drug induced lower extremity edema

The most appropriate next step in the management of this patient is to discontinue pregabalin and initiate duloxetine. In most patients with lower extremity edema, a detailed history and physical examination will suggest the cause. The most common causes of lower extremity edema include venous obstruction or insufficiency, heart failure (including right-sided heart failure secondary to pulmonary disease), cirrhosis, and nephrotic syndrome and hypoalbuminemia of other etiologies. Certain drugs and classes of drugs are frequent causes of edema. Direct vasodilators (minoxidil, hydralazine, calcium channel blockers, α-blockers) may produce edema by several mechanisms, including arteriolar dilatation (increases intracapillary pressure) and activation of the renin-angiotensin-aldosterone system (sodium retention). The thiazolidinediones, such as pioglitazone and rosiglitazone, stimulate sodium reabsorption by the sodium channels in the cortical collecting tubule cells. NSAIDs increase renal sodium reabsorption by inhibition of renal vasodilatory prostaglandins. Pregabalin is a calcium channel blocker and likely produces edema by the same mechanism as other calcium channel blockers; it is associated with peripheral edema in up to 17% of cases. In drug-induced edema, removal of the offending agent is the treatment of choice. This patient would benefit from switching pregabalin to a different fibromyalgia drug that is not associated with peripheral edema, such as duloxetine.

This patient's lower extremity edema is associated with the vasodilatory effects of pregabalin and not volume overload (no jugular venous distension, S3, or pulmonary crackles). In this situation, the use of diuretics can lead to volume depletion, electrolyte disorders, and kidney dysfunction. Discontinuing the drug responsible for the edema is a better strategy.

Duplex Doppler ultrasonography is a useful tool in the evaluation of deep venous thrombosis (DVT). However, DVT typically produces unilateral edema. Additionally, this patient has no risk factors for DVT (prolonged immobilization, cancer, previous DVT) and lacks supporting findings, such as calf swelling, tenderness, and superficial venous dilation.

Although compression stockings may help reduce edema, removal of the offending agent will likely resolve this patient's edema and obviate the need for compression stockings. Furthermore, compression stockings have poor adherence rates because of high cost, discomfort, and the difficulty that patients experience in donning and removing the stockings.