (IST-3), following NINDS dosing scheme for

alteplase, patients enrolled with 6 hours of symptoms onset, there was a significant

improvement in functional outcome in the Oxford Handicap score (0 to 2, alive and

independent) (OR 1.27; 95% confidence interval 1.10–1.47). There were more

deaths at 7 days in the alteplase group though. ITS-3 included patients >80 years of

age in comparison to ECASS-III and a broader blood pressure eligibility.

67 Because

P.C. presented to the ED within 3 hours of the onset of his stroke symptoms, he is a

candidate for alteplase therapy in accordance with the NINDS study protocol making

sure the patient has no exclusion criteria based on Table 61-6.

CASE 61-2, QUESTION 4: What general treatment interventions should be made for P.C.?

In addition to the general supportive therapy needed for a hospitalized patient,

several issues are important to the proper management of a stroke patient.

Assessing vital signs and ensuring stabilization of airway, breathing and

circulation is the initial part of the evaluation. Intubation and mechanical ventilation

may be required to ensure adequate ventilation and to protect the airways from

aspiration. Careful attention should be given to fluid and electrolyte control.

Excessive hydration or inadequate sodium supplementation may result in

hyponatremia, potentially causing cerebral edema. This can result in compression

and displacement of brain tissue which can disrupt cerebral perfusion. In addition,

hyponatremia can produce seizures, which increases the metabolic demand on

compromised neurons. Thus, 0.9% saline or lactated Ringer’s are the preferred fluids

in patients at risk for cerebral edema.

53

Attention to body temperature needs to be given. Studies have shown that even

small increases in temperature are associated with worse outcomes after acute

stroke.

68

,

69 Hypothermia is neuroprotective, and a reduction in body temperature of

0.26°F can be beneficial in stroke patients.

53

,

70 Use of antipyretics, such as

acetaminophen, are advised to maintain normal or slightly subnormal body

temperatures.

Another metabolic parameter that must be followed carefully is the serum glucose

concentration, because hyperglycemia may adversely affect ischemic infarction

outcomes. A review of multiple studies on the effects of hyperglycemia in acute

stroke concluded that hyperglycemia results in poor outcomes and increased

mortality.

71

If hyperglycemia is detected, appropriate insulin therapy should be

initiated to keep the serum glucose concentration less than 140 mg/dL without causing

hypoglycemia.

53

Caution should be exercised in the acute management of P.C.’s blood pressure.

Decreasing the blood pressure too rapidly will compromise cerebral blood flow and

expand the region of ischemia and infarction, whereas hypertension may place him at

a greater risk for cerebral hemorrhage, especially if a thrombolytic agent is used.

However, a study comparing treated and untreated patients who were hypertensive in

association with an acute stroke failed to demonstrate any difference in outcomes

between the groups.

72

For patients with a systolic blood pressure greater than 185 mm Hg or diastolic

blood pressure greater than 110 mm Hg, who are otherwise candidates for

intravenous fibrinolytic treatment, labetalol, nitroglycerin paste, or intravenous

nicardipine should be used to reduce the blood pressure to these goals before starting

alteplase.

53 A reasonable goal is to lower blood pressure by 15% during the first 24-

hours after onset of stroke. After administration of alteplase, a systolic blood

pressure should be kept less than 180/105 mm Hg to limit the risk of intracranial

hemorrhage. Specific blood pressure management recommendations are outlined for

the management of acute ischemic stroke patients (Table 61-5). In other patients, the

only consensus on blood pressure control is that treatment is required when pressures

exceed 220/120 mm Hg. If there is a clinical deterioration of neurologic function

associated with the reduction of blood pressure, the infusion rate of the

antihypertensive agent should be slowed or the drug discontinued. After the first 24

hours of stroke onset, maintenance antihypertensive therapy can then be initiated

using an oral agent, such as a thiazide diuretics, calcium-channel antagonist or ACEI

or ARB. The reader is referred to more detailed discussion of hypertension

management in Chapter 9.

The general daily needs of the patient should be assessed and provided on an asneeded basis. These include nutrition, urination, defecation, delirium, and prevention

of deep venous thrombosis, and decubitus ulcers. Neurologic deficits will

compromise the ability of many patients to adequately meet these needs, increasing

the necessity for medical assistance.

CASE 61-2, QUESTION 5: Should anticoagulation or antiplatelet agents be used acutely in P.C.?

Several studies have evaluated the use of anticoagulants in the treatment of acute

strokes. However, most of these studies are poorly designed or underpowered to

determine the efficacy of these agents.

HEPARIN AND HEPARINOIDS

Three studies have evaluated the use of heparin in acute stroke.

73–75

In one doubleblind study, heparin doses were adjusted to maintain the partial thromboplastin time

(aPTT) at 1.5 to 2 times control and continued for 7 days.

73 There were no significant

differences in death at 7 days, no differences in functional ability 1 year after the

stroke, and a greater mortality rate at 1 year for heparin-treated patients. Another

study compared aspirin, subcutaneous heparin (5,000 international units or 12,500

international units BID), both, and neither treatments for patients with acute ischemic

stroke.

74 There was no reduction of mortality or morbidity for patients receiving

either dose of heparin. Heparin use has also been studied in progressing stroke

(stroke with evolving neurologic symptoms), and no benefit was demonstrated with

its use.