Dextrose Administration Research Articles

Hospital Hypoglycemia: Not Only Treatment But Also Prevention

To propose a strategy, applicable on general hospital wards, for prevention of hypoglycemia in hospitalized patients. Although the mortality rate among hospitalized patients with hypoglycemia has been shown to be 22.2 to 27% in series that included patients with diabetes, some investigators have shown that hypoglycemia is not an independent predictor of mortality. Outside the critical care setting, the comparative risks of hyperglycemia and hypoglycemia and the relationship of hospital hypoglycemia to intensification of glycemic control have not been determined. The reported incidence of hospital hypoglycemia ranges from 1.2% for hospitalized adults to 20% for nonpregnant patients with diabetes admitted without a metabolic emergency. Among patients receiving antihyperglycemic therapy, the literature describes precipitating events--usually a sudden change of caloric exposure-- and predisposing conditions for hypoglycemic episodes. Hospital hypoglycemia is predictable, and it is preventable by measures other than undertreatment of hyperglycemia. Physician orders for antihyperglycemic therapy should be written and, if necessary, be revised so as to respond to the presence of predisposing conditions for hypoglycemia. A ward-based protocol or hospital-wide policy should establish the appropriate response to triggering events. Within the time frame of action of previously administered antihyperglycemic drugs (after abrupt interruption of caloric exposure), the threshold for preventive intravenous administration of dextrose is a glucose concentration of 120 mg/dL.

Effectiveness of octreotide in a case of refractory sulfonylurea-induced hypoglycemia

The use of sulfonylurea medications in the treatment of type 2 diabetes mellitus is common. Patients who present to the Emergency Department after ingestion of excessive amounts of suflonylurea medications often have hypoglycemia refractory to dextrose administration. Standard care includes the administration of dextrose, glucagon, and diazoxide. Recently, the use of octreotide has been described as an alternative treatment in these patients. We present a case of a 20-year-old woman who ingested 900 mg of glyburide causing refractory hypoglycemia resistant to treatment with intravenous dextrose, glucagon, and diazoxide. Octreotide administration rapidly reversed hypoglycemia allowing patient stabilization and eventual discharge without any significant adverse events.

Dextrose is absorbed by rectum in hypoglycemic rats

The objective of this study was to determine the efficacy of the rectal administration of dextrose in raising the serum glucose in a hypoglycemic rat model. A randomized, prospective, controlled experimental study was performed using 18-h fasted, acutely anesthetized Harlan Sprague-Dawley rats made hypoglycemic by the intravenous infusion of insulin at 3 U/kg/h for 2 h. At 1 h into the infusion, study rats received 1, 2, or 3 g/kg of 50% dextrose solution infused into the rectum using a balloon tipped catheter. Control animals received an equivolume, equi-osmolar (as compared to the 3 g/kg dose) amount of polyethylene glycol (PEG)-400 by rectum. Blood glucose (BG) measurements were made using blood obtained from the portal vein and a femoral artery. Intravenous insulin administered at 3 U/kg/h consistently produced BG levels 60% of baseline at 60 min and 80% of baseline at 120 min. BG levels in portal and arterial circulation increased after rectal dextrose. In general, portal venous values were greater than arterial after rectal dextrose. The greatest increase was seen 30 min after dextrose by rectum in animals receiving 3 g/kg. A 50% dextrose administered by rectum in hypoglycemic rats is absorbed in quantities sufficient to raise BG in the arterial and portal circulation.

Can paramedics safely treat and discharge hypoglycemic patients in the field?

To determine whether paramedics can safely treat and discharge insulin-dependent diabetic patients experiencing uncomplicated hypoglycemic events, we conducted a prospective, observational study with a convenience sample of diabetic patients whose hypoglycemia resolved after intravenous administration of dextrose and before they were transported by paramedics. On-line medical control was contacted to obtain approval and informed consent for participation from interested patients who met all eligibility criteria for the study. Participating patients were given instructions upon discharge from the study and were contacted by telephone 24 hours later to ascertain their medical outcomes and their opinions of the study protocol. We enrolled a total of 36 patients with 38 incidents of hypoglycemia. Of these, 91% reported no complications after discharge. Two patients developed recurrent hypoglycemia but treated themselves and did not require further emergency care. One further patient was found unresponsive on the morning following discharge and was subsequently admitted to a long-term care facility with hypoglycemic encephalopathy. Of the study participants, 85% were very satisfied with not being transported to an emergency department (ED) and 91% were very satisfied with the care they had received. All (100%) of the patients surveyed favored a permanent protocol allowing discharge of hypoglycemic patients without admission to an ED. We conclude that paramedics successfully treated, without complication, most of the patients with uncomplicated hypoglycemic events who were examined in our study. These patients generally preferred discharge without transportation to an ED. (Am J Emerg Med 2003;21:115-120. Copyright 2003, Elsevier Science (USA). All rights reserved.)

Neonatal Care of the Infant of the Diabetic Mother

After completing this article, readers should be able to: 1. Describe the most significant factor influencing neonatal morbidity in the diabetic pregnancy. 2. Characterize the impact of maintaining as normal a metabolic state as possible on the potential for perinatal and neonatal complications. 3. Describe the optimal location and services for delivery of a diabetic parturient. 4. Characterize the evaluation of an infant of a diabetic mother who requires resuscitation after birth. 5. Delineate the factor that most increases the chance of successful management of an infant of a diabetic mother in a regular nursery setting. Although many infants of diabetic mothers (IDMs) have an uneventful perinatal course, there is still an increased risk of complications, even in the infant born to the woman who has gestational diabetes. This discussion highlights specific factors that are critical in the immediate care of the IDM in the delivery room, in the nursery, and after discharge from the hospital. The care of this neonate builds on the pathophysiologic concepts presented in “The Infant of the Diabetic Mother” also appearing in this issue and other recent reviews of the subject. (1)(2) The physician responsible for the care and delivery of the parturient must inform the neonatologist, pediatrician, or their designee responsible for the care of the neonate of the mother’s condition well in advance of delivery to ensure optimal care of the newborn. Among the specific factors that are of utmost importance are the type of diabetes and degree of maternal control, prior pregnancy history, and complications occurring during the pregnancy, including data about fetal monitoring for determination of fetal size and maturation. This information allows the physician caring for the neonate to anticipate many, if not most, of the potential fetal and neonatal complications and assist in determining if a neonatologist needs to be present …

ENVIROGEN RECEIVES NASDAQ NOTIFICATION

We report a patient from a consanguineous family who presented with transient acute liver failure and biochemical patterns suggestive of disturbed urea cycle and mitochondrial function, for whom conventional genetic and metabolic investigations for acute liver failure failed to yield a diagnosis. Whole exome sequencing revealed a homozygous 12-bp deletion in PCK1 (MIM 614168) encoding cytosolic phosphoenolpyruvate carboxykinase (PEPCK); enzymatic studies subsequently confirmed its pathogenic nature. We propose that PEPCK deficiency should be considered in the young child with unexplained liver failure, especially where there are marked, accumulations of TCA cycle metabolites on urine organic acid analysis and/or an amino acid profile with hyperammonaemia suggestive of a proximal urea cycle defect during the acute episode. If suspected, intravenous administration of dextrose should be initiated. Long-term management comprising avoidance of fasting with the provision of a glucose polymer emergency regimen for illness management may be sufficient to prevent future episodes of liver failure. This case report provides further insights into the (patho-)physiology of energy metabolism, confirming the power of genomic analysis of unexplained biochemical phenotypes.

Hyperglycemic but not normoglycemic global ischemia induces marked early intraneuronal expression of β-amyloid precursor protein

Preischemic hyperglycemia is known to accentuate acute ischemic injury to neurons, microglia, and endothelia. In the present study, we used a monoclonal antibody to the N-terminal portion of β-APP to examine how the immunoreactivity of this normal membrane glycoprotein is differentially influenced by transient cerebral ischemia when carried out under normoglycemic vs. hyperglycemic conditions. Anesthetized, physiologically regulated rats received 12.5 min of global forebrain ischemia by bilateral carotid artery occlusions plus systemic hypotension. Hyperglycemia was induced by intraperitoneal dextrose administration prior to ischemia. One or three days later, brains were examined by β-APP immunohistochemistry. Ischemia under hyperglycemic conditions led to the robust, widespread intraneuronal expression of β-APP immunoreactivity in neocortex, hippocampus, thalamus, and striatum of all 11 rats; this was most prominent at 24 h postischemia. Compared to rats with normoglycemic ischemia, numbers of β-APP-immunopositive neurons in the parietal cortex of hyperglycemic rats were increased by 5.9 fold at 24 h, and by 10.6 fold at 3 days postischemia. β-APP-immunopositive neurons in hyperglycemic rats often exhibited striking morphological alterations typical of ischemic necrosis; however, no β-APP immunoreaction was observed in zones of frank infarction. Brains of normoglycemic rats ( n=11), by contrast, showed only weak β-APP immunostaining in occasional non-necrotic pyramidal neurons of parietal neocortex; no necrosis was present in thalamus. In sham-operated hyperglycemic rats, β-APP immunostaining of thalamic neurons was somewhat increased at 24 h. Western analysis revealed that the hyperglycemia-induced intraneuronal overexpression of β-APP was not associated with an overall increase in tissue levels. The results of this study demonstrate that transient forebrain ischemia under hyperglycemic conditions leads to the early intraneuronal expression of β-APP within neuronal populations showing a heightened susceptibility to hyperglycemia-induced accentuation of ischemic injury. Our data suggest that β-APP or its metabolites may be involved in the injury process.

Stress-Induced Hyperglycemia

Stress hyperglycemia is common and likely to be associated with at least some of the same complications as hyperglycemia in true diabetes mellitus, such as poor wound healing and a higher infection rate. The predominant cause is the intense counterregulatory hormone and cytokine responses of critical illness, often compounded by excessive dextrose administration, usually as TPN. Although randomized data suggesting benefit of controlling hyperglycemia in hospitalized patients are paltry, prospective controlled trials are feasible and should be initiated. In the interim, the practice at the authors' institution is to use insulin to lower plasma glucose concentrations to a safe range of 150 mg/dL to 200 mg/dL in all patients.

Acute Hypoglycemia following Combined Spinal-Epidural Anesthesia (CSE) in a Parturient with Diabetes Mellitus

Chief ResidentProfessorDepartment of AnesthesiologyUniversity of TennesseeMemphis, TennesseeJKR50@aol.comTo the Editor:—Intrathecal opioids, with or without local anesthetics, are commonly administered to parturients for analgesia in early labor. Women in labor have increased cortisol and epinephrine concentrations, which are known to stimulate hyperglycemia. 1With the onset of pain relief from neuraxial analgesia, a significant decrease in the concentration of catecholamines has been shown to occur, 2possibly preventing an increase in blood sugar. 1We report a case of acute hypoglycemia after onset analgesia in a diabetic parturient after combined spinal–epidural anesthesia (CSE).The patient was a 26-yr-old woman, gravida 6 para 4, at 38 weeks’ gestation with class 2 gestational diabetes mellitus controlled by diet only. She had no other medical problems. She was admitted in active labor and requested regional anesthesia for labor and delivery. Her blood sugar concentration ranged from 94 to 121 mg/dl, and her blood pressure (BP) ranged from 118/70 to 126/76 mmHg throughout pregnancy. One hour before combined spinal-epidural anesthesia, her blood sugar concentration was 121 mg/dl. Her BP at this admission ranged from 138/68 to 146/72 mmHg, her heart rate ranged from 88 to 110 beats/min, and an electrocardiogram showed a normal sinus rhythm.After hydration with 1,000 ml lactated Ringer’s solution, the block was performed with the patient in the sitting position. A 17-gauge epidural needle was advanced into the epidural space at the L3–L4 interspace, and a 25-gauge pencil-point needle was passed through the epidural needle into the subarachnoid space. A mixture of 25 μg fentanyl and 1.25 mg plain bupivacaine was injected intrathecally, and the spinal needle was withdrawn. An epidural catheter was threaded into the epidural space to a depth of 3 cm. At this time, the patient told us that her contractions were no longer painful. Her BP and heart rate were unchanged. A test dose of 3 ml lidocaine, 1.5%, with 1:200,000 epinephrine was injected into the epidural catheter. Approximately 2 min after the test dose, there was a sudden increase in her heart rate from 110 to 138 beats/min; her BP remained unchanged. Although the delayed tachycardia did not fit the classic definition of a positive response to the test dose, we decided to replace the epidural catheter, which was accomplished easily with the patient still in the sitting position. While the second epidural catheter was being secured to her back, the patient suddenly felt dizzy and became pale and diaphoretic and her BP decreased to 62/48 mmHg. No drug had been administered through the catheter at this time. The heart rate remained at 140–146 beats/min with sinus tachycardia. The patient was placed in the supine position and turned to her left side, and oxygen was administered via facemask. Fluids were infused rapidly, and a total of 50 mg ephedrine was administered intravenously in divided doses in 2 to 3 min. BP increased to 112/53 mmHg, but the patient continued to experience dizziness and “feeling faint.” There was no evidence of motor block, and sensory level to pin prick was at the T10 dermatome. At this time, her blood sugar was 57 mg/dl. With rapid administration of 5% dextrose, blood sugar increased to 128 mg/dl, and all symptoms were alleviated. The epidural catheter was subsequently used to provide pain relief for labor for several hours, and she delivered a healthy infant with an Apgar score of 9 and 9 at 1 and 5 min.Rapid onset of intense analgesia after CSE can decrease the BP to levels before the onset of painful contractions in parturients, but it seldom causes profound hypotension as in this patient. Decreased venous return resulting from aortocaval compression and sympathectomy can also cause hypotension. In our patient, aortocaval compression was unlikely because the procedure was performed with the patient in the sitting position. With a sensory level of T10, the sympathetic block can extend a few segments higher, causing a decrease in the BP. However, even after the restoration of BP with fluids and ephedrine, the patient remained dizzy and diaphoretic. The symptoms disappeared with the rapid administration of intravenous dextrose. In this patient, blood sugar levels had been stable before CSE placement, necessitating no insulin therapy. The cause of acute hypoglycemia and its relation, if any, to profound hypotension after CSE is unclear. We speculate that the abrupt decrease in the levels of catecholamines and cortisol associated with the rapid onset of analgesia from intrathecal opioids may have triggered these rare events in this patient.

Increased Aquaporin-4 Immunoreactivity in Rat Brain in Response to Systemic Hyponatremia

The present study was undertaken to assess whether the protein and mRNA expression levels of the glial water channel aquaporin-4 (AQP4) undergo downregulation and whether there is a subcellular redistribution of AQP4 protein in rat brain in response to systemic hyponatremia and brain edema. Systemic hyponatremia was induced for 4 or 48 h by combined administration of hypotonic dextrose i.p. and 8-deamino-arginine vasopressin (dDAVP) s.c. Semiquantitative immunoblotting of membrane enriched fractions showed significantly increased immunoreactivity to 164 ± 12% (n = 6) and 153 ± 12% (n = 6) of control levels in brain after 4 or 48 h of systemic hyponatremia, respectively. Similarly, immunoblots of cerebellar samples revealed an increase in AQP4 immunoreactivity to 136 ± 6% (n = 6) and 218 ± 44% (n = 6) of control levels, after 4 or 48 h of hyponatremia. In contrast, AQP4 mRNA levels were unchanged after 4 h of severe hyponatremia (104 ± 14% of control levels; n = 17), indicating that there are no changes in AQP4 expression in response to systemic hypoosmolarity. Immunocytochemistry and high-resolution immunogold electron microscopy revealed highly polarized labeling of AQP4 in astrocyte end-feet surrounding capillaries and forming the glia limitans. This pattern of labeling was not changed whereas an increased labeling intensity of AQP4 could be observed in response to hyponatremia. In conclusion, hyponatremia causes a pronounced and rapid increase in AQP4 immunoreactivity that is not accompanied by any increase in AQP4 mRNA expression. The increased AQP4 immunosignal may reflect secondary conformational modifications of AQP4 protein, leading to enhanced antibody binding. This post-translational modification of AQP4 may participate in the adaptation of cerebral tissue to systemic hyponatremia.

Hyperglycemia triggers massive neutrophil deposition in brain following transient ischemia in rats

Myeloperoxidase (MPO) immunohistochemistry was used to ascertain the role of polymorphonuclear leukocytes in hyperglycemia-induced accentuation of brain injury after transient ischemia. Rats received 12.5 min of normothermic global cerebral ischemia by bilateral carotid occlusion plus hypotension. Hyperglycemia was induced before ischemia by intraperitoneal dextrose administration. Quantitative MPO immunohistochemistry was performed at 24 h and 3 days postischemia. Brains of normoglycemic-ischemic animals contained almost no MPO activity. By contrast, striking numbers of MPO-positive cells were present in brains studied 24 h after hyperglycemic ischemia, both within pial and parenchymal vessels and within the parenchyma. MPO deposition tended to subside at 3 days. These results indicate that hyperglycemia triggers the early, massive deposition of neutrophils in the postischemic brain – an event that may contribute to exacerbation of injury.

Brain adaptation to water loading in rabbits as assessed by NMR relaxometry.

The present study was undertaken to investigate the cerebral adaptation to hypoosmolar stress in adult Pannon white rabbits by applying proton nuclear magnetic resonance relaxometry. Progressive hyponatremia was induced by combined administration of hypotonic dextrose in water and 8-deamino-arginine vasopressin over a hydration period of 3, 24, and 48 h. Each group comprised five animals. After completing the hydration protocols, blood was taken to determine plasma osmolality (freezing point depression) and sodium concentration (ion-selective electrode) and, at about the same time, T2-weighted images were made. After the in vivo measurements, the animals were killed and brain tissue samples were obtained to measure water content (desiccation method) and T1 and T2 relaxation times (proton nuclear magnetic resonance method). Free and bound water fractions were calculated by using multicomponent fits of the T2 relaxation curves. It was shown that brain water content and T1 relaxation time remained unchanged despite the progressing hyponatremia. By contrast, T2 relaxation time increased steadily from the control value of 100.2 +/- 7.7 ms to attain its maximum of 107.5 +/- 8.5 ms (p < 0.05) after 48 h of hydration. Using biexponential analysis, fast and slow components of the T2 relaxation curve could be distinguished that corresponded to the bound (T21) and free (T22) water fractions. In response to hyponatremia, the bound water fraction was markedly depressed from 6.5 +/- 3.0% to 3.6 +/- 0.9% (3 h, p < 0.05) and 3.9 +/- 0.8% (24 h, p < 0.05); then it approached the initial value of 5.3 +/- 2.5% by the end of the hydration period of 48 h. It is concluded that restructuring of brain water is a contributory factor to the successful adaptation to hypotonic environment.

The effect of dextrose administration on glucose production and lipolysis in volunteers with neural blockade (T7-S1)

The effect of dextrose administration on glucose production and lipolysis in volunteers with neural blockade (T7-S1)

The “two bag system” for variable intravenous dextrose and fluid administration: Benefits in diabetic ketoacidosis management

A case-controlled retrospective analysis compared the “two bag system,” based on the euglycemic clamp technique, versus the traditional “one bag” method for intravenous diabetic ketoacidosis management. The two bag system can provide more cost-effective intravenous dextrose and fluid delivery and enhance quality of care by improving the efficiency, timeliness, and flexibility of overall control. (J Pediatr 1999;134:376-8)

Endoscopic Ultrasound Localization of a Pancreatic Insulinoma: Case Report and Review of the Localization Techniques

A 23-year-old male was referred to our hospital for evaluation of new-onset seizures. Signs and symptoms of neuroglycopenia, including weakness, dizziness, and confusion, appeared during fasting and resolved promptly with intravenous dextrose administration. Insulin, proinsulin, and C-peptide levels were consistent with a diagnosis of insulinoma. Screening tests for multiple endocrine neoplasia type 1 and surreptitious sulfonylurea uses were negative. Preoperative localization of the insulinoma by transabdominal ultrasonography, computed tomography, and indium-111 octreoscanning were unsuccessful. Endoscopic ultrasonography (EUS) identified a 6- to 7-mm tumor at the juncture of the head and body of the pancreas. Surgical exploration confirmed the preoperative localization, and an 8-mm tumor was simply enucleated. The patient has been free of symptoms for 18 months since surgery. This report describes the utility of EUS to localize a solitary pancreatic insulinoma and provides a comparison of EUS and other preoperative localization techniques.

Patterns and problems of adult total parenteral nutrition use in US academic medical centers.

To determine the pattern of total parenteral nutrition (TPN) use in US academic medical centers because TPN in adults may be associated with complications related to excessive glucose (dextrose) administration and a respiratory quotient greater than 1.0. Two surveys of the University HealthSystems Consortium (n = 106, 74 members and 32 network partners using TPN) to determine TPN formulas and amounts of TPN nutrients given to 2 hypothetical abdominal trauma patients (1 man and 1 woman), each of whom weighed 70 kg. Amounts of dextrose, amino acids, and fat and rates of administration of TPN. In the first survey, 80% (59/74) of members and 41% (13/32) of network partners of the University HealthSystems Consortium reported using TPN formulas with more than 20% dextrose; half used 25% dextrose. In the second survey, the mean (+/-SD) TPN dextrose concentrations were 190+/-43 and 170+/-45 g/L (902+/-204 and 807+/-214 mmol/L), with amino acid concentrations at 40 to 50 g/L, in the male and female patients, respectively. The amounts of amino acids and glucose given, when referred to body cell mass in the male and female patients, were equivalent. In 26% (22/86) of the institutions surveyed, the amounts of glucose given in TPN were high enough (>4.48 mg/kg per minute) to produce a respiratory quotient greater than 1.0. A standard TPN formula was derived as 4.25% amino acids, 15% dextrose, and 20% fat emulsion, at a rate to provide required calories. Excessive TPN glucose administration, found in at least one fourth of US academic medical centers, suggests use of a TPN formula with no more than 15% dextrose, administered at a rate to provide no more than 4 mg/kg of glucose per minute.

Hypoglycaemia: a major biochemical complication in eclampsia- its risk factors and prognostic value

Summary In this two year prospective study, random blood glucose levels were determined in 52 eclamptic patients and 38 controls, at the University of Maiduguri Teaching Hospital and Specialist Hospitals in Maiduguri, Nigeria. Eclamptic mothers had lower glucose levels (mean value = 3.5 mmol/l) than controls (mean value = 6.8 mmol/l) ( P 0.001). Nineteen eclamptics (36.5%) had hypoglycaemic glucose levels (mean value = 2.3 mmol/l). These values returned to normal following intravenous administration of dextrose. Risk factors for hypoglycaemia identified in these mothers included lack of antenatal care, unsupervised labour at home, labour lasting more than 14 hours, obstructed labour, maternal hyperpyrexia, convulsions four or more times, deranged liver function especially HELLP syndrome (syndrome of haemolysis, elevated liver enzymes and low platelet count), poor energy supply in labour, low socio-economic class status and anaemia. A scoring panel derived from these risk factors was tested on a separate group of 48 eclamptics and this was found to be 96% sensitive. Infusion of 50% dextrose reversed coma in seven of eight comatose eclamptics and corrected fetal heart rate irregularities in 13 of 15 hypoglycaemic eclamptics. Seven of nine patients who suffered from posteclamptic psychosis had hypoglycaemic glucose levels. Three mothers with hypoglycaemia and HELLP syndrome died after developing hyperglycaemia following infusions of 50% and 10% dextrose. Hypoglycaemia should be considered a major biochemical complication of eclampsia. Its risk should be identified and its treatment be considered in the protocol of the management of eclamptics.

Inter- and intraindividual variability of the response to intravenous glucose tolerance testing in cats

Abstract Objective To evaluate inter- and intraindividual variation in results of the intravenous glucose tolerance test in cats. Animals 19 healthy specific-pathogen-free-derived cats were allotted to group A (n = 13), which was accustomed, and group B (n = 6), which was unaccustomed to having blood drawn. Procedure Blood samples were collected for glucose and insulin assays before and 5, 10, 15, 30, 45, and 60 minutes after IV administration of 500 mg of dextrose/kg of body weight. Glucose half-life (t1/2) and disappearance coefficient (K), and the acute-phase insulin response (Ins0-10) were calculated. Inter- and intraindividual variability was as-sessed by calculating the coefficient of variation for test variables. Results Comparing the 2 tests, there were no significant differences in glucose and insulin concentrations prior to dextrose administration or in t1/2, K, or Ins0-10. However, compared with group-A cats, cats in group B had significantly (P &lt; 0.05) longer t1/2 and lower K and Ins0-10 values, which was attributed to increased stress in these cats. Overall, the interindividual variability was 62.8% for K, 54.6% for t1/2, and 76.0% for Ins0-10. Mean intraindividual variability was 32.0 (range, 0.1 to 72.0)% for K and t1/2, and 45.8 (range, 4.0 to 179.5)% for Ins0-10. There was only a moderate correlation in results between the 2 tests (rs = 0.59 for t1/2 and K, rs = 0.58 for Ins0-10). Conclusion The variability in results of intravenous glucose tolerance tests in cats suggests caution is necessary in interpreting results of a single test in individuals. (Am J Vet Res 1996;57:1294-1298)

The Poisoned Patient With Altered Consciousness

In the assessment and management of the potentially poisoned patient with altered consciousness, the most consequential and controversial interventions occur during the first 5 minutes of care. In this review article, the risks and benefits of standard diagnostic and therapeutic interventions are presented to guide clinicians through this critical period of decision making. Data for discussion were obtained from a search of English-language publications referenced on MEDLINE for the years 1966 to 1994. Older literature was included when pertinent. Search terms included poisoning, overdose, toxicity, naloxone, glucose, thiamine, and flumazenil. Only large trials were used for determinations of diagnostic utility and efficacy. Small trials, case series, and case reports were reviewed extensively for adverse effects. Trials were reviewed for overall methodology, inclusion and exclusion criteria, sources of bias, and outcome. Analysis favors empirical administration of hypertonic dextrose and thiamine hydrochloride to patients with altered consciousness. Although rapid reagent test strips can be used to guide this therapy, they are not infallible, and they fail to recognize clinical hypoglycemia that may occur without numerical hypoglycemia. Administration of naloxone hydrochloride should be reserved for patients with signs and symptoms of opioid intoxication. Flumazenil is best left for reversal of therapeutic conscious sedation and rare select cases of benzodiazepine overdose.

Accuracy of fingerstick glucose determination in patients receiving CPR.

Recent demonstration of the dangers of hyperglycemia in the setting of cerebral hypoperfusion has resulted in recommendations to abandon the long-standing practice of empiric administration of dextrose to patients with altered mental status. Patients receiving basic cardiopulmonary resuscitation (CPR) have been identified as being at particular risk from inappropriate administration of dextrose. We conducted a prospective trial to determine whether the blood glucose of 50 patients receiving CPR could be accurately assessed using a portable rapid-reagent device in the emergency department (ED). We analyzed both capillary and venous blood samples in the rapid-reagent system, using laboratory analysis of venous blood to define the patient's true blood glucose level. Capillary blood analysis identified 8 patients as hypoglycemic; only 3 of these patients were truly hypoglycemic, and 2 patients identified as hypoglycemic by fingerstick were actually hyperglycemic on laboratory analysis. The only instance in which a patient was classified differently by venous rapid-reagent and laboratory analysis occurred when a patient assessed as normoglycemic (169 mg/dL) by the laboratory had a venous rapid-reagent glucose reading of 182 mg/dL (hyperglycemic). We recommend that venous (rather than capillary) blood be used to analyze blood glucose in all patients receiving CPR before dextrose administration is considered.