Case history

Case history

A 20-year-old man is brought to the accident and emergency department with abdominal pain, nausea, and vomiting with increasing polyuria, polydipsia, and drowsiness since the previous day. He was diagnosed with type 1 diabetes 2 years previously. He mentions that he ran out of insulin 2 days ago. Vital signs on admission are: BP 106/67 mmHg, heart rate 123 beats per minute, respiratory rate 32 breaths per minute, temperature 37.1°C (98.8°F). He is drowsy. Physical examination reveals Kussmaul breathing (deep and rapid respiration due to ketoacidosis) with acetone odour and mild generalised abdominal tenderness without guarding or rebound tenderness. Initial laboratory data are: blood glucose 25 mmol/L, arterial pH 7.24, PCO2 25 mmHg, bicarbonate 12 mmol/L, WBC count 18.5 × 10⁹/L, sodium 128 mmol/L, potassium 5.2 mmol/L, chloride 97 mmol/L, serum urea 11.4 mmol/L, creatinine 150.3 micromol/L, blood ketones (beta-hydroxybutyrate) 4.8 mmol/L. 

Other presentations

It is now well recognised that new-onset type 2 diabetes can present with diabetic ketoacidosis (DKA). These patients are typically individuals with obesity and undiagnosed hyperglycaemia, impaired insulin secretion, and insulin resistance. After treatment of the acute hyperglycaemic episode with insulin, beta-cell function and insulin sensitivity often improve, allowing discontinuation of insulin therapy. Many can subsequently be managed with oral agents or lifestyle modification alone, with approximately 40% remaining insulin-independent 10 years after the initial episode of DKA.[4]​ These patients do not exhibit the autoimmune laboratory findings characteristic of type 1 diabetes.[1][5]​​​​​ This condition has been described as 'type 1 and 1/2' (or 'type 1 and a half') diabetes, 'Flatbush' diabetes, 'atypical diabetes', or 'ketosis-prone' diabetes. 

Otherwise, it is rare for DKA to develop spontaneously in patients with type 2 diabetes. When it does occur, it is usually precipitated by missed or inadequate insulin doses or associated with infection, severe illness, trauma, surgery, or the use of certain drugs (e.g., sodium-glucose cotransporter-2 [SGLT2] inhibitors or the dual SGLT1/SGLT2 inhibitor sotagliflozin).[6][7]

An extreme hyperosmolar state resembling hyperosmolar hyperglycaemic state (HHS) may also occur in combination with DKA, particularly in type 1 diabetes.[8][4][9][10]​ It is estimated that one third of hyperglycaemic emergencies have a hybrid DKA-HHS presentation.[6]

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