Urine Ketone Research Articles

ODP165 Atypical DKA? Think Cannabis!

Abstract Diabetic ketoacidosis (DKA) can be life threatening if not recognized and treated promptly. DKA is characterized by hyperglycemia, acidosis, ketosis and elevated anion gap. The presence of these metabolic derangements is essential to make the diagnosis. The use of cannabis has been associated with atypical acid-base profile in DKA which may contribute to confusion in diagnosis and treatment. Case A 20-year-old man with type 1 diabetes since age 10 presented to the emergency department with 4 days of nausea, vomiting and elevated blood glucose (BG). Emesis occurred up to 6 times daily and started 2 days prior to hyperglycemia. He was unable to correct BG with rapid acting insulin. Moderate urine ketones were present. He denied symptoms of diarrhea, fever, sore throat, runny nose or cough and reported adherence to insulin regimen. Physical exam was remarkable for dry mucous membranes and mild epigastric tenderness. Lab evaluation showed BG of 268 (70-110mg/dL), sodium 133 (135-145 mmol/L), potassium 3.6 (3.5- 5.1 mmol/L), chloride 95 (98-107 mmol/L), bicarbonate 22 (22-32 mmol/L), creatinine 0.8 (0.6–1.2 mg/dL), Anion gap 16, beta-hydroxybutyrate 3.38 (<0.27 mmol/L). He had normal white blood cell count and infectious work up was unremarkable. The patient was started on continuous IV fluids and was managed with intermittent subcutaneous rapid acting insulin in addition to basal insulin. After anion gap closure he was transitioned to his home doses of insulin. Prior to discharge, the patient discretely asked about the effects of smoking marijuana on BG and subsequently disclosed he had increased his use of marijuana recently. Discussion Diabetic keto-alkalosis may present as a result of recurrent vomiting that leads to gastric acid loss. Cannabis use has been linked to an increased risk of diabetic keto-alkalosis. The underlying mechanism is hypothesized to be related to cannabis effects on the stomach causing delayed gastric emptying and leading to cyclic nausea and vomiting. One study conducted to investigate acid-base parameters seen in atypical DKA in Type 1 Diabetes referred to this as "Hyperglycemic Ketosis due to Cannabis Hyperemesis Syndrome" (HK-CHS) recommending obtaining urine drug screen in patients with atypical DKA 1 . Attention should be drawn to this phenomenon as cannabis use has grown with its legalization in many states. Individuals with T1D presenting with ketosis but normal or elevated pH and/or serum bicarbonate may confuse clinicians and delay proper diagnosis. When the patient does not disclose cannabis use voluntarily, taking a thorough social history is critical to making the correct diagnosis. Reference: 1. Akturk HK, Snell-Bergeon J, Kinney GL, Champakanath A, Monte A, Shah VN. Differentiating diabetic ketoacidosis and hyperglycemic ketosis due to cannabis hyperemesis syndrome in adults with type 1 diabetes. Diabetes Care 2021 December 8,: dc211730 Presentation: No date and time listed

RF32 | PSUN67 Recurrent Acute Pancreatitis Secondary to Hypertriglyceridemia in an Adolescent With Type 2 Diabetes, Symptomatic Hypocalcemia, and COVID-19 Infection

Abstract Introduction Hypertriglyceridemia is the third most common cause of acute pancreatitis, leading to increased morbidity and mortality. Hypocalcemia is a frequent complication of pancreatitis, attributed to saponification of calcium by the release of pancreatic lipase. Free fatty acids are released by the breakdown of triglycerides, then react with extracellular calcium, forming fatty acid salts that deposit in the retroperitoneum and reduce calcium availability.1 We present a case of an adolescent female with recurrent episodes of acute pancreatitis, hypertriglyceridemia, and hypocalcemia. Her first presentation of pancreatitis coincided with new-onset type 2 diabetes, while this third episode with COVID-19. Case An 18-year-old morbidly obese female with type 2 diabetes, hypertriglyceridemia, hepatomegaly, and recurrent acute pancreatitis was admitted for a third episode of pancreatitis secondary to severe hypertriglyceridemia. On admission, triglycerides were 3213 mg/dL (reference 35-134mg/dL), lipase 12,721 units/L (145-226u/L), amylase 323 units/L (<106u/L), AST 90 units/L (10-26u/L), and ALT 109 units/L (19-49u/L). A1C was 7.5%, blood glucose 301 mg/dL, bicarbonate 25 mmol/L, and large urine ketones. Initial calcium was 8.7 mg/dL (9.0-10.7mg/dL) and albumin 4.0 gm/dL (3.8-5.6gm/dL). The next day, she developed hypocalcemia with numbness and tingling. Serum calcium was 5.3mg/dL, ionized calcium 0.74 mmol/L (1.12-1.37mmol/L), and albumin <0.6 gm/dL. 25-hydroxy vitamin D level was 16.5 ng/mL (30-100). QTc was 470 ms (350-440ms). She was transferred to pediatric intensive care and initiated on an insulin drip at 0.1 units/kg/hour for hypertriglyceridemia. She received four IV calcium gluconate boluses (1000-2000 mg each). Symptoms improved within one day. Triglycerides decreased to 642 mg/dL, calcium and albumin normalized, and subcutaneous insulin regimen was resumed. She started vitamin D 3000 IU daily and elemental calcium carbonate 26 mg/kg/day. During her hospitalization, she was found to be COVID-19 positive and had become hypoxemic requiring 2.5 liters of oxygen. Upon resolution, she was discharged with outpatient follow-up. Of note, there is a strong maternal family history of type 2 diabetes and hypertriglyceridemia. The mother had three strokes in her forties. The patient has not previously undergone pancreatitis genetic testing. Discussion To conclude, this case affirms the importance of detecting hypertriglyceridemia-induced pancreatitis early on and improved outcomes with insulin drips. It is important to determine triggers for recurrent pancreatitis in those with underlying genetic etiologies of hypertriglyceridemia. Additionally, it is crucial to monitor for secondary hypocalcemia, particularly given the risk for prolonged QT interval and ventricular arrhythmias. Lastly, the COVID-19 pandemic may be associated with more severe presentations of pancreatitis. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 12:30 p.m. - 12:35 p.m.

Diabetic ketoacidosis induced by nivolumab in invasive mucinous adenocarcinoma of the lung: a case report and review of the literature

Nivolumab is the first programmed cell death receptor 1 (PD-1) inhibitor approved in China. Compared with chemotherapy, nivolumab has shown advantages of good efficacy and safety in the treatment of a variety of tumors. However, due to its short time of use in China and lack of safety experience, clinical understanding of its adverse reactions has not been sufficiently elucidated. In recent years, cases of diabetic ketoacidosis caused by nivolumab have been reported in the emergency department, which has aroused our concern. Here we present a serious case of diabetic ketoacidosis in a 69-year-old woman with invasive mucinous adenocarcinoma of the lung, which occurred following therapy with the PD-1 inhibitor nivolumab and dendritic cell/cytokine-induced killer cell (DC/CIK) immunotherapy. She presented with diabetic ketoacidosis 5 days after the second cycle of nivolumab administration. The patient presented with dry mouth symptoms, a maximum blood glucose of 511.2 mg/dL, hemoglobin A1c (HbA1c) level of 7.4%, urine ketone body value of 3+, and extracellular fluid residual alkali level of -3.8 mmol/L. Normal saline and insulin was initiated. The patient had no history of obesity or family history of diabetes. She received a single dose of 3.75 mg of dexamethasone treatment during this period of time which resulted in cough improvement, but did not explain the onset of the diabetes. She was treated with insulin, sitagliptin phosphate tablets and acarbose tablets. Diabetic ketoacidosis was considered an immune-related toxicity caused by nivolumab, and consequently, treatment with nivolumab was suspended. Patient was maintained under insulin treatment with a blood glucose levels normalization. The incubation period of nivolumab-induced diabetic ketoacidosis is dispersive and the clinical risk is high. Patients need life-long insulin therapy. Blood glucose and HbA1c should be monitored routinely before and during nivolumab immunotherapy to avoid the occurrence of diabetic ketoacidosis. After the occurrence of diabetic ketoacidosis, insulin should be used to actively control blood glucose and do a good job in medication education to ensure long-term compliance of patients. Nivolumab should only be initiated if the patient has a clinical benefit under stable glucose control.

EVALUATION OF CLINICAL AND LABORATORY FINDINGS OF PATIENTS APPLYING TO THE EMERGENCY DEPARTMENT DUE TO RENAL COLIC IN RAMADAN, A SINGLE CENTER STUDY

OBJECTIVE: We aimed to evaluate the demographic, laboratory and radiological results of patients who applied to the emergency department due to renal colic (RC) during Ramadan.MATERIAL AND METHODS: This retrospective cross-sectional study included patients applied to emergency department (ED) with a diagnosis of RC during 2019 Ramadan and the 1 month preceding Ramadan. Age, sex, the hour of application, the results of urinalysis (erythrocyturia, leukocyturia, ketonuria, and urine density), presence of stones on radiological imaging and the location of the stone in the urinary system were recorded. The patients were grouped into three groups as the patients in the month preceding Ramadan (Group 1, n=83); patients fasting in Ramadan (Group 2, n=55); and patients not fasting in Ramadan (Group 3, n=37).RESULTS: Of the study population, 52.6% applied in Ramadan and 47.4% in the preceding month. There was no significant difference between the groups with respect to mean age, urinary leukocytes, urinary ketone, presence of stones and location of stones (p>0.05). Urinary erythrocytes were significantly lower in Group 3. The proportion of men and frequency of patients' admission between 16-24 hours in Group 2 was higher than the other groups. Urine density of Group 1 was found to be significantly lower than groups 2 and 3, but there was no difference between groups 2 and 3.CONCLUSIONS: It was found that fasting patients applied to the emergency department most frequently between the hours of 4 p.m. and 12 a.m. due to renal colic. Urinary erythrocytes were found significantly less in Group 3. In addition, we think that the high urine densities of the patients who applied during Ramadan are not related to fasting but to the increasing air temperature.

SUDDEN LOSS OF VISION: A RARE PRESENTATION OF DIABETIC KETOACIDOSIS IN THE ICU

SUDDEN LOSS OF VISION: A RARE PRESENTATION OF DIABETIC KETOACIDOSIS IN THE ICU

IMMUNE CHECKPOINT INHIBITOR-INDUCED DIABETIC KETOACIDOSIS: A RARE SIDE EFFECT

IMMUNE CHECKPOINT INHIBITOR-INDUCED DIABETIC KETOACIDOSIS: A RARE SIDE EFFECT

Wolcott Rallison Syndrome

Background: Wolcott–Rallison Syndrome (WRS) is a rare autosomal recessive disorder characterized by permanent neonatal diabetes mellitus, skeletal dysplasia, hepatic dysfunction, and other systemic associations. Clinical Description: A 3-month-old infant with a history of fever and poor oral intake presented with severe dehydration, acidosis and 3+ urine ketones and was diagnosed to have sepsis and diabetic ketoacidosis (DKA). He also developed acute kidney injury (AKI) with blood urea 118 mg/dL and serum creatinine 1.5 mg/dL. Management: The child was ventilated, stabilized, and managed for DKA with fluids and insulin as per guidelines. AKI was managed with peritoneal dialysis. Genetic analysis revealed homozygous mutation in eukaryotic translation initiation factor 2-alpha kinase 3 gene consistent with the diagnosis of WRS. A close follow-up was kept with regular screening for other associated manifestations. Central hypothyroidism was detected first followed by skeletal dysplasia and chronic kidney disease. Growth retardation and developmental delay are also present. Conclusion: Neonatal diabetes cases need an early genetic work up and watchful follow-up for the manifestation of other possible associated features.

A Literature Review of the Therapeutic Perspectives of Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitor-Induced Euglycemic Diabetic Ketoacidosis.

Euglycemic diabetic ketoacidosis (DKA), a side effect of sodium-glucose cotransporter-2 (SGLT2) inhibitors, is a triad of high metabolic anion gap acidosis, raised serum and urine ketones, and serum glucose <250 mg/dl. SGLT2 inhibitors cause a carbohydrate deficit by glucosuria, which leads to an increased glucagon/insulin ratio, the metabolic shift from glucose to lipid utilization causing ketogenesis, and hence euglycemic DKA. Additional factors like the ketogenic diet, illness, surgery, and pregnancy contribute to precipitating these episodes. Keywords searchincluded "Euglycemic DKA and SGLT2 inhibitors" in PubMedand Google Scholar, to compile data from existing articles that provide information on the withholding and restarting period of the drug after a euglycemic DKA episode. SGLT2 inhibitors, used in the treatment of type 2 DM, have an average half-life of 11-13 hours, so most articles suggested withholding the drug three days before any elective surgery but some articles suggested a longer withholding period based on other precipitating factors contributing to euglycemic DKA. Hence, we came up with patient inclusion criteria and concomitant therapies review that we need to consider in making this decision. In addition, a multidisciplinary approach is required when laying out guidelines for restarting the drug to have a unanimous approach. After reviewing the existing literature, it is clear that concrete guidelines are required to decide on drug withholding and restarting periods after a euglycemic DKA episode, as they vary among different institutions and different specialties. We believe it is crucial to consider patient inclusion criteria and concomitant therapies in forming those guidelines.

Selective Determination of n-Hexane and Methyl Ethyl Ketone (MEK) in Urine by Magnetic-Silica Aerogel-Based Molecularly Imprinted Polymers (MIPs) with Gas Chromatography – Flame Ionization Detection (GC-FID)

Co-exposure to n-hexane and methyl ethyl ketone (MEK) may induce neurotoxicity in humans. Since biomonitoring of exposed chemicals is a powerful hygienic way of controlling chemical risk, a new molecularly imprinted polymer (MIP) is reported in this study. Polymerization was carried out upon the surface of magnetic silica aerogel (Si@Fe3O4) using 2-octanone as a dummy template to prepare Si@Fe3O4-MIP. The synthesized MIP was characterized by scanning electron microscopy (SEM), Fourier transform infrared (FT-IR) spectrometry thermogravimetric analysis (TGA), Brunauer–Emmett–Teller (BET) analysis, and vibration sample magnetometry (VSM). The reported method was utilized for the selective extraction of n-hexane and MEK from humane urine using gas chromatography – flame ionization detection (GC-FID). The highest selectivity coefficient of Si@Fe3O4-MIP was obtained for n-hexane and MEK. The validity of solid phase extraction (SPE)-based Si@Fe3O4-MIP was confirmed by the recovery (> 93.6%) and acceptable reproducibility was obtained with relative standard deviations between 1.6 and 8%. The limit of quantifications (LOQ) for n-hexane and MEK were 1.5 and 128 µg/L, respectively. The validated SPE-based Si@Fe3O4-MIP is suggested for determining n-hexane and MEK in urine of shoemaker workers for biomonitoring purposes.

Diabetic ketoacidosis in pregnancy

Pregnancy with diabetic ketoacidosis (DKA) increases maternal and perinatal morbidity and mortality. DKA is a rare complication of pregestational diabetes mellitus (DM) or gestational diabetes mellitus (GDM) during pregnancy. However, it could be life-threatening for the mother and fetus without correct diagnosis and treatment. This paper reports a case of DKA in 25 years old Female with 26/27 weeks gestational ages. This was the second pregnancy with bad obstetric history. The patient has a history of DM from a previous pregnancy. The diagnosis of DKA is based on the presence of hyperglycemia, ketone in urine, and metabolic acidosis. After aggressive fluid replacement, intravenous insulin therapy, correction of acidosis and electrolyte imbalance, the patient showed significant improvement. The baby was born spontaneously induced by oxytocin drip, with a birth weight of 900g, APGAR scores 0, and maceration grade 2. After being treated for six days in the intensive care unit and observed for three days in the ward, the patient was allowed to be outpatient in good condition. Rapid restoration of glycemic control is essential to prevent death in pregnant women with diabetes mellitus diabetic ketoacidosis.

Effect of Acupressure at P6 on Nausea and Vomiting in Women with Hyperemesis Gravidarum: A Randomized Controlled Trial.

Hyperemesis gravidarum is characterized by severe nausea and vomiting. This study aims to illustrate the efficacy of acupressure at P6 in treating nausea and vomiting in hyperemesis gravidarum. This parallel randomized controlled trial was conducted from 2016–2017 in a tertiary hospital. Hospitalized women with ≤16 weeks of gestation and moderate to severe nausea and vomiting classified using a modified PUQE score were randomly assigned in a 1:1 ratio to either apply an acupressure wristband at the P6 point three times daily or to receive regular doses of intravenous antiemetics. The primary outcome was differences in modified PUQE scores among the groups. The secondary outcomes were differences in the rate of urine ketone clearance and the frequency of requiring rescue antiemetics. Ninety women were equally randomized into two groups, with no dropout. There was a statistically significant difference in the degrees of nausea and vomiting between the groups at 8, 16, and 24 hours post-admission (p8hours= 0.001, p16hours = 0.006, and p24hours = 0.001). The requirement of antiemetics and the rate of urine ketone clearance between the two groups were also statistically significant, at p = 0.001 and p = 0.02 respectively. There were no side effects in either group. The P6 acupressure was efficacious in alleviating nausea and vomiting among hyperemesis gravidarum women. The trial was retrospectively registered on ClinicalTrials.gov (NCT05175079).

Laser printing based colorimetric paper sensors for glucose and ketone detection: Design, fabrication, and theoretical analysis

Regular monitoring of glucose and ketone contents in the body is vital for diabetic patients. Although estimation of the ketone content is necessary for proper healthcare monitoring, the research on the detection of ketone bodies is still nascent. Moreover, inaccurate eye-estimations and reliability are the key limitations of the widely used methodologies for estimating glucose in urine. Hence, simple procedures for fabricating reliable sensors are crucial for on-demand healthcare monitoring. Herein, we posit that a commercially available laser printer, without any added modifications, can be used to make paper-based sensors for colorimetric estimation of glucose and ketone in urine. We conducted a comprehensive experimental investigation to optimize the device designs for rapid estimation of the biomarkers. Also, for the first time, we present a detailed dynamic model of the flow-field in a variable cross-section paper device while considering the species transport and reaction kinetics within the porous media. Finally, we performed experiments with real urine samples to validate that our devices could detect results with zero false negatives. We believe that our present investigation and methodology can enable rapid and reliable fabrication of paper-based sensors for several fundamental studies and applications on affordable and non-invasive healthcare monitoring.

CHARGE syndrome presenting with persistent hypoglycemia: case report and overview of the main genetic syndromes associated with neonatal hypoglycemia

BackgroundCHARGE syndrome (CS) is an autosomal dominant genetic condition whose recognition in the neonatal period is complicated by considerable phenotypic variability. Pediatric patients with genetic disorders have a known high incidence of hypoglycemia, due to many concurring factors. To date, neonatal hypoglycemia is a feature poorly explored in the literature associated with CS. This paper adds to the existing literature on hypoglycemia in CS and provides a brief review of the mechanisms through which CS, as well as the main genetic syndromes associated with neonatal hypoglycemia, may determine it.Case presentationThe patient was a term newborn, first-born daughter to non-consanguineous parents. At birth, axial hypotonia with slight hypertonia of the limbs, and dysplastic auricles were noted. The incidental finding of asymptomatic hypoglycemia led to the initiation of glucose infusion on the II day of life, continued for a total of 8 days (maximum infusion rate: 8 mg/kg/min). In-depth endocrinological examinations showed poor cortisol response to the hypoglycemic stimulus, with normal GH values, thyroid function and ACTH. In view of the suspected hypoadrenalism, oral hydrocortisone therapy was initiated. Inappropriately low values of plasmatic and urinary ketones supported the hypothesis of concomitant transient hyperinsulinism, not requiring therapy. A brain MRI was performed, documenting thinning of the optic nerves, non-displayable olfactory bulbs and dysmorphic corpus callosum. An eye examination revealed bilateral chorioretinal coloboma. Temporal bone CT scan showed absence of the semicircular canals. The unexpected findings of coloboma and absence of semicircular canals led to the suspicion of CS, later confirmed by the molecular analysis of CHD7.ConclusionsIt seems important to consider CS in the differential diagnosis of persistent hypoglycemia in newborns with specific anomalies. At the same time, it is advisable to consider the risk of hypoglycemia in children with CS, as well as other genetic syndromes. Awareness of the many possible causes of hypoglycemia in newborns with genetic conditions may help steer the investigations, allowing for an appropriate and timely treatment.

Inborn Errors of Ketogenesis: Novel Variants, Clinical Presentation, and Follow-Up in a Series of Four Patients.

Inborn errors of ketogenesis are rare disorders that result in acute and fulminant decompensation during lipolytic stress, particularly in infants and children. These include mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase (HMGCS) deficiency and HMG-CoA lyase (HMGCL) deficiency. In this series, we describe the clinical, biochemical, and molecular profiles of four patients along with dietary interventions and their outcomes on a long-term follow-up. Two patients each of HMGCS and HMGCL deficiency were evaluated with clinical history, biochemical investigations, including tandem mass spectrometry (TMS) and urine gas chromatography-mass spectrometry (GCMS). Molecular analysis was performed by whole-exome sequencing, as well as exon array validated by long-range polymerase chain reaction. All individuals were diagnosed with acute metabolic decompensation in the early infancy period except one with HMGCL deficiency who had the first presentation at 5 years of age. Central nervous system manifestations, severe metabolic acidosis, hyperammonemia, hypoglycemia with a normal lactate, and absence of urinary ketones were observed in all the affected individuals. The disorder was life-threatening in three individuals and one succumbed to the illness. TMS was nonspecific and urine GCMS revealed dicarboxylic aciduria in HMGCS deficiency. Both the patients with HMGCL deficiency demonstrated elevated 3 hydroxyisovaleryl carnitine levels in TMS and metabolites of leucine degradation in urine GCMS. We identified five novel variants that included a large deletion involving exon 2 in HMGCL gene. There was no evidence of long-term neurological sequelae in the living individuals. Diet with moderation of fat intake was followed in two individuals with HMGCS deficiency. Low leucine and protein diet with moderation of fat intake was followed in the individual with HMGCL deficiency. All affected individuals are thriving well with no further major metabolic decompensation.

The role of serum ADAMTS-1 levels in Hyperemesis Gravidarum

BackgroundWe aimed to investigate the levels of ADAMTS-1, which is secreted from the extracellular matrix during trophoblastic invasion in hyperemesis gravidarum (HEG).MethodsIn this cross-sectional study, we compared 45 HEG patients aged between 21 and 34 in terms of ADAMTS-1 levels with a control group consisting of 44 healthy pregnant women. The demographic characteristics and several laboratory parameters of the patients were recorded. Both groups were also compared in terms of ketonuria. We evaluated the correlation between ADAMTS-1 levels and ketonuria.ResultsThe 2 groups were matched in terms of age, gestational age, gravidity, parity, and body mass index. Some inflammatory markers, such as neutrophil count, MPV, PDW, and PCT levels, were significantly higher in the HEG groups compared to the control group (all p < 0.05). However, mean MCV and serum TSH levels were statistically significantly lower in this group (both p < 0.001). ADAMTS-1 levels were 12.6 ± 1.4 ng/ml in the HEG group and 6.2 ± 1.6 ng/ml in the control group (p < 0.001). It was significantly and positively correlated with urine ketone, neutrophil count, and PDW, whereas negatively correlated with MCV and TSH value in the HEG group. ROC analysis showed that a threshold value of 11.275 ng/ml for ADAMTS-1 predicted HEG patients with a sensitivity of 60% and specificity of 95.5%.ConclusionADAMTS-1 serum levels are increased in HEG patients, and there is a positive correlation between ADAMTS-1 levels and ketonuria.

Diabetic ketoacidosis as a complication of methanol poisoning; a case report

IntroductionDiabetic ketoacidosis (DKA) is a complication of diabetes presenting with high anion gap metabolic acidosis. Methanol poisoning, on the other hand, is a toxicology emergency which presents with the same feature. We present a case of methanol poisoning who presented with DKA.Case presentationA 28-year-old male was referred to us with blurred vision and loss of consciousness three days after ingestion of 1.5 L of an unknown mixture of bootleg alcoholic beverage. He had history of insulin-dependent diabetes and had neglected his insulin shots on the day prior to hospital admission due to progressive loss of consciousness. Vital signs were normal and venous blood gas analysis showed severe metabolic acidosis and a methanol level of 10.2 mg/dL. After eight hours of hemodialysis, he remained unresponsive. Diabetic ketoacidosis was suspected due to positive urine ketone and blood sugar of 411 mg/dL. Insulin infusion was initiated which was followed by full awakening and extubation. He was discharged completely symptom-free after 4 weeks.ConclusionsDiabetic ketoacidosis and methanol poisoning can happen simultaneously in a diabetic patient. Given the analogous high anion gap metabolic acidosis, physicians should pay particular attention to examination of the diabetic patients. Meticulous evaluation for both conditions is highly recommended.

129-LB: The Impact of a Passive Alert on Screening for Euglycemic Diabetic Ketoacidosis in Hospitalized Patients Using an Sodium–Glucose Cotransporter 2 Inhibitor

The use of sodium-glucose cotransporter-2 (SGLT2) inhibitors has recently been associated with euglycemic diabetic ketoacidosis (euDKA) . The absence of hyperglycemia can delay recognition of euDKA. We aimed to increase screening rates for euDKA by implementing a passive alert to providers in the EHR (built as a BestPractice Advisory [BPA] on the Epic Storyboard) if an emergency department or hospitalized patient taking an SGLT2 inhibitor was at risk for euDKA. Criteria were blood glucose &amp;lt;250 mg/dL, SGLT2 inhibitor on the home medication list or initiated in the hospital, lack of an insulin infusion, and one of the following labs indicating acidosis: 1) anion gap &amp;gt;12 with serum bicarbonate &amp;lt;18 mmol/L, 2) urine ketones ≥ 3+, or 3) serum ketones ≥ 2 mmol/L. We conducted a retrospective review of the alert from implementation on 5/15/2021 until 12/13/2021. Of the 76 patients who triggered the alert, 13 (18%) had euDKA confirmed and 5 (7%) may have had it but were not evaluated for it. The alert introduced in the electronic health record successfully identified patients taking an SGLT2 inhibitor who were at risk for euDKA and may serve as a safety net to reduce delayed recognition of this serious condition. Disclosure D. Soliman: None. R. Musser: None. J. P. Jackson: None. J. German: None. S. Carlson: None. K. H. Odonnell: None. T. Setji: None.

80-LB: At Home, Monitoring Device for Prevention and Interception of Diabetic Ketoacidosis Events in Children

Diabetic ketoacidosis (DKA) is often the first sign of type 1 diabetes (T1D) , especially in those children under the age of 3, with 55-100% of those in this age range diagnosed in DKA. Furthermore, 10-12% of children diagnosed with Stage 3 T1D are 3 or less, highlighting a critical need to identify those children at highest risk of a potentially life threatening DKA event at diagnosis. Commercially available urine analysis strips are not easily used with young children, so a simpler solution is urgently needed for early detection of DKA. In order to change the T1D diagnosis and treatment paradigm, we have developed a non-invasive monitoring solution that integrates into a child’s everyday routine and can alert caretakers real time when some of the early indicators of diabetes and DKA arise. The solution comprises of a single use sensing pad and a reusable Bluetooth® connected device which together fit into standard diapers. The pad collects urine and saturates two specialized colorimetric biosensor membranes which react with glucose and ketones. The device detects sufficient saturation of the biosensors and at a prescribed optimal time point, takes a reading via a photodetector to quantify the color change. Data is then sent to a mobile app which converts the readings to glucose &amp; ketone levels using an algorithm. It sends alerts to the child’s caregiver if values indicate a threshold limit of ketones have been met, which can be early signs of diabetes or DKA. The data captured by the device can be stored and analyzed over time, so caregivers and healthcare providers may know days or weeks in advance if their child is headed toward diabetes, hoping to fend off a DKA event. This feature may provide an earlier and less precipitous diagnosis and treatment, rather than experiencing a life-threatening emergency. This at home, mobile smart monitoring solution provides a practical solution for at-home, real-time monitoring of urine glucose and ketones in young children at risk of developing T1D. Disclosure S. L. Edgar: None. A. Paunescu: None. M. Dong: Employee; Johnson &amp; Johnson.

A Term Neonate with Multiorgan Dysfunction, Severe Metabolic Acidosis, and Hyperkalemia.

A Term Neonate with Multiorgan Dysfunction, Severe Metabolic Acidosis, and Hyperkalemia.

Clinical and Dietary Determinants of Ketosis During Long-Term Fasting in 1610 Subjects

ObjectivesThe health-promoting effects of fasting are increasingly documented. Long-term fasting according to the Buchinger Wilhelmi program (200 kcal/day, approximately 30 grams of carbohydrates) elicits various health-improving effects. The metabolic switch from glucose to fat oxidation is associated with an elevation in urine ketone concentrations (ketonuria). We hypothesised that inter-individual differences in ketonuria are due to variations in daily intake of carbohydrate facultative supplements. We further hypothesised that changes in ketonuria are linked to the beneficial effects of therapeutic fasting on an individual basis, and that these could be predicted from a person’s demographic data and metabolic status before they entered the fasting program. MethodsWe evaluated daily variations in carbohydrate intake and ketonuria in a group of 1610 subjects during a 4 to 21-day fasting period. Ketosis was estimated non-invasively in urine with Ketostix strips. Unsupervised hierarchical clustering of ketonuria was used to stratify patients as subgroups. Random Forest classification was performed using R package Caret. Differences in the effects of fasting between the different subgroups were model-predicted estimated marginal means. ResultsKetonuria was less intense in individuals who consumed honey and/or juice, which corresponded to a daily carbohydrate intake of approximately 30 grams. Participants with high ketonuria were younger, had lower blood urea concentrations, and lower HDL levels, before they entered the fasting program. Subjects excreting the largest amounts of ketones in their urine had a larger decrease in blood glucose levels, glycated haemoglobin (HbA1c) levels, body weight and waist circumference, and a larger increase in blood uric acid concentrations, in the group of patients. ConclusionsWe showed that even a low level carbohydrate intake influences ketonuria during long-term fasting. The course of ketonuria could be predicted based on a patient’s characteristics before they entered the fasting program. Individuals with the most intense ketonuria presented the most pronounced metabolic changes during long-term fasting. Altogether, our study paves the way to the establishment of personalised long-term fasting strategies. Funding SourcesThis study was funded by Amplius GmbH, Überlingen, Germany.