Diabetic Ketoacidosis

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Diabetes and Sex written for patients

See also the separate Childhood Ketoacidosis article.

Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] 

  • Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks).
  • Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA).
  • Bicarbonate below 15 mmol/L and/or venous pH less than 7.3.

However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] 

DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] 

However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their their first presentation of diabetes.[3] 

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Precipitating conditions

There may be no obvious precipitating factor but possible factors include:[2] 

  • Infection.
  • Discontinuation of insulin (unintentional or deliberate).
  • Inadequate insulin.
  • Cardiovascular disease - eg, stroke or myocardial infarction.
  • Drug treatments - eg, steroids, thiazides or sodium-glucose co-transporter 2 (SGLT2) inhibitors.

Any physiological stress (including pregnancy, trauma or surgery) has the potential to initiate DKA. Medication (notably corticosteroids, sympathomimetics, alpha-blockers, beta-blockers and diuretics) may provoke an episode of DKA. Some women are more likely to go into DKA at the time of menstruation.[4]

The diagnosis is not always apparent and should be considered in anyone with diabetes who is unwell.[2] 

Taking a history should not delay the time to treatment. Check capillary blood glucose and blood gases promptly. If these suggest DKA then immediately begin resuscitation and management.

DKA usually develops within 24 hours. DKA typically presents with polyuria and polydipsia, vomiting, dehydration and, if severe, an altered mental state, including coma. Other signs and symptoms include weight loss, weakness and lethargy, Kussmaul respiration (deep hyperventilation) and acetone smell (like pear drops) on the breath.[2] 


  • Unwell, dehydrated with a tendency for rapid deterioration. There will be signs of gross dehydration such as:
    • Dry mucous membranes.
    • Decreased skin turgor/skin wrinkling.
    • Sunken eyes.
    • Slow capillary refill.
    • Tachycardia with weak pulse.
    • Hypotension.
  • Check temperature, pulse and blood pressure.
  • Smell the breath for the characteristic fruity/musty odour of ketones - the smell is akin to pear drops or nail-polish remover.
  • Respiratory compensation of acidosis can lead to tachypnoea or Kussmaul respiration (very deep, slowly rhythmic breathing).
  • Examine the chest for signs of pneumonic consolidation.
  • Check cardiovascular system for signs of cardiac failure, pericardial rub and murmurs.
  • Examine the abdomen to identify any intra-abdominal precipitant.
  • Assess mental status and orientation.
  • Perform a screening neurological examination.
  • Check the skin surface for evidence of abscesses, boils or other rashes.
  • Capillary blood glucose (remember to send a plasma glucose also).
  • Urine dipstick testing shows marked glycosuria and ketonuria (also send urine for microscopy and culture).
  • Assay of blood ketones is more sensitive and specific in detecting ketonaemia but is not always available.
  • Blood tests:
    • Plasma glucose will be elevated.
    • FBC - raised WCC is often seen but this does not necessarily indicate sepsis, as it may occur in DKA.
    • Electrolytes - Na+ may be high due to dehydration, low due to interference of glucose/ketones with assay, or normal; K+ may be high due to the effect of acidosis, normal or occasionally low but overall there is cell depletion of K+.
    • Urea and creatinine - elevated due to prerenal acute kidney injury or where renal impairment is the primary cause.
    • Arterial blood gases - metabolic acidosis with low pH and low HCO3; pCO2 should be normal but can be depressed by respiratory compensation; low pO2 may indicate a primary respiratory problem as a precipitant.
    • Cardiac enzymes - if myocardial ischaemia/infarction is suspected - eg, troponin.
    • Creatine kinase - rhabdomyolysis may also exist (also increased in myocardial infarction).
    • Amylase - if pancreatitis is suspected.
    • Blood cultures.
  • 12-lead ECG.
  • CXR.
  • Abdominal X-ray - if indicated by history and examination.
  • CT/MRI scan of the head - if there is impairment of consciousness or focal neurology.
  • Lumbar puncture - may be indicated if meningitis is a possible precipitant.

Plasma osmolality and anion gap

  • Plasma osmolality - should be checked, or calculated (see box, below). It is increased in both DKA and hyperosmolar hyperglycaemic non-ketotic coma (HONK), as both are hyperosmolar states. However, in HONK it is much higher .
  • Calculate the anion gap (as detailed in box, below), which should be elevated (>13 mmol/L).
Calculating plasma osmolality
  • Plasma osmolality = 2 ([Na mmol/L] + [K mmol/L]) + [Urea mmol/L] + [glucose mmol/L].
  • Should be higher than 290 mOsm/kg in cases of DKA. If it is higher than 320 mOsm/kg and there is not significant ketonaemia/ketonuria then HONK may be the diagnosis.
Calculating the anion gap
  • Anion gap = ([Na mmol/L] - ([Cl mmol/L] + [HCO3 mmol/L]).
  • Anion gap is elevated at >13 mmol/L in DKA.

Assessment of severity

The presence of one or more of the following may indicate severe DKA:[1] 

  • Blood ketones over 6 mmol/L.
  • Bicarbonate level below 5 mmol/L.
  • Venous/arterial pH below 7.0.
  • Hypokalaemia on admission (under 3.5 mmol/L).
  • Glasgow coma scale (GCS) less than 12.
  • Oxygen saturation below 92% on air (assuming normal baseline respiratory function).
  • Systolic BP below 90 mm Hg.
  • Pulse rate over 100 or below 60.
  • Anion gap above 16.

Initial management and monitoring

  • Immediate resuscitation as required.
  • Put the patient on SaO2 monitor, continuous ECG monitor and blood pressure/heart rate monitor.
  • Obtain large-bore peripheral intravenous (IV) access or insert central venous catheter.
  • Urinary catheterisation is usually carried out to monitor urine output and will also allow urinalysis.
  • Low molecular weight heparin and thromboembolic deterrent (TED) stockings are given prophylactically (but see local guidelines). These should be considered for those who are obtunded or comatose, or have other risk factors for venous thromboembolism, although as yet there are no concrete trial data to support this approach.
  • In unconscious, drowsy or vomiting patients, consider passing a nasogastric tube.

General management issues[1] 

Special patient groups
The following groups of patients need specialist input as soon as possible and special attention needs to be paid to their fluid balance:

  • The elderly.
  • Pregnant women.
  • Young people aged 18-25 years.
  • Heart or kidney failure.
  • Other serious comorbidities.

Fluid administration and deficits
The most important initial intervention is appropriate fluid replacement followed by insulin administration. The main aims for fluid replacement are to restore circulatory volume, remove ketones and correct electrolyte imbalance. Typical deficits in DKA in adults are water 100 ml/kg, Na+ 7-10 mmol/kg, Cl- 3-5 mmol/kg and K+ 3-5 mmol/kg.

The deficit should be replaced as crystalloid. In patients with kidney failure or heart failure, as well as the elderly and adolescents, the rate and volume of fluid replacement may need to be modified. The aim of the first few litres of fluid is to correct any hypotension, replenish the intravascular deficit, and counteract the effects of the osmotic diuresis with correction of the electrolyte disturbance.

Insulin therapy
A fixed-rate IV insulin infusion calculated on 0.1 units/per kg body weight/hour is recommended. Insulin has several effects but the most important are the suppression of ketogenesis, reduction of blood glucose and correction of electrolyte disturbance.

Metabolic treatment targets
The recommended targets are a reduction of the blood ketone concentration by 0.5 mmol/L/hour, an increase of the venous bicarbonate by 3.0 mmol/L/hour, a reduction of capillary blood glucose by 3.0 mmol/L/hour and to maintain K+ between 4.0 and 5.5 mmol/L. If these rates are not achieved then the insulin infusion rate should be increased.

IV glucose concentration
The focus should be on clearing ketones as well as normalising blood glucose. 
When plasma glucose is below 12 mmol/L then replace normal saline with 5% dextrose to prevent over-rapid correction of blood glucose and hypoglycaemia. 10% glucose may be required. It is important to continue 0.9% sodium chloride solution to correct circulatory volume. It is quite often necessary to infuse these solutions concurrently. Glucose should be continued until the patient is eating and drinking normally.

Treat any precipitating illness

  • Measures to actively detect a precipitating cause should be pursued.
  • One clue to the possibility of an unrecognised underlying cause is if the pH and anion gap fail to improve despite the aforementioned measures. In this case, review insulin therapy and consider other further investigations - eg, serial ECGs in silent cardiac ischaemia.
  • If an underlying cause is identified then it should also be treated, as appropriate.
  • If there are reasonable clinical grounds to suspect infection as the precipitant then appropriate antibiotic therapy should be given (usually broad-spectrum blind treatment); routine antibiotics are not advised.

To reduce the risk of catastrophic outcomes in adults with DKA, ensure that monitoring is continuous and that review covers all aspects of clinical management at frequent intervals.[5] 

  • Patients should ideally be managed in an HDU type of setting, or even ITU if they are severely unwell.
  • Electrolytes and venous bicarbonate must be checked at least every 1-2 hours for the first 2-4 hours and then 2- to 4-hourly thereafter (frequency will depend upon the individual clinical scenario).
  • Monitor hourly fluid balance.
  • Monitor capillary blood glucose every hour with an aim to reduce plasma glucose by 3-5 mmol/L/hour.
  • Plasma glucose should also be checked regularly, as capillary blood glucose may be inaccurate in DKA.
  • If capillary/plasma glucose has not fallen by at least 4 mmol/L in the first hour then check adequacy of rehydration and patency of infusion lines; if these are not at fault then double the dose of insulin for the next hour.
  • When plasma glucose is <12 mmol/L then replace normal saline with 5% dextrose to prevent over-rapid correction of blood glucose and hypoglycaemia.
  • Cerebral oedema:
    • Cerebral oedema causing symptoms is relatively uncommon in adults during DKA, although asymptomatic cerebral oedema may be common.
    • Cerebral oedema usually occurs within a few hours of the initiation of treatment. It presents in the first 24 hours with headache, behavioural changes and urinary incontinence, progressing to abrupt neurological deterioration and coma.
    • Cerebral oedema associated with DKA is more common in children than in adults.[6] 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.
  • Pulmonary oedema:
    • Pulmonary oedema has only been rarely reported in DKA. Pulmonary oedema usually occurs within a few hours of the initiation of treatment.
    • Elderly patients and those with impaired cardiac function are at particular risk and monitoring of central venous pressure should be considered.
  • Iatrogenic hypoglycaemia: severe hypoglycaemia is also associated with cardiac arrhythmias, acute brain injury and death.
  • Iatrogenic hypokalaemia.
  • Cardiac dysrhythmia due to electrolyte disturbance (particularly K+) or metabolic acidosis.
  • Myocardial suppression due to metabolic acidosis.
  • Venous thromboembolism.
  • Myocardial infarction (may be a cause or a complication of DKA).
  • Diabetic retinopathic changes may be seen prior to or after therapy for DKA.
  • Hypophosphataemia - rarely has significant clinical effects. Although there is a large loss of total body phosphate in DKA, there is no evidence of benefit of phosphate replacement but phosphate measurement and replacement should be considered in the presence of respiratory and skeletal muscle weakness.
  • Adult respiratory distress syndrome.
  • Mortality rates have fallen significantly in a period of 20 years - from 7.96% to 0.67%. The mortality rate is still high in developing countries and among non-hospitalised patients.
  • Prognosis worsens with age and the nature and severity of the underlying precipitating pathology (particularly myocardial infarction, sepsis and pneumonia).
  • The presence of coma at presentation, hypothermia or persistent oliguria are poor prognostic indicators.
  • Cerebral oedema remains the most common cause of mortality, particularly in young children and adolescents.
  • The main causes of mortality in the adult population include severe hypokalaemia, adult respiratory distress syndrome and comorbid states such as pneumonia, acute myocardial infarction and sepsis.
  • Patients with established type 1 diabetes should be given as much information as possible about risk factors for DKA and how to monitor their own glucose and ketone levels.
  • Education programmes for patients with diabetes, particularly concerning what to do in cases of illness ('sick day rules'). See separate Diabetes and Intercurrent Illness article.
  • Structured educational programmes provide advice on how to avoid omitting insulin, increasing insulin doses if unwell and when to test for ketones.
  • Patients should be advised to measure their ketone levels if they are unwell, as this may identify early ketosis, which can be addressed by increasing insulin doses. They should also be encouraged to seek medical attention if levels are increased.
  • Testing ketones in capillary blood has not been shown to be better for preventing DKA than urine testing.
  • People with recurrent DKA may have underlying precipitating factors and psychological support may be beneficial.
  • Drugs such as SGLT2 inhibitors should be used with caution in people at high risk of DKA.

Further reading & references

  1. Management of Diabetic Ketoacidosis in Adults 2nd Edition; Joint British Diabetes Societies Inpatient Care Group (September 2013).
  2. Misra S, Oliver NS; Diabetic ketoacidosis in adults. BMJ. 2015 Oct 28;351:h5660. doi: 10.1136/bmj.h5660.
  3. Misra S, Oliver N, Dornhorst A; Diabetic ketoacidosis: not always due to type 1 diabetes. BMJ. 2013 Jun 10;346:f3501. doi: 10.1136/bmj.f3501.
  4. Ovalle F, Vaughan TB 3rd, Sohn JE, et al; Catamenial diabetic ketoacidosis and catamenial hyperglycemia: case report and review of the literature. Am J Med Sci. 2008 Apr;335(4):298-303.
  5. Type 1 diabetes in adults: diagnosis and management; NICE Guidelines (August 2015)
  6. Bialo SR, Agrawal S, Boney CM, et al; Rare complications of pediatric diabetic ketoacidosis. World J Diabetes. 2015 Feb 15;6(1):167-74. doi: 10.4239/wjd.v6.i1.167.
  7. Gosmanov AR, Gosmanova EO, Dillard-Cannon E; Management of adult diabetic ketoacidosis. Diabetes Metab Syndr Obes. 2014 Jun 30;7:255-64. doi: 10.2147/DMSO.S50516. eCollection 2014.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Sean Kavanagh
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
1542 (v25)
Last Checked:
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