DKA and HHS — SAQ

Stem

A 19-year-old with type 1 diabetes presents with 24 hours of vomiting and abdominal pain. He has been taking less insulin because he is not eating. He is drowsy, RR 30/min with deep sighing breaths, HR 120, BP 95/60, capillary glucose 28 mmol/L. Capillary ketones 5.8 mmol/L. ABG: pH 7.12, HCO3 8 mmol/L, PaCO2 2.8 kPa. Potassium is 3.3 mmol/L. ECG shows U waves. ^[1]

Questions

a) Confirm the diagnosis using biochemical criteria and name the acid–base disorder. (2 marks)

• Diabetic ketoacidosis: hyperglycaemia (glucose typically >11 mmol/L), ketonaemia (ketones ≥3 mmol/L) or ketonuria, and metabolic acidosis (pH <7.3 and/or HCO3 <15) (1.5). ^[1]
• Acid–base: high-anion-gap metabolic acidosis with respiratory compensation (Kussmaul; low PaCO2) (0.5).

b) Outline the first-hour fluid and insulin plan, including the potassium issue. (4 marks)

• ABCDE; large-bore IV access; monitor; search for trigger (infection, omission of insulin) (0.5).
• 0.9% sodium chloride fluid resuscitation — e.g. 1 L over first hour if shocked/hypovolaemic (adjust for age/HF) (1). ^[1]
• Do not start insulin until K+ is known — JBDS requires senior review and additional potassium below 3.5 mmol/L, JBDS requires senior review and additional potassium below 3.5 mmol/L, and the 2024 ADA/EASD consensus advises delaying insulin until potassium exceeds 3.5 mmol/L (replace at 10 mmol/h): here K+ is 3.3 with ECG changes — replace potassium first while fluids run, with cardiac monitoring (1.5).
• Fixed-rate IV insulin infusion 0.1 units/kg/h once K+ safe — JBDS adds 40 mmol KCl per litre for potassium 3.5–5.5 mmol/L (1).

c) List resolution criteria for DKA and two major treatment complications. (2 marks)

• Resolution: ketones <0.6 mmol/L AND venous pH >7.3 (JBDS: do not use bicarbonate as a marker at this stage); patient eating — give subcutaneous fast-acting insulin at a meal and stop the IV infusion 30–60 minutes later (1). ^[1]
• Complications: hypokalaemia, hypoglycaemia, cerebral oedema (especially young), fluid overload, hyperchloraemic acidosis from saline, thrombosis (1 for any two well stated).

d) How does HHS differ from DKA in biochemistry and initial fluid emphasis? (2 marks)

• HHS: marked hyperglycaemia (often ≥30 mmol/L) and very high osmolality (≥320 mOsm/kg), minimal ketones, pH usually >7.3; older T2 phenotype (1). ^[2]
• Fluids are the mainstay; insulin is often delayed/low-dose until glucose fall plateaus with fluids; correct osmolality slowly; watch thrombosis risk (1).

References4ShowHide

1. [1]Dhatariya KK; Joint British Diabetes Societies for Inpatient Care The management of diabetic ketoacidosis in adults: An updated guideline from the Joint British Diabetes Society for Inpatient Care Diabet Med, 2022.PMID 35224769
2. [2]Mustafa OG, Haq M, Dashora U, Castro E, Dhatariya KK; Joint British Diabetes Societies (JBDS) for Inpatient Care Group Management of Hyperosmolar Hyperglycaemic State (HHS) in Adults: An updated guideline from the Joint British Diabetes Societies (JBDS) for Inpatient Care Group Diabet Med, 2023.PMID 36370077
3. [3]Umpierrez GE, Davis GM, ElSayed NA, et al. Hyperglycemic Crises in Adults With Diabetes: A Consensus Report Diabetes Care, 2024.PMID 39052901
4. [4]Savage MW, Dhatariya KK, Kilvert A, et al. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis Diabet Med, 2011.PMID 21255074