An ischemic stroke is characterized by an injury of the brain parenchyma due to lack of oxygen. It usually manifests as one or more acute neurological deficits.
Every year around 800.000 strokes happen in US, with 90% of them being ischemic strokes. Since this condition is an important cause of morbidity and mortality, aspects of its diagnosis and treatment are discussed below.
Different pathological mechanisms can cause a stroke, such as:
Cardioembolism (e.g. atrial fibrillation)
Atherosclerosis of large vessels
Occlusion of small vessels
Other causes (e.g. sickle cell disease, arterial dissection)
One or more acute neurological deficits may occur, depending on the area affected.
Anterior Cerebral Artery Stroke:
Hemiparesis or hemiplegia of the contralateral leg and pelvic floor musculature
Sensory loss of contralateral lower extremity
Apraxia (difficulty to execute learned movements)
Primitive reflex (grasp reflex and sucking reflex)
Middle Cerebral Artery Stroke:
Hemiparesis or hemiplegia of the lower half of the contralateral face and upper extremities (lower extremity not as common)
Sensory loss of contralateral face and upper extremity
Ataxia of contralateral extremities
Aphasia (expressive, receptive or global)* aphasia occurs if the stroke occurs in the dominant side
Apraxia (difficulty to execute learned movements)
Conjugate eye deviation (to the side of the lesion)
Posterior Cerebral Artery Stroke:
Contralateral homonymous hemianopsia
Prosopagnosia (inability to recognize faces, including self-recognition)
Chorea, intention tremor or hemiballismus
Dysdiadochokinesia (impaired ability to perform rapid, alternating movements )
Loss of balance and coordination
Regardless of the territory affected, headache is not a common feature in ischemic strokes and it is more common on hemorrhagic events.
The diagnosis should be focused on the early identification of the problem with history and physical examination.
During the acute setting the provider should try to exclude other causes that may cause neurological dysfunction and mimic a stroke (e.g. hypoglicemia, hypoxia, drug use, delirium, migraine with aura).
As soon as the stroke suspicion appears, brain imaging (CT scan without contrast is quick and therefore the method of choice in most places) should be obtained to exclude hemorrhagic stroke A.S.A.P. (since the patient may be elegible for trombolytic therapy). Acutely during an ischemic stroke a CT scan may show nothing or an area or hypodensity. The main purpose of the CT scan is, therefore, exclude an hemorrhagic lesion.
During the admission, other tests should be obtained, including:
Echocardiogram, useful to look for cardiac abnormalities or thrombus.
Carotid Doppler is important to evaluate for carotid stenosis (MRA or CTA may also be used for this purpose).
Other relevant tests include CBC with platelets, coagulation studies (PT, PTT), lipid panel, kidney function, metabolic panel, arterial blood gases, among others.
Many hospitals have a stroke team that should be activated as soon as there is a suspicion of stroke.
Airway (intubation of comatose patients), breathing (proper oxygenation/ventilation) and circulation (treating of hypotension) should be guaranteed. Cardiac monitoring should be provided in the first 24h to look for arrhythmias.
After a quick assessment through history and physical examination and imaging that excludes hemorrhagic stroke, the proper treatment should be offered.
Some patients (patients with a persistent and measurable neurological deficit, age >=18 years and symptoms that started less than 3 to 4.5 hours ago) can benefit from thrombolytics, alteplase specifically, as long as they don’t have contra-indications to thrombolytics. The alteplase dose is calculated as follows: 0.9mg/kg (max. of 90mg). 10% is given as IV bolus and the remainder is infused over 1h.
In patients with up to 6h of symptoms, intra-arterial endovascular thrombolysis may be considered. Intra-arterial thrombectomy may also be used in strokes due to large artery occlusion, also up to 6h of symptoms.
The patient should not receive anything by mouth (NPO) since dysphagia should be excluded with swallowing assessment before oral medications or diet is attempted. If the patient is not able to swallow, a nasoenteral tube or gastrostomy may be placed to provide nutrition, hydration and some medicaitons.
Hypertension should be tolerated up to 220mmHg for SBP and 120mmHg for DBP if the patient is not going to receive thrombolytics. If the patient is going to receive thrombolytics, his BP should be maintained below 185/110mmHg before the treatment and <180/105mmHg for 24h after the treatment. If the levels are above that, the patient should receive parenteral medication (e.g. labetalol-TRANDATE 10-20mg bolus that may be repeated q10-15min – max. 300mg total, or continuous infusion 2-8mg/min; OR nicardipine-CARDENE 5mg/h (dose may be increased by 2.5mg q15minutes up to 15mg/h until desired effect). When IV medication is used, the goal is to have a reduction of no more than 15% during the first 24h. After 24h, medication for chronic hypertension may be started (or resumed).
Glucose should be maintained between 140-180mg/dL.
Prevention of VTE is important and should be provided for all patients. Intermittent pneumatic compression (IPC) is the method of choice if the patient was mobile in the past 72h before the stroke. Prophylactic dose of enoxaparin (LOVENOX, 40mg SC daily) may be used in addition to IPC or alone, but should not be used for 24h after the administration of TPA.
As soon as hemorrhagic stroke is excluded and if a thrombolytic is not going to be used, early aspirin therapy (160-325mg/day) should be provided within 48h. Aspirin should not be given in the first 24h if thrombolytics (IV or intra-arterial) are used. Patients with stroke due to intracranial large artery atherosclerosis may receive dual therapy with aspirin + clopidogrel for up to 90 days (all other cases should receive aspirin alone as mentioned).
After the acute stage, other appropriate treatments may be provided according to the etiology. Patients with carotid artery stenosis may be treated with endarterectomy or stenting. Patients with atrial fibrillation should receive oral anticoagulation.
After the acute event, secondary prevention should be provided. That is done through the treatment of risk factors such as hypertension, diabetes, smoking, hyperlipidemia, and arrhythmias.
Patients should receive aspirin (50-100mg/day) or clopidogrel (75mg/day).
Statins (e.g. atorvastatin 80mg/day) should be provided, regardless of cholesterol levels.
SOURCES & FURTHER READING:
- Jauch E et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2013;44:870-947.
- AHA. Current Treatment Approaches for Acute Ischemic Stroke.
- Carrol CBO et al. What is the Role for Intra-Arterial Therapy in Acute Stroke Intervention? Neurohospitalist. 2015 Jul; 5(3): 122–132.
- Ma Q et al. Intravenous versus Intra-Arterial Thrombolysis in Ischemic Stroke: A Systematic Review and Meta-Analysis. PLoS One. 2015; 10(1): e0116120.
- Diagnosis and Initial Treatment of Ischemic Stroke. Institute for Clinical Systems Improvement. 2016.
- Mukherjee D. Guidelines for Early Management of Acute Ischemic Stroke | Ten Points to Remember. ACC. Jun 30, 2015.
- Saver JL. Intra-arterial thrombolysis. Neurology. 2001;57(5 Suppl 2):S58-60.