MON-586 - Edema after Starting an Insulin Pump, A Diagnostic Challenge of Insulin-Induced Edema

Insulin-induced edema (IIE) is a rare but recognized complication of insulin therapy. It mostly occurs in newly diagnosed diabetes patients requiring insulin therapy or in those intensifying existing insulin treatment. The exact pathophysiology is unclear. Also, evidence regarding its duration and optimal management is limited. Most reported cases, associated with insulin pump therapy, were in patients with type 1 diabetes mellitus. Here, we present a case of IIE that, to our knowledge, is the second reported case of edema developing in a patient with type 2 diabetes mellitus (T2DM) on insulin pump.
Our patient is a 40-year-old woman with obesity and poorly controlled T2DM using insulin for twelve years. Her HbA1c varied from 6.8% to 13.5% over time due to inconsistent basal-bolus insulin use. She was started an automated closed-loop continuous subcutaneous insulin pump. At the time of insulin pump initiation, her HbA1c was 13.5% and weight was 83.4 kg. In automated mode, she was initially requiring 100 units/day through insulin pump. Three months later, HbA1c improved to 8.4%. Weight increased to 88.4 kg. After four months of pump use, she developed bilateral lower extremities edema which rapidly progressed to generalized edema and anasarca, with mild exertional shortness of breath. Lab evaluation revealed normal renal, hepatic, and thyroid function: creatinine 0.89 mg/dL (ref:0.57-1.00), Albumin 4.1 g/dL (ref:3.9-4.9), urine creatinine 57.2 mg/dL, Alb/Creatinine Ratio < 5 mg/g (ref:0-29), TSH 1.790 uIU/mL (ref:0.450-4.500). Electrolytes and liver enzymes were normal.
Cardiac evaluation showed normal echocardiogram findings with no pericardial effusion and a negative treadmill stress test for ischemia. After excluding cardiac, renal, and hepatic etiologies, the diagnosis of insulin-induced edema was made.
Resolution of her edema was gradual and took nine months. Treatment included furosemide with only minimal improvement, adjusting her insulin pump glucose targets to the maximum of 120 mg/dL to reduce her total insulin use combined with compression stockings, and supportive care.

Pathophysiology of IIE is not well understood, though the most proposed mechanism is antidiuretic effect of insulin and sodium retention. Other causes are increased vascular permeability and transient hyperaldosteronism. IIE has been reported with all forms of insulin therapy and typically improves with diuretics, supportive care, and adjusting insulin dose. In cases related to insulin pump therapy, increasing the blood glucose target and reducing the daily insulin dose temporarily may help with IIE reduction.
Although, most cases of IIE develop soon after initiating or changing insulin therapy, our case demonstrates that edema may also happen months after insulin initiation. Research is needed to clarify incidence, risks, pathophysiology, and more directed treatments.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*