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At least 19 recordsLinked to original sources
PubMed1992

Studies on asphyxia: morphological research for the aid of diagnosis of asphyxia using light and electron microscopy and immunohistochemical methods.

The lattice-form structure and/or tubular myelin can be found in the debris-like structure which is the pinkish substance in the alveolar space in the Hematoxylin & Eosin stained sections. These findings were obtained by using rats in the air containing oxygen of 5% or mixing and/or contaminating each of methane, carbon dioxide, carbon monoxide and freon gases. The immunohistochemical detection using the monoclonal mouse antibody against human pulmonary surfactant (PS) apoprotein is of highly useful. The positive reaction products observed in the alveolar space indicate the localization of the tubular myelin. The data suggest that the PS appears when the inhaled air contains oxygen in low concentration. The immunohistochemical method using the antibody against human PS apoprotein is worth applying for the diagnosis of oxygen deficiency including the respiratory distress syndrome (RDS) of the new born. We conclude that the appearance of the positive reaction products suggests that, at least, the air did not come in contact with the surface of alveoli, which leads us to the diagnosis of death was from oxygen deficiency, even if we are at the stage when the mode of death is undetermined.

Animals↗
PubMed1992

The clinical diagnosis of asphyxia responsible for brain damage in the human fetus.

OBJECTIVE: Our objective was to review the clinical findings in infants who died in the perinatal period with brain damage attributable to asphyxia. STUDY DESIGN: The neuropathologic findings in 208 perinatal deaths have been reviewed. Thirty cases (22 fetal, eight newborn) had evidence of white matter or neuronal necrosis due to asphyxia. The clinical course of the pregnancy in 22 cases with brain damage attributable to fetal asphyxia were examined. RESULTS: The diagnosis of asphyxia was confounded by several factors: (1) asphyxia may occur at any time in the last half of pregnancy, (2) 50% of the antepartum asphyxia occurred when the pregnancy had no risk factors, (3) periodic fetal assessment in the complicated preterm pregnancies failed to identify the asphyxial episodes in the remaining cases of antepartum asphyxia, and (4) indicators of fetal asphyxia in the cases of intrapartum fetal asphyxia were obtained after the central nervous system injury had occurred. CONCLUSION: These findings highlight the difficulty in the diagnosis of fetal asphyxia at a stage that could permit intervention to prevent brain damage.

Adult↗
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↗
PubMed1975

The effect of phenobarbital on asphyxia in the newborn monkey.

This study characterizes the circulatory changes associated with asphyxia in the newborn monkey and examines the effect of phenobarbital on asphyxia. The time to last gasp and duration of total asphyxia as well as heart rate at the start of resuscitation were the same in the phenobarbital-treated and untreated infants. Initial cardiac output was the same in both groups; there was a profound drop in cardiac output with asphyxia which was the same in both groups. Organs which preferentially receive a greater percentage of cardiac output during asphyxia are heart, total brain, and adrenal glands. Organs receiving a decreased percentage of cardiac output during asphyxia are kidneys, liver, and gastrointestinal tract. Cerebral hemisphere flow as a percentage of cardiac output is maintained during asphyxia, whereas paleoencephalon flow as a percentage of cardiac output increases significantly. These data confirm the circulatory redistribution of cardiac output in response to asphyxia described previously in the monkey fetus. The treated infants did not show the prolongation of time to last gasp reported in the monkey fetus; the dose of phenobarbital we used, although adequate to produce sedation, may have been too low to demonstrate the protective effect.

Adrenal Glands↗
PubMed1991

How much of neonatal encephalopathy is due to birth asphyxia?

In the literature on neonatal encephalopathy, the pervasive assumption is that once infants with major malformations or infections have been excluded, most of the remaining cases are due to birth asphyxia. Assessing the proportion of neonatal encephalopathy that is due to asphyxia during birth is difficult because of problems in defining asphyxia and neonatal encephalopathy and in recognizing the cause of neonatal neurologic illness. Available evidence indicates that neonatal neurologic signs are not strongly related to obstetric complications, signs of fetal distress, or biochemical markers usually considered to indicate perinatal asphyxia. Most studies that have sought positive evidence of independent markers of intrapartum asphyxia have found them to be absent in a large majority of neurologically symptomatic neonates. We conclude that the proportion of neonatal encephalopathy that is asphyxial in origin is not known but warrants examination, especially in view of the probable need in the near future to identify, on the basis of evidence available in the first hour or so of life, suitable candidates for clinical trials of powerful but risky treatments of birth asphyxia.

Asphyxia Neonatorum↗
PubMed1976

[Fetal and neonatal asphyxia].

The literature data and the author's own observations justify the conclusion that asphyxia of the fetus and newborn is the most common cause of death in the perinatal period. The author discusses the significance of asphyxia of the fetus and newborn as the main disease or the principal cause of death. The author suggests that the type of asphyxia of the fetus or newborn in every concrete case should be indicated in the pathologoanatomic diagnosis on the basis of physiology of intrauterine and extrauterine life. In case of asphyxia it is suggested that the question concerning the presence (or absence) of the underlying disease--fetopathy, pre-existing the asphyxia condition--should be considered. In case of asphyxia of the newborn the author recommends to bear in mind the anatomic substrate responsible for impairment of the act of breathing of the newborn. In most cases this substrate is represented by pneumopathies--noninflammatory changes in the lungs of the newborn. Pneumopathies of the newborn include deep aspiration of the amniotic content, atelectasis, edema and hemorrhages, hyaline membranes.

Asphyxia Neonatorum↗
PubMed1975

Effects of asphyxia and potassium on canine and feline electrocardiograms.

The effects of asphyxia and potassium on the electrocardiogram (ECG), lead II, were recorded from dogs and cats anesthetized with sodium pentobarbital and halothane. Electrocardiographic recordings were made during control periods, during asphyxia (occluded endotracheal tube), during infusion of an isotonic KCl solution and during infusion of an isotonic NaCl solution. Arterial and venous blood gas partial pressures (PaCO2, PvCO2, PaO2 and and PvO2), plasma Na+ and K+ concentrations, heart rate and mean arterial blood pressure were measured during control periods, asphyxia and during the periods of infusion. The vagi were severed to assess the effect of vagal tone on the ECG changes. The characteristic ECG changes during asphyxia and the electrolyte imbalances resulting from infusion of isotonic KCl and NaCl were determined during sodium pentobarbital and halothane anesthesia in both dogs and cats. The combination of halothane and high PCO2 caused cardiac arrhythmias. Spontaneous recovery from ventricular fibrillation, as a result of hyperkalemia, was recorded from cats. Disappearance of the P waves, which is characteristic of hyperkalemia, was infrequent in this study and the U waves associated with hypokalemia were not found. Severing the vagi did not alter the ECG changes characteristic of asphyxia, hyperkalemia and hypokalemia. It was found that asphyxia and infusion of fluids high or low in potassium can produce ECG changes in both dogs and cats that can be correlated with blood gas partial pressure changes or plasma potassium concentrations.

Anesthesia, Inhalation↗
PubMed1976

The effects of asphyxia on afferent activity recorded from the cervical vagus in the duck.

Recordings were made of nervous activity from duck arterial chemoreceptors, arterial baroreceptors and pulmonary receptors during steady-state conditions (normoxic normocapnia, hypoxia, and hypercapnia) and apnoeic asphyxia. Arterial chemoreceptors were stimulated by hypoxia and intra-arterial KCN injection and showed an increasing discharge throughout asphyxia. During the first 2 min of asphyxia the time course of the development of asphyxic bradycardia paralleled that of the increase in arterial chemoreceptor discharge. Arterial baroreceptors discharged at a constant latency from the heart beat when mean arterial pressure was constant, while a drug-induced increase in mean arterial pressure was associated with a reduced latency and increased baroreceptor activity per heart-beat. During asphyxia mean arterial pressure often rose so that, despite the effect of bradycardia, baroreceptor activity per heart-beat and activity per unit time increased. Pulmonary receptors showed a linear relationship (negative slope) between discharge rate and % CO2 in inspired air and usually stopped firing in apnoeic asphyxia. The initiation and maintenance of diving bradycardia are discussed in terms of these results.

Animals↗
PubMedDate not supplied

Foetal co-relates and mode of delivery in asphyxia neonatorum.

A prospective study was conducted on consequitively born live births for determining the role of certain foetal factors and mode of delivery on asphyxia neonatorum. The difference in the incidence of neonatal asphxia in 1208 singleton births (8.5%) and in the 66 multiple births (9.7%) was statistically significantly (p less than 0.01). Among the singleton live births a significantly increased incidence of asphyxia was recorded in preterms when compared to term and post term babies collectively (p less than 0.001). Small for date babies were at a greater risk for asphxia neonatorum when compared to babies weighing appropriate for gestational age (p less than 0.001). An inverse relationship was observed between birth weight and asphyxia neonatorum. A significant difference was seen in the occurrence of neonatal asphyxia between babies weighing less than 2000 g. and those weighing more than 2000 g. (p less than 0.001). The incidence was significantly influenced by mode of delivery, being highest in vaginal breech delivery followed in decreasing frequency by forceps and normal vaginal delivery. Among vaginal breech delivered neonates those weighing greater than or equal to 2500 g were at the highest risk. Evidence of foetal distress and meconium stained amniotic fluid had a low predictability of asphyxia being 35.0% and 40.0% respectively though both were statistically significant (p less than 0.001).

Asphyxia Neonatorum↗
PubMed1975

Clinical characteristics of pregnancies complicated by intrapartum fetal asphyxia.

The clinical characteristics of 124 pregnancies complicated by intrapartum fetal asphyxia have been reviewed. The evidence of fetal asphyxia tends to appear earlier in patients with maternal medical and obstetric complications than in those with labor complications. Evidence of clinical fetal distress was present in 36 per cent and was not related to the severity of the asphyxia. Low Apgar scores occurred in 40 per cent of infants with moderate asphyxia and in 80 per cent of infants with severe asphyxia at delivery. In the newborn infants, clinical evidence of cerebral abnormality was observed in 3 per cent, and evidence of the respiratory distress syndrome was seen in 3 per cent of the study group.

Acidosis↗
PubMed1978

Intrapartum fetal asphyxia: a preliminary report in regard to long-term morbidity.

This is a preliminary report of a prospective follow-up study of 42 infants who had episodes of intrapartum fetal asphyxia at delivery identified by an acid-base assessment and a control group of 69 babies who had no evidence of intrapartum fetal asphyxia. The newborn infants were mature at delivery. There were no major neurologic disabilities in the asphyxia group. The pattern of physical growth and the mental and physical development indices of the babies of the asphyxia group were similar to those of the control group babies at 12 months of age. Results have not as yet indicated that the mature fetus with at least a terminal episode of asphyxia will exhibit evidence of handicap due to central nervous system injury.

Asphyxia Neonatorum↗
PubMed1975

Fetal asphyxia due to umbilical cord compression. Metabolic and brain pathologic consequences.

Term monkey fetus 1620 sustained 50 min of rapidly developing severe asphyxia which began immediately after its in utero version. The arterial blood pO2 decreased from a normal value of 34 to 11-12 mm Hg while the blood pH fell from 7.35 to 6.70. During this asphyxia, hemoglobin-oxygen saturations below 5% were recorded. The complete collapse of the umbilical circulation several minutes prior to the reoxygenation of the fetus added an episode of total asphyxia. With reoxygenation following delivery, fetal cardiovascular performance improved rapidly though over an hour was required for recovery from the severe acidosis. The animal prospered but was found moribund on the 13th postnatal day due to dehydration. Brain examination after euthanasia revealed severe paracentral cortical and basal ganglia damage. Damage also appeared symmetrically in nuclei in the lower brain stem and in thalamus. These three zones of injury are attributed to the partial, the partial combined with the total, and the total asphyxia, respectively. The present case makes clear that compression of the umbilical cord may cause damage of a variety of types depending on the severity and duration of the asphyxia induced. It also demonstrates the possibility of recovery from a systemic acidosis where the pH values have fallen to levels below 6.70 for up to an hour.

Animals↗
PubMed1992

Role of excitatory amino acid antagonists in the management of birth asphyxia.

Birth asphyxia is an important cause of permanent neuro-developmental disability. Asphyxia sets in course a progression of intracellular events which culminates in neuronal death, and this process may take up to 48 h to complete. Entry of calcium into the neurone appears to be the key to the cell death, and it is known that during asphyxia, excessive glutamate is released which stimulates the voltage-dependent N-methyl-D-aspartate (NMDA) receptor to open with an accumulation of excess intracellular calcium. MK-801 is a very effective NMDA receptor antagonist, and it has been shown that this drug prevents or significantly reduces the extent of cortical neurone infarction following experimental asphyxia in 7-day-old rat pups. Unfortunately, MK-801 is toxic to the pup, but newer NMDA receptor antagonists may offer the opportunity for neuroprotection in the human infant who has suffered severe birth asphyxia.

Amino Acids↗
PubMed1978

Body colour response of the carp (Cyprinus carpio) during asphyxia.

The body colour of immobilized carp was photoelectrically measured simultaneously with heart rate in order to examine one of the effects of asphyxia on autonomic functions of the cutaneous region. 1) Asphyxia induced marked body colour darkening and bradycardia. 2) Adequate increase in cardiac vagal activity was recorded during asphyxic bradycardia. 3) After atropine injection, body colour darkening, as in intact fish, was observed during asphyxia while heart rate was not changed. 4) After transection of anterior spinal cord, asphyxic stimulation did not induce body colour darkening. It is concluded that body colour darkening mediated by nervous pathways was observed during asphyxia simultaneously with the definite bradycardia. This response of body colour has provided the first indication for responses in cutaneous autonomic systems within the responses of the fish co-ordinated as a whole to asphyxia.

Animals↗
PubMedDate not supplied

[Relation between fetal hypoxia, neonatal asphyxia and hypoxic-ischemic encephalopathy].

Clinical data, duration of labour, mode of delivery and possibilities of fetal heart rate monitoring in predicting perinatal asphyxia and neonatal encephalopathy in 143 consecutively delivered asphyxiated infants and 143 paired healthy infants are analyzed. Perinatal asphyxia occurred in only 2.6% of normal pregnancies and significantly more frequently in pregnancies complicated by gestosis. It is far more common in children subject to operative deliveries (15-20%) and when labour lasts longer than 12 hours, either in vertex or breech presentations. The occurrence of encephalopathy is less frequent in children delivered by cesarean section (1.6%) and almost three times more frequent than in vaginal breech deliveries. In asphyxiated children delivered vaginally, significantly more frequently CTG scores were prepathologic (38% versus 3.4%). In the cesarean section group the differences are not significant in prepathologic CTG scores but are highly significant when CTG scores were pathologic (36% versus 2.7%). The mean duration of the pathologic heart rate pattern is significantly longer in mild asphyxia in comparison to the control group (45 minutes versus 12.5 minutes). In moderate asphyxia the pathologic CTG pattern lasted 72.1 minutes and in severe asphyxia 52 minutes.

Asphyxia Neonatorum↗
PubMedDate not supplied

Production of fetal asphyxia by maternal psychological stress.

Several lines of evidence indicate that maternal psychological stress leads to adverse pregnancy outcome in rhesus monkey. Chronic anxiety causes an increased stillbirth rate, fetal growth retardation, and altered placental morphology. On another time scale, lightening of maternal anesthesia during surgery produces an impaired fetal oxygenation while re-institution of anesthesia ameliorates the fetal asphyxia. The present study, for the first time, demonstrates a relationship between specific episodes of meternal psychological stress and exacerbation of fetal asphyxia in utero. Eight term pregnant rhesus monkeys were anesthetized with sodium pentobarbital. Catheters were placed both into the maternal and the fetal femoral arteries for the continuous recording of blood pressure and heart rate and for the intermittent campling of maternal and fetal blood. An open-ended catheter recorded intrauterine pressures. Following a complete repair, the anesthesia of the mothers was allowed to lighten. As the mothers awakened, the fetuses invariably showed the developemnt of fetal asphyxia. A fetal acidosis developed and the fetal oxygenation and repair of acidosis. Studies while the mothers were fully awake showed the repeated and regular development of episodes of heightened fetal asphyxia produced by episodes of stressful stimulation of the mothers. Episodes of maternal psychological stress led to changes in both fetal vital signs and blood chemical findings. These alterations in fetal state regularly followed the onset of the episodes of psychological stress by 50 seconds. These changes also usually remitted 50 seconds following the termination of the periods of stress. These results demonstrated a direct and unequivocal relationship between meternal psychological stress and fetal asphyxia. It is assumed the maternal stress produces impairments in the circulation to the uterus through an increased sympathetic nervous system activity and a shunting of the maternal blood-flow from the abdominal viscera to other organs as occurs in the fight-orflight reaction.

Animals↗