morphine and Cerebral-Palsy

Intrapartum asphyxia is defined as metabolic acidemia measured at birth with pH less than 7.00 and base deficit greater or equal to 12 mmol/l. Neonatal complications of intrapartum asphyxia include multiorgan failure and neonatal encephalopathy. Most severe consequences are death and neurological or sensorial impairment. Cause of permanent neurological impairment can be attributed to intrapartum asphyxia if three criteria are met: intrapartum history of a threatening event with acute fetal heart rate deterioration, biological markers of asphyxia, neonatal encephalopathy. Moderate to severe neonatal encephalopathy in asphyxiated term infants is associated with a high risk of cerebral palsy (especially quadriplegic or dyskinetic type) and/or cognitive disorders. Prognosis of neonatal encephalopathy can be accurately assessed by MR imaging.

Topics: Acidosis; Apgar Score; Biomarkers; Brain Diseases; Cerebral Palsy; Female; Fetal Blood; Fetal Hypoxia; Heart Rate, Fetal; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Lactic Acid; Magnetic Resonance Imaging; Meconium; Multiple Organ Failure; Nervous System Diseases; Pregnancy; Ultrasonography

A review of meconium pathophysiology and its contribution to the incidence of postnatal neurological handicap.. Reviewed article.. Department of Gynaecology and Obstetrics, Charles University and Faculty Hospital Plzen, Czech Republic.. Meconium can be a cause of infant neurological handicap. Two main pathogenetic pathways are mentioned. 1. Meconium (and its components: bile acids) may have a direct vasoconstrictive effect on umbilical and placental vessels. This way still remains controversial. 2. Meconium as a possible cause of intraamniotic infection results in a release of fetal cytokines (TNF alpha, IL-1 beta, IL-6), which can damage myelinogenesis in periventricular white matter.. Meconium in premature labour is a higher risk factor compared to term delivery. 41% of premature infants were diagnosed as having CP when meconium was present compared to 10% in the same group with clear amniotic fluid. The incidence in term pregnancy with meconium present is 0.4% compared to 0.3% in a population without any obstetrical risk.. Ultrasonographically found periventricular leukomalacia is the most reliable sign of subsequent cerebral palsy or other neurological sequelae.

Topics: Amniotic Fluid; Brain Damage, Chronic; Cerebral Palsy; Chorioamnionitis; Female; Humans; Infant, Newborn; Leukomalacia, Periventricular; Meconium; Placenta; Pregnancy

In this article, the authors examine whether indicators commonly used to recognized birth asphyxia are specific to asphyxial states, and whether these allow recognition of a severity of asphyxia sufficient to pose a risk of irreversible brain injury. Characteristics recognizable within the first hours after birth are focused on because these characteristics will be of most use in clinical decisions regarding use of potential new therapies for asphyxia.

Topics: Amniotic Fluid; Apgar Score; Asphyxia Neonatorum; Biomarkers; Blood Gas Analysis; Brain Diseases; Causality; Cerebral Palsy; Decision Making; Female; Heart Rate, Fetal; Humans; Infant, Newborn; Meconium; Predictive Value of Tests; Pregnancy; Pulmonary Gas Exchange; Severity of Illness Index

To evaluate the obstetric antecedents of cystic periventricular leukomalacia and transient echodense periventricular lesions among preterm infants.. A cohort study of preterm singleton infants born between 25 and 33 weeks gestation.. Pavia, Italy.. Three hundred and forty-nine infants admitted to a Division of Neonatal Intensive Care who were screened for periventricular leukomalacia.. The obstetric factors in infants with either cystic periventricular leukomalacia or transient echodense periventricular lesions were compared to those in infants with negative cranial ultrasonographic findings. Stepwise multiple logistic regression analysis was used to evaluate the association between risk factors and outcomes adjusting for confounders.. The prevalence of cystic periventricular leukomalacia and transient echodense lesions was 5.7% (20/349) and 14% (49/349), respectively. The main risk factors for cystic leukomalacia were first trimester haemorrhage (OR 4.49; 95% CI 1.63-12.39), maternal urinary tract infection on admission (OR 5.71; 95% CI 1.91-17.07), and neonatal acidosis (pH < 7.2) at birth (OR 5.97; 95% CI 1.93-18.52). Meconium-stained amniotic fluid (OR 3.95; 95% CI 1.42-10.98) and long term (> 72 hours) ritodrine tocolysis (OR 2.54; 95% CI 1.28-5.05) were associated with an increased risk of echodense lesions. The likelihood of overall leukomalacia (cystic plus echodense periventricular lesions) was increased among cases with meconium-stained amniotic fluid (OR 4.06; 95% CI 1.65-10.0), long-term ritodrine tocolysis (OR 2.56; 95% CI 1.38-4.72), maternal infection (OR 1.73; 95% CI 1.0-3.0), and acidosis at birth (OR 1.98; 95% CI 1.0-3.98).. This study confirms that maternal infection, acidosis at birth, and meconium-stained amniotic fluid increase the risk of periventricular leukomalacia in preterm infants. Long-term ritodrine use seems to increase the risk for transient echodense lesions.

Topics: Acidosis; Adult; Cerebral Hemorrhage; Cerebral Palsy; Cohort Studies; Female; Fetal Membranes, Premature Rupture; Humans; Infant, Newborn; Leukomalacia, Periventricular; Meconium; Obstetric Labor, Premature; Pregnancy; Risk Factors; Ritodrine; Tocolytic Agents; Urinary Tract Infections

To estimate the risk for cerebral palsy in preterm infants in relation to the presence of meconium in the amniotic fluid (AF).. A cohort study was conducted of 404 consecutive preterm infants delivered between 24 and 33 weeks' gestation at a single institution. Sociodemographic and clinical data were collected at birth. The diagnosis of cerebral palsy was made at 2 years' corrected age. Politomous logistic regression models were used to evaluate the odds for cerebral palsy while adjusting for potential confounders.. The overall prevalence of cerebral palsy among survivors was 11.6% (40/345). The cerebral palsy rate was 41.2% (7/17) among infants who were meconium-stained at birth and 10% (33/328) among those who were not (P = .006 by Fisher exact test). After adjustment for potential confounders (gestational age and fetal gender), the odds ratio of cerebral palsy among infants delivered to women with meconium-stained AF was 6.9 (95% confidence interval 2.32, 20.81, P = .001) relative to those delivered to women with clear AF.. The results of the present study support the view that the presence of meconium in the AF is a gestational age-independent risk factor for cerebral palsy among preterm infants.

Topics: Amniotic Fluid; Cerebral Palsy; Cohort Studies; Female; Gestational Age; Humans; Infant, Newborn; Infant, Premature, Diseases; Logistic Models; Meconium; Prevalence; Risk Factors; Socioeconomic Factors

Markers currently used to identify infants at highest risk for perinatal hypoxic-ischemic cerebral injury are insensitive in predicting the subsequent occurrence of neonatal seizures and/or neurodevelopmental sequelae, ie, cerebral palsy. To facilitate therapeutic strategies, early identification of the infant at highest risk for developing seizures secondary to hypoxia ischemia or asphyxia is critical, particularly if novel but potentially toxic therapies currently under experimental investigation become available for clinical use.. Ninety-six inborn term infants considered at high risk for having neonatal seizures secondary to hypoxia ischemia or asphyxia and admitted to the neonatal intensive care unit directly after labor and delivery were prospectively evaluated. Markers of high risk included the presence of moderate to thick meconium-stained amniotic fluid (MSAF), fetal heart rate (FHRT) abnormalities abruptio placentae, intubation and positive pressure ventilation in the delivery room (DR), chest compressions and epinephrine administration as part of resuscitation, a 5-minute Apgar score of 5 or less, umbilical cord arterial pH of 7.00 or less, and/or a base deficit of -14 mEq/L or more negative.. Seizures developed in 5 (5.2%) of the 96 infants. High-risk markers included FHRT abnormalities only (n=36), FHRT abnormalities and MSAF (n=20), MSAF only (n=23), abruptio placentae (n=6), intubation in the DR (n=44), intubation in the neonatal intensive care unit (n=22), chest compressions (n=2), 5-minute Apgar scores of 5 or less (n=21), umbilical cord arterial pH of 7.00 or less (n=21), and base deficits of -14 mEq/L or more negative (n=19). By univariate analysis, significant relationships with seizures were found with Apgar scores, the need for intubation in the DR, umbilical cord arterial pH, and base deficit. Combinations of the identified risk markers showed a strong relationship with seizures with the following odds rations (ORs), 95% confidence limits, sensitivity, specificity, and positive predictive values (PPVs): (1) low cord pH and intubation, OR, 163 (confidence limits, 7.9 and 3343.7); sensitivity, 100%; specificity 94%; and PPV, 50%; (2) low cord pH and low 5-minute Apgar score, OR, 39 (confidence limits, 3.9 and 392.5); sensitivity, 80%; specificity, 91%; and PPV, 33.3%; and (3) low pH, intubation, and low 5-minute Apgar score, OR, 340 (confidence limits, 17.8 and 6480.6); sensitivity, 80%; specificity, 98.8%; and PPV, 80%.. A combination of high-risk postnatal markers, specifically, a low 5-minute Apgar score and intubation in the DR in association with severe fetal acidemia, facilitates the identification within the first hour of life of term infants at highest risk for developing seizures secondary to perinatal asphyxia.

Topics: Abruptio Placentae; Acid-Base Imbalance; Adrenergic Agonists; Amniotic Fluid; Apgar Score; Asphyxia Neonatorum; Brain Ischemia; Cardiopulmonary Resuscitation; Cerebral Palsy; Epinephrine; Female; Fetal Blood; Forecasting; Heart Rate, Fetal; Humans; Hydrogen-Ion Concentration; Hypoxia, Brain; Infant, Newborn; Intensive Care, Neonatal; Intubation, Intratracheal; Meconium; Positive-Pressure Respiration; Pregnancy; Prospective Studies; Risk Factors; Seizures

To determine if meconium in the amniotic fluid (AF) can cause cerebral palsy by stimulating umbilical and placental blood vessels to constrict.. Brain injury patterns were analyzed in 43 children whose exposure to meconium in the AF was their only identified risk for quadriplegic cerebral palsy. The times their injuries occurred were established by following lymphocyte counts in their blood after birth.. All 43 had cerebral cortical and subcortical brain damage of the type produced by late gestational ischemia and hypoxemia. The time between the onset of injury and birth ranged from 2-38 hours. The neonates were severely acidotic at birth when birth occurred within 12-14 hours after ischemia and hypoxemia began. Thereafter, the acidosis receded as the time between its start and birth increased, presumably because vasoconstriction had ended. Severe acidosis did not recede in nine children whose cerebral palsy was due to disorders that kept them hypoxemic until birth.. Meconium in the AF may sometimes initiate vasoconstriction that leads to ischemic, hypoxemic cerebral palsy.

Topics: Acidosis; Amniotic Fluid; Brain Ischemia; Cerebral Palsy; Erythroblasts; Erythrocyte Count; Fetal Blood; Fetal Diseases; Humans; Hydrogen-Ion Concentration; Hypoxia; Infant, Newborn; Lymphocyte Count; Meconium; Time Factors; Umbilical Cord; Vasoconstriction

Analyses were undertaken to determine the causes of cerebral palsy in a prospective study of 43,437 full-term children. Presumed causes were found for about 71% of the 34 quadriplegic and 40% of the 116 nonquadriplegic patients with cerebral palsy. Risk estimates based on predictive models, adjusted for multiple factors, suggest that 53% of the quadriplegic patients with cerebral palsy could be attributed to congenital disorders, 14% to birth asphyxia, and 8% to other identified disorders. Thirty-five percent of the nonquadriplegic patients with cerebral palsy could be attributed to congenital disorders and 6% to other disorders. In the victims of cerebral palsy, characteristic consequences of birth asphyxia were more often the result of nonasphyxial disorders. These included meconium in the amniotic fluid, low 10-minute Apgar scores, neonatal apnea spells, seizures, persisting neurologic abnormalities, and slow head growth after birth.

Topics: Aged; Amniotic Fluid; Apgar Score; Asphyxia Neonatorum; Central Nervous System Diseases; Cerebral Palsy; Child; Confidence Intervals; Congenital Abnormalities; Humans; Infant; Infant, Newborn; Meconium; Prospective Studies; Risk Factors

Chronically meconium-stained fetuses may ultimately suffer cerebral palsy and other devastation. The mechanism is unknown. Innocuous pregnancy complications may cause some fetuses to discharge meconium, which may become hazardous, independently of aspiration. We herein report previously undescribed, meconium-induced umbilical and placental vascular necrosis. To investigate whether meconium causes vasocontraction, we tested umbilical vein tissue with an isometric transducer connected to a polygraph. The specimens were suspended in a 30-mL organ bath with Krebs solution (pH, 7.4; temperature, 37 degrees C; under aeration with 95% O2 and 5% CO2). We exposed the tissue to meconium and compared meconium-induced vasocontraction with that induced by Krebs solution and 10(-5) molar serotonin. Meconium maximally produced 62.9% of serotonin-induced vasocontraction. Krebs solution and boiled meconium did not produce vasocontraction. We hypothesize that meconium may cause placental and umbilical cord vasocontraction, cerebral and other fetal hypoperfusion, and major poor outcome.

Topics: Asphyxia Neonatorum; Cerebral Palsy; Cerebrovascular Circulation; Female; Humans; Hypoxia, Brain; Infant, Newborn; Ischemia; Meconium; Meconium Aspiration Syndrome; Muscle, Smooth, Vascular; Placenta; Pregnancy; Pregnancy Outcome; Risk Factors; Vasoconstriction