Case 1: Management of Acute Thrombotic Cerebrovascular Accident Post Recombinant Tissue Plasminogen Activator Therapy
A 59-year-old Hispanic man presented with right upper and lower extremity weakness, associated with facial drop and slurred speech starting 2 hours before the presentation. He denied visual disturbance, headache, chest pain, palpitations, dyspnea, dysphagia, fever, dizziness, loss of consciousness, bowel or urinary incontinence, or trauma. His medical history was significant for uncontrolled type 2 diabetes mellitus, hypertension, hyperlipidemia, and benign prostatic hypertrophy. Social history included cigarette smoking (1 pack per day for 20 years) and alcohol intake of 3 to 4 beers daily. Family history was not significant, and he did not remember his medications. In the emergency department, his vital signs were stable. His physical examination was remarkable for right-sided facial droop, dysarthria, and right-sided hemiplegia. The rest of the examination findings were insignificant. His National Institutes of Health Stroke Scale (NIHSS) score was calculated as 7. Initial CT angiogram of head and neck reported no acute intracranial findings. The neurology team was consulted, and intravenous recombinant tissue plasminogen activator (t-PA) was administered along with high-intensity statin therapy. The patient was admitted to the intensive care unit where his hemodynamics were monitored for 24 hours and later transferred to the telemetry unit. MRI of the head revealed an acute 1.7-cm infarct of the left periventricular white matter and posterior left basal ganglia. How would you manage this case?
This case scenario presents a patient with acute ischemic cerebrovascular accident (CVA) requiring intravenous t-PA. Diagnosis was based on clinical neurologic symptoms and an NIHSS score of 7 and was later confirmed by neuroimaging. He had multiple comorbidities, including hypertension, diabetes, dyslipidemia, and smoking history, which put him at a higher risk for developing cardiovascular disease. Because his symptoms started within 4.5 hours of presentation, he was deemed to be a candidate for thrombolytics. The eligibility time line is estimated either by self-report or last witness of baseline status.
Ischemic strokes are caused by an obstruction of a blood vessel, which irrigates the brain mainly secondary to the development of atherosclerotic changes, leading to cerebral thrombosis and embolism. Diagnosis is made based on presenting symptoms and CT/MRI of the head, and the treatment is focused on cerebral reperfusion based on eligibility criteria and timing of presentation.
Symptoms include alteration of sensorium, numbness, decreased motor strength, facial drop, dysarthria, ataxia, visual disturbance, dizziness, and headache.
The main goal of thrombotic stroke management is restoration of blood supply to the brain using intravenous thrombolytics. Ensuring a stable airway, breathing, and circulation should be the first step, followed by focused clinical history and neurologic assessment. Intravenous (IV) thrombolytics are indicated within 3 hours of symptom onset with no contraindications. Treatment with t-PA between 3.5 and 4 hours has been used in select group. CT of the head should be performed to exclude hemorrhage, and fingerstick glucose should be checked before administration of t-PA. Although immediate laboratory testing (complete blood count, coagulation panel, cardiac enzymes, and drug toxicology) and ECG can be performed, they should not delay the time to t-PA. Early use of t-PA results in better outcomes and is considered a quality measure in stroke care. The use of stroke scales such as the NIHSS helps to quantify the degree of neurologic deficit and change in clinical status. Blood pressure control with a systolic pressure ≤185 mm Hg and diastolic pressure ≤110 mm Hg should be achieved for at least 24 hours prior to initiating intravenous thrombolytics in those who are eligible. After t-PA use, blood pressure should be maintained at <180/105 mm Hg. All other antithrombotic agents should be kept on hold after 24-hour t-PA until repeat CT of the head rules out intracranial hemorrhage.
Eligibility for t-PA
Age ≥18 years
Clinical diagnosis of ischemic stroke causing neurologic deficit
Time of symptom onset <4.5 hours
Absolute contraindications to t-PA
Intracranial hemorrhage on CT
Clinical presentation suggests subarachnoid hemorrhage
Neurosurgery, head trauma, or stroke in past 3 months
Uncontrolled hypertension (>185 mm Hg systolic or >110 mm Hg diastolic)
History of intracranial hemorrhage
Known intracranial arteriovenous malformation, neoplasm, or aneurysm
Active internal bleeding
Suspected/confirmed endocarditis
Known bleeding diathesis
Abnormal blood glucose (<50 mg/dL)
Relative contraindications to t-PA
Only minor or rapidly improving stroke symptoms
Major surgery or serious nonhead trauma in the previous 14 days
History of gastrointestinal or urinary tract hemorrhage within 21 days
Seizure at stroke onset
Recent arterial puncture at a non-compressible site
Recent lumbar puncture
Post–myocardial infarction pericarditis
Pregnancy
Additional warnings to t-PA use >3 hours after stroke
Age >80 years
History of prior stroke and diabetes
Any active anticoagulant use (even with international normalized ratio <1.7)
NIHSS >25
CT shows multilobar infarction (hypodensity in greater than one-third of cerebral hemisphere)
Key Points
Suspect an acute ischemic CVA in a patient with risk factors presenting with neurologic deficit and neuroimaging reporting ischemic changes. Use formal stroke scales such as the NIHSS for clinical and treatment guidance.
Therapy should include reperfusion therapy in those who are eligible, statins, antiplatelet agents, blood pressure control, and risk factors modification.
Timing is a determining factor for reperfusion therapy, which is associated with better outcomes, and excluding intracranial hemorrhage must be done prior to any other intervention.
A 69-year-old Hispanic woman was brought to the emergency department for new-onset left-sided facial droop, slurred speech, and left hemiplegia that started 5 hours prior to arrival. She had never experienced these symptoms before. Her medical history included atrial fibrillation, hypertension, hyperlipidemia, and diabetes mellitus. The patient denied any history of smoking, alcohol, or illicit drug use. She mentioned that she does not like to take her medications, which include aspirin, apixaban, lisinopril, and metformin. On presentation, her vital signs were noted to be a blood pressure of 220/113 mm Hg, heart rate of 81 bpm, respiratory rate 16 of breaths/min, and temperature of 98.3°F. On physical examination, she was alert and oriented. Significant neurologic examination included facial asymmetry with nasal fold deviation to the right, dysarthria, and motor strength and sensations severely reduced on the left side and more significantly reduced in the upper extremity. Her National Institutes of Health Stroke Scale (NIHSS) score was calculated as 8. Laboratory data were remarkable for glucose of 315 mg/dL and normal coagulation profile. The initial CT of the head was unremarkable. ECG showed atrial fibrillation with slow ventricular response. She was started on intravenous nicardipine infusion, and rectal aspirin was given. A repeat CT of the head and MRI showed multiple areas of ischemic infarct involving the frontal parietal and occipital areas bilaterally. She was transferred to the telemetry unit. How would you manage this case?
This case describes a cardioembolic cause of ischemic stroke. History of atrial fibrillation with nonadherence to anticoagulation is a key here to diagnose the etiology. In addition, the head CT finding of multiple areas of brain involvement bilaterally is another clue toward the diagnosis. In this case, atrial fibrillation is already diagnosed; otherwise, investigation for underlying arrythmia through event monitor should be performed. Echocardiogram should be performed to rule out intracardiac thrombus.
Embolic stroke is caused by the formation of a thrombus in an artery, vein, heart chamber, or heart valve. It can also be caused by nonthrombotic material such as infected vegetation, valvular calcifications, cardiac tumors (eg, myxoma, papillary fibroelastoma, sarcoma), fibrocartilaginous material, air, or fat. Other emboli can have both thrombotic and nonthrombotic material. Cardioembolic cerebrovascular accidents (CVAs) are associated with a high recurrence rate and poor outcomes compared to other types of CVA.
Signs and symptoms are similar to those of other types of cerebral vascular disease. However, cardiopulmonary symptoms such as palpitations, chest pain, lightheadedness, and dyspnea may be present.
Management of cardioembolic stroke includes identification of its cause. Arrythmia such as atrial fibrillation is the most commonly associated etiology. Continuous telemetry monitoring using Holter and implantable loop recorder can be performed. Echocardiogram has a pivotal role in recognizing cardiac thrombus and vegetations, with utilization of transesophageal echocardiogram for better assessment of the left atria and ascending aorta. Use of anticoagulation in the setting of atrial fibrillation and intracardiac thrombus has been shown to prevent recurrence. Treatment of the underlying cause should be implemented, along with risk factor control using aspirin, statins, and antihypertensives.
Improvement in stroke recurrence has been observed with use of non–vitamin K antagonist oral anticoagulants in patients with nonvalvular atrial fibrillation. Closure of the left atrial appendage is a nonpharmacologic alternative, especially in patients at higher risk of hemorrhagic stroke, that has shown promising results.
Key Points
Acute neurologic symptoms with imaging evidence of multiple areas of infarct not limited to a single vessel territory are suspicious for cardioembolic stroke.
Cardiac arrythmias should be considered in the diagnostic evaluation of ischemic stroke.
Left ventricular thrombus and valvular vegetations can be identified using echocardiogram.
Anticoagulation can help prevent recurrent events.
A 52-year-old woman was brought to the hospital by her sister for sudden weakness of her left hand followed by left-sided facial drop and slurring of speech. The symptoms started 6 hours prior to her presentation. She denied fever, trauma, fall, dizziness, and palpitations. Her medical history included hypertension and hyperlipidemia. No relevant family history was found. She admitted use of cocaine 1 week prior and denied alcohol intake or smoking history. On arrival to the emergency department (ED), her vital signs were noted as blood pressure of 126/82 mm Hg, heart rate of 73 bpm, respiratory rate of 16 breaths/min, and temperature of 98.5°F. Physical examination was remarkable for lethargy but ability to follow commands, left nasolabial fold drooping, 1/5 left upper extremity weakness, and 3/5 left lower extremity. The rest of the examination was noncontributory. Stroke code was activated in the ED. National Institutes of Health Stroke Scale (NIHSS) score was 10. Initial CT of the head revealed no evidence of acute intracranial hemorrhage or ischemia. She beyond the window for tissue plasminogen activator because her symptoms started 6 hours prior. Laboratory testing was significant for elevated cardiac enzymes, and drug screen was positive for cocaine and cannabinoids. She was transferred to the telemetry floor. How would you manage this case?
This case presents an acute cerebral infarction involving the middle cerebral artery territory. The patient’s head MRI showed restricted diffusion with apparent diffusion coefficient (ADC) signal drop-off seen in the right temporoparietal cortex and subcortical white matter consistent with acute middle cerebral artery (MCA) infarction. The patient was beyond the window for thrombolysis and thus was treated with aspirin, high-intensity statin, blood pressure control, and risk factors modification (specifically cocaine cessation) for secondary stroke prevention. Stroke panel consists of head MRI, ultrasound of carotid artery, ECG, echocardiogram, swallow evaluation, and physical therapy.
The most commonly affected territory in a cerebral infarct is the MCA territory (the parietal lobe, the temporal lobe, and the internal capsule and thalamus), which is related to the area size and its direct flow from the internal carotid artery, leading to the easiest pathway for thromboembolism. MCA infarcts, as opposed to thrombotic infarcts, are generally embolic and typically from the heart or carotid artery. Other risk factors for MCA stroke are similar to those for strokes affecting other locations and include hypertension, hyperlipidemia, diabetes, and cardiac and carotid artery disease.
The development of malignant MCA infarction (extending beyond 50% of the MCA territory) is a life-threatening edema that usually develops 1 to several days after infarction and has a mortality rate of up to 80% in conservatively treated patients.
Symptoms include contralateral hemiparesis and hemisensory loss, hemianopia, aphasia (expressive [anterior MCA territory infarct], receptive [posterior MCA infarct], or global [extensive infarction]) when affecting the dominant hemisphere, and neglect when the affecting nondominant hemisphere. Early severe neurologic symptoms (hemiparesis, gaze deviation, and higher cortical signs) followed by headache, vomiting, papilledema, and reduced consciousness may predict a malignant course.
CT is useful for predicting the development of malignant brain swelling. The presence of early signs of infarction in a CT implies a worse prognosis.
Hyperdense MCA sign: Earliest visible sign of MCA infarction seen within 90 minutes after the event; a direct visualization of thromboembolic material within the lumen
MCA dot sign (Sylvian fissure sign): Represents a thromboembolism within a segmental branch of the MCA located within the Sylvian fissure (M2 segment)
Insular ribbon sign: Loss of normal gray-white differentiation
Cortical sulcal effacement
Obscuration of lentiform nucleus or caudate nucleus: Seen as early as 1 hour after occlusion and visible in 75% of patients at 3 hours
Large areas of hypodensity (defined as >50% of the MCA territory): Predictive of fatal brain swelling
MRI demonstrates the typical distribution of affected tissue or occlusion of the vessel, measured by diffusion-weighted imaging or ADC mapping.
Treatment of an MCA infarct is similar to that of infarcts affecting any other territory, with the exception that due to the size of the involved area, which results in space-occupying brain swelling due to vasogenic cerebral edema, patients with malignant MCA stroke are offered decompressive craniectomy as a lifesaving procedure. Osmotic agents (hypertonic saline solutions, mannitol, and glycerol) and steroid therapy are also used to reduce edema and minimize tissue shifts and may be beneficial for bridging to surgical intervention. However, no significant improvement in outcomes has been achieved with these modalities.
Use of stroke scales identifies patients eligible for intravenous thrombolytic or endovascular intervention and those with an elevated risk for complications such as intracerebral hemorrhage. The addition of antithrombotic agents such as aspirin within 48 hours of symptom onset has been shown to reduce complications, disability, and recurrence of stroke. Use of statins in acute stroke management is not supported by evidence.
For patients who are not treated with thrombolytics, blood pressure can be treated in the presence of a systolic or diastolic blood pressure >220 or >120 mm Hg, respectively; active ischemic coronary disease; aortic dissection; congestive heart failure; hypertensive encephalopathy; or preeclampsia/eclampsia. Fluid management, glucose control, swallowing assessment, physical therapy, and behavioral and lifestyle modifications are important components of stroke care. Management in a stroke unit has been associated with better outcomes.
Key Points
Large-vessel stroke occurs mainly due to the blockage in carotid vessels with sudden embolization.
Intravenous thrombolytics should be used if the eligibility criteria are met.
Risk factor modification, use of antiplatelets, and lipid-lowering therapy should be considered in management.
A 49-year-old woman was brought to the emergency department 45 minutes after she developed slurred speech and numbness and weakness in the right arm that resolved before arriving to the hospital. She denied any headache, blurry vision, palpitations, loss of consciousness, neck pain, or trauma. Her medical history included iron deficiency anemia and hyperlipidemia. Her medications included birth control pills and iron tablets. Family history was not significant for stroke and vascular events. She denied smoking or alcohol or illicit drug use. On arrival, vital signs were noted as blood pressure of 190/100 mm Hg, heart rate of 105 bpm, temperature of 98.8°F, and respiratory rate of 16 breaths/min. Her complete physical examination including neurologic examination was unremarkable. Laboratory testing was significant for moderate microcytic anemia and elevated total cholesterol and low-density lipoprotein levels. Electrolytes, coagulation panel, and drug screen were negative. CT of the head did not show any significant changes. She was transferred to the telemetry floor for further management. How would you manage this case?
This case describes a transient ischemic attack (TIA) in a middle-age woman with risk factors including uncontrolled hypertension and hyperlipidemia who presented with neurologic deficits that resolved within 24 hours. The diagnosis of TIA was made after excluding other causes on neuroimaging such as acute cerebrovascular accident, spinal disease, tumors, and multiple sclerosis. The patient was managed conservatively with stroke core measures and risk factor modification.
TIA is defined as a transient episode of neurologic dysfunction secondary to a focal brain, spinal cord, or retinal ischemia, without acute infarction. Traditionally defined TIA (ie, time based, lasting <24 hours) is associated with a high early risk of recurrent stroke (approximately 4% to 10% in the first 2 days after TIA). The ABCD2 score (Table 7.4.1) was designed to identify patients at high risk of ischemic stroke in this time period, but its predictive performance is not optimal. The diagnosis of TIA (in the absence of tissue infarction) is clinical and based on a determination that the cause of the symptoms is a brain ischemia rather than another cause. Diagnosis can be challenging and is usually subjective because the symptoms are transient, often minor, and highly variable.
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