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PubMed2005

The effect of mild hypothermia on insulin-like growth factors after severe asphyxia in the preterm fetal sheep.

OBJECTIVES: Persistent reductions in insulin-like growth factor I (IGF-I) levels in the preterm infant are strongly associated with increased risk of retinopathy and other complications, and may result from exposure to severe hypoxia. The effects of a potential new treatment for hypoxic-ischemic encephalopathy, cerebral hypothermia, on the responses of the IGF axis to hypoxia are unknown. The aim of this study was to examine the effects of prenatal asphyxia and cerebral hypothermia on changes in IGF-I and -II, IGF-binding protein 1 (IGFBP-1), and insulin levels. METHODS: Fetal sheep at 0.7 of gestation underwent either sham asphyxia and sham cooling (n = 7), asphyxia induced by 25 minutes of complete umbilical cord occlusion alone (n = 8), or asphyxia and head cooling (n = 8, extradural temperature 29.5 +/- 2.6C [vs 39.4 +/- 0.3C; P < .05]). Fetuses were studied for 3 days post-insult, during which time fetal blood samples were taken for endocrine measurements. RESULTS: There were no IGF axis changes during occlusion. Plasma IGF-I levels significantly decreased between 6 hours and 48 hours after asphyxia and IGF-II levels by 10 hours, in both asphyxia groups. IGFBP-1 rose from 4 hours, reaching a peak at 10 hours and returning to control values by 48 hours in the normothermia group, and by 24 hours in the hypothermia group. Insulin levels decreased between 2 hours and 10 hours after asphyxia in both asphyxia groups, and subsequently normalized. CONCLUSIONS: This study demonstrates for the first time that transient asphyxia in the preterm sheep fetus is associated with a significant decrease in IGF-II as well as IGF-I during recovery, and that these responses are not altered by mild systemic hypothermia.

Animals↗
PubMed2001

The prediction and prevention of intrapartum fetal asphyxia in term pregnancies.

OBJECTIVE: This study was undertaken to examine the roles of clinical risk scoring, electronic fetal heart rate monitoring, and fetal blood gas and acid-base assessment in the prediction and prevention of intrapartum fetal asphyxia in term pregnancies. STUDY DESIGN: The outcomes of 166 term pregnancies with biochemically confirmed fetal asphyxia (umbilical artery base deficit at delivery, >12 mmol/L) were examined. This population included 83 pregnancies delivered abdominally matched with 83 pregnancies delivered vaginally. Antepartum and intrapartum clinical risk factors and neonatal complications were documented. Fetal assessments included fetal heart rate patterns in the fetal heart rate record and fetal capillary blood gas and acid-base assessments. Fetal asphyxia was classified as mild, moderate, or severe on the basis of umbilical artery base deficit (cutoff >12 mmol/L) and neonatal encephalopathy and other organ system complications. RESULTS: Fetal asphyxial exposures were as follows: mild, 140; moderate, 22; and severe, 4. Intervention and delivery during the first or second stage of labor occurred in 98 of the 166 pregnancies. Predictive fetal heart rate patterns were the primary indication leading to intervention and delivery during the first or second stage of labor. Clinical risk factors when present were secondary indications in the clinical decision to intervene. Fetal blood gas and acid-base assessment was a useful supplementary test in 41 pregnancies. Intervention and delivery may have prevented the progression of mild asphyxia in 78 pregnancies and may have modified the degree of moderate or severe asphyxia in 20 pregnancies. CONCLUSION: Although fetal heart rate patterns will not discriminate all asphyxial exposures, continuous fetal heart rate monitoring supplemented by fetal blood gas and acid-base assessment can be a useful fetal assessment paradigm for intrapartum fetal asphyxia. Such an assessment paradigm will not prevent all cases of moderate or severe fetal asphyxia. However, prediction and diagnosis with intervention and delivery during the first or second stage of labor could prevent the progression of mild asphyxia to moderate or severe asphyxia in some cases.

Acid-Base Imbalance↗
PubMed1993

Acute asphyxia affects neutrophil number and function in the rat.

OBJECTIVES: Previous studies in adults suggest that various types of physiologic stress appear to decrease phagocytic cell function. Adherence and chemotaxis of, and phagocytosis and bacterial killing by, neonatal neutrophils are altered compared with adult neutrophil function. Stresses encountered by the fetus and neonate, such as asphyxia, were hypothesized to further alter neonatal neutrophil function. To investigate the impact of asphyxia on systemic immunity, we developed a rat model of acute asphyxia and evaluated the effect of asphyxia on neutrophil number and function. DESIGN: Prospective, laboratory study. SETTING: Research laboratory. SUBJECTS: Adult female Wistar rats. INTERVENTIONS: Exposure to CO2 and cold stress. MEASUREMENTS AND MAIN RESULTS: Arterial blood gas, blood glucose, neutrophil number, neutrophil-mediated, complement-dependent bacterial phagocytosis and killing were determined. After a 20-sec exposure to CO2 and cold stress (dry ice vapors), adult rats developed acute respiratory acidosis (pH 6.89 +/- 0.26, PaCO2 220 +/- 183 torr [29.3 +/- 24.3 kPa]), and mild hypoxia (60 +/- 20 torr [8.0 +/- 2.7 kPa]) followed by significant metabolic acidosis (base deficit = -12.0 +/- 1.5). Neutrophil number slowly increased and reached statistical significance by 72 hrs (5.0 +/- 1.5 x 10(3)/mm3) compared to controls (2.9 +/- 1.6 x 10(3)/mm3) (p = .03). Phagocytosis and killing of group B streptococci by neutrophils isolated immediately after asphyxia were significantly impaired (p = .03), and this decrease in function lasted for 24 hrs after asphyxia (p = .04), as measured by two different in vitro complement and antibody-mediated functional assays. CONCLUSIONS: After brief exposure to CO2 and cold stress, rats developed an acute respiratory acidosis and subsequent metabolic acidosis similar to acute asphyxia. Neutrophil number did not increase until 72 hrs after asphyxia. However, neutrophil-mediated phagocytosis and killing of bacteria were immediately impaired. We speculate that asphyxia may increase the risk for sepsis secondary to altered neutrophil function.

Acidosis↗
PubMed1989

Regional cerebral blood flow response during and after acute asphyxia in newborn piglets.

The hemodynamic response during and after acute asphyxia was studied in 14 newborn piglets. An apnea-like asphyxial insult was produced in paralyzed mechanically ventilated piglets by discontinuing ventilation until the piglets became bradycardic (heart rate less than 80 beats/min). Seven piglets had organ blood flow measured by microspheres at control, during asphyxia (PO2 = 16 +/- 11 Torr, pH = 7.31 +/- 0.07, PCO2 = 47 +/- 9 Torr), and during recovery from asphyxia. During acute asphyxia, rapid organ blood flow redistribution occurred, producing decreased renal and skeletal muscle blood flow, while coronary blood flow increased. Although total brain blood flow changed little during asphyxia, regional cerebral blood flow (rCBF) analysis revealed significant nonhomogeneous blood flow distribution within the brain during asphyxia, with decreases to the cerebral gray and white matter and the choroid plexus, whereas brain stem structures had increased flow. During recovery with reventilation, total brain blood flow increased 24% above control, with a more uniform distribution and increased flow to all brain regions. The time course of rCBF changes during acute asphyxia was then determined in seven additional piglets with CBF measurements made sequentially at 30-60 s, 60-120 s, and 120-180 s of asphyxia. The vasoconstriction seen in cortical structures, concurrent with the reduction in skeletal and kidney blood flow, known to be sympathetically mediated, suggest a selective reflex effect in this brain region. The more gradual and progressive vasodilation in brain stem regions during asphyxia is consistent with chemical control. These findings demonstrate significant regional heterogeneity in CBF regulation in newborn piglets.

Animals↗
PubMed1992

Brain cell membrane dysfunction following acute asphyxia in newborn piglets.

Brain cell membrane function during and following single and repeated episodes of asphyxia was investigated. Asphyxia in 24 anesthetized, paralyzed, mechanically-ventilated newborn piglets was produced by stopping ventilation for 2-3 min followed by recovery with reventilation. Measurements of cerebral Na+,K(+)-ATPase activity and of lipid peroxidation products, conjugated dienes and fluorescent compounds, were made during control (n = 12), asphyxia (n = 5), recovery after a single asphyxia event (n = 4), and recovery following 7 repeated asphyxia episodes (n = 3). Cerebral Na+,K(+)-ATPase activity remained unchanged from control during asphyxia (14.57 +/- 2.43 compared to 15.33 +/- 4.27 mumol Pi/mg protein/h, mean +/- SD), but was significantly reduced both during recovery after single (3.87 +/- 1.66) and after repeated (2.59 +/- 1.58) asphyxias, representing a 73 and 82% reduction in enzyme activity, respectively. Conjugated dienes and fluorescent compounds were similarly unchanged during asphyxia compared to control, but increased during recovery from single and from repeated episodes. Decreased cerebral Na+,K(+)-ATPase activity, simultaneous with an increase in lipid peroxidation products, reflects significant cellular membrane damage consistent with oxygen free radical formation during the recovery from acute asphyxia in the newborn piglet.

Animals↗
PubMed1997

Changes in cerebral cyclic nucleotides and cerebral blood flow during prolonged asphyxia and recovery in newborn pigs.

Cerebrovascular reactivity is preserved after acute severe asphyxia/reventilation in piglets. We hypothesize that prolonged, partial asphyxia with hypotension causes loss of cerebrovascular reactivity and altered cerebral hemodynamics during recovery. We investigated the changes in cerebrospinal fluid cAMP and cGMP, pial arteriolar diameters and flow, and cerebral blood flow during 1 h of asphyxia and 1 h of recovery. During asphyxia, blood pressure decreased from 10 +/- 0.7 to 4.7 +/- 0.3 kPa and increased during recovery to 6 +/- 0.7 kPa. cAMP increased 3-fold by 20 min of asphyxia, returning to baseline at 40 min of asphyxia. During recovery, cAMP increased 2-fold initially, followed by a decrease to 50% below baseline. cGMP increased after 20 min of asphyxia, with maximum levels observed at 40 min; reventilation resulted in a transient increase in cGMP. Pial arteriolar diameters increased at the onset of asphyxia, then decreased toward baseline; during recovery, a similar pattern occurred. Blood flow to the cerebrum (microspheres) decreased during asphyxia and remained very low during recovery. Pial arteriolar flow but not pial arteriolar diameters followed the changes in cortical cerebral blood flow (i.e. virtually no flow during recovery). During recovery, pial arteriolar reactivity to isoproterenol and histamine decreased significantly. We conclude that 60 min of asphyxic-hypotensive insult results in alterations of cerebral cAMP metabolism which may compromise cellular communications during recovery. Prolonged asphyxia induces "no-reflow" during recovery, even when partial pressures of arterial CO2 and O2 have returned to baseline values, and blood pressure is within the autoregulatory range.

Animals↗
PubMed2003

Asphyxia aggravates systemic hypotension but not pulmonary hypertension in piglets with meconium aspiration.

Meconium aspiration and birth asphyxia are both separately connected to significant pulmonary and systemic hemodynamic changes in newborns, but, although these insults frequently coexist, their combined effects on the neonatal circulation are still controversial. To determine the pulmonary and systemic circulatory changes induced by pulmonary meconium contamination with concurrent asphyxia, 41 anesthetized and ventilated newborn piglets (10-12 d) were studied for 6 h. Eleven piglets were instilled with a bolus of human meconium intratracheally, and 10 piglets had meconium instillation with immediate induction of an asphyxic insult. Eight piglets had only asphyxia and 12 ventilated piglets served as controls. Meconium instillation (with and without asphyxia) resulted in a sustained decrease in the oxygenation, which remained, however, on the control level in the asphyxic group. Although meconium insufflation (with and without asphyxia) increased pulmonary artery pressure and vascular resistance progressively during the study period, the meconium-induced hypertensive effect was actually diminished by additional asphyxia. Asphyxia alone did not have any effect on these pulmonary hemodynamic parameters. On the other hand, whereas systemic arterial pressure and vascular resistance remained on the control level after meconium instillation alone, asphyxia (with and without pulmonary meconium insult) resulted in a sustained fall in systemic pressure already by 4 h. Our data thus indicate that although the coexisting asphyxia seems to moderate the meconium aspiration-induced pulmonary hypertensive response, this additional asphyxic insult does not affect the associated hypoxemia, but rather significantly exacerbates systemic hypotension.

Acute Disease↗
PubMed2004

Declining diagnosis of birth asphyxia in California: 1991-2000.

OBJECTIVE: Birth asphyxia is recognized as an important cause of neonatal morbidity and mortality. Whether advances in perinatal care have altered the incidence of birth asphyxia is unknown. We determined the incidence of birth asphyxia diagnoses made over a 10-year period in California. METHODS: In a population-based retrospective cohort study of 5,364,663 live births, we determined the incidence and case fatality of birth asphyxia between 1991 and 2000. Using a statewide administrative hospital discharge database, we identified all newborn admissions that generated a diagnosis of birth asphyxia (International Classification of Diseases, Ninth Revision, Clinical Modification codes 768.5, 768.6, or 768.9) or a diagnosis that overlaps with birth asphyxia, such as congenital encephalopathy or fetal distress. We determined incidence and in-hospital case fatality rates adjusted for birth weight and demographic characteristics and stratified by associated perinatal complications. RESULTS: The 24 330 newborns who received a diagnosis of birth asphyxia yielded a population incidence of 4.5 per 1000 live births. Black ethnicity (relative risk [RR]: 1.3; 95% confidence interval [CI]: 1.2-1.3), male gender (RR: 1.2; 95% CI: 1.1-1.2), and low socioeconomic status (RR: 1.2; 95% CI: 1.1-1.2) all were associated with increased risk. The diagnosis of birth asphyxia decreased by 91% from 14.8 to 1.3 per 1000 live births during the study years. This decrease could not be explained by an increased diagnosis of overlapping conditions. Overall case fatality was 4%, and the majority of deaths in infants >2000 g occurred in the presence of congenital anomalies, cord abnormalities, or maternal hemorrhage. In newborns <2000 g, case fatality was highest in the presence of chorioamnionitis (48%). CONCLUSION: The diagnosis of birth asphyxia has decreased dramatically in recent years. The factors that are responsible for this decline are unclear and deserve additional investigation.

Asphyxia Neonatorum↗
PubMed2000

Perinatal asphyxia: multivariate analysis of risk factors.

UNLABELLED: Perinatal asphyxia contributes greatly to neonatal mortality and morbidity. In developing countries, the need for risk assessment in perinatal asphyxia is obvious because of the high birth rate and limited perinatal resources. OBJECTIVE: To determine the incidence and risk factors of perinatal asphyxia in infants who were delivered from mothers with high-risk conditions. STUDY DESIGN: A prospective study over a 5-year period from 1993 to 1997 was performed at a tertiary level, referral hospital. PATIENTS AND METHOD: Nine hundred and sixty-one infants who were delivered from 878 high-risk mothers were recruited. All of the risk factors that might have contributed to asphyxia were identified and recorded. Univariate and stepwise multiple logistic regression analysis was performed to identify significant factors that might have contributed to asphyxia, the odds ratios and 95 per cent confidence interval were computed. RESULTS: Abnormal fetal heart rate pattern, thick meconium stained amniotic fluid, and premature delivery, were three common risk factors for asphyxia. The mean gestational age was 37.6 +/- 3.5 weeks, 10.5 per cent (101/961) were infants less than 33 weeks. The incidence of asphyxia was 9.7 per cent and was highest (26.7%) in infants less than 1000 g. By univariate analysis, significant relationships between perinatal factors and asphyxia were found among birth weight, gestational age, premature and breech delivery but stepwise multiple logistic regression analysis revealed that only birth weight was significantly associated with perinatal asphyxia. CONCLUSION: In countries where resources are limited, a neonatal resuscitation team should be available for very low birth weight infants, premature and breech delivery.

Adult↗
PubMed1997

[Perinatal differences in relation to the severity of perinatal asphyxia].

OBJECTIVE: Despite the widespread use of the term perinatal asphyxia, there is little uniformity in the clinical definition of asphyxia, which makes comparison of incidence, treatment and outcome very difficult. The aim of this study was to know the perinatal differences of perinatal asphyxia in relation to its severity (severe and non-severe). PATIENTS AND METHODS: A prospective epidemiological study of perinatal asphyxia in fullterm infants born in our hospital between November 1991 and February 1995 was carried out. Perinatal asphyxia was graded as non-severe (1 minute Apgar score < or = 6 and/or umbilical artery pH < 7.20, with abnormal fetal heart rate patterns and/or meconium-stained amniotic fluid and the need for immediate neonatal resuscitation) and severe (1 minute Apgar score < or = 3 and umbilical artery pH < 7.10). The perinatal variables were graded as prenatal (gestational and obstetric), neonatal (resuscitation, general data of the newborn and organic manifestations of asphyxia) and postneonatal (neurologic sequelae at follow-up). RESULTS: During the study period there were 3.343 fullterm live births. Perinatal asphyxia developed in 156 cases (31 severe and 125 non-severe), with an incidence of 4.66 cases per 100 fullterm newborns. Neurologic manifestations (hypoxic-ischemic encephalopathy) during the neonatal period were present in 25.6% and extraneurological manifestations (hypoxic-ischemic disease) in 41.7% of the cases. The incidence of neurologic sequelae, in 115 asphyxiated full-term infants followed for at least 12 months, was 16.5% (19 cases). The main differences between severe and non-severe perinatal asphyxia were: chronic maternal diseases, distocic deliveries, thick meconium-stained amniotic fluid, all of the variables of neonatal resuscitation (Apgar score, umbilical artery pH, etc.), neurological and extraneurological (mainly pulmonary, digestive and cardiologic) manifestations during the neonatal period and neurological sequelae at follow-up. CONCLUSIONS: The main perinatal differences in relation to the severity of perinatal asphyxia were important in clinical management of asphyxiated newborns (neonatal resuscitation and systemic manifestations) and in their follow-up (early detection of neurologic sequelae).

Asphyxia Neonatorum↗
PubMed2004

Reflections on the occurrence and significance of antepartum fetal asphyxia.

This chapter documents the growing evidence of the occurrence and significance of antepartum fetal asphyxia. Perinatal mortality studies demonstrate that the majority of fetal deaths, including those due to asphyxia, occur in the antepartum period. Epidemiological studies of cerebral palsy conclude that a minority of cases of cerebral palsy are due to intrapartum fetal asphyxia and implicate antenatal events, including asphyxia. Cordocentesis studies have confirmed that antepartum fetal asphyxia occurs in the growth-restricted fetus and might contribute to the increase of stillbirths and cerebral palsy in these children. Blood gas and acid-base studies in the immature fetus have demonstrated the increased prevalence of fetal asphyxia, and particularly of moderate or severe asphyxia, of which the majority might occur in the antepartum period. The ultimate determination of the prevalence and significance of antepartum fetal asphyxia requires the development of a non-invasive specific measure of fetal asphyxia.

Cerebral Palsy↗
PubMed1997

Perinatal asphyxia induces long-term changes in dopamine D1, D2, and D3 receptor binding in the rat brain.

We have investigated the long-term effects of 15-16 min or 19-20 min of perinatal asphyxia on D1, D2, and D3 receptors (analyzed by quantitative autoradiography) in the mesotelencephalic dopamine systems of the 4-week-old rat. Perinatal asphyxia reduced D1 antagonist binding ([3H]SCH 23390 in the presence of ketanserine) in the accumbens nucleus, the olfactory tubercle, and the substantia nigra and increased D1 agonist binding ([3H]dopamine in the presence of spiperone) in the accumbens nucleus and the olfactory tubercle. No changes in D2 antagonist binding ([123]iodosulpride) were found, whereas D2 agonist binding ([3H]N-propylnorapomorphine, [3H]NPA) was reduced in the posterior part of the caudate-putamen, and following 19-20 min of asphyxia it was also reduced in the accumbens nucleus. D3 agonist binding (R/S-(+/-)-2-(N,N-di[2,3(n)-3H] propylamino)-7-hydroxy-1,2,3,4-tetrahydronaphthalene, [3H]7-OH-DPAT) was increased in the anterior part of the caudate-putamen following 15-16 min but not 19-20 min of asphyxia. The results indicate that perinatal asphyxia reduced the number of D1 receptors and increased D1 agonist affinity in the accumbens nucleus and the olfactory tubercle and reduced the number of D1 receptors in the substantia nigra. The number of D2 receptors was unchanged by asphyxia, whereas the D2 agonist affinity was reduced in the caudate-putamen and in the accumbens nucleus. D3 agonist binding was increased in the caudate-putamen selectively following 15-16 min of asphyxia. In conclusion, asphyxia during birth induces long-term changes in the binding characteristics of dopamine receptors in the mesotelencephalic dopamine systems, which may contribute to previously reported behavioral changes.

Animals↗
PubMed1995

Neonatal urinary uric acid/creatinine [correction of ceratinine] ratio as an additional marker of perinatal asphyxia.

UNLABELLED: The diagnosis and evaluation of perinatal asphyxia can be problematic and objective means of assessing its severity are lacking. To study the validity of urinary uric acid as a marker of the degree of perinatal asphyxia, the ratio of urinary uric acid to creatinine (UA/Cr) in urine specimens obtained after birth was measured in two groups of infants. Eighteen term infants with Apgar scores < or = 5 at 5 min and/or an umbilical cord blood pH < or = 7.2, and a base deficit > or = 12 meq/l were compared to 50 healthy controls. The severity of the perinatal asphyxia was determined by using an ASPHYXIA SCORE. The UA/Cr was higher in the asphyxiated group when compared to controls. (2.06 +/- 1.12, vs. 0.64 +/- 0.48; P < 0.001). Within the perinatal asphyxia group, a significant correlation was found between the UA/Cr ratio and the asphyxia score. (r = 0.86, P < 0.01). CONCLUSION: Infants with perinatal asphyxia have a significantly higher urinary UA/Cr ratio. This may be used as an indicator of the severity of perinatal asphyxia.

Asphyxia Neonatorum↗
PubMed2000

Effect of prolonged asphyxia on skin blood flow in fetal lambs.

OBJECTIVE: To determine the effect of a prolonged period of asphyxia on skin blood flow, a potential indicator of fetal cardiovascular responses to asphyxia, in the chronically catheterized fetal lamb. METHODS: Eight chronically instrumented pregnant ewes were studied at 118 +/- 1 days' gestation. After a control period, fetal acid-base status was assessed and regional blood flows were determined with dye-labeled microspheres. Fetal asphyxia was then induced by partial umbilical cord occlusion, decreasing fetal arterial oxygen pressure to 15 torr while maintaining pH above 7.28. Fetal cardiovascular status was monitored continuously. Fetal acid base status was evaluated every 10-15 minutes during cord occlusion. Regional blood flow determinations were repeated after 90 minutes of stable asphyxia. Results are expressed as the mean +/- standard error. Student t test for paired data was used to compare hemodynamic, acid-base, and regional blood flow determinations before cord occlusion and after 90 minutes of asphyxia. RESULTS: There was a significant increase in blood flow to the fetal scalp from a control value of 52 +/- 8 mL per minutes per 100 g to 175 +/- 30 mL per minute per 100 g at 90 minutes of asphyxia (P =.01). Similarly, there was an increase in blood flow to the skin overlying the fetal hindquarter from 39 +/- 12 mL per minute per 100 g during control to 153 +/- 47 mL per minute per 100 g at asphyxia (P =.038). CONCLUSION: In the chronically instrumented fetal lamb, a 90-minute period of asphyxia produced by partial cord occlusion resulted in a significant increase in blood flow to the fetal skin.

Animals↗
PubMed2003

Impact of perinatal asphyxia on the GABAergic and locomotor system.

Perinatal asphyxia can cause neuronal loss and depletion of neurotransmitters within the striatum. The striatum plays an important role in motor control, sensorimotor integration and learning. In the present study we investigated whether perinatal asphyxia leads to motor deficits related to striatal damage, and in particular to the loss of GABAergic neurons. Perinatal asphyxia was induced in time-pregnant Wistar rats on the day of delivery by placing the uterus horns, containing the pups, in a 37 degrees C water bath for 20 min. Three motor performance tasks (open field, grip test and walking pattern) were performed at 3 and 6 weeks of age. Antibodies against calbindin and parvalbumin were used to stain GABAergic striatal projection neurons and interneurons, respectively. The motor tests revealed subtle effects of perinatal asphyxia, i.e. small decrease in motor activity. Analysis of the walking pattern revealed an increase in stride width at 6 weeks of age after perinatal asphyxia. Furthermore, a substantial loss of calbindin-immunoreactive (-22%) and parvalbumin-immunoreactive (-43%) cells was found in the striatum following perinatal asphyxia at two months of age. GABA(A) receptor autoradiography revealed no changes in GABA binding activity within the striatum, globus pallidus or substantia nigra. We conclude that perinatal asphyxia resulted in a loss of GABAergic projection neurons and interneurons in the striatum without alteration of GABA(A) receptor affinity. Despite a considerable loss of striatal neurons, only minor deficits in motor performance were found after perinatal asphyxia.

Animals↗
PubMed2005

Management of birth asphyxia in home deliveries in rural Gadchiroli: the effect of two types of birth attendants and of resuscitating with mouth-to-mouth, tube-mask or bag-mask.

OBJECTIVES: To evaluate the effect of home-based neonatal care on birth asphyxia and to compare the effectiveness of two types of workers and three methods of resuscitation in home delivery. STUDY DESIGN: In a field trial of home-based neonatal care in rural Gadchiroli, India, birth asphyxia in home deliveries was managed differently during different phases. Trained traditional birth attendants (TBA) used mouth-to-mouth resuscitation in the baseline years (1993 to 1995). Additional village health workers (VHWs) only observed in 1995 to 1996. In the intervention years (1996 to 2003), they used tube-mask (1996 to 1999) and bag-mask (1999 to 2003). The incidence, case fatality (CF) and asphyxia-specific mortality rate (ASMR) during different phases were compared. RESULTS: During the intervention years, 5033 home deliveries occurred. VHWs were present during 84% home deliveries. The incidence of mild birth asphyxia decreased by 60%, from 14% in the observation year (1995 to 1996) to 6% in the intervention years (p<0.0001). The incidence of severe asphyxia did not change significantly, but the CF in neonates with severe asphyxia decreased by 47.5%, from 39 to 20% (p<0.07) and ASMR by 65%, from 11 to 4% (p<0.02). Mouth-to-mouth resuscitation reduced the ASMR by 12%, tube-mask further reduced the CF by 27% and the ASMR by 67%. The bag-mask showed an additional decrease in CF of 39% and in the fresh stillbirth rate of 33% in comparison to tube-mask (not significant). The cost of bag and mask was US dollars 13 per averted death. Oxytocic injection administered by unqualified doctors showed an odds ratio of three for the occurrence of severe asphyxia or fresh stillbirth. CONCLUSIONS: Home-based interventions delivered by a team of TBA and a semiskilled VHW reduced the asphyxia-related neonatal mortality by 65% compared to only TBA. The bag-mask appears to be superior to tube-mask or mouth-to-mouth resuscitation, with an estimated equipment cost of US dollars 13 per death averted.

Asphyxia Neonatorum↗
PubMed1998

Low-dose flunarizine does not affect short-term fetal circulatory responses to acute asphyxia in sheep near term.

Asphyxia is one of the major causes of perinatal brain damage and neuronal cell loss, which may result in psychomotor deficits during later development. It has been shown previously that the immature brain can be protected from ischemic injury by flunarizine, a class IV calcium antagonist. However, cardiovascular side-effects of flunarizine, when applied at the dosages used in those studies, have been reported. Recently, the present authors were able to demonstrate that even by injecting flunarizine at a far lower dosage (1 mg kg-1 estimated bodyweight) neuronal cell damage, caused by occlusion of both carotid arteries for 30 min, can be reduced in fetal sheep near term. The aim of the present study was, therefore, to examine whether low-dose flunarizine affects fetal cardiovascular responses to acute asphyxia in sheep near term. Ten fetal sheep were chronically instrumented at a mean gestational age of 132 +/- 1 days (term is at 147 days). Fetuses from the study group received a bolus injection of flunarizine (1 mg kg-1 estimated fetal weight) 60 min before asphyxia, whereas the solvent was administered to the fetuses from the control group. Organ blood flows, physiological variables and plasma concentrations of catecholamines were measured before, during and after a single occlusion of uterine blood flow for 2 min (i.e. at 0, 1, 2, 3, 4, and 30 min). Before asphyxia, the distribution of combined ventricular output and physiological variables, as well as concentrations of catecholamines, in fetuses from the control group were in the normal range for chronically prepared fetal sheep near term. During acute asphyxia there was a redistribution of cardiac output towards the central organs accompanied by a pronounced bradycardia and a rapid increase in arterial blood pressure. After asphyxia circulatory centralization did not resolve quite as rapidly as it developed, but was almost completely recovered at 30 min after the insult. There were nearly no differences in the time course of physiological and cardiovascular variables measured before, during and after acute intrauterine asphyxia between the control and study groups. From the present study it was concluded that low-dose flunarizine does not affect short-term fetal circulatory responses to acute asphyxia in sheep near term.

Adrenal Glands↗
PubMed1995

Assessing the contribution of birth asphyxia to cerebral palsy in term singletons.

In a geographically-based study, we investigated the risk of cerebral palsy following intrapartum asphyxia at term, and the contribution of intrapartum asphyxia at term to the overall rate of cerebral palsy. We used stringent criteria for identifying intrapartum asphyxia, while recognising that the initial hypoxial insult might have occurred in the antenatal period. In the first part of the investigation, a cohort of 160 term, singleton infants, with a low (< or = 3) 1-minute Apgar score, was followed to the age of 5 years. Six infants in the cohort had presumed intrapartum asphyxia, of whom two died in the neonatal period, three had spastic quadriparesis, profound developmental delay and visual impairment, and one was unimpaired. The frequency of cerebral palsy associated with birth asphyxia was estimated as one in 3700 full-term livebirths. To assess the impact of birth asphyxia on the overall rate of cerebral palsy, all cases of cerebral palsy born in the study period were identified. Of the 30 cases, the three identified in the follow-up study were the only ones whose impairment could be attributed to birth asphyxia in a full-term birth. Birth asphyxia at term therefore was associated with 10% [95% confidence interval (CI) 2.1, 26.5] of all cases of cerebral palsy and with 20% (95% CI 4.3, 48.1) of the 15 cases of cerebral palsy in children born at term.

Apgar Score↗