disorders and prioritize care accordingly.
Blood pressure control among stroke patients is an area of controversy and active investigation. Perfusion to the ischemic brain following a stroke is dependent on arterial blood pressure to maintain cerebral perfusion. Thus, hypotension or a relatively low blood pressure for a patient with chronic hypertension could theoretically adversely affect needed cerebral perfusion to at‐risk areas (e.g., penumbra). In fact, many patients experience hypertension immediately after a stroke, and studies have indicated that hypertension usually resolves spontaneously within a few hours. Yet, systolic blood pressure greater than 185 mmHg has been associated with increased risk of ICH among patients who subsequently receive fibrinolytic therapy. Blood pressure control is also postulated to be helpful in reducing hematoma expansion among ICH patients. In general, blood pressure management is best deferred until the patient is in a more controlled environment, such as an ED, where invasive monitoring is possible. If there are compelling reasons to lower a patient’s blood pressure in the field, such as coexisting pulmonary edema, for example, great care must be taken not to over‐correct. A suitable initial target is a 10% reduction of systolic blood pressure, but not lower than 150 mmHg.
Box 18.1 Mimics of stroke
Bell palsy
Complex migraine
Conversion disorders
Encephalopathy
Hypoglycemia
Labyrinthitis
Ménière disease
Postictal (Todd) paralysis
Ramsay–Hunt syndrome
Box 18.2 Inclusion and exclusion criteria for intravenous tPA
Inclusion criteria
Ischemic stroke onset within 4.5 h of drug administration
Measurable deficit on NIH Stroke Scale examination
Head CT does not show hemorrhage or nonstroke cause of deficit. Patient’s age is >18 years
Exclusion criteria
Minor or rapidly improving symptoms
Seizure at onset of stroke
Major surgery within 14 days
Prior stroke or serious head trauma with past 3 months
Known history of intracranial hemorrhage
Sustained blood pressure >185/110 mmHg
Aggressive treatment necessary to lower blood pressure
Symptoms suggestive of subarachnoid hemorrhage
Gastrointestinal or genitourinary hemorrhage in last 21 days
Arterial puncture at a noncompressible site within 7 days
Heparin administration within 48 h with elevated aPTT
Prothrombin time >15 s
Platelet count <100,000 μL
Serum glucose <50 mg/dL or >400 mg/dL
Relative contraindications
Large stroke with NIH Stroke Scale score >22
CT shows evidence of large MCA territory infarction (sulcal effacement or blurring of gray‐white junction in greater than one third of MCA territory)
Relative contraindications for the 3‐ to 4.5‐h treatment window
History of prior stroke and diabetes mellitus
NIH Stroke Scale >25
Oral anticoagulant use regardless of INR
Age >80 years
INR, international normalized ratio; MCA, middle cerebral artery; NIH, National Institutes of Health; aPTT, activated partial thromboplastin time.
Source: Miller J, Hartwell C, Lewandowski C. 2012, Stroke treatment using intravenous and intra‐arterial tissue plasminogen activator. Curr Treat Options Cardiovasc Med. 2012; 14:273–83. © 2012, Springer Nature.
Some literature suggests that placing the patient supine may increase cerebral perfusion, but it also increases intracranial pressure, and this remains an area of uncertainty and investigation. Obviously, supine positioning is not advised in a patient who has clinical evidence of elevated intracranial pressure. As always, the risk of aspiration must be considered as well [13].
Ultimately, the goals for prehospital care of the stroke patients include rapid evaluation, stabilization, neurologic examination, and expedited transport to an appropriate destination hospital [15]. Early communication to the destination hospital is important. Studies have shown that such notification gives time for the stroke team to arrive in the ED and decreases the time from ED arrival to computed tomography (CT) imaging and increased rates of IV tissue plasminogen activator (tPA) administration [16, 17].
Definitive treatment options
Sussman and Fitch reported the first use of IV thrombolytics to treat acute ischemic stroke in the late 1950s [18]. However, early studies using either streptokinase or urokinase resulted in high incidences of ICH. Therefore, these therapeutic agents were abandoned for the treatment of stroke until the 1970s, when advanced imaging technology could rule out the possibility of ICH prior to thrombolytic administration and allow for a more definitive diagnosis of ischemic stroke. Unfortunately, high rates of ICH secondary to streptokinase treatment persisted in later trials, and ultimately led to the early termination of the Multicenter Acute Stroke Trial‐Italy (MAST‐I) and Multicenter Acute Stroke Trial‐Europe (MAST‐E) in the mid‐1990s, as well as the abandonment of streptokinase as a viable ischemic stroke treatment option [19]. Around the same time as the MAST‐E trial, several trials of tPA, which was thought to have a better risk–benefit profile compared to other thrombolytics, were conducted and failed to demonstrate favorable outcomes.
However, it was felt that the use of tPA held promise if a correct dose and the right population of patients were selected [19]. In 1995, the NINDS trial demonstrated improved functional outcomes at 3 months as measured by the National Institutes of Health Stroke Scale score, the modified Rankin score (mRS), and other neurologic assessment tools in highly selected ischemic stroke patients treated within 3 hours of symptom onset [20]. Patients treated with tPA were 30% more likely to have minimal to no disability at 3 months compared with patients treated with placebo (absolute benefit of 12%; number needed to treat [NNT] = 8), which was found to persist at 12 months [20, 21]. Based upon these findings, in 1996, the U.S. Food and Drug Administration approved the use of intravenous tPA for the treatment of acute ischemic stroke within 3 hours of the onset
