PRACTICAL DIABETES VOL. 30 NO. 4 COPYRIGHT © 2013 JOHN WILEY & SONS 167

Review

Euglycaemic ketoacidosis in patientswith and without diabetes

AbstractKetoacidosis in individuals with diabetes is usually associated with a raised plasma glucoseconcentration. However, ketoacidosis in diabetes can occur with normal (≤11mmol/L) plasmaglucose levels. Ketoacidosis is also seen in patients who do not have diabetes, most commonlyin pregnancy or following alcoholic binges, rarely with starvation, anorexia nervosa or inbornerrors of metabolism. The aim of this review is to compare the clinical features, pathophysiologyand management of these conditions.

Common clinical features due to a raised anion gap metabolic acidosis are seen. Reducedcarbohydrate intake is a usual contributor to ketogenesis. Treatment is primarily withintravenous glucose, insulin if there is insulin deficiency and potassium as needed. The value ofusing bedside monitors to measure β-hydroxybutyrate levels both for diagnosis andmonitoring of response to treatment is emphasised. Early recognition of ketoacidosis andtreatment with glucose rather than saline is important for optimum outcome. Copyright ©2013 John Wiley & Sons.

Practical Diabetes 2013; 30(4): 167–171

Key wordseuglycaemic ketoacidosis; diabetes; pregnancy ketoacidosis; alcoholic ketoacidosis

Francine Le Neveu1

MBChB, Academic FY1 Trainee

Brython Hywel1MBChB, Core Medical Trainee

John N Harvey1

MD, FRCP, Senior Lecturer in Diabetes, Endocrinology& Metabolism

1Department of Endocrinology & Diabetes, WrexhamAcademic Unit, Bangor University, UK

Correspondence to: Dr John N Harvey, MD, FRCP, Gladstone Centre,Maelor Hospital, Wrexham LL13 7TD, UK; email: johnnharvey@btinternet.com

Received: 13 July 2012Accepted in revised form: 1 March 2013

IntroductionThere are a variety of potentialcauses of a metabolic acidosis. Themost common is diabetic ketoacido-sis (DKA), typically seen in type 1 dia-betes and due to either absoluteinsulin deficiency (at diagnosis orcaused by missed injections) or relative insulin deficiency (in inter-current illness). It is not alwaysappreciated that DKA can occur inthe presence of only mildly-elevatedplasma glucose levels or even normalglucose levels (euglycaemic DKA).The absence of hyperglycaemia canlead to diagnostic difficulty.

In this article we briefly revieweuglycaemic ketoacidosis as it hasbeen reported in patients both withand without diabetes. The potentialcauses are listed in Table 1.

DiagnosisIdentifying metabolic acidosiscause: use of the anion gapThe cause of a metabolic acidosis isnot always clear. Calculation of theanion gap can be informative.Measured as the sum of the meas-ured cations Na+ and K+ minus thesum of the measured anions Cl-and HCO3- the normal value is14mmol/L (range 10–18). The dif-ference is due to negatively chargedproteins, organic acids, phosphate

and sulphate ions. Metabolic acidosiswith normal anion gap is seen in bicarbonate losses via the gut (diarrhoea, pancreatic fistula,ureterosigmoidostomy) or kidney(renal tubular acidosis, treatmentwith acetazolamide), ingestion ofhydrochloric acid or substances thatgenerate it (ammonium chloride,arginine hydrochloride). Bicarb -onate losses are replaced byincreased renal reabsorption of chloride, maintaining ionic balancebut with acidosis. Metabolic acidosiswith high anion gap is caused byingestion or endogenous synthesis ofacids, particularly organic, where theanions are not normally measured.Ketoacidosis is the most commoncause. Metabolic acidosis with posi-tive anion gap is also seen in lacticacidosis, uraemic acidosis, poisoningwith salicylate, methanol or ethyleneglycol and in D-lactic acidosis due tolactobacillus overgrowth.

Definition of euglycaemic diabeticketoacidosis The term ‘euglycaemic diabeticketoacidosis’ was first used in 1973to describe a group of patients at the‘extreme of metabolic decompensa-tion’.1 The use of the term has beenchallenged on the basis that the con-dition is not a separate entity from

DKA but simply a different presenta-tion of the same process.2 The definition has changed over theyears. In 1973 Munro et al. definedeuglycaemic DKA as blood glucose<16.7mmol/L (300mg/dl) andplasma bicarbonate <10mmol/L.1More recent American DiabetesAssociation consensus statementshave suggested a definition of<13.9mmol/L in association withketoacidosis.3 Current UK state-ments have recommended diagnos-tic criteria for DKA of glucose>11mmol/L with acidosis (venousbicarbonate <15mmol/L and/orvenous pH <7.3) due to keton-aemia.4 The International Societyfor Pediatric and AdolescentDiabetes uses the same definition of DKA.5 Thus, glucose values≤11mmol/L in this setting may beregarded as indicating euglycaemicketoacidosis.6,7

Pseudo-euglycaemiaThe term pseudo-euglycaemiarefers to a measurement artefact in which the plasma glucose is erroneously measured as being inthe normal range. It occurs inpatients with severe hypertriglyceri-daemia. This can lead to late diag-nosis of DKA.8,9

Clinical syndromes and theirmanagementEuglycaemic diabetic ketoacidosisMunro et al. reported 37 cases ofyoung (age 10–28 years) type 1 dia-betic patients as having euglycaemicketoacidosis. Sixteen of these casespresented with a plasma glucose<11.1mmol/L thus fulfilling currentcriteria. In the Munro series, 32 ofthe cases reported vomiting over thetwo previous days. The remainderreported a reduced carbohydrateintake (nausea or other reason).Twenty-seven patients had contin-ued to take or increased their insulin dosage.1

Jenkins and colleagues studied atotal of 722 consecutive cases ofDKA. Of these, 14 episodes wereeuglycaemic with blood glucose con-centration <10mmol/L and bicar-bonate <15mmol/L at presentation.In the Jenkins series, the factorswhich precipitated euglycaemicketoacidosis were similar to those in hyperglycaemic DKA except that

euglycaemia was seen only once witha new diagnosis of diabetes. As inMunro’s series, most patients witheuglycaemic ketoacidosis had takentheir normal insulin dose or more in the 12 hours before admission.2Reports of euglycaemic ketoacidosisindicate vomiting and reduced calorie intake result in levels of glycaemia closer to normal.10 Forexample, in a 52-year-old diabeticman reported by Davies et al., whopresented with vomiting and wasdehydrated and pyrexial with a back-ground of chronic renal failure,blood glucose was 5.6mmol/L, pH7.19, bicarbonate 12.4mmol/L.11

In another case, a 35-year-old patient with type 1 diabetes had not eaten for two to three weeks dueto severe depression. He presentedwith a four-day history of nausea and vomiting, with pH 7.3, bicar-bonate 10mmol/L, anion gap +29,ketonuria and blood glucose5.8mmol/L.7

Studies have been undertaken toelucidate the metabolic changesunderlying euglycaemic ketoacido-sis. In subjects with type 1 diabetes,Burge et al. were able to show that fasting in the presence ofinsulin deficiency is associated withdecreased hepatic glucose produc-tion compared with the post-pran-dial state. Lipolysis and ketogenesisprogressed more rapidly in thefasted state. This was associated with, and is probably the result of, elevated levels of glucagon and catecholamines.12

The treatment of euglycaemicketoacidosis in diabetic individuals is similar to that of patients who areinitially hyperglycaemic and consistsof fixed-rate intravenous (IV) insulininfusion, 10% glucose (when bloodglucose is <14mmol/L), potassiumand monitoring of plasma ketones,aiming for a reduction of at least0.5mmol/L per hour.4

Starvation euglycaemicketoacidosisThus, there is some overlap with starvation ketoacidosis since starva-tion is a major contributory factor in the development of euglycaemicketoacidosis in diabetes. In the non-diabetic individual, reduced dietarycarbohydrate also leads to the use ofalternative energy sources. Free fattyacid (FFA) release from adipose tissue triglyceride stores is increased.The increased availability of FFA andan elevated glucagon/insulin ratioresults in generation of ketones bythe liver as starvation continues.Although ketosis is common in starvation, acidosis is rare. After afew days, ketone body levels mayreach 4–6mmol/L but usually donot exceed this since utilisation (bymany tissues) equals production.Ketone bodies are a major fuel formuscle during starvation and thereare urinary losses also. However,Owen et al. reported a 24-year-oldmale who had not eaten for threedays prior to presentation with 24 hours of vomiting followed bypersistent nausea. Arterial pH was7.09, bicarbonate 7.2mmol/L andglucose 6mmol/L. His conditiononly improved when transfused with glucose rather than the initialfluid resuscitation using Hartmann’ssolution. Thus it is possible forketone production to generatesevere acidosis in starvation.13 Thisphenomenon has been seen inanorexia nervosa also.

Pregnancy-related euglycaemicketoacidosisThe most common presentation oftrue euglycaemic DKA is in associa-tion with pregnancy. The presenta-tion is similar to hyperglycaemiccases with a history of dyspnoea,nausea and vomiting sometimes pre-ceded by infection.14 Patients usuallyhave gestational diabetes mellitus(GDM) or the development ofketoacidosis leads to the diagnosis of GDM.15,16 Ketoacidosis is rare ininsulin-treated diabetic pregnancy.17

Physiological changes that occur inpregnancy may contribute to thedevelopment of ketoacidosis inGDM (see below).

Cases of euglycaemic ketoacid o-sis have been reported in pregnantpatients who have no history of

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• Diabetic euglycaemic ketoacidosis• Non-diabetic euglycaemic ketoacidosis

– Starvation– Pregnancy related– Alcohol – Inborn errors of metabolism

Table 1. Causes of ketoacidosis

Causes of euglycaemic ketoacidosis

diabetes, nor fit the diagnostic crite-ria for GDM.18,19 As in the other situations, the euglycaemic ketoaci-dosis is usually secondary to nauseaand vomiting and a period of starva-tion/fasting which here is eitherdirectly related to the pregnancy orsupplementary to it. There may beadditional precipitating factors asillustrated by the following examplefrom our own practice.

A healthy 33-year-old, who was 30weeks’ pregnant with her secondchild, presented with a week-long history of flu-like symptoms, produc-tive cough and rigors. On examina-tion, her blood pressure was 103/53,respiratory rate 30 and temperature39.1oC, with lobar pneumonia andsubsequent empyema. She requiredinotropic support on the intensivetherapy unit. She had had urinaryketones since admission and herplasma β-hydroxybutyrate concen-tration was 5.3mmol/L (normal:<0.42mmol/L). Glucose levels werenormal throughout. Arterial pH was7.32, base excess -12 with a compen-sated metabolic acidosis, lactate0.8mmol/L (normal: <2.1mmol/L),and eGFR >60ml/min. Her non- diabetic ketoacidosis was successfullytreated with IV insulin 6 units/hourand 10% glucose IV with potassium. On day nine of admission, a 31-weekgestation infant was successfullydelivered.

Pregnancy results in significantalterations in fuel metabolism.Glucose is transported to the fetusby facilitated diffusion. Amino acids,particularly alanine, cross the pla-centa by active transport. Maternalfasting glucose concentration islower than in the non-pregnantstate, whereas plasma ketone con-centrations are higher and FFAs elevated after an overnight fast. Thishas been referred to as ‘acceleratedstarvation’ such that glucose is preferentially available to the fetusand alternative fuels are available for maternal consumption. Thephysiological response to fasting inthe third trimester is very differentfrom the non-pregnant state withreductions in plasma glucose,insulin and alanine and a greaterand more rapid rise in FFAs andketones.20 In Metzger et al.’s studythere was a strong correlationbetween fasting plasma FFA and

β-hydroxybutyrate, indicating thepotential for patients in the laterstages of pregnancy to developketoacidosis after starvation in theabsence of diabetes.20

The mainstay of treatment ofketoacidosis in non-diabetic preg-nancy has been IV fluid resuscitationincluding 10% glucose. Insulin,bicarbonate and phosphate havesometimes been used in addi-tion.18,19 Glucose infusion has beenshown to reduce β-hydroxybutyratelevels during ketonuric labour.21

Alcohol-related euglycaemicketoacidosisEuglycaemic ketoacidosis occurs inassociation with alcohol consump-tion. Typically, there has been heavydrinking followed by prolongedvomiting – for example, the 48-year-old female non-diabetic patientdescribed by Piya et al. who pre-sented with dyspnoea, vomiting andmalaise for three days havingabruptly stopped drinking alcoholprior to admission on a backgroundof alcohol excess.22 The blood glu-cose concentration was 9.8mmol/Lwith a high anion gap metabolic aci-dosis, pH 7.17, lactate 1.5mmol/Land capillary ketones 5.2mmol/L.

Alcohol has also been seen as a contributory cause in diabeticpatients presenting with euglycaemicketoacidosis. Alcoholic ketoacidosismay be more common in diabetes.Navaravong et al. reported a femalepatient with type 2 diabetes who presented with dyspnoea and wasfound to have a blood glucose of 4.8mmol/L, anion gap 37, pH7.24, urinary ketones present withplasma β-hydroxybutyrate elevated at 17.85mmol/L. The ketosis wasthought to be due to depleted hep -atic glycogen stores and increasedsympathetic activity.23

The primary ketone present inalcoholic ketoacidosis is β-hydroxy-butyrate. In a series of 23 cases of metabolic acidosis in alcoholicpatients, Fulop et al. found levels up to 7.8mmol/L.24 In alcoholicketoacidosis β-hydroxybutyrate isgenerated in preference to aceto- acetate so the diagnosis is facilitatedby modern meters that measure this metabolite. The classical nitro-prusside test detects acetoacetaterather than β-hydroxybutyrate.

Lactic acidosis occurs in patientswith liver disease and in acute inter-current illness, so may be seen in thesame patient population at risk ofalcoholic ketoacidosis and some-times in conjunction with it.24

Alcoholic ketoacidosis may beassociated with hypoglycaemia as aresult of consumption of NAD by themetabolism of alcohol to acetate.The resulting excess of NADHcauses the conversion of pyruvate tolactate such that pyruvate is notavailable for gluconeogenesis. Thegeneration of excess ketones ismainly due to starvation but conver-sion of acetate to ketone bodies may also contribute. Lipolysis is augmented by increased cate-cholamines and low insulin levelsproviding more FFA substrate.

Alcoholic ketoacidosis respondswell to glucose infusion. If there is noresponse, then lactate and β-hydrox-ybutyrate concentrations should be monitored.

Inborn errors of metabolismKetoacidosis is a feature of a numberof inherited metabolic conditionsseen in childhood. The combinationof ketoacidosis and hyperglycaemiasuggests type 1 diabetes, but organicacidurias (propionic acidaemia,methyl malonic acidaemia, isovalericacidaemia) and ketolytic defects (e.g. thiolase deficiencies) can alsoexhibit ketoacidosis in combinationwith hyperglycaemia and glycosuria.Measurement of lactate and ammo-nia levels helps to distinguish these.The combination of ketoacidosis andhypoglycaemia suggests defects ofgluconeogenesis or glycogen degra-dation (glycogen storage disease),maple syrup urine disease or adrenalinsufficiency. The congenital lacticacidoses also cause ketoacidosis. Adiagnosis of fasting ketoacidosis orketotic hypoglycaemia should bequestioned if there is associatedmetabolic acidosis.

Approximately 50% of patientswith inborn errors of intermediarymetabolism will present late: in latechildhood, adolescence or adult-hood. Symptoms are often intermit-tent and may include episodes of coma, focal neurological signs,seizures, apparently behaviouralsymptoms, vomiting, abdominalpain and liver dysfunction. It seems

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Review

likely that some chronic neurologicdisorders currently labelled asdegenerative will in time be identi-fied as variant forms of inbornerrors of metabolism.25

DiscussionEuglycaemic ketoacidosis is anuncommon occurrence. Althoughketones are regularly measured in diabetic patients, they may not be inother clinical situations or their signif-icance may not be appreciated suchthat the diagnosis can be easily missedin individuals who do not have dia-betes. Patients with diabetes candevelop other forms of metabolic aci-dosis or have acidosis due to multiplecauses (respiratory acidosis, uraemicacidosis, lactic acidosis most com-monly). Of patients with DKA,10–15% also have lactic acidosis bydefinition (lactate >5mmol/L, pH<7.2). Thus, measurement of plasmaketone concentration can have signif-icant diagnostic value. Modern bed-side plasma ketone monitors are nowreadily available (Optium, AbbottLabs; GlucoMen LX Plus, MenariniDiagnostics) such that ketosis andketoacidosis can be quantified. Thesemeters detect β-hydroxybutyraterather than the acetone/acetoacetatedetected by standard urine testing.

There are similarities betweenthe above syndromes of eugly-caemic ketoacidosis. In the non-diabetic state, starvation or poorintake due to vomiting is primarilyresponsible for lack of glucose andsuppression of insulin secretion. In diabetic individuals, there is adeficiency of insulin or insulinaction in addition. Thus treatment

is similar also, being based on IVglucose combined with insulin ifthere is insulin deficiency. The com-mon pathophysiology is shown inFigure 1.

In diabetic patients, the key difference in initial treatment is theuse of glucose rather than theemphasis on saline in hypergly-caemic DKA. This is analogous to

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• Alcoholism• Nausea of pregnancy, labour • Anorexia nervosa, starvation of any cause

• Inadequate insulin dosing in diabetes• Resistance to insulin action in pregnancy• Intercurrent illness

• Catecholamines, glucagon

• In pregnancy: preferential transport ofglucose and amino acids to the fetus

• In alcoholism: preferential consumptionof NAD limits gluconeogenesis

Common pathophysiology Other factors

Figure 1. Ketoacidosis: pathophysiology common to the clinical syndromes and additional factors

Diagnosis• Diabetic ketoacidosis (DKA) can occur in the absence of hyperglycaemia thus

measurement of ketones on a capillary sample is of value• Euglycaemic ketoacidosis occurs in the absence of diabetes, most commonly in association

with pregnancy or alcoholism• In non-diabetic patients, consider ketones as the unmeasured acid in high anion gap

acidosis• Modern bedside meters to measure plasma ketones are a valuable tool for diagnosis and

monitoring progress. They need to be more widely used• Other causes of metabolic acidosis are common and can occur simultaneously with

ketoacidosis. The anion gap calculation and direct measurement of ketones are useful here• In infants and young children, ketoacidosis is seen with some rare inborn errors of

metabolism

Treatment• Early recognition and treatment with dextrose is important (in adults). Insulin is not

necessarily required in the absence of diabetes• In hyperglycaemic DKA glucose is required when the plasma glucose falls below 14mmol/L• Frequent monitoring of these patients is required

Learning points

Table 2. Diagnosis and treatment learning points

Reduced carbohydrate intake

Reduced insulin secretion/action

Increased counter-regulatory hormones

Reduced hepaticglycogen stores.

Impairedgluconeogenesis

Increased fatty acid release

Increased ketone production

Ketoacidosis

the situation in the management ofhyperglycaemic DKA where 10%glucose 125ml/hour is now recom-mended when the blood glucosefalls below 14mmol/L.4 The mostcommon cause of adverse outcomein euglycaemic ketoacidosis is initialtreatment with saline without glu-cose. In patients not known to havediabetes, glucose concentrationsshould also be monitored and if anincrease is seen with glucose treat-ment the patient has uncontrolleddiabetes and insulin is required inaddition.

The lessons in diagnosis andmanagement for practitioners arelisted in Table 2.

In summary, there are issues ofdiagnostic difficulty and diagnosis issometimes delayed in these condi-tions where ketoacidosis occurs out-side the classical hyperglycaemic situation. The aim of this report has been to bring together some ofthe published case reports and tobriefly summarise similarities inmetabolic derangement, diagnosisand treatment.

Declaration of interestsThere are no conflicts of interestdeclared.

References1. Munro JF, et al. Euglycaemic diabetic ketoacidosis.

BMJ 1973;2:578–80.2. Jenkins D, et al. Euglycemic diabetic ketoacidosis:

does it exist? Acta Diabetol 1993;30:251–53.3. Kitabchi AE, et al. Hyperglycemic crises in adult

patients with diabetes. Diabetes Care 2009;32:1335–43.

4. Savage MW, et al. Diabetes UK PositionStatements and Care Recommendations: JointBritish Diabetes Societies Guideline for the man-agement of diabetic ketoacidosis. Diabet Med2011;28:508–15.

5. Wolfsdorf J, et al. Diabetic ketoacidosis in childrenand adolescents with diabetes. Pediatr Diabetes2009;10(Suppl 12):118–33.

6. McNulty SJ, English P. Euglycaemic diabetic ketoaci-dosis [Letter]. Pract Diabetes Int 2002;19:63.

7. Joseph, F, et al. Starvation induced true diabeticeuglycemic ketoacidosis in severe depression. J GenIntern Med 2008;24:129–31.

8. Rumbak MJ, et al. Pseudonormoglycemia in diabeticketoacidosis with elevated triglycerides. Am JEmerg Med 1991;9:61–3.

9. Baldwin L, et al. Spurious euglycaemia in severediabetic ketoacidosis. Lancet 1992;340:1407–8.

10. De P, Child DF. Euglycaemic diabetic ketoacidosis –is it on the rise? Pract Diabetes Int 2001;18:239–40.

11. Davies RG, et al. Euglycaemic diabetic ketoacidosis.Hospital Med 2003;64:557–8.

12. Burge MR, et al. Short-term fasting is a mechanismfor development of euglycemic ketoacidosis

during periods of insulin deficiency. J ClinEndocrinol Metab 1993;76:1192–8.

13. Owen D, et al. A patient with an unusual aetiology of a severe ketoacidosis. Intensive Care Med 2008;34:971–2.

14. Franke B, et al. A case of euglycaemic diabetic ketoaci-dosis in pregnancy. Diabet Med 2001;18:858–9.

15. Clark JDA, et al. Normoglycaemic ketoacidosis in awoman with gestational diabetes. Diabet Med1991;8:388–9.

16. Deepak D, et al. A case of euglycaemic diabeticketo acidosis in pregnancy – a reply. Diabet Med2002;19:699.

17. Kilvert JA, et al. Ketoacidosis in diabetic pregnancy.Diabet Med 1993;10:278–81.

18. Burbos N, et al. Severe metabolic acidosis as a con-sequence of acute starvation in pregnancy. ArchGynecol Obstet 2009;279:399–400.

19. Patel A, et al. Acute starvation in pregnancy: a causeof severe metabolic acidosis. Int J Obstet Anesth2011;20:253–6.

20. Metzger BE, et al. Accelerated starvation and theskipped breakfast in late normal pregnancy. Lancet1982;i:588–92.

21. Morton KE, et al. A comparison of the effects of fourintravenous solutions for the treatment of ketonuriaduring labour. Br J Obstet Gynaecol 1985;92:473–9.

22. Piya MK, et al. Ketoacidosis: not always diabetic.Diabet Med 2010;27(Suppl 1):P200.

23. Navaravong L, et al. An obscuring cause of wide-anion gap metabolic acidosis in alcoholic patient:an interesting case. J R Soc Med 2009:102:294–5.

24. Fulop M, et al. Alcoholic ketosis. Alcohol Clin ExpRes 1986;10:610–5.

25. Fernandes J, et al. Inborn Metabolic Diseases:Diagnosis and Treatment, 3rd edn. Berlin: Springer,2000.

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Book review

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Edited by Ali El SolhPublished by Wiley-Blackwell, 2012254 pages, price £84.50 (hardback)ISBN: 978 0 470 655900Website: www.wiley.com

Critical care management of the obese patient