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Severe Hypoglycemia (severe + hypoglycemia)

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Medical Sciences	94%

Selected Abstracts

Severe hypoglycemia during intensive insulin therapy

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2009
K.-M. KAUKONEN
Background: Tight glycemic control reduces mortality in surgical intensive care patients and in long-term medical intensive care patients. A large study on intensive insulin therapy was prematurely discontinued due to safety issues. As the safety of intensive insulin therapy has been questioned, we screened all patients during a 17-month period to reveal the incidence of hypoglycemia and its effects on the outcome of the patients. Methods: All patients treated between February 2005 and June 2006 in two intensive care units (ICUs) of a tertiary care teaching hospital were included in the study. A nurse-driven intensive insulin therapy with a target blood glucose level of 4,6 mmol/l had been introduced earlier. The patients were divided into two groups according to the presence of severe hypoglycemia (,2.2 mmol/l). Results: One thousand two hundred and twenty-four patients (1124 treatment periods) were included. During the study period, 61,203 blood glucose measurements were performed, 2.6% of which were below and 52.6% above the target range. Severe hypoglycemia (glucose ,2.2 mmol/l) occurred in 25 patients (36 measurements). The incidence was 0.06% of the measurements and 2.3% of the patients. The median age, sex, Acute Physiology And Chronic Health Evaluation II, Simplified Acute Physiology Score II, diagnosis category, ICU or hospital length of stay did not differ between the groups. The hospital mortalities were 25% and 15% in patients with or without severe hypoglycemia, respectively (P=0.16). Conclusion: Severe hypoglycemia during intensive insulin therapy is rare in clinical practice compared with previous clinical trials. [source]

A reduction in severe hypoglycaemia in type 1 diabetes in a randomized crossover study of continuous intraperitoneal compared with subcutaneous insulin infusion

DIABETES OBESITY & METABOLISM, Issue 11 2009
A. Liebl
Aim: Continuous intraperitoneal insulin infusion (CIPII) with the DiaPort system using regular insulin was compared to continuous subcutaneous insulin infusion (CSII) using insulin Lispro, to investigate the frequency of hypoglycemia, blood glucose control, quality of life, and safety. Methods: In this open, randomized, controlled, cross-over, multinational, 12-month study, 60 type 1 diabetic patients with frequent hypoglycemia and/or HbA1c > 7.0% with CSII were randomized to CIPII or CSII. The aim was to obtain the best possible blood glucose while avoiding hypoglycemia. Results: The frequency of any hypoglycemia was similar (CIPII 118.2 (SD 82.6) events / patient year, CSII 115.8 (SD 75.7) p = 0.910). The incidence of severe hypoglycemia with CSII was more than twice the one with CIPII (CIPII 34.8 events / 100 patient years, CSII 86.1, p = 0.013). HbA1c, mean blood glucose, and glucose fluctuations were not statistically different. Treatment-related severe complications occurred mainly during CIPII: port infections (0.47 events / patient year), abdominal pain (0.21 events / patient year), insulin underdelivery (0.14 events / patient year). Weight gain was greater with CSII (+ 1.5 kg vs. , 0.1 kg, p = 0.013), quality of life better with CIPII. Conclusions: In type 1 diabetes CIPII with DiaPort reduces the number of severe episodes of hypoglycemia and improves quality of life with no weight gain. Because of complications, indications for CIPII must be strictly controlled. CIPII with DiaPort is an alternative therapy when CSII is not fully successful and provides an easy method of intraperitoneal therapy. [source]

Evidence for a vicious cycle of exercise and hypoglycemia in type 1 diabetes mellitus

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2004
A. C. Ertl
Abstract Exercise is a cornerstone of diabetes management as it aids in glycemic control, weight management, reducing blood pressure, and improving the quality of life of patients. Unfortunately, owing to the complexity and difficulties of regulating exogenous insulin in a physiologic manner during exercise, physical activity often results in hypoglycemia in patients with type 1 diabetes mellitus (type 1 DM). When glucose levels fall below threshold glycemic levels, neuroendocrine, autonomic nervous system (ANS), and metabolic glucose counterregulatory mechanisms are activated. These hypoglycemic counterregulatory mechanisms in type 1 DM can be blunted irreversibly by disease duration or by acute episodes of prior stress. These reduced (or absent) counterregulatory responses result in a threefold increase in severe hypoglycemia when intensive glycemic control is implemented in type 1 DM 1. Much recent work has been focused on determining the in vivo mechanisms responsible for causing the increased incidence of severe hypoglycemia in type 1 DM. Studies from several laboratories have demonstrated the role played by episodes of antecedent hypoglycemia in producing blunted glucose counterregulatory responses during subsequent exposures of hypoglycemia. Until recently, the mechanisms responsible for exercise related hypoglycemia in type 1 DM have been attributed to relative or absolute increases of insulin levels or incomplete glycogen repletion after physical activity. Owing to the qualitative similarity of neuroendocrine, ANS, and metabolic responses to hypoglycemia and exercise, we have hypothesized that neuroendocrine and ANS counterregulatory dysfunction may also play an important role in the pathogenesis of exercise-related hypoglycemia in type 1 DM. Vicious cycles can be created in type 1 DM, where an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and ANS responses to a subsequent episode of either stress, thereby creating further hypoglycemia (Figure 1). This article will review the recent work that has studied the contribution of counterregulatory dysfunction to exercise-induced hypoglycemia in type 1 DM. Copyright © 2004 John Wiley & Sons, Ltd. 1. Reciprocal vicious cycles may be created in type 1 diabetes mellitus (type 1 DM), whereby an episode of hypoglycemia or exercise can feed forward to downregulate neuroendocrine and autonomic nervous system responses to a subsequent episode of either stress, thereby creating further hypoglycemia [source]

Diabetes management in the new millennium using insulin pump therapy

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S1 2002
Bruce W. Bode
Abstract Current goals of therapy of type 1 and 2 diabetes are to achieve near normal glycemia, minimize the risk of severe hypoglycemia, limit excessive weight gain, improve quality of life and delay or prevent late vascular complications. As discussed in this review, insulin pump or continuous subcutaneous insulin infusion (CSII) therapy provides a treatment option that can dramatically aid in achieving all of these goals. In comparison to multiple daily injections (MDI), CSII uses only rapid-acting insulin, provides greater flexibility in timing of meals and snacks, has programmable basal rates to optimize overnight glycemic control, can reduce the risk of exercise-induced hypoglycemia, and enhances patients' ability to control their own diabetes. Most important, in adults and adolescents with type 1 diabetes, CSII has been shown to lower HbA1c levels, reduce the frequency of severe hypoglycemia and limit excessive weight gain versus MDI without increasing the risk of diabetic ketoacidosis. Similarly positive results are being seen with CSII in adults with type 2 diabetes. The effectiveness of CSII and improvements in pump technology have fueled a dramatic increase in the use of this therapy. Practical guidelines are presented for selection of patients, initiation of treatment, patient education, follow-up assessments and troubleshooting. The recent introduction of methods for continuous glucose monitoring provides a new means to optimize the basal and bolus capabilities of CSII and offers the hope of the development of a feedback-controlled artificial pancreas. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Differential effects of low glucose concentrations on seizures and epileptiform activity in vivo and in vitro

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2006
Anne Kirchner
Abstract In vivo, severe hypoglycemia is frequently associated with seizures. The hippocampus is a structure prone to develop seizures and seizure-induced damage. Patients with repeated hypoglycemic episodes have frequent memory problems, suggesting impaired hippocampal function. Here we studied the effects of moderate hypoglycemia on primarily generalized flurothyl-induced seizures in vivo and, using EEG recordings, we determined involvement of the hippocampus in hypoglycemic seizures. Moderate systemic hypoglycemia had proconvulsant effects on flurothyl-induced clonic (forebrain) seizures. During hypoglycemic seizures, seizure discharges were recorded in the hippocampus. Thus, we continued the studies in combined entorhinal cortex,hippocampus slices in vitro. However, in vitro, decreases in extracellular glucose from baseline 10 mm to 2 or 1 mm did not induce any epileptiform discharges. In fact, low glucose (2 and 1 mm) attenuated preexisting low-Mg2+ -induced epileptiform activity in the entorhinal cortex and hippocampal CA1 region. Osmolarity compensation in low-glucose solution using mannitol impaired slice recovery. Additionally, using paired-pulse stimuli we determined that there was no impairment of GABAA inhibition in the dentate gyrus during glucopenia. The data strongly indicate that, although forebrain susceptibility to seizures is increased during moderate in vivo hypoglycemia and the hippocampus is involved during hypoglycemic seizures, glucose depletion in vitro contributes to an arrest of epileptiform activity in the system of the entorhinal cortex,hippocampus network and there is no impairment of net GABAA inhibition during glucopenia. [source]

Switch to oral hypoglycemic agent therapy from insulin injection in patients with type 2 diabetes

GERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 4 2008
Takashi Okamoto
Aim: We aimed to determine the feasibility of substituting thiazolidinedione-based therapy for insulin injection therapy in patients with type 2 diabetes. Methods: Thirty-six subjects (17 men and 19 women) aged 67.8 ± 11.3 years with an average insulin dose of 0.46 ± 0.17 U/kg bodyweight, a duration of insulin therapy of 6.1 ± 8.2 years and an average hemoglobin A1c (HbA1c) of 6.8 ± 1.3% were switched from insulin injection therapy to pioglitazone, glimepiride and voglibose combination therapy. Results: The number of subjects achieving HbA1c levels of less than 7% at 4 months was 30. The success rate of switch therapy was 83% (30/36). HbA1c was significantly reduced from 6.7 ± 1.3% to 5.9 ± 0.7% at 4 months after the switch (P < 0.01) in 32 patients who completed the planned 4-month study. No adverse effects including heart failure, liver dysfunction or severe hypoglycemia were observed. The insulin dose and the maximum blood glucose on the switch day were significantly lower and the age was significantly higher in the subjects who achieved HbA1c less than 7% at 4 months compared to those who did not (P < 0.05). Conclusion: Thiazolidinedione-based oral combination therapy may efficiently and safely substitute relatively high-dose insulin injection therapy in patients with type 2 diabetes. [source]

Incidence of severe hypoglycemia with tight glycemic control: the higher the better?

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2009
M. J. Schultz
No abstract is available for this article. [source]

Severe hypoglycemia during intensive insulin therapy

From congenital hyperinsulinism to diabetes mellitus: the role of pancreatic ,-cell KATP channels

PEDIATRIC DIABETES, Issue 2 2005
Khalid Hussain
Abstract:, Pancreatic ,-cell adenosine triphosphate (ATP)-sensitive potassium (KATP) channels play a pivotal role in linking glucose metabolism to regulated insulin secretion. KATP channels are hetero- octameric complexes comprising two subunits Kir6.2 and sulfonylurea receptor 1 (SUR1). Changes in the intracellular concentration of nucleotides (ATP) cause alterations in the resting and opening state of the KATP channels. Loss-of-function mutations in the genes encoding the two subunits of KATP channels lead to the most common form of congenital hyperinsulinism (CHI). This causes persistent and severe hypoglycemia in the neonatal and infancy period. CHI can cause mental retardation and epilepsy if not treated properly. On the other hand, now there is evidence of an association between polymorphisms in the Kir6.2 gene and type 2 diabetes mellitus, mutations in the Kir6.2 gene and neonatal diabetes mellitus, and mutations in the SUR1 gene and diabetes mellitus. Interestingly, for reasons that are unclear at present, mice knockout models of KATP channels are different from the human phenotype of CHI. This article is a review focusing on how abnormalities in the pancreatic ,-cell KATP channels can lead to severe hypoglycemia on the one hand and diabetes mellitus on the other. [source]

A prospective study of severe hypoglycemia and long-term spatial memory in children with type 1 diabetes

PEDIATRIC DIABETES, Issue 2 2004
Tamara Hershey
Abstract:, In a previous retrospective study, severe hypoglycemia (SH) was associated with decreased long-term spatial memory in children with type 1 diabetes mellitus (T1DM). In this study, we tested the hypothesis that prospectively ascertained SH would also be associated with decreased spatial long-term memory over time. Children with T1DM (n = 42) and sibling controls (n = 25) performed a spatial delayed response (SDR) task with short and long delays and other neuropsychological tests at baseline and after 15 months of monitoring. Extreme glycemic events and other medical complications were recorded prospectively during follow-up. Fourteen T1DM children experienced at least one episode of SH during the follow-up period (range = 1,5). After controlling for long-delay SDR performance at baseline, age, gender, and age of onset, the presence of SH during the prospective period was statistically associated with decreased long-delay SDR performance at follow-up (semipartial r = ,0.38, p = 0.017). This relationship was not seen with short-delay SDR or with verbal or object memory, attention, or motor speed. These results, together with previously reported data, support the hypothesis that SH has specific, negative effects on spatial memory skills in T1DM children. [source]

Insulin glargine improves hemoglobin A1c in children and adolescents with poorly controlled type 1 diabetes

PEDIATRIC DIABETES, Issue 2 2003
Anne Jackson
Abstract:, The pediatric diabetes team at the University of Minnesota made a clinical decision to switch patients with type 1 diabetes with a hemoglobin A1c level greater than 8.0% to insulin glargine in an effort to improve glycemic control. Retrospective chart analysis was performed on 37 patients 6 months after the switch to insulin glargine therapy. Results:, After 6 months, the average hemoglobin A1c level in the entire cohort dropped from 10.1 ± 2.0 to 8.9 ± 1.6% (p = 0.001). Thirty patients responded with an average hemoglobin A1c drop of 1.7 ± 1.5%, from 10.3 ± 2.2 to 8.6 ± 1.5% (p < 0.001). Seven patients did not respond to insulin glargine therapy, with an average hemoglobin A1c rise of 1.0 ± 0.8% from a baseline of 9.5 ± 1.0% to 10.4 ± 1.4% (p = 0.01). The greatest response was seen in children with an A1c > 12.0%, who dropped their hemoglobin A1c by 3.5 ± 1.9%. Compared with responders, non-responders had significantly less contact with the diabetes team in the form of clinic visits and telephone conversations both before and after initiation of glargine therapy. Sixty-two per cent of patients received insulin glargine at lunchtime, when injections could be supervised at school. Three episodes of severe hypoglycemia occurred after initiation of insulin glargine therapy. Conclusions:, Insulin glargine substantially improved glycemic control in children and adolescents with poorly controlled type 1 diabetes. This response was most remarkable in those with a baseline hemoglobin A1c level > 12.0%, and may have been related to increased supervision of injections. [source]

Intravenous glycerol therapy should not be used in patients with unrecognized fructose-1,6-bisphosphatase deficiency

PEDIATRICS INTERNATIONAL, Issue 1 2003
YUKIHIRO HASEGAWA
AbstractBackground: In Asian countries, glycerol solution that contains fructose (5%) is often used for management of brain edema. However, glycerol and fructose may cause severe hypoglycemia and metabolic acidosis in patients with fructose-1,6-bisphosphatase (FBPase) deficiency, even under stable conditions. The aim of the present study was to determine whether glycerol solution was used for brain edema during acute metabolic decompensation of hypoglycemia and metabolic acidosis in patients with unrecognized FBPase deficiency in Japan and to examine a long-term prognosis of the patients who had this kind of severe metabolic decompensation with or without glycerol therapy. Methods: A retrospective study of 20 children with FBPase deficiency was conducted, based on their medical records. Results: Six of the 20 children were given glycerol solution for the presence or possibility of brain edema during acute metabolic decompensation of hypoglycemia and metabolic acidosis; two of the six patients administered with glycerol were given dialysis. In four patients treated with glycerol alone without dialysis, two had no brain edema before glycerol administration but it developed later after the administration. These four patients treated with glycerol alone died or developed severe neurological complications. Fourteen patients who were not treated with glycerol solution had no brain edema and showed good prognosis. Conclusion: Glycerol solution, which contains fructose in Asian countries including Japan, should not be used as an osmotic agent for treatment of brain edema in patients who have hypoglycemia and retention-type metabolic acidosis, until FBPase deficiency is ruled out by measuring blood concentration of lactate. [source]

Prolonged Insulin Independence After Islet Allotransplants in Recipients with Type 1 Diabetes

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 11 2008
M. D. Bellin
We sought to determine the long-term outcomes in type 1 diabetic recipients of intraportal alloislet transplants on a modified immunosuppressive protocol. Six recipients with hypoglycemia unawareness received one to two islet infusions. Induction therapy was with antithymocyte globulin (ATG) plus etanercept for tumor necrosis factor-, blockade. Recipients received cyclosporine and everolimus for maintenance immunosuppression for the first year posttransplant, with mycophenolic acid or mycophenolate mofetil subsequently substituted for everolimus. Recipients have been followed for 1173 ± 270 days since their last infusion for islet graft function (insulin independence, hemoglobin A1c levels and C-peptide production) and for adverse events associated with the study protocol. Of the six recipients, five were insulin-independent at 1 year, and four continue to be insulin-independent at a mean of 3.4 ± 0.4 years posttransplant. None of the six recipients experienced recurrence of severe hypoglycemia. Measured glomerular filtration rate decreased from 110.5 ± 21.2 mL/min/1.73 m2 pretransplant to 82.6 ±19.1 mL/min/1.73 m2 at 1 year posttransplant. In conclusion, islet transplants restored insulin independence for a mean of >3 years in four of six recipients treated with ATG and etanercept induction therapy and with cyclosporine and, initially, everolimus for maintenance. Our results suggest this immunosuppressive protocol may allow long-term graft survival. [source]

Has Time Come for New Goals in Human Islet Transplantation?

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2008
R. Lehmann
The enthusiasm regarding clinical islet transplantation has been dampened by the long-term results. Concerns about the associated risks of life-long immunosuppression and the striking imbalance between potential recipients and available donor pancreata warrant changes in some of the current goals. Islet transplantation will never be a cure of type 1 diabetes in the majority of patients with no secondary complications, but is a valid option for a limited number of patients with brittle diabetes waiting for an organ or after organ transplantation. Furthermore, insulin independence should not be the main goal of islet transplantation, but avoidance of severe hypoglycemia and good glycemic control, which can be achieved with a relatively small functional beta-cell mass. Therefore, initially one islet infusion is sufficient. Retransplantation at a later time point remains an option, if glucose control deteriorates. Efforts to improve islet transplantation should no longer focus on islet isolation and immunosuppression, but rather on the low posttransplant survival rate of islets caused by activation of the coagulation pathway and the limited oxygen delivery to the islets. Transplantation of smaller islets be it naturally small or size tailored reaggregated islets has the potential to facilitate these processes. [source]

Basal insulin switch from NPH to glargine in children and adolescents with type 1 diabetes

PEDIATRIC DIABETES, Issue 3pt2 2008
Minna Päivärinta
Background:, Insulin glargine is a long-acting insulin analogue increasingly used instead of neutral protamine Hagedorn (NPH) insulin in young subjects with type 1 diabetes. Objective:, We evaluated the clinical course of diabetes in children and adolescents who were switched from NPH to insulin glargine. Methods:, Between August 2003 and November 2004, a total of 76 subjects were switched to glargine in our clinic, treating 340 children with type 1 diabetes. All the subjects had been receiving insulin NPH, and their serum C-peptide levels had been non-detectable for at least 1 yr. Data were collected retrospectively, and 12,18 months after the change, experiences with glargine were inquired using a questionnaire. Seven subjects (9.2%) discontinued glargine before 12 months, and seven refused to participate. Results:, Data for 62 subjects were analyzed. At the switch (0 months), their mean age was 12.7 yr (range 5.1,17.5), mean duration of diabetes was 6.7 yr (range 1.8,14.3), and mean hemoglobin A1c was (HbA1c) 9.2%. Twelve months later (+12 months), the mean HbA1c remained similar (9.2%), the proportion of long-acting insulin was smaller (47.7 vs. 58.1%; p < 0.001), and the daily insulin dose was lower (0.97 vs. 1.05 IU/kg; p < 0.001). The number of injections was lower at +12 months (17.7% with more than five injections vs. 64.5%; p < 0.001). No differences were seen in weight for height or the number of severe hypoglycemias. Most subjects who continued with glargine for ,12 months considered glargine better than NPH. Conclusions:, A switch to insulin glargine retains a similar glycemic control and does not change the number of severe hypoglycemias. [source]