Stroke is the leading cause of disability and fourth greatest cause of death in the United States. Of the 800,000 annual strokes in the United States, 85% are acute ischemic strokes (AIS). The remaining 15% are intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH). Intensive care issues pertinent to the care of AIS include the recognition and diagnosis of stroke, the provision of fibrinolytics and/or endovascular management, as well the medical management in the 24 hours posttreatment, management of cerebellar or large hemispheric infarcts (LHIs), and considerations in the management of a critical stenosis of a cervical arterial vessel.
History and Physical Examination
AIS is the result of a sudden loss of blood flow within a vascular region of the brain, retina, or spinal cord due to arterial vessel occlusion. The flow is most often compromised by the development of an atherosclerotic clot (ie, thrombosis) or sudden occlusion by a clot from a distant source (ie, embolism). The contemporary definition includes imaging findings of an acute infarction, even if clinical symptoms are not observed. Clinical symptoms of stroke are highly heterogeneous and variable (Table 48B–1) and are objectively scored using the National Institutes of Health Stroke Scale (NIHSS) (Table 48B–2). Presentations associated with a delay in stroke diagnosis included mild symptoms (NIHSS < 4), severe symptoms (NIHSS > 25), strokes affecting multiple vascular territories, isolated aphasia, posterior circulation symptoms, and young age. Symptoms typically begin suddenly, but a stuttering presentation can be seen in the setting of a partially occluded large vessel. The patient's last known well time (LKWT, ie, when they did not have any stroke symptoms) must be aggressively, thoroughly, and creatively sought (eg, using last social media interaction).
Table 48B–1Common signs and symptoms of acute ischemic stroke. ||Download (.pdf) Table 48B–1 Common signs and symptoms of acute ischemic stroke.
Hemiparesis, monoparesis, or (rarely) quadriparesis (in brainstem stroke)
Monocular or binocular visual loss
Visual field deficits
Vertigo (rarely in isolation)
Sudden decrease in the level of consciousness
Table 48B–2National institutes of health stroke scale (NIHSS). ||Download (.pdf) Table 48B–2 National institutes of health stroke scale (NIHSS).
|Item ||Category ||Description ||Score Range |
|1a ||Level of consciousness (LOC) ||Alert, drowsy, stuporous, coma ||0-3 |
|1b ||LOC questions (month, age) ||Answers both, one, or none correctly ||0-2 |
|1c ||LOC commands (open and close eyes, grip and release hand) ||Obeys both, one, or none ||0-2 |
|2 ||Best gaze ||Normal, partial palsy, forced deviation ||0-2 |
|3 ||Best visual (visual fields) ||Normal, partial hemianopia, complete hemianopia, bilateral hemianopia ||0-3 |
|4 ||Facial palsy ||Normal, minor, partial, complete ||0-3 |
|5a ||Motor arm, left ||No drift, drift, some effort against gravity, no effort against gravity, no movement ||0-4 |
|5b ||Motor arm, right ||No drift, drift, some effort against gravity, no effort against gravity, no movement ||0-4 |
|6a ||Motor leg, left ||No drift, drift, some effort against gravity, no effort against gravity, no movement ||0-4 |
|6b ||Motor leg, right ||No drift, drift, some effort against gravity, no effort against gravity, no movement ||0-4 |
|7 ||Limb ataxia ||None, present in one limb, present in both ||0-2 |
|8 ||Sensory ||Normal, mild to moderate loss, severe to complete loss ||0-2 |
|9 ||Best language ||No aphasia, mild to moderate aphasia, severe aphasia, mute with global aphasia ||0-3 |
|10 ||Dysarthria ||Normal, mild to moderate dysarthria, severe dysarthria ||0-2 |
|11 ||Extinction and inattention ||No neglect, partial, complete ||0-2 |
| ||Total ||n/a ||0-42 |
The physical examination is focused on cataloging a very accurate NIHSS, exploring for etiologies of stroke mimics, and findings suggestive of contraindications to intravenous (IV) thrombolysis (eg, scar from recent surgery).
The ideal diagnostic approach utilizes lean processing, with a prioritization of diagnostics that are critical for the decision to offer thrombolysis with IV recombinant tissue plasminogen activator (IV-rtPA) (see treatment, later). A list of comprehensive diagnostics is found in Table 48B–3. Critical immediate diagnostics are a blood glucose and noncontrast head computed tomography (NCHCT) to rule out hypoglycemia and an intracranial hemorrhage, respectively. The remaining diagnostics should be immediately obtained, but stroke specialists will not uncommonly make decisions to offer IV-rtPA based on patient-related factors, rather than waiting for the results. This is to hasten the provision of thrombolysis, as a 15-minute delay in treatment is associated with worsened outcomes, even if within 3 hours of symptom onset and within an hour of hospital presentation.
Table 48B–3Acute ischemic stroke diagnostics. ||Download (.pdf) Table 48B–3 Acute ischemic stroke diagnostics.
|On Presentation ||During Admission |
| || |
Transthoracic echocardiography (TTE) with bubble study
Cervical and intracranial vessel imaging (MRA, CTA, DSA, or Carotid Dopplersb)
LE Dopplers/CT pulmonary Angiographyd
Rheumatologic work upe
The timing of CT angiography (CTA) of the head and neck, CT perfusion, and/or magnetic resonance imaging (MRI) is dependent on local protocols and patient specific conditions. The acquisition of these images should never delay the administration of thrombolysis. A diagnosis of AIS is most commonly confirmed using MRI through interpretation of the diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) sequences. An acute stroke (< 7 days) has occurred when a specific region of the brain is bright (hyperintense) on DWI and dark on ADC. Magnetic resonance angiography (MRA) is also able to characterize the cerebral and cervical vasculatures.
Acute treatment of AIS consists of restoring blood flow to the compromised neuronal tissue. The first step is to determine eligibility for thrombolysis with IV-rtPA, which should be administered as soon as possible to all patients that meet inclusion/exclusion criteria (Table 48B–4) at a dose of 0.9 mg/kg, maximum dose 90 mg, with 10% bolused over 1 minute, and the remainder dripped over 1 hour. If possible, consent should be obtained, although if the patient is unable to consent and a legal representative is not available, IV-rtPA should be administered, as the benefits outweigh the risks of treatment and the degree of benefit is time-dependent. If a stroke mimic (ie, neurologic change concerned for AIS) is suspected, but cannot be definitely determined, and no contraindications exist, IV-rtPA administration should not be delayed.
Table 48B–4Inclusion/exclusion criteria for intravenous recombinant tissue plasminogen activator in acute ischemic stroke. ||Download (.pdf) Table 48B–4 Inclusion/exclusion criteria for intravenous recombinant tissue plasminogen activator in acute ischemic stroke.
|Inclusion Criteria |
Diagnosis of ischemic stroke causing measurable neurologic deficit
Neurologic signs not clearing spontaneously to baseline
Neurologic signs not minor and isolateda
Symptom onset less than 4.5 hours from initiation of IV rtPA (see below additional exclusion criteria for the 3.0-4.5 hour window)
|Exclusion Criteria |
History and physical
Symptoms suggest subarachnoid hemorrhage
Significant head trauma or prior stroke in the previous 3 months
Arterial puncture at noncompressible site in previous 7 days
History of previous intracranial hemorrhage
Intracranial neoplasm, AVM, or aneurysm
Recent intracranial or intraspinal surgery
Elevated blood pressure (systolic >185 mm Hg or diastolic >110 mm Hg)
Active internal bleeding
Stroke suspected to resulting from a septic embolus (eg, infective endocarditisa)
Platelet count less than 100,000/μL
Heparin received within 48 hours with aPTT above the upper limit of normal
Current use of Vitamin K Antagonist with INR >1.7 or PT >15 s
Current use of direct thrombin inhibitors or direct factor Xa inhibitors with elevated sensitive laboratory tests (eg, aPTT, INR, platelet count, ECT, TT, or appropriate factor Xa activity assays)
Blood glucose concentration less than 50 mg/dL (2.7 mmol/L)
Head CT demonstrates multilobar infarction (hypodensity >1/3 cerebral hemisphere)
|Relative Exclusion Criteria |
Minor or rapidly improving stroke symptoms
Seizure at onset with postictal residual neurological impairments
Major surgery or serious trauma within previous 14 days
Gastrointestinal or urinary tract hemorrhage within previous 21 days
Acute myocardial infarction within previous 3 months
|Exclusion Criteria for the 3 to 4.5 hour Time Window |
More than 80 years of age
Use of oral anticoagulants, regardless of the INR
Baseline NIHSS score of more than 25
History of stroke and diabetes
AIS secondary to large vessel occlusions (LVOs), particularly those with large clots (> 8 mm), respond poorly to IV-rtPA alone. Recent randomized controlled trials (RCTs) have concluded that endovascular treatment (EVT) of AIS improves outcomes in those with anterior circulation LVOs (ie, internal carotid artery [ICA] terminus and middle cerebral artery [MCA] M1). Identification and selection of candidates for this therapy can involve clinical assessment, CTA, or MRA. The administration of IV-rtPA should never be delayed for the acquisition of angiography. Based on these new data, American Heart Association/American Stroke Association (AHA/ASA) AIS guidelines now make the class 1 recommendation that EVT should be provided to AIS patients with an ICA or M1 occlusion who are more than 17 years of age, receiving IV-rtPA and have a prestoke modified Rankin Score (mRS) of 0 to 1 (see Table 48B–5), NIHSS greater than 5 (Table 48B–2), and Alberta stroke program early CT score (ASPECTS) greater than 5 (see Table 48B–6), and who can have EVT initiated (ie, groin puncture) within 6 hours of their LKWT. Patients should never be observed for a response to IV-rtPA who meet the indications for EVT. As with IV-rtPA, time to endovascular recanalization has been shown to be a predictor of outcomes.
Table 48B–5Modified rankin scale. ||Download (.pdf) Table 48B–5 Modified rankin scale.
|Score ||Clinical Symptoms |
|0 ||No symptoms at all |
|1 ||No significant disability despite symptoms; able to carry out all usual duties and activities |
|2 ||Slight disability; unable to carry out all previous activities, but able to look after own affairs without assistance |
|3 ||Moderate disability; requiring some help, but able to walk without assistance |
|4 ||Moderately severe disability; unable to walk without assistance and unable to attend to own bodily needs without assistance |
|5 ||Severe disability; bedridden, incontinent, and requiring constant nursing care and attention |
|6 ||Dead |
Table 48B–6Alberta stroke program early CT score (ASPECTS). ||Download (.pdf) Table 48B–6 Alberta stroke program early CT score (ASPECTS).
|Region ||Anatomic Location ||Head CT Level |
|C ||Caudate head || |
|LN ||Lentiform nuclear or putamen || |
|IC ||Posterior limb of internal capsule || |
|I ||Insular cortex ||Third ventricle |
|M1 ||Frontal operculum (anterior MCA territory) || |
|M2 ||Anterior temporal lobe (lateral to insula) || |
|M3 ||Posterior temporal lobe || |
|M4 ||Anterior MCA, superior to M1 || |
|M5 ||Lateral MCA, superior to M2 ||Lateral ventricles, superior to third ventricle |
|M6 ||Posterior MCA, superior to M3 || |
Of note, the first 3 endovascular trials did not find a benefit, which has been attributed to the poor recanalization rates with the early generation devices. The 5 most recent RCTs, all of which were positive, used newer generation stent retrievers that achieve a much higher rate of vessel recanalization. Although the strongest recommendations were made for those with a mRS of 0 to 1, NIHSS of greater than 5, and ASPECTS of greater than 5, those that fail to meet these criteria should not be interpreted as having an absolute contraindication to EVT. Rather, a class IIb recommendation was issued that it may be reasonable to acutely revascularize some patients with a M1 or ICA occlusion within 6 hours of LKWT, who do not meet all of the ASPECTS, NIHSS, and mRS criteria. More distal MCA (M2, M3), anterior cerebral artery (ACA), basilar artery, and posterior cerebral artery (PCA) occlusions can also be considered for EVT, but the degree of benefit is less certain, as they were either less prevalent or not included in the recent RCTs. Lastly, patients with contraindications to IV-rtPA, but within the 6-hour time window, can be considered for acute EVT (eg, international normalized ratio [INR] > 1.7).
During and after the administration of reperfusion therapy (IV-rtPA or endovascular) the patient requires frequent reassessment, with careful attention to their neurologic status and blood pressure (BP). BP parameters must be vigilantly maintained (< 180/105). All antiplatelet (AP) and anticoagulant (AC) medications are held for at least the first 24 hours. Aspirin, which has been shown to reduce stroke reoccurrence and mortality, should be provided 24 hours after IV-rtPA or EVT if the patient is neurologically stable and neuroimaging does not demonstrate hemorrhagic conversion of the infarct. In some circumstances, BP targets maybe more strict after EVT with full revascularization (thrombolysis in cerebral infarction 3 or 2b flow).
BP targets in patients not receiving IV-rtPA are less clear. Current guidelines support gentle BP reduction if the systolic BP (SBP) greater than 220 mm Hg or the diastolic BP is greater than 120 mm Hg. If performed, a modest goal should be set, so as to avoid expanding the infarct by hypoperfusing penumbral tissue, particularly in those with untreated LVOs.
Large Hemispheric Infarction
AIS secondary to the occlusion of a cervical or large proximal intracranial vessel, such as the carotid terminus (ICA-t) or MCA, is termed LHI. Although LHIs only account for 10% of all AIS, their mortality rate is 15% to 80% and the majority of survivors have significant disability. Clinical manifestations include hemiparesis, homonymous hemianopsia, ipsilateral gaze deviation, aphasia (usually with left LHIs), and agnosia and left-sided neglect (with right LHIs).
The large area of infarcted brain tissue produces substantial clinical defects at ictus. Over the following 24 to 96 hours (and less commonly up to 10 days) cytotoxic edema (CE) develops, causing the tissue to enlarge, which then compresses, distorts, and herniates neighboring uninfarcted tissues. Unaffected cerebral vessels can be pinched or kinked by the herniating infarcted brain, expanding the territory of infarction.
The first clinical sign of cerebral edema is a decline in the level of arousal. This is followed by ipsilateral or contralateral leg weakness (due to compression of the anterior cerebral artery in the setting of subfalcine herniation). Alternatively or later, findings of uncal herniation (see Chapter 48A—Principles of Neurosciences Critical Care) are seen, during which time the PCA may be compressed expanding the area of infarction. The lateral forces may also compress the third ventricle, producing an obstructive hydrocephalus and its associated symptoms.
The management of LHI includes therapies aimed to minimize the development of CE and identifying candidates for decompressive hemicraniectomy (DC). Strategies that mitigate CE include keeping the head of bed elevated to 30° and the neck in a neutral position, avoiding hypervolemia, and maintaining normothermia, normonatremia, normoglycemia, and normocarbia. The infusion of dextrose containing and hypoosmotic solutions must not occur.
Empiric administration of hyperosmotic solutions is not an uncommon practice, but evidence is lacking to support its efficacy. Aggressively maintaining the serum blood glucose below 125 mg/dL may lead to an increase in infarct size, so a goal of 140 to 180 mg/dL is recommended. Seizure prophylaxis is not indicated, but continuous video electroencephalogram (cvEEG) monitoring can be considered, particularly in patients with fluctuations in mental status. Corticosteroids do not have a proven role in the management of LHI. Dual AP therapy and therapeutic anticoagulation should be held, but subcutaneous heparin or low-molecular-weight heparin should be used for venous thromboembolism (VTE) prophylaxis.
Unfortunately, the available evidence is not able to fully predict which patient is going to have cerebral edema. Intracranial pressure (ICP) monitoring is of limited utility and is not typically performed. Instead the neurologic examination is performed at frequent, regular intervals. Older patients have some degree of cerebral atrophy; therefore they are less likely to deteriorate even if cerebral edema occurs, while the opposite holds true for the younger patient. Risk factors for cerebral edema and subsequent neurologic deterioration include female gender, nausea and vomiting on presentation, congestive heart failure, history of hypertension, leukocytosis, and initial NIHSS greater than 20 in dominant LHI or greater than 15 in nondominant LHI. Neuroimaging findings suggesting increased risk are summarized in Table 48B–7.
Table 48B–7Neuroimaging findings associated with an increased risk of neurologic deterioration in large hemispheric infarction. ||Download (.pdf) Table 48B–7 Neuroimaging findings associated with an increased risk of neurologic deterioration in large hemispheric infarction.
|Imaging ||Timing ||Finding |
|MRI DWI sequence ||6 hours after onset ||Infarct > 80 mL |
|MRI DWI sequence ||Within 14 hours of onset ||Infarct > 145 mL |
|NCHCT ||Within 6 hours of onset ||Frank hypodensity > 1/3 of MCA territory |
|NCHCT ||Admission ||Dense MCA |
|NCHCT ||Within 48 hours of onset ||MLS > or = 5 mm |
|NCHCT or MRI ||Any point ||Involvement of multiple vascular territories |
|NCHCT or MRI ||Any point ||Infarct of 50% of MCA territory |
|NCHCT or MRI ||Any point ||MCA infarct involves the basal ganglia |
|CTA head, MRA head, catheter angiography ||Any point ||Occlusion at the carotid terminus |
|CTA head, MRA head, catheter angiography ||Any point ||Incomplete circle of Willis |
|CTA head or catheter angiography ||Any point ||Marginal leptomeningeal collaterals |
In the event that hemispheric swelling occurs causing symptomatic neurologic deterioration, the initial response is to provide therapies that reduce cerebral edema, such as bolus hyperosmolar therapy (eg, 30 mL of 23.4% hypertonic saline or 1-1.5 mg/kg of 20% mannitol). See Chapter _____ for further guidance on the management of cytotoxic cerebral edema/intracranial hypertension. Ultimately, 70% to 80% of patients will die with maximal medical therapy in the absence of early surgical intervention (ie, DC).
Five randomized control trials have explored the efficacy of early DC in LHI. Overall results demonstrate a reduction in mortality (from ~70% to ~20%) and an improvement in functional outcomes in those 18 to 60 years of age. A recent trial demonstrated a similar reduction in mortality in older patients (61-82 years of age), although functional outcomes were not improved. When a DC is performed it should create a bony window of greater than or equal to 12 cm in the anterior-posterior dimension, with a medial border 1 cm lateral to the superior sagittal sinus and inferior border at the floor of the middle cranial fossa. The dura is then opened with cruciate incision (ie, durotomy). Although the timing of DC was not uniform among the published data, a consistent benefit was seen if it was performed within 48 hours of stroke onset in those experiencing neurologic deterioration. It is uniformly felt that once deterioration occurs, DC should be performed promptly, as unreversed herniation will produce irreversible brainstem injury. Although the evidence for its efficacy is not clear more than 48 hours after stroke onset, it is similarly felt that if deterioration occurs, benefits are likely to be seen.
When considering DC, patients and families must be aware that the procedure is not restorative. That is, it is a lifesaving procedure that may help reduce the degree of loss in functionality in the young patient (< 60 years of age), while strictly striving to save the life of the older patient, who will most likely be left moderately to severely disabled at 12 months (ie, mRS of 4 or 5, see Table 48B–5.) It is best to inform the patient and family of their possible candidacy for the procedure on admission to the ICU. That way if deterioration does occur, they will not be forced to make a hasty decision under duress. Furthermore, neurosurgery should be engaged on admission to avoid unnecessary procedural delays in the event of neurologic deterioration.
Similar to LHI, cerebellar strokes are subject to swelling and mass effect leading to herniation. Although they are smaller infarcts, their infratentorial location and juxtaposition to the fourth ventricle lends less room for their growth. Small increases in volume can compress the fourth ventricle, producing obstructive hydrocephalus. Further swelling will directly compress the brainstem.
As with LHI, similar measures to reduce the likelihood of swelling apply. If neurologic deterioration occurs, ICP lowering therapies can temporarily reverse the mass effect of the swelling, but ultimately surgical intervention is required. Obstructive hydrocephalus from fourth ventricular obstruction is often addressed with the placement of an external ventricular drain (EVD), but this will cause the swollen cerebellum to herniate upward, compressing and kinking the brainstem, producing local ischemia and potentially infarction of the midbrain and pons. Therefore, a suboccipital craniectomy (SOC) should be performed immediately after or simultaneously with EVD placement, which will allow for the swollen cerebellum to temporarily herniate extracranially. In contrast to LHI, nearly 3/4 of patients with large cerebellar infarcts will have very good outcomes.