A 45-year-old man with a 2-month history of progressive headache presented to the emergency department with nausea, vomiting, visual disturbance, and confusion for 1 day. He denied fever, weakness, numbness, shortness of breath, and flulike symptoms. He had significant medical history of hypertension and was on a β-blocker in the past, but a year ago, he stopped taking medication due to an unspecified reason. The patient denied any history of tobacco smoking, alcoholism, and recreational drug use. The patient had a significant family history of hypertension in both his father and mother. Physical examination was unremarkable, and at the time of triage, his blood pressure (BP) was noted as 195/123 mm Hg, equal in both arms. The patient was promptly started on intravenous labetalol with the goal to reduce BP by 15% to 20% in the first hour. The BP was rechecked after an hour of starting labetalol and was 165/100 mm Hg. MRI of the brain was performed in the emergency department and demonstrated multiple scattered areas of increased signal intensity on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images in both the occipital and posterior parietal lobes. There were also similar lesions in both hemispheres of the cerebellum (especially the cerebellar white matter on the left) as well as in the medulla oblongata. The lesions were not associated with mass effect, and after contrast administration, there was no evidence of abnormal enhancement. In the emergency department, his BP decreased to 160/95 mm Hg, and he was transitioned from drip to oral medications and transferred to the telemetry floor. How would you manage this case?
The patient initially presented with headache, nausea, vomiting, blurred vision, and confusion. The patient’s BP was found to be 195/123 mm Hg, and MRI of the brain demonstrated scattered lesions with increased intensity in the occipital and posterior parietal lobes, as well as in cerebellum and medulla oblongata. The clinical presentation, elevated BP, and brain MRI findings were suggestive of hypertensive emergency, more specifically hypertensive encephalopathy. These MRI changes can be seen particularly in posterior reversible encephalopathy syndrome (PRES), a sequela of hypertensive encephalopathy. BP was initially controlled by labetalol, and after satisfactory control of BP, the patient was switched to oral antihypertensive medications.
Hypertensive emergency refers to the elevation of systolic BP >180 mm Hg and/or diastolic BP >120 mm Hg that is associated with end-organ damage; however, in some conditions such as pregnancy, more modest BP elevation can constitute an emergency. An equal degree of hypertension but without end-organ damage constitutes a hypertensive urgency, the treatment of which requires gradual BP reduction over several hours. Patients with hypertensive emergency require rapid, tightly controlled reductions in BP that avoid overcorrection. Management typically occurs in an intensive care setting with continuous arterial BP monitoring and continuous infusion of antihypertensive agents.
An expedited evaluation for the cause of hypertension as well as assessment for the presence of end-organ failure, including encephalopathy, focal neurologic deficits (including vision changes), myocardial ischemia, heart failure, and acute kidney injury, should be performed. Diagnostic studies should be driven by clinical suspicion.
Optimal therapy, including the choice of agent and the BP goal, varies according to the specific hypertensive emergency. It is generally unwise to lower the BP too quickly or too much because ischemic damage can occur in vascular beds that have become habituated with the higher level of BP (ie, autoregulation). For most hypertensive emergencies, mean arterial pressure should be reduced gradually by approximately 10% to 20% in the first hour and by a further 5% to 15% over the next 23 hours. This often results in a target BP of <180/<120 mm Hg for the first hour and <160/<110 mm Hg for the next 23 hours (but rarely <130/<80 mm Hg during that time frame).
The major exceptions to gradual BP lowering over the first day are as follows:
The acute phase of an ischemic stroke: The BP is usually not lowered unless it is ≥185/110 mm Hg in patients who are candidates for reperfusion therapy or ≥220/120 mm Hg in patients who are not candidates for reperfusion (thrombolytic) therapy.
Acute aortic dissection: The systolic BP should be rapidly lowered to a target of 100 to 120 mm Hg (to be attained in 20 minutes) to reduce aortic shearing forces.
Intracerebral hemorrhage: Goals of antihypertensive therapy in such patients are variable and are discussed elsewhere.
After a suitable period (often 8 to 24 hours) of BP control at target in the intensive care unit, oral medications are usually given, and the initial intravenous therapy is tapered and discontinued.
Key Points
Hypertensive encephalopathy or PRES presents with nausea, vomiting, blurry vision, and headache.
MRI features of scattered changes in the occipital area are characteristic of PRES.
Gradual control of BP is the cornerstone of management.
A 55-year-old man was brought to the emergency department after he developed sudden onset of shortness of breath for 1 day associated with difficulty in sleeping and even speaking full sentences. He had 2 prior hospitalizations with the same complaint during which he was noted to have a hypertensive emergency that was treated with antihypertensive medications. He denied fever, flulike symptoms, chest pain, and vomiting. His medications included lisinopril, amlodipine, and furosemide. He stated that he is adherent on medications. He had a significant medical history of poorly controlled chronic hypertension. He did not know his family history. Social history was significant for current cigarette smoking of 1 pack per day for the past 30 years. In the emergency department, the initial blood pressure reading was 230/150 mm Hg with room air oxygen saturation of 92%. The patient was found to be in mild distress. Complete physical examination showed bilateral rales in all lung fields with audible S4 heart sound. The rest of the physical examination was unremarkable. ECG showed left ventricular hypertrophy, and chest x-ray showed diffuse interstitial pattern infiltrates suggestive of pulmonary edema. Laboratory data showed elevated creatinine, troponin, and pro-B-type natriuretic peptide (pro-BNP). He was started on nasal oxygen inhalation, and 1 intravenous dose of furosemide was administered. He started feeling significant improvement, and the BP decreased to 170/110 mm Hg. He was transferred to the telemetry floor for further management. How would you manage this case?
This patient presented with flash pulmonary edema in the setting of hypertensive emergency. The typical presentation, the examination findings, and improvement with diuretic are characteristic for renovascular hypertension. Another important aspect in this case is the recurrent hospitalizations with similar complaints, especially after initiation of an angiotensin-converting enzyme inhibitor (ACEI), and this patient should be evaluated for renal artery stenosis. Elevated troponin and pro-BNP are suggestive of fluid overload status.
Kidney disease can be a complication of hypertension, which can lead to organ damage. The presence of renovascular disease cannot predict renovascular hypertension (ie, renal artery stenosis). Renovascular hypertension is identified by acute kidney injury as a result of renal hypoperfusion, leading to a renin-angiotensin surge that ultimately causes vasoconstriction and hypertension. Renin/aldosterone levels will be high in renal artery stenosis, but with bilateral involvement, they can be normal or low, causing volume-dependent hypertension. The most common cause of renal artery stenosis is atherosclerosis. Fibromuscular dysplasia is a rare cause and usually suspected in young woman.
Recurrent flash pulmonary edema with creatinine elevation even with controlled blood pressure is the most common presenting feature. The symptoms can be worsened by the recent initiation of an ACEI. Renal bruit is an insensitive examination finding that can be observed in a few cases.
Duplex ultrasound can be an initial screening test, with the gold standard diagnostic tests being CT or magnetic resonance angiography. Use of contrast is generally avoided unless surgical intervention is planned. Renin/aldosterone levels do not aid in diagnosis.
Treatment strategy includes aggressive cardiovascular risk factor modification. Percutaneous intervention with angioplasty and stenting can be considered in select patients with recurrent flash pulmonary edema, bilateral renal artery stenosis, or fibromuscular dysplasia. The clinical studies have not shown any benefit of intervention over medical therapy. Blood pressure control should be optimized in these patients.
Key Points
Recurrent flash pulmonary edema is the initial presentation of renovascular hypertension, along with creatinine elevation especially after initiation of ACEI.
Duplex ultrasound is the initial screening test for the diagnosis.
Treatment includes management of blood pressure and other cardiovascular risk factors.
A 52-year-old woman was brought to the emergency department after being found walking in the middle of a freeway on a ramp. She was given intramuscular haloperidol by emergency medical personnel for agitation on the way to the hospital. Her medical history was notable for polysubstance use. On physical examination in the emergency department, she was alert and restless. Vitals were noted as temperature of 38.2°C (100.8°F), blood pressure of 210/124 mm Hg, pulse rate of 124 bpm, respiration rate of 14 breaths/min, and oxygen saturation of 97% breathing ambient air. Her pupils were symmetric, dilated, and reactive to light. Slight tremor of the hands was noted. No tongue fasciculations were observed. The skin was warm and diaphoretic. The chest was clear to auscultation. The patient was given intravenous benzodiazepines and started on fluids, and cultures were sent. Laboratory studies revealed a serum creatine kinase level of 6600 U/L, an increase in creatinine level from a baseline of 0.9 mg/dL to 1.4 mg/dL, and a normal troponin level. Urinary toxicology was positive for cocaine. Fractional excretion of sodium was <1%. An ECG revealed sinus tachycardia without ischemic changes. After initial control of blood pressure with diltiazem, the patient was admitted to the telemetry floor for further workup and management. How would you manage this case?
In this case, the combination of hypertension, tachycardia, fever, diaphoresis, mydriasis, and rhabdomyolysis is most consistent with sympathomimetic intoxication. Common causes of sympathomimetic intoxication include cocaine, amphetamines, ephedrine, and caffeine. In this patient, recent use of cocaine was suspected to be the reason behind the patient’s presentation because urine toxicology was positive for cocaine. Clinical presentation, history of cocaine use, physical examination findings, and urine toxicology results were suggestive of sympathomimetic intoxication caused by cocaine use. The patient was treated with gentle hydration, benzodiazepines, and antihypertensive medications.
Sympathomimetic toxicity is commonly seen in the United States, either due to overdose of over-the-counter medications (ephedrine-based cough syrup) or street drugs such as cocaine and methylamphetamines. These drugs exert psychological and physiologic toxic effects, leading to central nervous system stimulation and organ damage. The toxic effects commonly encountered on a medical floor are psychosis, seizure, acute kidney injury, coronary vasospasm, rhabdomyolysis, hypoglycemia, and hypertensive crisis.
Symptoms include tachycardia, hypertension, diaphoresis, seizure, hyperthermia, nausea, vomiting, agitation, and combativeness.
The diagnostic process includes a routine laboratory test to check thyroid function, ECG, measurement of creatine kinase levels and electrolytes, and kidney function test. Imaging of the head can be done based on neurologic findings. Urine drug screen should be performed; however, some of the newer drugs cannot be detected on routine toxicology screening. Blood cultures and other septic workup can be obtained to exclude other etiologies of fever.
Treatment strategy consists of benzodiazepines as first-line therapy for sympathomimetic intoxication. Experience in patients with cocaine-induced hypertension suggests use of β-blockers can paradoxically worsen hypertension due to loss of β-mediated vascular smooth muscle relaxation. Given these concerns with cocaine, it is reasonable to avoid β-blockers, such as propranolol, in sympathomimetic intoxication in general. Furthermore, acute kidney injury can be due to a combination of hypertensive renal crisis or dehydration and rhabdomyolysis, which would mandate hydration and rapid, tightly controlled blood pressure reduction. Another aspect of management is monitoring for arrythmia on telemetry to prevent any cardiac event in 24 to 48 hours. Patient should also be monitored for seizures.
Key Points
Sympathomimetic toxicity is commonly observed in the United States, with presenting symptoms including agitation, bizarre behavior, tremors, hypertension, and seizures.
Routine assessment of thyroid function, creatine kinase, kidney function, and electrolytes should be performed.
Benzodiazepine as the first-line treatment, control of blood pressure, and prevention of organ damage are the cornerstones of management.
A 55-year-old African American man was sent to the emergency department from the primary care physician’s clinic for markedly elevated blood pressure not controlled with clinic medications. He went to the clinic for follow-up of uncontrolled blood pressure. The blood pressure in the clinic was noted as 190/120 mm Hg and was equal in both arms. He stated that he took his medications in the morning. This was his third clinic visit with uncontrolled blood pressure. He remained asymptomatic otherwise. His only medical history was hypertension. His medications included amlodipine 10 mg, lisinopril 20 mg, and hydrochlorothiazide 25 mg. He reported no smoking, no over-the-counter medication use, and no substance abuse. Family history was significant for a brother with diabetes. He denied chest pain, shortness of breath, abdominal complaints, and urinary complaints. Physical examination was significant for severe hypertension with blood pressure of 215/125 mm Hg and heart rate of 75 bpm. Body mass index (BMI) was noted as 27 kg/m2. Otherwise, his examination was unremarkable. Initial laboratory data showed creatinine of 1.5 mg/dL (baseline 1.2 mg/dL); otherwise, no lab abnormalities of acute significance were noted. He was given 1 dose of intravenous labetalol in the emergency department, and the blood pressure came down to 160/95 mm Hg. He was transferred to the telemetry floor for further evaluation. How would you manage this case?
This case described the management of resistant hypertension. Poorly controlled blood pressure despite use of 3 medications should be evaluated for resistant hypertension. Although the patient was adherent to his medications, the blood pressure was still uncontrolled. First, measures should be taken to exclude pseudo-resistance by assuring proper technique, detailed review of the medication list and over-the-counter medications use, and assessing for white coat hypertension and lifestyle-related causes. In this case, the blood pressure was controlled with home medications in the hospital. In addition, the patient had recently started using nonsteroidal anti-inflammatory drugs, for the headache, which could a cause of his poorly controlled blood pressure.
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