Wednesday, May 26, 2021

Hypertensive Encephalopathy Case File

Posted By: Medical Group - 5/26/2021 Post Author : Medical Group Post Date : Wednesday, May 26, 2021 Post Time : 5/26/2021
Hypertensive Encephalopathy 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 17
A 55-year-old man is brought in to the emergency department (ED) by his wife for altered mental status (AMS). She states that for the past day, he has been confused and unsteady when he walks. The patient has a history of hypertension (HTN) and hyperlipidemia. He complains of headache and blurry vision. On examination, he is alert and oriented to person only. On fundoscopy, the optic discs appear hyperemic and swollen, with a loss of sharp margins. His neurologic examination is nonfocal and otherwise has a normal physical examination. The patient’s vital signs are a blood pressure of 245/140 mm Hg, heart rate of 95 beats per minute, respiratory rate of 18 breaths per minute, oxygen saturation of 98% on room air and he is afebrile.

 What is the most likely diagnosis?
 What is the best management?

Hypertensive Encephalopathy

Summary: 55-year-old man with a history of hypertension that presents with AMS, headache, and blurry vision with a blood pressure of 245/140 mm Hg. His physical examination is significant for bilateral papilledema and AMS.
  • Most likely diagnosis: Hypertensive encephalopathy.
  • Best management: Confirm the diagnosis by ruling out ischemic or hemorrhagic stroke, infection, and mass lesion. Lower blood pressure with intravenous (IV) medications and check for evidence of other end-organ damage.

  1. Identify the presentation of various hypertensive emergencies.
  2. Recognize the difference between a hypertensive urgency and emergency.
  3. Understand how to manage blood pressure in hypertensive emergencies.

This is a 55-year-old man with AMS, papilledema, and severe hypertension. This presentation is most likely hypertensive encephalopathy, which is defined as the presence of neurologic abnormalities secondary to acute elevation in blood pressure. In the past, hypertensive encephalopathy and malignant hypertension have been used interchangeably. The latter term, however, was removed from the national blood pressure guidelines. Hypertensive encephalopathy is one of many forms of hypertensive emergency. It is critical for the physician to manage the patient’s blood pressure if there is evidence of end-organ dysfunction. This is in contrast to blood pressure management in hypertensive urgency.

Once the patient’s airway, breathing, and circulation (ABCs) are addressed, the first step in management is to obtain a noncontrast head computed tomography (NCHCT) to rule out the presence of mass lesion and hemorrhagic or ischemic stroke. Once these diagnoses are eliminated and the diagnosis of hypertensive encephalopathy is established, the focus should turn to lowering the blood pressure. Intravenous antihypertensives should be administered to lower the patient’s blood pressure. The goal is not to normalize the blood pressure because this can lead to cerebral ischemia secondary to hypoperfusion. Instead, the goal is to reduce the MAP by 20% to 25% over the first hour. Various antihypertensive agents are available to manage this disorder. This is in contrast to typical blood pressure management in patients with long-standing hypertension who do not have acute end-organ damage. Sodium nitroprusside, labetalol, and nicardipine are the first-line agents for lowering blood pressure in the setting of hypertensive encephalopathy. Sodium nitroprusside is administered as an IV infusion starting at a rate of 0.25 μg/kg/min and can be increased to a maximum of 10 μg/ kg/min. Labetalol is administered as an IV bolus of 20 mg, which can be repeated. It can also be administered as an IV infusion at a rate of 0.5 to 2.0 mg/min. Nicardipine is administered at 5 mg/h, and can be increased by 2.5 mg/h every 5 minutes to a maximum of 30 mg/h.

Approach To:
Hypertensive Emergencies

HYPERTENSION: Defined as blood pressure greater than or equal to 140/90 mm Hg.

HYPERTENSIVE EMERGENCY: The presence of acute end-organ damage in the setting of elevated blood pressure.

HYPERTENSIVE URGENCY: The presence of elevated blood pressure, without evidence of acute, ongoing end-organ damage. It requires urgent, but not emergent, blood pressure reduction.

HYPERTENSIVE ENCEPHALOPATHY: Transient neurologic symptoms associated with elevated blood pressure.

PREECLAMPSIA: Elevated blood pressure (140 mm Hg systolic or 90 mm Hg diastolic) in a pregnant patient accompanied by proteinuria, edema, or both occurring after 20 weeks of gestation. Preeclampsia in a patient with preexisting essential hypertension is diagnosed if systolic BP has increased by 30 mm Hg or if diastolic BP has increased by 15 mm Hg.

SEVERE PREECLAMPSIA: Severe hypertension, excess proteinuria, oliguria, cerebral or visual disturbances, pulmonary edema, impaired liver function, epigastric or right upper quadrant pain, thrombocytopenia or fetal growth restriction.

ECLAMPSIA: Seizure activity or coma unrelated to other cerebral conditions in a pregnant patient with preeclampsia.

Hypertension is found in 20% to 30% of adults in developed countries. Hypertension is more common in men than in women, and blood pressure seems to increase with age. The incidence of hypertension is 1.5 to 2.0 times greater in African Americans than in Caucasians. Hypertension is defined as two readings of greater than 140/90 mm Hg on two different occasions. Hypertensive emergencies will occur in approximately 1% of these individuals and account for approximately 2% to 3% of all ED visits. The most common risk factor in hypertensive emergencies is a history of hypertension.

Hypertensive urgencies are acute elevations in blood pressure without the signs or symptoms of acute end-organ damage. Previously, it was believed that hypertensive urgencies required immediate, aggressive blood pressure reduction. However, no studies demonstrated a benefit of this management and the potential for harm exists. The elevated blood pressure in this circumstance should be reduced over days to weeks and the patient can be discharged from the ED and followed up in 24 to 48 hours as an outpatient.

The pathophysiology of hypertensive end-organ damage is not completely understood. Current theory holds that the acute rise in blood pressure leads to a series of vascular events, which causes end-organ damage. In hypertensive encephalopathy it is believed that the acute rise in blood pressure causes endothelial cell dysfunction in the brain’s vascular supply leading to cerebral edema. Hypertensive encephalopathy can manifest clinically as visual changes, papilledema, focal neurologic deficits, and seizure. Hypertensive encephalopathy is an uncommon clinical entity. In order to establish the diagnosis, more common causes of altered mental status must be ruled out, including, but not limited to, meningitis, encephalitis, ischemic or hemorrhagic stroke, mass lesion, and toxic ingestion.

The diagnosis of hypertensive emergency requires evidence of acute end-organ dysfunction that is attributable to an elevation in blood pressure. This dysfunction can manifest through multiple organ systems and includes acute myocardial infarction, aortic dissection, acute left ventricular failure, acute pulmonary edema, cerebral infarction or hemorrhage, acute renal failure, preeclampsia/ eclampsia, symptomatic microangiopathic hemolytic anemia, and hypertensive encephalopathy.

It is critical to differentiate a hypertensive emergency from urgency. This is accomplished through a focused history, physical examination, and appropriate ancillary tests. A detailed medical history must be obtained to determine if the patient has underlying renal, cardiac, or endocrine manifestations. The patient’s current medications must be known and the possibility of ingestion of illicit drugs or other substances must be considered. In particular, obtaining history about the use of cocaine or other sympathomimetic substances (phenylephrine, monoamine oxidase inhibitors) is crucial as it significantly alters the treatment regimen (β-blockers must be avoided in the setting of sympathomimetic use). Elucidate any symptoms related to end-organ damage such as chest pain (myocardial infarction, aortic dissection), dyspnea (congestive heart failure, pulmonary edema), anuria (renal failure), visual changes (papilledema, retinal hemorrhages), altered mental status, and seizures. For patients more than 20 weeks pregnant or who recently gave birth, investigate symptoms of preeclampsia.

The physical examination should also assess for signs of end-organ damage. Fundoscopy can reveal papilledema, retinal hemorrhages, and exudates. Cardiovascular examination can identify signs of heart failure such as jugular venous distension, an S3 gallop, pulmonary rales, and extremity edema. Neurologic examination should evaluate the mental status and signs of focal deficits.

Ancillary testing varies in the patient with hypertensive emergency depending on the patient’s symptoms and which end-organ is affected. An ECG and cardiac enzymes should be obtained in patients suspected of having a myocardial infarction. Electrolytes including creatinine (Cr) and blood urea nitrogen (BUN), hemoglobin, and proteinuria and red blood cell casts on urinalysis may point toward renal failure or glomerulonephritis. A chest radiograph may aid in the diagnosis of congestive heart failure, pulmonary edema, and aortic dissection. A head CT scan should be obtained in all patients who present with altered mental status or a focal neurologic deficit in order to rule out a mass lesion, ischemic and hemorrhagic stroke.

Hypertensive Disease in Pregnancy
Preeclampsia is a unique form of hypertensive emergency, which occurs in pregnant patients. The exact pathophysiology is unknown but it is characterized by an abnormal vascular response to placental implantation. It is associated with increased systemic vascular resistance, activation of the coagulation system, platelet aggregation, and endothelial cell dysfunction. Predicting which patients will develop preeclampsia or eclampsia is difficult but epidemiologic studies have identified several risk factors including chronic hypertension and nulliparity.

Various organ systems can be affected, especially with severe elevation in blood pressure. Damage to the renal glomerular system leads to proteinuria and eventually, renal failure. Hepatic function is compromised and can lead to periportal hemorrhagic necrosis, subcapsular hematoma, or hepatic rupture. Disorders of coagulation may occur as hemolytic-uremic syndrome. A percentage of women suffering from preeclampsia go on to develop HELLP syndrome characterized by Hemolytic anemia, Elevated Liver enzymes and Low Platelet count. Eclampsia is characterized by tonic-clonic seizures in addition to the above multiorgan system involvement. Vasospasm and impairment of the autoregulation system in the brain can cause cerebral edema, thrombosis, hemorrhage, blindness, seizure, or coma.

Management primarily focuses on stabilization of the mother through control of blood pressure and progression to eclampsia. Hydralazine is the antihypertensive agent of choice in preeclampsia and eclampsia. The goal should not be to normalize the blood pressure because this can lead to placental insufficiency (inadequate blood flow to the fetus). Target blood pressure is approximately 160/100 mm Hg. When hydralazine is ineffective, labetalol is the second-line medication for treating hypertension. Delivery is the only definitive treatment for preeclampsia. The gestational age and the severity of the disease must be considered so the risks and benefits of delivery versus expectant management can be assessed.

Management of Hypertensive Emergencies
Hypertensive emergency is a true medical emergency. Immediate evaluation and management is critical to limit morbidity and mortality. The patient should be placed on a cardiac monitor and an intravenous line should be started. After the ABCs are assessed and stabilized, treatment begins by making the patient comfortable, consequently eliminating contributing factors that may exacerbate hypertension such as pain, urinary retention, and hypoxia. Patients require immediate administration of antihypertensive medications to prevent irreversible end-organ damage (except in the case of acute ischemic stroke). As the elevation in blood pressure is being addressed, definitive measures should be taken to address any complications.

Understanding the concept of autoregulation is essential in the management of hypertensive emergencies. Autoregulation serves to maintain a constant, effective blood flow and perfusion to end organs, despite large variations in pressure. In the brain, autoregulation acts by adjusting cerebral blood flow within the brain microcirculation. Extensive studies of cerebral circulation demonstrate that cerebral blood flow (CBF) is maintained across wide variations of systemic blood pressure by vasoconstriction and vasodilatation in normotensive patients. Because it is difficult to measure CBF accurately, especially regional differences and requirements, the cerebral perfusion pressure (CPP) is used as a surrogate indicator for monitoring. The CPP is the pressure gradient required to perfuse the cerebral tissue. CPP is calculated as the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP):


where MAP can be approximated as: diastolic blood pressure + ([systolic blood pressure − diastolic blood pressure]). Local cellular oxygen demands can be met and regional cerebral blood flow maintained over a wide range of CPP (between 50 and 150 mm Hg in a normally functioning system).

In individuals with chronic hypertension, the CBF remains constant at higher CPP. However, if MAP, and thus CPP, drops into normal ranges, CBF precipitously declines leading to cerebral hypoperfusion. Although not as well studied, it is theorized that rapid, large declines in blood pressure in chronically hypertensive patients would lead to hypoperfusion of other end organs as well.

Common Antihypertensive Agents Used in Hypertensive
Emergencies (Table 17–1)
Sodium nitroprusside: It is a potent peripheral vasodilator that decreases preload and afterload by dilating both arteries and veins that cause an immediate decrease in blood pressure. The recommended starting IV dose is 0.25 μg/kg/min and titrated to desired clinical response and blood pressure. Because of its rapid action and potency, intra-arterial monitoring is recommended when starting an infusion. Some drawbacks to this medication include its metabolism to a toxic cyanide compound. It is also associated with reflex tachycardia and coronary steal in the setting of acute coronary syndrome.

Labetalol: It is a selective alpha-1 adrenergic and nonselective beta-adrenergic blocker. It lowers systemic vascular resistance while maintaining renal, coronary, and cerebral blood flow. Unlike other vasodilators, labetalol causes minimal reflex tachycardia. It is contraindicated in patients with acute asthma, COPD, and heart failure, heart block, and sympathomimetic drug abuse (eg, cocaine). Intravenous boluses of labetalol require 2 to 5 minutes to begin lowering the blood pressure. If a single bolus of 20 mg does not achieve the desired blood pressure reduction after 10 minutes, either repeated boluses at twice the original dosage can be given or an IV infusion can be started and titrated to the desired blood pressure.

Esmolol: It is a short-acting selective beta-1 adrenergic blocker. It has a rapid onset and short duration of action. These properties make it easy to titrate. Esmolol is effective in blunting the reflex tachycardia induced by nitroprusside. It carries the same contraindications as other β-blockers (see Labetalol). Standard dosing is an IV bolus of 500 μg/kg followed by a continuous infusion of 50 μg/kg/min, which can be increased by 50 μg/kg/min every 4 to 5 minutes until the desired blood pressure is obtained.

common antihypertensive agents

Should be administered with a ß-blocker to avoid reflex tachycardia.

Nicardipine: It is a dihydropyridine calcium channel blocker (CCB). It may have unique benefits in hypertensive encephalopathy as it crosses the blood-brain barrier (BBB) to vasorelax cerebrovascular smooth muscle and minimizes vasospasm, especially in subarachnoid hemorrhage. Nicardipine is contraindicated in patients with advanced aortic stenosis. The main adverse effect is abrupt reduction in blood pressure and reflex tachycardia, which can be harmful in patients with coronary heart disease. The initial infusion rate is 5 mg/h, increasing by 2.5 mg/h every 5 minutes to a maximum of 30 mg/h. Once the target BP is reached, downward adjustment by 3 mg/h should be attempted as tolerated.

Nitroglycerin: It is a potent vasodilator that acts mainly on the venous system. It decreases preload and also increases coronary blood flow to the subendocardium. Nitroglycerin can be administered as a paste, sublingual spray, dissolvable tablet, or an infusion. It has a rapid onset and is considered the drug of choice in hypertensive emergencies in patients with cardiac ischemia, left ventricular dysfunction, and pulmonary edema. The recommended starting IV infusion dose is 5 to 15 mcg/min and titrated to desired clinical response. It is not recommended in patients with severe aortic stenosis, left ventricular outflow obstruction, or inferior wall myocardial infarction because of the chance of precipitating cardiovascular collapse.

Fenoldopam: It is a selective peripheral dopamine type 1 (D1) agonist that has recently been added to the list of medications used in the treatment of hypertensive emergencies. It causes both vasodilation and natriuresis. Fenoldopam is administered as an IV infusion with a starting dose of 0.1 to 0.3 μg/kg/min and can be increased in increments of 0.05 to 0.1 μg/kg/min every 15 minutes to targeted effect. It has the advantage of increasing renal blood flow and improving creatinine clearance. As a result, fenoldopam may be the drug of choice in treating hypertensive emergencies in the setting of impaired renal function. It is contraindicated in patients with increased intraocular pressure.

Hydralazine: It lowers blood pressure by a direct vasodilatory effect on arteriolar smooth muscle. The exact mechanism of this effect is unknown. It is the preferred treatment by obstetricians in treating preeclampsia/eclampsia for decades, but has fallen out of favor for treatment of hypertension in other conditions. Hydralazine can cause reflex tachycardia and CNS and myocardial ischemia. Another downside of hydralazine is that while the half life is 3 to 6 hours, the total duration of effect is up to 36 hours and can be unpredictable. The recommended starting dose is 5 to 10 mg IV bolus, which can be repeated every 10 to 15 minutes.

Enalaprilat: It is the active IV form of enalapril, an angiotensin-converting enzyme (ACE) inhibitor. Enalaprilat lowers systemic vascular resistance, pulmonary capillary pressure, and heart rate while increasing coronary vasodilation. It has minimal effect on cerebral perfusion pressure. Some studies have found enalaprilat to be particularly useful in hypertensive emergency with acute pulmonary edema (APE). ACE inhibitors are contraindicated in pregnancy. The dose of enalaprilat is 1.25 mg IV bolus over 5 minutes and can be repeated every 6 hours. Enalaprilat cannot be titrated to effect.

Conditions Associated With Hypertensive Emergencies
Hypertensive encephalopathy: The initial goal is to rapidly lower the blood pressure by no more than 20% to 25% of the MAP. More aggressive lowering of the blood pressure can lead to hypoperfusion and ischemia as discussed above. More normalization of the blood pressure may be contemplated over 24 to 48 hours. The preferred medication is nitroprusside, labetalol, or nicardipine.

Acute cerebral infarction or hemorrhage: There is continued controversy as to when and how much elevated blood pressure should be lowered in patients with ischemic stroke. In fact, a recent multicenter, randomized control trial in Europe failed to demonstrate any benefit of lowering blood pressure in acute stroke and showed a trend towards harm. For patients who are candidates for thrombolytic therapy, blood pressure should be lowered to less than 185/110 mm Hg and maintained to less than 180/105 mm Hg for the next 24 hours. Otherwise, for patients who are not thrombolytic candidates, cautious lowering of pressure greater than 220/120 mm Hg is generally accepted, being careful to avoid lowering it too much or too rapidly as to induce drops in cerebral perfusion and cause greater ischemia. The preferred medications include labetalol, nitroprusside, and nicardipine.

Acute myocardial infarction: The goal in lowering the blood pressure in these cases is to decrease cardiac work by decreasing afterload and increasing coronary perfusion pressure. The preferred medications include nitroglycerin and β-blockers.

Aortic dissection: It is critical to lower blood pressure rapidly in this condition to limit progression of the dissection. Acute aortic dissection represents the only hypertensive emergency where rapid, aggressive blood pressure reduction is indicated. The goal is to maintain arterial pressure as low as possible without compromising end-organ perfusion. The preferred medications include labetalol alone. If this does not adequately lower blood pressure it should be used in combination with sodium nitroprusside.

Preeclampsia/eclampsia: The most commonly used agent in the past was hydralazine. However, obstetricians are using labetalol more frequently because it has similar efficacy and fewer side effects. In addition, magnesium sulfate is generally administered for seizure prophylaxis, though it has not been shown to lower blood pressure in hypertensive pregnant patients.


17.1 A 55-year-old man presents to the ED with complaints of a severe headache, diplopia, and vomiting. His blood pressure is 210/120 mm Hg upon arrival. Which of the following is the best next step?
A. Observe the blood pressure and recheck in 1 hour, and supportive measures for the headache and vomiting.
B. Obtain a head CT scan, give an antihypertensive such as nicardipine, and admit to the intensive care unit.
C. Give intravenous furosemide to decrease the blood pressure.
D. Give lorazepam to help the patient relax.

17.2 A 54-year-old woman presents to the ED requesting medication refi lls on her antihypertensive medications. She has been out of her medications for 2 weeks and cannot get an appointment with her private physician until next week. She normally takes atenolol and hydrochlorothiazide. Her blood pressure is 190/100 mm Hg. The patient has no complaints. She has been waiting for 4 hours and is in a hurry to get back to work. Which of the following is the most appropriate next step?
A. Change her medications to a calcium channel blocker.
B. Admit to the intensive care unit and initiate intravenous nitroprusside.
C. Give her a prescription for her medications, instruct her to take them immediately, and have her follow-up in 48 hours.
D. Counsel the patient on the dangers of her noncompliance, admit to the hospital, and begin the patient on intravenous labetalol.

17.3 A 38-year-old man presents to the ED after a motor vehicle collision. After complete evaluation it is determined that he sustained a fractured right tibia. The patient has a history of hypertension for which he is on pharmacologic treatment. The patient is writhing on the gurney in pain. His blood pressure is 210/104 mm Hg. The patient has no complaints except for right leg pain. Which of the following is the most appropriate next step in management?
A Pain control and monitor the patient’s blood pressure.
B. Start a β-blocker and monitor the patient’s blood pressure.
C. Call a social worker because of suspected drug or alcohol abuse.
D. Admit the patient to the hospital to get his blood pressure under control.


17.1 B. This man has hypertensive encephalopathy, which is a medical emergency. He has symptomatic hypertension causing end-organ damage. A head CT scan should be obtained prior to starting treatment to rule out any intracranial pathology. The appropriate treatment is IV antihypertensive medications to decrease his mean arterial pressure by 20% to 25% over 1 hour.

17.2 C. This patient has hypertensive urgency. She has no symptoms related to her elevated blood pressure and no signs of end-organ damage. The patient should restart her medications and have her blood pressure reassessed in 48 hours.

17.3 A. Although this man has a history of hypertension, he is in excruciating pain, which could be causing his elevated blood pressure. The appropriate treatment is to control the pain, have the leg set back into place, and monitor his blood pressure. The blood pressure should decrease once his pain is controlled.


 Hypertensive emergency is defined as markedly elevated blood pressure in the presence of end-organ damage, whereas hypertensive urgency is markedly elevated blood pressure without end-organ effects.

 One of the most common reasons for hypertensive emergency is patient noncompliance with antihypertensive medication.

 It is critical to cautiously lower blood pressure to avoid inducing a hypoperfusion state that leads to cerebral ischemia.

 Patients with hypertensive emergency should be admitted to a monitored setting, preferably an intensive care unit.


Amin A. Parenteral medication for hypertension with symptoms. Annals Emerg Med. 2008;51(3 Suppl): S10-S15. Epub 2008 Jan 11. 

Blumenfeld JD, Laragh JH. Management of hypertensive crises: the scientific basis for treatment decisions. Am J Hypertension. 2001;14(11 Pt 1):1154-1167. 

Chobanian AV, Bakris GL, Cushman WC, et al. The seventh report of the Joint National Committee on Prevention, Detection and Evaluation, and Treatment of High Blood Pressure, The JNC 7 Report. NIH Publication No. 04-5230. 2004. 

Cotton DB, Gonik B, Dorman KF. Cardiovascular alterations in severe pregnancy induced hypertension: acute effects of intravenous magnesium sulfate. Am J Obstet Gynecol. 1984;148:162-165. 

De Gaudio AR, Chelazzi C, Villa G, Cavaliere F. Acute severe arterial hypertension: therapeutic options. Curr Drug Targets. 2009;10(8):788-798. 

Fisher ND, Williams GH. Hypertensive vascular disease. In: Kasper DL, Braunwald E, Fauci AS, Hauser Sl, Longo DL, Jameson JL, eds. Harrison’s Principles of Internal Medicine. 16th ed. New York, NY: McGraw-Hill :1463-1481. 

Flanigan JS, Vitberg D. Hypertensive emergency and severe hypertension: what to treat, who to treat, and how to treat. Med Clin North Am. 2006;90(3):439-451. 

Frakes MA, Richardson LE. Magnesium sulfate therapy in certain emergency conditions. Am J Emerg Med. 1997;15:182-187. 

Lipstein H, Lee CC, Crupi RS. A current concept of eclampsia. Am J Emerg Med. 2003;21:223-226. 

Marik PE, Varon J. Hypertensive crises: challenges and management. Chest. 2007;131(6):1949-1962. 

McCoy S, Baldwin K. Pharmacotherapeutic options for the treatment of preeclampsia. Am J Health Syst Pharm. 2009;66(4):337-344. 

Pancioli AM. Hypertension management in neurologic emergencies. Annals Emerg Med. 200;51(3 Suppl):S24-S27. Epub 2008 Jan. 

Powers DR, Papadakos PJ, Wallin JD. Parenteral hydralazine revisited. J Emerg Med. 1998;16(2):191-196. 

Rhoney D, Peacock WF. Intravenous therapy for hypertensive emergencies, part 1. Am J Health Syst Pharm. 2009;66(15):1343-1352. 

Rhoney D, Peacock WF. Intravenous therapy for hypertensive emergencies, part 2. Am J Health Syst Pharm. 2009;66(16):1448-1457. 

Sandset EC, Bath PM, Boysen G, et al; SCAST Study Group. The angiotensin-receptor blocker candesartan for treatment of acute stroke (SCAST): a randomised, placebo-controlled, double-blind trial. Lancet. 2011;377:741.


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