[Shoulder dystocia: Guidelines for clinical practice--Short text]. / Dystocie des épaules : recommandations pour la pratique clinique--Texte court.

OBJECTIVES: To determine the available evidence to prevent and treat shoulder dystocia to attempt to decrease its related neonatal and maternal morbidity. MATERIALS AND METHODS: The PubMed database, the Cochrane Library and the recommendations from the French and foreign obstetrical societies or colleges have been consulted. RESULTS: Shoulder dystocia, defined as a vaginal delivery that requires additional obstetric maneuvers to deliver the fetus after the head has delivered and gentle traction has failed, complicates 0.5-1 % of vaginal deliveries. Risks of brachial plexus birth injury (LE3), clavicle and humeral fracture (LE3), perinatal asphyxia (LE2), hypoxic-ischemic encephalopathy (LE3) and perinatal mortality (LE2) are increased after shoulder dystocia. Its main risk factors are previous shoulder dystocia and macrosomia, but they are poorly predictive; 50 % to 70 % of shoulder dystocia cases occur in their absence, and the great majority of deliveries when they are present are not associated with shoulder dystocia. No study has proven that the correction of these risk factors (except gestational diabetes) would reduce the risk of shoulder dystocia (SD). Physical activity is recommended before and during pregnancy to reduce the occurrence of some risk factors for shoulder dystocia (grade C). In obese patients, physical activity should be coupled with dietary measures to reduce fetal macrosomia and weight gain during pregnancy (grade A). In case of gestational diabetes, diabetes care is recommended (diabetic diet, glucose monitoring, insulin if needed) (grade A) as it reduces the risk of macrosomia and shoulder dystocia (LE1). In order to avoid shoulder dystocia and its complications, only two measures are proposed. Induction of labor is recommended in case of impending macrosomia if the cervix is favourable and gestational age greater than 39 weeks of gestation (professional consensus). Cesarean delivery is recommended before labor in case of EFW greater than 4500g if associated with maternal diabetes (grade C), EFW greater than 5000g in the absence of maternal diabetes (grade C), history of shoulder dystocia associated with severe neonatal or maternal complications (Professional consensus), and finally during labor, in case of fetal macrosomia and failure to progress in the second stage, when the fetal head is above a +2 station (grade C). In case of shoulder dystocia, it is recommended not to pull excessively on the fetal head (grade C), do not perform uterine expression (grade C) and do not realize inverse rotation of the fetal head (professional consensus). McRoberts' maneuver, with or without a suprapubic pressure, is recommended in the first line (grade C). In case of failure, if the posterior shoulder is engaged, Wood's maneuver should be performed preferentially; if the posterior shoulder is not engaged, delivery of the posterior arm should be performed preferentially (professional consensus). It seems necessary to know at least two maneuvers to perform in case of shoulder dystocia unresolved by the maneuver of McRoberts (professional consensus). Pediatrician should be immediately informed in case of shoulder dystocia. The initial clinical examination should search complications such as brachial plexus birth injury or clavicle fracture (professional consensus). In absence of neonatal complication, monitoring of the neonate is not modified (professional consensus). The implementation of a practical training using simulation and concerning all caregivers of the delivery room is associated with a significant reduction in neonatal (LE3) but not maternal (LE3) injury. CONCLUSION: Shoulder dystocia remains a non-predictable obstetrics emergency. All physicians and midwives should know and perform obstetric maneuvers if needed quickly but without precipitation. A training program using simulation for the management of shoulder dystocia is encouraged for the initial and continuing formation of different actors in the delivery room (professional consensus).

Increasing incidence of abnormal glucose tolerance in women with prior abnormal glucose tolerance during pregnancy: DIAGEST 2 study.

AIMS: Mild blood glucose abnormalities during pregnancy may be linked to later glucose tolerance abnormalities or diabetes mellitus. Our aim was to determine the prevalence of diabetes mellitus (DM), impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) 6.75 years after delivery in women with differential blood glucose status during pregnancy. METHODS: We compared long-term outcomes among control women (n = 221), women with abnormal glucose tolerance during pregnancy (AGT; n = 322) and women with gestational diabetes (GDM; n = 466) who participated in DIAGEST 1. Women were recruited from 15 public maternity units in France. Clinical parameters could be determined in 155 control, 220 AGT and 338 GDM subjects. Rates of DM, IGT, IFG and 'Any Abnormality' were compared between the groups (American Diabetes Association criteria). RESULTS: Adherence to follow-up was 70.7%. Rates of DM, IGT and IFG were respectively 0.9% DM, 2.1% IGT and 3.6% IFG in the control group; rates in the AGT group were 6.3%, 11.3% and 6.3%. In GDM women, the rates of DM, IGT and IFG were, respectively, 18.0%, 13.4% and 8.5%. Predictors for DM were previous GDM, medical history of hypertension, age at delivery > or = 33 years, family history of diabetes, fasting glucose during pregnancy > or = 5.5 mmol/l and the severity of hyperglycaemia during pregnancy defined by the number of abnormal blood glucose values fasting, 1, 2 and 3 h during the glucose tolerance test at diagnosis of GDM. CONCLUSION: This study has identified a high prevalence of glucose tolerance abnormalities after AGT during pregnancy. Compared with GDM women, women with AGT have an intermediate risk of later diabetes.

Diabetes mellitus and dementia.

Alzheimer's disease (AD) and diabetes mellitus (DM) are two of the most common and devastating health problems in the elderly. They share a number of common features amongst which high prevalence after 65 years, important impact of patient's quality of life, substantial health care costs. Reviews on the epidemiological studies on cognitive impairment in patients with DM found evidence of cross-sectional and prospective associations between type 2 DM and moderate cognitive impairment, on memory and executive functions. There is also evidence for an elevated risk of both vascular dementia and AD in patients with type 2 DM, albeit with strong interaction of other factors such as hypertension, dyslipidaemia and ApoE genotype. DM is an independent predictor of post-stroke dementia. DM being an atherogenic risk factor, it may increase the risk of dementia through associations with stroke, causing vascular dementia. In addition, vascular reactivity may be adversely affected by advanced glycosylation end products resulting in more subtle perfusion abnormalities. Cerebrovascular disease may exacerbate AD through direct interactions between the two pathological processes or through cognitive impairment secondary to cerebrovascular disease "unmasking" AD at an earlier stage than it would otherwise become apparent. The increased risk of AD may also be mediated by the exacerbation of B-amyloid neurotoxicity by advanced glycosylation end products identified in the matrix of neurofibrillary tangles and amyloid plaques in AD brains, or associations with insulin functions. Decreased cholinergic transport across the blood-brain barrier observed in diabetic animals may exacerbate cognitive impairment in AD. Many interventions could reduce the cognitive decline associated with DM, yet not enough are taken into account so far.

[Iron overload and insulin resistance]. / Relations entre surcharges en fer et insulinorésistance.

There is increasing evidence that moderately elevated body iron stores, below levels commonly found in genetic hemochromatosis, may be associated with adverse health outcomes. Genetic hemochromatosis, characterized by transferrin saturation (TS) greater than 45%, is most often linked to homozygosity of the HFE C282Y allele. The phenotype is also modulated by mutations of more recently discovered genes (including ferroportin, hemojuvelin, hepcidin, and transferrin receptor) and environmental factors (including alcohol, viruses, diet, blood loss). Iron overload without hemochromatosis is characterized by high levels of serum ferritin and normal TS, as seen in dysmetabolic hepatosiderosis. Elevated serum ferritin levels predict incident type 2 diabetes in prospective studies and have been associated with hypertension, dyslipidemia, glucose tolerance disturbances, central adiposity, and metabolic syndrome. High ferritin levels are not synonymous with iron overload and may in some cases be a simple marker of insulin resistance.

[Epidemiological data and screening criteria of the metabolic syndrome]. / Données épidémiologiques et critères de dépistage du syndrome métabolique.

THREE DEFINITIONS: The metabolic or X syndrome is defined by an association of metabolic anomalies leading to an increased risk of cardiovascular complications. Today, there are at least 3 definitions of X syndrome: those of WHO, EGIR and NCEP. To varying degrees they associate increased abdominal fat, hypertension, glucose tolerance abnormality (ranging from hyperinsulinism to diabetes), and hypertriglyceridemia with low HDL cholesterol. FROM AN EPIDEMIOLOGICAL POINT OF VIEW: The prevalence of metabolic syndrome depends on the definition used and varies with the country or ethnic group considered. About 25% of the US and 10% of the French adult populations are concerned. THE RISK OF COMPLICATIONS: According to clinical trials, people with metabolic syndrome have a 2 to 4-fold increase in risk for coronary heart disease. Some of them have a particularly high risk (association of most features of the syndrome, association of an increased waist circumference and hypertriglyceridemia, presence of biological markers such as elevated C-reactive protein or microalbuminuria). Metabolic syndrome is also associated with a 4-fold increase in risk for developing diabetes.

[Insulin resistance physiopathology]. / Physiopathologie de l'insulinorésistance.

AMONG THE BIOLOGICAL MEDIATORS OF INSULIN RESISTANCE: two compounds released by the adipocyte are found, such as free fatty acids and tumor necrosis factor-alpha. They are incriminated in the deleterious role of visceral adiposity on the metabolic parameters. INTRA-CELL CORTISOL: Attention is also focused on the potential implication of cortisol in the genesis of metabolic syndrome, because cortisol is a potent antagonist of the effect of insulin and its presence in excess enhances visceral obesity and insulin resistance. GENETIC ASPECTS: Although no major locus has yet been identified, recent findings of several mutations or polymorphisms in genes acting in different regulation systems (adiponectin, PPARgamma2) also provide an interesting insight into the pathogenesis of this syndrome. Moreover, there is growing epidemiological evidence that intra-uterine factors could induce a so-called programming of the individual that may, at least in part, account for the difficulties encountered by the classical genetic approach.

[Treatment principles for the metabolic syndrome]. / Principes thérapeutiques du syndrome métabolique.

GENERAL PRINCIPLES: The general progression throughout the world in type 2 diabetes has lead medical Authorities to develop mass screening but also prevention measures, notably for "high-risk" subjects such as those exhibiting a metabolic syndrome. Studies on the topic have shown that preventing type 2 diabetes was possible via lifestyle changes, possibly in association with pharmacological therapy (metformine, acarbose, thiazolidinediones, orlistat). The other therapeutic stakes in the context of the metabolic syndrome also concern the management of all identified cardiovascular risk factors. REGARDING HYPERTENSION: there are currently no specific recommendations available in the framework of metabolic syndrome, with regard to lowering blood pressure and how to obtain it. However there is evidence that patients may benefit from the strict control of blood pressure (< or =130/85 mm Hg). REGARDING DYSLIPIDEMIA: LDL cholesterol remains the main target, with a goal depending on individual cardiovascular risk (<1 or 1.30 g/l in the case of metabolic syndrome). Statins are of major interest in this context. However, it is also established that normalisation of triglycerides and HDL cholesterol contributes to the improvement of cardiovascular Issues. The respective indications for fibrates or fibrate/statin associations still need to be defined in primary as in secondary prevention.