See also

Diabetes insipidus
Diabetes mellitus: management of unwell children with established diabetes at home
Diabetes mellitus: management of unwell children with established diabetes in hospital
Diabetes mellitus: new presentation
Diabetes mellitus and surgery
Hyperosmolar hyperglycaemic state

Key points

1. Diabetic ketoacidosis (DKA) may be the initial presentation of type 1 diabetes mellitus (T1DM)
2. Cerebral injury is the key life-threatening complication of DKA
3. Treatment goals are correction of dehydration and acidosis, reversing ketosis, gradually normalising blood glucose and electrolytes, and monitoring for acute complications
4. Children with DKA have depleted total body potassium regardless of the initial serum potassium level
5. Measured serum sodium may be low due to osmotic dilution in hyperglycaemia, corrected sodium levels should be calculated and monitored

Background

• The biochemical criteria for diagnosis of DKA are all three of
  • Serum glucose >11 mmol/L
  • Venous pH <7.3 or bicarbonate <18 mmol/L
  • Ketonaemia (ketones ≥3 mmol/L) or ketonuria (ketones ≥2+ on urinalysis)
• Children with hyperglycaemia (BGL >11 mmol/L) +/- ketosis who are not acidotic can be managed with subcutaneous insulin according to local guidelines for new presentation diabetes mellitus (see Diabetes mellitus: new presentation)
• Consider Hyperosmolar hyperglycaemic state (HHS) in hyperglycaemic children with altered conscious state who are not acidotic. Diagnostic criteria are
  • severe hyperglycaemia BGL >33.3 mmol/L
  • pH >7.25
  • serum bicarbonate >15 mmol/L
  • absent or mild ketonemia (ketones <3 mmol/L), mild ketonuria (ketones <2+ on urinalysis)
  • serum osmolality >320 mOsm/kg

Incidence is increasing with greater prevalence of type 2 diabetes in adolescents. Fluid deficits are typically more severe than DKA and early specialist involvement (paediatric endocrinologist/intensivist) is advised, prior to the initiation of insulin

• Euglycaemic ketoacidosis is a clinical syndrome occurring both in type 1 and type 2 diabetes mellitus characterized by
  • BGL <14 mmol/L
  • Metabolic acidosis (arterial pH <7.3, serum bicarbonate <18 mmol/L)
  • Ketonaemia ≥3 mmol/L

Can be caused by starvation, a low carbohydrate diet or off-label use of SLGT2-inhibitors. Consult a specialist early regarding management

Precipitants for DKA

• Inadequate insulin in a child or adolescent with known diabetes eg missed insulin doses, insulin pump failure
• First presentation of T1DM
• Illness in a child with known T1DM

Assessment

• History and examination are directed towards
  • Assessment of severity
  • Assessment of level of consciousness
  • Identifying potential precipitants
  • Detecting complications of DKA
• Vital signs including blood pressure
• Weigh child, compare with recent weight if available

Children with DKA will be dehydrated, however clinical estimates of volume depletion based on physical exam are often inaccurate, as acidosis may exacerbate peripheral shutdown

Assess level of dehydration

Investigations

Bloods - insert IV cannula when taking bloods

• Serum glucose level
• Venous blood gas
• Point of care blood ketones
• UEC, calcium, magnesium, phosphate
• FBE
• The following bloods are part of a diagnostic work up for first presentation T1DM. Collect with initial blood sampling if able, otherwise during initial admission:
  • Diabetes autoantibodies: anti-GAD, anti-IA2, zinc transporter 8
  • Coeliac serology and IgA
  • TSH, FT4

Urine

• Dipstick for ketones, glucose and urinalysis
• Culture if clinical suspicion of UTI

If there are clinical signs of infection, consider additional testing as part of septic workup

Once DKA is confirmed, the following biochemical monitoring should be put in place to guide ongoing management. These will continue until resolution of DKA

• Hourly: BGL, bedside ketone testing
• At 2 hours and 2-4 hourly thereafter: VBG, UEC, Ca, Mg, PO4

Severity of DKA

Management

Goals of treatment

1. Correct dehydration
2. Reverse ketosis, correct acidosis and normalise blood glucose levels
3. Monitor for complications of DKA and its treatment
   • Cerebral oedema
   • Hypo/hyperkalaemia
   • Hypoglycaemia
4. Identify and treat any precipitating cause

Airway/breathing/circulation

See Resuscitation

Note: It is rare for children with DKA to require intubation and ventilation. Maintaining respiratory compensation after intubation can be complex and early critical care advice prior to embarking on intubation is advised

Supportive measures and monitoring

• Nurse head up
• Continue to monitor airway safety in children with reduced conscious state Consider inserting an NGT to reduce risk of aspiration
• Keep nil by mouth until child is alert, and preferably until acidosis resolves Children can be given ice to suck on for comfort
• Insert second IVC to use as a blood sampling line, take initial diagnostic bloods if not drawn with initial IVC insertion
• Administer supplemental oxygen for children with severe circulatory impairment or shock
• Cardiac monitoring for assessment of ECG changes related to potassium levels
  • hyperkalaemia: peaked T waves, widened QRS
  • hypokalaemia: flattened or inverted T waves, ST depression, PR prolongation)
  • See ECG Interpretation
• Consider antibiotics for febrile children with signs of infection
• Consider urinary catheter for children who are unconscious to allow strict monitoring of fluid balance. Weighing nappies can be used for strict fluid balance for children who are unable to urinate on demand

Timeline of monitoring and management

1. Correct dehydration

Children with DKA will be dehydrated. Clinical estimates of fluid deficits are subjective and often inaccurate, thus most children can initially be safely commenced on the 'mild' or 'moderate' fluid rate (see below)

A bolus of 10 mL/kg 0.9% sodium chloride can be given over 30 minutes to children who are tachycardic with delayed central capillary refill

• This should be followed by a reassessment of central capillary refill and vital signs (NB acidosis results in poor peripheral perfusion)

Initial fluid replacement

Commence rehydration with 0.9% sodium chloride

• Measure urine output
• Use fluid containing 40 mmol/L potassium chloride if the serum potassium ≤5.5 mmol/L and the child is passing urine
• If anuric or serum potassium >5.5 mmol/L, do not use potassium containing fluids until this has improved

Keep nil by mouth until child is alert and acidosis has resolved (pH ≥7.3)

• Children can be given ice to suck on for comfort

Initial fluid rates (mL/hr) based on degree of dehydration

The fluid rates below represent maintenance plus replacement of hydration deficit over a 48-hour period.

Prior fluid resuscitation should be factored into fluid replacement, especially if the child has received >20 mL/kg. Discuss with a senior doctor

Fluid adjustments

Frequent monitoring of electrolytes, glucose, and osmolality will guide fluid composition and infusion rates. IV fluids containing 0.9% sodium chloride should be continued for at least the first 6 hours

The three key parameters to monitor and manage are

• glucose
• potassium
• sodium

Osmolality can be calculated using the following formula:

Osmolality = 2 x (serum sodium + serum potassium) + glucose + urea

Glucose

• BGL will decrease rapidly during initial rehydration/volume expansion and continue to decrease once the insulin infusion is started
• Once BGL is ≤15 mmol/L change fluids to 0.9% sodium chloride with 5% glucose and potassium chloride (maximum 60 mmol/L) as required
• Aim to keep the BGL between 5-10 mmol/L
• If BGL falls below 5 mmol/L or is falling rapidly (>5 mmol/L/hour) in the range between 5-15 mmol/L and the child remains acidotic, increase the glucose content to 10%
• Insulin infusion rate should only be decreased if BGL continues to fall despite glucose concentration of 10%

Potassium

• Children with DKA have a deficit of total body potassium however serum potassium levels may be normal, high, or low
• Treatment with insulin will shift potassium to the intracellular space rapidly resulting in hypokalaemia if potassium is not replaced
• Start potassium chloride at a concentration of 40 mmol/L, increasing to a maximum 60 mmol/L if required to maintain serum potassium in the normal range (depending on local protocols)
• If the child is hypokalaemic (K+ <3.0 mmol/L) replace potassium prior to commencement of insulin
• Once insulin is commenced, a repeat serum potassium should be measured within one hour and two- to four-hourly thereafter
• Caution
  • Use pre-mixed fluid bags containing potassium where possible avoid the need for manipulation or addition of concentrated potassium solutions to IV fluids
  • Do not add potassium chloride to a bag that is already hanging

Sodium

Measured sodium is depressed by the dilutional effect of hyperglycaemia

• Calculate corrected sodium with formula below:
  • Corrected sodium = measured sodium + 0.4 x (glucose – 5.5) mmol/L ie 3 mmol/L sodium to be added for every 10 mmol/L of glucose above 5.5 mmol/L
• Extremes of corrected sodium (Na <125 mmol/L or Na >150 mmol/L) should be discussed with a senior doctor early
• If a hypotonic solution is required, minimum sodium chloride content should be 0.45%

IV fluids can be ceased once pH and bicarbonate have normalised (pH >7.3, HCO3 >18) and the child is able to tolerate oral intake (this usually coincides with insulin being changed to subcutaneous injections)

Phosphate

• Hypophosphataemia is common during treatment and is primarily influenced by the degree of acidaemia
• Severe hypophosphataemia is uncommon as intracellular stores are usually adequate
• If phosphate level is below 0.32 mmol/L, IV phosphate replacement should be considered as per local protocols. See Hypophosphataemia guideline
• Calcium levels require close monitoring if IV phosphate is administered

2. Reverse ketosis and correct acidosis

IV rehydration should be commenced one hour prior to starting an insulin infusion

Insulin

To make up the insulin infusion:

• Add 50 units of clear/rapid acting insulin (Actrapid HM or Humulin R) to 49.5 mL of 0.9% sodium chloride to form a 1 unit/mL solution via syringe pump

    or

• Add 50 units of clear/rapid acting insulin (Actrapid HM or Humulin R) to 500 mL 0.9% sodium chloride to form a 0.1 unit/mL solution

Initial insulin infusion rates

• Do not use an insulin bolus at the initiation of therapy
• An insulin infusion rate of 0.05 units/kg/hour should be considered for:
  • Children undergoing inter-hospital transfer (limited access to biochemical monitoring)
  • Children less than 5 years old
  • Children with BGL <15 mmol/L at the time of commencement of the insulin infusion
• All other children with DKA should be commenced at a rate of 0.1 units/kg/hour

Practical points

• Insulin infusions should be run as a sideline with the rehydration fluids via a three-way tap, provided a syringe pump is used. Ensure the insulin is clearly labelled
• Adequate insulin must be continued to clear ketones and correct acidosis
• Aim to keep the blood glucose between 5-10 mmol/L by increasing the fluid glucose concentration to 10% before adjusting the insulin infusion rate
• Changing from an insulin infusion to subcutaneous insulin
  • Can be done when child is alert, eating and metabolically stable (pH >7.3, HCO3 >18)
  • Ideally just prior to a meal
  • Discuss the dose and regimen with the endocrinologist/paediatrician on call, or see Diabetes mellitus- new presentation
  • Continue the insulin infusion for 30 to 60 minutes after the first subcutaneous injection of rapid-acting insulin, then cease

Subcutaneous insulin in mild DKA

In children with mild DKA it may be appropriate to commence subcutaneous insulin in consultation with local endocrine or paediatric team

• Commence 0.1 units/kg Actrapid or Novorapid subcutaneous injection, then 0.1 units/kg every 2 hours (or as directed by the treating endocrine team)
• When acidosis has corrected change to Actrapid or Novorapid 0.1 units/kg every 4-6 hours

3. Monitor for complications of DKA and its treatment

The most important complications of DKA and its treatment are

• Cerebral injury
• Acute kidney injury
• Hypoglycaemia
• Hypo/hyperkalaemia
• Hypo/hypernatraemia
• Hypophosphataemia

Cerebral injury

Background

• Some degree of subclinical cerebral oedema is present during most episodes of DKA
• The degree of cerebral oedema that develops in DKA correlates with the degree of dehydration and hyperventilation at presentation
• Clinically significant cerebral injury usually develops within the first 12 hours
• Mortality and severe morbidity rates are very high without early treatment
• If cerebral injury is suspected, this should be immediately discussed with a senior doctor

Epidemiological risk factors

• First presentation diabetes
• Long history of poor control
• Age <5 years

Biochemical risk factors at presentation

• Severe hypocapnia
• Severe acidaemia
• Increased urea

Signs

• Early: headache, irritability, lethargy, vomiting worsening after therapy initiated
• Later: depressed consciousness, incontinence, thermal instability
• Very late: bradycardia, increased BP, respiratory impairment

Treatment

• Discuss with consultant on call and liaise with intensive care or paediatric retrieval service to discuss transfer
• Nurse head up
• Reduce fluid infusion rate by one-third
• Give hyperosmolar therapy if clinically significant cerebral injury is apparent, do not wait for cerebral imaging
  • Mannitol 20% (0.2 g/mL) dose: 0.5 g/kg IV over 20 minutes
    OR
  • 3% sodium chloride 3 mL/kg IV over 15 minutes
  • If no response within 15 minutes, discuss with intensive care specialist to consider repeated doses

Hypoglycaemia

A BGL <4.0 mmol/L should be treated with additional glucose as below

• 10% glucose IV bolus 2 mL/kg (repeat if required) and change rehydration fluids to include 10% glucose, with potassium chloride (maximum 60 mmol/L) as required
• Do not discontinue the insulin infusion
• If hypoglycaemia occurs despite use of 10% glucose in preceding two hours, decrease insulin infusion from 0.1 unit/kg/hr to 0.05 units/kg/hr (or to 0.03 units/kg/hr, if previously on 0.05 units/kg/hr)
• Continue with 10% glucose in fluids until BGL is stable between 5-10 mmol/L
• Oral treatment for hypoglycaemia may be used if pH ≥7.3 and the child is alert and able to tolerate oral intake

• Recheck BGL after 15-20 mins and give another serve of high GI oral carbohydrate if BGL still <4.0 mmol/L. If oral treatment has been used discuss timing of transition to sub-cutaneous insulin and oral diet with endocrinologist/consultant on call

4. Identify and treat precipitating cause

Assess for underlying infections and consider antibiotics after obtaining relevant cultures if appropriate.

In children with known T1DM the most common cause of DKA is omission of or significant reduction in recent insulin doses, or intercurrent illness

Other things to consider

Persisting Acidosis

If the acidosis is not correcting, consider the following

• Insufficient insulin to resolve ketosis (check insulin delivery)
• Inadequate rehydration
• Sepsis
• Hyperchloraemic acidosis (secondary to IV fluids)
• Salicylates or other substances that cause metabolic acidosis

Bicarbonate

• Only appropriate for children with life threatening hyperkalaemia or requiring inotropic support
• Discuss with intensive care specialist prior to administration

Consider consultation with local paediatric team when

• All children with DKA
• All newly diagnosed diabetes mellitus

Consider transfer when

Intensive care monitoring is recommended for

• Children <2 years of age
• Coma
• Cardiovascular compromise
• Seizures
• Signs of cerebral oedema
• Severe acidosis (pH <7.1 or HCO3 <5)

Children and adolescents with DKA should be managed in a unit that has

• Access to laboratory services for frequent and timely evaluation of biochemical variables
• Experienced nursing staff trained in monitoring and management of DKA in children and adolescents
• A paediatrician, endocrinologist, or critical care specialist with training and expertise in the management of paediatric DKA. Where such expertise is not available on-site, telephone advice should be sought from the appropriate specialists

The care required is beyond the level of comfort or resources of the local hospital

For emergency advice and paediatric or neonatal ICU transfers, see Retrieval Services

Last updated July 2025

Reference List

1. Glaser N, Fritsch M, Priyambada L et al. ISPAD Clinical Practice Consensus Guidelines 2022: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes. 2022; 23( 7): 835- 856. doi:10.1111/pedi.13406
2. Kuppermann N, Ghetti S, Schunk J, et al. Clinical trial of fluid infusion rates for pediatric diabetic ketoacidosis. N Engl J Med. 2018; 378(24):2275-2287. doi: 10.1056/NEJMoa1716816