Emergency Medicine Stroke Case File

Emergency Medicine Stroke Case File

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 14

A 59-year-old man with a history of hypertension presents to the emergency department (ED) with right-sided paralysis and aphasia. The patient’s wife states he was in his normal state of health until one hour ago, when she heard a thud in the bathroom and walked in to find him collapsed on the floor. She immediately called emergency medical services, who transported the patient to your ED. En route, his fingerstick blood sugar was 108 mg/dL. On arrival in the ED, the patient is placed on monitors and an IV is established. His temperature is 36.8 ºC (98.2°F), blood pressure is 169/93 mm Hg, heart rate is 86 beats per minute, and respiratory rate is 20 breaths per minute. The patient has a noticeable left-gaze preference and is verbally unresponsive, although he will follow simple commands such as raising his left thumb. He has a normal neurologic examination on the left, but on the right has a facial droop, no motor activity, decreased deep tendon reflexes (DTRs), and no sensation to light-touch.

⯈ What is the most likely diagnosis?

⯈ What is the most appropriate next step?

⯈ What is the best therapy?

ANSWER TO CASE 14:

Stroke

Summary: This is a 59-year-old man with acute onset of aphasia and right-sided paralysis 70 minutes prior to arrival in the ED.

• Most likely diagnosis: Stroke
• Most appropriate next step: CT scan of the head
• Best therapy: Thrombolytics

ANALYSIS

Objectives

1. Recognize the clinical findings of an acute stroke.
2. Understand the diagnostic and therapeutic approach to suspected stroke patients.
3. Be familiar with the National Institutes of Health (NIH) Stroke Scoring system.

Considerations

This 59-year-old man presents with an acute onset of focal neurologic deficits, which are typical for a cerebrovascular accident (CVA). Management priorities include: ABCs, stabilization of vitals, and a careful history and physical to distinguishing CVA from other etiologies which may present similarly, such as hypoglycemia. Nonenhanced CT is used to quickly determine whether the CVA is ischemic or hemorrhagic. If the event is ischemic, the patient may be a candidate for thrombolytic administration. The goal is to complete an evaluation and, if the patient is eligible, initiate treatment within 60 minutes of the patient’s arrival to the ED.

Approach To:

Suspected Stroke

DEFINITIONS

STROKE: The rapid development of the loss of brain function due to a disturbance in the blood vessels supplying the brain. It is also referred to as a cerebrovascular accident (CVA).

TRANSIENT ISCHEMIC ATTACK (TIA): Occurs when the blood supply to a particular area of the brain is interrupted. Often referred to as a “mini stroke,” the symptoms of a TIA typically last minutes to hours, but resolve within 24 hours.

THROMBOLYTICS: Medications that act to degrade clots and are used in the treatment of myocardial infarctions, pulmonary embolisms, and strokes.

NATIONAL INSTITUTES OF HEALTH STROKE SCALE: A bedside assessment tool that provides a reproducible, quantitative measurement of the strokerelated neurologic deficit.

CLINICAL APPROACH

Stroke is a serious and common disorder, which affects over 795,000 persons in the United States each year. It remains the third leading cause of death in the United States and the number one cause for disability. Twenty percent of persons affected will die within 1 year. Many of the surviving victims are left with neurologic deficits and may be unable to care for themselves.

Stroke is a term that describes the loss of perfusion to a territory of the brain, resulting in ischemia and a corresponding loss of neurologic function. Symptoms vary widely depending on the type of infarct, the location, and the amount of brain involved (Tables 14–1 and 14–2). Strokes are classified as either ischemic or hemorrhagic. Eighty percent of strokes are ischemic—due to the blockage of a blood vessel secondary to thrombosis or embolism. They are generally seen in patients older than the age of 50 and present with the sudden onset of focal neurologic deficits. Hemorrhagic strokes are typically seen in younger patients and are due to intraparenchymal or subarachnoid cerebral vessel bleeding.

The history and physical examination remains the cornerstone to evaluating stroke patients. The symptoms may include weakness, numbness, or discoordination of the limbs or face, cranial nerve palsies, dysarthria, or cognitive impairments such as aphasia or neglect. It is critical to find out the exact onset of stroke symptoms

as thrombolytics can only be given within a 4.5-hour window from the onset of symptoms. If the patient is unable to communicate or awoke with symptoms, the physician must determine when the patient was last awake and “normal.”

Strokes are more common in the elderly (75% occur in patients older than 75 years), males, and African Americans. Other risk factors for stroke include a history of transient ischemic attack (TIA) or previous stroke, hypertension, atherosclerosis, cardiac disease (eg, atrial fibrillation, myocardial infarction, valvular disease), diabetes, carotid stenosis, dyslipidemia, hypercoagulable states, tobacco and alcohol use.

It is possible, although challenging, to clinically infer the location of the anatomic insult to the clinical presentation by correlating symptoms with circulatory region (Figure 14–1). For instance, aphasia usually corresponds to a left hemispheric stroke; neglect generally indicates a right hemispheric stroke; crossed signs (eg, right-sided facial droop with left-sided extremity weakness) typically indicate brainstem involvement.

The evaluation should include the use of the NIH Stroke Scale (NIHSS) (Table 14–3), a standardized system that measures the level of impairment caused

Figure 14–1. Anatomy of brain and blood flow.

Reproduced from the National Institutes of Health, 2000.

by stroke. It measures several aspects of brain function such as consciousness, vision, sensation, movement, speech, and language. A score above 20 to the maximal score of 42 represents a severe stroke. Current guidelines allow strokes with scores above 4 to be treated with tPA.

Many hospitals have a “Stroke Team” or a “Code Stroke” protocol that facilitates the prompt diagnosis and treatment of stroke patients as the treatment of stroke is highly time sensitive. The National Institute of Neurological Disorders and Stroke (NINDS) has established door-to-treatment time frames in responding to acute stroke. These include a physician evaluation within 10 minutes of arrival, specialist/neurologist notification within 15 minutes, CT of head within 25 minutes and CT interpretation within 45 minutes. For ischemic strokes, the guideline for the administration of rtPA (recombinant tissue-type plasminogen activator) in eligible patients is within 60 minutes, within the “golden hour” of stroke care (See Table 14-4).

Diagnostic Studies:

Most of the diagnostic studies in acute stroke patients are used to exclude other etiologies for neurologic impairments and identify possible contraindications to tPA administration. An oxygen saturation is needed to exclude hypoxia as etiology of neurologic impairments. Because cardiac abnormalities are common among stroke patients, an ECG should be obtained. The most common dysrhythmia is atrial fibrillation. Although further cardiovascular studies will ultimately be performed, they should be done as an inpatient so that the acute care of the patient is not delayed. Another critical bedside test that should be performed is a capillary blood glucose (CBG). Hypoglycemia is a known mimicker of acute stroke and this condition can be rapidly ruled out with a normal glucose level.

Blood tests usually include a complete blood count including platelets (platelets should also be above 100,000 per mm³ to administer thrombolytics), coagulation studies, and cardiac markers. Coagulation studies are important on patient with anticoagulation who are supratheraputic and at higher risk for an intracerebral bleed.

Patients with suspected strokes should undergo diagnostic imaging, commonly a non-contrast head CT scan. Because of the difficulty in clinically differentiating a hemorrhagic from an ischemic stroke—the CT is vital for ruling out an intracerebral

^aRecombinant tissue plasminogen activator (rtPA) should be used with caution in individuals with severe stroke symptoms,

NIHSS > 22.

Data from Adams HP, Brott TG, Furlon AJ, et al. Guidelines for thrombolytic therapy for acute stroke, Circulation.

1996;94:1167.

bleed, which is an absolute contraindication to thrombolytic therapy. An early CT finding in ischemic stroke is loss of the grey-white differentiation due to increased water concentration in ischemic tissues—leading to a loss of distinction among the basal ganglia nuclei, gyri swelling, and sulcal effacement. Another early CT finding is increased density within the occluded vessel, which represents the thrombus.

Other imaging modalities such as contrast-enhanced CT and MRI may equal CT’s efficiency in detecting intracerebral hemorrhage. MRI is superior to CT for the demonstration of subactute and chronic hemorrhage, and gradient-echo MR can also detect other vascular lesions such as malforations and amyloid angiopathy. However, the length of these studies may delay the time-sensitive administration of tPA.

Differential Diagnoses

The differential for stroke is broad and may include:

Neurologic entities such as seizure/Todd’s paralysis, complicated migraine headaches, nonconvulsive status epilepticus, flares of demyelinating disorders such as multiple sclerosis, or spinal cord lesions. 

Toxic/metabolic abnormalities such as hypo- and hyperglycemia, hypo- or hypernatremia, drug overdose, and botulism.

Infectious etiologies such as systemic infection, Bell palsy, meningitis/encephalitis, Rocky Mountain spotted fever, and brain abscess.

Cardiac or vascular causes such as hypertensive encephalopathy, carotid/aortic/ vertebral artery dissection, subarachnoid hemorrhage, cerebral vasculitis.

Other etiologies such as tumor, sickle cell cerebral crisis, depression or psychosis, and heat stroke.

Treatment

Stroke patients are managed as critically ill patients. Management imperatives include: assessment and stabilization of the ABCs, formal evaluation for possible thrombolytic administration, and addressing comorbid conditions such as hypertension.

Alteplase (intravenous recombinant tissue-type plasminogen activator: rtPa) may help restore tissue perfusion in ischemic stroke and is the only FDA approved thrombolytic for stroke. The NIH/National Institute of Neurological Disorders and Stroke (NINDS) study in 1995 found that Alteplase improved functional outcomes at 3 months compared to placebo if given within three hours of symptoms onset. In May 2009, the American Heart Association/American Stroke Association (AHA/ASA) guidelines for the administration of rtPA following acute stroke were revised to expand the window of treatment from 3 hours to 4.5 hours to provide more patients with an opportunity to receive benefit from this effective therapy.

Recent studies have suggested that there may be a longer therapeutic window for the administration of thrombolytics. However, earlier administration is always better as “time is brain”—nervous tissue is lost as the stroke progresses. rtPa is usually administered 0.9 mg/kg with a maximum dose of 90 mg, with 10% of the dose administered as an IV bolus and the remainder infused over 60 minutes. Furthermore, neither heparin nor aspirin is used during the initial 24 hours. However, thrombolytics should not be withheld from a patient who has recently taken aspirin. Additionally, endovascular therapies such as intra-arterial and mechanical thrombolysis are being used for a subset of patients with acute ischemic stroke. See Table 14–4.

Elevated blood pressures are generally left untreated to maintain cerebral perfusion pressure. However, systolic blood pressure >220 mm Hg and diastolic blood pressures >120 mm Hg are best treated with easily titratable agents such as IV labetalol and nitrates. The blood pressure should not be lowered more than 25 percent of the presenting mean arterial blood pressure. The treated blood pressure should be below 185/110 mm Hg for rTPA administration.

Treatment of hemorrhagic stroke is different and includes blood pressure control with antihypertensives such as nimodipine, possibly reversing any anticoagulation with cryoprecipitate or platelets, and consultation with a hematologist and neurosurgeon.

COMPREHENSION QUESTIONS

14.1 A 58-year-old man experienced a neurologic deficit and is diagnosed as having a stroke. Which of the following is the most likely etiology?

A. Ischemic

B. Hemorrhagic

C. Drug-induced

D. Trauma-induced

E. Metabolic-related

14.2 An 80-year-old man is being evaluated for possible thrombolytic therapy after presenting with 2 hours of right arm weakness and aphasia. Which of the following is a contraindication for thrombolytic therapy?

A. Bilateral cerebral infarct

B. Hemorrhagic stroke

C. Hypertension-related stroke

D. Age of 80 years

14.3 An otherwise healthy 65-year-old woman is taken to the ED with probable stroke. Which of the following are the most urgent diagnostic studies?

A. Coagulation studies

B. ECG and cardiac enzymes

C. Bedside blood glucose and CT scan of the head

D. MRI of the head with and without contrast

14.4 A 67-year-old woman is seen in the emergency room with left arm weakness and right facial droop. Her blood pressure is 180/105 mm Hg. Which of the following is the best management for the hypertension?

A. Lower the blood pressure to less than 160/80 mm Hg by giving a small dose of labetalol.

B. Lower the blood pressure to less than 120/80 mm Hg.

C. No intervention for her blood pressure, but continue to monitor.

D. Lower the blood pressure to below 160/80 mm Hg if she is eligible for tPA.

ANSWERS

14.1 A. Ischemia is the most common etiology of stroke (due to thrombosis, embolism, or hypoperfusion) and is responsible for up to 80% of strokes.

14.2 B. Indications for tPA administration include an ischemic stroke with a clearly defined time of onset, measurable neuralgic deficit, and a baseline CT with no evidence of intracranial hemorrhage. Contraindications for tPA therapy vary and include: seizure at the time of stroke, history of intracranial hemorrhage, persistent blood pressure >185/110 mm Hg despite antihypertensive therapy, recent surgery or GI bleed, recent MI, pregnancy, or elevated aPTT or INR due to heparin or warfarin use, platelet count <100,000, etc.

14.3 C. Bedside blood glucose and CT scan of the head are the most urgent diagnostic studies in evaluating possible stroke patients. Coagulation studies, a complete blood count or platelet count should not delay tPA administration unless the patient is taking anticoagulation or has suspected thrombocytopenia. Noncontrast head CT is generally the initial imaging study, not MRI, to exclude hemorrhage or tumor as a cause of neurologic deficits. Though MRI provides more information, its cost, limited availability, restricted patient access, and other contraindications such as patient claustrophobia or metal implants limit its use.

14.4 C. Emergency administration of antihypertensive agents should be withheld in acute stroke to maintain cerebral perfusion pressure, unless the blood pressure is greater than 220/120 mm Hg. Patients are eligible for tPA with BP < 185/110 mm Hg. If patients have concurrent conditions that require acute lowering of blood pressure such as aortic dissection, hypertensive encephalopathy, acute renal failure, or congestive heart failure, a reasonable goal is to lower their mean arterial pressure 15% to 25% within the first 24 hours.

CLINICAL PEARLS

⯈ Strokes may present in a variety of ways, and the differential diagnosis of stroke is broad. Clinicians must take a careful history, including the time of onset of symptoms. The NIHSS measures the impairment due to stroke.

⯈ A bedside glucose measurement and a CT scan of the head are the most urgent diagnostic studies in suspected stroke.

⯈ Treatment is aimed at stabilizing the ABCs, evaluating for possible thrombolytic administration, and addressing comorbid conditions such as hypertension.

References

Adams HP Jr, del Zoppo G, et al. 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. Guidelines for the early management of adults with ischemic stroke. Stroke. 2007;38:1655-1711. 

Asimos AW. Code stroke: a state-of-the-art strategy for rapid assessment and treatment. Emerg Med Prac. 1999;1(2):1-24. 

Del Zoppo GJ, Saver JL, Jauch EC, Adams HP Jr. Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen activator: a science advisory from the American Heart Association/American Stroke Association. Stroke. Aug 2009;40(8):2945-2948. 

Diedler J, Ahmed N, Sykora M, et al. Safety of intravenous thrombolysis for acute ischemic stroke in patients receiving antiplatelet therapy at stroke onset. Stroke. Feb 2010;41(2):288-294. 

Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008;359(13):1317-1329. 

Huang P, Khor GT, Chen CH, et al. Eligibility and rate of treatment for recombinant tissue plasminogen activator in acute ischemic stroke using different criteria. Acad Emerg Med. 2011;18(3):273-278. 

Latchaw R, Alberts M, Lev M. Recomendations for imaging of acute ischemic stroke: a scientific statement from the American Heart Association. Stroke. 2009;40;3646-3678. 

Lewandowski C, Barsan W. Treatment of acute ischemic stroke. Ann Emerg Med. 2001;37(2):202-216. 

The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study G. Generalized efficacy or tPA for acute stroke. Stroke. 1997;28:2119-2125. 

The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study G. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995;333(24):1581-1587. 

Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine. 5th ed. New York, NY: McGraw-Hill; 2000:1430-1439. 

U.S. Centers for Disease Control and Prevention and the Heart Disease and Stroke Statistics—2007 Update, published by the American Heart Association. Available at: http://www.strokecenter.org/ patients/stats.htm. Accessed April, 2011.

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