You have a new patient!
Mrs. A, a 63-year-old female, was brought to the emergency department by her daughter after she noticed that her mother was unable to speak normally, and her face was droopy on the right side. Upon arrival, Mrs. A was lying on a stretcher in no acute distress. The daughter reported that her symptoms started suddenly about 30 minutes ago.
Vital signs showed a blood pressure of 170/90 mmHg, heart rate of 90 beats per minute, respiratory rate of 18 breaths per minute, Temperature is 36.6 C (98 F), and oxygen saturation of 98% on room air. The patient had a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus. On neurological examination, Ms. A was found to have right-sided facial droop, right arm pronator drift, and slurred speech. The NIH Stroke Scale (NIHSS) score was 8.
What do you need to know?
Importance
Acute ischemic stroke (AIS) is a major public health concern that affects millions of people worldwide. Stroke, ischemic or hemorrhagic, is the third most common cause of disability and the second most common cause of death worldwide [1]. It is estimated that 12.2 million strokes occur around the world annually, with the vast majority being ischemic [1,2]. Early recognition and management of acute ischemic stroke are vital as outcomes are directly tied to the time between the onset of symptoms and initiation of treatment. For every hour treatment is delayed, the brain loses as many neurons as it does in approximately 3.6 years of normal aging, which has led to the adage “time is brain” [3]. Therefore, emergency department physicians must be well-versed in diagnosing and managing acute ischemic stroke to maximize patient outcomes. The main goals in the acute management of ischemic stroke are to minimize ischemic damage to the penumbra, treat any complications because of the infarction, and diagnose the etiology to prevent a recurrence. The primary objectives of this chapter are to present a thorough overview of the major ideas and practices involved in the early evaluation and treatment of acute ischemic stroke in the emergency room.
Epidemiology
Understanding epidemiology can help elucidate risk factors that can result in faster recognition of stroke and its acute management. The vast majority of strokes occur beyond the 5th decade, with the age of onset being lower in low to middle-income countries [4]. In an acute setting, it is critical to identify if a stroke is ischemic or hemorrhagic, as treatment varies significantly [4,11]. This risk increases significantly with age, along with other lifestyle factors. These factors are listed in the table below (with the highest risk factors listed in descending order.)
Table 1. Modifiable and Non-modifiable risk factors for stroke [1,4–6]
Modifiable Risk Factors | Non-Modifiable Risk factors |
Hypertension | Prior history of stroke or TIA |
Cigarette smoking | Age ≥ 65 years |
Diabetes mellitus | Sex ♂ > ♀ |
Atrial Fibrillation | Family History |
Carotid artery stenosis | Genetic disorders (e.g., sickle cell) |
Dyslipidaemia | Migraine with aura |
Obesity and Metabolic syndrome | |
Diet/Nutrition | |
Sedentary Behavior | |
Alcohol/Recreational drug use (e.g. cocaine) | |
Coagulopathy | |
Hormone Replacement Therapy/OCP |
Pathophysiology
Acute ischemic strokes can occur due to thrombotic or embolic causes. One common link behind all the risk factors discussed above is that, in one form or another, they cause damage or dysfunction to blood vessels in the brain, reducing blood flow to the brain. Consequently, the parenchyma of the brain is unable to carry out its metabolic functions, which eventually leads to necrosis [7]. The exact mechanisms of how different risk factors contribute to stroke vary, but they ultimately all result in the damage of blood vessels in the brain. While there are many causes behind the damage of blood vessel walls, atherosclerosis and Virchow’s triad- blood stasis, endothelial injury, and hypercoagulability- remain the primary pathological process behind the vast majority of strokes [6,7]. For example, in Hypertension, the high pressures in the vessels cause shearing of the endothelial lining of blood vessel walls, which can result in rupture or thrombus formation. As the atherosclerotic plaques grow and become more advanced, they can lead to blood flow obstruction and turbulence, which can promote blood stasis. Blood stasis, in turn, can increase the risk of thrombosis within the affected blood vessel. The formation of a thrombus can obstruct blood flow to the brain and cause a stroke [7].
Similarly, smoking can cause inflammation and oxidative stress on blood vessels, causing an inflammatory response that ultimately results in the narrowing of the vessels and thrombus formation [8]. This framework also explains why older individuals are at higher risk since they have an increased prevalence of the modifiable risk factors listed in Table 1. [9]. Etiologies arising from circulatory system issues outside the brain require additional urgent management [5].
Medical History
A good history remains a key cornerstone in evaluating and managing stroke patients. Most typical presentations of strokes will be older adults presenting with acute onset focal neurological deficits. Patients might present with complaints of sudden onset speech difficulties, vision, sensation, strength, or coordination [10]. The acuity of neurologic dysfunction should clue physicians that stroke is an important differential. Another vital component when suspecting stroke is determining the time since the onset of symptoms. If this is unknown, then the last time the patient was seen well or at their neurological baseline can be used as a surrogate [11]. This step is critical as it helps determine whether the patient is within the window for reperfusion therapy and endovascular thrombectomy [5]. The 6S mnemonic list in Table 2. can be utilized to help clue clinicians that the patient might be having a stroke [12]:
Table 2. 6S mnemonic detailing core signs of stroke
S | Sudden onset |
S | Slurred speech |
S | Side weakness (unilateral deficits in face, arm, or leg) |
S | Spinning (Vertigo) |
S | Severe headache |
S | Seconds (time since symptoms started) |
The presence of this constellation should cue physicians to the immediate need for further evaluation of a serious process requiring labs and neuroimaging. The collection of symptoms can also give clues as to which vascular territory might be affected and can prompt the clinician to evaluate for further signs in that territory to help confirm the location. A general gestalt listed in Table 3. below can be used to help clinicians orient themselves as to which general vascular territory in the brain might be affected and what questions/exam findings to further probe for. The table is not exhaustive or mutually exclusive, and a more detailed discussion of the lesion site and associated neurologic findings is presented in the physical exam section.
Table 3. List of deficits and their associated territories [13]
Vascular territory | Associated deficits |
Anterior Cerebral Artery (ACA) | Feet and legs |
Middle Cerebral Artery (MCA) | Hands, Arms, Face, and Speech |
Posterior Cerebral Artery (PCA) | Visual |
Vertebrobasilar Artery (Brainstem) | Crossed signs (Contralateral hemiplegia & ipsilateral cranial nerve abnormalities) |
Cerebellar Arteries | Coordination |
The pace and course of symptoms can clue clinicians into the different subtypes of stroke that may be affecting the patient. Acute ischemic strokes due to embolic sources tend to occur suddenly, and the maximal deficit is perceived during this time. However, etiologies due to thrombosis tend to fluctuate and progress stepwise [14].
Other crucial components of medical history to assess are the risk factors mentioned in Table 1. They can help determine the precipitating factor for the stroke and can help guide management. For example, if the patient has a history of atrial fibrillation or carotid artery stenosis, then that could explain an embolic cause for the stroke and would require a more extensive workup along with additional management measures. Hypertension should also be sought out as it is the number one modifiable risk factor for stroke [2,6]. A review of current medications is also important because it can affect management. If a patient has been on anti-coagulation medications, then that is a strict contraindication for thrombolytics in stroke as it may lead to a hemorrhagic conversion [15]. In patients with acute ischemic stroke, a detailed medical history is crucial in directing the diagnostic and therapeutic decision-making process.
Physical Examination
Based on history, a focused physical and neurological exam can aid in localizing the lesion and provide clues as to the cause. Time is brain, and therefore, clinical suspicion of acute ischemic stroke should be rapidly confirmed with physical exam findings to minimize the time between the door to neuroimaging and recognize candidates for reperfusion therapy or endovascular thrombectomy [5,11,15]. As in all emergent cases, airway, breathing, circulation, disability, and exposure (ABCDE) should be prioritized in that order before attending to other steps in management. The physical exam should be tailored based on history to save time.
For example, if there is a history of atrial fibrillation, then a cardiac exam should be conducted to look for murmurs that might indicate an embolic cause. Patients with a history of atherosclerosis risk factors should also be examined for bruits in the neck that may reveal an embolic source. Papilledema on ocular exam may signify possible hemorrhagic stroke or cerebral edema as a complication of stroke that requires immediate intervention [16]. A neurologic exam is vital to confirm clinical suspicion of stroke and rule out other stroke mimics such as hypoglycemia or Bell’s palsy. Deficits on the exam can help point the clinician to the location of the lesion and the severity of the prognosis [13]. Table 4 below can be used to help localize the lesion based on clinical symptoms.
Table 4. A non-exhaustive list of common brain lesions and associated symptoms [13]
Vascular Territory | Common Neurologic Findings |
Anterior Cerebral Artery (ACA) |
|
Middle Cerebral Artery (MCA) |
|
Posterior Cerebral Artery (PCA) |
|
Anterior inferior cerebellar artery (AICA) |
|
Posterior inferior cerebellar artery (PICA) |
|
Vertebrobasilar system lesion (brainstem) |
|
The National Institutes of Health Stroke Scale (NIHSS) is one of the most studied and validated scales in clinical practice that should be used to provide a structured and quantifiable neurologic examination [5,11,12,16]. It includes 11 items (Table 5) and can be done in less than 10 minutes. The scale can quantify neurologic deficits and provide information about patient outcomes [17]. Facial paresis, arm weakness, and abnormal speech on the NIHSS are the most predictive findings for acute ischemic stroke [18].
Table 5. Snapshot of the National Institute of Health Stroke Scale (NIHSS) [5,19]
Instructions | Scale Definition |
1a. Level of consciousness (LOC) | 0 = Alert 1 = Drowsy- arousable by minor stimulation to obey, answer, or respond 2 = Obtunded; requires repeated stimulation to attend or is obtunded and requires strong or painful stimulation to make movements (not stereotyped). 3 = Unresponsive; Responds only with reflex motor or autonomic effects or unresponsive, flaccid, and areflexic. |
1b. Orientation Questions (2) | 0 = Answers both questions correctly. 1 = Answers one question correctly. 2 = Answers neither question correctly. |
1c. Response to commands (2) | 0 = Performs both tasks correctly 1 = Performs 1 task correctly 2 = Performs neither |
2. Gaze | 0 = Normal horizontal movements 1 = Partial gaze palsy 2 = Complete gaze palsy |
3. Visual fields | 0 = No visual field defect 1 = Partial hemianopia 2 = Complete hemianopia 3= Bilateral hemianopia |
4. Facial movement | 0 = Normal 1 = Minor facial weakness 2 = Partial facial weakness 3= Complete unilateral palsy |
5. Motor function (Arm) 5a. Left arm 5b. Right arm
| 0 = No drift 1 = Drift before 10 s 2 = Falls before 10 s 3= No effort against gravity 4=No movement |
6. Motor function (Leg) 6a. Left leg 6b. Right leg
| 0 = No drift 1 = Drift before 10 s 2 = Falls before 10 s 3= No effort against gravity 4=No movement |
7. Limb ataxia | 0 = No ataxia 1 = Ataxia in 1 limb 2 = Ataxia in 2 limbs 3= No effort against gravity 4=No movement |
8. Sensory | 0 = No sensory loss 1 = Mild sensory loss 2 = Severe sensory loss |
9. Language | 0 = Normal 1 = Mild aphasia 2 = Severe aphasia 3= Mute or global aphasia |
10. Articulation | 0 = Normal 1 = Mild dysarthria 2 = Severe dysarthria |
11. Extinction or inattention | 0 = Absent 1 = Mild loss (1 sensory modality lost) 2 = Severe loss (2 modalities lost) |
Vital signs play a critical role in the evaluation and management of acute ischemic stroke and conditions that may mimic stroke. Temperature, in particular, is a key parameter, as abnormalities can influence neurological function and mimic or exacerbate stroke symptoms. Hyperthermia (elevated body temperature) is associated with worsened outcomes in stroke patients due to increased metabolic demand and potential exacerbation of ischemic injury. On the other hand, hypothermia (lowered body temperature) can also cause altered mental status, which may resemble stroke-like presentations. Monitoring and correcting these temperature abnormalities is essential to optimize neurological recovery and rule out underlying infections or systemic conditions. Additionally, blood pressure, heart rate, respiratory rate, and oxygen saturation must be carefully assessed, as significant deviations can indicate complications such as increased intracranial pressure, arrhythmias, or hypoxia, which can impact stroke presentation and management.
Alternative Diagnoses
The differential diagnosis for acute-onset focal neurologic deficits, such as those found in acute ischemic stroke, is broad, and it is important to have a framework to rule out other causes. The VIINDICATES mnemonic (Table 6) can be useful in grouping the most frequent and important causes of acute neurologic dysfunction [20].
Table 6. Non-exhaustive differential diagnosis of acute ischemic stroke [21]
Vascular | Hemorrhagic stroke, cerebral venous thrombosis, arteriovenous fistulas, aneurysms |
Infectious | Meningitis, Encephalitis, Progressive multifocal leukoencephalopathy |
Immune system dysfunction/autoimmune | Multiple Sclerosis, Bell palsy, Guillain-Barré syndrome, Anti-NMDA encephalitis |
Neoplasm | Brain tumors, paraneoplastic syndromes, lung cancer |
Drugs | Alcohol withdrawal, drug intoxication (opioids, barbiturates, etc.) |
Cerebral/Neurologic | Transient ischemic attack (TIA), syncope, seizure, postictal paralysis, migraine aura |
Trauma | Traumatic brain injury, Subdural hematoma, epidural hematoma, Brown-Séquard syndrome |
Endocrine/Metabolic | Diabetic Ketoacidosis, hyponatremia, hypoglycemia |
Social/Psychiatric | Conversion disorder, malingering |
The clinician must pay close attention to the physical exam and medical history results that may favor one of these diagnoses over another to distinguish between them. Timing is critical and it is important to understand if the symptoms appeared suddenly or have been slowly brewing over time [12,16,21].
Acing Diagnostic Testing
When suspicion of acute ischemic stroke is high, time is of the essence due to the time limitations of thrombolytics or mechanical thrombectomy. Therefore, oxygen saturation, finger stick blood glucose, non-contrast head CT and angiography should be prioritized over all other tests as they are the only requirements before the administration of thrombolytics [5,11]. Oxygen saturation can help rule out hypoxia as a cause of neurological dysfunction [12,21]. Blood glucose is important as it can rule out hypoglycemia, DKA, or hyperosmolar hyperglycaemic state, which can all present like symptoms of stroke and can worsen outcomes with the administration of thrombolytics [22]. Neuroimaging is essential because it can help differentiate acute ischemic stroke from a hemorrhagic stroke, which has very different management. Neuroimaging can also rule out most other differential diagnoses discussed earlier when combined with physical history and exam. Loss of grey-white differentiation is an early CT finding in ischemic stroke, while increased density within the occluded vessel can represent a thrombus (Figure 1) [5,13,15,16,23].
Complete blood counts and coagulation studies should not delay the administration of thrombolytic therapy unless there is a high suspicion of coagulopathy or a history of the patient being on anticoagulating agents [5,12,16].
Electrocardiogram and cardiac markers such as troponin are also important to rule out cardiac causes. They may illuminate a source for emboli, such as atrial fibrillation, but this should not delay neuroimaging [5].
Other non-urgent lab tests that may be indicated depending on patient presentation include [5,10]:
Complete Metabolic Panel (CMP): Assesses electrolyte imbalances, renal function, and glucose levels, which are critical in stroke patients to rule out mimicking conditions (e.g., hypoglycemia) and to ensure safe administration of interventions like thrombolysis.
Blood Alcohol Level and Toxicology Screen: Helps identify substances that might contribute to altered mental status or stroke-like symptoms, such as intoxication or drug use, which can influence treatment decisions and prognosis.
Pregnancy Test in Women of Childbearing Age: Mandatory before imaging procedures involving radiation (e.g., CT) or medications (e.g., thrombolytics), as these might pose risks to a fetus.
Arterial Blood Gas (ABG): Assesses oxygenation, ventilation, and acid-base status. Useful in patients with suspected respiratory compromise or to evaluate hypoxia, which may exacerbate neurological deficits.
Chest Radiograph (CXR): Evaluates for underlying or concurrent conditions such as pneumonia, aspiration, or cardiac issues (e.g., heart failure) that could complicate stroke management.
Lumbar Puncture (LP): Performed if a hemorrhage is strongly suspected but not visible on a CT scan. Helps detect xanthochromia or elevated red blood cell count, which are indicative of subarachnoid hemorrhage.
Electroencephalogram (EEG): Recommended if seizures are suspected, as post-stroke seizures or seizure-like activity can mimic stroke symptoms or complicate recovery.
Urinalysis and Blood Cultures: Indicated in febrile patients to identify infections, such as urinary tract infections or sepsis, which might cause or exacerbate stroke-like presentations and impact recovery.
Blood Type and Cross-Match: Necessary if there is coagulopathy requiring reversal with fresh frozen plasma or if massive blood transfusion is anticipated in cases of hemorrhagic transformation.
MRI: Provides superior imaging of the brain compared to CT, identifying small or early infarcts and areas of ischemia. MRI is particularly valuable for stroke patients with ambiguous CT findings.
Risk Stratification
The presence of certain red flags, such as severe headache, papilledema, neck stiffness, loss of consciousness, or rapidly worsening neurological deficits, may indicate a worse outcome and the need for more aggressive management. These symptoms may indicate that the lesion has affected certain vital regions in the brain or there has been a conversion to hemorrhagic stroke [5,11]. Severe hypo/hyperglycemia (glucose < 50 mg/dL or > 400 mg/dL) or hypertension (> 185/110 mm Hg) also indicate a poor outcome as these need to be managed before reperfusion therapy can be utilized, which results in further neurologic insult [5]. The NIHSS score can be utilized to predict outcomes such as disability, recurrent stroke, or death. The higher the NIHSS score, the more severe the stroke and the worse the prognosis. In general, patients with an NIHSS score of 0-4 have a good prognosis, while those with a score of 20 or higher have a higher risk of death or severe disability [5,17,24].
Management
Stroke patients are treated as critically ill patients and require urgent management. This includes assessing and stabilizing the patient’s airway, breathing, and circulation (ABCs), conducting a thorough evaluation to determine whether thrombolytic therapy is appropriate, and addressing any underlying medical conditions, such as hypertension, that may complicate treatment [5,12,16].
Airway and breathing can be compromised due to damage to areas central to consciousness, breathing, or swallowing as listed in Table 7.
Table 7. Possible locations of lesions compromising the airway [25]
Levels of Consciousness | Breathing | Swallowing |
Thalami | respiratory centers in the cortex, pons, and medulla | Medulla & brainstem connections |
Limbic system | Pons |
|
Reticular formation in the brainstem | Medulla |
|
Damage to any of these areas requires securing the airway and maintaining breathing by positing the head of the bed to 30° to prevent aspiration. The specific approach will depend on the severity of the patient’s presentation [25]. Assessing the level of consciousness can provide valuable information to guide judgment. If a patient is awake, alert, and responsive, then they may be able to secure their airway and provide adequate ventilation on their own. Respiratory rate and effort should be assessed by looking for the rate of breathing, use of accessory muscles, or increased work of breathing. Airway patency can be determined by looking for signs of obstruction, such as snoring or stridor [16]. If oxygen saturation is below 94%, supplemental oxygen should be provided. Oxygen support is not beneficial if saturation is above 94% [5]. It is important to note that the neurologic exam can be severely limited if the patient requires intubation. Therefore, the clinician should pick up on subtle signs since the interaction with the patient began that can clue the physician on the baseline status, such as language function or any asymmetric motor activity, before the patient is pharmacologically paralyzed to be intubated [10].
Once breathing is secured, the next step is to ensure circulation is not compromised. Patients presenting with acute ischemic stroke frequently will be hypertensive as this is the body’s natural response to reperfuse the ischemic regions [16]. However, it is also not uncommon for patients to present with hypotension and hypovolemia. Due to the time-sensitive nature of acute ischemic stroke, correcting blood pressure takes priority [5]. When a patient with acute ischemic stroke has severe hypertension (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg), it may be necessary to lower their blood pressure to a safe level as administration of thrombolytics at this level can lead to hemorrhage [15]. Medications such as intravenous labetalol, nicardipine, or clevidipine can be used for cautious reduction (Table 8).
Table 8. Drug dosing for treatment of arterial hypertension in acute ischemic stroke [5]
Labetalol | 10–20 mg IV over 1–2 min, may repeat 1 time |
Nicardipine | 5 mg/h IV, titrate up by 2.5 mg/h every 5–15 min, maximum 15 mg/h; when desired BP reached, adjust to maintain proper BP limits |
Clevidipine | 1–2 mg/h IV, titrate by doubling the dose every 2–5 min until desired BP reached; maximum 21 mg/h |
In randomized controlled trials (RCTs) of intravenous (IV) thrombolytics, patients were required to have a systolic blood pressure <185 mm Hg and a diastolic blood pressure <110 mm Hg before treatment and <180/105 mm Hg for the first 24 hours after treatment [5]. Therefore, it is reasonable to aim for the blood pressure targets used in the RCTs of IV alteplase. In contrast, for patients with mild to moderate hypertension, it is generally advised to withhold blood pressure-lowering medications in the first few hours after the onset of stroke. This is because the rapid reduction in blood pressure can decrease cerebral perfusion and worsen ischemic injury [7].
Following stabilization, neuroimaging and lab tests discussed in the diagnostic test are prioritized to further aid in management. Figure 2 summarizes the steps discussed so far.
Once the diagnosis of acute ischemic stroke has been established, the next step is to figure out if the patient is eligible for thrombolysis (Table 9).
Table 9. Inclusion and exclusion criteria for rtTPA [5,15]
Inclusion Criteria |
|
Strict Exclusion Criteria |
|
Intravenous recombinant tissue plasminogen activator (tPA) agents such as Alteplase or Tenecteplase should be used (Table 10) [5,15,26]. Mechanical thrombectomy may be indicated if a large artery occlusion (LVO) is causing a stroke, and it has been less than 24 hours since symptom onset. The eligibility for mechanical thrombectomy and thrombolysis in individuals with ischemic stroke is assessed separately. Patients may be qualified for one, both, or neither of these treatments depending on the timing of their appearance (4.5 hours for thrombolysis, 24 hours for mechanical thrombectomy) [5,27]. However, if the patient is not eligible for either chemical thrombolysis or mechanical thrombectomy, immediate dual antiplatelet therapy (DAPT) with agents such as aspirin and clopidogrel should begin [5,28]. In the acute management of ischemic stroke (even if caused by atrial fibrillation [AF]), parenteral anticoagulation (e.g., intravenous heparin) should not be used because it increases the chance of hemorrhagic conversion [5,11].
Table 10. Dosing for rtTPA in the management of acute ischemic stroke [5]
Alteplase | IV 0.9 mg/kg over 60 minutes (max. dose 90 mg), with an initial 10% of dose given as a bolus over 1 minute |
Tenecteplase | IV 0.25 mg/kg as a bolus, max. dose 25 mg |
Aspirin | 160 to 325 mg loading dose, followed by 50 to 100 mg daily (for 21 days) |
Clopidogrel | 300 to 600 mg loading dose, followed by 75 mg daily (for 21 days) |
Special Patient Groups
When a patient presents with symptoms of acute ischemic stroke, clinical considerations differ based on age and special patient groups. Pediatric patients may experience stroke due to congenital heart disease, sickle cell disease, or infections. Symptoms may be less obvious and include seizures, vomiting, and headaches [29]. Diagnosis of stroke in pregnant patients is challenging, and thrombolytic agents may increase the risk of hemorrhage in both the mother and fetus [30]. Special patient groups, including those with sickle cell anemia or undergoing surgery, may also be at increased risk of stroke and require careful management. Treatment options should be carefully considered in these patient groups with an understanding of the potential risks and benefits [31].
When To Admit This Patient
Patients with acute ischemic stroke are generally admitted to the hospital for further investigations and treatment [5]. Early discharge may be considered for patients with mild symptoms, no significant comorbidities, and a low risk of complications, provided they have a reliable caregiver and access to appropriate follow-up care. Severe or progressive symptoms, significant comorbidities, or high risk of complications require admission to a stroke unit or critical care unit [5,16]. Discharge decisions should be based on a careful assessment of clinical status, risk of complications, and social circumstances. Clear instructions on medication, follow-up care, and stroke prevention strategies should be provided, along with safety-netting arrangements for timely and appropriate care if complications or worsening symptoms occur after discharge [5,32].
Revisiting Your Patient
Based on the initial assessment, Mrs. A is presenting with symptoms that are consistent with a stroke. The patient’s daughter reported that the symptoms started suddenly, and upon examination, Mrs. A has right-sided facial droop, right arm drift, and slurred speech. Her past medical history is significant for hypertension, hyperlipidemia, and type 2 diabetes mellitus. The NIHSS score of 8 indicates a moderate to severe stroke. Immediate management includes stabilizing the patient’s vital signs and providing supportive care, including oxygen and intravenous access. Given the suspicion of a stroke, a non-contrast head CT scan should be obtained to rule out a hemorrhagic stroke. Mrs. A should be considered for thrombolytic therapy with alteplase as she is within the appropriate time window, and there are no contraindications.
Authors
Hassan KHURAM BS, MS
Hassan Khuram is a 4th year medical student at Drexel University College of Medicine, with a background in psychology, biotechnology, and business of healthcare. He graduated Magna Cum Laude with a Bachelor of Science in Psychology from Virginia Commonwealth University and a Master of Science in Biotechnology from Georgetown University. He is passionate about neurocritical care, medical education, and bioethics. He has an extensive background in research, having conducted studies on various subjects, including substance misuse, Parkinson's disease, mindfulness meditation and more. He has published articles on neurological emergencies and ethical issues in neurological care.
Parker MADDOX BA, MS
Parker Maddox is a fourth-year medical student at Sidney Kimmel Medical College at Thomas Jefferson University in Philadelphia. He graduated from the University of Virginia with a double major in Biology and Chemistry and went on to obtain a master’s degree in Biophysics and Physiology at Georgetown University. Since arriving to medical school, Parker has developed a passion for Emergency Medicine and has performed research on a wide range of topics including early sepsis recognition, pandemic viruses including Coronavirus 2019 and Monkeypox, ischemic stroke, Bell’s palsy, and international ECMO critical care protocol. This work has yielded multiple publications and a presentation at the Society for Academic Emergency Medicine (SAEM) 2022 Conference.
Scott GOLDSTEIN, DO, FACEP, FAEMS, FAAEM, EMT-PHP
Dr. Scott Goldstein started his medical career at New York College of Osteopathic Medicine in New York where he received his Doctorate of Osteopathy and continued his training at Einstein Healthcare Network in the field of Emergency Medicine, Philadelphia. Dr. Goldstein is dual-boarded through the American Board of Emergency Medicine in Emergency Medicine and Emergency Medicine Services (EMS). He currently works at a Level 1 academic trauma center, Temple University Hospital, in Philadelphia where he is the Chief of EMS and Disaster Medicine. He has continued to be an active member of the education community and EMS community where he holds the title of Fellow of American College of Emergency Medicine through ACEP, Fellow of the Academy of Emergency Medical Services through NAEMSP and Fellow of the American Academy of Emergency Medicine through AAEM. His current academic title is one of Clinical Associate Professor of Emergency Medicine at Lewis Katz School of Medicine at Temple University.
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Reviewed and Edited By
Arif Alper Cevik, MD, FEMAT, FIFEM
Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.
