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 253 records · Page 14Linked to original sources

Diagnosis of birth asphyxia on the basis of fetal pH, Apgar score, and newborn cerebral dysfunction.

Imprecise diagnosis of birth asphyxia coupled with uncertainties about causal factors for neurologic abnormalities in the newborn have greatly fueled the current litigation crisis in obstetrics. Our goal was to more precisely define birth asphyxia based on fetal condition as measured by umbilical artery blood pH, Apgar scores, and neurologic condition of newborns. We selected for study 2738 patients with singleton pregnancies with cephalic presentations who were delivered of infants at term to avoid complications such as prematurity, which may affect infant outcome independent of birth condition. The basis for study of these particular patients were defined criteria for high risk and an indicated arterial cord pH value. A total of five infants demonstrated cerebral dysfunction as evidenced by seizures during the neonatal period. Infection was linked to seizures in three of these infants; one infant had neonatal asphyxia and only one infant's clinical course could be attributed solely to birth events (uterine rupture). Stratification of umbilical artery blood pH values, Apgar scores, and combinations of these dependent variables in relation to newborn clinical outcomes revealed that infants must be severely depressed at delivery before birth asphyxia can be reliably diagnosed. Such depression includes Apgar scores less than or equal to 3 at 1 and 5 minutes plus umbilical artery pH values less than 7.00.

Acid-Base Equilibrium↗

Intrapartum asphyxia in the preterm fetus less than 2000 gm.

The incidence of intrapartum asphyxia in the preterm fetus less than 2000 gm (6%) is greater than that in the mature fetus (2%). Severe antepartum hemorrhage is the only clinical marker predictive of asphyxia in the preterm fetus. Marked deceleration patterns and particularly late decelerations may be of predictive value for asphyxia. However, many intrapartum asphyxial episodes are not identified on the basis of clinical observations. Consistent diagnosis of intrapartum asphyxia in the preterm fetus requires routine umbilical cord blood gas and acid-base assessment at delivery.

Asphyxia Neonatorum↗

Markers of acute and chronic asphyxia in infants with meconium-stained amniotic fluid.

OBJECTIVE: Cord blood pH, lactate, hypoxanthine, and erythropoietin levels have all been used as markers of either acute or chronic asphyxia. We sought to determine whether these index values were significantly different in infants with or without meconium-stained amniotic fluid. STUDY DESIGN: Fifty-six pregnant women in spontaneous labor at term were divided into two groups on the basis of the presence or absence of meconium-stained amniotic fluid. All meconium-stained fluid was centrifuged, and the volume percentage of particulate matter (i.e., meconium) was recorded. Umbilical artery blood and mixed arterial and venous cord blood were obtained at each delivery. Lactate, hypoxanthine, and erythropoietin levels were measured. Statistical analysis included Student t test and rank sum statistics where appropriate. Normal and Spearman correlation coefficients were also used. RESULTS: There were no significant differences in mean umbilical artery pH (7.26 +/- 0.06 vs 7.25 +/- 0.10), lactate levels (32.8 +/- 10 mg/dl vs 30.4 +/- 14.2 mg/dl), and hypoxanthine levels (13.4 +/- 6.7 mumol/L vs 14.0 +/- 6.0 mumol/L) in newborns with meconium (n = 28) compared with controls (n = 28). Erythropoietin levels were significantly greater in newborns with meconium (median 39.5 mIU/ml vs 26.8 mIU/ml, p = 0.039). There was no correlation between the amount of particulate matter and any marker of asphyxia. CONCLUSIONS: There was no correlation between markers of acute asphyxia (i.e., umbilical artery blood pH, lactate, or hypoxanthine) and meconium. However, erythropoietin levels were significantly elevated in newborns with meconium-stained amniotic fluid. This latter marker may better correlate with chronic asphyxia.

Acute Disease↗

Fetal heart rate variability and cerebral oxygen consumption in fetal sheep during asphyxia.

This study was designed to examine the relationship between fetal heart rate variability and fetal cerebral oxygen uptake. Fetal sheep were chronically prepared with catheters and electrodes to determine cerebral blood flow (microsphere method), cerebral arteriovenous oxygen difference, and the electrocardiogram. An adjustable occluder was placed on the maternal common internal iliac artery to induce fetal asphyxia by reducing uterine blood flow. Fetal heart rate variability tended to decrease in the first 11 min of asphyxia, when cerebral oxygen consumption was approximately 53% of control. Despite stable cerebral oxygen consumption and worsening metabolic acidosis, however, fetal heart rate variability progressively returned towards normal by 36 min. There was no relationship between the depression of FHR variability and the degree of reduction of cerebral oxygen consumption. Nor was there any relationship between an alteration in regional cerebral blood flow or myocardial blood flow and the return of FHR variability with increasing duration of asphyxia. We conclude that there is an association between loss of fetal heart rate variability and reduced cerebral oxygen consumption, but the reduced variability does not persist with time at this degree of reduced cerebral metabolism in fetal sheep. This appears to be at variance with human clinical experience. Among the explanations for this may be insufficiently severe asphyxia, a species difference, removal of an inhibitor to FHR variability, or progressive use of other substrates for metabolism.

Animals↗

Effect of asphyxia on the frequency and amplitude modulation of synchronized renal nerve activity in the cat.

A computerized peak detection algorithm was used to retrieve new information about changes in the characteristics of renal nerve activity (RNA) with asphyxia in anesthetized cats. The algorithm scanned the series of RNA voltages for significant increases followed by significant decreases in a small cluster of voltage values. Once each synchronized RNA peak had been detected, its corresponding amplitude, width, and peak-to-peak interval were calculated. The peak-to-peak interval showed two rhythms of synchronized discharge: one between 200-500 ms accounting for 38 +/- 3% of intervals and a higher 20-180 ms frequency (52 +/- 5% of intervals). Asphyxia did not change the periodicity distribution despite increases in arterial pressure. The peak amplitude of RNA, reflecting the number of active fibers, was unimodally distributed and was increased 39 +/- 9% with asphyxia. The shape of the distribution was unchanged. The width of the synchronized activity was also unimodally distributed, mean 79 +/- 3 ms, and increased by asphyxia to 99 +/- 5 ms. The results indicate that the control of the periodicity and amplitude of synchronized discharge appear to be independent and are differentially affected by chemoreceptor input.

Animals↗

Reduction of blood PO2 decrease and PCO2 increase during asphyxia by paramedian reticular nucleus in cats.

Effects of activation of paramedian reticular nucleus (PRN) on the systemic arterial blood pressure (SAP), heart rate, renal nerve activity (RNA), and changes of the partial pressure of the arterial blood oxygen (PO2) and carbon dioxide (PCO2) during asphyxia were studied in cats anesthetized with chloralose (40 mg/kg) and urethane (400 mg/kg). During a 35-s period of asphyxial anoxia, SAP and RNA increased while heart rate decreased significantly. The arterial blood PO2 decreased by 64.6 +/- 4.7% while the PCO2 increased by 54.6 +/- 6.3%. Electrical stimulation of PRN produced a mild to moderate decrease of the SAP, heart rate, and RNA, but arterial PO2 and PCO2 did not change significantly. When PRN was stimulated simultaneously with asphyxia, increases of SAP and RNA and changes of blood gases subsequent to asphyxia reduced significantly. Arterial PO2 decreased only 54.0 +/- 4.9% while the PCO2 increased 39.4 +/- 10.5% (p < 0.01). Similar effects were observed in the venous blood from inferior vena cava. In addition, when the arteriovenous difference of PO2 and PCO2 was compared, simultaneous PRN stimulation during asphyxia produced a higher PO2 reserve (66.3%) and less PCO2 production (-7%) than without PRN stimulation; PO2 54.2%, PCO2 (-2.9%). The results suggest that PRN is a structure that can exert inhibition over a wide spectrum of body functions; not only autonomic system but probably also metabolism.

Animals↗

Hemodynamic responses to asphyxia in spontaneously breathing newborn term and premature lamb.

The comparative effects of asphyxia were studied in spontaneously breathing premature and full term newborn lambs. The premature lambs exhibited significantly higher baseline blood flow to several organs. Asphyxia induced similar changes in regional organ blood flow in preterm and term newborn lambs. Regional differences were found in baseline brain blood flow with an increase from cephalad to caudad. Asphyxia resulted in preferential increases in blood flow to the lower brain structures (cerebellum, medulla, midbrain, and spinal cord). Blood flow to most organs returned to baseline 140 min after recovery from asphyxia.

Animals↗

Foreign body asphyxia: a preventable cause of death in the elderly.

BACKGROUND: To assess the prevalence of food/foreign body asphyxia in the elderly Viennese population in order to reduce the incidence of these fatal events. METHODS: This is an autopsy-based, retrospective study in Vienna, Austria. Participants included all nonhospitalized (n =200) cases of choking in 1984 to 2001, from a total 42,745 consecutive autopsies performed at the Institute of Forensic Medicine. In addition, data from hospitalized adult cases of fatal choking (n =73) in 1984 to 2001, from the mortality registrar of Vienna, were included. RESULTS: The nonhospitalized choking victims were analyzed according to age (18 to 64 vs >/=65 years), sex, circumstances of death, and predisposing factors. Hospitalized cases were analyzed according to age, sex, and whether an autopsy was already performed by pathologists at the institution where they died. In the study period, 273 adults died of food/foreign body asphyxia, 73% of them out of the hospital and 27% in hospitals. Food/foreign body asphyxia in the elderly was characterized by a significantly higher asphyxiation of soft/slick foods (p <0.007) with agomphiasis (p <0.002), occurring most frequently during lunch (49%), and in 2.5% during feeding of neurologically impaired. In contrast, younger individuals choked significantly more often on large pieces of foreign material (p <0.002) and showed a significantly higher rate of blood alcohol concentration (p <0.001). CONCLUSIONS: This study demonstrates that semisolid foods are the cause of a large number of asphyxiations, especially among the elderly. Knowledge of the fact that semisolid foods are a high-risk factor in elderly individuals should be distributed in public and private healthcare systems, and awareness could be a first step in reducing the incidence of food/foreign body asphyxia.

Adolescent↗

Free fatty acid metabolism in the air-breathing African catfish (Clarias gariepinus) during asphyxia.

In several waterbreathing fish species, hypoxia induces a decrease in plasma free fatty acid (FFA) levels as opposed to an increase in air-breathing mammals. We hypothesised that this change is coupled to the mode of breathing. Therefore, we followed the metabolic response of cannulated air-breathing African catfish to an 8-h asphyxia period. The hematocrit and hemoglobin increased significantly upon asphyxia. However, no change was observed in the mean cellular hemoglobin concentration, indicating that more erythrocytes were brought into circulation. A continuous increase in plasma lactate concentration during asphyxia showed permanent activation of anaerobic glycolysis, pointing to a persistent oxygen shortage. Plasma glucose levels did not change, but FFA levels decreased significantly upon asphyxia with a concomitant increase in plasma noradrenaline levels. Thus, these results suggest that in the air-breathing African catfish noradrenaline mediated a decrease in plasma FFA levels similar to that in waterbreathing fish species.

Africa↗

The brassiere 'sign' - a distinctive marker in crush asphyxia.

The diagnosis of crush asphyxia typically relies on a history of chest or abdominal compression with the finding of skin petechiae and congestion. The following three cases of crush asphyxia demonstrate a distinctive pattern of petechiae and congestion associated with close-fitting clothing: Case 1, a 49-year-old woman who was crushed under a large hay bale; Case 2, a 35-year-old woman who was crushed between a wall and a car; Case 3, a 49-year-old woman who was crushed between a crane and the side of a truck. At autopsy in all three cases there were facial, conjunctival, neck and upper anterior chest petechiae. However, few or no petechiae, and reduced congestion, were observed in areas beneath the victims' brassieres. Deaths in these cases were all due to crush asphyxia, with the pattern of petechiae on the chests of the victims influenced by close-fitting clothing that had compressed cutaneous vasculature. This brassiere 'sign' provided a readily observable and easily recordable sign of crush asphyxia due to chest compression, and illustrated that vascular engorgement is necessary for the development of petechiae in these circumstances.

Accidents↗

Complex character analysis of heart rate variability following brain asphyxia.

In the present study Renyi entropy and L-Z complexity were used to characterize heart rate variability (HRV) of rats that were suffered from brain asphyxia and ischemia. Two groups of rats were studied: (a) rats (n=5) injected with NAALADase inhibitor, 2-PMPA, which has been proven neuroprotective in asphyxia injury and (b) control subjects (n=5) without medication. Renyi entropy and L-Z complexity of the R-R intervals (RRI) at different experiment stages were investigated in the two groups. The results show that both measures indicate less injury and better recovery in the drug injection group. The dynamic change of 90 min RRI signal after the asphyxia was investigated. The sudden reduction of the two parameters shows their sensitivity to the asphyxia insult.

Animals↗

Upper airway EMG responses to acute hypoxia and asphyxia are impaired in streptozotocin-induced diabetic rats.

Obstructive sleep apnoea (OSA) is a major clinical disorder that is characterised by multiple episodes of upper airway obstruction due to failure of the upper airway dilator muscles to maintain upper airway patency. The incidence of OSA is high in many endocrine disorders including both insulin-dependent and non-insulin-dependent diabetes but the reasons for this are not known. We wished to test the hypothesis that central respiratory motor output to the upper airway muscles is preferentially impaired in a rat model of diabetes mellitus. Sternohyoid (SH) and diaphragm (DIA) EMG activities were recorded in control and streptozotocin (STZ)-induced diabetic rats during normoxia, hypoxia (7.5% O2 in N2) and asphyxia (7.5% O2 and 3% CO2) under pentobarbitone anaesthesia. SH EMG responses to acute hypoxia and asphyxia were significantly impaired in STZ-induced diabetic rats compared to control animals (+47.1 +/- 5.7 vs. +11.7 +/- 1.9% during hypoxia in control and diabetic animals respectively and +56.5 +/- 7.9 vs. +15.7 +/- 5.0% during asphyxia). However, DIA EMG responses to hypoxia and asphyxia were not different for the two groups. We propose that the higher prevalence of OSA in diabetic patients is related to preferential impairment of cranial motor output to the dilator muscles of the upper airway in response to physiological stimuli.

Analysis of Variance↗

Magnesium sulfate therapy during asphyxia in near-term fetal lambs does not compromise the fetus but does not reduce cerebral injury.

OBJECTIVE: Our purpose was to investigate (1) the safety of fetal magnesium sulfate treatment and (2) possible beneficial effects on the brain during perinatal asphyxia. STUDY DESIGN: In 20 chronically instrumented fetal lambs (gestational age 125.8 +/- 3.5 days) four total umbilical cord occlusions for 5 minutes were repeated at 30-minute intervals. Fetuses received either saline solution (n = 11) or magnesium sulfate (n = 9) as a bolus of 300 mg intravenously 2 hours before occlusions, followed by an infusion of 100 mg/hr until 1 hour after occlusions. RESULTS: In the treated fetuses plasma magnesium levels rose from 0.85 +/- 0.20 to 2.23 +/- 0.40 mmol/ L. Occlusions induced asphyxia, associated with mortality; 4 of 11 fetuses in the control group versus 1 of 9 in the magnesium-treated group died (not significant). Fetal electroencephalographic activity decreased and cerebral impedance increased during occlusions. Maximum spike and seizure activity occurred 5 to 10 hours after asphyxia. Neuronal loss was primarily localized in the corpus striatum. Magnesium caused no alterations in blood pressure, heart rate, or cerebral and peripheral blood flow, nor did it influence electrophysiologic responses or neuronal loss. CONCLUSIONS: Administration of magnesium sulfate was safe but did not offer significant cerebral protection from asphyxia in the near-term fetal lamb.

Animals↗

Prediction of perinatal asphyxia with nucleated red blood cells in cord blood of newborns.

OBJECTIVE: To determine normal level of nucleated red blood cells (NRBC) per 100 white blood cells (WBC) in cord blood of term non-asphyxiated newborns and to investigate variations in NRBC counts in perinatal asphyxia. METHODS: A total of 75 cases were studied. Levels of NRBC per 100 WBC in umbilical venous blood were compared between 26 asphyxiated newborns (group I) and 49 non-asphyxiated newborns (group II). Correlation with neonatal outcome was also evaluated. RESULTS: The mean (+/-S.D.) NRBC per 100 WBC level in umbilical blood of newborns in group I was 16.5+/-6.4, range 3-25; whereas that in group II was 8.6+/-7.01, range 1-26. This difference was statistically significant (P<0.001). A statistically significant negative correlation existed between NRBC level and markers of acute intrapartum asphyxia, Apgar score and umbilical arterial pH (r=-0.50, P<0.001 and r=-0.48, P<0.001, respectively). Positive correlation was demonstrated with evidence of chronic antepartum asphyxia, presence of pregnancy induced hypertension and intrauterine growth restriction (r=2.66, P=0.02). A high NRBC count in umbilical blood correlated with poor early neonatal outcome. CONCLUSIONS: The level of NRBC per 100 WBC correlates both with acute as well as chronic antepartum asphyxia. Further, it can be used as a reliable index of early neonatal outcome.

Apgar Score↗

Noninvasive diagnosis of neonatal asphyxia and intraventricular hemorrhage by Doppler ultrasound.

The cerebrovascular hemodynamic alterations in asphyxia and intracerebral-intraventricular hemorrhage were determined by monitoring the pulsatile flow changes in the anterior cerebral arteries using Doppler ultrasound. The pulsatility index measurements, which were calculated from the recorded changes in Doppler frequency shifts, were obtained in four groups of newborn infants with the following diagnoses: Group I--normal term (n=21); Group II--asphyxia (n=12); Group III--IC-IVH (n=14); and Group IV--asymptomatic preterm (n=11). There was no significant difference between PI values of Groups I and IV. Compared to normal term infants, those diagnosed as having asphyxia had significantly lower PI measurements and those with IC-IVH had significantly higher PI values than the asymptomatic pretern infants. Serial Doppler studies were also performed in 22 preterm infants with respiratory distress. One-half of these infants subsequently developed IC-IVH. Prior to hemorrhage, their PI measurements were significantly lower than those who did not eventually have the complication. The low PI values in asphyxia and prior to the onset of IC-IVH indicate vasodilation and decreased resistance to blood flow. In IC-IVH, the high PI measurements denote the opposite. In infants with respiratory distress in the presence of significant vasodilation and lowered vascular resistance, CBF may increase to excessive levels, resulting in IC-IVH.

Asphyxia Neonatorum↗

Intrapartum asphyxia: a rare cause of cerebral palsy.

Data on all children with spastic cerebral palsy (N = 183) and on a matched group of control children (N = 549) born in Western Australia between 1975 and 1980 were compared to investigate the relationship between birth asphyxia and spastic cerebral palsy. Information on perinatal events for both the children with cerebral palsy and the control subjects was collected by means of epidemiologic methods to reduce bias. An association between clinically observed perinatal signs of birth asphyxia and spastic cerebral palsy was found (relative risk 2.84; 95% confidence interval 1.85 to 4.37). The population-attributable risk proportion was 14.1%. The likelihood of birth asphyxia's causing perinatal brain damage was assessed by two independent observers using defined criteria. It was estimated that in only about 8% (15/183) of all the children with spastic cerebral palsy was intrapartum asphyxia the possible cause of their brain damage. The contribution of intrapartum events and obstetric mismanagement to overall cerebral palsy rates is probably less than was previously thought.

Apgar Score↗

Multiple organ involvement in perinatal asphyxia.

OBJECTIVES: (1) To evaluate the frequency and spectrum of severity of multisystem dysfunction after perinatal asphyxia and (2) to analyze the relationship between the clinical and biochemical markers of perinatal asphyxia and multiorgan involvement. STUDY DESIGN: Seventy-two consecutive term newborn infants with perinatal asphyxia were studied prospectively. Systematic neurologic, renal, pulmonary, cardiac, and gastrointestinal evaluations were performed. Involvement of each organ was classified as moderate or severe. RESULTS: Involvement of one or more organs occurred in 82% of the infants; the central nervous system (CNS) was most frequently involved (72%). Severe CNS injury (7 infants) always occurred with involvement of other organs, although moderate CNS involvement was isolated in 14 infants. Renal involvement occurred in 42%, pulmonary in 26%, cardiac in 29%, and gastrointestinal in 29% of the infants; 15% neonates had renal failure and 19% had respiratory failure. The Apgar scores at 1 and 5 minutes were the only perinatal factors related to the number of organs involved and the severity of involvement; the Apgar score at 5 minutes had the stronger independent association. No relationship or organ dysfunction was found with the umbilical cord arterial blood pH, meconium-stained amniotic fluid, umbilical cord abnormalities, presentation, or type of delivery. CONCLUSIONS: Our findings indicate that the Apgar score at 5 minutes, in infants who have other criteria for asphyxia, is the perinatal marker that may best identify infants at risk of organ dysfunction.

Apgar Score↗

Adrenocorticotropin counteracts the increase in free radical blood levels, detected by electron spin resonance spectrometry, in rats subjected to prolonged asphyxia.

We investigated the influence of the adrenocorticotropic fragment 1-24 [ACTH-(1-24)] on the blood levels of highly-reactive free radicals in a rat model of prolonged asphyxia. Anesthetized animals were endotracheally intubated and mechanically ventilated with room air; after a 10 min stabilization period, the ventilator was turned off to induce asphyxia for 5 min; then, the ventilator was turned back on, and, simultaneously, the rats were intravenously treated with either ACTH-(1-24) (160 microg/kg in a volume of 1 ml/kg) or equivolume saline. Free radicals were detected in arterial blood by electron spin resonance spectrometry using an ex vivo method that avoids injection of the spin-trapping agent employed (alpha-phenyl-N-tert-butylnitrone). Arterial pressure, electrocardiogram (ECG) and electroencephalogram (EEG) were monitored for the 60 min observation period, or until prior death. At the end of the 5 min period of respiratory arrest, blood levels of free radicals were about four times higher than those of the basal, pre-asphyxia condition, arterial pressure had dramatically decreased, ECG showed marked bradycardia and signs of ischemic damage and the EEG had become isoelectric. Treatment with ACTH-(1-24) produced an immediate normalization of the blood levels of free radicals, associated with a restoration of cardiovascular function and full recovery of EEG within 30-45 min; all the saline-treated rats, on the other hand, died within 6.89 +/- 0.96 min. These results provide direct evidence that in a severe condition of prolonged asphyxia there is a rapid and massive production of highly-reactive free radicals and suggest that the resuscitating effect of adrenocorticotropin fragments in severe hypoxic conditions may be largely due to the inhibition of free radical overproduction during tissue reoxygenation.

Adrenocorticotropic Hormone↗