Seishi Furukawa

Circulatory disturbances during the first postnatal 24 hours in extremely premature infants 25 weeks or less of gestation with histological fetal inflammation.

Aim:  To investigate the effect of pre‐existing fetal inflammation on hemodynamics during the first postnatal 24 h in extremely premature infants ≤25 weeks of gestation.

Galantamine, an acetylcholinesterase inhibitor, reduces brain damage induced by hypoxia-ischemia in newborn rats.

Our aim is to elucidate whether galantamine, known as an acetylcholinesterase inhibitor, reduces brain damage induced by hypoxia‐ischemia (HI).

Activation of acetylcholine receptors and microglia in hypoxic-ischemic brain damage in newborn rats

OBJECTIVE We previously showed that acetylcholine receptor (AChR) agonist reduced hypoxic-ischemic brain damage in the newborn rats. To further investigated the interaction between hypoxia and chorinergic anti-inflammatory pathway, we examined the effect of AChR antagonist on brain damage and to see the relation between microglial activation and protective effect of AChR agonist. STUDY DESIGN Seven-day-old Wistar rats were divided into 2 groups, one receiving AChR antagonists to see if they have deleterious effects on hypoxic-ischemic brain damage, and the other receiving AChR agonist, carbachol, to investigate the emergence of microglia in the hippocampus. Rats were subjected to left carotid artery ligation followed by 8% hypoxia. Brains were analyzed histologically and immunohistochemically. RESULTS Antagonists of AChRs significantly enhanced brain damage in 1-h hypoxia-ischemia. In particular, the nicotinic AChR antagonist showed a marked enhancement of brain damage compared to the saline controls (p<0.01). The hippocampal CA1 was most vulnerable to any AChR antagonists, while the cortex was least vulnerable and only responsive to a higher dose of non-selective nAChR antagonist. Carbachol showed significantly less accumulation of microglia in the hippocampus than the saline controls (p<0.01) in hypoxia-ischemia. CONCLUSION An AchR-responsive pathway in the brain plays an important role in modifying perinatal brain damage, in which microglial accumulation may be involved.

Acetylcholine receptor agonist reduces brain damage induced by hypoxia-ischemia in newborn rats.

Objective: The newborn rat model has been developed to elucidate the mechanism and management of perinatal brain damage. Our study hypothesis is that an acetylcholine receptor agonist (carbachol) reduces hypoxia-ischemia (HI)-induced brain damage in a well-established newborn rat model. Study design: 7-day-old Wistar rats were divided into 3 groups at random: carbachol preinjection and HI (Carb/HI), saline preinjection and HI (Saline/HI), and only HI (HI). Rats were subjected to left carotid artery ligation followed by 2 hours of hypoxia (8% oxygen). We injected carbachol or saline before hypoxic loading. After 7 days, we checked for brain damage. Results: In the cerebral cortex, 25% of the Carb/HI group showed mild neural damage, and the remaining 75% showed no damage. In contrast, more than 80% of the Saline/HI and HI groups had severe neural damage. Similarly, neural damage significantly decreased in Carb/HI compared with Saline/HI and HI for CA1, CA2, CA3, and the dentate gyrus of hippocampal regions. Conclusion: Acetylcholine receptor agonist has a potent effect by reducing perinatal brain damage induced by HI in newborn rats.

Independent uterine contractions in simultaneous twin pregnancy in each horn of the uterus didelphys

The mechanism of synchronizing uterine contractions is not fully understood. We present a case of twin pregnancy in a uterus didelphys and objectively analyze the synchrony of bilateral uterine contractions. A 32‐year‐old woman, with a history of vaginal septal resection during her previous vaginal delivery, became pregnant with twins in a uterus didelphys in which each uterine horn had one fetus. At 37 weeks and 6 days, the first baby was delivered vaginally. The second baby was delivered by cesarean section due to recurrent late decelerations. Operative findings confirmed the didelphys uterus. We retrospectively reviewed the timing of contractions of both uteruses. The timing was determined by visual analysis as synchronous if both uteruses contracted within 5 s. Otherwise, contractions were considered solitary. Both uterine horns contracted independently in 90% of the incidence throughout labor and delivery. From this rare case of an ‘experiment by nature’, we speculated that the myometrium must be histologically connected in order to synchronize uterine contractions.

The impact of cesarean section on neonatal outcome of infants born at 23 weeks of gestation

OBJECTIVE Determine the impact of cesarean section (CS) on neonatal outcome of infants born at 23weeks of gestation. METHODS A retrospective study was performed involving 34 infants born at 23weeks and 91 infants born at 24-26weeks. Indications necessitating delivery were severe pregnancy induced hypertension, non-reassuring fetal heart rate patterns (NRFHRs), or intrauterine infection (IUI). Obstetrical indication for CS included NRFHR and breech presentation. Poor outcome included neonatal death or cerebral palsy. Univariate and multiple logistic analyses were performed to determine the effect of CS for obstetrical indications on poor outcome. RESULTS The incidence of poor outcome was significantly higher at 23weeks (number of poor outcomes/total number: 22/34) compared to that (31/91) at 24-26weeks (p<0.01). The incidence of a poor outcome was significantly higher at 23weeks for infants having NRFHR (11/16) compared to those at 24-26weeks (15/43, p=0.02). However, the incidence of a poor outcome was similar in infants with IUI (6/10 at 23weeks versus 5/11 at 24-26weeks, p=0.41). Vaginal birth in cases of obstetrical indication for CS at 23weeks was associated with higher risk of a poor outcome (odds ratio: 8.2). In contrast, the risk at 24-26weeks was not higher (OR, 0.8). After adjustment using variables of vaginal birth and IUI, vaginal birth significantly affected poor outcome (OR, 13.0). CONCLUSION Poor neonatal outcome was closely related to the mode of delivery, suggesting that CS for obstetrical indication at 23weeks may improve neonatal outcome.

Risk-Based Screening for Thyroid Dysfunction during Pregnancy

Objective. We conducted the study to see the incidence of thyroid dysfunction in women with obstetrical high-risk factors. Methods. We retrospectively reviewed medical charts of high-risk pregnant women who had examination for thyroid function during pregnancy. Women were divided according to clinical presentation, symptoms of thyroid disease and those with a personal history of thyroid disease (thyroid disease, n = 32), intrauterine growth restriction (IUGR, n = 115), diabetes mellitus (diabetes, n = 115), hypertension (n = 63), intrauterine fetal death (IUFD, n = 52), and placental abruption (abruption, n = 15). The incidence of thyroid dysfunctions including hyperthyroidism or hypothyroidism was compared. Results. The overall prevalence of thyroid dysfunction was 24.7%. The incidence of thyroid dysfunction in each group was as follows: 31% in thyroid disease, 25% in IUGR, 30% in diabetes, 27% in hypertension, 12% in IUFD, and 7% in abruption. Except IUFD, the incidence was not statistically significant from the group of thyroid disease (thyroid disease versus IUFD, P = 0.03 by χ 2 test). Thyroid disease represented for only 10% of all thyroid dysfunctions. Conclusion. Testing of women with a personal history or current symptoms of thyroid disease during pregnancy may be insufficient to detect women with thyroid dysfunction, who will become at high-risk pregnancy.

Fetal heart rate patterns related to neonatal brain damage and neonatal death in placental abruption

Aim:  The aim of this study was to determine the correlation between non‐reassuring fetal heart rate (NRFHR) patterns and poor neonatal outcome in placental abruption.

Perinatal death and neurological damage as a sequential chain of poor outcome

Objective: We investigated the risk factors of perinatal death and neurological damage. Methods: Perinatal death and neurological damage were retrospectively investigated using a population-based study of 108 024 deliveries from 1998 to 2007. Main factors studied were asphyxia, growth restriction and preterm delivery < 34 weeks of gestation, since these three factors were most often associated with poor prognosis. The impact of each factor was identified by multiple regression analyses. Results: There were 459 perinatal deaths (4.3/1000) and 220 neurological damages (2.0/1000). Preterm delivery accounted for 50% of perinatal deaths and neurological damage, whereas it constituted 2.6% of total births. Multiple regression analyses showed that prematurity < 34 weeks (10-fold), asphyxia (10-fold) and growth restriction (2-fold) were independent and significant risk factors associated with poor outcomes, and that the magnitude was similar throughout the three consecutive critical events of fetal death, neonatal death and neurological damage. Conclusions: Prematurity < 34 weeks, asphyxia and growth restriction are independent and persistent risk factors from perinatal death to neurological damage.

Is the Perinatal Outcome of Placental Abruption Modified by Clinical Presentation

Objective. The purpose of this study was to elucidate the impact of the clinical presentation on perinatal outcome in placental abruption. Study Design. A retrospective study was performed in 97 placental abruptions. Placental abruptions were classified according to clinical presentation: pregnancy-induced hypertension (HT, n = 22), threatened premature labor and/or premature rupture of membranes (TPL/ROM, n = 35), clinically low risk (LR, n = 27), and others (n = 13). Perinatal outcomes were compared among the HT, TPL/ROM, and LR groups. Results. The HT had significantly higher incidence of IUGR, IFUD, and low fibrinogen. The TPL/ROM had less severe disease. However, the LR had significantly higher incidence of IUFD, low UA pH < 7.1, low Apgar score of <7 at 5 min, and low fibrinogen. Conclusion. Disease severity in placental abruption is likely to depend on the clinical presentation.