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 793 records · Page 44Linked to original sources
PubMed1980

Cardiogenic shock associated with perinatal asphyxia in preterm infants.

Fetal and neonatal biophysical and biochemical changes were studied in four preterm infants who developed cardiogenic shock as a result of severe perinatal asphyxia. Fetal distress was documented by the presence of severe late and variable decelerations associated with decreased fetal heart rate variability. Severity of fetal acidosis was decumented by scalp and umbilical cord blood pH. Apgar scores at 1, 5, and 10 minutes were all equal to or less than 5. Although the clinical findings shortly after birth resembled respiratory distress syndrome, it was possible to make a primary diagnosis of cardiac failure with the recognition of cardiomegaly, hepatomegaly, electrocardiographic changes of myocardial hypoxia, decreased myocardial contractility, elevated central venous pressure, and severe lactic acidosis. The treatment of heart failure, including use of inotropic agents, resulted in rapid improvement in the clinical condition, with reversal of the abnormal findings within 24 to 36 hours. Concomitant with this improvement, the increase in arterial blood pressure was paralleled by increase in peripheral (toe) temperature.

Asphyxia Neonatorum↗
PubMed1988

Clinical trial of naloxone in birth asphyxia.

To determine whether endogenous opiates play a role in the pathogenesis of perinatal asphyxia, a blinded clinical trial of naloxone, a competitive opiate receptor blocker, was undertaken in infants with low 1-minute Apgar scores. Of 85 infants with 1-minute Apgar score 0 to 3, 44 received an injection of naloxone (approximately 0.4 mg/kg) and 41 received saline solution. In 108 infants with 1-minute Apgar score 4 to 6, 54 received naloxone and 54 saline solution. In neither group was there a significant effect of naloxone on respiratory frequency or heart rate up to 30 minutes after injection, nor at 24 hours of age. In both groups active muscle tone of upper and lower limbs was increased by naloxone, a response that may not be beneficial in the face of inadequate oxygen delivery to vital organs. We conclude that naloxone at this dose had no readily apparent benefit in the resuscitation of the asphyxiated newborn infant.

Adult↗
PubMed1989

School performance of survivors of neonatal encephalopathy associated with birth asphyxia at term.

School performance testing was completed at 8 years of age on 145 children who had had neonatal encephalopathy associated with birth asphyxia as term infants and on a comparison peer group of 155 children. The prospectively identified clinical categories of encephalopathy for the neonates were 56 mild (hyperalertness, hyperexcitability), 84 moderate (lethargy, hypotonia, suppressed primitive reflexes), and 5 severe (stupor, flaccidity, absent primitive reflexes). The mortality rate to 8 years of age was 13%. The incidence of impairment, which included cerebral palsy, blindness, cognitive delay, convulsive disorder, and severe hearing loss, was 16% among those assessed at 8 years (75% of survivors). Intellectual, visual-motor integration, and receptive vocabulary scores, as well as reading, spelling, and arithmetic grade levels for those with moderate or severe encephalopathy, were significantly below (p less than 0.01) those in the mild encephalopathy or peer comparison groups. Predictors of reading performance for the study group included category of encephalopathy, birth weight for gestational age, native language, and mother's educational level (multiple R = 0.58). Nonimpaired survivors of moderate encephalopathy were more likely to be more than one grade level delayed than were children from the peer group (reading 35% vs 15%, spelling 18% vs 8%, arithmetic 20% vs 12%, p less than 0.01). Thus children who had moderate and severe neonatal encephalopathy are at risk for physical and mental impairment and reduced school performance. Children with mild encephalopathy had school performance scores similar to those of their peers.

Asphyxia Neonatorum↗
PubMed1977

Perinatal asphyxia and renal failure in neonatal patients.

Herein we discuss oliguria and azotemia in neonatal patients associated with perinatal complications, including difficult labor and delivery, and respiratory asphyxia. Renal failure in these patients is accompanied by proteinuria, microscopic hematuria and red blood cell casts, and it generally resolves in 7 to 10 days. Umbilical aortography can be helpful in determining the presence of normal kidneys in these patients.

Asphyxia Neonatorum↗
PubMed1998

Deficient transcription of subunit RPA 40 of RNA polymerase I and III in heart of rats with neonatal asphyxia.

RNA polymerases transcribe nuclear genes for ribosomal RNA thus representing ribosomal biogenesis. RNA polymerase I transcribes class I genes, coding for large ribosomal RNA and is located in the nucleolus. RNA polymerase III transcribes class III genes, those that encode a number of small ribosomal RNA molecules. Both RNA polymerases form ribosomal biogenesis in a concerted action and have a common subunit, RPA40, essential for function and integrity. The aim of our study was to study the influence of hypoxia/asphyxia on transcription of this subunit as deterioration of ribosomal biogenesis may not be compatible with life. To test this hypothesis we used a nonsophisticated model of neonatal asphyxia. Rat pups were exposed to various asphyctic periods up to twenty minutes and heart tissue was taken for the evaluation of mRNA RPA40 levels, pH measurements and histological evaluation of the nucleolus by silver staining. mRNA RPA40 levels gradually decreased with the length of the asphyctic period paralleling the decrease of pH. Silver staining was remarkably decreased at the asphyctic period of 20 minutes. Our findings of decreased transcription of this essential RNA polymerase subunit indicate impairment of the ribosomal RNA synthetizing machinery and the histological findings suggest its structural relevance. This is the first in vivo observation of deteriorated RNA polymerase in asphyxia/hypoxia.

Actins↗
PubMed1999

Histological changes and neurotransmitter levels three months following perinatal asphyxia in the rat.

The involvement of excitatory amino acids (EAA) in the pathogenesis of hypoxic-ischemic states is well-documented. Information on the role of overexcitation by EAA in perinatalasphyxia (PA), however, is limited and data from adult models cannot be directly extrapolated to immature systems. Moreover, most adult models of ischemia are representing stroke rather than PA. We decided to study long term effects in a non-invasive rat model of PA resembling the clinical situation three months following the asphyctic insult. Morphometry on Nissl - stained sections was used to determine neuronal death in frontal cortex, striatum, hippocampus CA1, hypothalamus and cerebellum L1, and the amino acids glutamate, glutamine, aspartate, GABA, taurine, arginine as well as histamine, serotonin and 5-hydroxy-indoleacetic acid were determined in several brain regions and areas. Morphometry revealed that neuronal loss was present in the hippocampal area CA1 in all groups with PA and that morphological alterations were significantly higher in the cerebellar granular layer. The prominent light microscopical finding in all areas of asphyctic rats studied was decreased Nissl-staining, suggesting decreased cellular RNA levels. Glutamate, aspartate and glutamine were significantly elevated in the hypothalamus of asphyctic rats probably indicating overstimulation by EAA. Excitotoxicity in this area would be compatible with findings of emotional / behavioral deficits observed in a parallel study in our model of PA. Our observations point to and may help to explain behavioral and emotional deficits in Man with a history of perinatal asphyxia.

Animals↗
PubMed2000

Effects of hypothermia and gender on survival and behavior after perinatal asphyxia in rats.

Previous studies in rats have demonstrated that perinatal asphyxia (PA) produces long-term morphological alterations, particularly affecting hippocampus. neostriatum, and cerebral cortex. These changes were prevented by applying hypothermia during the asphyctic insult. Because these cerebral areas are involved in cognitive and motor functions, the aim of the present study was to determine whether periods of PA during normothermia or hypothermia produces long-term behavioral impairments in rats of both sexes. The cognitive and motor functions were studied using the spatial Morris water maze (MWM) task at 1.5 months, and the open field at 5 months, respectively. The present study revealed that female rats had a higher survival rate than males after PA in normothermic conditions (p < 0.014). and that hypothermia drastically prolonged the time of survival in both sexes (p < 0.001). There were no differences in learning and memory functions between groups or male and female rats when tested with MWM. Rats subjected to hypothermia treatment did not show differences in the MWM compared to controls. A lower locomotor activity in the open field test was only observed in male rats that suffered 15 and 20 min of PA in normothermia (p < 0.05). Hypothermia treatment prevented this hypoactivity. PA in females, even if severe, did not affect the motor activity. The data of both behavioral tests showed differences between sexes, i.e., the female rats learned the MWM task slower, and were more active in the open field. This work lends further support for the hypothesis that hypothermia can prevent mortality as well as long-term sequelae induced by PA.

Animals↗
PubMed1986

Cerebral artery Doppler ultrasonography for prediction of outcome after perinatal asphyxia.

43 term infants with clinical neurological manifestations of intrapartum asphyxia and who survived for more than 2 days were studied sequentially, while in hospital, with doppler ultrasound examination of the anterior cerebral arteries. 36 survivors with post-asphyxial encephalopathy were followed up for a median of 18 months and none who had had normal doppler measurements (defined by results in 49 non-asphyxiated babies) became seriously handicapped. Of the 18 infants with abnormal waveforms 12 had an adverse outcome (death or handicap). In the asphyxiated infants, doppler examination predicted outcome with an accuracy of 86%. The prediction of adverse outcome by abnormal doppler showed a sensitivity of 100% and a specificity of 81%. All abnormal results had occurred by 62 hours from birth.

Asphyxia Neonatorum↗
PubMed1986

Comparison of two methods of predicting outcome in perinatal asphyxia.

In a follow-up study of 122 full-term infants in whom postasphyxial encephalopathy occurred the incidence of death or severe handicap was 1 in 1000 deliveries. The abilities of two methods of diagnosing intrapartum asphyxia to predict outcome at a median age of 2.5 years were compared. A decision matrix calculation was undertaken to assess the sensitivity and specificity of low Apgar score and postasphyxial encephalopathy. A 10 min Apgar score less than or equal to 5 was the most sensitive of six different Apgar ratings in predicting adverse outcome (sensitivity 43%, specificity 95%) but even this was much less sensitive than the presence of moderate or severe encephalopathy in predicting death or severe handicap (sensitivity 96%).

Apgar Score↗
PubMed1987

Proptosis and diplopia following traumatic asphyxia.

We describe a previously unreported complication of traumatic asphyxia. An 11-year-old boy developed proptosis and diplopia following a crush injury in an automatic garage door. Computed tomography scan confirmed displacement of the eye. There was no retrobulbar hemorrhage or skull fracture, and the proptosis appeared secondary to traumatic displacement of orbital fat. Proptosis and diplopia resolved completely over six weeks. Visual disorders may be overlooked as a complication of trauma.

Accidents, Home↗
PubMed1997

Thyreoglobulin and violent asphyxia.

The concentration of thyreoglobulin (tg) was determined for death caused by hanging, strangulation by ligature, and throttling. Cases of sudden death (traumatic aortic rupture, penetrating wounds of the heart) were used for comparison. The mean values in cases of hanging (149.9 +/- 202.3 ng/ml), strangulation by ligature (193.1 +/- 173.3), manual strangulation (561.6 +/- 173.9) are distinguishable from violent acute deaths (23.3 +/- 27.6) and living healthy individuals (17.3 +/- 16.1). By means of statistical comparisons, significant differences were found between throttling and strangulation by ligature and between throttling and hanging (adjusted P < 0.001). In connection with examination of the bodies high tg values can be regarded as a vital reaction in obstructive asphyxia.

Asphyxia↗
PubMed1988

Brain energy metabolism in two kinds of total asphyxia: an in vivo phosphorus nuclear magnetic resonance spectroscopic study.

Brain energy metabolism was studied in vivo by means of 31P-NMR spectroscopy in newborn mice during and after 20-minutes exposure to either pure carbon dioxide gas or nitrogen gas. In the N2 group, the brain ATP concentration remained almost normal throughout the experiment, while it showed a 30% reduction in the CO2 group. The brain concentration of phosphocreatine dropped to about 20% of the control value during the asphyxia in both groups, and its recovery was significantly delayed in the CO2 group compared to in the N2 group. Tissue acidosis and Pi accumulation were more remarkable and prolonged in the CO2 group.

Adenosine Triphosphate↗
PubMed1994

Peripartum asphyxia.

The abysmal survival rates for the first barking foals described more than 60 years ago were probably due to the cumulative effects of asphyxia on multiple organ systems. Successful treatment of asphyxiated foals requires recognition of periparturient conditions associated with the syndrome and appreciation of the spectrum of clinicopathologic complications that can ensue.

Animals↗
PubMed1992

Traumatic asphyxia compounding craniofacial trauma.

Traumatic asphyxia is a condition characterized by cervicofacial petechiae, subconjunctival ecchymosis and other possible accompanying problems particularly ophthalmic, thoracic and cardiovascular injuries. While the facial petechiae per se are of little consequence, the attendant injuries to other organ systems can be serious and even fatal. Craniofacial injuries also present with fatal ecchymosis and haematoma formation due to the underlying skeletal injuries which may require active management. Clinicians managing trauma patients should be well aware of these two different entities which may occur separately or simultaneously so as to ensure correct and adequate treatment.

Accidents, Occupational↗
PubMed1995

Perinatal asphyxia: assessing its causal role and timing.

Perinatal asphyxia, whether prenatal, intrapartum, or neonatal is thought to be a significant contributor to newborn morbidity and mortality as well as long-term neurological deficits. Development of an intrapartum tool/test that can reliably identify and discriminate between varying degrees of fetal acidemia and suggest whether it is respiratory or metabolic in nature would be highly desirable. This article critically reviews the available experience with the currently available monitoring techniques and the significance of abnormalities of fetal and intrapartum measurements with respect to the predictive value of the observations available to the clinician.

Acidosis, Respiratory↗
PubMed2004

Life-long effects of perinatal asphyxia on stress-induced proteins and dynamin 1 in rat brain.

In previous work, we have shown that perinatal asphyxia (PA) in the rat leads to life-long neurotransmitter deficits and impairment of cognitive functions and behavior. This observation made us examine protein expression in hippocampus of rats with PA at the end of the life span. We applied a well-documented and characterized animal model of PA. Pups, normoxic and asphyxiated for 20 min, were brought up until the age of 24 months and then were sacrificed. Hippocampal tissue was dissected from the brains, and proteins were run on two-dimensional gel electrophoresis with in-gel digestion and subsequent identification of proteins by MALDI-TOF followed by quantification of protein spots by specific software. In hippocampus of rats with PA, the stress proteins protein disulfide isomerase A3 precursor and stress-induced phosphoprotein-1 were significantly increased, whereas the microtubule-associated protein dynamin-1 was significantly reduced. Increased stress protein levels may represent long-term effects of PA or, alternatively, could reflect conditioning of the stress protein machinery known to occur as a neuroprotective principle following hypoxic-ischemic conditions. Decreased dynamin-1 levels may be considered as a long-term effect on the exocytotic system possibly reflecting or leading to impaired neuronal transport and vesicle-trafficking in PA of the rat of advanced age.

Aging↗