Hypertension: Hypertension crisis (Hypertension, hypertensive emergencies, hypertensive urgency, malignant hypertension)
Does this patient have hypertensive crisis
What is hypertensive crisis? What are some terms to describe it?
- How common is the occurrence of hypertensive crisis?
- What are risk factors?
- Presentation of hypertensive crisis
- Diagnosis of hypertensive crisis
- Physical examination
- Examination of the ocular fundus
- Basic laboratory tests
- When to order work-up for secondary causes in setting of hypertensive crisis
How should patients with hypertensive crisis be managed?
- Initial therapeutic goals for blood pressure reduction
- Different parenteral drugs that can be used in the initial treatment
- Sodium nitroprusside
- Nifedipine, Clonidine
- What particular agent should be used in the management of specific hypertensive crises?
- Hypertensive encephalopathy
- Ischemic stroke
- Intracranial hemorrhage (ICH)
- Acute hypertensive heart failure
- Acute myocardial infarction
- Acute aortic dissection
- Acute renal failure
- Postoperative hypertension
- What should be the next step in the management once the initial blood pressure control has been achieved?
- What happens to patients with hypertension crisis?
What is the evidence?
Does this patient have hypertensive crisis
Hypertensive crisis is present if the elevated blood pressure (BP) is complicated by progressive target organ dysfunction, e.g., heart failure, coronary vascular disease, aortic dissection, encephalopathy, acute renal failure, intracranial or subarachnoid hemorrhge or fundoscopy reveals hypertensive neuroretinopathy indicative of malignant hypertension.
What is hypertensive crisis? What are some terms to describe it?
Hypertension crisis is the turning point in the course of hypertension at which acute management of the elevated BP will improve the short-term and long-term prognosis. Following JNC 7 definitions, a hypertensive crisis occurs when systolic BP (SBP) rises above 180 mmHg or a diastolic BP (DBP) above 120 mmHg. JNC 8 has not made any changes in the definition. However, truly there is no critical level of blood pressure that defines the presence of hypertensive crisis. An acute increase in blood pressure in previously normotensive individual can precipitate a hypertensive crisis at a diastolic blood pressure as low as 100 to 110 mmHg. Conversely, very high diastolic blood pressure may persist for many years in patients with essential hypertension without the development of hypertensive crisis.
Today a large number of different terms have been applied to define acute severe elevations in BP, and the current terminology is somewhat confusing. These include hypertensive emergency, hypertensive urgency, malignant hypertension and accelerated hypertension.
Hypertensive emergencies represent severe elevations in BP that are complicated by evidence of progressive target organ dysfunction and require immediate BP reduction (not necessarily to normal levels) to prevent or limit target organ damage. This definition of hypertensive emergency includes malignant and accelerated hypertension as well and does not distinguish between them.
Hypertensive urgency is a condition in which severe uncontrolled hypertension (generally, SBP >179 mmHg or a DBP >109 mmHg) is observed in a patient who may have evidence of previous end-organ damage related to hypertension, but in whom there exists no evidence of ongoing or imminent target organ dysfunction related to the current episode of hypertension. Although long-term control of BP in this setting can prevent complications due to stroke, myocardial infarction, or congestive heart failure, there is no evidence that acute reduction of blood pressure results in any improvement in short or long term prognosis. Unfortunately, the term “urgency” is a misnomer and has led to overly aggressive management of many patients with severe, uncomplicated hypertension. Aggressive treatment with intravenous drugs or even oral agents, such as clonidine or nifedipine, to rapidly lower BP can lead to cumulative effects causing hypotension, sometimes following discharge from the emergency room. A more appropriate clinical term to describe this condition is severe uncomplicated hypertension, because there is no need for urgent reduction of blood pressure as would be required in patients with true hypertensive crises.
Malignant hypertension is a clinical syndrome characterized by marked elevation of BP with widespread acute arteriolar injury (hypertension induced arteriolitis). Fundoscopy reveals hypertensive neuroretinopathy with striate (flame-shaped) hemorrhages, cotton-wool (soft) exudates, and often papilledema. Regardless, the degree of BP elevation, or presence of cerebral malfunction (encephalopathy, intracerebral or subarachnoid hemorrhage), or renal failure, malignant hypertension cannot be diagnosed in the absence of hypertensive neuroretinopathy. Some authors have defined malignant hypertension based on the presence of papilledema and have used the term accelerated hypertension when hemorrhages and cotton wool spot occur in the absence of papilledema. However, it is now accepted that the prognosis is the same in hypertensive patients with striate hemorrhage and cotton wool spots whether or not papilledema is present. In this regard, the World Health Organization has recommended that accelerated hypertension and malignant hypertension be regarded as synonymous terms for the same disease.
Because the terms emergent, urgent and accelerated hypertension have caused considerable confusion in the diagnosis and management of true hypertensive crisis, it is preferable to utilize only the following terms to define hypertensive crises: (a) Malignant hypertension and (b) Hypertensive crisis in the setting of benign hypertension with acute end-organ damage complications (acute TOD but no hypertensive neuroretinopathy).
The rationale for distinguishing malignant hypertension from benign hypertension with acute complications is that the malignant hypertension is a distinct clinical and pathological entity with hypertensive neuroretinopathy and other evidence of widespread acute arteriolar injury that left untreated, leads to rapid and relentless progression to end stage renal disease (ESRD) or death in less than 1 year. Even in the current era of more awareness and aggressive management of BP, the annual all-cause mortality per 100 patient-year remains significantly higher in malignant hypertension patients (2.6) compared with normotensive (0.2) and hypertensive (0.5) controls (both P <0.01); and ESRD or >50% decline in renal function has been reported in 31% of patients after s median of 67 months of follow-up in patients with malignant hypertension. Clinical scenarios with severe hypertension not accompanied by hypertensive neuroretinopathy or acute target organ damage (TOD), such as severe uncomplicated hypertension or benign hypertension with chronic stable complications, should not be categorized in hypertensive crisis.
The spectrum of hypertensive crises, where acute management of elevated blood pressure plays a decisive role in the eventual outcome and other categories of severe hypertension, is outlined in
Spectrum of hypertensive Crises
How common is the occurrence of hypertensive crisis?
It has been estimated that of the more than 65 million hypertensive patients in the United States, approximately 1% will experience a hypertensive crisis during their life time. Nearly 3.2% of patients presenting to the emergency room (ER) have a hypertensive crisis. In recent decades, the widespread use of antihypertensive therapy has reduced the incidence of hypertensive crises substantially. Hypertensive crises, including hypertensive emergency and urgency admissions to ER, were reported to be 4.6/1,000 in a recent multicenter Italian epidemiological study. Nonetheless, the 5-year survival rate among all patients who present with a hypertensive crisis is 74%. Men are affected twice as frequently as women.
Blacks have an increased incidence of essential hypertension compared to whites and also have increased incidence of malignant hypertension.
What are risk factors?
Hypertension of virtually any etiology (essential or secondary) can enter into the crisis phase. The most common cause for a hypertensive crisis is chronic hypertension with an acute exacerbation resulting from medication noncompliance. However, in 8% of hypertensive crisis and 28% of hypertensive urgencies (severe uncomplicated hypertension) presenting to the emergency room, the patients are unaware of a prior diagnosis of hypertension. The presence of de novo malignant hypertension almost always indicates an underlying secondary cause of hypertension.
A variety of secondary causes of HTN can lead to a hypertensive crisis including:
Renal parenchymal disease
Pregnancy (preeclampsia and eclampsia)
Central nervous system disorders
Systemic illnesses with renal involvement, such as: systemic lupus erythematosis, scleroderma, microangiopathic hemolytic anemia (TTP/HUS), endocrine disorders such as Cushing disease, primary aldosteronism, or a pheochromocytoma, and autonomic hyperactivity in spinal cord/head injuries, or cerebrovascular accident infarction/ hemorrhage can precipitate a crisis.
In previously normotensive individuals, the use of drugs such as oral contraceptives, cocaine, phencyclidine, monoamine oxidase inhibitors with tyramine or other agents such as linezolid, nonsteroidal anti-inflammatory drugs, or amphetamines puts them at jeopardy.
Poorly controlled hypertension in a patient requiring emergency surgery is a hypertensive crisis because of the increased cardiovascular risk that accompanies inadequate pre-operative BP control and the accompanying perioperative increase in catecholamine levels and increased vascular resistance. Severe postoperative hypertension is another risk factor for hypertensive crisis requiring immediate BP control because it can cause hypertensive encephalopathy or intracranial hemorrhage, or jeopardize the integrity of vascular suture and lead to postoperative hemorrhage.
Severe hypertensive crisis can also occur in patients with extensive burn injury or children receiving high-dose cyclosporine for allogenic bone marrow transplantation. In quadriplegic patients, hypertensive crisis may develop due to autonomic hyperreflexia from stimulation of nerves below the level of spinal cord injury. Hypertensive crises may also complicate acute rejection or transplant renal artery stenosis in patients with renal allograft.
Presentation of hypertensive crisis
The most common non-specific symptoms are:
Less common presenting symptoms include:
The specific symptoms related to end organ damage include:
Chest pain (myocardial ischemia or MI)
Back pain (aortic dissection)
Dyspnea (pulmonary edema or congestive heart failure)
Altered consciousness (hypertensive encephalopathy)
Young black men with malignant hypertension may present with advanced renal dysfunction in the absence of any dramatic clinical symptoms.
Diagnosis of hypertensive crisis
In patients presenting with severe hypertension, a thorough clinical assessment is of utmost importance to differentiate a hypertensive crisis from severe uncomplicated hypertension and guide appropriate therapy (
Determination of type of hypertensive crisis.
A detailed history is essential. it is vital to inquire about the onset, duration, and severity of hypertension, a history of prior end-organ damage, associated symptoms, recreational drug and alcohol use, a list of medications (antihypertensive regimen with dosing and over-the-counter preparations), and compliance with the antihypertensive regimen
Physical examination must be directed toward the cardiovascular and neurological systems. BP must be measured in both arms to detect any significant differences. Other tests include peripheral pulse exploration for absence or delay (which would suggest aortic dissection), cardiac and lung auscultation (S3, rales), assessment of volume status and mental status, and examination for focal or lateralizing neurologic signs that are infrequent in hypertensive encephalopathy and usually suggest some other cerebrovascular disease (hemorrhage, embolism, or atherosclerotic thrombosis).
Examination of the ocular fundus
Examination of the ocular fundus is of great importance in the assessment of hypertensive crisis to diagnose malignant hypertension. The appearance of striate (flame-shaped) hemorrhage and cotton-wool (soft exudates) spots with or without papilledema (Figure 2) closely parallels the development of severe arteriolar damage (fibrinoid necrosis and proliferative endarteritis) in malignant hypertension. Striate hemorrhage and cotton-wool spots result from high intravascular pressure and ischemic infarction of nerve fiber bundles in retina, respectively and most commonly occur within three disc diameter of the optic disc. In contrast, dot hemorrhage and hard exudates as a result of benign hypertensive retinal arteriosclerosis, usually occur in the periphery of the fundus.
Basic laboratory tests
Basic laboratory tests, including serum electrolytes, blood urea nitrogen, creatinine, complete blood count, electrocardiogram, chest X-ray, and urinalysis should be obtained to evaluate for potential secondary causes of hypertension and to define the extent of target organ damage. Malignant hypertension can cause nephrotic range proteinuria and gross or microhematuria. In contrast significant proteinuria and hematuria are rare in other types of hypertensive crisis. However, the level of protein excretion is of little value in the differentiation of primary malignant hypertension from malignant hypertension due to secondary causes.
Microangiopathic hemolytic anemia as evidenced by a decreased platelet count and either an increased lactate dehydrogenase or presence of schistocytes is common in patients with malignant hypertension and is strongly associated with renal dysfunction. Thrombotic microangiopathy in the setting of malignant hypertension should be distinguished from TTP and HUS. Patients with malignant hypertension have less impressive thrombocytopenia, higher blood pressure, neuroretinopathy changes that are not usually observed in HUS/TTP and more favorable renal prognosis with aggressive management of blood pressure. In addition, activity of ADAMTS13 in most patients with TTP is much lower than in patients with malignant hypertension, being 0 – 5% of normal.
When to order work-up for secondary causes in setting of hypertensive crisis
Rule out renovascular hypertension in all the cases of malignant hypertension, once it has been treated successfully. Rule out pheochromocytoma and primary hyperaldosteronism if symptoms of catecholamine excess and hypokalemia persist for more than a year after malignant hypertension phase has resolved. Renal biopsy is indicated if nephritic urinary sediment and/or nephrotic range proteinuria are present. Complete evaluation for the secondary causes should also be performed if hypertensive crisis occurs at age <30 years with out any risk factor (family history, smoking, obesity, drug abuse, oral contraceptives, CKD, sleep apnea), or >50 years, or resistant hypertension or no history of noncompliance with medication.
How should patients with hypertensive crisis be managed?
Initial therapeutic goals for blood pressure reduction
There are no absolute guidelines for the initial BP goal. There is a theoretical risk of cerebral hypoperfusion from impaired autoregulation during rapid reduction of BP. However, the proven benefit of acute reduction of BP in hypertensive crisis clearly outweighs the theoretic risk of cerebral ischemia. In general, an initial BP reduction to 160 to 170 mm Hg systolic, and 100 to 110 mm Hg diastolic or to a mean arterial pressure of 120 to 130 mm Hg over 2-4 hours can be safely accomplished.
Alternatively, the initial antihypertensive therapy can be individualized and reduction of mean arterial BP by 20% should be the initial goal for first 1-2 hours. This goal should be achieved using the parenteral antihypertensives. The use of potent parenteral agents with rapid onset and short duration of action has obvious advantages. If overshoot hypotension or neurologic sequelae develop, they can be quickly reversed by allowing the BP to stabilize at a higher level. During the reduction of BP with parenteral antihypertensives, the patient should be monitored closely for evidence of cerebral or myocardial hypoperfusion (yawning, nausea, hyperventilation or chest pain).
Some patients, particularly those with normal kidney function, may have some element of volume depletion because of the preceding pressure natriuresis that occurred in the setting of very high BPs. Thus, in the absence of clinical signs of volume overload, some volume expansion with intravenous saline solution will help to suppress renin secretion and to prevent significant hypotension with initiation of vasodilator therapy.
Different parenteral drugs that can be used in the initial treatment
Parenteral drugs that can be used in initial treatment are summarized in
Parenteral drugs for initial treatment of hypertensive crises
Sodium nitroprusside is a potent intravenous hypotensive agent with an immediate onset (seconds to 2 minutes) and brief duration of action (1 to 3 minutes). It causes vasodilation of both arteriolar and venous vessels resulting in decrease of both systemic vascular resistance (SVR) and venous return. The combined decrease in preload and afterload reduces left ventricular wall tension and myocardial oxygen demand.
Sodium nitroprusside is the first-choice agent for the majority of hypertensive emergencies including hypertensive encephalopathy, heart failure due to acute diastolic dysfunction, aortic dissection, and adrenergic crisis. The initial infusion rate should be 0.5 µg/kg/minute and the flow rate is increased in increments of 1 µg/kg/minute every 2 to 3 minutes until the desired hypotensive response is obtained. The average effective dose of sodium Nitroprusside is 3.0 µg/kg/minute (range 0.5 to 10 µg/kg/minute).
Sodium nitroprusside is rapidly metabolized with a reported half life of 3 to 4 minutes to a short lived intermediate cyanide, which is converted to thiocyanate by the liver in a reaction in which thiosulfate acts as a sulfur donor. Thiocyanate is excreted unchanged by the kidney with a half life of 1 week in patients with normal renal function. The most important adverse effect of sodium nitroprusside is intoxication with thiocyanate, which can occur when this agent is administered for more than 48 to 72 hours, particularly in patients with renal or liver dysfunction. When these factors are present, thiocyanate levels should be monitored and infusion should be discontinued if the plasma level exceeds 10 mg/dL.
Thiocyanate intoxication presents with nausea, vomiting, tinnitus, muscle cramps, hyperreflexia, disorientation, and psychosis. Treatment of thiocyanate toxicity includes administration of hydroxycobalamin and sodium thiosulfate infusions, and in chronic renal failure dialysis may be indicated. Cyanide poisoning is a very rare complication. Extravasation can cause local tissue necrosis.
Fenoldopam is a selective dopamine receptor (DA1) agonist and decreases SVR. It also increases renal blood flow and causes natriuresis and aquauresis. It is six times more potent than dopamine in causing renal vasodilatation. Its dosage adjustment is not required in renal and hepatic insufficiency. This agent has a rapid onset of action (within 10 minutes) and ease of BP titration.
Fenoldopam must be administered as an intravenous infusion and not as a bolus. The initial dose is 0.1 µg/kg/minute, the increments must not exceed 0.1 µg/kg/minute at 20-minute intervals, and the highest dose should not exceed 1.7 µg/kg/minute. It does not cause rebound hypertension, and therefore it can be withdrawn by tapering off or stopping its administration abruptly. It has the advantage of not requiring a line for intra-arterial BP monitoring. Its main indications are severe hypertension with renal failure, acute hypertensive heart failure, and hypertensive crisis of pregnancy. Fenoldopam is contraindicated in the setting of glaucoma. Side effects include headache, flushing, dizziness, tachycardia or bradycardia, hypokalemia, and local phlebitis. It should be avoided in patient with sulfa allergy.
Labetalol has selective α1- and nonselective β-blocking properties resulting in decrease in systemic vascular resistance without an appreciable change in cardiac output. After intravenous injection, the full antihypertensive effect occurs within 5 to 10 minutes and duration of action ranges from 2.0 to 6.5 hours. It can be administered as intravenous bolus with an initial dose of 20 mg over 2 minutes with 20 mg increments every 10 minutes interval until the desired response or maximum total dose of 300 mg has been given. Labetalol can also be given by continuous infusion, begun at 2 mg/minute with maximum dose of 300 mg. It needs decrease in dose in patients with live dysfunction, however, need no modification in renal insufficiency.
Because of its longer duration of action and less predictable hypotensive response with risk of overshoot hypotension, labetalol is not the ideal drug for treatment of hypertensive crisis. Labetalol is contraindicated for heart failure, heart block, and chronic obstructive pulmonary disease and for hypertensive crisis following coronary artery bypass graft surgery. Life threatening hyperkalemia has been reported in patients with renal failure, thus labetalol should be used cautiously in this setting. This agent has been used in the setting of hypertensive crisis of pregnancy because little placental transfer occurs
Esmolol is an ultra short-acting cardioselective β-blocker with an elimination half-life of approximately 9 minutes. It decreases arterial pressure by decreasing heart rate and myocardial contractility, and thus cardiac output. The onset of action of esmolol is within 60 seconds with duration of action of 10-20 minutes; however since it is metabolized by red blood cell esterase, in anemia its half-life increases. Esmolol is available for intravenous use both as a bolus and as an infusion.
Esmolol is particularly useful in severe post-operative hypertension which is associated with activation of sympathetic nervous tone. Typically, the drug is administered as a 500-1000 µg/kg loading dose over 1 minute, followed by an infusion starting at 50 µg/kg/minute and increasing up to 300 µg/kg/minute as necessary. Esmolol is contraindicated in patient with chronic obstructive pulmonary disease, heart failure, bradycardia and patients already on β-blocker therapy.
Nicardipine is a second-generation, dihydropyridine derivative calcium-channel antagonist with high vascular selectivity, and strong cerebral and coronary vasodilator activity. The onset of action of intravenous nicardipine is from 5 to 15 minutes, with duration of action of 4 to 6 hours. The initial infusion rate is 5 mg/hour, increasing by 2.5 mg/hour every 5 minutes to a maximum of 15 mg/hour until the desired blood pressure control is achieved. Since, nicardipine increases both stroke volume and coronary blood flow with a favorable effect on myocardial oxygen balance, it is particularly useful in patients with coronary artery disease and systolic heart failure. In addition, this agent has been recommended in the American Heart Association and American Stroke Association’s guidelines for the treatment of ischemic stroke when diastolic blood pressure is >120 mm Hg or the systolic blood pressure is >220 mm Hg.
Clevidipine is a new short-acting intravenous third-generation dihydropyridine calcium-channel blocker, which is a selective arterial vasodilator with very little or no effect on the myocardial contractility or chronotropy and venous capacitance. In the Phase III trials, clevidipine was effective in controlling BP in the settings of perioperative cardiac surgery and severe hypertension and was associated with minimal adverse effects. Its potential advantages consist of its short half-life, affording greater acute titratibility.
Clevidipine should be initiated at a dose of 1 to 2 mg/h and then titrated (usually doubled every 90 seconds) until the desired BP is attained. As BP approaches the target, the increase in dose should be less than double and the dosing interval should be lengthened to every 5 to 10 minutes. The action of clevidipine is independent of renal or hepatic functional status. Clevidipine is contraindicated in patients with allergies to soybeans, soy products, eggs, or egg products; and patients with defective lipid metabolism.
Nitroglycerine is a potent venodilator and only at high dose affects arterial tone. It reduces blood pressure by reducing preload and cardiac output. Intravenous nitroglycerine has an onset time of 2-5 minutes, duration of action of ~10-20 minutes and is eliminated by hepatic metabolism in ~1-4 minutes. It is generally not considered as a first line therapy for hypertensive crisis because of its low efficacy. Low dose administration (~60 mg/minute) may, however, be used as an adjunct to other intravenous antihypertensives in emergencies associated with acute coronary syndrome or pulmonary edema.
Phentolamine is a nonselective α-adrenergic blocking agent and is useful in the management of pheochromocytoma in conjunction with concomitant β-adrenergic blocker. The onset of action is within 2 to 3 minutes with duration of action of 15 to 30 minutes. The initial dose is intravenous injection of 1 mg with subsequent boluses of 1 to 5 mg are administered up to a total of dose of 20 to 30 mg or till desired blood pressure.
Enalaprilat is an intravenous angiotensin converting enzyme inhibitor and because of its slow onset and long duration of action, is a poor choice for use in a hypertensive crisis. In addition, it has potential to cause renal failure, and hyperkalemia in circulatory decompensated states.
Nifedipine immediate release formulations and oral clonidine loading must be abandoned as a treatment option in the management of hypertensive crisis because of erratic effect on BP.
Sodium nitroprusside and possibly fenoldopam are preferable agents because of their rapid onset, short duration of action and ease of titratibility. The main goal of treatment is to decrease mean arterial pressure by 20% or diastolic BP to 100 to 110 mm Hg in the first hour.
There is no good data from randomized controlled trial to guide blood pressure management in the hyperacute phase of ischemic stroke. However, there is consensus that BP must not be reduced in ischemic stroke patients unless they are candidates for thrombolytics. When thrombolytic treatment is planned for ischemic stroke, the BP must be <180/105 mm Hg. If the BP is >220/120 it would be acceptable to gradually reduce the BP in 24 to 48 hours. When diastolic BP is >140 mm Hg, Nicardipine or fenoldopam should be administered in order to decrease diastolic BP 10% to 15% in 12 to 24 hours. Recently published studies, where patients were enrolled as long as 30 to 48 hours after stroke onset, do not show any significant difference in mortality and functional outcome with aggressive hypertension treatment.
Intracranial hemorrhage (ICH)
For patients presenting with ICH, acute lowering of SBP to 140 mmHg is generally considered safe and results of the recent INTERACT2 study supports this recommendation. However, in the absence of elevated intracranial pressure, the recommended BP target is 160/90 mmHg. Despite the theoretic risk of elevation of intracranial pressure sodium nitroprusside remains the drug of choice because it allows cautious, graded blood pressure reduction. Fenoldopam and clevidipine are other options but experience with them is limited.
Acute hypertensive heart failure
Sodium nitroprusside is the preferred drug because it reduces both preload and afterload. The target is to reduce BP to normal or near-normal levels. The role of Clevidipine is being studied in large ongoing clinical trials for this indication.
Acute myocardial infarction
Intravenous β-blocker therapy (Esmolol, Labetolol) should be considered in all the patients unless contraindications such as bradycardia, heart failure or COPD are present. Intravenous nitroglycerine can be used as adjunct therapy to increase coronary blood flow.
Acute aortic dissection
In this condition, systolic BP must be reduced to 100 to 120 mm Hg as soon as possible, by means of a combined treatment with sodium nitroprusside and a β-blocker (Esmolol or metoprolol). β-blockade must be established first, before starting the nitroprusside infusion. An alternative agent is labetalol, which may be used as the only treatment because it has both β- and α-blocking effects. Heart rate must be maintained between 60 and 80 beats/minute.
This condition, either mild or severe, is managed best with a policy of delivery at or beyond 37 or 34 weeks’ gestation, respectively. Intravenously administered labetalol or hydralazine have long been considered first-line medications; however, hydralazine use can be associated with severe hypotension and maternal and fetal complications. An updated opinion of ACOG committee adds oral nifedipine as a first-line therapy since it has shown to provide good BP control with lower number of doses and less time needed. Careful monitoring is advisable with simultaneous use of magnesium sulfate since both are calcium antagonists. The aim is to decrease diastolic BP to 80 to 100 mm Hg. Severe preeclampsia should be treated with intravenous magnesium to prevent progression to eclampsia. Sodium nitroprusside is relatively contraindicated in pregnancy.
Acute renal failure
Fenoldopam is preferred agent because of its renal vasodilating property. Sodium nitroprusside and labetalol should be carefully used in this setting because of possible thiocyanate poisoning and hyperkalemia respectively.
Phentolamine is the treatment of choice; however sodium nitroprusside is equally effective. Once BP has been controlled, esmolol can be used to control the tachycardia or arrhythmias.
Clevidipine is the agent of choice because of its rapid onset and short duration of action with limited effect on cardiac preload and output. Over the years, experience has increased with favorable results; however, cost is an issue.
What should be the next step in the management once the initial blood pressure control has been achieved?
Oral antihypertensive agents should be initiated as soon as the patient has been stabilized and is able to tolerate medications by mouth, along with gradual tapering off of parenteral agent. Although all other agents may be effective in the long-term management of patients with hypertensive crisis, the cornerstone of initial oral therapy should be an arteriolar vasodilator such as hydralazine, sustained release nifedipine, or minoxidil. Vasodilators may cause reflex tachycardia with increase in cardiac output and blunt the hypotensive response. Therefore, treatment with β-adrenergic blockers is usually also required. Vasodilators also cause renal salt and water retention and hence the tolerance to hypotensive effect by volume overload. Thus, although diuretics may not be required for the initial management, they are usually required as a part of the long-term maintenance antihypertensive regimen.
After BP has been controlled with parenteral therapy and while the infusion is continued, hydralazine (100 mg) and metoprolol (50 mg) are administered orally. As the oral agents become effective and BP declines, the parenteral infusion is tapered. Brief interruption of the infusion can be used to assess the hypotensive response to oral agents. If after 6 to 8 hours the DBP remains higher than 100 mm Hg, a second dose of hydralazine (100 mg) should be given. The metoprolol dose is increased as needed to maintain adequate β-blockade (heart rate, 60-80 beats/min).
If BP is not controlled with hydralazine at a dose of 100 mg twice daily, minoxidil should be substituted for hydralazine. The starting dose of minoxidil (2.5 mg) is increased by 2.5 mg to 5 mg every 6 to 8 hours until the blood pressure is adequately controlled. The usual effective dose is 5 to 10 mg twice a day. As the blood pressure is brought under control with oral agents, the infusion is gradually weaned.
When the convalescing patient is mobilized, upright BP should be carefully monitored to avoid orthostatic hypotension. A diuretic, usually furosemide at a starting dose of 40 mg twice daily, is added to vasodilator regimen when it becomes evident that salt and water retention is beginning to occur. The goal is to reduce BP below <160/100 by the time of discharge with ultimate goal to reduce blood pressure <130/80 over next 2-3 months.
What happens to patients with hypertension crisis?
Fibrinoid necrosis of the arterioles is the classical hallmark of malignant hypertension. The characteristic finding is the deposition of the fibrinoid material in the media and occasionally in the intima. The small arteries reveal proliferative endarteritis or onionskin lesions consisting of intimal thickening, these lesions result in moderate to severe luminal narrowing and distant ischemia. In addition to the kidney, the vascular beds of the pancreas, gastrointestinal tract, liver, retina, brain, myocardium, prostate and skeletal muscles are frequently involved. In other types of hypertensive crisis the pathological changes are those of the benign hypertension i.e. hyaline arteriosclerosis. The arteriolar wall is thickened by homogenous eosinophilic material that narrows the lumen. Arteries may show medial hypertrophy with reduplication of elastic laminae.
In malignant hypertension developing in the setting of essential hypertension, the glomeruli may have focal and segmental fibroid necrosis, however, the percentage of involved glomeruli is typically only 5% to 30%, unlike chronic glomerulonephritis with superimposed malignant hypertension where the glomerular involvement is more diffuse and global.
What is the evidence?
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