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  • 1. Resident Grand Rounds Series Editor: Mark A. Perazella, MD Hypertensive Urgency and Emergency Chirag K. Vaidya, MD Jason R. Ouellette, MD A 52-year-old man presented to the emergency department complaining of worsening occipital headache and confusion. He reported experiencing numbness and weakness involving the right side of his body as well as blurry vision over the past 12 hours. His past medical history was pertinent for hypertension, bilateral renal artery stenosis, cocaine abuse, and hyperlip- idemia. On arrival, his blood pressure was 213/134 mm Hg. On physical examination, he was confused. Papilledema was seen on fundoscopic examination. He had mild motor weakness (4/5) in the right upper extremity. Laboratory studies revealed the following: serum potassium, 3.1 mEq/L; blood urea nitrogen, 36 mg/dL; and serum creatinine, 2.5 mg/dL (baseline creatinine, 1.5 mg/dL). Electrocardiogram revealed left ventricular hypertrophy by voltage criteria and nonspecific ST-T wave abnormalities in the lateral leads. Computed tomography scan of the head without contrast revealed diffuse bilateral white matter changes consistent with hypertensive encephalopathy. The patient was admitted to the intensive care unit and started on intravenous nitroprusside. Blood pressure decreased to 190/100 mm Hg over the first 3 hours and neurologic symptoms resolved within 5 hours. He was switched to his usual oral regimen on the third day of hospital admission and was discharged home on the fifth day with controlled blood pressure.H ypertension is an extremely common dis- without progressive target organ dysfunction.4 Notably, order in modern Western societies, with an these definitions do not specify absolute blood pres- age- and sex-adjusted prevalence of approxi- sure levels as hypertensive urgency or emergency may mately 28% in North America.1 Physicians occur with a modest increase in blood pressure in pre-in clinical practice are likely to encounter patients with viously normotensive persons (eg, during pregnancy orhypertensive urgency and emergency. Although im- with acute cocaine intoxication).proved management of chronic hypertension has de-creased the lifetime incidence of hypertensive crisis to etiology anD PatHoPHysiologyless than 1%, patients presenting with severe hyperten- Severe elevations in blood pressure may develop desion represent up to 25% of all patients presenting to novo or may complicate underlying essential or second-urban emergency departments.2 One-year and 5-year ary hypertension (Table 1). In white patients, 20% tomortality following untreated hypertensive emergency 30% of cases of hypertensive urgency or emergency areare 70% to 90% and 100%, respectively.3 With ad- secondary to uncontrolled essential hypertension, whileequate blood pressure control, these mortality rates in black patients, the percentage is as high as 80%.5decrease to 25% and 50%, respectively.3 This article The initiating factor in hypertensive emergency andreviews the approach to appropriately diagnosing and urgency is poorly understood. A rapid rise in blood pres-managing hypertensive urgency and emergency. sure associated with increased systemic vascular resistance is thought to be the triggering event.6 The rate of changeDefinition in blood pressure is directly related to the likelihood that Hypertensive emergency (crisis) is characterized by a se-vere elevation in blood pressure (> 180/120 mm Hg)complicated by evidence of impending or progressivetarget organ dysfunction.4 Examples of target organ Dr. Vaidya is chief resident, Internal Medicine Residency Program,dysfunction include coronary ischemia, disordered Saint Mary’s Hospital, Waterbury, CT, and a clinical instructor, Yale University School of Medicine, New Haven, CT. Dr. Ouellette is associatecerebral function, cerebrovascular events, pulmonary program director, Internal Medicine Residency Program, Saint Mary’sedema, and renal failure. Hypertensive urgency, on the Hospital, Waterbury, CT, and a clinical instructor, Yale Universityother hand, is a severe elevation in blood pressure School of Medicine, New Haven, CT.www.turner-white.com Hospital Physician March 2007 43
  • 2. Va i d y a & O u e l l e t t e : H y p e r t e n s i v e U r g e n c y & E m e r g e n c y : p p . 4 3 – 5 0 Table 1. Causes of Hypertensive Emergency TakE HomE PoinTs Essential hypertension • Distinguishing between hypertensive emergency Renal disease (associated with acute target organ damage) and Parenchymal disease urgency (no target organ damage) is crucial to Chronic pyelonephritis appropriate management. Primary glomerulonephritis • Diagnosis of hypertensive emergency requires a Vascular/glomerular disease thorough history (evidence of target organ dam- Systemic lupus erythematous age, illicit drug use, and medication compliance) Systemic sclerosis as well as a complete physical examination, basic Renal vasculitides (microscopic polyarteritis nodosa, laboratory data, and electrocardiogram to assess Wegener’s granulomatosis) for the presence of target organ damage and deter- Tubulointerstitial nephritis mine its severity. Renovascular disease • In general, hypertensive urgency is managed using Renal artery stenosis oral antihypertensive drugs in outpatient or same- Fibromuscular dysplasia day observational settings, while hypertensive emer- Atherosclerotic renovascular disease gency is managed in an intensive care unit or other monitored settings with parenteral drugs. Macroscopic polyarteritis nodosa • The initial goal in hypertensive urgency is a reduc- Drugs tion in mean arterial pressure by no more than Abrupt withdrawal of a centrally acting α2-adrenergic agonist (cloni- 25% within the first 24 hours using conventional dine, methyldopa) oral therapy; in hypertensive emergency, mean Phencyclidine, cocaine or other sympathomimetic drug intoxication arterial pressure should be reduced approximately Interaction with monoamine oxidase inhibitors (tranylcypromine, 10% during the first hour and an additional 15% phenelzine, and selegiline) within the next 2 to 3 hours. Pregnancy • Various medications are available for the treatment Eclampsia/severe pre-eclampsia of hypertensive emergency; specific target organ involvement and underlying patient comorbidities Endocrine dictate appropriate therapy. Pheochromocytoma Primary aldosteronism Glucocorticoid excess Renin-secreting tumorsan acute hypertensive syndrome will develop, with rapid Central nervous system disordersincreases over a short period of time increasing the likeli- CVA infarction/hemorrhagehood of a syndrome.7 The endothelium plays a central Head injuryrole in blood pressure homeostasis, mainly by modulat- Adapted with permission from Kitiyakara C, Guzman NJ. Malignant hy-ing vascular tone via secretion of substances such as nitric pertension and hypertensive emergencies. J Am Soc Nephrol 1998;9:135.oxide and prostacyclin.8 Stretch of the vessel wall duringsignificant blood pressure elevation causes activation CVA = cerebrovascular accident.of the renin–angiotensin system, which also appears tobe an important factor in the development of severelyelevated blood pressure. When there is a sustained or Diagnosissevere elevation in blood pressure, the compensatory Distinguishing between hypertensive emergency (as-endothelial vasodilatory response is turned off, lead- sociated with acute target organ damage) and urgencying to endothelial decompensation, which results in a (no target organ damage) is a crucial step in appropri-further rise in blood pressure and endothelial damage. ate management of these conditions as managementThis process leads to a self-sustaining cycle, resulting in a differs between them. The history and physical ex-progressive increase in resistance and further endothelial amination are extremely important in determining thedysfunction.9 The Figure outlines the underlying patho- severity of an acute hypertensive crisis syndrome andphysiology of hypertensive emergency. guiding further management. Laboratory data and44 Hospital Physician March 2007 www.turner-white.com
  • 3. Va i d y a & O u e l l e t t e : H y p e r t e n s i v e U r g e n c y & E m e r g e n c y : p p . 4 3 – 5 0 Endocrine disorders severe hypertension Essential hypertension Pregnancy Renal disorders Drugs Critical level or rapid rate of rise and increased vascular resistance Endothelial damage Spontaneous natriuresis ↑ Endothelial permeability Intravascular volume depletion Platelet and fibrin deposition Increase in vasoconstrictors Decrease in vasodilators, (renin–angiotensin, nitric oxide, prostacyclin catecholamines) Fibrinoid necrosis and intimal proliferation Further increase in blood pressure Severe blood pressure elevation Tissue ischemia End-organ dysfunctionFigure. Pathophysiology of hypertensive emergencies. (Adapted with permission from Kitiyakara C, Guzman NJ. Malignant hypertensionand hypertensive emergencies. J Am Soc Nephrol 1998;9:135.)other diagnostic tests such as electrocardiogram and anti-inflammatory drugs, certain herbal products); andchest radiograph can provide important information illicit drug use (cocaine, methamphetamine, ephe-regarding possible end-organ damage. dra). Patients should be asked specifically whether they abruptly stopped taking β blockers or central sympa-History tholytic agents as abrupt cessation of these medica- The history should include information regarding tions may lead to rebound hypertension. In addition,when the patient was diagnosed with hypertension; patients should be asked about symptoms suggestive ofbaseline blood pressure; the presence of previous end- end-organ compromise, including chest pain (myocar-organ damage, in particular renal and cerebrovascular dial ischemia/infarction, aortic dissection), shortness ofdamage; details regarding antihypertensive therapy breath (acute pulmonary edema secondary to left ven-and compliance with the regimen; intake of over-the- tricular failure), back pain (aortic dissection), and neu-counter medications (sympathomimetics, nonsteroidal rologic symptoms such as headache and blurry vision.www.turner-white.com Hospital Physician March 2007 45
  • 4. Va i d y a & O u e l l e t t e : H y p e r t e n s i v e U r g e n c y & E m e r g e n c y : p p . 4 3 – 5 0Neurologic symptoms may be due to intracerebral or serum creatinine concentrations should be measuredsubarachnoid hemorrhage or hypertensive encephalop- to evaluate for renal impairment. Hypokalemic meta-athy. Hypertensive encephalopathy is an acute organic bolic alkalosis may be seen as a result of intravascularbrain syndrome or delirium related to cerebral edema volume depletion and secondary hyperaldosteronism.believed to result from loss of cerebral vascular auto- Comparison of the measured serum creatinine valueregulatory function in the setting of severely elevated with baseline values should be done to evaluate for theblood pressure. It is characterized by headache, nausea, presence of acute and/or chronic kidney disease.and vomiting initially, followed by altered mental statusand/or seizure if hypertension is not treated. other Diagnostic tests An electrocardiogram should be obtained in all pa-Physical examination tients with hypertensive crisis as it may reveal evidence Blood pressure should be measured in both arms as of myocardial ischemia or infarction in the acute settinga significant discrepancy between arms (> 20 mm Hg as well as evidence of left ventricular hypertrophy duein systolic blood pressure) is suggestive of aortic dissec- to chronic hypertension. A chest radiograph should betion. In addition, blood pressure should be measured obtained to evaluate for pulmonary vascular congestionin both the supine and standing positions to assess as well as a widened mediastinum, which suggests aorticvolume status as patients presenting with hypertensive dissection. Urinalysis and urine sediment examinationemergency may be intravascularly volume depleted to evaluate for hematuria and/or cellular casts alsodue to pressure natriuresis. Head and neck examina- should be done. A computed tomography scan of thetion must include a complete fundoscopic examina- head without contrast should be performed in any pa-tion, as grades III (flame-shaped hemorrhages, fluffy, tient with neurologic symptoms, which include changewhite cotton wool spots, and yellow-white exudates) in mental status or focal neurologic signs suggestive of aand IV (papilledema with blurring of the disk margins cerebrovascular accident or hemorrhage.accompanied by hemorrhages and exudates) retinopa-thy are the hallmarks of hypertensive emergency. ManageMent Cardiovascular examination includes auscultation An important issue in the management of patientsfor new murmurs. A diastolic murmur consistent with with hypertensive urgency or emergency is how quicklyaortic insufficiency may support the diagnosis of aortic and to what degree to lower the blood pressure; how-dissection. Mitral regurgitation may develop secondary ever, there are no high-quality prospective studies thatto ischemic rupture of a papillary muscle. Signs sugges- address these questions. Management should be tai-tive of heart failure (elevated jugular venous pressure, lored to the individual patient based not only on abso-S3 gallop) also should be sought. The presence of rales lute blood pressure number, but also on the presenceon pulmonary examination suggests vascular congestion or absence of end-organ damage.6and pulmonary edema. Evidence of atherosclerotic dis-ease in any vascular bed, especially in smokers, should Hypertensive Urgencyheighten suspicion for renovascular hypertension due to General principles. In general, hypertensive urgencycritical renal artery stenosis. A systolic/diastolic abdomi- can be managed using oral antihypertensive agentsnal bruit suggests renovascular disease as the underlying in an outpatient or same-day observational setting, al-cause of hypertension. though this approach may not be appropriate when A careful neurologic examination should always be patient follow-up is difficult or unpredictable. Treatmentcompleted. The presence of focal neurologic signs in- is initiated with very low doses of oral agents using in-dicate ischemic or hemorrhagic stroke. Delirium or a cremental doses as needed and avoiding large startingflapping tremor is suggestive of hypertensive encepha- doses that may result in excessive blood pressure reduc-lopathy. Hypertensive encephalopathy is a diagnosis of tion. Avoiding excessive reduction is especially impor-exclusion; other causes that must be ruled out include tant in patients who are at highest risk for hypotensivestroke, subarachnoid hemorrhage, and mass lesions. complications, such as the elderly, patients with severe peripheral vascular disease, and those with known se-laboratory testing vere atherosclerotic cardiovascular and intracranial dis- Baseline investigations include a complete blood ease. The initial goal is to reduce blood pressure to 160/count with peripheral smear for the presence of schis- 110 mm Hg over several hours to days using conven-tocytes, which may suggest microangiopathic hemolytic tional oral therapy.10 Mean arterial pressure should beanemia. Serum electrolytes, blood urea nitrogen, and reduced by no more than 25% within the first 24 hours46 Hospital Physician March 2007 www.turner-white.com
  • 5. Va i d y a & O u e l l e t t e : H y p e r t e n s i v e U r g e n c y & E m e r g e n c y : p p . 4 3 – 5 0using conventional oral therapy. Antihypertensive agents ing the safety of calcium channel blockers concludedused to treat hypertensive urgency are described below. that “short-acting nifedipine should be used with great Specific agents. Captopril is an angiotensin-converting caution (if at all), especially at higher doses, in the treat-enzyme (ACE) inhibitor with an onset of action begin- ment of hypertension.”15ning within 15 to 30 minutes and a maximum drop inblood pressure occurring between 30 and 90 minutes. Hypertensive emergencyCaptopril is given as a 25-mg oral dose initially, followed General principles. Treatment of hypertensive emer-by incremental doses of 50 to 100 mg 90 to 120 minutes gency is tailored to each individual case based on thelater. Significant adverse effects include cough, hypoten- extent of end-organ damage as well as other comorbidsion, hyperkalemia, angioedema, and renal failure (es- conditions (Table 2 and Table 3). Blood pressure man-pecially in patients with bilateral renal artery stenosis, in agement in this setting requires the use of parenteralwhom it should be avoided). drugs, as precise and rapid control of blood pressure The calcium channel blocker nicardipine is one of is critical. These patients should always be managed inthe few therapies used in the setting of hypertensive an intensive care unit or other settings that allow con-urgency that has been evaluated in a randomized con- tinuous monitoring of blood pressure. The ideal ratetrolled trial and has demonstrated statistical superior- of blood pressure lowering is unclear, but reducing theity over placebo. In a study that randomly assigned 53 mean arterial pressure by 10% during the first hourpatients with urgent hypertension to nicardipine or and an additional 15% within the next 2 to 3 hours hasplacebo, effective blood pressure control was observed been recommended.16 More rapid reduction in bloodin 65% of the treatment group compared with 22% of pressure may result in cardiac or cerebrovascular hypo-the placebo group (P = 0.002).11 The usual oral dose is perfusion.30 mg, which can be repeated every 8 hours until the Pressure natriuresis may cause volume depletion intarget blood pressure is achieved. Onset of action is patients with hypertensive emergency, and administer-½ to 2 hours. Common adverse reactions include pal- ing vasodilator medications to these patients can leadpitations, flushing, headache, and dizziness.11 to precipitous drops in blood pressure. Patients with Labetalol has mixed α1- and β-adrenergic blocking volume depletion should receive intravenous (IV)properties and an onset of action within 1 to 2 hours. saline to restore intravascular volume and shut off theA wide dose range has been studied in different popu- renin-angiotensin-aldosterone system. Management oflations, making generalization difficult. In a random- specific emergencies is discussed in the following sec-ized study of 36 patients, groups receiving 100, 200, or tions.300 mg orally had significant decreases in both systolic Neurologic emergency. Common neurologic emer-and diastolic blood pressure.12 In general, the starting gencies in the setting of hypertensive crisis includedose is 200 mg orally, which can be repeated every 3 hypertensive encephalopathy, intracerebral hemor-to 4 hours.12 Common side effects include nausea and rhage, and acute ischemic stroke. Severe hypertensiondizziness. is very common in the setting of acute stroke, and Clonidine is a central sympatholytic (α2-adrenergic there is controversy surrounding the goal blood pres-receptor agonist) agent with an onset of action within sure. In intracerebral hemorrhage, there is typically15 to 30 minutes and a peak effect within 2 to 4 hours. disruption of the cerebral autoregulation of blood flowA typical oral regimen is a 0.1 to 0.2 mg loading dose in the area of the bleed, and blood flow and oxygenfollowed by 0.05 to 0.1 mg every hour until target delivery are dependent on systemic perfusion pres-blood pressure is achieved, up to a maximum dose of sure. The American Heart Association recommends0.7 mg. Common side effects include sedation, dry treating hypertension in the setting of an intracerebralmouth, and orthostatic hypotension. bleed only when blood pressure is more than 180/ Nifedipine is a calcium channel blocker with a peak 105 mm Hg.17 Mean arterial pressure should be main-effect within 10 to 20 minutes. Short-acting nifedipine is tained below 130 mm Hg.17not approved by the US Food and Drug Administration In patients with ischemic stroke, perfusion pressurefor treating hypertension, and major concerns have distal to the obstructed vessel is low, and compensatorybeen raised over its safety in the treatment of hyper- vasodilatation of these blood vessels occurs to maintaintensive urgency due to reports of unpredictable drops adequate blood flow. A higher systemic pressure isin blood pressure and associated risk of stroke.13,14 In required to maintain perfusion in these dilated blood1995, an ad hoc panel convened by the National Heart, vessels. Most patients, irrespective of pre-ischemicLung, and Blood Institute to review evidence regard- blood pressure control, experience a sustained rise inwww.turner-white.com Hospital Physician March 2007 47
  • 6. Va i d y a & O u e l l e t t e : H y p e r t e n s i v e U r g e n c y & E m e r g e n c y : p p . 4 3 – 5 0Table 2. Parenteral Drugs Used for Treatment of Hypertensive Emergencies mechanism Durationagent of action Dose onset of action adverse Effects/PrecautionsSodium Nitric oxide com- 0.25–10 µg/kg/min IV Immediate 2–3 min after Nausea, vomiting, nitro- pound, direct arterial infusion infusion Thiocyanate and cyanide intoxication prusside and venous vasodi- Increased intracranial pressure lator Methemoglobinemia Delivery sets must be light resistantFenoldo- Dopamine-1 receptor 0.1–0.3 µg/kg/min IV < 5 min 30 min Headache, flushing, tachycardia pam agonist infusion Local phlebitis mesyl- Mild tolerance after prolonged infusion ate May reduce serum potassium ECG changes: nonspecific T-wave changes/ventricular extra systolesNitroglyc- Nitric oxide com- 5–100 µg/min IV 2–5 min 5–10 min Headache, tachycardia, flushing erin pound; direct arte- infusion Methemoglobinemia rial and venodilator Requires special delivery system due to (mainly venous) drug binding to tubingEnalaprilat ACE inhibitor 0.625–2.5 mg every Within 30 12–24 hr Acute renal failure in patients with 6 hr IV min bilateral renal artery stenosis Prolonged half-lifeHydrala- Direct vasodilation of 5–20 mg IV bolus or 10 min IV 1–4 hr IV Tachycardia, flushing, headache zine arterioles with little 10–40 mg IM; repeat 20–30 min Sodium and water retention effect on veins every 4–6 hr IM Increased intracranial pressure Aggravation of anginaNicardi- Calcium channel 5–15 mg/hr IV infusion 1–5 min 15–30 min, but may Tachycardia, headache, flushing pine blocker exceed 4 hr after Local phlebitis prolonged infusion Aggravation of anginaEsmolol β-Adrenergic blocker 500 µg/kg bolus injec- 1–2 min 10–30 min Hypotension, nausea tion IV or 50– Asthma 100 µg/kg/min by First-degree atrioventricular block infusion. May repeat Heart failure bolus after 5 min or increase infusion rate to 300 µg/kg/minLabetalol α-, β-Adrenergic 20–80 mg IV bolus 5–10 min 3–6 hr Bronchoconstriction blocker every 10 min; 0.5– Heart block 2.0 mg/min IV infusion Vomiting, scalp tingling Heart failure exacerbationPhentol- α-Adrenergic receptor 5–15 mg IV bolus 1–2 min 10–30 min Tachycardia, flushing, headache amine blockerAdapted with permission from Vidt D. Hypertensive crises: emergencies and urgencies. The Cleveland Clinic disease management project. 12 Jan2006. Available at www.clevelandclinicmeded.com/diseasemanagement/nephrology/crises/crises.htm. Accessed 2 Feb 2007; and National HighBlood Pressure Education Program. The seventh report of the Joint National Committee on prevention, detection, evaluation, and treatment ofhigh blood pressure. Bethesda (MD): Dept. of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute;2004. NIH Publication No. 04–5230.ACE = angiotensin-converting enzyme; ECG = electrocardiogram; IM = intramuscular; IV = intravenous.blood pressure during cerebral ischemia, including this setting, mean arterial pressure should be loweredtransient ischemic attack. Therefore, in patients with by 15% to 20%.18ischemic stroke, blood pressure should be carefully Hypertensive encephalopathy is a severe end-organobserved for the first 1 to 2 hours to determine if it will manifestation of the hypertensive process. Gradualspontaneously decrease. Only a persistently mean arte- lowering of the blood pressure frequently leads torial pressure over 130 mm Hg or a systolic blood pres- rapid improvement of neurologic symptoms. If pa-sure over 220 mm Hg should be carefully treated. In tients do not improve within 6 to 12 hours, evaluation48 Hospital Physician March 2007 www.turner-white.com
  • 7. Va i d y a & O u e l l e t t e : H y p e r t e n s i v e U r g e n c y & E m e r g e n c y : p p . 4 3 – 5 0for other causes of the encephalopathic process should Table 3. Drug of Choice in Treatment of Specific Types ofbe undertaken. Hypertensive Emergencies Cardiac emergency. Major cardiac emergencies in Type of second-linethe setting of hypertensive crisis include acute myo- Emergency Drug of Choice Drugscardial ischemia or infarction, pulmonary edema, and neurologicaortic dissection. Patients presenting with a hyperten- Hypertensive en- Nitroprusside Labetalol orsive emergency involving myocardial ischemia or in- cephalopathy nicardipinefarction are typically treated with nitroglycerin as older Subarachnoid Nimodipine Labetalol orstudies have shown that it reduces myocardial oxygen hemorrhage nicardipineconsumption and increases flow beyond the stenotic CVA Labetalol Nitroprusside,coronary area.19 In the absence of significant heart fail- enalaprilature, β-blockers (eg, labetalol, esmolol) also should be Renalused to control blood pressure. Acute kidney injury Nicardipine Fenoldopam In the setting of acute aortic dissection, an IV Cardiacβ-blocker (eg, labetalol or esmolol) should be given Aortic dissection β-Blocker + nitroprusside Labetalol, tri-first, followed by a vasodilating agent, classically IV methaphannitroprusside. These agents are used to lower the sys- Pulmonary edema Nitroglycerin Nitroprussidetolic blood pressure to a goal of less than 120 mm Hg ± ACE inhibitorwithin 20 minutes. The order of administration is criti- Cardiac ischemia Nitroglycerin ± β-blocker Nitroprusside,cal as giving vasodilators alone can lead to increased labetalolshear stress in the vessel wall as a result of increased adrenergic crisisdP/dt with vasodilatation as well as subsequent reflex Pheochromocytoma Nitroprusside +tachycardia, increasing the risk of further dissection. β-blocker Phentolamine CocainePharmacologic therapy is usually a temporary bridgeto more definitive surgical treatment of dissection. Eclampsia Methyldopa Hydralazine Magnesium sulfate (do Typical treatment of pulmonary edema includes IV not use with calciumadministration of diuretics followed by IV administra- channel blocker)tion of an ACE inhibitor (usually enalaprilat) and ni-troglycerin. Sodium nitroprusside may be used if these Adapted with permission from Varon J, Marik PE. The diagnosis and management of hypertensive crises. Chest 2000;118:221.agents do not adequately control blood pressure. Hyperadrenergic states. Patients with catechol- ACE = angiotensin-converting enzyme; CVA = cerebrovascular ac-amine excess in settings such as pheochromocytoma, cident.cocaine or amphetamine overdose, monoamine oxi-dase inhibitor–induced hypertension, or clonidine a consequence of hypertensive emergency. Acute kid-withdrawal syndrome can present with hypertensive ney injury can present with proteinuria, microscopic he-crisis syndrome. In pheochromocytoma, initial blood maturia, oliguria, and/or anuria. Optimal treatment ispressure control can be achieved with sodium nitro- controversial. Although IV nitroprusside is widely used,prusside (arterial vasodilator) or with IV phentolamine it can cause cyanide or thiocyanate toxicity. Parenteral(ganglion-blocking agent).20 β-Blockers may be added fenoldopam mesylate (a dopamine-1 receptor agonist)for improved blood pressure control but should never has shown promising results and enhanced safety. Usebe used alone until α blockade is achieved as para- of fenoldopam avoids potential cyanide or thiocyanatedoxical hypertension may occur. Hypertension due toxicity associated with infusion of nitroprusside in theto clonidine withdrawal is best treated initially with setting of renal failure and also improves renal functionresumption of clonidine followed by the addition of as measured by creatinine clearance.16other drugs described above. Benzodiazepines havebecome one of the first-line agents in the setting of ConClUsioncocaine intoxication. They reduce the heart rate and Hypertensive urgency and emergency are associ-blood pressure through their anxiolytic effects and ated with significant morbidity and mortality. Promptare therefore recommended in patients with cocaine- recognition and early treatment is crucial in prevent-associated ischemia who are hypertensive, tachycardic, ing or halting progressive target organ damage. Fre-or anxious. quent monitoring that is typically only feasible in the Kidney failure. Acute kidney injury can be a cause or intensive care unit is necessary to achieve appropriatewww.turner-white.com Hospital Physician March 2007 49
  • 8. Va i d y a & O u e l l e t t e : H y p e r t e n s i v e U r g e n c y & E m e r g e n c y : p p . 4 3 – 5 0therapeutic endpoints. Treatment must be tailored to stress-mediated nitric oxide production by endothelialeach patient, based on the presence of specific target cells. Am J Physiol 1994;267(3 Pt 1):C753–8.organ damage and underlying comorbidities. The ben- 10. Keith NM, Wagener HP, Barker NW. Some different types of essential hypertension: their course and prognosis. Amefits of treating severe hypertension must be weighed J Med Sci 1939;197:332–43.against the risk of excessive blood pressure lowering. 11. Habib GB, Dunbar LM, Rodrigues R, et al. EvaluationThere are no high-quality prospective studies that ad- of the efficacy and safety of oral nicardipine in the treat-dress how quickly and to what degree blood pressure ment of urgent hypertension: a multicenter, randomizedshould be lowered. Extensive counseling should be double-blind, parallel, placebo-controlled trial. Am Heartprovided to patients upon discharge, especially if non- J 1995;129:917–23.compliance with medications contributed to the hyper- 12. Gonzalez ER, Peterson MA, Racht EM, et al. Dose-tensive crisis syndrome. HP response evaluation of oral labetalol in patients presenting to the emergency department with accelerated hyperten-RefeRenCes sion. Ann Emerg Med 1991;20:333–8.1. Wolf-Maier K, Cooper RS, Banegas JR, et al. Hyperten- 13. Rehman F, Mansoor GA, White WB. “Inappropriate” phy- sion prevalence and blood pressure levels in 6 European sician habits in prescribing oral nifedipine capsules in hos- countries, Canada, and the United States. JAMA 2003; pitalized patients. Am J Hypertens 1996;9(10 Pt 1):1035–9. 289:2363–9. 14. Grossman E, Messerli FH, Grodzicki T, Kowey P. Should a2. Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. moratorium be placed on sublingual nifedipine capsules Hypertensive urgencies and emergencies. Prevalence and given for hypertensive emergencies and pseudoemergen- clinical presentation. Hypertension 1996;27:144–7. cies? JAMA 1996;276:1328–31.3. Webster J, Petrie JC, Jeffers TA, Lovell HG. Accelerated 15. National Heart, Lung, and Blood Institute. New analyses hypertension—patterns of mortality and clinical factors regarding the safety of calcium-channel blockers: a state- affecting outcome in treated patients. Q J Med 1993;86: ment for health professional from the National Heart, 485–93. Lung, and Blood Institute. Bethesda (MD): U.S. Dept. of4. National High Blood Pressure Education Program. The Health and Human Services; 1995. seventh report of the Joint National Committee on preven- 16. Elliot WJ. Clinical features and management of selected tion, detection, evaluation, and treatment of high blood hypertensive emergencies. J Clin Hypertens (Greenwich) pressure. Bethesda (MD): Dept. of Health and Human 2004;6:587–92. Services, National Institutes of Health, National Heart, 17. Broderick JP, Adams HP Jr, Barsan W, et al. Guidelines for Lung, and Blood Institute; 2004. NIH Publication No. the management of spontaneous intracerebral hemor- 04–5230. rhage: a statement for healthcare professionals from a spe-5. Yu SH, Whitworth JA, Kincaid-Smith PS. Malignant hyper- cial writing group of the Stroke Council, American Heart tension: aetiology and outcomes in 83 patients. Clin Exp Association. Stroke 1999;30:905–15. Hypertens A 1986;8:1211–30. 18. Lick DR, Grotta JC, Lamki LM, et al. Should hypertension6. Vaughan CJ, Delanty N. Hypertensive emergencies. Lan- be treated after acute stroke? A randomized controlled cet 2000;356:411–7. trial using single photon emission computed tomography.7. Finnerty FA Jr. Hypertensive encephalopathy. Am J Med Arch Neurol 1993;50:855–62. 1972;52:672–8. 19. Kaplan JA, Jones EL. Vasodilator therapy during coronary8. Furchgott RF, Zawadzki JV. The obligatory role of endo- artery surgery. Comparison of nitroglycerin and nitroprus- thelial cells in the relaxation of arterial smooth muscle by side. J Thorac Cardiovasc Surg 1979;77:301–9. acetylcholine. Nature 1980;288:373–6. 20. Kitiyakara C, Guzman NJ. Malignant hypertension and hy-9. Kuchan MJ, Jo H, Frangos JA. Role of G proteins in shear pertensive emergencies. J Am Soc Nephrol 1998;9:133–42. Call FoR sUbmissions: RESIDENT GRAND ROUNDS sERiEs The editors of Hospital Physician are currently seeking clinical review articles for the Resident Grand Rounds series. This series is designed to provide residents with concise clinical review articles focusing on the diagnosis and management of acute, complex conditions frequently encountered in the care of inpatients. The format consists of a brief case scenario and focused discussion of diagnosis and management. Length is approximately 3500 words. We are particularly interested in topics from the following clinical areas but would consider topics in areas not listed: • Critical Care Medicine • Hematology • Otolaryngology/ENT Surgery • Rheumatology • General Surgery • Obstetrics/Gynecology • Psychiatry • Urology Residents and fellows are encouraged to contribute to this series under the guidance of a faculty mentor, who must be closely involved in the writing process. Authors interested in contributing are asked to contact the Editor, Robert Litchkofski (rlitchkofski@turner-white.com), or the Series Editor, Mark A. Perazella, MD (Mark.Perazella@Yale.edu) to obtain author guidelines and discuss the appropriateness of their topic. Copyright 2007 by Turner White Communications Inc., Wayne, PA. All rights reserved.50 Hospital Physician March 2007 www.turner-white.com