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PubMed2001

Asphyxia-induced release of alpha-melanocyte-stimulating hormone in newborn pigs.

Asphyxia and reperfusion induced changes in the plasma and cerebrospinal fluid (CSF) concentrations of alpha-melanocyte-stimulating hormone (alpha-MSH) were studied in newborn pigs using a specific radioimmunoassay technique. Cardiovascular and metabolic failure induced by neonatal asphyxia resulted in a 3-fold, significant (P < 0.05) increase in plasma alpha-MSH levels, whereas the hormone concentration in CSF was significantly (P < 0.05) reduced by 50% during postasphyxial reperfusion. Our data indicate an asphyxia-induced release of alpha-MSH, and suggest a discordant regulation of plasma and CSF concentrations in newborn pigs.

Animals↗
PubMed2002

Vasopressin and epinephrine are equally effective for CPR in a rat asphyxia model.

Epinephrine has been administered as a drug essential for cardiopulmonary resuscitation (CPR). Recently, vasopressin has been reported to be more effective than epinephrine for CPR in a ventricular fibrillation (VF) model. As a different myocardial pathology is speculated to exist between the VF model and the asphyxia model, we investigated whether vasopressin is also effective in a rat asphyxia model. Twenty-one Sprague-Dawley male rats were divided into three groups: vasopressin 0.8 U/kg (Vaso-Gr), epinephrine 0.05 mg/kg (Epi-Gr), and saline same volume as the other two drugs (Sal-Gr). Five minutes after suffocation induced by obstruction of the tracheal tube, CPR was performed using each drug. Although only one animal survived (17%) in the Sal-Gr, 6/7 (85%) survived in both Vaso-Gr and Epi-Gr (P<0.01). Vasopressin is as effective as epinephrine for CPR in asphyxia-induced rats.

Animals↗
PubMed2002

Vasopressin with delayed combination of nitroglycerin increases survival rate in asphyxia rat model.

Recently, vasopressin has been reported as a more effective drug than epinephrine (adrenaline) for cardiopulmonary resuscitation (CPR). However, vasopressin decreases myocardial blood flow (MBF) because of its strong vasoconstriction, to maintain better coronary perfusion pressure (CPP) compared with epinephrine. Nitroglycerin is well known to be able to maintain MBF and increase survival rate. In a VF model, vasopressin combined with nitroglycerin maintained CPP; however, low survival rates were observed compared with vasopressin alone. We investigated the effectiveness of the delayed use of nitroglycerin combined with vasopressin in a severe asphyxia model. Fourteen Sprague-Dawley male rats were divided into two groups: vasopressin 0.8 U/kg alone (V-Gr.), and nitroglycerin 0.3 microg/kg 45 s after the administration of 0.8 U/kg vasopressin (VN-Gr.). Six min after asphyxia induced by obstructing the tracheal tube, CPR was performed in two ways. Three animals resuscitated in the V-Gr. (42%) and six/seven (84%) in the VN-Gr. (P<0.05). In the 6 min of asphyxia rat model, vasopressin combined with delayed nitroglycerin is more effective than vasopressin alone.

Animals↗
PubMed1991

Prediction of the prognosis in neonatal asphyxia by photo-evoked eyelid microvibration.

Neonatal asphyxia causes hypoxic-ischemic encephalopathy and may damage the central nervous system. We studied neonatal asphyxia with photo-evoked eyelid microvibration (PEMV) which is a blink reflex elicited by photic stimuli. The latency of PEMV changed according to the severity of encephalopathy and the degree of unconsciousness. All of the neonate who had showed disappearance of PEMV died. When the prolonged latency persisted, the infant had a strong probability of sustaining neurological sequelae. PEMV provides useful information for predicting the outcome of neonatal asphyxia.

Asphyxia Neonatorum↗
PubMed1998

The syndrome of acute near-total intrauterine asphyxia in the term infant.

Eleven term infants sustained an acute, near-total intrauterine asphyxia at the end of labor. Imaging studies documented a consistent pattern of injury in subcortical brain nuclei, including thalamus, basal ganglia, and brainstem; in contrast the cerebral cortex and white matter were completely or relatively spared. This pattern of injury correlated with the acute and long-term neurologic syndromes in these patients. Four patients had a severe neonatal encephalopathy that included prominent signs of brainstem dysfunction. The other seven patients had a moderate neonatal encephalopathy. Three of these patients had dystonia consistent with basal ganglia injury; all seven remained normocephalic and had good cognitive outcomes consistent with sparing of cerebral cortex and white matter. Finally, in all 11 patients, injury to organs other than the brain was usually subtle. The distribution of injury in these patients reflects the hierarchy of metabolic needs that are unmet after a severe, sudden disruption of substrate supply as occurs in an acute, severe asphyxia. Thus, the higher metabolic rate of the brain compared with other organs explains the significant neonatal encephalopathy with relative sparing of nonbrain organs. Similarly, the higher metabolic rate of subcortical nuclei compared with cerebral hemispheres explains the preponderance of subcortical damage. This clinical and imaging syndrome is in contrast with that seen in more prolonged but less severe intrauterine asphyxia, in which shunting of blood flow from nonbrain organs to the brain and from cerebral hemispheres to the thalamus and brainstem renders nonbrain organs and cerebral hemispheres most vulnerable.

Asphyxia Neonatorum↗
PubMed1999

The use of hypothermia: a role in the treatment of neonatal asphyxia?

Perinatal asphyxia remains one of the most devastating neurologic processes. Although the understanding of the pathophysiology after perinatal asphyxia is extensive, there are few therapeutic interventions available to prevent or even mitigate the devastating process that unfolds after injury. The search for a safe and efficacious therapy has prompted scientists and clinicians to consider various promising therapies. One such therapy is therapeutic hypothermia. On the basis of adult, pediatric, and animal research, there is increasing evidence to suggest that therapeutic hypothermia may be an effective intervention to lessen the secondary neuronal injury that ensues after a hypoxic-ischemic insult. In this article the historic and modern-day uses of therapeutic hypothermia are first reviewed. The pathophysiology of neonatal asphyxia is examined next, with emphasis on the changes that occur when therapeutic hypothermia is implemented. Potential side-effects of the therapy in the neonate and the debate over systemic vs selective hypothermia are discussed. Lastly, although hypothermia as a potential treatment modality for neonates with hypoxic-ischemic encephalopathy is supported by numerous studies, the need for well-designed multicenter trials with detailed patient entry criteria and therapeutic conditions is emphasized.

Adult↗
PubMedDate not supplied

Long-term effects of acute perinatal asphyxia on rat maternal behavior.

In this study we used a rat model of graded perinatal asphyxia to study the long-term consequences of this manipulation on rat maternal behavior at adulthood. Rats were delivered by cesarean (C) section and the pups, still in the uterus horns, were placed into a water bath at 37 degrees C for periods of 0 (controls) or 20 min (asphyxia). Subsequently, female pups were given to surrogate mothers, weaned at 21 days postnatally and then left undisturbed until adulthood, when they were mated. Once they gave birth, on postnatal days (Pnds) 1, 3, 5, 7, 9, 11 and 13 they were observed in the home cage five times per day to assess their maternal behavior in an undisturbed condition. In addition, maternal behavior was observed for 30 min in a novel cage on Pnds 4 and 8. Perinatal asphyxia affected maternal behavior in the home cage, hypoxic females being more often found outside the nest area and performing more often behaviors such as self-grooming. Principal component analysis confirmed a more 'active' behavioral profile for hypoxic females. Hypoxic mothers were characterized by a longer latency to perform on-nest behavior and by a reduced frequency of pup retrieval and licking in the novel cage. No significant differences in corticosterone secretion in response to an acute stressor were found in dams belonging to the different treatments or in the body weights of the offspring. These results are suggestive of an arousal deficit due to perinatal hypoxia and point to the dopaminergic system as a potential neurochemical target for an early hypoxic insult.

Age Factors↗
PubMed1996

[Cerebral palsy and perinatal asphyxia in full term newborn infants].

Actual data on the frequency of cerebral palsy (CP) and "infirmité motrice cérébrale" (IMC), and their relationship with perinatal asphyxia and perinatal managements, are presented. In France, the frequency of IMC at 9 years of age, approximates 1 per thousand, for the 1972, 1976, 1981 generations. Three surveys, two English and one Australian, show an association between perinatal asphyxia and CP. However computation of percent attributable risk indicates that asphyxia can explain only one case of CP out of six among term neonates. These surveys show also that 10% of CP only could be prevented by improving perinatal managements. This, in addition to other factors such as the increase in survival of very preterm babies, explains the absence of a significant reduction of CP frequency despite improvements in the perinatal care.

Adolescent↗
PubMed1999

Relation between proton magnetic resonance spectroscopy within 18 hours of birth asphyxia and neurodevelopment at 1 year of age.

The aim of the study was to test the hypotheses that elevated cerebral lactate, detected by proton spectroscopy performed within 18 hours of suspected birth asphyxia, is associated with adverse outcome, and that increased lactate can be used to predict adverse outcome. Thirty-one term infants suspected of having had birth asphyxia and seven control infants underwent proton magnetic resonance spectroscopy, using three-dimensional chemical shift imaging, within 18 hours of birth. Adverse outcome was defined as death or neurodevelopmental impairment at 1 year of age or more. Nine infants had an adverse outcome. The other 22 and all of the control infants remained normal. Median (range) lactate/creatine plus phosphocreatine (lactate/creatine) ratios in the abnormal, the normal, and the control group were 1.14 (0.17 to 3.81), 0.33 (0 to 1.51), and 0.05 (0 to 0.6) respectively (P=0.003). Lactate/creatine >1.0 predicted neurodevelopmental impairment at 1 year of age with sensitivity of 66% and specificity of 95%, positive and negative predictive values of 86% and 88%, and a likelihood ratio of 13.2. Elevated cerebral lactate/creatine within 18 hours of birth asphyxia predicts adverse outcome.

Asphyxia Neonatorum↗
PubMed2003

White matter injury following systemic endotoxemia or asphyxia in the fetal sheep.

White matter injury is the most frequently observed brain lesion in preterm infants. The etiology remains unclear, however, both cerebral hypoperfusion and intrauterine infections have been suggested as risk factors. We compared the neuropathological outcome, including the effect on oligodendrocytes, astrocytes, and microglia, following either systemic asphyxia or endotoxemia in fetal sheep at midgestation. Fetal sheep were subjected to either 25 minutes of umbilical cord occlusion or systemic endotoxemia by administration of Escherichia coli lipopolysaccharide (LPS O111:B4, 100 ng/kg, IV). Periventricular white matter lesions were observed in 2 of 6 asphyxiated fetuses, whereas the remaining animals showed diffuse injury throughout the subcortical white matter and neuronal necrosis in subcortical regions, including the striatum and hippocampus. LPS-treatment resulted in focal inflammatory infiltrates and cystic lesions in periventricular white matter in 2 of 5 animals, but with no neuron specific injury. Both experimental paradigms resulted in microglia activation in the white matter, damaged astrocytes, and loss of oligodendrocytes. These results show that the white matter at midgestation is sensitive to injury following both systemic asphyxia and endotoxemia. Asphyxia induced lesions in both white and subcortical grey matter in association with microglia activation, and endotoxemia resulted in selective white matter damage and inflammation.

Animals↗
PubMed2004

Postnatal lactate as an early predictor of short-term outcome after intrapartum asphyxia.

OBJECTIVES: To compare the predictive value of pH, base deficit and lactate for the occurrence of moderate-to-severe hypoxic ischaemic encephalopathy (HIE) and systemic complications of asphyxia in term infants with intrapartum asphyxia. STUDY DESIGN: We retrospectively reviewed the records of 61 full-term neonates (> or =37 weeks gestation) suspected of having suffered from a significant degree of intrapartum asphyxia from a period of January 1997 to December 2001. The clinical signs of HIE, if any, were categorized using Sarnat and Sarnat classification as mild (stage 1), moderate (stage 2) or severe (stage 3). Base deficit, pH and plasma lactate levels were measured from indwelling arterial catheters within 1 hour after birth and thereafter alongwith every blood gas measurement. The results were correlated with the subsequent presence or absence of moderate-to-severe HIE by computing receiver operating characteristic curves. RESULTS: The initial lactate levels were significantly higher (p=0.001) in neonates with moderate-to-severe HIE (mean+/-SD=11.09+/-4.6) as compared to those with mild or no HIE (mean+/-SD=7.1+/-4.7). Also, the lactate levels took longer to normalize in these babies. A plasma lactate concentration >7.5+/-mmol/l was associated with moderate-or-severe HIE with a sensitivity of 94% and specificity of 67%. The sensitivity and negative predictive value of lactate was greater than that of the pH or base deficit. CONCLUSIONS: The highest recorded lactate level in the first hour of life and serial measurements of lactate are important predictors of moderate-to-severe HIE.

Asphyxia Neonatorum↗
PubMed2006

Mild hypothermia via selective head cooling as neuroprotective therapy in term neonates with perinatal asphyxia: an experience from a single neonatal intensive care unit.

OBJECTIVE: The objective of this study was to determine the efficacy of mild hypothermia via selective head cooling as a neuroprotective therapy in term infants with perinatal asphyxia. STUDY DESIGN: Full-term newborns who had 5 min Apgar scores <6, first arterial blood gas pH<7.10 or BD>15 mEq/l, and with the clinical signs of encephalopathy were enrolled within 6 h after birth. Patients were randomized to receive mild hypothermia treatment via selective head cooling for a total of 72 h or receive routine treatment as a control. Brain hypoxic-ischemic injury was quantified based on the head computed tomographic scan (CT scan) at postnatal age 5-7 days and a Neonatal Behavioral Neurological Assessment (NBNA) score at 7-10 days of life. RESULTS: A total of 58 patients (30 hypothermia, 28 control) completed the study. Hypothermia was well tolerated in this study and attenuated the hypoxic-ischemic brain injury due to perinatal asphyxia. Head CT scan demonstrated moderate to severe hypoxic-ischemic changes in only 4/30 cases from the hypothermic group. In contrast, 18/28 cases in the control group showed moderate to severe hypoxic-ischemic changes (chi (2)=15.97, P<0.01). Brain hypothermia also significantly improved the NBNA score (32+/-2 in the hypothermic group vs 28+/-3 in the control group, P<0.01). CONCLUSIONS: Our results suggest that selective head cooling may be used as a neuroprotective therapy in term neonates with perinatal asphyxia. A long-term follow-up study is needed to further validate the results of this study.

Apgar Score↗
PubMed2000

Accidental asphyxia in bed in severely disabled children.

OBJECTIVE: To determine whether there are specific situations which may increase the risk of accidental asphyxia during sleep in children with physical and mental disabilities. METHODOLOGY: Review of all cases where death was attributed to accidental asphyxia caused by unsafe sleeping situations in children listed in the Department of Histopathology database over a 10-year period from March 1989 to February 1999. RESULTS: A total of 26 cases were found (M:F, 19:7; age range, 1-48 months; average age, 7.4 months). Of those cases, two involved children with significant mental and physical impairment. Case 1: A 4-year-old boy with Klippel-Trenaunay-Weber syndrome, macrocephaly and severe developmental delay, was found dead with his head hanging over a wooden board attached to the side of his bed. Case 2: A 4-year-old boy with lissencephaly and severe developmental delay was found dead wedged between a retractable mesh cot side and the side of his bed. In both cases the devices resulting in death had been put in place to prevent the boys from falling out of bed. CONCLUSIONS: Accidental asphyxia in physically and mentally impaired children may be caused by devices that have been used to prevent injury from falling out of bed. Careful assessment of the specific developmental problems that children suffer should be undertaken before their beds are modified. It may be safer for these children either to have no barrier, or to have drop-sided cots/beds that meet recognized safety standards.

Accidents, Home↗
PubMedDate not supplied

Fatal unintentional traumatic asphyxia in childhood.

OBJECTIVE: The present study was undertaken to examine specific features of unintentional traumatic asphyxial deaths in childhood. METHODS: Coronial files and records at the Forensic Science Centre in Adelaide, South Australia, were examined over a 35-year period from 1966 to 2000 for all cases of traumatic asphyxial death occurring in children under the age of 17 years. RESULTS: Six cases of unintentional fatal traumatic asphyxia were identified. All of the victims were boys with an age range of 2-15 years (mean 6.8 years) and all were found dead at the scene. Fatal traumatic asphyxia resulted from entrapment beneath a chest of drawers, beneath a table tennis table, between a pile of wooden pallets and a metal fence, between a conveyor belt and its frame, and under a motor vehicle (in two cases). CONCLUSIONS: Fatal traumatic asphyxia in childhood is a rare event, with younger children commonly being trapped by furniture or by industrial equipment while playing, and older children being trapped under motor vehicles in similar circumstances to adult traumatic asphyxial deaths. Unsupervised play of young children around heavy and potentially unstable pieces of furniture may be dangerous, particularly if more than one child is present. Unsupervised play of young children in industrial yards should be avoided.

Accidents↗
PubMed2002

Randomized controlled trial of magnesium sulfate infusion for severe birth asphyxia.

OBJECTIVE: To determine whether postnatal MgSO(4) infusion (250 mg/kg per day) for 3 days is both safe and able to improve outcome in infants with severe birth asphyxia, as had been suggested by a small pilot study. METHODS: A multicenter randomized controlled trial was conducted. Entry criteria included 5-min Apgar score of seven or less and either failure to initiate spontaneous respiration at 10 min after birth because of asphyxia, or occurrence of clinically apparent seizures within 24 h after birth. Number of subjects was calculated to detect a 50% reduction in incidence of adverse outcomes. RESULTS: Distributions of perinatal factors, neonatal baseline characteristics and severity of hypoxic-ischemic encephalopathy were similar in treated and control groups. No significant differences were observed in duration of clinical seizures, or need for assisted ventilation. Survival with normal results of cranial computed tomography, electroencephalography and establishment of oral feeding by 14 days of age, was significantly more frequent in the treated group than in the control group (12/17 vs 5/16, P = 0.04). No significant differences in blood pressure, heart rate or respiratory rate were observed between groups. CONCLUSION: Postnatal MgSO(4) infusion as above is safe and can improve short-term outcome in infants with severe birth asphyxia.

Asphyxia Neonatorum↗
PubMed2003

Hypoxia activates the human placental vascular endothelial growth factor system in vitro and in vivo: up-regulation of vascular endothelial growth factor in clinically relevant hypoxic ischemia in birth asphyxia.

OBJECTIVE: We investigated the influence of acute hypoxia on the placental vascular endothelial growth factor system in vitro and in vivo in acute birth asphyxia compared with pregnancies that were complicated by preeclampsia and with healthy control subjects. STUDY DESIGN: Messenger RNA levels for vascular endothelial growth factor, flt-1, and KDR were measured by TaqMan real-time polymerase chain reaction in human placental choriocarcinoma cells (BeWo) that were exposed to hypoxia (1% oxygen, 5% carbon dioxide, 94% nitrogen) and in placental tissue of neonates with birth asphyxia (n = 20), newborn infants of mothers with preeclampsia (n = 20), and gestational age-matched control subjects. Immunhistologically, placental vascular endothelial growth factor protein expression was compared among the groups. RESULTS: In BeWo cells, vascular endothelial growth factor, flt-1 and KDR messenger RNA increased in a time-dependent manner in response to hypoxia. In vivo, vascular endothelial growth factor/beta-actin and KDR/beta-actin messenger RNA were significantly higher in placental tissue of newborn infants with severe hypoxic-ischemic encephalopathy than with newborn infants with mild or no hypoxic-ischemic encephalopathy and control subjects. In chronic placental hypoxia (preeclampsia), vascular endothelial growth factor and both receptors were found to be up-regulated. Increased placental vascular endothelial growth factor expression was confirmed by immunohistologic examination. CONCLUSION: The vascular endothelial growth factor system is up-regulated in response to placental hypoxia and is assumed to be a potential early indicator of severe birth asphyxia.

Actins↗
PubMed1991

Birth asphyxia and hypoxic-ischaemic encephalopathy: incidence and severity.

Clinically significant birth asphyxia was assessed over a 3-year period in a tertiary referral hospital in Nigeria. The overall incidence was 26.5/1000 live births of whom 12.1/1000 showed severely abnormal features comprising persistent seizures and coma. There was no appreciable difference in incidence for the consecutive years of the study. There was a marked involvement of infants who had suffered intrauterine growth retardation: 51 (30.7%) of these were asphyxiated, whereas only 3% were large for gestational age. The Apgar scoring system seemed not to have compared well with the clinical presentation of hypoxic-ischaemic encephalopathy from birth asphyxia. Much needs to be done to improve health care delivery and reduce the incidence of birth asphyxia.

Apgar Score↗
PubMed2006

Dynamics of hepatic enzyme activity following birth asphyxia.

AIM: To investigate: 1) the occurrence of hypoxic hepatitis in full-term infants after birth asphyxia, 2) the temporal enzyme pattern in asphyxiated newborn infants, and 3) whether the degree of hypoxic hepatitis, as reflected by the rise in aminotransferase, correlates with the severity of the asphyxia and CNS symptomatology. METHODS: Serum aminotransferases, lactate dehydrogenase, gamma-glutamyl transferase, total and conjugated bilirubin, cholinesterase activity, albumin, international normalized ratio (INR), and nucleated red blood cell count were prospectively measured in full-term asphyxiated newborn infants (n=26). Samples were collected three times during the first 72 h and once between days 6 and 12 after birth. Samples from healthy newborns (n=56), collected 24-172 h after birth, served as controls. RESULTS: In 12 of the 26 asphyxiated infants, a serum alanine aminotransferase (S-ALAT) pattern compatible with hypoxic hepatitis was found. Five infants showed increased S-ALAT activity but with a different pattern. Similar patterns were seen in serum aspartate aminotransferase (S-ASAT). S-ALAT and -ASAT concentrations 0-72 h after birth correlated significantly with severity of hypoxic-ischaemic encephalopathy. CONCLUSION: Birth asphyxia can induce an enzyme pattern in serum compatible to hypoxic hepatitis. There seems to be a correlation between aminotransferases in serum and the extent of CNS injury.

Alanine Transaminase↗