Accelerated hypertension definition

Accelerated hypertension definition DEFAULT

Malignant hypertension: does this still exist?

Malignant hypertension (MHT) is the most severe form of hypertension. It was originally defined by two major features: extremely high blood pressure with the diastolic blood pressure above 130 mmHg at the time of the diagnosis and hypertensive retinopathy grades III or IV in the Keith et al.'s classification [1].

More recently, the definition of MHT has been reconceptualized to emphasis multi-organ damage [2, 3]. Indeed, overall prognosis in patients with MHT mainly depends on the function of kidney, brain, and heart [3]. As the earlier diagnosis and appropriate antihypertensive treatment result in significant improvement of prognosis [4], it is of the utmost importance to set reliable diagnostic criteria. Hence, the proposed new definition presents MHT as a group of disorders with out of range elevation in blood pressure with the concomitant damage of at least three different target organs [3]. Considering the disease entity in a broader perspective will allow to increase the detection and estimate the real prevalence of this hypertensive emergency.

The principals of prompt detection, systemic evaluation, and effective management are the key to improve the long-term prognosis.

Epidemiology

In general population the prevalence of MHT is relatively low with annual incidence rate of around 2 per 100,000 of Caucasian population [5, 6]. Greater disease predisposition and worse prognosis is observed in the Afro-American population (7.3 new cases per 100,000 of population per year) [6]. There is also no significant difference in MHT prevalence between developed and developing countries [7, 8].

As a hypertensive emergency MHT might develop in patients with prior history of essential hypertension, but in up to 60% cases MHT occurs de novo with no differences in signs and symptoms or long-term survival [9].

In the past, MHT had an unfavorable prognosis and without adequate treatment, mortality rate in MHT was around 80% at 2 years [10]. Importantly, 5-year survival among MHT patients has improved dramatically over the decades and for patients diagnosed after 1997 it is now more than 90% [11]. When compared malignant and non-MHT all-cause mortality is higher, with kidney failure as the main cause of death among patients with MHT [12, 13]. Nevertheless, since the new, more effective antihypertensives are in use, current prognosis performs better [2]. Despite the overall decrease, the prevalence has been roughly stable for the last 40 years [4].

Diagnostic difficulties

MHT may pose a diagnostic challenge whilst early diagnosis is essential for prompt treatment [3, 14]. As emphasized, the MHT has a significantly worse prognosis than the non-MHT, and it appears this difference is mainly due to renal insufficiency resulting in end-stage renal disease. Moreover, the main diagnostic problem is caused by the lack of obvious symptoms which flag out patients who require further investigation, that is fundoscopy. The latter is an essential examination required to establish an initial diagnosis based on the original criteria. Thus, retinal fundoscopy should be performed in all patients presenting with severely increased blood pressure on examination [2]. It is due to the fact that typical retinal changes are dynamic, start to regress immediately upon the implementation of the antihypertensive treatment and do not persist for longer than 2–3 months [2, 15].

Although in some cases, when patients present with extreme signs of blood pressure elevation, such as hypertensive encephalopathy and MHT is suspected, Grade 3–4 ocular changes might be absent during their initial examination [16]. There are also other disorders which might cause papilledema or retinal hemorrhages, such as severe anemia, ineffective endocarditis, or connective tissue disorders [17]. Not to mention also diabetic retinopathy, which is a leading cause of sight impairment and retinal changes [18]. All the above disrupt and complicate the differential diagnosis. As the clinical presentation of MHT is often delayed, the presence of ocular fundus changes before initiating treatment should not be a determinant [3]. Moreover, changes in the vision correspond to the renal function impairment [19, 20].

The common cause of the described alternations is systemic microvascular dysfunction. An important pathological feature of MHT is endothelial dysfunction and fibroid necrosis of arterioles, that obviously concerns various tissues and affects many organs, especially key ones, that is kidney, heart, and brain [2, 21]. This premise lay the foundation for the evolution of definition in which the concept of multi-organ damage, described as hypertensive target organ damage (TOD), was introduced [2, 3, 21]. Other diagnostic criteria required are the presence of damage of at least three different target organs (kidney, heart, brain, and small vessels) and out of range elevation in systolic and diastolic blood pressure.

Renal abnormalities are the most common evidence of TOD and constitutes an independent determining factor in prognosis [22]. MHT exerts various impacts on the kidney, from elevated serum creatinine and proteinuria to acute renal failure as a first presentation of MHT [23, 24]. Moreover, renal ischemic changes are aggravated by hemolysis and low plate platelet count, resulting from thrombotic microangiopathy [3, 25].

In the heart, the impairment of cardiac structure and function is so evident that it is referred as hypertensive heart disease [26]. It includes left ventricular hypertrophy, cardiomegaly, systolic and diastolic dysfunction, and finally heart failure [9, 27]. Even atrial fibrillation is said to be a certain presentation of TOD [27].

Prevention of neurological deficits is a crucial goal in MHT treatment, especially because of their often-asymptomatic course and limited diagnostic possibilities. However, the most life-threatening condition, hypertensive encephalopathy, is a rare emergency with sudden onset of symptoms that facilitates differential diagnostics [2, 28].

Treatment

The hypertensive emergencies require immediate intervention to lower blood pressure [29]. It is important to reduce the blood pressure in appropriate pace, which is ~20–25% decrease within several hours [30]. Too rapid blood pressure reduction may result in severe multi-organ ischemia caused by hypoperfusion and failure of autoregulation mechanisms [16, 31]. The conventional “normal” level of blood pressure should not be aimed at acute presentation with MHT [32]. First line pharmacological agents are labetalol and nicardipine. Alternatively nitroprusside and urapidil can be used as safe and effective treatment of MHT [30], as recommended by the ESC position document. Labetalol is an alpha 1 adrenergic receptor and nonselective beta-adrenergic receptor blocker. Its main advantage is capacity to both maintenance of cardiac output and reduction of peripheral resistance with preservation of cerebral, renal, and coronary blood flow [33]. Nicardipine, a dihydropyridine derivative calcium channel blocker with cerebral and coronary vasodilatory activity, increases stroke volume and coronary blood flow and it is especially recommended for patients with coronary artery disease[34]. Alternatively, some groups use very low oral dose of angiotensin-converting enzyme inhibitors [35] or renin–angiotensin system blockers [36] titrated over 48 h, to prevent excessive fall in blood pressure. Although the preferable therapeutic approach for each patient depends on clinical presentation, the optimal clinical care is often be provided in the intensive care units to ensure adequate monitoring and treatment adjustments [37].

New definition

The original definition of MHT was focused only on visual disturbance and did not include other evidence of organ damage [1]. Such TOD, especially the severity of renal impairment, is pivotal in overall prognosis [38]. Along with the development of techniques for TOD assessment, a new definition has been widened to include the presence of impairment in at least three different organs including kidney, heart, brain, and microangiopathy [3]. They constitute various clinical presentations of the same disease entity [2, 3].

The current 2018 ESC/ESH Guidelines for the management of arterial hypertension present new, broadened approach to the hypertensive emergencies [29]. A collective group of “hypertension urgencies and emergencies” was distinguished with a strong emphasis on magnitude of organ damage, described as hypertension-mediated organ damage [29]. Besides, the term of “malignant hypertension” was clarified as it refers to the poor prognosis when untreated [29]. It characterizes the condition of severe hypertension with concomitant retinopathy, microangiopathy, disseminated intravascular coagulation, encephalopathy, acute heart failure, or acute deterioration in renal function [29]. Updated guidelines also offer greater range of diagnostic possibilities depending on target organs affected and symptoms, divided on common and specific tests [29]. Hence, common diagnostic tests including 12-lead ECG, hemoglobin, platelet count, fibrinogen, creatinine, eGFR, urine albumin:creatinine ratio were included for routine testing with fundoscopy as a crucial part of the diagnostic workup. Specific tests such as troponin, CK-MB, echocardiography, CT or MRI brain, urine drug screen, etc., undeniably contribute to improvement in general management of MHT [2, 39].

Conclusions

Although general improvements in diagnosis of MHT has been made, this is still a common emergency, especially in the developing countries due to the growing population, undiagnosed hypertension, and low level of health care services. Moreover, the diagnosis is established when the target organ impairment occur therefore this condition is related to much worse outcome than the nonmalignant forms of hypertension [3].

Despite better prognosis and significantly improved survival rates, patients with MHT remain at high risk. Not only do they require special attention during hospitalization, but also after discharge, which include screening for secondary hypertension and frequent follow-up visits.

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Author information

Affiliations

  1. Liverpool Centre for Cardiovascular Science, University of Liverpool, Liverpool John Moores University and Liverpool Heart & Chest Hospital, Liverpool, UK

    Magdalena Domek, Jakub Gumprecht, Gregory Y. H. Lip & Alena Shantsila

  2. Department of Internal Diseases, Diabetology and Nephrology, Silesian Medical University, Zabrze, Poland

    Magdalena Domek

  3. Department of Cardiology, Congenital Heart Diseases and Electrotherapy, Silesian Medical University, Silesian Centre for Heart Diseases, Zabrze, Poland

    Jakub Gumprecht & Gregory Y. H. Lip

  4. Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark

    Gregory Y. H. Lip

Corresponding author

Correspondence to Alena Shantsila.

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Domek, M., Gumprecht, J., Lip, G.Y.H. et al. Malignant hypertension: does this still exist?. J Hum Hypertens34, 1–4 (2020). https://doi.org/10.1038/s41371-019-0267-y

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1. Description of the problem

What every clinician needs to know

Severe hypertension is a common scenario encountered in intensive care patients. The role of the clinician is to establish the etiology and to determine whether blood pressure reduction may be detrimental or desirable.

Table I. Classification of hypertension

Two terms describe conditions associated with acute severe elevations in systemic arterial pressure when rapid reduction in blood pressure is required.

A hypertensive emergency is defined by the onset or progression of end-organ damage pertaining to the cerebrovascular, cardiovascular or renovascular system. Expeditious control of blood pressure is necessary to prevent catastrophic organ damage and should be carried out over a period of minutes to hours but not necessarily aiming for normal values.

Hypertensive urgencies are distinguished by the lack of end-organ damage; however, gradual blood pressure reduction over hours or days is indicated. Untreated hypertensive urgencies may evolve as sustained high blood pressure can lead to end-organ damage.

Accelerated hypertension and malignant hypertension also denote end-organ damage; however, they are characterized by pathognomonic changes. Accelerated hypertension is defined by retinal damage, including hemorrhages, exudates and arteriolar narrowing. The additional presence of papilloedema constitutes malignant hypertension, which is usually associated with diastolic blood pressure greater than 140 mmHg.

Table I summarizes the classification of high blood pressure. Hypertensive emergencies would usually be associated with values in the grade 3 range; however, there is no set blood pressure above which a hypertensive emergency is inevitable. Wide inter-person variability means that some people may tolerate high pressures unharmed in the short term.

In the long-term management of hypertension, if a person’s systolic and diastolic blood pressures fall into different categories, then the higher value should be used to quantify risk and guide treatment. There are no data in this respect for hypertensive emergencies, but intuitively the same principle should apply.

Table II. Hypertensive emergencies

It is important to carefully consider what the patient’s normal blood pressure may be before appropriate diagnostic and management plans can be instigated. In patients without pre-existing hypertension, a crisis can occur at lower than expected values.

Excessive lowering of blood pressure below the organ’s autoregulatory threshold can exacerbate ischemia and worsen outcome.

Patients presenting with neurological syndromes can deteriorate rapidly and therefore need re-assessment on a regular basis.

In catecholamine excess states unopposed alpha-adrenergic stimulation (i.e. beta-blockade without alpha-blockade) can cause life-threatening vasoconstriction.

Clinical features

It is important to acknowledge that hypertension per se is asymptomatic, and therefore the symptoms and signs of a hypertensive emergency will relate to the organ systems involved.

Cerebrovascular manifestations

Hypertensive encephalopathy most commonly presents with global phenomena of headache, nausea and vomiting, which progress to visual disturbances with or without retinal changes, focal neurological deficits, seizures that may be focal or generalized, coma and death.

Onset of symptoms is usually gradual and although blood pressure will be markedly elevated from the patient’s baseline, it may be lower than that associated with other target organ injury.

Hypertension is implicated in acute ischemic or hemorrhagic stroke and subarachnoid hemorrhage (SAH) causation. Onset of symptoms will be sudden and as with encephalopathy can range from headache (often very severe) to coma.

In addition to the original insult, further neurological deterioration can occur in all these patients due to evolving cerebral edema; ischemic strokes can be complicated by hemorrhagic transformation; and patients with SAH may rebleed or develop hydrocephalus or vasospasm, which may also cause ischemic infarcts.

This picture is complicated by the pathophysiological changes that occur in relation to any brain injury. Cerebral autoregulation is disrupted and adequate perfusion of the injured area relies heavily on mean arterial pressure; therefore, even in the absence of precipitating hypertension, a hypertensive response occurs in the majority of patients.

This presents a challenge in the management of hypertensive crises, where on one hand blood pressure reduction is necessary, but excessive lowering will exacerbate ischemia and secondary brain injury.

Cardiovascular manifestations

Acute coronary syndromes (ACS) constitute unstable angina, non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation MI (STEMI). MIs may be asymptomatic, particularly in susceptible groups such as the elderly or diabetics, or may present with chest pain and/or dyspnea, particularly in the context of low-cardiac-output states, pulmonary edema or congestive cardiac failure.

Back pain with or without chest pain should alert the physician to the possibility of aortic dissection. Other symptoms and signs related to acute aortic dissection will depend upon the location and extent of tearing and can result in ischemia of any organ or limb.

A syndrome of excessive catecholamine release, myocardial stunning and heart failure is a recognized complication of SAH. This completely reversible neurogenic myocardial stunning is associated with a wide spectrum of left ventricular wall motion abnormalities.

It also includes a subset of patients who exhibit classical tako-tsubo cardiomyopathy (a complex of apical ballooning and akinesia with basal sparing and hyperkinesis), which typically affects postmenopausal women in response to stress.

Renal manifestations

After diabetes mellitus, hypertension is the second most common cause of chronic renal impairment. The earliest signs of renovascular disease will be reductions in glomerular filtration rate (GFR) and microproteinuria.

Severe renal failure may present with a range of clinical symptoms, including general malaise, uremic delirium and fluid overload. Patients are often oligurio-anuric; laboratory tests will show elevations in urea and creatinine, and electrolyte abnormalities frequently include hyperkalemia. In scleroderma renal crisis urine output may be normal.

Key management points

Therapeutic priority is to reduce blood pressure to a pre-determined safe range promptly. The desired speed and degree of reduction will depend on the presence and type of end-organ damage.

In essential hypertension, blood pressure control can be achieved over a period of weeks to months with the aim of minimizing the long-term complications of chronic hypertension. In hypertensive urgencies it is adequate to reach target parameters over a period of hours to days. Oral medication is used, the choice of which will depend on patient demographics and underlying comorbidities.

Conversely, in hypertensive emergencies blood pressure reduction is required within minutes or hours at the most. The patient should be managed in a level 2 or 3 environment, invasive blood pressure monitoring is paramount, and short-acting intravenous drugs that can easily be titrated should be used.

In the absence of RCT evidence, a generally recommended goal is to reduce mean arterial pressure by 20-25% or diastolic pressure to 100-110mmHg. Excessive lowering of BP may lead to organ ischemia and infarction.

2. Emergency management

The patient should be stabilized according to the established principles of airway and breathing, and then attention can be focused on the circulation.

The history, examination and investigations obtained (as detailed below under ‘diagnosis’) will guide clinicians as to the precise nature of the problem and help establish specific therapeutic targets.

Neurological emergencies

Hypertensive encephalopathy: is entirely reversible and symptoms should begin to resolve within 6-12 hours of blood pressure control. MAP should be reduced by 25% over a few hours but no more than 20% in the first hour.

Acute ischemic strokes: treatment is not indicated unless the SBP is greater than 220 mmHg or DBP is greater than 120 mmHg. If a patient fulfills the criteria for thrombolysis, then BP should be reduced to SBP less than 185 mmHg and DBP less than 110 mmHg before fibrinolytics are administered and then maintained at SBP less than 180 mmHg and DBP less than 105 mmHg for the next 24 hours.

Intracerebral hemorrhage: new evidence using target SBP of 140 mmHg suggests that early BP control is well tolerated and can limit hematoma size. Current guidelines, however, recommend maintaining MAP less than 110 mmHg or SBP less than 160 mmHg except where radiological evidence of raised intracranial pressure exists, where targets will be higher: MAP less than 130 mmHg or SBP less than 180 mmHg.

SAH: management presents a particular challenge as blood pressure needs to be reduced to prevent re-bleeding but maintained high enough to minimize vasospasm. This problem is abolished following successful protection of the lesion, such as clipping or coiling of an aneurysm, when BP priorities will shift to vasospasm prevention. Nimodipine is used to help prevent vasospasm and will cause hypotension, especially if given intravenously; however, it is not indicated for the treatment of hypertension with SAH per se.

Cardiovascular emergencies

ACS: Treatment is indicated if SBP is greater than 160 mmHg or DBP is greater than 100 mmHg. Myocardial work reduction can be achieved by reducing heart rate and blood pressure, and in combination will limit infarct size.

While vasodilation is desirable, diastolic pressure should be adequate to support coronary perfusion and drugs that cause coronary artery dilatation are preferred. Thrombolysis is contraindicated if SBP is greater than 180 mmHg or DBP is greater than 100 mmHg.

Use: GTN + beta blocker +/- analgesia.

Acute left ventricular failure: hypertension increases myocardial work and exacerbates diastolic dysfunction; thus, vasodilation is the treatment of choice. It is a great misconception that immediate diuresis is necessary, as these patients are often intravascularly depleted from renin-induced natriuresis as well as catecholamine and angiotensin II-mediated vasoconstriction.

A rapid relief of symptoms may be observed with furosemide, but this is largely due to its pulmonary and systemic vasodilatory properties. Cardiac output monitoring should be employed to make accurate assessment of volemic status to determine whether the patient will benefit from fluid challenging or diuresis.

Use: Vasodilator +/- diuretic +/- ACE inhibitor.

Aortic dissection: vasodilators that cause a reflex tachycardia will increase the rate of pressure change (dP/dt) and risk tear extension. The aim is for SBP less than 110 mmHg.

Use: Analgesia + beta-blocker with vasodilator. Avoid beta-blocker with aortic regurgitation or cardiac tamponade. Calcium channel blockers can be used to control heart rate when beta-blockade is undesirable.

Renal emergencies

Evaluation to establish the cause/effect relationship is crucial. Blood pressure should be lowered using vasodilators but in specific situations alternative drugs may be indicated. In scleroderma renal emergencies ACE inhibitors are effective in 90% of cases and can promote renal recovery.

Usually ACE inhibitor use in the acute setting is contraindicated as renal dysfunction is exacerbated, particularly in patients with hyperkalemia and uremia. Post renal transplantation, calcium channel blockers, which may reverse cyclosporine-associated renal vasoconstriction, are preferred.

Management points not to be missed

Some neurological emergencies may be masked by cardiovascular complications – for example, a patient with severe acute heart failure and left bundle branch block (LBBB) who was thought to have an acute MI may have been thrombolysed as her drowsiness was thought to be due to a low-cardiac-output state. Further history determined that the patient was well until sudden onset of severe headache and vomiting, after which she became short of breath. A CT brain scan revealed a subarachnoid hemorrhage.

Drugs and dosages

Vasodilators

Contraindications: Neurological emergencies: cerebral vasodilation and worsen edema.

Name: Nitroglycerin/glyceryl trinitrate

Action: Venodilator at low dose. At higher doses: dilator of both veins and arteries, including coronary arteries.

Indication: ACS, aortic dissection, heart failure.

IV Dose: Initial: 0.25-0.5 mcg/kg/min, Max: 8-10 mcg/kg/min.

Name: Nitroprusside

Action: Arteriolar and venous vasodilator

Indication: Most hypertensive emergencies

Contraindication: Pregnancy. Caution in ACS.

IV Dose : 0.25-10 mcg/kg/min

Other: Risk of cyanide toxicity with doses greater than 2 mcg/kg/min, prolonged infusions lasting more than 24-28 hours and in renal impairment.

Name: Hydralazine

Action: Arteriolar dilator.

Indication: Pre-eclampsia. Pregnancy.

Contraindication: Neurological emergencies.

IV Dose: 0-10 mg every 20-30 min. Max: 20 mg.

Beta-blockers

Name: Labetalol

Action: Alpha and beta adrenoceptor blockade.

Indication: Most hypertensive emergencies.

Contraindication: Acute heart failure, asthma.

IV Dose: Infusion: 0.5-2 mg/min; Bolus: 5-80 mg every 10 min.

Name: Esmolol

Action: Short-acting selective beta-1 blockade (t1/2 is 8 minutes).

Indication: ACS. Unknown beta-blocker tolerance.

Contraindication: Severe heart failure.

IV Dose: 25-50 mcg/kg/min. Loading dose 250-500 mcg/kg over 3 minutes.

Other classes of drugs

Name: Nicardipine

Action: Calcium channel blocker.

Indication: Most hypertensive emergencies.

Contraindication: Acute heart failure. Caution in ACS..

IV Dose: 5-15 mg/hr.

Name: Fenoldapam

Action: Peripheral dopamine-1 antagonist.

Indication: Most hypertensive emergencies.

Contraindication: Caution in glaucoma.

IV Dose: 0.1 mcg/kg/min.

Name: Phentolamine

Action: Alpha-adrenergic blocker.

Indication: Catecholamine excess: pheochromocytoma, cocaine.

IV Dose: 5-10 mg every 5-15 minutes.

Oral drugs

Name: Enalaprilat

Action: Short-acting ACE inhibitor.

Indication: Acute LV failure, scleroderma crisis.

Contraindication: Non-scleroderma renal failure. Caution in ACS.

Oral Dose: 1.25-5 mg every 6 hours.

Name: Diltiazem

Action: Calcium channel blocker, reduces A-V nodal conduction, causes coronary artery dilatation.

Indication: Aortic dissection.

Contraindication: Acute heart failure, ACS.

Oral Dose: 30-120 mg q6-8h. Modified-release preparation not indicated in the acute setting.

3. Diagnosis

A detailed history and examination are the first steps in establishing a diagnosis. Thereafter a list of differentials will guide the choice of investigations. All patients presenting acutely will have ‘routine’ observations and investigations performed.

Hypertension history should include previous diagnosis and duration of hypertension; medication and compliance with medication; use of over-the-counter drugs that are sympathomimetic or illicit drugs, particularly cocaine; enquire about herbal remedies. Establish the presence of chronic end-organ damage, previous hospitalization or emergency treatment.

Routine observations: GCS, BM for glucose, respiratory rate, oxygen saturations, heart rate, BP.

Routine investigations: Electrolytes, urea and creatinine, full blood count. ECG and CXR

Establishing a specific diagnosis

Blood pressure parameters should be confirmed by at least two separate readings and should be measured in both arms. A difference of more than 20 mmHg would raise the suspicion of aortic dissection. If the patient is well enough the supine and standing or supine and sitting BP measurements may help determine if the patient is intravascularly fluid depleted.

If there is doubt about the accuracy of the recordings, as with cuff/patient size incompatibility or severe arrhythmias, intra-arterial blood pressure measurement should be considered.

Salient points in the history and examination not to be missed are described below, but the points listed are by no means exhaustive.

Diagnostic approach to a patient with this problem

Neurological presentations

History: Time of onset may be crucial (e.g. for ischemic stroke thrombolysis). Speed of onset and evolution of symptoms. Presence of visual disturbance, meningismus or seizure activity.

Examination: Establish pupillary size and reflexes; ocular palsies; presence of focal deficits. Fundoscopy for papilloedema or retinal changes may help distinguish a hypertensive emergency from an urgency.

Investigations:

CT brain scan: is the initial investigation of choice in most countries and will usually demonstrate the presence of any blood. Ischemic lesions often do not show up on early imaging, and thus CT may need to be repeated at a later date. CT signs of generalized cerebral edema include loss of gray/white matter differentiation, effacement of sulci and compression of ventricles.

Localized edema is represented by the above as well as areas of low attenuation. Unilateral lesions associated with significant mass effect may cause midline shift. CT imaging cannot exclude the presence of raised intracranial pressure, but the absence of radiological signs makes it less likely. A finding of posterior leukoencephalopathy (edema of the subcortical white matter in the parieto-occipital region) is characteristic of hypertensive encephalopathy.

Other imaging: Rarely necessary in the immediate setting but may help establish definitive diagnosis.

MRI will delineate cortical lesions more accurately than CT. Diffusion-weighted imaging (DWI) can show ischemic abnormalities very early and is the gold standard in some centers. CT angiography is required to look for cerebral aneurysms or arteriovenous malformations. Future stroke protocols will incorporate CT perfusion and angiography when a patient suspected of having a stroke has a normal plain CT.

Cardiovascular presentations

History: Onset and nature of chest pain. Presence or absence of back pain is essential as many aortic dissections may mimic ACS. Anticoagulation in aortic dissection can have catastrophic consequences.

Examination: Feel peripheries to assess perfusion, look for signs of RV and LV failure. Palpate bilaterally upper limb and lower limb pulses.

Investigations: ECG should be compared with any previous records in the patient’s notes. Serial ECGs may be required to distinguish old from evolving ischemic changes. Arrhythmias and LVH may be apparent. A chest radiograph may show an enlarged cardiac profile, pulmonary edema or widened mediastinum.

Echocardiography will provide information about regional wall motion abnormalities, structural abnormalities and cardiac function. CT angiography is the gold standard for diagnosing aortic dissection, although a dissection flap may be visualized with TTE but more so with TOE.

Renal presentations

Often diagnosed after laboratory investigation results have been obtained. Other investigations include: Urinalysis (UA) to detect hematuria or proteinuria. Urine microscopy to detect small quantities of RBC not detected on UA or RBC casts. A 24-hour urine collection is required to quantify micro-albuminuria. A renal USS may be required to exclude urinary tract obstruction.

Other investigations

  • Urinary toxicology screen.

  • Urinary beta-HCG for pregnancy.

  • Urinary catecholamines for suspected pheochromocytoma.

  • CTA or Doppler USS of renal arteries or renal biopsy for suspected primary renal disease.

  • Endocrine tests may be indicated to establish etiology of hypertension.

Following stabilization of the patient, the etiology of the hypertensive crisis needs to be established to guide further management.

Table III. Causes of hypertensive emergencies

Pathophysiology

Elevations in systemic vascular resistance are responsible for arterial hypertension, but the precise pathophysiological mechanisms are incompletely understood. Three processes account for the raised systemic vascular resistance:

  • Increased concentrations of circulating catecholamines.

  • Increased activity of the sympathetic nervous system.

  • Activation of the renin-angiotensin system.

Hypertension can also occur as a result of augmented left ventricular contractility or substantial intravascular volume expansion. Blood pressure is related to cardiac output by the following equation:

Mean Arterial Pressure = Cardiac Output x Systemic Vascular Resistance

Failure of the delicate homeostatic mechanisms that control these systems precipitates the hypertensive crisis. As SVR rises, the stressed vessel wall releases humoral vasoconstrictors, initiating a perpetual cycle of endothelial damage with subsequent activation of intravascular clotting cascades, the development of obliterative vascular lesions, proliferative arteritis and ultimately fibrinoid necrosis with further release of vasoactive mediators.

If this cycle is not interrupted, the vascular injury and autoregulatory dysfunction lead to a state of relative organ ischemia.

General discussion

The latest data show that the majority of patients (83%) presenting with an hypertensive emergency will exhibit single-organ dysfunction, 14% will have two-organ involvement, while multiorgan manifestations are uncommon. Cerebrovascular manifestations predominate, followed closely by cardiovascular disorders.

Table IV. Manifestations of hypertensive emergencies in order of frequency

Central nervous system (CNS)

Cerebral blood flow is normally maintained at constant levels through a wide range of perfusion pressures, approximately between MAP 50-150 mmHg. This autoregulation is maintained by myogenic, metabolic and humoral mechanisms.

Myogenic: wall stress is preserved in accordance with LaPlace’s law, which describes the relationship between the transmural pressure difference, the vessel radius, the wall thickness and wall tension, and is summed up by the following equation: Tension= (Pressure difference x Radius) ÷ Thickness.

Metabolic: At areas of low flow, substances such as nitric oxide, hydrogen ions, carbon dioxide and adenosine will accumulate, resulting in vasodilation with subsequent washout.

In addition to this metabolic build-up, during inflammation kinins are produced that also act to relax smooth muscle. Cerebral autoregulation is disrupted by brain injury; therefore, cerebral blood flow relies more heavily on perfusion pressure.

Cerebral Blood flow = Mean Arterial Pressure – Intracranial Pressure.

Patients with longstanding hypertension have the higher cerebrovascular resistance resulting in a right shift of the flow-pressure curve in the central nervous system. They can tolerate higher MAPs before there is disruption of their autoregulatory systems, but are more prone to ischemia at lower pressures.

Cardiovascular

Acute elevations in blood pressure disrupt the balance between myocardial oxygen supply and demand. Supply depends upon coronary blood flow, oxygen content of arterial blood and the position of the oxy-hemoglobin dissociation curve. Demand is determined by afterload (systolic arterial pressure), preload (left ventricular end-diastolic pressure), myocardial contractility and heart rate.

Acute hypertension can cause acute myocardial dysfunction. In chronic hypertension, left ventricular wall hypertrophy occurs, necessitating higher filling pressures resulting in relative diastolic dysfunction. LaPlace’s law can also be applied to explain left ventricular dysfunction in dilated cardiomyopathy; the increased radius requires the ventricle to generate greater tension in order to produce the same pressure.

Both these scenarios increase myocardial work and predispose to ischemia and ventricular failure. In primary myocardial dysfunction, hypertension occurs as a result of the sympathoadrenal response to pain, anxiety, hypoxemia and increased work of breathing.

Acute aortic dissection initiates with vessel wall tearing, which results in blood flow between the inner smooth intimal layer and the tunica media. Extension of the tear depends on the rate of change of aortic pressure (dP/dt) influenced by blood pressure, myocardial stroke volume and heart rate.

Blood pressure parameters will vary depending on the extent and location of the tear, and while hypertension may be present, a significant proportion of cases may present with severe hypotension, especially in the context of aortic rupture.

Renal

Renal blood flow is also autoregulated in a manner similar to CBF. Alterations in renal blood flow affect the renin-angiotensin system, which regulates the release of potent vasoconstrictors.

Renovascular disorders can occur secondary to systemic hypertension; as a result of renal artery stenosis; and due to intrinsic renal disease such as glomerulonephritis, particularly in younger patients or less frequently in association with specific disease processes such as scleroderma.

Hypertension is common following renal transplantation; however, in the early post-transplant period it may be a manifestation of graft ischemia, rejection or immunosuppressant toxicity.

Other conditions

Pre-eclampsia

Pre-eclampsia is a severe form of pregnancy-induced hypertension (i.e. that occurring after 20 weeks’ gestation) associated with multiple organ dysfunction. It is a common complication, occurring in 7% of pregnancies, and is the second most common cause of maternal mortality after thromboembolic disease.

Diagnostic features are high blood pressure (SBP > 160 and DBP > 110) and proteinuria greater than 5 g in 24 hours. Severe peripheral edema occurs but as edema is very common in pregnancy it is no longer used as a disease hallmark.

Oliguria fewer than 500 mls in 24 hours and thrombocytopenia (platelets < 100,000) are common. Other features are headaches, visual disturbances, hyper-reflexia, clonus, and seizures (eclampsia); pulmonary edema; epigastric or hypochondrial pain and HELLP (hemolysis, elevated liver enzymes and low platelets) may occur.

Pre-eclampsia is an ischemic condition that can affect any organ; however, the precise etiology remains unclear. Pathophysiological changes include:

Uteroplacental inadequacy: the normal vasodilatation of the placental vessels after the third trimester does not occur. Instead, vasoconstrictors are released to ensure placental perfusion; these vasoactive drugs have been identified in the placental and amniotic fluid as well as the blood. The vessels may become atherosclerotic.

Primary endothelial damage: results in increased production of thromboxane A2 and decreased prostacyclin, leading to further vasoconstriction.

Ischemic damage: increased platelet turnover and deposition of microvascular thrombin can lead to disseminated intravascular coagulation. Fibrinoid ischemic necrosis occurs in the placenta, cerebral, hepatic and renal vascular beds, causing multiple organ failure.

Immune complexes: occur due to inadequate maternal antibody response to the antigenic fetus.

Treatment: Magnesium sulfate infusion is the initial treatment of choice and is continued for 72 hours. Magnesium levels may be monitored in the laboratory, with the targets being 2-4 mmol/l; nevertheless, clinical monitoring of power and reflexes for signs of toxicity is essential.

Labetalol and hydralazine are second-line agents. Delivery of the fetus is the only cure and will be undertaken in severe life-threatening cases regardless of gestation.

Pheochromocytoma

Pheochromocytomas are benign neuroendocrine tumors that arise from chromaffin cells, 90% of which occur within the adrenal glands. Excess catecholamine release causes high blood pressure with periodic attacks of severe hypertension, tachycardia and diaphoresis that can last minutes or days.

Treatment is surgical excision; however, perioperative control of blood pressure is crucial, as both the surgical incision and handling of the tumor can result in a hypertensive crisis. The preferred agent is phentolamine, a potent alpha-adrenergic antagonist, with or without beta-adrenergic blockade. Labetalol is safe; however, beta-blockade without alpha-blockade is absolutely contraindicated.

Perioperative hypertension

Preoperative hypertension is often due to anxiety, and it is important to allow the patient some time to relax before a second measurement is obtained. Such acute elevations can be successfully treated with anxiolytic medication such as temazepam.

Preoperative hypertension is associated with significant cardiovascular morbidity; therefore, in patients with persistently elevated blood pressure, current recommendations are to postpone elective surgery if SBP is greater than 180 or DBP is greater than 110 mmHg and refer the patient for blood pressure management.

Postoperative hypertension may be due to pain, nausea, anxiety, hypoxemia, hypercarbia or hypervolemia. These reversible causes should be considered and treated before pharmacological agents are used.

Epidemiology

The World Health Organisation (WHO) has listed high blood pressure as the first cause of death worldwide.

The incidence of chronic hypertension among adults in the developed world is approximately 30% and has been increasing over the past three decades in North America, probably because of the strong association with obesity, whereas it has remained stable in England since 2003.

In all other aspects, statistics from both the USA and the UK largely concur, but the precise figures depend on the definition of hypertension, the values of which are lower in the USA. The prevalence of hypertension is up to 4% higher in men than in women, particularly in the younger and middle-aged groups. Westerners of African or Caribbean descent have 1.5-2.0 times greater risk of developing hypertension than Caucasians.

Universally blood pressure increases with age; it is more pronounced in females and it rises most rapidly over the age of 60. Systolic hypertension is more prevalent in the elderly and has a greater association with cardiovascular disease than diastolic hypertension.

It is well recognized that the monitored treatment of hypertension reduces the risk of subsequent complications. In people over 60, treatment reduced the risk of myocardial infarction, stroke and all-cause mortality if only the systolic value or both systolic and diastolic values were targeted. In those over 80, treatment did not reduce the risk of death but reduced stroke.

Estimates suggest that between 1% and 5% of hypertensive people will develop a hypertensive crisis. There are no data to prove that treating chronic hypertension prevents hypertensive crises, but this would be a reasonable extrapolation since over 90% of patients presenting with a hypertensive emergency have had a previous diagnosis of hypertension.

The prevalence of hypertensive emergencies is reflected by the prevalence of chronic hypertension in the community; therefore, hypertensive emergencies are more common in the elderly, in males and in those of Afro-Caribbean origin.

What's the evidence?

“The task force for the Management ofArterial Hypertension of the European Society of Hypertension (ESH) andof the European Society of Hypertension. 2007 Guidelines for the Management of Arterial Hypertension”. European Heart Journal. vol. 28. 2007. pp. 1462-536.

Aram, V. Chobanian, George, L. Bakris, Henry, R. Black. “The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure: The JNC7 Report”. JAMA. vol. 289. 2003. pp. 2560-72.

Fink, MP, Abraham, E, Vincent, JL, Kochanek, PM. Textbook of Critical Care. 2005. pp. 21-26.

Vaughan, CJ, Delanty, N. “Hypertensive Emergencies”. Lancet.. vol. 256. 2000. pp. 411-7.

Flanigan, JS, Vitburg, D. “Hypertensive Emergencies and Severe Hypertension: What to Treat, Who to Treat and How to Treat”. Med Clin North Am.. vol. 90. 2006. pp. 439-51.

Panioli, AM. “Hypertension Management in Neurological Emergencies”. Ann Emerg Med. vol. 51. March 2008. pp. S24-7.

Anderson, CS, Huang, Y, Wang, JG. “Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial”. Lancet Neurol. vol. 7. May 2008. pp. 391-9.

Marik, PE, Varon, J. “Hypertensive crises: challenges and management”. Chest. vol. 131. 2007. pp. 1949-62.

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Malignant Hypertension

Continuing Education Activity

Malignant hypertension is a term that has been used to describe patients with elevated blood pressure (BP) and multiple complications with poor prognoses. Today, the term hypertensive crisis is used to describe patients who present with severe BP elevations as follows: Systolic blood pressure and (SBP) greater than 180 mm Hg and Diastolic blood pressure (DBP) greater than 120 mm Hg). The diagnosis can be further classified as a hypertensive emergency when severe elevation in BP is associated with end-organ damage or hypertensive urgency when severe hypertension occurs without it. This activity reviews the cause of malignant hypertension, its pathophysiology and highlights the role of the interprofessional team in its management.

Objectives:

  • Outline the causes of malignant hypertension.

  • Describe the presentation of a patient with malignant hypertension.

  • Summarize the treatment of malignant hypertension.

  • Review the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by malignant hypertension.

Access free multiple choice questions on this topic.

Introduction

Malignant hypertension is a term that has been used to describe patients with elevated blood pressure (BP) and multiple complications (End organ damage) with a poor prognosis. Today, the term hypertensive crisis is used to describe patients who present with severe BP elevations as follow:

  • Systolic blood pressure (SBP) greater than 180 mm Hg 

  • Diastolic blood pressure (DBP) greater than 120 mm Hg) 

The diagnosis can be further classified as a hypertensive emergency when severe elevation in BP is associated with end-organ damage or hypertensive urgency when severe hypertension occurs without it. Prompt treatment of BP can prevent a hypertensive emergency and, consequently, serious life-threatening complications.[1][2][3][4]

To make a diagnosis of malignant hypertension, papilledema has to be present. In malignant hypertension, the key is to lower the blood pressure within a few hours.

Etiology

There are multiple causes of malignant hypertension (hypertensive crisis), including the following:

  • Medication noncompliance

  • Renovascular diseases, such as renal artery stenosis, polyarteritis nodosa, and Takayasu arteritis

  • Renal parenchymal disease including glomerulonephritis, tubulointerstitial nephritis, systemic sclerosis, hemolytic-uremic syndrome, systemic lupus erythematosus

  • Endocrine dysfunction, such as pheochromocytoma, Cushing disease, primary hyperaldosteronism, renin-secreting tumor

  • Coarctation of aorta; drugs or other exposures, including cocaine, phencyclidine, sympathomimetics, erythropoietin, cyclosporine

  • Antihypertensive medication withdrawal

  • Amphetamines

  • Central nervous system disorders, such as head injury, cerebral infarction, and cerebral hemorrhage

Epidemiology

Hypertensive emergencies are unusual, with a projected incidence of 1 to 2 cases per million per year. However, a recent investigation showed that the estimated number of visits due to this condition and the rate per million per adult emergency department (ED) visits have more than doubled from 2006 to 2013. Few examples include eclampsia (2%), cerebral infarction (39%), and acute pulmonary edema (25%).

Pathophysiology

Hypertensive emergencies occur when a relatively rapid elevation of BP develops in a short period. An increase in systemic vascular resistance by increasing vasoconstriction mechanisms through renin-angiotensin activation, pressure natriuresis, hypoperfusion, and ischemia are the most common culprits of end-organ damage. The classic vascular feature is fibrinoid necrosis of the small vessels. In addition, red cell destruction is common as they pass through these obstructed vessels leading to microangiopathic hemolytic anemia. Another feature of a hypertensive emergency is the loss of autoregulation in the brain, which can present as hypertensive encephalopathy.

History and Physical

Most patients have persistently elevated BP for years before presenting with the hypertensive emergency. Initial questioning should focus on finding indicators related to end-organ damage, including headaches, nausea or vomiting, visual disturbances, chest or back pain, dyspnea, orthopnea, or visual disturbances. Review all prescription and nonprescription medications, adherence, and time from the last dose. Ask about recreational drug use, such as amphetamines, cocaine, phencyclidine.

On physical exam, confirm BP on both arms using an appropriately-sized blood pressure cuff. Funduscopic exam findings may include hemorrhages, exudates, or papilledema. Assess for murmurs and gallops or other signs of heart failure. Look for evidence of pulmonary edema, abdominal bruits. Neurological findings can include stupor, seizures, delirium, agitation.[5][6][7]

Evaluation

The history and physical examination are really important in patients presenting with a very elevated BP or an acute rise over a previously normal baseline, even if the presenting BP is less than 180/120 mm Hg. Furthermore, the following evaluation should be performed to find the presence of end-organ damage in association with targeted clinical symptoms or signs:

  • Electrocardiography

  • Chest x-Ray

  • Urinalysis

  • Electrolytes and creatinine

  • Cardiac biomarkers, when the acute coronary syndrome is suspected

  • Toxicology screen

  • CT/MRI of the brain, when head injury, neurologic symptoms, hypertensive retinopathy, nausea, or vomiting are present

  • Contrast CT/MRI of the chest or TEE, if aortic dissection is suspected

It is often easiest to categorize hypertensive emergencies by the organ that is being damaged. The evaluation above can usually identify the at-risk target organ and direct both the target BP and the promptness with which the target is achieved.

The cardiac exam may reveal the presence of an MI, CHF, or pulmonary edema. Concentric left ventricular hypertrophy is often present, including the 4th heart sound. Always check the blood pressure in both arms to rule out aortic dissection. Patients may also have bruit in the neck and groin.

CNS exam may reveal a headache, visual changes, vomiting, confusion, and seizures. The eye exam may reveal soft exudates, flame-shaped hemorrhages, and papilledema.

The renal exam may present with oliguria, and the GI symptoms may include nausea, vomiting, and vague abdominal pain.

Treatment / Management

Adequate therapy, including the choice of the medication and the BP target, changes depending on the specific hypertensive emergency and the affected organ.[8][9][10][11]

It is not recommended to decrease the BP too fast or too much, as ischemic damage can occur in vascular territories that have become habituated with the elevated level of BP. However, for most hypertensive emergencies, mean arterial pressure (MAP) should be reduced by approximately 10 to 20% within the first hour and by another 5% to 15% over the next 24 hours. This often results in a target BP of less than 180/120 mm Hg for the first hour and less than 160/110 mm Hg for the next 24 hours, but rarely less than 130/80 mm Hg during that time frame.

Common intravenous (IV) medications and doses used to treat hypertensive emergencies include:

  • Nicardipine, initial infusion rate 5 mg per hour, increasing by 2.5 mg per hour every 5 minutes to a maximum of 15 mg per hour

  • Sodium nitroprusside, 0.3 to 0.5 mcg/kg/minute, increases by 0.5 mcg/kg per minute every few minutes as needed to a maximum dose of 10 mcg/kg per minute.

  • Labetalol 10 to 20 mg IV followed by bolus doses of 20 to 80 mg at 10-minute intervals until a target blood pressure is reached to a maximum 300-mg cumulative dose

  • Esmolol, initial loading dose 500 mcg/kg/minute over 1 minute, then 50 to 100 mcg/kg/minute to a maximum dose of 300 mcg/kg per minute.

If there is any possibility of over or underestimating BP using frequent noninvasive cuff measurements or if the end-organ damage is life-threatening, consider arterial catheterization for precise, second-to-second measurements allowing for more careful medication titration.

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

  • Acute phase of an ischemic CVA: The BP is usually not treated unless it is greater than 185/110 mmHg in patients whose reperfusion therapy could be an option or greater than 220/120 mm Hg in patients who might not qualify for it. Consider labetalol or nicardipine infusion.

  • Acute aortic dissection: The SBP should be lowered to 120 mm Hg within 20 minutes, and a target heart rate around 60 beats per minute to reduce aortic shearing forces. Treatment usually requires a beta-blocker and a vasodilator. Options include esmolol, nicardipine, or nitroprusside.

  • An intracerebral hemorrhage: The goals of therapy are different and depend on the location and surgical approach.

  • Acute myocardial ischemia: Nitroglycerin is the drug of choice; do not use if the patient has taken phosphodiesterase inhibitors, including sildenafil or tadalafil, within the past 48 hours.

After a suitable period, often 8 to 24 hours, of BP control at a target, oral medications are usually given, and the initial intravenous therapy is tapered and discontinued.

Differential Diagnosis

  • Acute kidney injury

  • Aortic coarctation

  • Aortic dissection

  • Chronic kidney disease

  • Eclampsia

  • Hypercalcemia

  • Hyperthyroidism

  • Pheochromocytoma

  • Renal artery stenosis

  • Subarachnoid hemorrhage

Staging

ACEP Guidelines for managing hypertension in the ED

  1. In asymptomatic patients with elevated BP, routine screening for end-organ damage is not recommended.

  2. In select patients (poor follow-up) screening for elevated creatinine may identify the renal injury.

  3. In asymptomatic patients with elevated BP, immediate medical intervention is not necessary.

  4. Selected patients with poor follow-up can be treated in the ED for elevated blood pressure.

  5. All patients with asymptomatic elevated BP should be referred to a cardiology outpatient clinic.

Prognosis

The prognosis of patients with malignant hypertension is guarded. Five-year survivals of 75% to 84% have been reported with treatment; without treatment, the life expectancy is less than 24 months. Most deaths are a result of heart failure, stroke, or renal failure.

Complications

Multiple complications can arise when target organs are affected, including encephalopathy, intracerebral hemorrhage, acute myocardial infarction, acute heart failure, pulmonary edema, unstable angina, dissecting aortic aneurysm, acute kidney injury, and vision loss.

Pearls and Other Issues

Most patients with severely elevated BP have no acute end-organ damage (hypertensive urgency). Nevertheless, some patients have signs and symptoms of acute, ongoing injury, which is recognized as hypertensive emergency or formerly as malignant hypertension.

It is generally not recommended to decrease the BP too quickly or too much as ischemic damage can occur in vascular territories that have become habituated with the elevated level of BP. For most hypertensive emergencies, the MAP should be reduced gradually by approximately 10 to 20% within the first hour and by a further 5% to 15% over the next 24 hours, with a final goal of approximately 25% reduction compared with baseline. 

Many patients have poorly controlled essential or secondary hypertension. Thus, long-term management turns out to be the primacy once the hypertensive crisis has been addressed.

Enhancing Healthcare Team Outcomes

The management of malignant hypertension requires an interprofessional team that includes an internist, nephrologist, cardiologist, and neurologist. Untreated, elevated blood pressure has high morbidity and mortality, including enormous healthcare costs. Therefore, the primary care providers, including the nurse practitioner, should regularly monitor blood pressure and emphasize medication compliance.

For asymptomatic patients, admission is not recommended. However, those with symptoms need to be monitored, and the specialists consulted to determine the presence of end-organ injury.

It is not recommended to decrease the BP too fast or too low, as ischemic damage can occur in vascular territories that have become habituated with the elevated level of BP. However, for the majority of hypertensive emergencies, mean arterial pressure (MAP) should be reduced by approximately 10% to 20% within the first hour and by another 5% to 15% over the next 24 hours.

All patients with hypertension should be encouraged to follow up in the outpatient clinic with a cardiology nurse. In addition, adherence to a low salt diet is beneficial. Finally, the interprofessional team members should continually encourage patients to remain compliant with their blood pressure medications and monitor their blood pressure at home.

Outcomes

The outcome for most patients with malignant hypertension in the short term is good, but in the long term, exacerbations are common. Strokes, vision loss, kidney damage, and adverse cardiac events are known to occur in a number of patients who are not compliant with therapy.[12] [Level V]

References

1.

Yong B, Power DA. Malignant Hypertension Causing a Pulmonary-Renal Syndrome. Case Rep Nephrol. 2018;2018:3273695. [PMC free article: PMC6311832] [PubMed: 30652035]

2.

Riemekasten G. [Progress in Systemic Sclerosis - Early, Targeted and Intensive Therapy is the Key to Success]. Dtsch Med Wochenschr. 2019 Feb;144(3):189-193. [PubMed: 30703839]

3.

Mir D, Ardabilygazir A, Afshariyamchlou S, Sachmechi I. Malignant Hypertension in Association with Low Estrogen Dose Oral Contraceptives: Case Report and Review of Literature. Cureus. 2018 Jul 13;10(7):e2978. [PMC free article: PMC6141051] [PubMed: 30237939]

4.

Dworakowska D, Grossman AB. Aggressive and malignant pituitary tumours: state-of-the-art. Endocr Relat Cancer. 2018 Nov 01;25(11):R559–R575. [PubMed: 30306782]

5.

Kimura N, Takekoshi K, Naruse M. Risk Stratification on Pheochromocytoma and Paraganglioma from Laboratory and Clinical Medicine. J Clin Med. 2018 Aug 27;7(9) [PMC free article: PMC6162838] [PubMed: 30150569]

6.

Manolis AA, Manolis TA, Mikhailidis DP, Manolis AS. Cardiovascular safety of oncologic agents: a double-edged sword even in the era of targeted therapies - Part 2. Expert Opin Drug Saf. 2018 Sep;17(9):893-915. [PubMed: 30126303]

7.

Zanatta E, Polito P, Favaro M, Larosa M, Marson P, Cozzi F, Doria A. Therapy of scleroderma renal crisis: State of the art. Autoimmun Rev. 2018 Sep;17(9):882-889. [PubMed: 30005860]

8.

Smith M. Refractory Intracranial Hypertension: The Role of Decompressive Craniectomy. Anesth Analg. 2017 Dec;125(6):1999-2008. [PubMed: 28806209]

9.

Brokmann JC, Rossaint R, Müller M, Fitzner C, Villa L, Beckers SK, Bergrath S. Blood pressure management and guideline adherence in hypertensive emergencies and urgencies: A comparison between telemedically supported and conventional out-of-hospital care. J Clin Hypertens (Greenwich). 2017 Jul;19(7):704-712. [PMC free article: PMC8031236] [PubMed: 28560799]

10.

Shah M, Patil S, Patel B, Arora S, Patel N, Garg L, Agrawal S, Jacobs L, Steigerwalt SP, Martinez MW. Trends in Hospitalization for Hypertensive Emergency, and Relationship of End-Organ Damage With In-Hospital Mortality. Am J Hypertens. 2017 Jul 01;30(7):700-706. [PubMed: 28430850]

11.

van der Merwe W, van der Merwe V. Malignant hypertension: a preventable emergency. N Z Med J. 2013 Aug 16;126(1380):39-45. [PubMed: 24126748]

12.

Liu S, Song A, Zhou X, Kong X, Li WA, Wang Y, Liu Y. Malignant pheochromocytoma with multiple vertebral metastases causing acute incomplete paralysis during pregnancy: Literature review with one case report. Medicine (Baltimore). 2017 Nov;96(44):e8535. [PMC free article: PMC5682838] [PubMed: 29095319]

Sours: https://www.ncbi.nlm.nih.gov/books/NBK507701/
Hypertensive Emergency (Common Cross-Cover Calls)

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 Table 1.

Table 1.
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

  • Renovascular disease

  • Renal infarction

  • 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:

  • Chest pain

  • Headache

  • Blurred vision

  • Weight loss

Less common presenting symptoms include:

  • Dizziness

  • Nausea

  • Dyspnea

  • Fatigue

  • Malaise

  • Epigastric pain

  • Polyuria

  • Gross hematuria

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)

  • Neurologic symptoms

  • Seizures

  • 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 (Figure 1).

Figure 1.
History

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

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 Table 2.

Table 2.
Sodium nitroprusside

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

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

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

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

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

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

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

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

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, Clonidine

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.

What particular agent should be used in the management of specific hypertensive crises?
Hypertensive encephalopathy

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.

Ischemic stroke

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.

Pre-eclampsia

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.

Pheochromocytoma

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.

Postoperative hypertension

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?

Pathological changes associated with hypertensive crisis
Vascular

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.

Renal

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.

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Hypertension definition accelerated

Hypertensive Emergencies

Accelerated hypertension is a hypertensive emergency. There is a recent increase in blood pressure to very high levels (≥180 mm Hg systolic and ≥120 mm Hg diastolic) resulting in target organ damage - usually seen as neurological (eg, encephalopathy), cardiovascular or renal damage. The term malignant hypertension used to be reserved for cases where papilloedema was present but the two terms are now often used interchangeably[1].

Where there is no evidence of target organ damage, the condition is a hypertensive 'urgency' rather than 'emergency' and treatment may be more gradual.

Finding accelerated hypertension and target organ damage in a patient demands urgent admission for assessment and treatment to lower blood pressure within hours in order to minimise further end-organ damage and reduce the risk of life-threatening events such as myocardial infarction, encephalopathy and intracerebral haemorrhage or subarachnoid haemorrhage. The National Institute for Health and Care Excellence (NICE) recommends same day referral for accelerated hypertension[1].:

  • With papilloedema and/or retinal haemorrhages; or
  • With life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury; or
  • In patients suspected of having a phaeochromocytoma (labile or postural hypotension, headache, palpitations, pallor, abdominal pain or sweating).

Epidemiology

There is a projected incidence of 1 to 2 cases per million per year, so this is not a common condition. However, a recent study of the number of visits to emergency departments with associated conditions or complications (eg, eclampsia, cerebral infarction and acute pulmonary oedema) doubled from 2006 to 2013[2].

Aetiology

Accelerated or malignant hypertension may be associated with any cause of secondary hypertension[3].

Presentation

This may be asymptomatic or may present with any of the many symptoms and/or signs of end-organ damage:

  • Headache.
  • Fits.
  • Nausea and vomiting.
  • Visual disturbance.
  • Chest pain.
  • Neurological deficit - eg, cerebrovascular event (CVE).
  • Bleeding due to disseminated intravascular coagulopathy (DIC).
  • Microangiopathic haemolytic anaemia.

Assessment[3]

The assessment and investigation of any patient thought to have accelerated hypertension should be undertaken urgently and by doctors with expertise in this field. This should include:

  • Full history - including:
    • Past medical history.
    • Full systems review.
    • Drug history including recreational drugs and over-the-counter herbal remedies.
  • Full examination - including:
    • Blood pressure measurements: lying, standing and in both arms (looking for coarctation or aortic dissection).
    • Fundoscopy - retinopathy: eg, grade III (flame haemorrhages, dot and blot haemorrhages, hard and soft exudates) to grade IV (papilloedema).
    • Cardiovascular examination: lying and standing blood pressure; look for signs of cardiac failure or pulmonary oedema, carotid or renal bruits, left ventricular heave, cardiac murmurs, third or fourth heart sounds.
    • Neurological examination.
  • Blood tests:
    • FBC ± clotting screen.
    • U&Es, creatinine.
    • Liver and TFTs.
    • Blood sugar measurement.
    • ± Cardiac enzymes and fasting blood lipids.
  • ± Ambulatory blood pressure monitoring.
  • Urine dip testing for protein and blood.
  • CXR: cardiac size, cardiac failure, etc.
  • ECG: left ventricular hypertrophy or left atrial enlargement.

Subsequent investigations may include:

  • CT/MRI scan of the head or kidneys.
  • Plasma renin activity.
  • Plasma aldosterone level.
  • 24-hour urine for vanillylmandelic acid (VMA) and metanephrine levels.
  • Auto-antibody levels - eg, antinuclear factor.

Management[1, 4]

General measures

The aim is to reduce the blood pressure over 24-48 hours. Patients usually have altered blood pressure autoregulation and if the blood pressure is reduced too fast, there may be organ hypoperfusion.

  • Initially, try to reduce the mean arterial pressure by approximately 25% over the first 24-48 hours.
  • An arterial line is helpful for continuous blood pressure monitoring.
  • There may be severe sodium and volume depletion; volume expansion with isotonic sodium chloride solution may be required.

Drugs

Initially, an intravenous (IV) route is usually used. Nitroprusside is often used as an IV drug but labetolol or nicardipine are alternatives which can be switched to oral formulations once blood pressure control is achieved. There is, however, some evidence that labetalol may produce a greater reduction in peripheral blood pressure in the immediate treatment of malignant hypertension[5].

Phentolamine is the drug of choice for a phaeochromocytoma crisis. Also available parenterally are diltiazem, verapamil and enalapril. Hydralazine is reserved for use in pregnant patients.

Prognosis[5]

Without treatment, accelerated hypertension may result in death within a year in over 90% of patients, as a result of end-organ damage - eg, myocardial infarction, CVE or renal failure. The prognosis has improved dramatically over the period of a few decades and with optimal treatment the five-year survival rate is >90%.

  • Astarita A, Covella M, Vallelonga F, et al; Hypertensive emergencies and urgencies in emergency departments: a systematic review and meta-analysis. J Hypertens. 2020 Jul38(7):1203-1210. doi: 10.1097/HJH.0000000000002372.

  • Pierin AMG, Florido CF, Santos JD; Hypertensive crisis: clinical characteristics of patients with hypertensive urgency, emergency and pseudocrisis at a public emergency department. Einstein (Sao Paulo). 2019 Aug 2917(4):eAO4685. doi: 10.31744/einstein_journal/2019AO4685.

  • Aronow WS; Treatment of hypertensive emergencies. Ann Transl Med. 2017 May5(Suppl 1):S5. doi: 10.21037/atm.2017.03.34.

  1. Hypertension in adults: diagnosis and management; NICE (August 2019)

  2. Janke AT, McNaughton CD, Brody AM, et al; Trends in the Incidence of Hypertensive Emergencies in US Emergency Departments From 2006 to 2013. J Am Heart Assoc. 2016 Dec 55(12). pii: JAHA.116.004511. doi: 10.1161/JAHA.116.004511.

  3. Naranjo M et al; Malignant Hypertension, StatPearls Publishing 2019

  4. Stanley A; Managing Hypertensive Emergencies, 2014 (downloadable pdf file).

  5. van den Bogaard B, Immink RV, Westerhof BE, et al; Central versus peripheral blood pressure in malignant hypertension effects of antihypertensive treatment. Am J Hypertens. 2013 Apr

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Accelerated Hypertension

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