Diabetic Ketoacidosis

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    This guideline has been adapted for statewide use with the support of the Victorian Paediatric Clinical Network

  • See also:      

    Diabetes mellitus 
    Diabetes phone calls 

    Diabetes mellitus and surgery          

    Key points

    1. Cerebral oedema is the key life-threatening complication of DKA
    2. When managing DKA, hypoglycaemia and hypo/hyperkalaemia are the other main complications which must be monitored for and treated
    3. Children with DKA are deplete in total body potassium regardless of the initial serum potassium level
    4. Measured serum sodium may be low due to osmotic dilution with glucose.  Corrected sodium levels should be calculated and monitored 


    The biochemical criteria for diagnosis of DKA are:

    • Serum glucose >11 mmol/L
    • Venous pH <7.3 or Bicarbonate <15 mmol/L
    • Presence of ketonaemia/ketonuria

    Children with hyperglycaemia (Blood glucose level (BGL) >11 mmol/L) +/- ketosis who are not acidotic can be managed with subcutaneous insulin (see Diabetes mellitus, new presentation, mildly ill).

    Hyperglycaemic children with altered conscious state who are not acidotic (pH of ≥7.3) and have little to no ketonaemia may have hyperglycaemic-hyperosmolar non-ketotic coma.  If this is a possibility, insulin should ONLY be given after discussion with local paediatric team and/or paediatric endocrinologist. 

    Precipitants for DKA

    • Inadequate insulin in a child or adolescent with known diabetes (eg missed insulin doses, insulin pump failure).
    • First presentation of Type 1 diabetes mellitus.
    • Illness. 


    History and examination are directed towards potential precipitants, assessment of severity, and detecting complications of DKA.

    Assessment of Dehydration

    Weigh child – compare to recent weight if available.


    • The degree of dehydration is often over-estimated in DKA, this may be compounded by peripheral shutdown due to acidosis.
    • Excessive fluid replacement may increase the risk of cerebral oedema.
    Degree of dehydration Clinical signs
    Assessment Percentage
    Mild <4% No clinical signs
    Moderate 4-7% Easily detectable dehydration – decreased tissue turgor, poor central capillary return
    Severe >7% Shock - Poor perfusion, rapid pulse, hypotension


    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


    Bloods - Insert an IV when taking bloods

    • Serum glucose
    • Urea, creatinine and electrolytes (sodium, potassium, calcium, magnesium, phosphate)
    • Venous gas (including bicarbonate)
    • FBE (haematocrit may be elevated as a marker of dehydration, WCC may be elevated as a stress response)
    • Blood ketones (bedside test, normal <0.6 mmol/L)
    • Consider investigations for precipitating cause: if clinical signs of infection consider septic work up
    • The following bloods are part of a diagnostic work up for first presentation T1DM: Insulin antibodies, GAD antibodies, ZnT8 antibodies, celiac screen (total IgA, anti-gliadin Ab, tissue transglutaminase Ab) TSH and fT4.  Collect these bloods with initial blood sampling if practical.  Please handover to admitting team if not done


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

    Consider ECG if potassium results will be delayed 

    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

    Severity of DKA Assessed based on the more severe of these parameters:
    Venous pH Bicarbonate (mmol/L)
    Mild <7.3 <15
    Moderate <7.2 <10
    Severe <7.1 <5


    Goals of Treatment:

    Sections below include:

    1. Correct dehydration
    2. Reverse ketosis, correct acidosis and glucose
    3. Monitor for complications of DKA and its treatment: Cerebral oedema, hypo/hyperkalaemia, hypoglycaemia
    4. Identify and treat any precipitating cause   


                See Resuscitation

    Supportive measures and monitoring

    • Nurse head up
    • In children with reduced conscious state monitor airway safety.  Consider inserting an NGT to prevent 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
    • 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 after obtaining appropriate cultures
    • 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 can’t urinate on demand

    Timeline of monitoring and management

    Timeline Observation/Investigation Management

    Assessment and ABC

    IV access and initial bloods including VBG

    Weigh child

    Start rehydration fluids

    Nurse head up

    Document passage of urine (ask child to void)

    0.9% sodium chloride +/- potassium
    1 hour

    Fluid balance

    Vital signs

    Neurological observations

    BGL and bedside ketones

    Start insulin infusion
    2 hours

    Fluid balance

    Vital signs

    Neurological observations, VBG,

    VBG and bedside ketones

    UEC (must check serum potassium within 1 hour of starting insulin infusion)

    Serum calcium, magnesium, phosphate

    Adjust fluids if required based on glucose and electrolytes
    3 hours

    Fluid balance

    Vital signs

    Neurological observations

    BGL and bedside ketones

    Adjust fluids if required based on glucose
    4 hours

    Fluid balance

    Vital signs

    Neurological observations

    VBG and bedside ketones


    Serum calcium, magnesium, phosphate

    Adjust fluids if required based on glucose and electrolytes
    5 hours

    Fluid balance

    Vital signs

    Neurological observations

    BGL and bedside ketones

    Adjust fluids if required based on glucose
    6 hours

    Continue the following hourly:

    Fluid balance

    Vital signs

    Neurological observations

    BGL and bedside ketones


    Continue the following 1-2 hourly:



    Continue the following 2-4 hourly:



    Serum calcium, magnesium, phosphate



    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 commenced on the “mild” or “moderate” fluid rate (see below).

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

    • This should be followed by a reassessment  
    • Acidosis results in poor peripheral perfusion so use central capillary refill with vital signs to assess response to fluids  

    Initial Fluid Replacement

    Commence rehydration with isotonic fluid eg 0.9% sodium chloride. 

    • Ask child to pass urine or remove nappy
    • Add 40 mmol/L potassium chloride to this fluid if the serum potassium ≤ 5.5mmol/L and the child is passing urine  
    • If anuric or serum potassium >5.5 mmol/L, do not add potassium to the fluids until this has resolved

    Keep nil by mouth until child is alert and acidosis has resolved. 

    • Children can be given ice to suck on for comfort.

    Intravenous or oral fluids that have been given at another facility may need to be factored into the assessment and calculation of fluid deficit and replacement. 

    • If the child has received more than 20 mL/kg, discuss the adjustment of fluids with the consultant.

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

    Weight (kg) Mild/nil dehydration (mL/hr) Moderate Dehydration (mL/hr) Severe Dehydration (mL/hr)
    5 24 27 31
    7 33 38 43
    8 38 43 50
    10 48 54 62
    12 53 60 70
    14 60 65 80
    16 65 75 85
    18 70 80 95
    20 75 85 105
    22 80 90 110
    24 80 95 115
    26 85 100 120
    28 85 105 125
    30 90 110 135
    32 90 110 140
    34 95 115 145
    36 100 120 150
    38 100 125 155
    40 105 130 160
    42 105 135 170
    44 110 135 175
    46 115 140 180
    48 115 145 185
    50 120 150 190
    52 120 155 195
    54 125 160 205
    56 125 160 210
    58 130 165 215
    60 133 171 220
    62 136 175 226
    64 139 179 232
    66 140 185 240
    68 145 185 245
    70 150 190 250

     Fluid Adjustments

    Frequent monitoring of electrolytes, glucose, and osmolality will guide fluid composition and infusion rates.  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


    • 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 5mmol/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%


    • 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, increase to a maximum 60 mmol/L if required to maintain serum potassium in the normal range
    • Once insulin is commenced, a repeat serum potassium should be measured within one hour and two to four hourly thereafter


    Measured sodium is depressed by the dilutional effect of hyperglycaemia

    Corrected sodium can be calculated with this formula:

    Corrected sodium  =  measured sodium  +  0.3 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.

    • 0.9% sodium chloride with glucose and potassium chloride (maximum 60 mmol/L) as required should generally be used for the duration of IV rehydration 
    • If a hypotonic solution is later thought to be required, discuss this with the paediatric endocrinologist on call.  The sodium chloride content should be at least 0.45% or greater
    • If measured sodium does not rise as the glucose falls during treatment or if hyponatraemia develops, this usually indicates excessive fluid correction which may increase the risk of cerebral oedema
    • Extremes of corrected sodium should be discussed with a senior doctor early

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


    • Phosphate replacement is rarely required (due to intracellular phosphate stores usually being adequate)
    • If phosphate levels drop below 0.32 mmol/L and/or symptoms of hypophosphataemia are present, IV phosphate replacement may be required
    • Calcium levels will need to be monitored if IV phosphate is administered

    2) Reverse ketosis and correct acidosis

    IV rehydration should be commenced prior to starting an insulin infusion.


    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.

    Initial insulin infusion rates

    • Children with DKA should generally be commenced at 0.1 units/kg/hour 
    • A reduced infusion rate of 0.05 units/kg/hour should be used 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

    Practical points

    • Insulin infusion can 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 changed when child is alert and metabolically stable (pH>7.3, HCO3 > 15)
      • Best time to change to subcutaneous insulin is just prior to a meal. Discuss the dose and regimen with the consultant on call
      • Continue the insulin infusion for 30 minutes after the first subcutaneous injection of rapid-acting insulin, then cease

    3) Monitor for complications of DKA and its treatment

    The most important complications of DKA and its treatment are:

    • Cerebral oedema
    • Hypoglycaemia
    • Hypo/hyperkalaemia
    • Hypo/hypernatraemia
    • Aspiration (if obtunded)

    Cerebral Oedema


    • Some degree of subclinical brain swelling is present during most episodes of DKA
    • Clinical cerebral oedema occurs suddenly, usually between 6-12 hours after starting therapy (range 2-24 hours)
    • Mortality and severe morbidity rates are very high without early treatment
    • If cerebral oedema is suspected, this should be immediately discussed with a consultant

    Risk Factors

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


    • Early: Headache, irritability, lethargy, vomiting
    • Later: depressed consciousness, incontinence, thermal instability
    • Very late: bradycardia, increased BP, respiratory impairment


    • Nurse head up
    • Reduce fluid infusion rate by one-third
    • Contact Paediatric, Infant and Perinatal Emergency Retrievals on 1300 137 650[KH14] 
    • Give mannitol immediately if cerebral oedema suspected – do NOT wait for cerebral imaging.
    • Mannitol 20% (0.2 g/mL) dose: 0.5 g/kg IV over 20 minutes (dose range: 0.25-1 g/kg), repeat if no improvement within 30-60mins.
    • Discuss with consultant on call and liaise with intensive care or paediatric retrieval service to discuss transfer.


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

    • 2 mL/kg 10% glucose IV bolus (repeat if required) and change rehydration fluids to include 10% glucose with 0.9% sodium chloride, 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 2 hours – decrease insulin infusion to 0.05 units/kg/hr (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 can be used if pH≥7.3 and the child is alert and able to tolerate oral intake. Use 4-5 Jelly beans or a serve of juice: 60 mL (5g carbohydrate) for children <25kg, 120 mL (10g carbohydrate) for children ≥25kg
    • Recheck BGL after 15-20mins and give another serve of juice or jelly beans 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 endocrinology / consultant on call

    4) Identify and Treat precipitating cause

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

    • Overall, infective precipitants are uncommon. 

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

    Other Things to Consider

    Persisting Acidosis

    If the acidosis is not correcting, consider the following:

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

    Rarely required


    • Discuss with consultant endocrinologist prior to administration
    • ONLY appropriate for children with life threatening hyperkalaemia or requiring inotropic support
    • May cause paradoxical CNS acidosis
    • Associated with increased risk of cerebral oedema
    • Sodium bicarbonate dose (mmol) = 0.15 x body weight (kg) x base deficit (mmol/L)
      • Administer IV over 30-60 minutes with cardiac monitoring
      • Reassess acid-base status and beware of hypokalaemia

    Consider consultation with local paediatric team for

    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)

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

    For emergency advice and paediatric or neonatal ICU transfers, call the Paediatric Infant Perinatal Emergency Retrieval (PIPER) Service: 1300 137 650.

    Information specific to RCH and Monash Children’s Hospital:

    Children with DKA should be discussed with the paediatric endocrinologist on-call 

    Last Updated November 2018