Hypertonic Glucose Infusion Research Articles

Severe Hypoglycemia Due To the Administration of Bromocriptine in a Non-diabetic Patient: A Case Study

The patient was a 24-year-old man with persistent vegetative state following severe traumatic brain injury due to a car accident, who was referred to the emergency department with ageneralized tonic-clonic seizure due to severe hypoglycemia. The patient was treated with phenytoin, levetiracetam, bromocriptine and enoxaparine. The patient was transferred to theIntensive Care Unit (ICU) for accurate monitoring. The patient in the ICU was treated with 100 cc/h of Dextrose 10% plus Intravenous antibiotic to treat urinary tract infection induced sepsis. The previous prescribed medications were also prescribed. Despite proper feeding through PEG tube and receiving 100 cc/h of Dextrose 10%, the patient’s blood glucose was dropped frequently below 50 mg/dl and hypertonic glucose infusion was several times required for treatment of hypoglycemia. Administration of bromocriptine as antidiabetic agent waseliminated after consultation with a neurologist surgeon. After bromocriptine discontinuation, hypoglycemia was resolved. In this non-diabetic patient, severe hypoglycemia occurred afteradministration of bromocriptine, which was an unusual complication in the non-diabetic patient treated with bromocriptine.

Effect of Intravenous Infusion of Hypertonic Glucose on the Treatment of Cows with Postpartum Anestrus

Effect of Intravenous Infusion of Hypertonic Glucose on the Treatment of Cows with Postpartum Anestrus

Effect of Intravenous Small-Volume Hypertonic Sodium Bicarbonate, Sodium Chloride, and Glucose Solutions in Decreasing Plasma Potassium Concentration in Hyperkalemic Neonatal Calves with Diarrhea.

BackgroundHyperkalemia is a frequently observed electrolyte imbalance in dehydrated neonatal diarrheic calves that can result in skeletal muscle weakness and life‐threatening cardiac conduction abnormalities and arrhythmias.HypothesisIntravenous administration of a small‐volume hypertonic NaHCO3 solution is clinically more effective in decreasing the plasma potassium concentration (cK) in hyperkalemic diarrheic calves than hypertonic NaCl or glucose solutions.AnimalsTwenty‐two neonatal diarrheic calves with cK >5.8 mmol/L.MethodsProspective randomized clinical trial. Calves randomly received either 8.4% NaHCO3 (6.4 mL/kg BW; n = 7), 7.5% NaCl (5 mL/kg BW; n = 8), or 46.2% glucose (5 mL/kg BW; n = 7) IV over 5 minutes and were subsequently allowed to suckle 2 L of an electrolyte solution. Infusions with NaHCO3 and NaCl provided an identical sodium load of 6.4 mmol/kg BW.ResultsHypertonic NaHCO3 infusions produced an immediate and sustained decrease in plasma cK. Hypertonic glucose infusions resulted in marked hyperglycemia and hyperinsulinemia, but cK remained unchanged for 20 minutes. Between 30 and 120 minutes after initiation of treatment, the most marked decrements in cK from baseline occurred in group NaHCO3, which were significantly (P < .05) larger during this period of time than in calves in group NaCl, but not group glucose. After 120 minutes, the mean decrease in cK from baseline was −26 ± 10%, −9 ± 8%, and −22 ± 6% in groups NaHCO3, NaCl, and glucose, respectively.Conclusions/Clinical ImportanceSmall‐volume hypertonic NaHCO3 infusions appear to have clinical advantages for the rapid resuscitation of hyperkalemic diarrheic calves, compared to hypertonic NaCl or glucose solutions.

Hypoglycémies sévères révélatrices d’un carcinome hépatocellulaire : une observation à Dakar (Sénégal)

ObjectiveHepatocellular carcinoma revealed by repeated and severe crises of hypoglycemia is rarely indicated in the literature; we report an observation in Dakar (Senegal).ObservationIt was about a Senegalese of 48 years admitted for hypoglycemic coma and to whom the clinical examination (tumoral hepatomegaly) and the biological explorations (alpha fetoprotein) and morphological (abdominal ultrasonography and CT scan) were in favour of advanced hepatocellular carcinoma. The treatment consisted in infusion of serum hypertonic glucose with strong doses of glucocorticoid. The evolution was fatal at the end of 10 days by uncontrollable repetitions of the hypoglycemia crisis with coma and generalized convulsions. Necropsy confirmed the diagnosis of advanced hepatocellular carcinoma.ConclusionHypoglycemia can be the initial clinical manifestation of hepatocellular carcinoma and it should be necessary to proceed to hepatic explorations during arisen unexplained hypoglycemia.

Liver abscess in neonates

Liver abscesses are rare in neonates with the majority resulting from an ascending infection via the umbilical and portal veins, haematogenous spread, or via the biliary tree, or via direct contiguous spread from neighbouring structures. They may present in unusual ways often presenting with ongoing sepsis and resulting in diagnostic difficulties. We present the clinical and radiological findings on six neonates with hepatic abscesses and underline the association with misplacement of umbilical line, association with hypertonic glucose infusions and TPN. A retrospective chart review made of six patients diagnosed with hepatic abscesses between 2000 and 2006. Methods included clinical and radiological review as well as evaluation of potential risk factors. Five of the six patients with neonatal liver abscess were of low birth weight and low gestational age (range 30-34 weeks), but one was post mature (42 weeks). Sex distribution was equal and two were HIV exposed (mother positive), two HIV negative with two having an unknown HIV status. Clinical signs included raised infective markers (CRP) (6) and non-specific signs of septicaemia (4), but a tender hepatomegaly (1) and abdominal distension with ileus (1) were also noted. Five were right-sided abscesses (2 associated with malposition of umbilical line) and one central in position. Predisposing factors included association with a misplaced umbilical line with high concentration glucose infusions (2) and tuberculosis was later diagnosed in one. Infective markers (CRP) remained high with positive blood cultures persisting in all. Causative organisms included Klebsiella (3) Staphylococcus (3) [one a multi-resistant staphylococcus (MRSA)], Gonococcus (1) and Enterobacter (1). Abdominal X-ray demonstrated a mal-positioned umbilical line in three patients (50%). Ultrasound (US) proved a reliable method of diagnosis although some difficulty was encountered in interpreting resolving abscesses and trans-diaphragmatic spread occurred in one. Three patients (50%) responded to antibiotic therapy alone, but interventional drainage was required in the remainder. Needle aspiration was successful in two of these, but one further patient had a radiologically placed pigtail drainage, but later required open drainage. This patient then developed trans-diaphragmatic spread and empyema requiring thoracoscopic decortication. Neonatal hepatic abscesses are rare but should enter the differential diagnosis of a neonate with ongoing sepsis. This study serves to draw attention to their association with misplaced central (umbilical) catheters. Failure to respond to antibiotic therapy necessitates interventional drainage.

Effect of Hyperosmolality on Vasopressin Secretion in Intradialytic Hypotension: A Mechanistic Study

Administration of a small volume of hypertonic solution has been used as an effective treatment for patients with intradialytic hypotension. Hypertonic solutions have been considered to act as plasma volume expanders. This clinical study examines whether arginine vasopressin (AVP) is involved in this mechanism of blood pressure control. Nonrandomized trial. 42 patients on long-term hemodialysis therapy at a single hospital. Effects of intravenous infusions of 20 mL of 10% saline, 20 mL of 50% glucose, 200 mL of 0.9% saline, or physiological doses of AVP were examined during intradialytic hypotension. Changes in plasma AVP levels, osmolality, plasma volume, and blood pressure were analyzed. Hypertonic saline infusion increased plasma osmolality (mean, 292.7 to 302.3 mOsm/kg H(2)O; P < 0.001), plasma AVP levels (3.9 to 7.8 pg/mL; P = 0.03), and mean arterial pressure (66.6 to 71.8 mm Hg; P = 0.01). The increase in plasma volume (2.3%; P = 0.03) was too small to increase blood pressure because of volume alone. Hypertonic glucose infusion yielded similar results. Isotonic saline infusion increased blood pressure with an abrupt increase in plasma volume (12.7%; P < 0.001). AVP infusion increased blood pressure and plasma AVP to levels similar to those induced by the hypertonic solutions. There are limitations in accurately measuring changes in plasma volume during hemodialysis. Results strongly suggest that the osmotic stimulation of AVP secretion by hypertonic solutions has an important role in increasing blood pressure in patients with intradialytic hypotension. Manipulating plasma AVP appropriately may help correct and prevent intradialytic hypotension.

Renal glucose reabsorption during hypertonic glucose infusion in female streptozotocin-induced diabetic rats

Information regarding the renal glucose transport capacity in diabetes mellitus is limited. These data are needed because two weeks following injection of streptozotocin (STZ), mRNA and protein levels of the glucose transporter, GLUT2, are upregulated in the proximal tubule of the rat. Therefore, we measured renal glucose transport and GLUT2 protein levels in female control rats, and in rats one (STZ-1), two (STZ-2), and three weeks (STZ-3) after STZ injection (65 mg kg −1, ip). Progressive amounts of glucose were infused into anesthetized rats via the femoral vein and renal clearances collected. The amount of glucose reabsorbed, factored by the glomerular filtration rate (GFR) was significantly greater in STZ-3 rats compared with all other groups. In addition, the amount of glucose reabsorbed factored by the amount of glucose filtered was decreased in STZ-1 and STZ-2 compared with controls but was increased in STZ-3. By contrast, renal GLUT2 levels were elevated in all the STZ-treated rats. These data suggest that other factors, functioning either in conjunction with or independent of GLUT2, are required to support an elevated renal glucose transport capacity.

Safety, Tolerability, and Efficacy of a Glucose-Insulin-Potassium-Magnesium-Carnitine Solution in Acute Myocardial Infarction

Fifty-four patients with AMI were treated with a front-loaded 15-hour infusion of hypertonic glucose, insulin, potassium, magnesium, and L-carnitine in addition to usual therapy. This metabolic solution was well tolerated, free of serious side effects, and reduced the incidence of morbid events.

Should Glucose Be Administered Before, With, or After Insulin, in the Management of Hyperkalemia?

To assess the hypokalemic effect of intravenous glucose (25 g i.v. in 5 min) followed by regular insulin (10 U) bolus, as well as the incidence of hypoglycemia, a well-known side effect of this intervention, nine uremic patients on maintenance hemodialysis were studied. Measurements were done of plasma potassium, glucose, insulin, and C-peptide before, and 15, 30, 45, and 60 min after glucose and insulin. The intervention induced a significant fall in plasma potassium level, a significant rise and then fall in plasma glucose, and a significant increase in the insulin and C-peptide levels. These data suggest that hypertonic glucose infusion should precede, not follow, the insulin bolus in the management of hyperkalemia. Such an approach is clinically effective and well tolerated, with no hypoglycemic side effects.

Nutritional regulation of insulin-like growth factor-binding protein gene expression in the ovine fetus and pregnant ewe.

The factors controlling the synthesis and degradation of the insulin-like growth factor-binding proteins (IGFBPs) during pregnancy are poorly understood. To clarify the roles of nutritional factors in the regulation of fetal and maternal IGFBP production, we examined the effects of fasting, refeeding, and glucose administration on plasma IGFBP concentrations and hepatic IGFBP mRNA levels in fetal lambs and pregnant ewes (n = 24). Maternal fasting for 3 days in late gestation stimulated a 50-100% increase in maternal plasma BP-1 concentrations (P < 0.05) and a 2- to 3-fold increase in fetal plasma BP-1 (P < 0.05), as determined by densitometric analysis of Western ligand blots. Fasting also stimulated a 40-70% increase in maternal plasma BP-2 concentrations (P < 0.05), but had no significant effect on fetal plasma BP-2 levels. Levels of hepatic BP-1 mRNA in the fetus and pregnant ewe during fasting paralleled plasma BP-1 levels, suggesting that fasting modulates fetal and maternal plasma BP concentrations at least in part through effects on hepatic gene expression. The effects of fasting on both mRNA and plasma levels of BP-1 and BP-2 were reversed by 3 days of refeeding and were prevented by glucose infusion during fasting. When ewes were made hyperglycemic by the infusion of hypertonic glucose, plasma BP-1 and BP-2 concentrations varied inversely with blood glucose concentrations. In addition, hyperglycemia reduced maternal liver BP-1 and BP-2 mRNA levels and fetal BP-1 mRNA levels by 50-65%. Direct administration of hypertonic glucose to the fetus decreased fetal plasma BP-1 levels acutely and reduced fetal BP-1 mRNA levels by 57%, but had no effect on fetal plasma BP-2 or fetal hepatic BP-2 mRNA levels. These findings indicate that glucose and other nutritional factors regulate gene expression and plasma levels of BP-1 and BP-2 in the pregnant ewe and BP-1 in the fetal lamb. The changes in expression of these IGFBPs during fasting and hyperglycemia may play roles in adaptation of the pregnant mother and fetus to metabolic stress.

Glucose infusion improves endogenous protein synthesis efficiency in multiple trauma victims

Metabolic costs of excessive nutritional support in stressed patients have been increasingly recognized. The decreased endogenous protein synthesis efficiency (PSE) following major injury has been attributed to the predominant need of amino acid precursors for gluconeogenesis. The present study tested the hypothesis that provision of glucose alone, not to exceed the resting energy expenditure (REE), for the first 4 to 5 days after trauma would be enough to restore PSE and stimulate the injured body to accept full nutrition. Eight severely injured, adult, hypermetabolic, and highly catabolic patients admitted to the Trauma Intensive Care Unit (TICU) served as our subjects. Integrated measurements of whole body fuel-substrate kinetics were obtained for energy metabolism (indirect calorimetry), protein kinetics (primed constant infusion of 15N-glycine), and glucose kinetics (labeled glucose infusions). Two studies were conducted on each same subject, one in the early flow phase of injury (48 to 60 hours after trauma) and a second after 4 to 5 days of hypertonic glucose (4.1 ± 0.5 mg/kg/min; 80% REE calories) infusion with electrolytes, trace elements, and minerals. Significant ( P < .05) increases in PSE (14%, 65% ± 2% to 74% ± 2%), plasma growth hormone and insulin levels, and respiratory quotient (RQ) (31%, 0.74 ± 0.03 to 0.97 ± 0.04), and decreases in endogenous glucose appearance rate (55%, 3.1 ± 0.5 to 1.4 ± 0.1 mg/kg/min), and negative N balance (48%, 219 ± 26 to 114 ± 15 mgN/kg/d) were observed. The results suggest that hypertonic glucose infusion alone may be sufficient for physiological adaptation in the immediate posttrauma days. This therapy restores normal PSE, which should protect the labile protein pool. Furthermore, this technique may be useful to “prime” the catabolic patient to make more efficient use of balanced nutritional solutions in the late “flow” phase of anabolic convalescence.

Effect of metabolic acidosis on glucose reabsorption in rats with acute hyperglycemia

The rate of reabsorption of glucose in the kidney is a factor to consider with respect to the degree of hyperglycemia in poorly controlled diabetics. The rate of reabsorption of glucose in the proximal tubule is driven by the electrochemical gradient for sodium across the luminal membrane. This gradient in the proximal tubule is also used to reabsorb a number of other substances, quantitatively the most important being bicarbonate. We wished to explore the hypothesis that acidosis, by reducing the filtered load of bicarbonate and therefore the reabsorption of bicarbonate in the proximal tubule, might permit an increased rate of reabsorption of glucose. Hyperglycemia was induced in rats by the infusion of hypertonic glucose. Reabsorption of glucose was measured by clearance methods and factored for glomerular filtration rate (GFR), which has a direct effect on the reabsorption of glucose. The reabsorption of glucose was increased in the kidney when the reabsorption of bicarbonate in the proximal tubule was decreased by either HCl-induced acidosis or the administration of a carbonic anhydrase inhibitor. This effect was independent of a change in GFR and the fractional excretion of Na, factors that may also lead to changes in the reabsorption of glucose by the kidney.

Inhibition of Gastric Acid Secretion by Jejunal Glucose and Its Relation to Osmolality and Glucose Load

Intrajejunal infusion of hypertonic glucose and hypertonic saline inhibits pentagastrin-stimulated gastric acid secretion in man. This effect is generally ascribed to the hyperosmolality of the solutions. Five volunteers were given 50 g glucose in osmolar concentrations of 2700 mosmol/l and 900 mosmol/l, and five were given 25 g glucose in osmolar concentrations of 2700 mosmol/l and 300 mosmol/l. Control studies with intrajejunal infusion of physiologic saline were performed in all subjects. Median inhibition of gastric acid secretion was 91% after 50 g glucose and 47% after 25 g glucose and was unrelated to the osmolar concentration. These findings suggest that the acid-inhibitory effect of intrajejunally administered glucose is related to the glucose load and not to the osmolar concentration. Plasma responses of intact neurotensin, immunoreactivity, NH2-terminal neurotensin immunoreactivity, enteroglucagon, and gastric inhibitory polypeptide were all related to the amount of glucose given. Glucagon and somatostatin, both of which are potent inhibitors of gastric secretion, were not released by intrajejunally administered glucose.

Amino Acid- and Glucose-Induced Cholestasis before and during Secretin Stimulation

To identify the mechanisms of reduced bile flow after hypertonic amino acid and glucose infusion, acute experiments were performed on anesthetized pigs. When secretin was not administered, amino acids or glucose reduced bile acid-dependent bile secretion to 65 +/- 3% of control. During secretin stimulation amino acids or glucose diminished bile acid-independent bile secretion to 78 +/- 2% of control. No changes in serum bilirubin, alanine aminotransferase, and aspartate aminotransferase were observed. Amino acids and glucose attack different mechanisms responsible for bile formation, but the result is that when secretin is not administered, biliary secretion of bile acids is reduced, and, accordingly, bile acid-dependent bile flow diminished. During secretin stimulation biliary NaHCO3 secretion is depressed, accounting for a fall in bile acid-independent bile flow. Amino acids exert no effect on bile acid secretion or, as a result, on bile acid-dependent bile flow after secretin infusion.

Intraosseous infusion of hypertonic glucose and dopamine.

Intraosseous infusion of drugs for resuscitation and of fluids has been advocated as an alternate emergency technique to intravenous infusion. The reliability of intraosseous infusion of many substances has not been established. Glucose and dopamine hydrochloride are two commonly used emergency drugs in pediatric practice that have not been carefully studied when administered into the bone marrow. In an animal model, we compared the response of an intraosseous injection of hypertonic glucose with that of an intravenous injection of hypertonic glucose. Serum glucose measurements following the injection revealed both routes of administration to be effective. A dopamine infusion was then administered through the bone marrow for 20 minutes. A statistically significant rise in blood pressure was observed two minutes after initiation of the infusion. Intraosseous infusion of hypertonic glucose and dopamine is an effective route by which to administer these medications and is potentially useful in emergency situations in which intravascular access is delayed.

The effects of glucose on myocardial substrate utilization in acute myocardial infarction or angina pectoris

Infusion of glucose-insulin-potassium during acute myocardial infarction has favorable clinical and hemodynamic effects, presumably as a result of decreased myocardial utilization of free fatty acids. In 14 patients with coronary artery disease, hypertonic glucose (a bolus of 10 g followed by infusion of a 30% glucose solution at a constant rate of 10 mg/ kg/min) was infused and arterial and coronary sinus levels of glucose, lactate and free fatty acids were measured before and after 15 and 30 minutes of infusion. Arterial glucose and lactate levels increased significantly after glucose infusion, whereas free fatty acid levels decreased significantly. Modest but significant correlations also existed between glucose arterial levels and the arterial-coronary sinus glucose difference (r = 0.53, p < 0.001); arterial lactate and the arterial-coronary sinus lactate difference (r = 0.35, p < 0.01); arterial free fatty acids; and the arterial-coronary sinus free fatty acid difference (r = 0.62, p < 0.001). These results with a hypertonic glucose infusion are similar to those reported after infusion of glucose-insulin-potassium without the potential for harmful adverse effects from infusions of insulin or potassium. Therefore, infusion of hypertonic glucose may be beneficial in patients with coronary artery disease. Further work is necessary to study its effects in different subgroups of patients with coronary artery disease.

Glucose infusion arrests the decompensatory phase of hemorrhagic shock.

Waning of hyperglycemia has been shown to be closely associated with the deterioration of mechanisms supporting homeostasis during hemorrhagic shock. However, the mechanisms which link plasma glucose levels to maintenance of homeostasis during hemorrhagic shock are not clear. The goal of the present study was to evaluate the importance of glucose to maintenance of compensatory mechanisms. This was undertaken by maintaining plasma glucose levels through infusion of hypertonic glucose (2-3 M) starting at the onset of decompensation during persisting hypovolemia. Administration of glucose at a rate of between 60 and 80 mumoles/min X kg arrested the fall in glucose concentration and significantly slowed or arrested the decompensatory phase. All of the saline infused control animals (n = 6) died within 3 hours after reaching their maximum shed blood volume, averaging 145 +/- 25 minutes, while two of the eight animals in the glucose infusion group died less than 4 hours after reaching the maximum shed blood volume. The remaining six animals were sacrificed between 270 and 397 minutes (average, 340 +/- 22 minutes) after reaching the maximum shed blood volume since decompensation was arrested. Compared to the saline-infused control group, animals receiving glucose infusion exhibited a more moderate acidosis, and the hemoconcentration which normally accompanies decompensation was also prevented. Since the increase in plasma osmolality and the fraction of the total osmolality change accounted for by glucose was less in the glucose-infused animals, these results suggest that the effect is not mediated through a glucose-related maintenance of a transcapillary osmotic gradient.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertonic glucose infusion causes splanchnic hyperemia in patients with cirrhosis

Hypertonic glucose infusion causes splanchnic hyperemia in patients with cirrhosis

The microvascular response of the neonatal mesentery to hypertonic feedings.

Using intravital microscopy we studied the responses of the jejunal and ileal mesenteric microcirculation to hypertonic meals in neonatal piglets. Test meals were infused through a cannulated segment of proximal jejunum. The intestinal segments were observed under conditions of controlled temperature and humidity, and the velocity of red blood cells through mesenteric arterioles was measured and blood flow calculated. Jejunal flow was not altered from baseline by saline or hypertonic mannitol infusion, while significant increases in flow were observed during hypertonic glucose infusion (3.8 X 10(-6) versus 10.7 X 10(-6) ml/s, p less than 0.01). Jejunal glucose infusion did not cause shunting from the ileal microcirculatory bed. We conclude that the infusion of hypertonic glucose causes an increase in jejunal blood flow, but does not result in a change in ileal flow. The increase in flow is a local phenomenon related to glucose absorption in neonatal piglets.

Glucose intolerance and amino acid imbalance in relation to changes in blood ketone body ratio in hepatectomized rabbits.

Glucose metabolism and plasma amino acid pattern were investigated in relation to arterial blood ketone body ratio (acetoacetate/3-hydroxybutyrate), which reflects liver mitochondrial redox state, in rabbits subjected to graded hepatectomy (25, 70 and 93%) and 70% hepatectomy with common bile duct obstruction. After partial hepatectomy, blood ketone body ratio decreased according to the extent of resected mass. Common bile duct ligation induced a further decrease in blood ketone body ratio in 70% hepatectomized rabbits. During a 6-hour hypertonic glucose infusion (0.7 g glucose/kg/h) which started 24 h after the operation, the blood glucose level remained between 230 and 280 mg/dl in 25 and 70% hepatectomized groups, while it increased linearly in 93% and jaundiced 70% hepatectomized groups. The plasma concentrations of alanine and proline as well as other amino acids increased as the blood ketone body ratio decreased. It is suggested that Krebs cycle and gluconeogenesis activities are inhibited as blood ketone body ratio decreases markedly resulting in an impaired glucose tolerance and amino acid imbalance.