On average, every 40 seconds someone in the USA has a stroke.
Age‐adjusted incidence of first ischemic stroke (per 100 000):
0.88 in whites.
1.49 in Hispanics.
1.91 in blacks.
Prevalence
About 6.6 million Americans >20 years of age have had a stroke, with an overall prevalence of 2.6%.
Global prevalence in 2010 was 33 million stroke survivors.
Pathophysiology
Ischemic infarction:
Uncoupling of metabolic demand for oxygen and glucose which exceeds delivery.
Mitochondrial production of ATP ceases and intracellular ATP stores become depleted rapidly.
The ischemic penumbra (zone of tissue between the infarct core and normal brain) experiences reduced blood flow but preserved cellular metabolism. The penumbra is the target for emergency revascularization.
As tissue infarcts, cells depolarize, leading to a large influx of calcium and sodium (induced by massive glutamate release, with stimulation of NMDA receptors) and an efflux of potassium.
Infarct core cells are destroyed by lipolysis, proteolysis, and disaggregation of microtubules due to metabolic failure.
Water moves into the cells following the influx of ions, and cytotoxic edema forms.
A secondary inflammatory response occurs in response to cell injury and death, further worsening cerebral edema.
Cerebral hemorrhage:
Disruption of tissue with the expanding hematoma.
Direct pressure effects.
Inflammatory response.
Raised ICP.
Hydrocephalus.
Subarachnoid hemorrhage:
Abrupt rise in ICP at time of aneurysm rupture often leads to global hypoperfusion resulting in loss of consciousness, and, in poor grade patients, diffuse brain injury.
Obstructive and/or communicating hydrocephalus may occur, compromising level of consciousness, memory, and cognition (Figure 27.3).
Delayed arterial vasospasm develops in 70% of patients, and can lead to delayed cerebral ischemia in up to 30% of patients.
Cerebral venous sinus thrombosis:
Venous outflow obstruction due to thrombosis of the venous sinuses may lead to venous infarction, ICH, and raised ICP.
Predictive/risk factors
Ischemic stroke/TIA
Hypertension.
Dyslipidemia.
Diabetes mellitus.
Atrial fibrillation.
Diffuse atherosclerotic disease.
Congestive heart failure.
Overweight and obesity.
Physical inactivity.
Obstructive sleep apnea.
Cigarette smoking.
Prothrombotic states.
Acute MI with LV thrombus.
Valvular heart disease.
Migraine.
Oral contraceptive use.
Intracerebral hemorrhage
Hypertension.
Cerebral amyloid angiopathy.
Anticoagulation and other forms of coagulopathy.
Chronic alcohol consumption.
Sympathomimetic drug use.
Fibrinolytic agents.
Vasculitis.
AVM.
Cerebral aneurysm
Formation:
Smoking.
Chronic alcohol consumption.
Female sex.
Hypertension.
Family history of first degree relatives with SAH.
Weak association: Marfan syndrome, neurofibromatosis I, Ehler–Danlos syndrome, fibromuscular displasia.
Rupture:
Large aneurysm size.
History of prior SAH.
Smoking.
Hypertension.
Cocaine and sympathomimetic abuse.
Prevention
Screening
Modifiable risk factor screening: hypertension, diabetes, hyperlipidemia, obesity, smoking, alcohol and drug use, physical inactivity.
Review history for possible sleep‐disordered breathing.
Atrial fibrillation: arterial pulse assessment followed by ECG in patients >65 years of age.
Asymptomatic carotid artery disease: consider carotid duplex scanning or other non‐invasive imaging in patients at high risk.
Non‐invasive screening for unruptured cerebral aneurysms in family members of SAH patients with ≥1 first degree relative with SAH or an intracranial aneurysm.
Healthy diet and physical exercise: 40 minutes a day 3–4 days per week.
Limitation of alcohol consumption: ≤2 drinks/day for men and ≤1drink/day for women.
Carotid artery stenosis (CAS):
Daily aspirin and a statin.
Asymptomatic: consider carotid endarterectomy (CEA) or stent in patient with >70% stenosis if the risk of peri‐operative stroke, MI, and death is low (<3%). CEA or CAS is not recommended in asymptomatic patients >85 years of age.
Symptomatic carotid stenosis: consider CEA or CAS for >70% stenosis in younger patients, while CEA is recommended for patients >70 years of age.
Atrial fibrillation: if the CHA2 DS2‐VASc score is 2 or higher anticoagulation is recommended (distinguish valvular versus non‐valvular AF).
Antiplatelet therapy:
Primary prevention:
Aspirin: daily aspirin 81 mg/day or higher is recommended in patients with high cardiovascular risk (10 year risk >10%).
Cilostazol may be used for the prevention of stroke in people with peripheral artery disease.
Secondary prevention
Short‐term combination therapy with aspirin plus clopidogrel may be considered for 21 days, or up to 6 months post stroke/TIA, then resuming single agent therapy.
Diagnosis
Differential diagnosis of acute ischemic stroke
Differential diagnosis
Features
Seizure
Eyes often look towards the hemiplegia rather than away, symptoms may ‘march’ from one limb to another, focal twitching may be noted, and may be globally impaired
Hypo‐ or hyperglycemia
May mimic stroke, but may have also features of global impairment, diaphoresis, or nausea
Mass/tumor
May mimic stroke; brain imaging required to distinguish
Hypertensive encephalopathy
Often have blurred vision, may be delirious without specific focal findings
Migraine
Symptoms may be associated with headache, and fluctuate. May have also more global impairment
Conversion disorder
Neurologic exam usually has non‐physiologic features
Subdural/epidural hematoma
May mimic acute stroke – CT imaging is required to distinguish this
Other toxic or metabolic encephalopathy
Patient may appear more globally impaired and have tremors or myoclonus, with or without a specific focal deficit
Typical presentation
Ischemic stroke or ICH: acute onset of new focal neurologic symptoms, which may be associated with headache, dizziness, nausea, and vomiting. Blood pressure is often elevated at presentation, and especially so with ICH. Patients with ICH often worsen over minutes to hours as clot expansion occurs.
SAH: sudden severe headache with transient loss of consciousness and nausea/vomiting. Mental status may return to normal, or may stay impaired. Mental status may worsen if hydrocephalus develops.
Clinical diagnosis
History
When was the patient last known to be well or time of onset of symptoms?
What were the initial symptoms and signs?
Review any vascular risk factors including diabetes.
Prior history of seizures.
Medications – anticoagulants and note time of last dose.
Any medical history that might exclude thrombolytic therapy.
Pre‐morbid functional status.
Physical examination
Neurologic exam:
Perform the NIH Stroke Scale (NIHSS).
Evaluate for signs of clinical seizures.
Cardiovascular: evidence of arrhythmia, congestive heart failure, variance in pulses, bruits.
Pulmonary: respiratory distress, neurogenic pulmonary edema, aspiration/inability to protect airway.
Stroke severity scales
The NIH Stroke Scale
Tested Item
Title
Responses and Scores
IA
Level of consciousness
0—Alert 1—Drowsy 2—Obtunded 3—Coma/unresponsive
1B
Orientation questions (2)
0—Answers both correctly 1—Answers 1 correctly 2—Answers neither correctly
1C
Response to commands (2)
0—Performs both tasks correctly 1—Performs 1 task correctly 2—Performs neither
Fingerstick glucose (note that this is the only test required before giving IV tissue plasminogen activator (tPA), unless a bleeding diathesis or liver failure is suspected, or if the patient is on warfarin).
Lumbar puncture – in cases of suspected SAH with negative head CT scan.
List of imaging techniques
Non‐contrast CT head: rule out blood, early infarct signs.
CT angiography head and neck: rapid scan done readily in the ER – evaluate for large vessel occlusion (LVO), ‘spot sign,’ or AVM with ICH, and cerebral aneurysm with SAH.
CT perfusion: rapid scan done readily in the ER – identify potential clot retrieval candidates in the setting of unknown time of onset of ischemic stroke with LVO.
MRI brain: can identify ischemic stroke, hemorrhage, and underlying lesions. In wake‐up stroke patients, identification of a DWI lesion in the absence of a corresponding FLAIR lesion can be used to identify potential candidates for tPA outside of the conventional 3 hour window.
MRA head and neck: consider special sequences for arterial dissection evaluation, and magnetic resonance venogram to evaluate for cerebral venous sinus thrombosis.
(Source: Emergency Neurological Life Support, Neurocritical Care Society)
Potential pitfalls/common errors made regarding diagnosis of disease
Patients with large hemispheric stroke or basilar artery occlusion may present with shaking limbs and altered consciousness, leading to a misdiagnosis of seizure as the primary event.
Atypical stroke symptoms, such as dizziness, difficulty walking without paralysis, a fluent aphasia appearing to the untrained eye as ‘confusion,’ and missed visual field loss or inattention have led to a delay in diagnosis.
Treatment
Treatment rationale
Ischemic stroke:
Restore cerebral blood flow as quickly as possible in patients presenting acutely.
IV thrombolysis in patients presenting up to 4.5 hours from onset. Newer protocols allow for thromboysis for wake‐up strokes that are DWI+ and FLAIR– on MRI.
Intra‐arterial mechanical thrombectomy (Figure 27.4) (LVO identified) up to 6 hours from onset (up to 24 hours for significant penumbra on CT perfusion or for basilar artery occlusion).
Hemorrhagic stroke:
Prevent clot expansion by controlling BP and reversing any coagulation defects.
Control ICP and cerebral edema.
Subarachnoid hemorrhage:
Stabilize the patient regarding airway and BP control, with the goal to avoid re‐rupture of the aneurysm.
Secure the aneurysm early.
Take measures to avoid symptomatic vasospasm once the aneurysm is secured.
When to hospitalize
All patients with TIA (ABCD2 score >3), acute stroke, ICH, or SAH are hospitalized.
TIA patients of low risk may be investigated as an outpatient (ABCD2 score ≤3 without another new indication, e.g. new atrial fibrillation).
Table of specific treatments for stroke
Treatment
Comments
Intravenous thrombolysis
Patient with acute stroke symptoms presenting within 3 hours of onset and with negative CT findings may be treated with IV tPA Patients presenting within 4.5 hours of onset with a negative CT scan and who are also of age <80, have an NIHSS <25, are not diabetic and have a prior history of stroke, and are not on anticoagulation may also be treated with IV tPA
Intra‐arterial clot retrieval or thrombolysis
Patients with suspected ischemic stroke with evidence of an LVO on CT angiography may be treated with IA tPA within 6 hours and IA clot retrieval within 8 hours of symptom onset
Craniotomy for clot evacuation
Patients presenting with posterior fossa ICH of ≥3 cm should undergo posterior fossa decompression and evacuation of the hematoma Patients with superficial lobar ICH with mass effect may benefit from open craniotomy to evacuate the hematoma
Craniotomy/clipping of cerebral aneurysm
Ruptured cerebral aneurysms with a wide neck that are not amenable to endovascular coiling, or of MCA location, should be treated with clipping of the aneurysm
Endovascular coiling of cerebral aneurysm
Ruptured cerebral aneurysms with a narrow neck amenable to coiling, and aneurysms of the posterior fossa should be treated with endovascular coiling
Hypertonic saline or mannitol for control of cerebral edema and elevated ICP
Hyperosmolar therapy, along with other measures such as head elevation, CSF drainage, and sedation
Hemicraniectomy and durotomy for malignant hemispheric infarction or ICH
For cases of refractory malignant brain edema and raised ICP, hemicraniectomy can be considered to prevent brain herniation
Ventriculostomy placement, lumbar drainage, or serial lumbar punctures
Hydrocephalus as a result of ICH or SAH may be managed with continuous or intermittent CSF drainage, depending upon the circumstances and patient
Prevention/management of complications
Aspiration pneumonia: dysphagia screening and aspiration precautions are required.
Deep venous thrombosis: subcutaneous unfractionated or low molecular weight heparin should be initiated within 24 hours of acute stroke.
