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  Etiology

  
  
  
  
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    Cardioembolic and other nonarteriosclerotic causes of cerebral infarction occur more commonly in patients admitted to the ICU and should be carefully sought by appropriate diagnostic tests.

    
    
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    In hypertensive patients with hemispheric lobar hemorrhages and in patients without hypertension, causes for intracerebral hemorrhage such as coagulopathies, arteriovenous malformations, or saccular aneurysms should be sought.

    
    
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    Nontraumatic spontaneous subarachnoid hemorrhage is almost always due to a ruptured saccular aneurysm and should be evaluated by arteriography.

  
  
  
  
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  Clinical and Laboratory Diagnosis

  
  
  
  
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    X-ray computed tomography (CT) is the diagnostic neuroimaging test of choice for patients with acute stoke. It is rapid, can be performed easily on acutely ill patients and acute intracerebral or subarachnoid hemorrhage are easily identified.

    
    
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    Lumbar puncture is the most sensitive test for detection of SAH; it should be performed when there is a strong clinical suspicion and a negative CT scan, or when CT is not available or feasible.

    
    
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    In suspected ischemic stroke, diffusion-weighted MRI can be helpful for improving diagnostic certainty when there is no clear history of an abrupt onset or the localization of the neurological findings is confusing. MRI has not been shown to be of value in selecting patients for thrombolytic therapy.

    
    
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    Early electrocardiographic (ECG) monitoring detects previously unsuspected atrial fibrillation in 3% to 5% of patients with acute cerebral ischemia.

    
    
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    Patients with transient ischemic attacks (TIAs) or mild stroke who are good surgical candidates for carotid endarterectomy should be evaluated for symptomatic carotid stenosis immediately since the risk of stroke can be as high as 1 in 20 within the first 2 days.

  
  
  
  
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  Treatment of Cerebral Infarction

  
  

  The following statements can be made based on good clinical trial data.

  
  
  
  
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    Routine use of supplemental oxygen does not reduce mortality.

    
    
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    Early treatment of hyperglycemia to achieve levels <7 mmol/L does not improve outcome.

    
    
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    In patients with systolic blood pressures of 160 to 200 mm Hg, pharmacological reduction of systolic pressure by 20 to 25 mm Hg within the first 24 hours is safe, but does not improve outcome.

    
    
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    In hemiplegic patients, subcutaneous low-dose heparin or enoxaparin reduces deep venous thrombosis.

    
    
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    Intravenously administered t-PA improves outcome in carefully selected patients with acute ischemic stroke when instituted within 4.5 hours of onset.

    
    
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    The clinical value of any intra-arterial pharmacological or mechanical revascularization therapy for acute ischemic stroke has not been demonstrated.

    
    
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    Aspirin 160 or 300 mg/d of aspirin begun within 48 hours of the onset of ischemic stroke results in a net decrease in further stroke or death.

    
    
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    Full anticoagulation with heparin or similar drugs in patients with acute ischemic stroke provides no clinical benefit in general or in any subgroup, including those with atrial fibrillation or other cardioembolic sources.

    
    
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    Hemicraniectomy reduces mortality in patients with large hemispheric infarcts and depressed level of consciousness who are operated within 48 hours of stroke onset.

  
  
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  Treatment of Intracerebral Hemorrhage

  
  

  The following statements can be made based on good clinical trial data

  
  
  
  
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    Prophylaxis for deep venous thrombosis with low-dose subcutaneous heparin or heparinoids may be instituted safely on the second day after the hemorrhage and reduces subsequent deep venous thrombosis if begun before day 4.

    
    
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    In patients with systolic blood pressure of 150 to 220 mm Hg, rapid pharmacological reduction of systolic pressure by 27 mm Hg within the first hour is safe but does not improve outcome.

    
    
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    Craniotomy and clot evacuation in patients with supratentorial ICH, either superficial or deep, is of no benefit.

  
  
  
  
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  Treatment of Subarachnoid Hemorrhage

  
  

  The following statements can be made based on good clinical trial data

  
  
  
  
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    Oral nimodipine at a dose 60 mg every 4 hours for 21 days after hemorrhage reduces poor outcome.

    
    
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    Early definitive treatment reduces the risk of rebleeding.

    
    
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    For aneurysms amenable to both endovascular coiling and surgical clipping, endovascular treatment is beneficial.

    
    
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    Intravascular volume contraction should be avoided.

  
  

Cerebrovascular diseases can be divided into three categories: cerebral ischemia and infarction, intracerebral hemorrhage, and subarachnoid hemorrhage. Cerebral ischemia and infarction are caused by processes that reduce cerebral blood flow. Reductions in whole brain blood flow due to systemic hypotension or increased intracranial pressure (ICP) may produce infarction in the distal territories or border zones of the major cerebral arteries. More prolonged global reductions cause diffuse hemispheric damage without localizing findings or, at its most severe, produce brain death. Prolonged regional reductions can lead to focal brain infarctions. Local arterial vascular disease accounts for approximately 65% to 70% of all focal brain infarctions. In most cases, arterial disease serves as a nidus for local thrombus formation with or without subsequent distal embolization. Focal arterial stenosis in combination with systemic hypotension is a very rare cause of focal brain infarction. Atherosclerosis is the most common cause of local disease in the large arteries supplying the brain. Disease of smaller penetrating arteries may cause small deep (lacunar) infarcts. While emboli arising from the heart cause approximately 30% of all cerebral infarcts in a general population, they assume more importance in ICU patients.¹ Atrial fibrillation is the most common of these causes. Atherosclerotic emboli following heart surgery, infective endocarditis, nonbacterial thrombotic endocarditis, and ventricular mural thrombus secondary to acute myocardial infarction or cardiomyopathy should all be considered in the appropriate circumstances. More rare causes of cerebral infarction must also be considered in the ICU. These include dissections of the carotid or vertebral artery (after direct neck trauma, “whiplash” injuries or forced hyperextension during endotracheal intubation), intracranial arterial or venous thrombosis secondary to meningeal or parameningeal infections, and paradoxical embolization from venous thrombosis via a patent foramen ovale.¹

Hemorrhage into the basal ganglia, thalamus, and cerebellum in middle-aged patients with long-standing hypertension is the most common type of intracerebral hemorrhage. In hypertensive patients with hemispheric lobar hemorrhages and patients without hypertension, other causes should be sought, such as arteriovenous malformations or saccular aneurysms.² Amyloid angiopathy becomes increasingly important in patients in the seventh, eighth, and ninth decades. These hemorrhages usually occur in the subcortical hemispheric white matter and may be multiple. Previous microhemorrhages in parietal and occipital lobes are often visible on magnetic resonance images. Hemorrhage due to anticoagulant and thrombolytic drugs may affect any part of the brain. Rarer causes of intracerebral hemorrhage occurring in patients with other systemic diseases include thrombocytopenia, hemophilia, and disseminated intravascular coagulation. Primary or metastatic brain tumors will rarely present as ICH.

Nontraumatic spontaneous subarachnoid hemorrhage (SAH) is almost always due to a ruptured saccular aneurysm. Aneurysms may also rupture into the brain parenchyma, producing intracerebral hemorrhage as well. Saccular aneurysms are most commonly located on the large arteries at the base of the brain. Both congenital and acquired factors appear to play a role in the postnatal development of aneurysms. Acquired factors include atherosclerosis, hypertension, and hemodynamic stress. In patients with infective endocarditis, mycotic aneurysms of more distal arteries may form and sometimes rupture. Other causes of SAH include ruptured arteriovenous malformations (cerebral and spinal) and fistulae, cocaine abuse, pituitary apoplexy, and intracranial arterial dissection.³ In some cases, particularly SAH ventral to the midbrain or restricted to cortical sulci, the cause cannot be determined.

The initial diagnostic evaluation of the patient with suspected stroke serves (1) to determine whether neurologic symptoms are due to cerebrovascular disease or to some other condition, such as peripheral nerve injury, intracranial infection, tumor, subdural hematoma, multiple sclerosis, epilepsy, or hypoglycemia; and (2) to distinguish among different types of cerebrovascular disease that require different treatments. The clinical history and examination remains the cornerstone of this process. Cerebrovascular disease typically produces focal brain dysfunction of sudden onset in a single location. The primary exception to this is aneurysmal SAH, which usually presents as a sudden onset of severe headache, with or without nausea, vomiting, or loss of consciousness. In some cases, a less severe aneurysmal hemorrhage may present as a headache of moderate intensity, neck pain, and nonspecific symptoms. A high index of suspicion is needed in order to avoid missing the diagnosis of SAH. Focal brain dysfunction may not always cause an obvious hemiparesis. Neurologic deficits such as neglect, agnosia, aphasia, visual field defects, or amnesia may be the only manifestations of brain infarction or hemorrhage. Multiple small brain infarcts may produce impaired consciousness with minimal or no focal neurologic deficits, mimicking metabolic, or toxic encephalopathy. The clinical distinction between cerebral infarction and intracerebral hemorrhage is unreliable as both produce sudden focal deficits. Large hemorrhages may produce vomiting or unconsciousness, but so may infarcts in the vertebrobasilar circulation. The initial neurologic examination provides a baseline for monitoring the subsequent clinical course. A thorough medical evaluation is necessary to detect systemic diseases that may be the cause of the cerebrovascular problem. Careful evaluation of the heart is imperative to detect conditions that might predispose to embolization, particularly atrial fibrillation, recent myocardial infarction, and more rarely, infective endocarditis.

X-ray computed tomography (CT) is the diagnostic neuroimaging test of choice for patients with acute stoke. It is rapid and can be performed easily on acutely ill patients. Acute intracerebral hemorrhage is easily identified by noncontrast CT. Cerebral infarction may not be demonstrated by CT for several days. If the infarct is small enough, it may never be apparent. Magnetic resonance diffusion weighted imaging is more sensitive than CT for lesion detection in the early period following ischemic infarction. Due to its higher resolution, magnetic resonance imaging (MRI) is also superior for detecting small infarcts (especially those in the posterior fossa) at any time. However, MRI is more cumbersome to perform in acutely ill patients because of longer imaging times, the need for special nonferromagnetic life support equipment, and the necessity of putting the entire body in the scanner. Demonstration of cerebral infarction by neuroimaging is rarely necessary, since the diagnosis often can be made reliably by the clinical presentation of the sudden onset of a focal brain deficit together with a negative CT scan to exclude hemorrhage and other conditions. MRI can be helpful for improving diagnostic certainty when there is no clear history of an abrupt onset or the localization of the neurological findings is confusing. Intravenous contrast administration increases the sensitivity for detecting diseases that may mimic stroke, such as tumor, chronic subdural hematoma, and abscess.

Diagnosis of border zone infarction due to systemic arterial hypotension is almost entirely dependent on the pattern of infarction shown by CT or MRI. Border zone infarctions are often asymmetrical and patchy; rarely is the entire border zone territory between the middle cerebral artery and posterior or anterior cerebral artery involved. Furthermore, the actual location of the border zone varies from person to person.⁴ When more than one area of acute infarction has occurred and all infarcted areas are within the border zones, systemic hypotension should be considered as a cause of infarction.

MRI has no advantage over CT in the demonstration of acute intracerebral hemorrhage, but it does have superior sensitivity for detecting subacute or chronic hemorrhage. MRI with contrast is the most sensitive way to detect a tumor underlying an ICH. Noncontrast CT has a sensitivity of >90% for detecting SAH when performed within 24 hours of hemorrhage. There is no role for standard MRI in the initial diagnosis of acute SAH since it is difficult to perform in an acutely ill agitated patient and it does not increase the likelihood of detecting SAH.

In the patient who is awake and alert with acute focal brain dysfunction and in whom noncerebrovascular causes can be excluded, the immediate distinction between cerebral infarction and cerebral hemorrhage may not be necessary if no emergent treatment of the stroke is planned. In certain situations, however, differentiation between infarction and hemorrhage may be critical. Patients with ischemic stroke whose time of onset can be determined to be less than 4.5 hours earlier and whose other medical problems do not preclude thrombolytic therapy, will benefit from treatment with intravenous tissue plasminogen activator (t-PA).^5,6 In this circumstance, emergency CT to exclude cerebral hemorrhage is imperative (see the section on treatment below). In the patient with decreased consciousness and a focal neurologic deficit, emergency CT may be critically important in identifying an intracranial tumor or subdural hematoma that requires emergency neurosurgical intervention.

Except in patients with cerebral venous thrombosis, hematologic evaluation of patients with ischemic stroke is rarely of value. Antiphospholipid antibodies are found in a high percentage of patients with arterial stroke, but they confer neither a worse prognosis nor is there a benefit of long-term anticoagulation.⁷ Acquired or hereditary hypercoagulable disorders have not been clearly linked to arterial ischemic stroke, whereas they are clearly of etiologic importance in cerebral venous thrombosis. In patients with intracranial hemorrhage, especially in the ICU, acquired hemorrhagic diatheses (eg, anticoagulant or thrombolytic drugs, thrombocytopenia) should always be considered and should be sought by appropriate laboratory testing when clinical suspicion indicates.

Lumbar puncture with cerebrospinal fluid (CSF) examination can be an extremely important test in the evaluation of the patient with apparent stroke, especially in patients with acquired immune deficiency syndrome (AIDS) or when there is infection elsewhere. Meningitis may cause stroke by producing thrombosis of arteries or cortical veins. CSF pleocytosis is common following septic embolism from infective endocarditis and can serve as a valuable clue to its presence. Lumbar puncture is the most sensitive test for detection of SAH; it should be performed when there is a strong clinical suspicion and a negative CT scan, or when CT is not available or feasible. CSF xanthochromia, which begins to develop after 4 hours and is reliably present at 12 to 24 hours, can help differentiate SAH from traumatic lumbar puncture.^8,9

Early electrocardiographic (ECG) monitoring detects previously unsuspected atrial fibrillation in 3% to 5% of patients with acute cerebral ischemia.^10-12 This information is clinically useful since the superiority of oral anticoagulation over aspirin for long-term secondary stroke prevention in this circumstance has been demonstrated.¹³ There is, however, no benefit for immediate anticoagulation in these patients.¹⁴ Transthoracic echocardiography can provide evidence of poor left ventricular function and, rarely, left ventricular thrombi. In patients without clinical cardiac disease (no previous history or signs or symptoms of cardiac disease, no ECG abnormalities, and normal cardiac silhouette on chest x-ray), left ventricular thrombi are vanishingly rare. Transesophageal echocardiography has made it possible to identify left atrial thrombi and atherosclerosis of the ascending aorta. Large aortic arch lesions are associated with an increased risk of stroke. The most common lesion detected by echocardiography in patients with stroke who have no other evidence of heart disease is patent foramen ovale with or without atrial septal aneurysm. Treatment implications are problematic (see below). ECG abnormalities are extremely common in patients with SAH. However, the clinical relevance of these abnormalities is questionable since they often do not correlate with echocardiographic abnormalities, histopathologic abnormalities, or serum markers of cardiac injury. Approximately 20% of patients with SAH have elevated serum troponin-I levels. Patients with elevated troponin-I levels should undergo echocardiography, as elevated troponin-I levels have been shown to be 100% sensitive and 86% specific for the detection of left ventricular dysfunction by echocardiography.¹⁵

Cerebral arteriography provides high-resolution images of both extracranial and intracranial vessels, which may be useful occasionally in the identification of causes of cerebral infarction such as arterial dissection. It is of little value for the diagnosis of isolated cerebral vasculitis due to the high prevalence of both false-positive and false-negative findings.¹⁶ Magnetic resonance arteriography (MRA), often overestimates the degree of stenosis, sometimes even portraying normal vessels as abnormal. In addition, MRA lacks the high resolution of conventional arteriography and cannot be used to exclude small aneurysms or abnormalities in distal arterial branches. In contrast, magnetic resonance venography has supplanted conventional catheter angiography for the detection of sagittal and lateral sinus venous thrombosis. In hypertensive patients with lobar intracerebral hemorrhage and in nonhypertensive patients with intracerebral hemorrhage in any location, arteriography may demonstrate vascular malformations or aneurysms.² CT angiography is almost as sensitive as arteriography for detecting causes of intracerebral hemorrhage but will occasionally miss a small arteriovenous malformation or fistula.^17-19 Cerebral arteriography plays an important role in the evaluation of the patient with SAH by confirming the existence of an aneurysm and providing the necessary information to plan a surgical approach. If CT or lumbar puncture demonstrates SAH, a four-vessel angiogram should be performed as soon as possible. A complete study is necessary to look for multiple aneurysms. If arteriography does not reveal a cause for SAH, it should be repeated in 1 to 2 weeks.

Doppler ultrasound of the carotid arteries is useful to screen for severe carotid stenosis at the cervical bifurcation in patients who are candidates for carotid endarterectomy. It is important to remember that the reliability of this technique varies from center to center. Patients with transient ischemic attacks (TIAs) or mild stroke who are good surgical candidates should be evaluated immediately since the risk of stroke following TIA can be as high as 1 in 20 within the first 2 days.²⁰ On the other hand, in patients with a completed stroke, there is usually no urgency in obtaining this information since carotid endarterectomy does not play a role in the management of acute stroke. Transcranial Doppler (TCD) studies can detect stenosis of intracranial vessels, but the value of this information in management decisions remains to be demonstrated.²¹ TCD can also detect increases in flow velocity in most patients with arteriographic vasospasm following SAH (see below).

The value of regional cerebral blood flow (CBF) measurements with positron emission tomography (PET), single photon emission computed tomography (SPECT), CT, or MRI in the diagnosis and treatment of patients with cerebrovascular disease remains to be demonstrated. Since the diagnosis of cerebral infarction can be made reliably by means of the clinical picture and a CT scan, it is rarely if ever necessary to demonstrate a defect on a CBF study. Furthermore, other conditions also may produce focal regional reductions of CBF. CBF measurement as an adjunct in deciding the appropriate therapeutic intervention in patients with stroke has not been shown to result in improved outcome. The combination of diffusion weighted imaging (DWI) and perfusion weighted imaging (PWI) in patients with acute ischemic stroke often reveals a central area of restricted diffusion surrounded by a larger area of low perfusion. The diffusion abnormality increases with time and its final boundaries correspond closely to the eventual infarct. These observations have led to the hypothesis that the area of perfusion-diffusion mismatch indicates tissue destined for infarction that may be salvaged by thrombolytic therapy. As of 2012, several clinical trials all have failed to demonstrate that treatment that decisions based on DWI-PWI magnetic resonance scans lead to better patient outcome.²²

CEREBRAL INFARCTION

Immediate supportive care of the patient with cerebral infarction requires attention to the patient’s airway, breathing, and circulation. Although most patients have preserved pharyngeal reflexes, those with brain stem infarction or depressed consciousness may require intubation for airway protection. Coexisting heart and lung disease are common. Respiratory and cardiac function should be assessed fully, and appropriate interventions performed to maintain perfusion and oxygenation. The use of supplemental inspired oxygen is rational only if the arterial oxygen content of the blood is decreased; routine use does not reduce mortality.²³ At the time of hospital admission, some patients may have mild intravascular volume depletion. In addition to normal maintenance requirements, careful fluid supplementation may be required. The composition of intravenous fluid (normal saline solution, one-half normal saline solution, or 5% glucose) makes no difference as long as serum electrolyte concentrations remain normal. Care should be taken to avoid hypo-osmolarity, which potentially could exacerbate brain edema. Early treatment of hyperglycemia to achieve levels <7 mmol/L does not improve outcome.²⁴ Systemic arterial hypertension is common following acute ischemic stroke. In most cases, blood pressure returns to baseline levels without treatment in a few days. There are no known hazards to the brain from this spontaneous transient elevation in systemic blood pressure. The value of treatment, if any, is unknown. Case reports describe sudden neurological deterioration when blood pressure is pharmacologically reduced.²⁵ In patients with systolic blood pressures of 160 to 200, a randomized trial has demonstrated that pharmacological reduction of systolic pressure by 20 to 25 mm Hg within the first 24 hours is safe as it did not cause more early neurological deterioration when compared to the natural decrease of 10 to 15 mm Hg, but neither did it improve death or dependency at 2 weeks.²⁶ There are insufficient data to permit designation of any target blood pressure levels as effective.^27,28 Continuing or stopping preexisting antihypertensive therapy for 2 weeks after acute ischemic stroke does not affect outcome.²⁹ When systemic hypertension causes organ damage elsewhere (eg, myocardial ischemia, congestive heart failure, or dissecting aortic aneurysm), careful and judicious lowering of the blood pressure with constant monitoring of neurologic status is indicated.

No clinical evidence or pathophysiologic rationale supports routine restriction to bedrest for patients with acute brain infarction. Prolonged immobility carries an increased risk of iliofemoral venous thrombosis, pulmonary embolism, and pneumonia. Patients should be out of bed and walking as soon as possible after a stroke. Occasionally, orthostatic hypotension with worsening of neurologic deficits will occur. In these cases, a more gradual program of ambulation should be instituted. In hemiplegic patients, subcutaneous low-dose heparin or enoxaparin should be administered to prevent iliofemoral venous thrombosis.³⁰ Alternating pressure antithrombotic stockings may provide benefit as well. In the case of pulmonary embolism or deep venous thrombosis, full anticoagulation with heparin or heparin-like drugs may be instituted. Fever may occur due to infection or other systemic causes. Central fevers due to hypothalamic disease are an exceedingly uncommon event and the search for other causes should be vigorously pursued. Animal studies have shown that even minor elevations in temperature of a few degrees poststroke can lead to worse brain damage. Maintaining normothermia through the use of antipyretics and cooling blankets makes good sense but is of unproven value. Trials of induced hypothermia with both external and internal cooling are now underway. It is important to remember that dysphagia occurs commonly, even with unilateral hemispheric lesions. Before oral feeding is instituted, each patient’s ability to swallow should be carefully checked. Institutions with formal dysphagia screening protocols have a reduced incidence of pneumonia.³¹ Incontinence is also common following acute stroke but the use of Foley catheters should be kept to a minimum because of the attendant increase in urinary tract infections. Careful attention must be given to the prevention of decubitus ulcers in bedridden patients.

Intravenously administered t-PA improves outcome in carefully selected patients with acute ischemic stroke when instituted within 4.5 hours of onset.^5,6 These findings were demonstrated in two separate studies: the NINDS Trial comprising patients within 0 to 3 hours of onset and the ECASS III Trial comprising patients within 3 to 4.5 hours of onset. Inclusion and exclusion criteria used in these trials were different and are listed in Tables 84-1 and 84-2. In both trials, patients received 0.9 mg/kg (90 mg maximum) of alteplase, 10% given as an initial bolus over 1 minute, followed by a continuous intravenous infusion of the remainder over 60 minutes. The infusion was discontinued if intracranial hemorrhage was suspected. In the NINDS 0- to 3-hour trial, all patients were admitted to a neurology special care area or ICU. Anticoagulant or antiplatelet drugs were not allowed for 24 hours. Nasogastric tubes and Foley catheters were avoided for 24 hours if possible. Blood pressure was monitored every 15 minutes for 2 hours, every 30 minutes for 6 hours, and then every 60 minutes for 16 hours. Blood pressure was kept below 180/105 mm Hg with labetalol or sodium nitroprusside. Symptomatic cerebral hemorrhage occurred more commonly in the group treated with t-PA (6%) than in the control group (<1%). Recommended treatment of symptomatic intracerebral hemorrhage included cryoprecipitate and platelet transfusion.³² In spite of this treatment, mortality at 3 months from ICH after t-PA was 75% in the NINDS trial.³³ Even taking into account the increased risk of intracerebral hemorrhage, there was no difference in mortality, and more t-PA-treated patients demonstrated an excellent neurologic outcome at 3 months by each of four separate outcome scales. The odds ratio for a favorable outcome due to treatment was 1.7. In the ECASS III 3- to 4.5-hour trial, anticoagulant or antiplatelet drugs were also not allowed for 24 hours with the exception that subcutaneous heparin (≤10,000 IU) or equivalent doses of low-molecular weight heparin was permitted for prophylaxis against deep-vein thrombosis. The odds ratio for a favorable outcome due to treatment was 1.3. Supporting evidence for these two pivotal trials is provided by retrospective analyses of small subgroups of patients enrolled <4.5 hours postevent in other trials.^34,35

Even though efficacy of IV t-PA has been demonstrated out to 4.5 hours, eligible patients should be treated as soon as possible since the benefit is time-dependent.³⁶

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