27: Stroke


CHAPTER 27
Stroke


Irene R. Boniece


Icahn School of Medicine at Mount Sinai, New York, NY, USA


Background


Disease classification



  • Acute ischemic stroke (AIS):

    • Cerebral infarction caused by occlusion of a cerebral artery, usually by thrombosis.
    • AIS is usually caused by thromboembolism.
    • Bleeding into an infarct is classified into hemorrhagic transformation (HT) and parenchymal hemorrhage (PH) (Table 27.1).

  • Transient ischemic attack (TIA):

    • A transient episode of neurologic dysfunction lasting less than 24 hours caused by temporary focal ischemia.
    • Most TIAs last <30 minutes.

  • Intracerebral hemorrhage (ICH):

    • Spontaneous, non‐traumatic bleeding into the brain parenchyma or ventricular system.
    • Most ICH is caused by chronic hypertension (Figure 27.1).

  • Subarachnoid hemorrhage (SAH):

    • Spontaneous, non‐traumatic bleeding into the subarachnoid space.
    • Most cases of SAH are caused by rupture of an intracranial ‘berry’ aneurysm.

Table 27.1 Classification of hemorrhagic infarction.



















Type Features
Hemorrhagic tranformation (HT) type I Isolated, scattered petechial hemorrhage
HT type II Confluent petechiae of blood throughout the infarct, without a space‐occupying effect.
Parenchymal hemorrhage (PH) type I: Confluent hemorrhage limited to ≤30% of the infarcted area with a mild space‐occupying effect.
PH type II: Confluent hemorrhage of ≥30% of the infarcted area with a significant space‐occupying effect.

Causes and mechanisms of stroke



  • Mechanisms of AIS:

    • Embolism (70%):

      • Cardiac:

        • Atrial fibrillation.
        • Left ventricular thrombus.
        • Atrial septal defect (paradoxical embolism).

          • Aortic atheroma.

      • Artery‐to‐artery embolism.
      • Embolic stroke of unknown source.

    • Large vessel atherosclerosis (10%):

      • Carotid bifurcation.
      • Intracranial stenosis of internal or middle cerebral artery (MCA).

    • Small‐vessel ‘penetrator’ infarction (i.e. lacunar infarction) (10%).
    • Arterial dissection.
    • Systemic hypotension (i.e. ‘watershed’ infarction) (5%).
    • Dural sinus thrombosis (i.e. venous infarction) (3%).
    • Others: non‐inflammatory vasculopathies (e.g. CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), Moyamoya disease), CNS vasculitis, hypercoaguable states, among others (2%).

  • Mechanisms of spontaneous ICH:

    • Hypertension (65%).
    • Amyloid angiopathy (15%).
    • Coagulopathy (15%).
    • Vascular malformation (arteriovenous malformation (AVM), AV fistula, or cavernous hemangioma) (5%).

  • Mechanisms of spontaneous SAH:

    • Cerebral aneurysm (80%).
    • Perimesencephalic non‐aneurysmal SAH (10%).
    • Intracranial dissection (5%).
    • Sympathomimetic drugs, coagulopathy, or idiopathic (5%).

Incidence/prevalence


Incidence



  • Around 795 000 people have a new or recurrent stroke per year, and more than 140 000 people die each year in the USA.
  • Worldwide, 15 million suffer a stroke each year, 5 million die and another 5 million are disabled.
  • Incidence by type:

    • 85% ischemic (Figure 27.2).
    • 10% intracerebral hemorrhage.
    • 5% non‐traumatic subarachnoid hemorrhage.

  • 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.
    • Inherited diseases:

      • Strong association: autosomal dominant polycystic kidney disease.
      • 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.

Primary and secondary prevention



  • Control of risk factors:

    • Hypertension, Diabetes, Hyperlipidemia, Obesity, Smoking cessation.

  • 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
2 Gaze 0—Normal horizontal movements
1—Partial gaze palsy
2—Complete gaze palsy
3 Visual fields 0—No visual field defect
1—Partial hemianopia
2—Complete hemianopia
3—Bilateral hemianopia
4 Facial movement 0—Normal
1—Minor facial weakness
2—Partial facial weakness
3—Complete unilateral palsy
5 Motor function (arm)

  1. a.Left
  2. b.Right
0—No drift
1—Drift before 5 seconds
2—Falls before 10 seconds
3—No effort against gravity
4—No movement
6 Motor function (leg)

  1. a.Left
  2. b.Right
0—No drift
1—Drift before 5 seconds
2—Falls before 5 seconds
3—No effort against gravity
4—No movement
7 Limb ataxia 0—No ataxia
1—Ataxia in 1 limb
2—Ataxia in 2 limbs
8 Sensory 0—No sensory loss
1—Mild sensory loss
2—Severe sensory loss
9 Language 0—Normal
1—Mild aphasia
2—Severe aphasia
3—Mute or global aphasia
10 Articulation 0—Normal
1—Mild dysarthria
2—Severe dysarthria
11 Extinction or inattention 0—Absent
1—Mild (1 sensory modality lost)
2—Severe (2 modalities lost)

The ICH score

This predicts mortality at 30 days:



  • GCS 3–4, 5–12, versus 13–15.
  • Age > or = 80 years.
  • Infratentorial ICH.
  • Volume >30 mL.
  • Presence of intraventricular blood.

SAH disease severity scores


  • Hunt and Hess grade:

    • 1 – no or minimal headache, mild neck stiffness.
    • 2 – moderate–severe headache, neck stiffness, cranial nerve palsy.
    • 3 – drowsy, minimal neurologic deficit.
    • 4 – stupor, moderate–severe hemiparesis.
    • 5 – deep coma, decerebrate.

Laboratory diagnosis


List of diagnostic tests



  • Basic metabolic panel.
  • CBC with platelet count.
  • PT, INR, and PTT.
  • 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.

Diagnostic algorithm (Algorithm 27.1)


Algorithm 27.1 Diagnosis of acute stroke


(Source: Emergency Neurological Life Support, Neurocritical Care Society)

Schematic illustration of the diagnosis of acute stroke.

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.

Management/treatment algorithms (Algorithms 27.227.4)


Algorithm 27.2 Management of acute ischemic stroke


(Source: Emergency Neurological Life Support, Neurocritical Care Society)

Schematic illustration of the management of acute ischemic stroke.

Algorithm 27.3 Management of intracerebral hemorrhage


(Source: Emergency Neurological Life Support, Neurocritical Care Society)

Schematic illustration of the management of intracerebral hemorrhage.

Algorithm 27.4 Management of subarachnoid hemorrhage


(Source: Emergency Neurological Life Support, Neurocritical Care Society)

Schematic illustration of the management of subarachnoid hemorrhage.

Special populations


Pregnancy


Intravenous thrombolysis with alteplase (tPA) – category C. Alteplase is only recommended for use during pregnancy when benefit outweighs risk.


Elderly


Age >80 years is a contraindication to treating acute stroke within 3–4.5 hours from onset of symptoms with IV tPA.


Prognosis


Nov 20, 2022 | Posted by in ANESTHESIA | Comments Off on 27: Stroke
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