Treatment of neonatal hypoglycemia with minibolus and intravenous glucose infusion

1980 ◽  
Vol 97 (2) ◽  
pp. 295-298 ◽  
Author(s):  
Lawrence D. Lilien ◽  
Rosita S. Pildes ◽  
Gopal Srinivasan ◽  
Sambasivarao Voora ◽  
Tsu F. Yeh
1977 ◽  
Vol 91 (5) ◽  
pp. 779-782 ◽  
Author(s):  
Lawrence D. Lilien ◽  
Luiz A. Grajwer ◽  
Rosita S. Pildes

2017 ◽  
Vol 19 (4) ◽  
pp. 517-523
Author(s):  
Amparo de la Peña ◽  
Corina Loghin ◽  
Xuewei Cui ◽  
Xin Zhang ◽  
Christoph Kapitza ◽  
...  

1989 ◽  
Vol 257 (2) ◽  
pp. E145-E157 ◽  
Author(s):  
J. Radziuk

The formation of hepatic glycogen by the direct pathway is assessed in humans 1) after a 12-h fast and oral loading (100 g) or 2) intravenous infusion (90 g) and 3) after a 24-h fast and the same oral glucose load. The methodology used is based on the double tracer method. [3–3H]glucose is infused at a constant rate for the determination of the metabolic clearance of glucose. [1–14C]glucose is administered with the glucose load. One hour after absorption or the intravenous glucose infusion is terminated, a glucagon infusion is initiated to mobilize the glycogen labeled with [1-14C]glucose and formed during the absorptive period. At this time a third tracer, [6-3H]glucose, is administered to measure glucose clearance. It was found that after the 12-h fast and oral glucose loading 7.2 +/- 1.1 g of hepatic glycogen appears to be formed directly from glucose compared with 8.4 +/- 1.0 g after the same load and a 24-h fast and 8.5 +/- 0.4 g after a 12-h fast and an equivalent intravenous glucose infusion. When the amount of label ([14C]glucose) mobilized that was not corrected for metabolic recycling was calculated, the data suggested that the amount of glycogen formed by gluconeogenic pathways was probably at least equal to that formed by direct uptake. It was also approximately 60% greater after a 24-h fast. It can be concluded that the amount of hepatic glycogen formed directly from glucose during glucose loading is not significantly altered by the route of entry or the extension of the fasting period to 24 h. The data suggest, however, that gluconeogenetic formation of glycogen increases with fasting.


2021 ◽  
Vol 47 (1) ◽  
Author(s):  
Fabio Meneghin ◽  
Martina Manzalini ◽  
Miriam Acunzo ◽  
Irene Daniele ◽  
Petrina Bastrenta ◽  
...  

Abstract Background Neonatal hypoglycemia is a common disorder especially in at-risk infants and it can be associated with poor long-term neurological outcomes. Several therapeutic interventions are suggested, from the implementation of breastfeeding to the glucose intravenous administration. Oral dextrose gel massaged into the infant’s inner cheek is a recent treatment option of asymptomatic hypoglycemia, after which oral feeding is encouraged. This approach seems to reduce the admission of infants to neonatal intensive care unit (NICU) so favouring maternal bonding and breastfeeding success at discharge. Methods In our ward, we prospectively compared a group of near-term neonates, (Gr2, n = 308) at risk for hypoglycemia, treated with an innovative protocol based on the addition of 40% oral dextrose gel (Destrogel, Orsana®,Italy) administered by massaging gums and cheek with historical matching newborns (Gr1, n = 389) treated with a formerly used protocol, as control group. The primary outcome was occurrence of NICU admission and the requirement of intravenous glucose administration; while discharge with full breastfeeding was the secondary outcome. Results In Gr1, 39/389 (10%) infants presented with asymptomatic hypoglycemia, 19/39 were transferred to the NICU, and 14/39 required intravenous glucose treatment. In Gr2, among the 30/308 infants with asymptomatic hypoglycemia managed according to the new protocol, 3/30 were transferred to the NICU and received intravenous glucose infusion. The mean duration of hospitalization respectively was 6.43 (± 6.36) and 3.73 ± 1.53 days (p <  0.001). At discharge, 7.7% of the infants in Gr1 and 30% of the infants in Gr2 were exclusively breastfed (p = 0.02). Considering Gr1 vs Gr2, the number of patients that were transferred to NICU was 19 (48.7%) vs 3 (10%) (p = 0.001) and the number of infants that needed intravenous glucose infusion was 14 (35.9%) vs 3 (10%) (p = 0.01), respectively. Conclusions In our population of near term infants, the introduction of 40% oral dextrose gel to the protocol, helped in the safe management of asymptomatic hypoglycemia and, at the same time, implemented breastfeeding.


PEDIATRICS ◽  
1973 ◽  
Vol 52 (1) ◽  
pp. 75-82
Author(s):  
Rosita S. Pildes ◽  
Daksha A. Patel ◽  
Menachem Nitzan

The present study was undertaken to determine the rate of glucose disposal in the pathogenesis of symptomatic neonatal hypoglycemia. Intravenous glucose (1 gm/kg) was injected rapidly into 11 hypoglycemic and eight control newborn infants. The percentage (mean ± SEM) disappearance rate per minute (Kt) was significantly higher (p &lt; 0.001) in the hypoglycemic newborn infants compared with that of the controls (2.8 ± 0.1 versus 1.2 ± 0.1, respectively). Baseline plasma insulin concentrations were significantly higher (p &lt; 0.01) in the hypoglycemic (16.8 ± 3.9µU/ml) than those of the controls (3.5 ± 1.0µU/ml). Baseline plasma growth hormone values in the hypoglycemic newborns were 16.6 ± 5.7 mµg/ml. Growth hormorne values rose in the hypoglycemic to 36 ± 10 mµg/ml at 10 minutes and to 64 ± 13 mµg/ml by 60 minutes.


1967 ◽  
Vol 55 (2) ◽  
pp. 305-329 ◽  
Author(s):  
Erol Cerasi ◽  
Rolf Luft

ABSTRACT In a previous paper it was shown that 15 out of 85 healthy subjects with a normal intravenous glucose tolerance demonstrated a low plasma insulin response to glucose infusion which was similar to that obtained in diabetic subjects. In the present paper it has been shown that the type of insulin response to glucose infusion was the same when the test was repeated. Low insulin responders to glucose infusion, as a group, also showed low insulin response to intravenous tolbutamide and oral glucose. This indicates that the type of insulin response is characteristic for a given subject irrespective of the stimulation used. There seemed to be no difference in the occurrence of diabetes in the family history of the groups of low and high insulin responders.


2019 ◽  
Vol 6 ◽  
pp. 2333794X1985741
Author(s):  
Mahdi Alsaleem ◽  
Lina Saadeh ◽  
Vasantha H. S. Kumar ◽  
Gregory E. Wilding ◽  
Lorin Miller ◽  
...  

There is variability in practice among care providers on feeding infants admitted with neonatal hypoglycemia (NH) for parenteral dextrose. We compared clinical outcomes in infants who were fed (NH-Fed) and hypoglycemic infants who were kept nothing per os (NPO) (NH-NPO) at the time of initiation of intravenous (IV) dextrose. We performed a retrospective review of all newborn infants admitted to the neonatal intensive care unit with NH for IV dextrose. Infants were grouped as per the feeding approach at initiation of IV dextrose: NH-Fed or NH-NPO infants. We found that infants in the NH-Fed group had lower maximum glucose infusion rate, less duration of glucose infusion therapy compared with the NH-NPO group, and significantly less number of days of hospital stay compared with the NH-NPO group (5.87 ± 1.4 days vs 4.9 ± 1.4 days, P < .006). In conclusion, feeding infants with hypoglycemia who require IV dextrose offers tangible benefits of shorter duration of parenteral dextrose and shorter length of hospitalization.


1982 ◽  
Vol 242 (2) ◽  
pp. E97-E101 ◽  
Author(s):  
A. D. Cherrington ◽  
P. E. Williams ◽  
N. Abou-Mourad ◽  
W. W. Lacy ◽  
K. E. Steiner ◽  
...  

The aim of this study was to determine whether a physiological increment in plasma insulin could promote substantial hepatic glucose uptake in response to hyperglycemia brought about by intravenous glucose infusion in the conscious dog. To accomplish this, the plasma glucose level was doubled by glucose infusion into 36-h fasted dogs maintained on somatostatin, basal glucagon, and basal or elevated intraportal insulin infusions. In the group with basal glucagon levels and modest hyperinsulinemia (33 +/- 2 micro U/ml), the acute induction of hyperglycemia (mean increment of 120 mg/dl) caused marked net hepatic glucose uptake (3.7 +/- 0.5 mg . kg-1 . min-1). In contrast, similar hyperglycemia brought about in the presence of basal glucagon and basal insulin levels described net hepatic glucose output in 56%, but did not cause net hepatic glucose uptake. The length of fast was not crucial to the response because similar signals (insulin, 38 +/- 6 micro U/ml; glucose increment, 127 mg/dl) promoted identical net hepatic glucose uptake (3.8 +/- 0.6 mg . kg-1 . min-1) in dogs fasted for only 16 h. In conclusion, in the conscious dog, a) physiologic increments in plasma insulin have a marked effect on the ability of hyperglycemia to stimulate net hepatic glucose uptake, and b) it is not necessary to administer glucose orally to promote substantial net hepatic glucose uptake.


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