IM Board Review

A 61-year-old man with fluctuating hypertension

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A 61-year-old man with type 2 diabetes mellitus on glimepiride therapy presented with somnolence and slurred speech. His capillary glucose level was 17 mg/dL and his serum glucose level was 28 mg/dL. He was treated with intravenous dextrose, and his glucose level promptly returned to normal.

He had been adherent to his medication regimen and denied overmedicating or accidental overdosing. Over the past 7 months, he had noted redness on his palms, a rash on his legs, intermittent moderate to severe headaches, weight loss, and decreased appetite. In addition, his blood pressure had been labile, which his physicians had attributed to autonomic instability. He had continued on the same dose of glimepiride despite losing weight.

His history included multivessel coronary artery disease treated with angioplasty and placement of multiple coronary stents; ischemic cardiomyopathy with a left ventricular ejection fraction of 28%; implantation of a cardioverter-defibrillator for secondary prevention of ventricular arrhythmia; an ischemic stroke; and multiple sclerosis complicated by bilateral blindness, with optic nerve involvement and autonomic instability, present for over a year and manifested by labile blood pressure. He was a long-time tobacco user. His daily medications included ticagrelor 90 mg, aspirin 81 mg, metoprolol 50 mg, ramipril 10 mg, simvastatin 20 mg, glimepiride 2 mg, and esomeprazole 40 mg. He needed help taking his medications.

At the time of hospital admission, his heart rate was 69 beats per minute with a regular rhythm, blood pressure 115/73 mm Hg, respiratory rate 11 breaths per minute with an oxygen saturation of 99% on room air, and oral temperature 34.7°C (94.5°F). He appeared to be in no distress.

Cardiovascular examination revealed no murmurs or gallops; there was mild nonpitting edema of the lower extremities. Pulmonary, abdominal, and neurologic examinations were unrevealing except for bilateral blindness. Vascular examination revealed no bruits. Results of a complete blood cell count and metabolic panel were normal except for a hemoglobin level of 9.9 g/dL (reference range 13.5–17.5) and a platelet count of 477 × 109/L (150–450).

Although he continued to receive the same medications he had been taking at home, his blood pressure fluctuated. On the second hospital day, it reached 186/135 mm Hg, at which time he also had palpitations, dyspnea, and crackles in the lower lobes of both lungs. Volume resuscitation on admission was suspected to have played a role, and he received furosemide, which improved his symptoms. But several hours later, his blood pressure rose again, and he became diaphoretic. Despite aggressive treatment with different antihypertensive agents, his blood pressure remained high and his symptoms persisted. Chest radiography showed no evidence of pulmonary edema. Because of his progressive dyspnea, the diagnosis of pulmonary embolism was entertained.


1. What could explain this patient’s high blood pressure?

  • A drug effect
  • Renovascular disease
  • Excess circulating catecholamines
  • Obstructive sleep apnea
  • Primary aldosteronism

Sympathomimetic drugs such as epinephrine, norepinephrine, dopamine, and vasopressin, which are used when hemodynamic support is required, can raise both systolic and diastolic blood pressure. Nonsteroidal anti-inflammatory drugs and nasal decongestants are common culprits in the community. However, our patient was using none of these drugs.

Renovascular disease is one of many causes of resistant hypertension, accounting for 8% of all cases.1,2 Despite fluctuations, the blood pressure often remains chronically elevated, its changes are less paroxysmal than in our patient, and a precipitating factor such as a dietary indiscretion is sometimes identified.1

Excess circulating catecholamines can be a result of stress, exogenous administration, or endogenous oversecretion. Our patient’s clinical presentation is highly suspicious for a high-catecholamine state, and this should be further evaluated.

Obstructive sleep apnea is common in patients with resistant hypertension, with an estimated prevalence as high as 60% in this group.3,4

Primary aldosteronism has an estimated prevalence of about 20% in patients evaluated for resistant hypertension.5


Computed tomographic angiography of the chest revealed no evidence of pulmonary emboli. There was mild dilation of the central pulmonary arteries and an incidental, incompletely imaged 4.7-by-3.4-cm mass of mixed attenuation in the right adrenal gland, with macroscopic fat within the lesion.

Figure 1. Computed tomography showed diffuse enlargement of the left adrenal gland (boxed area), but no discrete mass.

Computed tomography (CT) of the abdomen with dedicated cuts through the adrenal glands revealed a 4.7-cm heterogeneous right adrenal mass with a density of 34 Hounsfield units (HU). The left adrenal gland appeared diffusely enlarged without a discretely seen mass, consistent with hyperplasticity (Figure 1).

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