A 66-year-old man comes to the physician for regular follow-up. He experiences mild fatigue but otherwise has no complaints. The patient has a history of hypertension, type 2 diabetes mellitus, hyperlipidemia, chronic kidney disease, and ischemic cardiomyopathy. His temperature is 36.7 C (98 F), blood pressure is 122/70 mm Hg, and pulse is 82/min. Physical examination shows moist mucous membranes. There is a 2/6 holosystolic murmur at the apex that is unchanged from a previous finding. He has trace bilateral lower-extremity edema. Laboratory results are as follows: Two months ago, his creatinine was 2.3 mg/dL. Electrocardiogram shows normal sinus rhythm without other abnormalities. Which of the following is the best next step in management of this patient?

Question

A 66-year-old man comes to the physician for regular follow-up.  He experiences mild fatigue but otherwise has no complaints.  The patient has a history of hypertension, type 2 diabetes mellitus, hyperlipidemia, chronic kidney disease, and ischemic cardiomyopathy.  His temperature is 36.7 C (98 F), blood pressure is 122/70 mm Hg, and pulse is 82/min.  Physical examination shows moist mucous membranes.  There is a 2/6 holosystolic murmur at the apex that is unchanged from a previous finding.  He has trace bilateral lower-extremity edema.  Laboratory results are as follows:  Two months ago, his creatinine was 2.3 mg/dL.  Electrocardiogram shows normal sinus rhythm without other abnormalities.  Which of the following is the best next step in management of this patient?

Quizplus · Accepted Answer

11ec25c8_d4e1_6226_bc81_67e12ae7b125_MD0003_00 This patient has hyperkalemia (K⁺ >5.0 mEq/L), which is most often due to decreased urinary potassium excretion. The most common etiologies of hyperkalemia are acute or chronic kidney disease and medications or disorders that impair the renin-angiotensin axis. Other etiologies include increased potassium movement out of cells (eg, uncontrolled hyperglycemia, metabolic acidosis) or increased tissue catabolism (eg, trauma, tumor lysis syndrome). Patients with chronic hyperkalemia may be asymptomatic until the potassium gradually rises >7.0 mEq/L. However, acute hyperkalemia can cause symptoms at lower levels. Patients may develop ascending muscle weakness with flaccid paralysis and electrocardiogram (ECG) changes (eg, peaked T waves, followed by short QT interval, QRS widening, and sine wave with ventricular fibrillation). > Initial evaluation of hyperkalemia includes ECG to evaluate for conduction abnormalities. Acute therapy (eg, calcium gluconate, insulin with glucose) is typically reserved for patients with ECG changes, potassium >7.0 mEq/L without characteristic ECG changes, or rapidly rising potassium due to tissue breakdown. However, this patient has a normal ECG and does not require calcium gluconate (Choice A). The next step is to exclude acute treatable secondary causes (eg, uncontrolled hyperglycemia, tumor lysis syndrome). Patients should then have a review of recent/current medications as they frequently can cause hyperkalemia. Common offending medications include nonselective beta-adrenergic blockers, potassium-sparing diuretics (eg, triamterene), angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, and nonsteroidal anti-inflammatory drugs. > (Choice B) Patients with persistent, unexplained hyperkalemia should be evaluated further for hypoaldosteronism with serum renin and aldosterone levels. However, this patient should first have a review of his medications. (Choice C) Uncontrolled hyperglycemia due to insulin deficiency can shift potassium out of cells to cause hyperkalemia. However, these patients tend to have significant hyperglycemia (>300 mg/dL) and anion gap metabolic acidosis due to ketoacidosis. This patient's absence of a low bicarbonate or significant hyperglycemia makes this less likely. (Choice D) Urinalysis has limited value for evaluating hyperkalemia. However, urine electrolytes can help differentiate renal from extra-renal causes of hyperkalemia and would be indicated if no offending medications are found. Educational objective: The most common causes of hyperkalemia include acute or chronic kidney disease, medications, or disorders impairing the renin-angiotensin axis. Common offending medications include nonselective beta-adrenergic blockers, potassium-sparing diuretics (eg, triamterene), angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, and nonsteroidal anti-inflammatory drugs. References: Management of hyperkalemia. (http://www.ncbi.nlm.nih.gov/pubmed/24087806) Hyperkalemia. (http://www.ncbi.nlm.nih.gov/pubmed/16445274)

A 66-Year-Old Man Comes to the Physician for Regular Follow-Up