Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Asphyxia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources
PubMed2006

Xenon preconditioning reduces brain damage from neonatal asphyxia in rats.

Xenon attenuates on-going neuronal injury in both in vitro and in vivo models of hypoxic-ischaemic injury when administered during and after the insult. In the present study, we sought to investigate whether the neuroprotective efficacy of xenon can be observed when administered before an insult, referred to as 'preconditioning'. In a neuronal-glial cell coculture, preexposure to xenon for 2 h caused a concentration-dependent reduction of lactate dehydrogenase release from cells deprived of oxygen and glucose 24 h later; xenon's preconditioning effect was abolished by cycloheximide, a protein synthesis inhibitor. Preconditioning with xenon decreased propidium iodide staining in a hippocampal slice culture model subjected to oxygen and glucose deprivation. In an in vivo model of neonatal asphyxia involving hypoxic-ischaemic injury to 7-day-old rats, preconditioning with xenon reduced infarction size when assessed 7 days after injury. Furthermore, a sustained improvement in neurologic function was also evident 30 days after injury. Phosphorylated cAMP (cyclic adenosine 3',5'-monophosphate)-response element binding protein (pCREB) was increased by xenon exposure. Also, the prosurvival proteins Bcl-2 and brain-derived neurotrophic factor were upregulated by xenon treatment. These studies provide evidence for xenon's preconditioning effect, which might be caused by a pCREB-regulated synthesis of proteins that promote survival against neuronal injury.

Animals↗
PubMed2000

Outcome after intrapartum asphyxia in term infants.

Investigatory techniques, particularly magnetic resonance (MR) imaging and spectroscopy, performed in the early neonatal period on infants suspected of intrapartum asphyxia i.e. abnormal fetal heart recording, poor cord gases, low Apgar scores and the need for resuscitation, or with neonatal encephalopathy or seizures, have allowed a much better understanding of the patterns of brain injury and the biochemical processes that follow these events. It is usually possible to distinguish these patterns from those seen in other, often confounding, diagnoses. This has allowed far more precision about the timing of insults and in the prediction of particularly motor, feeding and visual outcome and to some extent intellectual outcome. Long-term neurological and psychometric follow-up of infants in whom detailed perinatal clinical histories and examination, haematological and biochemical investigation and MR brain scans are obtained will allow even more accurate prediction of outcome in the future. Such studies also help to validate standardized neonatal and infant clinical neurological examinations, making them useful tools to predict outcome.

Asphyxia Neonatorum↗
PubMed2000

MR patterns of hypoxic-ischemic brain damage after prenatal, perinatal or postnatal asphyxia.

The relationship between MR patterns of brain damage and type or timing of perinatal hypoxia-ischemia was studied. MR images of 104 children with evidence of bilateral posthypoxic-ischemic brain damage and neonatal records were reviewed. Three different MR patterns were found. Periventricular leukomalacia occurred in 73 children, in 82% after a history of subacute or chronic hypoxia-ischemia, in 71% after preterm birth. Predominant lesions of basal ganglia and thalamus occurred in 21 children, in 95% preceded by acute profound asphyxia, in 85% after term birth. Multicystic encephalopathy occurred in 10 infants, in 70% preceded by mild signs of hypoxia-ischemia, followed by an unexpectedly severe encephalopathy, in 60% after term birth. Statistical analysis showed that the patterns of injury were primarily related to the type of hypoxia-ischemia. We conclude that the type of hypoxia-ischemia, rather than the postconceptional age at occurrence determines the pattern of brain injury.

Asphyxia Neonatorum↗
PubMedDate not supplied

[Birth asphyxia - an unsolved problem of perinatal medicine].

Birth asphyxia is defined as a severe disturbance of oxygen supply to the fetus, which develops during the first or second stage of labor. The diagnosis is confirmed by a severe metabolic acidosis in the umbilical cord blood, a persistent low Apgar as well as functional disturbances as a result of hypoxic damage in various organs including the central nervous system. Apart from morbidity and mortality in the neonatal phase long term effects are of considerable significance. Only 10 - 15 % of all cerebral palsy cases developing after delivery at term are a consequence of a hypoxic encephalopathy developing during the process of labor and delivery. For a long time it was ignored, that a number of pregnancy pathologies may lead to brain damage, which could also produce the typical symptoms of cerebral palsy. An abrupt disturbance of oxygen supply may be a result of cord compression, a premature separation of the placenta or of rupture of the uterus. These situations are in general easily recognized by typical clinical symptoms together with a sudden drop in fetal heart rate with a persistent bradycardia. In these cases it is only possible to prevent hypoxic brain damage, if the fetus can be delivered by emergency caesarian section within 15 - 20 minutes after the acute event. Diagnosis and evaluation of subacute or chronic forms of insufficient supply of oxygen of the fetus in labor is considerably more difficult. Reliability of continuous heart rate monitoring of the fetus during labor as well as validity of certain heart rate changes for the detection of developing hypoxia is a matter of ongoing dispute. In the presence of clearly pathological heart rate patterns hypoxic damage may already have occurred. Suspicious or "non-reassuring" heart rate alterations are frequent and only in a small percentage a real threat to the fetus in form of severe hypoxia will develop. Up until now there is no clear scientific proof that a combination of continuous fetal heart rate monitoring with additional tests can prevent hypoxic damage to the fetus. Future efforts should be directed towards improving reliability of the description of fetal heart rate patterns, the validity of the information provided by heart rate changes as well as the proof of the benefit of continuous monitoring of the fetus during labor and delivery as a means of preventing severe hypoxia and its consequences to fetal health.

Asphyxia Neonatorum↗
PubMedDate not supplied

[Can subpartal fetal acidosis be avoided? Investigations on the complex causes of intrauterine asphyxia].

OBJECTIVE: The extent to which faulty medical treatment and defective apparatus are concomitant causes for the development of subpartal acidosis was investigated in a retrospective study. At the same time, the incidence of acidosis in the Lippe-Detmold Hospital, Department of Gynaecology and Obstetrics, its morbidity and mortality were analysed. METHODS: Data from all case histories of neonates with acidosis (pH in the umbilical artery < 7.100) who were born between 1 st January 1992 and 31 st December 1998 at the Department of Gynecology and Obstetrics at the Lippe-Detmold Hospital were evaluated electronically. Analytical measurements of blood gases (pH, pCO 2 and pO 2 ) in umbilical artery and venous blood were available from all cases. The base excess was corrected by computations according to Siggaard-Andersen and R. Zander for the actual oxygen saturation. The delivery cardiotocograms (CTG) were appraised qualitatively. Equipment defects, mistakes on the part of doctors and/or midwives (including the head of the department) were recorded after critical analysis of each individual case and documented in accordance with a key. The neonatal data were taken from the files of the paediatric division of the hospital (head of the department Dr. K. Wesseler). RESULTS: In seven years under report, 9.876 babies were born, 156 (1.58 %) of whom showed a pH of less than 7.100 in the umbilical arterial blood. The mean actual pH value was 7.047 +/- 0.058, and the oxygen-corrected base excess was - 16.3 +/- 3.2 mmol/l. Correction of the base excess resulted in a numerical lowering by about 2.0 mmol/l. The rate of premature births was 17.4 %. One newborn baby died of hypoxic shock (0.67 %). 94 % of these neonates could be discharged in a healthy condition. 4.6 % still showed symptoms on discharge. Disorders of respiratory adaptation were the most prominent feature in morbidity from acidosis (about 18 %). Only two babies showed neonatal convulsions. Renal, cardiac and haemostaseological complications were rarely observed. Only 5 (3.9 %) of the 128 neonates with available recordings did not show any pathological changes in the CTG. 26.4 % of all acidoses had to be designated as "pure fate". In a further 35 % medical mistakes could not be discerned. Consequently, 61.4 % of the acidoses had to be designated as "unavoidable". In the remaining roughly 40 %, inadequate cardiotocographical knowledge, inattentiveness, defective equipment etc. clearly played a causal role. In the severe cases (pH in the umbilical artery < 7.000), medical mistakes were much more frequent (50 %). CONCLUSIONS: Three-fifths of all subpartal acidoses in this study have a fateful nature, i.e. they cannot be prevented even by optimal professional management in good time. About two-fifths are avoidable if appropriate equipment and trained staff are available around the clock. Use of cardiotocography alone enables the threat of asphyxia to be detected in 97 % of the cases. The short-term prognosis of subpartal acidosis is good provided very low pH values (< 6.900) can be avoided. In perinatological studies, the base excess value should be corrected by computation. "Quality control" worthy of the name should include critical single-case analysis at least in severe acidosis.

Acidosis, Respiratory↗
PubMed1991

[Inner ear changes in fetal asphyxia].

Deafness following complications of pregnancy and obstetrics occurs frequently. The temporal bones of stillborn or neonates who died several days after delivery have often been examined, and haemorrhage and serous labyrinthitis have been found in infections, diabetes and trauma. In this study, pathological findings in the temporal bones of foetuses who died of chronic asphyxia in utero are described. 7 out of 15 cases had no labyrinthine pathology. Four had haemorrhage into the tissue or into perilymphatic or endolymphatic spaces. Likewise, four had developed eosinophilic precipitates in the liquid spaces of the inner ear. If the foetus survives such phases of hypoxia in utero, this might be the morphological correlate of developing deafness. Similar findings in infections such as rubella or cytomegalovirus infection are discussed.

Asphyxia Neonatorum↗
PubMed1988

Neonatal depression and birth asphyxia in the low birthweight neonate.

In 392 low birthweight neonates, acidosis as evident from umbilical artery pH 7.1 or less was strongly associated with Apgar score 6 or lower at 1 minute. However, most cases that were depressed (Apgar score 6 or lower at 1 minute) were not acidotic. Neonatal depression was most strongly and directly correlated with gestational age. Neonatal depression and birth asphyxia are distinct entities.

Acidosis↗
PubMed1985

The very low birthweight infant: incidence and significance of low Apgar scores, "asphyxia," and morbidity. Findings at delivery.

Cord blood gas determinations were made on arterial and venous blood from 78 babies weighing less than 2000 gm at birth, including 52 weighing 1500 gm or less. Correlations were made with Apgar scores and intrapartum events as well as with birthweight (BW) and gestational age (GA). Significant differences were seen between mean BW, GA, and Apgar scores for survivors versus nonsurvivors but only BW and GA were found to affect mortality. The incidence of low Apgar scores, which was high, was inversely related to BW and GA. Correlations between cord blood gases and Apgar scores were poor, most newborns showing normal gases irrespective of Apgar scores. The authors conclude that the term "asphyxia" is an overused explanation for low Apgar scores among very low birthweight babies; they believe it should be reserved for those depressed states proved to be associated with disturbed respiratory physiology.

Apgar Score↗
PubMed1992

Cerebral blood flow velocity and failure of autoregulation in neonates: their relation to outcome of birth asphyxia.

Using the continuous wave Doppler technique, we examined the pulsatility index (PI) of the anterior cerebral artery in 14 asphyxiated infants. We also measured the blood pressure (BP) and fontanel pressure (FP) and calculated the cerebral perfusion pressure (CPP). According to the neurological prognosis, we divided the 14 infants into two groups and studied correlation of each factor. In the good-prognosis group (n = 11), PIs are within normal limits. There is a negative correlation between BP, CPP and PI, suggesting that the autoregulation of cerebral blood flow has been lost. On the other hand, there is no significant correlation between BP, CPP and PI in the poor-prognosis group (n = 3). These infants are thought to have lost the autoregulation, but their cerebral blood flow is not pressure-passive. Not only BP but also brain edema, vasodilation, and possibly other factors may contribute to determine the cerebral blood flow. Concerning FP, no remarkable correlations are found between two groups. It is therefore very important to monitor the PI, BP, FP in asphyxiated infants even if the degree of asphyxia is mild.

Asphyxia Neonatorum↗
PubMed2005

Pathological findings in the temporal bone of newborn infants with neonatal asphyxia.

Hypoxia in adults frequently causes damage to the brain, but not the inner ear. However, hypoxia in neonates with inadequate blood-inner ear barrier function causes damage to the inner ear, leading to hearing loss and equilibration disorder. Clinically, asphyxiated neonates sometimes have the complication of sensorineural hearing impairment at high frequencies. Many reports suggest that this problem is caused by hypoxic encephalopathy. However, it is not clear whether inner ear disorders are present. In this report we examined the inner ear pathology of four asphyxiated neonates using serial sections of temporal bone. The subjects (n=4) were 1-13-day-old neonates with pregnancy periods of 24-36 weeks. Their fetal growth curves were within the normal range. There was one case each of twin pregnancy, placental abruption, placenta previa and meconium aspiration syndrome. For the case of severe neonatal asphyxia, damage to the inner ear included the degeneration and disappearance of outer hair cells of the organ of Corti and edematous changes in the stria vascularis. Degeneration of spiral ganglion and vestibular ganglion cells was observed in two of the other cases.

Asphyxia Neonatorum↗
PubMed2003

Long term production of reactive oxygen species during perinatal asphyxia in the rat central nervous system: effects of hypothermia.

The formation of oxygen-derived free radicals in hypoxic and ischemic/reperfused brains has been proposed as an important step that links brain injury to neuronal death. Previously, we have demonstrated that reactive oxygen species (ROS) production was significantly increased in rat neostriatum during acute perinatal asphyxia (PA) in pups. In this article, we have studied the time course of ROS production in the neostriatum and neocortex of adult rats subjected to PA using electron spin resonance spectrometry (ESR) in order to record ROS production. Further more, we analyzed the actions of hypothermia on ROS release in pups and adult rats. We used for this study 6-month-old rats that suffered sub-severe and severe PA when they were pups. The most significant production of ROS was detected either in the neostriatum or neocortex at 19 and 20 min of PA. Hypothermia during 20 and 100 min at 15 degrees C prevented ROS formation either in pups and adult rats. These data further support the concept that free radicals may contribute to the brain injury alterations and that hypothermia can prevent long-term sequelae induced by PA.

Animals↗
PubMed2006

Neostriatal cytoskeleton changes following perinatal asphyxia: effect of hypothermia treatment.

Long-term changes of different types of neurofilaments (NF) and glial fibrillar acid protein (GFAP) were studied in neostriatal rat subjected to perinatal asphyxia (PA) under normothermic and hypothermic (15 degrees C) conditions, using immunohistochemistry for light and electron microscopy. Neostriatal neurons of 6-month-old rats that were subjected to 19 and 20 min of PA, showed an increase of NF 200 kDa immunostaining mainly in the axon fascicles in comparison with the control and hypothermia groups. In contrast, no alterations were seen with NF68 and NF160 neurofilament antibodies. Furthermore, the same PA groups showed astroglial cells with enhanced GFAP immunoreactivity, evidencing a typical astroglial reaction with a clear hypertrophy of these cells. A quantitative image analysis confirmed these observations. Hypothermic treated animals did show neither astroglial nor neuronal cytoskeletal changes in comparison to the control group. These findings showed that PA produces chronic cytoskeletal alterations in the neostriatum cells that can be prevented by hypothermia.

Analysis of Variance↗
PubMed1997

Autoerotic asphyxia: a case report.

Autoerotic asphyxia is the induction of a state of oxygen deficiency to enhance sexual excitement and orgasm. It has been practiced for centuries, and there are many reports of fatalities. The authors report a case of a living participant that shows a number of characteristics different from those of fatalities. The case study also raises doubt about the conventional view that participants have no wish to die. We feel that further case studies of living participants will lead to a greater understanding of the practice and will facilitate treatment.

Adult↗
PubMed2001

Comparison of brainstem auditory evoked responses recorded at different presentation rates of clicks in term neonates after asphyxia.

UNLABELLED: This study examined whether high presentation rates of clicks while recording brainstem auditory evoked responses (BAER) can improve the detection of central auditory impairment in asphyxiated neonates using the BAER. The BAER was analysed at different presentation rates of clicks within the first week after birth in 38 term neonates who suffered perinatal asphyxia. At the routinely used 21 s(-1) clicks all BAER wave latencies increased significantly (ANOVA, p < 0.05-0.01). After excluding five neonates who had a significantly elevated BAER threshold, only wave V latency increased slightly (p < 0.05). The interpeak intervals of I-V and III-V also increased slightly (both p < 0.05). Similar results were found at 51 s(-1) clicks. As the clicks were increased to 91 s(-1), the III-V interval increased more significantly (p < 0.01) and the III-V/I-III interval ratio also increased significantly (p < 0.01). In particular, wave V amplitude reduced more significantly than that in normal term controls (p < 0.01). Compared with values in the controls, wave V amplitude reduced by 4.5%, 12.2% and 24.7% at 21, 51 and 91 s(-1) clicks, respectively. CONCLUSION: Although a moderate increase in the rate (e.g. 51 s(-1)) while recording the BAER did not improve the detection of hypoxic-ischaemic auditory impairment, a significant increase (e.g. 91 s(-1)) did, which mainly indicates an abnormal reduction in wave V amplitude.

Asphyxia Neonatorum↗
PubMed1999

Glycine and other neurotransmitter amino acids in cerebrospinal fluid in perinatal asphyxia and neonatal hypoxic-ischaemic encephalopathy.

The aim of this study was to evaluate the concentrations of neurotransmitter amino acids in the cerebrospinal fluid (CSF) of asphyctic newborns, and to establish whether these concentrations are related to the degree of hypoxic-ischaemic encephalopathy (HIE). Levels of glutamate, aspartate, glycine and taurine in CSF were measured in 48 full-term newborns during the first 2 d of life. Thirty-nine of these newborns had birth asphyxia and were divided into three groups: 11 without HIE, 19 with mild HIE and 9 with moderate HIE. None suffered from severe HIE. They were compared with a control group of 9 non-hypoxic newborns. Determinations of the amino acids in CSF were made by chromatography and expressed as micromol/l (mean+/-SD). CSF glycine value was related to erythrocyte count, and CSF taurine value was related to its plasmatic level. Levels of CSF glycine were related to the severity of HIE (p=0.020): control (12.08+/-4.04 micromol/l), without HIE (12.49+/-4.04 micromol/l), mild HIE (12.14+/-3.83 micromol/l), and moderate HIE (19.1+/-10.08 micromol/l; p < 0.05 versus mild HIE), even after removing the influence of red cells in CSF.

Analysis of Variance↗
PubMed2005

How much and for how long does the neonatal myocardium suffer from mild perinatal asphyxia?

Cardiac troponins can be useful in monitoring cardiac injury following perinatal distress. We report here an increase of cardiac troponin I (cTnI) to 2.84 microg/l at 3 weeks (age-related median: 0.07 microg/l) followed by normalization in a newborn with an uneventful clinical course after resuscitation at birth. Serial echocardiographs showed normal cardiac function. Such a time course of cTnI, not previously reported, could be due to either a greater sensitivity of biochemical markers than of instrumental tools or birth asphyxia. Larger studies are needed

Asphyxia Neonatorum↗
PubMed1990

Risk assessment in birth asphyxia.

In developing countries the need for a risk approach in neonatology is obvious because of a high birth rate, high neonatal mortality rate, and limited availability of resources. Quantification of risk, with selected antepartum, intrapartum factors, clinical, and post-mortem findings was done by calculating odds ratio, attributable risk, and 95 per cent confidence limits in 1811 babies, 541 of which were asphyxiated. Primigravidity, history of perinatal death, pregnancy induced hypertension, and antepartum haemorrhage carried higher risk. Abnormal fetal heart rate and meconium passage in amniotic fluid correctly predicted high risk of birth asphyxia. Decreasing risk in premature/low birth weight babies without increase in abdominal deliveries suggested that caesarean sections were unnecessary in preterm deliveries. Clinical monitoring of asphyxiated newborns was adequate enough.

Apgar Score↗
PubMed1986

An unusual case of compression asphyxia and smothering.

Scene investigation is an important part of the medicolegal autopsy. In many cases the cause of death cannot be determined without knowledge of the circumstances. A case is presented in which the diagnosis of compression asphyxia and smothering was made only after analysis of the scene findings.

Asphyxia↗