Insulin edema and acute neuropathy are rare side effects of insulin initiation or rapid improvement in glycemic control. Both conditions occurring simultaneously are very rare and there are no previous data on truncal neuropathy as a dominant feature. A 35-year-old lady, who presented with an infected, necrotic fourth finger and was admitted for debridement and antibiotics, developed diabetic ketoacidosis. Past medical history included latent autoimmune disease of adults. She was non-compliant with medication and had experienced significant weight loss (37 kg; body mass index (BMI) 15.1 kg/m 2 ). She was glutamic acid decarboxylase antibody positive, with poor glycemic control (HbA1c 133 mmol/mol (14.3%)). She was treated with intravenous and then subcutaneous insulin. From day 3, she developed significant pitting edema to her umbilicus. She was treated with furosemide 40 mg once daily and fluid restriction. Other causes of edema were excluded. Peak weight gain was 5 kg and edema resolved 2 weeks later. She also developed a painful sensory neuropathy over dermatomes T12-L2 on day 5, which persisted for several months before resolution. Magnetic resonance imaging was normal and nerve conduction studies showed generalized diabetic sensorimotor neuropathy. This is the first report of edema and truncal neuropathy developing secondary to insulin initiation and a rapid improvement in glycemic control. Our case was particularly susceptible due to poor glycemic control, low bodyweight, hepatic dysfunction and low serum albumin. This case highlights the importance of being aware of the rare complications of insulin therapy, particularly in susceptible patients.