DKA and HHS — Clinical Case

DCE Long Case

Candidate brief

Patient: Mr Liam Chen, 19 years old, university student.

Presenting complaint: Two days of vomiting, abdominal pain and increasing drowsiness. His mother found him difficult to rouse this morning.

Past history: Type 1 diabetes diagnosed aged 9. Two previous admissions with DKA in the last 12 months, both after stopping insulin.

Current medications: Insulin glargine 24 units at night, insulin aspart 8 units with meals.

Social history: Lives with his mother. Reports significant study stress; she reports he has been missing insulin doses over the last month.

Examination findings:

• GCS 13, drowsy but rousable
• RR 28 with deep, sighing respirations; SpO2 97 percent on room air
• HR 118, BP 96/60, temperature 37.9 degrees Celsius
• Dry mucous membranes
• Soft abdomen with epigastric tenderness
• Fruity odour to breath
• Crackles at the left base

Investigations:

• Capillary glucose 31 mmol/L
• Venous pH 6.98, bicarbonate 6 mmol/L
• Beta-hydroxybutyrate 7.8 mmol/L
• Sodium 130, potassium 5.8, chloride 92, urea 12 mmol/L, creatinine 110 micromol/L
• Chest X-ray: left lower lobe consolidation

Candidate's structured presentation (model)

Problem list:

1. Severe DKA. His beta-hydroxybutyrate above 6.0 mmol/L, pH below 7.0 and bicarbonate below 10 mmol/L fall in the consensus severe band, for which the suggested level of care is the intensive care unit. ^[1]

2. Pneumonia. Worldwide, infection is the most common precipitating factor for DKA, occurring in 14 to 58 percent of cases. ^[1]

3. Abdominal pain. It may be a result of the DKA or an indication of its precipitating cause, and needs further clinical evaluation if it is not resolved with the resolution of dehydration and metabolic acidosis. ^[1]

4. Recurrent DKA. In patients with recurrent DKA, up to 75 percent of admissions have been attributed to insufficient use of insulin therapy, such as missed insulin doses. ^[1]

Management plan:

Monitoring. Capillary glucose every 1 to 2 hours; blood every 4 hours for electrolytes, phosphate, creatinine, beta-hydroxybutyrate and venous pH until resolution of DKA. ^[1]

Fluids. In adults without renal or cardiac compromise, start isotonic saline or balanced crystalloid solutions at an initial rate of 500 to 1,000 mL/h during the first 2 to 4 hours. Fluid replacement should correct estimated deficits within the first 24 to 48 hours. ^[1]

Insulin. Fixed-rate intravenous insulin infusion at 0.1 units/kg/h. Once glucose falls below 13.9 mmol/L, add 5 to 10 percent dextrose and reduce the infusion to 0.05 units/kg/h, continuing until the ketoacidosis is resolved. ^[1]

Potassium. Start replacement after potassium falls below 5.0 mmol/L, to maintain 4 to 5 mmol/L; measure potassium 2 hours after starting insulin and every 4 hours thereafter. ^[1]

Resolution and transition. Ketones below 0.6 mmol/L with venous pH of 7.3 or more or bicarbonate of 18 mmol/L or more; allow an overlap of 1 to 2 hours between subcutaneous insulin and stopping intravenous insulin. ^[1]

Before discharge. Education on insulin administration and sick day advice must be provided or reinforced, and patients should receive an adequate supply of insulin. ^[1]

Examiner discussion questions

Q: "His anion gap is 32. Will you use it to decide when the DKA has resolved?"

"No. An anion gap above 12 mmol/L indicates a high anion gap acidosis consistent with DKA, but hyperchloraemic normal anion gap acidosis is common after treatment and can be mistaken for persistent DKA. The consensus does not use the anion gap as a resolution criterion." ^[1]

Q: "Why might his urine ketones look worse tomorrow?"

"The consensus notes that reliance on urine ketone testing can overestimate the severity of ketonemia later in the course of DKA, when beta-hydroxybutyrate is being cleared and converted into acetoacetate. For monitoring the response to therapy it recommends direct measurement of venous or capillary beta-hydroxybutyrate." ^[1]

Q: "What complications of treatment will you watch for?"

"Hypoglycaemia, which occurred in 16 to 28 percent in DKA studies; hypokalaemia, below 3.5 mmol/L in about 55 percent of people with DKA; normal anion gap acidosis in recovery; and, rarely in adults, cerebral oedema." ^[1]

Q: "Does his age matter for cerebral oedema?"

"In Glaser's study of children with DKA, low arterial carbon dioxide, high serum urea nitrogen and bicarbonate treatment were associated with cerebral oedema. In adults, the consensus describes cerebral oedema as rare and advises a low threshold for brain imaging if mental status changes." ^{[5] [1]}