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PubMed1993

Possible neuroprotective properties of flunarizine infused after asphyxia in fetal lambs are not explained by effects on cerebral blood flow or systemic blood pressure.

Neuroprotective properties of the calcium channel blocker flunarizine have been reported after hypoxic-ischemic insults in immature, infant, and adult rats. However, its effect on fetal regional cerebral blood flow (rCBF) and systemic blood pressure after severe asphyxia is not known. In 15 fetal lambs (3 to 5 d after surgery; gestational age at the experiment, 123.2 +/- 2.5 d), arterial oxygen content was progressively reduced to 30% by restriction of uterine blood flow with an inflatable balloon occluder around the maternal common internal iliac artery. The rCBF was measured with radioactive microspheres at baseline condition, after 1 h of severe asphyxia, and at 30 and 120 min in the recovery phase. Immediately after the end of the occlusion period, fetuses randomly received either flunarizine or its solvent (0.5 mg/kg estimated fetal weight). No differences in rCBF changes between groups were observed during and after asphyxia. Changes in arterial blood pressure or fetal heart rate due to flunarizine could not be demonstrated either. Only five fetuses (33%) survived this degree of asphyxia longer than 24 h: four of the flunarizine-treated group and one of the control group. It is unlikely that this possible protective property of the drug is caused by its influence on rCBF, arterial blood pressure, or fetal heart rate in the phase immediately after asphyxia.

Acid-Base Imbalance↗
PubMedDate not supplied

[Risk factors for neonatal asphyxia in neonates weighing more than 1000 grams]

OBJECTIVE: To evaluate some of the risk factors for neonatal asphyxia in neonates weighing more than 1000 grams. METHODS: In a population of 13.385 consecutive deliveries, from January 1991 to December 1994, 135 newborns with neonatal asphyxia were compared with 135 without the disease, in a casecontrol study, matched by birth weight, at the Neonatology Unit of the Pediatric Department of the Universidade Estadual de Campinas (UNICAMP). The statistical analysis employed was bivariate and multiple by logistic regression, and expressed as odds ratio (OR) with 95% confidence intervals. RESULTS: In the bivariate analysis, the factors significantly associated with asphyxia were: abruptio placentae [OR = 8.00 (1.07-353.4)], cesarean section [OR = 2.94 (1.64 -5.55)], breech presentation [OR = 3.33 (1.54 - 7.98)], abnormal fetal heart rates [OR = 4.88 (2.25-12.08)], prolonged rupture of membranes [OR = 4.33 (1.19-23.71)], a meconial hemorrhagic or infected amniotic fluid [OR = 9.00 (3.58 - 29.03)], oligohydramnios or polyhydramnios [OR =5.00 (1.88 - 16.76), use of anesthesia [OR = 2.56 (1.41 - 4.89)] and general anesthesia [OR = 14.00 (2.13 - 598.8)], male sex [OR = 2.06 (1.12 - 3.92)] and a gestational age of less than 37 weeks [OR = 3.29 (1.37 - 9.07). After multiple analysis, abnormal amniotic fluid, oligohydramnios or polyhydramnios, and anesthesia were the only factors associated with neonatal asphyxia, and more than six prenatal visits was a protector factor. CONCLUSIONS: Obstetrical, perinatal and neonatal clinical events are associated with neonatal asphyxia, that concerted efforts to provide adequate prenatal care, optimal assistance during delivery and birth, and appropriate neonatal intensive care should significantly reduce neonatal morbidity and mortality.

Journal Article↗
PubMed1984

Does glucose administration affect the cerebral response to fetal asphyxia?

This study was designed to test whether the fetal brain has an increased resistance towards asphyxia at high levels of blood-glucose, compared with low levels. 35 fetal sheep were exteriorized and investigated under general anesthesia. Cerebral blood flow (CBF) was estimated with the 133Xenon-washout method. Cerebral uptake of oxygen, glucose, and lactate was measured. Somatosensory evoked potentials (SEP) were recorded. The fetuses were subjected to controlled asphyxia by ventilating the ewes with gas mixtures low in oxygen. The blood sugar levels of the fetuses were varied over a four-fold range. During normal oxygenation of the fetus variations in the blood glucose concentration induced considerable changes in the cerebral glucose uptake, whereas CBF and oxygen uptake were unaffected. During asphyxia, hyperglycemia was associated with rapid development of acidosis and reduction in cerebral oxygen consumption together with deterioration of the neurophysiological characteristics of the brain. Far from being beneficial during asphyxia, fetal hyperglycemia appeared to reduce the tolerance of the fetal brain towards asphyxia. This report together with other evidence provides support for the view that extra glucose might be disadvantageous for the asphyxiated fetus.

Animals↗
PubMed1991

Effects of acute asphyxia on brain energy metabolism in fetal guinea pigs near term.

In a previous study we suggested that--unlike other forms of asphyxia--acute asphyxia caused by arrest of uterine blood flow is accompanied by a fall in oxygen delivery to the fetal brain (Jensen et al., 1987). This may change cerebral energy metabolism by causing an increase in the glycolytic rate. To test this hypothesis we studied the time course of the changes in the levels of high-energy phosphates and glycolytic intermediates in the cerebral cortex of unanaesthetized fetal guinea pigs near term before and after 2 and 4 min of acute asphyxia. During asphyxia there was a progressive fall of adenosine triphosphate, creatine-phosphate, glucose and fructose-1,6-diphosphate concentrations, whereas adenosine diphosphate, adenosine monophosphate and lactate concentrations increased. Pyruvate concentrations did not change. We conclude that fetal cerebral energy metabolism becomes increasingly anaerobic during acute asphyxia caused by arrest of uterine blood flow, because oxygen delivery to the fetal brain falls.

Animals↗
PubMed1990

Fetal asphyxia stimulates an increase in fetal plasma catecholamines and [Met]-enkephalin-arg6-phe7 in the late-gestation sheep fetus.

We have investigated whether enkephalin-containing peptides and catecholamines are increased in fetal plasma during periods of reduced uterine blood flow which produce moderate fetal asphyxia (i.e. hypoxemia, hypercapnia and acidemia). Experiments (n = 16) were performed in 11 ewes between 121-139 days gestation. In 8 experiments a clamp placed around the common iliac artery of the ewe was adjusted to produce a 50% reduction in the partial pressure of arterial oxygen (PO2) in fetal plasma for 30 min between 121-125 days gestation (n = 4) and between 131-139 days gestation (n = 4). Control (n = 8) experiments were performed when the arterial clamp was not adjusted. There was no significant effect of asphyxia on fetal plasma noradrenaline concentrations before 126 days gestation. After 130 days gestation during asphyxia, fetal plasma noradrenaline concentrations increased significantly from 2.20 +/- 0.72 pmol/ml (-15 min) to 14.06 +/- 0.75 pmol/ml (+5 min). The fetal adrenaline response to asphyxia did not change with increasing gestational age and after 130 days gestation fetal plasma adrenaline increased significantly from 1.48 +/- 0.46 pmol/ml (-15 min) to 4.05 +/- 1.22 pmol/ml (+10 min). Met-enkephalin-arg6-phe7 immunoreactivity was measurable (25-117 pg/ml) in all pre-experimental fetal sheep plasma samples collected between 121-139 days gestation. There was no specific effect of asphyxia on fetal plasma [Met]-enkephalin-arg6-phe7-IR before 130 days gestation. However after 130 days gestation, there was a significant increase in fetal plasma (Met-enkephalin Arg-6-phe7-IR above baseline values, when compared to control experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Lung liquid secretion, flow and volume in response to moderate asphyxia in fetal sheep.

The effects of moderate fetal asphyxia, induced by constriction of the maternal common internal iliac artery, on lung liquid secretion, tracheal fluid efflux and lung liquid volume have been investigated in unanaesthetized fetal sheep (111-142 days) in utero. During periods of fetal asphyxia the percent oxygen saturation, PO2, pH, and PCO2 of fetal carotid arterial blood changed from 57.2 +/- 1.3% (mean +/- SEM), 22.9 +/- 0.6 mmHg, 7.35 +/- 0.01 and 45.6 +/- 1.0 mmHg to 26.3 +/- 0.5% (P less than 0.001), 14.7 +/- 0.2 mmHg (P less than 0.001), 7.28 +/- 0.02, (P less than 0.001) and 47.8 +/- 0.4 mmHg (P less than 0.02), respectively. Fetal asphyxia, over 6 h, decreased the efflux of tracheal fluid from 7.07 +/- 0.47 ml/h to 3.97 +/- 0.36 ml/h (P less than 0.01) and, over 4 h, decreased the rate of lung liquid secretion from 9.42 +/- 1.76 ml/h to 4.91 +/- 1.54 ml/h (P less than 0.005), whereas it had no significant effect on lung liquid volume. The incidence of fetal breathing movements decreased from 52.9 +/- 2.5% to 22.6 +/- 3.5% during 6-h periods of fetal asphyxia. Thus, although fetal asphyxia decreased the net production of lung liquid, lung liquid volume was maintained probably, because the net efflux of fluid from the lungs via the trachea decreased to a similar extent.

Animals↗
PubMed1975

Maternal psychological stress and fetal asphyxia: a study in the monkey.

Fifteen pregnant rhesus monkeys near term were anesthetized with pentobarbital. Catheters were placed into the right femoral arteries of the mother and fetus, the fetuses being retained in utero. After repair of all incisions, the mothers were placed on their sides and allowed to recover from anesthesia. As they awakened, their fetuses regularly developed blood chemical and, frequently, vital signs changes indicative of deepening asphyxia. In eight cases, anesthesia was reinstated with intravenous pentobarbital, 30 mg. per kilogram. This caused an immediate and significant improvement in oxygenation of the fetus in all instances. The remaining animals were transferred to restraining chairs where the blood chemical and cardiovascular statuses of the mothers and fetuses were followed over the next 3 to 72 hours. During this time, the mothers, fully awake, were subjected to both "contrived" and "incidental" episodes of psychological stress stimulation. In the majority of instances, these periods of stress to the mothers caused episodes of bradycardia and hypotension in their fetuses. These induced vital signs changes of the fetuses appeared regularly about 50 seconds after the beginning of the periods of stress stimulation of the mother. Similarly, the vital signs changes frequently began returning toward more normal values with 1 to 2 minutes after the alleviation of maternal stress. Blood samples drawn in single cases before, during, and after recovery from bradycardia identified an associated increase in asphyxia of the fetuses. These episodic aggravations of the already existent fetal asphyxia of the fetuses. These episodic aggravations of the already existent fetal asphyxia brought about by stress stimulation of the mother are interpreted as resulting from activation of the maternal sympathetic nervous system causing vasoconstriction throughout the abdominal viscera and an accompanying retardation in intervillous space perfusion.

Acid-Base Equilibrium↗
PubMed1977

Intrapartum fetal asphyxia: clinical characteristics, diagnosis, and significance in relation to pattern of development.

The clinical and fetal heart rates and acid-base characteristics and their sequelae have been reviewed in 587 patients. The relevant clinical factors in the asphyxia group were the preterm fetus, the intrauterine growth retarded fetus, maternal toxemia, and midforceps delivery. The duration of the developing metabolic acidosis in the asphyxia group ranged from terminal to the last two hours of labor. Marked patterns of total decelerations and moderate and marked patterns of late decelerations are of predictive value in the diagnosis of intrapartum fetal asphyxia with a trend to an increased incidence in the longer duration categories, between four and two hours prior to delivery, and a significant increase in all categories during the last two hours of labor. The significance of intrapartum fetal asphyxia to the newborn infant is evident from the low Apgar scores, increased incidence of moderate and severe respiratory distress syndrome, and central nervous system complications in the asphixia group in relation to the normal group.

Acid-Base Equilibrium↗
PubMedDate not supplied

Acute fetal asphyxia and permanent brain injury: a retrospective analysis of current indicators.

OBJECTIVE: To determine whether a term neonate who has had sufficient intrapartum asphyxia to produce persistent brain injury will manifest the following four criteria: profound acidemia (arterial pH <7.00), an APGAR score < or =3 for 5 min or longer, seizures within 24 h of birth, and multiorgan system dysfunction. METHODS: Singleton, liveborn, neurologically impaired neonates > or =37 weeks gestation who lived at least 6 days and had sufficient documentation of current intrapartum asphyxia criteria were retrospectively analyzed. Of these infants, solely neonates with acute fetal asphyxia due to a sudden prolonged FHR deceleration that lasted until delivery from a catastrophic event, e.g., uterine rupture, cord prolapse, were included. Organ system dysfunction was defined by separate criteria for each organ system. Dysfunction in one or more was defined as multiorgan system dysfunction. RESULTS: Of the 292 eligible infants in the registry, 47 satisfied the entry criteria. In these 47 neonates, 10 (21%) satisfied all 4 criteria for intrapartum asphyxia. CONCLUSIONS: Our retrospective study suggests that currently used indicators to define permanent fetal brain injury are not valid.

Apgar Score↗
PubMed2005

Fluid restriction for term infants with hypoxic-ischaemic encephalopathy following perinatal asphyxia.

BACKGROUND: Current recommendations to control the consequences of hypoxic-ischaemic encephalopathy following perinatal asphyxia include the careful management of fluids, with avoidance of fluid overload and thus avoidance of cerebral oedema. Recommendations for fluid restriction in a neonate are based on the experience of restricting fluid intake in adults or older children. The extrapolation from studies in adults, older children and animals to the human neonate is fraught with hazard due to the different physiology and mechanisms of injury. OBJECTIVES: The objective of this review was to determine the effects of fluid restriction on short-term (mortality within the first 28 days of life, grade of hypoxic ischaemic encephalopathy, electrolyte disturbances, renal function, seizure activity) and long-term outcomes (death during the first year of life, CT or MRI changes, or severe neurodevelopmental disability at or equal to 12 months of age or more) in term infants following perinatal asphyxia. Subgroup analyses were planned on the basis of the severity of the resulting hypoxic-ischaemic encephalopathy, degree of fluid restriction, and length of fluid restriction. SEARCH STRATEGY: Searches were undertaken of MEDLINE October 2004 back to 1966, CINAHL back to 1966, the Oxford Database of Perinatal Trials and the Cochrane Central Register of Controlled Trial (CENTRAL, The Cochrane Library, Issue 3, 2004). Searches were made of previous reviews including cross-references and abstracts. The search was not limited to the English language; reports in foreign languages were translated. SELECTION CRITERIA: Randomised or quasi-randomised trials of fluid restriction in term newborn infants with perinatal asphyxia. DATA COLLECTION AND ANALYSIS: No studies were found meeting the criteria for inclusion in this review. MAIN RESULTS: No studies were found meeting the criteria for inclusion in this review. AUTHORS' CONCLUSIONS: Given that fluid restriction for the treatment of hypoxic ischaemic encephalopathy following perinatal asphyxia is recommended in standard textbooks, there is a need for randomised, controlled trials to establish if this practice affects mortality and morbidity. As it may not be ethical to include neonates with acute renal failure in a randomised trial, these babies will have to be excluded from the trial. These studies should investigate the effects of fluid management on outcomes such as mortality, seizure activity, evidence of cerebral damage on histology, and effects on renal function and electrolytes.

Asphyxia Neonatorum↗
PubMed2000

Brain RNA polymerase and nucleolar structure in perinatal asphyxia of the rat.

Ribosomes are integral constitutens of the protein synthesis machinery. Polymerase I (POL I) is located in the nucleolus and transcribes the large ribosomal genes. POL I activity is decreased in ischemia but nothing is known so far on POL I in perinatal asphyxia. We investigated the involvement of POL I in a well-documented model of graded systemic asphyxia at the level of activity, mRNA, protein, and morphology. Caeserean section was performed at the 21st day of gestation. Rat pups still in the uterus horns were immerged in a water bath for asphyctic periods from 5-20 min. Brain was taken for measurement of pH, nuclear POL I activity, and mRNA steady state, and protein levels of RPA40, an essential subunit of POL I and III. Silver staining and transmission electron microscopy with morphometry when appropriate were used to examine the nucleolus. Brain pH and nuclear POL I activity decreased with the length of the asphyctic period while POL-I mRNA and protein levels were unchanged. Accompanying the decrease in brain pH we found significant changes of nucleolar structure in the course of perinatal asphyxia at the light and electron microscopic level. As early as ten min following the asphyctic insult, morphological disintegration of the nucleolus was observed. The changes became more dramatic with longer duration of perinatal asphyxia. We conclude that severe acidosis may be responsible for decreased POL activity and for disintegration of nucleoli in neurons. This condition may lower the ribosome content in neonatal neurons and impair protein synthesis.

Animals↗
PubMed1994

Neuro-pathophysio-biochemical profiles of neonatal asphyxia.

Neurological and neuroelectrophysio-biochemical profiles were evaluated in newborn lambs exposed to severe temporary asphyxia. Isoelectric EEG, marked disturbances of phosphorus magnetic resonance spectrum (31P-MRS), and significant brain intracellular acidosis (pHi) were noted during asphyxia. Following resuscitation, the presence of early postasphyxic blood-brain-barrier (BBB) opening was associated with a marked transient increase in intracranial pressure (ICP), a 50% neonatal mortality and a 67% incidence of severe asphyxic encephalopathy. In contrast, those lambs exposed to the same magnitude of asphyxia, but without early BBB opening experienced neither death nor severe neurological deficits. Further, these lambs showed a rapid progressive normalization of the 31P-MRS and pHi, despite, the lack of EEG recovery in the first hour following resuscitation. Thus, the present study depicts that the early postasphyxic BBB disruption following temporary neonatal asphyxia is associated with poor prognosis.

Acid-Base Equilibrium↗
PubMed1986

Auditory brainstem response in neonates with asphyxia and intracranial haemorrhage.

Auditory brainstem response (ABR) was used to assess possible brainstem damage in 76 neonates with asphyxia and intracranial haemorrhage (ICH). Fifty-eight neonates had ICH, 52 had neonatal asphyxia and 34 of these patients had both. Eighty-nine percent of the patients with neonatal asphyxia showed some abnormal patterns in response, the major one being an increase in the threshold of wave V. In the ICH group, abnormal patterns were observed in 62.5%, among whom the prolongation of the I-V interpeak latency (IPL) and of wave V latency was seen more frequently than the increase of threshold of wave V. In the case of neonatal asphyxia associated with ICH, both the prolongation of the latency and the increase of threshold were observed equally. These abnormalities of ABR were associated with worsening clinical condition and conversely normalized gradually following the improvement of the underlying disease. Especially the I-V IPL, wave V latency and the threshold of wave V could serve as indicators of the treatment.

Asphyxia↗
PubMed1997

Delayed neuronal death following perinatal asphyxia in rat.

The consequences of perinatal asphyxia on the rat brain were studied 80 min to 8 days after birth with hematoxylin-eosin and in situ DNA double-strand-breaks labeling histochemistry. Asphyxia was induced by immersing fetus-containing uterus horns, removed from ready-to-deliver Sprague-Dawley rats, in a water bath at 37 degrees C for various time periods (0-22 min). Spontaneous- and cesarean-delivered pups were used as controls. Perinatal asphyxia led to a decrease in the rate of survival, depending upon the length of the insult. No gross morphological changes could be seen in the brain of either control or asphyctic pups at any of the studied time points after delivery. However, in all groups, nuclear chromatin fragmentation, corresponding to in situ detection of DNA fragmentation, was observed at different stages. Nuclear fragmentation in control pups showed a specific distribution that appeared to be related to brain maturation, thus indicating programmed cell death. A progressive and delayed increase in nuclear fragmentation was found in asphyctic pups, which was dependent upon the length of the perinatal insult. The most evident effect was seen in frontal cortex, striatum, and cerebellum at postnatal day 8, although changes were also found in ventral-posterior thalamus, at days 1 and 2. Thus, nuclear chromatin fragmentation in asphyctic pups indicates a delayed post-asphyctic neuronal death. The absence of signs of inflammation or necrosis suggests that delayed neuronal cell death following perinatal asphyxia is an active, apoptosis-like phenomenon.

Animals↗
PubMed2005

Effects of perinatal asphyxia on cell survival, neuronal phenotype and neurite growth evaluated with organotypic triple cultures.

The effect of perinatal asphyxia on brain development was studied with organotypic cultures from substantia nigra, neostriatum and neocortex. Asphyxia was induced by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 20 min. Following asphyxia, the pups were nursed by a surrogate dam and sacrificed after three days for preparing organotypic cultures. Non-asphyxiated caesarean-delivered pups were used as controls. Morphological features and cell viability were recorded during in vitro development. At day in vitro (DIV) 24, the cultures were treated for immunocytochemistry using antibodies against the N-methyl-D-aspartate receptor subunit 1 (NR1) and tyrosine hydroxylase (TH). While in vitro survival was similar in cultures from both asphyxiated and control animals, differences were observed when the neuronal phenotype was assessed. Compared to controls, the total number of NR1-positive neurons in substantia nigra, as well as the number of secondary to higher level branching of TH-positive neurites from asphyxiated pups were decreased, illustrating the vulnerability of the dopaminergic systems to perinatal asphyxia.

Animals↗
PubMed1975

The acid-base and biochemical characteristics of intrapartum fetal asphyxia.

The maternal and fetal acid-base, lactate, and pyruvate characteristics during the course of labor and at delivery were studied in 124 patients delivered of an infant with evidence of metabolic acidosis at delivery. This metabolic acidosis is principally caused by hyperlactatemia resulting from the tissue oxygen debt accompanying fetal asphyxia. Hypoxemia was one mechanism contributing to this fetal asphyxia and tissue oxygen debt. This evidence of fetal asphyxia developed during the last half and principally during the last two hours of the intrapartum period. Acid-base assessment of fetal blood with identification of a metabolic acidosis will provide an accurate objective diagnosis of intrapartum fetal asphyxia.

Acid-Base Equilibrium↗
PubMed1977

Intrapartum fetal heart rate profiles with and without fetal asphyxia.

Fetal heart rate profiles for periods up to 12 hours prior to delivery have been reviewed in 515 patients with a fetus at risk. Mechanisms other than fetal asphyxia will cause fetal heart rate decelerations, and fetal asphyxia may in some instances develop in the absence of total or late decelerations. However, an increasing incidence of total decelerations and late decelerations and particularly a marked pattern of total decelerations and late decelerations are of value in the prediction of fetal asphyxia. Fetal heart rate deceleration patterns can predict the probability of fetal asphyxia at the time of initial intervention, while a progression of fetal heart rate deceleration patterns in the individual fetus can be of assistance in the subsequent scheduling of serial acid-base assessments during labor.

Asphyxia↗
PubMed1983

Cerebral palsy and mental retardation in relation to indicators of perinatal asphyxia. An epidemiologic overview.

Although intrapartum asphyxia is established as an important cause of perinatal loss, there is little consensus as to how much of the burden of neurologic handicap in the community is attributable to intrapartum and neonatal asphyxia, as measured clinically. A review of the available epidemiologic information suggests that the role of perinatal events in the genesis of severe mental retardation and cerebral palsy is not as large as popularly thought. Of all neurologic handicaps, cerebral palsy bears the closest relationship to adverse perinatal events, but at least 50% of all cases have no documented depression at the time of birth. No more than 15% of severe mental retardation can be attributed to perinatal events. Severe mental retardation without cerebral palsy does not appear to be attributable to birth asphyxia. The majority of even quite severely asphyxiated babies suffer no detectable neurologic or intellectual sequelae. These epidemiologic observations suggest that resuscitative efforts in mature newborn infants ought not to be too quickly abandoned for fear of late sequelae. At the same time, obstetric intervention based solely on concern for later neurologic development cannot be justified. The most appropriate justification for antenatal and intrapartum monitoring of fetal condition are the established associations of indicators of fetal asphyxia with fetal and neonatal death, and with morbidity in the neonatal period.

Apgar Score↗