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PubMed1998

High-dose phenobarbital therapy in term newborn infants with severe perinatal asphyxia: a randomized, prospective study with three-year follow-up.

OBJECTIVE: To determine whether 40 mg/kg phenobarbital given to term infants with severe asphyxia would result in a lower incidence of seizures in the newborn period and an improved neurologic outcome. METHODS: We conducted a randomized, controlled, prospective study. Entry criteria included (1) an initial arterial pH less than or equal to 7.0 with a base deficit 15 mEq/L or more, (2) Apgar score less than or equal to 3 at 5 minutes of age, or (3) failure to initiate spontaneous respiration by 10 minutes of age. Sample size was calculated to detect a 50% reduction in the incidence of neonatal seizures. RESULTS: No differences were present between treatment and control groups with respect to severity of asphyxia assessed by initial arterial pH, base excess, cerebrospinal fluid lactate dehydrogenase concentration or detection of CSF creatine kinase of its BB isoenzyme. Seizures occurred in 9 of 15 infants in the treatment group and 14 of 16 infants in the control group (p = 0.11). No adverse effects were observed from phenobarbital on heart rate, respiratory rate, blood pressure, or arterial blood gas values. Three-year follow-up revealed normal outcome in 11 of 15 infants in the treatment group and 3 of 16 in the control group (p = 0.003). CONCLUSION: Phenobarbital, when administered in a dose of 40 mg/kg intravenously over 1 hour in term, severely asphyxiated newborn infants appeared to be safe and was associated with a 27% reduction in the incidence of seizures and a significant improvement in neurologic outcome at 3 years of age.

Anticonvulsants↗
PubMed2001

Brain fatty acids in perinatal asphyxia.

In hypoxic or ischemic states the release of fatty acids is proposed to have several harmful effects on brain structure and function. We therefore decided to study brain FFA in a simple, clinically related animal model resembling intrauterine perinatal asphyxia (PA). Cerebral blood flow (CBF), brain fatty acids (C14:0, C16:1, C16:0, C18:1, C1 8:0, sigma C), plasma glucose, lactate, beta-hydroxybutyrate (beta-OHB), non-esterified fatty acids (NEFA) and insulin were determined in PA and compared to the normoxic state. Brain C 14:0 FFA were not significantly different from normoxic rats. Brain FFA C 16:0 were comparable between groups but significantly decreased at 20 min of PA. C 18:0 FFA showed a trend to increase with the length of PA reaching significance at 10 min of asphyxia only and were declining at 20 min, however, not significantly. Brain C 16:1 and C 18:1 FFA concentrations were comparable between groups. The parameters cerebral blood flow, glucose and lactate showed a stepwise and significant increase with the length of PA, whereas beta-HOB, NEFA and insulin showed no changes. CBF, glucose and lactate showed a strong association whereas other parameters failed to correlate with each other. Only inconsistent trends of increased brain FFA were found and the association between brain glucose and brain FFA could be ruled out. Although CBF was manifold and significantly elevated in PA, brain FFA pattern suggests that the increase of CBF is obviously not mediated by brain FFA. We conclude that FFA may not be involved in the early phase-pathogenesis of PA.

Animals↗
PubMed1999

Genes involved in the pathophysiology of perinatal asphyxia.

Mechanisms in the pathogenesis of perinatal asphyxia (PA) at the gene level are only beginning to be elucidated, although gene hunting using differential display has revealed differences in gene expression between hypoxic and normoxic cells in vitro. As no information on gene expression was available from in vivo studies, we decided to use a non-invasive and clinically relevant animal model of PA for mRNA hunting applying the subtractive hybridization method. mRNAs from normoxic rat brain and brain of rat pups with 20 min of asphyxia were isolated and compared by this technique. The resulting subtracted mRNAs were converted to cDNA, sequenced and identified by gene bank data. A series of transcripts representing transcription factors, transporters, metabolic factors, were found to be up- or downregulated providing insight into mechanisms of PA, and on the other hand, genes with unknown functions could be given a preliminary role i.e. in PA. Results obtained with this powerful tool are now challenging quantitative determination of these genes and gene products at the protein and activity level to confirm their role in PA.

Animals↗
PubMed1995

Autoerotic asphyxia in adolescents.

The death of a child or young adult is always tragic, regardless of the cause. Cases of autoerotic asphyxia are often labeled as suicide, or are underreported because of embarrassment of relatives or misidentification of the initial clinical manifestations. It may be that autoerotic asphyxial death is far more common than realized. Many emergency nurses and physicians lack adequate knowledge about this phenomenon to make an accurate diagnosis. Family members are often reluctant or unwilling to provide enough data surrounding the circumstances in which the patient was found, and the cause of death is mislabeled as suicide. Autoerotic asphyxia is frequently labeled as a sexual aberrancy and an act that society would rather not acknowledge. But there are a number of implications for emergency nurses, such as prevention and sensitive support of family in the emergency department, that demand our attention.

Adolescent↗
PubMed1999

An international network for evaluating neuroprotective therapy after severe birth asphyxia.

Animal studies have shown great promise in their applicability to potentially neuroprotective therapies for severe birth asphyxia in human babies. It is now necessary to consider a strategy to evaluate some or all of these techniques within the context of human neonatal randomized control trials (RCT). We have set up a pilot study for an international RCT of mature babies with severe asphyxia (defined by an Apgar score of 5 or less at 10 minutes) and have shown that we can recruit from 120 centers in 17 countries an average of three babies a week, which is the required number to undertake a study over a 2-year period with sufficient power to show a significant improvement in outcome. Particular attention must be given in future studies to the size of improvement in outcome required, generalizability of entry criteria, and the appropriate measure of functional outcome in treated babies.

Animals↗
PubMed1990

Risk factors for birth asphyxia and brain damage in pregnancy and labour.

In this review the patho-physiology and risk factors of birth asphyxia are discussed. Simple and appropriate, but scientifically sound, technology for the prevention of birth asphyxia is described. This can be used at home, in the community, in health sub-centres and health centres to identify and assess risk factors so that appropriate referral can be made. Based on experience in developing countries, actions which can be performed by the mother, relatives, neighbours, traditional birth attendants and nurses and midwives are described.

Asphyxia Neonatorum↗
PubMed2002

Effect of asphyxia on the pupils of brain dead subjects.

The pupils dilate following cardiac arrest but the mechanism is unknown. If pupillary dilation represents inadequate blood supply to the midbrain, pupil size might be a rough guide to the adequacy of the resuscitation effort. The brain dead organ harvest patient presents a unique opportunity to study pupillary activity in the absence of an intact midbrain and to examine the effects of asphyxia on the pupil. Because the midbrain is dead in these subjects, the pupil has no supraspinal autonomic control and following aortic cross clamp, no blood can be delivered to the orbit. Ten brain dead patients scheduled for organ harvest were studied. Pupil size was measured from the right eye every minute for 9 min before and every minute for 10 min following aortic cross-clamp. Dapiprazole eye drops were instilled into the left eye at least 1 h before cross clamp in five cases and pupillary measurements were intermittently taken before and after cross clamp. Pupil size was stable before cross clamp. Following cross clamp, the pupil dilated in all cases, reaching 10.6 mm in one case. Mean dilation was 1.8+/-0.9 mm. Time to peak dilation was 4.3+/-1.4 min and latency of dilation was 1.4+/-1.2 min. Dapiprazole eye drops prevented the pupillary dilation in contralateral eye of the five cases in which it was used. The cause of this sympathetic activity is either a short burst of neuronal activity in the peripheral sympathetic system innervating the dilator muscle, or release of stored norepinephine from the presynaptic terminals, as asphyxia intervenes.

Adrenergic alpha-Antagonists↗
PubMed2003

Association between brain tissue pH and brain injury during asphyxia in piglets.

BACKGROUND: Acidosis may contribute to brain injury from asphyxia, but its role is unclear. In order to evaluate the association between brain acidosis and cerebral injury, we subjected piglets to hypoxia and hypotension (HYP-HOTN) or hypoxia alone (HYP) to inflict varying amounts of brain damage. We hypothesized that piglets with a more severe brain injury would have a lower brain pH. METHODS: Piglets had a pH microprobe inserted into the cerebral cortex. HYP animals breathed 5-8% O(2)/7% CO(2) for 30 min with mean arterial pressure (MAP) maintained at >40 mmHg. HYP-HOTN animals breathed the same gas for 30 min, but during the last 15 min, MAP was reduced to 25-30 mmHg by withdrawing blood. After 4 h of recovery, the animals were perfusion-fixed and pathology assessed. Somatosensory-evoked potentials (SEP) were also monitored. RESULTS: HYP-HOTN piglets had more neuropathology than HYP animals. During the last 15 min of injury, brain pH in the HYP-HOTN group was significantly higher than that in HYP. However, recovery of brain pH was prolonged in the HYP-HOTN animals. The amount of time for brain pH to recover to > or =7.00 correlated very well with both the degree of neuropathology and SEP recovery. The reduction in brain pH, either absolute or relative to baseline, was not associated with the severity of damage. CONCLUSIONS: The time needed for brain pH to recover after asphyxia, but not its severity, was associated with the amount of brain injury. Further study is warranted to determine whether immediate restoration of brain pH will reduce brain damage.

Acidosis↗
PubMed1998

Brain derived neurotrophic factor is increased in cerebrospinal fluid of children suffering from asphyxia.

Brain derived neurotrophic factor (BDNF) is a neurotrophic factor that is relatively highly expressed in developing and adult brain. Whereas clinical determinations of nerve growth factor (NGF) in human serum and cerebrospinal fluid (CSF) in different conditions have been undertaken there are no reports on levels of BDNF in human CSF. Here we show that BDNF is increased in CSF of neonatal children suffering from asphyxia which is characterised by periods of brain hypoxic-ischemia. In contrast to BDNF, levels of CSF NGF were largely decreased in these children. The present results show that BDNF can be detected in human CSF and that the levels increase following hypoxic-ischemic brain injury. As suggested by animal studies the increased BDNF might counteract neuronal damage observed in these patients following asphyxia.

Apgar Score↗
PubMed1991

Prognostic value of early somatosensory evoked potentials for adverse outcome in full-term infants with birth asphyxia.

SEPs were examined during the first weeks of life in 34 infants with mild to severe birth asphyxia, in an attempt to provide a more accurate prediction of neurodevelopmental outcome. Normal, delayed and absent responses were compared with the infant's acute clinical condition, imaging findings using different imaging techniques and neurodevelopmental outcome. All infants with normal SEPs were normal at follow-up. All but two of the infants with a delayed or absent response died or suffered from severe neurological sequelae. A delayed or absent N1 latency carried a risk for death or severe handicap of 71 and 100%, respectively, compared with 25 and 89% for moderate or severe encephalopathy on neurological assessment, and 29 and 85% for moderate or severe changes seen using different imaging techniques. SEPs may provide useful additional information when assessing the infant with birth asphyxia.

Asphyxia Neonatorum↗
PubMed1998

Birth asphyxia.

The term Birth asphyxia covers a number of clinical and physiological definitions. Birth asphyxia is a relatively common clinical event. In the majority of cases the outcome in terms of brain damage and future development of the child is excellent. However, a small number of children go on to develop patterns of brain damage which are then associated with disability. The article seeks to provide a basic understanding of the various mechanisms involved in producing injury.

Asphyxia Neonatorum↗
PubMed1999

Oxidative stress, brain white matter damage and intrauterine asphyxia in fetal lambs.

In order to examine the role of oxidative stress in asphyxia-induced perinatal brain damage, near-term fetal lambs were subjected to umbilical cord occlusion for approximately 60min until fetal arterial pH diminished to less than 6.9 and base excess to less than -20 meq/l. The levels of superoxide, hydrogen peroxide, glutathione (GSH) and thiobarbiturate-reactive substances (TBARS) within brain grey and white matter were determined at 72h to correlate with morphological changes. Although the topography and extent of brain damage varied somewhat from case to case, ranging from focal infarction in grey or white matter to subtle and patchy alterations of white matter, the telencephalic white matter appeared to bear the brunt of damage as compared to other regions. The parietal white matter, in particular was often the seat of early pathological changes that could be seen in isolation. These white matter changes were accompanied by significant increases in hydrogen peroxide and TBARS levels as compared to those in grey matter. In another set of experiments, 8 different brain regions were assayed for TBARS, GSH and superoxide dismutase (SOD). A highly significant rise in the levels of TBARS was again noted in the parietal and frontal white matter. SOD levels were higher in the frontal and parietal white matter, basal ganglia and cerebellum. Cerebral cortical and hippocampal neurons were relatively unaffected until accompanied by more severe damage to grey and white matter at other sites. These results suggest that the developing telencephalic white matter appears to be most vulnerable to the effects of intrauterine fetal asphyxia and that oxidative stress may be a major contributing factor in the pathogenesis of perinatal hypoxic-ischemic encephalopathy.

Animals↗
PubMed2003

Selective head cooling with hypothermia suppresses the generation of platelet-activating factor in cerebrospinal fluid of newborn infants with perinatal asphyxia.

Hypoxic-ischemic encephalopathy (HIE) remains one of the most important neurologic complications in the newborn. Several experimental and clinical studies have shown that hypothermia is the most effective means known for protecting the brain against hypoxic-ischemic brain damage. Furthermore, recent data have suggested that platelet-activating factor (PAF) could play a pathophysiologically important role in the progression of hypoxic-ischemic brain injury. The aim of the present study was to investigate the role of head cooling combined with minimal hypothermia in short-term outcome of infants with perinatal asphyxia. In addition, we have examined the effect of head cooling combined with minimal hypothermia on PAF concentrations in cerebrospinal fluid (CSF) after hypoxic-ischemic brain injury. The group of asphyxiated infants (Group 1) consisted of 21 full-term (gestational age >37 weeks). These infants were randomized and divided into either a standard therapy group (Group 1a; n=10) or cooling group (Group 1b; n=11). Head cooling combined with minimal hypothermia (rectal temperature 36.5-36 degrees C) was started as soon as practicable after birth. The infants were cooled for 72h and then were rewarmed at 0.5 degrees C/h. The control group (Group 2) consisted of seven full-term infants and none of these infants showed any sign of asphyxia. To measure PAF concentration in CSF, CSF with lumbar puncture was collected into tubes immediately before the cooling (1-3h after birth) and again after 36h. We had no evidence of severe adverse events related to hypothermia. In Group 1a, two infants died after 72h of life; however, all newborn infants in Group 1b survived. Convulsion required treatment in three infants of standard therapy group (1a); none of the infants in Group 1b had clinical seizure activity. Abnormal EEG patterns were found in four infants of Group 1a; no EEG abnormalities were noted in Group 1b (P<0.05). On admission (before cooling), PAF concentration in CSF of asphyxiated infants was found to be significantly higher when compared with that of control (P<0.001). Mean PAF concentration before initiation of the study was similar in the two asphyxiated groups (Group 1a vs. 1b) (P>0.05). Obtained PAF level in CSF after 36h, showed a profound decline in cooling group of infants compared to Group 1a infants (P<0.01). In conclusion, the present study suggests that cerebral cooling with minimal hypothermia started soon after birth has no severe adverse effects during 72-h cooling period and that short-term outcome of infants are encouraging. Our results also support the hypothesis PAF an important mediator in hypoxic-ischemic brain injury and demonstrate that head cooling combined with minimal hypothermia reduces the normal increase in PAF following hypoxic-ischemic brain injury in full-term infants.

Asphyxia Neonatorum↗
PubMed1995

Animal models of perinatal asphyxia: contributions, contradictions, clinical relevance.

Animal models have contributed immensely to our understanding of hypoxic ischemic encephalopathy in the newborn. A number of animal models have been used, including both primate and subprimate species. Although the Rhesus monkey model has a dramatically similar pathological distribution of brain injury when compared with the human, other pathologic processes secondary to asphyxia may be more appropriately assessed in other species. The maxim that because primates are closer on the phylogenetic tree to humans than are subprimates all observations in the primate are applicable to the human is simply not true. Understanding of the neurochemical consequences of asphyxia in the past decade have arisen from experiments primarily in the neonatal rat. We have come to understand that not only is the hypoxic event of major significance, but that, once reperfused, reoxygenation causes further injury. Free-radical generation following reperfusion may be massive and may further contribute to cell membrane injury. These observations have lead to rational theoretic approaches to the treatment of hypoxic ischemic brain injury. On the other hand, previously used treatments such as osmotic agents and glucocorticoids would appear to be not only inefficacious but hazardous in the treatment of hypoxic ischemic brain injury. The role of nitric oxide (NO) in the pathogenesis of brain injury is yet uncertain, but there is little doubt that it plays a significant role. Although survival of the immature animal subjected to hypoxic environment is longer than in the mature animal, the central nervous system of the immature animal is more sensitive to glutamate and N-Methyl-D-aspartate (NMDA) receptor-mediated injury.

Acidosis, Respiratory↗
PubMed2003

Mechanical asphyxia by three different mechanisms.

We report the case of death of a 75-year-old Caucasian woman, produced by three different ways of mechanical asphyxia: smothering and strangulation by hand and traumatic asphyxia by thoracic compression. All these criminal offences were carried out by one single assailant who compressed the mouth and the nose of the victim with the left hand, squeezed her neck with the right hand and pressed her thorax with the knees.

Aged↗
PubMed2003

Sexual asphyxia by hanging--a case report and a review of the literature.

A case of sexual asphyxial death by hanging is presented. A 35-year-old male, found dead lying on his face in a bed of a truck cab, had hanged himself from a window frame using a leather belt. He was completely naked. There were pornographic and sadomasochistic magazines beneath his face, opened to pages depicted nude photographs of a woman. Autopsy findings revealed a ligature mark on the neck and petechial hemorrhages in the conjunctivae, but there were no hemorrhages in the neck muscles or fractures of the hyoid bone or the thyroid cartilage. The alcohol levels in the blood and urine were 0.78 and 0.45 mg/ml, respectively. The circumstances suggested that his death was accidental, and due to asphyxia by hanging performed to enhance sexual gratification during masturbation. Sexual asphyxia is reviewed and discussed.

Accidents↗
PubMed2001

The pediatric neurologist as expert witness with particular reference to perinatal asphyxia.

The frequency of litigation related to alleged medical malpractice is increasing in Canada. For the neurologist, involvement in such litigation most often takes place in the context of acting as an expert witness and, for the pediatric neurologist, the most common clinical situation for which expertise is requested is that of possible perinatal asphyxia. The medical expert's primary role is to provide necessary guidance and assistance to the court, which may permit the rendering of decisions that are scientifically valid. This article will review the attributes of the medical expert witness. Aspects of perinatal asphyxia cases under litigation that commonly require the assistance of pediatric neurology expertise such as etiology, timing, extent of disability and life expectancy will also be reviewed in detail. The aim is to provide for the neurologist a clearer understanding of the responsibilities inherent in this increasing professional role.

Asphyxia Neonatorum↗
PubMed1998

Adverse effects of early phenobarbital administration in term newborns with perinatal asphyxia.

Taking advantage of the lack of consensus in our neonatal unit regarding the early (prior to the onset of signs of hypoxic-ischaemic encephalopathy) administration of phenobarbital to term infants with perinatal asphyxia, we evaluated the possible cerebral sparing effect of phenobarbital by doing a retrospective case-control analysis. Fifty-seven infants who received 10 mg/kg loading dose of phenobarbital within one hour following resuscitation and before the onset of signs of hypoxic-ischaemic encephalopathy were compared with 91 infants who did not to determine the effect of early phenobarbital on the incidence of subsequent seizures, and mortality in the perinatal period. Early phenobarbital was associated with a threefold (P < 0.025) increase in the incidence of subsequent seizures, and consequently a trend towards increased mortality. Seizures per se were associated with almost a 20-fold increase in mortality (P < 0.0001). These findings suggest that early phenobarbital administration may produce adverse rather than beneficial effects following asphyxia. Because this is an observational study; these results need to be confirmed by appropriate randomized trials in similar clinical settings.

Anticonvulsants↗