7. Ischemic stroke
We speak now in the four main components of acute ischemic stroke care. The topics on prevention of complications and recovery and rehabilitation are applicable to both ischemic and hemorrhagic stroke patients.
An ischemic stroke is death of brain tissue due to interruption of blood flow to a region of the brain, caused by occlusion of a cerebral or cervical artery or, less likely, a cerebral vein.
The etiology of the ischemic stroke is important to help determine the best treatment to prevent another stroke. However, regardless of etiology, initial therapy is for the most part the same, and so initially, the most important thing is to implement the acute measures described later.
The first important task is to differentiate between ischemic and hemorrhagic stroke, which can be done with a head CT. Detailed brain and vascular imaging are critically important but should not delay assessment for TPA candidacy. There are things that can mimic stroke.
A focused history should quickly exclude stroke mimics. Unless the presentation is atypical or a stroke mimic is suggested, one should assume it is a stroke and proceed with the determination of whether or not the patient is a candidate for acute therapy. A detailed diagnostic evaluation should be deferred.
7.4 The four components of ischemic stroke care
There are four components to caring for people with acute ischemic stroke. At every point, you should be thinking about the four issues:
(1) Acute therapy and optimization of neurological status.
(2) Etiological work-up for secondary prevention.
(3) Prevention of neurological deterioration or medical complications.
(4) Recovery and rehabilitation.
We present the four components in brief, and then there are longer discussions on the following topics:
- TPA therapy.
- Neurological deterioration.
- Stroke prevention.
7.5 Acute therapy and optimization of neurological status
The main goal of therapy is to get the artery open and re-establish blood flow. You should always ask yourself if you are doing everything possible to optimize blood flow to regions of cerebral ischemia.
7.5.1 Intravenous recombinant tissue plasminogen activator (TPA)
In this course, we will refer to recombinant tissue plasminogen activator as TPA, because that is what it is usually called in the busy emergency department. However, the reader should be aware that this drug is also referred to as rt-PA, t-PA, tPA, alteplase (generic name) or Activase (trade name).
- Intravenous TPA is the only FDA-approved treatment for ischemic stroke in the
. It is approved under safety monitoring in the European Union. Intra-arterial (IA) thrombolysis is a rescue therapy that is being used in several centers under various research protocols. A variety of neuroprotective agents (hypothermia, other drugs) are presently under investigation to try to decrease infarct size, but none is FDA-approved at this time. USA
- The current guideline is that TPA should be given if the patient meets criteria for treatment. Details of the protocol we speak later.
7.5.2 Concurrent Diagnostic Testing
Determination of stroke etiology is usually deferred until after starting TPA therapy. However, while considering or instituting TPA, concomitant information about vascular and tissue status may be helpful. For instance, detection of large-artery occlusion or stenosis is particularly helpful in planning acute recanalization strategies and risk stratification for recurrent stroke or neurological deterioration.
The following diagnostic tests may be helpful in determining the stroke mechanism; however, the need to do acute studies depends on a balance of availability of therapy, time requirement, clinical suspicion, and cost.
Transcranial Doppler ultrasound (TCD) can be performed to detect occlusion, recanalization, and reocclusion of the large intracranial arteries in real time and can be brought to the patient’s bedside in the emergency department.
CT angiography (CTA) can quickly provide a snapshot of the entire cerebral arterial anatomy, and can diagnose intracranial and extracranial stenoses, aneurysms, or dissections.
It is important to know the patient’s creatinine prior to the administration of IV contrast and exclude a contrast allergy. MR angiography (MRA) of the neck and circle of Willis provides the same information as CTA without risk of contrast. However, patients must be cooperative to hold still for several minutes, and those with a pacemaker and somewith aneurysm clips or stents may not be eligible for MRI scanning. MR imaging (MRI) of the brain can provide substantial information on stroke localization, age, bleeding, and tissue status. However, the same caveats apply as with MRA.
Do not treat hypertension acutely unless:
(1) The patient was treated with TPA or
(2) The patient has acute hypertensive end organ damage (congestive heart failure, myocardial infarction, hypertensive encephalopathy, dissecting aortic aneurysm, etc.)
(3) Systolic or diastolic pressures are above 220 or 120mmHg respectively
If you are going to treat hypertension, consider using a short acting agent that will wear off quickly or be turned off in case BP drops too much, such as:
- Labetalol (Trandate, Normodyne) 10 – 20mg IV
- Nicardipine (Cardene) 5 mg/hr IV infusion as initial dose;
- Titrate to desired effect by increasing 2.5mg/hr every 5 minutes to maximum of 15 mg/hr
- Goal: Blood pressure reduction by 10–15%.
Other options for maintenance of cerebral perfusion
- Normal saline for IV fluids – to maintain euvolemia and because it is isotonic and will not cause fluid shifts:
- Consider normal saline 500 cc bolus over 20 – 30 minutes.
- Consider hetastarch (Hespan, Hextend) for volumeexpansion:
- Hetastarch 500 cc over 1 hour; then
- Consider hetastarch 250 cc IV every 8 hours. Monitor jugular venous pressure and input/output. Watch for fluid overload.
- Consider phenylephrine (Neo-Synephrine) drip, or other pressors, in ICU for induced hypertension.
7.5.3 Antiplatelet and Anticoagulant Therapy as an Acute Treatment for Ischemic Stroke
Both antiplatelet and anticoagulant therapy are often considered in the acute therapy of ischemic stroke, and one or both may be appropriate, but randomized trials have shown that anticoagulants should not be routinely employed acutely. Trials have shown that antiplatelets have only a modest benefit, and no studies have yet shown the benefit of urgent antiplatelet treatment.