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PubMed1989

Perinatal risk factors in birth asphyxia: relationship of obstetric and neonatal complications to neonatal mortality in 16,365 consecutive live births.

Over a period of one year, 16,365 consecutively live born neonates were prospectively studied for evidence of birth asphyxia using the requirement of greater than one minute of positive pressure ventilation for identifying infants suffering from birth asphyxia. Asphyxia occurred in 2.8% of all neonates. Multivariate analysis of high risk factors associated with increased risk of asphyxia showed that low birth weight was the most significant predictor of asphyxia: asphyxia occurred in 68% of infants of less than 1,000 g birth weight and decreased to 1.2% in infants of 3-4 kg birth weight. Perinatal risk factors associated with a higher incidence of asphyxia include: postmaturity, birth weight (less than or equal to 2.5 kg) and with the presence of maternal and/or obstetric complications. The impact of asphyxia on neonatal mortality was most pronounced in more mature infants and the mortality was increased 3 fold in infants of less than 34 week gestation and greater than 27 fold for infants greater than 38 week gestation. Of the asphyxiated neonates, intrauterine growth retardation, fetal macrosomia, hypothermia, hyaline membrane disease, seizures, hypoglycemia and hyponatremia were significantly associated with an increased risk of death.

Adolescent↗
PubMed1980

Serotonin metabolism in neonatal rat brain during asphyxia and recovery.

Neonatal rats were exposed to 20 or 30 min of total or partial oxygen deprivation. During asphyxia and subsequent recovery the endogenous levels of tryptophan and 5-hydroxytryptamine (5-HT, serotonin) were measured. The activity of tryptophan hydroxylase, the first and rate limiting enzyme in the 5-HT synthesis pathway, was studied in vivo by measuring the accumulation of 5-hydroxytryptophan (5-HTP) after inhibition of aromatic L-amino acid decarboxylase with NSD 1015. During asphyxia there was a decrease in tryptophan hydroxylase activity in the whole brain and various regions studied. The levels of tryptophan, 5-HTP and 5-HT all increased after 30 min of recovery from asphyxia. In the whole brain, 5-HTP and 5-HT levels were normal 2 h after anoxia while tryptophan levels normalized more slowly to reach control values after 6 h. In the regional brain study, the 5-HTP levels returned quickly to control levels after asphyxia in the striatum and midbrain but not in the brainstem and hemispheres regions. The whole brain 5-HTP and 5-HT levels did not differ from controls 24 to 48 h after the asphyxia. Although the neonatal nervous system exhibits a great resistance to asphyxia, the metabolism of the neurotransmitter 5-HT is affected already during a short period of asphyxia and subsequent recovery. As 5-HT is ascribed important neurotransmitter functions, this might be relevant to the neurological sequelae of human asphyxia neonatorum.

5-Hydroxytryptophan↗
PubMed1967

Pulmonary vasoconstriction and changes in heart rate during asphyxia in immature foetal lambs.

1. The effect of changing the composition of pulmonary arterial blood on the pulmonary vasoconstrictor response to asphyxia was studied in immature foetal lambs of approximately 90 days gestation age.2. When normal foetal carotid arterial blood (withdrawn before asphyxia) was introduced during asphyxia, the pulmonary vasoconstriction was rapidly and wholly relieved as soon as this blood reached the lung. This did not happen when blood was used which had been withdrawn during asphyxia.3. Conversely introduction into a pulmonary artery of a foetal lamb during recovery, of arterial blood withdrawn during asphyxia, caused an immediate return of pulmonary vasoconstriction.4. These phenomena could not be explained by the generation of vasodilator agents such as bradykinin, acetylcholine, histamine or isoprenaline.5. During asphyxia injection of normal foetal arterial blood into the left atrium did not cause pulmonary vasodilatation, but did elicit a large increase in heart rate.6. Neither the pulmonary vasoconstriction during asphyxia, nor its relief by normal foetal arterial blood, nor the changes in heart rate were affected by previous bilateral vagotomy or administration of atropine or hexamethonium.7. It was concluded that, in immature foetal lambs, the effect of asphyxia in causing pulmonary vasoconstriction was mainly, if not exclusively, by a local action within the lungs, and that the bradycardia during asphyxia was mainly due to the fall in P(O2) acting locally upon the heart.

Acetylcholine↗
PubMed2000

Neurocirculatory consequences of intermittent asphyxia in humans.

We examined the neurocirculatory and ventilatory responses to intermittent asphyxia (arterial O(2) saturation = 79-85%, end-tidal PCO(2) =3-5 Torr above eupnea) in seven healthy humans during wakefulness. The intermittent asphyxia intervention consisted of 20-s asphyxic exposures alternating with 40-s periods of room-air breathing for a total of 20 min. Minute ventilation increased during the intermittent asphyxia period (14.2 +/- 2.0 l/min in the final 5 min of asphyxia vs. 7.5 +/- 0.4 l/min in baseline) but returned to the baseline level within 2 min after completion of the series of asphyxic exposures. Muscle sympathetic nerve activity increased progressively, reaching 175 +/- 12% of baseline in the final 5 min of the intervention. Unlike ventilation, sympathetic activity remained elevated for at least 20 min after removal of the chemical stimuli (150 +/- 10% of baseline in the last 5 min of the recovery period). Intermittent asphyxia caused a small, but statistically significant, increase in heart rate (64 +/- 4 beats/min in the final 5 min of asphyxia vs. 61 +/- 4 beats/min in baseline); however, this increase was not sustained after the return to room-air breathing. These data demonstrate that relatively short-term exposure to intermittent asphyxia causes sympathetic activation that persists after removal of the chemical stimuli. This carryover effect provides a potential mechanism whereby intermittent asphyxia during sleep could lead to chronic sympathetic activation in patients with sleep apnea syndrome.

Adult↗
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↗
PubMed2000

Preservation of cerebrovascular tone and reactivity by sodium channel inhibition in experimental prolonged asphyxia in piglets.

Sodium channels using cAMP as a second messenger play a role in the regulation of cerebral circulation and metabolism. Cerebrospinal fluid (CSF) cAMP levels have been shown to correlate with the degree and duration of hypoxic injury and outcome and to be an indicator of cerebral vascular reactivity. We hypothesize that sodium channel inhibition either before or at termination of experimental asphyxia will attenuate cerebrovascular alterations and maintain CSF cAMP levels. Three groups of piglets with closed cranial windows were studied: asphyxia or group 1 (n = 5) and two treatment groups. Pigs were treated with 50 mg/kg of sodium channel blocker before asphyxia (group 2, n = 6) and after the termination of asphyxia and start of reventilation (group 3, n = 6). Asphyxia was sustained over 60 min by ventilating piglets with 10% O2 gas mixture and decreasing minute ventilation followed by 60 min of reventilation with room air. Every 10 min, pial arterial diameters were measured, and CSF samples were collected for cAMP determination. Vascular reactivity to topically applied isoproterenol (10(-4) M) was evaluated 60 min after recovery. During asphyxia, cAMP levels in group 2 peaked and declined at a later time with mean values remaining significantly higher than those of groups 1 and 3. During reventilation, CSF cAMP concentrations were highest in group 3 and lowest in group 1. Pial arteriolar dilation occurred during asphyxia in all three groups but to a lesser degree in the pretreated group compared with groups 1 and 3. Pial arteriolar reactivity to isoproterenol postasphyxia was preserved in both groups 2 and 3. In summary, in newborn pigs, pretreatment with sodium channel blocker resulted in higher CSF cAMP levels and a lesser degree of pial arteriolar dilation during prolonged asphyxia. Pretreatment or treatment at reventilation restored vascular tone and reactivity.

Animals↗
PubMed2006

[Clinical study on improving the diagnostic criteria for neonatal asphyxia].

OBJECTIVE: Diagnosing neonatal asphyxia solely according to Apgar score may lead to misdiagnosis. The aim of this study was to explore new and more accurate diagnostic criteria for neonatal asphyxia. METHODS: Totally 10 376 live born neonates in our hospital were consecutively enrolled into the study. The following five items related to birth asphyxia, i.e., antepartum high-risk factors, Apgar scores, umbilical artery blood pH, organ injury, differential diagnosis on the causes of low Apgar score cases were examined and registered. The relationship among the first 4 items were analyzed. By differential diagnosis, the sensitivity and specificity of each index on diagnosing asphyxia and their complementary value on each other were investigated. RESULTS: The items correlated well with each other (P < 0.01 or < 0.05) but were not entirely parallel and consistent; they could complement but could not substitute for each other. The sensitivity of antepartum high-risk factors, low Apgar scores, umbilical artery blood pH < 7.00 and organ injury was 100%, 100%, 44.44% and 100%, while the specificity was 17.99%, 98.90%, 96.05% and 96.62%, respectively. Of the 230 low Apgar score cases in this series only 50.9% coincided with asphyxia. For the 230 cases, when low Apgar score was combined with umbilical artery blood pH < 7.00, the sensitivity and specificity were 41% and 99.1% and when low Apgar score was combined with umbilical artery blood pH < 7.20, the sensitivity and specificity were 100% and 29.20%, respectively. After organ injury was added, the specificity was increased to 65.49%. When differential diagnosis was further added to exclude the other causes of low Apgar score cases, the misdiagnosis rate was minimized. CONCLUSION: Up to now, no single accurate index for diagnosing neonatal asphyxia is available. In order to increase diagnostic bases and reduce misdiagnosis, the criteria of sole Apgar score should be replaced by multi-index diagnostic criteria. Based on the present study, a set of integrated diagnostic criteria for neonatal asphyxia is proposed: (1) prenatal high-risk factors, (2) low Apgar scores (respiratory depression must present), (3) umbilical artery blood pH < 7.00, if only pH < 7.20, the items (2) (4) (5) must be present, (4) hypoxic-ischemic organ injury (at least one organ dysfunction), (5) the other causes of low Apgar scores should be excluded. The last 4 indexes should all be met and the first one serves as reference. If multi-organ (three or more organs) dysfunction and (or) hypoxic-ischemic encephalopathy are present, severe asphyxia can be diagnosed.

Apgar Score↗
PubMed1993

Asphyxia of the newborn in east, central and southern Africa.

Very scanty information is available in East, Central and Southern Africa on the incidence and risk factors associated with asphyxia of the newborn. A multicentre prospective study involving 4267 deliveries in eight countries was undertaken over a three month period, in maternity units of the central hospitals to determine the incidence; maternal, service and logistic risk factors for asphyxia of the newborn as determined by an abnormally low apgar score. 30% of births were by primigravida mothers, of whom 67% were teenagers. A birth by a teenager had a higher risk for low birth weight. Overall incidence of low birth weight was 13.9%. The overall incidence of asphyxia of the newborn was 22.9% while that associated with low birth weight (i.e. babies weighing less than 2500 grams) was 29.3% compared with 21.5% among the normal birth weight babies. Low birth weight contributed a large proportion of the high neonatal mortality of 15.9% compared to 1.8% for normal birth weight babies by 24 hours after birth. The mean mortality by 24 hours post delivery was 3.8%. Obstetrical complications are important risk factors for asphyxia of the newborn. Among the important risk factors are those associated with prolonged labour and intra partum accidents. The incidence of risk for asphyxia broadly was 21.3%, which is very close to the actual incidence of asphyxia of 22%. Lack of referral contributed to increased risk of asphyxia. In a significant proportion of infants, resuscitation measures taken were inappropriate. The stillbirth rate was 3.0% while the incidence of externally evident congenital malformations was 1.2%. There is urgent need to institute appropriate measures to prevent and manage asphyxia of the newborn in the region. These should include identification of the at risk mother, proper referral and management while adhering to correct established procedures. There is also need to develop appropriate and relevant technologies for perinatal and neonatal care through research undertaken in the region. It is also concluded that the co-operation and joint effort between the obstetricians, paediatricians and the nursing staff who all contributed to the collection of this data is a cost effective approach to research in perinatal health and consequently in instituting interventions.

Adolescent↗
PubMed1996

[Perinatal asphyxia, hypoxic-ischemic encephalopathy and neurological sequelae in full-term newborns: an epidemiological study (1)].

INTRODUCTION: Perinatal asphyxia, and its neurologic manifestations (hypoxic-ischemic encephalopathy) is the most important cause of brain injury and neurologic sequelae in full-term infants. OBJECTIVE: The aim of this study was to know the incidence of perinatal asphyxia, hypoxic-ischemic encephalopathy and neurologic sequelae in our full-term infants. MATERIAL AND METHOD: Prospective epidemiologic study of perinatal asphyxia in full-term infants born in Universitary Hospital San Juan (Alicante, Spain) between November 1991-February 1995. Perinatal asphxyia was graded as non severe (1-minute Apgar score < or = 6 and/or umbilical artery pH < 7.20, with abnormal fetal heart rate patterns and/or meconiumstained amniotic fluid, and the need for immediate neonatal resuscitation) and severe (1-minute Apgar score < or = 3 and umbilical artery pH < 7.10). Hypoxic-ischemic encephalopathy was graded as mild, moderate and severe based on classification of Levene and Sarnat & Sarnat. Neurologic sequelae in 12-24 months follow-up was graded as mild, moderate and severe based on classification of Finer and Amiel-Tison. RESULTS: During the study period there were 3.342 full-term, live births. Perinatal asphyxia developed in 156 (31 severe and 125 non-severe), with an incidence of 4.66 cases per 100 full-term newborns. Neurologic manifestations was present in 25.6% of 156 term infants with perinatal asphyxia: 40 cases of hypoxic-ischemic encephalopathy (mild in 30, moderate in 5 and severe in 5). The incidence of hypoxic-ischemic encephalopathy was 1.19 cases per 100 full-term infants. The asphyctic newborns were regularly assessed. Ten infants was lost to follow-up. The incidence of neurologic sequelae, in 115 asphyxiated full-term infants follow-up at least 12-24 months, was 16.5%. CONCLUSIONS: Despite the widespread use of the term perinatal asphyxia, there is little uniformity on the clinical definition of asphyxia, which makes comparison of incidence, treatment and outcome very difficult. The main epidemiologic differences in the studies of perinatal asphyxia and hypoxic-ischemic encephalopathy are due to little agreement on their definition. A consensus is necessary.

Apgar Score↗
PubMedDate not supplied

[Delayed-onset dystonia due to asphyxia in the perinatal period].

The phenomenon of delayed-onset dystonia following presumed "static" brain injuries was described after stroke and head trauma. Burke et al. described a different category of secondary dystonia, where perinatal injury (asphyxia) caused minimal or no immediate neurological deficit, with the delay of years before dystonia emerged. This type of dystonia following perinatal injury has been termed "delayed onset dystonia due to static encephalopathy of childhood". According to the definition of dystonia, we were able to select 5 patients with the aetiologic diagnosis of perinatal asphyxia from the group of 347 out- and inpatients (1.4%) treated for various types of dystonia at the Movement Disorders Department (Institute of Neurology, CCS, Belgrade) from November 1986 to November 1994. At onset of dystonia the mean age of patients was 13.2 years (range from 10 to 17), with combined initial involvement of the arm and neck in 3 patients. The period from the onset of the disease to the maximum severity lasted 8.2 years (range from 4 to 14), resulting in segmental brachial dystonia in 3, hemidystonia and generalized dystonia in one patient each (Table 1). The adverse perinatal events are described in Table 2. Three of our patients had delayed achievements of developmental milestones. All patients were regularly schooled and had preserved intellectual capacities, except the patient 3 whose achievements were below average (IQ = 86). Different drugs were administered (Table 3), but moderate effects were achieved only with trihexyphenidyl in two patients (daily doses of 24 mg and 30 mg, respectively), and baclofen (80 mg p.d.) in one patient. In this study we describe 5 new patients who fulfilled the criteria for the diagnosis of delayed-onset dystonia due to perinatal asphyxia (Tables 1 and 2). We accepted the approach of Saint-Hilaire et al. to suggest a relationship between perinatal asphyxia and later occurrence of dystonia in our 5 patients. However, coincident occurrence of a primary dystonia with a static encephalopathy of childhood due to perinatal asphyxia cannot be excluded. This phenomenon of delayed appearance of dystonia was also described in other forms of static cerebral injury; i.e. stroke, head trauma or anoxic brain damage. Interestingly enough, age at the time of anoxia or brain insults seemed to be crucial for the development of dystonia: those who suffer acute brain insults during childhood or early life are more likely to develop dystonia than the older patients. Therefore, the "static" nature of encephalopathy induced by perinatal asphyxia is questionable. Finally, this study strengthens the suggestion that perinatal asphyxia can lead to delayed-onset dystonia, and, since "some of these patients closely resemble cases of idiopathic torsion dystonia, the prior occurrence of asphyxia should be used as a criterion of exclusion for that diagnosis".

Adolescent↗
PubMed2002

Dopamine for prevention of morbidity and mortality in term newborn infants with suspected perinatal asphyxia.

BACKGROUND: Perinatal asphyxia remains an important condition with significant mortality and long-term morbidity. Multisystem involvement including hypotension and low cardiac output is common in infants with perinatal asphyxia. Dopamine is commonly used for infants with hypotension of any etiology, with the goal of improving cardiac output and preventing its detrimental consequences. OBJECTIVES: To determine if dopamine, compared to placebo, no treatment, volume or another inotrope reduces morbidity and mortality in term newborn infants with suspected perinatal asphyxia. SEARCH STRATEGY: The standard search strategy of the Neonatal Review Group was used. Searches were conducted of the Oxford Database of Perinatal Trials, Cochrane Controlled Trials Register (The Cochrane Library, Issue 1, 2002), MEDLINE (1966 to March 2002), previous reviews including cross references, abstracts and conference proceedings (Perinatal Society of Australia and New Zealand 1998-2002 and Pediatric Academic Societies meetings 1998-2001). SELECTION CRITERIA: Randomised controlled trials comparing dopamine with placebo, no treatment, other inotropic agents, or volume in infants greater than 36 weeks gestation. Perinatal asphyxia could be suspected on the basis of a cord blood pH < 7.0, cord blood base excess < -16 mEq/L or 5 minute Apgar score < 6. DATA COLLECTION AND ANALYSIS: Standard methods of the Cochrane Neonatal Review Group with use of relative risk (RR), risk difference (RD) and weighted mean difference (WMD). The fixed effects model using RevMan 4.1 was used for meta-analysis. Data from individual studies were only eligible for inclusion if at least 75% of participants were followed up. MAIN RESULTS: Only one study (DiSessa 1981) was eligible. This study compared low dose dopamine at 2.5 mcg/kg/min with placebo (dextrose in water). This study enrolled 14 term infants with a 5 minute Apgar <6 and a systolic BP >=50 mmHg at a mean of 10 hours age. Seven infants only were randomised to treatment with dopamine and seven to receive placebo. No significant differences between these two groups were found for mortality or long term neurodevelopmental outcome. Length of hospitalisation was not significantly different between the two groups. No study was found that examined the effect of dopamine in infants with evidence of cardiovascular compromise, nor were any studies identified in which dopamine was compared to other inotropic agents for term infants with suspected asphyxia. REVIEWER'S CONCLUSIONS: There is currently insufficient evidence from randomised controlled trials that the use of dopamine in term infants with suspected perinatal asphyxia improves mortality or long-term neurodevelopmental outcome. The question of whether dopamine improves outcome for term infants with suspected perinatal asphyxia has not been answered. Further research is required to determine whether or not the use of dopamine improves mortality and long-term morbidity for these infants and if so, issues such as which infants, at what dose and with what co-interventions should be addressed.

Asphyxia Neonatorum↗
PubMed2007

Nicotinamide prevents the effect of perinatal asphyxia on dopamine release evaluated with in vivo microdialysis 3 months after birth.

The present study shows that nicotinamide prevents the long-term effect of perinatal asphyxia on dopamine release monitored with in vivo microdialysis in the neostriatum of 3-month-old rats. Perinatal asphyxia was induced by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 16 or 20 min. Sibling, spontaneous, and caesarean-delivered pups were used as controls. Saline or nicotinamide (0.8 mmol/kg, i.p.) was administered to control and asphyxia-exposed animals 24, 48, and 72 h after birth. After weaning, the rats were randomly distributed in laboratory cages for animal care under standard ad libitum laboratory conditions. Approximately 3 months after birth, control and asphyxia-exposed animals were implanted with microdialysis probes into the lateral neostriatum for measuring extracellular monoamine and metabolite levels with HPLC-coupled to an electrochemical detection system under basal, D-amphetamine, and K(+)-depolarising conditions. There was an asphyxia-dependent decrease of extracellular dopamine levels, mainly observed during the periods when D-amphetamine (100 microM) or KCl (100 mM) was added into the perfusion medium. Compared to that observed in caesarean-delivered controls, the effect of D-amphetamine on dopamine levels was decreased by approximately 30 and 70% in animals exposed to 16 and 20 min of perinatal asphyxia, respectively. The effect of K(+)-depolarisation was decreased by 45 and 83% in animals exposed to the same periods of asphyxia, respectively. Both effects were prevented by nicotinamide, even if the treatment started 24 h after the insult. The present results support the idea of nicotinamide as an interesting molecule, useful for protecting against anoxia/ischemia occurring at neonatal stages. Nicotinamide can help to restore NADH/NAD+ depletion, but also to inhibit PARP-1 overactivation, a mechanism of action that has attracted attention, representing a novel target for neuroprotection following insults involving energy failure.

Amphetamine↗
PubMed1995

Short-term effects of perinatal asphyxia studied with Fos-immunocytochemistry and in vivo microdialysis in the rat.

In the present study, the short-term consequences of various perinatal asphyctic periods were studied at the peripheral and CNS levels in the rat. Perinatal asphyxia was induced in rat pups delivered by caesarean section within the last day of gestation, by placing the uterus horns including the fetuses in a water bath at 37 degrees C for various periods of time (0-23 min). Following asphyxia, the uterus horns were opened. The pups were then removed and stimulated to breathe. Subcutaneous levels of pyruvate (Pyr), lactate (Lact), glutamate (Glu), and aspartate (Asp) were monitored with microdialysis 40 min after delivery. In parallel experiments, the pups were sacrificed 80 min after delivery. The brains were removed, fixed, cut, and processed for Fos immunocytochemistry. The number of Fos-immunoreactive (IR) cells in different brain structures was counted under light microscopy. Subcutaneous levels of Pyr, Lact, Glu, and Asp increased following perinatal asphyxia, as compared to caesarean-delivered pups or to spontaneously delivered controls. A maximum increase in Pyr levels (approximately threefold) was observed with 2-3 min of asphyxia, while Lact levels increased along with the length of asphyxia. A maximum increase in Glu and Asp levels (approximately threefold) was observed with 10-11 min of asphyxia. Fos-IR nuclei were predominantly found in the piriform cortex, and in the cortical amygdaloid complex. In some cases, mainly in pups exposed to asphyxia, Fos-positive cells were also seen in other tele-diencephalic structures.

Amino Acids↗
PubMed1996

Long-term effect of perinatal and postnatal asphyxia on developing human auditory brainstem responses: brainstem impairment.

Long-term effect of perinatal and postnatal asphyxia on the developing auditory brainstem was investigated in children, particularly those who exhibited residual neurodevelopmental deficits, by analyzing the central components of brainstem auditory evoked responses (BAER). The major abnormalities in the BAER were a reduction of wave V amplitude, followed by a decrease in V/I amplitude ratio, while abnormalities in interpeak intervals were relatively rare. These findings suggest that asphyxia could result in residual neural dysfunction of the brainstem but does not appear to exert any major long-term effect on neuronal transmission. BAER abnormalities occurred more frequently in the children with residual neurodevelopmental deficits than those without these deficits after perinatal asphyxia. The occurrence of BAER abnormalities was related to the duration as well as the degree of asphyxia. No significant difference was found in the abnormalities of the central BAER components between the children after perinatal asphyxia and those after postnatal asphyxia, suggesting that perinatal and postnatal asphyxia exerts a similar long-term effect on the developing central nervous system.

Asphyxia Neonatorum↗
PubMed2005

The pathological features and circumstances of death of lethal crush/traumatic asphyxia in adults--a 25-year study.

A 25-year retrospective study of cases of crush/traumatic asphyxia autopsied at Forensic Science SA, Adelaide, Australia from 1980 to 2004 was undertaken. A total of 79 cases of crush asphyxia was found consisting of 63 males (80%) and 16 females (20%). The age range of the males was 19-86 years (mean=41.8 years) and of the females was 19-75 years (mean=38.6 years). In 18 cases the exact circumstances of death were unclear, leaving 61 cases in which details of the fatal episode were available. Major categories included vehicle crashes (N=37), industrial accidents (N=9), farm accidents (N=6) and entrapment beneath vehicles (N=5). Forty of the 79 victims (51%) had only very minor bruises and abrasions; 28 (35%) had evidence of chest compression with rib and sternal fractures and large areas of soft tissue bruising of the chest; 7 cases (9%) had other significant injuries or findings that had contributed to death. All of these victims had signs of crush asphyxia in the form of intense purple congestion and swelling of the face and neck, and/or petechial hemorrhages of the skin of the face and/or conjunctivae. The pattern of pathological findings of crush asphyxia was not influenced by the presence or absence of concomitant serious or lethal injuries. In 4 cases (5%) where the circumstances of the lethal episode were those of crush asphyxia there were no characteristic pathological findings. This study has shown that a high percentage of crush asphyxias may be caused by vehicle accidents. It has also demonstrated that on occasion fatal crush asphyxia may have to be a diagnosis of exclusion, made only when there are characteristic death scene findings, and no evidence of lethal natural diseases or injuries at autopsy, with negative toxicological screening.

Adult↗
PubMed1998

Physiologic and histologic changes in near-term fetal lambs exposed to asphyxia by partial umbilical cord occlusion.

OBJECTIVES: Our purpose was to characterize the histologic changes in the asphyxiated fetal lamb brain and to correlate the severity of these changes with fetal physiologic parameters during and after asphyxia. STUDY DESIGN: Seventeen near-term fetuses were used for analysis: control group without manipulation (n = 4, 132 +/- 1.1 days of gestation at autopsy, mean +/- SEM), sham-asphyxia control group (n = 3, 132 +/- 1.3 days), and asphyxiated group, which successfully survived 72 hours after asphyxia (n = 10, 130 +/- 1.0 days). Asphyxia was produced by umbilical cord occlusion lasting for approximately 60 minutes until fetal arterial pH diminished to < 6.9 and base excess to < -20 mEq/L. Fetal heart rate, blood pressure, and electrocorticographic activity were continuously monitored. The fetuses were killed 72 hours after asphyxia, and the brains were fixed in formalin and processed for histologic and immunocytochemical studies. RESULTS: Neuropathologic changes varied from case to case, ranging from almost total infarction of cortical and subcortical structures to extremely subtle and patchy white matter alterations characterized by slight vacuolization of the white matter or slight to moderate increases in cellularity confined to the junction of cerebral cortex and white matter. Even fetuses that showed full recovery of all physiologic parameters, including electrocorticographic activity, demonstrated subtle but distinct white matter lesions. The gray matter, including the hippocampal neurons, was generally spared in these cases. Electrocorticographic parameters, duration of hypotension during asphyxia, and delayed recovery of blood lactate concentrations correlated well with the histologic grading of brain damage. CONCLUSIONS: Asphyxia by partial umbilical cord occlusion in near-term fetal lambs produces variable neuropathologic changes. The mildest change is a white matter lesion characterized by vacuolization and loss of myelin or by increased cellularity in the damaged regions.

Animals↗
PubMed2000

In vivo electrical activity of brainstem neurons in fetal rats during asphyxia.

To see changes in the activity and the sensitivity to glutamate of fetal brain neurons during asphyxia, the electrical activity of brainstem neurons was recorded extracellularly in fetal rats which were still connected with the dams by the intact umbilical cord. In urethan-anesthetized pregnant rats, fetal asphyxia (2-10 min) was induced by occluding the umbilical cord with a surgical clip, while reperfusion of the umbilical blood flow was performed by local application of a relaxant of blood vessels to the occlusion site. The spontaneous discharge of fetal brainstem neurons was suppressed for a long period of time by umbilical cord occlusion. The suppression of the firing occurred 48-150 (78+/-7) s after the start of umbilical cord occlusion, and lasted even after fetal cortical PO(2) recovered to control level after reperfusion. The changes occurred with a marked reduction in spike amplitude. A similar suppression was observed for the spikes induced by iontophoretic application of glutamate, although fetal brainstem neurons were extremely sensitive to glutamate before asphyxia. The suppression of the spontaneous spikes became more notable and longer when asphyxia was repeated. These findings suggest that the long-lasting suppression of fetal neurons during asphyxia may contribute to a reduction of cellular energy requirements in the fetal brain, thereby playing a role in the resistance of fetal neurons to brain damage caused by asphyxia. Furthermore, the reduced sensitivity of fetal neurons to glutamate during asphyxia may also contribute to prevent brain damage due to excitotoxity of glutamate.

Action Potentials↗
PubMed2000

C-fos gene expression in rat brain around birth: effect of asphyxia and catecholamines.

At birth, the mammalian nervous system must adapt rapidly to the new conditions it encounters in the extra-uterine environment. One aspect of this adaptation, known as arousal, is mediated by catecholamines, the levels of which in the brain increase rapidly after birth. The pattern of gene expression also changes. Shortly after birth, expression of the immediate early gene c-fos, known to reflect general neural activity, is up-regulated. Furthermore, asphyxia often occurs in connection with birth. In order to examine the effects of this phenomenon on the expression of c-fos, as well as on the rate of noradrenaline (NA) turnover, asphyxia was induced in rat pups delivered by caesarean section. Northern blot analysis and in situ hybridization revealed that the increase in expression of c-fos in certain areas of the brain was greatly enhanced by asphyxia of moderate duration; whereas more prolonged asphyxia lowered the level of c-fos mRNA. Asphyxia had a similar effect on the rate of NA turnover. Adrenergic receptor antagonists administered prior to birth attenuated the birth-related induction of c-fos mRNA. However, the potentiation of c-fos expression by asphyxia was not altered by these antagonists. Therefore, we propose that while catecholamines play an important role in the induction of c-fos in the brain at birth, the effects of asphyxia involve a different mechanism.

Adrenergic Antagonists↗