Abstract: Objectives To compare the Conventional, Specified, Expanded and Combined Apgar scoring systems in predicting birth asphyxia and the adverse early neurologic outcomes. Methods This prospective cohort study was conducted on 464 admitted neonates. In the delivery room, after delivery the umbilical cord was double clamped and a blood samples was obtained from the umbilical artery for blood gas analysis, meanwhile on the 1- , 5- and 10- minutes Conventional, Specified, Expanded, and Combined Apgar scores were recorded. Then the neonates were followed and intracranial ultrasound imaging was performed, and the following information were recorded: the occurrence of birth asphyxia, hypoxic Ischemic Encephalopathy (HIE), intraventricular hemorrhage (IVH), and neonatal seizure. Results The Combined-Apgar score had the highest sensitivity (97%) and specificity (99%) in predicting birth asphyxia, followed by the Specified-Apgar score that was also highly sensitive (95%) and specific (97%). The Expanded-Apgar score was highly specific (95%) but not sensitive (67%) and the Conventional-Apgar score had the lowest sensitivity (81%) and low specificity (81%) in predicting birth asphyxia. When adjusted for gestational age, only the low 5-minute Combined-Apgar score was independently associated with the occurrence of HIE (B = 1.61, P = 0.02) and IVH (B = 2.8, P = 0.01). Conclusions The newly proposed Combined-Apgar score is highly sensitive and specific in predicting birth asphyxia and also is a good predictor of the occurrence of HIE and IVH in asphyxiated neonates.

Abstract: Objective: This study was performed to determine the occurrence of hypoxic hepatitis in full-term neonates after perinatal asphyxia and to correlate between the rise in enzymes and severity of asphyxia with Apgar score and hypoxic ischemic encephalopathy (HIE) grading of the neonates. Method and material: This prospective case-controlled study was conducted in a tertiary-level hospital in India for a period of 12 months. The study group A comprised 70 newborns suffering from birth asphyxia, while 30 healthy neonates were included in group B (control). All biochemical parameters of liver function, ie, serum alanine transferase (ALT), aspartate transferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), total protein, serum albumin, bilirubin (total and direct), and international normalized ratio (INR), were measured on postnatal days 1, 3, and 10 in both study and control groups. Results: In group A, 22.8% newborns had severe (Apgar score 0–3), 47.1% had moderate (Apgar score 4–5), and 30% had mild (Apgar score 6–7) birth asphyxia at five minutes. In all, 14.28% babies were in HIE stage I, 25.73% babies were in HIE stage II, and 11.42% babies were in HIE stage III. The rest of the newborns, 48.57%, were normal. The prevalence of liver function impairment was seen in 42.85% of asphyxiated neonates. On day 1, ALT, AST, ALP, LDH, PT, and INR were significantly higher, and total protein and serum albumin were significantly lower in group A than in group B. However, ALT and AST correlated well with increasing severity of HIE score. On day 3, there was a rising trend observed in the concentration of mean LDH as HIE staging of neonates progressed from stage 0 to stage III, and among various HIE stages, the difference in LDH was statistically significant. Conclusion: We concluded that AST, ALT at 24 hours, and LDH at 72 hours of animation can be a utilitarian diagnostic tool to differentiate asphyxiated neonates from non-asphyxiated neonates and to discover the severity of perinatal asphyxia because of easy accessibility and feasibility of tests. The outcomes of this survey would be useful for physicians who receive neonates for whom birth details are not easily documented as most of the time the referred newborn infants lack asphyxia history either because the attendants do not know clearly the whole birth history or it was an unattended delivery, or the referring healthcare professional has not been observant because of legal threats. The neurological assessment also becomes difficult and inconclusive as ventilator treatment, sedative drugs, and anticonvulsant therapy would produce an evaluation of severity of hypoxic ischemic brain disease and neurological insult difficult.

Abstract: Background: Troponin is a protein of the troponin-tropomyosin complex in myocardium and it is considered an highly sensitive marker of myocardial necrosis both in adults and newborns with perinatal asphyxia. Some studies assume that high troponin levels in adults without signs of myocardial necrosis could be conditioned by some factors, such as hemolysis, turbidity, and hyperbilirubinemia. Case presentation: We report a case of a term female newborn of Caucasian race, with high troponin levels in absence of neonatal asphyxia and without clinical or instrumental signs of myocardial ischaemia. Conclusion: Hyperbilirubinemia might be a factor that could interfere with assessment of sieric troponin T. This might suggest that levels of troponin T should be trusted only when they are associated with signs of other conditions suggesting heart damage or respiratory distress.

Abstract: Background Perinatal asphyxia (PA) is a leading cause of mortality and morbidity in newborns: its prognosis depends both on the severity of the asphyxia and on the immediate resuscitation to restore oxygen supply and blood circulation. Therefore, we investigated whether measurement of S100B, a consolidated marker of brain injury, in salivary fluid of PA newborns may constitute a useful tool for the early detection of asphyxia-related brain injury.

Abstract: Introduction: Neonatal period is a very vulnerable period of life due to many problems. India alone contributes to about 25% of neonatal mortality around the world. In spite of advances in perinatal and neonatal care, neonatal mortality is still high in developing countries. This study was undertaken to study the disease pattern and outcome of neonates admitted to the neonatal intensive care unit (NICU) of a tertiary care teaching hospital, Mandya. Study Design: Retrospective study of medical records for 1 year (January 2014-December 2014). Materials and Methods: Neonates admitted to NICU, Mandya Institute of Medical Scienes, Mandya during the study period were included in the study; the data were recorded in predesigned proforma. The data were analyzed using appropriate statistical tool. Results: A total of 1487 neonates were admitted to NICU during the study period, 54 neonates left against medical advice, 79 were referred to other centers hence excluded from analysis. The ratio of the males to female admitted was 1.45:1. The major causes of morbidity were neonatal sepsis (28.8%), respiratory distress syndrome (RDS) (23.85%), birth asphyxia (17.72%), neonatal jaundice (7.02%), and meconium aspiration syndrome (5.47%). In this study, overall mortality rate was 7.16%. Most of the deaths were due to RDS (43.3%), birth asphyxia (37.11%), neonatal sepsis (8.25%), and congenital anomalies (8.25%). Neonates with birth weight <1500 g had poor outcome compared to neonates with birth weight more than 2500 g. Conclusion: This study identifi ed prematurity, low birth weight, neonatal sepsis, and birth asphyxia as major causes of morbidity and RDS, birth asphyxia as the major contributors to the neonatal mortality. Improving antenatal care, maternal health and timely referral of high risk cases to tertiary care hospital will help to improve neonatal outcome.

Abstract: Background Whether being small for gestational age (SGA) increases the risk of adverse neurodevelopmental outcome in premature infants remains controversial. Objective to study the impact of SGA (birthweight < percentile 10) on cognition, behavior, neurodevelopmental impairment and use of therapy at 5 years old. Methods This population-based prospective cohort included infants born before 32 weeks of gestation. Cognition was evaluated with the K-ABC, and behavior with the Strengths and Difficulties Questionnaire (SDQ). Primary outcomes were cognitive and behavioral scores, as well as neurodevelopmental impairment (cognitive score < 2SD, hearing loss, blindness, or cerebral palsy). The need of therapy, an indirect indicator of neurodevelopmental impairment, was a secondary outcome. Linear and logistic regression models were used to analyze the association of SGA with neurodevelopment. Results 342/515 (76%) premature infants were assessed. SGA was significantly associated with hyperactivity scores of the SDQ (coefficient 0.81, p < 0.04), but not with cognitive scores, neurodevelopmental impairment or the need of therapy. Gestational age, socio-economic status, and major brain lesions were associated with cognitive outcome in the univariate and multivariate model, whereas asphyxia, sepsis and bronchopulmonary dysplasia were associated in the univariate model only. Severe impairment was associated with fetal tobacco exposition, asphyxia, gestational age and major brain lesions. Different neonatal factors were associated with the use of single or multiple therapies: children with one therapy were more likely to have suffered birth asphyxia or necrotizing enterocolitis, whereas the need for several therapies was predicted by major brain lesions. Discussion In this large cohort of premature infants, assessed at 5 years old with a complete panel of tests, SGA was associated with hyperactive behavior, but not with cognition, neurodevelopmental impairment or use of therapy. Birthweight <10th percentile alone does not appear to be an independent risk factor of neurodevelopmental adverse outcome in preterm children.

Abstract: The mechanism by which the healthy heart and brain die rapidly in the absence of oxygen is not well understood. We performed continuous electrocardiography and electroencephalography in rats undergoing experimental asphyxia and analyzed cortical release of core neurotransmitters, changes in brain and heart electrical activity, and brain–heart connectivity. Asphyxia stimulates a robust and sustained increase of functional and effective cortical connectivity, an immediate increase in cortical release of a large set of neurotransmitters, and a delayed activation of corticocardiac functional and effective connectivity that persists until the onset of ventricular fibrillation. Blocking the brain’s autonomic outflow significantly delayed terminal ventricular fibrillation and lengthened the duration of detectable cortical activities despite the continued absence of oxygen. These results demonstrate that asphyxia activates a brainstorm, which accelerates premature death of the heart and the brain.

Abstract: BACKGROUND: Asphyxia is considered an important cause of morbidity and mortality in neonates. This condition can affect many vital organs including the central nervous system and may eventually lead to death or developmental disorders. OBJECTIVES: Considering the high prevalence of asphyxia and its adverse consequences, the present study was conducted to evaluate the risk factors for birth asphyxia and assess their correlation with prognosis in asphyxiated infants. PATIENTS AND METHODS: This two-year follow-up cohort study was conducted on 260 infants (110 asphyxiated infants and 150 healthy neonates) at Mashhad Ghaem Hospital during 2007 - 2014. Data collection tools consisted of a researcher-designed questionnaire including maternal and neonatal information and clinical/laboratory test results. The subjects were followed-up, using Denver II test for 6, 12, 18, and 24 months (after discharge). For data analysis, t-test was performed, using SPSS version 16.5. P value ≤ 0.05 was considered statistically significant. RESULTS: Of 260 neonates, 199 (76.5%) and 61 (23.5%) cases presented with normal neonatal outcomes and with abnormal neonatal outcomes (developmental delay), respectively. Variables such as the severity of asphyxia (P = 0.000), five-minute Apgar score (P = 0.015), need for ventilation (P = 0.000), and severity of acidosis at birth (P = 0.001) were the major prognostic factors in infants with asphyxia. Additionally, prognosis was significantly poorer in boys and infants with dystocia history (P = 0.000). CONCLUSIONS: Prevalence of risk factors for developmental delay including the severity of asphyxia need for mechanical ventilation, and severity of acidosis at birth, dystocia, and Apgar score were lower in surviving infants; therefore, controlling these risk factors may reduce asphyxia-associated complications. Language: en

Abstract: OBJECTIVE: To date, no study has systematically investigated the impact of drowning-induced asphyxia on hemostasis Our objective was to test the hypothesis that asphyxia induces bleeding by hyperfibrinolytic disseminated intravascular coagulation DESIGN: Observational study SETTING: A 2,100-bed tertiary care facility in Vienna, Austria, Europe PATIENTS: All cases of drowning-induced asphyxia (n = 49) were compared with other patients with cardiopulmonary resuscitation (n = 116) and to patients with acute promyelocytic leukemia (n = 83) Six drowning victims were investigated prospectively To study the mechanism, a forearm-ischemia model was used in 20 volunteers to investigate whether hypoxia releases tissue plasminogen activator INTERVENTIONS: None MEASUREMENTS AND MAIN RESULTS: Eighty percent of patients with drowning-induced asphyxia developed overt disseminated intravascular coagulation within 24 hours When compared with nondrowning cardiac arrest patients, drowning patients had a 13 times higher prevalence of overt disseminated intravascular coagulation at admission (55% vs 4%; p CONCLUSIONS: The vast majority of drowning patients develops overt hyperfibrinolytic disseminated intravascular coagulation, partly caused by hypoxia induced tissue plasminogen activator release Antifibrinolytics and heparinase partially reverse the abnormal clotting patterns Severe activated partial thromboplastin time prolongation may be a marker of combined hyperfibrinolytic afibrinogenemia and autoheparinization in drowning-related asphyxiaThis is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 40 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited The work cannot be used commercially Language: en

Abstract: About 25% of seizures in the neonatal period have causes other than asphyxia, ischaemia or intracranial bleeding. Among these are primary genetic epileptic encephalopathies with sometimes poor prognosis and high mortality. In addition, some forms of neonatal infant seizures are due to inborn errors of metabolism that do not respond to common AEDs, but are amenable to specific treatment. In this situation, early recognition can allow seizure control and will prevent neurological deterioration and long-term sequelae. We review the group of inborn errors of metabolism that lead to newborn/infant seizures and epilepsy, of which the treatment with cofactors is very different to that used in typical epilepsy management.

Abstract: Background and Aims: Decreasing mortality in sick and ventilated neonates is an endeavor of all neonatologists. To reduce the high mortality in this group of neonates, identification of risk factors is important. This study was undertaken to find out the indications of ventilation and complications in ventilated neonates and also study possible predictors of outcome. Subjects: Age Methods: Neonates consecutively put on mechanical ventilation during the study period (October 2011 to November 2013) enrolled. Primary disease of the neonates along with complications present listed. Clinical and laboratory parameters analyzed to find the predictors of mortality. Results: Total 300 neonates were ventilated. 52% were male. Mean age, weight, and gestational age were 21 ± 62 h, 2320 ± 846.2 g, and 35.2 ± 4.9 weeks, respectively. 130 (43%) neonates died. Respiratory distress syndrome (RDS) (31.1%), sepsis (22.7%), and birth asphyxia (18%) were the most common indications for ventilation. Mortality in ventilated patients with sepsis, pneumonia, RDS or birth asphyxia was 64.7%, 60%, 44.6%, and 33.3%, respectively. Weight P 2 , or PCO 2 did not have a significant association with mortality. On logistic regression, gestation Conclusions: Weight <2500 g, gestation <34 weeks, initial arterial pH <7.1, shock, pulmonary hemorrhage, apnea, hypoglycemia, neutropenia, and thrombocytopenia were significant predictors of mortality in ventilated neonates.

Abstract: Background: Midazolam is used as an anticonvulsant in neonatology, including newborns with perinatal asphyxia treated with hypothermia. Hypothermia may affect the safety and effectiveness of midazolam in these patients. Objectives: The objective was to evaluate the anticonvulsant effectiveness and hemodynamic safety of midazolam in hypothermic newborns and to provide dosing guidance. Methods: Hypothermic newborns with perinatal asphyxia and treated with midazolam were included. Effectiveness was studied using continuous amplitude-integrated electroencephalography. Hemodynamic safety was assessed using pharmacokinetic-pharmacodynamic modeling with plasma samples and blood pressure recordings (mean arterial blood pressure) under hypothermia. Results: No effect of therapeutic hypothermia on pharmacokinetics could be identified. Add-on seizure control with midazolam was limited (23% seizure control). An inverse relationship between the midazolam plasma concentration and mean arterial blood pressure could be identified. At least one hypotensive episode was experienced in 64%. The concomitant use of inotropes decreased midazolam clearance by 33%. Conclusions: Under therapeutic hypothermia, midazolam has limited add-on clinical anticonvulsant effectiveness after phenobarbital administration. Due to occurrence of hypotension requiring inotropic support, midazolam is less suitable as a second-line anticonvulsant drug under hypothermia.

Abstract: Introduction: Cerebral palsy (CP) is the most common physical disorder of children. Causes like jaundice and birth injury though are decreasing; complications resulting from the survival of low birth weight babies are replacing some of the older etiologies. Hence, this study was planned. Objectives: The objective was to study the clinical patterns, predisposing factors, and co-morbidities in children with CP. Materials and Methods: The present study is a hospital based prospective study conducted from January 2012 to January 2013 in children presenting to neurodevelopmental clinic at a tertiary care teaching hospital in India. Hundred cases with clinical features suggestive of CP were included in the study. Cases were evaluated by history, clinical examination, and necessary investigations. Results: Results of the study showed 81% of spastic, 12% of hypotonic, 5% of dystonic, and 2% of mixed CP cases. The mean age of presentation was 2 year, 2 month, and male to female ratio of 1:2. Pregnancy-induced hypertension (PIH) was the most common antenatal complication observed in 6%. Four percent had neonatal sepsis and 19% were born premature. Associated co-morbidities were mental retardation (55%), seizure disorder (46%), visual problems (26%), hearing problems (19%), and failure to thrive (47%). Discussion: Sex distribution observed in our study was male to female ratio of 1.2, which was comparable with a multicenter study in Europe. PIH was observed in 6% of cases, which was comparable with prior studies. Birth asphyxia was observed in 43% of cases. Eighty-one percent of the cases constituted a spastic variety of CP which was comparable to other studies. Conclusion: Perinatal asphyxia was the important etiological factor. We found preventable intranatal causes (60%) and antenatal causes (20%) forming a significant proportion. Co-morbidities were significantly observed in our study.

Abstract: Asphyxia during delivery produces long-term deficits in brain development. We investigated the neuroprotective effects of marine collagen peptides (MCPs), isolated from Chum Salmon skin by enzymatic hydrolysis, on male rats with perinatal asphyxia (PA). PA was performed by immersing rat fetuses with uterine horns removed from ready-to-deliver rats into a water bath for 15 min. Caesarean-delivered pups were used as controls. PA rats were intragastrically administered with 0.33 g/kg, 1.0 g/kg and 3.0 g/kg body weight MCPs from postnatal day 0 (PND 0) till the age of 90-days. Behavioral tests were carried out at PND21, PND 28 and PND 90. The results indicated that MCPs facilitated early body weight gain of the PA pups, however had little effects on early physiological development. Behavioral tests revealed that MCPs facilitated long-term learning and memory of the pups with PA through reducing oxidative damage and acetylcholinesterase (AChE) activity in the brain, and increasing hippocampus phosphorylated cAMP-response element binding protein (p-CREB) and brain derived neurotrophic factor (BDNF) expression.

Abstract: Birth asphyxia, which causes hypoxic-ischemic encephalopathy (HIE), accounts for 0.66 million deaths worldwide each year, about a quarter of the world's 2.9 million neonatal deaths. Animal models of HIE have contributed to the understanding of the pathophysiology in HIE, and have highlighted the dynamic process that occur in brain injury due to perinatal asphyxia. Thus, animal studies have suggested a time-window for post-insult treatment strategies. Hypothermia has been tested as a treatment for HIE in pdiglet models and subsequently proven effective in clinical trials. Variations of the model have been applied in the study of adjunctive neuroprotective methods and piglet studies of xenon and melatonin have led to clinical phase I and II trials(1,2). The piglet HIE model is further used for neonatal resuscitation- and hemodynamic studies as well as in investigations of cerebral hypoxia on a cellular level. However, it is a technically challenging model and variations in the protocol may result in either too mild or too severe brain injury. In this article, we demonstrate the technical procedures necessary for establishing a stable piglet model of neonatal HIE. First, the newborn piglet (< 24 hr old, median weight 1500 g) is anesthetized, intubated, and monitored in a setup comparable to that found in a neonatal intensive care unit. Global hypoxia-ischemia is induced by lowering the inspiratory oxygen fraction to achieve global hypoxia, ischemia through hypotension and a flat trace amplitude integrated EEG (aEEG) indicative of cerebral hypoxia. Survival is promoted by adjusting oxygenation according to the aEEG response and blood pressure. Brain injury is quantified by histopathology and magnetic resonance imaging after 72 hr.

Abstract: Objectives: Magnesium historically has been used for treatment and/or prevention of eclampsia. Considering the low body mass index of Indian women, a low-dose magnesium sulfate regime has been introduced by some authors. Increased blood levels of magnesium in neonates is associated with increased still birth, early neonatal death, birth asphyxia, bradycardia, hypotonia, gastrointestinal hypomotility. The objective of this study was to assess safety of low-dose magnesium sulfate regimen in neonates of eclamptic mothers treated with this regimen. Materials and Methods: This was a cross-sectional observational study of 100 eclampsia patients and their neonates. Loading dose and maintenance doses of magnesium sulfate were administered to patients by combination of intravenous and intramuscular routes. Maternal serum and cord blood magnesium levels were estimated. Neonatal outcome was assessed. Results: Bradycardia was observed in 18 (19.15%) of the neonates, 16 (17.02%) of the neonates were diagnosed with hypotonia. Pearson Correlation Coefficient showed Apgar scores decreased with increase in cord blood magnesium levels. Unpaired t-test showed lower Apgar scores with increasing dose of magnesium sulfate. The Chi-square/Fisher's exact test showed significant increase in hypotonia, birth asphyxia, intubation in delivery room, Neonatal Intensive Care Unit (NICU) care requirement, with increasing dose of magnesium sulfate. (P ≤ 0.05). Conclusion: Several neonatal complications are significantly related to increasing serum magnesium levels. Overall, the low-dose magnesium sulfate regimen was safe in the management of eclamptic mothers, without toxicity to their neonates.

Abstract: Many asphyxiated newborns still develop brain injury despite hypothermia therapy. The development of brain injury in these newborns has been related partly to brain perfusion abnormalities. The purposes of this study were to assess brain hyperperfusion over the first month of life in term asphyxiated newborns and to search for some histopathological clues indicating whether this hyperperfusion may be related to activated angiogenesis following asphyxia. In this prospective cohort study, regional cerebral blood flow was measured in term asphyxiated newborns treated with hypothermia around day 10 of life and around 1 month of life using magnetic resonance imaging (MRI) and arterial spin labeling. A total of 32 MRI scans were obtained from 24 term newborns. Asphyxiated newborns treated with hypothermia displayed an increased cerebral blood flow in the injured brain areas around day 10 of life and up to 1 month of life. In addition, we looked at the histopathological clues in a human asphyxiated newborn and in a rat model of neonatal encephalopathy. Vascular endothelial growth factor (VEGF) was expressed in the injured brain of an asphyxiated newborn treated with hypothermia in the first days of life and of rat pups 24-48 h after the hypoxic-ischemic event, and the endothelial cell count increased in the injured cortex of the pups 7 and 11 days after hypoxia-ischemia. Our data showed that the hyperperfusion measured by imaging persisted in the injured areas up to 1 month of life and that angiogenesis was activated in the injured brain of asphyxiated newborns.

Abstract: The present study aimed to assess the prognostic value of early amplitude-integrated electroencephalogram (aEEG) in late preterm infants who were born at a gestational age between 34 0/7 and 36 6/7 weeks for the prediction of neurobehavioral development. Late preterm infants (n = 170) with normal, mild, and severe asphyxia underwent continuous recording of aEEG for 4–6 h starting 6–8 h after delivery. The recordings were analyzed for background pattern, sleep-wake cycle (SWC), and seizures. Survivors were assessed at 18 months by neurological examination and Bayley Scales of Infant Development II. The incidence of adverse neurological outcome in the asphyxia group was significantly higher than in the normal group. For late preterm infants in the asphyxia group, abnormal aEEG pattern had a predictive potential of neurological outcomes with sensitivity of 78.57 % (specificity, 87.80 %; positive predictive value [PPV], 68.75 %; negative predictive value [NPV], 92.31 %; power, 85.45 %). Non-SWC and intermediate SWC significantly were increased (25.45 and 52.73 %, respectively) in the asphyxia group vs. the normal group. SWC pattern had neurological prognosis value in the asphyxia group with sensitivity of 64.29 % (specificity, 87.80 %; PPV, 64.29 %; NPV, 87.80 %; power, 81.82 %). Conclusion: Early aEEG patterns are important determinants of long-term prognosis of neurodevelopmental outcome in asphyxiated late preterm infants.

Abstract: Objective Total tau (T-tau), phosphorylated tau (p-Tau) and Beta-Amyloid 1-42 (AB42) in Cerebrospinal Fluid (CSF) are useful biomarkers in neurodegenerative diseases. The aim of the study was to investigate the role of these and other CSF biomarkers (T-tau, p-Tau, AB42, S100B and NSE), during hypoxia-reoxygenation in a newborn pig model. Design Thirty newborn pigs were included in a study of moderate or severe hypoxia. The moderate hypoxia group (n = 12) was exposed to global hypoxia (8% O2) until Base excess (BE) reached -15 mmol/l. The pigs in the group exposed to severe hypoxia (n = 12) received 8% O2 until BE reached -20 mmol/l or mean Blood Pressure fell below 20 mm Hg, The control group (n = 6) was kept at room air. For all treatments, the CSF was collected at 9.5 hours after the intervention. Results The level of AB42 in CSF was significantly lower in the pigs exposed to severe hypoxia compared with the control group, 922(SD +/-445)pg/ml versus. 1290(SD +/-143) pg/ml (p Interpretation This is the first study to our knowledge that demonstrated a significant drop in AB42 in CSF after neonatal hypoxia. Whether or not this has an etiological basis for adult neurodegenerative disorders needs to be studied with additional experiments and epidemiological studies. AB42 and S100B are significantly changed in neonatal pigs subjected to hypoxia compared to controls and thus may be valuable biomarkers of perinatal asphyxia.

Abstract: What Is Known about this Subject? Diffusion-weighted MRI has demonstrated changes in the corpus callosum of term neonates with perinatal asphyxia. The severity of cerebral changes demonstrated using diffusion-weighted MRI is difficult to assess without measuring values of the Apparent Diffusion Coefficient (ADC). What Is New? ADC values of the anterior part of the corpus callosum are slightly higher than of the posterior part in full term infants with perinatal asphyxia. Low ADC values of the corpus callosum were associated with an adverse outcome in infants with perinatal asphyxia. In infants treated with hypothermia lower ADC values than with normothermia were associated with a poor outcome, supporting neuroprotective effects of hypothermia Background Using MRI, changes can be detected in the corpus callosum (CC) following perinatal asphyxia which are associated with later neurodevelopmental outcome. Aim To study the association between the apparent diffusion coefficient of water (ADC) in the CC on MRI in neonates with perinatal asphyxia and neurodevelopmental outcome at 18 months of age. Subjects, Methods Of 121 infants 32 (26%) died and 13 (11%) survived with an adverse neurological outcome. Sixty-five (54%) received therapeutic hypothermia. MRI was performed within 7 days after birth using a 1.5 T or 3.0 T system, and ADC values were measured in the anterior and posterior CC. The association between ADC and composite outcome (death or abnormal neurodevelopment) was analyzed for both normothermia and hypothermia cases using receiver operating characteristics. Results ADC values of the posterior CC were lower than of the anterior part (mean difference 0.050 x 10(-3) mm(2)/s, p Conclusion Low ADC values of the posterior part of the corpus callosum are associated with an adverse outcome in term or near term neonates with perinatal asphyxia. Therapeutic hypothermia slightly modifies this association, showing that lower values were needed for an adverse outcome.

Abstract: In adults and in very preterm neonates, systemic infection is a well-recognised cause of encephalopathy. Although the manifestations of encephalopathy are very similar in the fetal inflammatory response and in acute hypoxic-ischaemic events, neonatal encephalopathy (NE) in term infants is more often attributed primarily to hypoxia-ischaemia rather than to infection. Is systemic infection an important etiological factor in NE in term and late preterm infants? A striking 1999 case report1 showed that placental infection with group B streptococcus can cause NE and that the clinical picture can closely mimic both immediate and later signs commonly assumed to indicate birth asphyxia. Many other reports describe associations of placental infections with encephalopathy in term neonates, suggesting that infection, or the resulting inflammation, can indeed underlie NE without an associated sentinel event causing asphyxia. This brief discussion considers the evidence of an infection-NE association, the difficulty of distinguishing infectious from non-infectious inflammation and the way forward. Most of the evidence relating infection to NE has concerned infections identified during the admission for delivery, usually defined histologically in the placenta, or clinically. Histological evidence includes chorioamnionitis, which is inflammation on the maternal side of the placenta and funisitis on the fetal side, with infiltration of the umbilical cord with inflammatory cells. Clinical evidence of infection includes maternal fever in labour, uterine tenderness, purulent discharge or fetal tachycardia. A third approach to identifying placental infection is by microbiological evaluation. Unfortunately, results of these approaches are often not in agreement,2 ,3 and multiple identification methods are rarely used in the same study. McDonald et al 4 compared placentas of 93 infants with NE with placentas of normal term controls (n=816) and of random controls (n=387), finding funisitis in 31.2% of NE placentas versus 5.4% and 4.4% of controls (p=0.002). Chorioamnionitis and villitis were …

Abstract: Perinatal asphyxia constitutes a prototype of obstetric complications occurring when pulmonary oxygenation is delayed or interrupted. A primary insult is first produced by the length of the time without oxygenation, leading to hypoxia/ischemia and death if oxygenation is not promptly established. A second insult is produced by re-oxygenation, eliciting a cascade of biochemical events for restoring function, implying, however, improper homeostasis. The effects observed long after perinatal asphyxia can be explained by over-expression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for oxidised nicotinamide adenine dinucleotide (NAD+) during re-oxygenation. Asphyxia also induces transcriptional activation of pro-inflammatory factors, including nuclear factor κB (NFκB) and its subunit p65, whose translocation to the nucleus is significantly increased in brain tissue from asphyxia-exposed animals, in tandem with PARP-1 overactivation, leading to the idea that sentinel protein inhibition constitutes a suitable therapeutic strategy. It is proposed that PARP-1 inhibition also down-regulates the expression of pro-inflammatory cytokines.

Abstract: Background and Purpose—Electroencephalographic recovery is predictive of outcome after perinatal hypoxia–ischemia, but it is unknown whether early changes in electroencephalographic can predict the response to therapeutic hypothermia in the preterm brain. Methods—0.7 gestation fetal sheep received umbilical cord occlusion or sham occlusion for 25 minutes, followed by sham hypothermia or whole-body cooling started either 30 minutes or 5 hours after occlusion and continued for 72 hours. Results—Early but not delayed hypothermia reduced neuronal loss and microglial induction in the striatum, with faster recovery of spectral edge frequency, reduced seizure burden, and less suppression of electroencephalographic amplitude (P<0.05). Conclusions—Recovery of higher electroencephalographic frequencies may be a biomarker of effective hypothermic neuroprotection in the preterm-equivalent brain.

Abstract: 2and/or did not cry immediately after delivery in the presence of neurologic symptoms, admitted into special care baby’s unit were studied. Of the 1163 babies admitted between 2010 and 2013, 415 (35.7%) were asphyxiated; 227 (54.7%) were males, 188 (45.3%) females, F:M was 1.2:1; However, 99 (23.9%) of the 415 asphyxiated babies died; 11 (11.1%) and 88 (88.9%) had moderate and severe asphyxia respectively. Also, 56 (56.6%) were males and 43 (43.4%) females. Significantly higher proportion of babies of mothers who had no antenatal care, mothers from low socioeconomic class 4 and 5, and who delivered outside the health facility (outborn) died ( p at least 0.001). More babies who suffered fetal distress, breech delivery and who had meconium stained liquor died (p is at least 0.04). Therefore, multiprong approach to reduce mortality from birth asphyxia is necessary like improvement of social status of women through educational and economic empowerment; provision of affordable, adequate, well equipped and cheap antenatal care to all pregnant mothers; provision of functional delivery health facilities to attend to mothers in labour to detect high risk mothers for better anticipatory care.

Abstract: The clinical evidence of neurological menifestations associated with asphyxia is described as hypoxic ischaemic encephalopathy (HIE). A variety of metabolic problems are present in asphyxiated newborns including hypoglycemia, hypocalcemia, hypomagnesemia and others metabolic abnormalities. Some of these biochemical disturbances may trigger seizure or potentiate further brain damage. This cross sectional case-control study was done in Mymensingh Medical College Hospital, to identify the association of hypoglycemia, hypocalcemia, hypomagnesemia in neonates with perinatal asphyxia. Study period was six months. Sample size was 60. Among total sample 30 term asphyxiated newborns of <24 hours age were case and equal number term healthy newborns <24 hours age were control. The main clinical presentations were delayed cry after birth along with respiratory distress, convulsion and absence of cry in asphyxiated newborns. Major physical findings were cyanosis, convulsion and tachypnoea in asphyxiated group. The mean value of serum calcium level was significantly lower in asphyxiated newborns (7.37 ± 0.10mg/dl) than control value (8.04±0.09mg/dl). Hypocalcemia was found among 23.33% babies in case group. On the contrary, hypocalcemia was found in single baby among control group. The mean value of serum magnesium was significantly lower in asphyxiated newborns (1.83 ± 0.04mg/dl) than control value (1.96 ± 0.05mg/dl). Hypomagnesemia was found among 3(10%) newborns but none was found among control group. Hypoglycemia was found in 7(23.33%) cases though the mean value of blood glucose was higher in case group (5.72 ± 0.62mmol/l) than control group (4.87 ± 0.15mmol/l) difference was not statistically significant. Combined hypoglycemia, hypocalcemia and hypomagnesemia were found in 1(3.33%) case; combined hypoglycemia and hypocalcemia were found in 2(6.67%) cases; and combined hypocalcemia and hypomagnesemia were found in 1(3.33%) case. During the study period, 3(10.0%) cases were expired but no death occurred among control group. This study shows isolated or combined hypoglycemia, hypocalcemia, hypomagnesemia are frequently found in newborns with perinatal asphyxia. So, it is necessary to monitor blood glucose, serum calcium and also serum magnesium among asphyxiated newborns for proper management.

Abstract: Background Neonatal encephalopathy following birth asphyxia is a major predictor of long-term neurological impairment. Therapeutic hypothermia is currently the standard of care to prevent brain injury in asphyxiated newborns but is not protective in all cases. More robust and versatile treatment options are needed. Angiogenesis is a demonstrated therapeutic target in adult stroke. However, no systematic study examines the expression of angiogenesis-related markers following birth asphyxia in human newborns.

Abstract: Background: Birth asphyxia occipital sinus common cause of mortality and morbidity and associated with various metabolic changes like hypoglycemia and hypocalcemia, hyperkalemia, hyponatremia, hyperphosphatemia. We conducted this study to evaluate changes in serum glucose and serum calcium in birth asphyxia. Objective: To study calcium and glucose levels in asphyxiated newborns of different severity in the early neonatal period and compare with controls. Materials and Methods: Calcium, glucose were estimated in serum samples of asphyxiated newborns of different severity and control group at 24 h of age. Results: The mean serum calcium level at 24 h of age is signifi cantly lower (8.31 ± 0.48 mg/dl vs. 9.47 ± 0.49 mg/dl; P < 0.001), mean serum glucose level was signifi cantly lower (54.4 ± 10.91 mg/dl vs. 76 ± 15.5 mg/dl; P < 0.001) in cases than control group. Among cases there was signifi cant negative correlation of serum calcium level and severity of asphyxia (P < 0.01) while there was highly signifi cant positive correlation of serum calcium with period of gestation (POG) and birth weight (P < 0.01). In the present study, there was a signifi cant negative correlation of serum glucose level and severity of asphyxia(P < 0.01) whereas highly signifi cant positive correlation was there of serum glucose with POG and birth weight. Conclusion: In the present study, it has been concluded that in birth asphyxia, there is highly signifi cant fall in serum calcium and glucose as compared to controls and proportional to degree of asphyxia.