Endocrine and metabolic · Hard
This case is fictional and exists for study. It describes no real patient.
24 years · female
A 24-year-old female with a 5-year history of Type 1 Diabetes Mellitus is brought to the emergency department by her family due to progressive nausea, persistent vomiting, and severe diffuse abdominal pain over the past 48 hours. She reports running out of her daily insulin cartridges 2 days ago. On initial clinical assessment, she appears lethargic, severely dehydrated, and exhibits deep, rapid sighing breathing with a fruity odor on her breath. Fluid resuscitation with intravenous 0.9% sodium chloride is immediately established.
Vital signs
- HR
- 118 bpm
- BP
- 96/60 mmHg
- RR
- 28/min
- Temp
- 37.1 °C
- SpO₂
- 98%
Examination findings
- Dry mucous membranes and markedly decreased skin turgor
- Generalized abdominal tenderness without guarding or rebound
- Deep, rapid respirations (Kussmaul breathing)
Investigations
| Blood Glucose | 26.2 mmol/L | reference: 4.0-7.8 |
| Venous pH | 7.12 | reference: 7.31-7.41 |
| Venous Bicarbonate | 11.0 mmol/L | reference: 22.0-29.0 |
| Blood Ketones | 5.2 mmol/L | reference: < 0.6 |
| Serum Potassium | 3.2 mmol/L | reference: 3.5-5.3 |
| Serum Sodium | 132 mmol/L | reference: 135-145 |
Question 1 of 3
Initial fluid resuscitation with 0.9% sodium chloride is underway. Given her lab results, particularly her serum potassium level of 3.2 mmol/L, what is the most appropriate next step regarding potassium and insulin management?
Insulin drives potassium into cells. In diabetic ketoacidosis, if serum potassium is < 3.5 mmol/L, starting insulin immediately can cause severe precipitous hypokalaemia leading to fatal cardiac arrhythmias. Potassium replacement must be initiated, and insulin held until K+ rises above 3.5 mmol/L. Starting insulin immediately without correcting potassium is dangerous. Insulin boluses are not recommended in UK national DKA guidelines. Sodium bicarbonate is not routinely recommended and can worsen intracellular acidosis and hypokalaemia.
Teaching point: Always check serum potassium before initiating fixed-rate intravenous insulin in DKA; if K+ < 3.5 mmol/L, replace potassium and delay insulin until K+ > 3.5 mmol/L.
Question 2 of 3
Four hours after starting appropriate fluid and insulin therapy, the patient's blood glucose drops to 13.1 mmol/L, but her blood ketones remain elevated at 3.8 mmol/L and venous pH is 7.21. Which management step should be taken next?
In DKA management, when blood glucose falls below 14.0 mmol/L, 10% glucose should be added to the fluid regime (typically at 125 mL/hr) while maintaining the fixed-rate intravenous insulin infusion (FRIII at 0.1 units/kg/hr). This prevents hypoglycaemia while allowing insulin to continue suppressing lipolysis and clearing ketoacidosis. Discontinuing FRIII or reducing its rate before ketoacidosis resolves will delay resolution. Replacing normal saline entirely with 5% dextrose does not deliver sufficient glucose or fluid volume compared to adding 10% glucose alongside crystalloid maintenance.
Teaching point: When blood glucose drops below 14 mmol/L in DKA, add 10% glucose infusion to prevent hypoglycaemia while continuing fixed-rate insulin until ketoacidosis resolves.
Question 3 of 3
Which set of findings best confirms that diabetic ketoacidosis has resolved, allowing the transition from intravenous to subcutaneous insulin?
Resolution of DKA is defined in UK national guidance (Joint British Diabetes Societies for Inpatient Care) as blood ketones < 0.6 mmol/L and venous pH > 7.30, in a patient who is alert and able to eat and drink; subcutaneous insulin is then given and the fixed-rate intravenous insulin infusion stopped at least 30 minutes later, so the patient is never left without insulin. Blood glucose alone or symptom improvement does not define biochemical resolution. Urine ketones lag behind blood ketones and should not be used to monitor resolution. Bicarbonate is deliberately not used as the endpoint: large volumes of 0.9% sodium chloride produce a hyperchloraemic acidosis that keeps bicarbonate suppressed after the ketoacidosis has cleared, so no bicarbonate threshold confirms resolution while blood ketones remain elevated., alongside a patient who is alert and able to eat/drink. Blood glucose alone or symptom improvement does not define biochemical resolution. Urine ketones lag behind blood ketones and should not be used to monitor DKA resolution. Bicarbonate of 15 mmol/L still indicates ongoing metabolic acidosis.
Teaching point: Resolution of DKA requires blood ketones < 0.6 mmol/L and venous pH > 7.30, not just normalization of blood glucose.
Key learning points
- In DKA, if serum potassium is below 3.5 mmol/L, potassium replacement must be given and insulin held until K+ is > 3.5 mmol/L to prevent dangerous arrhythmias.
- When blood glucose drops below 14 mmol/L during DKA treatment, add 10% glucose infusion alongside 0.9% NaCl and maintain the fixed-rate intravenous insulin infusion.
- DKA resolution is defined biochemically by blood ketones < 0.6 mmol/L and venous pH > 7.30, at which point the patient can be transitioned to subcutaneous insulin after eating.
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