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PubMed1981

Fetal cardiovascular reactions during labour and asphyxia modified by adrenergic receptor agonists and antagonists.

In the human fetus the adrenergic system develops morphologically at an early stage. The development of adrenergic receptors occurs to a large extent before birth. The human fetus is capable of a large production of catecholamines, particularly during the last two months of fetal life. Normal labour and delivery elicits an increased release of catecholamines, a reaction that is markedly enhanced by asphyxia. beta-Receptor stimulants not only relax the uterine smooth muscle but also tend to modify the concentration of surfactant in lung fluid. beta-Receptor blocking agents, both non-selective and cardioselective, create a problem in clinical medicine since they provide an effective means of treating hypertension in pregnancy. Theoretical implications of such treatment present a risk to the fetus. Experimental evidence from the fetal sheep preparation indicate that beta-receptor blockade carriers an immediate risk to the severely asphyxiated fetus when the blockade is induced acutely. In this situation heart muscle contractility, heart rate and cardiac output fall abruptly while the capacity for anaerobic glycolysis is greatly diminished. Even though such acute animal experiments are far removed from clinical practice the results suggest that great caution should be exercised in the use of adrenergic blocking agents in obstetric practice.

Adrenergic beta-Agonists↗
PubMed1986

Granule cell deficit in the mouse cerebellum after total asphyxia.

The cerebellar granule cell continues to proliferate after birth in the mouse as well as in the human being. Total asphyxia in the neonatal period in 40 mice resulted in a 13% reduction in the granule cell number and a 7% reduction in the Purkinje cell number. Differential effects on granule cell and Purkinje cell populations were noted when particular cerebellar lobules were examined.

Animals↗
PubMed1987

Parasagittal infarction in neonatal asphyxia.

A patient is described who suffered a bilateral hemorrhagic infarction in the parasagittal cerebrum following neonatal asphyxia. This case confirms experimental results that show the parasagittal cerebrum is especially vulnerable to ischemic damage in newborns.

Asphyxia Neonatorum↗
PubMed1989

Hypoxic-ischemic spinal cord injury following perinatal asphyxia.

The role of spinal cord injury in the pathogenesis of abnormal motor signs (depressed tone and reflexes) following severe perinatal hypoxia-ischemia was prospectively evaluated by clinical, electrophysiological, and neuropathological examinations in 18 asphyxiated neonates. All infants had an abnormal mental status (lethargy or coma), and seizures were present in 12. Neuromuscular examinations revealed hypotonia or flaccidity and hyporeflexia or areflexia in all infants. Neuropathological examinations of the cerebrum and spinal cord were conducted in the 12 neonates who expired. Cerebral pathological findings included cortical neuronal necrosis in 10 of 12 and subcortical white matter injury in 5 of 12. All infants with coma or seizures displayed diffuse cortical injury, but no injury conformed to a parasagittal "watershed" distribution. Spinal cord gray matter displayed prominent ischemic necrosis in 5 patients who were typically flaccid and areflexic. Electromyographic examinations of all 6 survivors were abnormal, consistent with recent injury to the lower motor neuron above the level of the dorsal root ganglion. We conclude that ischemic injury to anterior horn cells within spinal cord gray matter is relatively common among hypotonic-hyporeflexic neonates following severe perinatal hypoxia-ischemia. Although the acute neurological syndrome of neonatal asphyxia is often overshadowed by prominent cerebral signs such as coma and seizures, the motor abnormalities may be partially attributed to concurrent spinal cord injury.

Asphyxia Neonatorum↗
PubMed1986

[The course of respiration in death caused by obstructive asphyxia].

Experiments were carried out on 30 dogs to investigate the course of respiration during obstructive asphyxia. They were asphyxiated by occlusion of the exposed trachea. Intrathoracic pressure, blood pressure in the femoral artery, electrocardiogram and electroencephalogram readings were registered. In most cases, the respiration course during the dyspnea stage by occlusion of the trachea generally had an inspiratory character. In a few animals, when the trachea was occluded in the expiratory phase, there were a few positive expiratory respirations with moderate inspiratory movement and thereafter the respirations were inspiratory during the dyspnea stage. The terminal respirations, which occurred 1-2 min before the circulatory breakdown, were generally inspiratory, but in a few dogs they were expiratory.

Airway Obstruction↗
PubMed1978

Association of neonatal respiratory distress with birth asphyxia and deficiency of red cell mass in premature infants.

Red cell mass (RCM) was estimated using 125I-labelled human serum albumin in 128 premature infants born after 26 to 36 weeks gestation. Infants of three different gestational periods (26--29, 30--32, and 33--36 weeks) with respiratory distress (RD) averaged lower one-minute Apgar scores and lower RCM than infants without RD (P less than 0.05). The incidence of RD was significantly (P less than 0.05) higher in infants with Apgar scores below 6 and in infants with RCM of less than 35 ml/kg than in the infants with greater values. The highest incidence of RD and the highest mortality rate were found in the infants with low Apgar scores and low RCM values. Prematures with similar Apgar scores showed a higher incidence of RD when RCM was low, and infants with similar RCM showed a higher incidence of RD when Apgar scores were low. Our results suggest that both birth asphyxia and deficiency of red cell mass interfere with postnatal cardio-respiratory adaptation. In high-risk premature infants, erythrocytes should be transfused when the venous haematocrit is below 0.459

Anemia↗
PubMed1984

Can perinatal asphyxia cause cerebral edema and affect cerebral blood flow velocity?

Cerebral blood flow velocity (C.B.F.V.) was estimated in 49 newborn babies by calculating the pulsatility-index (P.I.) of the anterior cerebral arteries (A.C.A.) using Doppler ultrasound. We studied the changes in P.I. of the A.C.A. in relation to the clinical condition in three full-term babies with evidence of cerebral edema (in one patient proved by autopsy) due to perinatal asphyxia. There was a relation between the level of consciousness and the P.I.; a low P.I. (a sign of arterial vasodilatation) occurred with a low level of consciousness, while higher P.I. values (reduced vasodilatation) were detected when improvement of consciousness occurred. The following explanation is given: cerebral edema causes an increase of intracranial pressure and venous obstruction. The cerebral perfusion decreases and cerebral function changes; stupor and coma occur. By vasodilatation the resistance of the cerebral arteries is lowered; the C.B.F.V. increases in an attempt to restore cerebral perfusion. The vasodilation is reflected in the low P.I. values, as we found in our three patients.

Adult↗
PubMed1993

Early pattern recognition in severe perinatal asphyxia: a prospective MRI study.

On the basis of MRI examinations in 88 neonates and infants with perinatal asphyxia, we defined 6 different patterns on T2-weighted images: pattern A--scattered hyperintensity of both hemispheres of the telencephalon with blurred border zones between cortex and white matter, indicating diffuse brain injury; pattern B--parasagittal hyperintensity extending into the corona radiata, corresponding to the watershed zones; pattern C--hyper- and hypointense lesions in thalamus and basal ganglia, which relate to haemorrhagic necrosis or iron deposition in these areas; pattern D--periventricular hyperintensity, mainly along the lateral ventricles, i.e. periventricular leukomalacia (PVL), originating from the matrix zone; pattern E--small multifocal lesions varying from hyper--to hypointense, interpreted as necrosis and haemorrhage; pattern F--periventricular centrifugal hypointense stripes in the centrum semiovale and deep white matter of the frontal and occipital lobes. Contrast was effectively inverted on T1-weighted images. Patterns A, B and C were found in 17%, 25% and 37% of patients, and patterns D, E and F in 19%, 17% and 35%, respectively. In 49 patients a combination of patterns was observed, but 30% of the initial images were normal. At follow-up, persistent abnormalities were seen in all children with patterns A and D, but in only 52% of those with pattern C. Myelination was retarded most often in patients with diffuse brain injury and PVL (patterns A and D).

Asphyxia Neonatorum↗
PubMed1994

Pulmonary giant cells and traumatic asphyxia.

A morphometrical analysis was performed to elucidate the significance of pulmonary polynuclear giant cells as a histological sign of asphyxiation. A total of 13 cases of homicidal strangulation of throttling, 8 cases of traumatic asphyxia due to chest compression and 10 control cases (cause of death: severe head injury, no signs of aspiration or other relevant pulmonary alterations, smokers and non-smokers) were investigated. The number of alveolar macrophages containing 1 or 2 nuclei and of polynuclear giant cells per microscopic field (0.000025 cm2) was estimated and a statistical evaluation was carried out. A considerable individual variation was observed in all groups with a tendency to higher numbers of cells in cases of smokers or advanced individual age. However, no significant differences were detectable in the content of alveolar macrophages and in particular of polynuclear giant cells between the asphyxiated individuals and the controls. Since polynuclear giant cells occurred in similar amounts in healthy, functionally normal lungs of non-asphyxiated individuals, the detection of such cells cannot be regarded as a reliable indicator for asphyxiation.

Adolescent↗
PubMedDate not supplied

Hemodynamics and myocardial electrolyte (k+/na+) metabolism early in hemorrhagic shock during asphyxia.

In tests on guinea pig hearts in situ asphyxia tolerance was found to be increased early in hemorragic shock four times control value. These results are suggestive of an energy saving mechanism in shock whereby the heart is not damaged out metabolically relieved. Myocardial analyses showed that, owing to shock-related cardiac relief, under a simultaneous asphyctic stress the intracellular potassium stock decreases later and markedly less.

Animals↗
PubMed1990

Severe neonatal asphyxia due to X-linked centronuclear myopathy.

Severe neonatal centronuclear myopathy is inherited as an X-linked condition characterized by primary asphyxia, extreme muscular hypotonia and absent spontaneous movements. We report seven cases from three families to point out the importance of diagnosis with regard to prognosis, outcome and genetic counselling. In hypotonic diseases, analysis of cerebrospinal fluid, electromyography, nerve conduction velocity creatine kinase and a skin biopsy for fibroblast cultures for metabolic investigations are usually carried out. Needle muscle biopsy is an additional valuable investigation to establish diagnosis. In all our patients we found an increased number of centrally located nuclei with perinuclear halos confirming the diagnosis of centronuclear myopathy. The diagnosis of this disorder will become of greater importance as soon as carrier detection and prenatal diagnosis by DNA-technology are routinely available.

Asphyxia Neonatorum↗
PubMed1983

[Intrapartum death or infanticide? A contribution to intrapartum asphyxia].

On occasion of the autopsy of a 32-34-week-old fetus delivered with fetal membrane intact (caul/amnion birth), heavy hypoxic changes in the cardiac muscle, the liver and the kidney epithelia were found. On the other hand, there was no sign of aspiration although a sign of aspiration was to be expected, as the fetus was lying in the amniotic fluids. The systematic examination of 68 cases of intrapartal deaths of various causes demonstrated that intrapartal aspiration in the amniotic fluid only takes place, when the function of the umbilical cord is obstructed. If pressure is lacking, as for example, in amniotic (fluid) substances, or meconium, in the respiratory tract is either found not at all, or only in small quantities. For the purposes of forensic medicine, this means that death by intrapartal asphyxia can also be assumed when findings demonstrate simultaneously that aspiration is absent and hypoxic changes of the organs are present.

Adolescent↗
PubMed1980

[The diagnostic significance of coagulated heart blood in cases of death by acute asphyxia (author's transl)].

In cases of death by asphyxia, such as strangulation, hanging, drowning, lack of oxygen, compression of the chest, and carbon monoxide poisoning, the frequency of the liquid and coagulated state of blood in the heart was examined. Coagulated blood in the right heart can be found in cases of strangulation, hanging, and drowning, if simultaneously an elevated blood alcohol was present. The diagnostic significance of this result is discussed.

Alcoholic Intoxication↗
PubMedDate not supplied

Free oxygen radicals--predictors of neonatal outcome following perinatal asphyxia.

The study was undertaken to evaluate the role of free oxygen radicals in asphyxiated neonates. Thirty term neonates appropriate for gestational age and with severe birth asphyxia (Apgar score of 3 or less at 1 minute of life) formed the study subjects. The levels of superoxide dismutase (SOD), glutathione peroxidase (GPx), creatine phosphokinase (CPK) and lipid peroxidase (LPO) in the CSF of these neonates were estimated between 12 and 48 hrs of life. Enzyme estimation was performed by standard methods and the results were analysed statistically using Multivariate Logistic Regression analysis and non parametric tests namely Kruskal Wallis test and Wilcoxon's rank sum test. Out of the thirty babies, 14 were observed to be neurologically normal, 9 had significant morbidity and 7 died. The SOD levels ranged from 12.4 to 140 units/ml, GPx from 128 to 1933 nmol/min/dl, CPK from 2 to 2098 IU/dl and LPO from 5.4 to 30.8 umol/hr/dl. The SOD and GPx levels had an inverse relationship whereas rise in LPO and CPK levels were directly proportional to the extent of neurological damage and ultimate clinical outcome. CPK levels higher than 140 IU/ml were lethal and associated with 100% mortality whereas all normal neonates had CPK below 37 IU/ml. The levels of antioxidant enzymes can reliably and significantly predict mortality and morbidity whereas level of an enzyme cannot confidently confer normalcy. Hence antioxidant enzyme levels with a cut off value can be a useful marker and serve as a prognostic indicator in times to come.

Asphyxia Neonatorum↗
PubMed1997

Short-term changes in NADPH-diaphorase reactivity in rat brain following perinatal asphyxia. Neuroprotective effects of cold treatment.

Perinatal asphyxia (PA) produces changes in nitric oxide synthase (NOS) activity in neuronal and endothelial cells of the striatum and neocortex. The changes were examined using a histochemical NADPH-diaphorase (NADPH-d) staining method. Newborn rats were exposed to severe PA at 37 degrees C and other groups were subjected to severe PA under hypothermic condition (15 degrees C) for 20 or 100 min, respectively. Quantitative image analysis was performed on the striatum and neocortex in order to count cell number of reactive neurons and to compare the pattern of staining between the different groups of animals. Severe asphyctic pups showed an important neuronal loss in striatum and neocortex that was reduced by hypothermia. NADPH-d(+) neurons with reactive processes were found in the lateral zone of the striatum and neocortex in asphyctic pups. Controls and hypothermic striatum showed rounded cells without reactive process, while no cells were stained in cortex. There was also an increase in NADPH-d activity in endothelial cells in severe asphyctic pups in striatum and neocortex vs control and hypothermically treated animals. Our data evidenced that an inappropriate activation of NOS in neuronal and endothelial cells induced by PA is related to neuronal injury. Hypothermia inhibits neuronal injury and may be a valuable neuroprotective agent.

Animals↗
PubMedDate not supplied

Influence of maternal nutritional status on mode of delivery and asphyxia neonatorum.

To assess the influence of maternal malnutrition on the mode of delivery and asphyxia neonatorum, a cross sectional survey of 615 women in the age group of 20-28 yrs at the time of delivery was done. Women with chronic ailments and complicated pregnancies were excluded. The mothers were then classified into three groups based on Weight Height Product Index (WHPI) namely well nourished (WN), moderately malnourished (MMN) and severely malnourished (SMN). The proportion of asphyxiated babies among the three groups did not differ (P greater than 0.05). Abnormal deliveries like caesarean section were more common among SMN group compared to WN group ((P less than 0.01). No such difference was made out between MMN and WN groups (P greater than 0.05).

Asphyxia Neonatorum↗
PubMed2006

Magnesium therapy in birth asphyxia.

OBJECTIVE: Glutamate plays a critical role in the hypoxic ischaemic neuronal death. Two mechanisms of glutamate- induced neuronal death have been identified. One is rapid cell death that occurs in minutes and the second is delayed cell death that occurs over hours and is initiated principally by the activation of the N-methyl D-Aspactate (NMDA) receptor. Magnesium (Mg) is an NMDA receptor blocker. Systemic administration of Mg after a simulated hypoxic ischaemic insult has been shown to limit neuronal injury in several animal models. However, before embarking on to the use of Mg for neuronal protection in the human neonate it is important to study the safety and side effects of Mg administration. METHODS: Forty terms, appropriate for gestational age babies with severe birth asphyxia (1 min Apgar score < 3 and 5 min Apgar score < 6), were randomly assigned to either the study group or the control group. Infants in both groups were treated as per unit protocol except that babies in the study group received intravenous injection of magnesium sulphate 250 mg/kg within half an hour of birth and subsequently 125 mg/kg at 24 and 48 hours of life. RESULTS: The mean cord blood serum Mg levels were 0.78 (+/- 0.047) mmol/L in the control group and 0.779(+/-0.045) mmol/L in the study group. The serum Mg levels at 3, 6, 12, 24, 48 and 72 hours of life were 1.87(+/-0.6), 1.65(+/-0.059), 1.468 (+/-0.91), 1.881 (+/- 0.053), 1.916 (+/- 0.053) and 1.493 (+/- 0.084) mmol/L respectively in the study group. All these values were significantly higher than those obtained in the control group (p< 0.001). No significant alterations in heart rate, respiratory rate, oxygen saturation and mean arterial pressure were seen, following magnesium infusion with either 250 mg/kg or 125 mg/kg dose. The serum Mg levels in the study group ranged between 1.493 (+/- 0.084) and 1.916(+/-0.053) mmol/L, which are considered to be in the neuroprotective range. CONCLUSION: Injection MgSO4 administered in a dose of 250 mg/kg and 125 mg/kg as an intravenous infusion is safe and the Mg levels obtained are in the range considered to be neuroprotective.

Asphyxia Neonatorum↗
PubMed1999

Cholinergic, monoaminergic and glutamatergic changes following perinatal asphyxia in the rat.

Perinatal asphyxia (PA) is considered to lead to a variety of brain disorders including spasticity, epilepsy, mental retardation, and minimal brain disorder syndromes and may form the basis for psychiatric and neurodegenerative diseases later in life. We examined markers for neuronal transmission involved in the pathomechanisms of PA and candidates as mediators for long-term sequelae. We tested tyrosine hydroxylase (TH) and the vesicular monoamine transporter (VMAT) representing the monoaminergic system, the vesicular acetylcholine transporter (VAChT), and the excitatory amino acid carrier 1 (EAAC1), a neuronal subtype of the glutamate transporter, using immunohistochemistry on brain sections of rats subjected to graded PA. Three months following the asphyxiant insult immunoreactive (IR)-TH was decreased in striatum, hippocampus, thalamus, frontal cortex, and cerebellum; IR-VMAT was increased, and IR-VAChT was decreased in striatum. IR-EAAC1 glutamate transporter was increased in frontal cortex. The cholinergic, monoaminergic, and glutamatergic changes, still observed 3 months after the asphyxiant insult, may reflect their involvement in the pathomechanisms of PA and indicate mechanisms leading to long-term complications of PA. The variable consequences on the individual markers in several brain regions may be explained by specific susceptibility of cholinergic, monoaminergic, and glutamatergic neurons to the asphyxiant insult.

Age Factors↗