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 at 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). On mental status examination, he is drowsy. Physical examination reveals Kussmaul's breathing (deep and rapid respiration due to ketoacidosis) with acetone odour and mild generalised abdominal tenderness without guarding and rebound tenderness. Initial laboratory data are: blood glucose 25.0 mmol/L (450 mg/dL), arterial pH 7.24, PCO2 25 mmHg, bicarbonate 12 mmol/L (12 mEq/L), WBC count 18.5 × 10⁹/L (18,500/microlitre), sodium 128 mmol/L (128 mEq/L), potassium 5.2 mmol/L (5.2 mEq/L), chloride 97 mmol/L (97 mEq/L), serum urea 11.4 mmol/L (32 mg/dL), creatinine 150.3 micromol/L (1.7 mg/dL), serum ketones strongly positive.
It is now well recognised that new-onset type 2 diabetes can manifest with DKA. These patients are obese and have undiagnosed hyperglycaemia, impaired insulin secretion, and insulin resistance. However, after treatment of the acute hyperglycaemic episode with insulin, beta-cell function and insulin effects improve, so these patients are able to discontinue insulin therapy and may be treated orally or by diet alone, with 40% remaining insulin-independent 10 years after the initial episodes of DKA. These patients do not have the typical autoimmune laboratory findings of type 1 diabetes. This type of diabetes has been labelled as 'type 1 and 1/2' or 'type 1 and a half' diabetes, 'Flatbush' diabetes, or 'ketosis-prone' diabetes. Conversely, an extreme hyperosmolar state similar to hyperosmolar hyperglycaemic state (HHS) has been reported in combination with DKA in type 1 diabetes.
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