Childhood Ketoacidosis

Authored by , Reviewed by Dr Adrian Bonsall | Last edited | Certified by The Information Standard

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Diabetic ketoacidosis (DKA) is the leading cause of mortality in childhood diabetes.[1]The primary cause of DKA is absolute or relative insulin deficiency:

  • Absolute - eg, previously undiagnosed type 1 diabetes mellitus or a patient with known type 1 diabetes who does not take their insulin.
  • Relative - stress causes a rise in counter-regulatory hormones with relative insulin deficiency.

DKA can be fatal

The usual causes of death are:

  • Cerebral oedema - associated with 25% mortality (see 'Cerebral odedema', below).
  • Hypokalaemia - which is preventable with good monitoring.
  • Aspiration pneumonia - thus, use of a nasogastric tube in the semi-conscious or unconscious is advised.
  • Deficiency of insulin.
  • Rise in counter-regulatory hormones, including glucagon, cortisol, growth hormone, and catecholamines.
  • Thus, inappropriate gluconeogenesis and liver glycogenolysis occur compounding the hyperglycaemia, which causes hyperosmolarity and ensuing polyuria, dehydration and loss of electrolytes.
  • Accelerated catabolism from lipolysis of adipose tissue leads to increased free fatty acid circulation, which on hepatic oxidation produces the ketone bodies (acetoacetic acid and beta-hydroxybutyric acid) that cause the metabolic acidosis.

A vicious circle is usually set up as vomiting usually occurs compounding the stress and dehydration; the cycle can only be broken by providing insulin and fluids; otherwise, severe acidosis occurs and can be fatal.

Biochemical criteria

The biochemical criteria required for a diagnosis of DKA to be made are:
  • Raised blood glucose >11 mmol/L.
  • Venous pH of <7.3 and/or bicarbonate <15 mmol/L.
  • Ketonaemia and ketonuria (urine dipsticks only detect the acetoacetic acid and not acetone or beta-hydroxybutyrate).

In young children, or partially treated children, DKA may also occur in association with near-normal glucose levels. 

  • There is wide geographic variation in the frequency of DKA at onset of type 1 diabetes; rates inversely correlate with the regional incidence of type 1 diabetes.
  • Frequencies range from 15% to 70% in Europe and North America.
  • DKA at diagnosis is more common in children aged under 5 years, and in children whose families do not have ready access to medical care for social or economic reasons.
  • The risk of DKA in established type 1 diabetes is 1-10% per per year The risk is increased in:
    • Children with poor metabolic control or previous episodes of DKA
    • Peripubertal and adolescent girls
    • Children with psychiatric disorders, including those with eating disorders
    • Children with difficult or unstable family circumstances
    • Children who omit insulin
    • Children with limited access to medical services
    • Insulin pump therapy (as only rapid- or short-acting insulin is used in pumps, interruption of insulin delivery for any reason rapidly leads to insulin deficiency)

Young children are more likely to have DKA as the first presentation of type 1 diabetes than older children.[4]Children with DKA may present with any or all of the following common features of the condition:

  • Dehydration.
  • Lethargy, confusion.
  • Polyuria ± polydypsia.
  • Weight loss.
  • Abdominal pain ± vomiting (may mimic a surgical abdomen).
  • Rapid, deep sighing (Kussmaul's respirations).
  • Ketotic breath - fruity, pear drops smell.
  • Fever - this is not normal for DKA and a source of sepsis must be sought.
  • Shock, coma (assess Glasgow Coma Scale).
  • Also look for any evidence of cerebral oedema (see 'Cerebral oedema', below), ileus or infection.

Other causes of metabolic acidosis:

Investigations should include:  

  • Capillary blood glucose - can be performed but the glucose level must be confirmed on plasma samples.
  • Renal function - may reveal a pattern consistent with dehydration; potassium may also be abnormal (If laboratory measurement of serum potassium is delayed, perform an ECG for baseline evaluation of potassium status).
  • Venous pH and bicarbonate.
  • Near-patient testing for blood ketones - this is superior to testing for urinary ketones.
  • Urine dipstick - looking for ketones and infection.
  • FBC - leukocytes increased with left shift (not necessarily caused by infection) - but fever is not normal in DKA.
  • LFTs.
  • Amylase - may be nonspecifically raised.
  • Measurement of blood beta-hydroxybutyrate concentration, if available, is useful to confirm ketoacidosis and may be used to monitor the response to treatment.
  • Consider blood and urine cultures, CXR, CSF, throat swab and other appropriate samples if there is any indication of possible infection.

Always look for precipitating causes - eg, urinary tract infection, chest infection, etc.

Severity of DKA

This can be divided according to the acidosis:  

  • Mild - pH <7.3 or bicarbonate <15 mmol/L
  • Moderate - pH <7.2 or bicarbonate <10 mmol/L
  • Severe - pH <7.1 or bicarbonate <5 mmol/L

The following is based on British Society for Paediatric Endocrinology and Diabetes (BSPED) recommended DKA guidelines:  

Always begin with resuscitation of the patient

  • A - level of consciousness; need for nasogastric tube (if semi-conscious or unconscious, aspirate and leave on open drainage).
  • B - provide 100% oxygen by a face mask.
  • C - insert IV cannulae (take bloods as above) and administer fluids if needed; attach cardiac monitor.
  • D - assess conscious level early on. All patients should have Glasgow Coma Score (GCS) assessment, or a modification of the verbal response score for younger children, and one-hourly neurological observations. If the patient is comatose or semi-conscious, consider cerebral oedema and institute treatment and arrange transfer to PICU/HDU (but do not delay therapy).

Correct dehydration[5]

See also the separate article on Dehydration in Children.

Ideally, weigh the patient to calculate exact fluid replacement. However, this may not be possible and either a recent weight can be used or an estimated weight. Weight can be estimated by calculating for the child's age or surface area. Serial weights may also help chart the child's progress.

Patients with <5% dehydration who are not clinically unwell, ie mild acidosis and no nausea or vomiting, can be given oral rehydration with subcutaneous insulin.

Assessing dehydration

  • Capillary refill time
  • Skin turgor
  • Abnormal respiratory pattern
  • Dry mucous membranes
  • Sunken eyes
  • Weak pulse
  • Cool peripheries
  • Hypotension and oliguria, which are late signs in children and indicate severe dehydration

Degree of dehydration

Severity, percentage estimated fluid loss
Clinical picture
Mild, 3%
Only just clinically detectable
Moderate, 5%
Dry mucous membranes and reduced skin turgor
Severe, 8%
Above plus sunken eyes and delayed capillary refill time
Severely ill usually with poor perfusion and thready rapid pulse (hypotension is not always present and is a late sign)

Overestimation is dangerous and must be avoided, and it is advised not to use >8% in calculations when estimating.

Fluid replacement

  • If the patient is severely dehydrated or shocked (quite rare): 10 ml/kg 0.9% normal saline as a bolus (may be repeated if necessary up to a maximum of 30 ml/kg).
  • Calculate the deficit (by weight or, less accurately, by clinical assessment) and replace over 48 hours along with usual maintenance requirements using 500 ml of 0.9% saline, initially containing 20 mmol KCl, which can later be changed to 0.45% saline with 5% glucose and 20 mmol KCl when the blood glucose (BG) has fallen to 12-15 mmol/L.
  • Because the severity of dehydration may be overestimated, it is important to know that the rate required will rarely exceed 1.5-2.0 times the usual daily requirement based on age, weight, or body surface area.
  • Neonatal patients may require larger volumes - eg, 100-150 ml/kg/24 hours.
  • Fluid replacement must be monitored, as some patients may experience a massive diuresis and this volume may need to be incorporated into the ongoing infusions.

Oral fluids should only be started once there is clinical improvement with no vomiting. This may precede the end of the 48-hour period; if so, then adjust the rate of IV infusion.

Replace insulin

Treatment with insulin is essential to return the blood sugar level to normal limits, and to prevent further lipolysis and ketogenesis. The current recommendations for insulin therapy are as follows:[5]

  • IV fluids and potassium replacement should occur for one to two hours before starting insulin, by which point the blood glucose should have started falling.
  • Early insulin has been associated with an increased chance of developing cerebral oedema.
  • Insulin should be given as an IV infusion at a dose of 0.1 U/kg/hour (some favour 0.05 U/kg/hour, especially in younger children). An initial bolus is not usually recommended.
  • After an initial, often sizable, drop in BG from rehydration the aim is to reduce the BG by ≤4 mmol/L/hour.
  • When the BG falls to 12-15 mmol/L, change fluids to 0.45% saline with 5% glucose. If the BG drops below 8 mmol/L, add a sideline of 10% glucose and titrate the BG to 8-12 mmol/L. Do not decrease the insulin infusion.
  • If the BG rises, reduce the amount of glucose infused and, if necessary, increase the insulin infusion.
  • If the pH and anion gap ( [Na+] ) - ( [Cl-]+[HCO3-] ) (normal range 10-18 mmol/L) fail to improve, review the insulin therapy and consider other causes - eg, infection, errors in insulin preparation, adhesion of insulin to tubing in dilute solutions.
  • In the rare event that IV administration cannot be used, insulin may be given intramuscularly or subcutaneously, although absorption may be variable due to poor perfusion.
  • Once pH is >7.3 and BG <14 mmol/L, the insulin dose can be reduced but not <0.05 U/kg/hour and it should not be stopped until the patient is clinically well.
  • In some centres, if the patient is on long-acting insulin, this may be continued (deal with the consultant in charge) but continuous subcutaneous insulin pumps should be discontinued temporarily.

Replace potassium 

  • There is always depletion in total body potassium, however the initial serum K values may not be low; instead, they can be normal-to-high, reflecting the transcellular shift caused by the ketoacidosis.
  • This masks the deficit which is uncovered once insulin has commenced.
  • Potassium replacement therapy should be started immediately if the patient is hypokalaemic, but should otherwise be started when insulin therapy is begun.
  • If the patient is hyperkalaemic, do not give potassium therapy until urine output has been documented.
  • Potassium replacement therapy should continue until IV fluids are no longer necessary.

Phosphate replacement 

  • Although serum phosphate levels fall as a result of the osmotic diuresis, and this fall is further aggravated by insulin therapy which encourages phosphate to enter cells, there is no evidence that replacement has clinical benefit.
  • If severe and associated with neurology, hypophosphataemia may be treated using potassium phosphate salts as an alternative to, or combined with, potassium chloride/acetate.
  • Replacement of phosphate may induce hypocalcaemia.

Bicarbonate infusion is rarely needed and should be considered jointly by the intensive care team, paediatricians and possibly the resuscitation team.


  • Femoral line insertion is associated with femoral vein thrombosis and these patients must be anticoagulated.
  • Anticoagulation may also be considered in other patients (eg, those who are significantly hyperosmolar) and this should be discussed with senior colleagues.


Children admitted with DKA must be monitored closely until their biochemistry has normalised. Monitoring should include:[5]
  • Measurements of pulse, respiratory rate and blood pressure - at least hourly.
  • Accurate fluid input/output documentation (catheterisation may be required) - at least hourly.
  • ECG monitoring - due to potential potassium imbalance.
  • Capillary blood glucose - hourly, but it must be checked regularly against venous glucose, as capillary levels may be inaccurate in DKA.
  • 1- to 2-hourly capillary blood ketones (if available); if not, test urine for ketones. Near-patient ketone testing is a fairly new addition to the guidelines. This will help confirm that the blood ketones are falling adequately. If it does not fall then check infusion lines, calculations and the dose of insulin. If these are all fine then consider sepsis or inadequate fluid replacement.
  • Twice-daily weights may be helpful
  • U&Es, BG, FBC, venous blood gas and osmolality - every 2-4 hours.
  • Neurological investigations looking for indications of cerebral oedema, such as headache, vomiting, rising blood pressure, confusion or irritability, slow heart rate, decreased oxygen saturation - at least hourly. If suspected, mannitol 0.5-1 g/kg IV should be given immediately over 20 minutes (or 5-10 ml/kg of 3% saline) and transfer to ICU for ongoing management and possible ventilation.
  • Children who have long duration of symptoms, any element of confusion or a compromised circulation should be admitted to a children's unit or HDU where staff have considerable experience in treating children with DKA.
  • Children aged less than 5 with new-onset type 1 diabetes are at high risk of developing cerebral oedema and should be referred for consideration for treatment in a PICU.[5]
  • The following are recommended criteria for admission to PICU/HDU:
    • Severe acidosis (pH <7.1) with marked hyperventilation
    • Severe dehydration or shock
    • Depressed consciousness with risk of aspiration from vomiting
    • Very young (ie aged <2 years)
    • Insufficient staffing on wards
  • In a child with established diabetes, whose parents have been trained in sick day management, hyperglycaemia and ketosis without vomiting or severe dehydration can be managed at home or in an outpatient healthcare facility (eg, emergency ward), provided an experienced diabetes team supervises the care.
  • Continue IV fluids until the patient is drinking and tolerating food.
  • Only change to subcutaneous insulin once blood ketones are <1.0 mmol/L (note urine ketones may still be present).
  • Stop insulin infusion 60 minutes after soluble or long-acting insulin or 10 minutes after rapid-acting insulin to avoid rebound hyperglycaemia.
  • Cerebral oedema is associated with nearly 25% mortality and usually manifests within the first 12 hours.
  • Risk factors include:
    • Younger age
    • New-onset diabetes mellitus
    • Longer duration of symptoms
    • Use of bicarbonate in management of ketoacidosis (now rarely used)
  • Patients develop:
    • Headache
    • Vomiting
    • Confusion or irritability
    • Rising blood pressure and bradycardia
    • Decreased oxygen saturation
    • Focal neurology - eg, cranial nerve palsies
    • Papilloedema - a late sign
  • Treatment:
    • Exclude hypoglycaemia
    • Mannitol 0.5-1 g/kg IV should be given immediately over 20 minutes - this may need to be repeated after 2 hours
    • Reduce rate of fluid administration - halve the maintenance dose and replace the deficit over 72 hours rather than 48 hours
    • Elevate the head of the bed
    • Transfer to ICU - may need intubation and ventilation
    • 5-10 ml/kg of 3% saline is an alternative
    • Alternative diagnoses may need to be considered (eg, thrombosis, haemorrhage, infection) and a CT brain scan will help delineate the cause

One core issue in cerebral oedema is early identification. Major and minor criteria have been put forth with improved detection rates.

  • Hypoglycaemia
  • Hypokalaemia
  • Systemic infections
  • Aspiration pneumonia
  • Appendicitis - consider if there is ongoing abdominal pain
  • Others - eg, pneumothorax, interstitial pulmonary oedema, hyperosmolar hyperglycaemia non-ketotic coma

When DKA is recognised and treated immediately, the prognosis is excellent. However, when a patient has prolonged or multiple courses of DKA or if DKA is complicated by cerebral oedema  then the prognosis can be very poor.[6]

The mortality rate of children with DKA in the UK is approximately 0.31%, with the majority of these deaths occurring as a result of cerebral oedema.

Cerebral oedema associated with DKA is more common in children than in adults. In the UK around 70-80% of diabetes-related deaths in children under 12 years of age are caused as a result of cerebral oedema.[7]

DKA at the time of diagnosis of type 1 diabetes may be associated with poor long-term metabolic regulation and residual beta cell function.[8]

Further reading and references

  1. Lokulo-Sodipe K, Moon RJ, Edge JA, et al; Identifying targets to reduce the incidence of diabetic ketoacidosis at diagnosis of type 1 diabetes in the UK. Arch Dis Child. 2014 Jan 6. doi: 10.1136/archdischild-2013-304818.

  2. Wolfsdorf J, Glaser N, Sperling MA; Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care. 2006 May29(5):1150-9.

  3. de Vries L, Oren L, Lazar L, et al; Factors associated with diabetic ketoacidosis at onset of Type 1 diabetes in children and adolescents. Diabet Med. 2013 Nov30(11):1360-6. doi: 10.1111/dme.12252. Epub 2013 Jul 9.

  4. Dunger DB, Sperling MA, Acerini CL, et al; European Society for Paediatric Endocrinology/Lawson Wilkins Pediatric Endocrine Society consensus statement on diabetic ketoacidosis in children and adolescents. Pediatrics. 2004 Feb113(2):e133-40.

  5. Olivieri L, Chasm R; Diabetic ketoacidosis in the pediatric emergency department. Emerg Med Clin North Am. 2013 Aug31(3):755-73. doi: 10.1016/j.emc.2013.05.004. Epub 2013 Jul 6.

  6. Management of Diabetic Ketoacidosis in Adults; Joint British Diabetes Societies Inpatient Care Group (March 2010)

  7. Fredheim S, Johannesen J, Johansen A, et al; Diabetic ketoacidosis at the onset of type 1 diabetes is associated with future HbA1c levels. Diabetologia. 2013 May56(5):995-1003. doi: 10.1007/s00125-013-2850-z. Epub 2013 Feb 7.

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