Dextrose Administration Research Articles

SAT-LB118 Euglycemic Diabetic Ketoacidosis in Type 2 Diabetes Mellitus

IntroductionDiabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes. It is characterized by the triad of hyperglycemia (>250mg/dL), high anion gap metabolic acidosis (HAGMA), and ketonemia. Rarely, it would present with normal or mildly increased glucose levels (<200mg/dL) making it a diagnostic challenge. We present a case of euglycemic DKA in type 2 diabetes mellitus (T2DM).Case PresentationA 77-year-old woman living in a nursing home with a history of T2DM treated with insulin glargine, but for the past three days refused medications with decreased caloric intake. There were no new medications or ingestion of alcohol or toxic substances. She then developed worsening altered mental status hence admission to the hospital. Her vital signs were within normal limits. Physical examination revealed no abdominal tenderness. Initial laboratory studies showed glucose 83 mg/dL, bicarbonate 10 mmol/L, and anion gap 23 meq/L. Urinalysis significant with trace ketones. The following day, further work-up was done remarkable with beta-hydroxybutyrate 8.3 mmol/L, lactic acid 0.8 mmol/L, and toxicology panel negative. Arterial blood gas showed pH 7.137, pCO2 14 mmHg, and bicarbonate 4.8 mmol/L. DKA protocol was initiated and she was treated with insulin drip, bicarbonate drip, and intravenous fluid administration with D5W. After two days, DKA resolved and was subsequently transitioned to subcutaneous insulin.DiscussionSimilar to the findings of Burge et al, our case showed that decreased caloric intake predisposes patients with diabetes mellitus to euglycemic DKA during periods of insulin deficiency. A proposed mechanism for the accelerated ketosis is due to the effects of elevated levels of glucagon or catecholamines on lipolysis. Other causes of euglycemic DKA include pregnancy, heavy alcohol use, SGLT2 inhibitors, cocaine abuse, pancreatitis, sepsis, and chronic liver disease. It is also important to rule out other causes of HAGMA. In our case, although she has decreased caloric intake, starvation ketoacidosis usually leads to serum bicarbonate levels >18mmol/L. Management is similar to DKA but important difference is the dextrose administration to prevent hypoglycemia.ConclusionEuglycemic DKA is a medical emergency that may be overlooked as patients present without marked hyperglycemia. Physicians should have a high suspicion as this may result in delayed management and potential adverse metabolic consequences.

An Unusual Presentation of Insulinoma: Confusion With Psychiatric Symptoms

Insulinoma is a rare but common functional neuroendocrine tumor that secretes an excess amount of insulin resulting in mostly fasting hypoglycemia but can also cause postprandial hypoglycemia. It usually presents with neuroglycopenic and autonomic sympathetic symptoms that resolve following the administration of dextrose. The patients may remain symptomatic from 1 week to as long as several decades before diagnosis. Insulinoma presenting with psychiatric symptoms has been documented in case/case series reports. Laboratory findings of elevated insulin and C-peptide level in the presence of hypoglycemia and absence of plasma sulfonylurea are suggestive of the diagnosis. Localization of the tumor is essential preoperatively. Surgery usually cures most of the patients, but a minority will have a recurrence especially with malignant insulinoma. The manuscript presents a case of insulinoma presenting with psychiatric symptoms without sympathetic symptoms that led to the delay of the diagnosis for 3 months as initially thought to be related to psychiatric problems. Pancreatic insulinoma was localized by computed tomography (CT) scan and confirmed with endoscopic ultrasound (EUS). The patient underwent successful resection of the tumor, and her symptoms were completely resolved. J Med Cases. 2020;11(5):142-144 doi: https://doi.org/10.14740/jmc3477

Effects of intravenous dextrose on preventing postoperative nausea and vomiting: A systematic review and meta-analysis with trial sequential analysis.

BackgroundIt is reported that postoperative nausea and vomiting, common general anesthesia complications, may be prevented by perioperative intravenous dextrose administration, but with controversial clinical effectiveness.ObjectiveTo evaluate perioperative intravenous dextrose for preventing postoperative nausea and vomiting through a systematic review and meta-analysis of randomized controlled trials with trial sequential analysis.Data sourcesMEDLINE, the Cochrane Central Register of Controlled Trials, Embase, Web of Science, clinicaltrials.gov, and the University Hospital Medical Information Network Clinical Trials Registry were searched from inception until 22 June 2019.Eligibility criteriaTrials investigating intravenous dextrose effects vs. placebos on postoperative nausea and vomiting in patients who underwent general anesthesia.ResultsEleven trials (1,250 patients) were included. All participants were ASA1-2. The nine trials included laparoscopic surgeries, and 92.2% of the participants were women. The timing of dextrose infusion was before, during, and after surgery in three, five, and three trials, respectively. Our results revealed intravenous dextrose administration significantly reduced postoperative nausea, but not vomiting, during early and late postoperative periods (risk ratio [95% confidence interval], early nausea: 0.76 [0.59–0.99], late nausea: 0.65 [0.48–0.89]; early vomiting: 1.00 [0.81–1.25], late vomiting: 0.96 [0.43–2.16]). Evidence quality was downgraded to low because the trial sequential analysis indicated more trials are needed for firm conclusions.ConclusionsCompared with placebos, perioperative intravenous dextrose administration may decrease postoperative nausea but not vomiting.Trial registrationUniversity Hospital Medical Information Network Clinical Trials Registry (registration number: UMIN000030901).

Hypoglycemia after Bariatric Surgery in Mice and Optimal Dosage and Efficacy of Glucose Supplementation.

The Roux-en-Y Gastric Bypass (RYGB) mouse model is a vital tool for studying the pathophysiology of bariatric surgery and contributes greatly to research on obesity and diabetes. However, complications including postsurgical hypoglycemia can have profoundly negative effects. Unlike in humans, blood glucose (BG) is not typically managed in postoperative rodents, despite their critical role as translational models; without this management, rodents can experience hypoglycemia, potentially impairing wound healing, decreasing survivability, complicating interpretation of research data, and limiting translational utility. In this project, we sought to identify an optimal method for minimally invasive administration of dextrose in C57BL/6N (n = 16; 8 male, 8 female) mice. To do so, we characterized BG pharmacokinetic profiles after subcutaneous and oral-transmucosal (OTM) administration of dextrose. Compared with OTM dosage, the subcutaneous route provided more consistent and reliable delivery of glucose and did not cause significant adverse reactions. We then evaluated the frequency of hypoglycemic events after RYGB in C57BL/6N mice (n = 16; 8 male, 8 female) and the effects of subcutaneous dextrose supplementation on morbidity and mortality. BG measurement and behavioral pain assessment (grimace test) were performed for 3 d after surgery. Hypoglycemic (BG ≤ 60 mg/dL) animals were assigned to dose (5% dextrose SC) or no-dose treatment groups. Nearly all (87%) mice became hypoglycemic; 2 of these mice died. No significant intergroup difference in grimace score or mortality was detected. Overall, our results demonstrate that hypoglycemia is a frequent adverse event after RYGB in mice and that subcutaneous injection of dextrose is a safe and effective way to manage hypoglycemia. Further studies are necessary to optimize the intervention threshold and optimal dosage; regardless, we recommend glycemic management after RYGB surgery in mice.

Dextrose administration may reduce the incidence of postoperative nausea and vomiting after laparoscopic cholecystectomy: a double blind randomized controlled trial.

Postoperative nausea and vomiting (PONV) is the most common and undesirable of the complications associated with anesthesia, leading to discomfort in patients and extended hospital stays. The present study evaluates and compares the effects of preoperative/intraoperative dextrose infusion on PONV in patients undergoing laparoscopic cholecystectomy (LC). This prospective, double-blind, randomized controlled study included 93 ASA I-II LC patients who were divided into three groups. Group P received a 10 mL/kg/h rate 5% Dextrose infusion, applied preoperatively for 30 minutes, followed by the same infusion rate of Ringer's lactate until the end of surgery. Group I received a 10 mL/kg/h rate of Ringer's lactate preoperatively for 30 minutes and the same infusion rate of 5% Dextrose during the operation. The control group (Group C) received a Ringer's lactate solution infusion in the pre- and intraoperative periods at a rate of 10 mL/kg/h. The demographic data, PONV, hemodynamic variables, pain scores, blood glucose (BG) values, and antiemetic and analgesic requirements of the participants were recorded. Preoperative BG values were similar in all groups, whereas intraoperative and postoperative BG levels were higher in Group P and Group I, respectively (P=0.020, P=0.010) than in Group C. The incidence of PONV was decreased in groups P and I (38.7% and 25.8%, respectively) compared to Group C (P=0.015). The antiemetic postoperative drug usage for 6 hours was significantly lower in Group P (P=0.005). Preoperative dextrose infusion may be suggested for PONV prophylaxis as a safe and effective method following LC.

Glucose related endocrine and metabolic responses following bolus intravenous hypertonic dextrose administration in Iranian fat-tailed ewes at different pre and post parturition periods

Providing glucose as primary metabolic fuel for maintenance, foetal growth and milk production may be considered necessary for protection against negative energy balance and metabolic disorders. Five adult Ghezel ewes were selected 4 weeks before their parturition and followed at 2 weeks before, 2 and 4 weeks and 2, 3 and 4 months after parturition. Dextrose 50% was administered at 500 mg/kg, 10 mL/kg/hour, and blood samples were collected from all ewes prior to and 1, 2, 3 and 4 hours after 50% dextrose infusion. Serum levels of glucose, beta-hydroxybutyric acid, non-esterified fatty acids, cholesterol, triglyceride, high, low and very low density lipoproteins, insulin, triiodothyronine, thyroxine, prolactin, cortisol and insulin like growth factor-1 were evaluated. Glucose and insulin were increased significantly and immediately following intravenous dextrose administration at all studied periods. The levels of beta-hydroxybutyric acid and non-esterified fatty acids were significantly decreased following dextrose infusion at all periods. Triiodothyronine was decreased in pregnant ewes and increased in non-pregnant, lactating ones. The significant increasing cortisol patterns were detected at 2 and 4 weeks before and 2 and 4 weeks after parturition following dextrose administrations. The decreasing patterns of insulin like growth factor-1 were seen in all studied periods. Prolactin was significantly increased following dextrose administration at 4 and 2 weeks before and 2 weeks after parturition. Bolus intravenous hypertonic dextrose administration could induce the obvious endocrine and metabolic responses in Ghezel ewes via providing a source of energy and the glucose is an important direct controller of metabolic interactions in Ghezel ewes.

Prophylactic administration of oral calcium carbonate during plateletpheresis: A bicentric prospective study

BACKGROUND:Administration of anticoagulant citrate and dextrose (ACD-A) chelates ionized calcium in blood and causes hypocalcemia in plateletpheresis donors. The aim of the study was to observe the effects of oral calcium (Ca) supplementation during plateletpheresis on various parameters related to calcium metabolism.MATERIALS AND METHODS:This study was performed between January 2014 and December 2014 on 200 plateletpheresis donors. They were divided into two groups. In group A donors (n=100), no prophylactic oral calcium supplementation was given. In group B (n=100) donors, 2000 mg of calcium was given one hour before the start of the procedure, 500 mg was given at the start of the procedure and 500 mg calcium was given just before the end of procedure. Biochemical parameters like serum total calcium (T Ca), serum total magnesium (T Mg) and ionized calcium level (iCa) were measured before and after the procedure. Relative risk of citrate toxicity was measured between the two groups.RESULTS:There was a significant fall in total calcium (pre 9.02 mg/dl, post 8.23 mg/dl,), ionized calcium level (pre 1.14 mmol/L, post 0.91 mmol/L) and total magnesium (pre 1.92 mg/dl, post 1.79 mg/dl) amongst the donors who did not receive prophylactic calcium supplementation. Despite calcium intake, in prophylactic calcium intake group, we did observe a significant drop in total magnesium (pre 2.04 mg/dl, post 1.94 mg/dl) and ionized calcium level (pre 1.25 mmol/L, post 1.12 mmol/L, p<0.01). We did observe a drop in total calcium level, however, this observation was not statistically significant. The risk (RR=5.44) of citrate toxicity was higher among group A donors.CONCLUSION:Prophylactic oral calcium carbonate supplementation would help in to reduce the risk of citrate toxicity. Therefore, we suggest for prophylactic oral administration of 3000 mg elemental calcium carbonate in three divided doses to make PP procedures uneventful.

56: Association of timing from steroid administration to delivery and neonatal outcomes in the late-preterm period

Administration of antenatal steroids for women at risk of late preterm birth reduces neonatal morbidity but results in more frequent neonatal hypoglycemia. The objective was to evaluate if there is an association between time from steroid administration to delivery and neonatal hypoglycemia. Retrospective cohort of all women with singleton pregnancies admitted between 34-36 6/7 weeks’ from 4/2016-4/2017 and received at least one dose of antenatal steroids. The exposure was steroid latency, defined as the time from first dose of betamethasone to delivery, examined categorically as < 48 versus ≥ 48 hours from receipt of first dose of betamethasone. The primary outcomes were neonatal hypoglycemia ≤35 mg/dL in the first day of life, admission to the NICU, and neonatal dextrose administration. Of the 302 women eligible for inclusion, 49 (16.2%) had a steroid latency ≥48 hours. Women who received steroids ≥48 hours before delivery were more likely to have preeclampsia (8.2% vs. 1.2%; p=0.015) and were more likely to undergo cesarean (38.8% vs 24.5%; p=0.039). They received betamethasone at an earlier gestation(35.2 ± 0.8 vs 35.7 ± 0.8; p=0.001) but delivered at a more advanced gestation(36.2 ± 0.9 vs 35.8 ± 0.9; p=0.002) than women with a < 48 hour steroid latency. There was no difference in the frequency of hypoglycemia ≤35 mg/dL (14.3% vs. 19.0%; p=0.437) by steroid latency, which remained non-significant after accounting for potential confounders (aOR 0.40, 95% CI 0.12-1.30). Steroid latency remained non-associated with hypoglycemia when examined as a continuous variable. NICU admission and IV dextrose administration were also not associated with steroid latency (Table). Although administration of antenatal steroids for women at elevated risk of delivery in the late preterm period has been reported to increase the risk for neonatal hypoglycemia, in this cohort, the amount of time from steroid administration to delivery is not associated with a greater likelihood of neonatal hypoglycemia or related neonatal events.

Associations between intra-arrest blood glucose level and outcomes of adult in-hospital cardiac arrest: A 10-year retrospective cohort study

AimWe attempted to examine the association between intra-arrest blood glucose (BG) level and outcomes of in-hospital cardiac arrest (IHCA). The interaction between diabetes mellitus (DM) and BG level as well as between dextrose administration and BG level were investigated. MethodsThis single-centred retrospective study reviewed IHCA patients between 2006 and 2015. Patients with measured intra-arrest BG levels were included. Multivariable logistic regression analyses were conducted. Generalised additive models were used to identify appropriate cut-off points for continuous variables. Interactions between independent variables were assessed during the model-fitting process. ResultsAmong the 580 included patients, 34 (5.9%) achieved neurologically intact survival. There were 197 DM patients (34.0%). The mean intra-arrest BG level was 191.5 mg/dl, with 57 patients (9.8%) experiencing hypoglycaemia (BG level ≤ 70 mg/dl). A total of 165 patients (28.4%) received a dextrose injection. An intra-arrest BG level ≤ 150 mg/dl was inversely associated with favourable neurological outcomes at hospital discharge (odds ratio [OR]: 0.28, 95% confidence interval [CI]: 0.11–0.73; p-value = 0.01). In analyses of interactions, non-DM × BG level ≤ 168 mg/dl was inversely associated with favourable neurological outcomes (OR: 0.30, 95% CI: 0.11–0.80; p-value = 0.02). There were no significant interactions between BG level and dextrose administration. ConclusionIHCA patients with intra-arrest BG level ≤ 150 mg/dl had worse neurological recovery. Intra-arrest hypoglycaemia might be a marker of critical illness. Dextrose administration was not shown to improve outcomes of IHCA patients with intra-arrest BG level ≤ 150 mg/dl, indicating the need to develop new therapeutics other than dextrose administration for these patients.

Predictors of Time-to-Repeat Point-of-Care Glucose Following Hypoglycemic Events in Hospitalized Patients.

Previous studies have shown low adherence to the recommendation to repeat point-of-care glucose (POCG) within 15 minutes following the treatment of inpatient hypoglycemia. We sought to evaluate whether patient and clinical factors may predict time-to-repeat (TTR) POCG following hypoglycemic events in hospitalized adult patients. This was a retrospective cross-sectional analysis of 22 226 index hypoglycemic (≤70 mg/dL) readings (of 993 395 total POCG samples) from 6226 hospital admissions within the Johns Hopkins Health System over three years. Time-to-repeat was defined as the difference in time (minutes) between the index POCG and the next POCG sample. Multivariable logistic regression was used to evaluate the association of TTR with clinical, patient, and hospital factors. The median (IQR) TTR was 49 (25-119) minutes, and 14.1% of index POCGs had a TTR ≤15. Severity of hypoglycemia, intensive care unit (ICU), intermediate care (IMC) and pediatrics admissions, and dextrose or glucagon administration were associated with higher adjusted odds of TTR ≤15 minutes. Admission to community hospitals, procedural units, surgery, and labor and delivery was associated with lower adjusted odds of TTR ≤15 minutes. Age, sex, insulin on board, secretagogue use, diabetes type, nutritional status, previous POCG value, and glycemic variability were not significantly associated. There is low adherence to the recommendation to repeat a POCG within 15 minutes following the treatment of inpatient hypoglycemia, which may be mediated by both patient and hospital factors. Further studies are needed to understand the mediators and implications of this practice variability.

Hypoglycaemic crisis induced by non-islet cell tumours in two dogs

Two dogs were admitted for the diagnosis and treatment of neoplasia (a hepatic and a mammary tumour, respectively), lethargy, quadriparesis and abnormal mentation with hypoglycaemia. The blood analyses showed severe hypoglycaemia (1.32 and 1.60 mmol/l, respectively). Although prompt treatment, including intravenous administration of dextrose, was initiated, the blood glucose concentrations were not restored to a normal range. After the diagnostic procedures, no aetiology other than the hepatic tumour identified by the abdominal radiography and ultrasonography, and a mammary tumour that might have caused the hypoglycaemia, were identified. Because there was a high suspicion of non-islet cell tumour-induced hypoglycaemia as a paraneoplastic syndrome, the dogs underwent a hepatic lobectomy and total mastectomy with an ovariohysterectomy, respectively. Within 12 hours after surgery, the blood glucose concentrations of both cases had normalised, even without the administration of dextrose. The histopathological examinations identified a hepatocellular adenoma and a mammary carcinoma, respectively. The endocrine analysis of the serum at admission revealed low serum insulin concentrations (&amp;lt; 1.44 pmol/l) and high serum concentrations of insulin-like growth factor 2 in both dogs. Therefore, the diagnosis in both dogs was confirmed to be non-islet cell tumour-induced hypoglycaemia. Both dogs remained alive without the recurrence of hypoglycaemia 24 months later. Previously, the administration of intravenous dextrose has been considered as the initial treatment in dogs with hypoglycaemia; however, this can temporarily ameliorate the clinical signs related to the non-islet cell tumour-induced hypoglycaemia and help the anaesthesia for the surgical tumour resection as an emergency. Therefore, the definitive treatment of non-islet cell tumour-induced hypoglycaemia might be rapid surgical intervention, which can be associated with good prognosis in dogs with severe non-islet cell tumour-induced hypoglycaemia.

Risk factors for intraoperative hypoglycemia in children: a retrospective observational cohort study.

Intraoperative hypoglycemia can result in devastating neurologic injury if not promptly diagnosed and treated. Few studies have defined risk factors for intraoperative hypoglycemia. The authors sought to characterize children with intraoperative hypoglycemia and determine independent risk factors. This retrospective observational single-institution study included all patients < 18 yr of age undergoing an anesthetic from January 1 2012 to December 31 2016. The primary outcome was blood glucose < 3.3 mmol·L-1 (60 mg·dl-1). Data collected included patient characteristics, comorbidities, and intraoperative factors. A multivariable logistic regression model was used to identify independent predictors of intraoperative hypoglycemia. Blood glucose was measured in 7,715 of 73,592 cases with 271 (3.5%) having a glucose < 3.3 mmol·L-1 (60 mg·dl-1). Young age, weight for age < 5th percentile, developmental delay, presence of a gastric or jejunal tube, and abdominal surgery were identified as independent predictors for intraoperative hypoglycemia. Eighty percent of hypoglycemia cases occurred in children < three years of age and in children < 15 kg. Young age, weight for age < 5th percentile, developmental delay, having a gastric or jejunal tube, and abdominal surgery were independent risk factors for intraoperative hypoglycemia in children. Frequent monitoring of blood glucose and judicious isotonic dextrose administration may be warranted in these children.

Neonatal Hypoglycemia and the Effects of Dextrose Gel

In 2011, the American Academy of Pediatrics published guidelines for the management of neonatal hypoglycemia. These were guidelines only, because no absolute blood glucose level has been associated with adverse neonatal outcomes. The implementation of these guidelines caused an increased number of admissions to the NICU for neonates with hypoglycemia in the institution. NICU admissions are costly, stressful to the newborn, disrupt parent–newborn bonding, and can negatively impact exclusive breastfeeding rates. In the Sugar Babies Study, the use of dextrose gel was reviewed for treatment of neonatal hypoglycemia in neonates 35 weeks or older gestational age and 48 hours or less of life. The study found a decrease in NICU admission rates, which provided more time for parent–infant bonding, and an increase in 2-week postbirth breastfeeding rates. A new hypoglycemia algorithm would be developed, including the administration of dextrose gel. Dextrose gel would be given to neonates with blood glucose levels less than 45 mg/dl, followed by a feeding of either breast milk or formula. Implementation was preceded by a vigorous educational intervention targeted to reach 85% of the nursing staff. Nurses were given a folder of materials, including a review of how to perform a heel stick; the new hypoglycemia algorithm; the procedure for dextrose administration; and the nursing policy and procedure for hypoglycemia. A demonstration was also provided for the disbursement and administration of dextrose gel. A physician’s order for dextrose gel was added to the Computerized Physician Order Entry (CPOE) system. The dextrose gel was also added to the medication delivery system. Implementation went smoothly, and an immediate effect was noted. Although we did not see a 73% decrease in NICU admissions, as noted in some of the literature, a significant decrease in NICU admissions occurred, with a concomitant improvement of exclusive breastfeeding rates. Dextrose gel administration is a viable alternative to feeding alone for neonates with hypoglycemia, with the results of a reduction in NICU admissions and improvement in exclusive breastfeeding rates. Perinatal nurses can have a significant impact on the NICU admission rates of neonates with hypoglycemia through the administration of dextrose gel in addition to breast milk or formula feeding.

SUN-315 Ketogenic Diet Unmasking a Case of Insulinoma

Background: Insulinoma is a rare, sporadic neuroendocrine tumor, with incidence of 4 cases per million people (1). It is often difficult to diagnose given presentation of vague symptoms and often lack of localization of tumor on initial imaging. Timely diagnosis is usually necessary as there is commonly total resolution with surgery. We present a unique case of ketogenic diet unmasking insulinoma in a young healthy male. Clinical Case: An obese otherwise healthy 47-year male presented to our institution with rapid onset altered mental status followed by syncope and witnessed seizure-like activity. He denied previous episodes, although recalled symptoms of diaphoresis and confusion at night since beginning the ketogenic diet one week prior. Initial evaluation demonstrated normal metabolic panel, thyroid function, cortisol level, and HbA1C value of 4.8%, however plasma glucose level was 30 mg/dL with a corresponding insulin level to 87.9 (2.6-24.9) mlU/mL. Initial trauma protocol CT did not reveal injuries and the pancreas appeared normal. Hypoglycemia resolved initially following dextrose administration, however, he had several repeat episodes of symptomatic hypoglycemia despite continuous IV dextrose infusion and eating an oral diet. Two hours into 72 hour fasting test, he developed symptoms of neuroglycopenia, glucose level of 38 mg/dl with insulin level of 76.6 mlU/mL and C-peptide level of 6.7 ng/mL (1.1-1.4 ng/mL). MRI abdomen revealed 2.2x1.5 cm T2-hyperintense, hypervascular lesion in the pancreatic body with restricted diffusion, compatible with neuroendocrine tumor. Endoscopic ultrasound was completed for surgical planning. Diazoxide was initiated while awaiting surgery. He underwent successful enucleation of solitary pancreatic head lesion with resolution of episodic hypoglycemia. Histopathology confirmed neuroendocrine tumor, immunostaining positive for insulin. Conclusion: While clinicians have used ketogenic diet in aiding patients with epilepsy, the recent trend of this very low carbohydrate, high-fat diet for weight loss has been controversial. Insulinoma can be a diagnostic challenge, given the typical clinical presentation is a prolonged course of vague symptoms. Our case is atypical given the rapid onset of symptoms, diagnosis and appropriate treatment within two weeks of starting ketogenic diet. Reference: (1) Mathur, A, et al. “Insulinoma”. Surg Clin North Am. 89.5. (2009)

MON-167 Hypoglycemia Prevention: A Quality Improvement Project to Reduce Inpatient Hypoglycemia Rate Following Treatment of Hyperkalemia

Background: The use of fixed doses of intravenous insulin and dextrose for hyperkalemia treatment is well-established. Iatrogenic hypoglycemia as a result of treatment although common, can have negative consequences. Literature reveals various practices to minimize hypoglycemia risk. Aim: Our aim was to minimize hypoglycemia risk by modifying the original hyperkalemia protocol that included Point of Care(POC) glucose at 0 and 60 minutes after insulin/dextrose, and educating providers on factors that increase hypoglycemia susceptibility, with the goal to reduce hypoglycemia by a percent-decrease of 10 within 3 months. Methods: We revised the hyperkalemia protocol to include hourly blood glucose monitoring at 0, 60, 120, and 180 minutes, allowing for additional dextrose administration. We educated providers and nurses about hyperkalemia management options including increased caution when treating patients with K<6.0, low baseline POC glucose, and low EGFR. We completed a 3-month pre-intervention retrospective analysis, and a 3-month post-intervention analysis and characterized patients based on the above factors. Fisher’s exact test was used to compare categorical variables and Wilcoxon rank sums was used for continuous variables. Results: Pre-intervention, 8.93% of treatments resulted in hypoglycemia, versus 7.55% post-intervention (p=0.807), which is a 15.5 percent-decrease post-intervention. The hourly-monitoring intervention revealed that 6 of 8 hypoglycemic events occurred after 120 minutes. Median EGFR amongst hypoglycemic patients was 20.8 pre-intervention, and 19.4 post-intervention (p=0.311). Among hypoglycemics, median baseline (time 0) glucose was 102 mg/dL pre-intervention versus 99 mg/dL post-intervention(p=0.563). Patients who did not become hypoglycemic had median glucose of 136 mg/dL pre-intervention and 138 mg/dL post-intervention(p=0.929). Conclusion: The decrease in hypoglycemia rate, after hourly monitoring and provider education, while not statistically significant, is clinically meaningful. Our study demonstrates that most hypoglycemic events occur in patients with low baseline POC glucose, low EGFR, and can occur beyond one hour after hyperkalemia treatment. With this change, patients are systematically treated in a controlled setting, instead of rescued when symptomatic. We recommend providers be cognizant of these factors and use hourly-monitoring for both prediction and prevention of hypoglycemia.

SUN-326 Hypoglycemia and Lactic Acidosis: The Deadly Signs of Untreated Non-Hodgkin's Lymphoma

Introduction The presentation of hypoglycemia with lactic acidosis is rare, though well-described. It is most commonly associated with hematologic malignancies and is attributed to the Warburg effect in which cells consume large amounts of glucose through the glycolytic pathway with lactic acid production, even in aerobic conditions. Clinical Case 64yo WM with cirrhosis due to hemochromatosis, atrial fibrillation, type 2 diabetes mellitus managed by diet, initially presented with weakness, malaise and thrombocytopenia. Imaging revealed splenomegaly, bilateral adrenal masses, and diffuse lymphadenopathy. He was admitted, given IV fluid hydration, and discharged to have outpatient lymph node biopsy. Prior to biopsy he developed worsening weakness, fatigue, shortness of breath, and hypoxia. Lactate was 8.1mmol/L, n=0.7-2.1. He was admitted for sepsis secondary to pneumonia. During hospitalization, he was noted to be hypoglycemic (serum glucose 40mg/dL), requiring continuous dextrose infusion and dextrose 50% boluses. Evaluation was consistent with insulin independent hypoglycemia with labs as follows: Insulin <1 microU/mL (2-25), c-peptide 0.65ng/mL (0.78-5.19), proinsulin 4.2pmol/L (3.6-22), beta-hydroxybutyrate 4.07mg/dL (0.2-2.8), glucose 49mg/dL then 44mg/dL 30 minutes after administration of glucagon. ACTH 8.1pg/mL (7.2-63) and cortisol 11mcg/dL then 14.8mcg/dL after cosyntropin stimulation. He was started on stress dose steroids. Lactic acidosis persisted and worsened (>15mmol/L). Repeat CT imaging was obtained to search for potential source of lactic acidosis, though none was found. It was later noted that increasing lactate levels occurred with increased dextrose administration. A perirenal lymph node biopsy was performed. Shortly after the procedure, the patient rapidly decompensated. He was started on continuous renal replacement therapy and given rasburicase for suspected tumor lysis syndrome. Despite these efforts, the patient died. Pathology later returned positive for Non-Hodgkin’s Lymphoma. Discussion In this case, hypoglycemia was initially confounded by a history of cirrhosis and possible adrenal insufficiency. However, no improvement with steroids and worsening of lactic acidosis with increasing dextrose administration demonstrated that hypoglycemia was due to the Warburg effect in the setting of undiagnosed Non-Hodgkin’s Lymphoma. Recognizing this phenomenon is imperative as it coincides with high mortality, and the treatment of underlying disease may be the only effective option. References Georges C. Elhomsy, et al; “Hyper-Warburgism,” a Cause of Asymptomatic Hypoglycemia with Lactic Acidosis in a Patient with Non-Hodgkin's Lymphoma, The Journal of Clinical Endocrinology & Metabolism, Volume 97, Issue 12, 1 December 2012, Pages 4311-4316.

Effect of a Standardized Treatment Panel on Hypoglycemic Events in Hospitalized Acute Hyperkalemic Patients Treated With Intravenous Regular Insulin.

Purpose: Regular insulin is a commonly utilized treatment option for acute hyperkalemia. Despite its benefit, hypoglycemia and associated morbidity/mortality remain important concerns. This institution recently created a treatment panel to standardize regular insulin dosing (0.1 unit/kg) and blood glucose (BG) monitoring in patients with acute hyperkalemia. The purpose of this study is to investigate whether the order panel reduces hypoglycemic events in adults treated with intravenous (IV) regular insulin for hyperkalemia and to determine the effect the treatment panel has on regular insulin dosing, serum potassium, BG monitoring, and dextrose supplementation. Methods: This retrospective study was performed at a single academic medical center. Adults receiving IV regular insulin for acute hyperkalemia were included if BG was assessed prior to and following regular insulin administration. Primary outcome was hypoglycemia within 4 hours of regular insulin administration. Secondary outcomes were the change from baseline serum potassium, frequency of severe hypoglycemia, BG checks within 30 minutes prior to and within 4 hours following insulin administration, regular insulin dosing, and administration of dextrose 50% in water (D50W) following regular insulin administration. Hypoglycemia and severe hypoglycemia were defined as a BG concentration of <70 mg/dL and <50 mg/dL, respectively. Results: One hundred sixty-five patients were included; 75 using the treatment panel and 90 not. Patients using the treatment panel received a lower median (interquartile range [IQR]) regular insulin dose (.10 [0.09-0.10 unit/kg] vs 0.11 [0.09-0.14 unit/kg], P = .004) and had more frequent BG checks during the 4 hours following regular insulin administration (median [IQR]: 4 [3-5] vs 2 [1-3], P < .001). Hypoglycemia (13.3% vs 27.8%, P = .024) and severe hypoglycemia (2.7% vs 11.1%, P = .038) occurred less frequently with the treatment panel. Similar decreases in serum potassium were noted following IV regular insulin administration. Conclusions: Acute hyperkalemic patients utilizing a standardized treatment panel for the dosing and monitoring of IV regular insulin experienced fewer hypoglycemic and severe hypoglycemic episodes and had similar potassium lower effects. The treatment panel decreased regular insulin dosing and increased BG monitoring prior to and following regular insulin administration.

Effect of in ovo feeding of amino acids and dextrose solutions on hatchability, body weight, intestinal development and liver glycogen reserves in newborn chicks.

Early development of the digestive tract is crucial for achieving maximal growth and development of chickens. This study examined the effects of in ovo (IO) feeding of 0.70 mL of dextrose (10.00% and 20.00%) or amino acids solutions into the yolk sac at day 14 of incubation on small intestine histomorphometry and histomorphology, intestinal development, hatchability, body weight, and liver glycogen reserves in newborn chicks. Results showed body weight in amino acid fed hatchlings was higher than control and dextrose groups non-significantly, but hatchability was lower in amino acid group than others. Also, diameter of glycogen vacuoles in all IO treatment groups was more than control. Administration of exogenous dextrose and amino acids solutions into the yolk sac enhanced intestinal development by increasing the size and surface area of the villi and changed villi shape as well. It seems that dextrose or amino acids solutions could improve the intestinal villi development, while they did not affect finger-like villi in jejunum.

Insulinoma: A Diagnostic Challenge!

Insulinoma is a common tumour arising from islets of Langerhans. Patients with insulinomas present with neuroglycopenic symptoms such as repeated episodes of headache, blurred vision, diplopia and lethargy especially with fasting or exercise. Seizures, coma and permanent brain damage results from severe hypoglycaemia. The present report is of a female who got admitted with the chief complaints of swaying on to one side since one month and slurring of speech, seizures and becoming drowsy for four days. Her laboratory values indicated repeated episodes of hypoglycaemia in spite of repeated administration of intravenous dextrose. A CT scan of pancreas revealed insulinoma and was treated by surgical resection. After surgery, patient’s symptoms subsided and she recovered well. The clinical manifestations of insulinoma mimic features of diabetes mellitus and neuropsychiatric disorders, hence a thorough investigation needs to be done to confirm the diagnosis.

Abstract 239: Frequency of Advanced Cardiac Life Support Medication Use and Association With Survival During In-Hospital Cardiac Arrest

Introduction: Resuscitation medication shortages are widespread across the US. We sought to determine the frequency and quantity of meds used during IHCA. Methods: Retrospective, single center, chart review at a large, urban teaching hospital. Adults over 18 who suffered IHCA between Jan 2017 and Mar 2018 were identified. Trained and supervised research assistants used a standardized data tool to extract data from the EMR. Primary outcome was the frequency and quantity of ACLS meds used during IHCA. Secondary outcomes included evaluating the association of med administration with ROSC and survival as well as the use of sodium bicarb with survival in patients with pre-existing end stage renal disease. Results: Criteria were met for 181 IHCA events. Demographics: 71% (128 of 181) black; mean age 65; and 46% (83 of 181) women. Epi was given in 86.7% (157 of 181) cases, with average cumulative dose of 4.2 mg, sodium bicarb given in 63.5% (115 of 181), average dose of 1.9 amps, calcium chloride given in 39.2% (71 of 181), average dose of 1.9 amps, amiodarone was given in 30.9% (56 of 181), average dose of 311.8 mg, and atropine was given in 13.8% (25 of 181), average dose of 1.3 amps. Administration of sodium bicarb was associated with lower rates of ROSC (OR 0.31, 95% CI 0.18 to 0.83) and lower survival (OR 0.31, 95% CI 0.13 to 0.73). Administration of mag sulfate was associated with lower rates of ROSC (OR 0.33, 95% CI 0.13 to 0.83), but no difference in survival (OR 0.34, 95% CI 0.10 to 1.14). Administration of epi, amiodarone, calcium, dextrose, or atropine was not associated with a change in rates of ROSC or survival. In patients with pre-existing ESRD (45 of 181), 73.3% (33 of 45) received sodium bicarb, with 51.5% (17 of 33) achieving ROSC, and 12.1% (4 of 33) surviving to discharge. In patients without ESRD (136 of 181), 60.3% (82 of 136) received sodium bicarb, with 65.9% (54/82) achieving ROSC, and 22.0% (18 of 82) surviving to discharge. (12.1% vs 22.0% p = 0.224). Conclusions: Substantial amounts of drugs with known recent shortage are used in IHCA with no significant increase in ROSC or survival to discharge. Administration of sodium bicarb during IHCA is associated with lower rates of ROSC and survival. These results may be due to confounders such as code duration.