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PubMed1977

Quality of survival after severe birth asphyxia.

Thirty-one children who survived severe birth asphyxia defined by a 1-minute Apgar score of 0, or a 5-minute Apgar score of less than 4, have been seen at age 5 to 10 years for neurological and psychological assessment. Their progress has been compared with that of controls matched for sex, birthweight, gestational age, and social class. 29(93%) of the 31 asphyxiated group and all the controls had no serious neurological or mental handicap. 2 were severely disabled and mentally retarded. Detailed studies of psychological function showed no significant differences between the two groups. 2 apparently stillborn infants have made normal progress. It was not possible to identify any perinatal factor which predicted the occurrence of serious handicap with certainty. We considered that the quality of life enjoyed by the large majority of the survivors was such as to justify a positive approach to the resuscitation of very severely asphyxiated neonates.

Asphyxia Neonatorum↗
PubMed1981

Hearing, speech, and language in survivors of severe perinatal asphyxia.

Hearing, speech, and language were studied in 26 children who survived severe perinatal asphyxia. The results of hearing tests showed that most children had a favourable outcome. Only 1 child had sensorineural deafness. Hearing loss in 6 others was due to middle-ear disease which resolved after treatment, and on retesting was found to be normal. The study also showed that neither gentamicin treatment nor incubator noise seemed to affect hearing. The results of speech and language assessment were less encouraging and about one-third of the children without serious mental or physical handicap had deficits in speech and language. It is suggested that the quality of life in such children could be improved if these deficits were detected early and adequately treated.

Asphyxia Neonatorum↗
PubMed1983

Umbilical venous blood pH: a useful aid in the diagnosis of asphyxia at birth.

Umbilical venous blood, and umbilical arterial blood pH, PO2, PCO2, and base excess were determined in 453 term infants at birth. The results indicate that umbilical venous blood pH, and umbilical arterial blood pH are significantly related to each another. Acidosis, as defined by an umbilical venous blood pH less than 7 X 27, is associated with a lower PO2, a raised PCO2, and a reduced buffer base when compared with PO2, PCO2, and buffer base associated with a normal pH (7 X 27-7 X 42), or alkalosis (pH greater than 7 X 42). The infant's condition at birth was recorded using modified Apgar scores, in which the gradings were vigorous (5-6), intermediate (3-4), or depressed (0-2). In the neonatal period, neurological abnormalities occurred in infants who had been in a depressed condition at birth in the presence of acidosis. Other infants, who had been in a depressed condition with a normal pH or alkalosis and the remaining infants who had an intermediate or a vigorous condition at birth, did not manifest neurological abnormalities in the neonatal period. Our findings suggest that measurement of umbilical venous blood pH, whose values correlate well with those of umbilical arterial blood pH, in infants who are in a depressed condition at birth improves the clinical assessment of the severity of asphyxia.

Acidosis↗
PubMed1984

Cord blood gases, birth asphyxia, and intraventricular haemorrhage.

The relation between intraventricular haemorrhage, Apgar scores, and cord blood gases was determined prospectively in 150 infants of 34 weeks' gestation, or less. Although there was no significant relation between birth asphyxia and subsequent haemorrhage, a consistent trend for lower Apgar scores in infants who developed haemorrhage was shown.

Apgar Score↗
PubMed1985

Medical management of raised intracranial pressure after severe birth asphyxia.

The effects of dexamethasone and 20% mannitol infusion in reducing raised intracranial pressure were assessed in severely asphyxiated newborn infants. Intracranial pressure was measured continuously by a percutaneously placed subarachnoid catheter, and cerebral perfusion pressure was calculated from this and blood pressure data. Dexamethasone treatment, assessed in seven infants, produced an overall fall in intracranial pressure which was sustained for at least six hours, but this was coincident with a simultaneous reduction in systemic blood pressure with no change in the cerebral perfusion pressure. Mannitol, studied on nine occasions, produced a fall in intracranial pressure in each case, together with an overall rise in cerebral perfusion pressure 60 minutes after starting the infusion; this was sustained for a further four hours. We can find little to support the routine use of dexamethasone in severe perinatal asphyxia but mannitol infusion seems of value in treating raised intracranial pressure associated with cerebral oedema.

Asphyxia Neonatorum↗
PubMed1990

Prediction of acute renal failure after birth asphyxia.

Twenty-one babies of 34-41 weeks' gestational age with birth asphyxia (5 minute Apgar score less than or equal to 5 or umbilical artery pH less than or equal to 7.2) were studied during the first two days of life to find out whether the urinary excretion of tubular markers of renal function is of value in the early diagnosis of acute renal failure. Urinary retinol binding protein, myoglobin, and N-acetyl-beta-D-glucosaminidase (NAG), expressed as a ratio with urinary creatinine, were measured and excretion profiles repeated at 3-6 days in 15 infants and at 7-14 days in 11 infants. Plasma creatinine concentration, creatinine clearance, plasma myoglobin concentration, and fractional sodium excretion were measured where possible in asphyxiated infants. Control data were obtained from 50 healthy infants: 28 gave urine samples alone, 17 urine and blood, and five blood alone. Normal urinary values were derived from 17, 25, and three infants, respectively, for the three time periods. The number of control samples was limited for ethical reasons. Four asphyxiated infants had acute renal failure (group 1), four had tubular dysfunction without glomerular disturbance (group 2) and 13 had normal renal function (group 3). Group 1 were clearly identified by greatly increased urinary retinol binding protein (greater than 27,000 micrograms/mmol creatinine) and myoglobin (greater than 1500 micrograms/mmol creatinine) excretion measured in the first two days of life. In control infants the range of excretion of retinol binding protein within the same time period was 3 to 967 micrograms/mmol creatinine and urinary myoglobin was undetectable. Excretion of NAG failed to discriminate between groups 1 and 2. Acute renal failure occurred only in infants who had heavy myoglobinaemia. Tubular dysfunction in group 2 was transient and not accompanied by plasma electrolyte disturbances. We conclude that measurement of urinary excretion of retinol binding protein or myoglobin after birth is helpful in the early diagnosis of acute renal failure.

Acetylglucosaminidase↗
PubMed1992

Somatosensory evoked potentials and outcome in perinatal asphyxia.

Somatosensory evoked potentials (SEP) can be measured in the term newborn infant and given an index of function in the areas of the brain most likely to be damaged in perinatal asphyxia. We studied the median nerve SEP in 30 asphyxiated term infants over the course of their encephalopathy and until discharge from the neonatal unit. Three types of response were noted: normal waveform, abnormal waveform, or absence of cortical response. Follow up of the survivors was undertaken at a mean age of 12 months by means of a Griffiths' assessment and neurological examination. Nine infants died of their asphyxial illness and one of spinal muscular atrophy. Of the 20 survivors, three have cerebral palsy, four have minor abnormalities, and 13 are neurodevelopmentally normal. There was a close correlation between outcome and SEP. All 13 infants with normal outcome had normal SEP by 4 days of age, whereas those with abnormal or absent responses beyond 4 days had abnormalities at follow up.

Asphyxia Neonatorum↗
PubMed2003

Perinatal asphyxia in the guinea pig leads to morphologic but not neurologic, cognitive, or behavioral changes.

BACKGROUND: In a recent publication, we described neurodegeneration along with neurotransmitter deficits and impaired differentiation in the guinea pig 3 months following severe perinatal asphyxia (PA). We were therefore interested in the clinical features in terms of neurology, cognitive functions, and behavior. METHODS: We tested the long-term effects of PA in an animal model, which in the rat are well documented and resemble the clinical situation. Examinations consisted of an observational battery for motor and reflex functions and the acoustic startle response setting. We tested cognitive functions in the multiple T-maze and evaluated behavior using the elevated plus maze and open field studies. RESULTS: No neurologic deficits were observed in the observational battery, including the acoustic startle response. Cognitive functions of memory and learning were not impaired in the multiple T-maze. In the open field and in the elevated plus maze, the system to test anxiety-related behavior, guinea pigs performed well. CONCLUSION: Our findings of patent neurology, cognitive functions, and behavior do not reflect the prominent morphologic findings of neurodegeneration. This is in agreement with corresponding studies on PA in the rat at the identical time point. We learned from this study that both test systems, although representing the standard in neuroscience, are either not sensitive enough or central nervous system lesions are clinically fully compensated.

Animals↗
PubMed2003

Perinatal asphyxia exerts lifelong effects on neuronal responsiveness to stress in specific brain regions in the rat.

BACKGROUND: Perinatal asphyxia (PA) causes irreversible damage to the brain of newborns and can produce neurologic and behavioral changes later in life. To identify neuronal substrates underlying the effects of PA, we investigated whether and how neuronal responsiveness to an established stress challenge is affected. METHODS: We used Fos expression as a marker of neuronal activation and examined the pattern of Fos expression in response to acute swim stress in 24-month-old rats exposed to a 20-minute PA insult. RESULTS: Swim stress produced a similar pattern of Fos expression in control and asphyxiated rats in 34 brain areas. Asphyxiated rats displayed a higher number of stress-induced Fos-positive cells in the nucleus of the solitary tract, parabrachial nucleus, periaqueductal gray, paraventricular hypothalamic nucleus, nucleus accumbens, caudate-putamen, and prelimbic cortex. No differences in the Fos response to stress were observed in other regions, including the locus ceruleus, amygdala, hippocampus, or septum. CONCLUSION: These data provide functional anatomic evidence that PA has lifelong effects on neuronal communication and leads to an abnormal, augmented neuronal responsiveness to stress in specific brain areas, particularly in the main telencephalic target regions of the mesencephalic dopamine projections, as well as in a functionally related set of brain regions associated with autonomic and neuroendocrine regulation.

Animals↗
PubMed1974

Water and electrolyte abnormalities in the human brain after severe intrapartum asphyxia.

In a necropsy study of brain water, sodium, and potassium concentrations is newborn infants, abnormalities were found in 10 out of 16 cases who were severely asphyxiated at birth. It is concluded that, although frank cerebral cortical necrosis is not often recognizable in perinatal deaths, early anoxic-ischaemic cerebral damage is frequent after intrapartum asphyxia. Diffuse cerebral swelling was associated with marked electrolyte disturbances and may be regarded as a feature of anoxic-ischaemic encephalopathy in asphyxiated newborn infants.

Asphyxia Neonatorum↗
PubMed2006

Term neonate prognoses after perinatal asphyxia: contributions of MR imaging, MR spectroscopy, relaxation times, and apparent diffusion coefficients.

PURPOSE: To retrospectively evaluate magnetic resonance (MR) imaging, hydrogen 1 (1H) MR spectroscopy, apparent diffusion coefficient (ADC), T1, and T2 measurements for prediction of late neurologic outcome in term neonates after severe perinatal asphyxia. MATERIALS AND METHODS: This study was approved by the local ethics committee. Informed consent from parents was not required. Thirty term neonates (12 boys, 18 girls; age range, 2-12 days) with severe hypoxic-ischemic encephalopathy were examined during the first 12 days of life with conventional and diffusion-weighted cerebral MR imaging, 1H MR spectroscopy with absolute quantification, and T1 and T2 measurements. Quantitative 1H MR spectroscopy, T1, and T2 data were acquired on one 10-mm slab positioned at the level of the basal ganglia. The neonates were assigned to one of two groups according to their late (>12-month follow-up) neurologic outcome: those with an unfavorable outcome-that is, death or severe disability-and those with a favorable outcome. Clinical data, MR signal intensity abnormalities, ADCs, 1H MR spectroscopy findings, and relaxation times were compared by using Chi2 testing and analysis of variance to individualize the prognostic indicators. RESULTS: The unfavorable (n=16) and favorable (n=14) outcome groups were similar in terms of clinical data (ie, Apgar scores, visceral hypoxic injuries), visualization of brain edema on MR images, and T1 and T2 relaxation times. Late unfavorable neurologic outcome was associated with a mixed pattern of cortical and basal ganglia signal intensity abnormalities on MR images (13 babies with unfavorable vs three babies with favorable outcomes, P=.001) and with decreased absolute N-acetylaspartate (NAA) and choline concentrations in all brain structures, especially the basal ganglia (mean NAA concentration: 2.72 mmol/L in unfavorable outcome group vs 4.66 mmol/L in favorable outcome group, P<5x10(-9)), as measured with MR spectroscopy. In the basal ganglia, an NAA concentration lower than 4 mmol/L indicated an unfavorable individual prognosis with 94% sensitivity and 93% specificity. Significantly reduced ADCs also were noted in the unfavorable outcome group, but only during the first 6 days of life. CONCLUSION: Conventional MR imaging findings, spectroscopically measured absolute NAA and choline concentrations, and ADCs are complementary tools for predicting the individual outcomes of severely asphyxiated term neonates.

Age Factors↗
PubMed1989

Two-phase change of sympathetic rhythms in brain ischemia, Cushing reaction, and asphyxia.

The present study was designed to determine the extent to which the brain stem neural networks, normally capable of synchronizing the sympathetic nerve discharge (SND) into 2- to 6- and 10-Hz rhythmic fluctuations, contribute to the control of autonomic reactions during brain hypoxia and/or hypercapnia. Vertebral, cardiac, and renal nerve discharges were recorded electrophysiologically in 34 anesthetized, curarized, and artificially ventilated cats. The sympathetic nerve responses to cerebral ischemia (elicited by reducing the blood supply to the brain), intracranial pressure elevation (Cushing reaction), and systemic asphyxia were tested with special focus on the rhythmic structure of the SND. It has been found that there are two phases of SND changes during cerebral ischemia differing mainly in the frequency content of the signals and less in the compound action potential amplitude. During the first phase the rhythmic generators controlling the tonic sympathetic outflow are more strongly activated, which is reflected in a stronger, more regular, and more widespread manifestation of these rhythms on the efferent neurograms. After some time the normal SND structure abruptly changes to a desynchronized activity with loss of the three main sympathetic rhythms and responsiveness to baroreceptor reflex activation. The same stereotyped changes can be observed regardless of the way in which the brain hypoxia and/or hypercapnia has been produced. Nor does the denervation of peripheral baro- and chemoreceptors substantially alter the general pattern of the responses.

Animals↗
PubMed1998

CO2 asphyxia increases plasma norepinephrine in rats via sympathetic nerves.

The objective of this study was to determine whether the plasma norepinephrine (NE) increase in rats exposed to CO2 asphyxia was due to adrenal gland release or sympathetic nerve ending (SNS) release. Plasma NE was measured by high-performance liquid chromatography in hypertensive and normotensive rats using the following protocol: control session, CO2 exposure, N2 exposure, reserpine + CO2, and adrenalectomy + CO2. Four strains of male and female rats were used: spontaneously hypertensive rats, Wistar-Kyoto rats, and two congenic strains with different Y chromosomes. The same rats were used throughout the experiment (n = 80). Blood pressure measured by aortic telemetry increased approximately 50-60 mmHg in response to CO2 in all strains. CO2 increased NE 6-10x in all strains and both genders. N2 produced a significant increase in NE (73% of CO2 response). Reserpine significantly decreased (67%) plasma NE after CO2. Adrenalectomy did not significantly reduce the NE response to CO2. In conclusion, the increase in plasma NE after CO2 was associated with SNS release and not adrenal medullary release, was mainly due to hypoxia, and was not a specific response to CO2.

Adrenalectomy↗
PubMed1998

Circadian rhythms in diving behavior and ventilatory response to asphyxia in canvasback ducks.

Underwater feeding behavior was measured in 10 captive canvasback ducks (Aythya valisineria) for 12 days under a 12:12-h light-dark photoperiod. Feeding activity exhibited a daily rhythm, with 76% of dives occurring at night. In separate experiments on six of these ducks, a circadian rhythm was observed in the duration of voluntary dives. Dives at night (14.7 +/- 0.7 s) were significantly longer than those during the day (10.7 +/- 0.7 s). These day-night differences in diving behavior were accompanied by day-night differences in respiratory responses to progressive asphyxia. In the same six ducks, ventilation increased exponentially as a function of inspired CO2 concentration during rebreathing in a closed-circuit barometric plethysmograph. The exponential rate constant for inspired ventilation was significantly smaller at night (0.23 +/- 0.02) than during the day (0.26 +/- 0.01). We suggest that intermittent apneic exercise is facilitated by reduced respiratory chemosensitivity and that the respiratory and behavioral control systems are synchronized by the circadian timing system in diving ducks.

Animals↗
PubMed1977

Respiratory patterns during progressive asphyxia in newborn rabbits.

During acute progressive asphyxia an abrupt transition occurs from regular respiratory efforts to primary apnea and gasping. To study this transition we measured inspiratory duration (TI), expiratory duration (TE), maximal inspiratory tracheal pressure (Pmax), electromyographic activity (EMG) of different muscle groups, and the electrocorticogram (ECoG) of 3- to 5-day-old rabbits following airway occlusion at functional residual capacity (FRC). The onset of primary apnea was associated with other central nervous system events as indicated by decerebrate posture and maximal EMG activity which were followed by relaxation, loss of EMG activity, and an isoelectric ECoG. Indices of inspiratory drive (Pmax and Pmax/TI) were preserved or accentuated following primary apnea despite a reduction of overall respiratory activity (frequency X Pmax). The onset of primary apnea appears to be due to interruption of the respiratory cycling controls rather than failure of the respiratory center which regulates inspiratory force. Gasping appears to be linked with progressive changes in respiratory patterns which are observed prior to primary apnea. These findings do not support the concept of a "gasping" center.

Airway Obstruction↗
PubMed1987

Phrenic and external intercostal motoneuron activity during progressive asphyxia.

Phrenic and external intercostal motoneuron activities were compared during progressive asphyxia induced by the interruption of artificial ventilation in the pentobarbital-urethan-anesthetized, gallamine-paralysed rabbit. The relative augmentation of inspiratory activity of the T1-T4 external intercostal nerves was significantly greater than that of the phrenic nerve during asphyxic hyperpnea. This was associated with a greater recruitment of intercostal than of phrenic motoneurons, particularly late in the hyperpneic phase immediately before the period of asphyxic apnea. However, peak and average discharge frequencies developed by intercostal motoneurons (n = 20) were only approximately 60% of those of the phrenic motoneurons (n = 28). Gasping respiration terminated the apneic period and was associated with a further intense recruitment of intercostal though not of phrenic motoneurons, but discharge frequencies developed by the intercostal motoneurons remained approximately 60% of those of the phrenic motoneurons. The instantaneous frequency profiles generated by the motoneurons often exhibited progressive changes during the terminal stages of hyperpnea (reduction in inspiratory duration and duty cycle and increases in inspiratory slope and discharge frequencies) such that much of the character of gasping respiration became evident before the apnea. Such smooth transitional sequences do not obviate the existence of an "independent gasping center" but do require that such a proposed center at least possess the capacity for interaction with those sites responsible for the generation of eupneic and hyperpneic respiration.

Action Potentials↗
PubMed2003

Transient cholestasis in newborn infants with perinatal asphyxia.

UNLABELLED: In asphyxiated newborn infants, cholestasis often leads to extensive investigations and a cause can rarely be found. OBJECTIVE: To assess the frequency of transient neonatal cholestasis in an unselected group of asphyxiated newborn infants in a mother-child centre. METHOD: Charts of 181 asphyxiated newborn infants born with appropriate birth weight for gestational age (AGA) or small weight for gestational age (SGA) at Sainte-Justine Hospital, Montreal, Quebec between 1989 and 1993 were reviewed. RESULTS: Transient neonatal cholestasis was found in 8.5% of asphyxiated AGA and 33% of SGA newborn infants, compared with 3.94% cholestasis of any etiology in nonasphyxiated SGA infants. Asphyxiated neonates born before the age of 35 weeks had an increased risk for transient neonatal cholestasis (odds ratio 2.84, CI 1.0-8.1) CONCLUSION: Transient neonatal cholestasis is associated with several contributing factors related to the severity of the neonatal distress. Asphyxia is frequently accompanied by cholestasis in this group of newborns and without symptoms other than uncomplicated cholestasis. Investigations should be focussed on conditions requiring immediate therapy.

Apgar Score↗
PubMed2001

Human perinatal asphyxia: correlation of neonatal cytokines with MRI and outcome.

Clinical studies of the preterm neonate and animal models of asphyxial brain injury both support a role for proinflammatory cytokines in central nervous system (CNS) injury. There are fewer studies of perinatal CNS injury in the full-term neonate. We have performed a prospective cohort study of full-term infants with perinatal asphyxia. Using archived neonatal blood samples, we have analyzed the serum levels of several proinflammatory cytokines. Preliminary results demonstrate an increase in IL-1, IL-6, and TNF-alpha in those children who are deceased at 1 year or who have a diagnosis of cerebral palsy versus those with normal neuromotor outcome. Further analysis will include correlations of cytokine levels with injury on MRI spectroscopy, with neonatal clinical markers of encephalopathy, and with later neurodevelopmental outcome.

Asphyxia Neonatorum↗