Acute stroke

    Last updated date: 13-Apr-2023

    Originally Written in English

    Acute Stroke

    Acute stroke

    Acute stroke is also known as a cerebrovascular accident, which is a description that most stroke neurosurgeons dislike. Stroke does not happen by chance. Brain attack is a superior and more significant term, similar in meaning to a heart attack.  As a consequence of preexisting cerebrovascular disease, acute stroke is characterized as the sudden emergence of localized neurological symptoms in a vascular area. Each year, 850,000 new brain attacks occur in the United States. Every one minute, a new stroke is developed. Stroke is the primary cause of mortality and disability in the United States. Strokes are divided into two categories. Ischemic stroke is the most common form, which is caused by a blockage in blood flow to a specific part of the brain. 84 percent of all acute strokes are caused by an ischemic stroke. Hemorrhagic strokes, which are triggered by the rupture of a blood artery, account for 16% of acute strokes. Intracerebral hemorrhage and subarachnoid hemorrhage, which account for around 5 percent of all strokes, are the two main kinds of hemorrhagic strokes.

    There are four basic forms of ischemic strokes, as per the TOAST categorization. Large vessel atherosclerosis, small vessel atherosclerosis (lacunar infarction), cardioembolic strokes, and cryptogenic (unknown cause) strokes are all examples of these conditions. Each has its own set of causes and pathophysiology. Irrespective of the nature of stroke, it's vital to remember that each minute that a major vessel ischemic stroke goes untreated results in the death of about two million cells. In understanding acute stroke and its management, this is the most crucial time is brain concept.

    Strokes can be caused by a variety of factors, including high blood pressure, arteriosclerosis, and emboli produced in the heart as a consequence of atrial fibrillation or rheumatic heart disease. Coagulation diseases, cervical arterial dissection, and different kinds of vasculitis may be added to the list of probable reasons in younger patients. Before giving any form of treatment in the case of a potential stroke manifestation, a thorough history and physical examination, as well as urgent brain neuroimaging, must be undertaken. One can improve his or her likelihood of a meaningful recovery by receiving prompt, specialized therapy based on the cause of the stroke, rehabilitation programs, and long-term lifestyle changes.



    Stroke is the sixth leading source of mortality in the United States, with 60 percent of strokes occurring outside of hospitals. A person has a stroke every one minute on average, and one person dies from a stroke every four minutes.  Stroke is among the most frequent causes of disability.

    In the United States, blacks had 1.5 times higher age-adjusted risk of stroke mortality than whites. Hispanics have a lower total stroke rate than whites and blacks, but they experience more lacunar lesions and strokes at a younger age.

    Men are more likely than women to have a stroke; white men have a stroke incidence of 63 per 100,000, with death occurring in 26 percent of cases, whereas women have a stroke incidence of 60 per 100,000 and a death rate of 39 %.

    Although stroke is commonly associated with the elderly, one-third of all strokes occur in those under the age of 60. Stroke risk rises with age, especially in patients over the age of 65, who account for 75 percent of all strokes.


    Acute Stroke Pathophysiology

    Acute Stroke Pathophysiology

    Atherosclerosis is the most prevalent and serious underlying condition that results in the development of an atherothrombotic plaque due to a build-up of low-density lipoprotein cholesterol in the brain's arteries. These plaques can cause distant ischemia of the brain by blocking or narrowing the neck or intracranial arteries. They are more likely to rupture. When a plaque ruptures, the underlying cholesterol crystals are exposed, attracting platelets and fibrin. Strokes in the distal arterial areas are caused by the release of fibrin-platelet dense emboli through an artery-to-artery embolic cascade. The underlying cardiac issue determines the nature of the cardiac cause of embolism. Clots in the left atrium are common in atrial fibrillation. These are clots with a lot of red blood cells in them. When emboli form during infective endocarditis, there may be tumor emboli in the left atrium and bacterial aggregates from vegetations.

    When an arterial obstruction occurs, the oxygen and nutrients transport to the neurons in the immediate vicinity is cut off. The Na+/K+ ATPase pumps fail due to the inability to go through aerobic metabolism and make ATP, resulting in a buildup of Na+ inside the cells and K+ outside the cells. Cell depolarization and subsequent glutamate discharge are caused by the buildup of Na+ ions. Glutamate activates the NMDA and AMPA receptors, allowing calcium ions to enter the cells. Continuous calcium influx causes neuronal activity and eventually cell death due to neurotoxic effects.

    There are no notable macroscopic changes in the first 12 hours. With neuronal cellular edema, there is cytotoxic edema due to energy generation failure. Diffusion-weighted MRI, which displays reduced diffusion as a result of neuronal cellular ballooning, can identify this early infarction phase. Vasogenic edema develops 6 to 12 hours after a stroke. FLAIR sequence MRI may be the best way to see this phase. Swelling of the infarcted region and elevations in intracranial pressure are caused by both cytotoxic and vasogenic edema. The invasion of phagocytes, which start clearing away the dead cells, follows. The injured brain tissues weaken and liquefy as a result of extensive phagocytosis, with peak liquefaction happening 6 months after the stroke. A dense network of glial fibers intermingled with capillaries and connective tissue forms several months after a stroke.

    With the inclusion of blood extravasation and washout, hemorrhagic strokes cause a similar type of cellular malfunction and synchronized processes of healing.


    Acute Stroke Causes

    Acute Stroke Causes

    A stroke can be caused by a number of different factors. Hypertension, diabetes mellitus, hypercholesterolemia, lack of physical activity, overweight, genetics, and cigarette smoking are some of the most frequent factors associated. The heart is a common source of cerebral embolism, especially in patients with cardiac arrhythmia (atrial fibrillation), valve diseases, structural defects, and chronic rheumatic heart disease. Emboli can get stuck in regions where there is already narrowing. Ischemic stroke and alcohol consumption have a strong association. Ischemic stroke is less likely in people who drink slightly to moderately, but it is far more likely in people who drink heavily. Alcohol consumption has a nearly linear connection with the risk of hemorrhagic stroke.

    Strokes in small vessels (lacunar infarctions) are most usually triggered by persistent, uncontrolled high blood pressure, which leads to lipo-hyalinosis and arteriolosclerosis. The basal ganglia, internal capsule, thalamus, and pons are all affected by any of these strokes. High blood pressure that is uncontrolled in these locations can result in hypertensive intracerebral hemorrhages.

    Hemorrhagic strokes account for about 16 percent of all strokes, with high blood pressure being the most common cause. Cerebral amyloid angiopathy, a disorder in which amyloid plaques form in small and medium arteries, making them stiff and more sensitive to rupture, is another cause of intracranial hemorrhage. Accumulation can occur anywhere, but it is most frequent in the frontal and parietal lobe areas. Aneurysms, arteriovenous malformations, cavernous malformations, capillary telangiectasia, and vasculitis are all common causes of acute intracranial hemorrhage, with aneurysms, arteriovenous malformations, capillary telangiectasias, venous angiomas, and vasculitis being the most common.


    Acute Stroke Symptoms

    Acute Stroke Symptoms

    The brain is time.  A quick yet complete history is the most important initial step in making a diagnosis. When a patient presents with acute, focal neurological impairments and/or a changed level of consciousness, a stroke should be considered a strong possibility. It's difficult to tell the difference between a hemorrhagic and an ischemic stroke based on clinical symptoms alone. Although a minor intracerebral hemorrhage can appear clinically exactly like a deep hemisphere ischemic infarction, it is more common that a headache and/or altered state of consciousness suggests a hemorrhage. The indications and symptoms obtained from the history and physical examination can be used to pinpoint the affected area. Hemiparesis, sensory impairments, vision changes, dysarthria, and facial droop are all common indications and symptoms. Strokes in the posterior circulation cause ataxia and vertigo to appear suddenly. Symptoms such as nausea, vomiting, headache, and blurred or double vision, which are typically associated with increased intracranial pressure, may potentially indicate a hemorrhagic stroke. In addition to obtaining information regarding the symptoms, the time of beginning must be determined in order to determine further treatment once an ischemic stroke diagnosis has been established.

    A neurologic examination is used to determine the location of the stroke, assess baseline function upon patient admission, rule out a transient ischemic attack or other issues that mimic stroke, and determine potential comorbidities. It consists of cranial nerve function, range of motion, and muscular strength assessments, sensory quality, vibratory sensation, cerebellar function, walking, language, mental state, and level of consciousness tests. The National Institutes of Health Stroke Scale is used to measure baseline function, which evaluates the level of awareness, visual and motor function, sensibility and attention, cerebellar function, and language ability.

    In addition to the neurologic examination, the paraspinal muscles are palpated and range of motion is tested to rule out indications of meningitis in the neck. A carotid bruit shows the presence of subclinical atherosclerosis. A fundus evaluation is done to examine for hypertensive changes, retinal hemorrhage, and thromboembolism, in addition to checking extraocular muscle activity and the visual field for visual abnormalities. The carotid, radial, femoral, and posterior tibial pulses are all palpated during a peripheral vascular assessment. Murmurs, rubs, gallops, and arrhythmias are all detected during a heart exam.

    Characteristics of a middle cerebral artery stroke include:

    1. Hemiparesis with hypesthesia on the opposite side (Weakness of arm and face is worse than in the lower limb)
    2. Turn your eyes to the side of the lesion.
    3. Hemianopsia on the ipsilateral side
    4. The dominant hemisphere is compromised by aphasia.
    5. Agnosia
    6. Inattention

    Anterior cerebral artery stroke has the following characteristics:

    1. Although speech is intact, there is a lack of control.
    2. The state of mind has changed.
    3. The ability to make decisions is hampered.
    4. Sensory impairments in the contralateral cortical hemisphere
    5. Legs have more contralateral weakness than arms.
    6. Urinary incontinence
    7. Apraxia of the gait

    Stroke of the posterior cerebral artery has the following features:

    1. Cortical loss of vision
    2. Homonymous hemianopia on the opposite side
    3. Changes in mental state
    4. Visual agnosia is a condition in which a person can’t discriminate what he is seeing
    5. Impairment of memory
    6. Stroke of the vertebral/basilar arteries features:
    7. Vertigo
    8. Visual field deficiencies and diplopia
    9. Dysarthria
    10. Syncope and nystagmus


    Acute Stroke Diagnosis

    Acute Stroke Diagnosis

    The most crucial first diagnostic tool used to establish the diagnosis and rule out any bleeding or hemorrhagic stroke is an emergency CT scan without contrast. A patient may be suitable for fibrinolytic therapy depending on the CT findings and the start of symptoms. The most accurate way to diagnose acute ischemia infarction is with MRI. It may accurately diagnose as well as indicate the infractions' size and location. Because of the time required to obtain the images and the limited availability, it is not recognized first-line scans. Other MRI procedures, such as the diffusion-perfusion mismatch, identify patients who benefit from reperfusion therapy beyond the first 4 to 6 hours of an acute ischemic stroke and characterize the area of the brain at risk (penumbra) that can be rescued with early treatment. An MRI is still prohibited if you have a cardiac pacemaker. The location of the obstruction in the vasculature can be determined with the help of a CT angiography. It can identify patients who need interventional thrombectomy treatment because of a major artery blockage. CT perfusion scan can also reveal the ischemic center and penumbra mismatch, which can help with revascularization decisions after the 6-hour frame has passed. The severity of carotid stenosis can also be determined via Doppler testing.

    Laboratory tests are done to evaluate the patient's baseline condition and to look for clues to the cause of the stroke. A metabolic panel, complete blood count, lipid panel, hemoglobin A1c, blood urine nitrogen, creatinine, albumin, and glomerular filtration rate are some of the fundamental laboratory tests. Random blood glucose, platelet count, and PT/PTT are all essential tests to assess if a patient is a candidate for Intravenous thrombolytic therapy. Other laboratories that may be requested in younger patients with stroke symptoms include a coagulation profile, rheumatoid factor, antinuclear antibodies, and other vasculitis biomarkers.

    In cryptogenic strokes, an ECG, echocardiogram, and extended ECG monitoring may be recommended to exclude a cardiac origin, particularly atrial fibrillation. To exclude a post-seizure condition, an EEG may be required.


    Acute Stroke Treatment

    Acute Stroke Treatment

    The patient's airway, breathing, and circulation must all be examined before any intervention can be performed. The next step is to determine whether or not he or she is suitable for alteplase. The parameters for exclusion are based on the American Heart Association/American Stroke Association's recommendations. Fibrinolytic therapy is used to break clots and restore blood flow to damaged areas. To be successful, the fibrinolytic must be given within 3 to 4 hours of the onset of symptoms, based on the exclusion criteria. During a stroke, the time is brain strategy is critical, and it necessitates a quick and collaborative treatment approach, just as it is during the management of myocardial infarction and sepsis. To shorten the time between diagnosis and therapy, mobile stroke facilities and telemedicine have been developed. Because endovascular therapy is now an option, the treatment timeline has recently been extended.

    Thrombolytic Therapy Criteria:

    • Symptoms indicate an ischemic stroke
    • No recent head trauma
    • No history of myocardial infarction in the previous 3 months
    • No gastrointestinal bleeding in the previous 21 days
    • No arterial puncture in the previous week
    • No major surgery within the previous 2 weeks
    • No history of an intracranial hemorrhage
    • Systolic blood pressure less than 185 mmHg or diastolic blood pressure less than 110 mmHg
    • No recent trauma or bleeding
    • Not on any oral anticoagulant
    • Blood glucose higher than 50 mg/dl

    Hemorrhage is a serious potential side effect of fibrinolytic therapy. Hemorrhagic conversion is divided into two subsets: hemorrhagic infarction and parenchymal hematoma. Parenchymal hematomas are less common than hemorrhagic infarctions. Increased infarction size, gray matter distribution, atrial fibrillation, and cerebral embolism, acute hyperglycemia, low platelet count, and inadequate collateral circulation are all major risk factors for this condition.

    There have been tremendous breakthroughs in acute stroke care in latest years. In patients with major artery occlusion in the anterior circulation, endovascular thrombectomy in the first 6 hours is substantially better than normal medical therapy, according to multiple studies. These advantages persisted regardless of geographic location or patient factors.

    In 2018, a major massive change in stroke care occurred once again. Endovascular thrombectomy revealed significant advantages in patients with major artery blockage in the arteries of the proximal anterior circulation. Using perfusion scanning, this study prolonged the stroke window in some patients from 15 to 23 hours. As a result, we can manage more patients for longer periods of time, up to 24 hours.

    Patients should be started on antiplatelet medication, such as aspirin, within 1 to 2 days of symptoms onset. To promote perfusion to the peri-infarction areas, blood pressure should be kept slightly increased during the first few days after a stroke. If diastolic blood pressure is over 220 mm Hg or systolic blood pressure is over 120 mm Hg, blood pressure should be reduced by no more than 15 percent. For Intravenous Alteplase therapy, blood pressure must be less than 180/110.

    During the patient's hospitalization, comorbidities must also be evaluated and treated. If the room air saturation is less than 95%, oxygen should be administered. Hypoglycemia and hyperglycemia should also be diagnosed and managed.

    Patients are admitted to a stroke unit, which is prepared and trained to manage and care for those who have suffered a stroke. Studies have demonstrated the superiority of stroke units over non-specialized units.  A multidisciplinary approach to acute stroke management is optimal, with the stroke neurologist, interventional neuroradiologist, speech pathologist, physiotherapist, occupational therapist, pharmacist, support worker, and nursing care team all contributing. Blood pressure care, swallowing assessment and aspiration preventative measures, Intravenous fluid with isotonic fluids, minimizing and treating fever actively, treating hyperglycemia, preventing infection and DVT prophylaxis, and early assessment and plan for subsequent rehabilitation are all part of the general care of a patient with acute stroke.


    Cerebral Edema Treatment

    Cerebral edema peaks 3-4 days after a stroke and can be detected using a non-contrast CT scan. An alteration in mental status, unconsciousness, or a change in pupil size could all be indicators. Mannitol is used to treat it; however, the use of corticosteroids is debatable. In most patients, patient positioning, hypothermia, hyperventilation, and hyperosmolar treatment will help.


    Seizures Treatment

    Within the first few days after an ischemic stroke, 5–25 percent of individuals experience seizures. Standard antiepileptic medications may be required to treat these seizures.


    Acute Stroke Prognosis

    After a stroke, the prognosis is complicated, with patient age, stroke degree, stroke cause, infarct area, and related comorbidities all playing a role. Complications from a stroke might also affect a patient's outcomes. Pneumonia, deep vein thrombosis, urinary tract infections, and pulmonary embolism are all common problems. Patients who do not have any issues during the first week, on the other hand, tend to have continuous neurological recovery. The majority of patients recover the greatest in the first 3 to 6 months following a stroke.



    Acute stroke

    Stroke continues to be associated with a high rate of morbidity and mortality. Furthermore, the financial burden on the health service is considerable. Despite the fact that there are therapies for strokes, the results are not always good, and many people are left irreversibly handicapped.

    The treatment of stroke is best accomplished with an interdisciplinary team that comprises the emergency department doctor, registered nurse, neurologist, radiologist, and stroke team. The objective is to determine whether the stroke is embolic or hemorrhagic before starting thrombolytic therapy. Physical, speech, and occupational therapy may be required for individuals who recover.

    It is critical to recognize a stroke as soon as possible. Nursing personnel must be trained to recognize probable stroke patients and notify a physician right away to assess the patient. Depending upon the nature of the diagnosis, physicians should collaborate with pharmacists to conduct quick medication interaction testing and then begin treatment as soon as possible.

    However, because it is more cost-effective, the attention is now on stroke prevention. All physicians are responsible for informing the public about ways to avoid strokes. Because uncontrolled high blood pressure is one of the risk factors for stroke, the pharmacist should advise patients to take their blood pressure medications. Patients should be educated by physicians, as well as nurses, on quitting smoking, consuming a good diet, getting regular exercise, and keeping a healthy body weight. 

    For those who have had a stroke, a support worker may be needed to ensure that the home is safe and that the patient has the necessary support structures. To educate the patient on what to consume, a dietary consultation should be scheduled. Some individuals may also require therapy in order to restore speech, musculature, and joint function. Improved outcomes and a higher quality of life can only be achieved through an interdisciplinary team strategy and open communication.