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PubMed1996

Maternal factors contributing to asphyxia neonatorum.

The objective was to identify maternal risk factors for birth asphyxia, and took the form of a retrospective study over 3 years of 15,964 deliveries. The antenatal and intrapartum course of 68 mothers who delivered babies with birth asphyxia was studied. Babies < 34 weeks/< or = 2000 g at birth were excluded. A 5-min Apgar score < 6 was regarded as abnormal. The incidence of asphyxia neonatorum was 4.6/1000. Most mothers (76 per cent), resided locally, booked (91 per cent), and had satisfactory antenatal clinic attendance (average seven visits). The distribution showed a disproportionately large number of grand multiparas (10 per cent). Labour was characterized by prolonged first (49 per cent) and second (36 per cent) stages with a high incidence of meconium in the amniotic fluid (47 per cent). Most deliveries (53 per cent) were by caesarian section of which 44 per cent were performed for fetal distress. Meconium aspiration was common (34 per cent). High risk signs in labour can be recognized. The judicious use of the partogram, fetal scalp blood pH, and amino-infusion are encouraged.

Asphyxia Neonatorum↗
PubMed1997

Decrease of heart protein kinase C and cyclin-dependent kinase precedes death in perinatal asphyxia of the rat.

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 phosphorylation by protein kinase C (PKC) represents another mechanism incriminated for cell death. We used an unsophisticated perinatal asphyxia model to study heart protein kinases PKC and cyclin dependent kinase (CDK). Tissue pH, ATP, the antioxidant enzymes superoxide dismutase, catalase, and glutathion peroxidase, lipid peroxidation products, carbonyls, and aromatic hydroxylation were also tested. Electron spin resonance was applied to demonstrate the possible presence of radical adducts. An ELISA method was used to determine cell death. PKC activity and mRNA decreased with the length of the asphyctic periods and were paralleled by CDK and pH, whereas cell death gradually increased. No evidence was found for the involvement of active oxygen species or a radical adduct, and no energy depletion was observed. We conclude that impaired protein phosphorylation and/or acidosis may play a role in the pathobiochemistry of death from perinatal asphyxia in the rat.

Animals↗
PubMed1994

Autoerotic asphyxia: the development of a paraphilia.

The authors studied five adolescent male practitioners of autoerotic asphyxia to determine contributors to its etiology. Extensive histories including detailed sexual histories were obtained from each boy. Their life histories suggested an early history of choking, in combination with physical or sexual abuse, was related to the development of autoerotic asphyxia. Each boy appeared to have paired choking with sexual arousal, and autoerotic asphyxia was a persisting behavior pattern for four of five boys. This sample is the largest study of living practitioners of this behavior and suggests the heretofore unmentioned history of either choking or abuse.

Adolescent↗
PubMed1985

Long-term followup after traumatic asphyxia.

Victims of traumatic asphyxia syndrome were studied to determine: mechanism of injury, severity of injury, characteristic physical stigmata, treatment, and long-term disability. Consecutive patients who sustained severe crush injuries with traumatic asphyxia in the 5-year period ending November 1984 were reviewed. Followup was established by personal examination or questionnaire. Severity of injury and disability were assessed by Injury Severity Score and questionnaire, respectively. Six patients, ranging in age from 4 to 65 years, were hospitalized from 4 to 150 days for traumatic asphyxia. The mechanism of injury in each case was severe crush by an object weighing greater than 1,000 pounds. All patients had associated injuries, often involving the thorax, and the mean Injury Severity Score was 14.5. Severe craniocervical cyanosis with petechiae was present in all patients. Four patients had temporary neurologic impairment. Despite severity of injury, no long-term disability was detected at an average followup of 4.4 years. No long-term survivors demonstrated residual cyanosis, petechiae, swelling, or neurologic sequelae. All had returned to work or school.

Adolescent↗
PubMed1988

Visual loss following traumatic asphyxia in children.

Two young children suffered loss of vision in separate incidents following traumatic asphyxia. Visual loss secondary to trauma can occur from a variety of causes. This is apparently the first description of traumatic asphyxia causing visual loss in children. In children, visual impairment is easily missed unless the degree of handicap is severe. All children should have their fundi and visual acuity assessed before discharge following significant trauma, including all episodes of traumatic asphyxia.

Asphyxia↗
PubMed1991

Cardiac injury complicating traumatic asphyxia.

During a 3-year period (1986-1989), 8 patients were seen at St. Louis University Medical Center exhibiting the stigmata of traumatic asphyxia. Fewer than 200 cases of traumatic asphyxia have been reported and there is only a single report of a cardiac injury. In this series, 3 of 8 (37.5%) patients were found to have an injury to the heart: two cardiac contusions and a ventricular rupture. Five patients were crushed in motor vehicle collisions, one by an elevator counterweight, and two patients by river barges. Injuries associated with these patients include pulmonary contusion, hemopneumothorax, traumatic pneumatocele, traumatic retinopathy, bone fractures, mental confusion, and liver contusion. There was one death in the series, a patient with rupture of the right ventricle and severe splenic and liver injuries. The cardiac status of the patients was evaluated by serial serum cardiac enzyme determinations, electrocardiograms, and echocardiography. This report illustrates the importance of complete cardiac evaluation in patients with traumatic asphyxia.

Accidents, Occupational↗
PubMed1995

Benign cervical prevertebral soft tissue swelling in traumatic asphyxia.

Two cases of benign cervical prevertebral soft tissue swelling following traumatic asphyxia are presented. Neither were associated with neck pain, neck tenderness, or mechanism of injury associated with cervical injury, and each resolved spontaneously. Traumatic asphyxia, which results in significant craniofacial swelling, may also result in swelling of the retropharyngeal soft tissues, which may be detected on cervical radiography. Cervical prevertebral soft tissue swelling in the setting of traumatic asphyxia should not be misinterpreted as suggestive of spinal injury in the absence of other findings.

Adult↗
PubMed1995

Somatosensory evoked potentials predict neurologic outcome in full-term neonates with asphyxia.

OBJECTIVE: To investigate the ability of somatosensory evoked potentials (SSEP) to predict neurologic outcome in term neonates with birth asphyxia. METHODOLOGY: Upper limb SSEP were performed on nine infants of 1-7 weeks of age who had perinatal asphyxia and an encephalopathy still present at 7 days of age. Comparison was made between the cranial ultrasound, electroencephalogram (EEG), SSEP and neurologic outcome at 9-36 months. RESULTS: Normal SSEP were found in four infants, all of whom were normal on neurologic follow up at 9-12 months. Neonatal EEG performed on two out of four of these infants were also normal, while cerebral oedema was seen on cranial ultrasound in three of the four studies. No SSEP response was seen initially in three infants, all of whom had adverse outcomes (one death, two with spastic diplegia). In contrast, their neonatal EEG had shown normal background rhythms, while two of the three cranial ultrasounds revealed oedema. For two infants the initial SSEP was absent over one hemisphere and just present over the other. Both children were abnormal on follow up at 10-12 months but did not have a hemiparesis. CONCLUSIONS: Upper limb SSEP appear more sensitive than EEG or cranial ultrasounds in predicting the short term neurologic outcome of neonates with asphyxia.

Asphyxia Neonatorum↗
PubMed2006

Neurodevelopmental outcome of infants with birth asphyxia treated with magnesium sulfate.

BACKGROUND: A neuroprotective effect of MgSO(4) has been shown in some animal models of perinatal hypoxic-ischemic brain damage. The aim of the present paper was to determine whether postnatal MgSO(4) infusion (250 mg/kg per day i.v. for 3 days, in combination with dopamine) is safe in infants with severe birth asphyxia, and also observe effects on neurodevelopmental outcome at 18 months. METHODS: Inclusion criteria were clinical history consistent with perinatal asphyxia; gestational age at least 37 weeks; 5 min Apgar score < or =6; failure to initiate spontaneous respiration within 10 min after birth; and symptoms of encephalopathy. On each day MgSO(4) was infused over 1 h in combination with dopamine (5 microg/kg per min). Changes in vital signs, clinical course of encephalopathy, laboratory variables, and adverse events were monitored. Infants were followed for 18 months. RESULTS: Thirty infants were studied. Mean birthweight was 2878 g; mean gestational age, 39.6 weeks, and median 5 min Apgar score, 3. All required endotracheal intubation for resuscitation. Median age at MgSO(4) initiation was 5 h. All infants had moderate or severe hypoxic-ischemic encephalopathy. Mean serum Mg(2+) concentration remained at least 1.3 mmol/L. MgSO(4) caused no change in physiological variables including mean arterial pressure. Two infants died as neonates, while six of 28 survivors had severe neurodevelopmental disability at 18 months; the remaining 22 had no neurodevelopmental disability. CONCLUSION: Postnatal infusion of MgSO(4) with dopamine caused no change in physiological variables. Deaths and severe sequelae were less frequent than in reported cases with the same grade of hypoxic-ischemic encephalopathy severity, and this treatment may improve neurodevelopmental outcome in infants with severe birth asphyxia.

Asphyxia Neonatorum↗
PubMed2006

Brain and cognitive-behavioural development after asphyxia at term birth.

Perinatal asphyxia occurs in approximately 1-6 per 1000 live full-term births. Different patterns of brain damage can result, though the relation of these patterns to long-term cognitive-behavioural outcome remains under investigation. The hippocampus is one brain region that can be damaged (typically not in isolation), and this site of damage has been implicated in two different long-term outcomes, cognitive memory impairment and the psychiatric disorder schizophrenia. Factors in addition to the acute episode of asphyxia likely contribute to these specific outcomes, making prediction difficult. Future studies that better document long-term cognitive-behavioural outcome, quantitatively identify patterns of brain injury over development and consider additional variables that may modulate the impact of asphyxia on cognitive and behavioural function will forward the goals of predicting long-term outcome and understanding the mechanisms by which it unfolds.

Asphyxia Neonatorum↗
PubMed1977

Clinical application of evoked electroencephalographic responses in newborn infants. I: Perinatal asphyxia.

Evoked electroencephalographic responses are useful for the study of cerebral maturation in full-term and pre-term newborn infants. In an attempt to achieve wider clinical application, 57 newborn infants with differing degrees of perinatal asphyxia were examined. Altogether 154 examinations were performed. In all of them photostimulation was used, and in 72 investigations somatosensory evoked responses were also recorded. The following results were obtained: (1) Visual evoked responses were affected in 85 per cent of the cases. Somatosensory evoked responses were affected less often - in 65 per cent of the newborn babies examined. The incidence and degree of deviations were related to the degree of asphyxia. (2) The most characteristic features of the evoked responses in asphyxiated infants were abnormal response patterns, increase of latency and poor photic driving. (3) On the basis of all alterations observed, a scoring system was developed which enabled quantitative evaluation. The evoked response risk-score correlated well with the degree of asphyxia. (4) Repeated observations were important: a permanently high risk-score at repeated investigations was a serious prognostic sign.

Asphyxia Neonatorum↗
PubMed1997

Intrapartum fetal asphyxia and the occurrence of minor deficits in 4- to 8-year-old children.

Term newborn infants, 48 of whom had mild intrapartum fetal asphyxia, and 43 controls were assessed between 4 and 8 years of age for evidence of selective brain damage and minor deficits. Measures of motor and cognitive development were obtained at 4 and at 6 to 8 years of age. Memory tests, including the Alternation Test and determinations of Extended Digit Span, Spatial Memory, and Paired Associate Learning, were given annually between 4 and 8 years of age. Assessments of the family, child health, and child behaviour were obtained. There were no differences between the asphyxia and control groups for motor or cognitive development or the serial tests of memory. The two groups did not differ in regard to family characteristics, child health, or child behaviour. These findings indicate that term newborn infants exposed to mild intrapartum fetal asphyxia do not have minor motor and cognitive deficits later in childhood.

Acidosis↗
PubMed1994

Clustering of perinatal markers of birth asphyxia and outcome at age five years.

OBJECTIVES: In a cohort of term infants with cerebral depression at delivery, to investigate the association of perinatal signs of birth asphyxia, particularly abnormal fetal heart rate patterns in labour, acidaemia, and serious neonatal encephalopathy, with neurodevelopmental outcome at age five years. DESIGN: Five year follow up study of a birth cohort. SETTING: Regional maternity hospital. SUBJECTS: One hundred and eighty-four singleton infants with a 1 min Apgar score < or = 3, born at term between January 1984 and September 1985. MAIN OUTCOME MEASURES: Neonatal death, cerebral palsy, and scores on a battery of neurodevelopmental tests at age five. RESULTS: Seven infants had a cluster of perinatal signs suggestive of birth asphyxia; all included serious neonatal encephalopathy. Three of these infants died neonatally, three had spastic quadriparesis with profound developmental delay, and one was unimpaired at the age of five. Among the remaining infants, no association was found between severely abnormal fetal heart rate patterns in labour and scores on neurodevelopmental tests, or between acid-base status at delivery and test scores. CONCLUSIONS: Birth asphyxia, identified by a cluster of abnormal perinatal signs, including serious neonatal encephalopathy, has a poor prognosis. If serious encephalopathy is not present, cerebral depression at birth preceded by abnormal fetal heart rate patterns in labour, or with acid-base derangement, is not predictive of later impairment.

Acid-Base Imbalance↗
PubMed1976

The effects of asphyxia on 5-hydroxytryptamine metabolism in the immature rat brain.

Five-day-old rats subjected to prolonged asphyxia at 37 degrees C show a slower rate of synthesis of 5-HT as measured by the accumulation of the amine after inhibition of monoamine oxidase. During recovery from asphyxia 5-HT synthesis is markedly stimulated when measured over a 50 or 90 min period. No change in 5-HT synthesis was observed in 5-day-old rats during recovery from cold exposure or immobilization. The results indicate that the persistent increase in synthesis that follows resuscitation may be related to asphyxia per se rather than to the stress component of the treatment.

Animals↗
PubMed1976

Effective pulmonary capillary blood flow in infants with birth asphyxia.

Effective pulmonary capillary blood flow was measured on the first day of life in twenty term infants with birth asphyxia and twenty-five normal term infants. The infants studied showed no clinical or laboratory evidence of respiratory distress. The mean effective pulmonary capillary blood flow of 121 ml/kg/min in the birth asphyxia group was significantly lower than the mean of 162 ml/kg/min in the normal group. The possible relationship of birth asphyxia and pulmonary hypoperfusion in the aetiology of the idiopathic respiratory distress syndrome is discussed.

Asphyxia Neonatorum↗
PubMed2005

Cortisol and ACTH responses to severe asphyxia in preterm fetal sheep.

It has been hypothesized that the hypothalamic-pituitary-adrenal (HPA) axis is immature in the preterm fetus and that this compromises their ability to adapt to hypoxic stress; however, there are few direct data. We therefore examined the effects of asphyxia on HPA responses in chronically instrumented preterm fetal sheep (104 days of gestation; term is 147 days), allocated to a sham control group (n = 7) or 25 min of complete umbilical cord occlusion (n = 8), followed by recovery for 72 h. During umbilical cord occlusion there was a rapid rise in ACTH levels (230.4 +/- 63.5 versus 14.1 +/- 1.8 ng ml(-1) in sham controls, 16-fold) and cortisol levels (7.4 +/- 4.9 versus 0.2 +/- 0.1 ng ml(-1), 31-fold), with further increases after release of cord occlusion. ACTH levels were normalized by 24 h, while plasma cortisol levels returned to sham control values 72 h after asphyxia. Fetal arterial blood pressure was elevated in the first 36 h, with a marked increase in femoral vascular resistance, and correlated positively with cortisol levels after asphyxia (P = 0.05). In conclusion, the preterm fetus shows a brisk, substantial HPA response to severe hypoxia.

Adrenocorticotropic Hormone↗
PubMed1970

Effect of asphyxia due to umbilical cord occlusion in the foetal lamb on leakage of liquid from the circulation and on permeability of lung capillaries to albumin.

1. Experiments were performed on foetal lambs, exteriorized at Caesarean section, to determine the effects of asphyxia on the leakage of liquid from the circulation and on the permeability of lung capillaries to albumin. Following a period of control observation (30-120 min) the foetus was asphyxiated by occlusion of the umbilical cord for 5-10 min and then allowed to recover while observations were continued for a further 20-80 min.2. Measurements were made of the lymph flow from the lungs, that had drained via the thoracic duct; of protein concentration in lymph and plasma; of arterial blood haematocrit, pH, P(O2) and P(CO2); and of arterial and left atrial pressures and heart rate. Human serum albumin labelled with (125)I was infused intravenously during the control period and (125)I count rates were followed in plasma and lymph throughout the experiment. Values for the transfer coefficient of albumin (E/V min(-1), i.e. interstitial fluid clearance of albumin per unit of lung interstitial fluid volume) were determined during control, cord-occlusion and post-occlusion periods.3. During cord occlusion arterial and left atrial pressure, haematocrit and plasma protein concentration all rose, returning to the control value by 20 min after release of cord occlusion. The haematocrit values indicated that about 9% of the blood volume was temporarily lost from the circulation. Lung lymph flow also increased, reaching a maximum in the 5 min period after release of occlusion and returning to the control level 15 min later. Values for E/V of albumin were at no time significantly different from those during the control period.4. It was concluded that acute foetal asphyxia produced by umbilical cord occlusion caused an increased leakage of liquid from the circulation in general. This effect was temporary and was probably due to an increase in capillary pressure during cord occlusion. The asphyxia had no persistent effect on the permeability of lung capillaries to albumin.

Albumins↗
PubMed1976

Outcome of very severe birth asphyxia.

The aim of this study was to establish the outcome of very severe birth asphyxia in a group of babies intensively resuscitated at birth. 48 infants, born between 1966 and 1971 inclusive, were selected; 15 were apparently stillborn and 33 had not established spontaneous respirations by 20 minutes after birth. One-half of them died, but 3 to 7 years later three-quarters of the survivors are apparently normal. Later handicap was associated with factors leading to prolonged partial intrapartum asphyxia, while acute periods of more complete asphyxia were not necessarily harmful.

Asphyxia Neonatorum↗