Developments in the management of diabetic ketoacidosis in adults: implications for anaesthetists

Abstract

Key points•Diabetic ketoacidosis (DKA) is a medical emergency and bedside capillary ketone testing allows timely diagnosis and identification of successful treatment.•0.9% saline with premixed potassium chloride should be the main resuscitation fluid on the general wards and in theatre; this is because it complies with National Patient Safety Agency recommendations on the administration of potassium chloride.•Weight-based fixed rate i.v. insulin infusion (FRIII) is now recommended rather than a variable rate i.v. insulin infusion (VRIII).•The blood glucose must be kept above 14 mmol litre−1 with the FRIII.•Precipitating factor(s) needs to be identified and treated. Surgery and also critical care may be indicated to manage the patient presenting with DKA. •Diabetic ketoacidosis (DKA) is a medical emergency and bedside capillary ketone testing allows timely diagnosis and identification of successful treatment.•0.9% saline with premixed potassium chloride should be the main resuscitation fluid on the general wards and in theatre; this is because it complies with National Patient Safety Agency recommendations on the administration of potassium chloride.•Weight-based fixed rate i.v. insulin infusion (FRIII) is now recommended rather than a variable rate i.v. insulin infusion (VRIII).•The blood glucose must be kept above 14 mmol litre−1 with the FRIII.•Precipitating factor(s) needs to be identified and treated. Surgery and also critical care may be indicated to manage the patient presenting with DKA. Diabetic ketoacidosis (DKA) is a medical emergency. The diagnostic triad is:DKA can occur in both type 1 and type 2 diabetes mellitus and, although preventable, it remains a frequent and life-threatening complication. Errors in the management of DKA are not uncommon and are associated with significant morbidity and mortality. The majority of mortality and morbidity in DKA are attributable to delays in presentation and initiation of treatment. Rapid recognition and treatment of DKA is critical. (i)Ketonaemia ≥3.0 mmol litre−1 or significant ketonuria (more than 2+ on urine sticks)(ii)Blood glucose >11.0 mmol litre−1 or known diabetes mellitus(iii)Bicarbonate <15.0 mmol litre−1, venous pH <7.3, or both. To overcome these concerns and to highlight current management strategies, the Joint British Diabetes Societies (JBDS) published guidelines in 2010. This was updated in consultation with the Intensive Care Society in September 2013.1Joint British Diabetes Societies Inpatient Care GroupThe Management of Diabetic Ketoacidosis in Adults. 2nd Edn. 2013http://www.diabetes.org.uk/Documents/About%20Us/What%20we%20say/Management-of-DKA-241013.pdfGoogle Scholar This article will review the pathophysiology of DKA and highlight the modern management of DKA that is relevant for anaesthetists. A summary of the JBDS guidelines pertinent to intensivists has been published.2Kohler K Levy N Management of diabetic ketoacidosis: a summary of the 2013 Joint British Diabetes Societies guidelines.J Intensive Care Soc. 2014; 15: 2-5Crossref Scopus (10) Google Scholar In England in 2010, there were 14 375 admissions to acute NHS trusts where DKA was the primary diagnosis. Subsequently, it was estimated that 13% of these patients were admitted to Intensive Care Units (2% of all general ICU admissions).3Rudd B Patel K Levy N Dhatariya K A survey of implementation of NHS diabetes guidelines for management of diabetic ketoacidosis in the intensive care units of the East of England.J Intensive Care Soc. 2013; 14: 60-64Crossref Scopus (5) Google Scholar Furthermore, the National Diabetes Inpatient Audit 2012 found that 0.5% of in-patients with diabetes actually developed DKA as an inpatient whilst in hospital.4Health and Social Care Information CentreNational Diabetes Inpatient Audit. 2012http://www.diabetes.org.uk/Documents/Reports/NaDIA-annual-report-2012-0613.pdfGoogle Scholar The mortality rate has decreased in some patient populations; however, in the elderly and in patients with comorbidities, it remains >5%. DKA results from a relative or absolute insulin deficiency with a concomitant increase in counter regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone. Hyperglycaemia ensues because of increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues. This is magnified by transient insulin resistance because of the hormone imbalance itself. The combination of insulin deficiency and increased counter regulatory hormones leads to the release of free fatty acids and their unrestrained oxidation in the liver to ketones. These ketones include acetone, 3-beta-hydroxybutyrate, and acetoacetate. The predominant ketone in DKA is 3-β-hydroxybutyrate. Hydrogen ions produced by the dissociation of the ketone bodies causes the metabolic acidosis.5Kitabchi AE Umpierrez GE Miles JM Fisher JN Hyperglycaemic crises in adult patients with diabetes.Diabetes Care. 2009; 32: 1335-1343Crossref PubMed Scopus (1092) Google Scholar Hyperglycaemia causes osmotic fluid shifts from intracellular to extracellular compartments. The glucose load in the glomerular tubules exceeds the renal threshold leading to glucosuria and an obligatory osmotic diuresis. This diuresis causes a loss of sodium, potassium, and phosphate along with water and glucose. The three most common causes are:Inadequate insulin therapy is the recognized cause of hospital-acquired DKA. This may be caused by inadequate prescription or administration of insulin, or insufficient monitoring of capillary blood glucose (CBG). (i)An underlying infection(ii)Missed insulin treatment(iii)First presentation of diabetes mellitus.6Causes of DKANHS Choices.http://www.nhs.uk/Conditions/diabetic-ketoacidosis/Pages/Causes.aspxGoogle Scholar The cause may occasionally necessitate emergency surgical treatment (e.g. appendicitis; infarcted bowel; incision and drainage of abscess; ectopic pregnancy). DKA occurs predominantly in patients with type 1 diabetes, but it can also develop in patients with ketone prone type 2 diabetes. There is a wide clinical spectrum in the presentation of DKA. DKA is a recognized cause of the acute abdomen, and this in itself can actually result in unnecessary emergency surgery. Presentation in type 2 diabetes is the same as in type 1 diabetes; however, some studies have found there to be a different biochemical presentation with a less severe acidosis and a tendency for normal initial serum potassium levels.7Newton CA Raskin P Diabetic ketoacidosis in type 1 and type 2 diabetes mellitus: clinical and biochemical differences.Arch Intern Med. 2004; 164: 1925-1931Crossref PubMed Scopus (159) Google Scholar Initial investigations fall into three categories:Ongoing investigations are then required to monitor the effect of treatment, and to ensure successful and safe treatment. (i)Establish diagnosis of DKA(ii)Baseline investigations(iii)Identify cause. As DKA is the triad of:The following investigations are mandatory. (i)Ketonaemia ≥ 3.0 mmol litre−1 or significant ketonuria (more than 2+ on urine sticks)(ii)Blood glucose >11.0 mmol litre−1 or known diabetes mellitus(iii)Bicarbonate <15.0 mmol litre−1, venous pH <7.3, or both. (i)Capillary ketone levels/urinalysis for ketones(ii)Blood sugar(iii)Blood gas for pH, bicarbonate, or both. In the past, diagnosis and successful treatment of DKA was guided by CBG with the erroneous assumption that correction of hyperglycaemia would be a marker for suppression of ketogenesis and successful reversal of acidosis. However, CBG is both a poor determinant of severity and a poor surrogate marker for successful treatment. Euglycaemic ketoacidosis is possible depending on the hepatic glycogen stores before the onset of DKA. This demonstrates the necessity for ketone monitoring. Ketone meters (Fig. 1) are now available for rapid testing for β-hydroxybutyrate at the bedside. Handheld ketone meters are operated in an identical fashion to bedside CBG meters. Results are available within 10 s allowing immediate differentiation between simple hyperglycaemia and ketotic states. Trials have found that the utilization of blood ketone testing is more effective than urine acetoacetate testing in improving diagnosis and their use is associated with a reduced time to recovery from DKA and shorter hospital stay.8Klocker AA Phelan H Twigg SM Craig ME Blood beta-hydroxybutyrate vs urine acetoacetate testing for the prevention and management of ketoacidosis in type 1 diabetes: a systematic review.Diabetic Med. 2013; 30: 818-824Crossref PubMed Scopus (75) Google Scholar To make the diagnosis, a blood gas is essential for the assessment of the acidosis and serum bicarbonate levels. Recent evidence has shown little difference between arterial and venous pH and bicarbonate.9Kelly AM The case for venous rather than arterial blood gases in diabetic ketoacidosis.Emerg Med Australas. 2006; 0: 64-67Crossref Scopus (40) Google Scholar These small differences are inconsequential to the diagnosis or management of DKA, and therefore the JBDS guidelines recommend the use of venous blood gases if the patient is managed on the ward, in order to prevent repeated arterial punctures. These include full blood count, urea, creatinine, potassium, sodium, chloride, CRP, and liver function tests. It is imperative to discover the cause of the DKA and investigations should be based on the clinical findings. Common investigations include ECG, blood cultures, amylase, and pregnancy test. To assure safe response to treatment, the following should occur hourly till resolution of the ketosis:To assure metabolic stability, the following should occur at a minimum of 2 hourly intervals until resolution of the ketosis: (i)CBG/arterial blood glucose (if arterial line sited)(ii)Capillary blood ketones. (iii)pH(iv)bicarbonate(v)potassium. DKA is a life-threatening condition and resuscitation along with initial treatment must occur simultaneously with clinical assessment. Appropriate history, examination, and investigations should be undertaken to diagnose the condition, identify the severity, and identify the cause. Initial management should focus on: (i)Airway protection, if required(ii)Fluid resuscitation(iii)Insulin administration(iv)Assessment of severity(v)Identification of cause. An airway, breathing, circulation, disability, exposure (ABCDE) approach will provide structure to the initial resuscitation. Appropriate venous access must be obtained. The most important initial therapeutic invention in DKA is fluid replacement followed by insulin administration. It is now universally agreed that crystalloids with a sodium concentration in the range of 130–154 mmol litre−1 should be used as the resuscitation fluid. In the UK, this is generally either 0.9% saline or Hartmann's solution. There is ongoing debate on which crystalloid is superior. There is evidence to suggest that the use of balanced crystalloid solutions are associated with a faster resolution of the metabolic acidosis and less hyperchloraemic metabolic acidosis.10Mahler SA Conrad SA Wang H Arnold TC Resuscitation with balanced electrolyte solutions prevents hyperchloraemic acidosis in patients with diabetic ketoacidosis.Am J Emerg Med. 2011; 29: 670-674Abstract Full Text Full Text PDF PubMed Scopus (99) Google Scholar11Chua H-R Venkatesh B Stachowski E et al.Plasma-Lyte 148 vs 0.9% saline for fluid resuscitation in diabetic ketoacidosis.J Crit Care. 2012; 27: 138-145Abstract Full Text Full Text PDF PubMed Scopus (92) Google Scholar However, balanced solutions such as Hartmann's solution contains insufficient potassium, and under NPSA rules, 3% potassium chloride should not be stored/added to fluids on the general wards.12National Patient Safety AgencyPotassium solutions: risks to patients from errors occurring during intravenous administration. 2002http://www.nrls.npsa.nhs.uk/resources/?entryid45=59882Google Scholar Therefore, the use of 0.9% saline with premixed potassium chloride is advocated for ward and theatre use. Critical care can both administer concentrated potassium centrally, and add potassium to Hartmann's solution. Thus, critical care may choose to use Hartmann's solution as the primary fluid for resuscitation. Table 1 is an example of a typical fluid replacement regimen for a previously well 70 kg adult. However, the exact rate of infusion should be formulated after clinical assessment of the individual patient. If the patient is shocked, the patient should receive an initial bolus of 500 ml over <15 min, and further fluid boluses dependent on clinical re-assessment.Table 1Typical fluid replacement regimen for a previously well 70 kg adult on the general wardFluid numberFluidRateInitial bag1 litre 0.9% saline1000 ml h−12nd bag1 litre 0.9% saline with premixed potassium chloride500 ml h−13rd bag1 litre 0.9% saline with premixed potassium chloride500 ml h−14th bag1 litre 0.9% saline with premixed potassium chloride250 ml h−15th bag1 litre 0.9% saline with premixed potassium chloride250 ml h−16th bag1 litre 0.9% saline with premixed potassium chloride150 ml h−1Further fluid1 litre 0.9% saline with premixed potassium chlorideClinical assessmentWith regular re-assessment Open table in a new tab Administration of i.v. human soluble insulin is mandatory. Classically the insulin has been titrated against the surrogate marker of the blood glucose using a variable rate i.v. insulin infusion (VRIII). The term ‘variable rate i.v. insulin infusion’ has now replaced the ambiguous and obsolete term ‘sliding scale’. It is now recognized that glucose levels are a poor surrogate marker for resolution of ketosis, and using the blood glucose as a marker to guide insulin therapy may (and does) lead to the erroneous action of reducing insulin whilst the patient is still highly ketotic. A fixed rate administration of i.v. insulin whilst the patient remains ketotic avoids this risk. Thus, recent evidence and guidelines suggest that a weight-dependent fixed rate i.v. insulin infusion (FRIII) should be administered, rather than the variable rate i.v. insulin infusion (VRIII). Table 2 summarizes the advantages and disadvantages of an FRIII.Table 2Advantages and disadvantages of an FRIIIAdvantagesDisadvantages (i)Faster resolution of DKA(ii)No titration of the insulin against the false surrogate marker of capillary glucose(iii)Complete resolution of DKA provided the FRIII is turned off once the ketone levels are <0.6 mmol litre−1Risk of hypoglycaemia if CBG is not measured hourly and additional glucose containing solutions not administered once CBG <14 mmol litre−1 Open table in a new tab The FRIII is administered via an infusion pump. The FRIII is constituted by adding 50 units of human soluble insulin (Actrapid®, Humulin S®) to 0.9% sodium chloride to make a final volume of 50 ml (1 unit ml−1). Ideally this should be provided as a ready-made infusion. The FRIII is then administered at a fixed rate of 0.1 unit kg−1 h−1 (i.e. 7 ml h−1 if weight is 70 kg). Weight should be estimated if not available, and pregnant patients should have their current weight used. Metabolic targets for the continuation of the current fixed rate insulin infusion are:If the above targets are not being achieved, it is necessary to reassess the patient and consider the causes of non-successful treatment. This may include:If it is deemed that unsuccessful treatment is secondary to insufficient insulin, the FRIII will need to be increased in increments of 1 unit h–1 until the targets are met. A maximum rate of 15 units h−1 is recommended. (i)Reduction of blood ketone concentration by >0.5 mmol litre−1 h−1(ii)If blood ketone measurement is not available, the venous bicarbonate should increase by 3.0 mmol litre−1 h−1(iii)Reduction in CBG by 3.0 mmol litre−1 h−1. (i)Non-administration of the insulin for any reason (e.g. tissued cannula, pump not running, anti-syphon valve not used, etc.).(ii)Ongoing co-morbidity that will need senior review(iii)Insufficient insulin. The FRIII should be continued until resolution of the ketosis. Resolution of DKA is defined as:Before stopping the FRIII, it is necessary to administer insulin in another form; otherwise, the patient will re-develop ketosis. The patient can either be recommenced on their usual regimen (if they are eating and drinking) or converted to a variable rate i.v. insulin infusion with concurrent administration of 5% dextrose in 0.45% saline with 0.15% potassium chloride. This transition should ideally be managed by the diabetes specialist team. (i)pH >7.3(ii)bicarbonate >15.0 mmol litre−1(iii)blood ketone level <0.6 mmol litre−1. To aid the transition from i.v. insulin to subcutaneous insulins, it now advised that the long-acting analogue insulins are continued. The long-acting analogue insulins are Levemir®, Lantus®, and Tresiba®. Some units are also beginning to experiment with the continuation of the long-acting human basal insulins such as Humulin I®, Insulatard®, and Insuman Basal®. Continuation of the long-acting insulins avoids rebound hyperglycaemia when the i.v. insulin is stopped and may subsequently reduce the length of stay.13Hsia E Seggelke S Gibbs J et al.Subcutaneous administration of glargine to diabetic patients receiving insulin infusion prevents rebound hyperglycemia.J Clin Endocrinol Metab. 2012; 97: 3132-3137Crossref PubMed Scopus (55) Google Scholar The FRIII should be continued until there is resolution of the ketosis; however, it may cause hypoglycaemia before resolution of the ketosis. Therefore, it is mandatory to perform hourly CBGs and to be prepared to give additional glucose once the CBG is <14 mmol litre−1. It is recommended that 10% glucose at 125 ml h−1 should be administered. In theatre, 20% glucose at 50 ml h−1 or 50% glucose may be administered. The rate of the primary resuscitation fluid may need to be altered to prevent fluid overload. Because of erratic and unpredictable insulin absorption, these devices should probably be stopped and disconnected during an episode of DKA, and only reinstated with diabetes specialist team input. Patients should be considered for critical care referral if any of the following criteria are present:It is often necessary to admit emergency surgical patients to a level 2 or 3 facility, both pre- and post-surgery. (i)Glasgow Coma Score (GCS) <12 or abnormal AVPU (alert, voice, pain, unresponsive) scale(ii)Blood ketones >6 mmol litre−1(iii)Bicarbonate level <5 mmol litre−1(iv)Venous/arterial pH <7.0(v)Hypokalaemia on admission (<3.5 mmol litre−1)(vi)Oxygen saturation <92% on air (assuming normal baseline respiratory function)(vii)Systolic BP below 90 mmHg(viii)Pulse over 100 or below 60 beats min(ix)Anion gap >16 [Anion gap = (Na+ + K+) – (Cl− + HCO3−) ]. Mortality from DKA in the UK has fallen significantly in the last 20 yr from 7.96 to 0.67%.1Joint British Diabetes Societies Inpatient Care GroupThe Management of Diabetic Ketoacidosis in Adults. 2nd Edn. 2013http://www.diabetes.org.uk/Documents/About%20Us/What%20we%20say/Management-of-DKA-241013.pdfGoogle Scholar Hypokalaemia, acute lung injury, and co-morbid states such as pneumonia, sepsis, and myocardial infarction are associated with increased mortality. Cerebral oedema remains the most common cause of death in DKA in children. The exact mechanism is uncertain; however, it is felt that cerebral oedema may be related to cerebral hypoperfusion before treatment, with subsequent vasogenic oedema occurring during DKA treatment as a result of reperfusion of previously ischaemic brain tissue (i.e. the osmotic fluctuations during DKA treatment do not play the primary causal role).14Watts W Edge JA How can cerebral edema during treatment of diabetic ketoacidosis be avoided?.Pediatric Diabetes. 2014; 15: 271-276Crossref PubMed Scopus (21) Google Scholar Table 3 summarizes the risk factors, signs and symptoms, immediate treatment and also the different strategies that are utilized by paediatricians to reduce the risk of cerebral oedema.15Wolfsdorf J Craig ME Daneman D et al.ISPAD clinical practice consensus guidelines 2009 compendium. Diabetic ketoacidosis in children and adolescents with diabetes.Pediatric Diabetes. 2009; 10: 118-133Crossref PubMed Scopus (241) Google ScholarTable 3Summary of risk factors, signs and symptoms, initial treatment of cerebral oedema, and the strategies used to minimize the risk of cerebral oedema in childrenRisk factors for cerebral oedemaSigns and symptomsInitial treatment of cerebral oedemaMajor differences in treatment of paediatric DKA to minimize risk of cerebral oedema (i)Younger age(ii)New onset diabetes(iii)Longer duration of symptoms(iv)Greater hypocapnia at presentation after adjusting for degree of acidosis(v)Increased serum urea nitrogen at presentation(vi)More severe acidosis at presentation(vii)Bicarbonate treatment for correction of acidosis(viii)An attenuated increase in measured serum sodium concentrations during therapy(ix)Greater volumes of fluid given in the first 4 h(x)Administration of insulin in the first hour of fluid treatment (i)Headache(ii)Slowing of heart rate(iii)Change in neurological status (restlessness, irritability, increased drowsiness, incontinence)(iv)Specific neurological signs (e.g. cranial nerve palsies)(v)Increase in blood pressure(vi)Decreased O2 saturation (i)Immediate i.v. mannitol or hypertonic 3% saline(ii)Reduce fluids by 1/3(iii)Intubation and ventilation and avoidance of aggressive hyperventilation(iv)CT to rule out other pathology (i)No i.v. boluses of insulin(ii)Commencement of i.v. insulin after 1 h of fluid treatment(iii)Gradual rather rapid restoration of normovolaemia (>48 h)(iv)Use of 0.9% saline initially (1st 4–6 h) and then consideration of saline with tonicity >0.45% according to serum sodium and osmolality. Open table in a new tab Initial serum potassium may be normal, raised or low in DKA. However, there is a total body potassium deficit. Potassium loss is caused by a shift from the intracellular to extracellular space in exchange for hydrogen ions which accumulate in acidosis. The extracellular potassium is then lost through osmotic diuresis. The initial litre of fluid should not have potassium added. Provided the serum potassium is <5.5 mmol litre−1, and the patient is not oliguric, subsequent fluids should have 40 mmol litre−1 of potassium chloride. Adequate fluid, potassium and insulin therapy will resolve the acidosis in DKA, but there may be disturbances of other electrolytes including bicarbonate, sodium, and phosphate. Generally, these electrolyte imbalances improve as the DKA is treated effectively. Typical fluid and electrolyte deficits are summarized in Table 4.Table 4Typical fluid and electrolyte deficits in adults with DKAWater100 ml kg−1Sodium7–10 mml kg−1Chloride3–5 mmol kg−1Potassium3–5 mmol kg−1 Open table in a new tab Ketosis causes delayed gastric emptying; therefore, the use of nasogastric tube may help protect the airway in those patients with an altered mental state, and those who require surgery and anaesthesia. A urinary catheter should be inserted in all patients with an altered mental state, those in a critical care setting or undergoing anaesthesia for monitoring of urine output and fluid balance. Oliguria is a sign of acute kidney injury. All patients should receive appropriate venous thromboembolism (VTE) risk assessment and subsequent prophylaxis. Dehydrated patients with DKA are at high risk of VTE. Both chemical (e.g. low-molecular-weight heparin) and physical (e.g. anti-embolic stockings) thromboprophylaxis should be considered. If infection is suspected appropriate antibiotic therapy should be commenced according to local policy. The diabetes specialist team must be involved in the care of those with DKA as soon as possible in the acute phase. Their involvement has been shown to reduce the length of stay and improve patient safety. If a surgical cause is identified, senior multidisciplinary review to discuss the optimal timing of surgery is required. It is also important to try and ensure that the clinical picture of an ‘acute abdomen’ is not secondary to the DKA in order to prevent needless surgery. The Royal College of Surgeons (RCS) document ‘Emergency Surgery, Standards for unscheduled surgical care’ provides a useful framework that promotes timely surgery but allows time for accurate diagnosis, initial treatment, and resuscitation.16The Royal College of Surgeons, EnglandEmergency survey. 2011http://www.rcseng.ac.uk/publications/docs/emergency-surgery-standards-for-unscheduled-care/@@download/pdffile/rcs_emergency_surgery_2011_web.pdfGoogle Scholar The standards are summarized below. Each patient must be managed individually, including the optimal time to operate. Unless the patient requires immediate surgery, preoperative resuscitation should occur with correction of the hypovolaemia, the metabolic acidosis, and the electrolyte imbalances. (i)Patients with ongoing haemorrhage require immediate surgery.(ii)Patients with septic shock who require immediate surgery are operated on within 3 h of the decision to operate as delay increases mortality significantly.(iii)Patients with severe sepsis (with organ dysfunction) who require surgery are operated on within a maximum of 6 h to minimize deterioration into septic shock.(iv)Patients with sepsis (but no organ dysfunction) who require surgery should have this within a maximum of 18 h.(v)Patients with no features to indicate systemic sepsis can be managed with less urgency but in the absence of modern and structured systems of care, delay will result in unnecessary hospital stay, discomfort, illness, and cost. Preoperative management should be focused on optimizing the patient for surgery. Furthermore, the senior anaesthetist must decide whether a VRIII or a FRIII will be used intra-operatively. If the anaesthetist decides to use the FRIII intraoperatively, as a minimum, provision must be made to have sufficient vascular access for the following:Central venous access should be obtained to guide fluid therapy and to facilitate the administration of multiple drugs and fluids. (i)Administration of the fixed rate i.v. insulin infusion via a pump(ii)Administration of the DKA resuscitation fluid (0.9% saline with 0.3% premixed potassium chloride via a pump may be the most appropriate) at the rate as guided by Table 1.(iii)Administration of the intra-operative resuscitation fluid(iv)Administration of anaesthetic bolus drugs(v)Administration of 20% glucose at 50 ml h−1 if the CBG is <14 mmol litre−1.(vi)Ability to check blood glucose, potassium, and pH at regular intervals (minimum hourly). Patients should be anaesthetized with full monitoring, with an arterial line in situ, and in theatre to facilitate continuous blood pressure monitoring post induction. An arterial blood gas (ABG) should be obtained before induction to give an indication of the degree of acidosis, and to ensure no hyperkalaemia, as succinylcholine is often used to facilitate intubation as part of a rapid sequence induction. Because of gastric stasis, the nasogastric tube should be aspirated before induction of anaesthesia. Patients should be intubated with a rapid sequence induction with cricoid pressure. In view of the hypovoalemic state and the acidosis, anaesthesia must be induced with a combination of drugs that promote cardiovascular stability. Regular (minimum hourly) monitoring of ABGs and blood glucose is mandatory. Patients should be ventilated to ensure no iatrogenic respiratory acidosis. Potassium needs to be kept within the normal range, and replaced as indicated. Blood glucose needs to be kept >14 mmol litre−1 whilst the patient is being treated with the FRIII. Consideration should be given to flow/cardiac output directed guided fluid therapy given the complex intra-operative fluid requirements of the surgical patient with DKA. After operation patients should receive nursing care in a level 2/3 environment until resolution of the DKA. The patient should receive their normal long-acting insulin analogue at the normal time. The Diabetes specialist teams will be able to assist in the transition from i.v. insulin to subcutaneous insulin and can provide further education and reinforce the ‘sick day rules' to the patient. (i)DKA is a life-threatening medical emergency characterized by the biochemical triad of ketonaemia, hyperglycaemia, and acidaemia.(ii)Bedside monitoring of capillary ketones, glucose, blood gases, and electrolytes should be used to make the initial diagnosis and guide subsequent management.(iii)Weight based fixed rate i.v. insulin infusion (FRIII) is now recommended rather than a variable rate i.v. insulin infusion (VRIII), and the blood glucose must be kept >14 mmol litre−1 with the FRIII.(iv)0.9% Saline with premixed potassium chloride should be the main resuscitation fluid on the general wards and in theatre. This is because it complies with National Patient Safety Agency recommendations on administration of potassium chloride.(v)Balanced electrolyte solutions are associated with a faster resolution of acidosis, but contain insufficient potassium to justify their safe use except in critical care.(vi)The cause of the DKA must be sought and surgery may be required.(vii)Critical care may be required.(viii)Continuation of long acting insulins may reduce complications during transition from i.v. to subcutaneous insulin.(ix)Early involvement of diabetic specialist teams is mandatory. N.L. is a member of the writing group for JBDS DKA guidelines. The associated MCQs (to support CME/CPD activity) can be accessed at https://access.oxfordjournals.org by subscribers to BJA Education.