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Managing Calcium Channel Blocker‐Related Peripheral Edema

A69-year-old woman was referred to the hypertension clinic with refractory stage 2 hypertension. She had been taking a diuretic for 20 years. Mild pedal edema occurred a year previously but had gotten worse following prescription of nifedipine 2 months before the initial hypertension clinic visit. The patient denied exertional dyspnea or paroxysmal nocturnal dyspnea. She complained of dry mouth and fatigue. Past medical history included transient ischemic attacks with a normal brain computed tomography scan and echocardiogram, hemiparkinsonism with a right-sided tremor, and hypothyroidism. Both of the patient’s parents, her two brothers, and her two sisters had hypertension. Medications at the time of her first hypertension clinic visit were levothyroxine 0.075 mg q.d., pramipexole dihydrochloride 1.5 mg t.i.d., clonidine 0.3 mg t.i.d., clopidogrel 75 mg q.d., losartan 50 mg b.i.d., amantadine 100 mg b.i.d., nifedipine extended release 30 mg q.d., and furosemide 40 mg q.d. Blood pressure (BP) was 184/92 mm Hg in both arms supine and 168/94 mm Hg in the left arm standing. Creatinine was 1.2 mg/ dL (normal range 0.7–1.3 mg/dL), potassium 4.0 mEq/ L (normal range 3.5–5.0 mEq/L), thyroid-stimulating hormone 3.3 IU/mL (normal range 0.4–4.0 IU/mL), and urinalysis was negative for protein. Twenty-fourhour urine collections for vanilmandelic acid, catecholamine, and metanephrine were normal. Initial hypertension clinic plans were to switch the furosemide to chlorthalidone 25 mg q.d. and to wean her from clonidine. Fatigue and dry mouth resolved, but pedal edema continued to be bothersome; a followup BP was 144/94 mm Hg. She refused to try a β blocker due to fear of alopecia. Nifedipine was changed to diltiazem extended release 120 mg q.d., and when seen in the hypertension clinic about 6 weeks later, her pedal edema had resolved and BP was 132/82 mm Hg.