Acute ischemic stroke is caused due to thrombotic or embolic occlusion of a cerebral artery. 

Sudden blood circulation loss in brain shows neurologic function loss in ischemic stroke cases. Cerebral hemispheres receive blood from three major paired arteries. 

Anterior and middle cerebral arteries from internal carotid arteries provide supply for anterior circulation. 

Posterior cerebral arteries from basilar artery provide supply in thalami, brainstem, and cerebellum for circulation. 

Strokes are divided into 2 types as:  

Hemorrhagic  

Ischemic 

Strokes are divided in 3 major subtypes: 

Large artery 

Small-vessel or lacunar 

Cardioembolic infarction 

Transient ischemic attack (TIA) is an acute episode of temporary neurologic dysfunction.  

The symptoms last for less than 1 hour to less than 30 minutes, but prolonged episodes can occur in some cases. 

Stroke is a major cause of disability and death in the US with around 795000 new or recurrent cases every year. 

WHO report shows 10 million cases globally, with 5 million deaths and 5 million permanent disabilities due to stroke. 

People with >55 years old shows stroke incidence rates from 4.2 to 6.5 per 1000 person. Stroke incidence higher in high-income country indigenous people. 

Acute strokes from blood vessel blockage causes cell oxygen deprivation and ATP depletion. ATP absence causes loss of energy for cell membrane gradients. 

Vascular occlusion causes varied ischemic regions in territory. Blood flow limited to residual flow and collateral supply. Certain brain regions prone to intracerebral hemorrhage include thalamus and putamen. 

TIA involve in temporary reduction of cerebral blood flow due to partial/total vessel occlusion from acute thromboembolic event or vessel stenosis. 

Causes of ischemic stroke are: 

• Age, Sex 
• Cerebral amyloidosis 
• Coagulopathy 
• Hypertension 
• History of migraine headaches  
• Fibromuscular dysplasia 

Prognosis post-acute ischemic stroke varies by stroke severity, premorbid condition, age, and poststroke complications. 

Cardiogenic emboli related to highest 1-month mortality in stroke. 

Analysed variables to determine factors linked with early stroke mortality. Ischemic stroke worsens outcome and morbidity at 3 months. 

Higher blood volume at onset predicts worse outcomes. Hematoma growth linked to poorer function and higher mortality. 

Detailed information including presenting symptoms and medical history of patient should be gathered. 

• Neurological Examination 
• Respiratory Examination 
• Cardiovascular Examination 

• Acute symptoms are: 
• Aphasia 
• Visual Disturbances 
• Diplopia 
• Dysarthria 
• Nausea and Vomiting 
• Seizures 
• Neck Stiffness 

Antipyretics recommended for febrile stroke patients to prevent neural damage from hyperthermia. 

Optimal blood pressure levels for acute hemorrhagic stroke patients are undefined, but high levels can worsen outcomes. 

Early intensive BP reduction in intracerebral hemorrhage treatment reduces hematoma growth in antithrombotic therapy recipients. 

Hematoma can cause elevated intracranial pressure, but frequency in intracerebral hemorrhage patients is unknown. 

Hemodynamics and reimaging for patients with deteriorating neurologic status. Those with hemorrhagic transformation or cerebral edema may decline clinically. 

Hypothermia showed promise in treating cardiac arrest survivors with specific conditions. 

Emergency Medicine

Blood glucose levels should be regularly monitored to maintain normal levels. High blood pressure should reduce to prevent worsening ischemia. 

Maintain oxygen saturation levels more than 94%. Isotonic saline is suggested to maintain hydration and electrolyte balance. 

Reduce stress and anxiety to maintain a quiet environment for patients. 

Proper education and awareness about ischemic stroke should be provided and its related causes, and how to stop it with management strategies. 

Appointments with a cardiologist and preventing recurrence of disorder is an ongoing life-long effort. 

Emergency Medicine

Alteplase: 

It promotes thrombolysis to convert plasminogen into plasmin, fibrin and fibrinogen. 

Emergency Medicine

Diazepam 

It modulates the postsynaptic effects of gamma-aminobutyric acid type A transmission in presynaptic inhibition. 

Phenytoin: 

It inhibits seizure activity in motor cortex and brainstem centers to prevent spread of seizures and grand mal episodes. 

Emergency Medicine

Aspirin: 

It blocks prostaglandin synthetase action to inhibit prostaglandin synthesis. 

Emergency Medicine

Warfarin: 

It is used to reduce the risk of death and thromboembolic events such as stroke or systemic embolization. 

Dabigatran: 

It inhibits clot-bound thrombin and thrombin-induced platelet aggregation. 

Emergency Medicine

Labetalol: 

It blocks beta1-, alpha-, and beta 2-adrenergic receptor sites to decrease BP.  

Emergency Medicine

Enalapril: 

It prevents the conversion of angiotensin I to angiotensin II which increases levels of plasma renin. 

Emergency Medicine

Nicardipine: 

It relaxes coronary smooth muscle and produces coronary vasodilation to improve myocardial oxygen delivery. 

Emergency Medicine

Nitroprusside sodium: 

It decreases peripheral vascular resistance to relax arteriolar smooth muscle.  

Emergency Medicine

Angioplasty and stenting are indicated in atherosclerotic stenosis cases. 

Ventriculostomy is performed to manage increased intracranial pressure due to hydrocephalus secondary stroke. 

Emergency Medicine

Initial assessment and stabilization phase includes stages of management as follows: 

Hyperacute phase within 0 to 6 hours 

Acute Phase within 6 to 24 hours 

Subacute Phase within 24 hours to 7 days 

Chronic Phase within 7 days and beyond 

Pharmacologic therapy is very effective in the treatment phase as it includes use of anticonvulsants, beta blocker, vasodilator, ACE inhibitors, anticoagulants and surgical intervention. 

In supportive care and management phase, patients should receive required attention such as lifestyle modification and rehabilitation. 

The regular follow-up visits with the cardiologist are schedule to check the improvement of patients along with treatment response.