Stroke

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1117 times

Chapter 62 Stroke

Corey R. Fehnel, MD , Ala Nozari, MD, PhD , Lee H. Schwamm, MD, FAHA

1 What is the definition of stroke?

Stroke is a sudden, focal neurologic syndrome due to cerebrovascular ischemia. Strokes are sudden, or apoplectic, by definition. A slow progression of neurologic symptoms should make the clinician consider alternative diagnoses. Strokes occur in two broad categories:

image Ischemic stroke due to arterial occlusion

image Hemorrhagic stroke due to vessel rupture

2 Name two common conditions that mimic stroke symptoms

Seizure and complicated migraine. Although at times difficult to distinguish, the clinician can often differentiate between these conditions on the basis of the temporal nature of symptom onset. Strokes generally produce a deficit that is sudden and maximal at onset. Seizures progress rapidly over a few seconds and may be associated with stereotyped motor movements and often impairment or loss of consciousness. Migraines can produce stereotypical visual, sensory, motor, or language symptoms in a predictable fashion because of the presumed mechanism of “cortical spreading depression” occurring over minutes. Spreading depression is an extracellular wave of neuronal depolarization thought to be related to rising levels of potassium concentration in the extracellular space that produces migratory symptoms as it spreads across the surface of the cortex.

3 What are the most important aspects of evaluating an acute ischemic stroke?

The last time the patient was known to be at his or her baseline is key to all acute stroke interventions. The earlier a thrombolytic can be given, the greater the chance for saving neurons and reversing disability. Three- and 4.5-hour windows for intravenous (IV) thrombolysis relate primarily to the risk of hemorrhage, whereas patients receiving thrombolytic treatment within 90 minutes of symptom onset have the greatest benefit. Time is brain.

4 Who should be administered IV recombinant tissue plasminogen activator (IVtPA)?

All patients seen within 3 hours of onset of acute neurologic deficit thought to result in significant disability (generally a National Institutes of Health Stroke Scale [NIHSS] score >3-4)and having intracerebral hemorrhage excluded by head computed tomography (CT) should be administered IVtPA.

5 Who should not receive IVtPA?

See Box 62-1.

Box 62-1 Contraindications for IVtPA

Absolute contraindications to IVtPA

image Presence of hemorrhage or large territory infarction on unenhanced head CT

image Central nervous system lesion with high likelihood of hemorrhage (tumor, vascular malformation, aneurysm, abscess, contusion)

image Known bacterial endocarditis

Relative contraindications to IVtPA (these are often interpreted widely and it may be reasonable to treat selected patients in the presence of one or more of these risk factors)

image Minor or rapidly improving symptoms

image Seizure at stroke onset

image Previous stroke or serious head trauma within 3 months

image Major surgery within 14 days or minor surgery within 10 days

image History of prior intracerebral hemorrhage

image Blood pressure >185/110 mm Hg (may be corrected with antihypertensive)

image Pregnant or less than 10 days post partum

image Arterial puncture at noncompressible site within 7 days

image International normalized ratio >1.7 (or prothrombin time >15/sec), partial thromboplastin time >40/sec, platelet count <100,000/μL

image Glucose <50 mg/dL or >400 mg/dL

image NIHSS score >22

6 Who are candidates for extended-window IVtPA?

Patients presenting between 3 and 4.5 hours after symptom onset may be candidates for extended-window IVtPA. There are additional exclusion criteria for extended-window tPA: age >80 years, NIHSS score >25, greater than one-third middle cerebral arteries (MCA) territory infarction by CT or magnetic resonance imaging (MRI), any oral anticoagulant use, prior stroke, or diabetes.

7 What are the benefits and risks of IVtPA?

IVtPA is supported by level I evidence and results in 30% reduction in disability at 3 months compared with placebo. Symptomatic hemorrhage rates vary depending on the study but range from 3% to 6%. An additional one in three patients given treatment with IVtPA will improve by one grade on the modified Rankin scale, and an additional one in eight will have complete reversal of deficits.

8 When should you consider intraarterial thrombolysis or a catheter-based clot retrieval?

Intraarterial interventions remain an experimental therapy for acute ischemic stroke, although use of direct lytics via intraarterial catheter has a limited recommendation based on the Prolyse in Acute Cerebral Thromboembolism (PROACT) trial. Use of this intervention varies by institution. Intraarterial administration of thrombolytics is limited to 6 hours from last seen well time, whereas mechanical retrieval tends to be limited to 8 hours from symptom onset. Patients generally must have more severe neurologic deficits (NIHSS score >6) and a proximal arterial occlusion to be considered for intraarterial therapy. Full-dose IVtPA is not a contraindication to patients undergoing a catheter-based intervention.

9 Describe the cerebral vasculature

Four arteries supply the brain. Two common carotid arteries bifurcate into external and internal segments. The internal segment penetrates the base of the skull and travels within the cavernous sinus. The carotid emerges from the sinus to bifurcate into anterior cerebral arteries (ACA) and MCA. The carotid arteries terminating in ACA and MCA branches compose the anterior circulation. The posterior circulation is supplied by two vertebral arteries traveling within the lateral foramina of the sixth to second cervical vertebrae, which then penetrate the dura mater and join at the midline at the level of the pons to form the basilar artery. The basilar bifurcates to form the posterior cerebral arteries (PCA). Anterior and posterior circulations are joined by the posterior communicating arteries creating the circle of Willis.

10 Describe a lacune and the common lacunar syndromes

A lacune literally means pit. Lacunar infarcts represent a series of small perforating vessel occlusions that result in clinical symptoms that differ from large artery infarctions. Lacunar strokes tend to be either motor or sensory and typically lack cortical findings such as alterations of consciousness or corticosensory modalities (i.e., graphesthesia, stereognosis). See Box 62-2.

Box 62-2 Lacunar syndromes

Pure motor weakness: Face, arm and leg all involved equally. No cognitive, sensory, or visual field loss. Usually in contralateral pons or internal capsule.

Pure sensory syndrome: Numbness or paresthesias of face, arm, and leg without cognitive, motor, or visual field cut. Most commonly localized to the contralateral ventroposterolateral or medial thalamus.

Ataxic hemiparesis: Contralateral ataxia and weakness without cognitive, sensory, or visual field cut. Localizes to posterior limb of internal capsule or pons.

Dysarthria or clumsy hand: Contralateral hand clumsiness. Face or tongue weakness and slurred speech. Localizes to the pons.

11 Describe the large artery infarction syndromes

See Box 62-3.

Box 62-3 Artery infarction syndromes

Anterior Circulation Syndromes

Carotid artery occlusion: Often associated with transient monocular blindness (amaurosis fugax) due to ophthalmic artery involvement. Key symptoms are reflected by MCA involvement and include contralateral hemiparesis of the face and arm more than the leg, as well as loss of corticosensory modalities. If dominant hemisphere is involved, aphasia is present. Nondominant hemisphere results in neglect. If patient has poor collaterals, this occlusion may produce hemiplegia of face, arm, and leg with gaze deviation and decreased level of arousal.

MCA: Proximal occlusions result in contralateral hemiparesis of the face and arm more than the leg, as well as loss of corticosensory modalities. If complete proximal occlusion occurs, symptoms may resemble the carotid artery syndrome. If dominant hemisphere is involved, aphasia is present. Nondominant hemisphere results in neglect. The MCA has two major branches:

Superior division: Results in anterior or Broca-type aphasia with more prominent motor symptoms of hemiparesis. Nondominant superior division occlusions spare language but result in anosognosia and aprosody of speech.
Inferior division: Results in posterior or Wernicke-type aphasia with more prominent deficit of language comprehension, contralateral visual field loss. Nondominant hemisphere inferior division occlusions result in neglect, poor visual-spatial constructions, and sometimes agitation.

PCA: Most commonly results in contralateral hemianopia. Detailed review of other features, which depend on laterality of the brain, is outside the scope of this chapter. Readers are instead referred to the bibliography.

ACA: Weakness of foot and leg more than arm or face.

Posterior Circulation Syndromes

Basilar artery

Top of the basilar: These patients are somnolent with small, poorly reactive pupils and multiple gaze palsies. The condition is sometimes associated with involuntary movements of the extremities (basilar fits) that may resemble convulsions or hallucinations. Patients may have quadriparesis and become “locked in.”

Pontine syndromes: Bilateral or crossed findings and gaze palsies (i.e., internuclear ophthalmoplegia) are key to localizing infarcts to the pons. These patients often have fluctuating symptoms in the early hours of the onset of symptoms.

Vertebral artery

Lateral medullary syndrome (Wallenberg): Vertigo, nystagmus, ipsilateral facial sensory loss, pharyngeal paresis, and Horner syndrome (autonomic dysfunction). Contralateral loss of pain and temperature to body and limbs.

Medial medullary syndrome: Ipsilateral tongue paresis (rarely seen), contralateral hemiparesis and posterior column dysfunction due to the medial lemniscus.

Cerebellar artery

Posterior inferior cerebellar artery: Vertigo, veering to ipsilateral side, ipsilateral limb ataxia, headache, and vomiting.

Superior cerebellar artery and anterior inferior cerebellar artery infarction rarely occur in isolation because of robust collaterals.

12 What is a watershed syndrome?

Infarction at border zones between major arterial territories typically occurs as the result of global brain hypoperfusion or hemispheric hypoperfusion (i.e., critical carotid stenosis). MCA-ACA is most common and results in a person in a barrel pattern of weakness affecting proximal greater than distal musculature.

13 How do infarcts resulting from venous sinus thrombosis (VST) differ from arterial strokes?

Visualized areas of infarction lie outside traditional arterial territories. Infarcts result from venous back pressure, have prominent vasogenic edema on imaging, and are often multifocal and associated with hemorrhage. VST is a less-common but significant cause of stroke in younger persons, particularly women. It is more common with venous thrombotic risk factors such as inherited hypercoagulable states (e.g., factor V Leiden mutation), and thrombophilia is encountered in approximately 80% of patients. Oral contraceptives in association with tobacco use, and late-term pregnancy or postpartum periods, present higher risk of VST. Despite the presence of hemorrhage, the risk of progression to devastating intracerebral hemorrhage appears to be lowered by anticoagulation with IV heparin. Treatment with heparin is not recommended for patients with isolated cortical vein thrombosis if the sinuses are patent.

14 How should blood pressure be managed in acute ischemic stroke?

A doctrine of permissive hypertension should be followed. Tissue bordering areas of infarction, or the penumbra, often has a loss of cerebral autoregulation and is at risk for hypoperfusion and hence further infarction in the setting of acutely lowered blood pressures (BP). The optimum BP goal for an individual patient depends on many factors, including baseline BP, pattern of cerebral collateral flow, and the degree of stenosis or occlusion of the intracerebral arteries. In the absence of evidence for other end-organ dysfunction (i.e., cardiac or renal), most clinicians tolerate BPs as high as 220/120 mm Hg. Pressures in excess of this are generally treated with labetalol or nicardipine as needed to gently lower the BP under careful observation for neurologic worsening. Aggressive treatment of hypertension in acute stroke often results in worsening of stroke symptoms and may result in greater disability. BP reduction occurs spontaneously outside the hyperacute period. Gradual pharmacologic reduction in BP can take place over several days after an acute stroke. The one exception to this rule is among patients who are candidates for IVtPA where the BP should be <185/110 mm Hg to start treatment and be maintained at <180/105 mm Hg for the 24 hours after treatment.

15 What is a transient ischemic attack (TIA)?

The traditional definition of TIA was any ischemic stroke symptom that resolved within 24 hours. However, the definition has come under scrutiny because most deficits lasting greater than 1 hour are likely to cause infarction that is visible by MRI. For this reason, many centers manage patients with TIA with the same urgency as patients with acute ischemic stroke. A TIA should be considered an opportunity to rapidly intervene with appropriate medical or surgical therapies to prevent disability from an impending larger or more disabling stroke.

16 What strokes require anticoagulation for secondary prevention?

Anticoagulation is often used liberally in clinical settings, although the data do not support its use in unselected patients. The strongest indications for permanent anticoagulation for secondary prevention of ischemic stroke are atrial fibrillation, acute myocardial infarction complicated by left ventricular mural thrombus, mechanical prosthetic heart valves, and hypercoagulable disorders. Short-duration anticoagulation of up to 3 months followed by antiplatelet therapy is often used in the setting of arterial dissection or with severe cardiomyopathy, although specific studies addressing these populations are limited. Patients with noncardioembolic stroke due to other causes (large artery disease, small vessel disease, cryptogenic) are generally best treated with antiplatelet therapy. No evidence suggests that increasing the dose of aspirin in patients who have a stroke while taking aspirin will provide additional benefit.

17 For what size infarctions should anticoagulation be withheld?

This decision requires balancing the risk of recurrent infarction with the risk of hemorrhagic transformation of the index infarction. In general, if the area of infarction is large (i.e., more than one third of the MCA territory) or involves the deep lenticulostriate perforators, anticoagulation is often held for several weeks to reduce the risk of hemorrhagic transformation. However, anticoagulation may be initiated sooner in settings of high risk of recurrent stroke.

18 Who should undergo hemicraniectomy for large hemispheric strokes?

Very large territory strokes (so-called malignant MCA infarcts) with >50% of MCA territory involved on imaging or a measured estimated volume of >150 mL and major neurologic disability on presentation pose a risk of death of cerebral edema and subsequent herniation. Current data suggest both a functional and survival benefit from early decompressive surgery within 48 hours of stroke onset in persons under the age of 60 years. However, the decision should still be made on a case-by-case basis for the individual patient given the significant nature of remaining disability.

19 What are the subtypes of primary hemorrhagic strokes?

Primary intracerebral hemorrhage may be classified according to cause or location. Hypertensive hemorrhages more commonly involve deep brain structures because of the location of small arteries arising of large main trunk vessels that are most prone to hypertensive injury over time. Specific locations from most common to less common are the caudate, thalamus, pons, and cerebellum. Hemorrhages due to deposition of amyloid protein in the arterial wall, known as amyloid angiopathy, are lobar in location and spare the deep tissues. Although less common, ruptured aneurysms may present as intraparenchymal hemorrhages with minimal or no subarachnoid blood, and CT or traditional transfemoral angiography should be considered when the hematoma overlies the sylvian cistern.

20 What BP goals should be met after acute intracerebral hemorrhage?

This remains an active area of research. Optimum BP after a spontaneous intracerebral hemorrhage likely depends on the individual’s normal BP range. Current guidelines suggest a target systolic blood pressure (SBP) of less than 160 mm Hg, although ongoing trials suggest that an SBP of less than 140 mm Hg is probably also safe.

21 Describe the tools used for reversal of anticoagulation in warfarin-associated intracerebral hemorrhage

Most centers currently use a combination vitamin K (safe, inexpensive, but slow reversal time) and fresh frozen plasma. A more rapid reversal is achieved with prothrombin complex concentrates and recombinant activated factor VII. Although these latter strategies rapidly correct measured laboratory abnormalities, it is unclear whether they provide long-term benefit over the traditional approaches. A randomized controlled trial of factor VII did not show clinical benefit despite promising phase II data and a reduction in hematoma growth. Practice varies significantly because of concerns over safety profile, cost, efficacy, and thrombotic complications.

22 When should an intracerebral hemorrhage be surgically evacuated?

Cerebellar hemorrhages require emergent surgical decompression, which has been shown to provide durable benefit. The role for surgical craniotomy and evacuation in spontaneous intracerebral hemorrhage in the supratentorial space is less clear, as a major randomized trial did not show benefit overall to early surgery, despite a trend toward benefit if the clot was located superficially.

23 Should patients with intracerebral hemorrhage receive empirical antiepileptic medications?

No data support the use of prophylactic antiepileptic drugs in spontaneous intracerebral hemorrhage. Some data suggest increased incidence of seizure within the first 7 days in the setting of traumatic intracerebral hemorrhage.

Key Points Strokeimage

1. Ischemic stroke is a medical emergency where treatment administered within accepted time frames (up to 4.5 hours for IVtPA) can dramatically improve functional outcome.

2. BP should not be treated in acute ischemic stroke unless it is greater than 220/110 mm Hg or SBP >185/110 mm Hg if IVtPA is to be administered.

3. Atrial fibrillation, acute myocardial infarction, mechanical heart valves, and hypercoagulable states are the proved indications for stroke prevention with therapeutic anticoagulation.

4. Intracerebral hemorrhage location suggests the likely cause with deep territory involvement suggesting hypertension and lobar location suggesting amyloid.

5. There is no role for surgical evacuation of spontaneous intracerebral hemorrhage in unselected patients. Cerebellar hemorrhage always warrants neurosurgical evaluation, and decompression should be undertaken in patients with declining examination results or large hemorrhages.

Bibliography

1 Adams H.P.Jr. Del Zoppo GD, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke. Circulation. 2007;115:e478–e534.

2 Broderick J., Connolly S., Feldmann E., et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults. Stroke. 2007;38:2001–2023.

3 Furie K.L., Kasner S.E., Adams R.J., et al. American Heart Association Stroke Council, Council on Cardiovascular Nursing, Council on Clinical Cardiology, and Interdisciplinary Council on Quality of Care and Outcomes Research. Guidelines for the prevention of stroke in patients with stroke or transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42:227–276.

4 Furlan A., Higashida R., Wechsler L., et al. Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA. 1999;282:2003–2011.

5 Hacke W., Kaste M., Bluhmki E., et al. and for the European Cooperative Acute Stroke Study (ECASS) investigators: Alteplase compared with placebo within 3 to 4.5 hours for acute ischemic stroke. N Engl J Med. 2008;359:1317–1329.

6 Johnston S.C., Albers G.W., Gorelick P.B., et al. National Stroke Association recommendations for systems of care for transient ischemic attack. Ann Neurol. 2011;69:872–877.

7 Levi M., Levy J.H., Andersen H.F., et al. Safety of recombinant activated factor VII in randomized clinical trials. N Engl J Med. 2010;363:1791–1800.

8 Marler J.R., Tilley B.C., Lu M., et al. Early stroke treatment associated with better outcome: the NINDS rt-PA stroke study. Neurology. 2000;55:1649–1655.

9 Mehdiratta M., Kumar S., Selim M., et al. Cerebral venous sinus thrombosis. In: Caplan L.R., ed. Uncommon Causes of Stroke. 2nd ed. New York: Cambridge University Press; 2008:497–504.

10 Mendelow A.D., Gregson B.A., Fernandes H.M., et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet. 2005;365:387–397.

11 The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995;333:1581–1587.

12 Ropper A.H., Samuels M.A. Cerebrovascular diseases. In Adams and Victor’s Principles of Neurology, 9th ed, New York: McGraw-Hill; 2009:660–746.

13 Smith W.S. Safety of mechanical thrombectomy and intravenous tissue plasminogen activator in acute ischemic stroke. Results of the multi Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trial part I. AJNR Am J Neuroradiol. 2006;27:1177–1182.

14 Steiner T., Rosand J., Diringer M. Intracerebral hemorrhage associated with oral anticoagulant therapy: current practices and unresolved questions. Stroke. 2006;37:256–262.

15 Vahedi K., Hofmeijer J., Juettler E., et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol. 2007;6:215–222.

Share this:

Related posts:

Intensive Care Unit Organization, Management, and Value Status Epilepticus Bronchoscopy Acute Bacterial Pneumonia Toxic Alcohol Poisoning Hemodynamic Monitoring