A 76-year-old woman with a history of hypertension, type 2 diabetes mellitus, coronary artery disease, heart failure with preserved ejection fraction, and atrial fibrillation comes to the office for a follow-up visit. The patient says, "I feel exhausted all the time, and my feet are often swollen at the end of the day. I have also gained several pounds over the past 3 months." She has had no chest pain, dyspnea, orthopnea, or dizziness. Her medications include low-dose aspirin, metoprolol, lisinopril, furosemide, metformin, insulin glargine, and a daily multivitamin supplement. The patient underwent electrical cardioversion for persistent atrial fibrillation 6 months ago and has since been taking amiodarone. Two months ago, anticoagulation was discontinued due to recurrent falls related to gait disturbance from diabetic neuropathy. Blood pressure is 134/70 mm Hg with no postural changes, pulse is 58/min and regular, and oxygen saturation is 96% on room air. Weight is 77 kg (170 lb), which is 4.5 kg (10 lb) more than her recorded weight a few months ago. With the head of the bed elevated to 30 degrees, the jugular venous pressure is 2 cm above the sternal angle. Hepatojugular reflux is absent. Lung fields are clear to auscultation. Trace edema is noted at the ankles. Decreased vibratory and light touch sensation is present in the distal lower extremities. The remainder of the physical examination is normal. Serum creatinine is 0.8 mg/dL, sodium is 132 mEq/L, and potassium is 3.7 mEq/L. Which of the following is the most appropriate next step in management of this patient?

Question

A 76-year-old woman with a history of hypertension, type 2 diabetes mellitus, coronary artery disease, heart failure with preserved ejection fraction, and atrial fibrillation comes to the office for a follow-up visit.  The patient says, "I feel exhausted all the time, and my feet are often swollen at the end of the day.  I have also gained several pounds over the past 3 months."  She has had no chest pain, dyspnea, orthopnea, or dizziness.  Her medications include low-dose aspirin, metoprolol, lisinopril, furosemide, metformin, insulin glargine, and a daily multivitamin supplement.  The patient underwent electrical cardioversion for persistent atrial fibrillation 6 months ago and has since been taking amiodarone.  Two months ago, anticoagulation was discontinued due to recurrent falls related to gait disturbance from diabetic neuropathy.  Blood pressure is 134/70 mm Hg with no postural changes, pulse is 58/min and regular, and oxygen saturation is 96% on room air.  Weight is 77 kg (170 lb), which is 4.5 kg (10 lb) more than her recorded weight a few months ago.  With the head of the bed elevated to 30 degrees, the jugular venous pressure is 2 cm above the sternal angle.  Hepatojugular reflux is absent.  Lung fields are clear to auscultation.  Trace edema is noted at the ankles.  Decreased vibratory and light touch sensation is present in the distal lower extremities.  The remainder of the physical examination is normal.  Serum creatinine is 0.8 mg/dL, sodium is 132 mEq/L, and potassium is 3.7 mEq/L.  Which of the following is the most appropriate next step in management of this patient?

Quizplus · Accepted Answer

Explanation: 11ec2b69_bece_15a7_8f63_d34cae31c0b4_MD0005_00 Amiodarone can cause thyroid dysfunction due to its high iodine content and intrinsic effects on thyroid metabolism. Both hypothyroidism and hyperthyroidism can occur, although the former is more common. The large iodine load suppresses synthesis of thyroid hormone (Wolff-Chaikoff effect), and amiodarone itself directly inhibits the conversion of T4 to T3. In patients with normal thyroid function, this can lead to a transient subclinical hypothyroidism in the first few months of amiodarone therapy. However, in patients with pre-existing chronic lymphocytic (Hashimoto) thyroiditis, it can cause overt and prolonged hypothyroidism. Conversely, amiodarone can cause hyperthyroidism due to increased thyroid hormone synthesis in patients with nodular thyroid disease or latent Graves disease (amiodarone-induced thyrotoxicosis type 1), or due to destructive thyroiditis with release of preformed thyroid hormone (amiodarone-induced thyrotoxicosis type 2). This patient's clinical (fatigue, weight gain, bradycardia) and laboratory (hyponatremia) features are likely due to hypothyroidism, and her serum TSH level should be checked. Patients on chronic amiodarone therapy should have periodic monitoring of TSH (every 3-4 months). (Choices A, B, and E) Mineralocorticoid receptor antagonists (eg, spironolactone, eplerenone) or escalating doses of loop diuretics (eg, furosemide) are indicated for certain patients with heart failure that is symptomatic despite therapy with an ACE inhibitor and a beta blocker. B-type natriuretic peptide is released from ventricular myocytes in response to high filling pressures and is useful for differentiating decompensated heart failure from other causes of dyspnea. However, this patient has no dyspnea or orthopnea, and her lung fields and jugular venous pressure are normal. Her other clinical features, including edema, are likely due to hypothyroidism. (Choice D) Hypothyroidism due to amiodarone can be easily treated with levothyroxine, although higher-than-normal doses may be required due to the decreased conversion of T4 to T3. Amiodarone need not be discontinued. Educational objective: Amiodarone can cause thyroid dysfunction due to its high iodine content and intrinsic effects on thyroid metabolism. Both hypothyroidism and hyperthyroidism can occur, with the former being more common. TSH levels should be monitored every 3-4 months in patients on chronic amiodarone therapy. References: Amiodarone-induced thyroid dysfunction. (http://www.ncbi.nlm.nih.gov/pubmed/24067547)

A 76-Year-Old Woman with a History of Hypertension, Type 2