Presentation of a clinical case A 58-year-old woman with known hypertension presents to the emergency department with headaches and blurred vision for the past 3 days. Her prescribed medications include amlodipine, hydrochlorothiazide, and lisinopril, but she acknowledges that her adherence is spotty and she has not taken any of those drugs for almost 3 weeks. She seems anxious but comfortable. The average sitting blood pressure, calculated from multiple measurements, is 242/134 mm Hg , and the heart rate is 68 beats/min. Fundus examination reveals arteriolar narrowing, bilateral flame hemorrhages, cottony infiltrates, and papilledema. Auscultation reveals a fourth heart sound. The rest of the exam is normal. The electrocardiogram shows left ventricular hypertrophy. Other laboratory tests and chest x-rays are normal. Emergency brain computed tomography (CT) shows heterogeneous attenuation of subcortical white matter in both posterior parieto-occipital regions, but without hemorrhage or infarction. How would you evaluate and treat this patient? |
| clinical problem |
Elevations in blood pressure above 180/110-120 mm Hg can cause acute injury to the heart, brain, and microvasculature. If there is target organ damage caused by acute hypertension, the condition is labeled a "hypertensive emergency" and requires immediate and aggressive treatment to limit the progression of the lesions.
In the absence of acute target organ damage there is no very defined terminology and management, and the author calls it "hypertensive emergency" ; This condition is 2-3 times more common than hypertensive emergency. Acute severe hypertension, sometimes with acute target organ damage, may also manifest perioperatively .
Both the absolute level reached by blood pressure and the rate of its rise determine the risk of target organ damage caused by acute hypertension.
Many patients with chronic hypertension have severe elevations in blood pressure for months or years without apparent effects, while more moderate sudden increases (e.g., 160/100 mm Hg in a previously normotensive patient) can cause serious injury, particularly in cerebral vessels (as occurs in eclampsia, pheochromocytoma, acute drug-induced hypertension or acute glomerulonephritis).
In the US, severe acute hypertension accounts for an estimated 4.6% of all emergency department visits and is a common reason for hospitalizations. It is more common in people >60 years old, black, uninsured, underinsured, or living in low-income areas.
US claims-based data indicate that hospitalizations for hypertensive emergencies have increased steadily over the past 20 years, but over time, in-hospital mortality has improved and currently ranges between 0.2% and 11%. Even in the absence of acute target organ damage, episodes of severe hypertension have long-term consequences .
In a study of 2,435 patients with a previous transient ischemic attack and an isolated systolic blood pressure >180 mm Hg (without symptoms) they showed an increased risk of stroke during the 3 years of follow-up, by a factor of 5, compared to those who did not have episodes of systolic blood pressure >140 mm Hg, regardless of usual blood pressures.
Similarly, a prospective cohort study showed that patients who had been hospitalized for a hypertensive emergency had a 50% higher risk of fatal and nonfatal cardiovascular events than controls, despite having similar blood pressure levels during follow-up.
In contrast to these long-term consequences, hypertensive emergencies do not appear to be associated with short-term adverse outcomes.
Although hospitalization rates are relatively high (up to 11% within 30 days of initial presentation), studies did not show increased risks of adverse outcomes days to several months after discharge from either the office or emergency department. .
A recent analysis of 58,535 doctor’s office visits of patients who had systolic blood pressure ≥180 mm Hg, diastolic blood pressure ≥110 mm Hg, or both (average, 182.5/96.4 mm Hg) showed a similar incidence of events cardiovascular in 6 months (0.9%) both hospitalized patients and prone patients who were discharged after the visit.
| Strategies and evidence |
A structured approach to the management of severe acute hypertension involves having key elements include accurate blood pressure measurement; careful evaluation of potential precipitants, symptoms, and evidence of end-organ damage, as well as therapeutic decisions based on the presence of symptoms or acute end-organ damage.
> Blood pressure measurement
Blood pressure should be measured in both arms and the thigh , using appropriate technique and validated devices. Most hospitals use automated devices that rely on oscillometric measurements.
Two large registry studies comparing oscillometric with intra-arterial measurements in critical care or surgical patients showed that oscillometric devices consistently underestimate blood pressure levels by up to 50-30 mm Hg, when recorded intra-arterial levels are >180/100 mmHg.
Auscultatory measurements using aneroid or mercury devices also have substantial discordance with intra-arterial measurements, in the high blood pressure ranges, even when meticulous technique is applied.
Due to the possible underestimation of the severity of hypertension, if there is evidence of damage to target organs and intravenous agents are required, the use of oscillometric (and auscultatory) devices is not recommended and the placement of an arterial catheter should be indicated.
Typically, in the absence of target organ damage, noninvasive oscillometric or auscultatory devices are used to guide treatment, despite their limitations.
> Determination of precipitating factors
Most patients who present with severe acute hypertension are already known hypertensive and have received treatment.
The most common precipitating factor is non-compliance with prescribed antihypertensive medications. In a large database, three-quarters of outpatients who were evaluated for a systolic pressure ≥180 mm Hg or a diastolic pressure ≥110 mm Hg already had a diagnosis of hypertension, and more than half had already been prescribed ≥2 antihypertensive agents .
In a prospective study of patients with hypertension, the most important predictor of a hypertensive crisis was lack of adherence to medication. These data underscore the importance of interventions that improve treatment adherence (e.g., use of blood pressure self-monitoring, opportunities for social support, and partnerships with health coaches, nurses, or pharmacists), although studies are still lacking to demonstrate that these interventions reduce the risk of severe acute hypertension.
Other common precipitating factors are excess sodium in the diet; the use of over-the-counter medications or illicit drugs (e.g., cocaine, amphetamines, sympathomimetic agents, nonsteroidal anti-inflammatory drugs, and high-dose glucocorticoids).
Anxiety or panic and acute stroke or heart failure can be both a cause and consequence of severe hypertension.
Patients with acute glomerulonephritis, preeclampsia, pheochromocytoma, or scleroderma may present with renal crisis with severe acute hypertension.
Among hospitalized patients, mobilization of intravenous infusion fluids, discontinuation of antihypertensive medications, pain, and urinary retention are considered common precipitants.
In patients who present without a clear precipitating factor or who meet criteria for refractory hypertension during follow-up, additional testing should be performed to investigate secondary causes of hypertension, such as renovascular disease, primary aldosteronism, excess glucocorticoids, pheochromocytoma and, in younger patients, coarctation of the aorta.
| Assessment of acute target organ damage |
Given the suspected diagnosis of acute damage to target organs, including lesions of the brain, heart and great vessels (aorta in particular), kidneys and microvasculature (including the retina), an important part of the initial evaluation is the evaluation of symptoms and signs and tests.
Diffuse microvascular injury ( also known as "malignant hypertension" ) manifests as severe retinopathy, acute kidney injury or microangiopathic hemolytic anemia, and thrombocytopenia. These characteristics can occur together or in isolation. In the absence of symptoms to guide evaluation, there is little data on the performance of diagnostic tests.
In a prospective study of 167 patients seen in the emergency department for triage diastolic blood pressure ≥100 mm Hg, routine metabolic panels revealed acute kidney injury requiring hospitalization in 7% of patients.
In retrospective studies, the results of most diagnostic tests obtained from patients without evidence of acute end-organ damage have been normal or simply reflected prolonged exposure to hypertension.
Still, it is common practice to obtain a basic metabolic panel to evaluate kidney function and electrolyte levels, a complete blood count to detect microangiopathy, a urinalysis to identify proteinuria or hematuria, and an electrocardiogram and troponin levels to rule out injury. asymptomatic myocardial
Patients without target organ damage are usually asymptomatic. Symptoms, when present, may include headache, atypical chest pain, dyspnea, dizziness, lightheadedness, and epistaxis.
| Treatment |
> Autoregulation of cerebral blood flow
Autoregulation of organ blood flow refers to physiological adaptations that allow organ perfusion to remain relatively constant across a wide range of blood pressure. In the context of severe acute hypertension, the most important thing is flow autoregulation ; This autoregulation is best studied in the brain, although the principles are applicable to most end organs.
In chronic severe hypertension , cerebral blood flow remains at levels similar to normal but its autoregulatory curve shifts to the right. This change allows patients to tolerate higher blood pressure levels without suffering cerebral edema, but confers a predisposition to hypoperfusion of the brain at substantially higher blood pressure levels than in normotensive individuals, although these curves are not consistent or predictable at all. individual level.
Limited data suggest that treatment of severe hypertension for several months may improve autoregulation moderately, while patients with mild to moderate hypertension (<180/110 mm Hg) recover autoregulatory responses a few weeks after the start of a treatment. effective therapy.
| Treatment of choice |
There are relatively few trials comparing different agents for hypertensive emergencies and urgencies. Treatment is, to a large extent, determined by an understanding of the pathophysiologic characteristics, the presence and type of target organ injury, the availability and costs of medications, and the physician’s experience with these agents. There is considerable variability in practice regarding the choice of medications.
> Hypertensive emergencies
All patients should be admitted to intensive care units and treated with intravenous antihypertensives, depending on the clinical scenario.
In the US, the most common drugs used are labetalol, nitroglycerin, icardipine, hydralazine, and nitroprusside . Of these medications, hydralazine has unpredictable effects, often leads to excessive lowering of blood pressure, and should generally be avoided as a first choice.
Comparative studies showed that nicardipine achieved blood pressure control faster with less variability in blood pressure (allowing blood pressure to remain closer to target) than labetalol, but there were no significant differences in adverse events or mortality.
A trial comparing clevidipine with nicardipine showed that clevidipine was associated with less variability than nicardipine. In the absence of studies comparing different rates of blood pressure reduction, management is based on the principles of self-regulation and guideline recommendations, which seek to achieve blood pressure reduction by no more than 20 to 25% during first hour, and then at 160/100-110 mm Hg for the next 2 to 6 hours .
Excessive reduction in blood pressure (systolic blood pressure <100-120 mm Hg) may occur in up to 10% of patients, and is associated with increased risk of death . If excessive blood pressure reduction occurs, intravenous drugs should be discontinued immediately , and in some cases, temporary use of vasopressors, intravenous fluids, or both is indicated.
Resumption or initiation of long-acting antihypertensive medications should be done concurrently with intravenous therapy to provide a smoother transition, shorten the need for intravenous and intensive care medications, and minimize the risk of rebound hypertension, which is also associated with with higher mortality.
The appropriate time to start or restart oral medications is uncertain. Because the risk of hypotension is greatest in the first 6 hours of intravenous therapy, a reasonable approach is to begin oral agents 6 to 12 hours after starting intravenous therapy.
Long-acting drugs are chosen according to standard guidelines for the management of chronic hypertension. Consensus recommendations are based on very limited data, while in some cases, when comparing the guidelines, it is found that they are not uniform.
| Hypertensive emergencies |
Most patients without acute target organ damage can be cared for on an outpatient basis.
Treatment with long-acting medications consistent with the guidelines should be initiated, reinstated, or adjusted, and initial stabilization follow-up scheduled. Experience indicates that most patients can tolerate normalization of blood pressure within 48 to 72 hours. , although some require longer periods due to dizziness, fatigue or mental slowness.
The recommended rate and intensity of blood pressure reduction varies depending on the presence of certain conditions, particularly aortic dissection, eclampsia, pheochromocytoma attacks, and intracerebral hemorrhage, requiring more aggressive approaches to limit the occurrence of injury. .
Ischemic stroke requires conservative management to avoid peri-infarct hypoperfusion and worse outcomes. between 1 and 7 days.
In a study of more than 500 patients presenting to the emergency department with severe hypertension, the blood pressure of almost one-third of the patients fell to less than 180/110 mm Hg ( before administration of the drug) after 30 minutes to remain silent and rest. If rest or control of anxiety or other precipitating factors is not achieved under these conditions, an oral antihypertensive agent may be indicated. In this context, intravenous medications are not indicated .
For patients with symptoms that appear to be related to hypertension but are not indicative of end-organ damage (e.g., headache, atypical chest pain, or epistaxis), it is reasonable to choose an oral agent with a more rapid onset of action, such as clonidine (0.1 to 0.3 mg), labetalol (200 to 400 mg), captopril (25 to 50 mg), prazosin (5 to 10 mg), or topical 2% nitroglycerin ointment (2.5 to 5cm).
The use of oral or sublingual nifedipine should be avoided due to the unpredictability of blood pressure reduction, possibly as a result of cardiovascular events.
Medications can be administered every 30 minutes until the target blood pressure is reached. A systematic review of comparative trials and cohort studies showed similar acute blood pressure reductions with different agents.
Clinical experience and descriptions of the acute effects of clonidine and labetalol suggest that they may be associated with less abrupt changes in blood pressure than other agents. Patients are usually discharged once symptoms have improved, which often coincides with a decrease in blood pressure ≤160-180/100-110 mm Hg.
| Areas of uncertainty |
Large randomized trials are lacking to identify the most effective treatment for hypertensive urgencies and emergencies in general, and for specific cases of underlying conditions. For treatment-naïve patients presenting to the emergency department, it has not yet been established whether or not antihypertensive medication should be prescribed upon discharge.
Currently, the American College of Emergency Physicians recommends initiating therapy in the emergency department only for those selected patients who are likely to have poor follow-up and recommends referral, while the remainder are discharged without initiating treatment. Although there is reasonable concern about inappropriate treatment of normotensive patients, failure to treat may represent a missed opportunity to minimize risks.
| Guides |
Recommendations for the management of severe acute hypertension are based on the main European and US guidelines. There are variations in the terminology and specific thresholds of arterial hypertension, but to define hypertensive urgencies and emergencies, they all recognize that the threshold critical is 180/110-120 mm Hg.
Regarding the management of hypertensive emergencies, there is general agreement on the rate of blood pressure reduction and the need to use intravenous drugs, with the patient admitted to an intensive care room.
| Conclusions and recommendations |
- The patient described in the vignette has severe acute hypertension complicated by posterior encephalopathy syndrome . This hypertensive emergency was precipitated by lack of adherence to antihypertensive treatment.
- The patient should be admitted to the intensive care unit and immediately begin treatment with continuous intravenous antihypertensive medication, with invasive monitoring of intra-arterial blood pressure. In this context, the agents of choice are nicardipine (or clevidipine) and labetalol.
- Given his relative bradycardia , the choice would be nicardipine. Although data are lacking to guide the appropriate rate of blood pressure reduction, it would be advisable to lower blood pressure by 20-25% in the first hour, with the plan to reach a blood pressure of approximately 160/100 mm Hg by 6 hours.
- At this point, if the patient has a good response and does not develop relative hypotension, amlodipine and lisinopril can be restarted, because stepwise additions may reduce the risk of excessive blood pressure reduction.
- The diuretic can also be restarted the next day. if necessary. After 18 to 36 hours, nicardipine would be discontinued, although under close monitoring of blood pressure.
- The patient can be discharged once her symptoms improve and hypertension remains controlled for at least 24 hours without intravenous treatment.
- You will be scheduled in the office for 1 week later.
- The author would not perform studies to evaluate the presence of secondary hypertension unless blood pressure remains uncontrolled during follow-up.
