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Official reprint from UpToDate www.uptodate.com ©2016 UpToDate

Evaluation and treatment of hypertensive emergencies in adults

Authors: William J Elliott, MD, PhD, Joseph Varon, MD, FACP, FCCP, FCCM, FRSMSection Editors: George L Bakris, MD, Norman M Kaplan, MDDeputy Editor: John P Forman, MD, MSc

All topics are updated as new evidence becomes available and our peer review process iscomplete.Literature review current through: Oct 2016. | This topic last updated: Aug 16, 2016.

INTRODUCTION AND TERMINOLOGY — Most patients with significantly elevated bloodpressure (systolic pressure ≥180 and/or diastolic pressure ≥120 mmHg) have no acute, end­organ injury (so called severe asymptomatic hypertension). Although some propose relativelyrapid initiation of antihypertensive therapy in this setting, there may be more risk than benefitfrom such an aggressive regimen. (See "Management of severe asymptomatic hypertension(hypertensive urgencies) in adults".)

By contrast, some patients with significantly elevated blood pressure have signs or symptoms ofacute, ongoing target­organ damage. Such patients have a hypertensive emergency.Hypertensive emergencies can develop in patients with or without preexisting chronichypertension [1,2]. Often, the diastolic pressure is ≥120 mmHg, but there is no specific thresholdsince individuals who develop an acute rise in blood pressure can develop symptoms if theprevious pressure was normal (such as in a pregnant woman who develops eclampsia or ayoung adult who develops acute glomerulonephritis).

The term "malignant hypertension" entered the medical lexicon in 1928 because, at that time,patients with this condition had a prognosis that was similar to patients with many cancers.However, antihypertensive therapies that can quickly and safely lower blood pressure haveimproved outcomes [3] and, therefore, the term is now used only by billing and codingpersonnel.

EVALUATION AND DIAGNOSIS — The history and physical examination in patients presentingwith a severely elevated blood pressure (or an acute rise in blood pressure over a previouslynormal baseline, even if the presenting pressure is <180/120 mmHg) should determine whetheror not any of the following are present [4]:

®

®

Acute head injury or trauma

Generalized neurologic symptoms, such as agitation, delirium, stupor, seizures, or visualdisturbances

Focal neurologic symptoms that could be due to an ischemic or hemorrhagic stroke

Flame hemorrhages, exudates (cotton­wool spots), or papilledema when direct funduscopyis performed, as these are consistent with grade III or IV hypertensive retinopathy and can

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In addition, the following tests may be performed to evaluate the presence of target­organdamage:

It is often easiest to categorize hypertensive emergencies by the target organ that is beingdamaged (eg, brain, heart). The evaluation above can usually identify the at­risk target organand can dictate both the target blood pressure and the rapidity with which the target is achieved.(See 'Treatment' below.)

Hypertensive emergencies are uncommon, with an estimated population incidence (based uponlarge claims databases) of one to two cases per million per year. A retrospective record reviewfrom one adult emergency department found that hypertensive emergencies accounted for lessthan 1 percent of all visits occurring during a single year [5]. Of these hypertensive emergencies,eclampsia was the least common (2 percent), whereas cerebral infarction (39 percent) andacute pulmonary edema (25 percent) were the most common, similar to the conclusions of aseparate report [6].

TREATMENT

be associated with hypertensive encephalopathy

Nausea and vomiting, which may be a sign of increased intracranial pressure

Chest discomfort, which may be due to myocardial ischemia or aortic dissection

Acute, severe back pain, which might be due to aortic dissection

Dyspnea, which may be due to pulmonary edema

Pregnancy, as such patients with severe hypertension could have preeclampsia or developeclampsia

Use of drugs that can produce a hyperadrenergic state, such as cocaine, amphetamine(s),phencyclidine, or monoamine oxidase inhibitors, or recent discontinuation of clonidine orother sympatholytic agents

Electrocardiography

Conventional chest radiography

Urinalysis

Serum electrolytes and serum creatinine

Cardiac enzymes (if an acute coronary syndrome is suspected)

Computed tomography (CT) or magnetic resonance imaging (MRI) of the brain (if headinjury, neurologic symptoms, hypertensive retinopathy, nausea, or vomiting are present)

Contrast­enhanced CT or MRI of the chest or transesophageal echocardiography (if aorticdissection is suspected)

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Overall approach to therapy — Optimal therapy, including the choice of agent and the bloodpressure goal, varies according to the specific hypertensive emergency [7,8].

It is generally unwise to lower the blood pressure too quickly or too much, as ischemic damagecan occur in vascular beds that have grown accustomed to the higher level of blood pressure(ie, autoregulation). For most hypertensive emergencies, mean arterial pressure should bereduced gradually by about 10 to 20 percent in the first hour and by a further 5 to 15 percentover the next 23 hours [8].

The major exceptions to gradual blood pressure lowering over the first day are:

After a suitable period (often 8 to 24 hours) of blood pressure control at target in the intensivecare unit, oral medications are usually given and the initial intravenous therapy is tapered anddiscontinued.

Neurologic emergencies — Severe hypertension with acute neurologic signs or symptoms isusually the most complicated and difficult clinical scenario, as the differential diagnosis includesvaried conditions that have disparate treatments, only some of which routinely involve loweringthe blood pressure:

The acute phase of an ischemic stroke – The blood pressure is usually not lowered unlessit is ≥185/110 mmHg in patients who are candidates for reperfusion therapy (table 1) or≥220/120 mmHg in patients who are not candidates for reperfusion therapy. (See "Initialassessment and management of acute stroke", section on 'Blood pressure management'.)

Acute aortic dissection – The systolic blood pressure is rapidly lowered to a target of 100to 120 mmHg (to be attained in 20 minutes) [9]. (See "Management of acute aorticdissection".)

Intracerebral hypertension – Goals of antihypertensive therapy in such patients are variableand are discussed elsewhere. (See "Spontaneous intracerebral hemorrhage: Treatmentand prognosis", section on 'Blood pressure'.)

Ischemic stroke – Patients with acute ischemic stroke­in­evolution are most often not givenantihypertensive drugs unless they are candidates for tissue plasminogen activator andtheir initial blood pressure is ≥185/110 mmHg or if their initial blood pressure is ≥220/120,even if they are not candidates for reperfusion therapy. The preferred antihypertensivemedications in this setting are discussed in detail elsewhere. (See "Initial assessment andmanagement of acute stroke", section on 'Blood pressure management'.)

Hemorrhagic stroke – Management of blood pressure in patients with spontaneousintracerebral hemorrhage and subarachnoid hemorrhage is complicated by competing risks(eg, reducing cerebral perfusion) and benefits (eg, reducing further bleeding). Aninternational trial involving 2839 subjects with onset of symptoms less than six hours prior topresentation and a baseline blood pressure of 150 to 200 mmHg found that lowering bloodpressure (within one hour) to <140 mmHg was safe and produced nonsignificant benefitson death and major disability [10] United States guidelines indicate that blood pressure­lowering therapy should be given in this setting if there are no contraindications [11].Intravenous labetalol and nicardipine are most often used as first­line agents, although

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Cardiac emergencies — The most common cardiac emergencies associated with severelyelevated blood pressure are acute left ventricular dysfunction with pulmonary edema and acutecoronary syndrome (including acute myocardial infarction).

Vascular emergencies — Vascular emergencies include acute aortic dissection and severehypertension in patients who have recently undergone vascular surgery.

shorter­acting drugs might be more advantageous. Management of blood pressure inpatients with hemorrhagic stroke is discussed in detail elsewhere. (See "Spontaneousintracerebral hemorrhage: Treatment and prognosis", section on 'Blood pressure' and"Treatment of aneurysmal subarachnoid hemorrhage", section on 'Blood pressure control'.)

Head trauma – Head trauma with increased intracranial pressure can produce severeelevations in blood pressure. Hypertension is usually treated in this setting only if thecerebral perfusion pressure (mean arterial pressure minus intracranial pressure) is >120mmHg and the intracranial pressure is >20 mmHg. (See "Evaluation and management ofelevated intracranial pressure in adults", section on 'Blood pressure control'.)

Hypertensive encephalopathy – In contrast to stroke and head trauma, the signs andsymptoms of hypertensive encephalopathy (eg, headache, confusion, nausea, vomiting)usually abate after the blood pressure is lowered (see "Moderate to severe hypertensiveretinopathy and hypertensive encephalopathy in adults"). In fact, hypertensiveencephalopathy is most often a diagnosis of exclusion, confirmed retrospectively when themental status improves after the blood pressure is lowered into the autoregulatory range.Thus, patients with suspected hypertensive encephalopathy should have their bloodpressure lowered by approximately 10 to 20 percent during the first hour of treatment.However, additional lowering should be gradual such that, compared with the initial bloodpressure upon presentation, the pressure is reduced by no more than 25 percent at the endof the first day of treatment. Commonly used medications in this setting include clevidipine,nicardipine, fenoldopam, and nitroprusside.

Acute heart failure – Patients with acute left ventricular dysfunction and pulmonary edemashould usually receive loop diuretics. An easily titratable vasodilator (eg, sodiumnitroprusside, nitroglycerin) is often added to reduce afterload. Drugs that increase cardiacwork (eg, hydralazine) or acutely decrease cardiac contractility (eg, labetalol or other betablocker) should be avoided. The goal of these therapies is amelioration of heart failure andimprovement in pulmonary edema, which can often be achieved with a 10 to 15 percentreduction in blood pressure. (See "Treatment of acute decompensated heart failure:General considerations".)

Acute coronary syndrome – Severe hypertension associated with an acute coronarysyndrome (including acute myocardial infarction) is appropriately treated with intravenousnitroglycerin, clevidipine, nicardipine, or esmolol to reduce the underlying coronary ischemiaand/or increased myocardial oxygen consumption and to improve prognosis [12]. (See"Overview of the acute management of ST elevation myocardial infarction" and "Overviewof the acute management of unstable angina and non­ST elevation myocardial infarction".)

Acute aortic dissection – Patients with acute aortic dissection are treated to rapidly reducethe blood pressure to a goal systolic of 100 to 120 mmHg within about 20 minutes of

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Renal emergencies — Severe hypertension may occasionally cause acute injury to the kidneys(acute hypertensive nephrosclerosis, formerly called "malignant nephrosclerosis"). Thiscondition is characterized by hematuria (usually microscopic hematuria, which is found inapproximately 75 percent of patients with hypertensive emergencies) [14] and an elevatedserum creatinine. It is important to determine whether or not these findings are recent since theymay predate the severe blood pressure elevation in some patients.

When renal injury occurs as a result of severe hypertension, the common pathologic findingsinclude fibrinoid necrosis of small arterioles and "onion skinning" of small renal arteries. Thehistologic changes are indistinguishable from other forms of the hemolytic­uremic syndrome(picture 1A­D); however, a kidney biopsy is seldom performed in such patients. The renalvascular disease leads to glomerular ischemia and activation of the renin­angiotensin system,possibly resulting in exacerbation of the hypertension.

Antihypertensive therapy often leads to worsening kidney function, sometimes requiring dialysis,although this reduction in kidney function may be reversed with long­term blood pressure control[15]. By contrast, fenoldopam is associated with a temporary improvement in renal function andis therefore a useful antihypertensive agent in patients with renal hypertensive emergencies.

Sympathetic overactivity resulting in hypertensive emergencies — Four causes ofsympathetic overactivity can lead to severe elevations of blood pressure and acute target­organdamage:

diagnosis (table 2), although this target is not based upon clinical trial evidence. Anintravenous beta blocker is given first (usually esmolol, but labetalol, propranolol, andmetoprolol can also be used) to reduce the heart rate below 60 beats per minute and theshear stress on the aortic wall [13]. In addition, a vasodilator (often nitroprusside orclevidipine) is typically required to quickly achieve the goal blood pressure. (See"Management of acute aortic dissection".)

Severe hypertension in patients with recent vascular surgery – Severe elevations of bloodpressure can threaten suture lines and, therefore, such patients are often treated withrapidly acting intravenous antihypertensive agents in an intensive care unit setting.Although this is common practice, no controlled studies have proven the benefit of thisintervention.

Withdrawal of short­acting antihypertensive agents (especially clonidine, propranolol, orother beta blockers) can be associated with severe hypertension and may mimic the signsand symptoms of pheochromocytoma. Typically, reinstitution of the recently discontinueddrug will lower the blood pressure. Oral clonidine will begin to lower blood pressure withinan hour; however, some beta blockers take much longer to lower the blood pressure and,therefore, short­acting intravenous medications are often required while waiting for thereinstituted beta blocker to achieve an effect. (See "Withdrawal syndromes withantihypertensive therapy".)

Ingestion of sympathomimetic agents (eg, tyramine­containing foods in patients who takechronic monoamine oxidase inhibitors [7], amphetamine­like compounds, cocaine, etc) canprecipitate severe hypertension and end­organ damage. Such patients can be treated with

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Unless a beta blocker was recently withdrawn, administration of a beta blocker alone iscontraindicated in these settings since inhibition of beta receptor­induced vasodilation canresult in unopposed alpha­adrenergic vasoconstriction and a further rise in blood pressure [16].(See "Clinical presentation and diagnosis of pheochromocytoma".)

Hypertensive emergencies during pregnancy — Intravenous magnesium sulfate,methyldopa, hydralazine, and labetalol have been widely used in pregnant women with severehypertension, which is usually due to preeclampsia or exacerbation of preexistent hypertension.Fenoldopam and nicardipine have also been used.

These issues as well as antihypertensive drugs that are contraindicated in pregnancy arediscussed in detail separately. (See "Management of hypertension in pregnant and postpartumwomen", section on 'Acute therapy'.)

ANTIHYPERTENSIVE DRUGS — An overview of the mechanism of action, doses, and routesof administration of many antihypertensive drugs that are often used for hypertensiveemergency is presented elsewhere. (See "Drugs used for the treatment of hypertensiveemergencies".)

FOLLOW­UP — Secondary causes of hypertension are more common in patients who have ahypertensive emergency compared with other hypertensive populations [17]. Thus, patients witha hypertensive emergency should be evaluated for common forms of secondary hypertensionand, if there are suggestive clinical clues, less common causes of secondary hypertension.Patients should be reminded that adherence to long­term antihypertensive drug therapy canreduce the risk of recurrent hospitalization for hypertensive emergencies.

The most important aspect of care for the patient with a hypertensive emergency is assuringthat high­quality outpatient follow­up is available, as many of the presenting problems (includingdialysis for end­stage renal disease) can improve greatly if the blood pressure is well controlledin the long term. A large proportion of patients without follow­up will return to the hospital with arepeated hypertensive emergency [1].

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials,"The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plainlanguage, at the 5 to 6 grade reading level, and they answer the four or five key questions apatient might have about a given condition. These articles are best for patients who want a

intravenous phentolamine or nitroprusside. (See "Evaluation and management of thecardiovascular complications of cocaine abuse".)

Pheochromocytoma can also produce severe hypertension and acute target­organdamage. The treatment of hypertension in pheochromocytoma is discussed separately.(See "Treatment of pheochromocytoma in adults".)

Severe autonomic dysfunction (eg, Guillain­Barré and Shy­Drager syndromes or acutespinal cord injury) is occasionally associated with hypertensive emergency. Such patientscan be treated with phentolamine, nitroprusside, or other agents. (See "Guillain­Barrésyndrome in adults: Treatment and prognosis", section on 'Blood pressure' and "Chroniccomplications of spinal cord injury and disease", section on 'Cardiovascular complications'.)

th th

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general overview and who prefer short, easy­to­read materials. Beyond the Basics patienteducation pieces are longer, more sophisticated, and more detailed. These articles are writtenat the 10 to 12 grade reading level and are best for patients who want in­depth informationand are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to printor e­mail these topics to your patients. (You can also locate patient education articles on avariety of subjects by searching on "patient info" and the keyword(s) of interest.)

SUMMARY AND RECOMMENDATIONS

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Basics links (see "Patient education: High blood pressure emergencies (The Basics)")

Most patients with significantly elevated blood pressure (systolic pressure ≥180 and/ordiastolic pressure ≥120 mmHg) have no acute, end­organ injury (so called severeasymptomatic hypertension). However, some patients with significantly elevated bloodpressure have signs or symptoms of acute, ongoing target­organ damage. Such patientshave a hypertensive emergency. (See 'Introduction and terminology' above.)

The history and physical examination in patients presenting with a severely elevated bloodpressure (or an acute rise in blood pressure over a previously normal baseline, even if thepresenting pressure is <180/120 mmHg) should seek to identify signs and symptoms ofacute target­organ damage; in addition, certain laboratory and, in some settings, imagingstudies may be needed. (See 'Evaluation and diagnosis' above.)

Optimal therapy, including the choice of agent and the blood pressure goal, variesaccording to the specific hypertensive emergency. It is generally unwise to lower the bloodpressure too quickly or too much, as ischemic damage can occur in vascular beds that havegrown accustomed to the higher level of blood pressure (ie, autoregulation). For mosthypertensive emergencies, mean arterial pressure should be reduced by about 10 to 20percent in the first hour and then gradually during the next 23 hours so that the finalpressure is reduced by approximately 25 percent compared with baseline. (See 'Treatment'above.)

The major exceptions to modest and gradual blood pressure lowering over the first 24hours are:

The acute phase of an ischemic stroke – The blood pressure is usually not loweredunless it is ≥185/110 mmHg in patients who are candidates for reperfusion therapy(table 1) or ≥220/120 mmHg in patients who are not candidates for reperfusiontherapy. (See "Initial assessment and management of acute stroke", section on 'Bloodpressure management'.)

•

Acute aortic dissection – The systolic blood pressure is rapidly lowered to a target of100 to 120 mmHg (to be attained in 20 minutes). (See "Management of acute aorticdissection".)

•

Spontaneous hemorrhagic stroke – The systolic blood pressure can be rapidly reducedif no contraindications exist. The goals of therapy vary according to the clinical setting.

•

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REFERENCES

1. Mayer SA, Kurtz P, Wyman A, et al. Clinical practices, complications, and mortality inneurological patients with acute severe hypertension: the Studying the Treatment of AcutehyperTension registry. Crit Care Med 2011; 39:2330.

2. Padilla Ramos A, Varon J. Current and newer agents for hypertensive emergencies. CurrHypertens Rep 2014; 16:450.

3. Katz JN, Gore JM, Amin A, et al. Practice patterns, outcomes, and end­organ dysfunctionfor patients with acute severe hypertension: the Studying the Treatment of AcutehyperTension (STAT) registry. Am Heart J 2009; 158:599.

4. Johnson W, Nguyen ML, Patel R. Hypertension crisis in the emergency department.Cardiol Clin 2012; 30:533.

5. Martin JF, Higashiama E, Garcia E, et al. Hypertensive crisis profile. Prevalence andclinical presentation. Arq Bras Cardiol 2004; 83:131.

6. Zampaglione B, Pascale C, Marchisio M, Cavallo­Perin P. Hypertensive urgencies andemergencies. Prevalence and clinical presentation. Hypertension 1996; 27:144.

7. Kaplan NM, Victor RG. Chapter 8: Hypertensive Crises. In: Kaplan's Clinical Hypertension,10th Ed, Lippincott, Williams & Wilkins, Philadelphia 2010. p.274.

8. Elliott WJ. Clinical features in the management of selected hypertensive emergencies.Prog Cardiovasc Dis 2006; 48:316.

(See "Spontaneous intracerebral hemorrhage: Treatment and prognosis", section on'Blood pressure'.)

A variety of antihypertensive drugs can be used to treat hypertensive emergencies; anoverview of the mechanism of action, doses, and routes of administration of these agents ispresented elsewhere. (See "Drugs used for the treatment of hypertensive emergencies".)

After a suitable period (often 8 to 24 hours) of blood pressure control at target in anintensive care unit, oral medications are usually given and the initial intravenous therapy istapered and discontinued. (See 'Overall approach to therapy' above.)

Secondary causes of hypertension are more common in patients who have a hypertensiveemergency compared with other hypertensive populations. Thus, patients with ahypertensive emergency should be evaluated for common forms of secondary hypertensionand, if there are suggestive clinical clues, less common causes of secondary hypertension.(See 'Follow­up' above.)

The most important aspect of care for the patient with a hypertensive emergency isassuring that high­quality outpatient follow­up is available. A large proportion of patientswithout follow­up will return to the hospital with a recurrent hypertensive emergency. (See'Follow­up' above.)

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9. Li JZ, Eagle KA, Vaishnava P. Hypertensive and acute aortic syndromes. Cardiol Clin2013; 31:493.

10. Anderson CS, Heeley E, Huang Y, et al. Rapid blood­pressure lowering in patients withacute intracerebral hemorrhage. N Engl J Med 2013; 368:2355.

11. Hemphill JC 3rd, Greenberg SM, Anderson CS, et al. Guidelines for the Management ofSpontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals Fromthe American Heart Association/American Stroke Association. Stroke 2015; 46:2032.

12. Lau J, Antman EM, Jimenez­Silva J, et al. Cumulative meta­analysis of therapeutic trialsfor myocardial infarction. N Engl J Med 1992; 327:248.

13. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis andmanagement of patients with Thoracic Aortic Disease: a report of the American College ofCardiology Foundation/American Heart Association Task Force on Practice Guidelines,American Association for Thoracic Surgery, American College of Radiology, AmericanStroke Association, Society of Cardiovascular Anesthesiologists, Society forCardiovascular Angiography and Interventions, Society of Interventional Radiology,Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation 2010;121:e266.

14. Elliott WJ, Weber RR, Nelson KS, et al. Renal and hemodynamic effects of intravenousfenoldopam versus nitroprusside in severe hypertension. Circulation 1990; 81:970.

15. González R, Morales E, Segura J, et al. Long­term renal survival in malignanthypertension. Nephrol Dial Transplant 2010; 25:3266.

16. Brown H, Goldberg PA, Selter JG, et al. Hemorrhagic pheochromocytoma associated withsystemic corticosteroid therapy and presenting as myocardial infarction with severehypertension. J Clin Endocrinol Metab 2005; 90:563.

17. Börgel J, Springer S, Ghafoor J, et al. Unrecognized secondary causes of hypertension inpatients with hypertensive urgency/emergency: prevalence and co­prevalence. Clin ResCardiol 2010; 99:499.

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GRAPHICS

Potential approaches to arterial hypertension in patients with acuteischemic stroke who are candidates for acute reperfusion therapy

Patient otherwise eligible for acute reperfusion therapy except that bloodpressure is >185/110 mmHg

Labetalol 10 to 20 mg intravenously over 1 to 2 minutes, may repeat one time; or

Nicardipine 5 mg/hour intravenously, titrate up by 2.5 mg/hour every 5 to 15 minutes,maximum 15 mg/hour; when desired blood pressure reached, adjust to maintain properblood pressure limits; or

Other agents (hydralazine, enalaprilat, etc) may be considered when appropriate

If blood pressure is not maintained at or below 185/110 mmHg, do not administer rtPA

Management to maintain blood pressure at or below 180/105 mmHg duringand after acute reperfusion therapy

Monitor blood pressure every 15 minutes for 2 hours from the start of rtPA therapy, then every30 minutes for 6 hours, and then every hour for 16 hours

If systolic blood pressure is >180 to 230 mmHg or diastolic is >105 to 120 mmHg:

Labetalol 10 mg intravenously followed by continuous infusion 2 to 8 mg/min; or

Nicardipine 5 mg/hour intravenously, titrate up to desired effect by 2.5 mg/hour every 5 to15 minutes, maximum 15 mg/hour

If blood pressure is not controlled or diastolic blood pressure >140 mmHg, considerintravenous sodium nitroprusside

rtPA: recombinant tissue­type plasminogen activator.

Reprinted with permission. Stroke. 2013: 44:870­947. Copyright © 2013 American Heart Association,Inc.

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European Society of Cardiology guidelines: Initial management ofpatients with suspected aortic dissection

Recommendation Class

1. Detailed medical history and complete physical examination (whenever possible) I

2. Intravenous line, blood sample (CK, troponin I, myoglobin, WBC, D­dimer, hematocrit,LDH)

I

3. ECG: documentation of ischemia I

4. Heart rate and blood pressure (BP) monitoring I

5. Pain relief (morphine sulphate) I

6. Reduction of systolic blood pressure using beta blockers (IV propranolol, metoprolol,esmolol, or labetalol)

I

7. Transfer to intensive care unit I

8. In patients with severe hypertension additional vasodilator (IV sodium nitroprusside totitrate BP to 100­120 mmHg)

I

9. In patients with obstructive pulmonary disease, blood pressure lowering with calciumchannel blockers

II

10. Imaging in patients with ECG signs of ischemia before thrombolysis if aorticpathology is suspected

II

11. Chest x­ray III

Classification

Class I: Conditions for which there is evidence and/or general agreement that a given procedureor treatment is useful and effective.

Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion aboutthe usefulness/efficacy of a procedure or treatment.

Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.

Class IIb: Usefulness/efficacy less well established by evidence/opinion.

Class III: Conditions for which there is evidence and/or general agreement that theprocedure/treatment is not useful and in some cases may be harmful.

Data reproduced with permission from Erbel, R, Alfonso, F, Boileau, C, et al, Eur Heart J 2001; 22:1642.

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Light micrograph showing acute hypertensivenephrosclerosis (formerly "malignant nephrosclerosis")

Light micrograph reveals fibrinoid necrosis in the preglomerular afferent arteriole(arrow) in acute hypertensive nephrosclerosis (formerly "malignantnephrosclerosis"). The normal muscle layer of the media has been replaced bythe fibrinoid material.

Courtesy of Helmut Rennke, MD.

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Light micrograph showing acute hypertensivenephrosclerosis (formerly "malignant nephrosclerosis")II

Mucoid intimal thickening and luminal narrowing in a small muscular renal artery(arrow) in the early stages of healing in acute hypertensive nephrosclerosis(formerly "malignant nephrosclerosis"). Similar changes can be seen in otherthrombotic microangiopaties, such as scleroderma and the hemolytic­uremicsyndrome.

Courtesy of Helmut Rennke, MD.

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Light microscopy showing thrombotic microangiopathywith onion­skin thickening of a muscular renal artery

Concentric onion­skin thickening of a muscular renal artery, leading to completeobliteration of the vascular lumen, during the later healing phase of previousfibrinoid injury in any of the forms of the hemolytic uremic syndrome, includingscleroderma and acute hypertensive nephrosclerosis (formerly called "malignantnephrosclerosis").

Courtesy of Carol Black, MD.

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Immunofluorescence microscopy showing fibrindeposition in thrombotic microangiopathy

Immunofluorescence microscopy in the hemolytic uremic syndrome shows fibrindeposition (bright yellow areas) in branches of a muscular renal artery.

Courtesy of Helmut Rennke, MD.

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Contributor Disclosures

William J Elliott, MD, PhD Consultant/Advisory Board: Novartis [Hypertension]. OtherFinancial Interest: Elsevier; Springer [Hypertension (book, journal)]. Joseph Varon, MD, FACP,FCCP, FCCM, FRSM Nothing to disclose George L Bakris, MD Grant/Research/Clinical TrialSupport: Bayer; Boehringer Ingelheim; Relypsa; Vascular Dynamics [Diabetic neuropathy,diabetes, hypertension (Empagliflozin, patiromer)]. Consultant/Advisory Boards: AstraZeneca;Bayer; Boehringer Ingelheim; Relypsa; Vascular Dynamics; Merck; Pfizer; NxStage [Diabeticneuropathy, diabetes, hypertension (Empagliflozin, patiromer)]. Norman M Kaplan,MD Nothing to disclose John P Forman, MD, MSc Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found,these are addressed by vetting through a multi­level review process, and through requirementsfor references to be provided to support the content. Appropriately referenced content isrequired of all authors and must conform to UpToDate standards of evidence.

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