Endocrine and metabolic · Moderate
This case is fictional and exists for study. It describes no real patient.
24 years · female
A 24-year-old female with known type 1 diabetes mellitus presents to the emergency department with a two-day history of generalized abdominal pain, persistent nausea, and repeated vomiting. Her partner notes she has been increasingly lethargic and confused over the past 12 hours. She was recently diagnosed with a urinary tract infection and admits to omitting her basal insulin doses due to poor oral intake. On examination, she appears acutely unwell, severely dehydrated with dry mucous membranes, reduced skin turgor, and deep, rapid respirations with a sweet, fruity odor on her breath. Abdominal examination reveals mild, diffuse tenderness without guarding or rebound.
Vital signs
- HR
- 118 bpm
- BP
- 94/62 mmHg
- RR
- 28/min
- Temp
- 37.8 °C
- SpO₂
- 97%
Examination findings
- Deep, rapid respirations (Kussmaul breathing)
- Fruity breath odor
- Dry mucous membranes and reduced skin turgor
- Mild diffuse abdominal tenderness without peritoneal signs
Investigations
| Venous Blood Gas pH | 7.18 pH units | reference: 7.31-7.41 |
| Venous Bicarbonate | 11.0 mmol/L | reference: 22.0-29.0 |
| Capillary Blood Glucose | 24.5 mmol/L | reference: 4.0-7.0 |
| Capillary Blood Ketones | 4.8 mmol/L | reference: <0.6 |
| Serum Potassium | 4.9 mmol/L | reference: 3.5-5.0 |
Question 1 of 3
Which of the following is the single most appropriate initial management step for this patient?
The primary initial intervention in diabetic ketoacidosis (DKA) is intravenous fluid resuscitation using 0.9% sodium chloride to restore intravascular volume and renal perfusion. Intravenous insulin boluses are not recommended as they increase the risk of hypokalaemia and cerebral oedema. Sodium bicarbonate is not recommended in adult DKA in the UK (JBDS-IP), at any pH: adequate fluid resuscitation and a fixed-rate intravenous insulin infusion correct the acidosis, whereas bicarbonate worsens hypokalaemia, can produce paradoxical CSF acidosis and delays ketone clearance. Dextrose is only introduced when blood glucose falls below 14 mmol/L.
Teaching point: The immediate priority in diabetic ketoacidosis management is fluid resuscitation with 0.9% sodium chloride.
Question 2 of 3
Which acid-base disturbance is demonstrated by this patient's clinical presentation and blood gas results?
DKA causes accumulation of unmeasured ketoacid anions (beta-hydroxybutyrate and acetoacetate), producing a high anion gap metabolic acidosis (pH < 7.30, low bicarbonate). Deep, rapid breathing (Kussmaul respiration) is the physiological respiratory compensation acting to blow off carbon dioxide and partially raise pH.
Teaching point: Diabetic ketoacidosis presents with a high anion gap metabolic acidosis and physiological compensatory hyperventilation.
Question 3 of 3
Two hours into treatment with intravenous fluids and a fixed-rate intravenous insulin infusion, the patient's capillary blood glucose decreases to 13.2 mmol/L, but capillary ketones remain elevated at 3.2 mmol/L. What is the most appropriate next action?
When blood glucose drops below 14 mmol/L during DKA management, intravenous 10% dextrose should be added to the fluid regimen to prevent hypoglycaemia while continuing the fixed-rate intravenous insulin infusion (FRIII). The insulin infusion must be maintained to suppress lipolysis and clear ketoacidosis until blood ketones fall below 0.6 mmol/L and venous pH exceeds 7.30.
Teaching point: Add 10% dextrose when blood glucose drops below 14 mmol/L in DKA while maintaining the fixed-rate insulin infusion to clear ketonaemia.
Key learning points
- Immediate fluid resuscitation with 0.9% sodium chloride is the critical first step in managing diabetic ketoacidosis.
- Fixed-rate intravenous insulin infusion (0.1 units/kg/hour) must be continued until ketoacidosis resolves (ketones < 0.6 mmol/L, pH > 7.30).
- Intravenous 10% dextrose should be added when blood glucose drops below 14 mmol/L to allow continued insulin administration without risking hypoglycaemia.
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