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We present the case of a 28-year-old male with a history of alcohol dependency and smoking, who presented with chest pain, shortness of breath, and altered sensorium. He exhibited severe metabolic acidosis, hypoglycemia, low platelet count, and acute kidney injury. Alcoholic ketoacidosis was suspected due to ketonuria, metabolic acidosis, and ketonemia, compounded by electrolyte abnormalities and radiographic findings of pneumonia., (This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

The last decade has been characterized by exciting findings on eu- or hypoglycemic ketosis and ketoacidosis. This review emphasizes the following five key points: 1. Since the traditional nitroprusside-glycine dipstick test for urinary ketones is often falsely negative, the blood determination of β-hydroxybutyrate, the predominant ketone body, is currently advised for a comprehensive assessment of ketone body status; 2. Fasting and infections predispose to relevant ketosis and ketoacidosis especially in newborns, infants, children 7 years or less of age, and pregnant, parturient, or lactating women; 3. Several forms of carbohydrate restriction (typically less than 20% of the daily caloric intake) are employed to induce ketosis. These ketogenic diets have achieved great interest as antiepileptic treatment, in the management of excessive body weight, diabetes mellitus, and in sport training; 4. Intermittent fasting is more and more popular because it might benefit against cardiovascular diseases, cancers, neurologic disorders, and aging; 5. Gliflozins, a new group of oral antidiabetics inhibiting the renal sodium-glucose transporter 2, are an emerging cause of eu- or hypoglycemic ketosis and ketoacidosis. In conclusion, the role of ketone bodies is increasingly recognized in several clinical conditions. In the context of acid-base balance evaluation, it is advisable to routinely integrate both the assessment of lactic acid and β-hydroxybutyrate., (© 2023. The Author(s).)

Upon both acute and prolonged alcohol intake, the brain undergoes a metabolic shift associated with increased acetate metabolism and reduced glucose metabolism, which persists during abstinence, putatively leading to energy depletion in the brain. This study evaluates the efficacy of ketogenic treatments to rescue psychiatric and neurochemical alterations during long-term alcohol withdrawal. Female mice were intermittently exposed to alcohol vapor or air for three weeks, during which mice were introduced to either a ketogenic diet (KD), control diet supplemented with ketone ester (KE) or remained on control diet (CD). Withdrawal symptoms were assessed over a period of four weeks followed by re-exposure using several behavioral and biochemical tests. Alcohol-exposed mice fed CD displayed long-lasting depressive-like symptoms measured by saccharin preference and tail suspension, as well as decreased norepinephrine levels and serotonin turnover in the hippocampus. Both KD and KE rescued anhedonia for up to three weeks of abstinence. KD mice showed higher latency to first immobility in the tail suspension test, as well as lower plasma cholesterol levels. Our findings show promising effects of nutritional ketosis in ameliorating alcohol withdrawal symptoms in mice. KD seemed to better rescue these symptoms compared to KE., (© 2024. The Author(s).)

Background: The diagnosis of alcoholic ketoacidosis (AKA) has traditionally been made based only on clinical history and the presence of severe metabolic acidosis with a high anion gap (AG); however, the concentration of beta-hydroxybutyrate (BOHB), a pivotal ketone body in AKA, is not evaluated in most cases. The aim of this study was to clarify the clinical spectrum of AKA in terms of the severity of ketoacidosis by using a point-of-care capillary BOHB measurement device., Methods: This retrospective case series was conducted at a Japanese private teaching hospital. Patients with suspected AKA, based on their clinical history, who underwent BOHB measurement using a point-of-care capillary measurement device in the emergency department, were included. Data on their clinical presentations, blood tests, and treatments were collected, described, and compared between patients with a BOHB concentration higher than 3.0 mmol/L (H-BOHB) and those with a concentration less than 3.0 mmol/L (L-BOHB)., Results: A total of 83 patients were included in this study. Sixty-eight patients were categorized as having H-BOHB and 15 as having L-BOHB. Nausea (71%), vomiting (71%), tachycardia (76%), and tachypnea (46%) were commonly observed at presentation. Hyponatremia (46%), hypokalemia (34%), hypomagnesemia (42%), and hyperphosphatemia (41%) were frequent electrolyte abnormalities upon presentation. Rehydration with balanced crystalloids and glucose-containing intravenous fluids, electrolyte supplementation, and thiamine replacement were the major treatments. The mean length of stay in the ICU and hospital were 4.4 and 7.0 days, respectively, with low overall mortality (1%). The H-BOHB and L-BOHB groups did not differ in terms of clinical data. Seventy percent of patients with L-BOHB had severe metabolic acidosis with a high AG due to hyperlactatemia (mean lactate concentration: 8.5 mmol/L)., Conclusions: We described the clinical features of AKA measured by using a point-of-care capillary BOHB measurement device. Although certain patients diagnosed with AKA based only on their clinical history had predominant lactic acidosis with minor elevations in BOHB concentration, the BOHB concentration had no effect on the clinical spectrum of AKA in this study., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Continuous renal replacement therapy (CRRT) is a dialysis modality used in critically ill patients with acute kidney injury (AKI). Although most dialysate and replacement fluids are dextrose-containing, CRRT-associated hypophosphatemia sometimes warrants the use of phosphorus-containing solutions which are dextrose free. The other less commonly used dextrose-free dialysate solutions are certain formulations of Prismasol and Prismasate. As glucose is a small molecule, which is readily cleared with dialysis, use of these solutions can result in increased caloric loss, net glucose deficit, and shifting of the metabolic pathway towards gluconeogenesis and ketogenesis. Starvation ketosis is usually a benign entity, however when combined with factors such as stress of critical illness, can produce metabolic acidosis which at times can be severe. We describe five patients who developed worsening metabolic acidosis despite adequate clearance from CRRT and were diagnosed with CRRT-associated ketoacidosis. Administration of dextrose-containing fluids or tube feeds promptly resulted in resolution of ketonemia and acidosis. Recognition of this entity is of great importance as the reflexive reaction to increase the prescribed dose of CRRT to improve the acidosis, in fact worsens the problem.

Obese asthmatics tend to have severe, poorly controlled disease and exhibit methacholine hyperresponsiveness manifesting in proximal airway narrowing and distal lung tissue collapsibility. Substantial weight loss in obese asthmatics or in mouse models of the condition decreases methacholine hyperresponsiveness. Ketone bodies are rapidly elevated during weight loss, coinciding with or preceding relief from asthma-related comorbidities. As ketone bodies may exert numerous potentially therapeutic effects, augmenting their systemic concentrations is being targeted for the treatment of several conditions. Circulating ketone body levels can be increased by feeding a ketogenic diet or by providing a ketone ester dietary supplement, which we hypothesized would exert protective effects in mouse models of inherent obese asthma. Weight loss induced by feeding a low-fat diet to mice previously fed a high-fat diet was preceded by increased urine and blood levels of the ketone body β-hydroxybutyrate (BHB). Feeding a ketogenic diet for 3 wk to high-fat diet-fed obese mice or genetically obese db/db mice increased BHB concentrations and decreased methacholine hyperresponsiveness without substantially decreasing body weight. Acute ketone ester administration decreased methacholine responsiveness of normal mice, and dietary ketone ester supplementation of high-fat diet-fed mice decreased methacholine hyperresponsiveness. Ketone ester supplementation also transiently induced an "antiobesogenic" gut microbiome with a decreased Fermicutes/Bacteroidetes ratio. Dietary interventions to increase systemic BHB concentrations could provide symptom relief for obese asthmatics without the need for the substantial weight loss required of patients to elicit benefits to their asthma through bariatric surgery or other diet or lifestyle alterations.

Purpose: Real-time continuous glucose monitoring (RT-CGM) provides information on glycemic variability (GV), time in range (TIR), and guidance to avoid hypoglycemia, thereby complimenting HbA1c for diabetes management. We investigated whether GV and TIR were independently associated with chronic and acute diabetes complications., Methods: Between September 2014 and January 2017, 515 subjects with type 1 diabetes using sensor-augmented pump therapy were followed for 24 months. The link between baseline HbA1c and CGM-derived glucometrics (TIR [70-180 mg/dL], coefficient of variation [CV], and SD) obtained from the first 2 weeks of RT-CGM use and the presence of complications was investigated. Complications were defined as: composite microvascular complications (presence of neuropathy, retinopathy, or nephropathy), macrovascular complications, and hospitalization for hypoglycemia and/or ketoacidosis., Results: Individuals with microvascular complications were older (P < 0.001), had a longer diabetes duration (P < 0.001), a higher HbA1c (7.8 ± 0.9 vs 7.5 ± 0.9%, P < 0.001), and spent less time in range (60.4 ± 12.2 vs 63.9 ± 13.8%, P = 0.022) compared with those without microvascular complication. Diabetes duration (odds ratio [OR] = 1.12 [1.09-1.15], P < 0.001) and TIR (OR = 0.97 [0.95-0.99], P = 0.005) were independent risk factors for composite microvascular complications, whereas SD and CV were not. Age (OR = 1.08 [1.03-1.14], P = 0.003) and HbA1c (OR = 1.80 [1.02-3.14], P = 0.044) were risk factors for macrovascular complications. TIR (OR = 0.97 [0.95-0.99], P = 0.021) was the only independent risk factor for hospitalizations for hypoglycemia or ketoacidosis., Conclusions: Lower TIR was associated with the presence of composite microvascular complications and with hospitalization for hypoglycemia or ketoacidosis. TIR, SD, and CV were not associated with macrovascular complications., (© The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: The study involved a female patient diagnosed with late-stage dementia, with chronic daytime somnolence (CDS) as a prominent symptom., Objective: To explore whether her dementia resulted from Type 3 diabetes, and whether it could be reversed through ketosis therapy., Methods: A ketogenic diet (KD) generating low-dose 100 μM Blood Ketone Levels (BKL) enhanced by a brief Ketone Mono Ester (KME) regimen with high-dose 2-4 mM BKLs was used., Results: Three sets of data describe relief (assessed by % days awake) from CDS: 1) incremental, slow, time-dependent KD plus KME-induced sigmoid curve responses which resulted in partial wakefulness (0-40% in 255 days) and complete wakefulness (40-85% in 50 days); 2) both levels of wakefulness were shown to be permanent; 3) initial permanent relief from CDS with low-dose ketosis from 6.7% to 40% took 87 days. Subsequent low-dose recovery from illness-induced CDS (6.9% to 40%) took 10 days. We deduce that the first restoration involved permanent repair, and the second energized the repaired circuits., Conclusion: The results suggest a role for ketosis in the elimination of CDS with the permanent functional restoration of the awake neural circuits of the Sleep-Wake cycle. We discuss whether available evidence supports ketosis-induced bioenergetics alone or whether other mechanisms of functional renewal were the basis for the elimination of CDS. Given evidence for permanent repair, two direct links between ketosis and neurogenesis in the adult mammalian brain are discussed: Ketosis-induced 1) brain-derived neurotrophic factor, resulting in neural progenitor/stem cell proliferation, and 2) mitochondrial bioenergetics-induced stem cell biogenesis., Competing Interests: The authors have no conflict of interest to report., (© 2021 – The authors. Published by IOS Press.)

Background: Alcoholic ketoacidosis (AKA) is defined by metabolic acidosis and ketosis in a patient with alcohol use. This is a common presentation in the emergency department (ED) and requires targeted therapies., Objective: This narrative review evaluates the pathogenesis, diagnosis, and management of AKA for emergency clinicians., Discussion: AKA is frequently evaluated and managed in the ED. The underlying pathophysiology is related to poor glycogen stores and elevated nicotinamide adenine dinucleotide and hydrogen. This results in metabolic acidosis with elevated beta-hydroxybutyrate levels. Patients with AKA most commonly present with a history of alcohol use (acute or chronic), poor oral intake, gastrointestinal symptoms, and ketoacidosis on laboratory assessment. Patients are generally dehydrated, and serum glucose can be low, normal, or mildly elevated. An anion gap metabolic acidosis with ketosis and electrolyte abnormalities are usually present on laboratory evaluation. Management includes fluid resuscitation, glucose and vitamin supplementation, electrolyte repletion, and evaluation for other conditions., Conclusions: Emergency clinician knowledge of the evaluation and management of AKA is essential in caring for these patients., (Published by Elsevier Inc.)

Sodium-glucose cotransporter-2 (SGLT2) inhibitors are drugs designed to lower plasma glucose concentration by inhibiting Na + -glucose-coupled transport in the proximal tubule. Clinical trials demonstrate these drugs have favorable effects on cardiovascular outcomes to include slowing the progression of CKD. Although most patients tolerate these drugs, a potential complication is development of ketoacidosis, often with a normal or only a minimally elevated plasma glucose concentration. Inhibition of sodium-glucose cotransporter-2 in the proximal tubule alters kidney ATP turnover so that filtered ketoacids are preferentially excreted as Na + or K + salts, leading to indirect loss of bicarbonate from the body and systemic acidosis under conditions of increased ketogenesis. Risk factors include reductions in insulin dose, increased insulin demand, metabolic stress, low carbohydrate intake, women, and latent autoimmune diabetes of adulthood. The lack of hyperglycemia and nonspecific symptoms of ketoacidosis can lead to delays in diagnosis. Treatment strategies and various precautions are discussed that can decrease the likelihood of this complication., (Copyright © 2021 by the American Society of Nephrology.)

Background: Euglycaemic ketoacidosis (EKA) is an infrequent but serious condition which usually follows a period of starvation, severe vomiting or illness in individuals with or without diabetes. Ketoacidosis is associated with materno-fetal morbidity and mortality necessitating prompt diagnosis and management. Physiological increases in insulin resistance render pregnancy a diabetogenic state with increased susceptibility to ketosis. COVID-19 is associated with worse clinical outcomes in patients with diabetes and is an independent risk factor for ketoacidosis in normoglycaemic individuals., Case Presentations: We describe two cases of SARS-CoV-2 positive pregnant women presenting with normoglycaemic metabolic ketoacidosis. Both cases were associated with maternal and fetal compromise, requiring aggressive fluid and insulin resuscitation and early delivery., Conclusion: We discuss possible physiology and propose a management strategy for euglycaemic ketoacidosis in pregnancy.

Nutritional ketosis has been proven effective for neurometabolic conditions and disorders linked to metabolic dysregulation. While inducing nutritional ketosis, ketogenic diet (KD) can improve motor performance in the context of certain disease states, but it is unknown whether exogenous ketone supplements-alternatives to KDs-may have similar effects. Therefore, we investigated the effect of ketone supplements on motor performance, using accelerating rotarod test and on postexercise blood glucose and R -beta-hydroxybutyrate ( R -βHB) levels in rodent models with and without pathology. The effect of KD, butanediol (BD), ketone-ester (KE), ketone-salt (KS), and their combination (KE + KS: KEKS) or mixtures with medium chain triglyceride (MCT) (KE + MCT: KEMCT; KS + MCT: KSMCT) was tested in Sprague-Dawley (SPD) and WAG/Rij (WR) rats and in GLUT-1 Deficiency Syndrome (G1D) mice. Motor performance was enhanced by KEMCT acutely, KE and KS subchronically in SPD rats, by KEKS and KEMCT groups in WR rats, and by KE chronically in G1D mice. We demonstrated that exogenous ketone supplementation improved motor performance to various degrees in rodent models, while effectively elevated R -βHB and in some cases offsets postexercise blood glucose elevations. Our results suggest that improvement of motor performance varies depending on the strain of rodents, specific ketone formulation, age, and exposure frequency.

Background: Sodium-glucose co-transporter-2 (SGLT2) inhibitors are increasingly used for the treatment of type 2 diabetes, but have been associated with ketoacidosis., Methods/results: We report a case series of three patients with latent autoimmune diabetes of the adult who presented with ketoacidosis, including one case with normal blood glucose levels, in the context of SGLT2 inhibitor use., Conclusions: Sodium-glucose co-transporter-2 inhibitors should be used with caution and close clinical monitoring in patients with latent autoimmune diabetes of the adult. A clinical risk score permits targeted autoantibody testing and should be undertaken prior to commencement of SGLT2 inhibitors or cessation of insulin., (Crown Copyright © 2020. Published by Elsevier Inc. All rights reserved.)

A 37-year-old woman who had 8 weeks post partum, breast feeding and on a low carbohydrate and high protein (ketogenic) diet, was admitted to the hospital with acute onset of nausea, vomiting and abdominal pain of 1-day duration. On admission, she was found to have high anion gap metabolic acidosis, elevated beta-hydroxybutyric acid level, normal glucose level and evidence of ketoacidosis. She was treated with lactated Ringer solution, along with dextrose 5% solution with the resolution of symptoms and metabolic derangement., Competing Interests: Competing interests: One of the coauthors (TM) reports personal fees and non-financial support from consultant of FUJIFILM Corp/Japan International Cooperation Agency (JICA), outside the submitted work., (© BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Ketosis is a metabolic situation involving an increase in blood and urine concentrations of ketones that, when prolonged, leads to acidosis. Moderate ketosis usually appears after a fast of a few hours, but its prolongation exposes to hyperketosis. Observation: A 25-year-old woman presented to the emergency department for cohercitive vomiting. She was fasting for a long time in a spiritual setting and had a restricted diet limited to water and vitamin supplements. Clinical and biological assessment was in favour of fasting ketoacidosis. Evolution was favorable with intravenous hydration, poly-ionic and micronutrient supplementation and a gradual resumption of oral feeding. Conclusion: We report the case of a patient with fasting ketoacidosis. Besides consequences of this ketoacidosis, the challenge was also in resuming oral feeding in order to avoid a potentially fatal inappropriate renutrition syndrome.

Negative animal health and performance outcomes are associated with disease incidences that can be labor-intensive, costly, and cumbersome for many farms. Amelioration of unfavorable outcomes through early detection and treatment of disease has emphasized the value of improving health monitoring. Although the value is recognized, detecting hyperketonemia (HYK) is still difficult for many farms to do practically and efficiently. Increasing data streams available to farms presents opportunities to use data to better monitor cow and herd health; however, challenges remain with regard to validating, integrating, and interpreting data. During the transition to lactation period, useful data are presented in the form of milk production and composition, milk Fourier-transform infrared (FTIR) wavelength absorbance, cow management records, and genomics, which have been employed to monitor postpartum onset of HYK. Attempts to predict postpartum HYK from test-day milk and performance variables incorporated into multiple linear regression models have demonstrated sufficient accuracy to monitor monthly herd prevalence; however, they lacked the sensitivity and specificity for individual cow diagnostics. Subsequent artificial neural network prediction models employing FTIR data and milk composition variables achieved 83 and 81% sensitivity and specificity for individual cow diagnostics. Although these results fail to reach the diagnostic goals of 90%, they are achieved without individual cow blood samples, which may justify acceptance of lower performance. The caveat is that these models depend on milk analysis, which is traditionally done every 4 weeks. This infrequent sampling allows for a single diagnostic sample for about half of the fresh cows. Benefits to farms are greatly improved if postpartum cows can be milk-tested weekly. Additionally, this allows for close monitoring of somatic cell count and may open the door for use of other herd health monitoring tools. Future improvements in these models may be achievable by maximizing sensitivity at the expense of specificity and may be most economical in disorders for which the cost of treatment is less than that of mistreating (e.g., HYK). Genomic predictions for HYK may be improved by incorporating genome-wide associated SNP and further utilized for precision management of HYK risk groups. Development and validation of HYK prediction models may provide producers with individual cow and herd-level management tools., (Copyright © 2020 American Dairy Science Association. Published by Elsevier Inc. All rights reserved.)

Background: Ketosis is a metabolic disorder often triggered by anorexia in animals fed on high energy diets. Although mostly described in pregnant female guinea pigs, under the name of pregnancy toxicosis; there is limited information on ketosis in males and non-pregnant females, often presented to clinics with anorexia or inappetence. The objective of this study was to observe progression of ketosis in guinea pigs, document the changes and evaluate diagnostic methods and a therapeutic approach., Results: Twenty eight adult guinea pigs (Cavia porcellus), castrated males and intact females of obese and slim body condition were fasted for 3 days and refed afterwards. The slim animals served as control group for body condition. Either slim and fat animals were divided into two treatment groups: half of them received fluid replacements with glucose subcutaneously, the other half did not receive any injection and served as treatment control. Serum beta-hydroxybutyrate, and urine acetoacetate and acetone were measured during and after fasting. Serum ALT, bile acids and liver histology were also analyzed after 7 days of refeeding (and therapy). Females and obese guinea pigs showed a significantly higher increase in ketone bodies in serum and urine. Obese, female, or animals not receiving therapy needed more time to regulate ketone bodies to normal levels than slim animals, males or animals receiving therapy. Liver histology revealed increased hepatocyte degeneration and higher glycogen content in obese animals and animals receiving therapy, and additionally more glycogen content in males. Only minor hepatic fat accumulation was documented. Bile acids showed good correlation to histological liver changes whereas ALT did not., Conclusions: Female and obese animals react more intensively to fasting. As preventive management, animals should be kept in adequate body condition, fasting should be avoided, and anorexia should be treated immediately. In such a case, urinary dip sticks to detect ketone bodies are a useful diagnostic tool. Glucose therapy leads to faster cessation of ketogenesis and should be recommended in cases of ketosis. However, it needs to be adjusted to avoid hepatocyte glycogen overload and degeneration. Measuring bile acids presents a valuable indicator of liver damage.

A 59-year-old woman unaware of having diabetes was transferred due to coma. Upon discovery at home, her consciousness on the Glasgow Coma Scale was E1V2M4, BP 95/84 mmHg, body temperature 34.7°C. On arrival at ER, height was 1.63 m, weight 97 kg, plasma glucose (PG) 1,897 mg/dL, HbA 1c 13.6%, osmolality 421 mosm/kg, arterial pH 7.185, lactate 6.34 mmol/L, β-hydroxybutyrate 7.93 mmol/L. With saline and regular insulin infusion, PG was lowered to 1,440 mg/dL at 2 hours and then to 250 mg/dL by Day 3, and consciousness normalized by Day 5. On admission, serum immunoreactive insulin (IRI) was undetectable (<0.03 U/mL), C-peptide immunoreactivity (CPR) undetectable (<0.003 ng/mL), and anti-glutamic acid decarboxylase antibody negative. Following the above-described treatment, fasting PG was 186 mg/dL and CPR 1.94 ng/mL, respectively, on Day 14; 2-h post-breakfast PG 239 mg/dL and CPR 6.28 ng/mL, respectively, on Day 18. The patient discharged on Day 18 with 1,800 kcal diet, 32 U insulin glargine and 40 mg gliclazide. Fifteen months later at outpatient clinic, her HbA 1c was 6.9% and 2-h post-breakfast PG 123 mg/dL and CPR 5.30 ng/dL with 750 mg metformin, 10 mg gliclazide and 18 U insulin glargine. Transient, but total cessation of insulin secretion was documented in a patient with type 2 diabetes under severe metabolic decompensation. Swift, sustained recovery of insulin release indicated that lack of insulin at the time of emergency was due to secretory failure, i.e., unresponsive exocytotic machinery or depletion of releasable insulin, rather than loss of beta cells.

Ketoacidosis is uncommon in non-diabetic women, but occurs in the postpartum period as a rare complication of continuing to breastfeed during periods of acute illness. We report a case of a lactating woman who presented with severe symptomatic ketoacidosis in the early postpartum period. We also review the pathophysiology and management of lactation ketoacidosis., (© 2019 Royal Australasian College of Physicians.)

Rationale: Dapagliflozin (a sodium-glucose cotransporter-2 [SGLT2] inhibitor) represents the most recently approved class of oral medications for the treatment of type 2 diabetes. Dapagliflozin lowers plasma glucose concentration by inhibiting the renal reuptake of glucose in the proximal renal tubules. In 2015, the US Food and Drug Administration released a warning concerning a potential increased risk of ketoacidosis in patients taking this medication., Patient Concerns: We present the case of a 23-year-old woman with type 2 diabetes treated with dapagliflozin (10 mg, once a day) for 2 years who presented to the emergency department with abdominal pain., Diagnoses: We diagnosed her with severe ketoacidosis with a normal glucose level (177 mg/dL) due to dapagliflozin, accompanying acute pancreatitis due to hypertriglyceridemia. We concluded that the precipitating factor for euglycemic ketoacidosis was pseudomembranous colitis., Interventions: She was treated with intravenous infusions of insulin, isotonic saline, and sodium bicarbonate as diabetic ketoacidosis treatment., Outcomes: She was in shock with severe metabolic acidosis. After continuous renal replacement therapy, the uncontrolled metabolic ketoacidosis was treated, and she is currently under follow-up while receiving metformin (500 mg, once a day) and short- and long-acting insulins (8 units 3 times and 20 units once a day)., Lessons: We report an unusual case of SGLT2 inhibitor-induced euglycemic ketoacidosis recovered by continuous renal replacement therapy in a patient with type 2 diabetes and recurrent acute pancreatitis due to hypertriglyceridemia. We diagnosed a rare complication of the SGLT2 inhibitor in a patient with type 2 diabetes in whom uncontrolled metabolic ketoacidosis could be effectively managed via continuous renal replacement therapy.

Spinal muscular atrophy (SMA) is a genetic neuromuscular disease characterized by progressive muscle weakness and atrophy. We report a case of a 36-year-old man with SMA type 3 who presented to our emergency department with epigastric pain and vomiting. He was found to have severe ketoacidosis on laboratory evaluation. The patient's symptoms and ketoacidosis resolved after dextrose infusion and a relatively small amount of sodium bicarbonate infusion. Given the severity of the ketosis that seemed inconsistent with moderate starvation alone, we postulate that there must have been other contributing factors besides moderate starvation that might explain the severity of acidosis in this particular patient. These factors include low muscle mass, disturbed fatty acid metabolism, hormonal imbalances and defective glucose metabolism. Ketoacidosis is an under-recognized entity in patients with neuromuscular diseases and requires a high index of suspicion for prompt diagnosis and management.

Starvation ketoacidosis (SKA) constitutes an important consideration in the pregnant patient who presents with profound metabolic acidosis. Pregnancy-related changes predispose the patient to develop SKA following relatively short periods (12 - 14 hours) of 'starvation'. Patients also typically look clinically well in relation to the significant metabolic derangements that accompany the condition. Prompt recognition and early institution of appropriate therapy is therefore extremely important in terms of optimising maternal and fetal outcome. We describe a pregnant patient with SKA who presented with profound euglycaemic ketoacidosis that resolved rapidly following the early initiation of appropriate therapy. Furthermore, appropriate therapy resulted in our patient avoiding the need for an emergency caesarean section, which is often reported in this scenario. The ensuing discussion addresses SKA in pregnancy, the unique features of our patient, and management considerations from a maternal and fetal perspective. We also discuss the various causes of ketoacidosis such as diabetic ketoacidosis (DKA), euglycaemic DKA, alcohol-induced euglycaemic ketoacidosis and SKA in pregnant patients.

Rationale: Pregnant women are more prone to ketosis due to the relative insulin resistance, accelerated lipolysis and increased free fatty acids., Patient Concerns: We report a pregnant woman with hyperlipidemia, who experienced severe metabolic acidosis after a short period of starvation., Diagnoses: Based on her clinical symptoms, exclusion diagnosis and therapeutic diagnosis, her condition was diagnosed as starvation ketoacidosis., Interventions: An emergency caesarean section under general anesthesia was implemented 2 hours after her admission. The metabolic acidosis was treated with fluid resuscitation using compound sodium lactate, bicarbonate, and 5% dextrose together with insulin 6U., Outcomes: Both mother and baby were discharged clinically well., Lessons: Starvation ketoacidosis may happen in special patient who was in pregnancy and with severe hypertriglyceridemia, after just one day fasting and vomiting.

Two female patients were admitted due to ketoacidosis. Serum glucose was moderately elevated. The patients exhibited abdominal and neurologic symptoms. Treatment consisted of metformin, insulin glargin and empagliflozin, as well as glimepiride, insulin detemir and empagliflozin, respectively. Treatment with intravenous fluid replacement, insulin, glucose, potassium and buffer solution led to a normalisation of pH and serum glucose levels. Our report describes two cases of atypical ketoacidosis with moderately elevated serum glucose during sodium-glucose co-transporter-2 (SGLT2) inhibitor therapy.

Objective: Determination of the frequency of subclinical hypocalcaemia, increased lipomobilisation and subclinical ketosis as problems in dairy herds and identification of possible risk factors., Material and Methods: Information was obtained from 51 dairy farms on husbandry, feeding, management of the cows and heifers, animal health and prophylactic treatments using a questionnaire. Blood samples from 20% of the cows and 30% of the heifers of each farm (= herd sample) were collected in the week ante partum (a. p.) for determination of serum calcium (Ca), magnesium (Mg), phosphorus (P) and non-esterified fatty acids (NEFA) concentrations and in the week post partum (p. p.) for measurement of serum β-hydroxybutyrate (BHB) concentration. For evaluation of the herd sample results, the percentage of animals with a laboratory value above a determined threshold value for the various parameters was calculated. When the percentage exceeded a certain threshold (alert) level, a herd problem was assumed. Alert levels from the literature and adapted levels were used., Results: For minerals, an adapted alert level of 10% was taken as a basis. In cows, the alert level for Ca, Mg, P (too low) and P (too high) was exceeded in 13.7%, 13.7%, 25.7% and 7.8% of the herd samples, respectively. NEFA (a. p.) and BHB (p. p.) had an adapted alert level of 30%. For NEFA, the alert level was exceeded by cows and heifers on 47.1 % and 51.0% of the farms, respectively. For BHB, the alert level was exceeded by cows and heifers on 33.3% and 13.7% of the farms, respectively. As risk factors, a too large group size for the transition cows (Ca, Mg), pasturing (Ca, BHB), one phasic feeding of dry cows (Mg, BHB) and a lack of a separated dry cow area (BHB) were identi fied. Risk factors for the heifers were no pasturing of the young stock (NEFA) and a low frequency of pushing up the diet in the feed bunk (BHB)., Conclusion and Clinical Relevance: Subclinical ketosis in cows and an increased lipomobilisation in heifers were frequent herd problems in the dairy herds studied and were asso ciated with husbandry, feeding and management. Therefore, these herd problems should be handled intensively in veterinary herd health programs with the aim to establish effective preventive measures., Competing Interests: Die Autoren erklären, dass kein Interessenkonflikt besteht., (Schattauer GmbH.)

Background: This study is to explore the clinical characteristics, laboratory diagnosis, and treatment outcomes in pediatric patients with non-diabetic ketoacidosis., Methods: Retrospective patient chart review was performed between March 2009 to March 2015. Cases were included if they met the selection criteria for non-diabetic ketoacidosis, which were: 1) Age ≤ 18 years; 2) urine ketone positive ++ or >8.0 mmol/L; 3) blood ketone >3.1 mmol/L; 4) acidosis (pH < 7.3) and/or HCO 3  < 15 mmol/L; 5) random blood glucose level < 11.1 mmol/L. Patients who met the criteria 1, 4, 5, plus either 2 or 3, were defined as non-diabetic ketoacidosis and were included in the report., Results: Five patients with 7 episodes of non-diabetic ketoacidosis were identified. They all presented with dehydration, poor appetite, and Kussmaul breathing. Patients treated with insulin plus glucose supplementation had a quicker recovery from acidosis, in comparison to those treated with bicarbonate infusion and continuous renal replacement therapy. Two patients treated with bicarbonate infusion developed transient coma and seizures during the treatment., Conclusion: Despite normal or low blood glucose levels, patients with non-diabetic ketoacidosis should receive insulin administration with glucose supplementation to correct ketoacidosis.

Alcoholic ketoacidosis - a review A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem in the emergency room. Over and above methanol- and ethylene glycol intoxication, alcoholic ketoacidosis is a common but less recognized etiology. The disorder occurs in alcoholics who have had a recent binge drinking followed by the abrupt cessation of alcohol consumption because of abdominal pain and vomiting, with resulting dehydration, starvation, and then a β-hydroxybutyrate dominated ketoacidosis. Laboratory results may be misleading as the common urine-ketone tests may be negative or only weakly positive, since they only respond to acetoacetate. The short-term prognosis is good if treatment including replacement of fluid, electrolytes, glucose and thiamine is provided. However, recent studies have indicated that alcoholic ketoacidosis may be a significant cause of mortality in patients with alcohol dependence.

Strict restriction of carbohydrates can induce symptomatic ketoacidosis. We herein report a 76-year-old demented woman who developed ketoacidosis after 1 month of abnormal eating behavior involving selectively eating hamburger steak (estimated carbohydrate =12.7 g/day). Laboratory tests showed high-anion-gap metabolic acidosis with elevated blood ketone levels. She was successfully treated with intravenous fluids followed by oral intake of a regular diet. She remained relapse-free after correcting her eating habits. Healthcare providers should know that abnormal eating behavior in demented people can lead to an extremely-low-carbohydrate diet and cause atypical ketoacidosis unexplained by diabetes, heavy alcohol intake, or starvation conditions.

Background: Alcoholic ketoacidosis (AKA) is a complex syndrome that results from disrupted metabolism in the setting of excessive alcohol use and poor oral intake. Dehydration, glycogen depletion, high redox state, and release of stress hormones are the primary factors producing the characteristic anion gap metabolic acidosis with an elevated β-hydroxybutyrate (β-OH) and lactate., Case Report: We present the case of a 47-year-old man who presented to the emergency department with metabolic acidosis and profoundly elevated lactate levels who had AKA. He recovered completely with intravenous fluids and parenteral glucose administration. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Emergency physicians should always consider the immediately life-threatening causes of a severe anion gap metabolic acidosis and treat aggressively based on the situation. This case highlights the fact that AKA can present with an impressively elevated lactate levels. Emergency physicians should keep AKA in the differential diagnosis of patients who present with a similar clinical picture., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Objective: Canagliflozin is a sodium-glucose co-transporter 2 (SGLT-2) inhibitor, one of a class of novel antiglycemic agents that are gaining in popularity in the treatment of diabetes., Methods: We describe a case in which a patient experienced difficult-to-treat metabolic ketoacidosis in the setting of canagliflozin use., Results: A 52-year-old man with type 2 diabetes mellitus developed profound ketoacidosis without overt hyperglycemia while taking canagliflozin. Despite initiation of an insulin infusion, the metabolic acidosis persisted for 3 days., Conclusion: Treatment with canagliflozin was associated with development of euglycemic ketoacidosis.

A prospective cohort study was conducted on 1,081 dairy goats from 10 commercial herds in Québec (Canada) to define prepartum hyperketonemia based on optimal blood β-hydroxybutyrate acid threshold values for the early prediction of pregnancy toxemia (PT) and mortality in late-gestation dairy goats. All pregnant goats had blood sampled weekly during the last 5wk of pregnancy. The blood was analyzed directly on the farm for β-hydroxybutyrate acid quantification using a Precision Xtra meter (Abbott Diabetes Care, Saint-Laurent, QC, Canada). Body condition scores on the lumbar region and sternum were noted. Each goat was classified as being at low (n=973) or high risk (n=108) of having PT by producers based on a standardized definition. The optimal threshold for predicting a PT diagnosis or mortality for each week before kidding was determined based on the highest sum of sensitivity and specificity. The association between hyperketonemia and subsequent PT was tested using a multivariable logistic regression model considering hyperketonemia at wk 4 prepartum, litter size, and body condition score at wk 4 prepartum as covariates, and herd and parturition cohort as random effects. The association between mortality and hyperketonemia was also tested using a logistic regression model accounting for the presence or absence of treatment during the last month of pregnancy. The hyperketonemia definition based on PT varied between ≥0.4 and ≥0.9mmol/L during the last 5wk prepartum. Goats affected by hyperketonemia at wk 4 prepartum and with a large litter size (≥3 fetuses) had 2.1 and 40.5 times the odds, respectively, of subsequent PT than other goats. Hyperketonemia definitions based on mortality varied between ≥0.6 and ≥1.4mmol/L during the last 4wk prepartum, and was ≥1.7mmol/L during the first week postpartum. Goats affected by hyperketonemia and treated by producers had 3.4 and 11.8 times the odds, respectively, of subsequent mortality than did other goats. These results showed that prepartum hyperketonemia could be defined in dairy goats using subsequent risks of PT or mortality during the last month of pregnancy., (Copyright © 2015 American Dairy Science Association. Published by Elsevier Inc. All rights reserved.)

We report a 55 year old Japanese man with a history of alcohol abuse, who was in a near fasting state for the previous few days.He was admitted to our hospital with abrupt disturbance of consciousness. He presented disturbance of consciousness with extreme hypoglycemia and ketoacidosis with high β-hydroxybutyric acid concentration. Taking into account his living history, we diagnosed with alcoholic ketoacidosis (AKA). Symptoms ameliorated with glucose injection and fluid loading. AKA patients show abdominal pain, nausea or vomiting, but they are usually alert and lucid despite the severe acidosis. This case, however, presented comatose status caused by hypoglycemia. Poor oral intake of this patient was assumed to be the cause of hypoglycemia. Alcoholism may cause hypoglycemia accompanying with AKA, due to a low carbohydrate intake, the inhibition of gluconeogenesis, and reduced hepaticglycogen storage as seen in this case. Here, we report a case of AKA that demonstrated hypoglycemia with the literature review.

Background: Purulent pericarditis is an acute and fulminant disease characterized by pus accumulation in the pericardial space. Its incidence has declined substantially and the common pathogen has changed since the beginning of the antibiotic era; however, it is still found in some patients with immunocompromised conditions., Case Report: We report a rare case in which the onset of diabetes mellitus presented as extremely high HbA1c concentration, ketoacidosis, multi-site abscesses and purulent pericarditis. After antibiotic therapy and pericardiocentesis, the purulent pericarditis still did not resolve and further intrapericardial thrombolytic therapy also failed. Finally, this patient was treated successfully by surgical debridement and pericardiectomy., Conclusion: In the immunocompromised state of severe hyperglycaemia, purulent pericarditis is a possible complication of uncontrolled infection. If purulent pericarditis cannot be cured using non-surgical treatments, such as antibiotic therapy, pericardiocentesis and intrapericardial thrombolytic therapy, a surgical pericardiectomy should be considered to avoid morbidity and mortality., (© 2014 The Authors. Diabetic Medicine © 2014 Diabetes UK.)

Unlabelled: The prevalence of diabetes is increasing significantly and, therefore, dental practitioners are having to manage diabetic patients on a more regular basis. Alongside the systemic effects on the various tissues and organs of the body, diabetes can adversely affect oral health and all clinicians should be aware of the issues that may arise., Clinical Relevance: Dental practitioners are almost guaranteed to encounter both diagnosed and undiagnosed diabetic patients. It is therefore important that they are aware of the oral signs and symptoms of disease and the reciprocal relationship between oral health and glycaemic control, so that diabetic patients are managed accordingly.

Chronic alcoholism is a frequently unrecognised cause of ketoacidosis. Most patients with alcoholic ketoacidosis present with normal or low glucose, but this condition can present with hyperglycaemia. This can lead to misdiagnosis of diabetes ketoacidosis and, therefore, inappropriate treatment with insulin. We describe a 37-year-old Caucasian woman with chronic pancreatitis secondary to excess alcohol consumption, admitted with abdominal pain and vomiting, fulfilling the criteria for diabetes ketoacidosis. She was treated according to diabetes ketoacidosis protocol and experienced a hypoglycaemic attack within an hour of initiation of insulin. On review of her history, she was found to have three similar episodes over the past 12 months. Alcoholic ketoacidosis can present with hyperglycaemia due to relative deficiency of insulin and relative surplus in counter-regulatory stress hormones including glucagon. Awareness of the syndrome with a detailed history helps to differentiate alcohol ketoacidosis from diabetes ketoacidosis and prevent iatrogenic hypoglycaemia.

Dairy cows pass through a period of negative energy balance as they transition from late gestation to early lactation. Poor adaptation through this period, expressed as excessively elevated concentrations of non-esterified fatty acids (NEFAs) pre- or post-partum and elevated concentrations of β-hydroxybutyrate post-partum, increases an individual animal's risk of post-partum disease, removal from the herd, reproductive difficulty, and reduced milk production. Field studies have shown that subclinical ketosis often affects 40% of cows in a herd although the incidence can be as high as 80%. Peak incidence occurs at 5 days in milk, and cows that develop subclinical ketosis in the first week of lactation have a higher risk of negative effects and reduced milk production than cows that develop subclinical ketosis in the second week of lactation. Herds with more than a 15-20% prevalence of excessively elevated concentrations of NEFAs and β-hydroxybutyrate in early lactation have higher rates of negative subsequent events, poorer reproduction, and lower milk yield than herds with a lower prevalence of negative energy balance. This paper reviews (1) strategies for testing of energy-related metabolites, (2) consequences of poor adaptation to negative energy balance (for individual animals and for herds), (3) treatment approaches for affected cows, and (4) economic considerations for testing and treating cows with poor adaptation to negative energy balance., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Ketoacidosis can occur most often as a result of uncontrolled diabetes mellitus. However, it can be seen with fasting and alcohol consumption, as well. Ketoacidosis in association with fasting has less severity, and ketoacid levels do not exceed 10 mEq/L. In the literature, there are a few reports about severe high anion gap acidosis that were associated with fasting. We report a case of pregnancy associated with high anion gap acidosis as a result of fasting.

Starvation ketosis outside pregnancy is rare and infrequently causes a severe acidosis. Placental production of hormones, including glucagon and human placental lactogen, leads to the insulin resistance that is seen in pregnancy, which in turn increases susceptibility to ketosis particularly in the third trimester. Starvation ketoacidosis in pregnancy has been reported and is usually precipitated by a period of severe vomiting. Ketoacidosis is likely to have important implications for fetal survival as ketoacidosis in women with type 1 diabetes mellitus is associated with intrauterine death. This article features four cases of women with vomiting in the third trimester of pregnancy associated with a severe metabolic acidosis. The mechanism underlying ketogenesis, the evidence for accelerated ketogenesis in pregnancy and other similar published cases are reviewed. A proposed strategy for management of these women is presented., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

The current paper presents the results of monitoring of 69 patients with acute respiratory viral infection, acetonemic syndrome. It was shown the effectiveness of inclusion of Reamberinum into complex therapy as a means for reduction of with acetonemic syndrome and for detoxic effect.