Diabetic Ketoacidosis (DKA)

JBDS-IP The Management of Diabetic Ketoacidosis in Adults. Last revised: Mar 2023.

BSPED Guideline for the Management of Children and Young People under the age of 18 years with Diabetic Ketoacidosis – 2021. Last updated: Nov 2024.

Article Last Updated:21/01/2026

Minor changes were made to incorporate the management of euglycaemic DKA as per JBDS guidance.

Date: 05/11/25

Paediatric DKA management added

Date: 29/11/2025

Background Information

Definition

DKA is an acute, life-threatening complication of diabetes mellitus, characterised by a triad of:

Hyperglycaemia
Ketosis
Metabolic acidosis

See below for its diagnostic criteria.

Pathophysiology

The trigger of DKA development is insulin deficiency + ↑ counter-regulatory hormones (glucagon, cortisol, growth hormone, catecholamines) ^[Ref]

Subsequent consequences: ^[Ref]

↓ Peripheral glucose uptake + ↑ hepatic gluconeogenesis → hyperglycaemia
↑ Lipolysis → ketogenesis (acetoacetic acid and beta-hydroxybutyric acid) → metabolic acidosis

Role of insulin:

Promote glucose uptake + inhibit hepatic gluconeogenesis (net effect = reduced blood glucose)
Inhibits lipolysis and ketogenesis

Role of counterary hormones:

Increase hepatic gluconeogenesis (increase blood glucose)
Stimulate lipolysis and ketogenesis

In DKA, there is less insulin and more counter-regulatory hormones.

Aetiology

Primarily affects those with T1DM as it is associated with insulin deficiency. ^[Ref]

Precipitators of DKA: ^[Ref]

Insulin deficiency
- New-onset T1DM (1/3 of children and adolescents present initially as DKA)
- Insulin omission / non-adherence

↑ Insulin demand (→ relative deficiency)
- Infection (esp. UTI and pneumonia)
- Trauma
- Surgery
- Systemic steroids

Complications

Electrolyte abnormalities: ^[Ref]

Phosphate / potassium disturbances
- On presentation (due to insulin deficiency/acidosis) → hyperphosphataemia/hyperkalaemia
  - Note: despite a normal/high potassium on presentation, total body potassium is depleted
  - Therefore, potassium supplementation is required even if initial levels are within range (see Management below)
- After insulin therapy (with correction of acidosis) → hypophosphataemia/hypokalaemia
  - Routine phosphate supplementation is not recommended, but replacement should be considered in patients with severe hypophosphatemia or symptoms
Hyponatraemia / hypomagnesaemia (from hyperglycaemia-induced osmotic diuresis)
Dehydration and hypovolaemia (can progress into AKI and shock)

Iatrogenic complications: ^[Ref]

Cerebral oedema (common in younger patients) – most common cause of mortality
- Cerebral oedema happens from rapid hyperglycaemia correction
- The rapid drop in plasma osmolality shifts water into brain cells
- Strict adherence to DKA protocols regarding fluid therapy is essential to prevent cerebral oedema

Hypoglycaemia (from insulin therapy)
- To prevent this, the insulin rate should be reduced and IV glucose should be added once plasma glucose drops below 14 mmol/L (see management below)

Pulmonary oedema and ARDS (from fluid overload)

Diagnosis

Clinical Features

DKA typically occurs in the context of T1DM.

Non-specific findings (in both DKA and HHS): ^[Ref]

Dehydration (e.g. dry mucous membrane, reduced skin turgor, tachycardia)
Polyuria, polydipsia (from hyperglycaemia)
Nausea and vomiting
Altered mental status
Fatigue / generalised weakness

Specific findings in DKA (absence in HHS): ^[Ref]

Rapid onset (<24 hours)
Abdominal pain (this occurs due to ketoacidosis irritating the peritoneum, thus it is absent in HHS)
“Pearl-drop” / fruity breath odour (from exhaled ketones)
Kussmaul respiration (compensatory hyperventilation in response to metabolic acidosis)

DKA Diagnostic Criteria

All 3 of the following must be present:

Component	Cut-off
Diabetic-	Capillary blood glucose >11 mmol/L
-Keto-	Capillary ketone ≥3 mmol/L, or Urine ketones 2+ or more
-Acidosis	Venous pH <7.3, and/or Bicarbonate <15 mmol/L

Euglycaemic DKA is increasingly common due to its association with SGLT-2 inhibitor use. Diagnostic criteria are as above, minus the hyperglycaemia.

Prevention

Patient Education

Emphasise sick-day rules:

NEVER stop insulin, and adjust insulin doses as instructed
Monitor blood glucose more frequently (every 2-4 hours)
Monitor ketones regularly (blood / urine)
Stay hydrated and eat easily digestible carbohydrates

Acute DKA Management

Step 1 – Fluid Resuscitation

Fluid replacement to rehydrate the patient is the FIRST PRIORITY in DKA management to restore circulatory volume and stabilise the patient. Although not the definitive management, it alone will not resolve DKA. Insulin is the definitive treatment, but fluids should always be given first. This is important in both exams and clinical practice.

If systolic BP <90 mmHg (i.e. patient is shocked) → fluid bolus (500 mL of 0.9% NaCl over 10-15 min)

Once systolic BP >90 mmHg (or >90 mmHg from the start):

Give 1L of 0.9% NaCl over 1 hour with NO potassium
Potassium only to be considered in 2nd bag onwards – see step 3 below

Step 2 – Insulin Therapy

Insulin is the definitive treatment that resolves DKA. However, note that insulin is NOT the first priority in managing DKA. The first priority is always fluid resuscitation.

Insulin’s main effects in treating DKA are:

Suppression of ketogenesis
Reduction of blood glucose
Correction of electrolyte disturbance

Commence fixed rate intravenous insulin infusion (FRIII)

Rate: 0.1 unit/kg/hour
Choice of insulin: short-acting insulin (JBDS recommends human soluble insulin – Actrapid® or Humulin S®)
Preparation: 50 units of insulin made up to 50 mL with 0.9% NaCl

Changes to Existing Insulin Therapy

Stop any short-acting insulin
Continue long-acting insulin (e.g. glargine, detemir, degludec) at usual dose and time

When Glucose Falls <14 mmol/L

Consider reducing the insulin rate to 0.05 units/kg/hour
Add 10% dextrose at 125 mL/hr

Step 3 – Ongoing Management

Continue FRIII and fluid replacement:

2nd bag of fluid: 1L of 0.9% NaCl over 2 hours + potassium replacement if ≤5.5 mmol/L
3rd bag of fluid: 1L of 0.9% NaCl over 2 hours + potassium replacement if ≤5.5 mmol/L
4th bag of fluid: 1L of 0.9% NaCl over 4 hours + potassium replacement if ≤5.5 mmol/L
5th bag of fluid: 1L of 0.9% NaCl over 4 hours + potassium replacement if ≤5.5 mmol/L
6th bag of fluid: 1L of 0.9% NaCl over 6 hours + potassium replacement if ≤5.5 mmol/L

Adherence to DKA fluid protocol is important to prevent cerebral oedema (from correcting hyperglycaemia too rapidly) and fluid overload complications (e.g. pulmonary oedema).

Potassium Replacement

Potassium replacement depends on potassium levels:

>5.5 mmol/L → no potassium replacement needed
3.5-5.5 mmol/L → 40 mmol/L of potassium infusion solution
<3.5 → senior review (as additional potassium required)

If the potassium delivery rate exceeds 20 mmol/hour, continuous cardiac monitoring is required.

Such that if 40 mmol/L of potassium replacement is indicated in the 2nd or 3rd bag of fluids, that corresponds to 20 mmol/hour as these fluids are 1L given over 2 hours. These patients would require cardiac monitoring.

Aims of Treatment

Ketone ↓ at least 0.5 mmol/L/hr / bicarbonate ↑ at least 3 mmol/L/hr
Blood glucose ↓ at least 3 mmol/L/hr
Maintain serum potassium in normal ranges

It is more important to be aware of what parameters to monitor, and their expected trend (i.e. what should go up and go down, to indicate treatment is working).

In clinical practice, these exact rates would be easily accessible, and in exams, the questions tend to assess one’s understanding of principles, rather than recalling exact cut-offs.

Euglycaemic DKA

Diagnostic Criteria/Definition

Euglycaemic DKA has the same diagnostic criteria as DKA, however, with a glucose level that does NOT meet the cut-off for DKA (i.e., glucose is <11 mmol/L)

Management

Fluid therapy /Insulin therapy/ Ongoing management (step 1-3) is the same as acute DKA (see above)
The only difference is when to start glucose/dextrose infusion
- Initiate dextrose/glucose infusion 10% straight away at 125 ml/hr alongside the FRIII (to prevent hypoglycaemia) – since glucose is already <14 mmol/L by definition
  - If glucose keeps falling despite 10% glucose, JBDS guidelines recommend reducing FRIII to 0.05 units/kg/hr to avoid hypoglycaemia

Post-DKA Resolution

Resolution Criteria

DKA should resolve by 24 hours (if not → seek senior review)

Resolution criteria:

Ketones <0.6 mmol/L, and
Venous pH >7.3

Management Post-Resolution

Convert to subcutaneous insulin
- Only discontinue the IV insulin infusion until 30 min after subcutaneous insulin has been given

Patient should be eating and drinking

Paediatric DKA

The BSPED has a specific guideline for the management of DKA in children and young people who are <18 y/o

The following section compares the similarities and main differences to adult DKA management

Similarities

Management Aspect	Details
Diagnosis	Same diagnostic criteria Hyperglycemia (generally glucose $> 11$ mmol/L or known diabetes) PLUS Ketonaemia (blood ketones $> 3.0$ mmol/L) PLUS Acidosis (venous pH $< 7.3$ or bicarbonate $< 15$ mmol/L)
Initial Priority	Restoration of circulating volume (fluid replacement) is the most important initial therapeutic intervention
Insulin Type/Method	Both use a Fixed Rate Intravenous Insulin Infusion (FRIII), typically made up of soluble human insulin (e.g., Actrapid or Humulin S) diluted in 0.9% sodium chloride solution
Potassium	If potassium is in the normal range: Both guidelines recommend a standard concentration of $40 mmol/L$ potassium chloride be added to the intravenous fluid bags (EXCEPT during initial fluid resuscitation / first bag) during the majority of the treatment phase
Glucose/Dextrose Addition	Both require adding glucose (dextrose) infusions once blood glucose levels fall below 14.0 mmol/L to prevent hypoglycemia while continuing the insulin infusion to suppress ketogenesis
Metabolic Targets	Same resolution rate criteria: 0.5 mmol/L/hour fall in ketones 3.0 mmol/L/hour rise in venous bicarbonate 3.0 mmol/L/hour fall in blood glucose
Resolution Criteria	Same DKA resolution definition: Blood ketones <0.6 mmol/L AND Venous pH <7.3
Transition to SC Insulin	Transition from intravenous to subcutaneous insulin should occur: Post-resolution PLUS Patient is alert and able to eat IV infusion should not be discontinued until 30 min after the subcutaneous dose has been given

Differences

Timing of Insulin Initiation (The Most Significant Difference)

Management Aspect	Adults	Children
Timing	Commence FRIII immediately (within the first 60 minutes) after fluid therapy has begun	Start intravenous insulin infusion 1–2 hours after beginning intravenous fluid therapy
Rationale	Effective suppression of ketogenesis is prioritised	Delay is implemented because there is some evidence that cerebral oedema is more likely if insulin is started early

Fluid Therapy

Management Aspect	Adults	Children
Initial Bolus (Non-Shocked)	1L 0.9% NaCl over the first 60 minutes	10 ml/kg bolus of 0.9% NaCl over 30 minutes
Bolus (Shocked Patients)	500 ml bolus of 0.9% NaCl over 10-15 minutes, repeated as needed	10 ml/kg bolus of 0.9% NaCl over 15 minutes, repeated as required up to 40 ml/kg
Potassium (response to low K+)	Insulin administration must be deferred if potassium is $< 3.0 mmol/L$ until potassium level is $> 3.0 mmol/l$	Insulin is commenced promptly alongside fluid resuscitation If potassium is $< 3.5 mmol/L$ , immediate senior review is required for additional potassium replacement

Definitions of ‘shock’ for initial DKA fluid resuscitation:

Adults: based on systolic blood pressure

SBP <90 → Shock
SBP ≥90 → Non-Shocked

Children: based on clinical signs (as outlined by APLS) rather than a single blood pressure threshold, including:

Tachycardia
Prolonged CRT
Poor peripheral pulses
Hypotension (late sign of shock)

Non-shocked children do NOT exhibit the above signs of shock, but may still be dehydrated.

Insulin Dosage

Management Aspect	Adults	Children
Starting Rate	Standard fixed rate is 0.1 units/kg/hour	Dosage can be 0.05 units/kg/hour OR 0.1 units/kg/hour Guideline states that 0.05 units/kg/hour would be sufficient in most cases, especially in children younger than 5 years, to reduce hypoglycemia incidence

References

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