Stroke

Chapter: Stroke
McMaster Section Editor(s): Robert Hart, Wieslaw Oczkowski
Section Editor(s) in Interna Szczeklika: Anna Członkowska, Marek Bodzioch
McMaster Author(s): Wieslaw Oczkowski
Author(s) in Interna Szczeklika: Anna Członkowska, Maciej Niewada
Additional Information

Definition, Etiology, Pathogenesis Top

Stroke is defined as an abrupt onset of focal brain, spinal cord, or retinal injury due to abnormalities of cerebral blood flow with clinical symptoms or signs lasting >24 hours and/or radiologic abnormalities of infarction or hemorrhage present on imaging studies. Subarachnoid hemorrhage (SAH) is also considered in the category of stroke, although the cerebral dysfunction is usually generalized.

Focal neurologic signs and symptoms that resolve spontaneously within 24 hours and without radiologic abnormalities are referred to as a transient ischemic attack (TIA).

On the basis of pathomechanism and etiology, stroke can be classified as:

1) Ischemic stroke (accounting for ~80% of strokes), which is usually due to an occlusion (often a transient occlusion with embolic strokes) of an artery and the resulting reduction of focal cerebral perfusion. Ischemic stroke may be caused by:

a) Atherosclerotic plaques (in situ plaque rupture with occlusion or artery-to-artery embolism) in the major arteries supplying the brain (aortic arch, carotid and vertebral arteries) or in large- and medium-size intracranial arteries.

b) Degenerative lesions/microatherothrombosis (in situ occlusion) in small penetrating arteries of the brain (lacunar stroke).

c) Cardiac embolism from atrial fibrillation (most frequently), ischemic heart disease (left ventricular aneurysm or cardiomyopathy), mitral or aortic valvular heart disease (rheumatic valvular disease, endocarditis, or artificial bioprosthetic or mechanical valves).

d) Less common causes, such as a patent foramen ovale (paradoxical embolism), arterial dissection, or coagulopathies.

Despite recent diagnostic advances, ~20% of ischemic strokes are found to be cryptogenic after diagnostic evaluation.

Hemorrhagic transformation of ischemic infarction occurs in 5% of patients after thrombolysis, but it can occur spontaneously in patients with cardioembolic stroke and a large infarction. Hemorrhagic infarct is often asymptomatic because it is due to bleeding into the already damaged tissue, but if severe, it can manifest clinically as deterioration in neurologic function and is managed as spontaneous intracerebral hemorrhage.

2) Hemorrhagic stroke (accounting for ~15%-20% of stroke cases), which may be caused by:

a) Intracerebral hemorrhage: Most commonly occurs due to bleeding from a ruptured penetrating intracranial vessel in the context of hypertension (weakened vessel due to degenerative changes and microaneurysmal formation), bleeding from rupture of a lobar vessel in the elderly (weakened vessel due to amyloid deposition), or rupture from an arteriovenous malformation.

b) SAH (accounting for ~5% of stroke cases): Most frequently occurs as a result of rupture of a saccular aneurysm at the base of the brain in the subarachnoid space and presents clinically with generalized brain dysfunction (headache, decreased level of consciousness [LOC]).

3) Cerebral venous thrombosis (accounting for <1% of stroke cases), which occurs as a result of thrombosis of intracranial venous sinuses, the deep venous system, and cortical veins, causing cerebral ischemia, infarction, and hemorrhage. The clinical presentation can be variable and include headache, seizures, focal signs, decreased LOC.

Risk factors: Hypertension, diabetes mellitus, dyslipidemia, tobacco smoking, physical inactivity, cardiac diseases, alcohol abuse, oral contraceptives, hormonal replacement therapy, pregnancy, migraine.

Clinical Features and Natural History Top

1. Symptoms of ischemic stroke depend on the location of the lesion. The Oxford classification identifies ischemic stroke subtypes based on the location and vascular territory:

1) Total anterior circulation infarct (TACI) involves the area supplied by the anterior and middle cerebral arteries and causes total anterior circulation syndrome (TACS): significant hemiparesis or sensory disturbances affecting one side of the body in ≥2 out of 3 areas (the face, upper extremities, lower extremities), aphasia, and homonymous hemianopsia.

2) Partial anterior circulation infarct (PACI) involves part of the anterior cerebral circulation and causes partial anterior circulation syndrome (PACS): motor or sensory symptoms in 1 or 2 out of the 3 areas mentioned above, or isolated aphasia.

3) Lacunar stroke (LACI) develops in the areas supplied by the penetrating arteries, most frequently in the basal ganglia, internal capsule, thalamus, or brainstem, and causes lacunar syndrome (LACS): usually limited to paresis or sensory disturbances in 2 out of 3 areas (the face, upper extremities, lower extremities). Isolated weakness involving all of the face, arm, and leg (pure motor stroke) is a relatively specific LACS.

4) Posterior circulation infarct (POCI) affects the vertebrobasilar system and manifests with cerebellar, brainstem, or occipital lobe signs and symptoms (posterior circulation syndrome [POCS]), including ataxia and nystagmus, cranial nerve palsies with contralateral motor/sensory deficits, or isolated homonymous hemianopia.

Symptoms of hemorrhagic stroke depend on the type and location of bleeding:

1) Intracerebral hemorrhage results in a variety of focal deficits depending on the location of the bleeding; it is typically associated with a prominent headache due to intracranial hypertension, but the headache does not usually have a thunderclap quality; it is not possible to differentiate it on clinical grounds from cerebral infarction, and imaging is required.

2) SAH should always be carefully excluded in each patient with a sudden and intense (thunderclap) headache (often described as “the worst ever in my life”). Usually, there are few focal neurologic signs, but more commonly, a change in the LOC is seen.

Cerebral venous thrombosis causes a wide range of clinical manifestations, and the area of the injury does not correspond to the area of arterial blood supply. Cerebral venous thrombosis may lead to focal neurologic symptoms or partial seizures, symptoms of increased intracranial pressure, altered mental status; and with involvement of the cavernous sinus, to abnormal eye movement (palsies of cranial nerves III and VI) with accompanying exophthalmos, retrobulbar pain, and eyelid edema.

2. Natural history: In the first hours or days following a stroke, the patient’s neurologic status may change. Up to 20% of patients with cerebral infarction will have worsening of their impairments in the first 24 to 48 hours (stroke in progression). In 5% to 10% of patients with ischemic stroke, a second stroke occurs early (new neurologic symptoms develop; it may be associated either with a new or the same blood supply area as the first stroke). In up to 10% of large cerebral infarctions (TACIs), hemorrhagic transformation may occur, usually in the first 48 hours, with possible neurologic worsening. In addition, large cerebral infarctions (TACIs) may show clinical worsening or decreased LOC due to cerebral edema between days 3 and 5. In the absence of these complications, most patients start to improve after the initial few days and the majority of motor recovery occurs over the first 2 to 3 months. The risk of stroke is about 10% in the first 30 days after a TIA, with half the events occurring in the first few days. Rapid identification of the stroke etiology and implementation of risk-reduction strategies in patients with an acute TIA are imperative.Evidence 1Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered to low due to the observational nature of data (before-after study) but increased to moderate due to a very large effect size. Rothwell PM, Giles MF, Chandratheva A, et al; Early use of Existing Preventive Strategies for Stroke (EXPRESS) study. Effect of urgent treatment of transient ischaemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet. 2007 Oct 20;370(9596):1432-42. Erratum in: Lancet. 2008 Feb 2;371(9610):386. Carasco-Alexander, Faye [corrected to Alexander, Faye C]. PubMed PMID: 17928046. Lavallée PC, Meseguer E, Abboud H, et al. A transient ischaemic attack clinic with round-the-clock access (SOS-TIA): feasibility and effects. Lancet Neurol. 2007 Nov;6(11):953-60. PubMed PMID: 17928270.

Diagnosis Top

Diagnostic Workup

1. Take a history: Carefully establish the exact time of the onset of symptoms, as this is crucial for determining the indications for thrombolytic treatment. Almost all stroke patients present with sudden and focal neurologic symptoms and signs.

2. Assess the vital signs (airway, breathing, circulation—ABCs): Respiration rate, blood pressure, heart rate (including electrocardiography [ECG]), and SaO2 (pulse oximetry).

3. Perform an efficient general examination: Look for evidence of trauma or other signs that may require immediate medical intervention. In patients with SAH, symptoms and signs of meningeal irritation (stiff neck) can be present.

4. Perform a focused neurologic examination: A standardized stroke scale, such as the National Institutes of Health Stroke Scale (NIHSS) (Table. Example of the application of...), is a tool that can quantify the degree of impairment, identify stroke location, quantify change in neurologic impairments, and predict the outcome. The NIHSS is useful in determining the prognosis after stroke and has become a common and reliable communication tool among clinicians.Evidence 2High Quality of Evidence (high confidence that we know true effects of intervention). Adams HP Jr, Davis PH, Leira EC, et al. Baseline NIH Stroke Scale score strongly predicts outcome after stroke: A report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology. 1999 Jul 13;53(1):126-31. PubMed PMID: 10408548. Lyden P, Raman R, Liu L, Emr M, Warren M, Marler J. National Institutes of Health Stroke Scale certification is reliable across multiple venues. Stroke. 2009 Jul;40(7):2507-11. doi: 10.1161/STROKEAHA.108.532069. Epub 2009 Jun 11. PubMed PMID: 19520998; PubMed Central PMCID: PMC2726278.

5. Assess blood glucose levels. Patients with hypoglycemia can present with a focal stroke-like picture.

6. Collect blood samples for a complete blood count (CBC), prothrombin time (PT), international normalized ratio (INR), activated partial thromboplastin time (aPTT), serum electrolytes, renal function tests, and serum biomarkers of myocardial infarction. Measure the thrombin time (TT) if the patient is suspected to be treated with a direct thrombin inhibitor or ecarin clotting time (ECT) if a direct factor Xa inhibitor is suspected. In selected patients, there might be specific indications to order hepatic function tests, toxicology screen, blood alcohol level, and pregnancy test.

7. Perform nonenhanced computed tomography (NECT) or magnetic resonance imaging (MRI) of the brain as soon as possible; these studies accurately differentiate ischemic stroke from hemorrhagic stroke, which cannot be reliably done on clinical grounds, and are crucial for both acute and chronic management. While MRI offers better resolution, NECT takes a shorter time to complete, can be performed in patients with metal implants, is less susceptible to motion artifacts, and in most cases provides enough information to make emergency treatment decisions. The sensitivity of computed tomography (CT) scanning in the first few hours after SAH is almost 100%. If the results of the head CT scans are normal or inconclusive and SAH is suspected based on the clinical presentation, perform a diagnostic lumbar puncture. Do not perform the lumbar puncture before you have excluded an intracranial space-occupying lesion with brain CT or MRI.

8. Further studies should be guided by the need to identify the pathomechanism of the stroke: carotid ultrasonography and/or CT angiography/magnetic resonance angiography for large vessel atherosclerosis and stenosis; echocardiography (transthoracic and/or transesophageal) for a cardioembolic source; prolonged cardiac monitoring for suspected atrial fibrillation. Other studies are guided by the clinical indication: chest radiographs for suspected aspiration pneumonia, or electroencephalography (EEG) for suspected epileptic disorders mimicking stroke.

Differential Diagnosis

Differential diagnosis includes a broad spectrum of diseases that may occasionally present with and produce focal neurologic symptoms or signs. Even in expert hands, >10% of patients diagnosed with ischemic stroke at the initial evaluation are found to have another disorder (most commonly seizure, migraine, or psychosomatic conversion disorder).

The CT or MRI brain scan reliably differentiates ischemia or infarction from hemorrhage. Most mass lesions, such as tumor, subdural hematoma, or abscess, are evident on brain imaging. Toxic and metabolic disorders simulating stroke become evident from their atypical presentation, examination, laboratory analyses, and progression of the disorder.

Treatment Top

Stroke is a medical emergency, a life-threatening condition that often results in severe and permanent neurologic impairment and disability. Therefore, stroke requires an urgent diagnosis and immediate treatment. A patient with suspected stroke should be urgently transported to a hospital that is experienced in providing stroke care, and preferably directly to a hospital with a dedicated stroke unit.Evidence 3Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Stroke Unit Trialists' Collaboration. Organised inpatient (stroke unit) care for stroke. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD000197. Review. Update in: Cochrane Database Syst Rev. 2013;9:CD000197. PubMed PMID: 17943737.

General Medical Treatment

1. Control the vital parameters: Immediately assess and stabilize airway, breathing, and circulation (ABCs). Patients with stroke may require mechanical ventilation and treatment of cardiac dysfunction in an intensive care unit setting.

2. Control blood pressure: In the early phase of stroke, blood pressures are frequently elevated, and then they spontaneously decrease after a few days. An excessive lowering of blood pressure may lead to a reduction in cerebral blood flow, resulting in an expansion of the ischemic lesion and deterioration of the patient’s neurologic status. Avoid rapid lowering of the blood pressure.

1) Usual indications for the use of antihypertensive drugs:

a) Patients with ischemic stroke eligible for thrombolysis: systolic blood pressure (SBP) >185 mm Hg or diastolic blood pressure (DBP) >110 mm Hg (Table. Treatment of hypertension in patients...).

b) Patients with ischemic stroke not eligible for thrombolysis: SBP >220 mm Hg or DBP >120 mm Hg (Table. Treatment of hypertension in patients...). The available evidence has failed to show benefit of lowering the SBP below certain thresholds (ie, 180 or 160 mm Hg).Evidence 4High Quality of Evidence (high confidence that we know true effects of intervention). He J, Zhang Y, Xu T, et al; CATIS Investigators. Effects of immediate blood pressure reduction on death and major disability in patients with acute ischemic stroke: the CATIS randomized clinical trial. JAMA. 2014 Feb 5;311(5):479-89. doi: 10.1001/jama.2013.282543. PubMed PMID: 24240777. ENOS Trial Investigators, Bath PM, Woodhouse L, Scutt P, et al. Efficacy of nitric oxide, with or without continuing antihypertensive treatment, for management of high blood pressure in acute stroke (ENOS): a partial-factorial randomised controlled trial. Lancet. 2015 Feb 14;385(9968):617-28. doi: 10.1016/S0140-6736(14)61121-1. Epub 2014 Oct 21. Erratum in: Lancet. 2015 Feb 14;385(9968):606. PubMed PMID: 25465108; PubMed Central PMCID: PMC4343308.

c) Patients with intracerebral hemorrhage: SBP >160 mm Hg (Table. Treatment of hypertension in patients...). It is probably safe to rapidly lower the SBP to 140 or less; however, the efficacy is unproven.

d) Patients with SAHSBP > 160 mm Hg.

e) Patients with elevated blood pressure associated with acute coronary syndromes, aortic dissection, heart failure, renal injury, or markedly reduced coagulability in the course of anticoagulant treatment: Blood pressure targets are based on the condition and urgency of the situation.

2) Choice of agents: The blood pressure is best controlled with IV drugs; examples: Table. Treatment of hypertension in patients..., Table. Treatment of hypertension in patients..., Table. Treatment of hypertension in patients.... Stroke is rarely accompanied by hypotension, which is usually associated with ischemic heart disease or may be a result of dehydration, bleeding (usually from the gastrointestinal tract), or pharmacotherapy. Correct the underlying cause of the hypotension, administer fluids, and, if necessary, manage the patient in an intensive care unit setting with vasopressors.

3. Correct any existing fluid and electrolyte disturbances (see Water and Electrolyte Disturbances).

4. Monitor blood glucose levels. Both hyperglycemia and hypoglycemia have adverse effects on the brain in the setting of acute stroke. In patients with hyperglycemia, restrict dietary carbohydrates; in patients with glucose levels ≥10 mmol/L, consider insulin treatment but with caution, to avoid hypoglycemia. In patients with hypoglycemia (<3.3 mmol/L), administer 25 mL of 50% glucose (dextrose) in a slow intravenous injection (low tonicity of a 5% glucose solution may cause brain edema).

5. Reduce the body temperature if it is >37.5 degrees Celsius. Fever is frequent in the first 48 hours post stroke and is associated with a less favorable prognosis. The source of fever, in particular infection, should be identified. Use acetaminophen (INN paracetamol) (up to 4000 mg/d) and surface cooling.

6. Monitor urine output: Urinary incontinence is common after acute stroke, and as many as 20% of patients with stroke have urinary retention. Bladder scanning and/or in-out catheterization should be ordered. Temporary catheterization may be indicated to monitor urine output and in the case of urinary retention; however, prolonged catheterization should be avoided if possible, as it is associated with an increased risk of infections.

7. Insert a nasogastric tube to provide oral medications otherwise not available intravenously in patients with dysphagia. Dysphagia is common after stroke; however, early feeding does not change the probability of a good outcome and may be deferred as long as hydration is maintained.

8. Start prophylaxis of venous thromboembolism for immobile patients with low-molecular-weight heparin (LMWH) (eg, enoxaparin 40 mg/d) rather than unfractionated heparin (UFH); consider pneumatic compression if anticoagulation is contraindicated.Evidence 5Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Sandercock PA, Counsell C, Tseng MC. Low-molecular-weight heparins or heparinoids versus standard unfractionated heparin for acute ischaemic stroke. Cochrane Database Syst Rev. 2008 Jul 16;(3):CD000119. doi: 10.1002/14651858.CD000119.pub3. Review. PubMed PMID: 18646059. CLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration, Dennis M, Sandercock P, Reid J, Graham C, Forbes J, Murray G. Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS 3): a multicentre randomised controlled trial. Lancet. 2013 Aug 10;382(9891):516-24. doi: 10.1016/S0140-6736(13)61050-8. Epub 2013 May 31. Erratum in: Lancet. 2013 Aug 10;382(9891):506. Lancet. 2013 Sep 21;382(9897):1020. PubMed PMID: 23727163.  (see Primary Prevention of Venous Thromboembolism).

9. Good nursing care and positioning can reduce the risk of aspiration pneumonia, other infections, and pressure ulcers.

10. Management of increased intracranial pressure or seizures: see Complications, below.

Specific Therapy for Ischemic Stroke

1. Acetylsalicylic acid (ASA): Administer ASA immediately in patients who do not receive fibrinolysis or 24 hours following fibrinolytic treatment; intracranial hemorrhage must be excluded by brain CT. Start with 160 to 325 mg/d, then reduce the dose to 81 mg/d.Evidence 6Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002 Jan 12;324(7329):71-86. Erratum in: BMJ 2002 Jan 19;324(7330):141. PubMed PMID: 11786451; PubMed Central PMCID: PMC64503. Some physicians add clopidogrel 300 mg as a loading dose followed by 75 mg/d for 21 days in patients after a minor ischemic stroke or a TIA at high risk of subsequent stroke.Evidence 7Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Moderate Quality of Evidence and a weak rather than strong recommendation due to indirectness to the North American population. Wang Y, Wang Y, Zhao X, et al; CHANCE Investigators. Clopidogrel with aspirin in acute minor stroke or transient ischemic attack. N Engl J Med. 2013 Jul 4;369(1):11-9. doi: 10.1056/NEJMoa1215340. Epub 2013 Jun 26. PubMed PMID: 23803136.

2. Fibrinolytic treatment: Recombinant tissue plasminogen activator (rtPA) 0.9 mg/kg (10% of the dose in IV injection over 1-2 minutes followed by the remaining 90% of the dose in IV infusion over 1 hour; maximum total dose, 90 mg).Evidence 8Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Wardlaw JM, Murray V, Berge E, et al. Recombinant tissue plasminogen activator for acute ischaemic stroke: an updated systematic review and meta-analysis. Lancet. 2012 Jun 23;379(9834):2364-72. doi: 10.1016/S0140-6736(12)60738-7. Epub 2012 May 23. Review. PubMed PMID: 22632907; PubMed Central PMCID: PMC3386494. Wardlaw JM, Murray V, Berge E, del Zoppo GJ. Thrombolysis for Acute Ischemic Stroke, Update August 2014. Stroke. 2014;45(11):e222–e225. doi:10.1161/STROKEAHA.114.007024.

1) rtPA may be used within 4.5 hours from the onset of an ischemic stroke that has caused clinically significant and measurable neurologic deficits. Note that the benefits of fibrinolytic therapy decrease as more time elapses from the onset of stroke to the administration of rtPA.

2) Exclusion criteria: Table. Thrombolytic therapy for ischemic stroke:....

3) Complications: The risk of symptomatic intracranial hemorrhage is increased in patients who receive rtPA (8% vs 2%), as is early death; however, death or dependency at 3 to 6 months is decreased in patients treated with rtPA.

3. For patients with occlusions of the proximal intracranial vessels (carotid artery, middle cerebral artery, anterior cerebral artery) as seen on CT angiography, including those who underwent fibrinolytic therapy, intra-arterial clot extraction with stent retrievers significantly improves the probability of good recovery; consideration should be given to treatment or transfer to an interventional stroke center if feasible.Evidence 9Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Berkhemer OA, Fransen PS, Beumer D, et al; MR CLEAN Investigators. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015 Jan 1;372(1):11-20. doi: 10.1056/NEJMoa1411587. Epub 2014 Dec 17. Erratum in: N Engl J Med. 2015 Jan 22;372(4):394. PubMed PMID: 25517348. Goyal M, Demchuk AM, Menon BK, et al; ESCAPE Trial Investigators. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med. 2015 Mar 12;372(11):1019-30. doi: 10.1056/NEJMoa1414905. Epub 2015 Feb 11. PubMed PMID: 25671798. Campbell BC, Mitchell PJ, Kleinig TJ, et al; EXTEND-IA Investigators. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med. 2015 Mar 12;372(11):1009-18. doi: 10.1056/NEJMoa1414792. Epub 2015 Feb 11. PubMed PMID: 25671797. Saver JL, Goyal M, Bonafe A, et al; SWIFT PRIME Investigators. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med. 2015 Jun 11;372(24):2285-95. doi: 10.1056/NEJMoa1415061. Epub 2015 Apr 17. PubMed PMID: 25882376.

4. Heparin:

1) Ischemic stroke: Administration of UFH or LMWH at therapeutic doses (the majority of immobilized patients require the use of heparin at prophylactic doses) is indicated only in exceptional cases: possibly in patients with stroke caused by cardioembolism, who are at high risk of a second embolism, as well as in patients with arterial dissection; even in these circumstances, there is no generally accepted evidence that the benefit from treatment outweighs the risk of increased bleeding.

2) Cerebral venous thrombosis: Start with heparin (UFH or LMWH) at therapeutic doses (Table. Dosage of low-molecular-weight heparin in...), then continue treatment with a vitamin K antagonist (VKA) (warfarin) for 3 to 6 months (INR, 2.0-3.0). Repeat venous imaging should be used to guide discontinuation of anticoagulation.Evidence 10Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to the low number of events. Coutinho J, de Bruijn SF, Deveber G, Stam J. Anticoagulation for cerebral venous sinus thrombosis. Cochrane Database Syst Rev. 2011 Aug 10;(8):CD002005. doi: 10.1002/14651858.CD002005.pub2. Review. PubMed PMID: 21833941. Saposnik G, Barinagarrementeria F, Brown RD Jr, et al; American Heart Association Stroke Council and the Council on Epidemiology and Prevention. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011 Apr;42(4):1158-92. doi: 10.1161/STR.0b013e31820a8364. Epub 2011 Feb 3. Review. PubMed PMID: 21293023.

3) Contraindications: Extensive ischemic infarction (eg, involving >50% of the area supplied by the middle cerebral artery), uncontrolled hypertension, hemorrhagic transformation of an ischemic infarction, and stroke complicating infective bacterial endocarditis.

Specific Therapy for Intracerebral Hemorrhage and Subarachnoid Hemorrhage

SAH requires a surgical clipping of the ruptured vessel and/or endovascular embolization using coils inserted into the aneurysm. Neurosurgical consultation should be obtained in all patients with SAH.

Surgical evacuation of an intracerebral hemorrhage is generally not recommended, except for selected patients with a cerebellar hematoma to prevent fatal brain stem compression and in patients with a large spontaneous superficial intracerebral hemorrhage with impending herniation. Neurosurgical consultation is recommended for most patients with intracerebral hemorrhage.

Rehabilitation

Rehabilitation plays a crucial role in the resolution of the neurologic deficits caused by stroke. The goals of rehabilitation are to prevent complications, minimize loss of function (impairment), and maximize activity and participation (disability and handicap). Patients should be admitted to and managed in a rehabilitation stroke unit by a multidisciplinary stroke team that includes the core disciplines of physiotherapy, occupational therapy, and speech language therapy.

Complications Top

Progressive stroke, brain edema, hemorrhagic transformation, and recurrent infarction are the neurologic causes of clinical deterioration.

1. Increased intracranial pressure and brain edema, which develops as early as 24 to 48 hours of stroke, after vascular reperfusion, usually peaks after 3 to 5 days. Increasing edema is a frequent cause of the worsening neurologic deficits (affecting about 10% of patients); it may lead to cerebral herniation and death.

Treatment:

1) Elevate the head of the bed at 20 to 30 degrees.

2) Provide a comfortable environment and prevent secondary complications (eg, adequate pain management, appropriate body positioning, shoulder protection in hemiplegic patients).

3) Prevent hypoxemia and maintain a normal body temperature.

4) Short-term hyperventilation (unproven efficacy for improving outcomes) may be used (provided the cerebral perfusion is good); lowering the PaCO2 by 5 to 10 mm Hg may decrease the intracranial pressure by 25% to 30%.

5) Pharmacologic treatment (unproven efficacy) might be considered only in the case of massive cerebral edema: IV mannitol 0.25 to 0.5 g/kg over 20 minutes (this may be repeated every 6 hours) or hypertonic saline. Glucocorticoids have not been shown to be effective.

6) In younger patients (<60 years old) with massive hemispheric cerebral infarction (greater than two-thirds of the middle cerebral artery territory), early decompressive craniectomy will decrease mortality from about 80% to 30% but with potentially severe residual disability; the decision should be guided by patients’ values and preferences.Evidence 11Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). High Quality of Evidence (high confidence that we know true effects of intervention). Vahedi K, Hofmeijer J, Juettler E, et al; DECIMAL, DESTINY, and HAMLET investigators. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol. 2007 Mar;6(3):215-22. PubMed PMID: 17303527. In older individuals (>60 years old) decompressive craniectomy increases survival but only at the expense of severe disability.Evidence 12Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due indirectness (difficulties in interpretation of severe disability). Jüttler E, Unterberg A, Woitzik J, et al; DESTINY II Investigators. Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke. N Engl J Med. 2014 Mar 20;370(12):1091-100. doi: 10.1056/NEJMoa1311367. PubMed PMID: 24645942.

7) Cerebellar infarction or hemorrhage is particularly dangerous and prone to life-ending herniation; close monitoring and early neurosurgical consultation should be obtained. Patients may require early craniectomy or ventricular drainage.

2. Epileptic seizures, which are usually partial or secondarily generalized partial seizures (rarely status epilepticus), may occur early or later after stroke in 5% to 15% of patients; recurrence is not uncommon. Treatment of seizures may require immediate control with IV lorazepam 2 to 4 mg (maximum dose, 8 mg), followed by phenytoin 15 to 20 mg/kg by IV infusion (maximum rate, 50 mg/min). Long-term treatment is preferred with either lamotrigine, carbamazepine, or gabapentin; drug choice is dependent on other patient factors.

3. Venous thromboembolism and pulmonary embolism: For prevention and treatment, see Deep Vein Thrombosis, Pulmonary Embolism, Primary Prevention of Venous Thromboembolism.

4. Infections:

1) Urinary tract infections occur in up to 15% of patients within the first 2 weeks of stroke and may be prevented by maintaining adequate fluid volume and avoiding unnecessary catheterization.

2) Respiratory infections most often occur in the context of dysphagia and more severe strokes in up to 7% of patients and are associated with increased mortality and a poor functional outcome. Assessment and monitoring for dysphagia, early mobilization, and early treatment of infection can improve outcomes.

5. Urinary and fecal incontinence: Urinary incontinence is present in up to 50% of patients early after stroke and persists in up to a third of patients 1 year later; avoid aggravating factors (eg, diuretics), treat urinary tract infections with appropriate antibiotics, and monitor for urinary retention. Constipation may occur in up to 50% of patients within the first month of stroke; proper hydration, monitoring, and mobilization may prevent complications.

6. Pressure ulcers: Due to immobility and incontinence, patients with stroke are at high risk of skin breakdown. Monitoring, skin protection, and positioning are the key preventive measures.

7. Spasticity is a velocity-dependent increase in tone that occurs after stroke. It can cause pain, decrease in function, and interfere with recovery; positioning, stretching, a range of motion exercises, and other physiotherapeutic interventions are the mainstay of treatment. Antispasmodic medication (avoiding benzodiazepines) and botulinum toxin injections are part of a comprehensive spasticity-management program.

8. Shoulder pain syndrome: A painful shoulder has many causes, including trauma, bursitis/tendonitis/capsulitis, rotator cuff tears, spasticity, and complex regional pain syndrome 1 or 2. Appropriate shoulder protection is necessary as a prophylactic measure; start physiotherapy and use analgesics if needed (glucocorticoid injections are not recommended unless there is a specific indication) Advise the patient (and the caregiver) how to get up from the bed without straining the affected shoulder and how to support the affected limb, especially if the limb is flaccid. Treatment of spasticity and the restoration of a normal range of motion require specialized procedures (avoid exercises using weights suspended over the head).

9. Falls: Falls may occur in 15% to 65% of stroke patients. Strategies for prevention of falls are necessary.

10. Malnutrition: Patients unable to eat on their own or with dysphagia are at risk for dehydration and malnutrition. Maintain adequate hydration and nutrition; introduce nasogastric, or percutaneous endoscopic gastrostomy (PEG) feedings if necessary and desired. Note that early nasogastric feeding is not associated with better outcomes.

11. Depression (affects ~30% of patients at different periods following stroke): Treatment with selective serotonin reuptake inhibitors (SSRIs) should be considered especially in the presence of any indications, as it may additionally decrease disability.Evidence 13Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due heterogeneity and the risk of bias. Mead GE, Hsieh CF, Lee R, et al. Selective serotonin reuptake inhibitors for stroke recovery: a systematic review and meta-analysis. Stroke. 2013 Mar;44(3):844-50. doi: 10.1161/STROKEAHA.112.673947. Epub 2013 Jan 29. Review. PubMed PMID: 23362083.

12. Delirium is common after stroke and affects up to a quarter of patients. An underlying cause aside from the stroke should be sought and treated if found.

Prevention Top

Secondary Stroke Prevention

1. Management of risk factors:

1) Hypertension: Start treatment with an angiotensin-converting enzyme inhibitor (ACEI) for stable patients after a few days (on average 7) targeting an SBP <140 mm Hg and a DBP <90 mm Hg;Evidence 14Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6105 individuals with previous stroke or transient ischaemic attack. Lancet. 2001 Sep 29;358(9287):1033-41. Erratum in: Lancet 2001 Nov 3;358(9292):1556. Lancet 2002 Jun 15;359(9323):2120. PubMed PMID: 11589932.Liu L, Wang Z, Gong L, et al. Blood pressure reduction for the secondary prevention of stroke: a Chinese trial and a systematic review of the literature. Hypertens Res. 2009 Nov;32(11):1032-40. doi: 10.1038/hr.2009.139. Epub 2009 Oct 2. Review. PubMed PMID: 19798097. for patients with lacunar stroke, a treatment target of an SBP <130 mm Hg is indicated.Evidence 15Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). SPS3 Study Group, Benavente OR, Coffey CS, Conwit R, et al. Blood-pressure targets in patients with recent lacunar stroke: the SPS3 randomised trial. Lancet. 2013 Aug 10;382(9891):507-15. doi: 10.1016/S0140-6736(13)60852-1. Epub 2013 May 29. Erratum in: Lancet. 2013 Aug 10;382(9891):506. Coffey, C S [aded]. PubMed PMID: 23726159; PubMed Central PMCID: PMC3979302. Initiate treatment with an ACEI (perindopril or ramipril) and/or a diuretic (eg, indapamide).

2) Glucose intolerance and diabetes mellitus: These are best assessed by measuring glycated hemoglobin (HbA1c). Follow treatment guidelines for nonstroke and mixed patient populations.

3) Hypercholesterolemia: High-dose statin treatment (eg, atorvastatin 80 mg/d) should be initiated in all patients with ischemic stroke or a TIA presumed to be of atherosclerotic origin.Evidence 16Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Amarenco P, Bogousslavsky J, Callahan A 3rd, et al; Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) Investigators. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med. 2006 Aug 10;355(6):549-59. PubMed PMID: 16899775. O'Regan C, Wu P, Arora P, Perri D, Mills EJ. Statin therapy in stroke prevention: a meta-analysis involving 121,000 patients. Am J Med. 2008 Jan;121(1):24-33. doi: 10.1016/j.amjmed.2007.06.033. Review. PubMed PMID: 18187070. The efficacy of treating to target is unproven.

4) Cessation of smoking: Continued smoking is associated with stroke recurrence. Behavioral therapy and pharmacotherapy are effective in treating tobacco dependence.

5) Screening for obesity, weight loss measures: Although screening is recommended, weight loss is of uncertain benefit.

6) Regular physical activity: Those patients who can and have no other contraindications should participate in moderate to vigorous intensity exercise 3 to 4 times per week for 40 minutes.

7) Obstructive sleep apnea syndrome (OSAS): There is a high prevalence of OSAS in patients with TIA and stroke. Consideration may be given to a sleep study and treatment (if indicated, with continuous positive airway pressure [CPAP]).

8) Alcohol: Light to moderate amounts of alcohol have protective effects (2 drinks per day for men, 1 drink per day for women). Heavier use is associated with an increased risk of ischemic and hemorrhagic stroke.

2. Antithrombotic treatment: Treatment is dependent on the presumed cause of stroke.

1) Noncardioembolic sources of TIA or stroke (extracranial atherosclerotic arterial disease, intracranial atherosclerotic arterial disease, lacunar disease): Use antiplatelet treatment, not anticoagulation.Evidence 17Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002 Jan 12;324(7329):71-86. Erratum in: BMJ 2002 Jan 19;324(7330):141. PubMed PMID: 11786451; PubMed Central PMCID: PMC64503. Options include ASA 81 to 325 mg/d, or clopidogrel 75 mg/d, or ASA 25 mg + extended-release dipyridamole bid. The combination therapy (ASA + dipyridamole) and clopidogrel have a similar efficacy. The combination of ASA 81 mg/d and clopidogrel 75 mg/d may be used for the first 90 days after TIA or stroke or in patients with intracranial disease; long-term treatment without other indications is associated with an increased risk of bleeding and should not be used.Evidence 18Strong recommendation (downsides clearly outweigh benefits; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Wang Y, Wang Y, Zhao X, et al; CHANCE Investigators. Clopidogrel with aspirin in acute minor stroke or transient ischemic attack. N Engl J Med. 2013 Jul 4;369(1):11-9. doi: 10.1056/NEJMoa1215340. Epub 2013 Jun 26. PubMed PMID: 23803136. Derdeyn CP, Chimowitz MI, Lynn MJ, et al; Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis Trial Investigators. Aggressive medical treatment with or without stenting in high-risk patients with intracranial artery stenosis (SAMMPRIS): the final results of a randomised trial. Lancet. 2014 Jan 25;383(9914):333-41. doi: 10.1016/S0140-6736(13)62038-3. Epub 2013 Oct 26. PubMed PMID: 24168957; PubMed Central PMCID: PMC3971471. Diener HC, Bogousslavsky J, Brass LM, et al; MATCH investigators. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet. 2004 Jul 24-30;364(9431):331-7. PubMed PMID: 15276392.

2) Cardioembolic sources of TIA or stroke (atrial fibrillation, cardiomyopathy, left ventricular thrombus, valvular heart disease [native, bioprosthetic, mechanical]): In patients with atrial fibrillation, long-term anticoagulation is indicated to prevent recurrent stroke.Evidence 19Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Hart RG, Pearce LA, Aguilar MI. Meta-analysis: antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation. Ann Intern Med. 2007 Jun 19;146(12):857-67. PubMed PMID: 17577005. Connolly SJ, Ezekowitz MD, Yusuf S, et al; RE-LY Steering Committee and Investigators. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med. 2009 Sep 17;361(12):1139-51. doi: 10.1056/NEJMoa0905561. Epub 2009 Aug 30. Erratum in: N Engl J Med. 2010 Nov 4;363(19):1877. PubMed PMID: 19717844. Patel MR, Mahaffey KW, Garg J, et al; ROCKET AF Investigators. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. N Engl J Med. 2011 Sep 8;365(10):883-91. doi:10.1056/NEJMoa1009638. Epub 2011 Aug 10. PubMed PMID: 21830957. Granger CB, Alexander JH, McMurray JJ, et al; ARISTOTLE Committees and Investigators. Apixaban versus warfarin in patients with atrial fibrillation. N Engl J Med. 2011 Sep 15;365(11):981-92. doi: 10.1056/NEJMoa1107039. Epub 2011 Aug 27. PubMed PMID: 21870978. Use a VKA or non-VKA oral anticoagulants (novel oral anticoagulants [NOACs]; apixaban, dabigatran, rivaroxaban). The target INR for a VKA is 2.5 (range, 2.0-3.0). NOACs are chosen based on the patient’s preference, tolerability, drug interactions, renal dysfunction, and time in range for VKA treatment. ASA 81 mg/d is indicated if anticoagulation is not possible; ASA 81 mg/d with clopidogrel 75 mg/d may also be considered if anticoagulation is not possible.Evidence 20Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). High Quality of Evidence (high confidence that we know true effects of intervention). ACTIVE Investigators, Connolly SJ, Pogue J, Hart RG, et al. Effect of clopidogrel added to aspirin in patients with atrial fibrillation. N Engl J Med. 2009 May 14;360(20):2066-78. doi: 10.1056/NEJMoa0901301. Epub 2009 Mar 31. PubMed PMID: 19336502. ASA 81 mg/d may be added to anticoagulation in patients with atrial fibrillation and an acute coronary syndrome or coronary stent. Anticoagulation with a VKA is indicated for a left ventricular thrombus; the target INR is 2.5 (range, 2.0-3.0).

3) Long-term anticoagulation with a VKA is recommended for the prevention of stroke in patients with mechanical heart valves; the intensity of anticoagulation varies by the valve position (aortic: INR, 2.0-3.0; mitral: INR, 2.5-3.5). The addition of ASA 81 to 100 mg/d in patients at a lower risk of bleeding decreases the risk of embolism. NOACs should not be used in patients with mechanical valves, as the agents increase the risk of embolism and bleeding.Evidence 21Strong recommendation (downsides clearly outweigh benefits; right action for all or almost all patients). High Quality of Evidence (high confidence that we know true effects of intervention). Eikelboom JW, Connolly SJ, Brueckmann M, et al; RE-ALIGN Investigators. Dabigatran versus warfarin in patients with mechanical heart valves. N Engl J Med. 2013 Sep 26;369(13):1206-14. doi: 10.1056/NEJMoa1300615. Epub 2013 Aug 31. PubMed PMID: 23991661. The risk of embolism and recurrent embolism is lower with bioprosthetic valves, and long-term anticoagulation over antiplatelet treatment may not be indicated.

4) Patients with dilated or restrictive cardiomyopathy (left ventricular ejection fraction ≤35%) in sinus rhythm and without a thrombus have a relatively low risk of recurrent embolism. Antiplatelet treatment rather than a VKA may be reasonable.Evidence 22Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). High Quality of Evidence (high confidence that we know true effects of intervention). Homma S, Thompson JL, Pullicino PM, et al; WARCEF Investigators. Warfarin and aspirin in patients with heart failure and sinus rhythm. N Engl J Med. 2012 May 17;366(20):1859-69. doi: 10.1056/NEJMoa1202299. Epub 2012 May 2. PubMed PMID: 22551105; PubMed Central PMCID: PMC3723382.

5) Other, less common sources of stroke are arterial dissection, aortic arch disease, patent foramen ovale (PFO), and cerebral vein and sinus thrombosis. One recent randomized trial compared antiplatelet treatment vs anticoagulation treatment in cervical (carotid or vertebral) arterial dissection and found no difference between these two treatments; however, the study was associated with major imprecision that precluded a clear recommendation.Evidence 23Low Quality of Evidence (low confidence that we know true effects of intervention). Quality of Evidence lowered due to the small number of events. CADISS trial investigators, Markus HS, Hayter E, Levi C, Feldman A, Venables G, Norris J. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015 Apr;14(4):361-7. doi: 10.1016/S1474-4422(15)70018-9. Epub 2015 Feb 12. Erratum in: Lancet Neurol. 2015 Jun;14(6):566. PubMed PMID: 25684164. Aortic arch disease has been associated with an increased risk of stroke, and in such cases antiplatelet therapy with statin therapy is suggested over anticoagulation.Evidence 24Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of intervention). Quality of Evidence lowered due to the small number of events. Amarenco P, Davis S, Jones EF, et al; Aortic Arch Related Cerebral Hazard Trial Investigators. Clopidogrel plus aspirin versus warfarin in patients with stroke and aortic arch plaques. Stroke. 2014 May;45(5):1248-57. doi: 10.1161/STROKEAHA.113.004251. Epub 2014 Apr 3. PubMed PMID: 24699050. A PFO can be a source of embolism with or without paradoxical embolism but is usually an “innocent bystander” (found in 23% of the general population): antiplatelet and anticoagulant therapy seem equally effective in preventing recurrence of stroke, and PFO closure is associated with an increased risk of procedural stroke without obvious long-term risk reduction.Evidence 25Weak recommendation (downsides likely outweigh benefits, but the balance is close or uncertain; an alternative course of action may be better for some patients). High Quality of Evidence (high confidence that we know true effects of intervention) Furlan AJ, Reisman M, Massaro J, et al; CLOSURE I Investigators. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. N Engl J Med. 2012 Mar 15;366(11):991-9. doi: 10.1056/NEJMoa1009639. PubMed PMID: 22417252. Meier B, Kalesan B, Mattle HP, et al; PC Trial Investigators. Percutaneous closure of patent foramen ovale in cryptogenic embolism. N Engl J Med. 2013 Mar 21;368(12):1083-91. doi: 10.1056/NEJMoa1211716. PubMed PMID: 23514285. Cerebral vein and sinus thrombosis is treated acutely with therapeutic doses of LMWH despite the possibility of hemorrhagic conversion of the venous infarctions.Evidence 26Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to the small number of events (imprecision). Coutinho J, de Bruijn SF, Deveber G, Stam J. Anticoagulation for cerebral venous sinus thrombosis. Cochrane Database Syst Rev. 2011 Aug 10;(8):CD002005. doi: 10.1002/14651858.CD002005.pub2. Review. PubMed PMID: 21833941. Long-term anticoagulation of this condition (3 months vs longer) is based on indirect evidence from other venous thrombosis territories and depends on individual patients’ circumstances (presence of precipitating factors or thrombophilias).

In the absence of carotid artery stenosis warranting revascularization or a major-risk cardioembolic source requiring anticoagulation (such as atrial fibrillation or a left ventricular thrombus), the 3 most important mainstays of secondary ischemic stroke risk reduction are blood pressure control, antiplatelet therapy, and high-dose statins.

3. Invasive treatment of carotid artery stenosis: see Carotid and Vertebral Artery Disease.

TablesTop

Table. Example of the application of the NIHSS as used in Hamilton Health Sciences. For a full scale, visit www.nihstrokescale.org.

1a. LOC

0

Alert

1

Drowsy

2

Stuporous

3

Comatose

1b. LOC questions

0

Answers both questions correctly

1

Answers 1 question correctly

2

Answers neither question correctly

1c. LOC commands

0

Performs both tasks correctly

1

Performs 1 task correctly

2

Performs neither task correctly

2. Best gaze

0

Normal

1

Partial gaze palsy

2

Forced deviation

3. Visual fields

0

No visual loss (or in coma)

1

Partial hemianopia

2

Complete hemianopia

3

Bilateral hemianopia

4. Facial palsy

0

Normal

1

Minor

2

Partial

3

Complete

5. Best motor: right arm

0

No drift

1

Drift

2

Some effort against gravity

3

No effort against gravity

4

No movement

6. Best motor: left arm

0

No drift

1

Drift

2

Some effort against gravity

3

No effort against gravity

4

No movement

7. Best motor: right leg

0

No drift

1

Drift

2

Some effort against gravity

3

No effort against gravity

4

No movement

8. Best motor: left leg

0

No drift

1

Drift

2

Some effort against gravity

3

No effort against gravity

4

No movement

9. Limb ataxia

0

Absent (or in coma)

1

Present in 1 limb

2

Present in ≥2 limbs

10. Sensory

0

Normal

1

Partial loss

2

Dense loss (or in coma)

11. Best language

0

No dysphasia

1

Mild

2

Severe dysphasia

3

Mute

12. Dysarthria

0

Normal articulation

1

Mild to moderate dysarthria

2

Unintelligible or worse

13. Neglect

0

No neglect (or in coma)

1

Partial neglect

2

Complete neglect

NIHSS total score

NIHSS scoring for aphasic and comatose patients:

1b) LOC questions: Aphasic and stuporous patients unable to state age or month = 2 points.

2. Best gaze: Conjugate gaze deviation overcome by voluntary or reflex movement = 1 point. Isolated eye nerve palsy = 1 point.

3. Visual fields: Visual field clear cut asymmetry = 1 point. Total blindness = 2 points.

4. Facial palsy: Facial asymmetry can be assessed in response to noxious stimuli.

5-8. Motor testing: Motor testing can be pantomimed for aphasic patients.

9. Limb ataxia: If cannot be demonstrated = 0 points.

10. Sensory: Asymmetry = 1 point. Bilateral sensory loss = 2 points. Patient in coma and with no response to pain = 2 points.

11. Best language: Patient in coma = 3 points.

12. Dysarthria: Scored only if audible speech is heard.

13. Neglect: Present if obviously more than blindness or sensory loss.

NIHSS, National Institute of Health Stroke Scale; LOC, level of consciousness.

Table. Treatment of hypertension in patients with recent ischemic stroke who are eligible for fibrinolytic treatment (examples; other medications are possible)

Before fibrinolytic treatment:

– Do not administer rtPA if BP cannot be maintained at or below 185/110 mm Hg

Patient eligible for rtPA administration except for SBP >185 mm Hg and/or DBP >110 mm Hg

– IV labetalol 10-20 mg over 1-2 min, may be repeated once
Or:
– IV nicardipine 5 mg/h, titrate up by 2.5 mg/h every 5-15 min (maximum rate, 15 mg/h). When target BP is achieved, adjust to maintain appropriate BP limits
Or:
– Other agents (eg, hydralazine, enalaprilat) when appropriate

During or after fibrinolytic treatment:

– Maintain BP at or below 180/105 mm Hg

– Monitor BP every 15 min for 2 h following the start of rtPA administration, then every 30 min for 6 h, and then every hour for 16 h

BP cannot be controlled with labetalol or nicardipine or DBP >140 mm Hg

– Admission to ICU

– Sodium nitroprusside IV 0.5 microg/kg/min

BP, blood pressure; DBP, diastolic blood pressure; ICU, intensive care unit; rtPA, recombinant tissue plasminogen activator; SBP, systolic blood pressure.

Table. Treatment of hypertension in patients with recent ischemic stroke who do not receive fibrinolytic treatment (examples, other medications are possible)

Blood pressure

Managementa

SBP <220 mm Hg and DBP <120 mm Hg

Do not use antihypertensive agents. Hold 50% of previously used beta-blockers, hold other antihypertensive medications. Consider antihypertensive treatment in patients with severe heart failure, aortic dissection, or symptoms of hypertensive encephalopathy (choice of agents: see Stroke)

SBP >220 mm Hg or DBP of 120-140 mm Hg

IV labetalol 10-20 mg over 1-2 min, may be repeated every 10 min (maximum total dose, 300 mg). Enalaprilat 0.625-1.25 mg every 6 h. IV nicardipine 5 mg/h, titrate up to target BP by 2.5 mg/h every 5-15 min (maximum rate, 15 mg/h)

DBP >140 mm Hg

– ICU admission

– IV sodium nitroprusside 0.5 microg/kg/min

a Target BP reduction is 10%-15%. Continuous BP monitoring is necessary. Onset, duration of action, and adverse effects of the drugs: see Table 4 in Essential Hypertension.

BP, blood pressure; DBP, diastolic blood pressure; ICU, intensive care unit; SBP, systolic blood pressure.

Table. Treatment of hypertension in patients with recent intracerebral hemorrhage (examples; other medications could be used [see also: Table 2 in Stroke, Table 3 in Stroke])

BP

Management

BP at presentation <160/90 mm Hg. ICP normal, no history of hypertension. Maintain BP <140/80 mm Hg

IV nicardipine 5 mg/h, titrate up by 2.5 mg/h every 5-15 min (max rate, 15 mg/h)

BP at presentation >160/90 mm Hg or history of hypertension. Maintain BP <160/90 mm Hg

IV nicardipine 5 mg/h, titrate up to target BP by 2.5 mg/h every 5-15 min (max rate, 15 mg/h)

If ICP is elevated, maintain cerebral perfusion pressure

ICU admission with ICP monitoring

BP, blood pressure; ICP, intracranial pressure; ICU, intensive care unit.

Table. Thrombolytic therapy for ischemic stroke: an example of exclusion criteria as used in Hamilton Health Sciences

Exclusion criteria for thrombolytic therapy with tPA for acute stroke order set

Goal: Door-to-needle time: 60 minutes

Absolute exclusion criteria: All answers must be “NO”

Onset of symptoms or the “last seen normal” is >4.5 hours

Yes

No

CT evidence of cerebral hemorrhage

Yes

No

Clinical presentation consistent with subarachnoid hemorrhage even if CT scan normal

Yes

No

Blood pressure >185/110 mm Hg and not treatable

Yes

No

Blood glucose levels <2.7 mmol/L (48.6 mg/dL)

Yes

No

Significant head trauma, brain surgery, or spinal surgery within 3 months

Yes

No

History of intracranial hemorrhage (in previous 6 months)

Yes

No

Recent minor stroke (1 month) or moderate to severe stroke (3 months)

Yes

No

Active internal, gastrointestinal, or urinary bleeding within 21 days

Yes

No

Arterial puncture at a noncompressible site in previous 7 days

Yes

No

Platelet count <100 x 109/L

Yes

No

IV heparin received within 48 hours, resulting in abnormally elevated aPTT >40 seconds

Yes

No

Low-molecular-weight heparin at full anticoagulant levels

Yes

No

Warfarin use with INR >1.7

Yes

No

Novel oral anticoagulants (rivaroxaban, dabigatran, apixaban) taken within previous 24 hours

Yes

No

Relative contraindications: Consider eligibility on an individual basis based on benefits/risks

Rapidly improving neurological signs or NIHSS <4

Yes

No

History of arteriovenous malformation or aneurysm

Yes

No

Profound stroke with obtundation, fixed eye deviation, and complete hemiplegia, or NIHSS >24

Yes

No

Acute cerebral infarct with ASPECT score ≤5

Yes

No

Recent large myocardial infarction or pericarditis within 3 months

Yes

No

Blood glucose levels >22.2 mmol/L (399.6 mg/dL)

Yes

No

Recent major surgery or trauma (cardiac, thoracic, abdominal, orthopedic) within 14 days

Yes

No

History of bleeding diathesis or liver failure

Yes

No

Seizure at onset of stroke with residual postictal neurological deficits

Yes

No

Pregnancy

Yes

No

Age <18 years

Yes

No

Summary eligibility assessment: All answers must be checked

1. The patient meets inclusion criteria: acute ischemic stroke symptom and symptom onset <4.5 hours.

Yes

No

2. The patient does not have any of the absolute exclusion criteria.

Yes

No

3. The patient may have one or more of the relative contraindications, but potential benefits of alteplase exceed potential risks.

Yes

No

Alteplase (rtPA) to be given (YES or NO):

Yes

No

aPTT, activated partial thromboplastin time; ASPECT, Alberta Stroke Program Early CT Score; CT, computed tomography; INR, international normalized ratio; NIHSS, National Institutes of Health Stroke Scale; tPA, tissue plasminogen activator.

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