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PubMed2000

Long term neurological and behavioral effects of graded perinatal asphyxia in the rat.

Perinatal hypoxic-ischemic states can cause irreversible damage to the brain, ranging from minimal brain dysfunction to death. Only few studies have been reported describing neurological, cognitive and behavioral deficits following perinatal asphyxia. We therefore decided to study long term effects of perinatal asphyxia in a well-documented animal model resembling the clinical situation. Caeserean section in rats was performed and the pups, still in the uterus horns, were placed into a water bath at 37 degrees C for periods of 5-20 min; pups were then given to surrogate mothers and examined at three month of age. Examinations consisted of a battery of motor and reflex tests, Morris water maze, multiple T-maze, elevated plus maze and open field studies. No abnormalities were found in rats even with long periods of perinatal asphyxia by neurological examination, in the open field and in mazes. Interestingly, in the elevated plus maze rats with long lasting exposure to hypoxia (15 and 20 min of asphyxia) showed reduced anxiety-related behavior. This finding may be relevant for the explanation of anxiety related disorders in adulthood with a tentative history in the perinatal period.

Animals↗
PubMed2002

Neonatal organ system injury in acute birth asphyxia sufficient to result in neonatal encephalopathy.

OBJECTIVE: To identify the proportion of major organ system injury in cases of acute intrapartum asphyxia that result in neonatal encephalopathy. METHODS: A prospectively maintained database was cross-referenced using medical record coding to identify diagnoses of acute intrapartum asphyxia, acute birth asphyxia, or neonatal encephalopathy over a 6-year period. An acute intrapartum asphyxial antecedent was validated with emphasis on excluding long-standing or chronic conditions where injury likely occurred before presentation. Injury pattern was evaluated using routinely available laboratory and imaging tests. RESULTS: Forty-six cases of acute peripartum asphyxia sufficient to result in the diagnosis of neonatal encephalopathy were identified. Clinical central nervous system injury resulting in encephalopathy was present in 100% of cases as it was an entry criteria; of these, 49% had electroencephalogram and 40% had imaging studies diagnostic of acute injury. Liver injury based on elevated aspartate transaminase or alanine transaminase levels occurred in 80%. Heart injury, as defined by pressor or volume support beyond 2 hours of life or elevated cardiac enzymes, occurred in 78%. Renal injury, defined by an elevation of serum creatinine to greater than 1.0 mg/dL, persistent hematuria, persistent proteinuria, or clinical oliguria, occurred in 72%. An elevation in nucleated red blood cell counts exceeding 26 per 100 white blood cells occurred in 41%. CONCLUSION: Using common diagnostic tests as markers of acute asphyxial injury, we noted that multiple organs suffer damage during an acute intrapartum asphyxial event sufficient to result in a neonatal encephalopathy.

Adult↗
PubMed2003

Neuroprotection by the cannabinoid agonist WIN-55212 in an in vivo newborn rat model of acute severe asphyxia.

This study was designed to evaluate the neuroprotective effect of the cannabinoid agonist WIN-55212 after inducing acute severe asphyxia in newborn rats. The left common carotid artery was ligated in anaesthetised 7-day-old Wistar rats, which were then asphyxiated by inhaling 100% nitrogen for 10 min. Pups recovering from asphyxia were s.c. administered vehicle (n=23), WIN-55212 (0.1 mg/kg, n=18), or WIN-55212 plus the CB1 receptor antagonist SR141716 (3 mg/kg, n=10). Pups undergoing a sham operation served as controls (n=12). Coronal sections of the brain were obtained on the 14th day after surgery and observed under light microscope after Nissl or Fluoro-Jade B (FJB) staining, to respectively quantify surviving or degenerating neurones in the CA1 area of the hippocampus and parietal cortex. Acute asphyxia led to early neurone loss amounting to 19% in the hippocampus and 29% in the cortex (both ANOVA P<0.05 vs. control). Delayed neurone loss occurred in the proportions 13% in the hippocampus and 20% in the cortex (both ANOVA P<0.05 vs. control). Neuronal loss was fully prevented by WIN-55212 administration. Co-administration of SR141716 failed to modify the protective effect of WIN-55212 on early neuronal death, but abolished the WIN-55212-induced prevention of delayed neuronal death. We conclude that when administered after acute severe asphyxia in newborn rats, WIN-55212 shows a neuroprotective effect, reducing both early and delayed neurone loss. This effect is achieved through two parallel CB1-dependent and -independent mechanisms.

Animals↗
PubMed1998

Interaction of methylprednisolone and transient asphyxia on the inner ear of the adrenalectomized rat.

Methylprednisolone has been shown clinically to have beneficial effects on certain types of hearing loss. In the current study, compound action potential (CAP) thresholds, endocochlear potentials (EPs), and potassium concentration (CK+) values in the endolymph were determined under conditions of transient asphyxia (45 seconds) and methylprednisolone treatment (24 hours) in bilateral adrenalectomized rats. Treatment with methylprednisolone significantly reduced the effect of transient asphyxia on CAP thresholds as compared with nontreated animals. Methylprednisolone did not alter the dramatic short-term reduction in the EPs produced by anoxia. Potassium concentrations in treated adrenalectomized rats were significantly lower before transient asphyxia than in nontreated adrenalectomized rats. In the nontreated rats, transient asphyxia induced a reduction in CK+ levels that was not seen in the methylprednisolone-treated animals. The data support the clinical application of methylprednisolone for certain forms of hearing loss and for potassium imbalance in the endolymph.

Adrenalectomy↗
PubMed1999

Dynamics of fetal circulatory responses to hypoxia and asphyxia.

This review will focus on the dynamic changes of the fetal circulation, the distribution of organ blood flow during normoxemia, and that during hypoxia and asphyxia caused by various experimental perturbations. Furthermore, the relation between oxygen delivery and tissue metabolism during oxygen lack as well as evidence to support a new concept will be presented along with the principal cardiovascular mechanisms involved. Finally, blood flow and oxygen delivery to the principal fetal organ will be examined and discussed in relation to organ function. The fetal circulatory response to hypoxaemia and asphyxia is a rapid centralization of blood flow in favour of the brain, heart, and adrenals and at the expense of almost all peripheral organs, particularly of the lungs, carcass, skin and scalp. This response is qualitatively similar but quantitatively different under various experimental conditions. However, at the nadir of severe acute asphyxia the circulatory centralization cannot be maintained. Then there is circulatory de-centralization, and the fetus will experience severe brain damage if not expire unless immediate resuscitation occurs. Future work in this field will have to concentrate on the important questions, what factors determine this collapse of circulatory compensating mechanisms in the fetus, how does it relate to neuronal damage, and how can the fetal brain be pharmacologically protected against the adverse effects of asphyxia?

Asphyxia Neonatorum↗
PubMed2003

Perinatal asphyxia impairs connectivity and dopamine neurite branching in organotypic triple culture from rat substantia nigra, neostriatum and neocortex.

The effect of perinatal asphyxia on brain development was studied with organotypic cultures from substantia nigra, neostriatum and neocortex. Asphyxia was induced by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 20 min. Following asphyxia, the pups were nursed by a surrogate dam and sacrificed after 3 days to prepare organotypic cultures. Non-asphyxiated caesarean-delivered pups were used as controls. Morphological features were recorded during in vitro development. At day in vitro (DIV) 24, the cultures were treated for histochemistry using fast red for cell nucleus labelling and antibodies against tyrosine hydroxylase for dopaminergic neurons. Compared to controls, cultures from asphyxiated pups revealed a diminished integration quantified during 21 DIV. After immunocytochemistry and camera lucida reconstruction, tyrosine hydroxylase-positive neurons showed a decreased number of neurites from secondary and higher level branching, demonstrating a vulnerability of the dopaminergic systems after perinatal asphyxia.

Animals↗
PubMed1982

The effect of artery ligation and asphyxia on auditory evoked brain stem response.

Auditory evoked brain stem response (ABR) was recorded in two groups of cats during artery ligation. Group A underwent bilateral ligation of the vertebral artery (V.A.) for 180 min after which bilateral ligation of the carotid artery (C.A.) was done. In group B animals, initially V.A. was bilaterally ligated and right C.A. was also ligated, then after the same period, left C.A. was additionally ligated. ABR changes were also observed under asphyxia induced by turning off the respirator. Ligation of V.A. bilaterally resulted in a trend toward prolongation of the ABR latencies (group A). Ligation of V.A. bilaterally and right C.A. resulted not only in a trend toward prolongation of the latencies, but also in an increase in the amplitude in wave III and V (group B). Asphyxia caused more rapid and remarkable changes in ABR than artery ligation. After the onset of asphyxia, temporary increase in the amplitude was observed before the waves deteriorated. ABR is affected by changes of the blood flow and asphixic condition. ABR changes possibly depend on the development of the collateral vessels, vasodilation effect, or increase in blood pressure after artery obstruction or sustained asphyxia.

Animals↗
PubMed1998

Maturation of peripheral and brainstem auditory function in the first year following perinatal asphyxia: a longitudinal study.

Maturation of peripheral hearing and auditory brainstem following perinatal asphyxia was investigated by longitudinal recording of brainstem auditory evoked potentials (BAEP) during the first year of life in affected infants. The general maturational course of the BAEP following asphyxia was similar to that in a control group of infants with normal births, although there were some abnormalities in the BAEP Response threshold elevation seen in a few asphyxiated infants improved significantly during the first 3 months. The interpeak intervals in the asphyxiated infants did not differ significantly from that of the control-group infants except in the first month, when the I-V and III-V intervals were significantly prolonged in the severe asphyxia group. In contrast, wave V amplitude and V/I ratio were always smaller when compared to that of the control-group infants. Amplitude reduction of wave V was more sustained than the prolonged I-V interval. Persistent hearing loss and brainstem auditory impairment were seen in 6.8% and 14.6% of the asphyxiated infants, respectively. These findings suggest that asphyxia does not interfere significantly with the maturation of the auditory system in most asphyxiated infants and that sustained peripheral hearing loss and brainstem impairment occur only in a small proportion of affected infants.

Age Factors↗
PubMed1998

Cooling and asphyxia differentially affect augmented noradrenaline turnover in the brain of the externalized rat foetus.

The object was to investigate the effect of various perinatal conditions particularly cooling and asphyxia on the noradrenaline (NA) turnover in the foetal rat brain. The ratios between the noradrenergic metabolite 3-methoxy-4-hydroxy phenyl-ethylene glycol-sulphate (MHPG) and noradrenaline were determined as indexes of NA-turnover in the cortex and the pons-medulla of the foetal rat brain using high pressure liquid chromatography (HPLC). Rat foetuses were externalized by caesarean section performed on a spinally anaesthesized highly pregnant rat mother. One uterine horn was used as control while the other was exposed to externalization, simulated uterine contractions, cooling or asphyxia. Externalization per se and simulated uterine contractions did not cause any significant change in the NA-turnover. Cooling at 25 degrees C for 20 min caused a significant increase in NA-turnover in the cortex while a significant decrease was observed after 10 min of asphyxia in both the cortex and the pons-medulla and after 15 min in the cortex. We conclude that externalization and simulated uterine contractions per se do not seem to affect the augmented NA-turnover at birth. Cooling caused an increase suggesting a potentiating role on NA-turnover in conjunction with the externalization. On the other hand NA-turnover was depressed by asphyxia, suggesting that the level of oxygen is important for NA neuron activity.

Animals↗
PubMed2003

Umbilical cord interleukin-6 levels are elevated in term neonates with perinatal asphyxia.

BACKGROUND: A correlation between elevation of pro-inflammatory cytokines and white matter injury or abnormal neurologic outcome has been established in the preterm infant. In the full-term neonate, few studies exist linking elevation of cytokines with encephalopathy and poor neurodevelopmental outcome. Our aims were to investigate if serum interleukin-6 concentrations in delivering mothers and their offspring at birth are associated with perinatal asphyxia, and to examine the relation of interleukin-6 levels to the severity of hypoxic-ischemic encephalopathy and to the neurological outcome. DESIGN AND METHODS: Serum interleukin-6 levels were measured at birth, 24 and 48 h of life in 50 consecutive term uninfected newborns with perinatal asphyxia and 113 randomly selected healthy term newborns, and at delivery in their mothers. RESULTS: The median cord interleukin-6 concentrations in the infants who developed hypoxic-ischemic encephalopathy was 376-fold as high as the values in the normal infants (P < 0.0001) and 5.5-fold as high as those in the infants with asphyxia who did not develop hypoxic-ischemic encephalopathy (P < 0.05). There was also a significant relationship between interleukin-6 and the degree of hypoxic-ischemic encephalopathy, and between interleukin-6 and neurodevelopmental outcome at 2 years of age. Regardless of outcome, in the asphyxiated infants the interleukin-6 values were significantly lower at both 24 and 48 h of life than at birth, with a significant decline from 24 to 48 h of life. Among mothers of the asphyxiated neonates, there were no significant differences in interleukin-6 concentrations between those delivering neonates with and without hypoxic-ischemic encephalopathy. CONCLUSIONS: Measurement of IL-6 concentrations in the umbilical cord of neonates with perinatal asphyxia may be useful to identify early, and in a relatively simple way, those who are most likely to have subsequent brain injury and adverse outcome.

Adult↗
PubMed2000

Stillbirths and neonatal encephalopathy in Kathmandu, Nepal: an estimate of the contribution of birth asphyxia to perinatal mortality in a low-income urban population.

We describe a prospective cross-sectional survey over a 12-month period in the principal maternity hospital of Kathmandu, Nepal, where over 50% of the local population deliver. The study aim was to estimate the contribution of birth asphyxia to perinatal mortality in this setting. During 1995, there were 14,371 livebirths and 400 stillbirths, a total stillbirth rate of 27 per 1000 total births. The fresh term (2000 g or more) stillbirth rate was 8.5 per 1000 total births [95% CI 7.1, 10.1]. Ninety-two cases of neonatal encephalopathy (NE) affecting term infants were detected (excluding those due to congenital malformations, hypoglycaemia and early neonatal sepsis). The birth prevalence of NE was 6.4 per 1000 livebirths [95% CI 5.2, 7.8]. There was evidence of intrapartum compromise in 63 (68%) of the cases of NE and 65 (76%) of the stillbirths, but only in 12 (12%) of controls. The cause-specific early neonatal mortality rate for NE was 2.1 per 1000 livebirths [95% CI 1.4, 3.0]. Combining the NE deaths and fresh stillbirths gives an upper estimate for term birth asphyxia perinatal mortality rate of 10.8 per 1000 total births [95% CI 9.2, 12.6], 24% of all perinatal deaths before hospital discharge. This study suggests that birth asphyxia remains an important cause of perinatal mortality in developing countries. The paper discusses the pros and cons of different strategies to reduce birth asphyxia in low-income countries.

Asphyxia Neonatorum↗
PubMed1999

Effects of acute asphyxia at birth on subsequent heat production capacity in newborn pigs.

The effect of acute asphyxia at birth on subsequent ability to produce heat was investigated in 30 newborn pigs. A model of experimentally induced asphyxia consisting of the prevention of breathing within the first four minutes of life was used. Blood was sampled from an umbilical artery catheter within the first 75 minutes of life for blood gas, pH, glucose, lactate and catecholamine analysis. After the treatment and 24 hours later, heat production capacity, shivering intensity and rectal temperature were measured 10 degrees C below thermoneutrality. Effects on blood gas parameters were severe but transient whereas alterations in carbohydrate metabolism were maintained during the first 75 minutes (P < 0.05). Acute asphyxia at birth induced only minor alterations of thermoregulatory abilities during the first day of life: rectal temperature was lower one hour after birth (P < 0.05) and the postnatal increase in heat production capacity was less pronounced than in controls. It is suggested that the lower viability usually reported for piglets suffering from asphyxia during delivery is most likely to result from reduced vigour and colostrum intake, as well as altered carbohydrate metabolism early after birth.

Animals↗
PubMed1985

Asphyxia and hyaline membrane disease in neonatal monkeys.

An animal model for studying the relationship between perinatal asphyxia and hyaline membrane disease (HMD) is described. The HMD developed in these Macaca mulatta (rhesus) and M. arctoides (stump tail) monkeys was clinically, physiologically, and histologically similar to that seen in human infants. The monkeys were delivered by cesarean section at a gestational age of 85-91% of term when surfactant, though present, was less than mature levels. Asphyxia at birth proved to be an important factor in disease development. Five minutes of asphyxia immediately before the first breath greatly increased the incidence and severity of HMD when compared to nonasphyxiated controls of a similar gestational age. Amniotic fluid L/S ratios did not differ significantly in the asphyxiated and control groups but data based on static pressure-volume studies of the excised lungs indicated that the surfactant activity of the asphyxiated group was significantly less. Lung maturity with regard to surfactant production appears to be a critical factor. The data from these experiments, together with data cited in the literature, strongly suggest that the lung and its surfactant system is most vulnerable to hypoxia and/or acidosis during the early stages of surfactant production. The asphyxiated non-human primate model used here should prove valuable for studying the pathogenesis of HMD and especially for further clarifying the relationship between perinatal asphyxia and HMD.

Amniotic Fluid↗
PubMed1996

Neuropsychological consequences of very low birth weight and asphyxia at term: follow-up until school-age.

This prospective, longitudinal study examined neuropsychological consequences of different conditions associated with risks of perinatal asphyxia. Four groups of children, 5 to 9 years of age, were studied: (1) very low birth weight (VLBW) children born small for gestational age (SGA) (n = 34); (2) VLBW children born appropriate for gestational age (AGA) (n = 43); (3) children with signs of birth asphyxia at term (birth asphyxia) (n = 36), and (4) control children (n = 45). Moderately and severely disabled children were excluded. The WISC-R and the NEPSY, a new neuropsychological assessment consisting of attention, language, motor, sensory, visuospatial, and memory subtests, were administered. The VLBW-SGA group had the poorest test results. The VLBW-AGA group was somewhat less impaired, whereas the birth asphyxia group performed at the control group level. Impairment, when present, tended to be diffuse in all groups, affecting psychometric intelligence, naming, visuo-motor performance, tactile finger discrimination, attention, and phonological analysis.

Asphyxia Neonatorum↗
PubMed2006

Reventilation with room air or 100% oxygen after asphyxia differentially affects cerebral neuropathology in newborn pigs.

AIM: To test if reventilation with room air (RA) or 100% oxygen (O2) after asphyxia would differentially affect neuronal damage in different brain areas of newborn pigs. METHODS: Anaesthetized piglets were subjected to 10 min asphyxia (n=27) or served as time controls (n=7). Reventilation started with either RA or O2 for 1 h, and was continued with RA for an additional 1-3 h. Cortical or cerebellar blood flow was assessed with laser-Doppler flowmetry (LDF). Haematoxylin/eosin-stained sections from six brain regions were prepared for blinded neuropathological examination and scoring. RESULTS: Asphyxia resulted in significant neuronal damage compared to time controls in all areas examined except the pons. O2 ventilation elicited greater neuronal lesions in the hippocampus and the cerebellum but smaller damage in the basal ganglia compared to RA. The assessed physiological parameters including the LDF signals were similar in both ventilation groups, except for PaO2 in the first hour of reventilation (RA 75+/-5 mmHg, O2 348+/-57 mmHg; p<0.05). Interestingly, however, reactive hyperaemia was much higher in the O2-sensitive cerebellum as compared with the cortex (1101+/-227 vs 571+/-73; p<0.05, area under the curve). CONCLUSION: O2 toxicity after asphyxia was demonstrated in the piglet hippocampus and cerebellum but not in the cerebral cortex or basal ganglia. The observed regional differences may be associated with local haemodynamic factors.

Air↗
PubMed1992

Factors associated with clinically significant perinatal asphyxia in the Malaysian neonates: a case-control study.

A 2-month prospective study was carried out in a Kuala Lumpur maternity hospital to determine the antenatal and intrapartum factors associated with perinatal asphyxia in the Malaysian neonates. The incidence of perinatal asphyxia was 18.7 per 1000 livebirths. Of the 75 asphyxiated neonates born during this period, 70 (93.3 per cent) were of term or post-term gestation. The incidence of perinatal asphyxia was more common in the neonates with one of the following characteristics: low birth weight (< 2500 g), breech delivery, or delivery by instrumentation or lower segment Caesarean section (P < 0.001). Conditional logistic regression analysis of the asphyxiated and the control neonates in a nested case-control study (after controlling for sex, race, birth weight, modes of delivery, and maternal gravida) showed that there were two associated factors which were of statistical significance. These were: small-for-gestation neonates and the presence of intrapartum problems. Our study suggests that to reduce the incidence of perinatal asphyxia, the common causes of small-for-gestation neonates and the common types of intrapartum problems should be identified to enable appropriate preventive measures to be carried out.

Asphyxia Neonatorum↗
PubMed1995

Birth asphyxia in a rural community of north India.

A community-based inquiry was conducted in a rural area of north India to estimate extent of the problem of birth asphyxia. Births and neonatal deaths were recorded in 54 villages. Trained field workers contacted birth attendants/family members within 15 days after the birth, and recorded the symptoms and signs related to birth asphyxia on a pre-coded questionnaire. Detailed descriptive history of birth events in chronological order was recorded in cases suspected to be asphyxiated or stillborn. Two pediatricians reviewed the case histories independently to assign the diagnosis. Out of the 1977 recorded livebirths, field workers suspected 53 babies to be asphyxiated, 39 of these were diagnosed as asphyxiated, four as not asphyxiated by both the experts, and 10 were considered as asphyxiated by one of the experts. Prevalence of birth asphyxia was estimated to be at least 2 per cent (39/1977). Case fatality in these cases was 74 per cent. The verbal diagnosis method adopted in this study can be used to compare the prevalence of asphyxia in community studies.

Asphyxia Neonatorum↗
PubMed2000

Plastic bag asphyxia in southeast Scotland.

Death resulting from plastic bag asphyxia has been recognized for >40 years, but relatively little is known about either its epidemiology or its pathophysiology. Over 15 years (1984-1998), 30 deaths were attributed to plastic bag asphyxia among the 14,560 autopsies performed in the Forensic Medicine Unit in Edinburgh. These 30 deaths involved 20 male and 10 female subjects, with an age range of 13 to 81 years. Eleven had some alcohol measurable in the blood, with four having levels >80 mg/dl. Only one individual appeared to have ingested a drug overdose, but inhaled substances within the plastic bag may have contributed to death in five cases. The absence of childhood accidental deaths may reflect successful preventive measures. The 3 accidental deaths involved adults (including 2 who died of autoerotic asphyxia), and the remaining deaths were 27 suicides. Of those who committed suicide, most (59%) had chronic psychiatric illness rather than chronic debilitating or terminal physical illness. In contrast with reports from the United States, publicity associated with "self-deliverance" did not result in an increased number of deaths from plastic bag asphyxia (4 deaths in this series). Analysis of the circumstances of all the deaths revealed them to be difficult to predict and hence prevent.

Accidents↗