Case history
Case history
A 20-year-old man is brought to the emergency department with abdominal pain, nausea, and vomiting with increasing polyuria, polydipsia, and drowsiness since the day before. 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 98.8°F (37.1°C). On mental status examination, he is drowsy. Physical examination reveals Kussmaul breathing (deep and rapid respiration due to ketoacidosis) with acetone odor and mild generalized abdominal tenderness without guarding and rebound tenderness. Initial laboratory data are: blood glucose 450 mg/dL, arterial pH 7.24, pCO₂ 25 mmHg, bicarbonate 12 mEq/L, WBC count 18,500/microliter, sodium 128 mEq/L, potassium 5.2 mEq/L, chloride 97 mEq/L, BUN 32 mg/dL, creatinine 1.7 mg/dL, serum ketones strongly positive.
Other presentations
It is now well recognized that new-onset type 2 diabetes can manifest with DKA. These patients are obese and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin resistance. However, after treatment of the acute hyperglycemic 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 following the initial episodes of DKA. These patients do not have the typical autoimmune laboratory findings of type 1 diabetes.[2] This type of diabetes has been labeled as "type 1 and ½" or "type 1 and a half" diabetes, "Flatbush" diabetes, or "ketosis-prone" diabetes. Otherwise, it is rare for DKA to develop spontaneously in patients with type 2 diabetes (who are not ketosis-prone), with it generally being precipitated by missed or inadequate insulin doses, or in association with infection, severe illness, trauma, surgery, or use of certain drugs (e.g., sodium-glucose cotransporter-2 [SGLT-2] inhibitors).[3] Conversely, an extreme hyperosmolar state similar to hyperosmolar hyperglycemic state (HHS) has been reported in combination with DKA in type 1 diabetes.[4][5][6][7]
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