Endocrinology

Hyperglycaemia in an unwell adult

High capillary glucose in an acutely unwell patient with or without known diabetes

Time-critical presentation5-stage reasoningCase walk-through

What to ask

Decide immediately whether this is ketoacidosis, a hyperosmolar state or stress hyperglycaemia.
  • Duration of polyuria, polydipsia, weight loss, vomiting and abdominal pain.
  • Insulin or oral agent omission, pump failure, missed basal dose.
  • Precipitants: infection, chest pain, steroids, alcohol, pregnancy, new drugs, surgery, fasting.
  • SGLT2 inhibitor use — glucose may be near normal in ketoacidosis.
  • Previous DKA episodes, psychosocial context and access to supplies.

Discriminators

  • Ketones decide the diagnosis, not the glucose value.
  • Days of gradual decline with profound dehydration and minimal ketones suggests a hyperosmolar state.
  • Vomiting plus abdominal pain in a diabetic patient is DKA until measured otherwise.

Case walk-through — Ketones 5.8, potassium 3.1

4 decisions · hard

Case vignette

A 19-year-old with type 1 diabetes has vomited all day after running out of insulin. Glucose 32 mmol/L, capillary ketones 5.8 mmol/L, venous pH 7.05, bicarbonate 6 mmol/L, potassium 3.1 mmol/L, pulse 122/min, blood pressure 96/58 mmHg. He weighs 60 kg and has had 1 L of 0.9% sodium chloride.

  1. 1

    Potassium is 3.1 mmol/L. What happens next?

  2. 2

    He weighs 60 kg. What is the fixed-rate insulin infusion rate?

    Answer the previous step to continue.

  3. 3

    Four hours later glucose is 12.5 mmol/L and ketones are 3.4 mmol/L. What do you change?

    Answer the previous step to continue.

  4. 4

    Ketones are 0.4 mmol/L, pH 7.34, bicarbonate 19 mmol/L and he is eating. How do you convert?

    Answer the previous step to continue.

Full checklist

Original structured checklist
  1. 1

    History

    • Duration of symptoms, insulin or oral agent omission, pump problems
    • Precipitants: infection, chest pain, steroids, alcohol, pregnancy, new drugs
    • SGLT2 inhibitor use — the glucose may be near-normal in DKA
    • Previous DKA episodes and psychosocial context
  2. 2

    Examination

    • Hydration, blood pressure, heart rate, mental state
    • Kussmaul respiration and ketotic breath
    • Full source search including feet, skin and chest
    • Abdominal examination — pain may be metabolic rather than surgical
  3. 3

    Initial tests

    • Capillary glucose and capillary beta-hydroxybutyrate in every unwell diabetic patient
    • Venous blood gas, urea and electrolytes, FBC, ECG
    • Anion gap, corrected sodium and calculated osmolality
    • Precipitant screen: cultures, chest radiograph, troponin, pregnancy test
  4. 4

    Differential

    • Diabetic ketoacidosis, including euglycaemic DKA
    • Hyperosmolar hyperglycaemic state
    • Stress hyperglycaemia in critical illness or steroid therapy
    • Newly diagnosed diabetes without acidosis
  5. 5

    Immediate treatment

    • DKA: 0.9% sodium chloride 1 L in the first hour, fixed-rate insulin 0.1 units/kg/h, potassium 40 mmol/L when 3.5-5.5
    • Add 10% glucose alongside saline once glucose falls below 14 mmol/L and continue insulin until ketones clear
    • Continue usual long-acting basal insulin throughout
    • HHS: slower fluid replacement with insulin used cautiously and osmolality change limited
    • Treat the precipitant and withhold metformin and SGLT2 inhibitors during the acute illness
  6. 6

    Follow-up

    • Convert to subcutaneous insulin only after resolution with an overlap
    • Diabetes specialist team review before discharge in every case
    • Structured sick-day education and a written personalised plan
    • Early outpatient review and address recurrent presentations

Demo content. Educational decision support only. Verify every dose, citation and recommendation against your national formulary and the primary source before clinical use.