Hypokalaemia is a dangerous complication in severe cases of eating disorders with self-induced vomiting and can result in rhabdomyolysis, cardiac arrhythmias, and death. Self-induced vomiting leads to hypokalaemia through two pathways. First, loss of gastric acid causes hypochloraemic metabolic alkalosis, which increases filtered bicarbonate load in the nephron (exceeding the tubular resorptive threshold), and subsequently increases distal sodium bicarbonate delivery. Secondly, hypovolaemia causes activation of the renin-angiotensin-aldosterone axis. Increased distal sodium delivery and mineralocorticoid activity together cause urinary potassium wasting. Standard management of severe hypokalaemia in patients with anorexia or bulimia nervosa and persistent self-induced vomiting includes intravenous replacement of potassium and correction of hypovolaemia. However, hypokalaemia is often refractory in eating disorder outpatients who have ongoing self-induced vomiting after discharge. We present a case of hypokalaemia due to anorexia nervosa, binge-purge subtype with self-induced vomiting successfully treated with a proton pump inhibitor (PPI) in addition to standard therapy.