Acute stroke is divided into two types:
ischemic (approximately 85% of cases)
hemorrhagic (approximately 15% of cases)
Ischemic stroke is a cerebrovascular occlusion that causes ischemic neuronal injury. The source of occlusion is typically either embolism or thrombosis.
(of the aortic arch, cervical arteries, large intracranial arteries, and small cerebral vessels)
(due to atrial fibrillation, low ejection fraction leading to ventricular thrombus, and “paradoxical” systemic venous embolism through a patent foramen ovale)
Other less-common causes include cervical artery dissection, endocarditis, vasculitis (systemic vs. primary central nervous system), reversible cerebral vasoconstriction syndrome (RCVS, or Call-Fleming syndrome), hypercoagulable states (e.g., systemic malignancy, antiphospholipid antibody syndrome, hemolytic–uremic syndrome/thrombotic thrombocytopenic purpura, nephrotic syndrome), global hypoperfusion, and vascular compression (herniation syndromes).
When a patient presents with symptoms suggestive of acute ischemic stroke, the primary and urgent goal is to determine whether he or she can safely receive intravenous tissue plasminogen activator (tPA) or benefit from other forms of arterial revascularization. Because these interventions are time-sensitive, the immediate workup should be focused and efficient and include the following:
All patients with suspected ischemic stroke should undergo a careful and focused neurologic assessment and evaluation using the National Institutes of Health Stroke Scale (NIHSS), a standardized physical examination template that quantifies the severity of the deficit for appropriate evaluation and documentation.
Focused history and physical examination:
The purpose of the focused history is to identify absolute and relative contraindications to tPA (see table below for full list). The evaluation should focus on the following:
last-seen well time
current use of anticoagulant/antiplatelet agents
current platelet count and international normalized ratio (INR)
prior intracranial bleeding or other major bleeding
current blood pressure
: Required STAT
to distinguish intracerebral hemorrhage from ischemic stroke. CT has high sensitivity for identifying acute intracranial hemorrhage but may not show early ischemic changes during the acute period. If imaging demonstrates hemorrhage, tPA is obviously contraindicated.
(not necessarily during the acute period):
This is highly sensitive for both acute intracranial hemorrhage and acute ischemic changes but slower, more expensive, and more susceptible to motion artifact than CT; may be contraindicated in some patients (e.g., patients with pacemakers or metal implants).
Imaging of the head and neck vessels may be useful to detect areas of stenosis, dissections, or occlusions. Vessel imaging may also guide intervention when intra-arterial therapy is being considered. Options for vessel imaging include CT of the head and neck vessels with arterial contrast (CTA) or magnetic resonance angiogram (MRA), which does not require constrast. Ultrasound of the neck vessels may be useful but does not provide good imaging of the intracranial and posterior neck vessels. In select cases, catheter-based angiography is performed.
When a cardioembolic source is suspected, transthoracic echocardiography is performed to evaluate for vegetation, mural thrombus, and presence of a patent foramen ovale. Transesophageal echocardiography is performed when atrial appendage clot is suspected.
Heart rhythm monitoring:
Ambulatory noninvasive ECG monitoring is often recommended after discharge if cause of stroke has not been identified; some studies suggest up to 16% of patients have newly detected atrial fibrillation detected only by Holter monitor.
Note: Young patients or patients without apparent risk factors warrant additional workup for unusual causes of stroke, including evaluation for a hypercoagulable state.
Ischemic penumbra: Initial stroke symptoms reflect the area of core infarction in addition to surrounding tissue with low perfusion (“penumbra”). This area of low perfusion surrounding the core area of infarction can be preserved if reperfusion is achieved rapidly. Otherwise, the area eventually becomes incorporated into the area of infarct. Therefore, revascularization interventions (e.g., tPA), when indicated, should be attempted as soon as safely possible.
The following image shows the progression over time (left to right) of reversible ischemic penumbra volume (green) to the irreversible infarct core (red):
(Source: Acute Ischemic Stroke, N Engl J Med 2007.)
tPA revascularization: Before giving tPA, a CT scan must be obtained to rule out hemorrhage. The time-sensitive decision regarding the use of tPA does not depend on MRI; CT is sufficient to rule out hemorrhage. If a patient presents early with no contraindications to therapy, intravenous tPA may be given to try to dissolve the clot. The Food and Drug Administration (FDA) currently has approved use of tPA within 3 hours after the stroke event, whereas current American Heart Association/American Stroke Association (AHA/ASA) guidelines recommend treatment up to 4.5 hours in selected patients. Note that the benefit of tPA decreases and the risk increases with time, so the earlier tPA is administered, the higher the likelihood of a positive neurologic outcome (“time is brain”). Understanding and inquiring about potential contraindications before administering tPA is important.
The following table lists inclusion and exclusion criteria for intravenous tPA therapy in patients with acute ischemic stroke:
(Source: Intravenous Thrombolytic Therapy for Acute Ischemic Stroke, N Engl J Med 2011.)
Important risk/benefit statistics to share when counseling patients and family members about tPA therapy:
Benefits: absolute increase in odds of neurologic improvements at 90 days of 11-13 percentage points.
Risk for intracerebral hemorrhage possibly causing neurologic deterioration or death is 6%.
Read more about thrombolysis for stroke in Clinical Pearls & Morning Reports.
Intra-arterial mechanical thrombectomy: Emerging evidence supports the use of intra-arterial mechanical thrombectomy (with a stent-retriever device) in patients with proximal large-vessel occlusions of the anterior circulation (intracranial internal carotid, middle cerebral, anterior cerebral) who present within 6 hours after their last-seen well time. Visualization of the cerebral vessels is required, either by CT angiography, MRA, or digital subtraction angiography. Mechanical thrombectomy should only be performed at stroke centers with experienced operators. Consideration of mechanical thrombectomy should not delay or influence the decision to give intravenous tPA (per AHA/ASA guidelines). Mechanical thrombectomy can follow intravenous tPA administration.
Read more in this blog post about intra-arterial treatment for acute ischemic stroke.
Complications of Acute Ischemic Stroke:
hemorrhagic transformation of the infarct bed (bleeding into the friable, newly infarcted tissue)
malignant cerebral edema (swelling of the infarcted tissue): When severe, this can cause shifting and herniation of the brain. Suboccipital craniotomy (for large posterior-fossa infarcts) and decompressive hemicraniectomy (for large middle-cerebral-artery infarcts) can be considered.
Note: Depending on the etiology, appropriate secondary-stroke prevention can be chosen (e.g., aspirin, anticoagulation, blood-pressure [BP] control, lipid-lowering agents).
Secondary prevention of stroke: The following table offers strategies for secondary prevention of stroke:
(Source: Secondary Prevention after Ischemic Stroke or Transient Ischemic Attack, N Engl J Med 2012.)
Fifteen percent of strokes are due to hemorrhagic stroke, either intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH).
Intracerebral hemorrhage is a neurologic emergency.
illicit drug use
rarer causes (e.g., bleeding into tumors, aneurysm rupture, other vascular malformations)
The AHA/ASA ICH guidelines recommend that workup of ICH focus on the factors listed in the following table:
Integral Components of the History, Physical Examination, and Workup of the Patient with ICH in the Emergency Department
CT indicates computed tomography; GCS, Glasgow Coma Scale; ICH, intracerebral hemorrhage; INR, international normalized ratio; and MRI, magnetic resonance imaging.
(Source: Guidelines for the Management of Spontaneous Intracerebral Hemorrhage, Stroke 2015. Reprinted with permission ©2014, American Heart Association, Inc.)
admission to ICU or dedicated stroke unit
STAT cerebral vascular imaging
(to assess for aneurysms, vascular malformation, and active extravasation of contrast; this so-called “spot sign” indicates ongoing bleeding that may predict expansion of the hemorrhage)
reversal of coagulopathy
if possible (agents include vitamin K, fresh frozen-plasma, prothrombin complex concentrates, and/or platelets, depending on why the patient is coagulopathic; reversal agents for direct oral anticoagulants are being investigated in randomized controlled trials [RCTs])
management of hypertension:
The Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial [INTERACT2] trial found no difference in hematoma growth, death, or major disability between standard of care BP control (<180 mm Hg systolic) and intensive management (<140 mm Hg systolic), but the intensive group had better functional outcomes as measured by the Rankin scale. (see related NEJM JW summary and this blog post)
The ATACH-2 Trial found that treatment of participants with intracerebral hemorrhage to achieve a target systolic blood pressure of 110 to 139 mm Hg did not result in a lower rate of death or disability than standard reduction to a target of 140 to 179 mm Hg, with no significant between-group difference in the ordinal distribution of the modified Rankin scale score at 3 months. (see related NEJM JW summary and this blog post)
2015 AHA/ASA recommendations (note: last updated prior to ATACH-2 trial):
For ICH patients presenting with systolic blood pressure (SBP) between 150–220 mm Hg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe and can improve functional outcome.
For ICH patients presenting with SBP >220 mm Hg, consider aggressive reduction of BP with a continuous intravenous infusion and frequent BP monitoring.
(avoid both hyper- and hypoglycemia)
treatment of fever
(may be reasonable based on animal studies, although no conclusive evidence exists from human studies)
management of seizures:
Treat clinical seizures or electrographic seizures on electroencephalograph (EEG) with antiepileptic drugs (AEDs).
There is no indication for prophylactic antiepileptic medications for intracerebral hemorrhage (several studies have found prophylaxis to be harmful). Note: A short course of prophylactic AED therapy is used in patients with subdural hematoma.
intracranial pressure (ICP) monitoring
should be considered in patients with Glasgow coma score (GCS) ≤8, clinical evidence of transtentorial herniation, or intraventricular hemorrhage or hydrocephalus. Cerebral perfusion pressure goal is usually 50–70 mm Hg.
referral for neurosurgery:
minimal evidence supports surgery for ICH except in the following specific situations:
Patients with cerebellar hemorrhage and neurologic deterioration from brain-stem compression and/or hydrocephalus should undergo surgical removal of hemorrhage as soon as possible (with concomitant administration of hyperosmolar therapy such as mannitol).
In deteriorating patients with supratentorial hematoma evacuation, surgery might be life-saving but efficacy is not established. The Surgical Treatment for Ischemic Heart Failure (STICH) trial showed no benefit from early decompressive surgery.
In patients with supratentorial ICH with coma, midline shift, or elevated ICP refractory to medical management, decompressive craniotomy with or without hematoma evacuation might reduce mortality.
other (nonacute) management:
Prevention of venous thromboembolism:
Patients with ICH are at high risk for venous thromboembolism, which should be managed with compression stockings and compression boots.
Assessment and management of dysphagia:
Some patients require feeding tube placement.
Subarachnoid Hemorrhage (SAH)
The most common cause of subarachnoid hemorrhage is aneurysm rupture or trauma. Other causes include vascular malformations.
SAH begins abruptly with the primary symptom of a sudden severe headache, classically described as a thunderclap or “the worst headache of my life.” Usually, no important focal neurologic signs appear at presentation unless bleeding occurs into the brain at the same time.
Severe headache may be associated with:
brief loss of consciousness
focal neurologic deficit
Diagnostic Algorithm for Subarachnoid Hemorrhage
(Source: Aneurysmal Subarachnoid Hemorrhage, N Engl J Med 2006.)
A patient’s first or worst headache or one that starts abruptly (“thunderclap”) should trigger suspicion for SAH and prompt workup, including imaging with CT of the head. Lumbar puncture (LP) should be performed in any patient with suspected SAH and negative results on head CT.
Misdiagnosis can occur in the absence of the classic signs and symptoms of SAH. The most common incorrect alternative diagnoses are migraine and tension-type headaches.
In the critical care setting, the main goals of treatment are:
secure the vascular malformation
prevent and manage vasospasm
treat other medical and neurologic complications
SAH Treatment Guidelines
(Source: Aneurysmal Subarachnoid Hemorrhage, N Engl J Med 2006.)