Dextrose Infusion Research Articles

Abstract #1397695: Use of Continuous Glucose Monitoring to Solve the Mystery of Pseudohypoglycemia

Hypoglycemia (glucose < 55 mg/dL) is uncommon in people without diabetes. Routine monitoring of blood glucose in hospitalized patients usually is performed by fingerstick point of care (POC) glucose testing via glucometer as a measure of capillary whole-blood glucose, correlating with venous plasma glucose. Pseudohypoglycemia is a consideration when POC glucose is low but plasma blood glucose is normal range. It can occur in the setting of impaired peripheral perfusion, such as in patients with Raynaud’s disease, shock, or peripheral vascular disease (PVD). A 63-year-old female was admitted for evaluation of uncontrolled hypertension. Her medical history was significant for previous myocardial infarction, atrial fibrillation, and heart failure with preserved ejection fraction. She had no history of Raynaud's phenomenon, diabetes (HbA1C 5.1%), or known PVD. During hospitalization, she had symptoms of anxiety, diaphoresis, tremors, nausea, forgetfulness, dizziness. POC glucose was 37 mg/dL and the patient was promptly treated with IV dextrose, negating a blood draw for a confirmatory venous plasma glucose. Several similar episodes occurred, even while on dextrose infusion prompting a hypoglycemia laboratory work-up. Off of dextrose, her POC glucose dropped to <50 mg/dL with insulin 97.7 uIU/mL, C-peptide 12.3 ng/mL and proinsulin of 77 pmol/L. However venous glucose was 173 ng/mL and thought to reflect treatment with dextrose prior to the blood draw. A second time, POC glucose was <50 ng/mL with insulin 48.9 uIU/mL and C-peptide 6.0 ng/mL which could support hyperinsulinemia but, again, venous plasma glucose was normal (113 mg/dL). Anti-diabetic medication and insulin antibody screening were negative. A continuous glucose monitoring system (CGMS) was placed on her abdomen to provide alternative peripheral glucose data. The patient manifested glucoses of 32/15/21 mg/dL by glucometer while simultaneous CGMS values were 110/126/156 mg/dL, confirming pseudohypoglycemia. In nondiabetic patients, hypoglycemia fulfilling Whipple’s triad be documented prior to initiating the complex evaluation for causes of hypoglycemia. Our patient is unusual because she did not have usual causes of pseudohypoglycemia such as Raynaud’s disease, diabetes, shock, or PVD. The inaccuracy of POC glucose measurements in patients with impaired microperfusion should be considered when the data are incongruent, as this can cause unnecessary investigations and prolonged length of stay. Should alternative blood glucose monitoring be required in these patients, CGM is a valuable technology.

Abstract #1401109: Quetiapine-induced Hypoglycemia in an Elderly Non-diabetic Patient with Dementia

Quetiapine is a second-generation antipsychotic agent (SGA) widely prescribed for the treatment of psychotic and mood disorders. In elderly patients, quetiapine is often used to treat psychotic symptoms associated with dementia. A metabolic syndrome phenotype of weight gain, hyperglycemia, and hyperlipidemia is a potential adverse effect of SGA’s, though hypoglycemia caused by SGA’s is documented. We report a case of quetiapine-induced hypoglycemia in a non-diabetic patient. A 79-year-old male with Lewy body dementia was admitted to hospital for management of a myocardial infarction. The patient had no history of diabetes mellitus, renal failure, or hepatic insufficiency, and nobody living with the patient was treated for diabetes. Plasma glucose on admission was 84 mg/dL. Quetiapine was started to control delirium, but within 24 h the patient had worsening confusion and a capillary blood glucose (CBG) measurement of 52 mg/dL. Symptoms improved with administration of dextrose, and the patient ultimately required a 10% dextrose infusion to maintain CBG’s >80 mg/dL. An ACTH-stimulation test (30 min stimulated cortisol 24.8 μg/dL, expected >18) and hypoglycemic medications panel (sulfonylureas and meglitinides) were unremarkable. Quetiapine was stopped, and hypoglycemia resolved. No hypoglycemia occurred during a subsequent 48-h diagnostic fast followed by a mixed meal tolerance test. Due to the patient’s advanced age and comorbidities, it was decided not re-challenge with quetiapine and observe for recurrence of hypoglycemia. Hypoglycemia is a rare complication of SGA’s, and diagnosis may be delayed or missed in patients with baseline confusion or agitation. In addition to quetiapine, there are case reports of hypoglycemia occurring during treatment with risperidone, olanzapine, aripiprazole, and paliperidone. Clozapine and olanzapine increase insulin release from isolated pancreatic islets in vitro, though quetiapine did not demonstrate this effect. However, endogenous hyperinsulinemia has been documented in case reports of quetiapine-induced hypoglycemia. The physiologic pathway by which SGA’s increase insulin release is unknown; some authors have focused on the antagonism of M1 muscarinic receptors, but the muscarinic M1 receptor antagonist pirenzepine has been demonstrated to reduce insulin secretion induced by the muscarinic receptor agonist carbachol from isolated rat pancreatic islets in vitro. Though the mechanism by which hypoglycemia occurs is unclear, this case demonstrates that hypoglycemia should be considered in patients with worsening mental status during treatment with SGA’s.

Case report - sulfonylurea poisoning mimicking vertebrobasilar acute ischemic stroke

Background: We report the case of sulfonylurea induced hypoglycemia manifesting as acute encephalopathy with focal neurological signs misdiagnosed as posterior circulation acute ischemic stroke (AIS) and discuss the potential effects of hypoglycemia on central nervous system, as well as its differentiation from AIS. Case presentation: A 64-year-old patient with type II diabetes treated with glimepiride was transferred to the Department of Neurology after the procedure of radical prostatectomy. On admission, the patient was unconscious with four limb paresis and bilateral Babinski sign. Non-contrast head CT and CT angiography vessels did not reveal any abnormalities. Due to exceeded therapeutic window the patient was disqualified from intravenous thrombolysis. At the admission hypoglycemia was observed and promptly corrected with the 5% dextrose infusion. For the next 72 hours repeated intravenous glucose infusions were needed to maintain its levels above 70 mg/dl. Based on the absence of ischemic changes on MRI and repeated decreases in glucose level for the next 3 days, glimepiride induced hypoglycemic encephalopathy was diagnosed. Within 24 hours of admission the patient regained consciousness and eventually presented four-limb paresis as a result of prolonged neuroglycopenia. Conclusions: Prolonged insufficient brain nutrition can result in permanent or long-lasting brain damage, manifesting as impaired consciousness and focal neurological signs. Perioperative sulfonylureas intake may result in prolonged hypoglycemia.

Congenital hyperinsulinism in a Nigerian infant: A case report and review of literature

Congenital hyperinsulinism, a rare genetic disorder characterized by excess insulin secretion even during hypoglycemic episodes, has two histological subtypes; diffuse and focal. Genotypes denote which of the two subtypes presents, and this is the first case being reported in Nigeria. The aims of this study were to report the first case of genetically confirmed compound heterozygote inheritance for two non-sense mutations in the ABCC8 gene in a Nigerian child and her family. A full-term average weight (7.5 lb) female baby presented with severe hyperinsulinemic hypoglycemia [HH] after birth and failed medical treatment with dextrose infusion. She had several hypoglycemic seizure episodes and spastic diplegic cerebral palsy, despite frequent feeding. Following physiotherapy, her spasticity was regressing and she was also able to say polysyllabic words. Genetic testing done 2 years after birth showed that her father was heterozygous for the ABCC8 non-sense mutation, P.W143*, and her mother was heterozygous for the P.Q416* ABCC8 mutation. This report shows the need for quick and early genetic testing for rare disorders and the possibility of collaboration with more specialized genetic laboratories. When diagnosed, diffuse or focal diazoxide unresponsive hypoglycemia may be treated by partial or complete pancreatectomy with the potential complication of diabetes mellitus later in life.

Prolonged diabetic ketoacidosis due to SGLT2 inhibitor use and low‐carbohydrate diet

AbstractA 59‐year‐old gentleman was admitted with diabetic ketoacidosis (DKA). His medication history included a sodium‐glucose co‐transporter 2 (SGLT2) inhibitor for the past six years. Relevant history includes undertaking a low‐carbohydrate diet for four months.In hospital he required a fixed rate insulin infusion for 25 hours and variable rate insulin infusion for a total of 32 hours to manage his ketonaemia. He received concomitant dextrose infusion and oral nutritional supplements throughout the course of his admission to replenish the likely depleted glycogen stores in his liver as a result of his diet.The case highlights the importance of identifying DKA early and treating the underlying cause. It also highlights the potential increasing prevalence of ketoacidosis which may occur as more patients are prescribed SGLT2 inhibitors and adhere to carbohydrate‐restricted diets. Copyright © 2023 John Wiley &amp; Sons.

The Quality of Preoperative Glycemic Control Predicts Insulin Sensitivity During Major Upper Abdominal Surgery: A Case-Control Study.

To examine the association of the quality of preoperative glycemic control and insulin sensitivity during major upper abdominal surgery. In cardiac surgery, glycated hemoglobin A1c (HbA1c), an indicator of glycemic control during the preceding 3 months, correlated with intraoperative insulin sensitivity. Furthermore, insulin resistance showed a significant association with adverse clinical outcomes. This study is a post hoc exploratory analysis of a randomized controlled trial in patients undergoing elective hepatectomy and receiving the hyperinsulinemic-normoglycemic clamp (HNC) as a potential intervention to reduce surgical site infections (ClinicalTrials.gov NCT01528189). Immediately before skin incision, the HNC was initiated by infusing insulin at the rate of 2 mU/kg/min. Dextrose was administered at rates titrated to maintain normoglycemia (4.0-6.0 mmol/L). The average of 3 consecutive dextrose infusion rates during steady state was used as a measure of insulin sensitivity. Primary outcome was the relationship between preoperative HbA1c and insulin sensitivity during surgery. Secondary outcomes were the associations of insulin sensitivity with the patient's body mass index (BMI) and postoperative morbidity. Thirty-four patients were studied. HbA1c (Y = -0.52X + 4.8, P < 0.001, R2 = 0.29), BMI (Y = -0.12X + 5.0, P < 0.001, R2 = 0.43) showed negative correlations with insulin sensitivity. The odds ratio of postoperative complications within 30 days of surgery for every increase in insulin sensitivity by 1 mg/kg/min was 0.22 (95% confidential interval, 0.06-0.59; P = 0.009). We demonstrate significant associations of the quality of preoperative glycemic control and body mass index with insulin sensitivity during hepatectomy. The degree of insulin resistance correlated with postoperative morbidity.

Nutrient Uptake by the Hindlimb of Growing Pigs Treated with Porcine Somatotropin and Insulin

The shift in nutrient partitioning induced by porcine somatotropin (pST) is accompanied by a decrease in insulin sensitivity for whole-body glucose uptake. The relative contribution of metabolic changes in the hindlimb was investigated in eight pigs (55 kg) that had received recombinant pST (120 μg/kg) or excipient (control) for 7 d. Uptake of metabolites by the hindlimb was measured under basal conditions and during hyperinsulinemic-euglycemic clamps at low [14 ng/(kg·min)] and high [360 ng/(kg·min)] insulin infusion rates. Dextrose infusion rate required to maintain euglycemia was used as an index of whole-body glucose uptake in response to exogenous insulin. Effects of pST on hindlimb and whole-body glucose uptake were evident only at physiological levels of insulin (basal and low insulin infusion rate). During the low rate of insulin infusion, dextrose infusion rate was 79% lower for pST-treated pigs and glucose uptake by the hindlimb was 59% lower compared with control pigs. The decrease in glucose uptake by the hindlimb was entirely accounted for by the estimated reduction in glucose utilization by adipose tissue of the hindlimb. Glucose:oxygen quotients were reduced during basal (57%) and low insulin infusion (63%) with pST treatment, indicating a change in the pattern of substrate utilization. This is consistent with the concept that pST directs nutrients away from adipose and towards muscle growth by altering the response of tissues to homeostatic signals such as insulin.

Levofloxacin-Induced Fatal Hypoglycaemia in a Non-Diabetic Patient: A Case Report

Levofloxacin, a broad-spectrum, third-generation fluoroquinolone antibiotic, is rarely reported to cause life-threatening adverse effects, such as severe hypoglycaemia resulting in a coma. This case concerns hypoglycaemia in an elderly, non-diabetic patient induced by levofloxacin. A 61-year-old male patient was admitted with severe hypoglycaemia. Past medical history revealed treatment with levofloxacin for pneumonia. During the hospital stay, the patient was treated with multiple doses of 25 g dextrose 50% (D50), 2 doses of 1 mg glucagon, and a continuous infusion of dextrose 10% (D10). The patient was discharged on the sixth day of admission in a stable condition with no clinical symptoms. Clinicians must be aware of this lesser-known adverse effect to ensure quick recognition and treatment with the proper adjuncts.

Computerized insulin protocol for intrapartum and postpartum glucose management in gravidas with Type 1 diabetes

Computerized insulin infusion calculators (IICC) improve glucose control in non-pregnant populations. Our IICC is an insulin sensitivity coefficient-based algorithm relying on point of care (POC) glucose values and the rate of change which allows for dynamic changes in insulin resistance. We evaluated the effectiveness of an IICC in achieving intrapartum and postpartum euglycemia in gravidas with Type 1 diabetes mellitus (T1DM). This retrospective study included gravidas with T1DM managed intrapartum and postpartum with IICC between 2016-2020. Patients were excluded if insulin infusion or POC glucose values were not available. Insulin infusion rate, POC glucose and neonatal data were obtained from the electronic medical record. Our primary outcome was the percentage of hourly glucose values within goal in the intrapartum period (80-119 mg/dL), and postpartum period (80-179 mg/dL). Secondary outcomes included intrapartum mild hyperglycemia (120-179 mg/dL) and hypoglycemia (< 60 mg/dL), hyperglycemia (≥ 180 mg/dL) for both time periods, and select neonatal outcomes. 39 patients (47 pregnancies) were included for analysis. Mean maternal age was 29.5 ± 5.3 years and first trimester HbA1c was 7.2 ± 1.4%. 39.3% (n=471) of the intrapartum glucose values and 68.7% (n=929) of the postpartum glucose values were in target (p< .0001)(Figure 1). The incidence of intrapartum mild hyperglycemia was 545 (46.3%). The incidence of hypoglycemia was 2.7% for both time periods while the incidence of hyperglycemia was 9.3% and 18.6% intrapartum and postpartum, respectively. Figure 2 shows the mean POC glucose values. Twenty-four (51.1%) neonates were admitted to the neonatal intensive care unit and 22 (46.8%) had hypoglycemia requiring dextrose infusion. To our knowledge, this is the first descriptive study of IICC use intrapartum and postpartum. The IICC performed better at achieving postpartum versus intrapartum glucose control, while having low rates of hyperglycemia and hypoglycemia. Development of a pregnancy specific IICC may improve peripartum glycemic control.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Postpartum intrauterine dextrose infusion: Effects on uterine health, metabolic stress, systemic inflammation, and daily milk yield in clinically healthy dairy cows

The objective of this study was to assess the effect of intrauterine dextrose infusion at 4 ± 1 d in milk (DIM) on the incidence of clinical metritis (CM), metabolic stress [i.e., body condition score (BCS), β-hydroxybutyrate (BHB) concentration, and subclinical ketosis incidence], systemic inflammation (i.e., haptoglobin concentration), and daily milk yield in clinically healthy postpartum dairy cows. Cows (n = 245) from a dairy farm located in southwest Pennsylvania were screened at 4 ± 1 DIM using a Metricheck (Simcro Tech Ltd.) device to assess vaginal discharge. In addition, overall cow health (e.g., lameness, abnormal breathing) and rectal temperature were assessed at this time. Cows (n = 134) that presented a clear dense vaginal discharge, were in clinically good health status, and had a normal rectal temperature (i.e., <39.7°C) were blocked by parity (primiparous = 64; multiparous = 70) and randomly assigned to 1 of 3 groups: (1) SAL (n = 45): 1 intrauterine infusion of isotonic saline solution (1 L/cow); (2) DEX (n = 44): 1 intrauterine infusion of a 50% dextrose solution (1 L/cow), or (3) CON (n = 45): cows remained untreated. Cows were re-screened at 7 d after enrollment (11 ± 1 DIM) using the Metricheck device to assess CM incidence (research clinical metritis incidence; RCMI). On-farm computer records (i.e., Dairycomp 305) were also used to collect clinical metritis incidence (farm clinical metritis incidence; FCMI). In addition, BCS was assessed and blood samples were collected at enrollment and at study d 7, 14, and 21. Furthermore, daily milk yield and clinical disease events for the first 60 DIM were collected from on-farm computer records. The data were analyzed using the MIXED and GLIMMIX procedures of SAS (SAS Institute Inc.) as a randomized complete block design. Although not significant, the RCMI and FCMI in DEX and SAL cows were on average 14.5 and 18.1 percentage points higher, respectively, compared with CON cows. The SAL cows had higher BHB and haptoglobin concentrations and higher incidence of subclinical ketosis compared with CON cows on study d 7. With regard to daily milk yield, there was a day by treatment interaction, where CON cows produced more milk on certain days compared with DEX and SAL cows. Based on these findings, authors conclude that intrauterine dextrose infusion in clinically healthy postpartum cows with normal vaginal discharge may be prejudicial for cow health and performance.

Predicting resolution of hypoglycemia with and without dextrose infusion in newborn infant of gestational diabetic mothers.

Neonatal hypoglycemia (NH) may lead to significant neurological impairment if left untreated. Infants of gestational diabetic mothers (IGDM) are at increased risk of early NH and need to be screened. However, it is challenging to predict management with or without intravenous dextrose once hypoglycemia is identified. We evaluated the association between hypoglycemia risk scores at 1-hour of life and the need for intravenous dextrose for hypoglycemia resolution in IGDM. This was a retrospective cohort study of IGDM born at a gestational age ≥35 weeks from January 2015 to December 2017. NH was the disease of interest. The outcomes were the association of hypoglycemia risk score (HRS) with and without intravenous dextrose for hypoglycemia resolution. Each infant's hypoglycemia risk score (HRS) was calculated using data extracted from the maternal and neonatal electronic medical records. Resolution of hypoglycemia with and without intravenous dextrose was compared between the low HRS (0-1) group and the high HRS (2-5) group. Sixty-five infants were included in the study with a mean gestational age of 38.2 ± 1 weeks for low HRS and 38.0 ± 2 weeks for high HRS. While more children with high HRS were delivered by cesarean section (p = 0.04), hypoglycemia resolved more frequently without intravenous dextrose in infants with low HRS (p = 0.03). IGDM is at increased risk of NH. The resolution of hypoglycemia without dextrose infusion is frequently associated with low HRS at 1-hour of life. Early identification using HRS of IGDM whose hypoglycemia will resolve with or without intravenous dextrose may help clinicians triage newborns to either stay in the nursery or transfer for more invasive care.

Insulin Secretion and β-Cell Function Are Preserved in Patients with Treated Hematological Malignancies

INTRODUCTION Cancer survivors are at elevated risk for developing type 2 diabetes mellitus, which decreases quality of life and increases mortality during cancer survivorship. Type 2 diabetes results from a combination of insulin resistance and decreased insulin secretion. Assessing pancreatic β-cell function by measuring insulin secretion dynamics in response to hyperglycemia can provide insight into the pathogenesis of type 2 diabetes. We investigated insulin secretion in patients with treated hematological malignancies and compared them to non-diabetic controls without cancer. We hypothesized that patients with hematological malignancies will have decreased insulin secretion compared to controls without cancer due to β-cell toxicity from previous treatment and chemotherapy. METHODS We evaluated insulin secretion in 16 non-diabetic adult patients with treated hematological malignancies using a hyperglycemic clamp, which assesses pancreatic β-cell function by measuring insulin secretion in response to hyperglycemia (200 mg/dL) maintained by a dextrose infusion. Clamp outcomes included first phase (T0-10 minutes), second phase (T90-120 minutes), and maximal (L-arginine stimulated) insulin response. The insulin sensitivity index (ISI) and disposition index (DI, a measure of the β-cell function to compensate for insulin resistance) were calculated. Controls (n=32) matched for age, sex, race, and body mass index (BMI) were selected 2:1 from a database of 154 hyperglycemic clamps in participants without diabetes or cancer. Demographic characteristics and clamp outcomes were compared using χ2, Wilcoxon rank-sum test, or linear regression. RESULTS Hyperglycemic clamps were performed in 48 individuals without diabetes (16 patients with treated hematological malignancies and 32 matched controls without cancer). Cancer survivors and controls without malignancy were well-matched for age, sex, race (Table 1). Myeloid malignancies were the most common diagnosis (n=11; 69%) with a median time from diagnosis to metabolic testing of 6 months. Treatment included cytotoxic chemotherapy (n=15; 94%), glucocorticoids (n=7; 44%), and radiation (n=1; 6%) with 7 (44%) patients achieving a remission prior to testing. Compared to controls, patients with malignancy had lower fasting glucose levels (93.0 mg/dL [IQR 86.3-96.6] vs 101.5 [IQR 94.9-107.6], p<0.001) and lower fasting insulin levels (11.5 uU/mL [IQR 9.3-15.0] vs 16.3 [IQR 12.3-21.5], p=0.023), suggesting greater insulin sensitivity within the cancer cohort. In univariable analysis, there were no significant differences between first and second phase insulin response between patients with or without treated hematological malignancies (Table 1). Cancer survivors had a higher maximal (L-arginine stimulated) insulin secretion (3606 uU/mL [IQR 3255-4594] vs 2278 [IQR 1900-3555], p=0.026) and a higher disposition index (2521 mg/kg/min [IQR 1986-3360] vs 1300 [IQR 939-1923], p=0.01) than in controls. Cancer survivors demonstrated a trend toward greater insulin sensitivity compared to controls (6.82 mg/kg/min per uU/mL [IQR 5.53-10.83] vs 4.98 [IQR 3.65-7.28], p=0.092). After adjustment for BMI and fasting glucose in linear regression models, both second phase (β=242.5, p=0.005) and maximal insulin secretion (β=1225.6, p=0.019) were greater in cancer survivors then in controls without cancer (Table 2). CONCLUSION Cancer survivors had higher maximal phase insulin secretion and disposition index (a measure of β-cell function adjusted for insulin resistance) compared to non-diabetic controls without cancer. Our data suggests that cancer survivors have preserved β-cell function following treatment of their hematological malignancies, contrary to our hypothesis. Longitudinal follow-up is needed to determine factors that promote diabetes susceptibility in cancer survivors. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

PSAT277 Glucocorticoid Therapy for Management of Hypoglycemia in the context of Non-Islet Cell Tumor-Induced Hypoglycemia

Abstract Background Non-islet cell tumor-induced hypoglycemia (NICTH) is a rare paraneoplastic syndrome which can cause recurrent hypoglycemia. There is no clear standard of care for management of hypoglycemia. Often, these patients have high morbidity and therefore surgical tumor resection is not always possible. Clinical case: This is the case of a 69 year-old male presenting with altered mental status in the context of hypoglycemia without clear etiology with an initial serum glucose level of 32 mg/dL (normal range 60-100 mg/dL) which quickly corrected after administration of intravenous glucose. He was found to have a large bowel obstruction with CT abdomen revealing an underlying neoplasm. Biopsy of suspected lesion on colonoscopy revealed colorectal adenocarcinoma. Repeated episodes of hypoglycemia complicated by seizures required inpatient management. Workup included serum insulin level which resulted in suppressed level (&amp;lt;1. 0 uU/mL, normal range 1.9-23. 0 uU/mL), low c-peptide level (0.1 ng/mL, normal range 1.1-4.4 ng/mL), low beta hydroxybutyrate level (0. 07 mmol/L, normal level &amp;lt;0.3 mmol/L), cortisol level of 43.7 mcg/dL, undetectable insulin like growth factor-1 (IGF-1) level (&amp;lt;10 ng/mL, normal range 59-230 ng/mL) and low insulin like growth factor-2 (IGF-2) level (66 ng/mL, normal range 333 - 967 ng/mL). IGF2: IGF1 ratio was 66 (ratio &amp;gt;10 is indicative for diagnosis of non-islet cell tumor hypoglycemia). Due to extremely poor oral intake and recurrent episodes of hypoglycemia despite continuous dextrose infusion, the patient was started on 20 mg prednisone daily. Eventually, 40 mg of intravenous methylprednisolone in addition to dextrose infusion was needed as maintenance therapy effectively preventing hypoglycemia. Given his poor functional status, the surgical and oncology team decided he was no longer a surgical or chemotherapy candidate. Eventually, palliative medicine was consulted and the patient was transitioned to comfort care with a plan for outpatient hospice. Conclusion NICTH should be suspected in any patient with hypoglycemia without clear etiology, especially if there are suggestions to NICTH such as known malignancy or newly diagnosed mass. Once NICTH is identified and a primary tumor is found, complete tumor resection represents ideal management, however, not always attainable. In such cases, dextrose infusion might be insufficient to prevent hypoglycemia and is not always the preferred option given the required long-term venous access. In these circumstances, early high dose glucocorticoids are safe and appear to successfully prevent hypoglycemic events. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

ODP315 Hypoglycemia: Neuroendocrine Tumor of the Pancreas with Liver Metastasis and Transformation to Insulinoma

Abstract Background Neuroendocrine tumors (NETs) are rare, can be found in any part of the body including the gastrointestinal tract, lung, and pancreas and have potential for metastasis. Clinical Case A 39-year-old male with stage IV high grade neuroendocrine tumor of the pancreas with metastasis to the liver and lymph nodes whose disease progressed despite treatment with systemic therapy who presented with severe hypoglycemia. Diagnosis and management of his hypoglycemia was difficult. For the diagnosis, patient's serum blood glucose did not always correlate with his capillary blood glucose via finger sticks, which lead to a delay in his diagnosis. Also, his diagnosis was not straight forward as he did not respond adequately to the glucagon following a serum glucose of less than 55 mg/dL (normal 70-110 mg/dL) during a diagnostic fast. Once critical labs were obtained, it took days for the results. In the interim, his hypoglycemia was managed with dextrose infusions at 10%, 20% and as high as 50%, frequent meals, and high dose steroids, yet he still had daily symptomatic hypoglycemia. A diagnosis of insulinoma was made with the following critical lab results: insulin 70.4 uIU/mL (2.6-24.9), C-peptide 12.6 ng/mL (1.1-4.4), proinsulin 407.6 pmol/L (0. 0-10. 0), beta-hydroxybutyrate &amp;lt;0. 050 mmol/L (0. 02-0.27), insulin antibodies &amp;lt;5. 0 uU/mL, negative sulfonylurea screen, insulin-growth factor-1 (IGF-1) 77 ng/mL (90-278), and insulin-growth factor binding protein three (IGF-BP3) 2133 ug/L (2571-5982). Patient was treated with both diazoxide and hepatic artery embolization to reduce tumor burden. His dose of diazoxide was titrated to maintain normoglycemia. He had mild tumor lysis syndrome that did not require dialysis. His hypoglycemia resolved within a few days of treatment and was discharged from the hospital with a continuous glucose monitor (CGM), diazoxide and hydrocortisone. It is our belief that transformation of the liver lesions to insulinoma was the cause of his hypoglycemia. Conclusion We recommend that patients with metastases from their neuroendocrine tumor who develop hypoglycemia be evaluated for insulinoma and if found should be treated with diazoxide and if not surgical candidates to consider hepatic artery embolization. Presentation: No date and time listed

PMON313 Hyperinsulinemic Hypoglycemia and Growth Hormone Deficiency Secondary to 20p11 Deletion

Abstract Introduction Hyperinsulinism (HI) and growth hormone deficiency (GHD) are known causes of hypoglycemia but not commonly found together. We present a 4-month-old boy with hypoglycemia found to have both HI and GHD with subsequent genetic diagnosis of 20p11 deletion. This deletion has been associated with panhypopituitarism. This case represents a few to report HI as a manifestation of this deletion. Treatment with both recombinant human growth hormone (rhGH) and Diazoxide led to blood glucose (BG) normalization. Clinical Case A 4-month-old, full-term, large for gestational age (96th percentile), born to a nondiabetic mother presented with hypoglycemic seizures. He had transient hypoglycemia at birth, normal newborn screen, and exclusively breastfeeding with normal growth and development. He had a negative 60-hour video EEG. Further work-up was significant for serum glucose of 54 mg/dL despite blood draw being 20 minutes after a breastfeed, prompting endocrinology evaluation. Physical exam showed no dysmorphism and normal genitalia. He had a serum glucose of 39 mg/dL while asymptomatic. Critical sample revealed detectable insulin (3.2 mcIU/mL), low beta hydroxybutyrate (145.6 mcmol/L) and low growth hormone (GH) (4.2 ng/dL). He had normal cortisol, lactic acid and ammonia. A glucagon challenge showed an increase in BG of 26 mg/dL (35--&amp;gt;61 mg/dL). He had a GH stimulation test with arginine (peak GH 3.8 ng/dL) and glucagon (peak GH 6.6 ng/dL). He had mildly elevated liver enzymes that resolved on repeat testing. Plasma amino acid, plasma acylcarnitine profile, urine organic acids, and brain MRI were normal. He was initially started on rhGH with continued hypoglycemia, hence, Diazoxide, and chlorothiazide were added. His BG was monitored until dextrose infusion was successfully weaned, while maintaining normoglycemia. Genetic testing with next-generation sequencing revealed 20p11.22-p11.21 deletion. He was discharged on Diazoxide (12 mg/kg/day), chlorothiazide, and rhGH (0.27 mg/kg/week). Conclusion It is important to determine the cause of hypoglycemia so specific treatment can be provided. HI is a common cause of hypoglycemia in infants due to abnormal insulin secretion in the pancreatic beta cells. GHD can also cause hypoglycemia and be associated with other pituitary hormone deficiencies. Evaluation of our patient's hypoglycemia revealed HI, GHD and 20p11 deletion. This deletion has been associated with hypoglycemia due to GHD and few reports with HI. This patient will need to be regularly screened for other pituitary hormone abnormalities. Other features of 20p11 deletion include cognitive delay, craniofacial dysmorphisms, gastrointestinal and genitourinary anomalies. While hypoglycemia is often the result of a single cause, this case shows that there are pathological conditions that can present with both GHD and HI, so the differential diagnosis for hypoglycemia should remain broad. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

ODP149 Hypertriglyceridemia-Induced Acute Pancreatitis in Second Trimester of Pregnancy

Abstract Background Acute pancreatitis (AP) during pregnancy is a rare, potentially life-threatening disease, with an incidence of 1 case per 1,000-10,000. Hypertriglyceridemia (HTG)-induced pancreatitis accounts for only 5% of cases. Here we describe a rare case of HTG-induced AP during the second trimester of pregnancy, which was treated with concurrent insulin and plasmapheresis. Clinical Case A 35-year-old multigravida female was admitted for preterm premature rupture of membranes at 26 weeks gestation. Symptoms began on day 8 of admission and included severe epigastric pain radiating to the back. On exam, there was significant epigastric tenderness on palpation. There were no xanthelasmas or tendon xanthomas seen. She was afebrile but tachycardic. Laboratory evaluation noted a triglyceride (TG) level of &amp;gt;5,680 mg/dL (n&amp;lt;150), amylase 201 U/L (n&amp;lt;100) and lipase 277 U/L (n&amp;lt;60), consistent with AP. She was euglycemic. CT of the abdomen showed interstitial edematous pancreatitis with a peripancreatic collection. She was placed on NPO and started on intravenous (IV) fluid therapy, in combination with IV insulin and 10% dextrose. The patient also underwent one session of plasmapheresis. TG levels downtrended rapidly to 3,585 mg/dL within 24 hours. Once TG levels decreased below 1,000 mg/dL, insulin and dextrose infusions were stopped, and combination therapy of fenofibrate, omega-3 fatty acids, and low-fat low-carbohydrate diet was started. At 28 weeks and 5 days gestation, a cesarean section was performed due to suspected fetal distress. The patient was discharged on fenofibrate and Omega-3 fatty acids with a TG level of 456 mg/dL. Genetic testing revealed a heterozygous variant in the LPL gene mutation (c.644G&amp;gt;A; p. Gly215Glu) and a heterozygous variant of uncertain significance (VUS) in the ABCA1 gene (c.1765G&amp;gt;A; p. Val589Ile). She had no known family history of hyperlipidemia or cardiovascular disease. Conclusion Lipoprotein lipase (LPL) deficiency is an autosomal recessive disorder caused by biallelic pathogenic mutations in the LPL gene. The heterozygous c.644G&amp;gt;A variant has been previously described in several patients with LPL deficiency, however its impact on the function of the LPL protein has not yet been clearly defined. The ABCA1 gene is associated with Tangier disease, characterized by very low HDL levels and HTG. The ABCA1 gene variant detected in this case is classified as VUS as its effect on the gene function is not yet known. Further investigation is warranted to understand the role of these variants in familial dyslipidemia. Aside from the described patient, only one other case report of HCT-induced AP treated with concomitant plasmapheresis and IV insulin therapy has been reported in the literature. There are no published guidelines regarding the optimal treatment for HTG-induced AP in pregnancy. Combined treatment modality with plasmapheresis and IV insulin seems to be effective, however, its risks and benefits should be carefully assessed. Presentation: No date and time listed

LBSUN255 Recurrent Hypoglycemia In A Patient With Beckwith-Wiedemann Syndrome Secondary To Insulinoma

Abstract Background Beckwith-Wiedemann Syndrome (BWS) is a genetic condition characterized by macrosomia, childhood tumors, and neonatal hypoglycemia and hyperinsulinemia. The cause of this hyperinsulinemic hypoglycemia is unknown, but it is believed to be caused by chromosomal mutations at 11p15.5 and genes encoding beta-cell ATP-sensitive potassium channels. In our case, we have an adult patient with a history of BWS who is experiencing hypoglycemia due to a different cause: an insulinoma. This is the first report of insulinoma in an adult with this syndrome. Case Presentation The patient is a 53-year-old male with a history of BWS. Due to shortness of breath, the patient was admitted and discovered to have new and severe systolic heart failure. Patient was started on beta blockers by cardiology. During his hospital stay, he developed hypoglycemia, with glucose levels in the 20s. As the hypoglycemia became more frequent, he was placed on dextrose. Dextrose was turned off to obtain hypoglycemia labs such as insulin, proinsulin, C-peptide, and hydroxybutyrate, but his blood sugar never fell below 80mg/dL. His hypoglycemia was attributed to a beta-blocker side effect or rebound from a dextrose infusion. He was discharged from hospital and sent home. After a loss of consciousness episode at home two weeks later, the patient was readmitted. When he arrived at the emergency department, his blood glucose level was 18mg/dL, and he was given dextrose. After being admitted to the hospital, dextrose was again discontinued, and blood glucose levels dropped to 45mg/dL on serum testing. At the time, C-peptide levels were elevated at 25.7ng/mL, B-hydroxybutyrate levels were 0. 06mmol/L, and insulin levels were above 700uIU/mL. At the time, the choice was between insulin autoantibody syndrome and insulinoma. The patient then had an abdominal computed tomography scan, which revealed a 3.7×2.9cm neuroendocrine tumor in the distal pancreas. Changes in the liver were found to be alarming for metastases, thus an MRI was conducted to confirm this. There was no sign of liver metastases on the MRI. In the interim, the patient was started on subcutaneous octreotide 50 mcg twice daily. Given the patient's underlying heart problems, diazoxide was not pursued. Octreotide was increased to 100mcg subcutaneously three times daily throughout his hospital stay, and he was discharged home with a continuous glucose monitor and intentions to operate later that month. Conclusions Although BWS has been linked to a higher risk of childhood malignancies, it's uncertain whether BWS could be a predisposing factor for the development of insulinoma. Because this is such a rare disorder, there is a paucity of information on predisposition or risk factors. However, the link between macrosomia and tumor growth in BWS suggests that there may be a predisposition to insulinoma that has yet to be investigated. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

PSUN251 Euglycemic DKA In A Patient Undergoing Major Surgery

Abstract Background Euglycemic DKA represents a diagnostic challenge as a lack of hyperglycemia can lead to a delay in recognition and administration of appropriate treatment. We present a case of euglycemic DKA in the setting of starvation and surgical stress in a patient with type 2 diabetes without SGLT2 inhibitor use. Clinical Case A 61-year-old type 2 diabetic woman presented with a two-day history of vomiting associated with abdominal pain. She was previously treated with glipizide, metformin, and sitagliptin, which had been discontinued months ago due to poor oral intake. CT imaging demonstrated a 12.4×11.2×10.5 cm pelvic mass with ascites and omental nodularity in the setting of a history of prior right granulosa cell tumor and mature cystic teratoma status post total abdominal hysterectomy with bilateral salpingo-oophorectomy. The patient subsequently developed hematemesis on hospital day 7, for which she was made NPO. She underwent EGD which demonstrated severe esophagitis and duodenitis. She was given an oral diet for one day, prior to resuming NPO status on hospital day 10 for exploratory laparotomy and tumor debulking. On hospital day 11, the patient's labs were notable for an anion gap metabolic acidosis (pH 7.26, n 7.4; CO2 16 mmol/L, n 20-31 mmol/L; anion gap 15 mmol/L, n 5-15 mmol/L), elevated beta-hydroxybutyrate (5.5 mmol/L, n 0.02-0.27 mmol/L), and a blood glucose range of 141-233 mg/dL (n 65-140 mg/dL). The patient was not on any scheduled insulin other than a low dose correctional scale with Lispro subcutaneously pre-meals and had not used SGLT2 inhibitors. There was no suspicion for alcohol toxicity or other poisoning given that the patient had been hospitalized. The lactate level was normal. Thus, the patient met criteria for euglycemic DKA likely secondary to prolonged fasting, exacerbated by the stress of major surgery. The patient was started on an insulin drip with dextrose infusion until the metabolic parameters improved, and she was transitioned to subcutaneous insulin. In diabetic patients unable to tolerate enteral nutrition or with enteral nutrition delays due to surgery, initiation of parenteral nutrition may prevent progression to euglycemic DKA. Ultimately, her pathology was consistent with metastatic granulosa cell tumor, and she was discharged to subacute rehabilitation. Conclusion Euglycemic DKA may be overlooked due to normoglycemia leading to a delay in the diagnosis and appropriate management. It is a medical emergency and should be treated with an intravenous insulin infusion and dextrose. It can be prevented in diabetic patients undergoing major surgical stress by ensuring adequate nutritional support.Reference: Modi, A., Agrawal, A. and Morgan, F., 2017. Euglycemic diabetic ketoacidosis: a review. Current diabetes reviews, 13(3), pp.315-321. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

ODP244 SGLT2 Inhibitor-Induced Euglycemic DKA and its Challenges

Abstract Introduction Sodium-glucose cotransporter type 2 inhibitors (SGLT2-i) have proven to be a gamechanger for patients with diabetes, cardiovascular, and renal disease. However, this class of medications confers an increased risk for adverse side effects such as genitourinary infections and, rarely, euglycemic diabetic ketoacidosis (EDKA). Studies have shown that the risk of euglycemic DKA from SGLT2 inhibitors increase sevenfold in patients with type 2 diabetes mellitus (T2DM) with an overall incidence of approximately 0.1%. These side effects need to be taken into consideration when prescribing this type of therapy. Case Description Case of a 61-year-old male, with hypertension, type 2 diabetes mellitus on glargine, insulin lispro and empagliflozin, adherent to his regimen. Also, patient had a history of CAD s/p PCI (2015), and urethral stricture with self-catheterization who presented to the ED complaining of genital pain of 4 days evolution. Patient had been treated at home with clindamycin without improvement of symptoms. Upon evaluation at ED, laboratories were remarkable for WBC: 25.90, glucose: 144mg/dL, sodium: 134mmol/L, potassium: 5.3mmol/L, CO2: 10mmol/L, ketones: large. Arterial blood gases with metabolic acidosis and anion gap: 26.3. [LAG1] Glycated hemoglobin was 6.8%. Urinalysis was significant for glucosuria 1000 mg/dL, SG 1. 036, 30 mg/dL of protein, negative for nitrites and leukocyte esterase, and few bacteria. Blood glucose levels remained between 145-194 the first 24 hours after admission. Urology service performed a penile exploration with the finding of bilateral corpus cavernosum abscesses that were drained and cultured. Patient was diagnosed with EDKA and started therapy with IV insulin infusion as per DKA protocol, however 10% dextrose infusion was required to continue insulin IV infusion until ketoacidosis resolution. Broad spectrum IV antibiotics were initiated. However, his clinical condition deteriorated and developed respiratory failure requiring mechanical ventilation. After 36 hours of insulin infusion, IV antibiotics and fluids, his anion gap normalized. Abscess and blood cultures reported Candida Glabrata. Antifungal therapy was started and after seven days, the patient's clinical condition improved with resolution of his sepsis and DKA, and was successfully extubated. Patient was discharged to a rehabilitation facility. Conclusion EDKA presents a diagnostic and treatment challenge. It should be suspected in patients with metabolic acidosis, ketonemia and under treatment with a SGLT2-i, even in the absence of hyperglycemia. Prompt treatment initiation with IV insulin infusion along with IV dextrose is important for resolution of DKA. Five-percent dextrose solution should be started and titrated as needed, but if ketoacidosis does not resolve, 10% dextrose can be considered to maintain the insulin infusion. Prescribing this class of hypoglycemic medication should be avoided in those who are clearly at high risk of this well-known complications. Patient education regarding early recognition and to seek early medical evaluation are essential. [LAG1]Anadir unidades Presentation: No date and time listed

ODP253 Utilizing EMR Optimization to Streamline Inpatient Blood Glucose Management and Improve Clinician Efficiency

Abstract Introduction Diabetes mellitus is a common disease that is prevalent in over 30.3 million people in the US. The annual cost of diabetes related inpatient care is over $97 billion. Poor glycemic control has been associated with increase hospital length of stay, increased cost and increased mortality. One of the challenges faced by clinicians in managing inpatient blood glucose is the lack of easy access to necessary data. The various pieces of information needed for comprehensive inpatient blood glucose management were in different parts of the EMR and required multiple clicks to access. The glucose flowsheet 2. 0 was created to remedy this problem. The flowsheet aggregated data necessary onto one screen and displayed it in a context specific manner. The flowsheet aimed to decrease the amount of time spent and the number of clicks needed to gather data clinicians need to manage blood glucose in inpatients. Method/Quality Improvement action: Glucose flowsheet 2. 0 aggregates the following information. Blood Glucose, Fingerstick Glucose, A1c, Dextrose infusions, Steroid (name/dosing), Tube feeds (name/rate), Nutritional Supplement (name//frequency), Percentage of Meal eaten, Vasopressors and Creatinine/GFR. After the flowsheet went live inpatient providers and nursing staff were sent an email educating them about the changes to diabetes flowsheet and how to access it. Six Months after the diabetes flowsheet went live a 6-question survey was sent to approximately 300 residents and advanced practitioners taking care of inpatients and received 69 responses. Results The survey had a response rate &amp;gt;20% with a confidence interval of 90% and less than 10% margin of error between the survey responders and the population of clinicians involved in adult inpatient management. 90.7% of survey respondents agreed/strongly agreed "flowsheet 2. 0 gives me relevant and up to date information needed manage blood glucose for hospitalized patients." 87.7% of respondents agreed/strongly agreed that "allows me to view more relevant diabetes and blood glucose related data than on one screen compared to glucose flowsheet 1. 0." 80% and 85% of participants agreed/strongly agreed that the flowsheet 2. 0 improved efficiency by reducing time needed and clicks required to gather necessary data for inpatient blood glucose management. 80.6% of respondents agreed/strongly agreed that "Glucose Flowsheet 2. 0 helps me to save time without compromising quality of diabetes care." 80.6% of respondents agreed/strongly agreed that "the changes implemented in the Glucose flowsheet 2. 0 makes it more likely for me to minimize, prevent, identify or correct errors". Clinicians found the optimization of EMR to be a net positive that saves time without compromising quality of care. This quality improvement project shows that data presented in EMR can be optimized in a context specific manner to improve clinicians’ sense of efficiency. Presentation: No date and time listed