Diabetic Ketoacidosis (DKA) is a life threatening emegency and requires prompt recognition and treatment. Dr David Ewins is a Consultant Physician in Endocrinology and Diabetes and talks with Scott about the approach to evaluating and managing DKA in adults as well as some of the finer points and controversies that exist.

Have a listen to the episode below or follow the links to iTunes or Podbean (non-iPhone users)


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What is DKA?

DKA is a life threatening medical emergency, which occurs usually in patients with type 1 diabetes mellitus due to a deficiency or lack of insulin. Rarely, it can also occur in those with other forms of diabetes (1,2).


Insulin usually impairs gluconeogenesis which occurs mainly in the liver, encourages glycogen formation from glucose, and promotes glucose uptake from the blood into the tissues of the body. It therefore acts to lower the blood glucose level (2,3).

In DKA, the deficiency of insulin causes the blood glucose to rise. But this is not the only consequence of the lack of insulin…………..

Insulin itself also has several anabolic effects including promoting the formation of fat from fatty acids and protein from amino acids.

With a lack of insulin, the opposite can occur and there is a breakdown of fat into fatty acids, and fatty acids into ketones. These ketones can be used to generate a small amount of energy, but are acidic. The insulin deficiency causes an excess of ketones to develop which cannot be buffered by the body and cause the blood to become more acidic, leading to Diabetic Ketoacidosis (DKA) (2,3).

If untreated, DKA can be fatal. Indeed, this was the cause of death of patients with Type 1 Diabetes before the discovery of insulin injections in the 1920s (4). If treated properly, sick patients presenting with DKA will normally make a full recovery.

DKA itself can be a presenting feature of type 1 diabetes or can be caused by poor compliance with insulin treatment in patients with diabetes. This includes deliberate or accidental omission of insulin injections (3,5).

DKA can also be caused by an acute illness including an infection, myocardial infarction or recent surgery. At times of an acute illness there is an increase in counter regulatory hormones, such as glucagon and adrenaline, which act to raise the blood glucose as part of the stress response. This is normally balanced by an increased of insulin, driving the glucose into the tissues so that it can be used. If there is a deficiency of insulin, the acute illness can then precipitate DKA through unopposed actions of these counter regulatory hormones (1,2,5).

A Typical Case


• 24-year-old female
• History of type 1 diabetes
• 3-day history of nausea, vomiting, and abdominal pain
• Capillary blood glucose measurement in the ED elevated at 23mmol/L
• Previous history of problems with insulin compliance, but states they have been taking their insulin and have recently had a 5-day course of amoxicillin from their GP for a ‘chest infection’
• On examination, appear to be taking deep, sighing breaths

Diagnosis of DKA

Firstly, in any acutely unwell patient, follow the ABCD approach. If DKA is suspected, assess the patient for any clinical features of DKA including the signs and symptoms of a raised blood glucose. The patient may have developed osmotic symptoms such as thirst, polyuria and polydipsia due to the osmotic diuresis caused by a raised blood glucose level (1,2).

As the patient becomes acidotic in DKA, they will try to compensate by hyperventilating, taking deep sighing breaths known as Kussmaul breathing. They are trying the produce a respiratory alkalosis by “blowing off” carbon dioxide and attempt to compensate for the metabolic acidosis of DKA. The acetone in the ketones can be smelt on their breath, which smells like pear drop sweets or nail varnish remover (2,3,5).

Biochemically, the blood glucose level is usually elevated. Rarely, in patients with long standing diabetes and a long unwell period, particularly with vomiting, there can be euglycameic acidosis and a blood glucose in normal range. The ketone level in the blood will be raised or significantly raised in the urine and the patient will be acidotic (see definition).

Diagnosis definition of DKA (from Joint British Diabetes Societies Guidelines) (1):
• Ketonaemia > 3.0mmol/L or significant ketonuria (more than 2+ on standard urine sticks)
• Blood glucose > 11.0mmol/L or known diabetes mellitus
• Bicarbonate (HCO3-) < 15.0mmol/L and/or venous pH < 7.3



Severe DKA would be characterised by the above features, but with:
• pH < 7.1
• Bicarbonate < 5mmol/L
• Ketones > 6mmol/L
• low potassium level at presentation <3.5mmol/L
• Impaired Glasgow Coma Scale (GCS) score < 12
• Haemodynamic compromise including a low Systolic Blood Pressure <90mmHg, or disturbance in heart rate (Pulse >100 or <60bpm)


Patients presenting with one or more of these features should be considered for referral and transfer to a Critical Care Unit (High Dependency Unit/Intensive Care Unit) providing closer monitoring and central venous access (7).


There are three main factors which need addressing:
1. Intravenous fluid resuscitation
2. Potassium replacement when appropriate
3. A Fixed Rate Intravenous Insulin Infusion (FRIII)

The patient should always be discussed with the senior doctor on call at an early stage and at subsequent stages if there are any clinical concerns about their condition. Additionally, the inpatient specialist diabetes team should be informed and involved in the care of the patient as soon as possible.

Intravenous Sodium Bicarbonate may be required, but is usually not necessary.
Most local hospital guidelines follow the Joint British Diabetes Society Guidelines (1). The guidelines are divided into different time periods.

Hour 1


Firstly, it’s important to assess the patient and make the diagnosis of DKA as discussed above. As for any critically unwell patient, an Airway, Breathing, Circulation (A,B,C) approach is best to identify any immediate problems to be addressed (8).

Early intravenous access is important for the provision of intravenous fluids. Patients with DKA are often profoundly dehydrated by up to 6-9L (15) and will require insertion of two large bore intravenous cannulae (1,3,5). In severe cases, central venous access may be required. In some cases, access can be so difficult that intraosseous access is required in the ED or acute setting.

Once access is established, bloods should be taken for:
• Urea and electrolytes – check renal function and assess the potassium level for guiding its replacement in fluids
• Glucose – usually raised for assisting diagnosis
• Ketones – for diagnosis/assessing severity
• Full Blood Count – assess for infection in terms of high or low white cell count, and systemic disturbance
• Venous Blood Gas (VBG) – for diagnosis/assessing severity

Local hospital policies will vary, but often there is a DKA order set of bloods which includes all the above and can be ordered as a set simultaneously to be taken immediately on admission, in Chester, we call this DKA0.

Immediate intravenous fluid resuscitation is required. Usually, normal saline (Sodium Chloride 0.9%) is used, with the first 1L being given over the first 30 to 60 minutes. As the fluids are commenced as soon as access is gained, the patient’s blood results will not be available and therefore potassium is not added to the first bag of fluids (1,5).

From the second bag of fluids onwards, intravenous potassium will be added to the fluids according to the latest serum potassium result.

The effect of insulin pushing potassium into the cells and correction of metabolic acidosis cause a drop in the serum potassium concentration. Hypokalaemia can cause corrected QT (QTc) prolongation on the ECG and there is a real risk of a hypokalaemic cardiac arrest. This is an early cause of death in DKA (1,2,3,5).

Therefore, potassium supplementation will be required in the further fluids, guided be the patient’s blood results. If the serum potassium is 3.5 to 5.5mmol/L, 40mmol of potassium chloride would be added per litre of intravenous fluid. No potassium would be added if the serum potassium is > 5.5mmol/L. If the potassium is < 3.5mmol/L, Critical Care advice should be sought for providing higher doses of intravenous potassium replacement (1,9).

After initiating fluids and potassium replacement, a Fixed Rate Intravenous Insulin Infusion (FRIII) should be commenced. This is commenced at 0.1 units/Kg/hour, so for most patients (e.g. 60-80Kg), this would work out as 6 to 8 units/hour. This is usually given in a syringe pump with 50 units of actrapid (short acting insulin) in 50ml of 0.9% Sodium Chloride and given at a fixed rate (1,5). As the concentration of insulin is 1 unit/ml, the fixed rate is equal to the number of units/Kg/hr required.

The FRIII must be continued until the ketoacidosis is corrected. If the patient is a known diabetic already on insulin therapy, it is important to prescribe their usual long acting insulin analogue at the same time. This makes converting them back to their usual subcutaneous insulin much easier by providing some background subcutaneous insulin (1,5).

If the patient has a decreased consciousness level, with GCS < 12, a critical care referral should be made and a nasogastric (Ryle’s) tube should be inserted for drainage of the stomach due to a high risk of aspiration.

A urinary catheter should be inserted for accurate measurement of urine output and assessment of the patient’s fluid balance (1,3).

The patient should be having continuous cardiac monitoring, and a chest x ray should be considered, in part to look for any focal consolidation or evidence of a low respiratory tract infection as a trigger for DKA. Blood cultures and urine cultures should also be sent, and any evidence of infection should be treated with prompt administration of intravenous antibiotics (1,5,10).

A pregnancy test should be performed in women of a child bearing age (1).

Hours 1-6


The patient’s blood tests should be repeated after 1 hour (Urea and Electrolytes, Glucose, Ketones, Venous Blood Gas) to assess their progress. Again, local hospital policies will vary, but there may be a DKA order set of bloods which includes all the above and can be ordered as a set simultaneously. At Chester, this is unsurprisingly DKA1

Hourly blood capillary glucose monitoring is essential.

The aim of the intravenous fluid resuscitation (+/- potassium) and FRIII is to treat the DKA by producing a steady rise in the venous bicarbonate level of 3mmol/L/hour, a steady fall in blood ketones of 0.5mmol/L/hour and to maintain the blood potassium level in the normal range.

After the first litre of intravenous fluids, the second and third litres of fluid (each with potassium replacement guided by the blood results) are usually given each over 1 to 2 hours, and the fourth and fifth litres of fluids (again with potassium replacement guided by the blood results) would be given more slowly, typically each over 4-6 hours, although this will depend upon the individual patient’s condition and clinical judgement as to their fluid balance.

The patient’s blood tests should be repeated after 4 hours (Urea and Electrolytes, Glucose, Ketones, Venous Blood Gas) to assess their progress and again there may be a DKA order set of bloods which can be ordered simultaneously.

The FRIII is continued until the acidosis is corrected. As a guide, this is until the pH is > 7.35, the venous bicarbonate is > 20 mmol/L, and the blood ketones are undetectable or <0.3mmol/L. The blood glucose level may start to drop with the FRIII. Therefore, to prevent the patient from becoming hypoglycaemic before the acidosis is corrected, a 10% dextrose intravenous infusion may need to be added at 125 ml/hour, to run alongside in addition to their current fluid when the glucose is below 14 mmol/L (1,5).

Any potential precipitating factors for the DKA should continue to be sought and treated as appropriate (1, 2,7).


Hour 6 onwards

The patient’s blood Urea and Electrolytes, ketones and bicarbonate would need to continue to be monitored, being checked at 6 and 12 hours.

The overall aim within this time is to assess whether the patient’s clinical condition is improving with continued management outlined above and that their biochemical tests are improving. Intravenous fluid replacement is continued with potassium replacement and insulin, being vigilant to avoid hypoglycaemia (1).

All cases of DKA should be discussed with a senior doctor. The patient should be assessed for any complications of the treatment of DKA. These include fluid overload (which may require critical care input for invasive monitoring to guide further fluids) and cerebral oedema, which be detected by a reducing conscious level (GCS should be monitored, remembering that a GCS <12 is an indication for critical care involvement) (1).

Again, the inpatient specialist diabetes team should be involved in the care of the patient as soon as possible.

The cause of the DKA can be assessed including whether the patient had accidentally or deliberately omitted insulin treatment. Again, look for any concurrent infection requiring treatment, or another precipitant including MI.

Usually, after 12 to 24 hours of treatment the patient’s biochemical blood tests will have returned to normal. The intravenous insulin infusion is continued until the patient is eating and drinking (1,3,5,7).

Conversion to Regular Insulin Prescription


Once the patient feels well, is biochemically back to normal and eating and drinking, provided their long acting subcutaneous insulin has been continued, their short acting insulin can be restarted at their usual dose just before their next meal.
Approximately 30 minutes after giving this, the intravenous insulin infusion can be stopped.

The patient then continues their usual insulin regime e.g. basal bolus regime: short acting subcutaneous insulin given with subsequent meals and a long acting subcutaneous insulin once daily (1,11).

If possible, it’s best to switch the patient back to their usual subcutaneous insulin during the day (i.e. before breakfast or lunch, rather than before their evening meal) to ensure continuity of care should there be subsequent fluctuations in their blood glucose level.


DKA with Insulin Pumps

These patients should be managed in exactly the same way as described above. Their subcutaneous insulin pump should be switched off, disconnected and taken down. This avoids confusion since the FRIII will be used to treat their DKA. As for any patient with DKA the inpatient specialist diabetes team should be informed as soon as possible.

Only the inpatient specialist diabetes team and the patient themselves would have knowledge of using an insulin pump so only these individuals should recommence this when appropriate following resolution of the DKA. This should be performed under the guidance of the diabetes specialist team.


Complications of DKA

There may initially be hyperkalaemia, particularly with severe dehydration, metabolic acidosis and renal impairment. Then, Hypokalaemia can be caused by the administration of insulin and correction of the metabolic acidosis. As discussed, hypokalaemia can be a cause of early death in DKA through cardiac arrest. It is important to closely monitor the patient’s potassium level, ensuring this is replaced in intravenous fluids as required (1,5,9).

Hypoglycaemia can occur through the administration of the FRIII, but this should be prevented through the administration of 10% dextrose alongside the intravenous fluids when the glucose is <14mmol/L. The FRIII should be continued at a fixed rate until the acidosis has resolved (1,5).

Cerebral oedema can occur, more often in paediatric patients but also in adult patients. This is thought to be caused by rapid changes in osmotic pressures as the patient is treated with the FRIII and fluids. This is a difficult condition to treat. Patients may initially develop a headache followed by a falling conscious level (GCS) due to increasing intracerebral pressure. This would be an indication for immediate referral to critical care for measures to try to decrease intracerebral pressure and treat the cerebral oedema (1,13).

Pulmonary oedema can occur particularly in elderly patients with heart failure and/ or renal impairment due to the large volume administration of fluids to treat the DKA. This may require critical care input for invasive monitoring to guide further fluids (1,2).




  1. Adjusting or removing the FRIII early. The FRIII should not be reduced or taken down until the DKA is fully treated. If the glucose is dropping <14mmol/L, 10% dextrose should be commenced usually at 125ml/hr and the FRIII should not be reduced.
  2. Inadequate potassium replacement. Potassium should be replaced in the intravenous fluids, guided by the close monitoring of the patient’s blood results as above.



Unless there are concerns regarding a critically ill patient, particularly a patient’s oxygenation or ventilation, a venous blood gas (VBG) and venous bicarbonate will provide all the information required for the management of DKA, and is more comfortable for the patient than an arterial blood gas (ABG) (1). Therefore, if a patient’s peripheral oxygen saturations are within normal range 94 to 98% or better on room air, with GCS 15, and there are no concerns regarding their ventilation, then VBG and venous bicarbonate will suffice.

The choice of intravenous fluids is still debated, but UK national guidance for the management of DKA on the ward recommends the use of 0.9% sodium chloride with potassium replacement as guided by the patient’s blood results (1). The purpose of this discussion is not to enter into the complex arguments around fluid management.

Use of IV Sodium Bicarbonate

This would be only be used with discussion with a senior doctor prior to considering it, if the pH is < 7 and is not improving after presentation



In summary, we have discussed the assessment and management of DKA in adult patients including the use of a FRIII. A document which is really useful for further essential reading is the Joint British Diabetes Society Guidelines on the management of DKA in adults (1).

For young people under the age of 18 years with DKA, a senior doctor oncall and the paediatric diabetes service should be contacted immediately and the BSPED DKA guidelines followed (14).

I’d like to thanks Dr Ewins for his time and effort in recording this podcast and the medical education department at Chester for their continued support.

Email any feedback or other aspects of diabetes you’d like covered foamdation@gmail.com

Twitter: @FOAMdation @scottymwilliams

Or you can complete the message form on the contact tab of the website

Speak soon,



1. The Management of Diabetic Ketoacidosis in Adults. Joint British Diabetes Societies Inpatient Care Group. Second Edition Update: September 2013 Accessed 5/7/17

2. Kasper, Fauci et al. Harrison’s Principles of Internal Medicine 19th edition. McGrawhill 2016

3. Kumar, Clark et al. Kumar and Clark’s Clinical Medicine 9th edition. Elsevier 2016

4. Banting F, Best C et al. Pancreatic extracts in the treatment of diabetes mellitus. CMAJ 1922;12:141–6

5. NICE guideline 17- Type 1 Diabetes in adults: diagnosis and management
Website https://www.nice.org.uk/guidance/ng17
Accessed 6/7/17

6. English P, Williams G. Hyperglycaemic crises and lactic acidosis in diabetes mellitus. Postgrad Med J 2004;80(943):253-261.

7. National Institute for Clinical and Healthcare Excellence. Acutely ill patients in hospital (CG50). http://www.nice.org.uk/CG50 2007
Accessed 5/7/17

8. Resuscitation Council (UK). Adult Advanced Life Support https://www.resus.org.uk/resuscitation-guidelines/adult-advanced-life-support/
Accessed 7/7/17

9. National Patient Safety Agency. Potassium solutions: risks to patients from errors occurring during intravenous administration. http://www.nrls.npsa.nhs.uk/resources/?entryid45=59882
Accessed 6/7/17

10. Surviving Sepsis Campaign http://www.survivingsepsis.org/SiteCollectionDocuments/SSC_Bundle.pdf
Accessed 5/7/17

11. Chowdhury T, Cheston H et al. Managing adults with diabetes in hospital during an acute illness. British Medical Journal 2017;357:528-531

12. Price H, Thomsett K et al. Developing best practice tariffs for diabetic ketoacidosis and hypoglycaemia. Pract Diab 2013; 30(1):6-8

13. Edge J, Jakes R et al. The UK case–control study of cerebral oedema complicating diabetic ketoacidosis in children. Diabetologia 2006; 49(9):2002-2009.

14. British Society for Paediatric Endocrinology and Diabetes. BSPED Recommended Guideline for the Management of Children and Young People under the age of 18 years with Diabetic Ketoacidosis 2015 https://www.bsped.org.uk/clinical/docs/DKAGuideline.pdf
Accessed 6/7/17

15. A Gosmanov et al, Management of Adult Diabetic Ketoacidosis. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 2014;7:255-264







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