Management of diabetic ketoacidosis
Introduction
Diabetic ketoacidosis (DKA) is the metabolic abnormality of type 1 diabetes. Near patient testing for the ketones is now readily available for monitoring allowing for a shift away from using glucose levels to drive treatment decisions in the management of DKA. National UK guidelines have been developed to reflect the development in technology.1 They are evidence based where possible but are also drawn from accumulated multiprofessional knowledge and consensus agreement.
Pathophysiology and diagnosis
DKA usually occurs as a consequence of insulin deficiency. This enhances hepatic glucose production. Enhanced fat breakdown increases serum free fatty acids that are then metabolised producing large quantities of ketones and metabolic acidosis. Fluid depletion is a serious problem caused by osmotic diuresis. Electrolyte shifts and depletion are, in part, related to the osmotic diuresis. Hyper- and hypokalaemia are particular dangers.
Absolute diagnostic criteria do not exist, however, the following are proposed: ketonaemia ≥3 mmol/l by ketone meter, or significant ketonuria (more than 2+ on standard urine sticks); blood glucose over 11 mmol/l or known diabetes mellitus; and venous bicarbonate (HCO3−) <15 mmol/l and/or venous pH <7.3.
Developments in management
Recent developments now allow us to focus on the underlying metabolic abnormality (ketonaemia), which simplifies the treatment of those who present with modest elevation of blood glucose but with acidosis secondary to ketonaemia ‘euglycaemic diabetic ketoacidosis’.2,3
Blood glucose is routinely checked at the bedside, but portable ketone meters now also allow bedside measurement of 3-beta-hydroxybutyrate.4–7 The resolution of DKA depends upon the suppression of ketonaemia, therefore the measurement of blood ketones now represents best practice in monitoring the response to treatment.8 Access to blood gas and blood electrolyte measurements is now usually available within a few minutes of blood being taken. Therefore glucose, ketones and electrolytes, including bicarbonate and venous pH, should be assessed at, or near, the bedside.
The involvement of diabetes specialist teams
Diabetes specialist team (DST) involvement shortens patient stay and improves outcomes.9 All patients should be reviewed by a member of the DST prior to discharge, not undertaking this is a governance issue.10
General management issues
There is universal agreement that the most important initial therapeutic intervention is appropriate fluid replacement followed by insulin administration. The main aims of fluid replacement are to:
restore circulatory volume
clear ketones
correct electrolyte imbalance.
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 rectification of electrolyte disturbance.
Assessment of severity
The presence of one or more of the following may indicate severe DKA and admission to a level 2/high dependency unit environment; insertion of a central line and immediate senior review should be considered:
blood ketones over 6 mmol/l
bicarbonate level below 5 mmol/l
venous/arterial pH below 7.1
hypokalaemia on admission (under 3.5 mmol/l)
Glasgow Coma Scale less than 12 or abnormal AVPU (Alert, Voice, Pain, Unresponsive) scale
oxygen saturation below 92% on air (assuming normal baseline respiratory function)
systolic blood pressure below 90 mmHg
pulse over 100 or below 60 bpm.
Insulin therapy and metabolic treatment targets
A fixed rate intravenous insulin infusion (FRIVII) calculated on 0.1 units/kg infusion is recommended. Patient demographics are changing and patients with DKA are now more likely to be obese or suffering with other insulin-resistant states, including pregnancy. This has led to the re-emergence of FRIVII in adults in the USA and international paediatric practice.11–13 The FRIVII may need to be adjusted; the recommended targets are:
reduction of the blood ketone concentration by 0.5 mmol/l/hour
if ketone meter not available, the venous bicarbonate should rise by 3 mmol/l/hour and capillary blood glucose fall by 3 mmol/l/hour
potassium should be maintained between 4.0 and 5.0 mmol/l.
Intravenous glucose concentration
The management should be focused on clearing ketones as well as normalising blood glucose. It is often necessary to administer an intravenous (iv) infusion of 10% glucose via an iv pump in order to avoid hypoglycaemia and permit the continuation of a FRIVII to suppress ketogenesis. Introduction of 10% glucose is recommended when the blood glucose falls below 14 mmol/l. It is important to continue 0.9% sodium chloride solution concurrently via an iv pump.
Continuation of long-acting insulin analogues
In the last few years the use of long-acting basal insulin analogues (insulin detemir – Levemir®, insulin glargine – Lantus®) has become widespread. Continuation of long-acting analogues during the initial management of DKA provides background insulin when the iv insulin is discontinued. This avoids rebound hyperglycaemia when iv insulin is stopped and should avoid excess length of stay.
Serious complications of DKA and its treatment
Hypokalaemia and hyperkalaemia are potentially life-threatening conditions during the management of DKA. There is a risk of acute renal failure associated with severe dehydration and it is therefore recommended that no potassium be prescribed with the initial fluid resuscitation or if the serum potassium level remains above 5.5 mmol/l. However, potassium will almost always fall as the DKA is treated with insulin, thus it is recommended that 0.9% sodium chloride solution with potassium 40 mmol/l (ready-mixed) is prescribed as long as the serum potassium level is below 5.5 mmol/l and the patient is passing urine.
If the serum potassium level falls below 3.5 mmol/l the potassium regimen needs review. All aspects of potassium use must comply with local and national guidance.14 Trusts need to ensure that they have local protocols in place, which allow for the safe administration of concentrated potassium injectables. Other serious complications include cerebral and pulmonary oedema which are discussed in the online document.1 Close attention to fluid balance and slower fluid replacement is recommended for younger adults; for children <18 years of age use the British Society for Paediatric Endocrinology and Diabetes DKA guidelines which can be found at: www.bsped.org.uk/professional/guidelines/docs/DKAGuideline.pdf
Hypoglycaemia
The blood glucose may fall very rapidly as ketoacidosis is corrected and a common mistake is to allow it to drop to hypoglycaemic levels. This may result in a rebound ketosis driven by counter-regulatory hormones. Severe hypoglycaemia is also associated with cardiac arrhythmias, acute brain injury and death. It is partly for this reason that 10% glucose is recommended.
Conclusion and summary
DKA is a medical emergency with a significant morbidity and mortality. It is now recommended that FRIVII be used with bedside measurement of metabolic parameters. The DST should always be involved as soon as possible and ideally within 24 hours because this has been demonstrated to be associated with a better patient experience and reduced length of stay.
In the management of diabetic ketoacidosis the following guidance should therefore be followed:
measure blood ketones, venous (not arterial) pH and bicarbonate and use results as treatment markers
monitor ketones and glucose using bedside meters, when available and operating within their quality assurance range
monitor electrolytes on blood gas analysers with intermittent laboratory confirmation
replace ‘sliding scale’ insulin with weight-based FRIVII
involve the DST as soon as possible
continue long-acting insulin analogues as normal.1
- Royal College of Physicians
References
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- Joint British Diabetes Societies Inpatient Care Group
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- Munro JF,
- Campbell IW,
- McCuish AC,
- Duncan LJP
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- Sheikj-Ali M,
- Karon BS,
- Basu A,
- et al.
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- Wallace TM,
- Matthews DR
- ↵
- Wiggam MI,
- O'Kane MJ,
- Harper R,
- et al.
- ↵
- ↵
- Clement S,
- Braithwaite SS,
- Magee MF,
- et al.
- ↵
- Kitabchi AE,
- Umpierrez GE,
- Miles JM,
- Fisher JN
- British Society for Paediatric Endocrinology and Diabetes (BSPED) guidelines for the management of DKA. www.bsped.org.uk/professional/guidelines/docs/DKAGuideline.pdf.
- ↵ International Society for Pediatric and Adolescent Diabetes. (IPSAD) 2007. www.ispad.org/FileCenter/10-wolfsdorf_Ped_Diab_2007,8.28-43.pdf.
- ↵
- National Patient Safety Authority
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- Introduction
- Pathophysiology and diagnosis
- Developments in management
- The involvement of diabetes specialist teams
- General management issues
- Assessment of severity
- Insulin therapy and metabolic treatment targets
- Intravenous glucose concentration
- Continuation of long-acting insulin analogues
- Serious complications of DKA and its treatment
- Hypoglycaemia
- Conclusion and summary
- References
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