Euglycemic Ketoacidosis Research Articles

Successful renal replacement therapy of extreme ertugliflozin and alcohol induced euglycaemic ketoacidosis

Successful renal replacement therapy of extreme ertugliflozin and alcohol induced euglycaemic ketoacidosis

The peri-operative implications of sodium-glucose co-transporter 2 inhibitors: a narrative review.

Sodium-glucose co-transporter 2 inhibitors are a novel class of antihyperglycaemic drugs used in the management of type 2 diabetes, that improve glycaemic control, cardiovascular outcomes and promote weight loss. They are also approved for the treatment of heart failure and chronic kidney disease in patients with or without diabetes. This narrative review discusses the peri-operative effects and implications of sodium-glucose co-transporter 2 inhibitors and gives an overview of current evidence and existing peri-operative guidelines. We conducted a literature review to identify peer-reviewed English language articles published since 2000, with further articles identified by reviewing the references of key papers. Peri-operative sodium-glucose cotransporter 2 inhibitor use carries a risk of euglycaemic ketoacidosis. Although clinically significant diabetic ketoacidosis remains a rare event, sodium-glucose co-transporter 2 inhibitors inhibitor-associated diabetic ketoacidosis has been observed across almost all surgical specialities. Ketoacidosis may present with any blood glucose level. Existing guidelines are inconsistent and may be a source of clinical confusion. Based on the half-life of sodium-glucose cotransporter 2 inhibitors, we recommend withholding treatment for 72 h before elective surgery (5 half-lives), with additional multidisciplinary input for specific procedures with dietary alterations and in patients with poorly controlled diabetes of cardiac/renal disease. In the event of emergency surgery or any surgery within 72 h of sodium-glucose cotransporter 2 inhibitor administration, we recommend pre-, intra- and postoperative blood ketone monitoring (6 hourly for 24 h post-surgery and until full oral diet is resumed). Sodium-glucose cotransporter 2 inhibitor treatment should only be resumed after resumption of full oral diet in the absence of ketosis.

Euglycemic Ketoacidosis Associated with SGLT-2 Inhibitors in Non-diabetic Patients-A Narrative Review.

Euglycemic ketoacidosis is an acute, life-threatening emergency that is characterized by euglycemia, metabolic acidosis, and ketonemia. It is a well-recognized adverse event in diabetic patients taking sodium-glucose cotransporter-2 inhibitor (SGLT-2 inhibitor). However, there is limited data on SGLT-2 inhibitor-related euglycemic ketoacidosis in non-diabetic patients. The mechanism behind SGLT-2 inhibitor-associated euglycemic ketoacidosis involves a general state of starvation or relative insulin deficiency, which exacerbates the mild baseline ketonemia caused by this class of medications while normoglycemia is maintained. The incidence of euglycemic ketoacidosis will likely increase with the increasing use of SGLT-2 inhibitors for various indications in addition to diabetes mellitus type 2, predominantly for congestive heart failure (CHF). Recognizing the signs and symptoms of this life-threatening condition is essential to treat it effectively. Our objective is to comprehensively revisit the pathophysiology of euglycemic ketoacidosis associated with SGLT-2 inhibitors and the risk factors for the condition, review the available data, and summarize the reported cases of euglycemic ketoacidosis in non-diabetic patients on SGLT-2 inhibitors. Our literature search identified five articles with six cases of euglycemic ketoacidosis in non-diabetic patients who were on SGLT-2 inhibitors for heart failure with reduced ejection fraction. The common risk factor in five out of the six cases was decreased oral intake due to acute illness, fasting, or a perioperative state.

Euglycemic diabetes ketoacidosis associated with SGLT-2 inhibitors - review of case reports

AIM: Sodium-glucose cotransporter 2 (SGLT-2) inhibitors have gained significant importance in the treatment of type 2 diabetes mellitus. One of the adverse effects while using SGLT-2 inhibitors is euglycemic ketoacidosis (euDKA) - acute life-threatening emergency. METHODS: The following review of case reports was based on articles published in 2023, obtained from the PubMed databases. Key search terms included “case report”, “sglt-2”, “sglt-2i”, “sodium-glucose cotransporter inhibitors”, “dka”. “eudka”, “euglycemic ketoacidosis”. RESULTS: In the literature, cases of euDKA correlated with the use of SGLT-2 inhibitors are described. CONCLUSION: There is a need for greater observation of the frequency of the adverse effects in patients taking sodium-glucose cotransporter inhibitors (SGLT-2i) and for raising awareness among doctors about the possibility of developing euglycemic diabetic ketoacidosis during the SGLT-2 inhibitors therapy.

A case of severe euglycemic ketoacidosis arising during dapagliflozin intake

A case of severe euglycemic ketoacidosis arising during dapagliflozin intake

Dapagliflozin Use in Children with Advanced Heart Failure Undergoing Heart Transplantation: A Matched Case-Control Study.

Dapagliflozin has been associated with euglycemic ketoacidosis in adults with diabetes contributing to poor outcomes when continued prior to surgery. It is unknown if preoperative use of dapagliflozin may lead to adverse events (AE) in nondiabetic children with advanced heart failure (HF) undergoing heart transplantation (HTx). We performed a single-center, matched case-control analysis of nondiabetic primary pediatric HTx recipients < 21years-old who underwent HTx and followed through postoperative day (POD) 3. Cases who received dapagliflozin leading up to HTx (n = 22) were matched by age and cardiac diagnosis to two historical controls who did not receive dapagliflozin (n = 44). Median age at HTx was 13.8years (range 0.36-20.7) and 48% were female. Cardiac diagnoses included cardiomyopathy (45%), Fontan failure (41%), and single ventricle status post stage I palliation (14%). Cases received median dapagliflozin dose of 0.17mg/kg once daily; therapy was stopped one day prior to HTx. There were no significant differences in blood glucose nadirs, arterial blood gas indices including nadirs of pH, bicarbonate, or peaks of arterial blood lactic acid POD0-3. Vasopressor, inotrope, and insulin infusion usage were not different. No patients were treated for severe hypoglycemia, euglycemic ketoacidosis, or urinary tract infections. There were no deaths. Length of stay in ICU and time from HTx to hospital discharge did not differ between cohorts. Use of dapagliflozin in children with advanced HF until HTx is not associated with AE in the immediate postoperative period nor increased length of hospitalization post-HTx. Potential cardiovascular benefits of dapagliflozin in patients awaiting HTx should be prioritized.

Euglycemic Ketoacidosis Induced by SGLT2 Inhibitor in Latent Autoimmune Diabetes in Adults: A Case Report

Background: Euglycemic ketoacidosis (EKA) is a medical condition characterized by the presence of ketoacidosis without significant hyperglycemia. It is particularly challenging to diagnose due to normal or near-normal blood glucose levels. SGLT2 inhibitors, used in managing type 2 diabetes mellitus, are known to cause EKA. This risk is increased in patients with latent autoimmune diabetes in adults (LADA), a type of Type 1diabetes presented in adult (Hybrid form of diabetes) Case Report: A 64-year-old male with a history of diabetes mellitus and hypothyroidism presented with shortness of breath, nausea, and dizziness. Despite taking Metformin, Glimepride, Thyroxin, and Empagliflozin, he had poor glycemic control (HbA1c 9%) Physical examination showed generalized vitiligo and tachycardia. Initial laboratory results revealed high anion gap metabolic acidosis with normal blood glucose, consistent with EKA. Extensive diagnostic workup confirmed the presence of LADA and SGLT2 inhibitor induced EKA. Result: The patient was diagnosed with type 1 diabetes mellitus (LADA) and EKA induced by SGLT2 inhibitors. Management included discontinuation of the SGLT2 inhibitor, initiation of insulin therapy, and monitoring of metabolic parameters. Conclusion: Euglycemic ketoacidosis induced by SGLT2 inhibitors in patients with LADA is a serious condition requiring prompt recognition and treatment. Clinicians should be vigilant in monitoring adult patients with diabetes and other autoimmune conditions who are on SGLT2 inhibitors for symptoms of ketoacidosis even when blood glucose levels are normal. Recommendations: Regular monitoring of blood ketone levels in patients on SGLT2 inhibitors. Consideration of alternative glucose-lowering therapies in patients with LADA. Education for patients and healthcare providers on the risks of EKA. Keywords: Euglycemic ketoacidosis, SGLT2 inhibitors, Latent autoimmune diabetes in adults, Diabetes management, Metabolic acidosis.

Sodium-glucose co-transporter-2 inhibitor-associated non-diabetic ketoacidosis: a case report

Ketoacidosis is considered an emergency metabolic disorder that can be triggered by starvation and alcohol consumption in addition to diabetes. We described an unusual case of ketoacidosis in a non-diabetic young man who presented to our hospital with a complaint of rapid and shallow breathing, weakness and nausea. Fourteen days back, due to heart failure, he started sodiumglucose co-transporter 2 inhibitors (SGLT2-i) in addition to fumarate bisoprolol, sacubitril/valsartan and eplerenone. Based on clinical examination, ketoacidosis was suspected, although his glucose and glycosylated hemoglobin levels were in range. Overall, based on the clinical and laboratory findings, the diagnosis of euglycemic non-diabetic ketoacidosis due to the use of the SGLT2- i was made and SGLT2-i has been discontinued. Although SGLT2-i are effective and safe drugs, it is advisable to carefully evaluate their use also in non-diabetic patients especially when hepatic fibrosis or incorrect eating habits are present.

Novel Approach to Continuation of Elective Procedures in People at Risk for Sodium-Glucose Cotransporter 2 Inhibitor-Associated Euglycemic Ketoacidosis.

Novel Approach to Continuation of Elective Procedures in People at Risk for Sodium-Glucose Cotransporter 2 Inhibitor-Associated Euglycemic Ketoacidosis.

Can euglycemic Diabetic Ketoacidosis Caused by SGLT2 Inhibitors be avoided in Covid-19 and other acute Infections?

We present a case of anion gap euglycemic diabetic ketoacidosis (EuDKA) in a patient with COVID-19 infection. Patients with diabetes mellitus are at increased risk of severe illness, and hyperglycaemia is associated with higher morbidity and mortality in patients infected with COVID-19. A 76-year-old male with diabetes mellitus treated with SGLT2 inhibitor tested positive for COVID-19 infection on day 3 after his admission. In the emergency room he had a high anion gap metabolic acidosis and a blood glucose of 248 mg/dl. His urine tested strongly positive for ketones. A diagnosis of euglycemic diabetic ketoacidosis was made and he was treated with intravenous insulin and normal saline; his antidiabetic medications were stopped. His metabolic acidosis gradually resolved, and he was discharged. Euglycemic diabetic ketoacidosis is a rare complication of COVID-19 infection. It is defined by the American Diabetes Association as the triad of anion gap metabolic acidosis with arterial pH <7.3, serum bicarbonate <18 mmol/l and ketonuria or ketonemia. It is a life-threatening complication which usually occurs in type 1 diabetes mellitus patients but may also occur in type 2 diabetes mellitus patients. As described earlier, it is associated with hyperglycaemia but if blood glucose is low or near normal but <250 mg/dl it is then named euglycemic diabetic ketoacidosis. Patients treated with SGLT2 inhibitors are at increased risk of euglycemic diabetic ketoacidosis. COVID-19 infection precipitated euglycemic diabetic ketoacidosis in our patient. SGLT2 inhibitors must be stopped when this adverse reaction occurs. As their use increases, the risk of this adverse reaction is higher as well. Their prescription should be restricted to trained physicians who are able to educate their patients and treat them appropriately in situations that may arise. COVID-19 infected patients are at increased risk of developing diabetic ketoacidosis or euglycemic ketoacidosis when treated with SGLT-2 inhibitors.It is practical to discontinue the drug at the onset of any symptoms consistent with acute infection to prevent the development of euglycemic diabetic ketoacidosis.

Dijabetična ketoacidoza u trudnoći

Diabetic ketoacidosis (DKA) is one of the most serious and life-threatening complications of diabetes mellitus (DM), especially when it occurs during pregnancy, with a prevalence ranging from 0.5% to 3%. Pregnancy is considered a susceptible environment for the development of this type of metabolic imbalance due to its inherent physiological changes. Unspecific symptoms (vomiting, diarrhea, abdominal pain, etc.), especially in pregnant women, and the fact that ketoacidosis can develop even with normal glucose values (defined as euglycemic ketoacidosis), often lead to a delayed diagnosis. Evidence suggests that timely diagnosis and appropriate management of ketoacidosis are crucial in preventing adverse outcomes for both the mother and the fetus. Fetal outcomes are often dichotomous, resulting in either fetal demise (miscarriage/stillbirth) with a prevalence of 10% to 35%, or the birth of a healthy baby, with possible complications primarily related to diabetes mellitus itself. Additionally, case reports of ketoacidosis developing even in non-diabetic women due to other diseases (such as acute pancreatitis, appendicitis), as well as in those with gestational diabetes mellitus (GDM), further emphasize the importance of considering this condition in everyday clinical practice. The aim of this paper is to further elucidate the causes and course of this complication, as well as the outcomes for both mother and fetus, to contribute to a better overall understanding.

Abstract 17641: Frequency of Reported Euglycemic Ketoacidosis With Sodium-Glucose Cotransporter-2 Inhibitors is Not Increased in Patients With Heart Failure: Analysis of US Food and Drug Administration Adverse Event Reporting System (FAERS)

Introduction: Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are first-line therapy for heart failure (HF) but have an associated risk for euglycemic ketoacidosis. Patients with HF exhibit many additional risk factors for euglycemic ketoacidosis. However, no data describes the incidence or risk of euglycemic ketoacidosis in HF. Hypothesis: Reported incidence of euglycemic ketoacidosis with empagliflozin and dapagliflozin is not higher in patients with HF compared to the general population. Methods: Cases of euglycemic ketoacidosis with empagliflozin and dapagliflozin (single or combination products) were identified in the Food and Drug Administration Adverse Event Reporting System (FAERS) from January 2022 to March 2023. HF was identified as those taking at least two of the listed medication categories (angiotensin converting enzyme inhibitor/angiotensin receptor blocker/angiotensin receptor neprilysin inhibitor, mineralocorticoid receptor antagonist, HF-approved beta blocker) with a loop diuretic or search terms related to cardiac failure from MedDRA. Cases with missing event date, age, gender, and reporter country were removed. Reporting rates of euglycemic ketoacidosis stratified by HF status were examined descriptively. Results: Out of 16,880 adverse event reports involving empagliflozin and dapagliflozin, a total of 432 (2.6%) cases of SGLT2 inhibitor-associated euglycemic ketoacidosis were identified (mean age 65±13 years, 55.6% male, and mean weight of 87±27 kg). Patients who developed euglycemic ketoacidosis were younger and of lower mean weight. The incidence of euglycemic ketoacidosis among patients without HF was 2.8% compared to 0.8% in patients with HF [OR 0.27, 95% CI (0.17, 0.44)]. Mortality or need for hospitalization was not increased in patients experiencing euglycemic ketoacidosis for both the HF cohort (mortality: 5.9% vs. 6.7%; hospitalization: 23.5% vs. 31.1%) and general population (mortality: 0.2% vs. 3.6%; hospitalization: 30.1% vs. 27.3%). Conclusions: Euglycemic ketoacidosis with empagliflozin and dapagliflozin was uncommon, does not appear to be more frequent in patients with HF compared to the general population, and does not appear to be associated with worse outcomes.

A Case report of the rare non-diabetic euglycaemic ketoacidosis (NDEK) in patient with acute pancreatitis

A Case report of the rare non-diabetic euglycaemic ketoacidosis (NDEK) in patient with acute pancreatitis

Pilot study of a ketogenic diet in bipolar disorder.

Recent evidence from case reports suggests that a ketogenic diet may be effective for bipolar disorder. However, no clinical trials have been conducted to date. To assess the recruitment and feasibility of a ketogenic diet intervention in bipolar disorder. Euthymic individuals with bipolar disorder were recruited to a 6-8 week trial of a modified ketogenic diet, and a range of clinical, economic and functional outcome measures were assessed. Study registration number: ISRCTN61613198. Of 27 recruited participants, 26 commenced and 20 completed the modified ketogenic diet for 6-8 weeks. The outcomes data-set was 95% complete for daily ketone measures, 95% complete for daily glucose measures and 95% complete for daily ecological momentary assessment of symptoms during the intervention period. Mean daily blood ketone readings were 1.3 mmol/L (s.d. = 0.77, median = 1.1) during the intervention period, and 91% of all readings indicated ketosis, suggesting a high degree of adherence to the diet. Over 91% of daily blood glucose readings were within normal range, with 9% indicating mild hypoglycaemia. Eleven minor adverse events were recorded, including fatigue, constipation, drowsiness and hunger. One serious adverse event was reported (euglycemic ketoacidosis in a participant taking SGLT2-inhibitor medication). The recruitment and retention of euthymic individuals with bipolar disorder to a 6-8 week ketogenic diet intervention was feasible, with high completion rates for outcome measures. The majority of participants reached and maintained ketosis, and adverse events were generally mild and modifiable. A future randomised controlled trial is now warranted.

Unusual case of concurrent metformin-associated lactic acidosis and euglycaemic ketoacidosis

Metformin-associated lactic acidosis (MALA) and euglycaemic diabetic ketoacidosis (EKA) are both life-threatening endocrine emergencies. MALA is a well-documented complication of anti-glycaemic therapy in diabetics while EKA is an increasingly recognized disease entity with the advent of use of sodium-glucose co-transporter-2 (SGLT-2) inhibitors. However, the occurrence of concurrent metformin-associated lactic acidosis and euglycaemic ketoacidosis (MALKA) is uncommon and rarely reported in the literature. We report an unusual case of MALKA, in a 74-year-old gentleman with no previous history of chronic kidney disease and SGLT-2 inhibitor use, who presented with altered mental status, acute renal failure and profound high anion-gap metabolic acidosis (HAGMA) with lactaemia, ketonaemia and normoglycaemia (pH 6.965, bicarbonate 3.1, creatinine 522, glucose 6.6, lactate 17.5, ketones &gt;8). The patient was initiated on intravenous insulin infusion with dextrose-containing drip and continuous renal replacement therapy (CRRT) in the intensive care unit (ICU). The patient had a prolonged hospital stay but was eventually discharged with a normalised renal function without need for long-term dialysis. The parallel occurrence of MALA and EKA suggest a metformin-associated inhibition of gluconeogenesis. This case highlights the importance of early recognition and investigation of concurrent diabetic ketoacidosis in the presence of MALA and vice versa as MALKA benefits from both prompt institution of parenteral glucose therapy and insulin infusion and consideration of initiation of haemodialysis.

Euglycaemic ketoacidosis after abdominal surgery: Implications of SGLT2 inhibitors for anaesthesiologists - A case study.

Euglycaemic ketoacidosis after abdominal surgery: Implications of SGLT2 inhibitors for anaesthesiologists - A case study.

Non-Diabetic Euglycaemic Ketoacidosis Secondary to SGLT2 Inhibition

Non-Diabetic Euglycaemic Ketoacidosis Secondary to SGLT2 Inhibition

915-P: Euglycemic Ketoacidosis in Type 1 Diabetes on an Automated Insulin Delivery System after Bariatric Surgery—A Case Series

Obesity is an increasing concern in patients with type 1 diabetes. Bariatric surgery is an effective option for weight loss and is associated with an improvement in metabolic complications. We report 2 cases of adults with type 1 diabetes using automated insulin delivery where laparoscopic sleeve gastrectomy was complicated post-operatively by euglycemic ketoacidosis. The first case was of a 28-year-old man using Control-IQ (HbA1c 7.3%, body mass index 40, and insulin requirements 0.98 Units/kg/day). His insulin requirements and carbohydrate intake decreased from 108 units and 208 grams respectively to 44 units and 8 grams during the preoperative liquid diet. His lack of carbohydrate consumption continued post-operatively. Two days after his surgery, he presented to the emergency department with nausea, where his glucose level was 12.8 mmol/L, venous pH level 7.30, venous bicarbonate concentration 20.9 mmol/L, and plasma beta-hydroxybutyrate 4.5 mmol/L. He was treated with intravenous hydration with supplementation dextrose with observation. The second case was of a 33-year-old woman using the MiniMed 770G (HbA1c 7.0%, body mass index 44, insulin requirements 0.4 units/kg/day). Post-operative day 16, she presented to the emergency department with nausea and vomiting. Her glucose level was 11.9 mmol/L venous pH was 7.31, venous bicarbonate was 17 mmol/L, and positive urinary ketones. Daily insulin requirements had reduced (from preoperatively to post-operatively) from 35.8 to 16.3 Units per day, with her carbohydrate intake from 86 to 33 grams. She was treated with intravenous insulin. Though euglycemic ketoacidosis is documented after bariatric surgery and starvation, automated insulin delivery (particularly unnoticed insulin changes) may have influenced glycemia and acidosis. Careful review of insulin administration, carbohydrate intake, and ketone monitoring is recommended in these cases. Disclosure M.Pasqua: None. M.Tsoukas: Speaker's Bureau; Novo Nordisk Canada Inc., Boehringer Ingelheim (Canada) Ltd., Eli Lilly and Company, Janssen Scientific Affairs, LLC, AstraZeneca, Sanofi. W.Hu: None.

#6212 SEVERE HYPERCHLOREMIC METABOLIC ACIDOSIS WITH SGLT-2 INHIBITORS IN PATIENTS WITH URINARY DIVERSION

Abstract Background and Aims Urinary diversion after cystectomy using autologous intestinal segments has been the gold standard treatment of benign and malignant diseases of urinary tract. The most frequent metabolic abnormalities is hyperchloremic metabolic acidosis, due to ammonium absorption alongside chloride gain and bicarbonate excretion in the bowel conduit. Sodium-glucose co-transporter-2 (SGLT2) inhibitors are a class of antihyperglycemic agents that recently revolutionized the paradigm of chronic kidney disease. It exerts its effect by preventing the reabsorption of filtered glucose from the tubular lumen, acting on the SGLT2 proteins in the renal proximal convoluted tubules, and thus promoting a greater urinary glucose excretion. The authors described 2 patients with bowel conduit and mild hyperchloremic metabolic acidosis, presented with severe metabolic acidosis short after starting SGLT2 inhibitors. Method Consultation of medical records. Results Case 1: 62-year-old male with an orthotopic neobladder since 2005, type 2 diabetes and nonspecific interstitial pneumonia. In 2018 arterial blood gas (ABG) was: pH 7.45, pO2 81, pCO2 28, HCO3- 19.3, Cl 107, AG 7.7 (normal albumin), K+ 3.25. In February 2022 he was sent to the emergency department (ER) from a Pneumology appointment, after an ABG showed an aggravated hyperchloremic metabolic acidosis: pH 7.25, pCO2 27.5, HCO3- 12, Cl 122, Na+ 143, K+ 3.74, AG 9, lactate 0.69, glucose 261, ketone bodies negative); blood workup added acute kidney injury (AKI), urea 81, creatinine 1.6. The patient medical history revealed: administration of 5 cycles of cyclophosphamide (7 months before) and the introduction of empagliflozin 10mg id, 10 months prior to this event, as an addition to Metformin 1000mg id. A progressive metabolic normalization was observed after the SGLT2 inhibitor was withdrawn and intravenous hydration. Case 2: A 63-year-old male with an ileal conduit since 2018 and type 2 diabetes. He had chronic renal disease since 2021 with serum creatinine 1.5-2. He presented with a 3-day history of lethargy and anorexia. He had started dapagliflozina 10mg id 10 months prior to this event. At admission the patient had normal vital signs, glasgow coma scale 15 and no major signs at observation. ABG showed severe hyperchloremic metabolic acidemia (pH 6.98, pCO2 20.5, pO2 124.4, HCO3- 4.7, Na 129, Cl 120, AG 4.3, K+ 3.54, glucose 200, lactate 0.5) alongside AKI, urea 209 and creatinine 2.8 and spot urine without ketone bodies. He was admitted for a short period to the intensive care unit, for intravenous sodium bicarbonate and hydration, on top of SGLT2 inhibitor suspension, with progressive clinical and metabolic resolution. Conclusion Chronic hyperchloremic metabolic acidosis is a frequent and known complication of urinary diversion, due to the reabsorption of solutes by the intestinal mucosa because of the presence of urine (ammonium and chloride absorption and bicarbonate excretion) and diarrhea and volume depletion due to reduced sodium absorption in the gout. Euglycemic Ketoacidosis is a well-known complication of SGLT2 Inhibitor therapy and was not this case as both patients had normal anion gap. Hyperchloremic acidosis as been rarely described but not so severe as we presented. Although both patients had AKI, was not severe. We hypothesize that SGLT2 inhibitors, could exacerbate the chronic hyperchloremic metabolic acidosis by increasing urinary sodium and glucose excretion, that could exacerbate volume depletion, diarrhea and hyperglycemia (and subsequent volume depletion). This are the first 2 cases reported of severe hyperchloremic metabolic acidosis in patients with orthotopic neobladder and SGLT2 inhibitors treatment. The physiopathology of this presentation needs to be studied.

Defining Physiological Ketosis Following Very-Low-Calorie Diets

IntroductionVery low-calorie diets (VLCDs) are used preoperatively in bariatric-metabolic surgery; however, this can lead to physiological ketosis. Euglycemic ketoacidosis is an increasingly recognized complication in diabetic patients on sodium-glucose-cotransporter-2 inhibitors (SGLT2i) undergoing surgery and requires assessment of ketones for diagnosis and monitoring. VLCD induced ketosis may confound monitoring in this group. We aimed to evaluate the influence of VLCD, compared to standard fasting, on perioperative ketone levels and acid-base balance. Materials and methodsTwenty-seven patients were prospectively recruited to the intervention group and 26 to the control group from two tertiary referral centres in Melbourne, Australia. Intervention group patients were severely obese (body mass index) (BMI) (≥35), undergoing bariatric-metabolic surgery, and prescribed 2 wk of VLCD preoperatively. Control group patients underwent general surgical procedures and prescribed standard procedural fasting only. Patients were excluded if diabetic or prescribed SGLT2i. Ketone and acid-base measurements were taken at regular intervals. Univariate and multivariate regression was utilised with significance defined as P < 0.005. ClinicalTrials.gov ID: NCT05442918. ResultsPatients on VLCD, compared to standard fasting, had an increased median preoperative (0.60 versus 0.21 mmol/L), immediate postoperative (0.99 versus 0.34 mmol/L) and day 1 postoperative (0.69 versus 0.21 mmol/L) ketone level (P < 0.001). Preoperative acid-base balance was normal in both groups, however VLCD patients were found to have a metabolic acidosis immediately postoperatively (pH 7.29 versus pH 7.35) (P = 0.019). Acid-base balance had normalized in VLCD patients on postoperative day 1. ConclusionsPreoperative VLCD resulted in increased pre- and postoperative ketone levels with immediate postoperative values consistent with metabolic ketoacidosis. This should be considered particularly when monitoring diabetic patients prescribed SGLT2i.