Neurodevelopmental outcome of late-preterm infants: Literature review.

Late-preterm infants are characterized by a birth term from 340/7 to 366/7 weeks of gestation. A foetal brain at 340/7 weeks of gestation weighs only 65% of the full-term newborn brain, which suggests a particular cerebral vulnerability to injury during this 6-week period. Epidemiological studies reporting the neurological outcomes of late-preterm infants exhibit large methodological heterogeneity that inhibits clarity on this issue. However, contradictory results and odds ratio values near neutral reveal probable moderate neurodevelopmental delay in late-preterm infants. This observation reflects the variable neurological outcomes of this population according to multiple perinatal factors. Therefore, the current challenge is to define efficient screening strategies to determine infants requiring specific follow-up.

[Biological monitoring and other explorations in the acute phase of a neonatal arterial ischemic stroke (excluding hemostasis)]. / Surveillance biologique et autres explorations à la phase aiguë d'un accident vasculaire cérébral ischémique du nouveau-né (hors hémostase).

Neonatal monitoring and other explorations required just after neonatal arterial ischemic stroke (NAIS) diagnosis remain elusive. This review attempts to propose guidelines on this topic. During neonatal period, three major contexts related to NAIS emerge: 1) Metabolic disorders including hypoglycemia; 2) Early post-natal infections; 3) Cardio-vascular anomalies. Different patient profiles have been defined (typical, atypical and at risk profiles). According to these profiles, a final decisional tree including biological monitoring and complementary explorations has been suggested to caregivers.

[Blood transfusion to pre-term neonates: What is new in the French guidelines since 2002?] / Transfusion de culot globulaire chez le nouveau-né grand prématuré : ce qui a changé dans les recommandations françaises depuis 2002.

This document updates the "Guidelines for the Administration of Blood Products: Transfusion of Infants and Neonates" published in 2002 by the French National Authority for Health (HAS). In doing so, it acknowledges changes in transfusion practices during the past decade, particularly with respect to safety issues and additional published transfusion-related guidelines. The major modifications concern irregular agglutinin screening indications before 4 months of age, a limitation of blood irradiation, and a non-recommendation for systematically checking for cytomegalovirus status. More precise thresholds for transfusion and an update of blood transfusion alternatives were also provided. Delayed cord clamping (>30s after birth) is recommended unless the neonate is asphyxiated and needs to be moved immediately for resuscitation.

[Neonatal arterial ischemic stroke: Review of the current guidelines]. / Accidents vasculaires cérébraux ischémiques artériels néonatals : synthèse des recommandations.

Neonatal arterial ischemic stroke (NAIS) is a rare event that occurs in approximately one in 5000 term or close-to-term infants. Most affected infants will present with seizures. Although a well-recognized clinical entity, many questions remain regarding diagnosis, risk factors, treatment, and follow-up modalities. In the absence of a known pathophysiological mechanism and lack of evidence-based guidelines, only supportive care is currently provided. To address these issues, a French national committee set up by the French Neonatal Society (Société française de néonatologie) and the national referral center (Centre national de référence) for arterial ischemic stroke in children drew up guidelines based on an HAS (Haute Autorité de santé [HAS]; French national authority for health) methodology. The main findings and recommendations established by the study group are: (1) among the risk factors, male sex, primiparity, caesarean section, perinatal hypoxia, and fetal/neonatal infection (mainly bacterial meningitis) seem to be the most frequent. As for guidelines, the study group recommends the following: (1) the transfer of neonates with suspected NAIS to a neonatal intensive care unit with available equipment to establish a reliable diagnosis with MRI imaging and neurophysiological monitoring, preferably by continuous video EEG; (2) acute treatment of suspected infection or other life-threatening processes should be addressed immediately by the primary medical team. Persistent seizures should be treated with a loading dose of phenobarbital 20mg/kg i.v.; (3) MRI of the brain is considered optimal for the diagnosis of NAIS. Diffusion-weighted imaging with apparent diffusion coefficient is considered the most sensitive measure for identifying infarct in the neonatal brain. The location and extent of the lesions are best assessed between 2 and 4 days after the onset of stroke; (4) routine testing for thrombophilia (AT, PC PS deficiency, FV Leiden or FII20210A) or for detecting other biological risk factors such as antiphospholipid antibodies, high FVIII, homocysteinemia, the Lp(a) test, the MTHFR thermolabile variant should not be considered in neonates with NAIS. Testing for FV Leiden can be performed only in case of a documented family history of venous thromboembolic disease. Testing neonates for the presence of antiphospholipid antibodies should be considered only in case of clinical events arguing in favor of antiphospholipid syndrome in the mother; (5) unlike childhood arterial ischemic stroke, NAIS has a low 5-year recurrence rate (approximately 1 %), except in those children with congenital heart disease or multiple genetic thrombophilia. Therefore, initiation of anticoagulation or antithrombotic agents, including heparin products, is not recommended in the newborn without identifiable risk factors; (6) the study group recommends that in case of delayed motor milestones or early handedness, multidisciplinary rehabilitation is recommended as early as possible. Newborns should have physical therapy evaluation and ongoing outpatient follow-up. Given the risk of later-onset cognitive, language, and behavioral disabilities, neuropsychological testing in preschool and at school age is highly recommended.

[Malignant pertussis and exchange transfusion]. / Coqueluche maligne et exsanguino-transfusion.

CASE REPORT: Malignant pertussis is a critical clinical state associated with fatal outcome in 70% of cases. The severity criteria are a lung infection with pulmonary hypertension and hyperleukocytosis usually above 50 G/L. We report the case of a 2.5-month-old girl hospitalized with critical pertussis in a pediatric intensive care unit. She had acute respiratory distress syndrome with pulmonary hypertension complicated by a bacterial secondary infection with Enterobacter cloacae managed by high-frequency oscillatory ventilation associated with pulmonary vasodilatation therapy. In the absence of clinical improvement and before considering extracorporeal life support, exchange transfusion was performed at day 9 to reduce hyperleukocytosis at 70 G/L. Exchange transfusion was successfully performed with a reduction of leukocytes to under 40 G/L followed by steady improvement of pulmonary function. Weaning from mechanical ventilation and discharge took place at day 23 and 38, respectively. COMMENTS: Exchange transfusion should be considered in infants suffering from malignant pertussis with extreme leukocytosis before hemodynamic failure to improve the survival prognosis.

[Atrial chaotic tachycardia during a respiratory tract infection due to NL63 coronavirus]. / Tachycardie atriale chaotique au cours d'une infection respiratoire à coronavirus NL63.

We report the case of a 3-month-old boy hospitalized with acute bronchiolitis. Respiratory distress was associated with cardiogenic shock caused by chaotic atrial tachycardia. The cause of bronchiolitis was a coronavirus NL63 viral infection, confirmed in nasopharyngeal aspirations. The patient required intensive care including diuretics (furosemide), anti-arrhythmic drugs (amiodarone and digoxin), and inotropic drugs (milrinone and levosimendan) associated with mechanical ventilation. The outcome was favorable in 10 days and the sinusal cardiac rhythm was completely restored at discharge.

[Long-term cerebral effects of perinatal inflammation]. / Conséquences cérébrales à long terme de l'inflammation périnatale.

Perinatal inflammation can lead to fetal/neonatal inflammatory syndrome, a risk factor for brain lesions, especially in the white matter. Perinatal inflammation is associated with increased incidence of cerebral palsy in humans and animal models and there is a strong relationship with increased incidence of autism and schizophrenia in humans. Perinatal inflammation causes acute microglial and astroglial activation, blood-brain barrier dysfunction, and disrupts oligodendrocyte maturation leading to hypomyelination. Inflammation also sensitizes the brain to additional perinatal insults, including hypoxia-ischemia. Furthermore, long after the primary cause of inflammation has resolved, gliosis may also persist and predispose to neurodegenerative diseases including Alzheimer's and Parkinson's disease, but this relation is still hypothetical. Finding of acute and chronic changes in brain structure and function due to perinatal inflammation highlights the need for treatments. As gliosis appears to be involved in the acute and chronic effects of perinatal inflammation, modulating the glial phenotype may be an effective strategy to prevent damage to the brain.

Gastrointestinal dysfunction in mice with a targeted mutation in the gene encoding vasoactive intestinal polypeptide: a model for the study of intestinal ileus and Hirschsprung's disease.

In 1970, Drs. Said and Mutt isolated a novel peptide from porcine intestinal extracts with powerful vasoactive properties, and named it vasoactive intestinal peptide (VIP). Since then, the biological actions of VIP in the gut as well as its signal transduction pathways have been extensively studied. A variety of in vitro and in vivo studies have indicated that VIP, expressed in intrinsic non-adrenergic non-cholinergic (NANC) neurons, is a potent regulator of gastrointestinal (GI) motility, water absorption and ion flux, mucus secretion and immune homeostasis. These VIP actions are believed to be mediated mainly by interactions with highly expressed VPAC(1) receptors and the production of nitric oxide (NO). Furthermore, VIP has been implicated in numerous physiopathological conditions affecting the human gut, including pancreatic endocrine tumors secreting VIP (VIPomas), insulin-dependent diabetes, Hirschsprung's disease, and inflammatory bowel syndromes such as Crohn's disease and ulcerative colitis. To further understand the physiological roles of VIP on the GI tract, we have begun to analyze the anatomical and physiological phenotype of C57BL/6 mice lacking the VIP gene. Herein, we demonstrate that the overall intestinal morphology and light microscopic structure is significantly altered in VIP(-/-) mice. Macroscopically there is an overall increase in weight, and decrease in length of the bowel compared to wild type (WT) controls. Microscopically, the phenotype was characterized by thickening of smooth muscle layers, increased villi length, and higher abundance of goblet cells. Alcian blue staining indicated that the latter cells were deficient in mucus secretion in VIP(-/-) mice. The differences became more pronounced from the duodenum to the distal jejunum or ileum of the small bowel but, became much less apparent or absent in the colon with the exception of mucus secretion defects. Further examination of the small intestine revealed larger axonal trunks and unusual unstained patches in myenteric plexus. Physiologically, the VIP(-/-) mice showed an impairment in intestinal transit. Moreover, unlike WT C57BL/6 mice, a significant percentage of VIP(-/-) mice died in the first postnatal year with overt stenosis of the gut.