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PubMed2005

ACOG Committee Opinion. Number 326, December 2005. Inappropriate use of the terms fetal distress and birth asphyxia.

The Committee on Obstetric Practice is concerned about the continued use of the term "fetal distress" as an antepartum or intrapartum diagnosis and the term "birth asphyxia" as a neonatal diagnosis. The Committee reaffirms that the term fetal distress is imprecise and nonspecific. The communication between clinicians caring for the woman and those caring for her neonate is best served by replacing the term fetal distress with "nonreassuring fetal status," followed by a further description of findings (eg, repetitive variable decelerations, fetal tachycardia or bradycardia, late decelerations, or low biophysical profile). Also, the term birth asphyxia is a nonspecific diagnosis and should not be used.

Asphyxia Neonatorum↗
PubMed1982

Effect of asphyxia on theophylline clearance in newborns.

The effect of asphyxia on theophylline clearance was studied in 30 newborns who were matched for gestational age, postnatal age, and the presence or absence of asphyxia. Asphyxiated newborns cleared theophylline at approximately half the rate of nonasphyxiated newborns. We found that, in order to achieve a steady-state plasma concentration of 8 mg/L of theophylline, asphyxiated neonates should receive 2.1 mg/kg/day, while nonasphyxiated neonates should receive 3.9 mg/kg/day.

Asphyxia Neonatorum↗
PubMed1997

Prediction of outcome after perinatal asphyxia.

Perinatal asphyxia at term remains a significant cause of infant death and neurodevelopmental impairment, probably causing 20% of all cases of cerebral palsy. This review examines indicators that can help determine the prognosis after suspected asphyxia in term infants, including obstetric information, clinical examination, and diagnostic methods based on neurophysiology, neuroimaging, and biochemistry. New data confirm that many frequently used indicators are generally not specific predictors, while simple electroencephalographic methods, magnetic resonance spectroscopy, and magnetic resonance imaging can have high positive predictive values even when used quite soon after birth.

Asphyxia Neonatorum↗
PubMed1998

Recent advances in developing neuroprotective strategies for perinatal asphyxia.

Perinatal asphyxia is the most important cause of acute neurologic injury in the newborn and occurs in approximately six per 1000 term live births. After resuscitation of an infant with birth asphyxia, the emphasis has been on supportive therapy; however, there is increasing evidence that a "therapeutic window" exists in the early hours following the insult, and perhaps for longer, when intervention can attenuate activation of the neurotoxic cascade that leads to delayed cell death hours, days or months later.

Asphyxia Neonatorum↗
PubMed2002

Cochleosaccular pathology after perinatal and postnatal asphyxia: histopathologic findings.

OBJECTIVE: This study describes the histopathologic findings of a patient with severe bilateral sensorineural hearing loss after perinatal and postnatal hypoxia and asphyxia. STUDY DESIGN: Histopathologic examination on the temporal bones. SETTING: The study was performed at the Elizabeth McCullough Knowles Otopathology Laboratory, Division of Otopathology, Department of Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. RESULTS: Histopathologic examination on the left temporal bone revealed severe atrophy of the organ of Corti throughout the entire cochlea, decrease in the number of the spiral ganglion cells especially in the basal turn, and mild atrophy of saccular macula. In the right temporal bone, similar abnormalities were observed in the inner ear, but the changes were milder than those in the left temporal bone. No other distinct pathologic finding was observed in either ear. CONCLUSION: These findings suggest that the presence of severe hypoxic ischemia causes cochleosaccular atrophy. To our knowledge, this is the first histopathologic case report describing the long-term effect of perinatal and postnatal hypoxia and asphyxia that produced cochleosaccular abnormalities in the human inner ear.

Asphyxia Neonatorum↗
PubMed2005

Sudden death due to asphyxia by esophageal polyp: two case reports and review of asphyxial deaths.

Asphyxia, not an uncommon cause of sudden death, may result from numerous etiologies. Foreign-body aspiration and strangulation are 2 extrinsic causes. Airway obstruction may also be caused by laryngeal edema, asthma, infection, or anaphylaxis. Chronic causes of asphyxia include musculoskeletal diseases (eg, muscular dystrophy, amyotrophic lateral sclerosis), neurologic disorders (eg, myasthenia gravis, multiple sclerosis), respiratory disease (eg, emphysema, chronic bronchitis), or tumors. The manner of death in cases of asphyxiation may be natural, accidental, homicide, or suicide. For the death investigator, determining the cause and manner of death can often be quite challenging. We report here 2 cases of an esophageal fibrovascular polyp causing sudden asphyxial death, review of the literature, and discussion of other differential diagnoses in the case of asphyxial death.

Adult↗
PubMed1977

Regional vascular responses to asphyxia in the rabbit.

Organ blood flow was measured in eight spontaneously breathing male New Zealand white rabbits exposed to a 50 min period of asphyxia. The results were compared with eight control animals. Cardiac output and arterial pressure did not change. There was increased flow to the heart, brain and diaphragm. Flow to the kidneys and adipose tissue was reduced. Flow to the gastro-intestinal tract, liver, skeletal muscle and carcass was unchanged. Prolonged moderate asphyxia produces preferential blood supply to vital organs and maintains flow to the skeletal musculature and the gastro-intestinal tract; their blood supply is diverted mainly from the kidneys. These changes are similar to those seen in haemorrhagic and endotoxic shock in the rabbit.

Animals↗
PubMed2006

Naloxone and epinephrine are equally effective for cardiopulmonary resuscitation in a rat asphyxia model.

BACKGROUND: It is not known whether naloxone is as efficacious as epinephrine during cardiopulmonary resuscitation (CPR). The aim of the study was to compare the effects of naloxone and epinephrine on the outcomes of CPR following asphyxial cardiac arrest in rats. METHODS: Cardiac arrest was induced with asphyxia by clamping the tracheal tubes. Twenty-four Sprague-Dawley rats were randomized prospectively into a saline group (treated with normal saline, 1 ml intravenously, n = 8), an epinephrine group (treated with epinephrine, 0.04 mg/kg intravenously, n = 8) or a naloxone group (treated with naloxone, 1 mg/kg intravenously, n = 8) in a blind fashion during resuscitation after asphyxial cardiac arrest. After 5 min of untreated cardiac arrest, conventional manual CPR was started and each drug was administered at the same time. RESULTS: The rates of restoration of spontaneous circulation (ROSC) were one of eight (12.5%), seven of eight (87.5%) and seven of eight (87.5%) in the saline, epinephrine and naloxone groups, respectively. The rates of ROSC in the epinephrine and naloxone groups were equal and significantly greater than that in the saline group (P = 0.01 and P = 0.01, respectively). CONCLUSION: The administration of naloxone or epinephrine alone may increase the resuscitation rate, and both drugs are equally effective for CPR in a rat asphyxia model. However, the mechanism by which naloxone produces its efficacy during CPR remains unclear and further experimentation will be necessary.

Animals↗
PubMed1991

Birth asphyxia associated oliguria: relationship to outcome at 1 year.

The relationship between the degree of oliguria following severe birth asphyxia and outcome at 12 months was examined in 31 infants. All 31 infants developed encephalopathy following severe birth asphyxia and 25 had oliguria for 24 h or more following delivery. Eighteen had persistent oliguria (i.e. greater than 48 h) and the remaining seven had transient oliguria (between 24 and 48 h). Poor outcome (death or neurological abnormality at 12 months) was significantly associated with the degree of oliguria. Encephalopathy, however, was found to be more closely correlated with poor outcome rather than duration of oliguria and a stepwise regression model confirmed that encephalopathy was the more powerful predictor of poor outcome. In those situations where an infant's degree of encephalopathy can not be assessed accurately (e.g. muscle relaxant use) the duration of oliguria may prove a useful prognostic indicator.

Asphyxia Neonatorum↗
PubMed1992

Perinatal features of birth asphyxia and neurologic outcome.

The perinatal events of 40 term newborn infants who had severe birth asphyxia were reviewed and correlated with the neurological outcome at a mean age of 2 1/2 years. Severe birth asphyxia was defined as an Apgar Score of less than or equal to 3 at 1 min. The majority (68.5%) of the babies had an abnormal fetal heart pattern before delivery. Persistent fetal bradycardia was most frequently associated with poor outcome. The neurological staging, the need for assisted ventilation for more than 24 hours and severe renal impairment were the best predictors of neonatal death or subsequent poor neurological outcome. The overall mortality was 10% and 15% of the surviving babies had varying degrees of neurological handicap.

Apgar Score↗
PubMed1980

Cerebrospinal fluid lactate dehydrogenase in infants with perinatal asphyxia.

Cerebrospinal fluid (CSF) lactate dehydrogenase was determined in 19 control infants without asphyxia (Group I), 24 infants with perinatal asphyxia (Group II), and 26 asphyxiated infants with seizures (Group III). Mean birthweights, gestational ages, CSF glucose, protein and red blood cells, and the ages at which the lumbar punctures were performed were not significantly different among the three groups. Mean CSF lactate dehydrogenase was significantly higher in Group III than in Groups I and II. Isoenzyme patterns indicated that the origin of the CSF lactate dehydrogenase was neuronal tissue, or a plasma transudate from increased permeability of the blood-brain barrier. There were 10 deaths due to anoxic encephalopathy in Group III, but none in Groups I or II. Follow-up of survivors at 10 to 30 months of age revealed neurological sequelae in three infants in Group I, two in Group II and five in Group III. Mean CSF lactate dehydrogenase in those with sequelae had not been significantly different from that of normal survivors; however, the mean was significantly higher in infants who died with anoxic encephalopathy compared with normal infants. These data indicate that CSF lactate dehydrogenase is significantly elevated in infants with fatal anoxic brain damage, and suggest that determinations may be of prognostic value in non-fatal cerebral hypoxia.

Asphyxia Neonatorum↗
PubMed1990

Power spectral analysis of the EEG of term infants following birth asphyxia.

The aim of this pilot study was to perform power spectral analysis of the EEGs of term infants following birth asphyxia, to establish its value as a prognostic indicator. 16 term infants were studied over an 18-month period. Power spectral analysis was performed on the EEGs of babies with signs of hypoxic-ischaemic encephalopathy at regular intervals during the first five days of life. It showed distinct changes following birth asphyxia, which were related to the eventual outcome of the babies. Absolute power was significantly reduced in the babies with poor outcome compared with those with good outcome, particularly in the delta bands.

Asphyxia Neonatorum↗
PubMed1992

Positional asphyxia in individuals with severe cerebral palsy.

The authors report the accidental death by positional asphyxia of three individuals with cerebral palsy occurring after they had been placed in bed for the night. During the five-year period between 1984 and 1989, 12 per cent of deaths from positional asphyxia in King County, Washington, involved individuals with cerebral palsy. Such accidents are similar to those occurring among healthy young children, perhaps because both groups have limited motor skills. Further research into accidents among disabled persons may clarify their special risks and possibly lead to modifications in bed design.

Accidents, Home↗
PubMed1994

Dyskinetic cerebral palsy and birth asphyxia.

Of 115 children with dyskinetic cerebral palsy (CP) in the Mersey region, 17 were born at term and at an appropriate weight for age, and have preserved cognitive abilities. 10 of these are likely to have sustained intrapartum asphyxial brain-damage as the cause of their CP. In such circumstances, a characteristic pattern is usually seen of severe fetal distress occurring late in labour, severe but short-lived birth asphyxia and only mild or moderate hypoxic-ischaemic encephalopathy. This clinical picture should be distinguished from the pattern of birth asphyxia which precedes the development of spastic quadriplegic CP.

Apgar Score↗
PubMed1995

Grating acuity and visual field development in infants following perinatal asphyxia.

Grating acuity and visual fields were assessed in 66 children who had had perinatal asphyxia (ASPH). Also tested were 41 healthy preterm children (H-PT). Subjects were tested at birth to one month, and four, nine, 12, 17, 24, 30 and 36 months corrected age. The mean acuity scores of the ASPH group were lower than those of the H-PT group at most test ages, and significantly so at 30 and 36 months. The mean visual field size of the infants in the ASPH group was significantly smaller than that of the H-PT group at nine, 12, 30 and 36 months. No significant effects were found for preterm vs term birth, gestational age at birth, degree of asphyxia and presence of strabismus. However, central nervous system abnormalities (intraventricular haemorrhage and periventricular leukomalacia) were related to deficits in acuity and visual field size.

Asphyxia Neonatorum↗
PubMed1999

Problems in the detection of intrapartum fetal asphyxia with intermittent auscultation.

We present 4 cases of severe intrapartum fetal asphyxia occurring during spontaneous unaugmented labours at term in low-risk women. In each case the baseline heart rate was completely normal, and the only indication of asphyxia was markedly decreased variability detected with electronic fetal heart rate monitoring. Correct action was taken in 3 cases that probably prevented fetal death or reduced neonatal morbidity. In no case would intermittent auscultation have been able to identify the compromised fetus.

Adolescent↗
PubMed1999

Group B streptococcus infection, not birth asphyxia.

This case illustrates 2 main points. Firstly, fetal infection can mimic exactly both the immediate and delayed signs of perinatal asphyxia. Secondly, the placenta may hold the key to the diagnosis of sepsis which may be made difficult in the neonate by labour ward practices such as the use of intrapartum and immediate newborn antibiotics. We strongly support the recommendation that newborn blood and fetal membrane cultures should always be obtained in babies with a diagnosis of 'intrapartum asphyxia and fetal distress' (1). To this we would add the recommendation that placental histology be performed in these circumstances.

Asphyxia Neonatorum↗
PubMed1987

Plasma catecholamine levels in preterm infants. Effect of birth asphyxia and Apgar score.

Catecholamine levels were measured in cord arterial blood from preterm infants. Relatively lower catecholamine levels were found in the preterm infants than in term infants, although no significant correlation was found between noradrenaline and adrenaline levels and either gestational age or birthweight. Significantly higher catecholamine levels were found after labour. Preterm females had significantly higher catecholamine levels than boys after asphyxia and tended also to have higher catecholamine levels without asphyxia, although not significant. Catecholamine levels were also significantly elevated in those infants with a low Apgar score (less than 7 at 5 min) and those who were acidotic (cord arterial pH less than 7.25). A good correlation was found between a low Apgar score and the presence of acidosis.

Apgar Score↗