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PubMedDate not supplied

[Relation between fetal hypoxia, neonatal asphyxia and hypoxic-ischemic encephalopathy].

Clinical data, duration of labour, mode of delivery and possibilities of fetal heart rate monitoring in predicting perinatal asphyxia and neonatal encephalopathy in 143 consecutively delivered asphyxiated infants and 143 paired healthy infants are analyzed. Perinatal asphyxia occurred in only 2.6% of normal pregnancies and significantly more frequently in pregnancies complicated by gestosis. It is far more common in children subject to operative deliveries (15-20%) and when labour lasts longer than 12 hours, either in vertex or breech presentations. The occurrence of encephalopathy is less frequent in children delivered by cesarean section (1.6%) and almost three times more frequent than in vaginal breech deliveries. In asphyxiated children delivered vaginally, significantly more frequently CTG scores were prepathologic (38% versus 3.4%). In the cesarean section group the differences are not significant in prepathologic CTG scores but are highly significant when CTG scores were pathologic (36% versus 2.7%). The mean duration of the pathologic heart rate pattern is significantly longer in mild asphyxia in comparison to the control group (45 minutes versus 12.5 minutes). In moderate asphyxia the pathologic CTG pattern lasted 72.1 minutes and in severe asphyxia 52 minutes.

Asphyxia Neonatorum↗
PubMedDate not supplied

Brain damage from perinatal asphyxia: correlation of MR findings with gestational age.

MR scans of 25 patients who suffered asphyxia at known gestational ages were reviewed retrospectively. The gestational ages of the patients at the time of asphyxia ranged from 24 to 46 weeks. The MR pattern of brain damage in patients with prolonged partial asphyxia was seen to evolve in a predictable manner corresponding to the known maturation of the brain and its vascular supply. Patients at 24- and 26-weeks gestational age had irregularly enlarged ventricular trigones with minimal periventricular gliosis. Patients at 28-34 weeks had variably dilated ventricles with periventricular gliosis. The 36-week neonate had mild cortical and subcortical atrophy and gliosis superimposed on deep white matter and periventricular gliosis. Term neonates had significant cortical and subcortical gliosis and atrophy in the parasagittal watershed areas. Postterm neonates (44-46 weeks) showed cortical and subcortical watershed gliosis and atrophy with sparing of the immediate periventricular region. Two children suffered cardiocirculatory arrest; their scans revealed a different pattern of brain damage, demonstrating primarily brainstem, thalamic, and basal ganglia involvement. MR appears to be a powerful tool in the assessment of brain damage resulting from perinatal asphyxia that gives important clues to the time and nature of the asphyxia.

Adolescent↗
PubMed1990

[Analysis of 366 cases of neonatal asphyxia].

366 cases of neonatal asphyxia were studied during 1983-1988. Different management regimes were used for neonatal asphyxia of different causes. The occurrence of neonatal asphyxia decreased from 4.9% in 1983 to 3.0% in 1988 in this hospital. Conversely, the occurrence of high risk pregnancy increased from 76.2% to 80.9% during the same period. Umbilical cord problems, hypertonic and too frequent uterine contractions, placental insufficiency and prolonged labor were the main causes of neonatal asphyxia. Use of magnesium sulphate for hypertonic contraction, correct estimation of fetal weight, and early diagnosis and selection of indications of C.S. are important for the prevention of neonatal asphyxia. Antepartum diagnosis and management of cord problems have already been discussed.

Asphyxia Neonatorum↗
PubMed1989

Birth asphyxia and neurodevelopmental outcome.

Thirty six neonates with severe birth asphyxia (Apgar score less than or equal to 3 at 1 min), 32 with moderate birth asphyxia (Apgar score 4 to 6 at 1 min) and 35 controls (Apgar score greater than or equal to 7 at 1 min) matched for weight and gestation were followed up prospectively for neurodevelopmental outcome. Fetal distress occurred more frequently in babies with severe birth asphyxia when compared to controls (p less than 0.05). Six neonates with severe birth asphyxia had abnormal neurological signs such as delayed sucking, hypo or hypertonia, apneic spell or seizures. Of these, only two had delayed developmental milestones (Developmental Quotient less than 70) and features of cerebral palsy. Both of these babies developed seizures during first 24 hours, did not suck and required gavage feeding. The study highlights the fact that a vast majority of survivors of birth asphyxia enjoy good quality of life thus emphasizing the need for vigorous management of asphyxiated babies at birth.

Apgar Score↗
PubMed1988

Hypoxanthine: a marker for asphyxia.

It has been hypothesized that hypoxanthine concentrations in the blood of newborn infants are a marker of asphyxia. To test this hypothesis, we measured serum hypoxanthine levels in relationship to perinatal and neonatal asphyxia, and compared arterial hypoxanthine levels with arterial pH and base deficit. We also compared hypoxanthine levels of survivors with those of asphyxiated non-survivors. Forty-two newborns were classified as asphyxiated by either of two methods: 1) Infants from whom umbilical cord hypoxanthine levels were taken were classified as asphyxiated if they had an Apgar score of 6 or less at 1 or 5 minutes, fetal heart rate below 100 beats per minute, or meconium-stained amniotic fluid; and 2) infants from whom peripheral arterial hypoxanthine samples were taken were classified by clinical assessment, whereby one author, blinded to the infants' hypoxanthine levels, prospectively assessed each patient's condition for evidence of asphyxia. Hypoxanthine levels correlated with increased base deficit (P less than .001; r = 0.8) and with decreased pH (P less than .001; r = -0.5). By both of our asphyxia classification methods, hypoxanthine levels were significantly higher (P less than .002) in the asphyxiated groups. We also noted a higher hypoxanthine level in asphyxiated non-survivors as compared with all survivors (P less than .02). We propose that serum hypoxanthine levels may help define asphyxia. Because hypoxanthine, when metabolized by xanthine oxidase, generates oxygen radicals that are highly destructive to tissue, hypoxanthine levels may have important therapeutic implications for asphyxiated patients.

Asphyxia Neonatorum↗
PubMed1987

Dynamic changes in organ blood flow and oxygen consumption during acute asphyxia in fetal sheep.

The effects of acute asphyxia on both the time course of blood flow changes in central and peripheral organs, including the skin, and the time course of changes in oxygen consumption were studied in 9 unanaesthetized fetal sheep in utero at 130 +/- 2 days of gestation during 4-min arrest of uterine blood flow. Blood flow distribution and total oxygen consumption were determined at 1-min intervals during asphyxia using isotope-labelled microspheres (15 micrograms diameter) and by calculating the decline of the arterial O2 content, respectively. During asphyxia peripheral blood flow including that to the skin, scalp, and choroid plexus decreased rapidly, whereas blood flow to the heart, brain stem and (in surviving fetuses only) adrenals increased slowly. Total oxygen consumption fell exponentially with time and was closely correlated with the fall in both arterial oxygen content and peripheral blood flow; the time courses of these changes were very similar to those of the decreasing blood flows to the skin and scalp. Blood flow within the brain was redistributed at the expense of the cerebrum and the choroid plexus; the total blood flow to the brain did not change. In the 5 fetuses that died during the recovery period adrenal blood flow failed to increase and, at the nadir of asphyxia, peripheral vessels dilated and central vessels constricted. We conclude that in fetal sheep near term during acute asphyxia the time course of changes in blood flow to central and peripheral organs is different; total oxygen consumption depends on arterial O2 content and peripheral blood flow; total blood flow to the brain does not change, but is redistributed towards the brain stem at the expense of the cerebrum and choroid plexus; fetal death is preceded by a failure of adrenal blood flow to increase, by peripheral vasodilatation, and by central vasoconstriction and skin blood flow validly indicates rapid changes in the distribution of blood flow and the changes in oxygen consumption that accompany it.

Animals↗
PubMed1983

Birth asphyxia: pathophysiologic events and fetal adaptive changes.

We have made significant advances toward understanding birth asphyxia and its effects upon neurologic development in the newborn and infant. The fetus is well adapted to compensate for moderate alterations in oxygen delivery. However, near lethal hypoxemia, prolonged exposure, and survival result in cell death and permanent neurologic sequelae. Neuroelectrical measurements such as the EEG and visual evoked potential provide insight into the acute alterations in nerve transmission during asphyxia, and in the recovery phase may ultimately provide information for long-term prognosis. These measurements are limited, however, by their inability once lost to distinguish cell inactivity from cell death. Permanent neurologic damage from asphyxia appears now to be a complex process in which severe hypoxemia precipitates a cascade of events leading to glycolysis, glycogenolysis, hypotension, and ultimately the accumulation of high concentrations of lactate at the cell level. As a consequence, cellular and extracellular fluid shifts produce cerebral edema, further impairment of cerebral circulation, and ultimately cell death. Clinical studies have helped to identify the newborn at high risk for neurologic impairment, but a cause-effect relationship remains unclear. That birth asphyxia can produce severe neurologic damage and death is generally accepted. Moreover, improper resuscitation of a severely depressed newborn increases the chance of permanent sequelae. The important clinical question is: Can one alter the natural course of asphyxia as has been alluded to through pharmacologic and ventilator manipulation? Answers to this question will depend upon continued study of the mechanisms of asphyctic damage in the central nervous system.

Acidosis↗
PubMed1984

Effects of asphyxia at birth on postnatal glucose regulation in the rat.

We have characterized the effect of a period of asphyxia at birth, followed by recovery, upon newborn rats. Asphyxiated pups were subjected to 3 to 5% (v/v) inspired oxygen during the first 20 min of life and then maintained in room air for 6 h. Control pups were maintained in room air throughout the 6-h period. Hypoxia produced severe asphyxia as reflected by a pH of 6.76 +/- 0.05, PaCO2 of 87 +/- 3 mm Hg and PaO2 of 15.4 +/- 4 mm Hg, and by a greatly increased blood lactate/pyruvate ratio. Plasma catecholamine concentrations in asphyxiated pups were elevated (epinephrine 13,866 +/- 250 pg/ml, norepinephrine 9611 +/- 1813 pg/ml) compared to control animals (epinephrine 973 +/- 234 pg/ml, norepinephrine 774 +/- 133 pg/ml) at 20 min. Asphyxia initially increased plasma glucose concentration, and then with recovery it fell below controls. Hepatic glycogen stores did not differ between asphyxiated and control pups. Plasma insulin concentrations remained elevated during asphyxia and the usual neonatal surge of plasma glucagon was significantly delayed. Neonatal asphyxia increases catecholamines, causes lactic acidemia, and alters insulin and glucagon levels. The interactions between these variables alters the normal pattern of glucose availability during the neonatal period.

Animals↗
PubMed1983

Asphyxia and gestational age.

Perinatal asphyxia at term is a major cause of mortality and morbidity. In many instances obstetric or maternal complications during pregnancy, labor, or delivery account for the asphyxia, but there is a group of infants in whom asphyxia occurs without any recognizable risk factors. The histories of 1602 infants were evaluated with these problems in mind. There were 547 infants without any complicating factors, 329 with obstetric complications, and 356 with miscellaneous maternal, fetal, and neonatal problems. The mean gestational age of these infants was 277.4 days. Fetal distress was noted in 183 cases without subsequent neonatal disease; the mean gestation of these infants was 282.7 days. Unexpected intrapartum asphyxia was observed in 187 instances with a mean gestation of 288.8 days. Those who died or had neurologic symptoms had the longest mean gestation, 291 days. Only 5% of the infants dying of unexpected perinatal asphyxia and less than 16% of those with neurologic symptoms were born before their due dates; approximately 64% of the infants with obstetric complications, miscellaneous problems, or no complications or morbidity were born before 280 days. The implications for management of pregnancy at or beyond 280 days are discussed.

Asphyxia Neonatorum↗
PubMed1995

-Neonatal asphyxia as the cause of brain damage in children?-.

The prevalence of cerebral palsy (CP) has increased over the last 15 years in most countries. This is explained by an improved survival of very low birth weight prematures. In term infants birth asphyxia is of minor significance as a cause for CP. In only 10% of all CP cases following delivery at term, birth asphyxia must be discussed as a possible cause. In premature deliveries events during the perinatal period are of greater significance for the later development of a CP. Only severe forms of oxygen deficit, leading to tissue damage in the brain and other organs with clinical symptoms during the first days of life, are of significance for the long term prognosis. Even in the presence of severe birth asphyxia the causal relationship with a psychomotor handicap is not proven, since brain damage may have developed during pregnancy before the onset of labour and may be the cause of birth asphyxia. Brain damage and birth asphyxia may be the result of a common pathology of pregnancy.

Asphyxia Neonatorum↗
PubMed1995

Profound asphyxia in the premature infant: imaging findings.

PURPOSE: To investigate imaging findings in premature infants who had profound asphyxia. METHODS: CT (three patients), MR (three patients), and ultrasonography (four patients) studies of five patients who had profound asphyxia before the postconceptional age of 32 weeks were retrospectively reviewed. The patients ranged from 1 day to 4 months old at the time of the imaging studies. An autopsy report was available in one patient. The results were compared with reports in the literature of patients with similar injuries at similar ages. RESULTS: Abnormalities of the thalami and basal ganglia were present in all infants examined with CT or MR. CT showed low attenuation in the basal ganglia and high attenuation (blood or calcium) in the thalami; thalamic cavitation and low attenuation of the upper brain stem were present in one infant. MR showed T1 and T2 shortening in the thalami in all patients. Variable MR changes were noted in the basal ganglia, ranging from diminished size with normal signal intensity to T1 and T2 shortening with normal size and complete cavitation. T1 and T2 shortening were seen in the dorsal brain stem in one patient. Sonography showed transient or persistent hyperechogenicity in the thalami in three patients and cavitation of the thalami in one patient. Damage to the perirolandic cortex was not present in any patient. CONCLUSION: Profound asphyxia before 32 weeks gestational age shows consistent injury to the thalami, basal ganglia, and brain stem that can be detected by all three imaging modalities. The pattern of injury seems to differ from that of partial asphyxia in premature infants and of profound asphyxia in term infants.

Asphyxia Neonatorum↗
PubMedDate not supplied

Production of fetal asphyxia by maternal psychological stress.

Several lines of evidence indicate that maternal psychological stress leads to adverse pregnancy outcome in rhesus monkey. Chronic anxiety causes an increased stillbirth rate, fetal growth retardation, and altered placental morphology. On another time scale, lightening of maternal anesthesia during surgery produces an impaired fetal oxygenation while re-institution of anesthesia ameliorates the fetal asphyxia. The present study, for the first time, demonstrates a relationship between specific episodes of meternal psychological stress and exacerbation of fetal asphyxia in utero. Eight term pregnant rhesus monkeys were anesthetized with sodium pentobarbital. Catheters were placed both into the maternal and the fetal femoral arteries for the continuous recording of blood pressure and heart rate and for the intermittent campling of maternal and fetal blood. An open-ended catheter recorded intrauterine pressures. Following a complete repair, the anesthesia of the mothers was allowed to lighten. As the mothers awakened, the fetuses invariably showed the developemnt of fetal asphyxia. A fetal acidosis developed and the fetal oxygenation and repair of acidosis. Studies while the mothers were fully awake showed the repeated and regular development of episodes of heightened fetal asphyxia produced by episodes of stressful stimulation of the mothers. Episodes of maternal psychological stress led to changes in both fetal vital signs and blood chemical findings. These alterations in fetal state regularly followed the onset of the episodes of psychological stress by 50 seconds. These changes also usually remitted 50 seconds following the termination of the periods of stress. These results demonstrated a direct and unequivocal relationship between meternal psychological stress and fetal asphyxia. It is assumed the maternal stress produces impairments in the circulation to the uterus through an increased sympathetic nervous system activity and a shunting of the maternal blood-flow from the abdominal viscera to other organs as occurs in the fight-orflight reaction.

Animals↗
PubMed1977

Late decelerations and brain tolerance of the fetal monkey to intrapartum asphyxia.

Eight monkey fetuses near term were subjected to regulated asphyxia during labor by mechanically constricting the maternal abdominal aorta and diminishing blood flow to the uterus. A magnitude of asphyxia was produced and maintained for an initial three hours that was close to but not sufficient to elicit late decelerations. The asphyxia was then augmented during a fourth hour to cause late decelerations of magnitudes of 5 to 15 per cent of the initial heart rate. After termination of the fourth hour of asphyxia, the fetuses were delivered by hysterotomy and provided intensive care. During the three to nine months of survival after birth, all animals were neurologically intact; on necropsy the brains were free of pathologic changes both grossly and microscopically. These results support the thesis that fetal heart rate monitoring during labor exhibits a sensitivity sufficient to diagnose asphyxia of the fetus of clinical significance before it reaches a magnitude that may cause permanent neurological injury. The results are particularly pertinent to those clinical circumstances where the decreases in intervillous space blood flow brought about by uterine contractions are accentuated due to low maternal blood pressure.

Animals↗
PubMed1995

Limitations in the clinical prediction of intrapartum fetal asphyxia.

OBJECTIVE: Our purpose was to demonstrate the predictive value of clinical risk scoring and fetal assessment for intrapartum fetal asphyxia. STUDY DESIGN: Intrapartum fetal asphyxia was defined by an umbilical artery buffer base < 34 mmol/L. The predictive value of 20 antepartum and intrapartum risk factors was examined in 1909 consecutive pregnancies. The predictive value of clinical risk factors with periodic fetal assessment was examined in a second population of 100 consecutive pregnancies with biochemically determined intrapartum fetal asphyxia. RESULTS: The incidence of intrapartum was 2.3%. Two problems were apparent in these studies. A significant proportion of intrapartum fetal asphyxia occurred in pregnancies with no risk factors. The positive predictive value of clinical risk factors was low, 3%, resulting in a large number of false positives requiring clarification. CONCLUSION: Screening and fetal assessment methods must be improved to ensure the early recognition of intrapartum fetal asphyxia that may require intervention during labor to avoid morbidity and mortality.

Delivery, Obstetric↗
PubMed2003

The effect of a global birth asphyxia on the ontogeny of BDNF and NGF protein expression in the juvenile brain.

Neurotrophic growth factors are strongly upregulated following brain injury in order to limit the amount of delayed apoptotic cell death. In particular, the neurotrophins NGF and BDNF are upregulated following injury and offer neuroprotection when administered after brain injury. Further, both growth factors are involved in the control of neural proliferation and plasticity during both development and recovery from injury. We used a model of global birth asphyxia in the rat to follow the ontogeny of BDNF and NGF protein levels within the normal and asphyctic hippocampus and cerebellum for the first 28 days of postnatal life. In contrast to what is seen in the injured adult brain, we see an early and long lasting decrease in NGF content within the asphyctic hippocampus, whereas cerebellar NGF content showed a delayed increase following asphyxia. Asphyxia also caused a delayed increase in BDNF content within the hippocampus but decreased BDNF levels within the cerebellum. Further, a comparison of the ontogeny of plasma corticosterone over development shows that endogenous BDNF protein levels are not sensitive to the dramatic increase in circulating corticosterone that occurs at the end of the stress hyporesponsive period. In summary, we find that perinatal birth asphyxia causes opposing changes in NGF and BDNF protein expression in a spatio-temporal-dependent manner. These results point to the need for more detailed studies on the mechanisms of action of BDNF and NGF within the developing brain before these can be used therapeutically following birth asphyxia in man.

Animals↗
PubMed1983

Breathing during sleep: the responses to asphyxia and prochlorperazine in normal subjects and patients with obstructive sleep apnea.

The effects of sleep and prochlorperazine (12.5 mg intravenous bolus) on the ventilatory and arousal responses to asphyxia were studied in normal subjects and patients with obstructive sleep apnea (OSA). The ventilatory response to asphyxia was reduced during non-rapid eye movement sleep in the six normal subjects studied (1.93 +/- 0.18 l min-1.% SaO2 awake vs. 1.01 +/- 0.10 l min-1.% SaO2 asleep; mean +/- SEM; p less than 0.01) (SaO2 = arterial oxygen saturation). In the two normal subjects studied during sleep following prochlorperazine administration, ventilatory responsiveness was increased (p less than 0.05) but arousal response to asphyxia was depressed (p less than 0.025). Although prochlorperazine increased waking ventilatory responsiveness to asphyxia in five of six patients with OSA (2.26 +/- 0.44 l min-1.% SaO2 vs. 4.77 +/- 1.39 l min-1.% SaO2; mean +/- SEM; p less than 0.01), the drug had no clinically significant effect on upper airway obstruction during sleep; in three patients, apnea frequency was slightly reduced but in four of six patients severity of hypoxemia during apnea was increased with drug administration. We conclude that prochlorperazine administration is unlikely to benefit patients with obstructive sleep apnea despite its ventilatory effects during wakefulness and sleep. This lack of effect may be explained by separate effects of the drug on ventilatory and arousal responses to asphyxia.

Adult↗
PubMed1978

Mechanisms of vascular changes in skeletal muscle during asphyxia in the cat.

Vascular responses in the hindlimb muscles of anesthetized paralyzed cats during systemic asphyxia were studied. The cats were ventilated with 10% O2-10% CO2-80% N2 for 10-20 min periods, while blood flow to the skinned hindlimb was monitored (electromagnetic flowmeter). Mean arterial pressure rose and hindlimb flow typically fell during asphyxia, implying increased vascular resistance. After sympathetic denervation of the hindlimb, resistance increased in some groups of animals, and did not change in others during asphyxia. Functional adrenalectomy did not alter these response characteristics. Resistance also did not changes significantly if the control resistance was first increased to the predenervation level by electrically pacing the lumbar sympathetic chain. In contrast, pronounced vasodilatation occurred during asphyxia after blocking of the alpha receptors in the hindlimb (phenoxybenzamine) or after systemic catecholamine depletion (reserpine). We conclude that the vasoconstriction in innervated muscle during asphyxia was caused in part by increased discharge of sympathetic constrictor nerves to the muscle vasculature, with augmentation from a humoral alpha agonist of nonadrenal origin, possibly norepinephrine released from sympathetic nerves throughout the body.

Adrenal Medulla↗
PubMed1993

The effect of adenosine transport inhibition on cardiovascular function and survival after severe asphyxia in fetal lambs.

When the energy demand exceeds the energy supply, anaerobic metabolism takes over and the ATP catabolite adenosine is generated. Adenosine acts as a coronary vasodilator, thereby increasing the oxygen supply to the heart. Its potential, however, is poorly exploited due to extensive catabolism. R-75231 inhibits transport of adenosine into endothelial cells, where it is catabolized, resulting in an elevation of interstitial adenosine concentrations. In 14 fetal lambs (3 to 5 d after surgery, gestational age 124.1 +/- 1.1 d), seven fetuses were pretreated with R-75231 (0.1 mg/kg estimated fetal weight as a bolus injection in the inferior vena cava), whereas the other seven served as controls. After 1 h of severe asphyxia, induced by restriction of uterine blood flow, those fetuses treated with R-75231 showed a faster normalization of aortal pH and, in contrast to the control group, did not develop tachycardia. The percentage increase in myocardial blood flow during asphyxia, measured with radioactive microspheres, was significantly higher in the R-75231-treated group compared with the control group (437 and 284%, respectively). In the control group, only three fetuses recovered and survived, whereas in the R-75231 group, all seven animals recovered after severe asphyxia. It is concluded that fetal lambs pretreated with R-75231 before the onset of severe asphyxia have an enhanced increase in myocardial blood flow during asphyxia, recover faster, and survive longer.

Adenosine↗