Dextrose Infusion Research Articles

Hypotension in Preterm Infants (HIP) randomised trial

ObjectiveTo determine whether restricting the use of inotrope after diagnosis of low blood pressure (BP) in the first 72 hours of life affects survival without significant brain injury at 36...

The Effect of Preoperative Oral Versus Parenteral Dextrose Supplementation on Pain, Nausea, and Quality of Recovery After Laparoscopic Cholecystectomy

PurposeEarlier studies suggest that carbohydrate loading is effective in reducing preoperative nausea. This study was conducted to investigate the effect of preoperative oral versus parenteral carbohydrate loading on the postoperative pain, nausea, and quality of recovery (QoR). DesignThree-arm randomized, single-blind clinical trial. MethodsIn this study, 95 adult patients scheduled for elective laparoscopic cholecystectomy were randomly assigned into three groups of preoperative intravenous dextrose 10% infusion, oral carbohydrate (OCH)–rich drink, and control. The pain and nausea severity scores were measured during recovery, 6 hours, and 24 hours thereafter. The 40-item QoR score was evaluated the day after surgery. FindingsIn recovery, nausea severity was comparable among three groups, whereas pain score in the OCH group was significantly less than the controls (P = .009). Pain score in patients who received intravenous dextrose was mediocre and not statistically different from two other groups. Six and 24 hours after surgery, nausea and pain scores in OCH and dextrose infusion groups were significantly lower than the control group (P < .05). The 40-item QoR score was significantly higher in intervention groups than control participants (P < .05). Blood glucose levels were comparable in three groups before and after surgery. ConclusionsPreoperative carbohydrate loading significantly improves the QoR after laparoscopic cholecystectomy without significant effect on blood glucose levels. Oral route more effectively controls nausea and pain than parenteral dextrose administration.

Critical Low Catastrophe: A Case Report of Treatment-Refractory Hypoglycemia following Overdose of Long-Acting Insulin

Overdose of long-acting insulin can cause unpredictable hypoglycemia for prolonged periods of time. The initial treatment of hypoglycemia includes oral carbohydrate intake as able and/or parenteral dextrose infusion. Refractory hypoglycemia following these interventions presents a clinical challenge in the absence of clear guidelines for management. Octreotide has sometimes been used, but its use is generally limited to sulfonylurea overdose. In this case report, we present a case of refractory hypoglycemia following an overdose of 900 units of long-acting insulin glargine that failed to respond to usual modes of therapy mentioned above. Stress-dose corticosteroids were then initiated, followed by subsequent improvement in IV dextrose and glucagon requirements and blood glucose levels. Hence, corticosteroids may serve as an adjunctive therapy in managing hypoglycemia and can be considered earlier in the course of treatment in patients with refractory hypoglycemia to prevent volume overload, especially when large volumes of dextrose infusions are required.

Profound Lactic Acidosis due to Dextrose Infusion and the Role of Thiamine

Profound Lactic Acidosis due to Dextrose Infusion and the Role of Thiamine

Physiologic Effects of Exogenous Dextrose in Murine Klebsiella pneumoniae Sepsis Vary by Route of Provision

Sepsis is characterized by a dysregulated immune response to infection. Nutrition is important in the care of septic patients, but the effects of specific nutrients on inflammation in sepsis are not well defined. Our prior work has shown benefits from early enteral dextrose infusion in a preclinical endotoxemia model of sepsis. In the current study, we extend our initial work to examine the effects of dextrose infusions, varying by route of administration, on inflammation and glycemic control in a more clinically relevant and translational model of Klebsiella pneumoniae (KP) bacteremia. Ten-week old C57BL6/J male mice (n = 31) underwent the implantation of indwelling vascular catheters, followed by inoculation with oropharyngeal KP. The mice were randomized 24 h after inoculation to (1) intravenous (IV) dextrose, (2) enteral dextrose, or (3) enteral saline (control) to study the effects on systemic inflammation, hemodynamics, and glycemic control. At 72 h, 77% of the control mice died, whereas IV dextrose induced 100% mortality, associated with increased inflammation, hyperglycemia, and hypotension. Enteral dextrose reduced mortality to 27%, promoted euglycemia, and reduced inflammation compared to IV dextrose. We conclude, in a bacteremic model of sepsis, that enteral (but not IV) dextrose administration is protective, suggesting that the route of nutrient support influences inflammation in sepsis.

Efficacy of Dose-Titrated Glucagon Infusions in the Management of Congenital Hyperinsulinism: A Case Series.

Background: Congenital hyperinsulinism (CHI), a rare disease of excessive and dysregulated insulin secretion, can lead to prolonged and severe hypoglycemia. Dextrose infusions are a mainstay of therapy to restore normal glycemia, but can be associated with volume overload, especially in infants. By releasing intrahepatic glucose stores, glucagon infusions can reduce dependency on dextrose infusions. Recent studies have reported positive outcomes with glucagon infusions in patients with CHI; however, to date, there are no reports describing the clinical utility of titrated doses of infused glucagon to achieve glycemic stability.Objective: To assess the potential clinical utility of dose-titrated glucagon infusions in stabilizing glycemic status in pediatric patients with CHI, who were managed by medical and/or surgical approaches.Methods: Patients with CHI (N = 33), with or without mutations in the ATP-sensitive K+ channel genes, ABCC8, and KCNJ11 requiring glucagon by dose titration in addition to intravenous dextrose and medical therapy with diazoxide/octreotide to achieve glycemic stability were recruited. Following glucagon titration and a 24-h glucose stable period, glucose infusion rate (GIR) was reduced over a 24-h period. Achievement of glycemic stability and decrease in GIR were considered end points of the study.Results: All patients achieved glycemic stability with glucagon infusion, demonstrating clinical benefit. GIR reduced from 15.6 (4.5) to 13.4 (4.6) mg/kg/min mean (SD) (p = 0.00019 for difference; n = 32; paired t-test) over 24 h. By univariate analysis, no individual baseline characteristic was associated with changes in the GIR. However, by baseline-adjusted modeling, mutational status of the patient (p = 0.011) was inversely associated with a reduction in GIR. Adverse events were infrequent with diarrhea possibly attributed to glucagon treatment in 1 patient. With long-term treatment following GIR reduction, necrolytic migratory erythema was observed in another patient.Conclusion: These data suggest that dose-titrated glucagon infusion therapy aids hypoglycemia prevention and reduction in GIR in the clinical management of patients with CHI.

Acute encephalopathy in children in Muzaffarpur, India: a review of aetiopathogenesis.

The acute encephalopathy occurring in children in Muzaffarpur, India, also recognised in other litchi-cultivating areas of India, Bangladesh, Vietnam and China, had previously been linked to litchi consumption. Recently, it has been identified as hypoglycaemic encephalopathy of an unusual aetiology with three key factors: undernutrition, prolonged fasting and litchi consumption. A second set of investigators has independently reconfirmed the diagnosis and the three-factor aetiology. Skipping the evening meal with an intake of large amounts of litchi in undernourished children is causative. Early-morning hypoglycaemia with an inadequate glycogen store leads to initiation of gluconeogenesis and fatty acid β-oxidation, but methylene cyclopropyl alanine and glycine present in the litchi aril block the fatty acid β-oxidation cycle. The outcomes are uncorrected hypoglycaemia and encephalopathy due to the entry of metabolic intermediates that cross the blood-brain barrier and affect neuronal function. Suggested measures include early 10% dextrose infusion. Awareness about the disease is of prime importance. The diagnosis and aetiopathogenesis are still under question from a part of the scientific community. This review was undertaken to present a comprehensive view of hypoglycaemic encephalopathy and to remove some of the lingering doubts.

SAT-117 Refractory Paraneoplastic Non Islet Cell Tumor Hypoglycemia (NICTH) from Hepatocellular Carcinoma Managed with Somatostatin Analogue and Glucocorticoids

Non islet cell tumor hypoglycemia (NICTH) is a rare paraneoplastic syndrome generally seen in tumors of mesenchymal and hepatic origin. This syndrome is characterized by life threatening hypoglycemia caused by over expression of high molecular weight insulin-like growth factor 2 (IGF 2). The main stay of treatment is surgical resection of the tumor with no clear medical management being reported as standard of care.We present the case of a 72 year old Cambodian man with no history of diabetes mellitus who presented to our institution with severe hypoglycemia complicated by a seizure and was found to have hepatocellular carcinoma (HCC). Hypoglycemia occurred during times of fasting. Laboratory evaluation revealed a serum glucose of 30mg/dl with insulin level of 2.2 mcIU/mL [2.6 - 24.9 mcIU/ml], C-Peptide of 0.17 ng/mL [0.80 - 3.85 ng/ml], BHB <0.1 mmol/L [0.0 - 0.3 mmol/L] and Proinsulin of <0.4 pmol/L [< or = 18.8 pmol/L]. Hypoglycemic agents screening was negative. Insulin Antibody was negative <0.4 U/mL [<0.4 U/mL] and adrenal insufficiency and hypothyroidism was ruled out. Patient was found to have an elevated IGF 2: IGF 1 ratio of 78 confirming the diagnosis of NICTH. IGF 2 level was 780 ng/ml [333 - 967 ng/ml] while IGF-1 was < 10 ng/ml [32-200 ng/ml] He was not a candidate for surgery due to portal vein involvement and tumor radioembolization was unsuccessful. Despite Prednisone dose of 10 mg twice daily and frequent complex carbohydrate meals, he still continued to have hypoglycemia ultimately requiring hospitalization. During hospitalization, he was treated with 50% dextrose infusion, 37.5 grams of dextrose gel every three hours and frequent small meals. Hypoglycemia remained refractory and a trial of diazoxide was ineffective. He was then started on octreotide with titration to 100mg every 8 hours with significant reduction in hypoglycemic episodes. He continues to remain on octreotide, Prednisolone 20mg twice a day, dextrose gel and dextrose infusion. Goal is to wean dextrose infusion and transition him to Pasireotide 40mg monthly.Hepatocellular carcinoma has been associated with NICTH in the literature. NICTH is characterized by an IGF2:IGF1 ratio >10 as there is no commercially available assay for big IGF II. Definitive treatment involves surgical resection or tumor debulking. Octreotide has antiangiogenic and antineoplastic properties and unfortunately, few studies have shown improved survival and quality of life in patients with advanced HCC. In the case of our patient, tumor was unresectable and NICTH improved with octreotide and prednisolone.

SAT-LB303 Severe Refractory Volume Overload With Diazoxide in the Treatment of Insulinoma

Background: Insulinoma is the most common neuroendocrine tumor (NET), occurring in 1-4 people per million. Surgical resection remains standard of care for symptomatic control and long-term remission. Where surgery is not feasible medical therapy with diazoxide and somatostatin analogues is used as supportive management. Case: A 88-year-old male with background hypertension, remote myocardial infarct and chronic kidney disease (CKD) (Cr 130-150 umol/L; N 60-115) was diagnosed with insulinoma following a presentation for confusion and CBG of 0.9 mmol/L. Diagnosis was confirmed by 72 hour fast with inappropriate insulin (85 pmol/L; N<95) and elevated c-peptide (1875 pmol/L; N 325-1090) with documented hypoglycemia (2.8 mmol/L). CT abdomen localized a 1.2 cm exophytic lesion in the pancreatic tail suggestive of insulinoma. Normal morning cortisol (547 nmol/L) excluded adrenal insufficiency. Initial management included resuscitation with dextrose infusions. Due to advanced age and high cardiac risk profile, the patient was not a candidate for surgical resection of the NET. Endoscopic ultrasound (EUS) ablation was deferred at time of initial hospitalization due to stabilization of hypoglycemia with high glycemic diet. An episode of nocturnal hypoglycemia prompted initiation of diazoxide 100 mg as an outpatient. Subsequent dyspnea (NYHA IV) developed and acute on chronic kidney injury (peak Cr 416 umol/L) with evidence of anasarca secondary to diazoxide use prompted readmission to hospital. With conversion to octreotide, discontinuation of diazoxide and treatment with multiple diuretics, volume overload did not improve. The patient was deemed not a candidate for intermittent hemodialysis and the decision was made to change goals of care. The patient died of complications of volume overload from cardiorenal syndrome 21 days after the initiation of diazoxide. Conclusion: Volume overload has been documented as a complication of diazoxide use in both hypoglycemia and hypertension, occurring in up to 50% of cases, however mortality is not common with supportive management.1, 2 Risk factors for refractory volume overload appear to include reduced ejection fraction, extremes of age and history of CKD3. Possible mechanisms for acute decompensation in CKD include increased unbound diazoxide levels, prerenal effect from hypotension and sodium retention4,5. This case highlights the need for close monitoring with diazoxide use in high risk patients. Clinicians should consider echocardiogram, close monitoring of clinical volume status and renal parameters.

MON-679 What’s in a Bottle? the Importance of Careful Medication Review to Prevent Life Threatening Hypoglycemia

Background: Over 1 in 9 emergency department (ED) visits are due to drug-related adverse events (1) and careful medication review is essential for patient safety. Clinical Case: A 73-year-old male presented to the ED after his family found him to be tremulous with a blood glucometer reading of 30 mg/dL. He was given glucagon and oral glucose however this did not help his blood glucose and he was brought in for further evaluation. He had a history of chronic kidney disease, hepatocellular carcinoma (HCC) and diabetes mellitus type 2 for which he was on no medication at the time of presentation. He reported being on Glipizide nine months ago. In the ED, he had a temperature of 98.3°F; pulse of 76 beats/min; respiratory rate of 18 breaths/min and blood pressure of 166/71. On physical examination, he was in no acute distress with normal neurologic, cardiac and respiratory exam. Laboratory workup was notable for glucose 40 mg/dL, HbA1c 5.0%, Cr 2.55 mg/dL, eGFR 24, ALT 7 IU/L and AST 23 U/L. CT abdomen and pelvis was consistent with known diagnosis of HCC. The patient was given 4 boluses of D50W and started on a continuous dextrose infusion along with octreotide infusion due to persistent hypoglycemia. Patient’s blood glucose improved one day later and he remained stable off the dextrose and octreotide infusions. Further laboratory evaluation revealed ACTH 9 pg/mL (ref 6-50), Random Cortisol 16.1 at 1:36pm, TSH 1.40uIU/ml, Free T4 1.09 ng/dL, Cosyntropin stimulation test at baseline 15.4 ug/dL; at 30 min 22 ug/dL; at 60 min 28.3 ug/dL and Beta-Hydroxybutyrate 0.11 mmol/L. With a blood sugar level of 32 mg/dL, he was found to have Insulin level 35.9 (ref 3.0-25.0mU/L), Pro-insulin 55.6 (ref < 18.8pmol/L) and C-peptide 9.21 (ref 0.8-3.85ng/mL). The patient’s family brought his medications for review with no clear discrepancies noted. Closer inspection of the tablets inside each pill bottle revealed that the pills inside the Docusate-Senna container did not match the description for the same but instead matched the description for Glipizide. The patient disclosed that he had emptied the Glipizide tablets into the bowel regimen container for “safe keeping” when it was discontinued. He was inadvertently taking two Glipizide tablets twice a day as the VNA had mistakenly used these pills to fill his pill box. This serious error in confirming the patient’s medications resulted in his severe hypoglycemia. His Sulfonylurea screen returned positive for Glipizide. Conclusion: Sulfonylureas, an essential component of diabetes management, have a dangerous side effect of hypoglycemia and errors in its administration can be fatal. Therefore, thorough medication reconciliation and review of the actual pills is essential to prevent such errors. Reference: Zed PJ, et al. Incidence, severity and preventability of medication-related visits to the emergency department: a prospective study. Can Med Assoc J. 2008;178(12):1563-1569.

SUN-698 Management of Hyperglycemia in an Adult Patient with Glycogen Storage Disease Type 1b

Background: Glycogen storage disease type 1b (GSD1b) is caused by a deficiency of glucose 6 phosphatase leading to glycogen deposition. The hallmark findings of GSD1b are hypoglycemia and lactic acidosis. GSD1b can be associated with hepatomegaly, hypertriglyceridemia, hematologic abnormalities, hypothyroidism, inflammatory bowel disease, proteinuria, and hypoglycemic seizures. Main stay of therapy is to avoid fasting and to ingest frequent feeds high in complex CHO. Raw cornstarch (CS) has been used for the treatment of hypoglycemia in GSD1b since the early 1980s. CS is digested slowly, providing a steady release of glucose allowing for more stable glucose levels over a longer period of time as compared with other sources of CHO. Adults may require more CS to maintain BG >70 mg/dL and lactate <2mmol/L during the night. We report a case of an adult patient with GSD1b admitted with inability to tolerate oral intake and found to have persistent hyperglycemia on admission requiring insulin therapy.Clinical Case: A 31 year old female with a history of GSD1b complicated by hypoglycemia, Crohn’s disease, chronic pancreatitis and neutropenia was admitted for abdominal pain, emesis and inability to tolerate CS. She was made NPO and was started on a dextrose drip to avoid hypoglycemia and hyperlactatemia. The rate of dextrose infusion was adjusted to maintain lactate levels <2 mmol/L. She developed persistent hyperglycemia with glucose values of 250–350 mg/dL. Laboratory evaluation revealed an HbA1c of 7.6% (reference [ref] 4.3–5.6%), C-peptide of 1.3 ng/mL (ref 0.8–3.9 ng/mL), lactate of 2.3–3.1 mmol/L (ref 0.5–2.2 mmol/L). BHB levels were normal (WNL). Anti-GAD, insulin and islet cell antibodies were negative. The main goal was to avoid hypoglycemia while keeping ketone and lactate levels WNL. The decision was made to start a regular insulin infusion at a constant rate of 1 u/hr to keep BG <180 mg/dL while on the dextrose infusion with close monitoring of lactate and BHB. Insulin and dextrose drip rates were adjusted based on BG. The ultimate goal was to determine total daily insulin requirements while ingesting her home CS doses and to transition to long acting insulin. Short acting insulin boluses were not used given risk of hypoglycemia. The patient’s unpredictable tolerance to CS made determining a fixed insulin dose challenging. She eventually managed to tolerate CS and was transitioned to 10 units of insulin Detemir twice daily. She was discharged with plans to get a CGM and a ketone meter. BG readings at home were between 140–170 mg/dL.Conclusion: We report a rare case of GSD1b and diabetes. The pathogenesis may be related to effects of chronic pancreatitis or metabolic syndrome. Treatment of hyperglycemia in patients with GSD1b is challenging given the heightened risk of fasting hypoglycemia. Treatment options are limited, and there are no data regarding the safe use of insulin in this patient population.

MON-LB123 Diagnosis and Management of Euglycemic DKA in the Setting of SGLT2 Inhibitor Use and Prostate Abscess

Introduction: SGLT2i has been associated with euglycemic DKA by increasing lipid oxidation and glucagon synthesis. In the event of an underlying infection, increased ketogenesis could lead to the presentation of DKA. Clinical case: A 35 year old male patient who was recently diagnosed with type 2 Diabetes mellitus after he presented to his primary care physician with increased urinary frequency, frothy urine. He was found to have a hemoglobin A1c of 12.5% and blood glucose 408 mg/dl. Urinalysis was negative for nitrites and leukocyte esterase. Patient endorsed to have one sexual partner and safe sexual practices. Urinary gonorrhea and chlamydia antigens were negative. He was diagnosed with diabetes mellitus and was started on ertugliflozin, exenatide and bactrim for possible UTI. Three days later, the patient presented to the ED with dysuria, polyuria, rectal pain, nausea and fatigue. Patient appeared to be in distress with tachypnea and tachycardia. Physical exam showed signs of dehydration. Laboratory evaluation revealed blood glucose at 185 mg/dL. Given the history of recent diagnosis of diabetes mellitus and SGLT2 inhibitor use, euglycemic DKA was suspected. ABG revealed metabolic acidosis (arterial blood gas pH 7.32, pCo2 20, pO2 130) with elevated anion gap of 24, HCO3 level of 10 mmol/L (reference range 22 - 28 mmol/L) and beta-hydroxybutyrate of 5.7 mmol/L (reference range 0 - 0.3 mmol/L). The lactate levels were normal. Wbc count 20,100. Urinalysis showed glucose 4+, ketones 4+, WBC 4, negative for infection. Computed tomography scan of his abdomen and pelvis with contrast showed 3.7 x 2.7 cm prostate abscess and acute cystitis. Patient was treated for euglycemic DKA with infusion of insulin and dextrose 10% with 0.45% NS. Careful monitoring of his blood sugar was required as it dropped with slight increase in infusion rate. He was started on ciprofloxacin for prostate abscess. Patient’s metabolic acidosis resolved and he showed clinical improvement. Endocrinologist was on consult. Patient was switched to insulin regimen for glycemic control. Conclusion: SGLT2i class of drugs has been increasingly used in the treatment of diabetes due to improved cardiovascular outcomes and renal protective effects. However, diagnosing DKA can be a concern while treating patients with this drug. While the SGLT2i is responsible for his euglycemic presentation, DKA was likely triggered by his prostate abscess. They can be used safely with extensive education to the physicians about euglycemic DKA presentation. Management requires starting D10 infusion along with insulin drip to avoid the risk of hypoglycemia.

SUN-677 The Warburg Effect: A Case of Persistent Hypoglycemia and Lactic Acidosis

Background: It is well established that malignant cells are able to metabolize glucose to lactate in the presence of oxygen, known as the Warburg effect (WE) - a rare metabolic complication of malignancies, presenting with lactic acidosis & hypoglycemia. It signifies a poor prognosis with high mortality rates. We present the case of a woman with malignancy who presented with persistent hypoglycemia requiring a dextrose drip and type B lactic acidosis. Clinical case: A 63-year-old female was referred to our institution for persistent hypoglycemia and lactic acidosis after being admitted to another hospital for a urinary tract infection. Her history was notable for generalized fatigue & weight loss. She had lactic acidosis (18-25mEq/L; Normal: 0.5–2.2mEq/L) despite stable hemodynamics that did not improve with resuscitation & antibiotics. Her hospital course was complicated by worsening mental status & non- hypoxic respiratory distress due to profound acidosis, requiring intubation. She required a dextrose infusion of up to 40g/hour to maintain normoglycemia and with the infusion, an increase in lactate level was noted. Workup to rule out insulin-dependent hypoglycemia, adrenal insufficiency, GH deficiency, MELAS, mesenteric ischemia & drug-related lactic acidosis was unremarkable. EEG was not suggestive of seizure activity. Initial labs were notable for elevated levels of CA-19-9 408U/mL (normal: 0–34), & CA 125 430U/mL (normal: 0–34) which were attributed to her newly diagnosed cirrhosis. However, the degree of her liver dysfunction was felt to be not severe enough to cause hypoglycemia. Imaging studies looking for tumors were unrevealing. A bone marrow biopsy done to rule out occult malignancy showed metastatic carcinoma with neuroendocrine features. Further treatment was not pursued by her family. Based on the diagnosis of metastatic cancer, it was felt that her persistent hypoglycemia was due to the Warburg effect. Conclusion: The Warburg effect (WE) is observed in cancers when the malignant cells utilize glycolysis over oxidative phosphorylation, regardless of oxygen content, for energy production. This involves aerobic glycolysis & lactic acid is its by-product. Cancer cells use more glucose via the glycolysis pathway to meet their demands leading to hypoglycemia & concurrent lactic acidosis despite normal oxygen levels. WE is a rare but severe complication of malignancies that signifies a poor prognosis. Patients with this complication need to be monitored closely until definitive treatment can be implemented. This case highlights the importance of maintaining a high clinical index of suspicion for diagnosing WE. Reference Elhomsy G. C., Eranki V., Albert S. G., 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. 2012;97(12):4311–4316.

MON-699 Artifactual Hypoglycemia in a Patient with Prolonged Hospital Stay for Neuroleptic Malignant Syndrome

Background: Hypoglycemia is rare in patients without diabetes. A low capillary glucose concentration is not sufficient to make a diagnosis of a hypoglycemic disorder. In fact, this has multiple sources of error. Fulfillment of Whipple’s triad is an essential step for establishing the diagnosis of a hypoglycemic disorder. Clinical case: A 47-year old Caucasian male with past medical history of paranoid schizophrenia was admitted to the ICU from an outside facility with catatonia and apneic spells following an acute change in mental status. He was diagnosed with neuroleptic malignant syndrome and Endocrinology was consulted after 137 days in the hospital for concerns of severe and recurrent hypoglycemia. The patient was non-verbal on evaluation and despite multiple capillary blood glucose readings of <70 mg/dL, including measurements as low as 29 mg/dL, he remained asymptomatic with absence of any clinical signs of an adrenergic response to hypoglycemic episodes. He was on continuous tube feeding through a PEG tube. The low capillary blood glucose measurements prompted rapid management with intravenous or oral dextrose based on the hypoglycemia protocol designed by the hospital. As a last resort, the patient was placed on a continuous dextrose infusion in addition to tube feeding to prevent hypoglycemia.Diagnostic evaluation: Following consultation, we ordered for a corresponding plasma glucose measurement to be done with any capillary blood glucose measurement of < 55 mg/dL prior to correction for hypoglycemia. For a capillary blood glucose measured at 48 mg/dL, corresponding plasma glucose was 95 mg/dL. Whipple’s triad was not fulfilled and no additional work up was pursued. We recommended calibration of the glucose monitors for the hospital unit where the patient was admitted with recommendations to stop monitoring capillary blood glucose in this patient in the absence of diabetes, signs/symptoms of hypoglycemia, medications implicated to cause hypoglycemia and ongoing nutrition with tube feeding. Follow-up: The patient remains in the hospital and is waiting placement at an extended care facility. Plasma blood glucose measurements remain within normal range.Clinical lesson: Artifactual hypoglycemia, though uncommon, is an important consideration when evaluating and managing hypoglycemia. Whipple’s triad is essential to make a diagnosis of true hypoglycemia. Several factors; patient, operator and machine-related, can impact measurements of capillary blood glucose measurements and often result in unnecessary treatment measures often causing inefficient and often preventable wastage of hospital resources and sometimes even harm the patient.

SAT-LB110 Sulfonylurea-Induced Hypoglycemia: To Use Octreotide or Not

Background: Sulfonylurea poisoning can cause sustained hypoglycemia refractory to intravenous dextrose. Traditional treatment for sulfonylurea induced hypoglycemia includes intravenous dextrose and glucagon as well as diazoxide in refractory cases. Octreotide is recommended for sulfonylurea poisoning in adult and pediatric patients with laboratory evidence of hypoglycemia.Clinical Case: An 89 year-old female with chronic kidney disease stage III, hypothyroidism, and diabetes mellitus type II, hypertension who presented with intractable nausea and diarrhea. Patient had been taking cefdinir for an UTI the prior week. On CT scan of the abdomen, colitis was demonstrated. Clostridium Difficile Assay was positive. She was incidentally found to have profound hypoglycemia with a blood glucose level of 30 mg/dL. Patient had hypoglycemia unawareness. Despite receiving 4 ampules of dextrose 50%, glucose level did not significantly improve. In the ED, patient was afebrile and hemodynamically stable. Her labs were significant for a hyponatremia of 125 mmol/L with an acute kidney injury [AKI] (Cr 1.94 mg/dL from 1.5 mg/dL). Patient was placed initially on a dextrose 5% normal saline infusion, but glucose levels continued to decline after brief response. Due to poor IV access, internal jugular central line was placed and patient was placed on D10NS infusion with good glycemic response. Patient had taken sulfonylurea despite not eating appropriately for 2 days. After 24 hours on D10 normal saline infusion, patient was able to maintain normal to slightly hyperglycemic levels with consistent carbohydrate diet. Her nausea and diarrhea had considerably improved after starting vancomycin 125 mg every 6 hours. Sulfonyurea was indefinitely discontinued.Conclusion: Patients presenting with sulfonylurea induced hypoglycemia complicated by poor PO intake, AKI, and infection can be safely treated with supportive measures like proper hydration, and dextrose infusion medication is appropriately metabolized by body without the need for octreotide infusion.

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).

SGLT 2 inhibitor induced euglycemic ketoacidosis

SGLT2 inhibitors are being increasingly prescribed for the treatment of type 2 diabetes mellitus. Apart from lowering HbA1c, they are also potentially beneficial in reducing body weight and blood pressure. The awareness among Indian doctors of the potentially fatal complication of SGLT2 inhibitor induced diabetic ketoacidosis may not be widespread. To complicate things further, the blood glucose levels may not be as high as would be expected in a case of diabetic ketoacidosis, making the diagnosis more challenging. We present a case of empagliflozin induced euglycemic ketoacidosis in a post Whipple’s surgery patient. A 52 years old man with upper abdominal pain was found to have a duodenal mass on evaluation. He was a known diabetic on tablets sitagliptin and empagliflozin. Patient underwent Whipple’s surgery for the duodenal mass. Patient had severe metabolic acidosis with ketosis in the immediate post-operative period with mild elevation of blood sugar. The common causes of ketoacidosis were eliminated and the diagnosis of drug induced ketoacidosis was clinched. Patient was successfully treated with intravenous fluids, dextrose and insulin infusion and discharged in good health. It is important to be aware of this adverse effect so that the correct treatment is instituted in a timely fashion.

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.

Embolization of a Complex Facial Arteriovenous Malformation, Balloon-Assisted Flow Arrest, and Controlled n-BCA Injection with Dextrose Push Technique: 2-Dimensional Operative Video.

N-butyl cyanoacrylate glue (n-BCA, Cerenovus, Irvine, California) is commonly used to treat arteriovenous malformation (AVM). Even though Onyx (ethylene vinyl alcohol, Medtronic, Dublin, Ireland) presents more controlled injection, n-BCA is colorless, thus preferable for treatment of superficial facial malformations. N-BCA injection into AVM can result in premature distal migration or early precipitation and reflux into the feeder vessels. Here we describe a trans-arterial balloon assisted technique embolization of a complex facial AVM with n-BCA. A 22-yr-old female with chronic oral/gum bleeding presented with a complex facial AVM. She underwent selective transarterial n-BCA balloon assisted treatment with dextrose push. Informed written consent was obtained. A Scepter dual lumen balloon (MicroVention, Aliso Viejo, California) and a Prowler microcatheter (Cerenovus) were introduced via a 6-French Envoy guide catheter (Cerenovus) selectively into the AVM feeder. The balloon was positioned 3 cm proximal to the Prowler microcatheter tip and fully inflated to create flow arrest. Diluted 25% concentration of n-BCA in Ethiodol Oil was injected through the Prowler microcatheter. The distal migration of the n-BCA was modulated with simultaneous injection of Dextrose 5% in water via the Scepter balloon. This resulted in a controlled glue injection without early distal glue migration (because of the flow arrest) nor early proximal glue precipitation or reflux (because of the dextrose infusion), obtaining complete cure of the complex facial AVM. Glue embolization with flow arrest and dextrose push allows well controlled injection, and it represents a valid option also for high flow vascular lesions.