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PubMed1990

Defective regulation of cerebral oxygen transport after severe birth asphyxia.

Cerebral artery Doppler ultrasonography was used to study the cerebral blood-flow velocity and cerebral oxygen transport of infants requiring a blood transfusion to correct anaemia. Mean flow velocity, pulsatility index and haemoglobin concentration were determined before and after transfusion. 11 stable preterm infants demonstrated an inverse relationship between haemoglobin concentration (or estimated arterial oxygen content) and mean flow velocity, indicating the presence of a homeostatic mechanism keeping brain oxygen transport within certain limits. Three infants with severe post-asphyxial encepalopathy had relatively high mean flow velocities and low pulsatility indices both before and after transfusion. There were no circulatory adjustments in response to an increase in haemoglobin concentration. Thus severe asphyxia at birth disrupted the homeostatic mechanism responsible for keeping brain oxygen transport constant. These findings stress the importance of close monitoring of arterial oxygen content, particularly for infants with severe post-asphyxial encephalopathy.

Asphyxia Neonatorum↗
PubMed1992

Relation between cerebral oxidative metabolism following birth asphyxia, and neurodevelopmental outcome and brain growth at one year.

Studies of cerebral oxidative metabolism were carried out by phosphorous magnetic resonance spectroscopy during the first week of life in 52 infants with clinical and/or biochemical evidence of birth asphyxia. 15 infants died and the 37 survivors were assessed by a wide range of neurodevelopmental tests at one year of age. The minimum recorded values for cerebral phosphocreatine/inorganic phosphate concentration ratio (an index of oxidative metabolism) were related to outcome. The results showed a significant relation between the extent of derangement of oxidative metabolism and the severity of adverse outcomes, including death, neurodevelopmental impairment and reduced head growth.

Adenosine Triphosphate↗
PubMed1975

Circulating levels of fibrin/fibrinogen degradation fragment E in normal pregnancy, and in association with intrauterine growth retardation and perinatal asphyxia.

Levels of fibrin/fibrinogen degradation products have been measured by aspecific and sensitive radioimmunoassay for degradation fragment E (FgE) in pregnant patients. Maternal FgE levels rose from the 16th week reaching a plateau at the 36th week in normal pregnancy. There was no correlation between maternal FgE levels and maternal age, parity or the occurrence of perinatal asphyxia. A minority of patients (5 per cent) with evidence of intrauterine growth retardation showed prolonged elevation of FgE levels.

Asphyxia Neonatorum↗
PubMed1982

Neurological normality after extreme birth asphyxia. Case report.

A case of extremely severe birth asphyxia is reported. In spite of successful resuscitation the arterial pH was still only 6.6 at the age of 1 h. Assessment at 3 years 10 months revealed that the child was not only completely normal, but was of superior intelligence. This case demonstrates the advisability of maintaining an optimistic approach even when very severe fetal acidosis is detected around the time of birth.

Acidosis↗
PubMed1990

Birth asphyxia and the intrapartum cardiotocograph.

The intrapartum cardiotocographs (CTGs) of 38 severely asphyxiated, term infants, born during a 17-month period, and those of 120 healthy term infants acting as controls were independently reviewed by three investigators who were unaware of the clinical outcome. Inter-observer agreement was good (Kappa statistic = 0.74, P less than 0.0001). The investigators found that cardiotocographic abnormalities were present in 33 of the asphyxiated infants (87%) and in 35 of the controls (29%) and predicted that the abnormalities were severe enough to lead to significant fetal metabolic acidosis at delivery in 23 asphyxiated infants (61%) and in 11 controls (9%). The differences between the two groups were highly significant (P less than 0.001). Using the traditional diagnostic criteria for fetal distress, the investigators found that fetal blood sampling was indicated in 58% of cases in the asphyxia group and in 20% of controls but was only performed in 16% of asphyxiated infants and in 8% of controls. Furthermore, the median response times of delivery suite staff for abnormal fetal heart rate patterns were similar whether the FHR changes, classified using Krebs' CTG scoring system, were moderate or severe: 80 min and 90 min, respectively. These findings suggest that interpretation of the intrapartum CTG continues to pose major problems for practising obstetricians.

Acidosis, Respiratory↗
PubMed1982

The importance of neonatal asphyxia and caesarean section as risk factors for neonatal respiratory disorders in an unselected population.

The risk of neonatal respiratory disorders was calculated in an unselected, total population together with the relative contributions of some factors found associated with an increased risk. Postnatal asphyxia, expressed as a low one minute Apgar score, and low gestational age were substantially, independent risk factors. Caesarean section added, though less markedly, to the risk of the above disorders.

Apgar Score↗
PubMed1983

Severe neonatal asphyxia. Incidence and prediction of outcome in the Stockholm area.

In Sweden during the 1970's the incidence of severe asphyxia (an Apgar score of 3 or less at 5 min) has decreased significantly from 3.22 to 2.56 per 1000 infants. A follow-up study was undertaken concerning 116 infants (40 preterm, 76 full-term) admitted to St. Göran's Children's Hospital during a 7-year period (1973-79). The mortality rate was 48% in preterm and 21% in full-term infants. Significant sequelae were present in 27% of the surviving full-term and 14% of the preterm infants. The three severely-handicapped preterm infants had other serious diseases as well whereas this applied to only one full-term infant. The predictors of sequelae included perinatal complications, late onset of spontaneous ventilation (greater than 20 min) and postnatal symptoms, such as seizures. Only two of 9 infants with regular breathing after 20 min and three of 16 infants with seizures were considered normal at follow-up.

Apgar Score↗
PubMed1984

Elevation of plasma concentrations of arginine vasopressin following perinatal asphyxia.

Hypoxic ischemic encephalopathy is a major cause of mortality in neonates. Studies in experimental subjects have shown differing responses of plasma arginine vasopressin to hypoxia. Plasma arginine vasopressin levels, serum osmolality, urine osmolality and fluid intakes were measured in thirteen asphyxiated and nineteen control newborn infants during the first seventy-two hours of life. In the asphyxiated infants plasma arginine vasopressin was found to be elevated as compared to control infants on days one (p less than 0.001) and two (p less than 0.007) but not on day three of life. Urine osmolality was also elevated in the study patients on days one (p less than 0.01) and two (p less than 0.001) but not on day three, in spite of equal intakes of fluid on day one in both groups and significantly diminished fluid intake on days two and three in the study patients. Serum osmolality was not different between the two groups on any day studied, and was felt to be on the basis of diminished intake in the study infants. The data presented in this study support the concept that arginine vasopressin release occurs following perinatal asphyxia in term newborn infants.

Arginine Vasopressin↗
PubMed1990

Delayed-onset dyskinetic 'cerebral palsy--a late effect of perinatal asphyxia?

A 12-year-old girl, born full term after severe pre- and peripartal asphyxia, with transient abnormal newborn neurology and slight motor development deviations but no cerebral palsy syndrome, is described. At the age of 5, she developed a slowly progressive dyskinetic hemisyndrome, initially uncoordinated hyperkinetic movements in her left arm, dystonic posturing then supervened. Since the age of 11, her right side had also slowly become involved. As extensive examinations excluded other causes, it is concluded that this case represents a delayed onset dyskinetic 'CP-syndrome' subsequent to a postanoxic non-progressive insult to the basal ganglia, but with a well compensated functional integrity before the age of 5.

Asphyxia Neonatorum↗
PubMed1996

Magnetic resonance imaging in children with neonatal asphyxia: correlation with developmental sequelae.

Magnetic resonance (MR) findings and developmental sequelae were examined in 60 patients with neonatal asphyxia. Nine patients with marked destruction of the cerebrum had the severest motor and mental disability. Six had lesions of the periventricular white matter and thalamus. Seven had border zone infarction with lesions of the white matter and thalamus. Nine had lesions of the middle-lateral part of the thalamus, putamen and peri-Rolandic area. Five with lesions of the thalamus, putamen and cerebral white matter had the severest motor and mental disability. Twenty with lesions of the thalamus and/or putamen had athetosis or clumsiness. Four with lesions of the opercular region, white matter and thalamus had feeding difficulty. Some correlation between MR findings and developmental sequelae was recognized.

Adolescent↗
PubMed1997

Transient elevation of aldosterone levels in perinatal asphyxia.

We measured plasma aldosterone levels in cord blood and peripheral blood collected 18-24 h after birth in 19 asphyxiated and 19 normal term newborn infants. The asphyxiated newborn infants had significantly higher aldosterone levels in cord blood than the normal newborn infants. At 18-24 h after birth there was no difference between the groups with respect to aldosterone levels. There was a positive significant correlation between aldosterone levels and PCO2 in cord blood by multiple linear regression analysis. There is a transient elevation of aldosterone levels in perinatal asphyxia.

Aldosterone↗
PubMed1966

Intracellular recording from cat spinal motoneurones during acute asphyxia.

1. Changes in membrane and action potentials of cat spinal motoneurones during acute asphyxiation and re-oxygenation were recorded with an intracellular technique.2. The asphyxial potential of the grey matter, which develops in the first 2-2.5 min of asphyxiation, can be expected to interfere with the membrane potential record. After correcting for this effect a gradual depolarization of the soma at a rate of 3-4 mV/min was found, commencing within a fraction of a minute after the start of asphyxiation.3. The orthodromic responses of the motoneurones were the most vulnerable to O(2) lack. They failed earlier than the responses to antidromic and to direct excitation of the cell through the micro-electrode. After failure of the orthodromic spike an excitatory post-synaptic potential remained for a short time. Failure of antidromic excitation began by the dropping out of the some dendritic potential, followed by the arrest of the initial segment response.4. It was concluded that the early arrest of orthodromic excitation is caused by presynaptic failure.5. All changes in membrane and action potentials were completely reversible by re-oxygenation after periods of asphyxia lasting from 4 to 6 min. The orthodromic response recovered markedly slower than the antidromic and direct ones.

Animals↗
PubMed1967

Effects of gestation and prenatal asphyxia on pulmonary surface properties of the foetal rabbit.

1. The pulmonary surface properties of foetal rabbits were studied after delivery by Caesarean section at 26-30 days and after normal delivery at term (31 days).2. Quasi-static pressure-volume curves were defined for the lungs and the surface properties of the same lungs were further studied both by the bubble-stability method and by means of a surface balance and trough. Results given by each method are compared and discussed.3. At the 26th day of gestation the pulmonary surface properties, characteristic of the animal at term, were not yet present. These properties were first evident on the 28th day.4. A period of 16 min intense prenatal asphyxia on the 28th day of gestation failed to produce a change in pulmonary surface properties.

Animals↗
PubMed1994

[Fulmonant group A streptococcal infection accompanied by massive pulmonary hemorrhage and subsequent asphyxia: a case report].

A case of fulminant group A streptococcal infection occurring in a 6-year-old Japanese child is reported. She was accompanied by massive pulmonary hemorrhage and subsequent asphyxia. She initially had pharyngalgia with fever. The cephalosporin antibiotic was given orally for 3 days. Three days after that recurrence of fever and pharyngalgia was noted. Twelve hours later tachypnea and a sudden onset of hemoptysis was noted. She manifested DOA (dead on arrival) and died in the emergency room. Autopsy revealed the presence of numerous cocci in the vessels and massive pulmonary hemorrhage. Streptococcus pyogenes was isolated from the blood. The serotype of this group A streptococcal organism was typed as M4, T4, which produces exotoxin type B and C, which was sensitive to the penicillins.

Asphyxia↗
PubMed1982

Naloxone reverses neonatal depression caused by fetal asphyxia.

Pregnant near-term rabbits were given an intravenous dose of saline or the opiate antagonist naloxone and then asphyxiated. The fetuses were delivered by cesarean section and evaluated for respiration, color, muscle tone, response to stimulation, and general activity at 1, 3, 5, 10, 15, and 30 minutes of age. The naloxone-treated pups had significantly better scores during the first 15 minutes after birth than the saline-treated pups. Naloxone did not adversely affect the scores of nonasphyxiated pups. These data suggest that endogenous opiates worsen the neonatal depression caused by intrauterine asphyxia and that this effect can be reversed by naloxone.

Animals↗
PubMed2005

Do hyperoxaemia and hypocapnia add to the risk of brain injury after intrapartum asphyxia?

BACKGROUND: Episodes of hyperoxaemia and hypocapnia, which may contribute to brain injury, occur unintentionally in severely asphyxiated neonates in the first postnatal hours. OBJECTIVE: To determine whether hyperoxaemia and/or hypocapnia during the first 2 hours of life add to the risk of brain injury after intrapartum asphyxia. METHODS: Retrospective cohort study in term infants with post-asphyxial hypoxic ischaemic encephalopathy (HIE) born between 1985 and 1995. Severe and moderate hyperoxaemia were defined as Pao(2) >26.6 and Pao(2) >13.3 kPa (200 and 100 mm Hg). Severe and moderate hypocapnia were defined as Paco(2) <2.6 and Paco(2) <3.3 kPa (20 and 25 mm Hg). Adverse outcome ascertained by age 24 months was defined as death, severe cerebral palsy, or any cerebral palsy with blindness, deafness, or developmental delay. With outcome as the dependent variable, multivariate analyses were performed including hyperoxaemic and hypocapnic variables, and factors adjusted for initial disease severity. RESULTS: Of 244 infants, 218 had known outcomes, 127 of which were adverse (64 deaths, 63 neurodevelopmental deficits). Multivariate analyses showed an association between adverse outcome and episodes of severe hyperoxaemia (odds ratio (OR) 3.85, 95% confidence interval (CI) 1.67 to 8.88, p = 0.002), and severe hypocapnia (OR 2.34, 95% CI 1.02 to 5.37, p = 0.044). The risk of adverse outcome was highest in infants who had both severe hyperoxaemia and severe hypocapnia (OR 4.56, 95% CI 1.4 to 14.9, p = 0.012). CONCLUSIONS: Severe hyperoxaemia and severe hypocapnia were associated with adverse outcome in infants with post-asphyxial HIE. During the first hours of life, oxygen supplementation and ventilation should be rigorously controlled.

Analysis of Variance↗
PubMed2005

Recovery of amplitude integrated electroencephalographic background patterns within 24 hours of perinatal asphyxia.

OBJECTIVE: To assess the time course of recovery of severely abnormal initial amplitude integrated electroencephalographic (aEEG) patterns (flat trace (FT), continuous low voltage (CLV), or burst suppression (BS)) in full term asphyxiated neonates, in relation to other neurophysiological and neuroimaging findings and neurodevelopmental outcome. METHODS: A total of 190 aEEGs of full term infants were reviewed. The neonates were admitted within 6 hours of birth to the neonatal intensive care unit because of perinatal asphyxia, and aEEG recording was started immediately. In all, 160 infants were included; 65 of these had an initial FT or CLV pattern and 25 an initial BS pattern. Neurodevelopmental outcome was assessed using a full neurological examination and the Griffiths' mental developmental scale. RESULTS: In the FT/CLV group, the background pattern recovered to continuous normal voltage within 24 hours in six of the 65 infants (9%). All six infants survived the neonatal period; one had a severe disability, and five were normal at follow up. In the BS group, the background pattern improved to normal voltage in 12 of the 25 infants (48%) within 24 hours. Of these infants, one died, five survived with moderate to severe disability, two with mild disability, and four were normal. The patients who did not recover within 24 hours either died in the neonatal period or survived with a severe disability. CONCLUSION: In this study there was a small group of infants who presented with a severely abnormal aEEG background pattern within six hours of birth, but who achieved recovery to a continuous normal background pattern within the first 24 hours. Sixty one percent of these infants survived without, or with a mild, disability.

Asphyxia Neonatorum↗