Initial Diagnosis and Management of Acute Ischemic Stroke


Period measured

Optimal time (min)

From ED arrival to emergency physician evaluation

10

From ED arrival to CT scan initiation

25

From ED arrival to CT scan interpretation

45

From ED arrival to initiation of therapy (80% compliance)a

60


Reproduced by permission of Stroke [1]

ED emergency department, CT computed tomography

aTarget should be compliance with these guidelines in at least 80% of cases




5.1 Establishing Time of Stroke Onset and History Taking


If stroke symptoms are recognized by emergency physicians, “stroke code” should be activated immediately. In some well-developed areas, emergency medical service (EMS) personnel are trained to identify stroke symptoms, and the stroke team could be alerted on the way to the hospital. Following stroke code activation, the exact time of symptom onset should be determined because time-dependent treatments are performed based on this information. Physicians should ask patients when the stroke symptoms began. However, the patient may not be able to talk about their symptoms or onset status due to neurologic deficits or comorbidities. In this situation, obtaining a detailed history from family members, witnesses who observed the onset of the stroke, and emergency medical personnel can provide valuable information. In addition, any observations of the patient during daily activities might be evaluated with cautious history taking, as a patient’s daily routine may aid in providing a stroke onset time. Cellular phone recordings could also verify the normal status of the patient. Because therapeutic intervention in this stage carries risk and requires rapid decision, the physician may contact responsible family members or a legally authorized representative to discuss the possible risks or benefits of the intervention.

Additional history about the patient should also be obtained quickly. Risk factors such as hypertension, diabetes mellitus, dyslipidemia, and cardiac disease, as well as migraine, seizure, trauma, drug abuse, alcohol abuse, pregnancy, and previous stroke history, should be noted. Medication history including the use of antithrombotics should be obtained. Intravenous thrombolysis exclusion criteria should be assessed in a timely manner. In addition, the patient’s weight is needed to determine the dose of recombinant tissue plasminogen activator (rtPA).


5.2 Physical Examination


After the airway, breathing, and circulation of the patient have been assessed and vital signs including blood pressure, heart rate, oxygen saturation, and temperature have been recorded, a more detailed physical examination should be performed. Ageneral physical examination is important to identify possible etiologic factors for ischemic stroke as well as possible complications and coexisting comorbidities. Examination of the face and head may reveal signs of trauma. Auscultation of the neck and chest may reveal carotid bruits and cardiac murmurs, arrhythmias, and rales, respectively. Skin and extremity examination may reveal a few signs specific to coagulopathies, platelet disorders, trauma, or embolic lesions. Because acute comorbidities may influence the selection of an acute treatment, a thorough but brief examination is necessary.


5.3 Neurologic Examination and Stroke Scales


The neurological evaluation of an acute stroke patient must be brief and efficient. An experienced neurologist should immediately assess the level of consciousness and breathing patterns. If patients are alert and able to respond to verbal stimuli, neurological examinations should be performed based on common stroke scales, such as the National Institutes of Health Stroke Scale (NIHSS) (Table 5.2). The scales have demonstrated their utility and can be administered by a broad spectrum of health providers [2]. Use of a standard stroke scale helps quantify the degree of neurological deficits and facilitate communication among stroke teams. When a patient’s consciousness is impaired, neurologists should uncover localizing and lateralizing signs. Deviation of the eyes or head, air-escaping pattern of the face, asymmetric withdrawal response to noxious stimuli, asymmetric brainstem reflexes, and asymmetric pathologic reflexes are examples of brain damage. A thorough neurological examination is necessary in patients who are unconscious to rule out conditions that may mimic stroke. Although intravenous rtPA use in stroke mimics does not show harmful effects, thrombolytic treatment of stroke mimics should be under 3% based on non-contrast-enhanced computed tomography (NECT) alone [3].


Table 5.2
National Institutes of Health Stroke Scale



















































































































































































Tested Item

Responses

Score

1a. Level of consciousness

Alert

0

Not alert, but arousable with minimal stimulation

1

Not alert, requires repeated stimulation to attend

2

Coma/unresponsiveness

3

1b. LOC questions (Ask patient the month and their age)

Answers both correctly

0

Answers one correctly

1

Both incorrect

2

1c. LOC commands (Ask patient to open and close eyes, make fist/let go)

Obeys both correctly

0

Obeys one correctly

1

Both incorrect

2

2. Best gaze (only horizontal movement)

Normal

0

Partial gaze palsy

1

Forced deviation

2

3. Visual fields testing

No visual field loss

0

Partial hemianopia

1

Complete hemianopia

2

Bilateral hemianopia (blind including cortical blindness)

3

4. Facial palsies (ask patient to show teeth or raise eyebrows and close eyes tightly)

Normal symmetrical movement

0

Minor paralysis (flattened nasolabial fold)

1

Partial paralysis (total or near-total paralysis of lower face)

2

Complete paralysis of one or both sides (absence of facial movement)

3

5. Motor function—arm (left, right)

Normal (extends arms 90 for 10 s without drift)

0

Drift

1

Some effort against gravity

2

No efforts against gravity

3

No movement

4

Untestable (joint fused or limb amputated)

9

 6. Motor function—leg (left, right)

Normal (hold leg 30° for 5 s without drift)

0

Drift

1

Some effort against gravity

2

No efforts against gravity

3

No movement

4

Untestable (joint fused or limb amputated)

9

 7. Limb ataxia

No ataxia

0

Present in one limb

1

Present in two limb

2

 8. Sensory (use pinprick to test arms, legs, trunk, and face—compare side to side)

Normal

0

Mild to moderate decrease in sensation

1

Severe to total sensory loss

2

 9. Best language (describe picture, name items, read sentences)

No aphasia

0

Mild to moderate aphasia

1

Severe aphasia

2

Mute

3

10. Dysarthria (read several words)

Normal articulation

0

Mild to moderate slurring of words

1

Near unintelligible or unable to speak

2

Intubated or other physical barrier

9

11. Extinction and inattention

Normal

0

Inattention or extinction to bilateral simultaneous stimulation in one of the sensory modalities

1

Severe hemi-inattention or hemi-inattention to more than one modality

2
 
Total score
 


5.4 Emergency Management of Stroke Patients



5.4.1 Brain and Vascular Imaging


Imaging of the brain with NECT is crucial to confirm the diagnosis of cerebral hemorrhage, which appears as an area of high density. It is widely used in almost all hospitals because it is inexpensive, noninvasive, and easily accessible. It is the single most important imaging modality because a decision of intravenous thrombolysis can be easily made, and it can also reveal brain tumors, which would be a contraindication to thrombolysis. NECT may show early signs of infarction such as a loss of gray-white matter interface among the nuclei of the basal ganglia and insular cortex. Cortical swelling by cerebral ischemia may produce sulcal effacement, and early arterial occlusion may show signs of a hyperdense vessel. When these signs of early infarct are present, the degree of ischemia will be more profound and the outcome will be poor [4].

Diffusion-weighted imaging (DWI) of the brain is the most sensitive and specific imaging for acute infarct even in the early stages of a stroke. It can differentiate an old infarction from a recent infarction and detect relatively small lesions in the brainstem, which are poorly visualized with NECT. In the hyperacute stage of ischemic stroke, visible diffusion lesions will include both regions of irreversible infarctions with more severe apparent diffusion coefficient (ADC) changes and regions of salvageable penumbra with less severe ADC changes. Standard MRI sequences (T1-weighted, T2-weighted, fluid-attenuated inversion recovery [FLAIR]) are relatively insensitive to acute stroke but may be useful to diagnose stroke mimics such as seizure and metabolic abnormalities. DWI/FLAIR mismatch has been recently suggested, especially in patients with unclear onset or wake-up stroke. It is a concept based on DWI changes beginning with the onset of stroke and FLAIR changes that are apparent after 3 h. However, it should only be used in specific conditions and on an individual basis [5]. Susceptibility-weighted imaging (SWI) and gradient echo imaging (GRE) are able to detect very small amounts of deoxyhemoglobin and intracerebral hemorrhages and microbleeds. Based on these MRI findings, they could be used as an initial imaging modality to evaluate acute stroke patients. However, if MRI scans are not readily available for 24 h, as in most hospitals, time should not be wasted waiting for MRI results.

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Oct 17, 2017 | Posted by in NEUROLOGY | Comments Off on Initial Diagnosis and Management of Acute Ischemic Stroke

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