Hypoglycemia Natural Treatments

Guide To Beating Hypoglycemia

Here's Just A Tiny Glimpse Of The Topics Covered: The 3 main types of hypoglycemia and which type you're most likely suffering from. How snacking on chocolate bars can actually make you Fat and worsen your condition! (If you thought those delicious dark brown bars were great energy- boosters.think again!) The No. 1 question most folks have when it comes to hypoglycemia and hyperglycemia. Why you should insist on a 6-hour Gtt and not a 5-hour one. ( Why it might not be a good idea to consult a doctor to confirm your hypoglycemia. Aside from taking a Gtt, what other methods can you use to determine whether or not you're suffering from this condition? Well, refer Chapter 4, Pgs. 23-26 to take a revealing 67-question test especially designed to find out if you've got the symptoms. An inspiring motivational exercise that will help you effectively banish all of your negative thoughts that prevent you from having peace of mind. 2 good reasons why you should keep a food journal. 3 powerful nutrients that limit the effect of glucose on your blood sugar level. This is vital to a hypoglycemic as it helps slow down the absorption of sugar in the food. The secret impulse that literally forces you to say 'yes' to a candy bar or chocolate whenever you feel the hunger pangs gnawing at you. 2 ingredients that are lethal to a hypoglycemic. 'Hidden sugars' you must know to avoid buying products that can easily worsen your condition. 8 essential rules of food planning that are crucial to your speedy recovery from hypoglycemia. Leave out one of them and it could hurt your chances of recovering. How to create a healthy food plan that's suitable for both vegetarian and non- vegetarian hypoglycemics. Most food plans only focus on non-vegetarians, but this one works great for everybody! Read more...

Guide To Beating Hypoglycemia Summary


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My Guide To Beating Hypoglycemia Review

Highly Recommended

The author has done a thorough research even about the obscure and minor details related to the subject area. And also facts weren’t just dumped, but presented in an interesting manner.

When compared to other e-books and paper publications I have read, I consider this to be the bible for this topic. Get this and you will never regret the decision.

Insulin and hypoglycemic compounds

The passage of plasma proteins across the human placental barrier in humans is a highly selective process. It cannot be predicted on a simple way based on physical properties, i.e. protein binding, lipid solubility or molecular weight. In diabetic pregnancy, the safe use of insulin, insulin analogs and oral hypoglycemic agents relies on the absence of transfer from maternal to fetal circulation. It has been known for years that free maternal insulin does not cross the materno-fetal barrier either in early or late pregnancy.97-99 In addition, the absence of significant transfer of insulin lispro100 makes insulins the primary therapeutic choices for treatment of pregnant women with diabetes. However, insulin-binding antibodies have been detected in newborn infants whose diabetic mothers received insulin therapy. This is due to increased titer of antibodies in insulin-treated mothers and, the higher the antibody titer of the mother the greater is the total insulin in the fetal...

Undetected hypoglycemia

Despite years of meticulous study, there is still a paucity of information regarding the optimal level of glycemia in diabetic pregnancy which clinicians should target to safely reduce maternal and perinatal morbidity. Strict metabolic control in this patient population has been associated with an increased risk of maternal hypoglycemia. Rosenn et al.8 reported significant hypoglycemia, defined as hypoglycemia requiring assistance from another person, in 71 of gravid patients with Type 1 diabetes with a peak incidence in the first trimester. In our study, using CGM, in Type 1 gravid patients, hypoglycemic events were recorded in 76 of the patients, most of the episodes were nocturnal, some of them asymptomatic.18 Interestingly, in all cases, an interval of 1-4 h preceded clinical manifestations. When GDM patients were assessed, hypoglycemic events were recorded in 58 of the patients, all of them insulin-treated.28 The impact of maternal hypoglycemia on human fetal development and...

CSII decreases the rates of hypoglycemia

Hypoglycemia is a major problem in pregnant women,8 secondary to both the intensification of insulin treatment and to the decline of the counter-regulatory response to hypoglycemia during pregnancy. Rates of severe hypoglycemia has been reported to reach 71 of pregnant women, in whom glycemic goals were set at 100 mg dL fasting and 140 mg dL at 90 min post-meal by Rosenn et al.9 They found an overall incidence of 6.68 episodes per patient per pregnancy of severe hypoglycemia, equivalent to an incidence of 894 episodes per 100 patient-years. The DCCT trial reported fewer cases 58 cases of severe hypoglycemia per 270 pregnancies. CSII has been consistent in showing reduction in hypoglycemia while maintaining low HbA1c. Bode et al.10 demonstrated a significant reduction in major hypoglycemic events during the first year of CSII use when hypoglycemic rates decreased from 138 episodes per 100 patient-years to 22 episodes a reduction that was sustained for at least 4 years.10 An...

Protective response to hypoglycemia

Falling plasma glucose concentrations are sensed in the hypothalamus and other regions of the brain as well as in the hepatic portal vein and the carotid artery. Glucose sensing in visceral sites sends the information to the brain via the cranial nerve (especially vagous nerve) and, as a result of a complex integration within the brain, these signals are responsible for the autonomic response (sympathetic and parasympathetic) organized within the hypothalamus. Through mechanisms that include increased autonomic activity, hypoglycemia causes reduced pancreatic beta-cell insulin secretion and increased alfa-cell glucagon secretion. Hypoglycemia, involving hypothalamo-hypophyseal neuroendocrine mechanisms, also causes an increased secretion of growth hormone and adrenocorticotropin. The exact mechanism involved in this process is not well known. The glucokinase-mediated sensing in pancreatic beta-cells remains the best characterized mechanism of response to glucose falling. Similar...

Lack of awareness of hypoglycemia

The inability of patients to recognize impending hypoglycemia is a major clinical problem in the management of insulin treated diabetes and it represents an important barrier to tight metabolic control especially in patients that have been encouraged to treat their diabetes intensively. Lack of awareness of hypoglycemia is a common long-term complication of diabetes. Epidemiological surveys in unselected population have reported that around 25 of subjects with Type 1 diabetes experience persistent or intermittent difficulty in recognizing hypoglycemia.28 In diabetic people with a long history of diabetes a reduced autonomic activation in response to hypoglycemia cause a lack of neurogenous alarm symptoms (hypoglycemia unawareness). This can lead to severe hypoglycemic crises without the typical alarm signs. Awareness of hypoglycemia is largely the result of sympathetic neural, rather than adrenomedullary, activation. The exact mechanism of hypoglycemia unawareness is not completely...

Hypoglycemic attacks

In pregnancy, diabetic women become more liable to hypo-glycemic attacks than before pregnancy. If they are under tighter glycemic control than before pregnancy, then they may even become less aware of their hypoglycemic attacks than they were previously. It may therefore be thought reasonable to discriminate against such women in terms of the activities in which they are allowed to participate. However, an English court has recently ruled as illegal, under the Disability Discrimination Act 1995, a high school's attempt to ban a diabetic student from a watersports holiday in France, on the grounds that there had been hypoglycemic attacks when the student was on an earlier skiing trip.9 In England, if a pregnant woman commits a crime when she is hypoglycemic, this fact may provide a valid and sufficient defence in law, although not for all offences (see later). In the case of R v. Padmore,10 a diabetic committed the crime of homicide when in a state of hypoglycemic automatism. The jury...

Carbohydrate metabolism

Glucose is the primary energy source of fetoplacental tissues. During early pregnancy, basal plasma glucose and insulin levels and hepatic gluconeogenesis are unchanged.1 However, during late pregnancy, the mother develops hypoglycemia, which is specially manifest under fasting conditions, when the rate of gluconeogenesis from different substrates is enhanced.2,3 The use of different substrates for such increased gluconeogen-esis is variable the conversion of glycerol to glucose rather than other more classical gluconeogenetic substrates like pyruvate or alanine is specially intense.4 The development of maternal hypoglycemia despite the enhanced gluconeogenesis and the reduced consumption of glucose by maternal tissues, due to her insulin-resistant condition, is the result of the high rate of placental transfer of glucose, which is greater than that of any other substrate (Figure 5.1).5 This preponderance of placental transfer of glucose over other metabolites has been demonstrated in...

4 Psychiatric Medication Use Near Term

Some medications may produce toxicity or withdrawal effects in the newborn. These include the selective serotonin reuptake inhibitors (e.g., fluoxetine, paroxetine), which have been linked with neonatal jitteriness, respiratory distress, and hypoglycemia (19,20), and benzodiazepines (e.g., clonazepam, diazepam, lorazepam), which can produce excessive

Fetal Risk Summary

No other reports describing the use of acarbose during human pregnancy have been located. Less than 2 of a dose is absorbed systemically, but several metabolites are absorbed in much greater proportions, and the embryo or fetal risk from any of these is unknown. Acarbose is normally used in combination with oral hypoglycemic agents, and these hypoglycemic drugs are not indicated for the pregnant diabetic as they may not provide good control in patients who cannot be controlled by diet alone (3). Carefully prescribed insulin therapy will provide better control of the mother's blood glucose, thereby preventing the fetal and neonatal complications that occur with this disease. High maternal glucose levels, as may occur in diabetes mellitus, are closely associated with a number of maternal and fetal effects, including fetal structural anomalies, if the hyperglycemia occurs early in gestation. To prevent this toxicity, most experts, including the American College of Obstetricians and...

38 nutritional requirements for the active pregnant woman

The Dietary Reference Intakes (DRIs) for macronutrient and micronutrient intakes have not been defined for the active pregnant woman compared with those who are sedentary. Protein requirements in pregnancy have been estimated at 1.1 g kg day (71 g day for someone 163 cm tall, weighing 65 kg.), while in active people there is a slightly higher estimated requirement of 1.2 to 1.4 g kg body weight per day 43 . The 2005 Dietary Guidelines for Americans recommend 20-35 of calories from fat, with most coming from polyunsaturated and monounsaturated fatty acids, while limiting intake of saturated fats to less than 10 of calories and keeping trans fatty acids as low as possible. Fat intake should not be restricted to less than 15 of energy requirements because fat is important not only as a source of calories, but also to aid in the absorption of fat-soluble vitamins and provides essential fatty acids 44 . Carbohydrate intake of 40-55 of energy requirements is needed to replace the muscle...

Fetal glucose transporters

GLUT1 is found throughout the fetal tissues and on all endothelial cells, and probably accounts for the majority of basal tissue glucose uptake from the fetal plasma. GLUT4 is found in the heart, adipose tissue, and skeletal muscle. In the fetal sheep, the GLUT1 protein concentration is up-regulated by hypoglycemia and hypoinsulinemia in skeletal muscle and adipose tissue, while there is no change in the brain.30 In contrast, hyperglycemia appears to down-regulate GLUT1 protein concentrations in most tissues. Insulin-responsive GLUT4 protein is up-regulated by hypoglycemia, but in response to hyperglycemia it is initially up-regulated and then down-regulated to normal or less than normal levels in skeletal muscle and adipose tissue.31,32 Acute hyperinsulinemia increases the whole fetal glucose utilization rate, principally in the heart and skeletal muscle,14 and decreases the fetal plasma glucose concentration,8 but it has been difficult to demonstrate in which organs this increased...

Kinetics of the glucose utilization rate in the fetus

In this situation, substrate supply (amino acids, glucose, fatty acids and triglycerides, and glycerol) is probably as or more important than insulin itself. The capacity for glucose utilization in the human fetus can only be estimated from measurements in prematurely born infants or in animal models such as the sheep. In preterm humans, doubling or even tripling of glucose utilization rate (GUR) from basal is possible.34 GUR in fetal sheep follows MichaelisMenten kinetics,8 and is relatively limited to a doubling of basal GUR. This capacity is variable, however, as increased entry of glucose into the fetal plasma from the placenta increases fetal glucose concentration and insulin secretion, which, in turn, augments fetal glucose utilization, thus limiting further increases in the fetal glucose concentration. Glucose and insulin clamp experiments in fetal sheep, in which glucose or insulin or both are infused until GUR reaches maximal rates, have shown that plasma...

Fetal insulin secretion

Fatty acids also stimulate fetal insulin secretion their concentrations are increased in pregnant diabetics and in their fetuses in late gestation, perhaps contributing to augmented fetal insulin secretion.43 Acute and chronic hypoglycemia, and probably hypoaminocidemia as well, diminish fetal insulin secretion.36 Responsible mechanisms are not known, although presumably glucose activates insulin gene response elements, and both glucose and amino acids are necessary to develop mechanisms that regulate insulin secretion from the pancreatic beta cell. In contrast to such variable hyperglycemic conditions that generally augment insulin secretion, sustained hypoglycemia usually diminishes fetal insulin secretion. For example, in fetal sheep in late gestation, fetal hypoglycemia produced by insulin infusion into the mother, produces normal to increased fetal pancreatic islet insulin content, but reduced fetal GSIS. Because these islets have normal glucose metabolism, ATP-activated...

Fetal amino acid uptake

Amino acids are actively concentrated in the trophoblast intracellular matrix by Na+ K+-adenosine triphosphate-(ATP)ase- and H+-dependent transporter proteins at the maternal-facing microvillous membrane of the trophoblast and then transported into the fetal plasma producing fetal-maternal plasma concentration ratios ranging from 1.0 to 5.0.77,85 This active transport process is decreased by hypoxia and hypoglycemia in vivo.86,87 In vivo studies also show that many amino acids are directly transported across

Kinetics of glucose uptake and transport by the placenta

Chronically hypoglycemic pregnant sheep in which fetal glucogenesis develops,9 thereby contributing glucose molecules to the fetal glucose pool and sustaining fetal glucose utilization at near-normal rates. As a result, the placental-to-fetal glucose concentration gradient and the placental-to-fetal glucose transfer rate are relatively reduced under these circumstances, uteroplacental glucose consumption is maintained at near-normal rates for the level of maternal glycemia. Thus, fetal glucose production can compensate for reduced maternal glucose supply and sustain placental as well as fetal glucose utilization requirements.

Birthweight criteria for normal fetal growth

The criteria for normal fetal growth are population specific, based on issues reviewed earlier. Therefore most reports describe fetal growth in relationship to population percentiles, most usually less than 10th centile as SGA or small for gestational age, 10th to 90th centile as AGA or appropriate or average for gestational age and LGA for large for gestational age, i.e. birthweight greater than the 90th centile. These may be further delineated for gender and race. IUGR usually implies a neonate that is SGA and in addition has evidence of decreased intrauterine growth such as an increased head to abdominal ratio (asymmetric IUGR) or physiologically hypo-glycemia at birth. At the other end of the birthweight spectrum, infants are often classified as macrosomic or overgrown if fetal weight is greater than 4000 g, although some define macrosomic if birthweight is greater than 4500 g. However, it has become apparent in the last 10 years that these criteria used to classify birthweight...

Can treatment of GDM improve adverse outcome

It is also unclear if the data were analyzed with the intent to treat group. Drexel et al.77 reported their efforts to prevent perinatal morbidity in GDM by tight metabolic control. Insulin therapy was initiated without a trial of diet alone if one or more values during the OGTT was 200mg dL. The therapeutic goals were capillary blood glucose concentration

Racial distribution of gestational diabetes mellitus

Recently, Silva et al.7 reported on ethnic differences in perinatal outcome of GDM. Neonates born to Native-Hawaiian Pacific-Islander mothers and Filipino mothers had four and two times the prevalence of macrosomia, respectively, compared with neonates born to Japanese, Chinese, and Caucasian mothers. These differences persisted after adjustment for other statistically significant maternal and fetal characteristics. Ethnic differences were not observed for other neonatal or maternal complications associated with GDM, with the exception of neonatal hypoglycemia and hyperbilirubinemia. the authors concluded that this finding emphasizes the need to better understand ethnic-specific factors in GDM management and the importance of developing ethnic-tailored GDM interventions to address these disparities.

Impaired glucose tolerance as a risk factor of adverse outcome

Nasrat et al.49 examined pregnancy outcome in 212 women with IGT and 212 women with normal glucose tolerance. They found a higher mean age and higher parity in the IGT group. The babies in this group also had higher birthweights, lower levels of capillary blood glucose and higher hematocrit. Nevertheless, the proportion of babies with birthweights 2 standard deviations (SD) above the mean, neonatal capillary blood glucose 28 mg dL and hematocrit 65 was equal in the two groups. Therefore, the authors concluded that IGT does not lead to any adverse outcome. Similar findings were reported by Ramtoola et al.,50 who failed to find an excess perinatal mortality in 267 pregnant women with IGT compared with a background population. The mean birthweight was significantly higher in the babies born to women with GDM and gestational IGT than in the background population, but not in the babies of women with pregestational diabetes. The incidence of macrosomia was highest in the GDM group and it...

Early gestational diabetes mellitus diagnosis as a risk factor

Early onset of GDM is a high-risk factor. Bartha et al.64 found that among 3986 pregnant women, those with early-onset GDM (n 65) were more likely to be hypertensive (18.46 vs. 5.88 , P 0.006), have higher glycemic values and greater needs for insulin therapy (33.85 vs. 7.06 , P 0.001) than those in whom diabetes developed later (n 170). All cases of neonatal hypoglycemia (n 4) and all perinatal deaths (n 3) were in this group. The women with early GDM also had an increased risk of postpartum diabetes mellitus, whereas those

Cognitive development in children of diabetic mothers

The research group at Northwestern University, Chicago, tested 73 pre-existing and 112 GDM infants for the relationship between maternal fasting plasma glucose and hemoglobin A1c during the second and third trimesters on neonatal performance on the Brazelton Neonatal Behavioral Assessment scale. The Brazelton scale has gained wide asseptance as one of the premier instruments for integrative characterization of nervous system function in the newborn.52 They found a significant correlation between glycemic control in three out of the four newborn behavioral dimensions on the scale. In each case, poor glycemic control was followed by a poor Brazelton rating of the neonate. The results were no different when gestational diabetic and pre-gestational diabetics were analyzed separately. Attribution of results to various prenatal events such as asphyxia, neonatal hypoglycemia or differences in socioeconomic status or ethnicity could not be made. Although the authors...

39fuel utilization in exercise and pregnancy

Measurements by indirect calorimetry reveal preferential use of carbohydrates during exercise in pregnancy 53 . The respiratory exchange ratio (RER) reflects the ratio between CO2 output and oxygen uptake (VO2). The RER provides information on the proportion of substrate derived from various macronutrients. For carbohydrate to be completely oxidized to CO2 and H2O, one volume of CO2 is produced for each volume of O2 consumed. An RER of 1 indicates carbohydrates are being utilized, while an RER of 0.85 indicates mixed substrate. Assessment of fuel utilization during pregnancy is important because of the possible effect of exercise-induced maternal hypoglycemia 53 . Such events are unlikely to occur during 45 min of moderate exercise, but could occur after 60 min of continuous moderate to strenuous exercise (Fig. 3.2). The tendency for higher respiratory exchange ratios during pregnancy and during exercise in pregnancy suggests a preferential utilization of carbohydrates. Soultanakis et...

Is there an associated increased adverse outcome in GDM

The infants of GDM women are at an increased risk for stillbirth and aberrant fetal growth (macrosomia and growth restriction) as well as metabolic (e.g. hypoglycemia and hypocal-cemia), hematological (e.g. bilirubinemia and polycythemia) and respiratory complications that increase neonatal intensive care unit admission rates and birth trauma (e.g. shoulder dystocia)19,20 (Table 14.1). Hypoglycemia The adverse outcomes most commonly associated with GDM include increased perinatal mortality, macrosomia, shoulder dystocia, birth trauma, pre-eclampsia, Cesarean section, neonatal hypoglycemia, hypocalcemia, hyperbilirubinemia, and polycythemia. In addition, there are long-term effects Clinicians must, therefore, consider the merits of establishing the diagnosis of GDM. Gestational diabetes, if untreated or not recognized, may be associated with an increased risk of intrauterine fetal death and commonly reported morbidities such as macrosomia, birth trauma, neonatal hypoglycemia,...

232 Selective adrenergic agonists

Adverse reactions in the fetus and the newborn (tremors, tachycardia, hypoglycemia, and hypokalemia) have been reported, especially when high doses of 32-agonists are used. The effects are less common when used by inhalation, and they are reversible. Raker and Flanagan reported a case of maternal and fetal tachycardia after inadvertanl inhalation of high doses of albuterol for 24 hours in week 33 (Baker 1997). The heart rale became normal after the discontinuation of albuterol.

Glucose alterations in gestational diabetes mellitus

To the delivery of a large baby, mainly both maternal perineal damage and birth trauma, including shoulder dystocia, Erbs palsy, etc. The hyperinsulinism remains in the newborn period and increases the risk of hypoglycemia, once the umbilical supply of glucose is suddenly arrested after delivery. Because of this process, the newborn will need frequent monitorization of blood glucose, early feeds and occasionally may require the intravenous administration of glucose. Hypoglycemia in the newborn, if not corrected, may lead to brain damage.41 Fetal macrosomia also increases the risk of obesity, Type 2 diabetes mellitus and cardiovascular diseases later on in life.42,43

Diagnostic oral glucose tolerance test

The primary objective was to specifically and independently determine associations between maternal glycemia and the risk of adverse pregnancy outcome. In a much smaller study, Gilmer and Beard reported values for area under the curve of a 2-h OGTT that could predict risk of neonatal hypoglycemia.64

Possible mechanisms of action of diabetes on the early embryo

Hyperglycemia induced excessive cell death in the ICM of rat blastocysts, which was characterized mainly by nuclear fragmentation. It was shown that these cells contain a large amount of the clusterin transcripts, a gene associated with apoptosis. The over-expression of clusterin in blastocysts of STZ diabetic rats indicates that these embryos may be affected by subtle disruptions in the expression pattern of critical developmental genes.16 Similar to the previous study, blasto-cysts from diabetic rats and mice showed increased nuclear chromatin degradation in the ICM cells.17,18 These and other studies demonstrate that in pre-implantation embryogenesis, hyperglycemia triggers increased apoptosis, especially at the blastocyst stage. Maternal hyperglycemia caused a decrease in the expression of facilitative glucose transporter genes such as GLUT1, GLUT2, and GLUT3, which was associated with the reduction in glucose transport to the embryo and a decrease in intra-embryonic free...

2823 Thiazide diuretics

Hydrochlorothiazide, chlorthalidone, mefruside, bemetizide, ben-droflumethiazide, butizide, chlorazanil, clopamide, indapamide, metolazone, polythiazide, quinethazone, trichlormethiazide, and xipamide are bcnzthiazide derivatives whose action depends on the Inhibition of absorption of sodium and chloride in the distal tubule area. These drugs cause a potassium loss and lead to a reduction in the plasma volume In addition, they inhibit the excretion of uric acid. Benzthiazides are well-absorbed in the intestinal tract and are excreted unchanged in the urine. They cross the placenta and, when they are given sub partu, can lead to electrolyte changes (hyponatremia, hypokalemia), to thrombopenia, and to reactive hypoglycemia in the newborn as a result of their diabetogenic effect on the mother. In addition, prolonged labor has been described as a result of the inhibitory action on the smooth muscles.

910monitoring and evaluation

At each prenatal visit, eating disorders screening may be conducted (see Table 9.4) along with measurement and documentation of parameters or outcomes related to nutrition interventions and diagnoses. Body weight and rate of weight gain should be tracked and evaluated. Adjustments in energy intake should be based on appropriateness of weight changes. Eating behaviors and dietary intake should be examined at each prenatal visit to assess the adequacy of dietary composition and patterns of intake. Changes in purging and nonpurging behaviors should be noted and addressed. Fingersticks to check hematocrit and glucose may be useful in the monitoring of iron status and hypoglycemia or hyperglycemia. In women with established eating disorders, urinalysis may detect starvation or dehydration as noted by urinary ketones, elevated specific gravity, and alkaline urine. Vital signs will show any change in general health status. Glucose tolerance testing should be conducted in the 24th to 28th...

Gestational diabetes mellitus

Daily blood glucose self-monitoring (SMBG) appears to be superior to intermittent office monitoring of plasma glu-cose.10 For women treated with insulin, various evidence indicates that postprandial monitoring is superior to pre-prandial monitoring. De Veciana et al.11 showed that postprandial glucose measurements were significantly better for predicting a lower daily insulin dose, HbA1c level, birthweight, and a reduced risk for Cesarean section, large for gestational age, and neonatal hypoglycemia. The most effective insulin regime for insulin therapy during pregnancy consists of four injections per day. In 1999, Nachum et al.41 compared the twice daily insulin injection regimen versus four daily in a cohort of more than 400 pregnant women with diabetes. They showed that a regime of four daily insulin injections improved metabolic control and perinatal outcomes better than the twice daily injections moreover, the intensified therapy did not increase the risk of hypoglycemia in the...

Pregestational diabetes

The desired outcome of the preconception phase of care is to lower HbA1c values to a level associated with optimal development during organogenesis. Epidemiological studies indicate that HbA1c test values up to 1 above normal are associated with rates of congenital malformations and spontaneous abortions that are not greater than rates in nondiabetic pregnancies. However, rates of each complication continue to decrease with even lower HbA1c test levels. Thus, the general goal for glycemic management in the preconception period and during the first trimester should be to obtain the lowest HbA1c test level possible without undue risk of hypoglycemia in the mother. In 2003 the ADA stated that the goal for metabolic control in diabetic pregnant should be less than 1 above the upper limit of the normal range.75 To obtain these values, there is need for an appropriate meal plan, self-monitoring of blood glucose (SMBG), self-administration of insulin and self-adjustment of insulin doses,...

Fetal complications of maternal hyperglycemia

Uncontrolled hyperglycemia primarily affects fetal growth on both extremes of the normal growth curve. In those diabetic mothers that have advanced vascular disease, fetal growth deceleration may occur due to placental insufficiency. Fetal growth deceleration is defined as those in lower 5th percentile on a growth curve adjusted for gestational age.18,19 Macrosomia defined as an absolute birthweight of greater than 4000-g or greater than the 90th percentile (adjusted for gender, ethnicity, and gestational age). Cesarean sections often must be performed when the baby is at term to reduce the risk of birth trauma such as Erb's palsy or Klumpke's paralysis.20 Cesarean sections also adds risk to the mother's health. As explained by the Pederson hypothesis,21 the effects of an intrauterine environment of hyperglycemia and hyperinsulinemia include hypoglycemia, organ developmental problems (especially gastrointestinal), erythrocytosis, iron redistribution, calcium and magnesium...

Glucose toxicity and the role of postprandial hyperglycemia

Fetal hyperinsulinemia may cause increased fetal body fat (macrosomia) and, therefore, a difficult delivery, or cause inhibition of pulmonary maturation of surfactant and, therefore, respiratory distress of the neonate. The fetus may also have decreased serum potassium levels caused by the elevated insulin and glucose levels, and may therefore have cardiac arrhythmias. Neonatal hypoglycemia may cause permanent neurological damage. There is also an increased prevalence of congenital anomalies and spontaneous abortions in diabetic women who are in poor glycemic control during the period of fetal organogenesis, which is nearly complete by 7 weeks postconception.

1042 Complications Associated with Preexisting Diabetes

Second- and third-trimester fetal complications include macrosomia, neonatal hypoglycemia, neonatal hypocalcemia, hyperbilirubinemia, polycythemia, respiratory distress syndrome, preterm delivery, and stillbirth. With the exception of stillbirth, other complications are more closely associated with infant morbidity than mortality. Neonatal hypoglycemia is a fetal serum glycemic level 65 at delivery, could lead to perinatal asphyxia. The risk of these conditions decreases if the mother maintains optimal glycemic control throughout pregnancy.

Definition of normoglycemia based on infant outcome

Previously, glucose control and targets for treatment were based on clinical judgment and concern for hypoglycemia. In fact, most clinicians preferred to maintain hyperglycemia rather than increase the risk of a hypoglycemic reaction. As tools and techniques improved to achieve near-normal glucose levels during pregnancy, the emphasis has changed to strive for the degree of maternal metabolic control that is associated with normal body size and proportions in full-term infants. Hellmuth et al.53 found that the frequency of hypo-glycemia, especially nocturnal hypoglycemia, was seen with a prevalence of 37 in the first trimester of pregnancies treated with intensified insulin therapy. Sacks et al.53 studied 48 Type 1 and 113 Type 2 diabetic women during pregnancy. They found that the mean glucose levels were higher in the Type 1 patients and at least one daily glucose level was

Oral antidiabetic agents Classification and characteristics

Can serious postprandial and fasting hypoglycemia be minimized because the drug duration of action is short enough or its dependence on plasma glucose levels sufficient Sulfonylureas have been used in the treatment of Type 2 diabetes since 1942 because of their capacity to cause hypo-glycemia by stimulating insulin release from pancreatic beta cells. Sulfonylureas bind to specific receptors on beta cells forcing closure of potassium adenosine triphosphate (ATP) channels and opening of calcium channels that cause an increase in cytoplastic calcium that stimulates insulin release. The major effect of these drugs is to enhance insulin secre-tion.26-31 Sulfonylureas may also further increase insulin levels by reducing hepatic clearance of the hormone, the main contributor to fasting hyperglycemia. Enhanced insulin secretion diminishes glucose toxicity and improves insulin secretion after meals, thus reducing postprandial hyperglycemia. These drugs can also enhance peripheral tissue...

Algorithms for management using continuous glucose monitoring

Kaufman et al.30 demonstrated that CGM could serve as a clinical tool for clinical decision-making and glycemic control in children with Type 1 diabetes. In another recent work, Hershkovitz et al.31 demonstrated the clinical implications of CGM use to assess and manage asymptomatic hypoglycemic events in children with glycogen storage disease. Jovanovic has showed that CGM profiles allowed the physician to identify glucose patterns and to better target diabetic treatment. In a pilot study, Yogev et al.33 studied eight women with diabetes in pregnancy, of whom six were Type 1 and 2 were GDM. Data derived from the CGM for 72 h were assessed and treatment was adjusted on the basis of the findings. Two to four weeks later, the patients were re-evaluated with CGM. In the second time period, a significant reduction in mean blood glucose, hypoglycemic events and duration of undetected hyperglycemia was demonstrated. Recently, Kerssen et al.34 reported that since there is a wide variability...

Insulin requirements during pregnancy

When a woman is pregnant, she must avoid both hypoglycemia and hyperglycemia. Severe hypoglycemia has been associated with an increased risk of maternal death.3 Hyperglycemia on the other hand, while it does not have an immediate affect on the mother, can have drastic affects on the fetus. Near the end of the first trimester of pregnancy, maternal insulin needs decrease. This decrease in insulin requirement was first noted by Jorgen Pedersen,1 who warned other physicians to be aware of hypoglycemic events in women with diabetes, as it might be a sign of pregnancy. While the insulin requirements drop in the end of the first trimester, the woman becomes more insulin resistant and will require increasing amounts of insulin to maintain glucose control throughout the remainder of the pregnancy.5 The amount of insulin required will almost double by the end of the third trimester.5

During diabetic pregnancy

In pregnant women with diabetes (Types 1 and 2) good metabolic control before and during pregnancy is essential to reduce maternal-fetal morbidity and mortality. To obtain and maintain an optimal daily glycemic profile and HbA1c levels to near normal values during pregnancy, women with diabetes are at increased risk of severe hypoglycemic episodes. Rosen and co-workers5 have reported that in a cohort of 84 pregnant women with Type 1 diabetes, 71 have had significant episodes of hypoglycemia requiring assistance from another person. The peak of incidence occurred from the 10th to 15th week of gestation and blood glucose fluctuations were more frequent in women who have experienced severe hypoglycemia, independently of HbA1c levels. In another observation performed in 55 Type 1 diabetic women,6 a prevalence of nocturnal hypoglycemic episodes (blood glucose

21717 Eye nose and ear drops

The carbonic anhydrase inhibitors brinzolamide, dorzolamide, and for systemic application, acetazulatnide, which are used for glaucoma therapy, have not been systematically studied. A new born of 34 weeks' gestation was tachypnoic, and a combined respiratory-metabolic acidosis, hypoglycemia, and hypokalemia was diagnosed. Its mother had been treated with 750 mg azetazolamide daily during the 3 days prior to delivery. There was 2.9pg ml in the blood of the newborn when this was measured 5 hours after birth - almost a therapeutic concentration (3-10 ig ml). There was no substance detectable on day 11. Further development of the child was uneventful (Ozawa 2001). There were no birth defects or postnatal disorders observed in the newborn of 12 women using, on average, 500 mg azetazolamide daily for idiopathic increased intracranial pressure. Nine of them were exposed during the first trimester (Lee 2005).

Diabetic retinopathy and perinatal outcome

Several investigators have addressed the issue of a possible relationship between diabetic retinopathy and perinatal outcome. Moloney et al.131 noted that maternal retinal hemorrhages or neovascularization were associated with increased infant morbidity. McElvy et al.147 performed a prospective study of 205 pregnant women with Type 1 diabetes. Development or progression of retinopathy during pregnancy was significantly associated with reduced fetal growth, manifested by lower mean birthweight and a higher rate of small for gestational age (SGA) and low birthweight (LBW) infants. There was no correlation between progression of retinopathy and gestational age at delivery, preterm delivery, respiratory distress syndrome, neonatal hypoglycemia, or neonatal death.

Counseling women with diabetic nephropathy

Careful counseling of the woman and her partner of the risk for herself and the newborn is important before the couple can take a well-considered decision regarding pregnancy. An updated diabetes status including hemoglobin A1c, risk of hypoglycemia, degree of retinopathy, serum creatinine, blood pressure, and proteinuria is necessary to estimate the risk for complications during pregnancy. The number of antihypertensive drugs to control the blood pressure sufficiently prior to pregnancy is also of importance, since there has to be room for further intensification of antihypertensive treatment in late pregnancy, if necessary.

Clinical manifestations

The clinical manifestations of neonatal hypoglycemia in IDM and IGDM are not specific, and there is no pathogno-monic sign. Symptoms may be neurologic (tremor, jitteri-ness, high-pitched cry, eye-rolling, convulsions), respiratory signs (cyanosis, tachypnea, apnea), cardiac-related (tachycardia, cardiomegaly, cardiac failure), digestive (refusal to feed), or metabolic (hypothermia, sweating), alone or in combination. However, many infants, even those with very low plasma glucose levels, are asymptomatic, probably because of the initial brain glycogen stores, although the exact biochemistry is still unclear. The characteristics of neonatal hypoglycemia in IDM are very early onset (first hour after birth) generally asymptomatic, non-recurrent and good response to i.v. glucose.9 However, some cases have been reported even after the first 24 h.13 There is no well-defined method for predicting which new-borns will have severe hypoglycemia, so all IDM and IGDM must be screened after birth....

Non Chromosomal Syndromes Associations and Sequences

Beckwith Wiedemann Syndrome

Another example of an infant with the typical macrosomia (birthweight of 3950 g), polycythemia (hematocrit 66 ) and hypoglycemia. Note the macroglossia, nevus flammeus over the glabellar region and the eyelids, and the prominent eyes with relative infraorbital hypoplasia. Figure 3.2. Another example of an infant with the typical macrosomia (birthweight of 3950 g), polycythemia (hematocrit 66 ) and hypoglycemia. Note the macroglossia, nevus flammeus over the glabellar region and the eyelids, and the prominent eyes with relative infraorbital hypoplasia.

Pump use during labor and delivery

Maintaining euglycemia during the peripartum is essential for the prevention of neonatal hypoglycemia. When the pregnant diabetic woman enters active labor the insulin requirements fall drastically while the glucose infusion rate necessary to maintain a blood glucose level of 70-90 mg dL was found to be constant at 2.55 mg kg min.39 Protocols for maintaining euglycemia during labor are usually based on i.v. infusion of glucose, to maintain glucose consumption, and low rate of insulin (1-4 U h) with no more subcutaneously administered insulin. The low rate of insulin required can be administered by the pump using a temporary fixed basal rate. Feldberg et al.,40 in a small trial, showed a decrease in neonatal hypoglycemia using CSII compared with an intravenous regimen. The choice between i.v. insulin protocol and continuation of CSII depends on the familiarity with insulin pumps and the practice at the maternity ward.

Breastfeeding and maternal diabetes

Although maternal hypoglycemia does not cause a reduction in breast milk lactose level, it does lead to increased secretion of epinephrine, which inhibits milk production and the ejection reflex. In addition, elevated acetone levels can be expressed in breast milk, placing stress on the newborn liver.55 As a result, the diabetic mother should be well instructed in order to achieve the right adjustment of diabetes to lactation, and to understand the issues of diet and insulin. These problems are not related to breastfeeding per se but to the overall management of diabetes.

Adverse perinatal outcome

Maternal hyperglycemia with resultant fetal hyperinsulinemia is central to the pathophysiology of diabetic complications in pregnancy. The infants of GDM women are at a 3 to 8 fold increased risk for stillbirth and aberrant fetal growth (macrosomia and growth restriction) and metabolic (eg, hypo-glycemia and hypocalcemia), hematologic (eg, bilirubinemia and polycythe-mia), and respiratory complications that increase neonatal intensive care unit admission rates and birth trauma (eg, shoulder dystocia) 7,8 .

Factors related to intrauterine growth

To further study the role of maternal blood glucose levels during pregnancy on fetal growth, Scholl et al.17 studied the influence of maternal blood glucose levels in nondiabetic women on the birthweight of their offspring. They found that mean weight of newborns increased by 50 g with maternal blood levels of 99-130 mg and by 200 g if blood levels were above 130 mg . However, higher maternal blood glucose levels were associated with a higher rate of pregnancy complications. On the other hand, maternal hypoglycemia was associated with reduced birthweight of term infants. All these studies show that hyperglycemia increases fetal weight and emphasize repeatedly the importance of good glycemic control during diabetic pregnancy.

Fetal assessment by ultrasound

Two trials were identified which sought to answer the question as to whether ultrasound could help to identify pregnant women with diabetes who were likely to benefit from an intervention. Buchanon et al.1 used the third trimester ultrasound to measure the fetal abdominal circumference in women with mild gestational diabetes mellitus (GDM). If the fetal abdominal circumference was large ( 75th centile), women were randomized either to continue with their diet or to start insulin in addition to their dietary therapy 59 women completed the study but no serious clinically important adverse outcomes were reported (Table 51.2). Rossi et al.2 also started insulin therapy when ultrasound measurements of the fetal abdominal circumference exceeded the 75th centile in women with mild, diet-controlled GDM 73 women had an ultrasound fetal abdominal circumference measurement at 28 and 32 weeks gestation, and 68 women had a single measurement at 32 weeks. There were no maternal hypoglycemic...

A Nausea and Vomiting Morning Sickness

(1) One of the most common discomforts of early pregnancy is possibly due to high levels of humanchorionic gonadotropin (HCG) or progesterone, cultural expectations, emotional factors, and hypoglycemic reaction as a result of increased basal metabolism due to the 24-hour a day fetal and maternal body functions, especially after a period of fasting (from night to morning). (a) Eat a high-protein snack at bedtime if it's a hypoglycemic attack.

Costeffectiveness of alternative approaches to diagnosing and treating GDM

Three studies have assessed the cost-effectiveness or cost-benefit of interventions in GDM. In one, the Northern California program, reimbursed charges were applied to the clinical outcomes of a prospective randomized trial of preprandial or postprandial blood glucose monitoring in GDM.33,34 GDM was treated with insulin in all 66 women. Although mean gestational ages at delivery were similar, the postprandial monitoring group had lower glycohemoglobin levels, significantly lower birthweights, less macrosomia, less neonatal hypoglycemia and fewer Cesarean deliveries.34 The program costs per case of GDM were slightly higher in the postprandial blood glucose monitoring group ( 3800) than in the preprandial blood glucose monitoring group ( 3600), but outcome costs per case of GDM were lower in the postprandial monitoring group ( 7500) compared to the

Blood glucose monitoring devices

The evaluation should include the analysis of the mean difference of the device reading, with respect to a reference procedure at low, medium and high blood glucose concentrations. Other items of the evaluation will include customer acceptability (size, weight, portability, calibration, duration of a test performance, economic cost). Then, a validation protocol using an adequate sample size of recruited patients will follow, covering a wide range of blood glucose levels from the hypoglycemic range to extreme hyperglycemia. Non-invasive or minimally invasive continuous monitoring of blood glucose is a high priority (both to detect unsuspected hypoglycemia and as a further step in the development of an artificial pancreas), allowing automatic measurement of blood glucose and adjustment of insulin administration (Figure 53.7). Transcutaneous sensors and implanted sensors use multiple detection systems enzymatic (e.g. glucose oxidase), electrode,...

461 preceptor blockers

Circulatory symptoms and hypoglycemia have been cited from time to time in connection with the intake of i-S-rcceptor blockers via mother's milk. In contrast to the experience with subpartu administration, such an effect is not very probable. Nevertheless, acebutolol, atenolol, and sotalol should be viewed critically because the low protein binding and primarily renal excretion allow for the possibility

Certification of diabetics

The present author has recently been involved in one such case. A family doctor had signed this certificate for a diabetic patient, but he signed negative answers to these two questions. He failed to mention that 5 years previously the patient had caused a motoring accident in which a heavy truck was driven through the central reservation of a major motorway, and that the episode was attributed to hypoglycemia. Thus, the doctor had signed false entries on the driving licence application, which misled the Driving and Vehicle Licensing Authority into issuing another heavy goods vehicle licence. A few months later the driver had a more serious trucking accident in which three people were killed two adults and one child. Again, this accident was attributed to hypoglycemia. On this occasion the driver was imprisoned for causing death by dangerous driving.

Breast Feeding Summary

Chlorpropamide is excreted into breast milk. Following a 500-mg oral dose, the milk concentration in a composite of two samples obtained at 5 hours was 5 pmg mL (G.G. D'Ambrosio, personal communication, Pfizer Laboratories, 1982). The effects on a nursing infant from this amount of drug are unknown, but hypoglycemia is a potential toxicity. 1. Smoak IW. Embryopathic effects of the oral hypoglycemic agent chlorpropamide in cultured mouse embryos. Am J Obstet Gynecol 1993 169 409-14. 2. Zucker P, Simon G. Prolonged symptomatic neonatal hypoglycemia associated with maternal chlorpropamide therapy. Pediatrics 1968 42 824-5. 8. Elliott B, Schenker S, Langer O, Johnson R, Prihoda T. Oral hypoglycemic agents profound variation exists in their rate of human placental transfer. Society of Perinatal Obstetricians Abstract. Am J Obstet Gynecol 1992 166 368. 9. Elliott BD, Schenker S, Langer O, Johnson R, Prihoda T. Comparative placental transport of oral hypoglycemic agents in humans a model of...

4119 Insulin and oral antidiabetics

Neither glibenclamide nor glipizide were detected in the breast-milk of three mothers. Hypoglycemia was not observed in any of the children. In another eight women receiving a single dosage of gliben clamide, no substance was found in milk. A high protein-binding of 98 could explain these results (Feig 2005). Only small amounts of metformin are found in mothers' milk the weight-adjusted dose for a fully breastfed child is 0.1-0.7 (Briggs 2005, Gardiner 2003, Hale 2002). Hypoglycemia was not reported in breastfed infants. Metformin concentrations in breast milk remained stable over the time of observation. Growth, motor-social development, and illness requiring a pediatrician's visit were assessed in 61 nursing infants (21 male, 40 female) and 50 formula-fed infants (19 male, 31 female) born to 92 mothers with polycystic ovary syndrome (PCOS) taking a median of 2.55 g metformin per day throughout pregnancy and lactation. At 3 and 6 months of age, the weight, height, and motor-social...

Etiology of perinatal mortality

Later in pregnancy, maternal hyperglycemia is translated into fetal hyperplasia of pancreatic islet cells and hyperinsu-linemia. Pedersen and colleagues29,30 linked this to early neonatal hypoglycemia. A series of studies by Salvesen et al.31,32 demonstrated that hyperinsulinemia is related to cord blood acidemia and hypoxemia. It is suggested that hypoxemia and academia are related to increased rates of stillbirth and neonatal death observed in the diabetic population. Furthermore, insulin has an anabolic effect on muscle and adipose tissue linked to fetal macrosomia.32,33 Macrosomia in its turn is related to increased risk of PNM and shoulder dystocia.34

Rabin Medical Center Petah Tiqva Israel

This major book gives a comprehensive review of the epidemiology, science and clinical management of gestation diabetes. Fully updated and revised, it contains new chapters on Fetal growth in normal and diabetic pregnancies Genetics Congenital anomalies Exercise Pharmacological management Insulin pump therapy Hypoglycemia The role of ultrasound for timing of delivery Thyroid and pregnancy Fetal origins of adult disease Metabolic syndrome and diabetes following gestational diabetes mellitus Psychological and social aspects

Glycated serum proteins

Main findings from the RCT demonstrated that patients with Type l DM managed by SBGM at home obtained similar results regarding glycemic control to those patients under intensive control in the hospital. Maternal and fetal outcomes were also similar in both groups. Women preferred lower use of the hospital and home management with SBGM. Particularly for GDM, monitoring blood glucose after meals, rather than before, contributed to better metabolic control and better fetal outcomes (there were fewer Cesarean sections for cephalopelvic disproportion, fewer cases of macrosomia and large-for-gestational-age infants, and fewer episodes of neonatal hypoglycemia).49 In addition, women who utilized SBGM were less likely to require hospital admission, leading to a substantial cost saving.

Images Of Pseudohermaphrodites

Images Pseudohermaphrodites

Micropenis with a normal scrotum in an infant who presented with severe hypoglycemia. This combination should alert one to the diagnosis of hypopituitarism. There is a higher incidence of hypopituitarism in patients with a variety of midline defects. Hypopituitarism was confirmed in this infant.

Ascites In Small Babies

People With Caudal Regression Syndrome

Classic facies of an infant of a diabetic mother. Note the shaved scalp with multiple venipuncture sites resulting from the need for intravenous glucose for hypoglycemia which occurs commonly in these infants. Therapy may also be required for hypocalcemia and hypomagnesemia.

Insulin infusion pumps

Insulin pumps during pregnancies complicated by diabetes are still in its infancy. Kitzmiller et al.58 showed that insulin pump therapy did improve glucose control and minimized clinically significant hypoglycemic events to 2.2 week. Coustan et al.59 then reported a randomized clinical trial of insulin pump therapy versus conventional therapy in pregnancies complicated by diabetes. They showed that there were no differences between the two treatment groups with respect to outpatients mean glucose levels, symptomatic hypoglycemia or HbAlC levels. Potter et al.57 studied continuous insulin infusion in the third trimester of eight pregnancies complicated by diabetes. Compared to historical controls, they concluded that diurnal variations of blood glucose concentrations were dampened. Leveno et al.62 performed a case controlled trial of insulin pump therapy versus literature intensified conventional therapy, and observed no significant differences between the groups for glucose control,...

Neurological and psychological development

Reports of long-term neurological deficits in the offspring of diabetic mothers include impaired visual motor function, Erb's palsy, seizure disorders, cerebral palsy, mental retardation, speech disturbances, reading difficulties, behavior disturbances and deafness.57-63 Mechanisms potentially involved in the occurrence of such problems are (1) birth trauma, especially trauma to the head and neck because of large infant size and shoulder dystocia 64 (2) prolonged, severe neonatal hypoglycemia, which may damage the central nervous system with potentially permanent deficits 65 (3) neonatal hyperbilirubinemia, which leads to kernicterus 57 and (4) abnormal fuel metabolism during gestation, which may cause long-term aberrations in neurological and psychological development.

Use of rapidacting insulin analogs in pregnancies complicated by diabetes

Postprandial glucose control in the patient with GDM is important to neonatal outcome.6-8 The Diabetes in Early Pregnancy (DIEP) Study identified 28.5 of infants from diabetic mothers who were 90th percentile in infant birth-weights.8 The birthweight in this 28.5 correlated positively with fasting blood glucose and A1C. When adjusted for fasting blood glucose and A1C, the nonfasting blood glucose concentration in the third trimester was an even stronger predictor of infant birthweight and fetal macrosomia. Combs et al.7 confirmed these findings, as they associated macrosomia with higher postprandial glucose concentrations obtained between weeks 29 and 32 of gestation. In addition, they described a higher risk of small-for-gestational-age (SGA) infants in those with lower (120 mg dL) was significantly lower in the lispro group. Overall metabolic control also improved significantly in the insulin lispro group, which showed the greatest absolute decrease in A1C levels as compared to the...

Problems with and solutions for the artificial pancreas

The main reason for the difficulty in finding a precise algorithm is two periods of delay associated with a closed-loop artificial pancreas. The first is the delay in the time it takes to obtain a reading from the subcutaneous glucose-monitoring device. This primary delay creates a difference between the true value of the capillary glucose in current time and the value that the glucose sensor reads in the interstitial fluid. If the sensor takes a measurement every 5 min (common for current continuous glucose monitoring systems), the capillary and interstitial glucose levels could be different by as much as 10 mg dL. While 10 mg dL is hardly a reason for much concern, the algorithm that controls the insulin pump may think blood glucose levels are still rising after a meal when in fact they have begun to fall. If the measurement of the sensor is not accurate to the time, the insulin pump could deliver the wrong amount of insulin, and cause either hypoglycemia if too much insulin is...

2159 Diabetes mellitus and pregnancy

Neonatal morbidity include macrosomia (an extremely large newborn) with immature organ functions or hypotrophy, and postpartum metabolic derangements of the newborn - especially hypoglycemia. Insulin action changes during the course of pregnancy. At 10-14 weeks' gestation, insulin sensitivity is slightly increased however, it then declines for the rest of the pregnancy, with insulin resistance being highest late in the third trimester, insulin sensitivity rebounds with the delivery of the placenta. In cases of pre-existing diabetes, these changes contribute to a degree of hypoglycemia in the first trimester and increased insulin requirements during later pregnancy, and reinstitution of the pre-pregnancy insulin requirement after delivery.

Prevalence Of Diabetes And Fertility

The reported prevalence of neonatal hypoglycemia in diabetic pregnancy varies because of variations in the definition of the disorder this is in addition to differences in methods of glucose examination, maternal control of diabetes during pregnancy and labor, and neonatal treatment, particularly feeding. It is not surprising in the light of these great variations that the previous figures for neonatal hypoglycemia in infants of diabetic mothers (IDM) have only historical significance. During the last 10 years, in well-controlled diabetic mothers and using the 'operational definition' of neonatal hypoglycemia, 1. Hypoglycemia the prevalence of early neonatal hypoglycemia was still high, particularly in those mothers who were long-standing diabetics. In 2000, Agrawal et al.10 reported 47 prevalence, but they used a threshold of only 2 mmol L (c. 34 mg ). Cordero et al1 noted a 47 prevalence in macrosomic IDM (Type 1) but only 20 in non-macrosomic infants. In infants of gestational...

Support for the fetal insulin hypothesis from monogenic diabetes studies

There has been strong evidence for the principle that genes resulting in monogenic diabetes have a large impact on fetal growth. In addition to the observation of glucokinase, which acts on glucose sensing (see above), there is also greatly reduced birthweight in mutations that reduce insulin secretion or action. The impact n fetal growth on monogenic diabetes mutations are outlined in Table 61.3. When hyperglycemia is detectable soon after birth due to reduced insulin secretion (e.g. Kir6.2 neonatal diabetes) it is not surprising that there is also reduced insulin secretion in utero and hence low birth-weight.42 More striking is that mutations in HNF-1P are associated with a 800g reduction in birthweight despite diabetes not usually developing until early adult life (Edghill and Hattersley, personal communication). This observation is compatible with the role of HNF-1P in pancreatic stem cells43 which is supported by loss of function mutations resulting in reduced pancreatic size and...

Insulin sensitivity and resistance in pregnancy

The development of resistance to the glucose-lowering effects of insulin is a normal phenomenon of pregnancy. In a pioneer study, Burt et al.10 demonstrated that pregnant women experience fewer hypoglycemic events in response to insulin infusion than non-gravid women. Accordingly, later research found women with normal pregnancies had progressively exaggerated insulin responses to ingested glucose, together with a slightly decreased glucose tolerance.11,12 Using the IVGTT model, Buchanan et al.13 and Cousins et al.14 demonstrated a significant (70 ) reduction in insulin sensitivity during the second trimester of normal pregnancy, with a return to normal values shortly after delivery. Ryan et al.2 were the first to report quantitative differences in insulin sensitivity between normal and diabetic pregnancies. Other researchers noted that insulin sensitivity was lower in patients with GDM than in patients with normal pregnancies at 12-14 weeks of gestation, before the point of maximal...

Recreational And Sports Activities

Ketosis and hypoglycemia are more likely to occur during prolonged strenuous exercise in pregnancy. Because of nausea, vomiting, or the feeling of fatigue that is prevalent in pregnancy, women may be unable to run long distances. In pregnancy, we advise the recreational athlete to reduce mileage to no more than 2 miles per day. This is a precautionary step intended to prevent complications such as hyperthermia or dehydration. Studies of women who averaged between 1.5 and 2.5 miles per day throughout pregnancy have shown no deleterious effects (6.7).

Treatment of Mood Disorders During Pregnancy

Other studies attribute the symptoms to antidepressant withdrawal. Case reports of neonatal withdrawal in neonates exposed to paroxetine have been published and describe transient symptoms of irritability, excessive crying, increased muscle tone, feeding problems, sleep disruption, and respiratory distress (Costei et al. 2002 Dahl et al. 1997 Nordeng et al. 2001 Stiskal et al. 2001). In a prospectively ascertained sample of 55 neonates exposed to paroxetine proximate to delivery (dose range 10-60 mg median 20 mg), 22 (n 12) had complications necessitating intensive treatment (Costei et al. 2002). The most common symptoms included respiratory distress (n 9), hypoglycemia (n 2), and jaundice (n 1), all of which resolved over 1-2 weeks without specific intervention. The extent to which other SSRIs (with longer half-lives) demonstrate similar risk for neonatal toxicity has yet to be explored. Furthermore, it is crucial to investigate other factors that modulate vulnerability to neonatal...

The early years

However, one could not expect White to have understood all that is known today about the biology of diabetic pregnancy, and she did not. She admitted, 'The cause of overgrowth of the fetus of the diabetic is not known,' although she certainly recognized the problem. Fifty-six per cent of Joslin patients' infants had birthweights 8 lb, compared with 9 of a control series presumably 8 lb, or c. 3600 g, represented infants large for gestational age (LGA) or the ninetieth cen-tile). She noted that 'The greatest growth of the embryo occurs in the last two months, at a time when the blood sugar is often normal,' which it surely was not. Another statement, now known to be wide off the mark, was 'Congenital defects are beyond our therapeutic control and are, we believe, related to a disease which is genetic in origin.' She later revised her opinion and in 1958 said that 'The 3 per cent mortality due to congenital anomalies can perhaps be lowered by avoiding such causes of anoxia as acidosis...


Maternal metabolic adaptations during pregnancy are mainly directed to maintaining a continuous availability of substrates to warrant fetal growth. Glucose, used as a primary energy source of fetoplacental tissues, is quantitatively the most important substrate crossing the placenta. During late pregnancy the mother develops hypoglycemia as a result of the high rate of placental transfer, despite of enhanced gluconeogenesis and reduced consumption of glucose. Amino acids cross the placenta against the gradient thanks to an active process. Fetal growth is sustained by the transfer of amino acids from maternal circulation. Protein metabolism changes gradually throughout gestation, and although during late pregnancy there is increased nitrogen retention, the mother develops hypoaminoacidemia, which is specially evident during fasting. Fat depot accumulation and maternal hyperlipidemia are characteristic features of pregnancy. Maternal adipose tissue lipoly-tic activity is increased and...

The urinary tract

From around 8 weeks there may be an increase in the frequency of micturition, owing to pressure from the enlarging uterus and increased vascularity of the bladder. Urine will be checked regularly at antenatal visits for the presence of protein, glucose and ketones, which should not be present. Protein could indicate a possible infection (very common during pregnancy) or occasionally pre-eclampsia. Glucose could indicate diabetes, as could the presence of ketones, though this may just be the result of low blood sugar.

Glucose transporters

Confined primarily to the microvillous membranes of the syncytiotrophoblast where it logically might confer directionality of glucose flux across the trophoblast to the fetus, or at least ensure trophoblast glucose uptake when maternal and fetal glucose concentrations are reduced, as it has a greater affinity for glucose than GLUT1.21 Despite considerable study, the regulation of placental glucose transporter expression and activity remain poorly defined.22-24 Placental GLUT1 is acutely up regulated by hypoxia and hyperglycemia, while acute hypoglycemia leads to down regulation. Chronic changes in glycemia, both hyper- and hypoglycemia, generally are associated with diminished expression.22 Thus maternal hyper-glycemia causes a time-dependent decline in the entire placental glucose transporter pool (GLUT-1 and GLUT-3). In contrast, maternal hypoglycemia decreases GLUT-1 but not GLUT-3, resulting in a relatively increased GLUT-3 contribution to the placental glucose transporter pool,...

Fetal glucogenesis

Tracer studies in humans68 and sheep10 have shown that when glucose tracer is infused into the mother the specific activity or enrichment ratio of tracer (labeled) glucose to non-labeled glucose in the fetal plasma is the same as in the maternal plasma. This demonstrates that the only source of glucose in the fetus is from the maternal plasma, otherwise, new glucose production into the fetal plasma from either the fetus itself or from the placenta would dilute the tracer glucose coming from the mother along with unlabeled glucose, thus lowering the fetal enrichment ratio. Furthermore, studies in fetal sheep have shown that the net uptake of glucose by the fetus from the placenta invariably is equal to the fetal glucose utilization rate, independently measured with glucose tracers.69 Thus, there is no evidence for fetal glucose production under normal conditions. Also, there is little if any fetal glucogenesis under the conditions of short-term (1-4 h) changes in maternal and fetal...

The GDM controversy

Since the late 1960s when O'Sullivan first suggested the term 'gestational diabetes', controversy has continuously surrounded this clinical entity even though it is associated with adverse pregnancy outcome, i.e. macrosomia, birth trauma, and neonatal hypoglycemia. Regardless of these serious results, opinions and anecdotes have been more prolific than research generated data on this issue. There is no consensus regarding diagnostic criteria, the utility of universal screening, or the association of gestational diabetes with perinatal morbidity and mortality. For example, Jarrett2 concluded that GDM is 'a non-entity' whose only clinical association is with an increased maternal risk of subsequent diabetes.1 The Scottish Intercollegiate Guidelines Network (SIGN) published a document regarding the management of diabetes in pregnancy in 2001. They reiterated that there is as yet no consensus on the definition, management or treatment of GDM, or the most appropriate strategies for...

Management of GDM

Dietary control is very important not only for GDM patients, but also for normal pregnant women. The incidence of macrosomia is about 5-10 in most Chinese hospitals. If GDM is not detected and managed properly, the incidence of macrosomia could be as high as 50 . But if dietary control is carried out strictly, most patients do not need insulin therapy and the incidence of macrosomia could be greatly reduced. The ideal dietary control should provide the necessary nutrition to both mother and fetus, achieve well-controlled glucose levels, and avoid hypoglycemia and ketosis. The ideal body weight (IBW height - 100) should be calculated first, and the daily calorie requirement is calculated according to the standard of 30-35 kcal kg. The proportions of carbohydrate, protein, and fat are 40-50, 25-30, and 25-30 , respectively. In order to counter-balance the effects of day and night fluctuation of anti-insulin hormones of pregnant women, GDM patients are advised to have five meals a day....

2629 Quinine

Especially in the last part of pregnancy, severe maternal hypoglycemia has been induced by quinine therapy. Recommendation. In pregnancy, quinine can be used for therapy of acute chloroquine-resistant falciparum malaria. The potential risk for the fetus due to the therapy is much less than the hazards due to the severe maternal disease. Attention should be paid to possible maternal hypoglycemia. Even though embryotoxic effects due to quinine in analgesic compounds are not to be expected, these agents should be avoided because they do not conform to good therapeutical practice.

2827 Mannitol

Diuretics are no longer part of the standard therapy for hypertension and edema during pregnancy they should only be used for particular indications. In such cases, hydrochlorothiazide is the diuretic of choice. Furosemide can also be given when treatment of heart or renal failure requires a diuretic. When therapy is long term, the mother's electrolytes and hematocrit should be monitored and the development of oligohydramnios ruled out. If treatment is continued throughout the pregnancy, hypoglycemia in the newborn should be determined. Mannltol may be used during pregnancy when an osmotic diuretic is necessary. Other benzthiazide derivatives, ethacrynic acid, amiloride, triamterene, and aldosterone antagonists should be avoided during pregnancy. If therapy with aldosterone antagonists is absolutely necessary, spironolactone should be chosen. None of the diuretics is an indication for interrupting the pregnancy.

Morning Sickness

Morning sickness, nausea, occasional vomiting, tiredness, and exhaustion are common to about 70 of pregnant women. It is vital to manage morning sickness during your pregnancy, because vomiting can interfere with anti-epileptic drug intake, absorption, and compliance. Most nausea occurs during the first trimester and goes away during the second trimester. Morning sickness does not always happen in the morning. You can get morning sickness for no apparent reason, and at any time of day. For some women, it might last longer than the early stage of pregnancy. Some women experience morning sickness throughout the entire 9 months. No one understands exactly what causes morning sickness, but many factors are known to contribute to morning sickness, including low blood sugar, low blood pressure, hormonal changes, nutritional deficiencies (vitamin B6 and iron), nutritional excess (spicy, sugary, and refined foods), fatigue, and stress. Ginger has been thoroughly researched, and may be taken...


Most cases of primary AI are diagnosed before pregnancy. During gestation, a new diagnosis should be considered in a case with classic symptoms of excessive fatigue, malaise, weight loss, vomiting, orthostasis, abdominal pain, hyperpigmentation, or biochemical disturbance 30,39,40 . Hypoglycemia, salt craving, malaise, seizures, or even coma should prompt testing of the HPA axis in pregnancy. Persistent vomiting can be mistaken for hyper-emesis gravidarum, potentially leading to a fatal outcome if left undiag-nosed 40 . Biochemical disturbance with hyponatremia is characteristic however, this is usually more severe than the mild hyponatremia (5-mmol L decrease) that occurs in normal pregnancy. Severe hyponatremia or metabolic acidosis is associated with poor outcomes, including fetal death 33 . Hyperkalemia was reported to be absent in several cases of newly diagnosed primary AI during pregnancy. This may reflect the increase in the RAS, rather than the severity of adrenocortical...

107 medications

A common insulin regimen is rapid-acting or short-acting insulin before breakfast and dinner, or before each meal and intermediate-acting before breakfast and at bedtime. Intermediate-acting insulin is not usually injected before dinner because of possible nocturnal hypoglycemia.

1081Sick Day Rules

Hypoglycemia is a concern if the woman is ill and consuming inadequate calories. All pregnant women with preexisting diabetes should be aware of hypoglycemia symptoms, which range from sweating, blurred vision, nervousness, anxiety, headache, weakness, or in severe cases, seizures or unconsciousness. The treatment for hypoglycemia depends on the severity of the symptoms. Mild-to-moderate symptoms are treated with 15 g of carbohydrate if the blood glucose level is


Insulin requirements usually decrease after delivery and it is not uncommon for the woman to forego insulin for the first 1-2 days after delivery. Insulin adjustments are necessary to prevent hypoglycemia. There are no contraindications to lactation for the woman with diabetes, and women should be encouraged to breastfeed. The meal plan is adjusted to include additional snacks to avoid hypoglycemia, which may be more frequent during lactation. Women with type 2 diabetes and choosing to breastfeed are advised to continue insulin therapy for the duration of lactation 35, 50 . Oral antidiabetic agents may resume once breastfeeding is terminated or if the woman chooses to formula feed her infant.

32 Anticonvulsants

Heart rate decelerations (34) and withdrawal symptoms of irritability, jitteriness, feeding difficulties, and abnormal tone (41) have been reported in neonates in association with valproate use near the time of delivery. Other complications among neonates include liver toxicity (42) and hypoglycemia (43). Reductions in neonatal fibrinogen levels have also been reported (44).

In diabetes

The defense mechanisms against hypoglycemia are clearly impaired in Type 1 diabetes. In fact, insulin deficient (Type 1 and advanced Type 2) diabetic patients are not able to decrease insulin levels and the loss of glucagon response to hypoglycemia is the most common defect in these patients. Under these conditions, epinephrine remains critical for counter-regulation. However, many Type 1 diabetic patients, especially after recurrent hypoglycemia and in the presence of long-term diabetes (10-20 years), suffer from reduced responses of epi-nephrine. Therefore, Type 1 diabetic patients with combined defect of glucagon and epinephrine are at about a 6-fold increased risk for severe iatrogenic hypoglycemia during intensive insulin therapy.13 Hypoglycemia in Type 2 diabetes is less frequent than in Type 1 because of insulin resistance and intact counter-regulation, at least in patients with a short duration of diabetes. As the duration of diabetes increases and beta-cell function...

Type 1 diabetes

Inappropriate hyperinsulinemia, either absolute or relative, is the initiating cause of hypoglycemia in diabetes mellitus. Hyperinsulinemia is the rule in diabetes mellitus, both Type 1 and Type 2, because of the therapeutic delivery of insulin into the peripheral rather than portal circulation and because of the empirical algorithms used to administer insulin. Absolute hyperinsulinemia, due to excessive levels of circulating insulin because of an excess of dosage or irregularity of absorption, causes hypoglycemia more frequently during the hours preceding meals or in the first morning hours. Relative hyper-insulinemia is due to other conditions such as delayed or inadequate diet (especially as far as the range of carbohydrates is concerned), physical exercise, renal failure, excessive alcohol consumption, delayed gastric emptying. In these conditions usually hypoglycemia occurs after meals.20 Nevertheless, as reported by the DCCT, the hyperinsulinemia can explain only a part of the...

Type 2 diabetes

Type 2 diabetes is characterized by insulin resistance and persistent beta-cell function, which allows insulin secretion to decrease as blood glucose falls, and apparently intact counter-regulation. Consequently, as reported in the literature,14 the rate of severe hypoglycemia is lower than in Type 1 diabetes. However, the UKPDS study showed that the frequency of hypo-glycemia increases over the years with a prolongation of the duration of insulin treatment.23 Patients with advanced Type 2 diabetes and long duration of insulin treatment have reduced glucagon and sympathoadrenal response to hypoglycemia.14 In people with Type 2 diabetes hypoglycemia is often a consequence of the pharmacological treatments with hypoglycemic agents that stimulate pancreatic insulin secretion (sulfonylureas, glinides). Drugs that act on insulin sensitivity (metformin and glitazones) do not cause hypoglycemia.

Diabetic pregnancy

Hypoglycemia during diabetic pregnancy is certainly linked to the intensified insulin treatment useful to reach and maintain the targets of glycemic control recommended in these women. Low blood glucose levels can expose women to the risk of hypoglycemia. Moreover, the impairment of glucose counter-regulation16-18 and other features such as an increase in insulin sensitivity during the first trimester of gestation,24 are important in determining an increase in hypoglycemic episodes during pregnancy. It is well known that the need for insulin increases progressively during pregnancy reaching a maximum, with the largest fluctuations, during the third trimester. In this context, a reduced metabolic clearance of insulin in the third trimester, as reported by Bjorklund et al.25 can reduce the recovery from hypoglycemia. Finally, nausea and vomiting, common in the first trimester, can contribute to hypoglycemia by reducing the ingestion of carbohydrate (Box 32.1).


In classical textbooks, hypoglycemia is usually defined as a plasma glucose concentration below 50-55 mg dL (2.7-3 mmol L).26 However, the glycemic thresholds responsible for the activation of the counter-regulatory system is already evident at a plasma glucose concentrations of 65-70 mg dL (3.6-3.8 mmol L).27 Thus a physiological definition of hypo-glycemia could be any glycemia below 65 mg dL. In diabetic people symptoms of hypoglycemia may shift upwards or downwards depending on antecedent glycemic control. According to the entity of the clinical presentation, hypo-glycemia can be classified as symptomatic, light-moderate and severe hypoglycemia both in pregnancy and outside pregnancy. Symptoms of hypoglycemia, which are the same during pregnancy, are divided into two categories neurogenic and neuroglycopenic (Figure 32.2). Neurogenic (autonomic) symptoms are triggered by a failing in glucose levels and cause patients to recognize that they are experiencing a hypoglycemic episode....

Fetal consequences

A series of experimental studies in animals have demonstrated a teratogenic effect of maternal hypoglycemia occurring during the embryogenesis. The exposure, in vitro, of mouse embryos to hypoglycemic milieu even for short periods (2 h) in the first stages of embryogenesis, resulted in malformations. This could be explained by the fact that younger embryos are very sensitive to hypoglycemia because they are dependent on uninterrupted glycolisis and do not have developed the ability for aerobic glucose metabolism.30,31 Studies regarding a potential teratogenic effect of hypoglycemia in pregnant women are few. Impastato et al.,32 more than 40 years ago, reported that six out of 19 normal pregnant women who received insulin coma therapy, for psychiatric disorders, during the early phase of pregnancy, had malformed fetus. The following clinical studies evaluating the potential teratogenic effect of maternal hypoglycemia in diabetic patients, as reported in Table 32.1, showed no increase...


Diabetic people should be educated to identify correctly the alarm symptoms of hypoglycemia and to treat themselves promptly to prevent progression to neuroglycopenia. All hypoglycemic episodes, even in the absence of symptoms, require treatment. The goal of the treatment is to increase the blood glucose to a safe level to avoid clinical consequences. Relatives, friends, teachers, and co-workers should be taught to recognize symptoms of hypoglycemia and, where there is doubt, they must immediately treat the person who may have hypoglycemia. Mild-to-moderate hypoglycemia is usually treated with food, oral glucose tablets, or sucrose solutions. It is sufficient to administer 15-20 g of glucose as glucose tablets (3-5 g 10 kg body weight) or soft drinks containing pure glucose to raise blood glucose by 65 mg dL (3 mmol L). Fruit juice is absorbed more slowly than glucose and is not as effective in raising the blood glucose levels as tablets or liquid glucose. Likewise, honey is less...

21510 Insulin

The endocrinc part of the pancreas produces and secretes insulin, glucagons, and somatostatin. Insulin is necessary for storage of metabolic substrates such as glucose, fatty acids, and amino acids. Glucagon is important for the reverse regulation in hypoglycemia. There is less information on the use of insulin aspart during pregnancy. A multinational European study compared the maternal and fetal complications of type I diabetic pregnant women on regular insulin (Actrapid ) (n 165) and on insulin aspart (n 157). Similar numbers of live births, fetal losses, and congenital anomalies were reported in both groups, as well as similar rates of neonatal hypoglycemia and infant birth characteristics. Overall glycemic control was similar, as well as the maternal and obstetric complications during pregnancy (Hod 2006). The other insulin analogs, insulin glulisin, insulin detemir, and insulin glargine, have rarely been used in pregnancies to date. The long-acting insulin glargine might worsen...

Available techniques

Figure 36.1 Para 1, normal pregnancy, spontaneous onset at 39 weeks gestation, oligohydramnios plus decreased fetal movements noted by the mother. Emergency Cesarean section for fetal distress at 17 43. Female 2900 g, Apgar score 1-3-5, cord artery data not obtained, cord vein data - pH 7.29, pCO2 6.5 kPa, BDecf (base deficit in the extra cellular fluid) 2.5 mmol l. Initial ventilation by mask followed by intubation, meconium in upper airways. Adequate breathing at 25 minutes of age. Marked hypoglycemia (0.5 mmol l) initially. No sign of meconium aspiration or RDS (respiratory distress syndrome). Increased neuromuscular tone but normal electroencephalogram. No suctioning reflex initially. Normal behavior after 4 days. Discharged home after 15 days. Figure 36.1 Para 1, normal pregnancy, spontaneous onset at 39 weeks gestation, oligohydramnios plus decreased fetal movements noted by the mother. Emergency Cesarean section for fetal distress at 17 43. Female 2900 g, Apgar score 1-3-5,...

Risk factors

The degree of neonatal hypoglycemia in IDM is affected by several maternal and neonatal factors. Early postnatal blood glucose concentrations have been negatively correlated with maternal blood glucose concentrations at delivery and to cord plasma glucose levels. Hypoglycemia did not occur when the maternal blood glucose at delivery was less than 7.1 mmol L (c. 120 mg ).6 Maternal glycemic control during labor and delivery is also important early postnatal hyperglycemia has been described in infants whose nondiabetic mothers received i.v. glucose during labor.6 Neonatal risk factors include perinatal distress, small for gestational age, polycythemia, and individual susceptibility.


The most accepted explanation for the development of neonatal hypoglycemia in IDM is the Pedersen hypothesis or the maternal hyperglycemia-fetal hyperinsulinemia theory.5 This hypothesis claims that even in women under close observation, the episodic diurnal hyperglycemia characteristic of diabetes is the major factor predisposing the fetus to hyperglycemia because of the direct relationship between the maternal and fetal blood glucose concentrations. The fetal hyperglycemia stimulates the release of insulin by fetal islet cells, giving rise to persistent fetal hyperinsulinemia. After birth, the hyperinsulinemia and inadequate or absence of glucose intake lead to neonatal hypoglycemia. Fetal hyperinsu-linemia is also associated with suppression of plasma free-fatty-acid levels and hepatic glucose output. Other hormones may also play a role. Defective counteregula-tion by catecholamines and or glucagon (i.e. failure of their release in response to hypoglycemia) results in both...


Early diagnosis and prompt and adequate therapy are essential to prevent the late consequences of severe neonatal hypo-glycemia in IDM. Studies in both animals and humans clearly show that severe, prolonged neonatal hypoglycemia leads to acute neurologic injury, often with permanent sequelae. The neuropathological findings in hypoglycemic brain damage include acute degeneration of neurons and glia cells throughout the cerebral cortex and especially the occipital lobes.14 The damage involves layers 2 and 3 (in contrast to ischemia, which usually affects pyramidal cells in laminae layers 3 and 5-6).15 On computed tomography (CT) and magnetic resonance imaging (MRI), extensive cerebral loss can be seen, most marked in the occipital regions (in contrast to hypoxic-ischemic injuries, in which parasagittal 'watershed' areas are more evident in the frontal and parieto-occipital regions). Long-term follow-up data are still lacking on IDM in general and asymptomatic hypoglycemic infants in...


No correlation was found between the medical status of the newborn infants (i.e. hypoglycemia, increased or decreased birthweight) and outcome of any of the associated variables in the children born to diabetic mothers. This emphasizes the importance of the environment of the child in the development


The present authors have identified a further 26 trials focusing on the use of insulin, either comparing its use with diet alone or with no treatment, or in trials comparing different types of insulin, different regimes of delivery of insulin or comparing insulin with oral hypoglycemics.5,19-43 The population of pregnant women in these studies were either gesta-tional or pregestational diabetics. glycemia.22,30-33,35,36 The incidence ranged from zero to a high rate of hypoglycemia, with 0 in four studies,22,30,32,36 7 in Nachum et al.'s33 study, 12.5 in Nosari et al.'s31 study and the high rate of 36.4 in Coustan et al.'s35 study. It is most likely that these large differences reflect the varying definitions of severe hypoglycemia rather than any true differences in quality of care. This is the reason why severe hypoglycemia is defined by the authors as one that causes unconciousness. In the three studies with cases of severe hypoglycemia, Coustan et al.35 defined it as an episode of...

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