Case Presentation: A 30-year-old female with medical history of constipation with chronic laxative use presented with complaints of peripheral edema and weight gain. Patient had been using stimulant laxatives for 4 years but stopped 1-week prior to presentation due to painless bright-red blood per rectum. She initially presented to the emergency department 7 days after stopping her laxatives with peripheral edema, progressive shortness of breath, orthopnea and a 19-lb weight gain. Physical exam showed abdominal distention and edema in bilateral lower extremities. Potassium was 3.3 mmol/L and NT-ProBNP was elevated at 676 pg/mL. Albumin was normal and her urinalysis was negative for protein. She received furosemide 40mg with improvement in edema and shortness of breath. She was seen two days later at her primary care clinic. At that time, her dyspnea had resolved, however she had persistent edema and minimal weight loss. Her physical exam showed abdominal distension and pitting edema of lower extremities. She had no elevated JVP, S3 or displaced PMI on exam. Her basic metabolic panel was within normal limits and she was started on 40mg of furosemide daily. An echocardiogram showed EF of 55-60% with mild mitral and tricuspid regurgitation. She returned to clinic one week later with resolution of her edema and had returned to her baseline weight.

Discussion: Stimulant laxatives are the most common class abused by patients with eating disorders [1]. Abuse of stimulant laxatives can lead to several medical complications as these have been shown to act like a diuretic at high doses [2]. It can induce sodium and free water loss and abrupt cessation can cause significant rebound edema [2,3]. A hyperaldosterone state can result after long term laxative induced hypovolemia, which when discontinued leads to a state of aldosterone-mediated renal retention [4]. Treatment involves loop diuretics. Aldosterone antagonists have also been used in management for patients who meet criteria for pseudo Bartter syndrome [2,4,5,6]. Patients with Pseudo-Bartter syndrome present with hypokalemia, metabolic alkalosis and edema. A loop diuretic was used as our patient had normal potassium and bicarbonate. Patients’ laxative use should be quantified upon initial encounter and they should be monitored closely for symptom development after cessation. Treatment duration was ill-defined in previous literature, however it is recommended that treatment is started at the onset of first identification of peripheral edema. In our case, treatment persisted until patient stated symptoms had resolved.

Conclusions: Abrupt cessation of high dose laxatives can cause edema and rapid weight gain. Our case report highlights a significant amount of weight gain which has been reported rarely. Optimal treatment approach remains ill defined at this time but is centered around diuretic use in patients with significant fluid overload.