You Have A New Patient!
A 63-year-old male is brought to the Emergency Department (ED) by paramedics with a chief complaint of transient right-sided weakness. He states that the weakness started suddenly while he was watering his garden, lasted about 15 minutes, and then resolved without any residual deficits. On examination, his temperature is 36°C, blood pressure is 150/90 mmHg, pulse is 81 beats/min, respiratory rate is 18 breaths/min, and oxygen saturation is 97% on room air.
The patient’s past medical history is remarkable for hypertension, diabetes mellitus, and hyperlipidemia. He also smokes half a pack of cigarettes daily.
What Do You Need To Know?
Importance
Transient Cerebral Ischemia (TCI) or Transient Ischemic Attack (TIA) is defined as a sudden onset of transient, focal neurological symptoms and/or signs that occur due to focal brain, spinal cord, or retinal ischemia, without acute infarction [1]. Neurological symptoms and signs are related to the ischemic area of the brain. TIA is a neurologic emergency because patients with TIA have an early high risk of subsequent stroke. Up to 80% of strokes after TIA are preventable. Therefore, early recognition and differentiation of TIA cases are important for early treatment, which reduces the possibility of stroke. In brief, TIA represents a great opportunity for the physician to prevent stroke. Early diagnosis and treatment are the key.
Epidemiology
TIA is an important clinical condition that is common worldwide. The total global incidence of TIA is approximately 1.19 per 1000 persons per year, and it has been observed that the incidence is higher (4.88 per 1000 persons) in older age groups (85–94 years) [2]. TIA is more common in Black and male populations than in White and female populations [3].
Pathophysiology
TIA is mainly caused by three mechanisms of pathophysiology: (1) intrinsic vascular (lacunar or small vessel) pathogenesis such as atherosclerosis, lipohyalinosis, inflammation, and amyloidosis; (2) embolism originating from the heart and extracranial large vessels; and (3) low-flow conditions such as insufficient blood flow to the brain, decreased perfusion pressure, and increased blood viscosity [4].
(1) Lacunar or small vessel TIA: These TIAs are usually due to atherosclerosis of the proximal vessels or lipohyalinosis of the distal vessels. Small vessel TIAs cause symptoms similar to the lacunar strokes that are likely to follow, such as weakness or numbness in the arms, legs, and face, which are recurrent and progressive.
(2) Embolic TIAs: These are characterized by a relatively longer duration of focal neurological symptoms. These TIAs are mostly the result of embolism from a specific source. Embolism can originate from larger arteries or from the heart. In one study, it was determined that the symptoms of embolic TIAs lasted longer (hours) than those of low-flow TIAs (lasting minutes) [5].
TIAs create specific symptoms according to the regions of the occluded vessel:
Anterior circulation embolic TIA: Larger emboli can occlude the middle cerebral artery stem and cause contralateral hemiplegia, cortical surface symptoms (aphasia and dysexecutive syndromes in the dominant hemisphere, anosognosia or neglect in the nondominant hemisphere). Smaller emboli can occlude branches of the middle cerebral artery and cause focal symptoms such as numbness, weakness, and/or heaviness of the hand and arm.
Posterior circulation embolic TIA: These emboli can cause transient ataxia, diplopia, dizziness, dysarthria, hemianopsia, quadrantanopia, numbness, and unilateral hearing loss. If the embolus lodges at the top of the basilar artery, stupor or coma may occur. If the embolus lodges in the distal branches of the posterior cerebral artery, it can cause memory loss or a homonymous field defect.
(3) Low-flow TIA occurs with an obstructive vascular process in any extracranial or intracranial artery and disruption of collateral flow in the area supplied by these arteries. Low-flow TIAs are usually of short duration (minutes) and recurrent [4].
Anterior circulation low-flow TIA: These TIAs usually produce symptoms of a similar character. They occur due to hemodynamically significant stenotic lesions, especially in the proximal internal carotid artery, middle cerebral artery, and internal carotid artery, where collateral flow from the circle of Willis is insufficient. Ischemia-related symptoms resulting from these lesions usually include weakness or numbness in the hands, arms, legs, face, tongue, and/or cheek. Recurrent aphasic syndromes occur when there is focal ischemia in the dominant hemisphere, and recurrent neglect occurs when there is focal ischemia in the nondominant hemisphere. Limb-shaking TIAs are a rare but classic hypoperfusion syndrome in which repetitive jerking movements of the arm or leg are due to severe stenosis or occlusion of the contralateral internal carotid or middle cerebral artery.
Posterior circulation low-flow TIA: Unlike anterior low-flow TIA, the symptoms of these TIAs are not stereotypical because many neuronal structures in the brainstem are located very close to each other. Posterior low-flow TIA symptoms include diplopia, eyelid drooping, inability to look up, dysarthria, dizziness, drowsiness, bilateral leg and arm weakness or numbness, a feeling of heaviness, and numbness on one side of the body or face.
The diagnosis of TIA is based on the clinical features of the transient neurological attack and neuroimaging findings [6]. The majority of TIA cases do not present when fully symptomatic. For this reason, the history reported by the patient and witnesses is very important in terms of diagnosis [7]. TIA patients may experience typical or atypical symptoms.
Typical TIA:
It consists of focal neurological symptoms of sudden onset and transient character, localized to a single vascular region in the brain. These symptoms include aphasia or dysarthria, transient monocular blindness (amaurosis fugax), hemianopia, hemiparesis, and/or hemisensory loss. In such cases, the probability of ischemia is relatively high. However, these symptoms may also occur due to non-ischemic causes such as seizures, migraines, and intracerebral hemorrhage.
Atypical TIA:
Clinical characteristics of transient symptoms considered to be atypical of an ischemic attack include the following [8-10]:
- Gradual progression of symptoms.
- Change of symptoms from one type to another.
- Disturbance of vision in both eyes, characterized by the occurrence of positive phenomena (positive symptoms are not normally experienced by most individuals and reflect an excess of normal functions, such as flashing lights).
- Isolated sensory symptoms with a focal distribution, especially in areas such as a finger, chin, or tongue.
- Attacks lasting less than 30 seconds.
- Isolated brainstem symptoms such as dysarthria, diplopia, or hearing loss.
- Amnesia and confusion.
- Incoordination of limbs.
Atypical TIAs with negative symptoms (negative symptoms mean loss of a neurological function, such as hearing loss or vision loss) have a high risk of recurrent stroke. For this reason, they should be handled and treated as typical TIAs [4].
Medical History
The most important question is the time of symptom onset because it guides the treatment. Patients and/or their relatives should also be questioned about neurological diseases and symptoms (such as migraine, epilepsy, previous attacks similar to this one, syncope, etc.), cardiovascular diseases (such as myocardial infarction, atrial fibrillation, carotid stenosis, etc.), metabolic disorders (such as diabetes, hyperlipidemia, etc.), hypertension, drug usage, smoking, and family history of cardiac and/or neurological diseases.
- Important points regarding the medical history of patients with TIA: Cardiovascular diseases, previous history of neurological attack or stroke, and drug usage.
- Risk factors for TIA: Older age, atrial fibrillation, atherosclerosis, diabetes mellitus, hypertension, hyperlipidemia, smoking, history of stroke, male gender, and Black race.
- Prognosis of TIA patients: The prognosis is defined by the risk of recurrent stroke. The risk of stroke after TIA varies according to several factors, including the time elapsed since the last TIA, the presence of vascular pathologies, and the presence of acute infarction on diffusion-weighted magnetic resonance imaging (DW-MRI). Stroke is most likely to occur in the first week after a TIA, with a 1.5–3.5% risk in the first 48 hours. Within 90 days, the risk of stroke rises to 40% [11–14]. Vascular pathologies such as large artery atherosclerosis, small artery disease, and cardio-embolic conditions increase the risk of recurrent stroke. Additionally, the presence of acute lesions on DW-MRI or chronic ischemic lesions on computed tomography (CT) increases the likelihood of recurrent stroke in TIA patients.
Physical Examination
A detailed neurological evaluation should be performed on the patient, including assessment of cranial nerves, strength and sensation, visual fields, language, gait, and coordination. A focal neurological deficit on exam should raise suspicion for TIA. In addition to the neurological exam, it is important to perform a thorough cardiovascular exam, listening closely for irregular rhythms, murmurs, and bruits on the carotids.
- Red flags: Bruits on the carotids, the presence of negative symptoms, and irregular rhythms.
Alternative Diagnoses
What other diseases can present with similar clinical features/conditions?
Seizures, migraines, metabolic disorders such as hypoglycemia, subarachnoid or intracerebral hemorrhage, subdural hematoma, syncope, and central nervous system (CNS) demyelinating disorders such as multiple sclerosis, etc., should come to mind in the differential diagnosis of TIA.
Which findings make TIA more probable?
Sudden onset of typical symptoms, presence of negative symptoms, and normal laboratory and imaging findings.
Which risk factors and findings make other diagnoses more probable or make this diagnosis less probable?
We can differentiate syncope, epileptic seizures, CNS demyelinating disorders, and migraine aura with a detailed history. In the differentiation of seizures, the lactate value in an arterial blood gas (ABG) test is also important. High lactate levels support the diagnosis of seizures. Intracranial hemorrhages and subdural hematomas have specific imaging findings.
Acing Diagnostic Testing
Bedside Tests
First, vital signs (body temperature, pulse rate, respiration rate, blood pressure, and peripheral oxygen saturation) of the patient should be measured and recorded. Then, as the first approach, in all patients presenting with neurological symptoms, the measurement of blood glucose at the bedside, along with checking electrolytes, PO2, PCO2, and lactate values in an arterial blood gas (ABG) test, and performing electrocardiography (ECG), are very valuable in terms of diagnosis and differential diagnosis.
Laboratory Tests
Complete blood count (CBC), biochemistry, and coagulation tests are usually performed in addition to blood glucose measurement and ABG. These tests are useful in distinguishing metabolic disorders such as hypoglycemia from TIA. Impaired coagulation tests are also helpful in guiding diagnosis and treatment.
Imaging
Patients who are symptomatic should be considered as having a stroke. A non-contrast head CT scan can be used to assess early ischemic signs and exclude intracerebral hemorrhage. In TIA, CT has low sensitivity and usually does not show any pathological findings. If CT is negative for mass lesions and intracranial hemorrhage, computed tomography angiography (CTA) and/or magnetic resonance angiography (MRA) can be used to investigate intracranial and extracranial vascular occlusions. If CTA and/or MRA are negative for large vessel occlusion and TIA is suspected, MRI should be obtained to evaluate for signs of ischemia/infarction. DW-MRI following MRI is the gold standard for acute ischemic stroke and distinguishes stroke from TIA. DW-MRI is valuable because it shows focal areas of cytotoxic edema, which are seen in acute stroke.
Risk Stratification
The ABCD2 score (age, blood pressure, clinical features, duration, and the presence of diabetes mellitus) is commonly used to determine stroke risk following TIA. Parameters evaluated in the ABCD2 score assign scores for certain clinical features (speech impairment and unilateral weakness) and duration of symptoms, in addition to risk factors such as age, blood pressure, and diabetes. However, studies have found that the ABCD2 score does not reliably distinguish between those with a low and high risk of recurrent stroke.
Alternatively, the Canadian TIA Score uses variables routinely obtained in the ED setting to classify patients into minimal, low, high, or critical risk categories, which are associated with the likelihood of developing a stroke in the week following a TIA. Using the Canadian TIA Score strikes a balance by allowing risk stratification based on history, clinical data points, and neuroimaging, and defines clear follow-up actions based on the patient’s predictive score. Compared to the ABCD2 score, the Canadian TIA Score has shown better predictability [15].
However, there are not enough studies on the Canadian TIA Score. For this reason, a risk stratification score alone should not be used to determine the management of patients. Instead, the decision regarding hospitalization versus discharge should be made within the greater clinical context.
Management
Initial Stabilization
In all patients presenting to the Emergency Department, the initial assessment should involve the “ABCDE” approach (assessment of Airway, Breathing, Circulation, Disability, and Exposure). If the patient is alert and responds with a normal voice, the airway is open. However, if there is no respiration despite effort, the airway must be secured by checking for a foreign body, performing airway-opening maneuvers (head-tilt and chin-lift or jaw-thrust), suctioning the airway, or even intubating if necessary. In TIA patients, altered mental status is a common cause of airway obstruction [16]. If breathing is insufficient and oxygen saturation is below 94%, supplemental oxygen should be administered [17].
Altered mental status could be a sign of decreased perfusion, so obtaining intravenous access and starting IV fluids, if indicated, should be performed (the best choice is isotonic fluid). Blood pressure measurements, performing an EKG, and auscultation for abnormal heart sounds, murmurs, and carotid bruits can provide clues to the etiology of the TIA. Patients should be evaluated for disability using the Glasgow Coma Score (GCS), evaluation of pupillary light reflexes, and checking for signs of lateralization.
As hypoglycemia is considered a TIA mimic, it must be checked and corrected immediately, and hyperglycemia should also be prevented. Patients should be evaluated for drug intake and toxic ingestions. All patients with impaired consciousness should undergo a complete physical examination, which includes removing their clothes to search for signs of bleeding, foreign bodies, and trauma [16].
Medications
Treatment is started according to risk stratification.
If the ABCD2 score is ≥4: Dual antiplatelet therapy (DAPT) is started.
- Aspirin (160 to 325 mg loading dose, followed by 50 to 100 mg daily) plus clopidogrel (300 to 600 mg loading dose, followed by 75 mg daily)
- Alternatively, aspirin (300 to 325 mg loading dose, followed by 75 to 100 mg daily) plus ticagrelor (180 mg loading dose, followed by 90 mg twice daily).
If the ABCD2 score is <4: Aspirin monotherapy is started.
- Aspirin (162 to 325 mg daily) [18, 19].
According to the Canadian TIA Score, patients are divided into four risk groups and managed as follows:
Minimal and Low Risk: Refer the patient to rapid outpatient assessment with a neurologist.
High Risk:
- Start or switch to DAPT (clopidogrel or dipyridamole + ASA).
- Initiate or control hypertension management.
- Refer the patient to neurology within 24 hours.
Critical Risk:
- Start or switch to DAPT (clopidogrel or dipyridamole + ASA).
- Start oral anticoagulation if the patient has atrial fibrillation.
- Start a statin class medication.
- Initiate or optimize control of hypertension.
- Admit the patient to the hospital and ensure referral to neurology within 24 hours [20].
Procedures
In patients with ongoing and disabling symptoms, emergent evaluation for IV thrombolysis and mechanical thrombectomy should be performed. Selected patients with recently symptomatic cervical internal carotid artery stenosis can significantly benefit from early carotid endarterectomy (within two weeks of a non-disabling stroke or TIA) [21].
Special Patient Groups
Stroke is a rare condition in the pediatric population, but all principles that apply to adults also apply to the pediatric population. Because the incidence of stroke increases with age, physicians should consider stroke in the management of undifferentiated geriatric patients.
In pregnant patients, physiological changes increase the risk of stroke, and there is significant maternal morbidity and mortality associated with stroke. However, a transient ischemic attack (TIA) is not a type of pregnancy-associated stroke, but it should be noted that TIAs precede strokes in up to 15% of cases [22].
When To Admit This Patient
Because of the high risk of stroke after TIA, patients diagnosed with TIA should be hospitalized for further etiological investigation and treatment.
Only selected patients with a completely normal physical examination, no ongoing disability, normal imaging (including MRI), and a low-risk score can be discharged if their neurology outpatient clinic visit is imminent and after aspirin therapy is started.
Discharged patients should be informed about TIA symptoms and encouraged to call Emergency Medical Services (EMS) and/or go to the nearest Emergency Department if these symptoms begin.
The main symptoms of a TIA can be remembered with the acronym FAST:
- Face – Drooping or numbness on one side of the face, inability to smile, or if the mouth or eye has drooped.
- Arms – Inability to lift both arms and keep them raised because of weakness or numbness in one arm.
- Speech – Slurred speech, inability to talk at all despite appearing to be awake, or difficulty understanding speech.
- Time – If any of these signs or symptoms is present, call Emergency Medical Services (EMS) immediately.
Revisiting Your Patient
The ABCDE approach was initiated as soon as the patient entered the ED. Since he is awake and does not show signs of difficulty breathing, his airway is considered open, and his breathing is considered normal.
Blood pressure is high, but pulse is within normal ranges. No murmur, abnormal sounds, or carotid murmur is detected on auscultation. Since hypoglycemia and hyperglycemia can mimic TIA, a bedside glucose level was measured and found to be 110 mg/dL (6.1 mmol/L).
A focused neurological examination was performed: pupils are equal and reactive, facial expressions appear appropriate, there is no drooping, and there is no slurring of speech. Muscle strength in his right arm is decreased, and muscle strength in his right leg is slightly decreased. There is no sensory deficit. The rest of the physical exam is unremarkable.
An electrocardiogram (EKG) was requested to check for acute pathologies and arrhythmias, such as atrial fibrillation, which is important in the etiology of TIA, and it demonstrates sinus rhythm. Since the history and physical examination are typical for an acute cerebrovascular accident, an intravenous (IV) catheter was inserted, and complete blood count (CBC), plasma urea nitrogen, creatinine, electrolytes, cardiac enzymes, and coagulation parameters (prothrombin time, activated partial thromboplastin time, and international normalized ratio [INR]) were ordered.
To exclude bleeding, the patient underwent a non-contrast brain tomography, which was interpreted as normal. The ABCD2 score was found to be ≥6. The patient was consulted with the neurology department. No focal neurological signs were detected in serial physical examinations. Thrombolytic therapy was not considered because the symptoms resolved, and the imaging was normal.
However, because the patient’s complaints were typical of stroke and/or TIA, due to comorbid diseases, and because he is not on antiplatelet therapy, he is considered to have a high risk for stroke. As a result, dual antiplatelet therapy (DAPT) was started, and the patient was transferred to the neurology service for further examination and treatment to elucidate the etiology.
Recommended Free Open Access Medical Education (FOAM) resources
- Zink J. (2022). Syncope and Syncope Mimics. EmDocs. Retrieved from http://www.emdocs.net/syncope-and-syncope-mimics/
- Chapman S. (2023). The Utility of MRI in the ED. EmDocs. Retrieved from http://www.emdocs.net/the-utility-of-mri-in-the-ed/
- Lanata E.P. (2021). TIA: Emergency Department Evaluation and Disposition. EmDocs. Retrieved from http://www.emdocs.net/tia-emergency-department-evaluation-and-disposition/
- Rezaie S. (2021). “Rebellion21: Canadian TIA Risk Score vs ABCD2”. REBEL EM blog. Retrieved from https://rebelem.com/rebellion21-canadian-tia-risk-score-vs-abcd2/
Authors
Omer Jaradat
Dr. Omer Jaradat is an Emergency Medicine Physician at Ahi Evran University Training and Research Hospital, Kirsehir, Türkiye. He is an enthusiast of emergency medicine and strongly believes in the generalist and collective approach of the specialty. He is particularly interested in global emergency medicine, emergency medicine education, and innovation. A dedicated follower and contributor to #FOAMed, he feels proud to be a member of the emergency medicine community.
Elizabeth DeVos
Dr. Haci Mehmet Caliskan is an Associate Professor of Emergency Medicine and an academician at Ahi Evran University, Kirsehir, Türkiye. He is deeply interested in emergency medicine education and is passionate about engaging students in the emergency medicine community. He is an advocate for fair and equitable medical care. His current professional interests include cardiovascular diseases, pulmonary medicine, and trauma. He takes Atatürk as an example in both his professional and social life.
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References
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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.
