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Stroke is one of the leading causes of disability in the USA. Timely acute interventions in the form of tPA and endovascular therapy have changed the landscape of acute stroke care. Having an organized and efficient system of care is extremely important for delivering acute stroke care. This chapter details the components of acute stroke care from the emergency room to the neurocritical care unit. The chapter covers pre- and post-tPA and endovascular care as well as post stroke complication management in the neurocritical care unit.
2 Cerebrovascular Emergency—Acute Stroke Diagnosis and Management
2.1 Epidemiology
Stroke is the fifth leading cause of death in North America
It is the leading cause of disability
795,000 people/year have a stroke in North America
2.2 Etiology
2.2.1 Nonmodifiable Risk Factors
Age
Sex
Race
Family history
2.2.2 Modifiable Risk Factors
Hypertension
Diabetes mellitus
Hyperlipidemia
Smoking
Excessive alcohol use
Obstructive sleep apnea
2.2.3 Stroke Subtypes
According to TOAST 9 classification there are five subtypes of ischemic stroke:
Large artery atherosclerosis
Cardioembolism
Small vessel occlusion (lacunar stroke)
Stroke of other determined etiology
Mechanical valves
Atrial fibrillation/flutter
Left atrial (LA) appendage thrombus
Left ventricular (LV) thrombus
Recent myocardial infarction (MI)
Dilated cardiomyopathy
Endocarditis/infection
Patent foramen ovale
Atrial septal aneurysm
Congestive heart failure
Vasculopathies
Hypercoagulable state
Stroke of undetermined etiology/cryptogenic
2.3 Common Clinical Presentations
Presentation depends on the vascular territory. See Table 2‑1.
F.A.S.T. is the acronym most associated with recognition of early stroke signs:
F = Facial weakness
A = Arm weakness
S = Speech difficulty
T = Time to call 9–1-1
Once in the emergency department a more thorough examination using the National Institutes of Health Stroke Scale (NIHSS) is completed (Table 2‑2).
2.4 Differential Diagnosis for Acute Ischemic Stroke
Intracerebral hemorrhage (ICH)
Subarachnoid hemorrhage (SAH)
Migraine with aura (most auras DO NOT last beyond 60 minutes nor present with loss of function)
Transient global amnesia
Postictal Todd’s palsy (history of epilepsy or prior Todd’s palsy, short duration with improvement)
Hypoglycemia (rapid improvement with glucose correction) 2
2.5 Acute Stroke Diagnosis, Treatment, and Management
2.5.1 Stroke Activation
(Fig. 2‑1)
ABC: airway, breathing, circulation
O2 saturation >94% (supplemental oxygen is not recommended if the patient is not hypoxic)
Finger-stick glucose should be >50
Intravenous (IV) access
History: Past medical, surgical, and medication (ask about antiplatelet and anticoagulant agents)
Check electrocardiogram (ECG)—rule out acute ST-elevation myocardial infarction (STEMI)
Send STAT labs: Coagulation panel and platelet
Perform focal stroke examination using NIHSS (Table 2‑2 and Fig. 2‑1 shows the pictures and sentences used for questions 9 and 10 on the scale.)
Check STAT computed tomography (CT) of head ( Fig. 2‑2 )
Rule out hemorrhage
Rule out large completed ischemic stroke
Identify acute middle cerebral artery (MCA) or basilar occlusion
Assess eligibility for IV tPA (Table 2‑3 and Fig. 2‑3)
If eligible, dosing for tPA is 0.9 mg/kg with a maximum dose of 90 mg.
A bolus of 10% is given over the first minute followed by the remaining dose over 1 hour.
If a patient is ineligible for tPA then administer 325 mg aspirin orally or 300 mg aspirin rectally (provided no hemorrhage on CT of head).
Blood pressure goals (Fig. 2‑4):
Blood pressure must be controlled prior to administering IV tPA to minimize the bleeding risk. Goal is <185/110.
With tPA administration, maintain a blood pressure (BP) goal of <180/105.
If tPA is NOT given then the BP goal should be < 220/110 during the first 24 hours.
Avoid agents like hydralazine, nitroprusside, and nitroglycerin due to their vasodilatory effect.
Fig. 2‑1 outlines the pathway for further imaging in patients with suspected large vessel occlusion or dense vessel on plain CT head. CT angiogram (CTA) of head and neck to identify artery occlusion and CT perfusion to evaluate size of core infarct and penumbra (Fig. 2‑5).