[Asphyxia neonatorum. I. On the etiology of asphyxia neonatorum].
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Acidosis, Respiratory↗
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[Nursing of infants with asphyxia neonatorum. Keypoints in nursing of infants with asphyxia neonatorum: from a physician's viewpoints].
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Asphyxia Neonatorum↗
[Sodium and potassium balance during the 1st days of life in the bodies of healthy newborn infants and in asphyxia neonatorum]f life in the bodies of healthy newborn infants and in asphyxia neonatorum].
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Asphyxia Neonatorum↗
Asphyxia due to oxygen deficiency by gaseous substances.
The determination of the cause of death in asphyxiation gas cases is very difficult because of the variation in circumstances surrounding such deaths. To clarify the cause of death and to identify the factors involved in asphyxia, the symptoms during asphyxia, the concentration of gases at the respiratory arrest, the time to death and the concentration of the gaseous substances in the tissues were studied using rats and six gases. Three inhalations were used: (1) rapid asphyxia (2-3 min) in the exposure chamber in which the oxygen was depleted completely, (2) prolonged asphyxia (20-25 min) by gradually depleted oxygen, and (3) asphyxia by the inhalation of gases saturated with a critical gas concentration, maintaining the O2 at 20% (60 min). In the rapid asphyxia groups, respiratory arrest occurred within 30 to 40 s, followed by cardiac arrest 2 or 3 min thereafter. Severe convulsions were observed only with the use of nitrogen. In the prolonged asphyxia groups, respiratory arrest occurred at the concentration of 4-5% O2 with non-toxic gases (N2, CH4, N2O, and propane). The toxic gases CO2 and Freon-22 produced respiratory arrest at the concentration of 6.6-8.0% O2 (60-67% CO2) and 13-14% of O2 (30-35% Freon-22), respectively. Variations in the concentrations of the gases among the tissues was observed according to the type of asphyxia, type of gas and the duration of exposure. The concentration of the fat-soluble gases in the adipose tissue showed marked variation according to the duration of the exposure. The distribution pattern of methane was different from those of the other gases, in which the variation of concentrations among the tissues except lung were little in both rapid and prolonged asphyxia. These phenomena were considered to be attributable to the solubility of the gaseous substances in blood and tissues. Atrophy in the alveoli was observed after the rapid asphyxia with CO2 and N2O. Local hemorrhaging in the lungs was also observed, especially in CO2 asphyxia. The risks of oxygen-depletion asphyxia are the rapid reaction of loss of consciousness and respiratory and cardiac arrest. This paper presents valuable findings for the diagnosis of the cause of death and estimating the situation of the accident in cases of asphyxia.
Animals↗
Influence of maternal, obstetric and fetal risk factors on the prevalence of birth asphyxia at term in a Swedish urban population.
BACKGROUND: The influence of maternal, obstetric and fetal risk factors on the prevalence of birth asphyxia at term in a Swedish urban population. OBJECTIVE: To investigate risk factors for Apgar score-defined birth asphyxia, birth asphyxia with hypoxic-ischemic encephalopathy and birth asphyxia-related death/disability. MATERIAL AND METHODS: Retrospective case-control study in term neonates with birth asphyxia defined as Apgar score < 7 at 5 min. Cases originating from nonasphyctic causes (e.g. infection, maternal sedation) were excluded. Hypoxic-ischemic encephalopathy was diagnosed according to criteria by Sarnat. Maternal, obstetric and fetal risk factors were registered in 225 cases of birth asphyxia diagnosed in 42 203 live births occurring in the urban Swedish population studied. A matched control group was used for statistical evaluation. RESULTS: Asphyxia was associated with single civil status, OR = 7.1 (95%CI 2.0, 27.6); intrauterine meconium release, OR = 4.1 (95%CI 1.8, 9.8); operative delivery, OR = 8.7 (95%CI 3.4, 24.6); breech delivery, OR = 20.3 (95%CI 3.0, 416.5); oxytocin augmentation, OR = 2.9 (95%CI 1.4, 6.3); cord complication, OR = 15.8 (95%CI 2.1, 341.5); external compression to assist delivery OR = 6.2 (95%CI 1.3, 45.7); and cardiotocography score, OR = 0.5 (95%CI 0.4, 0.6). Normal fetal heart rate variability, OR = 0.4 (95%CI 0.2, 0.6), repeated late decelerations irrespective of amplitude or repeated variable decelerations, OR = 29.4 (95%CI 5.7, 540.8) or occasional late or variable decelerations, OR = 2.2 (95%CI 1.3, 3.8), and no accelerations, OR = 5.2 (95%CI 2.0, 16.4), were associated with asphyxia. Operative or instrumental delivery was more common in all three asphyxia groups compared with controls. Leanness was a risk factor for asphyxia and for hypoxic-ischemic encephalopathy. Maternal age, smoking and illnesses, time of delivery (day/night, seasonal) and previous caesarean section were not associated with birth asphyxia. CONCLUSIONS: An association between neonatal asphyxia and cardiotocography parameters, intrauterine meconium release, operative delivery, breech delivery, single civil status, oxytocin augmentation, cord complication, external compression to assist delivery and neonatal leanness was found. Abnormal fetal heart rate variability, repeated late decelerations irrespective of amplitude or repeated variable decelerations, occasional late or variable decelerations and no accelerations were associated with asphyxia.
Apgar Score↗
Cochlear inner hair cells: effects of transient asphyxia on intracellular potentials.
Intracellular potentials were recorded from inner hair cells in the guinea pig cochlea. Transient asphyxia was induced by interrupting respiration for brief periods. Asphyxia caused a hyperpolarization of the resting membrane potential (resting Em). The hyperpolarization averaged 2.9 mV for 30 s asphyxias and 5.7 mV for 45 s asphyxias. The membrane potential recovered quickly after normal ventilation was resumed. Asphyxia also induced a rapid and profound decrease of the d.c. receptor potential in response to moderate intensity tone bursts at the characteristic frequency of the inner hair cell. At maximal depression, the receptor potential was reduced about 60% for a 30 s asphyxia and 100% for a 45 s asphyxia. The receptor potential recovered slowly after normal ventilation was resumed. A similar percent reduction and time course of recovery were observed for the a.c. receptor potential. In recordings from the same animals, the round window compound action potential (CAP) was as severely depressed by asphyxia as the hair cell receptor potentials. The time course of recovery for the CAP was similar to the slow recovery of the d.c. receptor potential. In contrast, the round window cochlear microphonics (CM) and the endolymphatic potential (EP) were affected less by asphyxia and recovered quickly after ventilation was resumed. Frequency tuning curves (FTCs) for the d.c. receptor potential were measured during the period of maximal receptor potential depression. These FTCs showed decreased tip sensitivity and a decrease in sharpness of tuning, as measured by the Q10. These changes were fully reversible. Low frequency (tail) segments of the FTCs were much less affected by asphyxia. The inner hair cell FTC changes during asphyxia were compared with neural FTC changes reported by other investigators. The similarities lead us to the conclusion that the inner hair cell and the auditory neural response to sound are equally sensitive to asphyxia.
Animals↗
Effects of perinatal asphyxia on the mesostriatal/mesolimbic dopamine system of neonatal and 4-week-old male rats.
The present study was undertaken in order to study the effects of perinatal asphyxia on tyrosine hydroxylase (TH) activity, dopamine levels and turnover, and dopamine metabolites (3,4-dihydroxyphenylacetic acid, DOPAC, homovanillic acid, HVA, and 3-methoxytyramine, 3-MT, analyzed by high-performance liquid chromatography, HPLC) measured in the basal ganglia of the 20- to 40-min-old newborn and 4-week-old male rat. Asphyxia was induced in pups by placing the fetuses, still in their uterus horns removed by hysterectomy from pregnant rats at full term, in a 37 degrees C water bath for 15-16 min or 19-20 min. Following asphyxia, the uterus horns were opened, and the pups were removed and stimulated to breathe. A 100% and 50-80% pup survival was obtained following 15-16 min and 19-20 min of asphyxia, respectively. Acute changes were studied in brains from newborn pups 20-40 min after delivery, and long-term changes were studied in brains from 4-week-old rats. No changes in TH-activity could be observed in the substantia nigra/ventral tegmental area (SN/VTA), the striatum, or the accumbens nucleus/olfactory tubercle (ACC/TUB), in the newborn or the 4-week-old rat. In the newborn rat, 19-20 min of asphyxia increased (as compared to controls) dopamine levels in the SN/VTA to 136 +/- 14% and in the ACC/TUB to 160 +/- 10%, indicating an increased synthesis and/or release of dopamine. DO-PAC levels were increased in the SN/VTA to 150 +/- 14% and in the ACC/TUB to 151 +/- 10%, and HVA levels were increased to 152 +/- 16% in the striatum and to 117 +/- 4% in the ACC/TUB. Following 15-16 min of asphyxia, dopamine levels were increased to 130 +/- 12% in the ACC/TUB, and DOPAC levels were increased to 135 +/- 6% and 130 +/- 12% in the SN/VTA and the ACC/TUB, respectively. This suggests that the increased dopamine levels may preferably reflect an increased release of dopamine following perinatal asphyxia. In the 4-week-old rat, dopamine levels were decreased in the SN/VTA to 71 +/- 4%, in the striatum to 52 +/- 8%, and in the ACC/TUB to 53 +/- 7%, following 19-20 min of perinatal asphyxia as compared to controls. No changes were observed in DOPAC, HVA, or 3-MT levels, indicating that the reduced dopamine levels reflect a reduced dopamine synthesis following perinatal asphyxia. A decrease in dopamine utilization was observed in the striatum to 15 +/- 8% and in the ACC/TUB to 9 +/- 13% following 19-20 min of perinatal asphyxia as compared to controls. This indicates that perinatal asphyxia produced long-lasting reductions in activity in the mesostriatal/mesolimbic dopamine systems in the 4-week-old rat.
3,4-Dihydroxyphenylacetic Acid↗
Comparison between hypothermia and glutamate antagonism treatments on the immediate outcome of perinatal asphyxia.
This study investigated the influence of temperature or glutamate antagonism on the immediate outcome of perinatal asphyxia. Perinatal asphyxia was produced by water immersion of fetus-containing uterus horns removed by cesarean section from ready to deliver rats. The uterus horns were kept in a water bath for different time periods, before the pups were delivered and stimulated to breathe. After delivery, the pups were assessed for behavior and for systemic glutamate, aspartate, lactate and pyruvate levels measured with in vivo microdialysis, or ex vivo for energy-rich phosphates, including adenosine triphosphate (ATP), in brain, heart and kidney. In a series of experiments, asphyxia was initiated in a water bath at 37 degrees C, before the pup-containing uterus horns were moved for different time intervals to a 15 degrees C bath. In another series of experiments, the mothers were treated with N-methyl-D-aspartate (NMDA) antagonist, dizocilpine (MK-801), or alpha-amino-3-hydroxy-methylisoxazole-4-propionic acid (AMPA) antagonist,2,3-dihydroxy-6-nitro-7-sulfamoyl benzo(f) quinoxalin NBQX) 1 h before hysterectomy and asphyxia at 37 degrees C. The rate of survival rapidly decreased following exposure to more than 16 min of asphyxia, and no survival could be observed after 22 min of asphyxia. An LD50 was estimated to occur at approximately 19 min of asphyxia. The outcome was paralleled by a decrease in ATP in kidney, followed by a decrease in heart and brain. A maximal decrease in ATP was observed after 20 min of asphyxia in all tissues. Systemic microdialysis revealed that glutamate, aspartate and pyruvate levels were increased with a peak after 5 min of asphyxia. In contrast, lactate levels increased along with the length of the insult. Survival was increased when the pup-containing uterus horns were moved from a 37 degrees C to a 15 degrees C bath, at 15 min of asphyxia (the LD50 was thus increased to 30 min). If the shift occurred at 10 or 5 min of asphyxia, the LD50 increased to 80 or 110 min, respectively. The effect of glutamate antagonism was minor compared to hypothermia; the best effect (an increase in the LD50 to approximately 22 min) was observed after combining AMPA and NMDA antagonists.
Adenosine Triphosphate↗
[Perinatal asphyxia, hypoxic-ischemic encephalopathy and neurological sequelae in full-term newborns. II. Description and interrelation].
INTRODUCTION: There have been several attempts to relate either perinatal asphyxia at birth or abnormal neurological findings after asphyxia in neonatal period (hypoxic-ischemic encephalopathy), to outcome. OBJECTIVE: To investigate, in full-term infants, the relation between perinatal asphyxia, hypoxic-ischemic encephalopathy and neurologic sequelae at follow-up, and to define the main neurologic sequelae (cerebral palsy, mental retardation, neonatal death). Material and method. Prospective epidemiologic study over perinatal asphyxia in term neonates born in Universitary Hospital San Juan (Alicante, Spain) between November 1991-February 1995. Perinatal asphyxia was graded as non severe (1-minute Apgar score < or = 6 and/or umbilical artery pH < 7.20, with abnormal fetal heart rate patterns and/or meconium-stained amniotic fluid, and the need for immediate neonatal resuscitation) and severe (1-minute Apgar score < or = 3 and umbilical artery pH < 7.10). Hypoxic-ischemic encephalopathy was graded as mild, moderate and severe based on classification of Levene and Sarnat & Sarnat. The abnormalities on psicomotor development are based in the neurologic 'alert signs' and in the neurologic sequelae; this sequelae was graded as mild, moderate and severe based on classification of Finer and Amiel-Tison. The relationships between these variables are studied by univariant and multivariant analysis (Cox's regression). RESULTS: The incidence of neurologic sequelae, in 115 asphyxiated full-term infants follow-up at least 12-24 months, was 16.5%; 4 cases of severe sequelae, 4 moderate and 11 mild. The overall asphyxia-related infant mortality rate was 0.87/1.000 live births. The main sequelae detected at follow-up was motor disability, and other disabilities like mental retardation, epilepsy, sensorial defects, were infrequents. The incidence of cerebral palsy was 0.87/1.000 live births, and 2.6% asphyctic term neonates. We found a statistically significant (p < 0.001) association between severity of perinatal asphyxia and/or evidence of hypoxic-ischemic-encephalopathy and the neurological development at follow-up. Of the several factors associated to risk of neurologic sequelae on univariant analysis, only two were independently associated on multivariant analysis: severe perinatal asphyxia (RR = 2.82; IC = 1.07-7.39) and postasphyctic encephalopathy (RR = 4.17; IC = 1.48-11.75). CONCLUSIONS: Most survivors of perinatal asphyxia do not have adverse sequelae. The best predictive tool for the neurological prognosis at follow-up was severe perinatal asphyxia at birth and evidence of encephalopathy in neonatal period. Our study confirm that perinatal asphyxia is infrequently the cause of cerebral palsy and mental retardation.
Asphyxia Neonatorum↗
Determining the contribution of asphyxia to brain damage in the neonate.
Studies in the research laboratory have demonstrated the complex relationship between fetal and newborn asphyxia and brain damage, a balance between the degree, duration and nature of the asphyxia and the quality of the cardiovascular compensatory response. Clinical studies would support the contention that the human fetus and newborn behave in a similar manner. An accurate diagnosis of asphyxia requires a blood gas and acid base assessment. The clinical classification of fetal asphyxia is based on a measure of metabolic acidosis to confirm that fetal asphyxia has occurred and the expression of neonatal encephalopathy and other organ system complications to express the severity of the asphyxia. The prevalence of fetal asphyxia at delivery is at term, 25 per 1000 live births of whom 15% are moderate or severe; and in the preterm, 73 per 1000 live births of whom 50% are moderate or severe. It remains to be determined how often the asphyxia recognized at delivery may have been present before the onset of labor. There is a growing body of indirect and direct evidence to support the contention that antepartum fetal asphyxia is important in the occurrence of brain damage. Although much of the brain damage observed in the newborn reflects events that occurred before delivery, newborn asphyxia and hypotension, particularly in the preterm newborn, may contribute to the brain damage accounting for deficits in surviving children.
Animals↗
[Significance of intrapartum asphyxia for the onset of fetal brain damage].
The prevalence of cerebral palsy is around 0.2% and has remained constant during the last 30 years. Retrospective case-control studies do not show a clear correlation between perinatal asphyxia and the development of cerebral palsy. Less than 10% of all cerebral palsy cases show signs of severe asphyxia during labour and delivery as the major pathological and likely cause for the brain damage. Severe cases of birth asphyxia with multiorgan defects and signs of hypoxic-ischaemic encephalopathy have a high mortality and the risk of permanent brain damage is increased by a factor of 10 to 30. Inspite of this, 90% of the survivors show normal development. The association between perinatal asphyxia and neuromotor developmental disturbances does not provide proof of a causal connection. Intrapartal abnormalities of foetal heart rate monitoring are not specific for foetal asphyxia and show only a limited correlation with the apgar and the cord blood pH. Foetal heart rate recording with pathological changes does not imply an elevated risk of later problems with neuromotor development and the widespread use of foetal heart rate monitoring during labour and delivery did not result in a significant reduction in the frequency of cerebral palsy. In addition to malformations, various forms of antinatal pathology like prematurity, intrauterine growth retardation and congenital infections are related to the development of brain damage. In each case of birth asphyxia, additional pathology like congenital infections or malformations in addition to changes in brain structure as a result of asphyxia must be ruled out using specific diagnostic methods like ultrasound, computed tomography and magnetic resonance. Furthermore, a careful documentation of the developmental phases is of fundamental importance for a final evaluation. In otherwise unremarkable deliveries at term, four conditions must be fulfilled to postulate a causal relationship between asphyxia and the development of cerebral palsy: The asphyxia must be severe. During the early neonatal period, clinical symptoms of moderate to severe hypoxic-ischaemic encephalopathy with functional impairment of other organs must be present. The neurological symptoms must be typical for intrapartal asphyxia. Documentation of diagnostic evaluation to rule out other forms of pathology must be complete (21).
Asphyxia Neonatorum↗
Antepartum fetal asphyxia in the preterm pregnancy.
OBJECTIVE: The objective of this report was to provide insight into the frequency and characteristics of antepartum fetal asphyxia in pregnancies that are delivered preterm. STUDY DESIGN: The characteristics of 30 pregnancies that were delivered preterm with biochemically confirmed antepartum fetal asphyxia (umbilical artery base deficit of >12 mmol/L) that were derived from >1 decade of experience in a single tertiary care obstetric unit were examined. Antepartum clinical characteristics, fetal assessment tests, and neonatal complications were documented. Fetal asphyxia was classified as mild, moderate, or severe on the basis of an umbilical artery base deficit (>12 mmol/L) and newborn encephalopathy and other organ system complications. RESULTS: Antepartum fetal asphyxia accounted for at least 34% of the fetal asphyxia in the pregnancies that were delivered preterm. Predictive criteria that led to intervention and diagnosis included clinical risk factors and, particularly, abnormal fetal assessment tests. The 50% incidence of moderate or severe asphyxia in the antepartum preterm pregnancies compares with 15% in term pregnancies. Moderate or severe asphyxia occurred with equal frequency with early and delayed intervention. CONCLUSION: Fetal asphyxia in pregnancies that were delivered preterm is present frequently before the onset of labor. Abnormal fetal assessment tests are valuable predictors of antepartum fetal asphyxia. The increased frequency of moderate and severe fetal asphyxia in the pregnancy that is delivered preterm implies a greater likelihood of long-term morbidity or death.
Asphyxia↗
Urinary uric acid/creatinine ratio as an additional marker of perinatal asphyxia.
PURPOSE: To study the validity of urinary uric acid (UA) as a marker of perinatal asphyxia in term and premature infants. METHODS: The urinary ratio of UA to creatinine (Cr) was obtained within 24 hours after birth in four groups of infants: 17 term infants and 18 premature infants with perinatal asphyxia, and 22 healthy term infants and 20 premature infants without perinatal asphyxia. Perinatal asphyxia was defined as an Apgar score of 3 or less at 1 minute or 5 or less at 5 minutes, and/or a first blood gas pH of less than 7.25 and a base deficit of at least 12 mmol/L. RESULTS: The urinary ratio of UA to Cr was significantly higher in term infants with perinatal asphyxia than in term infants without asphyxia (1.53 +/- 0.71 vs 0.73 +/- 0.45; p < 0.005). The same result was found between premature infants with and without perinatal asphyxia (3.89 +/- 1.84 vs 2.45 +/- 0.88; p < 0.01). The urinary ratio of UA to Cr in premature infants was significantly higher than in term infants. When the urinary ratio of UA to Cr was greater than 0.95, perinatal asphyxia was identified with a sensitivity of 80% and a specificity of 71% in term infants. In premature infants, a cut-off value of UA/Cr for perinatal asphyxia of 2.9 had a sensitivity of 71% and a specificity of 70%. CONCLUSIONS: The results of this study indicate that the urinary ratio of UA to Cr may be used as an additional marker of perinatal asphyxia in term and premature infants. In comparison with other markers such as xanthine, hypoxanthine, and ascorbic acid, it is a simple, quick, and inexpensive way to detect hypoxic episodes in a neonatal intensive care unit within 24 hours after birth.
Asphyxia Neonatorum↗
[The changes in free radical and prostaglandin metabolism in newborn infants with asphyxia].
Blood plasma thromboxane-B2 (TXB2) and 6-keto-PGF1 alpha levels were determined by radioimmunoassay technique during the first six to sixteen hours of life in 16 newborn infants with severe asphyxia, 18 newborn infants with mild asphyxia and 27 normal term neonates. Plasma lipid peroxidation (LPO) content was measured by TBA-colour-contrast method in 15 infants with severe asphyxia, 17 infants with mild asphyxia and 24 healthy term newborn infants. The results showed that blood plasma LPO, TXB2 and 6-keto-PGF1 alpha levels in infants suffering from severe asphyxia were higher than those in infants with mild asphyxia and normal infants (P < 0.01), but no significant difference was noted between the mild asphyxia group and normal control group (P > 0.01). These suggest that production of free radicals is increased and prostaglandin metabolism is triggered in the infants with severe asphyxia, that cerebral ischemia and hypoxia caused by asphyxia contributes to the augmented production of prostaglandins and free radicals, and that accumulation of free radicals and prostaglandin enhances brain damage and the metabolism of arachidonic acid appears to be an important source of the free radicals in infants with intrauterine asphyxia.
6-Ketoprostaglandin F1 alpha↗
Effect of perinatal asphyxia on systemic and intracerebral pH and glycolysis metabolism in the rat.
The effects of perinatal asphyxia on systemic and brain pH and glycolysis metabolism were studied in the rat. Perinatal asphyxia was induced by immersing pup-containing uterus horns, obtained by cesarean section from rats within the last day of gestation, in a water bath at 37 degrees C for various periods of time (0-23 min). Subcutaneous levels of pyruvate (Pyr), lactate (Lact), glutamate (Glu), and aspartate (Asp) were monitored with microdialysis 40-80 min after delivery. In parallel experiments, the pups were sacrificed 40 min after delivery and the heart and brain were removed for measuring pH. Brain (striatum) Pyr, Lact, Glu, and Asp levels were also analyzed. A decrease in the rate of survival was first observed following asphyctic periods longer than 16 min, and no survival could be observed after 22 min of asphyxia. In control (cesarean-delivered) pups, heart and brain pH were 7.36 +/- 0.01 (N = 8) and 7.30 +/- 0.01 (N = 8), respectively. Significant decreases in pH were first observed following 5-6 and 10-11 min of asphyxia, in heart and brain, respectively. In both regions pH decreased along with the length of asphyxia, but a decrease below 7 was only observed in the brain, following asphyctic periods longer than 16 min. A significant increase in subcutaneous Lact levels was first observed following 2-3 min of asphyxia, with a maximum after 20-21 min of asphyxia. In the brain, the increase in Lact levels was delayed compared to that observed in subcutaneous tissue. Pyr and Asp levels increased in subcutaneous tissue following perinatal asphyxia and decreased in brain tissue following > 15 min of asphyxia. Glu levels were increased subcutaneously by moderate (5-16 min) asphyctic periods, but, in the brain, were only transiently increased by 10-11 min of asphyxia. Thus, changes in systemic pH, glycolysis, and excitatory amino acid metabolism are observed following shorter asphyctic periods than are changes in the brain. In particular, increases in subcutaneous Lact levels precede: (i) a decrease in brain pH, (ii) an increase in brain Lact levels, (iii) a decrease in the rate of survival, and, probably, (iv) brain damage. It is suggested that monitoring Lact levels by subcutaneous microdialysis is a useful method for predicting the outcome produced by hypoxic-ischemic insults.
Animals↗
The clinical diagnosis of asphyxia responsible for brain damage in the human fetus.
OBJECTIVE: Our objective was to review the clinical findings in infants who died in the perinatal period with brain damage attributable to asphyxia. STUDY DESIGN: The neuropathologic findings in 208 perinatal deaths have been reviewed. Thirty cases (22 fetal, eight newborn) had evidence of white matter or neuronal necrosis due to asphyxia. The clinical course of the pregnancy in 22 cases with brain damage attributable to fetal asphyxia were examined. RESULTS: The diagnosis of asphyxia was confounded by several factors: (1) asphyxia may occur at any time in the last half of pregnancy, (2) 50% of the antepartum asphyxia occurred when the pregnancy had no risk factors, (3) periodic fetal assessment in the complicated preterm pregnancies failed to identify the asphyxial episodes in the remaining cases of antepartum asphyxia, and (4) indicators of fetal asphyxia in the cases of intrapartum fetal asphyxia were obtained after the central nervous system injury had occurred. CONCLUSION: These findings highlight the difficulty in the diagnosis of fetal asphyxia at a stage that could permit intervention to prevent brain damage.
Adult↗
The prediction and prevention of intrapartum fetal asphyxia in preterm pregnancies.
OBJECTIVE: This study was undertaken to examine the contribution of electronic fetal heart rate monitoring in the prediction and prevention of intrapartum fetal asphyxia in the preterm pregnancy. STUDY DESIGN: The outcome of 40 pregnancies with biochemically confirmed intrapartum fetal asphyxia (ie, an umbilical artery base deficit >12 mmol/L) was examined. This included 20 pregnancies that were delivered abdominally matched with 20 pregnancies that were delivered vaginally. Antepartum and intrapartum clinical risk factors and newborn complications were documented. The interpretation of the fetal heart rate record as determined by the responsible clinicians was recorded. Fetal asphyxia was classified as mild, moderate, or severe on the basis of an umbilical artery base deficit of >12 mmol/L and newborn encephalopathy and other organ system complications. RESULTS: Fetal asphyxia was classified as mild in 21 pregnancies and as moderate or severe in 19 pregnancies. The fetal heart rate record was predictive of fetal asphyxia in 27 pregnancies and nonpredictive in 11 pregnancies. The predictive fetal heart rate record was the primary indication for intervention in 21 of the 24 pregnancies that were delivered by cesarean delivery in the first stage or operative vaginal delivery in the second stage of labor. Newborn outcome may have been influenced by intervention and delivery because of a predictive fetal heart rate record in 10 pregnancies with mild fetal asphyxia and in 9 pregnancies with moderate or severe fetal asphyxia. CONCLUSION: Electronic fetal monitoring is a useful screening test for the prediction of intrapartum fetal asphyxia in the preterm pregnancy. A predictive fetal heart rate record was the principle indication that led to intervention and delivery. A prediction of fetal asphyxia that leads to intervention and delivery may prevent or modify moderate or severe newborn morbidity as the result of fetal asphyxia.
Cesarean Section↗
Long-term effect of perinatal and postnatal asphyxia on developing human auditory brainstem responses: peripheral hearing loss.
Peripheral hearing was assessed by examining brainstem auditory evoked responses (BAER) in children who suffered perinatal or postnatal asphyxia, particularly in those with residual neurodevelopmental deficits, to investigate the long-term effect of asphyxia on the developing auditory sensitivity. The BAER data were collected at least 6 months after the episode of asphyxia. Of the children who suffered perinatal asphyxia, hearing loss was found more frequently in those who exhibited residual neurodevelopmental deficits (17.1%) than in those who did not (6.3%), but this difference did not reach statistical significance. This implied that the long-term effect of perinatal asphyxia on the peripheral auditory system and its effect on the central nervous system may be relatively discrete or not closely correlated. The occurrence of hearing loss did not appear to be closely related to the degree of perinatal asphyxia, although hearing loss occurred more frequently in the children after severe asphyxia compared to those after mild asphyxia. There was no evidence for permanent hearing loss in the children who survived severe, prolonged postnatal asphyxia and exhibited residual neurodevelopmental deficits. These findings suggest that a critical period of particular sensitivity to the effect of hypoxia may exist during the development of the human peripheral auditory system. This period may range from some time prenatally to some time shortly after birth, probably the third postnatal month. After that, hypoxia is unlikely to lead to permanent hearing loss.
Age Factors↗