Acute Stroke (Cerebrovascular Accident)

Article Author:
Genti Shatri
Article Editor:
Benjamin Senst
Updated:
12/19/2018 6:38:53 AM
PubMed Link:
Acute Stroke (Cerebrovascular Accident)

Introduction

A cerebrovascular accident, more commonly known as a “stroke,” is broadly classified as either ischemic or hemorrhagic. In either category, the end result is a loss of blood flow and nutrients and oxygen to a region of the brain, resulting in neuronal damage and subsequent neurological deficits. There are numerous causes of stroke, such as prolonged hypertension, arteriosclerosis, and emboli that have formed as a result of atrial fibrillation or rheumatic fever. In younger patients, the possible list of causes may be broadened to include clotting disorders and various forms of vasculitis.  In the event of a possible stroke presentation, a precise history and physical must be performed alongside emergent neurological imaging before administering any form of treatment. With early, focused treatment based on the stroke etiology, rehabilitation programs, and long-term lifestyle changes, one can maximize his/her chances for a meaningful recovery.[1]

Etiology

There is a multitude of etiologies that can lead to a stroke. One of the most common causes is the formation of a plaque secondary to low-density lipoprotein cholesterol (LDL) build up. Some of the most common risk factors include hypertension, diabetes mellitus, and smoking. Thrombi can also develop at the bifurcation sites of the internal carotid, middle cerebral arteries, and the basilar arteries. Emboli commonly originate from the heart, especially in patients with preexisting heart arrhythmias (atrial fibrillation), valvular disease, structural defects (atrial and ventricular septal defects) and rheumatic fever. Emboli usually lodge in areas of preexisting stenosis.[2]

Strokes that occur in small vessels are most commonly caused by chronic, uncontrolled hypertension and arteriosclerosis. These strokes occur in the basal ganglia, internal capsule, thalamus, and pons. Uncontrolled hypertension in these areas can also lead to small hemorrhages.[3]

About 20% of all strokes are classified as hemorrhagic, with the etiology being most commonly uncontrolled hypertension. Other causes of hemorrhagic strokes include cerebral amyloid angiopathy, a disease in which amyloid plaques deposit in small and medium vessels, which causes vessels to become rigid and more vulnerable to tears. Deposition can occur anywhere, but they occur most commonly on the surfaces of the frontal and parietal lobes. The structural integrity of vessels is another important consideration in hemorrhagic stroke etiology, with aneurysms, arteriovenous malformations, cavernous malformations, capillary telangiectasias, venous angiomas, and vasculitis being more common reasons for stroke.[4]

Epidemiology

In the United States, stroke is the fifth common cause of death, and 60% of strokes occur outside of hospitals. On average, every 40 seconds, a person suffers from a stroke, and every 4 minutes, there is one death caused by a stroke.[5] Stroke is a leading cause of disability.[6]

Pathophysiology

When a blockage or bleed occurs, the immediately adjacent neurons lose their supply of oxygen and nutrients. The inability to go through aerobic metabolism and produce ATP causes the Na+/K+ ATPase pumps to fail, leading to an accumulation of Na+ inside the cells and K+ outside the cells. The Na+ ion accumulation leads to cell depolarization and subsequent glutamate release. Glutamate opens NMDA and AMPA receptors and allows for calcium ions to flow into the cells. A continuous flow of calcium leads to continuous neuronal firing and eventual cell death via excitotoxicity.[7]

In the first 12 hours, there are no significant macroscopic or microscopic changes. Twelve hours after the stroke, cytotoxic and vasogenic edema develop, neuronal cell bodies swell, and myelinated fibers disintegrate. Tissues swell as phagocytic cells clear away the dying cells. Extensive phagocytosis causes softening and liquefaction of the affected brain tissues, with peak liquefaction occurring 6 months post-stroke. Several months after a stroke, astrocytes form a dense network of glial fibers mixed with capillaries and connective tissue.[8][9]

Hemorrhagic strokes lead to the same type of cellular dysfunction and concerted events of repair with the addition of blood extravasation and resorption.[10]

History and Physical

A thorough history is an absolutely critical first step toward making a diagnosis. A stroke should be high on the differential for a patient presenting with sudden, focal neurological deficits and/or altered level of consciousness. Based on clinical presentation alone, it is almost impossible to differentiate between a hemorrhagic or ischemic stroke. The signs and symptoms elicited from the history and physical can aid in localizing the affected region. Common signs and symptoms include hemiparesis, sensory deficits, diplopia, dysarthria, and facial droop. Strokes that are more posterior present with a sudden onset of ataxia and vertigo. Symptoms commonly attributed to increased intracranial pressure, such as nausea, vomiting, headache, and blurred or double vision, may provide evidence supporting a hemorrhagic stroke. In addition to gathering information about the symptoms, one needs to establish the time of their onset to decide whether fibrinolytic therapy is an option once the diagnosis of ischemic stroke is confirmed.[11]

A neurological exam is performed to ascertain stroke location, establish baseline function upon hospital admission, rule out a transient ischemic attack (TIA) and other stroke mimickers, and deduce potential comorbidities. It is composed of testing cranial nerve function, the range of motion and muscle strength, sensory integrity, vibratory sense, cerebellar function, gait, language, mental status, and level of consciousness. Baseline function is determined via the National Institutes of Health Stroke Scale (NIHSS), which focuses on the level of consciousness, visual and motor function, sensation and neglect, cerebellar function, and language capabilities.[12]

In addition to the neurological exam, the neck is examined to rule out signs of meningitis via palpation of the paraspinal musculature and testing the range of motion. Besides testing extraocular muscle function and the visual field for visual defects, a fundus examination is performed to check for retinal hemorrhage, tears, and emboli. A peripheral vasculature exam includes palpation of the carotid, radial, femoral, and posterior tibial pulses. A cardiac exam is also performed to detect murmurs, rubs, gallops, or arrhythmias.[13]

Evaluation

Emergency CT without contrast is one of the first diagnostic tools utilized to confirm the diagnosis and rule out any bleeds or a hemorrhagic stroke. Based on the CT results and symptom onset, a patient may be a candidate for fibrinolytic therapy. The diffusion-perfusion mismatch describes the area of tissue at risk ("penumbra") that can be saved with early treatment and identifies patients that benefit from reperfusion therapy.[14][15] A diffusion-weighted MRI is obtained within the first 12 hours of patient presentation, but it is not considered to be the first line of imaging due to the time needed to obtain the images. There are also several contraindications for an MRI, with one of the most common ones being an implantable pacemaker. A CT angiogram aids in localizing the blockage in the vasculature. Doppler studies can also be utilized to determine the degree of carotid stenosis.[16]

Labs are also drawn to determine the patient’s baseline health and provide potential clues toward stroke etiology. Some of the basic labs include a metabolic panel, complete blood count with differential, lipid profile, hemoglobin A1c (HbA1c), blood urine nitrogen (BUN), creatinine, albumin, and glomerular filtration rate (GFR). In younger patients presenting with stroke symptoms, other labs that might be ordered include a coagulation panel, rheumatoid factor (RF), anti-nuclear antibodies (ANA), and other markers for vasculitis.[17]

An ECG and 24-hour ECG monitoring are performed to rule out a cardiac etiology. An EEG may also be warranted to rule out a post-seizure state.[18]

Treatment / Management

Before any treatment can be administered, the patient must be assessed for stable airway, breathing, and circulation. The patient must also be assessed to determine whether he/she is a candidate for alteplase (rt-PA). The exclusion criteria are based on guidelines from the American Heart Association/American Stroke Association. Fibrinolytic therapy aims to dissolve the clot and restore blood flow to the affected regions. The fibrinolytic must be administered within 3 to 4.5 hours after symptom onset to be effective, depending on exclusion criteria. As with the treatment of myocardial infarction and sepsis care, during a stroke the "time is brain" approach is important and requires a fast treatment response. Mobile stroke units and telemedicine have evolved to reduce time to treatment onset.[19][20][21] The time frame for treatment has recently been expanded due to the option of endovascular treatment.[22]

A notable potential complication after fibrinolytic therapy is hemorrhagic transformation. Hemorrhagic transformation is classified as hemorrhagic infarction and parenchymal hematoma, each with 2 subsets. Hemorrhagic infarctions occur more often than parenchymal hematomas. Predictive factors for the occurrence of this complication include increased infarction area, gray matter location, atrial fibrillation, and cerebral embolism, acute hyperglycemia, low platelet count, and poor collateral circulation.[23]

Within 24 to 48 hours of symptoms onset, patients should be placed on anti-platelet therapy, typically 325 mg of aspirin orally. Blood pressure should be maintained slightly elevated for the first few days after a stroke to counter vasoconstriction. Blood pressure should also be lowered by no more than 15% if diastolic blood pressure is over 220 mm Hg or if systolic blood pressure is over 120 mm Hg. Comorbidities also need to be addressed and managed during the patient’s hospital stay.[24]

Patients are admitted to the stroke unit that is equipped and trained to treat and care for people with stroke. The superiority of stroke units compared to non-specialised units has been proven in studies.[25]

Differential Diagnosis

The differential diagnosis is broad and can include stroke mimics such as TIA, metabolic derangement (in other words, hypoglycemia, hyponatremia), hemiplegic migraine, infection, brain tumor, syncope, and conversion disorder.[26]

Prognosis

The prognosis after a stroke is multifactorial, with patient age, stroke severity, stroke etiology, infarct location, and associated comorbidities being significant contributing factors. Stroke complications can also impact a patient’s prognosis. Common complications include pneumonia, deep vein thrombosis, urinary tract infections, and pulmonary embolism. However, patients who do not experience any complications within the first week tend to experience steady neurological improvement. The majority of patients experience the most improvement during the first 3 to 6 months after a stroke.[22]

Enhancing Healthcare Team Outcomes

During the time-dependent early stroke phase and rehabilitation, stroke care involves an interprofessional team to prevent the disease.[27] Once the diagnosis of stroke is made, the patient may need extensive physical rehabilitation, speech therapy and/or a dietary consult. For those who recover function within 3 months, the prognosis is good, but for those with residual neurological deficits, the outcome is guarded.