Prediction of hypoxic-ischemic brain damage in full-term neonates with acute encephalopathy, using two different brain proteins, electroencephalogram and magnetic resonance imaging

The Objective of this study was to evaluate the usefulness of serum levels of two different brain proteins; Neuron specific enolase [NSE] and Creatinine brain specific kinase [CK-BB], electroencephalography [EEC], Conventional MRI imaging and diffusion-weighted MR imaging [DWMRI] for the early diagnosis of ischemic brain injury and prediction of hypoxic brain damage. A total of 30 term newborns were included in this study, 20 with neonatal encephalopathy and 10 normal cases. Clinical evaluation of neonatal condition and neurological outcomes was done. Serum estimation of NSE and CK-BB was done at 0, 12 and 24 hours after admission. Electroencephalography [EEC] was done at a median date of 1.17 days. Magnetic resonance imaging [MRI] both conventional and diffusion weighted were also done. EEC and MRI were done for the study group cases. The Apgar score at 2 minutes has highest specificity with a good negative predictive value of severe brain injury. Arterial blood base deficit have the highest sensitivity and highest negative predictive values. The highest significance was evident at 12 hours values of both NSE and CK-BB. A combination of NSE at 12 h with arterial blood pH [cutoff value, <6.9] or arterial blood base deficit [cutoff value, >17 mM/L] increased the positive predictive value and specificity. Bad outcomes as severe degree or death are usually associated with severe findings of both diffusion weighted MRI and background trace of EEG. The early EEG changes distinguish between those infants with a normal or abnormal outcome. MRI gives more specific information about the type and severity of brain lesion. The 12 hour values of NSE and CK-BB have a good predictive power either alone or combined with other clinical tests or investigations. This early determination is becoming increasingly important with the advent of hypothermia and other potential neuroprotective therapies for the treatment of HI brain injury in the asphyxiated newborn

Cardiac troponin T as a diagnostic marker of hypoxic myocardial injury in sick full-term and preterm neonates

Perinatal asphyxia is associated with cardiac dysfunction; this may be secondary to myocardial ischemia. Also, in preterm infants with respiratory distress syndrome, cardiac function is negatively influenced by the severity of lung disease. Cardiac troponin T [cTnT] is the ideal marker used in the detection of myocardial injury. The aim of the present work was to provide evidence of the usefulness of cTnT in the diagnosis of myocardial injury in neonates after intrauterine hypoxia or with respiratory distress syndrome. Forty five neonates were enrolled in the study and were divided into three groups: group I, fifteen full-term neonates with perinatal asphyxia; group II, fifteen preterm neonates with respiratory distress syndrome; and control group, fifteen healthy full term neonates. Arterial blood gases were measured for sick neonates; serum cTnT was assayed and echocardiography was performed for all neonates. Serum cTnT levels were significantly higher in sick neonates [groups I and II] than the control group [P<0.001]. There was significant correlation between cTnT levels and arterial blood gases [pH, PO[2], PCO[2], HCO[3]] and also with echocardiographic parameters of ventricular function [FS% and EF%] [P<0.01]. cTnT is a useful diagnostic marker used for assessment of post hypoxic myocardial injury in fullterm neonates with perinatal asphyxia or preterm neonates with respiratory distress syndrome

Prediction of hypoxic-ischemic brain damage in full-term neonates with acute encephalopathy, using two different brain proteins electroencephalogram and magnetic resonance imaging

The Objective of this study was to compare the usefulness of serum levels of two different brain proteins; Neuron specific enolase [NSE] and Creatinine brain specific kinase [CK-BB], electroencephalography [EEG], Conventional MRI imaging and diffusion-weighted MR imaging [DWMRI] for the early diagnosis of ischemic brain injury and prediction of hypoxic brain damage. The study was performed at Tanta University Hospitals, Neonatology Unit. The study design was a cross sectional one. A total of 30 term newborns, 20 with neonatal encephalopathy and 10 normal cases were included in the study. Clinical evaluation of neonatal condition and neurological outcomes was done. Serum estimation of NSE, CK-BB was done at 0, 12 and 24 hours after admission. Electroencephalography [EEG] was done at a median date of 1.17 days. Magnetic resonance imaging [MRI] both conventional and diffusion weighted were also done. EEG and MRI were done for the study group cases. The results showed that the Apgar score at 2 minutes has highest specificity with a good negative predictive value of severe brain injury. Arterial blood base deficit have the highest sensitivity and highest negative predictive values. The highest significance was evident at 12 hours values of both NSE and CK-BB. A combination of NSE at 12 h with arterial blood pH [cutoff value, <6.9] or arterial blood base deficit [cutoff value, >17 mM/L] increased the positive predictive value and specificity. Bad outcomes as severe degree or death are usually associated with the moderate to severe findings of both MRI and background trace of EEG. Bad outcomes as severe degree or death are usually associated with severe findings of both diffusion weighted MRI and background trace of EEG. The early EEG changes distinguish between those infants with a normal or abnormal outcome. MRI gives more specific information about the type of brain lesion. The 12 hour values of NSE and CK-BB have a good predictive power either alone or combined with other clinical tests or investigations. Combined biochemical testing and EEG may give very good indicators about neonatal outcomes. This early determination is becoming increasingly important with the advent of hypothermia and other potential neuroprotective therapies for the treatment of HI brain injury in the asphyxiated newborn

Neonatal cerebrospinal fluid plasminogen and plasminogen activator inhibitor-1 assay as predictors of post hemorrhagic hydrocephalus

Massive intraventricular hemorrhage [IVH] in neonates is followed by progressive ventricular dilatation in 55-80% of cases if the infant survives. The initial mechanism of post hemorrhagic hydrocephalus [PHH] is thought to be obstruction by multiple small blood clots of the channels of the cerebrospinal fluid [CSF] to areas of absorption. Plasminogen activator inhibitor-1 [PAI-1] is the principal regulator of fibrinolysis in blood and one of the most highly controlled of the fibrinolytic components. The aim of this study is to measure plasminogen and plasminogen activator inhibitor-1 levels in the CSF of the neonates after IVH to assess endogenous fibrinolytic activity and to predict the development of post hemorrhagic hydrocephalus. Fifteen full term and preterm neonates with IVH were enrolled in the study. Ten neonates without IVH were used as a control group. Cranial ultrasound was performed at age of 2 weeks and 2 months. Plasma and CSF plasminogen and PAI-1 levels were assessed for these neonates. The results revealed that CSF PAI-1 was significantly higher in infants with IVH than in the controls [P<0.001]. There was no significant difference in the CSF and plasma plasminogen between infants with IVH and controls [p>0.05]. CSF PAI-1 was significantly higher in infants with PHH than in infants with post hemorrhagic ventricular dilatation [p<0.05], with a sensitivity [100%] and specificity [100%]. CSF PAI-1 is a very sensitive and specific parameter than CSF plasminogen for prediction of PHH in neonates with IVH, and this might be useful to evaluate the specific therapeutic programs of these neonates

Predictability of neonatal infection in cases of preterm premature rupture of membranes by interleukin-6 estimation: antenatal bed side test from vaginal fluid versus neonatal serum testing at birth and after 24 hours

The Objective of this study was to assess the predictability of interleukin 6[IL-6] for neonatal infection, in women with preterm premature rupture of membranes [PPROM] using a bed side test from vaginal fluid versus neonatal serum testing at birth and after 24 hours. The study was a cross sectional one and enrolled 73 women who were hospitalized for PPROM. The gestational age at study entry ranged between 28 and 35 completed weeks of gestation that was confirmed from history and/or by a first-trimester ultrasonograhy. Maternal routine investigations as serum C reactive protein [CRP] and IL-6 detection in vaginal fluid were done. Neonatal examination and assessment was done. Initial neonatal outcomes as Apgar score, neonatal infections and neonatal cranial ultrasound were assessed. Neonatal CRP and IL-6 were also estimated. The results showed that neonatal infections were more frequent for babies of women with IL-6-positive vaginal samples [29.7% vs 8.3%; P=0.02]. The sensitivity of vaginal testing of IL-6 for predicting neonatal infection was 79%; its specificity was 56%; its positive predictive value was 30%, and its negative predictive value was 92%. The mean neonatal IL-6 at 0 hour was significantly higher in babies of the vaginally positive than the vaginally negative mothers [P<0.01]. The sensitivity of IL-6 at 0 hour for predicting neonatal infection was 99%; specificity was 91.4%; positive predictive value was 57.4%, and negative predictive value was 92%. The sensitivity at 24 hours was 67.4%; specificity was 69.3%; positive predictive value was 50%, and negative predictive value was 63%. Estimation and detection of IL-6 with both the qualitative vaginal secretions bedside test and at birth neonatal serum are of great value in the prediction of neonatal infection in cases of PPROM. This cytokine may reflect the insult that the fetus had been exposed to: hence affection of the fetal brain. Antenatal detection and early at birth estimation are of medico legal importance, which may protect obstetricians and pediatricians from alleged intrapartum or early neonatal mismanagement

Prediction of infants who may develop bronchopulmonary dysplasia in preterm babies with respiratory distress syndrome

The objective of this study was to test the neonatal polymorphism of TNF alpha to measure the day one levels of sL-selectin, sE-selectin and sICAM-1 in sera of neonate and placenta growth factor in cord blood, for the prediction of development of bronchopulmonary dysplasia [BPD]. The study design was a cross sectional one. Forty preterm neonates with respiratory distress and 10 normal full term neonates were enrolled. The neonates were divided into 2 subgroups; 15 who developed bronchopulmonary dysplasia and 25 without. Sampling was done and diagnostic evaluation of all parameters was accomplished. The results proved that infants. None of the infants with BPD carried the AA TNF- alpha -238 genotype, compared with 3 infants without BPD, and only 1 infant with BPD carried the GA TNF- alpha -238 genotype, compared with 7 infants without BPD. Higher sE-selectin has a diagnostic ability [sensitivity 73%, specificity 76%] higher PLGF has a sensitivity of 67% and specificity 68%. Combination of both, improved specificity to 80%. If we add to them, cases which have absence of GA TNF- alpha -238 genotype, we have got a very high sensitivity [93%] but with lower specificity. Combined all data supported a specificity 80% with a sensitivity of 86%. What had been found in this study might clarify the role of adhesion molecules, P1GF and TNF polymorphism as biological marker to determine which premature infants with RDS are at risk for development of BPD and to permit early intervention and might provide a new therapeutic target to prevent BPD

Serum intercellular adhesion molecule-1 and interleukin-10 in asthmatic children

The objective of the present study was to investigate serum, intercellular adhesion molecule-I [sICAM-1] and interleukin-10 [IL-10] in asthmatic children in correlation with immunoglobulin E [IgE]. Thirty asthmatic children and ten controls were enrolled. Using enzyme linked immunosorbent assay [ELISA] sIACM-1, IL-10 and total IgE levels were determined during acute attacks, and 2 weeks after remission [stable asthma]. The results of the present study showed that sICAM-1 and total IgE increased significantly in children during acute attacks Vs controls [P<0.05], while IL-10 decreased significantly in children during acute attack Vs controls [P<0.05]. On the other h and, in stable asthma sICAM-1, IL-10, and total IgE all return to levels comparable with controls. IL-10 correlated significantly in a negative manner with sICAM-1 and total IgE levels. While sICAM-1 correlated positively with total IgE levels We can conclude that sICAM-1 might play a remarkable Pathophysiology role in controlling the severity of asthmatic paroxysm, whereas IL-10 is protective against asthma. The present data open the door in the very near future for therapeutic intervention in pediatric asthma using anti-inflammatory agents could act by blocking ICAM-1 molecules and administration of IL-10 as a novel therapy