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PubMed2000

Ventilatory sensitivity to mild asphyxia: prone versus supine sleep position.

AIMS: To compare the effects of prone and supine sleep position on the main physiological responses to mild asphyxia: increase in ventilation and arousal. METHODS: Ventilatory and arousal responses to mild asphyxia (hypercapnia/hypoxia) were measured in 53 healthy infants at newborn and 3 months of age, during quiet sleep (QS) and active sleep (AS), and in supine and prone sleep positions. The asphyxial test mimicked face down rebreathing by slowly altering the inspired air: CO(2), maximum 5% and O(2), minimum 13.5%. The change in ventilation with inspired CO(2) was measured over 5-6 minutes of the test. The slope of a linear curve fit relating inspired CO(2) to the logarithm of ventilation was taken as a quantitative measure of ventilatory asphyxial sensitivity (VAS). Sleep state and arousal were determined by behavioural criteria. RESULTS: At 3 months of age, prone positioning in AS lowered VAS (0.184 prone v 0.269 supine, p = 0.050). At newborn age, sleep position had no effect on VAS. Infants aged 3 months were twice as likely to arouse to the test than newborns (p = 0.013). Placing infants prone as opposed to supine increased the chances of arousal 1.57-fold (p = 0.035). CONCLUSION: Our findings show 3 month old babies sleeping prone compared to supine have poorer ventilatory responses to mild asphyxia, particularly in AS, but the increased prevalence of arousal is a protective factor.

Arousal↗
PubMed1999

Correlation of basal ganglia magnetic resonance spectroscopy with Apgar score in perinatal asphyxia.

BACKGROUND: Brain metabolite levels are measured by proton magnetic resonance spectroscopy (1H MRS) and include N-acetylaspartate (NAA), creatine (Cr), choline (Cho), and lactate and the ratios NAA to Cho and Cr (NAA-ChoCr), NAA-Cr, NAA-Cho, and Cho-Cr. Brain metabolite levels may correlate with the degree of neonatal asphyxia. OBJECTIVE: To determine which brain metabolite ratios have the strongest correlation with the Apgar scores in infants with possible asphyxia; whether the correlation is stronger with basal ganglia (BG) or anterior border-zone metabolites; and whether a combined approach using routine MR imaging (MRI), diffusion-weighted MRI, and MRS can be used to evaluate the severity of neonatal asphyxia. METHODS: Twenty infants with 1-minute Apgar scores of 6 or less were studied at 2 to 28 days of age. The MRS variables were compared with routine and diffusion-weighted brain MRI. Clinical variables and MRS findings were subjected to factor analysis and stepwise multiple regressions to determine interrelationships. RESULTS: The BG region NAA-Cho and NAA-ChoCr ratios correlated with the 1-minute (P<.001) and 5-minute (P = .01 for NAA-Cho; P = .006 for NAA-ChoCr). There was no correlation between metabolite levels and the 10-minute Apgar scores. The stongest predictions exist between the 1-minute Apgar scores and the NAA-Cho and NAA-ChoCr ratios. In the anterior border zone, the only correlation was between the 1-minute Apgar score and the NAA-Cho ratio, but there was a strong age effect in these data. Lactate was found in the BG of 3 infants, all of whom had 5-minute Apgar scores of 6 or less. Three patients had focal lesions on MRI; 2 of these had elevated lactate levels in the abnormal region; and the third, who had an intrauterine stroke, had no lactate in the region. CONCLUSIONS: Correlations between NAA-Cho and NAA-ChoCr ratios and the 1- and 5-minute Apgar scores are stronger in the BG region than in the frontal border zone. The presence or absence of lactate may indicate the severity of the brain insult, and the combination of MRS, MRI, and diffusion-weighted MRI may assist in localizing and predicting a long-term brain injury.

Apgar Score↗
PubMed1999

Oxidative stress in newborn infants with and without asphyxia as measured by plasma antioxidants and free fatty acids.

A rapid perfusion of oxygen in infants at birth may cause an increase of oxidative stress. To assess this possibility, we measured levels of blood plasma antioxidants and free fatty acids in 20 normal infants at 0, 1, 3, and 5 days after birth. Plasma levels of the most reactive antioxidant, ascorbic acid, decreased daily to equilibrium values at days 3 and 5. Percentages of oxidized form of coenzyme Q-10 (%CoQ-10) in total coenzyme Q, another good marker of oxidative stress, in infants (25-31%) were significantly higher than those in healthy young adults (4.5%). Plasma levels of total free fatty acids (FFA) in normal infants were highest at day 1 and decreased rapidly thereafter. The content of polyunsaturated fatty acids (PUFA) in total FFA was lowest at day 1 and then increased. Since PUFA are susceptible to oxidation, these changes in FFA composition suggest that oxidative stress is most evident at the initial day of neonatal life. Furthermore, it appears that mono-unsaturated fatty acids such as oleic and palmitoleic acids increase in response to the oxidative loss of PUFA. Similar changes in plasma antioxidants, FFA levels, and FFA compositions were observed in 9 infants with asphyxia. Values of %CoQ-10 in infants with asphyxia were significantly greater than those in normal infants, suggesting that infants with asphyxia have elevated oxidative stress.

Adult↗
PubMed2002

Perinatal asphyxia induced neuronal loss by apoptosis in the neonatal rat striatum: a combined TUNEL and stereological study.

Perinatal asphyxia can lead to cell damage in various regions of the brain, such as the neostriatum. In this study, we investigated the mechanism of cell death that leads to neuron loss in the neostriatum of rat pups. Asphyxia was induced by immersing fetus-containing uterus horns in a water bath at 37 degrees C for 20 min. This led to an increase in mortality rate (+/- 40%) compared to control pups (0%). TUNEL-positive cell profiles were visible in all groups at postnatal day (P) 2, P8, and P15, peaking at P8. A significant increase of 40% at P8 and 45% at P15 in the number of TUNEL-positive cell profiles was observed in asphyctic rats compared to control rats. Nuclear condensation and fragmentation was visible with the DNA stain Hoechst 33342. Furthermore, laser-scanning confocal microscopy showed multiple DNA fragments in TUNEL-positive cell profiles. We found a decrease of 16% in the total number of striatal neurons in the asphyctic pups compared to the control pups at 21 days postasphyxia using stereology. These data show that asphyxia causes exaggerated apoptotic cell death during the first week of life and as a consequence a small amount of neuron loss in the neostriatum.

Aging↗
PubMed1999

Upregulation of the aromatic amino acid decarboxylase under neonatal asphyxia.

Perinatal hypoxic-ischemic cerebral injury is a major determinant of neurologic morbidity and mortality in the neonatal period and later in childhood. There is evidence that the dopaminergic system is sensitive to asphyxia. However, the respective enzyme activities have not yet been measured in the living neonatal brain. In this study, we have used 18F-labeled 6-fluoro-L-3,4-dihydroxyphenylalanine (FDOPA) together with positron-emission tomography (PET) to estimate the activity of the aromatic amino acid decarboxylase (AADC), the ultimate enzyme in the synthesis of dopamine (DA), in the brain of newborn piglets. Simultaneously, the cerebral blood flow (CBF) was measured with colored microspheres. Asphyxia elicited an up to threefold increase of the CBF. Despite this, the blood-brain transfer of FDOPA as well as the clearance rate constants from brain were unchanged. However, the synthesis rate of FDA from FDOPA was significantly increased in frontal cortex, striatum, and midbrain. This increase of the AADC activity and the decrease of monoamine oxidase activity may contribute to the increase of extracellular DA during asphyxia which is expected to be involved in severe disturbances of neuronal metabolism, e.g., by generating free radicals.

Algorithms↗
PubMed1992

The possible risk of bilirubin encephalopathy as predicted by plasma parameters in neonates with previous severe asphyxia.

The study group consisted of nine mature newborn infants with a previous history of severe asphyxia and a control group of 18 mature, healthy newborns with the same postnatal age and sex. The object of the investigation was to compare the possible risk of development of bilirubin encephalopathy between the two groups as estimated by plasma parameters. The asphyxia group had a significantly lower reserve albumin concentrations for binding of monoacetyldiaminodiphenyl sulphone (P = 0.008), a measure of binding of unconjugated bilirubin, and significantly lower total albumin concentrations (P = 0.02). No significant difference was observed in unconjugated bilirubin concentration. It is suggested that mature newborns with previous severe asphyxia are at a slightly increased risk of developing bilirubin encephalopathy over and above the well-known risk associated with increased permeability of the blood brain barrier.

Asphyxia Neonatorum↗
PubMed2000

A traumatic asphyxia in a child.

PURPOSE: Traumatic asphyxia in a child is rare and the pathophysiology is different from that occurring in an adult. We report a case of traumatic asphyxia in a child who recovered without specific treatment, even though chest and abdominal compression was severe. CLINICAL FEATURES: A three-year-old boy (14.2 kg) was run over by the rear wheel of a Jeep. He was under the tire for about three minutes and then was transferred to our hospital. When he arrived, he was lethargic with Glasgow Coma Scale of E3V4M6 (coma score of 13). He was cyanotic in his face and had a tire mark from the left shoulder to the right abdomen, petechiae on the head, face, conjunctiva and chest, oral bleeding, and facial edema. Serum concentrations of liver enzymes were increased and microhematuria was detected. However, no injuries were seen in the brain, eye, chest, or abdomen. Cyanosis disappeared in a few hours. Facial and thoracic petechiae disappeared in three days and that of the conjunctiva in five days. He was discharged from hospital on the 13th day without any disturbances. CONCLUSION: We present a three-year-old boy with traumatic asphyxia. He had no complications although he received severe thoraco-abdominal compression by a Jeep.

Asphyxia↗
PubMed2004

Social withdrawal, neophobia, and stereotyped behavior in developing rats exposed to neonatal asphyxia.

Perinatal asphyxia is a concern for public health and may promote subtle neuropsychiatric disorders. Anoxic insults to neonatal rats cause long-lasting neurobehavioral deficits. In the present study, we focussed on changes in emotional behaviors as a consequence of neonatal asphyxia in Wistar rats. Newborn pups (24 h after birth) underwent a single 30-min exposure to a 100% N2 atmosphere (or air). The offspring was tested for a) locomotor and exploratory activity with or without a d-amphetamine challenge (0, 1, or 2 mg/kg) on postnatal day (pnd) 15; b) social interactions and novelty seeking during adolescence; c) levels of the brain-derived neurotrophic factor (BDNF). In the open-field test (pnd 15), N2-exposed pups injected with the high (2 mg/kg) amphetamine dose exhibited reduced levels of locomotor hyperactivity, and a more marked involvement in stereotyped behaviors. Individual differences emerged in the locomotor response to the novelty-seeking test: two subgroups of rats (separated on the basis of the median value) showed either arousal/attraction or avoidance/inhibition in response to free-choice novelty. The N2-exposed group showed a more marked novelty-induced avoidance and inhibition. Time devoted to allogrooming and play-soliciting behaviors was reduced, whereas object exploration was increased. Levels of BDNF were reduced in the striatum of N2-exposed rats, suggesting poorer synaptic performance of dopamine pathways. In conclusion, these findings suggest an increased risk of developing social withdrawal, neophobia and behavioral stereotypies (common symptoms found in schizophrenia and autism) as a consequence of neonatal asphyxia in preterm humans.

Analysis of Variance↗
PubMed1975

The incidence of fetal asphyxia in six hundred high-risk monitored pregnancies.

Six hundred high-risk monitored obstetric patients were reviewed for evidence of fetal asphyxia at delivery. The over-all incidence was 20 per cent, i.e., 8 times the incidence in a normal obstetric population. Highly significant indicators of risk for asphyxia were severe toxemia (79 per cent), prematurity with further medical or obstetric complications (36 per cent), and clinical fetal distress, particularly meconium staining with fetal heart rate abnormality (33 per cent). All obstetric, medical, or gestational complications in this review were associated with an increased risk for fetal asphyxia when compared to that in a normal obstetric population.

Asphyxia Neonatorum↗
PubMed1984

Changing patterns of birth asphyxia and trauma over 20 years.

Comparison of birth asphyxia and trauma in the same obstetric service during periods 18 years apart shows some reassuring and some disquieting findings. Liberalized cesarean sections, electronic monitoring of fetal heart in labor, and replacement of opiate sedation by epidural anesthesia have had their effect. There has been dramatic reduction in perinatal death and neonatal encephalopathy due to birth asphyxia and trauma and only rarely do affected infants now develop permanent cerebral injury. Severe birth asphyxia, defined by need for prolonged ventilation, has, however, remained unchanged in frequency. Unexpectedly, fractures and paralyses have dramatically increased. The major hazard today for the term infant is the use of midforceps, which has become much more common in parallel with the increased use of pain relief by continuous epidural anesthesia.

Anesthesia, Obstetrical↗
PubMed1990

Predicting neonatal morbidity after perinatal asphyxia: a scoring system.

Predicting immediate neonatal morbidity after perinatal asphyxia has been difficult. A review of asphyxiated neonates greater than or equal to 36 weeks' gestation admitted to The Children's Hospital Newborn Intensive Care Unit in 1983 was conducted to devise a scoring system that would rapidly predict organ dysfunction observed in the immediate neonatal period. Comparison of potential score components to morbidity by multiple regression analysis yielded significant association with abnormalities in fetal heart rate monitoring, the 5-minute Apgar score, and neonatal base deficit. A scoring system was devised whose sensitivity (93.8%) and specificity (81.3%) were more predictive than any of its individual components. Prospective analysis in a similar population in 1984 validated its ability to distinguish severe from moderate morbidity after asphyxia. Positive predictive value for the score in the combined study groups (n = 98) was 79% and the negative predictive value was 83%. The scoring system may offer a rapid and accurate prediction of organ dysfunction in the immediate neonatal period after asphyxia.

Asphyxia Neonatorum↗
PubMed1982

Cerebral arterio-venous difference for hypoxanthine and lactate during graded asphyxia in the fetal lamb.

Hypoxanthine (HX) and lactate are degradation products from energy-rich intracellular substrates (ATP and glycogen), and their concentration will increase during anaerobic conditions, such as fetal asphyxia. In this study the accumulation of the two metabolites in blood during asphyxia was studied in 7 acutely exteriorized fetal lambs. The arterio-venous difference of HX and lactate over the brain was related to the function of the fetal brain as reflected by the somato-sensory evoked electroencephalogram potentials (SEP). Increased concentrations of HX in plasma and lactate in blood occurred simultaneously with deterioration of the SEP and the 3 variables correlate highly significantly. During normoxia, a net cerebral influx was found for HX, which in combination with severe asphyxia gradually changed to a net efflux. A linear correlation was found between the cerebral arterio-venous differences of HX and the impairment of the SEP. No such correlation existed for lactate. The results suggest, that the fetal brain has a high threshold for degrading its energy-rich intracellular purines.

Animals↗
PubMed1982

Prognostic value of the electroencephalogram in neonatal asphyxia.

In order to determine whether an EEG early in the course of asphyxia neonatorum is of any more value than the neurological examination in predicting outcome we reviewed case histories of 38 infants with asphyxia neonatorum. The EEG background activity was valuable in predicting outcome. Normal and maturationally delayed EEGs were associated with normal outcomes while low voltage, electrocerebral inactivity and burst suppression EEGs were highly correlated with severe neurological sequelae. Epileptiform activity was not as predictive of outcome as background activity. Although initial normal neurological examinations were associated with normal developmental and neurological outcomes, moderately and severely abnormal infants had more variable courses. A single EEG done early in the course of asphyxia neonatorum is a more sensitive predictor of outcome than the neurological examination.

Asphyxia Neonatorum↗
PubMed1982

Development of sympathetic ganglionic neurotransmission in the neonatal rat. Pre- and postganglionic nerve response to asphyxia and 2-deoxyglucose.

To determine the time course of development of neurotransmission in the sympathetic ganglion of the rat, pre- and postganglionic activity was recorded from the cervical sympathetic trunk in anesthetized neonatal and mature preparations. Tonic activity and responses to two stimuli, cellular hypoglycemia induced by 2-deoxyglucose and asphyxia, which are known to evoke CNS-mediated sympathetic activation in mature rats were measured. In 2-11-day-old neonates, tonic preganglionic activity recorded from the cervical sympathetic nerve and responses to hypoglycemia and asphyxia were comparable to or greater than that in mature rats. In 17-19-day-old neonates these variables were elevated to twice the adult value. In contrast, tonic postganglionic activity recorded from the internal carotid nerve was barely detectable through 5 days of age and there was no response to hypoglycemia. During asphyxia, maximum postganglionic impulse frequency and total number of impulses discharged were 10-20% of the mature value through the 5th postnatal day and the duration of the postganglionic response was only 25% of the preganglionic response. Tonic postganglionic activity and response to stimuli were equivalent to those in mature rats by the 10th postnatal day. The compound action potential evoked in the postganglionic axons by direct electrical stimulation was comparable in 4-5 and 10-13 day-old rats. In the concluded that functional ganglionic neurotransmission is established in the neonatal rat between the 5th and 10th postnatal day. The relation between biochemical changes associated with maturation of the postganglionic neuron, ganglionic synaptogenisis and neurotransmission is discussed. It is concluded that synaptogenisis and onset of neurotransmission are causally associated with development of CNS regulation of postganglionic activity and end organ response rather than with maturation of the postganglionic neuron and that cholinergic excitation of the postganglionic neuron adequate to evoke action potentials is not essential to initiate maturation of the neuron.

Animals↗
PubMed1995

Repeated asphyxia causes loss of striatal projection neurons in the fetal sheep brain.

Repeated episodes of cerebral hypoxia-ischemia can cause primarily striatal neuronal loss in the developing brain. We investigated the effect of repeated episodes of asphyxia on specific neuronal sub-populations of the basal ganglia in late-gestation fetal sheep. Asphyxia was induced in 10 fetal sheep (118-126 days gestation) by occluding the umbilical cord for 5 min. This procedure was repeated four times at 30 min intervals and the brains were fixed 3 days later for histopathology. Immunohistochemical markers were used to identify various populations of neurons in the striatum. Antibodies to calbindin were used to stain the GABAergic medium-sized striatal projection neurons and antibodies to somatostatin and parvalbumin to identify striatal interneurons. Striatal projection neurons to the globus pallidus were recognized by enkephalin immunoreactivity, while the striatonigral terminals were identified in the substantia nigra pars reticulata by substance P immunohistochemical labelling. The results showed a marked loss of calbindin staining in the striatum, evident by both reduced cell numbers and a decrease in neuropil staining. The number of parvalbumin immunoreactive cells was also reduced in the striatum, while somatostatin interneurons were selectively preserved. In addition, immunostaining for enkephalin in the globus pallidus and for substance P in the substantia nigra was markedly reduced. These results show that the stiatal GABAergic medium-sized projection neurons are severely affected by recurrent episodes of asphyxia. These findings are confirmed and extended by the results demonstrating that both the enkephalin/GABA striatopallidal and the substance P/GABA stiatonigral pathways are affected. The results of this study therefore suggest that the efferent striatal projections to the globus pallidus and to the substantia nigra may be involved in asphyxial episodes resulting in cerebral palsy.

Animals↗
PubMed1993

Does hypoxemia prevent brain damage in birth asphyxia?

The clinical syndrome of hypoxic ischemic encephalopathy (HIE) which occurs in association with birth asphyxia, is thought to represent a reperfusion injury consequent upon the generation of cytotoxic oxygen derived free radicals. It has recently been suggested that resuscitation of asphyxiated infants with unrestricted oxygen may aggravate the brain damage by causing hyperoxia and increased free radical production. To determine whether sustained hypoxemia may be protective in birth asphyxiated infants, we investigated the relationship between HIE and persistent pulmonary hypertension of the neonate (PPHN). The latter condition is also related to intrauterine and intrapartum birth asphyxia but is associated with persistent hypoxemia in the infant. In a retrospective analysis of 39 asphyxiated neonates admitted to the neonatal intensive care unit, we found that 28 had HIE, 10 had PPHN and only 1 had both HIE and PPHN. We therefore suggest that the hypoxemia due to PPHN may limit the production of oxygen derived free radicals in asphyxiated neonates and hence protect against the development of HIE. These findings lend support to current research into air vs. oxygen resuscitation for infants with birth asphyxia.

Asphyxia Neonatorum↗
PubMed1991

Acute neonatal morbidity and long-term central nervous system sequelae of perinatal asphyxia in term infants.

Twenty-eight term neonates with severe perinatal asphyxia were referred to a tertiary neonatal intensive care unit (NICU). The morbidity of asphyxia included involvement of the pulmonary (n = 24 infants), central nervous system (n = 22), renal (n = 15), cardiac (n = 14), metabolic (n = 13) and hematologic (n = 10) systems. The majority of neonates had more than three organ systems involved. Twenty-four neonates survived the neonatal course and at NICU discharge all system effects other than the central nervous system had resolved. At 5 years (60 months), 14 children had a normal neurologic examination, 9 had spastic quadriplegia and one had hemiplegia. Nine children had a McCarthy General Cognitive Index (GCI) greater than or equal to 84, 3 had a GCI between 68 and 83 and 12 scored less than 67. Neonatal seizures, renal problems, microcephaly at 3 months, and post-neonatal seizures were associated with an abnormal neurologic outcome or a GCI less than 67. A neurologic examination during the first year of life may reveal whether children with birth asphyxia will be relatively normal at age 5 years or whether they will show considerable delay.

Analysis of Variance↗
PubMed1988

Traumatic asphyxia in New Mexico: a five-year experience.

Compression of the chest causing facial petechiae, violaceous facial hue, subconjunctival hemorrhages, and frequent mental status abnormalities has been termed traumatic asphyxia. We identified 35 such cases occurring in the State of New Mexico from 1980 to 1985 from records of the Office of the Medical Investigator (n = 30) and from cases presenting to the University of New Mexico Trauma Center (n = 5). Among those found at highest risk for traumatic asphyxia were people ejected from motor vehicles, men working under cars that were inadequately supported and fell onto the victims, children under the age of 5 years who were crushed under household furniture, and people involved in construction activities. Traumatic asphyxia following a moving motor vehicle accident was significantly associated with alcohol ingestion (p less than 0.001). Preventive and therapeutic strategies should focus on the groups and events identified.

Accidents↗