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PubMed1966

Causes of birth asphyxia and trauma.

Causes of birth asphyxia and trauma were determined in the 208 most severely affected infants of 10,995 consecutive live births; 159 infants had cerebral disturbances, 39 had fractures and palsies, and 10 had fractures or palsies in addition to cerebral disturbances. Most frequent causes of birth asphyxia and trauma were: prolonged labour, midforceps or breech delivery in full-term infants; abruption placentae, difficult breech delivery, and maternal sedation in premature infants; and unattended precipitate deliveries in immature infants. Asphyxia following normal labour and delivery usually occurred in infants with fetal malnutrition.Improved obstetrical management with more frequent use of Cesarean section delivery might have been of value in preventing much of this fetal injury.Asphyxia and trauma due to complications of delivery were twice as frequent on the ward as on the private service. This may have been due in part to a lower Cesarean section rate on the ward service. A monthly review of birth asphyxia and trauma is recommended to help maintain a high standard of obstetrical practice.

Abruptio Placentae↗
PubMed1981

Death by railway accident: incidence of traumatic asphyxia.

Eleven people were killed in a railway accident. Four of them died of severe blunt injury, three of moderate injuries combined with traumatic asphyxia and suffocation. Four of the victims were only slightly injured but showed distinct signs of traumatic asphyxia. An extensive pulmonary microembolism syndrome consisting of bone-marrow and fat embolism was found in these cases. Comparing the morphologic findings after suffocation by thoracic compression and traumatic asphyxia the authors attribute independent pathophysiologic significance to traumatic asphyxia. The importance of autopsies and histologic examinations in railway accidents is emphasized.

Accidents↗
PubMed1995

[Acute complications in full term neonates with severe neonatal asphyxia].

The acute systemic complications of perinatal asphyxia, defined as an umbilical artery pH at birth of 7.10 or less, were evaluated in fifty full-term newborn infants. We also investigated the prenatal complications that lead to asphyxia, and the relationship between Apgar score and cord pH. Asphyxia or fetal distress was not identified in 56% of the cases. The most common condition associated with asphyxia was prolonged labor followed by abruptio placentae. About half of the babies studied, suffered some degree of renal and brain dysfunction; 24% had severe respiratory disease. Myocardial failure was present in 24%. Regarding metabolic complications, the most frequent was hypocalcemia, present in 44%. On the other hand, there was no correlation between Apgar score and cord pH. Mortality was 22%. The main cause of death was Persistent Pulmonary Hypertension.

Abruptio Placentae↗
PubMedDate not supplied

Decreased respiratory tolerance from intermittent asphyxia in rat sucklings.

To study the respiratory tolerance of rat pups to intermittent asphyxia induced by exposure to closed rebreathing, we randomized newborn rats from four litters into two treatment groups. Respiratory tolerance was defined as the time interval during asphyxia until the first episode of 30 seconds of apnea. Rats in the experimental group were asphyxiated once daily during the first 4 days of life. Rats in the control group were asphyxiated once on day 4 of life. Pups exposed to intermittent asphyxia had a significant reduction in respiratory tolerance compared with that of littermates asphyxiated once at the same age. These findings suggest that the ability of the young mammal to withstand re-exposure to asphyxia may be impaired.

Analysis of Variance↗
PubMed1997

Decrease of brain protein kinase C, protein kinase A, and cyclin-dependent kinase correlating with pH precedes neuronal death in neonatal asphyxia.

BACKGROUND: Acidosis, energy depletion, overstimulation by excitatory amino acids, and free radical-mediated reactions are the major, current concepts for the explanation of damage and death resulting from asphyxia. Impaired protein phosphorylation by protein kinase C represents another mechanism incriminated in cell death. METHODS: We used a nonsophisticated perinatal asphyxia model to study brain (frontal cortex) pH, ATP, protein kinases PKC, PKA, and cyclin-dependent kinase. We used o-tyrosine, a marker for hydroxyl radical attack, and LPO 586, a spectrophotometric assay, to study lipid peroxidation products. The antioxidant enzymes catalase, superoxide dismutase, and glutathione peroxidase were used in the frontal cortex. In addition, a cell death ELISA and histology to evaluate cell death were performed. RESULTS: Brain pH and protein kinases were decreasing with the length of the asphyctic periods, and energy depletion was shown by a drop of ATP levels, whereas no evidence for the involvement of free radical-mediated mechanisms was obtained. Cell death was shown by the cell death ELISA as early as 10 minutes after the asphyctic period, and histologically, cell death could be revealed but not before day 8 after asphyxia. CONCLUSION: Acidosis and/or impaired protein kinases, but not free radical mechanisms, may play a role in the pathobiochemistry of cell death in neonatal asphyxia of the rat.

Adenosine Triphosphate↗
PubMed1993

Effects of asphyxia on the fetal lamb brain.

OBJECTIVE: Our purpose was to study the effect of fetal asphyxia on the release of hypoxanthine and xanthine in cerebrospinal fluid and on brain histologic characteristics. STUDY DESIGN: In seven fetal lambs (3 to 5 days after surgery, gestational age 124.3 +/- 2.6 days) asphyxia was induced by restriction of uterine blood flow. RESULTS: Fetal pH and base excess were reduced to 6.99 +/- 0.02 and -17.6 +/- 0.9 mmol/L, respectively. Cerebral blood flow increased during asphyxia and returned to normal in the recovery phase. Maximum concentrations of cerebrospinal fluid hypoxanthine and xanthine were reached in the normoxemic recovery phase. This high level of substrates during normoxemia facilitates oxygen free radical formation and may thus aggravate postasphyctic brain damage. Histologic evaluation of the brain 3 days after the insult showed a variable degree of edema. Coagulative neuronal changes, characteristic of irreversible cell death, were only occasionally detected. These changes were most obvious in the Purkinje cells of the cerebellum. CONCLUSIONS: Fetal asphyxia induced by uterine blood flow restriction is associated with high levels of cerebrospinal fluid hypoxanthine and xanthine in the recovery phase. Microscopically detectable brain damage, although not extensive, is mainly located in the cerebellum.

Animals↗
PubMed1995

Effect of asphyxia on the composition of cationic elements in the perilymph.

To elucidate the role of free radicals in the cochlea, cationic elements in the perilymph of the scala tympani in normal and asphyxic guinea pigs were measured by an inductively coupled plasma atomic emission spectrometer. The concentrations of 7 cationic elements (i.e., calcium, copper, iron, magnesium, phosphorus, lead and zinc) were measured simultaneously in a sample of the perilymph taken before, during and after asphyxia. There was no significant change in these cationic elements during asphyxia for 3 min. In contrast to the stationary level during asphyxia, the iron concentration was significantly elevated at 5 min after re-ventilation following asphyxia and decreased rapidly toward the pre-asphyxic level thereafter, although no significant change was observed in other cationic elements. These results were comparable to the theory of non-protein-bound iron accumulation produced by an O2-dependent mechanism during re-perfusion.

Animals↗
PubMed1987

Enzyme-linked immunosorbent assay for determination of plasma thyroglobulin and its application to post-mortem diagnosis of mechanical asphyxia.

A high sensitive enzyme-linked immunosorbent assay (ELISA) for determination of plasma thyroglobulin was devised and applied to the postmortem diagnosis of mechanical asphyxia. The sensitivity of the present ELISA was 5 ng/ml. All of the 15 victims who died from causes other than mechanical asphyxia showed plasma thyroglobulin levels lower than 200 ng/ml (99.8 +/- 37.9 ng/ml), while 12 out of 14 victims of mechanical asphyxia showed the levels higher than 200 ng/ml (2100 +/- 3450 ng/ml in 14 victims). Thus, the present ELISA appears to be useful for postmortem diagnosis of mechanical asphyxia.

Adolescent↗
PubMed2003

Effects of recombinant human superoxide dismutase during reoxygenation with 21% or 100% oxygen after cerebral asphyxia in newborn piglets.

OBJECTIVE: Superoxide radicals (O2-) are generated during reoxygenation following asphyxia, possibly more when higher concentrations of O2 are used during resuscitation. Superoxide dismutase (SOD) is an antioxidant enzyme, which scavenges O2-. We tested the hypothesis that a single intravenous dose of recombinant human Cu,Zn SOD (rhSOD) could influence microcirculation and biochemical markers of asphyxia in piglets reoxygenated with 21% or 100% O2 after combined cerebral hypoxemia-ischemia-hypercapnia. METHODS: Anesthetized newborn piglets were randomized to asphyxia (n = 40) or control (n = 3). Asphyxia was induced by ventilation with 8% O2, adding CO2, and temporary occlusion of both common carotid arteries. After 20 min, 16 piglets received rhSOD 5 mg/kg intravenously and reoxygenation with 21% O2 (rhSOD, 21%; n = 8) or 100% O2 (rhSOD, 100%; n = 8), and 24 piglets received saline and reoxygenation with 21% O2 (21%, n = 13) or 100% O2 (100%, n = 11). The cortical microcirculation was assessed by laser Doppler flowmetry, and glutamate in the striatum and hypoxanthine in the cortex were measured by in vivo microdialysis. RESULTS AND CONCLUSION: rhSOD peaked in plasma after 5 min. No rhSOD was detected in brain tissue. There were no significant differences between rhSOD and non-rhSOD groups in any measured variable.

Animals↗
PubMed1980

Cerebral energy metabolism in diving and non-diving birds during hypoxia and apnoeic asphyxia.

1. Cerebral energy metabolism during apnoeic asphyxia and steady-state hypoxia was compared in ducks and chickens; ducks tolerate apnoeic asphyxia 3-8 times longer than chickens. 2. Fluctuations in the reduced form of respiratory chain nicotinamide adenine dinucleotide (NADH) were monitored from the left cerebral hemisphere by a noninvasive fluorometric technique and used as an indicator of mitochondrial hypoxia. NADH fluorescence was expressed in aribtrary units (a.u.) where 100 a.u. was defined as the fluorescence change from normoxia to anoxia. Electroencephalogram (e.e.g.) and surface Po2 were recorded from the right hemisphere. 3. After 1 min of asphyxia NADH fluorescence increased by 37 a.u.+/-3.60 S.E. of mean (n=54) in paralysed chickens and 8 a.u.+/-1.41 (n=55) in aralysed ducks. After 2 min the fluorescence increased by only 15 a.u.+/-1.95 in ducks. 4. Both species showed an isoelectric e.e.g. when fluorescence increased by approximately 35 a.u., indicating that anaerobic ATP production in ducks did not maintain brain function (e.e.g.) for a greater accumulation of respiratory chain NADH. 5. At a given decrease in tissue Po2 ducks and chickens showed the same level of NADH increase, indicating that both species are equally dependent on tissue Po2 for the maintenance of redox state. 6. We conclude that biochemical adjustment which enhance anaerobic ATP production and/or prolong oxidative phosphorylation during progressive hypoxia are not responsible for increased cerebral tolerance to apnoeic asphyxia in the duck.

Anaerobiosis↗
PubMed1989

Role of endogenous opioids in the cardiovascular responses to asphyxia in fetal sheep.

Intravenous administration of the opioid receptor antagonist naloxone to asphyxiated fetal sheep increases the arterial blood pressure. We examined the hypothesis that endogenous opioids modify the cardiac output distribution during asphyxia due to changes in the vascular resistance of some fetal organs. Thirteen fetal sheep (0.8-0.9 of gestation) were chronically catheterized. Fetal asphyxia was induced by reducing the uterine blood flow with an inflatable occluder around the common internal iliac artery to approximately 50% of control for 40 min. Naloxone solution or the solvent alone was added for the last 20 min. Asphyxia caused hypertension, and the fetal arterial blood pressure further increased when asphyxiated fetuses received naloxone. Heart, brain, and adrenal blood flows increased due to the increase in blood pressure, with no changes in their vascular resistances. In contrast, kidney and carcass blood flows decreased, and their vascular resistances increased. We conclude that endogenous opioids inhibit the vasoconstriction of these vascular beds during fetal asphyxia.

Acid-Base Equilibrium↗
PubMed1998

The cerebral hemodynamic response to asphyxia and hypoxia in the near-term fetal sheep as measured by near infrared spectroscopy.

This study examined the hypothesis that the cerebrovascular response to asphyxia of the late gestation sheep fetus is characterized by an increase in cerebrovascular resistance and a fall in cerebral blood flow (CBF) rather than the fall in resistance and increase in CBF which occurs in acute hypoxemia. In eight unanesthetized late gestation fetal sheep (123- to 125-d gestation) we evaluated continuous changes in carotid blood flow (CaBF) as an index of global CBF and total cerebral Hb concentrations as an index of global cerebral blood volume (CBV) using ultrasound flow probes and near infrared spectroscopy respectively. Asphyxia was induced by rapid and complete occlusion of the umbilical cord for 10 min. We also examined the fetal response to 1 h of acute 9% isocapnic hypoxia for comparison purposes. During hypoxia we observed a sustained increase in CaBF (p < 0.05) and CBV (p < 0.01) and a fall in carotid vascular resistance (p < 0.05). During asphyxia there was no significant rise in CBV, a fall in CaBF (p < 0.05), and a rise in carotid vascular resistance (p < 0.01). CaBF fell at a time when mean arterial pressure was elevated (p < 0.01). These data strongly suggest that fetal CBF does not increase and may even fall during severe asphyxia of rapid onset. Furthermore, our near infrared spectroscopy data show that the relative changes in total cerebral Hb concentrations may reflect the type and severity of the insult to which the fetus is exposed.

Animals↗
PubMed1984

Maternal beta-adrenoceptor blockade reduces fetal tolerance to asphyxia. A study in pregnant sheep.

Maternal and fetal beta 1-adrenoceptor blockade was induced in sheep by infusing i.v. 11 pregnant ewes with metoprolol in doses producing maternal plasma concentrations of metoprolol comparable to those obtained in clinical use. Ten other ewes and their fetuses served as controls. Under acute anaesthesia the fetus was exteriorized and subjected to two levels of controlled asphyxia by intermittent, complete obstruction of the maternal placental blood flow. Fetal haemodynamic reactions were assessed by measuring fetal heart rate, cardiac contractility, cardiac output and cerebral blood flow. The metabolic reactions were evaluated from blood gases, pH, lactate and hypoxanthine concentrations, while the electrophysiological status of the brain was evaluated from the somatosensory evoked EEG potentials (SEP). Already during the period of moderate asphyxia the beta-blocked fetuses demonstrated a blunted haemodynamic response, in comparison with the control fetuses, resulting in an accelerating lactic acidosis, signs of a breakdown of intra-cellular energy-rich phosphates and an impaired cerebral function. During the period of severe asphyxia, both groups of fetuses exhibited signs of extensive cerebral deterioration. During the ensuing recovery phase, 80% of the control fetuses regained their brain function, as assessed by SEP, whereas this was true for only 30% of the beta 1-blocked fetuses. It is concluded that the ovine fetus relies heavily on greatly increased sympatho-adrenal activity to adapt itself to asphyxia and that blockade of the fetal beta 1-adrenoreceptors by maternal medication is a hazard to the potentially asphyctic fetus.

Adrenergic beta-Antagonists↗
PubMed1992

Cerebral energy metabolism in immature and mature guinea pig fetuses during acute asphyxia.

In immature fetuses circulatory centralization caused by acute asphyxia is less effective than that in mature fetuses (Jensen & Berger, 1991). This suggests that cerebral oxygenation may be poor in immature fetuses during asphyxia. On the other hand cerebral oxygen consumption is lower in immature than that in mature fetuses. To determine, whether or not there is an imbalance between oxygen supply and demand in one or the other group, we compared the time course of the changes of cerebral concentrations of both high-energy phosphates and glycolytic intermediates between immature and mature guinea pig fetuses during acute asphyxia caused by arrest of uterine blood flow. The fall in the cerebral concentrations of adenosine triphosphate and glucose, and the rise in those of adenosine monophosphate and lactate were slower in immature than in mature fetuses. There were no differences between the levels of cerebral adenosine diphosphate and creatine phosphate of the two groups. From these results we conclude that during acute asphyxia the imbalance between cerebral oxygen supply and demand is less marked in immature than in mature fetuses.

Acute Disease↗
PubMed1990

Cerebral oxygen consumption during asphyxia in fetal sheep.

Cerebral blood flow and cerebral arteriovenous oxygen content difference were measured in 17 fetal sheep, and cerebral oxygen uptake was calculated. The measurements were made under control conditions and after profound fetal asphyxia induced of uterine blood flow for up to 90 min. In 14 of the fetal sheep, sequential measurements were made to examine hemodynamic changes and cerebral oxygen consumption at comparable intervals up to 36 min of asphyxia. These fetuses initially had elevated blood pressure and lowered heart rate became hypoxemic, hypercarbic, and acidotic. There was an initial decrease in cerebral oxygen consumption. Sequential measurements, however, showed a relative stability in this decreased oxygenation during 4 to 36 min of asphyxia despite a progressive metabolic acidosis. The cerebral fractional oxygen extraction remained unchanged despite a mean pH of 6.98 at 36 min. The calculated cerebral oxygen uptake during asphyxia in all 17 sheep was grouped according to whether the ascending aortic oxygen content was greater or less than 1.0 mmol/l. In the first group with mean ascending aortic oxygen content of 1.3 mmol/l, blood flow to the brain was increased and cerebral oxygen consumption was 85% of control. In the second group with mean arterial blood oxygen content of 0.8 mmol/l, there was a narrowing of the arteriovenous oxygen content difference, but no further increase in cerebral blood flow. Cerebral oxygen consumption was only 48% of control in this more asphyxiated group. We conclude that the degree of hypoxemia in the second group represents a point where physiologic mechanisms cannot compensate, and may be associated with neuronal damage.

Adrenal Glands↗
PubMed1987

Fetal sympathetic activity, transcutaneous PO2, and skin blood flow during repeated asphyxia in sheep.

To improve detection of fetal distress, we examined whether increased fetal sympathetic activity during repeated episodes of asphyxia decreases skin blood flow, which can be monitored by recording transcutaneous PO2. Sympathetic activity was assessed by relating catecholamine concentrations in the fetal plasma to blood gas, acid-base, and heart rate variables which are commonly used to determine fetal distress. Fifteen experiments were conducted on 8 anaesthetised fetal sheep in utero between 125 and 145 days of gestation (term is at 147 days). They were subjected to 11 consecutive episodes of asphyxia of 30 (n = 3), 60 (n = 9), or 90 (n = 3) s over 33 min, achieved by arrest of uterine blood flow. Blood samples were drawn at 0, 33, and 60 min to determine arterial blood gases, acid base-balance, and concentrations of lactate, glucose, norepinephrine, and epinephrine. Fetal transcutaneous PO2, relative local skin blood flow, heart rate, arterial blood pressure, and arterial O2 saturation were recorded continuously. Fetal plasma concentrations of norepinephrine and epinephrine increased logarithmically as the duration of repeated asphyxia, anaerobic metabolism, and glucose concentrations increased, and as the mean O2 saturation, transcutaneous PO2, and local skin blood flow decreased. We conclude that during repeated episodes of asphyxia in fetal sheep near term, a significant increase in sympathetic activity can be detected indirectly by transcutaneous PO2 monitoring, because sympathetic activation reduces skin blood flow.

Animals↗
PubMed1979

[Morphologic changes in the brain after sustaining asphyxia during labor (pathogenesis of mental retardation)].

An analysis was accomplished of pathomorphological changes in the brains of 10 newborns, who died of intranatal asphyxia and of 1 adult brain with mental retardation, due to asphyxia during delivery. The dynamics of hypoxic changes of an irreversible character in the brain of the newborn and the existence of chronic hypoxic encephalopathy with pronounced cellular devastation in the late period of asphyxia indicate common genesis of the pathological process in the brain, conditioning its progression. The role of intranatal asphyxia in the pathogenesis of changes in postnatal development of neuropsychic activity is discussed.

Age Factors↗
PubMed2000

Homicidal asphyxia.

Homicides due to asphyxia are relatively uncommon. To better understand the presentation of such cases, the files of the Bexar County Medical Examiner's Office were reviewed from January 1, 1985, through December 31, 1998, for all such homicides. A total of 133 cases were found. The largest category was ligature strangulation with 48 deaths (21 male, 27 female). Petechiae were present in the conjunctivae and/or sclerae in 86% of the cases; fractures of the hyoid and/or thyroid cartilage were present in 12.5%. There were a total of 41 deaths from manual strangulation (27 female, 14 male). Petechiae were present in 89% of the cases. In cases of manual strangulation, fractures of the hyoid, thyroid, or cricoid cartilage were found in all the male victims and slightly more than one half of the female victims. Twenty-six cases of suffocation were found; 20 of the victims were < or =2 years of age. Only 1 of these children had petechiae and/or scleral hemorrhage. Five deaths were due to choking. Three of the deaths involved adults who were gagged; 2 deaths involved infants with foreign material pushed into the mouth. Other categories of asphyxia were as follows: 9 deaths due to more than one form of asphyxia; 1 death due to hanging, and 3 deaths due to drowning. Rape was the motive in 66% of the female victims of ligature strangulation and 52% of those due to manual strangulation.

Adult↗