DKA - paediatric



Key points

Vigilance for the most important complications of DKA treatment is important:

  1. Hypoglycaemia (Glucose <4mmol/l).
  2. Hypo/hyperkalaemia.
  3. Cerebral oedema - commonly seen at 4-12 hours after treatment initiation because of rapid changes in serum osmolality (see effective osmolality). Most deaths in DKA occur in young people as a result of cerebral oedema.
  4. Worsening acidosis due to hypovolaemia or lack of insulin.

Advice

  • Don’t treat with insulin in the first hour
  • Add or increase Dextrose concentration of the IV fluid if the glucose is falling to fast (>5mmol/l) or going to low (<17mmol/l add 5%, <8mmol/l increase to 7.5% then 10%). Insulin infusion remains the same unless serum glucose continuing to fall despite 10% dextrose.
  • Add KCL 20mmol/l in 500ml 0.9% Saline when K <5.5mol/l and recent history of urination.
  • Give 0.9% saline boluses of 10ml/kg if clinically shocked.

Approach


Guide for increasing the percentage glucose in a bag:

Glucose 50% is used to increase the glucose concentration.

These calculations are based on adding glucose to a 5% dextrose / 0.9% Saline 500ml bag.

Guide for increasing % glucose in a bag
%w/v glucose required  Vol to be withdrawn from infusion bag Vol of glucose 50% to be added to infusion bag
7.5% 28ml 28ml
10% 55ml 55ml
12.5% 82.5ml 82.5ml

DKA is defined as

↑glucose (plasma glucose >11 mmol/l)

Ketonaemia >3mmol/L

pH < 7.3

DKA treatment goals

  • Correct acidosis and reverse ketosis.
  • Correct dehydration.
  • Monitor for complications of DKA (cerebral oedema).
  • Restore blood glucose to near normal.
  • Identify and treat any precipitating event.

Resuscitation

Airway

Ensure that airway is patent and secure airway if child is comatose. Pass N/G tube, on free drainage, if comatose or persistent vomiting.

Breathing

Titrate supplemental Oxygen to achieve SpO2 >94%.

Circulation

2 large bore IV cannulae, take baseline bloods (see "below).

  • If child is volume depleted but not shocked, give 10mls/kg 0.9% saline over 30 mins (as a bolus).
  • Reassess capillary refill time and heart rate.
  • ± repeat bolus 10mls/kg 0.9% saline.
  • Senior input is required if considering need for a third bolus of 10mls/kg 0.9% saline.

Confirm Diagnosis

History: Polydipsia and polyuria. Weight loss, abdominal pain and drowsiness.

Examination: Acidotic respirations, dehydration, drowsiness, ileus. Fever is not part of DKA and suggests sepsis as a precipitant and investigations should be sent as indicated by signs and symptoms e.g. MSU, Blood cultures, CXR etc.

Initial investigations

  • Plasma glucose.
  • VBG – Arterial samples are not required.
  • U&E: Calculate corrected sodium and effective osmolality.
  • If this is a first presentation of DKA, send samples for:
    • HbA1C.
    • TFT and anti-TPO.
    • Anti-GAD, ZnT8 and anti-IA2 antibodies.
    • IgA and TTG.

Initial management

Check weight – this should nearly always be possible to measure in the ED.

Record level of consciousness using GCS.

Assess degree of dehydration. Do not estimate more than 8% dehydration in calculations.

Degree of dehydration
Mild, 3% is only just clinically detectable
Moderate, 5% dry mucous membranes, ↓skin turgor
Severe, 8% above with sunken eyes, poor capillary return
± shock may be severely ill with poor perfusion, thready rapid pulse (↓BP is not likely and is a very late sign)

Monitoring

Monitoring during therapy
Continuous
  • ECG monitoring
½ hourly
  • Neuro obs, including consciousness (using modified GCS) and heart rate, in children under age 12
  • Or in children and young people with a pH <7.1 (↑ risk cerebral oedema)
1 hourly
  • Vital signs (or more frequently if indicated)
  • Neuro obs (escalate immediately if headache or change in conscious level or behaviour)
  • Blood glucose and blood ketone levels
2 hourly
  • Electrolytes (x2) (and calculate corrected sodium)/VBG/Lab glucose until acidosis reversed
  • Review fluid composition and rate following each result
  • May be able to check 4 hourly after substantial clinical improvement
Accurate
  • Documentation of fluid input and output
Twice daily
  • Weights

Consider ITU admission

If severe DKA (pH <7.1, Shock, decreased GCS, age <2 years of age) or if staffing on the ward is insufficient to allow adequate monitoring.

Where PICU or HDU do not exist within the admitting hospital, transfer to another hospital for such care (unless ventilatory support becomes necessary) may not be appropriate. However, ALL children with DKA are high-dependency patients and require a high level of nursing care, usually 1:1 even if on general paediatric wards.


Physical examination

Look for evidence of cerebral oedema (Irritability, cushings triad, unequal pupils, decreased GCS) and infection.


Continue management

Fluids

Volume of fluid

By this stage, the circulating volume should have been restored and the child no longer in shock. If not, give a further 10 ml/kg 0.9% saline (to a maximum of 30 ml/kg) over 30 minutes. (discuss with a consultant if the child has already received 30 ml/kg).

Otherwise, once circulating blood volume has been restored, calculate fluid requirements as follows:

Requirement = Maintenance + Deficit – fluid already given.

Deficit (litres) = % dehydration x body weight (kg)
Ensure this result is then converted to ml.

For most children, use 5% to 8% dehydration to calculate fluids.

Neonatal DKA will require special consideration and larger volumes of fluid than those quoted may be required, usually 100-150 ml/kg/24 hours).

APLS maintenance fluid rates over-estimate requirement, particularly at younger ages. Add calculated maintenance (for 48 hrs) and estimated deficit, subtract the amount already given as resuscitation fluid, and give the total volume evenly over the next 48 hours. i.e.
Hrly rate = 48 hr maintenance + deficit – resusc. fluid already given / 48.

Maintenance requirements
Weight  
0-12.9kg 80 ml/kg/24 hrs
13-19.9kg 65 ml/kg/24 hrs
20-34.9kg 55 ml/kg/24 hrs
35-59.9kg 45 ml/kg/24 hrs
>60kg 35 ml/kg/24 hrs

Example :

A 20 kg 6 year old boy who is 8% dehydrated, and who has already had 20ml/kg saline, will require:71mls/hr.

Do not include continuing urinary losses in the calculations at this stage.

For a method of calculating fluid rates which can be printed out for the child’s medical record.

Example fluid requirements
8% x 20kg = 1600 mls deficit
plus 55 mls x 20kg = 1100 mls maintenance (day 1)
  1100 mls maintenance (day 2)
= 3800 mls
minus 20kg x 20ml 400mls resusc. fluid
= 3400 mls over 48 hrs = 71 mls/hour

Type of fluid

Initially use 0.9% saline with 20 mmol KCl in 500 ml, and continue this NaCl for at least 12 hours.

Once the blood glucose has fallen to 14 mmol/l add glucose to the fluid.

A bag of 500 ml 0.9% saline with 5% glucose and 20 mmol KCl should be available from Pharmacy. If not, make up a solution as follows - withdraw 50ml 0.9% sodium chloride/KCl from 500ml bag, and add 50ml of 50% glucose (this makes a solution which is approximately 5% glucose with 0.9% saline with potassium).

If the plasma sodium is falling, continue with Normal saline (with or without glucose depending on blood glucose levels). Some have suggested that Corrected Sodium levels give an indication of the risk of cerebral oedema. If you wish to calculate this, go to: http://www.strs.nhs.uk/resources/pdf/guidelines/correctedNA.pdf.

Corrected sodium levels should rise as blood glucose levels fall during treatment. If they do not, then continue with Normal saline and do not change to 0.45% saline.

Aim for a gradual reduction in glucose level of <5mmol/l/hr. If glucose is falling too quickly i.e. >5mmol/hour or if it drops below 17mmol/l change the IV fluid to 5% dextrose and 0.9% saline.

If the blood glucose continues to fall >5mmol/hour or falls to less than 8 mmol/l change the IV fluid to 7.5% dextrose and 0.9% saline. The concentration can be further increased in increments to 10% dextrose and then 12.5% dextrose should the glucose continue to fall rapidly or remain <8mmol/l. If the blood glucose continues to drop in spite of a 12.5% dextrose infusion consider halving the insulin infusion rate. In practice, this usually only occurs when the ketones have cleared.

If the glucose falls below 4mmol/l, give a 2ml/kg bolus of 10% dextrose, increase the dextrose concentration to 7.5% / 10% / 12.5% if not already done and recheck the BSL in 15 minutes.

Oral fluids

Keep nil PO until significant clinical improvement and correction of acidosis. Subtract from total fluid required.

Potassium

Total body potassium is always depleted. Potassium levels will fall once insulin is commenced. Commence potassium supplementation with 20mmol KCl per 500ml of fluid as soon as initial resuscitation is finished unless anuria is suspected, peaked t waves on ECG or K > 5.5mmol/l.

Check U&E's 2 hours after resuscitation is begun and then at least 4 hourly, and alter potassium replacements accordingly. More potassium than 40 mmol/l is occasionally required.

Use a cardiac monitor and observe frequently for T wave changes.

Insulin

Continuous low dose insulin is the optimal method. Generally the dose is 0.1units/kg/hr but lower doses can be considered in toddlers due to concerns around increased insulin sensitivity in the age group.

Insulin infusion:

  • Add 50 units of Actrapid to 49.5 ml normal saline (concentration of 1 unit per ml) deliver via a syringe pump.
  • Connect via a Y connector to the fluids already running.
  • Run the infusion at 0.1 iu / kg / hour (0.1ml/kg/hr).
  • Continue until pH >7.3.

Please see Fluids section on advice around when to increase the dextrose concentration of the maintenance fluid.

Continue insulin infusion until child drinking and eating normally. Discontinue insulin infusion 30 minutes after first subcutaneous injection to allow time for the subcutaneous insulin to start working and avoiding rebound hyperglycaemia.

If biochemical parameters do not improve, reassess and review fully. Is there underlying sepsis, errors in insulin prescription or preparation, a tissued IV line?

Once rehydration fluids and potassium are running, blood glucose levels will start to fall. Do not start insulin until intravenous fluids have been running for at least an hour.

Continuous low-dose intravenous infusion is the preferred method. There is no need for an initial bolus.

Make up a solution of 1 unit per ml. of human soluble insulin (e.g. Actrapid) by adding 50 units (0.5 ml) insulin to 50 ml 0.9% saline in a syringe pump. Attach this using a Y-connector to the IV fluids already running. Do not add insulin directly to the fluid bags.

The solution should then run at 0.1 units/kg/hour (0.1ml/kg/hour).

  • Once the blood glucose level falls to 14mmol/l, change the fluid to contain 5% glucose (generally 0.9% saline with glucose and potassium. Do not ↓ the insulin. The insulin dose needs to be maintained at 0.1 units/kg/hour to switch off ketogenesis
  • Do not stop the insulin infusion while glucose is being infused
  • If the blood glucose falls below 4 mmol/l, give a bolus of 2 ml/kg of 10% glucose and increase the glucose concentration of the infusion. Insulin can temporarily be reduced for 1 hour
  • Once the pH is above 7.3, the blood glucose is down to 14 mmol/l, and a glucose-containing fluid has been started, consider reducing the insulin infusion rate, but to no less than 0.05 units/kg/hour
  • If the blood glucose rises out of control, or the pH level is not improving after 4-6 hours consult senior medical staff and re-evaluate (possible sepsis, insulin errors or other condition), and consider starting the whole protocol again

For children who are already on long-acting insulin (especially Glargine (Lantus)), your local consultant may want this to continue at the usual dose and time throughout the DKA treatment, in addition to the IV insulin infusion, in order to shorten length of stay after recovery from DKA.

For children on continuous subcutaneous insulin infusion (CSII) pump therapy, stop the pump when starting DKA treatment.


Sodium and Osmolality:

A rapid fall in effective plasma osmolality and/or sodium during therapy may be associated with cerebral oedema. Aim for slow correction of no more than 0.5mmol/hr.

Where effective osmolality = 2 X (Na+K) + Glucose.

Hyperglycaemia causes falsely low plasma sodium levels. Sodium falls 2mmol/l for every 5.5mmol/l rise in glucose.

Corrected Sodium = Measured Na + (2X (glucose – 5.5) / 5.5).

If the initial corrected sodium is >150mmol/l, a slower rehydration rate should be considered.

If actual serum sodium falls during treatment consider slowing the rehydration rate or increasing the sodium concentration and increase vigilance for signs of cerebral oedema.

Bicarbonate

This is rarely, if ever, necessary. Discuss with senior staff.

There is no evidence that bicarbonate is either necessary or safe in the management of DKA. It may exacerbate CNS acidosis, tissue hypoxia and osmolar load. Its only purpose is to improve cardiac contractility in severe shock. Persistent acidosis usually reflects insufficient resuscitation, inadequate insulin or sepsis.

Bicarbonate should only be considered if pH <6.9 and impaired cardiac contractility after discussion with senior medical staff.

Anticoagulation prophylaxis

There is a significant risk of femoral vein thrombosis in young and very sick children with DKA who have femoral lines inserted. Therefore consideration should be given to anticoagulating these children with 100 units/kg/day as a single daily dose of Fragmin.

Children who are significantly hyperosmolar might also require anticoagulant prophylaxis (discuss with your consultant).


Continuing management

Urinary catheterisation should be avoided but may be useful in the child with impaired consciousness.

  • Documentation of fluid balance is of paramount importance. All urine needs to be measured accurately. All fluid input must be recorded (even oral fluids)
  • If a massive diuresis continues fluid input may need to be increased. If large volumes of gastric aspirate continue, these will need to be replaced with 0.9% saline with KCl
  • Check biochemistry, blood pH, and lab. blood glucose 2 hours after the start of resuscitation, and then at least 4 hourly. Review the fluid composition and rate according to each set of electrolyte results

If acidosis is not correcting, consider the following:

  • insufficient insulin to switch off ketones
  • inadequate resuscitation
  • sepsis
  • hyperchloraemic acidosis
  • salicylate or other prescription or recreational drugs

Use near-patient ketone testing to confirm that ketone levels are falling adequately. If blood ketones are not falling, then check infusion lines, the calculation and dose of insulin and consider giving more insulin.

Consider sepsis, inadequate fluid input and other causes if sufficient insulin is being given.

Insulin management once ketoacidosis resolved

Continue with IV fluids until the child is drinking well and able to tolerate food. Only change to subcutaneous insulin once blood ketone levels are below 1.0 mmol/l, although urinary ketones may not have disappeared completely.

Discontinue the insulin infusion 60 minutes (if using soluble or long-acting insulin) or 10 minutes (if using Novorapid or Humalog) after the first subcutaneous injection to avoid rebound hyperglycaemia. Subcutaneous insulin should be started according to local protocols for the child with newly diagnosed diabetes, or the child should be started back onto their usual insulin regimen at an appropriate time (discuss with senior staff).


Cerebral oedema

The cause of cerebral oedema during therapy of DKA remains unclear. The results of a recent randomised controlled trial demonstrated that neither the rate nor the sodium chloride content of intravenous fluids significantly influenced neurologic outcomes in children presenting in DKA (please see Appendix 2 controversies for further details).

Early insulin administration (in the first hour of fluid management of DKA) has been shown to increase the risk of cerebral oedema so it is recommended that children receive fluids only in the first hour of treatment.

Risk Factors (cerebral oedema):

Younger children (< 5 years old), first presentation, severe dehydration (+ high urea), Hypernatraemia, Measured Sodium that fails to rise with treatment.

  • Incidence 0.5-0.9% episodes of D.K.A. with 21-24 % mortality.
  • Most commonly occurs in first 24 hours, usually 4-12 hours after treatment begins but may occur at 24-48 hours.
  • Pathophysiology of cerebral oedema in DKA is still poorly understood but epidemiological studies show greater risk when children are treated with insulin in the first hour of treatment.
  • Treat as such if any suspicion.

Signs/symptoms (cerebral oedema):

Headache, irritability, restlessness, drowsiness, incontinence (in a previously continent child) or specific neurological signs.

Cushings triad: Hypertension, bradycardia, irregular respirations.

Late signs: Seizures, papilloedema, unequal pupils, respiratory arrest.

Management (cerebral oedema):

  • Exclude hypoglycaemia.
  • Nurse at 45 degrees head up.
  • Contact Consultant immediately.
  • Hypertonic saline 3% 3ml/kg over 10 minutes.
  • Doses may need to be repeated if no response.
  • Reduce maintenance fluid by a third and deliver rehydration fluid over 72 hours (rather than 48hours).
  • Transfer to ICU and consider need for transfer to a tertiary PICU.
  • Arrange Neuroimaging (CTB or MRI) in discussion with PICU and neurosurgical team as other intracerebral pathology can present in the same way (e.g. cerebral venous thrombosis).

Other complications

  • Hypoglycaemia and hypokalaemia – avoid by careful monitoring and adjustment of infusion rates. Consideration should be given to adding more glucose if BG falling quickly even if still above 4 mmol/l
  • Systemic Infections – Antibiotics are not given as a routine unless a severe bacterial infection is suspected
  • Aspiration pneumonia – avoid by nasogastric tube in vomiting child with impaired consciousness

Continuing abdominal pain is common and may be due to liver swelling, gastritis, bladder retention, ileus. However, beware of appendicitis and ask for a surgical opinion once DKA is stable. A raised amylase is common in DKA.

Other problems are pneumothorax ± pneumo-mediastinum, interstitial pulmonary oedema, unusual infections (e.g. TB, fungal infections), hyperosmolar hyperglycaemic non–ketotic coma, ketosis in type 2 diabetes. Discuss these with the consultant on-call.



Content By Dr Rory O'Brien, Dr Íomhar O' Sullivan 11/06/2019. Last review Dr ÍOS 16/06/21.