Hospital Medicine

Ischemic stroke

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Ischemic Stroke

I. What every physician needs to know.

Ischemic stroke manifests as neurologic deficits resulting from reduction in cerebral perfusion below the limits of electrical activity in a focal region of brain. Without resumption of blood flow this can progress inexorably to permanent infarction.

Early evaluation focuses on correct diagnosis of ischemia and identification of patients who are candidates for thrombolytic therapy to resume perfusion. Supportive care during hospitalization focuses on optimal management of blood pressure, glycemic control, and electrolytes. Prevention of secondary injury such as aspiration pneumonia, venous thromboembolism, and catheter related infection is paramount during hospitalization. A diligent search for underlying etiology of the stroke is necessary in order to tailor secondary prevention measures.

Anticoagulation for cardioembolic stroke and antiplatelet therapy for thrombotic stroke along with statin and long term titration to normal blood pressure reduce risk of second stroke. Carotid stenosis offers another target for intervention. Hospitalization offers the chance to complete evaluation of underlying etiology, assess rehabilitation needs, provide patient education, and initiate the therapeutic plan to reduce the chance of second events. Coordinated care during hospitalization, following evidence-based guidelines, effective transitions that promote adherence to therapy after discharge, and appropriate follow-up to titrate to long term goals is critical to improve outcomes.

II. Diagnostic Confirmation: Are you sure your patient has Ischemic Stroke?

At presentation ischemic stroke is a clinical diagnosis. Focal neurologic deficits are the hallmark of ischemic stroke, and the deficits seen will depend on the function of the brain supplied by the occluded vessel. Non-contrast computed tomography (CT) is not sensitive for early stroke, and magnetic resonance imaging (MRI) with diffusion weighted imaging (DWI) may not be available in time to inform hyperacute management decisions such as whether to deliver thrombolysis. Some centers use advanced CT imaging including CT perfusion and CT angiogram (CTa) to aid in decision making on presentation.

Subsequent imaging tests confirm or refute the clinical diagnosis of stroke. Non-contrast CT of the brain will usually be negative in early ischemic stroke or show only blurring of the grey-white junction. In some cases a hyper dense signal in an artery can signal occlusive clot. Acute non-contrast CT is used more to rule out hemorrhage than to rule in ischemia which in itself is essential and adequate to initiate antiplatelet treatment based on the clinical diagnosis of stroke.

Over time CT images will evolve into demonstration of edema and eventual loss of volume in the area of infarction. Advanced CT imaging with contrast can show asymmetric delay in time the contrast takes to reach the area of brain occluded by clot or even a point of occlusion on CTa. Sensitivity is limited, especially for small or posterior circulation strokes due to low spatial resolution and fewer cuts through the brain than conventional CT imaging.

MRI with diffusion weighted imaging is the most sensitive test for acute ischemic stroke although it is not always available or timely on patient presentation. MRI with diffusion weighted images will confirm a diagnosis of stroke when obtained during hospitalization.

After the diagnosis of ischemic stroke has been confirmed, the next step is to establish the most likely etiology of the stroke with implications for optimal secondary prevention regimen. One classification scheme divides ischemic stroke into five categories:

1. Cardioembolic

2. Large vessel atherosclerotic or thrombotic

3. Small vessel occlusion (lacunar infarct)

4. Other (hypercoagulable state, vasculitis, dissection, sickle cell, etc.)

5. Undetermined

A. History Part I: Pattern Recognition:

Weakness and/or sensory loss represent the most common presentation of ischemic stroke. Hemiparesis combined with sensory loss is characteristic of occlusion of the contralateral carotid or middle cerebral artery. Neglect can be seen in lesions on the non-dominant hemisphere (usually the right brain), and aphasia can be seen in dominant hemisphere lesions (usually the left brain) impacting Wernicke’s or Broca’s area.

Posterior cerebral artery infarcts tend to give homonymous hemianopsia, and anterior cerebral artery infarcts often lead to contralateral motor defects at times in combination with abulia (loss of motivation). Lacunar infarcts of the internal capsule may yield isolated sensory or motor weakness often in a distribution larger than would be expected for the volume of infarction due to the high density of motor and sensory fibers passing through this region.

Posterior circulation (basilar and vertebral arteries) infarcts may present with loss of consciousness (almost always with other deficits), ataxia, vertigo, diplopia, loss of coordination, or cranial nerve defects. Retinal artery occlusion leads to amaurosisfugax classically described as a shade lowering over the vision in one eye.

Unlike some of its mimics, the pattern of ischemic stroke is usually rapid development (over minutes) of focal negative neurologic deficits. Headache may be seen, but this is more typical for migraine, hemorrhage, or other space occupying lesion. Positive symptoms such as paresthesias or scotomata, slow development of deficits over hours to days, or generalized weakness suggest alternate etiology.

B. History Part 2: Prevalence:

According to the 2012 Heart Disease and Stroke Statistics, an American suffers a stroke every 40 seconds, and stroke causes one in every 18 deaths in the United States. There are 795,000 strokes each year, of which 185,000 are second events. Seven million Americans have a history of stroke, but the incidence of stroke appears to be declining.

African Americans have increased risk of stroke compared to White and Asian populations in the United States.

Each stroke costs more than $140,000 to care for over a lifetime, and the combination of direct and indirect stroke cost to society is 40.9 billion dollars.

Risk factors for stroke are prevalent including hypertension (present in 1/3 of all adults with less than half adequately controlled), diabetes mellitus (8% of the population), hyperlipidemia (15% of the population), and tobacco abuse (approximately 20% of the population). Other risk factors include advanced age, carotid stenosis, or excessive alcohol use. Cardiac disease including cardiomyopathy, valve disease, or atrial fibrillation increase risk of cardioembolic stroke.

C. History Part 3: Competing diagnoses that can mimic Ischemic Stroke.

Mimics of stroke are legion. As early identification of stroke is of vital importance, stroke centers are willing to accept a degree of false alerts in order to avoid missing true strokes. The most common mimics of stroke include complex migraine, seizure with post-ictal phenomena, systemic infection (delirium), brain tumors, and toxic/metabolic disturbances such as hypoglycemia or hyponatremia.

Other stroke mimics include conversion disorder, vestibular dysfunction, brain hypoperfusion due to cardiac disturbance, syncope, trauma, subdural hematoma, infectious encephalitis, transient global amnesia, dementia/acute confusion, peripheral mono-neuropathy (such as Bells palsy or compression neuropathy), demyelinating disease, spinal cord injury or lesion, parkinsonism, myasthenia gravis, or hypertensive encephalopathy.

Particular vigilance is merited for seizure with post-ictal paresis, complex migraine, and conversion disorder as these diagnoses are most likely to fool the clinician into treating with thrombolytic therapy.

D. Physical Examination Findings.

A rapid but thorough neurologic exam is paramount. The National Institute of Health Stroke Scale (NIHSS) is a method of rapidly assessing the severity of defects and offers a means of organizing the focused stroke neurologic exam.

This assessment scores patients on 11 domains of neurologic function including level of consciousness, gaze palsy, visual field deficits, facial palsy, abnormal motor exam of the arms, abnormal motor exam of the legs, ataxia, sensory deficits, language defects (aphasia), dysarthria, and extinction/inattention.

Free training on how to perform the NIHSS assessment is available at http://learn.heart.org/ihtml/application/student/interface.heart2/nihss.html

The global score on the NIHSS assists in conveying the severity of deficits and also organizing description of the domains of deficit for comparison between examiners.

E. What diagnostic tests should be performed?

On physical exam, focal deficits of motor function, sensation, cranial nerves, coordination, language, or visual field suggest stroke.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Complete blood count (CBC), Basic metabolic panel (BMP), prothrombin time (PT), partial thromblastin time (PTT), international normalized ratio (INR), and blood glucose.

On presentation testing is designed to evaluate for contraindications to thrombolysis (coagulopathy, thrombocytopenia) or severe electrolyte disturbances that could mimic stroke (perturbation of glucose or sodium).

Electrocardiogram (ECG) to establish the presence of atrial fibrillation as an indication for anticoagulation. Follow-up telemetry or Holter monitoring can capture episodic atrial fibrillation.

Fasting lipid panel for evaluation of modifiable risk factors for secondary prevention.

Erythrocyte sedimentation rate (ESR) is indicated in cases where temporal arteritis is suspected (elderly patient, jaw claudication, temporal artery tenderness).

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

All patients with suspected stroke require brain imaging. The choice of initial imaging modality is dictated by speed, availability, and whether the patient presents within the time frame for thrombolytic treatment.

For patients presenting within the thrombolytic window non-contrast brain CT allows hemorrhage to be ruled out rapidly. Non-contrast CT is not sensitive for ischemic stroke although blurring of grey-white junction can be an early sign. Hyper dense signal in a cerebral artery can suggest acute clot. Non-contrast head CT serves primarily to rule out hemorrhagic stroke rather than rule in ischemic stroke.

Advanced CT imaging including CT perfusion studies and CT angiogram may be employed acutely to provide additional information suggesting a region of infarction or target for intra-arterial therapy. Asymmetry in time for contrast to reach the brain suggests ischemic stroke on the side with delay. Preserved blood volume in the area of delay in contrast flow may suggest salvageable brain tissue. Advanced CT imaging studies can provide support for thrombolysis but will miss small or lacunar infarcts due to low special resolution and because CT perfusion is analyzed in selected cuts of brain and does not image all regions of the brain.

MRI with diffusion weighted images is the most sensitive test for acute ischemic stroke and would be appropriate follow-up to initial CT scan. In some centers MRI is the first line imaging modality. Areas of acute ischemia will show up as hyperintensity on diffusion weighted images.

All patients who are reasonable candidates for carotid revascularization should have carotid imaging using ultrasound, CTa, or magnetic resonance angiogram (MRA).

Transcranial Doppler may be ordered as a supplemental test to evaluate posterior circulation stenosis, but this is rarely required.

Echocardiogram is indicated to evaluate for cardioembolic etiology such as left heart thrombus, valve disease, vegetations, or shunt. Yield is highest in patients with suggestion of cardiac disease on physical exam, ECG, and chest radiography.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Carotid imaging is not indicated for patients who would not be candidates for carotid intervention such as those who already know they would not consent to the procedure or patients with limited life expectancy.

A patent foramen ovale is present in a quarter of the healthy population. Bubble studies to evaluate for patent foramen ovale are of limited utility in elderly patients with alternate plausible explanations for stroke.

A hypercoagulability panel should only be ordered on patients with a significant family history of thrombophilia or unexplained stroke in a young patient. Only 1% to 4.8% of strokes are due to hypercoagulable states. This expensive evaluation has limited utility in the general stroke population.

III. Default Management.

1. Rapid assessment of history and physical. Is stroke most likely diagnosis?

2. Establish time last known normal. If within thrombolytic window proceed with evaluation for tPA candidacy.

3. Initial labs (CBC, basic metabolic panel, and coagulation studies) and CT imaging to rule out contraindications to thrombolysis - treat if eligible as soon as possible.

4. Admit and evaluate for likely etiology of stroke (MRI with DWI, echocardiogram, ECG/Telemetry, carotid imaging or MR angiogram). Provide supportive care to maximize perfusion to at risk brain and reduce risk of complications (catheter associated infections, aspiration pneumonia, venous thromboembolism).

5. Identify modifiable targets for secondary prevention (anticoagulation for cardioembolic versus antiplatelet therapy for non-cardioembolic, blood pressure optimization, statin therapy, carotid intervention, smoking cessation, and lifestyle) and begin treatment to achieve secondary prevention goals.

6. Assess and implement plan for rehabilitation of neurologic deficits. Educate patient and family about stroke.

7. Discharge with good communication to next level provider about secondary prevention goals.

A. Immediate management.

Immediate management of ischemic stroke focuses on delivery of thrombolysis within 60 minutes of presentation for patients who meet criteria.

  • Vital signs. Blood pressure must be brought to less than 185/110 millimeters mercury (mmgHG) for thrombolysis.

  • Physical examination using National Institute of Health Stroke Score to quantify stroke deficit severity. Strokes with minimal or rapidly resolving deficits may not merit thrombolytic treatment.

  • Rapid history focusing on time from last known normal, symptoms, allergies, and medical illness or medications that would preclude use of thrombolysis.

  • Laboratory evaluation for stroke mimics or contraindications to thrombolysis.

  • Fingerstick blood glucose, BMP, CBC, PTT, PT/INR.

  • ECG and troponin.

  • Other tests to consider on a case-by-case basis include pregnancy test, arterial blood gas (ABG), Liver function panel, toxicology screen and blood alcohol level.

  • Non-contrast CT of brain to rule out hemorrhage. Some centers will choose more advanced imaging to aid in the thrombolysis decision such as CT perfusion/CTa or go directly to MRI. Regardless of the modality used, the goal time from triage to interpretation of brain imaging is less than 45 minutes.

Contraindications to IV thrombolysis:

  • Minor or rapidly spontaneously clearing symptoms.

  • Patient last known normal more than 4.5 hours before intravenous (IV) recombinant tissue plasminogen activator (rTPA) can be administered (previously 3 hours).

  • Very large strokes have increased risk of hemorrhagic conversion and represent a “caution” for TPA.

  • Intracranial or subarachnoid hemorrhage.

  • Head trauma, prior stroke, or myocardial infarction in the last 3 months.

  • Any history of intracranial bleeding.

  • Gastrointestinal or urinary hemorrhage in the last 3 weeks - Major surgery in the last 2 weeks.

  • Arterial puncture at a noncompressible site in the last week.

  • Blood pressure greater than 185/110 mm Hg by the time thrombolysis administered (medications may be used to achieve target BP goal).

  • Active bleeding or acute fracture.

  • INR>1.7, heparin use with elevated aPTT, or platelet count < 100,000 cells/microliter.

  • Blood glucose < 50 milligrams/deciliter (mg/dl) or seizure at onset (to reduce the chance of treating a stroke mimic).

Based on the information obtained a decision can be made for use of thrombolysis. Options are:

1. IV tPA is recommended by the American Heart Association/American Stroke Association (AHA/ASA) for use up to 4.5 hours from time the patient was last known normal (previously approved to 3 hours but extended to 4.5 hours based on the ECASSIII trial). 0.9 milligrams/kilogram (mg/kg) with 10% given as a bolus over 1 minute then the remainder given over 60 minutes (maximum dose 90 mg).

2. Intraarterial tPA can be used up to 6 hours from time last known normal.

3. Mechanical thrombolysis can be used up to 8 hours from time last known normal.

Some experts recommend consideration of thrombolysis beyond these time thresholds for patients with posterior circulation strokes such as basilar artery occlusion with locked in syndrome.

Regardless of the maximum threshold for treatment, restoration of cerebral blood flow should occur as fast as possible as patients with ischemic stroke have been estimated to irreversibly lose 1.9 million neurons each minute of ongoing ischemia. Time is brain.

For patients who do receive thrombolysis, post-treatment blood pressure should be maintained less than 180/105 mm Hg (approximately one third of thrombolysis patients will require active blood pressure reduction in the first 24 hours to achieve this goal).

In the hyperacute stroke period, blood pressure should be allowed to run high but maintained less than 220/120 mm Hg for patients who did not receive thrombolysis (permissive hypertension).

If blood pressure is being reduced in the hyperacute period, drop should not exceed 10-15% due to worsening of ischemia associated with over correction. Particular care should be attended to avoiding precipitous reduction in blood pressure in patient with critical carotid or intracranial vessel stenosis.

Hyperglycemia worsens brain tissue injury by causing increased tissue acidosis due to anaerobic metabolism in the ischemic tissue. Hence, dextrose in IV fluids is best avoided in the first 24 hours. During hospitalization blood glucose should be ideally maintained below 180 mg/dl, whilst avoiding any hypoglycemia.

Interruption of statin therapy acutely after stroke worsens outcomes, and every effort should be made to obtain early enteral access to avoid this. High intensity statin therapy is recommended for all patients with stroke irrespective of their baseline low density lipoprotein (LDL) level. Only Atorvastatin 40-80 mg and rosuvastatin 20 mg qualify as high intensity therapy.

Hyponatremia worsens cerebral edema and stroke can induce syndrome of inappropriate antidiuretic hormone (SIADH). Based on this, the use of hypotonic fluid in the hyperacute stroke period is discouraged.

Fever is harmful in stroke patients, and aggressive measures to seek out and treat causes of fever and reduce temperature to normal is indicated.

Urinary catheter associated infections are the most common complication after stroke and avoidance or early removal is suggested to reduce this risk.

Aspiration pneumonia is the second most common complication after ischemic stroke. Swallow evaluation, aspiration precautions, good oral hygiene, and vaccinations for pneumonia and influenza can reduce the risk of aspiration pneumonia by half.

Deep venous thrombosis (DVT) is a common complication of stroke with hemiplegia, but with SQ heparin/low molecular weight (LMWH) prophylaxis the rate of symptomatic DVT can be reduced to only about 1%.

Aspirin should be administered in the hyperacute stroke period (immediately if not using thrombolysis or 24 hours after thrombolysis) either orally after the patient has passed the swallow evaluation or via nasogastric (NG) or rectal route.

Early use of therapeutic dose heparin or LMWH does not improve outcomes and is discouraged in the hyperacute stroke period as it increases rate of hemorrhagic conversion to an equal degree that it reduces early second ischemic events. This is true even in stroke of cardioembolic etiology. Whether early therapeutic anticoagulation benefits patients in certain subgroups such as critical carotid stenosis, carotid dissection, or clot visible in the left heart is hotly debated in the absence of adequate randomized trial data for these sub-populations.

B. Physical Examination Tips to Guide Management.

Initial physical exam should focus on the neurologic and cardiopulmonary examination. The examination may be done in two stages: a rapid evaluation on presentation designed to provide adequate information to make the decision on thrombolysis; and a second examination after CT scan of the brain designed to complete the comprehensive physical examination.

Some elements of the exam may suggest alternative explanation for symptoms such as cardiac arrhythmia as an explanation for syncope or dizziness, evidence of tongue lacerations or diffusely tender muscles as a clue to seizure.

Other elements of the exam may offer clues as to the etiology of the seizure including irregular rhythm, jugular venous distension, murmurs, or cutaneous signs of systemic microemboli (splinter hemorrhages, Roth spots, Osler nodes, Janeway lesions) as indication of cardioembolic source of embolism. Carotid bruits are signs of potential large artery embolism. Temporal artery tenderness, bruits, or loss of pulses could be a sign of temporal arteritis.

Finally the physical should be used to detect signs of co-morbid illness that will affect general supportive care (jaundice to indicate hepatic disease, wheezing to suggest pulmonary illness, etc.).

Monitoring neurologic status with emphasis on the areas of initial deficit at least every 4 hours is prudent to detect worsening after admission.

New neurologic deficits or worsening in the early post stroke period can be a sign of new ischemic event, drop in blood pressure causing decreased flow to the ischemic penumbra (the at risk area of brain surrounding the core of infarction), development of cerebral edema, or hemorrhagic conversion. Repeat brain imaging is indicated if new or worsening deficits develop.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

MRI with diffusion weighted images is indicated for stroke patients to define the area of ischemia and provide clues to etiology (multiple infarcts in different vascular territories suggests cardioembolic source).

In addition to ECG, telemetry monitoring should be done during hospitalization to detect paroxysmal atrial fibrillation. 5% of patients with normal sinus rhythm on initial ECG will be found to have atrial fibrillation with subsequent holter/telemetry monitoring.

Carotid imaging (ultrasound, CTA, or MRA) is indicated for patients with ischemic stroke who would be candidates for carotid endarterectomy CEA or carotid stenting.

Echocardiogram is indicated in all patients with suspected cardioembolic etiology or cryptogenic stroke. Inclusion of bubble study to detect right to left shunt through a PFO is appropriate for patients with stroke at a young age or cryptogenic stroke. Transesophageal echocardiography has greater sensitivity, but given increased cost and risk this is usually reserved for young patients with otherwise unexplained stroke.

Fasting lipid panel should be done during hospitalization for baseline record, though all patients will need to be started on high dose statin therapy unless contraindicated.

Hypercoagulability panels are reasonable for patients with cryptogenic stroke or family history of hypercoagulability but are of low yield in changing management for the typical stroke. Antiphosholipid syndrome and hyperhomocysteinemia are the hypercoagulable states most associated with stroke.

ESR is reasonable for patients with suspicion of temporal arteritis.

Most patients do not require electroencephalogram (EEG) or lumbar puncture. These tests can be ordered If diagnosis of stroke versus mimic such as seizures or infectious encephalopathy is uncertain.

D. Long-term management.

Patients with cardioembolic stroke should be treated with anticoagulation. This reduces rates of further strokes by approximately 65%. Warfarin titrated to goal INR 2-3 is most commonly chosen (2.5-3.5 for mechanical heart valves). Combination of warfarin with aspirin is recommended for patients with mechanical heart valves who suffer stroke on warfarin, but routine combination therapy is not recommended for atrial fibrillation.

Dabigatran 150 mg oral (po) twice a day (bid) or Rivaroxaban 20 mg p. daily are alternative agents approved for prevention of stroke in patients with atrial fibrillation. Use of these alternative oral anticoagulants acutely in the post-stroke period has not been studied. For patients with contraindication to anticoagulation, an antiplatelet agent represents a less effective alternative with lower bleeding risk than full anticoagulation. Combination of aspirin and clopidogrel has similar bleeding risk compared to anticoagulation and so is not recommended for patients who are not using anticoagulation due to potential for bleeding.

Patients with non-cardioembolic stroke should be treated with antiplatelet therapy. Aspirin 81 mg p daily, combination aspirin/dipyridamole 25/200 extended release (ER) po bid, or clopidogrel 75 mg po daily are all acceptable first line treatment options. Studies suggest aspirin-extended-release-dipyridamole and clopidogrel are more effective at preventing vascular events than aspirin monotherapy. Aspirin/dipyridamole (Aggrenox®) has a 40% incidence of headache and hence tolerability could be an issue. Previously, high cost was an issue for clopidogrel but now a cheaper generic version is available. Direct comparison between aspirin/dipyridamole and clopidogrel did not reveal difference in efficacy at stroke prevention. Studies like the MATCH trial have shown that in the longterm (beyond 90 days after stroke), combination treatment with aspirin and clopidogrel does not provide any further prevention in recurrent stroke than monotherapy with either alone, but on the other hand significantly increased incidence of life threatening bleeding episodes. Whilst it is clear that there is no role for combination antiplatelet therapy in the long term, more recent studies have supported use of dual antiplatelet therapy in the immediate 1 to 3 months after an ischemic cerebrovascular event. Hence, the current recommendation has been updated to use a combination of aspirin 81 mg and clopidogrel 75 mg for the first 30 days following a transient ischemic attack (TIA) or minor ischemic stroke (NIHSS<4) followed thereafter by monotherapy (preferably clopidogrel or Aggrenox® rather than aspirin).

For ischemic stroke occurring in the territory of a stenotic large “intracranial” artery, the dual antiplatelet therapy with aspirin and clopidogrel is extended to 90 days. Vascular stenting of such a vessel has shown no additional benefit over medical management alone based on the SAMPRISS trial.

Choice of initial agent should be individualized based on patient preference, tolerance to side effects, ability to afford medication, and ease of adherence. A patient with a stroke on aspirin is a reasonable candidate for switch to an alternative antiplatelet agent.

Anticoagulation has been studied and found no more effective and with increased bleeding compared to antiplatelet therapy for non-cardioembolic stroke (including intracranial stenosis). Combination of clopidogrel and aspirin gives increased bleeding risk without further reduction in stroke and is not recommended over monotherapy. No therapy provides 100% risk reduction, so second strokes can occur despite appropriate antithrombotic therapy.

Patients with >50% carotid stenosis on the same side as the infarction are potential candidates for CEA (first line) or carotid stent assuming the operator has acceptable complication rates (<6%), and the occlusion is not already complete. Patients with stenosis of >70% get more benefit than patients with stenosis of 50-69%. Patients with less than 50% stenosis on the symptomatic side or less than 70% stenosis on the asymptomatic side are not appropriate for carotid intervention.

High dose, high potency statin is indicated for all patients with ischemic stroke as described above.

While relative permissive hypertension (upto 220/110 mm Hg) is recommended to preserve perfusion to the ischemic penumbra during the hyperacute stroke period, once this period has passed blood pressure reduction should begin. The goal for hypertension control is to achieve a blood pressure of < 140/90 mm Hg prior to discharge.

Therapy evaluation is necessary to assess need for ongoing rehabilitation during and after hospitalization. In general, patients with stroke have the greatest deficits in the first few days and recovery of some function is common, but hard to predict.

E. Common Pitfalls and Side-Effects of Management.

All antithrombotics increase the risk of bleeding.

Warfarin - multiple drug and dietary interactions. Difficult to maintain reliably in therapeutic range. Requires monitoring at least monthly. Rare complications include warfarin skin necrosis.

Dabigatran - Expensive and dyspepsia can be a common side effect. No reversal agent. Myocardial infarction rates may be higher than with warfarin so may not be good choice for patients with coronary artery disease.

Rivaroxaban - Expensive. No reversal agent. Non-inferior to warfarin but not demonstrated better in terms of stroke rates or overall bleeding complications.

Aspirin - gastrointestinal side effects, particularly ulceration, at higher doses.

Aspirin/dypridamole ER - More expensive than aspirin. Requires twice daily dosing. Headache is a common side effect, seen in up to 40%.

Clopidogrel - More expensive than aspirin. Only good antiplatelet option for patients with aspirin allergy. Thrombotic thrombocytopenic purpura (TTP) is a rare complication.

Statins - Myopathy is a common side effect. Rarely can cause rhabdomyolysis. Hepatotoxicity can be seen in 2-3% of patients on high dose high potency statin after acute vascular event.

A. Renal Insufficiency.

Imaging choices that do not require IV contrast are preferred for the patient with impaired renal function (example would be carotid ultrasound instead of CT angiogram/MRA with gadolinium).

Angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blocker (ARBs) would be first line antihypertensives in this population.

B. Liver Insufficiency.

Increases risk of bleeding with warfarin.

C. Systolic and Diastolic Heart Failure.

ACE inhibitors/ARBs and beta blockers would be preferred first line antihypertensive agents in this population.

D. Coronary Artery Disease or Peripheral Vascular Disease.

Troponin monitoring is reasonable as 16% of patients with stroke will have elevation in troponin and 2-4.5% will trigger acute myocardial infarction.

Clopidogrel is more effective than aspirin for all cause prevention of vascular events in this population.

Beta blocker would be first line antihypertensive agents in this population.

E. Diabetes or other Endocrine issues.

Maintenance of blood glucose less than 200 mg/dl is recommended. Combination of scheduled pre-meal short acting insulin with correction factor based on degree of hyperglycemia is a good option potentially in combination with basal long acting insulin. Oral hypoglycemics are not good choices for the acute post-stroke period as change in neurologic status will necessitate resumption of nothing by mouth (NPO) status. Metformin has no role in the acute stroke period due to risk of lactic acidosis when combined with IV contrast. ACE inhibitors or ARBs would be first line antihypertensive therapy in patients with diabetes.

F. Malignancy.

Interventions such as carotid endarterectomy, which exchange short term increased risk of stroke or myocardial infarction in return for long term reduction in stroke rates, do not have a good tradeoff for patients with limited life expectancy due to cancer.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD).

ABG may be reasonable for patients with active lung disease during initial stroke evaluation as hypercapnea could be confused for stroke symptoms. Chest x-ray (CXR) as part of initial evaluation is indicated for patients with lung disease. Attention to oxygen saturation is important as hypoxia will be detrimental to vulnerable brain tissue in the penumbra.

Beta blockers should be avoided in patients with bronchospasm.

I. Gastrointestinal or Nutrition Issues.

Patients with stroke often have impaired swallow, which increases the risk for aspiration pneumonia. All patients with stroke should be evaluated for swallow function prior to any oral intake including medications. Enteral tube feeding may be needed in the post-stroke period while the degree of swallow function recovery is assessed. Percutaneous endoscopic gastrostomy (PEG) tube is required for patients who do not regain safe swallow but this can be deferred for 1-2 weeks while recovery of safe swallow function is assessed.

J. Hematologic or Coagulation Issues.

Coagulopathy or thrombocytopenia is a contraindication for IV thrombolysis and presents increased risk for bleeding when combined with antithrombotic therapy for stroke secondary prevention.

K. Dementia or Psychiatric Illness/Treatment.

Medications with daily dosing would be preferred in context of psychiatric illnesses that impair adherence.

A. Sign-out considerations While Hospitalized.

Communication of deficits observed such as the NIHSS allows the cross-covering clinician to objectively assess change in neurologic status. Goal blood pressure and interventions to take if patient is not at goal should be communicated or better yet included in the standing orders.

B. Anticipated Length of Stay.

Length of stay for stroke is 5.3 days (last reported in 2007).

C. When is the Patient Ready for Discharge.

A stroke patient is ready for discharge when the evaluation for etiology and institution of secondary prevention measures has been completed, the patient has a stable deficit trajectory, rehabilitation needs are assessed, and patient education has been completed.

1. When should clinic follow up be arranged and with whom.

Stroke patients may follow-up with primary care, with neurology, or both. A follow-up appointment preferably within 2 weeks should be established prior to discharge. The follow-up provider should have clear communication as to the long term goals for secondary prevention to re-enforce adherence and titrate therapy.

  • Anti-thrombotic agent chosen for secondary prevention.

  • Goal for long-term blood pressure - Normotensive is goal for most patients.

  • Goal for long-term lipid control - LDL <70 mg/dl or 50% reduction from pre-treatment levels.

  • Goal for long-term glycemic control - Glycosylated hemoglobin (HbA1c)<7 % is recommended.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

Fasting lipid profile should be completed during hospitalization in addition to the other tests described earlier to evaluate for appropriate secondary prevention measures.

E. Placement Considerations.

During hospitalization a physical therapy/occupational therapy/speech evaluation should assess rehabilitation needs in order to make an informed decision as to the appropriate discharge location (home +/- home therapy, Skilled Nursing Facility, or acute inpatient rehabilitation).

F. Prognosis and Patient Counseling.

Stroke is the leading cause of serious long term disability in the United States. One year after a stroke, 16%-35% of patients will have died. Within 5 years of a first stroke, 6-25% of patients will have suffered a second stroke.

Patients must be counseled on signs and symptoms of stroke and importance of immediate evaluation via emergency medical services (EMS) for new strokes. Emphasize the limited time window for intervention. Patients should understand their personal risk factors for stroke and take responsibility for working with their outpatient clinician in reaching secondary prevention goals for blood pressure and LDL. Patients should understand their discharge medication regimen and be aware of risks and potential side effects. Patients should be counseled on their follow-up plan.

Exercise is associated with decreased risk of stroke and all patients should engage in 30 minutes of moderate-intensity exercise at least 1-3 days each week as able based on their deficits with weight loss being prudent for overweight patients (goal body mass index [BMI] of 18.5 to 24.9 kilogram/meter squared [kg/m2]). Low salt healthy balanced diet should be recommended. Heavy drinkers should moderate alcohol use. Smoking cessation counseling is critical for patients abusing tobacco.

A. Core Indicator Standards and Documentation.

The Joint Commission has quality metrics for ischemic stroke that have been harmonized with the stroke Get-With-The-Guidelines quality measures:

  • Venous thromboembolism prophylaxis within 48 hours of admission

  • Discharged on antithrombotic therapy

  • Anticoagulation therapy for atrial fibrillation/flutter

  • Thrombolytic therapy administered for appropriate candidates

  • Antithrombotic therapy by end of hospital day 2

  • Discharged on a statin medication

  • Swallow evaluation prior to any oral intake including medications (under evaluation as a reportable quality metric)

  • Stroke education complete

  • Smoking cessation counseling (standard for all patients and not stroke specific)

  • Assessed for rehabilitation

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

A mathematical model of optimal adherence over 5 years to secondary prevention measures for non-cardioembolic stroke including high potency antiplatelet agent, high dose statin, aggressive blood pressure control, diet, and exercise suggests 90% risk reduction of second strokes could be possible. Adherence and aggressive titration to achieve these goals is critical.

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