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Stroke, Acute
Scott A. Drummond Jr., DO, DABR
image BASICS
A cerebrovascular accident (CVA) is an infarction or hemorrhage in the brain.
DESCRIPTION
Stroke is the sudden onset of a focal neurologic deficit(s) resulting from either infarction or hemorrhage within the brain.
  • Two broad categories: ischemic (thrombotic or embolic; 87%) and hemorrhagic (13%)
  • Hemorrhage can be intracerebral or subarachnoid.
  • System(s) affected: neurologic; vascular
  • Synonym(s): CVA; cerebral infarct; brain attack
  • Related terms: transient ischemic attack (TIA), a transient episode of neurologic dysfunction due to focal ischemia without permanent infarction on imaging (see topic “Transient Ischemic Attack [TIA]”)
Pediatric Considerations
  • Cardiac abnormalities (congenital heart disease, paradoxical embolism, rheumatic fever, bacterial endocarditis)
  • Metabolic: homocystinuria, Fabry disease
EPIDEMIOLOGY
Incidence
Annual incidence in the United States is ˜795,000.
Prevalence
  • Prevalence in the United States: 550/100,000
  • Predominant age: Risk increases >45 years of age and is highest during the 7th and 8th decades.
  • Predominant sex: male > female at younger age, but higher incidence in women with age ≥75 years
ETIOLOGY AND PATHOPHYSIOLOGY
  • 87% of stroke is ischemic, three main subtypes for etiology: thrombosis, embolism, and systemic hypoperfusion. Large vessel atherothrombotic strokes are commonly related to the origin of the internal carotid artery. Small vessel lacunar strokes are commonly due to lipohyalinotic occlusion. Embolic strokes are largely from a cardiac source (due to left atrial thrombus, atrial fibrillation, recent MI, valve disease, or mechanical valves) or ascending aortic atheromatous disease (>4 mm).
  • 13% of stroke is hemorrhagic; most commonly due to HTN. Other causes include intracranial vascular malformations (cavernous angiomas, AVMs), cerebral amyloid angiopathy (lobar hemorrhages in elderly), and anticoagulation.
  • Other causes include fibromuscular dysplasia (rare), vasculitis, or drug use (cocaine, amphetamines).
Genetics
Stroke is a polygenic multifactorial disease, with some clustering within families.
RISK FACTORS
  • Uncontrollable: age, gender, race, family history/genetics, prior stroke or TIA
  • Controllable/modifiable/treatable
    • Metabolic: diabetes, dyslipidemia
    • Lifestyle: smoking, cocaine use, amphetamine use
    • Cardiovascular: hypertension, atrial fibrillation, valvular heart disease, endocarditis, recent MI, severe carotid artery stenosis, hypercoagulable states, and patent foramen ovale
GENERAL PREVENTION
Smoking cessation, regular exercise, weight control to maintain nonobese BMI and prevent type 2 diabetes, use alcohol in moderation, control BP, and manage hyperlipidemia; use of antiplatelet agent, such as aspirin, in high-risk persons; treatment of nonvalvular atrial fibrillation with dose-adjusted warfarin or dabigatran, apixaban, and rivaroxaban
COMMONLY ASSOCIATED CONDITIONS
Coronary artery disease is the major cause of death during the first 5 years after a stroke.
image DIAGNOSIS
PHYSICAL EXAM
  • Assess airway, breathing, and circulation (ABC).
  • Anterior (carotid) circulation: hemiparesis/hemiplegia, neglect, aphasia, visual field defects
  • Posterior (vertebrobasilar) circulation: diplopia, vertigo, gait and limb ataxia, facial paresis, Horner syndrome, dysphagia, dysarthria, alternating sensory loss
DIFFERENTIAL DIAGNOSIS
  • Migraine (complicated)
  • Postictal state (Todd paralysis)
  • Systemic infection, including meningitis or encephalitis (infection also may uncover or enhance previous deficits)
  • Toxic or metabolic disturbance (hypoglycemia, acute renal failure, liver failure, drug intoxication)
  • Brain tumor, primary or metastases
  • Head trauma, encephalopathy
  • Other types of intracranial hemorrhage (epidural, subdural, subarachnoid)
  • Trauma, septic emboli
DIAGNOSTIC TESTS & INTERPRETATION
Primarily used to narrow differential and identify etiology of stroke
Initial Tests (lab, imaging)
  • Serum glucose level, including fingerstick testing (REQUIRED to exclude hypo- and hyperglycemia) (1)[B]
  • ECG
  • CBC, including platelets
  • Electrolytes, including BUN and creatinine
  • Coagulation studies: PT, PTT, INR
  • Markers of cardiac ischemia
  • Emergent brain imaging with noncontrast CT (or brain MRI with diffusion weighted [DW-MRI]) to exclude hemorrhage can be lifesaving (1)[A].
  • Subsequent multimodal CT (perfusion CT, CTA, unenhanced CT) or MRI to improve diagnosis of acute ischemic stroke
Follow-Up Tests & Special Considerations
Consider LFT, tox screen, blood alcohol, ABG, lumbar puncture if suspected subarachnoid hemorrhage (SAH), EEG if suspect seizures, blood type and cross.
  • DW-MRI is more sensitive than CT for acute ischemic stroke; however, MRI also is better than CT for diagnosis of posterior fossa lesions (2)[B].
  • Emergent treatment (IV thrombolysis) should NOT be delayed to obtain advanced imaging studies.
  • Follow-up imaging of carotid vessels with Doppler ultrasound, CTA, or MRA of head and neck should be completed.
Diagnostic Procedures/Other
Echocardiogram (transthoracic and/or transesophageal) in patients with increased suspicion for cardioembolic source. In cryptogenic stroke patients, prolonged ECG monitoring should be performed with a 30-day event monitor.
Test Interpretation
Early CT findings: hyperdense MCA sign (increased attenuation of proximal portion of the MCA; is associated with thrombosis of MCA), loss of graywhite matter differentiation, sulcal effacement, loss of insular ribbon
image TREATMENT
  • BP closely monitored in the first 24 hours (1)[A]
    • Antihypertensives should be withheld unless systolic BP >220 mm Hg or diastolic BP >120 mm Hg, with a goal to lower BP by ˜15% during first 24 hours if treatment is indicated. If thrombolytic therapy is to be initiated, BP must be <185/110 mm Hg prior to thrombolytics.
    • In acute spontaneous intracranial hemorrhagic stroke, goal for BP control is 160/90 mm Hg or target MAP 110 (see topic, “Subarachnoid Hemorrhage” for details on BP management). With suspicion for elevated ICP, BP should be reduced with goal to keep cerebral perfusion pressure between 61 mm Hg and 80 mm Hg.
    • Antihypertensive medications should be restarted 24 hours after stroke onset for patients with a history of hypertension who are neurologically stable.
  • Exclusion criteria for thrombolysis within 3 hours of onset include:
    • Symptoms suggestive of SAH
    • Head trauma or prior stroke within 3 months
    • MI within 3 months
    • GI or gastric ulcer hemorrhage within 21 days
    • Major surgery within 14 days
    • Arterial puncture at noncompressible site within 7 days
    • Any history of intracranial hemorrhage
    • Elevated BP (systolic >185 mm Hg and diastolic >110 mm Hg)
    • Active bleeding or acute trauma on examination
    • Taking anticoagulant and INR ≥1.7
    • Activated PTT not in normal range if heparin received during previous 48 hours; platelet count <100,000 mm3
    • Blood glucose concentration <50 mg/dL
    • Seizure with postictal residual neurologic impairment
    • Multilobar infarction on CT (hypodensity >1/3 cerebral hemisphere)
    • Patient or family members not able to weigh and understand potential risks and benefits of treatment
  • P.995

  • Extended exclusion criteria for thrombolysis within 4.5 hours include per AHA/ASA guidelines:
    • Age >80 years
    • All patients taking oral anticoagulants regardless of INR
    • National Institute of Health (NIH) Stroke Scale >25
    • History of stroke and diabetes
  • Antiplatelet agents: Oral aspirin (initial dose, 325 mg) should be started within 24 to 48 hours (1)[A].
MEDICATION
First Line
  • BP management (parameters under “Treatment”) options include:
    • Labetalol 10 to 20 mg IV over 1 to 2 minutes, which may be repeated once
    • Nicardipine infusion 5 mg/hr, titrate up by 2.5 mg/hr at 5- to 15-minute intervals to maximum of 15 mg/hr; reduce to 3 mg/hr when target BP is reached
  • Thrombolysis, IV administration of rtPA: Infuse 0.9 mg/kg, maximum dose 90 mg over 60 minutes with 10% of dose given as bolus over 1 minute.
    • Admit to ICU or stroke unit, with neurologic exams every 15 minutes during infusion, every 60 minutes for next 6 hours, then hourly until 24 hours after treatment.
    • Discontinue infusion and obtain emergent CT scan if severe headache, angioedema, acute hypertension, or nausea and vomiting develop.
    • Measure BP every 15 minutes for first 2 hours, every 30 minutes for next 6 hours, then every hour until 24 hours after treatment. Maintain BP < 185/105. Follow-up CT at 24 hours before starting anticoagulants or antiplatelet agents.
  • Antiplatelet: aspirin 325 mg/day within 48 hours, or 24 to 48 hours after thrombolytic therapy (1)[A]
Second Line
Carotid endarterectomy (CEA) for carotid artery stenosis rarely is indicated emergently. CEA is indicated for stenosis >70% ipsilateral to TIA or incomplete stroke lesion and may be indicated for 50-69% stenosis in carefully selected patients, depending on risk factors.
ISSUES FOR REFERRAL
Follow-up with neurologist 1 week after discharge, with subsequent follow-up based on individual circumstances
ADDITIONAL THERAPIES
  • Prophylactic antibiotics are not recommended.
  • Deep vein thrombosis (DVT) prophylaxis should be instituted for immobilized patients.
  • Corticosteroids are not recommended for cerebral brain edema.
  • Statin use should be continued without interruption following acute stroke (1)[B].
  • At discharge, patient should be referred for physical therapy, occupational therapy, and speech therapy, as necessary.
SURGERY/OTHER PROCEDURES
  • Ventricular drain may be placed for patients with acute hydrocephalus secondary to stroke (most commonly due to cerebellar stroke).
  • Decompressive surgery is recommended for major cerebellar infarction; it should be considered for malignant middle cerebral artery infarction, especially if the patient is <60 years of age.
  • Consider mechanical embolus removal with a cerebral infarction device in carefully selected patients, with evidence of potentially salvageable tissue on advanced imaging.
COMPLEMENTARY & ALTERNATIVE MEDICINE
Acupuncture starting within 30 days from stroke onset may improve neurologic functioning.
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
  • Observe closely within first 24 hours for neurologic decline, particularly due to cerebral edema.
  • Keep head of bed at least 30 degrees when elevated ICP is suspected. Patients with ischemic stroke may benefit from a horizontal bed position during the acute phase.
  • Monitor cardiac rhythm for at least first 24 hours to identify any arrhythmias.
  • Airway support and ventilatory assistance may be necessary due to diminished consciousness or bulbar involvement; supplemental oxygen should be reserved for hypoxic patients. Consider elective intubation for patients with malignant edema.
  • Correct hypovolemia with normal saline.
  • All patients should be kept NPO until a formal swallow evaluation has been performed; to reduce risk of aspiration pneumonia, maintain elevated head of bed to 30 degrees.
  • Hypoglycemia can cause neurologic dysfunction; rapidly correct during initial evaluation.
  • Hyperglycemia within first 24 hours after stroke is associated with poor functional outcomes and AHA/ASA guidelines: insulin treatment for patients with glucose levels >140 to 180 mg/dL (1)[C].
  • In patients with ICH secondary to anticoagulant use, correction of an elevated INR is necessary with use of IV vitamin K and fresh frozen plasma or prothrombin concentrate complex. Factor VII infusion should be used in patients needing urgent surgical intervention (i.e., those with cerebellar hemorrhage who are neurologically deteriorating).
  • DVT prophylaxis (1)[B]
  • Maintain oxygen saturation >94% (1)[C].
  • Early use of physical therapy and discharge planning for rehabilitation need and placement
IV Fluids
IV hydration with maintenance amounts of normal saline until swallowing status is assessed; monitor fluid balance closely.
Nursing
  • Regular neurologic exams more frequent in first 24 hours (every 1 to 2 hours)
  • Fall precautions; frequent repositioning to prevent skin breakdown
Discharge Criteria
Medically stable, adequate nutritional support, neurologic status stable or improving
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
  • Secondary prevention of stroke with aggressive management of risk factors
  • Platelet inhibition using aspirin, clopidogrel, or aspirin plus extended-release dipyridamole (Aggrenox) based on physician and patient preference
Patient Monitoring
Follow-up every 3 months for 1st year, then annually.
DIET
Patients with impaired swallowing should receive nasogastric or percutaneous endoscopic gastrostomy feedings to maintain nutrition and hydration.
PATIENT EDUCATION
National Stroke Association (800-STROKES or http://www.stroke.org)
PROGNOSIS
Variable, depends on subtype and severity of stroke; NIH stroke scale may be used for prognosis.
REFERENCES
1. Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013;44(3): 870-947.
2. Chalela JA, Kidwell CS, Nentwich LM, et al. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007;369(9558):293-298.
Additional Reading
&NA;
Yew KS, Cheng EM. Diagnosis of acute stroke. Am Fam Physician. 2015;91(8):528-536.
Codes
&NA;
ICD10
  • I63.9 Cerebral infarction, unspecified
  • I61.9 Nontraumatic intracerebral hemorrhage, unspecified
  • I63.50 Cereb infrc due to unsp occls or stenos of unsp cereb artery
Clinical Pearls
&NA;
  • Unless stroke is hemorrhagic or patient is undergoing thrombolysis, BP should not be lowered acutely to maintain perfusion of penumbra region.
  • IV thrombolysis should be considered in eligible patients with neurologic deficits that do not clear spontaneously within 3 to 4.5 hours of symptom onset.
  • DW-MRI is more sensitive than conventional CT for acute ischemic stroke. MRI is also better than CT for diagnosis of posterior fossa lesions.