Worldwide, stroke is the second most common cause of mortality and the third most common cause of disability.(1) Globally, the incidence of stroke due to ischemia is 68 percent, while the incidence of hemorrhagic stroke (intracerebral hemorrhage and subarachnoid hemorrhage combined) is 32 percent, reflecting a higher incidence of hemorrhagic stroke in low-and middle-income countries.(2) Men have a higher incidence of stroke than women at younger but not older ages, with the incidence reversed and higher for women by age 75 years and older.(3)
According to World Health Organization estimates, 5.5 million people died of stroke in 2002, and roughly 20% of these deaths occurred in South Asia.(4)
In Pakistan, stroke and transient ischemic attacks (TIA) are highly prevalent. A recent community-based survey suggested an estimated 21.8% prevalence of stroke and / or TIA in an urban slum of Karachi.(5) Stroke-specific fatality has been reported between 7% and 20% in various studies from Pakistan. Upto 63% of all stroke patients develop complications and upto 89% are dependent for activities of daily living.(6) The estimated annual incidence of stroke in Pakistan is 250 / 100,000, which is projected to an estimate of 350,000 new cases every year.(7)
Stroke is classified into two major types:
- Brain ischemia due to thrombosis, embolism, or systemic hypoperfusion
- Brain hemorrhage due to intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH)
Approximately 80 percent of strokes are due to ischemic cerebral infarction and 20 percent to brain hemorrhage.
ISCHEMIC STROKE: Acute ischemic strokes result from vascular occlusion secondary to thromboembolic disease. Ischemia causes cell hypoxia and depletion of cellular adenosine triphosphate (ATP). Without ATP, there is no longer the energy to maintain ionic gradients across the cell membrane and cell depolarization. Influx of sodium and calcium ions and passive inflow of water into the cell lead to cytotoxic edema.(8,9,10)
ISCHEMIC CORE AND PENUMBRA: An acute vascular occlusion produces heterogeneous regions of ischemia in the affected vascular territory. Local blood flow is limited to any residual flow in the major arterial source plus the collateral supply, if any. Affected regions with cerebral blood flow of lower than 10 mL / 100 g of tissue / min are referred to collectively as the core. These cells are presumed to die within minutes of stroke onset.(11)
Zones of decreased or marginal perfusion (cerebral blood flow < 25 mL / 100g of tissue / min) are collectively called the ischemic penumbra. Tissue in the penumbra can remain viable for several hours because of marginal tissue perfusion.(11)
ISCHEMIC CASCADE: On the cellular level, the ischemic neuron becomes depolarized as ATP is depleted and membrane ion-transport systems fail. Disruption of cellular metabolism also impairs normal sodium-potassium plasma membrane pumps, producing an intracellular increase in sodium, which in turns increases intracellular water content. This cellular swelling is referred to as cytotoxic edema and occurs very early in cerebral ischemia.
Cerebral ischemia impairs the normal sodium-calcium exchange protein also found on cell plasma membranes. The resulting influx of calcium leads to the release of a number of neurotransmitters, including large quantities of glutamate, which in turn activates N -methyl-D-aspartate (NMDA) and other excitatory receptors on other neurons.
These neurons then become depolarized, causing further calcium influx, further glutamate release, and local amplification of the initial ischemic insult. This massive calcium influx also activates various degradative enzymes, leading to the destruction of the cell membrane and other essential neuronal structures.(12) Free radicals, arachidonic acid, and nitric oxide are generated by this process, which leads to further neuronal damage.
Ischemia also directly results in dysfunction of the cerebral vasculature, with breakdown of the blood-brain barrier occurring within 4-6 hours after infarction. Following the barrier’s breakdown, proteins and water flood into the extracellular space, leading to vasogenic edema. This produces greater levels of brain swelling and mass effect that peak at 3-5 days and resolve over the next several weeks with resorption of water and proteins.(13,14)
Within hours to days after a stroke, specific genes are activated, leading to the formation of cytokines and other factors that, in turn, cause further inflammation and microcirculatory compromise.(12) Ultimately, the ischemic penumbra is consumed by these progressive insults, coalescing with the infarcted core, often within hours of the onset of the stroke.
Infarction results in the death of astrocytes, as well as the supporting oligodendroglial and microglial cells. The infarcted tissue eventually undergoes liquefaction necrosis and is removed by macrophages, with the development of parenchymal volume loss. A well-circumscribed region of cerebrospinal fluid like low density, resulting from encephalomalacia and cystic change, is eventually seen. The evolution of these chronic changes may be seen in the weeks to months following the infarction.
HEMORRHAGIC TRANSFORMATION OF ISCHEMIC STROKE: Hemorrhagic transformation represents the conversion of an ischemic infarction into an area of hemorrhage. This is estimated to occur in 5% of uncomplicated ischemic strokes, in the absence of fibrinolytic treatment. Hemorrhagic transformation is not always associated with neurologic decline, with the conversion ranging from the development of small petechial hemorrhages to the formation of hematomas that produce neurologic decline and may necessitate surgical evacuation or decompressive hemicraniectomy.
Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed, producing petechial hemorrhage or more frank intraparenchymal hematoma.(8,15,16)
Spontaneous hemorrhagic transformation of an ischemic infarct occurs within 2–14 days postictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely to occur with larger infarct volumes.(8,17,18) Hemorrhagic transformation is also more likely following administration of rt-PA in patients whose baseline noncontrast CT (NCCT) scans demonstrate areas of hypodensity.(19,20,21)
POSTSTROKE CEREBRAL EDEMA AND SEIZURES: Although clinically significant cerebral edema can occur after anterior circulation ischemic stroke, it is thought to be somewhat rare (10-20%).(21) Edema and herniation are the most common causes of early death in patients with hemispheric stroke.
Seizures occur in 2-23% of patients within the first days after ischemic stroke.(21) A fraction of patients who have experienced stroke develop chronic seizure disorders.
In intracerebral hemorrhage, bleeding occurs directly into the brain parenchyma. The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension. Other mechanisms include bleeding diatheses, iatrogenic anticoagulation, cerebral amyloidosis, and cocaine abuse.
Intracerebral hemorrhage has a predilection for certain sites in the brain, including the thalamus, putamen, cerebellum, and brainstem. In addition to the area of the brain injured by the hemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the hematoma. A general increase in intracranial pressure may occur.
SUBARACHNOID HEMORRHAGE: The pathologic effects of subarachnoid hemorrhage (SAH) on the brain are multifocal. SAH results in elevated intracranial pressure and impairs cerebral autoregulation. These effects can occur in combination with acute vasoconstriction, microvascular platelet aggregation, and loss of microvascular perfusion, resulting in profound reduction in blood flow and cerebral ischemia.(22)
SIGNS AND SYMPTOMS:
Sometimes a stroke develops gradually. But it is more likely to have one or more sudden warning signs like these:
- Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.
- Sudden confusion, trouble speaking, or difficulty understanding speech.
- Sudden trouble seeing in one or both eyes.
- Sudden trouble walking, dizziness, loss of balance, or lack of coordination.
- Sudden severe headache with no known cause.
The FAST test is a quick way to check someone for symptoms.
- Face: Ask the person to smile. Does one side of the face droop?
- Arms: Ask the person to raise both arms. Does one arm drift downward? Or is one arm unable to raise up?
- Speech: Ask the person to repeat a simple phrase. Is his or her speech slurred or strange?
- Time: If any of these signs observed, emergency help needed immediately.
Patient assessment and management during the acute phase (first few hours) of an ischemic stroke will be reviewed here.
INITIAL ASSESSMENT: Time is of the essence in the hyperacute evaluation of stroke patients. The history, physical examination, serum glucose, oxygen saturation, and a noncontrast CT scan are sufficient in most cases to guide acute therapy. Other tests are considered based upon individual patient characteristics, but the absence or unavailability of any additional tests need not be a reason to delay therapy if otherwise indicated.
AIRWAY, BREATHING AND CIRCULATION: Assessing vital signs and ensuring stabilization of airway, breathing, and circulation is part of the initial evaluation of all patients with critical illness, including those with stroke.(23) Patients with increased intracranial pressure due to hemorrhage, vertebrobasilar ischemia, or bihemispheric ischemia can present with a decreased respiratory drive or muscular airway obstruction. Hypoventilation, with a resulting increase in carbon dioxide, may lead to cerebral vasodilation and elevate intracranial pressure.
In these cases, intubation may be necessary to restore adequate ventilation and to protect the airway from aspiration; this can be especially important in the presence of vomiting, which occurs commonly with increased intracranial pressure, vertebrobasilar ischemia, and intracranial hemorrhage. Patients with adequate ventilation should have the oxygen saturation monitored.
HISTORY AND PHYSICAL: Establishing the time of ischemic stroke symptom onset is critical because it is the main determinant of eligibility for treatment with intravenous thrombolysis and endovascular thrombectomy.(24) For patients who are unable to provide a reliable onset time, symptom onset is defined as the time the patient was last known to be awake and free of stroke symptoms.(23) For patients presenting within the therapeutic window for thrombolysis (less than 4.5 hours from symptom onset) or endovascular thrombectomy (less than 6 hours from symptom onset), the history needs to be accurate but rapid; contraindications to thrombolytic treatment should also be assessed.
The history and physical examination should be used to distinguish between other disorders in the differential diagnosis of brain ischemia. As examples, seizures, syncope, migraine, hypoglycemia, or drug toxicity can mimic acute ischemia.(23) The most difficult cases involve patients with the combination of focal signs and altered level of consciousness. It is important to ask the patient, relative, or any reliable informant whether the patient takes insulin or oral hypoglycemic agents, has a history of epilepsy, drug overdose or abuse, or recent trauma.
Diagnosing an intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH) as soon as possible can be lifesaving.(25,26) The history may be helpful in this regard. The presence of onset headache and vomiting favor the diagnosis of ICH or SAH compared with a thromboembolic stroke, while the abrupt onset of impaired cerebral function without focal symptoms favors the diagnosis of SAH. Another important element of the history is whether the patient takes anticoagulant drugs. Even with these clues, diagnosing intracranial hemorrhage on clinical grounds is very imprecise, so early neuroimaging with a CT or MRI scan is critical. CT is preferred at most centers, as it can be obtained very rapidly and is effective at distinguishing between ischemic and hemorrhagic stroke. It is important to assess and stabilize vital physiologic functions before sending the patient for an imaging study.
The physical examination should include careful evaluation of the neck and retroorbital regions for vascular bruits, and palpation of pulses in the neck, arms, and legs to assess for their absence, asymmetry, or irregular rate. The heart should be auscultated for murmurs. The lungs should be assessed for abnormal breath sounds, bronchospasm, fluid overload, or stridor.
The skin should be examined for signs of endocarditis, cholesterol emboli, purpura, ecchymoses, or evidence of recent surgery or other invasive procedures, particularly if reliable history is not forthcoming. The funduscopic examination may be helpful if there are cholesterol emboli or papilledema. The head should be examined for signs of trauma. A tongue laceration may suggest a seizure.
In cases where there is a report or suspicion of a fall, the neck should be immobilized until evaluated radiographically for evidence of serious trauma. Examination of the extremities is important to look for evidence of systemic arterial emboli, distal ischemic, cellulitis, and deep vein thrombosis; the latter should raise the possibility that the patient is receiving anticoagulant treatment.
NEUROLOGIC EVALUATION: The neurologic examination should attempt to confirm the findings from the history and provide a quantifiable examination for further assessment over time. Many scales are available that provide a structured, quantifiable neurologic examination. One of the most widely used and validated scales is the National Institutes of Health Stroke Scale (NIHSS), composed of 11 items adding up to a total score of 0 to 42; defined cutpoints for mild, moderate, and severe stroke are not well established, but cut-points of NIHSS score <5 for mild, 5 to 9 for moderate, and ≥10 for severe stroke may be reasonable.
The three most predictive examination findings for the diagnosis of acute stroke are facial paresis, arm drift / weakness, and abnormal speech (a combination of dysarthria and language items derived from the NIHSS).(27,28) The NIHSS score on admission has been correlated to stroke outcome.(29,30) and its use is recommended for all patients with suspected stroke.(31)
IMMEDIATE LABORATORY STUDIES: All patients with suspected stroke should have the following studies urgently as part of the acute stroke evaluation:(23,25)
- Noncontrast brain CT or brain MRI
- Finger stick blood glucose
- Oxygen saturation
Other immediate tests for the evaluation of ischemic and hemorrhagic stroke include the following: (23,25)
- Complete blood count including platelets
- Cardiac enzymes and troponin
- Serum electrolytes, urea nitrogen, creatinine
- Prothrombin time and international normalized ratio (INR)
- Activated partial thromboplastin time
However, fibrinolytic therapy for acute ischemic stroke should not be delayed while awaiting the results of hematologic studies unless the patient has received anticoagulants or there is suspicion of a bleeding abnormality or thrombocytopenia.
The following laboratory studies are appropriate in selected patients:(23,25,26)
- Liver function tests
- Toxicology screen
- Blood alcohol level
- Pregnancy test in women of child-bearing potential
- Arterial blood gas if hypoxia is suspected
- Chest radiograph if lung disease is suspected
- Lumbar puncture if subarachnoid hemorrhage is suspected and head CT scan is negative for blood; note that lumbar puncture will preclude administration of tPA, though tPA should not be given if there is suspicion for subarachnoid hemorrhage as the cause of the symptoms
- Electroencephalogram if seizures are suspected
- Thrombin time and or ecarin clotting time if known or suspected that the patient is taking direct thrombin inhibitor or direct factor Xa inhibitor
Chest radiography, urinalysis and blood cultures are indicated if fever is present. We also suggest blood for type and cross match in case fresh frozen plasma is needed to reverse a coagulopathy if ICH is present.
In order to limit medication dosage errors, particularly with the use of alteplase, an accurate body weight should be obtained early during the urgent evaluation.(32)
NEUROIMAGING: Urgent brain imaging with CT or MRI is mandatory in all patients with sudden neurologic deterioration or acute stroke. In the evaluation of the acute stroke patient, imaging studies are necessary to exclude hemorrhage as a cause of the deficit, and they are useful to assess the degree of brain injury and to identify the vascular lesion responsible for the ischemic deficit. Some advanced CT and MRI technologies may be able to distinguish between brain tissue that is irreversibly infarcted and that which is potentially salvageable, thereby allowing better selection of patients who are likely to benefit from therapy.
CARDIAC STUDIES: Electrocardiography (ECG) is important for detecting signs of concomitant acute cardiac ischemia. This test is particularly important in the setting of stroke, as patients with ischemic stroke frequently harbor coronary artery disease but may not be able to report chest pain.
Stroke alone can be associated with ECG changes. The sympathetic response to stroke can lead to demand-induced myocardial ischemia. In large strokes, especially subarachnoid hemorrhage, there are centrally mediated changes in the ECG. The ECG and cardiac monitoring are important for the detection of chronic or intermittent arrhythmias that predispose to embolic events (e.g. atrial fibrillation) and for detecting indirect evidence of atrial / ventricular enlargement that may predispose to thrombus formation.
PALLIATIVE CARE: Palliative care is an important component of comprehensive stroke care. Some patients with severe strokes die during the initial hospitalization, others will be severely disabled and palliative care can begin to address the patient's and family's short- and long-term needs. Some patients have advance directives providing instructions for medical providers in the event of severe medical illness or injury.
STROKE MANAGEMENT ISSUES: Early key management issues that often arise in acute stroke include blood pressure control, fluid management, treatment of abnormal blood glucose levels, swallowing assessment, and treatment of fever and infection.
FLUIDS: Intravascular volume depletion is frequent in the setting of acute stroke, particularly in older adult patients,(33) and may worsen cerebral blood flow. For most patients with acute stroke and volume depletion, isotonic saline without dextrose is the agent of choice for intravascular fluid repletion and maintenance fluid therapy.(34) In general, it is best to avoid excess free water (e.g. as in ½ isotonic saline) because hypotonic fluids may exacerbate cerebral edema in acute stroke and are less useful than isotonic solutions for replacing intravascular volume.
HYPOGLYCEMIA: Hypoglycemia can cause focal neurologic deficits mimicking stroke, and severe hypoglycemia alone can cause neuronal injury. It is important to check the blood sugar and rapidly correct low serum glucose (<60 mg / dL or 3.3 mmol / L) at the first opportunity. Normoglycemia is the desired goal while avoiding marked elevation of serum glucose.(23)
HYPERGLYCEMIA: Hyperglycemia may augment brain injury by several mechanisms including increased tissue acidosis from anaerobic metabolism, free radical generation, and increased blood brain barrier permeability. Several lines of evidence point to the deleterious effects of elevated glucose in acute stroke:(35)
- Hyperglycemia worsens ischemic damage in animal models of stroke
- Glucose reduction decreases ischemic damage in experimental models
- Acute hyperglycemia is associated with reduced salvage of penumbral tissue and greater final infarct size by neuroimaging(36)
- Hyperglycemia is associated with reduced benefit from recanalization with thrombolytic therapy and higher odds for symptomatic intracerebral hemorrhage(37)
The American Heart Association / American Stroke Association guidelines for acute ischemic stroke recommend treatment for hyperglycemia to achieve serum glucose concentrations in the range of 140 to 180 mg / dL (7.8 to 10 mmol / L).(23) The European Stroke Initiative guidelines recommend treatment for glucose >180 mg / dL (>10 mmol / L).(38)
SWALLOWING ASSESSMENT: Dysphagia is common after stroke and is a major risk factor for developing aspiration pneumonia. It is important to assess swallowing function prior to administering oral medications or food.
HEAD AND BODY POSITION: During the acute phase of stroke, the position of the patient and the head of bed should be individualized with respect to the risk of elevated intracranial pressure and aspiration, and the presence of comorbid cardiopulmonary disease.
It is recommended to keep the head in neutral alignment with the body and elevating the head of the bed to 30 degrees for patients in the acute phase of stroke who are at risk for any of the following problems:
- Elevated intracranial pressure (i.e. intracerebral hemorrhage, cerebral edema >24 hours from stroke onset in patients with large ischemic infarction)
- Aspiration (e.g. those with dysphagiaand / or diminished consciousness)
- Cardiopulmonary decompensation or oxygen desaturation (e.g. those with chronic cardiac and pulmonary disease)
It is suggested to keep the head of bed flat (0 to 15 degree head-of-bed position) for patients in the first 24 hours after ischemic stroke onset who are not at risk for elevated intracranial pressure, aspiration, or worsening cardiopulmonary status.
Keeping the patient flat is a temporary measure that should be discontinued in most patients after 24 to 48 hours. National guidelines favor early mobilization because it lessens the likelihood of major complications such as pneumonia, deep vein thrombosis, pulmonary embolism, and pressure sores after stroke.(23) Exceptions may include those who exhibit neurologic deterioration upon assuming more upright postures. For this reason, close observation is recommended when patient position is altered,(23) as during the transition from lying to sitting and standing.
FEVER: Fever may contribute to brain injury in patients with an acute stroke. The source of fever should be investigated and treated, and antipyretics should be used to lower temperature in febrile patients with acute stroke.(23,25) It is suggested to maintain normothermia for at least the first several days after an acute stroke.(39) However, the clinical utility of this approach has not been established.
BLOOD PRESSURE MANAGEMENT:
ACUTE ISCHEMIC STROKE: Special considerations apply to blood pressure control in patients with acute ischemic stroke who are eligible for thrombolytic therapy. Before lytic therapy is started, treatment is recommended so that systolic blood pressure is ≤185 mmHg and diastolic blood pressure is ≤110 mmHg.(23) The blood pressure should be stabilized and maintained at or below 180 / 105 mmHg for at least 24 hours after thrombolytic treatment.
For patients with ischemic stroke who are not treated with thrombolytic therapy, most consensus guidelines recommend that blood pressure not be treated acutely unless the hypertension is extreme (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg), or the patient has active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute renal failure, or pre-eclampsia / eclampsia.(23,40) When treatment is indicated, cautious lowering of blood pressure by approximately 15 percent during the first 24 hours after stroke onset is suggested.(23)
Current guidelines suggest that it is reasonable to restart antihypertensive medications 24 hours after stroke onset in patients with preexisting hypertension who are neurologically stable, unless a specific contraindication to restarting treatment is known.(23)
If acute antihypertensive therapy is needed, intravenous agents are generally used.
Current guidelines note that vasopressors may be used to improve cerebral blood flow in rare cases when systemic hypotension is producing neurologic impairment, with close neurologic and cardiac monitoring.(23)
ACUTE HEMORRHAGIC STROKE: In both intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH), the approach to blood pressure management must take into account the potential benefits (e.g. reducing further bleeding) and risks (e.g. reducing cerebral perfusion) of blood pressure lowering.
CHOICE OF ANTIHYPERTENSIVE AGENT: In the acute phase of stroke, there is no clear evidence to support the use of any specific antihypertensive agent to achieve recommended blood pressure goals.(23) Consensus guidelines suggest intravenous labetalol and nicardipine as first-line antihypertensive agents if pharmacologic therapy is necessary in the acute phase, since they allow rapid and safe titration to the goal blood pressure.(23)
Intravenous nitroprusside should be considered second-line therapy since it carries added theoretical risks of increasing intracranial pressure or affecting platelet function.
ACUTE THERAPY: For eligible patients with acute ischemic stroke, intravenous alteplase is first-line therapy, provided that treatment is initiated within 4.5 hours of clearly defined symptom onset. Because the benefit of alteplase is time dependent, it is critical to treat patients as quickly as possible. Eligible patients with a large artery occlusion presenting within 6 hours of symptom onset should receive endovascular thrombectomy.
ISCHEMIC STROKE MANAGEMENT: In addition to intravenous thrombolysis with alteplase and endovascular thrombectomy, a number of interventions for ischemic stroke are associated with either reduced disability, complications, or stroke recurrence, including:
- Antithrombotic therapy with aspirin initiated within 48 hours of stroke onset
- Prophylaxis for deep venous thrombosis and pulmonary embolism
- Antithrombotic therapy at discharge
- Lipid lowering with high intensity statin therapy
- Blood pressure reduction after the acute phase of ischemic stroke has passed
- Behavioral and lifestyle changes including smoking cessation, exercise, weight reduction for obese patients, and a Mediterranean style diet
STATIN THERAPY: For patients with acute ischemic stroke, it is suggested to start or continue statin treatment as soon as oral medications can be used safely. There is clear evidence that long-term intensive statin therapy is associated with a reduced risk of recurrent ischemic stroke and cardiovascular events.
SEROTONIN-REUPTAKE INHIBITORS (SSRIS): There is some evidence from small randomized controlled trials suggesting that early initiation of selective serotonin-reuptake inhibitors (SSRIs) after ischemic stroke for patients with hemiparesis but without depression enhances motor recovery and reduces dependency.(41,42,43) Larger trials are needed to determine the role of SSRIs for promoting recovery after ischemic stroke.
NEUROPROTECTIVE AGENTS: The rationale for the use of neuroprotective agents is that reducing the release of excitatory neurotransmitters by neurons in the ischemic penumbra may enhance the survival or these neurons. Despite very promising results in several animal studies, however, clinical trials have thus far failed to confirm consistent benefit.(44-48)
STROKE UNIT CARE: Evidence suggests that patients with acute stroke have better outcomes when admitted to a hospital unit that is specialized for the care of patients with all types of acute stroke, including ischemic, intracerebral hemorrhage, and subarachnoid hemorrhage.(49-52)
GOALS OF THERAPY:
Immediate goals include minimizing brain injury, treating medical complications, and moving toward uncovering the pathophysiologic basis of the patient's symptoms.
To review “The American Heart Association (AHA) /American Stroke Association (ASA) guidelines for acute ischemic stroke”, please click on below link:
To review “European Stroke Initiative guidelines”, please click on below link:
CONSULTATION AND COUNSELLING:
A stroke team or an experienced professional who is sufficiently familiar with stroke should be available within 15 minutes of the patient's arrival in the Emergency Department. Other consultations are tailored to individual patient needs. Often, occupational therapy, physical therapy, speech therapy, and physical medicine and rehabilitation experts are consulted within the first day of hospitalization.
Consultation of cardiology, vascular surgery, or neurosurgery may be warranted based on the results of carotid duplex scanning, neuroimaging, transthoracic and transesophageal echocardiography, and clinical course. During hospitalization, additional useful consultations include the following:
- Home health care coordinator
- Rehabilitation coordinator
- Social worker
- Psychiatrist (commonly for depression)
A number of behavioral and lifestyle modifications may be beneficial for reducing the risk of ischemic stroke and cardiovascular diseases. These include smoking cessation, limited alcohol consumption, weight control, regular aerobic physical activity, salt restriction, and a Mediterranean diet.
SMOKING CESSATION: All patients who are recent or current tobacco smokers should be counseled routinely to quit smoking.
ALCOHOL CONSUMPTION: All patients with ischemic stroke or TIA who are heavy drinkers should eliminate or reduce their alcohol consumption because of the increased risk of stroke and high morbidity associated with alcoholism.
PHYSICAL ACTIVITY AND EXERCISE: For patients with ischemic stroke or TIA who are capable of regular exercise, suggest moderate to vigorous intensity physical exercise most days of the week for at least 40 minutes. Moderate intensity exercise is defined as activity sufficient to break a sweat or noticeably raise the heart rate (e.g. walking briskly, using an exercise bicycle)
DIET: Emerging evidence suggests that dietary interventions, and in particular a Mediterranean diet improves outcomes in patients with established cardiovascular disease. Mediterranean-type diet that emphasizes the intake of vegetables, fruits, whole grains, low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, and nuts. It limits the intake of sweets, sugar-sweetened beverages, and red meats. Calories from saturated fat should be limited to 5 to 6 percent and calories from trans-fat should be reduced. For patients who would benefit from blood pressure lowering, a reduction in sodium (no more than 2400 mg per day) is also suggested.
WEIGHT REDUCTION: Weight reduction for obese patients is potentially beneficial for improved control of other important parameters, including blood pressure, blood glucose, and serum lipid levels ultimately preventing stroke.
MANAGING UNDERLYING CONDITIONS:
If patient is suffering from any condition which is known to increase risk of stroke such as high cholesterol, high blood pressure, atrial fibrillation, diabetes or a transient ischaemic attack (TIA), ensuring the condition is well controlled is also important in helping prevent strokes.
- Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012; 380:2095.
- Krishnamurthi RV, Feigin VL, Forouzanfar MH, et al. Global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990-2010: findings from the Global Burden of Disease Study 2010. Lancet Glob Health 2013; 1:e259.
- Writing Group Members, Mozaffarian D, Benjamin EJ, et al. Heart Disease and Stroke Statistics-2016 Update: A Report From the American Heart Association. Circulation 2016; 133:e38.
- World Health Organization (WHO). The Atlas of Heart Disease and Stroke. http://www.who.int/cardiovascular_diseases/resources/atlas/en/
- Kamal AK, Itrat A, Murtaza M, Khan M, Rasheed A, Ali A, et al. The burden of stroke and transient ischemic attack in Pakistan: a community-based prevalence study. BMC Neurol 2009; 9:58.
- Farooq MU, Majid A, Reeves MJ, Birbeck GL. The epidemiology of stroke in Pakistan: past, present, and future. Int J Stroke 2009; 4:381-9.
- Khealani BA, Wasay M. The burden of stroke in Pakistan. Int J Stroke 2008; 3:293-6
- Donnan GA, Fisher M, Macleod M, Davis SM. Stroke. Lancet. 2008 May 10. 371(9624):1612-23.
- Dirnagl U, Iadecola C, Moskowitz MA. Pathobiology of ischaemic stroke: an integrated view. Trends Neurosci. 1999 Sep. 22(9):391-7.
- Yuan J, Yankner BA. Apoptosis in the nervous system. Nature. 2000 Oct 12. 407(6805):802-9.
- Latchaw RE, Yonas H, Hunter GJ, Yuh WT, Ueda T, Sorensen AG, et al. Guidelines and recommendations for perfusion imaging in cerebral ischemia: A scientific statement for healthcare professionals by the writing group on perfusion imaging, from the Council on Cardiovascular Radiology of the American Heart Association.Stroke. 2003 Apr. 34(4):1084-104.
- Kasner SE, Grotta JC. Emergency identification and treatment of acute ischemic stroke.Ann Emerg Med. 1997 Nov. 30(5):642-53.
- Gotoh O, Asano T, Koide T, Takakura K. Ischemic brain edema following occlusion of the middle cerebral artery in the rat. I: The time courses of the brain water, sodium and potassium contents and blood-brain barrier permeability to 125I-albumin. Stroke. 1985 Jan-Feb. 16(1):101-9.
- Bell BA, Symon L, Branston NM. CBF and time thresholds for the formation of ischemic cerebral edema, and effect of reperfusion in baboons. J Neurosurg. 1985 Jan. 62(1):31-41.
- Mullins ME, Lev MH, Schellingerhout D, Gonzalez RG, Schaefer PW. Intracranial hemorrhage complicating acute stroke: how common is hemorrhagic stroke on initial head CT scan and how often is initial clinical diagnosis of acute stroke eventually confirmed?.AJNR Am J Neuroradiol. 2005 Oct. 26(9):2207-12
- Lyden PD, Zivin JA. Hemorrhagic transformation after cerebral ischemia: mechanisms and incidence.Cerebrovasc Brain Metab Rev. 1993 Spring. 5(1):1-16
- Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group.N Engl J Med. 1995 Dec 14. 333(24):1581-7
- Nighoghossian N, Hermier M, Adeleine P, Blanc-Lasserre K, Derex L, Honnorat J, et al. Old microbleeds are a potential risk factor for cerebral bleeding after ischemic stroke: a gradient-echo T2*-weighted brain MRI study.Stroke. 2002 Mar. 33(3):735-42
- González RG. Imaging-guided acute ischemic stroke therapy: From "time is brain" to "physiology is brain".AJNR Am J Neuroradiol. 2006 Apr. 27(4):728-35
- Albers GW, Amarenco P, Easton JD, Sacco RL, Teal P. Antithrombotic and thrombolytic therapy for ischemic stroke: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.Chest. 2004 Sep. 126(3 Suppl):483S-512S
- [Guideline]Adams HP Jr, del Zoppo G, Alberts MJ, Bhatt DL, Brass L, Furlan A, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. 2007 May. 38(5):1655-711.
- Kim EY, Na DG, Kim SS, Lee KH, Ryoo JW, Kim HK. Prediction of hemorrhagic transformation in acute ischemic stroke: role of diffusion-weighted imaging and early parenchymal enhancement.AJNR Am J Neuroradiol. 2005 May. 26(5):1050-5
- Jauch EC, Saver JL, Adams HP Jr, 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.
- Demaerschalk BM, Kleindorfer DO, Adeoye OM, et al. Scientific Rationale for the Inclusion and Exclusion Criteria for Intravenous Alteplase in Acute Ischemic Stroke: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2016; 47:581.
- Hemphill JC 3rd, Greenberg SM, Anderson CS, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2015; 46:2032.
- Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke 2012; 43:1711.
- Kothari R, Hall K, Brott T, Broderick J. Early stroke recognition: developing an out-of-hospital NIH Stroke Scale. Acad Emerg Med 1997; 4:986.
- Goldstein LB, Simel DL. Is this patient having a stroke? JAMA 2005; 293:2391.
- Generalized efficacy of t-PA for acute stroke. Subgroup analysis of the NINDS t-PA Stroke Trial. Stroke 1997; 28:2119.
- Adams HP Jr, Davis PH, Leira EC, et al. Baseline NIH Stroke Scale score strongly predicts outcome after stroke: A report of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Neurology 1999; 53:126.
- Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke 2007; 38:1655.
- Michaels AD, Spinler SA, Leeper B, et al. Medication errors in acute cardiovascular and stroke patients: a scientific statement from the American Heart Association. Circulation 2010; 121:1664.
- Rodriguez GJ, Cordina SM, Vazquez G, et al. The hydration influence on the risk of stroke (THIRST) study. Neurocrit Care 2009; 10:187.
- Burns JD, Green DM, Metivier K, DeFusco C. Intensive care management of acute ischemic stroke. Emerg Med Clin North Am 2012; 30:713.
- Lindsberg PJ, Roine RO. Hyperglycemia in acute stroke. Stroke 2004; 35:363.
- Parsons MW, Barber PA, Desmond PM, et al. Acute hyperglycemia adversely affects stroke outcome: a magnetic resonance imaging and spectroscopy study. Ann Neurol 2002; 52:20.
- Bruno A, Levine SR, Frankel MR, et al. Admission glucose level and clinical outcomes in the NINDS rt-PA Stroke Trial. Neurology 2002; 59:669.
- European Stroke Initiative Executive Committee, EUSI Writing Committee, Olsen TS, et al. European Stroke Initiative Recommendations for Stroke Management-update 2003. Cerebrovasc Dis 2003; 16:311.
- Ginsberg MD, Busto R. Combating hyperthermia in acute stroke: a significant clinical concern. Stroke 1998; 29:529.
- National Institute for Health and Clinical Excellence. Stroke: The diagnosis and acute management of stroke and transient ischaemic attacks. Royal College of Physicians, London 2008. http://www.nice.org.uk/CG068 (Accessed on February 01, 2011).
- Mead GE, Hsieh CF, Lee R, et al. Selective serotonin reuptake inhibitors (SSRIs) for stroke recovery. Cochrane Database Syst Rev 2012; 11:CD009286.
- Chollet F, Tardy J, Albucher JF, et al. Fluoxetine for motor recovery after acute ischaemic stroke (FLAME): a randomised placebo-controlled trial. Lancet Neurol 2011; 10:123.
- Mead GE, Hsieh CF, Hackett M. Selective serotonin reuptake inhibitors for stroke recovery. JAMA 2013; 310:1066.
- Dávalos A, Alvarez-Sabín J, Castillo J, et al. Citicoline in the treatment of acute ischaemic stroke: an international, randomised, multicentre, placebo-controlled study (ICTUS trial). Lancet 2012; 380:349.
- Reza Noorian A, Nogueira R, Gupta R. Neuroprotection in acute ischemic stroke. J Neurosurg Sci 2011; 55:127.
- Sahota P, Savitz SI. Investigational therapies for ischemic stroke: neuroprotection and neurorecovery. Neurotherapeutics 2011; 8:434.
- Tymianski M. Can molecular and cellular neuroprotection be translated into therapies for patients?: yes, but not the way we tried it before. Stroke 2010; 41:S87.
- Ginsberg MD, Palesch YY, Hill MD, et al. High-dose albumin treatment for acute ischaemic stroke (ALIAS) Part 2: a randomised, double-blind, phase 3, placebo-controlled trial. Lancet Neurol 2013; 12:1049.
- Candelise L, Gattinoni M, Bersano A, et al. Stroke-unit care for acute stroke patients: an observational follow-up study. Lancet 2007; 369:299.
- Meretoja A, Roine RO, Kaste M, et al. Effectiveness of primary and comprehensive stroke centers: PERFECT stroke: a nationwide observational study from Finland. Stroke 2010; 41:1102.
- Di Carlo A, Lamassa M, Wellwood I, et al. Stroke unit care in clinical practice: an observational study in the Florence center of the European Registers of Stroke (EROS) Project. Eur J Neurol 2011; 18:686.
- Stroke Unit Trialists' Collaboration. Organised inpatient (stroke unit) care for stroke. Cochrane Database Syst Rev 2013; :CD000197.