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Management of perinatal asphyxia is one of those rare opportunities in clinical medicine when death or life-long disability can be prevented with several minutes of skillful and judicious action. Fetal and neonatal asphyxia is approached most successfully as a joint obstetric, pediatric, and anesthetic effort. This article reflects the team approach to perinatal asphyxia.
1. This study analyzes variations of oxygen tension induced by asphyxia in the myocardium (MpO2) and coronary sinus blood (CSpO2) of the anesthetized open-chest dog. Oxygen tension was measured polarographically and arterial blood pressure and coronary blood flow were recorded simultaneously. 2. Asphyxia increased arterial pressure and coronary blood flow but decreased both MpO2 and CSpO2. 3. During the reoxygenation phase, arterial pressure and coronary flow decreased gradually. Reoxygenation induced a rapid but transient increase in CSpO2 above control levels. In contrast, MpO2 returned gradually to the basal state. 4. The mechanism(s) involved in the differential effects of asphyxia followed by reoxygenation on MpO2 and CSpO2 remain to be elucidated.
This study was undertaken to investigate the effects of neonatal asphyxia on brain development, with special reference to the kinetics of neuronal proliferation by using autoradiography. For 30 minutes, two-day-old suckling mice, Jcl:ICR strain, were put into a chamber which was constantly flushed with 100% CO2 gas. After the exposure to asphyxia, 29% of the mice survived. Cell cycle studies were carried out at two days and at seven days on the external matrix cells, the precursor of the granule cells, at the external granular layer of the cerebellum from CO2-exposed and control mice by 3H-thymidine autoradiography. At two days the generation time of the control mice was about 15 hours, whereas that of the asphyxiated mice was about 17 hours. The prolongation of the generation time in the asphyxiated mice was caused mainly by a delay in the G2 phase. This prolongation was apparent for about five days and thereafter growth caught up. These results suggest that neonatal asphyxia has an adverse effect on cerebellar neuronal proliferation that may revert to normal spontaneously in older animals.
The effects of vagosympathectomy, asphyxia, hypoxia and hypercapnia on the breathing of anaesthetised pigs are described. Vagosympathectomy caused changes in cardiovascular variables and in the pattern of breathing characteristic of the loss of stretch receptor activity. After vagosympathectomy the linear relationship between tI and tE was abolished. Hypoxia in intact animals produced changes in minute ventilation by peripheral chemoreceptor drive. When this drive was removed by vagosympathectomy the central depressing effects of hypoxia were revealed as a slowing of breathing and reduction in minute volume. The central depressing effect of hypoxia on respiration was very potent in the pig and very clearly seen in asphyxia. Vagosympathectomy caused a reduction in frequency of breathing and respiratory arrest occurred when a dead space of only moderate size was used. Breathing slowed from the moment of connection of the dead space to produce respiratory arrest within 2 min. The pig lung has been considered similar to the human lung on morphometric and physiological grounds but these results show that there are very important species differences in response to asphyxia.
Noradrenaline content was measured in the cerebrospinal fluid of 17 full-term and 16 premature newborns with or without perinatal asphyxia. Upon the effect of asphyxia the noradrenaline content of cerebrospinal fluid exhibited a more than three-fold increase (from 2.61 +/- 1.45 microgram/l to 10.86 +/- 4.02 micrograms/l) in mature newborns, but it decreased to about half of the control value in premature babies (from 2.39 +/- 0.72 microgram/l to 1.25 +/- 0.70 microgram/l). The observations emphasize the role of central noradrenergic structures in the organization of asphyxia-induced stress-response and in the regulation of adaptation to extrauterine life.
The serum bilirubin concentration was studied in 114 full term and 199 preterm babies suffering from either perinatal asphyxia or idiopathic indirect hyperbilirubinaemia, in order to establish the effect of asphyxia on the serum bilirubin level. Infants with any other disease causing non-physiologic jaundice were excluded. It was found that perinatal asphyxia per se does not exaggerate hyperbilirubinaemia either in full term or in preterm babies. Weight loss correlated significantly with the peak bilirubin concentration in all groups of patients. This would suggest the possible role of feeding and hydration in the genesis of hyperbilirubinaemia.
Asphyxia produced by discontinuing of artificial respiration for 3-5 min in curarized cats, was well tolerated by some neurons of the cerebral and hypothalamus cortex even when repeated a few times with the interval between asphyxias from 40 to 60 min. In most cases neurons even increased their resistance against subsequent effect of acute oxygen insufficiency preserving for a longer time the spontaneous impulse activity during the second and the third asphyxia.
We measured maternal venous (MV), umbilical arterial (UA) and umbilical venous (UV) cortisol levels of 180 pregnancies at term, and investigated especially cases of fetal distress and neonatal asphyxia. No fetal distress and no neonatal asphyxia cases followed spontaneous vaginal deliveries (94), cesarean sections (18) or breech extractions (6). In cesarean section delivery, the cortisol levels of three individual samples were lower than in other modes of deliveries. The cortisol level of the umbilical artery was significantly higher than that of the umbilical vein in spontaneous vaginal delivery and cesarean section delivery. When spontaneous vaginal deliveries were classified into the fetal distress group and no fetal distress group, the cortisol levels of the umbilical artery and umbilical vein in the former group were significantly higher than those in the latter group. Furthermore, regardless of fetal distress there were significant positive correlations between the cortisol levels of MV & UA, MV & UV, and UA & UV. In addition, as the cortisol level of the maternal vein increased, the umbilical arterial-venous cortisol ratio (UA/UV) gradually approached 1.0. These data suggest that in fetal distress or neonatal asphyxia, the fetus may produce cortisol for itself independent of the mother.
The pathophysiology of respiration and hemodynamics during the agonal period of death by obstructive asphyxia was investigated. Experiments were carried out on ten dogs that were strangulated by ligature (seven cases) or asphyxiated by occlusion of the intubation tube (three cases). The following parameters were registered: Blood pressure in the arteria femoralis and arteria pulmonalis, electrocardiogram, endotracheal pressure, respiratory frequency, electroencephalogram. These were the most important findings: (a) An excessive and distinctly biphasic hypertonic reaction takes place after strangulation by ligature whereas occlusion of the intubation tube results in a slight increase of arterial blood pressure. (b) After occlusion of the tube more than after strangulation the endotracheal pressure becomes deeply negative during the inspiration trials. (c) After cessation of respiration a distinct pulmonary arterial hypertension develops in both forms of obstructive asphyxia. (d) The paralysis of the respiratory center takes place after about 4 min at the same time when the circulatory breakdown develops. The final cardiac failure occurs after about 9-10 min. The dysregulation of respiration and hemodynamics in the agony of obstructive asphyxia can be differentiated from other shock models. This results in special morphological alterations of the lung tissue which have been described elsewhere.
Perinatal asphyxia is one of the major causes of cerebral injury in neonates. It may be due to the increased endogenous opioid-like substances (OLS) in the body. The levels of three OLS, namely leucine-enkephalin (LEK), beta-endorphin (beta-EP) and dynorphin A1-13 (DynoA1-13) of 44 cases with neonatal asphyxia were studied by radioimmunoassay. The OLS level in plasma and cerebral spinal fluid (CSF) were higher in asphyxiated group than those in the control group, especially in asphyxiated cases with fetal distress. The OLS levels of CSF were also higher in cases with cerebral injury than in those without cerebral injury, while the levels of OLS in plasma had no difference in these two groups. The relationship between OLS levels and asphyxia and cerebral injury is also discussed.
We examined changes in plasma during drowning and hanging to determine the mechanism of acute asphyxia. Rabbits were used for the acute drowning and hanging experiments (using artificial sea water or fresh water for the former and complete or incomplete hanging for the latter). The plasma was examined for changes in haptoglobin and total protein contents. For acute drowning, the haptoglobin level reduced dramatically after one minute of inhalation of artificial sea and fresh water by about 46.0% and about 61.0%, respectively. Total protein content showed the same pattern of reduction. Afterward, haptoglobin remained generally unchanged but the total protein content returned to the original level 3 minutes after inhalation. For the handing, the haptoglobin level reduced within 1 minute. When respiratory arrest was near, both haptoglobin and total protein contents rose gradually. The changes in the haptoglobin level caused by hanging were similar to those that occur in acute asphxia when the air passage is completely obstructed and in subacute asphxia when the air passage is strangulated. Totally different and unique patterns were seen in association with drowning in comparison with obstructive asphyxia. These results suggested that the pathological physiology of acute drowning is different from that of fatal neck compression or other types of acute asphyxia.
In this article, the authors examine whether indicators commonly used to recognized birth asphyxia are specific to asphyxial states, and whether these allow recognition of a severity of asphyxia sufficient to pose a risk of irreversible brain injury. Characteristics recognizable within the first hours after birth are focused on because these characteristics will be of most use in clinical decisions regarding use of potential new therapies for asphyxia.
Nuclear magnetic resonance imaging and spectroscopy have added significant new information about the newborn brain during and following asphyxia. NMR imaging has permitted sequential in vivo analysis of CNS maturation in the perinatal period that is superior in anatomic resolution, and especially in the characterization of myelination, to either cranial ultrasound or radiographic computed tomography. As a result, the accurate detection and recognition of the brain lesions associated with hypoxic-ischemic encephalopathy is now possible, including PVL, cerebral infarction, intraparenchymal and intraventricular hemorrhage, and delayed myelination. This has improved our understanding of the associated potential risk for abnormal neuro-developmental outcome with specific lesions. NMR spectroscopy has provided a metabolic window into the biochemical events during and following asphyxia. 31P MRS captures the phosphorous metabolites as levels rise and fall and shift in relation to each other to maintain cellular energy homeostasis in the face of oxygen depletion. Meanwhile, proton NMR spectroscopy promises to sustain the metabolic purview beyond the immediate cellular response to asphyxia to the chronic adaptation phase. Appropriately applied, this noninvasive technology may yet enable us to identify brain injury that is reversible in sufficient time to intervene and to diagnose accurately what is irreversible for timely prognostication. Furthermore, the integration of clinical imaging and spectroscopy capabilities is both feasible and desirable; information provided by each being mutually complementary. Imaging could improve spectroscopy interpretation by identifying the observed tissue, whereas MRS should clarify diagnosis of anatomic lesions detected by MRI. Advances in spatial resolution and speed of data acquisition may soon make integrated MRI/MRS a clinical reality.
BACKGROUND: Birth asphyxia is a major cause of neonatal mortality. An understanding of the determinants of mortality among asphyxiated neonates will help formulate effective management protocols. METHODS: One hundred and fifty consecutive neonates with birth asphyxia (apnoea or gasping respiration at 1-minute of age) were prospectively studied. The association of the outcome variable, namely, mortality before discharge, was documented in relation to a number of clinically important risk factors. RESULTS: The neonatal mortality of 24.7% (37/150) among asphyxiated neonates was 34.5-times compared to that of the non-asphyxiated population (p < 0.001). The mortality rates in preterm-and term-asphyxiated neonates were 47.8% and 6%, respectively (p < 0.0001). The relative risk of mortality increased progressively with increased birth-weight. On univariate analysis, prematurity, low birth-weight, respiratory distress, severity of asphyxia, hypoxic-ischaemic encephalopathy, apnoea, acidosis and seizures were found to be significant risk factors of death. However, on step wise regression analysis, prematurity emerged as the most significant determinant of mortality. The highest positive predictive value (58.3%) for mortality was documented for hypoxic-ischaemic encephalopathy. CONCLUSION: A significant reduction in mortality among asphyxiated neonates will require aggressive management of prematurity-related neonatal complications and hypoxic-ischaemic encephalopathy.
In the current legal climate, the recognition of cerebral palsy or other major brain dysfunction in a child is likely to lead to a malpractice action against the obstetrician who delivered the child. Perinatal asphyxia is usually considered the most likely cause of the brain damage, and the obstetrician is presumed by the lawyer either to have failed to recognize the fetal asphyxia or to have ignored it. In this essay, the illogic in this reasoning is discussed. While fetal asphyxia clearly can cause fetal brain damage, the infrequency of this relationship is stressed. The dilemma faced by the obstetrician as a result of modern perinatal care is discussed.
The diagnosis of fetal asphyxia requires a blood gas and acid-base assessment demonstrating a significant metabolic acidosis. However, the fetus may tolerate an asphyxial insult without central nervous system injury because of the fetal cardiovascular adaptation to hypoxemia. Prediction of the significance of an asphyxial insult to the fetus requires a measure of both the duration and degree of the asphyxia as well as an expression of the fetal compensatory response to the asphyxia.
The action of asphyxia and aminooxyacetic acid (AOAA) on the crossed olivocochlear bundle (COCB), was investigated, in particular, the slow change evoked by COCB stimulation, often called the crossed olivocochlear potential (COCP). Terminating artificial respiration caused the COCP to fall within 2 min to 0.25 mV. It remained at this level for an additional 4 min before declining to zero. If artificial respiration was reinstated, before 3 min had elapsed, the COCP recovered completely within 5 min. Administration of AOAA (40 mg/kg, i.v.) produced a slow reduction in the endocochlear potential (EP) to about 10 mV in 60 min. The COCP initially declined after AOAA administration but fully recovered by the time the EP plateaued at 10 mV. The results with asphyxia could be explained solely by a reduction of the EP; however, in light of the different results observed with AOAA, one might hypothesize an additional action of asphyxia at the efferent nerve-ending-hair cell synapse.
OBJECTIVE: Our goal was to update our experience with nucleated red blood cells as a marker for fetal asphyxia and to determine whether a relationship exists between the presence of nucleated red blood cells and long-term neurologic impairment. STUDY DESIGN: Nucleated red blood cell data from 153 singleton term neurologically impaired neonates were compared with cord blood nucleated red blood cells of 83 term nonasphyxiated newborns. Newborns with anemia, intrauterine growth restriction, and maternal diabetes were excluded. The group of neurologically impaired neonates was separated into the following subgroups: group I, persistent nonreactive fetal heart rate pattern from admission to delivery (n = 69); group II, reactive fetal heart rate on admission followed by tachycardia with decelerations and absent variability (n = 47); group III, reactive fetal heart rate on admission followed by an acute prolonged deceleration (n = 37). The first and highest nucleated red blood cell value and the time of nucleated red blood cell disappearance were assessed. RESULTS: The mean number of initial nucleated red blood cells was significantly higher in the group of neurologically impaired neonates (30.3 +/- 77.5, range 0 to 732 per 100 white blood cells) than in the control group (3.4 +/- 3.0, range 0 to 12 per 100 white blood cells) (p < 0.000001). When the group of neurologically impaired neonates was separated on the basis of timing of the neurologic impairment, distinct nucleated red blood cell patterns were observed. Significant differences were obtained between each of the three groups of neurologically impaired neonates and the normal group, with respect to initial nucleated red blood cells (group I, 48.6 +/- 106.9; group II, 11.4 +/- 9.8; group III, 12.6 +/- 13.4; p < or = 0.000002). Maximum nucleated red blood cell values were higher in group I (mean 51.5 +/- 108.9) than in groups II and III combined (mean 12.7 +/- 11.9) (p = 0.0005). Group I also had a longer clearance time (119 +/- 123 hours) than groups II and III combined (mean 59 +/- 64 hours) (p < 0.001). CONCLUSION: Our ongoing study indicates that nucleated red blood cells identify the presence of fetal asphyxia. When fetal asphyxia is present, distinct nucleated red blood cell patterns are observed that relate to the timing of fetal injury. In general, intrapartum injuries are associated with lower nucleated red blood cell values. Thus our data continue to support the concept that nucleated red blood cell levels may assist in determining the timing of fetal neurologic injury.