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PLAB 1 (Professional and Linguistic Assessments Board Part 1)

6.2 Diabetic Emergencies: DKA & Hyperosmolar Hyperglycaemic State

Q: A 24-year-old woman with type 1 diabetes is admitted to the acute medical unit with vomiting and abdominal pain. Her weight is 60 kg. Bedside investigations confirm diabetic ketoacidosis: capillary blood glucose is 24.2 mmol/L, capillary blood ketones are 4.8 mmol/L, and a venous blood gas shows a pH of 7.18 and bicarbonate of 11.2 mmol/L. She has just completed her initial 1-litre infusion of 0.9% sodium chloride over 1 hour. Repeat laboratory results show a serum potassium of 4.2 mmol/L. What is the most appropriate fluid prescription for her second litre of intravenous fluid?

0.9% sodium chloride with 40 mmol potassium chloride over 2 hours. Prescribing 0.9% sodium chloride with 40 mmol potassium chloride (KCl) over 2 hours is the standard Joint British Diabetes Societies (JBDS) recommendation. The patient's serum potassium is 4.2 mmol/L (within the target replacement range of 3.5–5.5 mmol/L). Because insulin drives potassium into cells and rehydration causes kaliuresis, failing to add potassium will lead to rapid, life-threatening hypokalaemia and cardiac dysrhythmias. The second bag of fluid in DKA is given over 2 hours. Dextrose should not be introduced until blood glucose falls below 14.0 mmol/L; giving 10% dextrose at this stage (blood glucose 24 mmol/L) would worsen hyperosmolality. Infusing unsupplemented 0.9% sodium chloride would precipitate profound hypokalaemia. Administering 20 mmol KCl over 1 hour provides inadequate potassium replenishment and infuses the fluid volume too rapidly for the second phase of DKA resuscitation.

Q: A 19-year-old man with type 1 diabetes is being treated for diabetic ketoacidosis with a fixed-rate intravenous insulin infusion at 0.1 units/kg/hour and 0.9% sodium chloride. Three hours into therapy, his capillary blood glucose has fallen from 26.0 mmol/L to 13.2 mmol/L. However, his capillary ketones remain elevated at 3.4 mmol/L, and venous blood gas shows a pH of 7.22 and bicarbonate of 13.0 mmol/L. What is the most appropriate next step in his medical management?

Add 10% glucose at 125 mL/h and consider reducing the insulin infusion to 0.05 units/kg/h. The correct step is to start 10% glucose at 125 mL/h alongside the 0.9% sodium chloride and keep the fixed-rate intravenous insulin infusion running, considering a reduction from 0.1 to 0.05 units/kg/h. The Joint British Diabetes Societies (JBDS) 2023 DKA guideline recommends this once capillary glucose falls below 14 mmol/L, because insulin is still needed to suppress lipolysis and clear ketones while glucose and the lower rate prevent hypoglycaemia. Stopping the insulin infusion, or cutting it to a trivial 0.02 units/kg/h with saline alone, would let ketoacidosis rebound. Transferring to subcutaneous insulin is premature: his ketones (3.4 mmol/L) and pH (7.22) do not meet the JBDS resolution criteria of ketones below 0.6 mmol/L and venous pH above 7.3.

Q: A 78-year-old nursing home resident with type 2 diabetes is brought to the emergency department with profound confusion and severe lethargy progressing over the past five days. Examination reveals dry mucous membranes, marked skin tenting, blood pressure of 88/54 mmHg, and heart rate of 118 bpm. Laboratory tests demonstrate: capillary blood glucose of 44.0 mmol/L, serum sodium of 148 mmol/L, potassium of 4.8 mmol/L, urea of 22.4 mmol/L, serum osmolality of 352 mOsm/kg, venous pH of 7.36, serum bicarbonate of 21 mmol/L, and capillary blood ketones of 0.4 mmol/L. What is the most appropriate initial therapy?

Intravenous fluid resuscitation with 0.9% sodium chloride and prophylactic low molecular weight heparin. Intravenous fluid resuscitation with 0.9% sodium chloride and prophylactic low molecular weight heparin (LMWH) is the essential initial management for hyperosmolar hyperglycaemic state (HHS). The primary therapeutic goal in HHS is gradual circulatory restoration and reduction of serum osmolality with crystalloids alone, aiming for a fall in osmolality of 3–8 mOsm/kg/hour and in glucose of no more than 5 mmol/L/hour. Because profound dehydration and extreme hyperviscosity create an immense risk of arterial and venous thrombosis, prophylactic LMWH is mandatory. Starting insulin before or without fluid resuscitation causes sudden intracellular water and glucose shifts, precipitating acute vascular collapse and cerebral hypoperfusion. Hypotonic 0.45% saline is not indicated initially unless serum sodium is rising despite fluid resuscitation, and rapid administration risks central pontine myelinolysis. Sodium bicarbonate is contraindicated in HHS as significant acidosis is absent and bicarbonate worsens intracellular hypokalaemia.

Key Takeaways

Diabetic ketoacidosis (DKA) is diagnosed by the biochemical triad of hyperglycaemia (blood glucose > 11.0 mmol/L or known diabetes), ketonaemia (blood beta-hydroxybutyrate ≥ 3.0 mmol/L or urine ketones ≥ ++), and metabolic acidosis (venous pH < 7.30 or bicarbonate < 15.0 mmol/L); euglycaemic DKA can occur in patients taking SGLT2 inhibitors.
The cornerstone of DKA management (JBDS protocol) is rapid crystalloid fluid resuscitation with 0.9% sodium chloride combined with a Fixed-Rate Intravenous Insulin Infusion (FRIII at 0.1 units/kg/h) based on actual body weight, while continuing long-acting subcutaneous basal insulin.
Potassium management in DKA requires strict adherence: omit potassium from the initial 1-litre bag; add 40 mmol KCl per litre bag if serum K+ is 3.5–5.5 mmol/L, omit KCl if K+ > 5.5 mmol/L, and seek senior review because additional potassium is needed if K+ < 3.5 mmol/L; never stop the insulin infusion.
Hyperosmolar Hyperglycaemic State (HHS) is characterized by severe hyperglycaemia (> 30 mmol/L), profound hyperosmolality (> 320 mOsm/kg), and severe dehydration without significant ketoacidosis; initial therapy is 0.9% NaCl fluid resuscitation alone (insulin 0.05 units/kg/h is added only if glucose ceases to fall), alongside mandatory prophylactic LMWH due to high thromboembolic risk.

Last updated: October 2026

Diabetic Emergencies: DKA & Hyperosmolar Hyperglycaemic State

Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycaemic State (HHS) represent life-threatening acute metabolic emergencies. Rapid diagnosis, prompt crystalloid rehydration, structured insulin administration, and vigilant electrolyte monitoring form the foundation of management according to Joint British Diabetes Societies (JBDS) and NICE guideline NG17/NG28.

Diabetic Ketoacidosis (DKA)

DKA results from an absolute or severe relative deficiency of circulating insulin combined with an excess of counter-regulatory hormones (glucagon, adrenaline, cortisol, and growth hormone). This hormonal imbalance accelerates lipolysis in peripheral adipocytes, releasing free fatty acids that undergo hepatic mitochondrial beta-oxidation into ketone bodies (acetoacetate and beta-hydroxybutyrate). Concurrently, hepatic gluconeogenesis and glycogenolysis cause severe hyperglycaemia, inducing osmotic diuresis, profound electrolyte depletion, and hypovolaemia.

The Diagnostic Triad

Diagnosis requires the simultaneous presence of three biochemical components:

Hyperglycaemia: Blood glucose > 11.0 mmol/L (or known diabetes mellitus).
Ketonaemia: Capillary blood beta-hydroxybutyrate ≥ 3.0 mmol/L (or urine ketones ≥ ++ on dipstick).
Acidosis: Venous blood gas (VBG) showing pH < 7.30 or serum bicarbonate < 15.0 mmol/L.

Important

Euglycaemic DKA: Patients taking SGLT2 inhibitors (dapagliflozin, empagliflozin, canagliflozin) can develop severe ketoacidosis with normal or only mildly elevated blood glucose levels (< 11.0 mmol/L). Glucosuria maintains near-normal glycaemia despite profound relative insulin deficiency and ongoing ketogenesis. When a patient on an SGLT2 inhibitor presents with nausea, vomiting, abdominal pain, or tachypnoea, blood ketones and venous blood gases must be checked immediately regardless of capillary glucose.

JBDS DKA Resuscitation Protocol

Management of DKA requires three concurrent interventions delivered in a high-dependency setting: intravenous crystalloid fluids, fixed-rate intravenous insulin, and potassium replacement.

1. Fluid Resuscitation

The average adult fluid deficit in DKA is 100 mL/kg (5–8 litres). The standard replacement fluid is 0.9% sodium chloride:

1st litre: Infuse over 1 hour (do NOT add potassium to this first bag).
2nd litre: Infuse over 2 hours (with KCl added based on serum potassium).
3rd litre: Infuse over 2 hours (with KCl).
4th litre: Infuse over 4 hours (with KCl).
5th litre: Infuse over 4 hours (with KCl).
6th litre: Infuse over 6 hours (with KCl).
Caution: In elderly patients, heart failure, or renal impairment, fluid rates must be modified to prevent fluid overload and pulmonary oedema.
Introducing 10% Dextrose: When capillary blood glucose drops below 14.0 mmol/L, immediately commence 10% glucose at 125 mL/hour alongside the 0.9% sodium chloride infusion, and (JBDS 2023) consider reducing the fixed-rate insulin infusion from 0.1 to 0.05 units/kg/hour to lower the risk of hypoglycaemia. Never stop the insulin infusion: insulin must continue to suppress ketogenesis and clear the acidosis, with glucose preventing hypoglycaemia.

2. Fixed-Rate Intravenous Insulin Infusion (FRIII)

Administer soluble human insulin (Actrapid or Humulin S) at a fixed rate of 0.1 units/kg/hour calculated from the patient's actual weight (prepared by adding 50 units of soluble insulin to 50 mL 0.9% NaCl, delivered via a syringe pump at 0.1 mL/kg/h).
Basal Subcutaneous Insulin Rule: DO NOT stop the patient's usual long-acting basal insulin (e.g., Lantus, Levemir, Tresiba, Toujeo). Basal insulin must be continued at its normal dose and timing to prevent rebound hyperglycaemia and ketoacidosis when the intravenous insulin infusion is eventually discontinued.

3. Potassium Replacement Protocol

Insulin drives potassium into cells, and rehydration dilutes serum potassium while increasing urinary kaliuresis. Without replacement, hypokalaemia develops rapidly, risking lethal ventricular arrhythmias.

Measured Serum Potassium (mmol/L)	Potassium Chloride (KCl) Replacement per 1-Litre Bag of 0.9% NaCl
> 5.5 mmol/L	Nil KCl added. Check serum potassium hourly.
3.5 – 5.5 mmol/L	Add 40 mmol KCl per 1-litre bag.
< 3.5 mmol/L	Seek immediate senior review: additional potassium is required (JBDS 2023). Concentrated potassium may need a high-dependency setting and central access; monitor potassium and ECG closely.

Monitoring Targets & DKA Resolution

Hourly monitoring: Capillary blood glucose and blood beta-hydroxybutyrate.
Venous blood gas (VBG) & electrolytes: Check at 2, 4, 8, 12, and 24 hours.
Physiological targets:
- Reduction of capillary blood ketones by ≥ 0.5 mmol/L/hour.
- Rise in venous bicarbonate by ≥ 3.0 mmol/L/hour.
- Fall in capillary blood glucose by ≥ 3.0 mmol/L/hour.
- Maintain serum potassium strictly between 4.0 and 5.0 mmol/L.
If targets are not met: Check line patency, verify infusion rates, and increase the FRIII rate by 1.0 unit/hour increments.

Criteria for DKA Resolution

DKA is resolved when all of the following criteria are met:

Capillary blood beta-hydroxybutyrate < 0.6 mmol/L, AND
Venous blood gas pH > 7.3.
JBDS 2023 advises not using bicarbonate as the marker of resolution, because 0.9% saline causes a hyperchloraemic acidosis that keeps bicarbonate low after the ketoacidosis has cleared.
Before converting to subcutaneous insulin, the patient should also be eating and drinking.

Note

Transition to Subcutaneous Insulin: Convert back to subcutaneous insulin only when the patient is ready to eat. Administer the patient's subcutaneous rapid-acting prandial insulin and basal insulin with a meal, and continue the FRIII for 30–60 minutes after the subcutaneous injection to avoid a gap in circulating insulin coverage.

Hyperosmolar Hyperglycaemic State (HHS)

Hyperosmolar Hyperglycaemic State (HHS) is an endocrine emergency typically occurring in older patients with type 2 diabetes. It is characterized by severe hyperglycaemia, extreme hyperosmolality, and profound dehydration in the absence of significant ketoacidosis.

Diagnostic Criteria for HHS

Severe hyperglycaemia: Blood glucose typically > 30.0 mmol/L.
Profound hyperosmolality: Serum osmolality > 320 mOsm/kg (calculated effective osmolality: $2 \times [\text{Na}^+] + \text{glucose}$ ). Total serum osmolality includes urea: $2 \times [\text{Na}^+] + \text{glucose} + \text{urea}$ .
Significant hypovolaemia and dehydration.
Absence of significant ketoacidosis: Venous pH > 7.30, serum bicarbonate > 15.0 mmol/L, and capillary blood ketones < 3.0 mmol/L.

Pathophysiological Differences

Unlike DKA, patients with HHS possess sufficient residual endogenous insulin secretion to suppress adipose lipolysis and hepatic ketogenesis, preventing severe metabolic acidosis. However, the insulin level is insufficient to promote peripheral glucose utilisation, leading to escalating hyperglycaemia over days to weeks. The resultant severe osmotic diuresis produces an average fluid deficit of 100–220 mL/kg (8–12 litres in a 70 kg adult).

Management Principles of HHS

Gradual Fluid Resuscitation: The cornerstone of HHS therapy is fluid replacement using 0.9% sodium chloride. The goal is to slowly expand circulating volume and reduce serum osmolality at a controlled rate of 3–8 mOsm/kg/hour.
- Caution on Rapid Osmolality Drops: Precipitous reduction of serum osmolality risks cerebral oedema and central pontine myelinolysis.
Insulin Administration: Unlike DKA, insulin should NOT be started immediately in HHS unless blood ketones are ≥ 1.0 mmol/L or significant acidosis is present. Fluid resuscitation alone lowers glucose through renal clearance and haemodilution. If blood glucose ceases to fall despite adequate rehydration, initiate a low-dose fixed-rate insulin infusion at 0.05 units/kg/hour.
Thromboprophylaxis: Dehydration and extreme hyperviscosity confer an immense risk of arterial and venous thromboembolism. Prophylactic low molecular weight heparin (LMWH) is mandatory for all patients with HHS unless contraindicated.

Comparison: DKA vs Hyperosmolar Hyperglycaemic State

Clinical / Biochemical Parameter	Diabetic Ketoacidosis (DKA)	Hyperosmolar Hyperglycaemic State (HHS)
Primary Population	Typically Type 1 Diabetes (younger, rapid onset < 24h)	Typically Type 2 Diabetes (older, insidious onset days–weeks)
Pathophysiology	Absolute insulin deficiency; unchecked lipolysis and ketogenesis	Relative insulin deficiency; suppressed lipolysis; massive osmotic diuresis
Capillary Blood Glucose	Usually 11.0 – 30.0 mmol/L (or < 11 in euglycaemic DKA)	Markedly elevated, typically > 30.0 mmol/L (often > 50 mmol/L)
Blood Ketones (Beta-hydroxybutyrate)	≥ 3.0 mmol/L (or urine ketones ≥ ++)	< 3.0 mmol/L (usually normal or mildly elevated)
Venous pH & Bicarbonate	pH < 7.30; Bicarbonate < 15.0 mmol/L	pH > 7.30; Bicarbonate > 15.0 mmol/L
Serum Osmolality	Variable, usually < 320 mOsm/kg	> 320 mOsm/kg
Typical Fluid Deficit	~100 mL/kg (~5–8 litres)	~100–220 mL/kg (~8–12 litres)
Primary Initial Therapy	0.9% NaCl + FRIII (0.1 units/kg/h) immediately	0.9% NaCl alone; add low-dose insulin (0.05 U/kg/h) only if glucose stops falling
Potassium Management	Strict titration; add 40 mmol KCl/L if K+ 3.5–5.5	Replace if K+ < 5.5 mmol/L; monitor closely
Thrombotic Risk	Moderate; give prophylactic LMWH	Extremely high; mandatory prophylactic LMWH

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JBDS DKA Fluid Resuscitation, Insulin Infusion, and Potassium Management Algorithm

Test Your Knowledge

A 24-year-old woman with type 1 diabetes is admitted to the acute medical unit with vomiting and abdominal pain. Her weight is 60 kg. Bedside investigations confirm diabetic ketoacidosis: capillary blood glucose is 24.2 mmol/L, capillary blood ketones are 4.8 mmol/L, and a venous blood gas shows a pH of 7.18 and bicarbonate of 11.2 mmol/L. She has just completed her initial 1-litre infusion of 0.9% sodium chloride over 1 hour. Repeat laboratory results show a serum potassium of 4.2 mmol/L. What is the most appropriate fluid prescription for her second litre of intravenous fluid?

0.9% sodium chloride with 40 mmol potassium chloride over 2 hours

10% dextrose with 40 mmol potassium chloride over 2 hours

0.9% sodium chloride with no added potassium over 2 hours

0.9% sodium chloride with 20 mmol potassium chloride over 1 hour

Test Your Knowledge

A 19-year-old man with type 1 diabetes is being treated for diabetic ketoacidosis with a fixed-rate intravenous insulin infusion at 0.1 units/kg/hour and 0.9% sodium chloride. Three hours into therapy, his capillary blood glucose has fallen from 26.0 mmol/L to 13.2 mmol/L. However, his capillary ketones remain elevated at 3.4 mmol/L, and venous blood gas shows a pH of 7.22 and bicarbonate of 13.0 mmol/L. What is the most appropriate next step in his medical management?

Discontinue intravenous fluids and transition immediately to subcutaneous basal-bolus insulin

Add 10% glucose at 125 mL/h and consider reducing the insulin infusion to 0.05 units/kg/h

Reduce the insulin infusion rate to 0.02 units/kg/h and continue 0.9% sodium chloride alone

Stop the insulin infusion until blood glucose rises above 15.0 mmol/L

Test Your Knowledge

A 78-year-old nursing home resident with type 2 diabetes is brought to the emergency department with profound confusion and severe lethargy progressing over the past five days. Examination reveals dry mucous membranes, marked skin tenting, blood pressure of 88/54 mmHg, and heart rate of 118 bpm. Laboratory tests demonstrate: capillary blood glucose of 44.0 mmol/L, serum sodium of 148 mmol/L, potassium of 4.8 mmol/L, urea of 22.4 mmol/L, serum osmolality of 352 mOsm/kg, venous pH of 7.36, serum bicarbonate of 21 mmol/L, and capillary blood ketones of 0.4 mmol/L. What is the most appropriate initial therapy?

Intravenous sodium bicarbonate infusion and immediate subcutaneous basal insulin

Immediate fixed-rate intravenous insulin infusion at 0.1 units/kg/h without intravenous fluids

Intravenous fluid resuscitation with 0.9% sodium chloride and prophylactic low molecular weight heparin

Rapid intravenous administration of 0.45% hypotonic saline over 30 minutes

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