Subependymal Germinal Matrix Research Articles

Posterior subependymal germinal matrix hemorrhage as a mild form of hemorrhage in extremely preterm infants: neurodevelopmental outcomes at corrected ages of 18-24 months.

This study aimed to explore the effects of both the presence and size of posterior subependymal germinal matrix hemorrhage (PS-GMH), considered a mild form of hemorrhage, on the neurodevelopmental outcomes of extremely preterm infants. A retrospective analysis was conducted on 221 extremely preterm infants, assessing their initial and term-equivalent age (TEA) cranial ultrasound (cUS) examinations from 2016 to 2021. Infants were classified based on the presence and size (small/large) of PS-GMH. Neurodevelopmental outcomes at corrected ages of 18-24 months were analyzed in 135 infants. PS-GMH was identified in 86.9% (192/221) of the infants, with 13.5% (26/192) exhibiting large PS-GMH. Among the 135 infants who were followed up, those with PS-GMH were found to have younger gestational ages (P<0.001) and a higher incidence of maternal chorioamnionitis (P=0.016) than those without PS-GMH. Significant differences were observed in the incidence of grade II intraventricular hemorrhage (IVH) on initial cUS (P=0.003) and ventriculomegaly at TEA cUS (P=0.026) across the groups with no PS-GMH, small PS-GMH, and large PS-GMH. The large PS-GMH group exhibited a higher occurrence of grade II IVH than the small PS-GMH group (P=0.006). However, ventriculomegaly incidence did not significantly vary with PS-GMH status. Neurodevelopmental outcomes were also not significantly different across PS-GMH statuses. The adjusted odds ratios for any neurodevelopmental impairment, compared to the no PS-GMH group, were 1.70 (95% confidence interval [CI], 0.40 to 7.26; P=0.471) for all PS-GMH, 1.61 (95% CI, 0.37 to 6.93; P=0.526) for small PS-GMH, and 3.84 (95% CI, 0.62 to 24.00; P=0.150) for large PS-GMH. PS-GMH was frequently observed in extremely preterm infants; however, it did not independently predict adverse neurodevelopmental outcomes.

Pharmacological Strategies and Surgical Management of Posthemorrhagic Hydrocephalus Following Germinal Matrix-Intraventricular Hemorrhage in Preterm Infants.

Germinal matrix-intraventricular hemorrhage (GM-IVH) is a detrimental neurological complication that occurs in preterm infants, especially in babies born before 32 weeks of gestation and in those with a very low birth weight. GM-IVH is defined as a rupture of the immature and fragile capillaries located in the subependymal germinal matrix zone of the preterm infant brain, and it can lead to detrimental neurological sequelae such as posthemorrhagic hydrocephalus (PHH), cerebral palsy, and other cognitive impairments. PHH following GM-IVH is difficult to treat in the clinic, and no levelone strategies have been recommended to pediatric neurosurgeons. Several cellular and molecular mechanisms of PHH following GM-IVH have been studied in animal models, but no effective pharmacological strategies have been used in the clinic. Thus, a comprehensive understanding of molecular mechanisms, potential pharmacological strategies, and surgical management of PHH is urgently needed. The present review presents a synopsis of the pathogenesis, diagnosis, and cellular and molecular mechanisms of PHH following GM-IVH and explores pharmacological strategies and surgical management.

Intraventricular Hemorrhage in Premature Infants: A Review of Risk Factors, Pathology, Treatment, and Prognosis

Abstract Intraventricular hemorrhage (IVH) in newborns is defined as bleeding within the ventricles, surrounded by the brain. This condition is most commonly observed in premature newborns and is directly proportional to gestational age; the smaller the gestational age, the higher the risk of IVH. It typically occurs in the subependymal germinal matrix, a highly vascularized area undergoing significant development in newborns and regression in full-term infants. The etiology is multifactorial and primarily attributed to the intrinsic fragility of the vascularization of the germinal matrix. Risk factors for IVH in premature infants include the immaturity of the cerebral vascular system, fluctuations in blood pressure, hypoxia, and oxidative stress. Furthermore, clinical factors such as respiratory distress syndrome, mechanical ventilation, and coagulation disorders contribute to the vulnerability of preterm infants to this complication. Regarding treatment, interventions can range from careful monitoring and medical support to surgical procedures such as cerebrospinal fluid drainage or ventriculoperitoneal shunting in severe cases. Pharmacological therapy, including the use of anti-inflammatory drugs, may be implemented to minimize brain injuries. Complications of IVH include obstructive hydrocephalus, non-obstructive hydrocephalus, post-hemorrhagic hydrocephalus, developmental disorders, cerebral palsy, and seizures. In conclusion, IVH in premature infants remains a complex and delicate issue in neonatology. An integrated approach covering both prevention and treatment is essential to minimize the negative impact of this complication on the neurological development of premature infants. Continuous research is necessary to develop innovative and effective strategies for managing this critical problem in neonatal medicine. Transfontanelar ultrasound remains the election method for diagnosis. Mild and moderate forms have shown favorable progression, while severe IVH has led to the development of post-hemorrhagic obstructive hydrocephalus.

Perspectives : Understanding the Pathophysiology of Intraventricular Hemorrhage in Preterm Infants and Considering of the Future Direction for Treatment.

Remarkable advances in neonatal care have significantly improved the survival of extremely low birth weight infants in recent years. However, intraventricular hemorrhage (IVH) continues to be a major complication in preterm infants, leading to a high incidence of cerebral palsy and cognitive impairment. IVH is primarily caused by disruption of the fragile vascular network of the subependymal germinal matrix, and subsequent ventricular dilatation adversely affects the developing infant brain. Based on recent research, periventricular white matter injury is caused not only by ischemia and morphological distortion due to ventricular dilatation but also by free iron and inflammatory cytokines derived from hematoma and its lysates. The current guidelines for the treatment of posthemorrhagic hydrocephalus (PHH) in preterm infants do not provide strong recommendations, but initiating treatment intervention based on ultrasound measurement values before the appearance of clinical symptoms of PHH has been proposed. Moreover, in the past decade, therapeutic interventions that actively remove hematomas and lysates have been introduced. The era is moving beyond cerebrospinal fluid shunt toward therapeutic goals aimed at improving neurodevelopmental outcomes.

Risk factors, trends of neurological disorders, and outcomes of neonatal periventricular hemorrhages

Periventricular hemorrhage is bleeding from the subependymal germinal matrix, which results in severe motor disorders, mental and speech developmental delay.Purpose. The study aims to evaluate risk factors, the trends of neurological disorders, and the outcomes of neonatal periventricular hemorrhage in children whose mothers were on gravidary anticoagulant and/or antiplatelet therapy.Material and methods. The study examined 160 newborns with PVH: Group I — 53 (37.9%) children born from pregnancy on the background of antiplatelet and/or anticoagulant therapy for hypercoagulation syndrome; Group II — 87 (62.1%) children born from pregnancy on the background of antiplatelet and/or anticoagulant therapy to treat degree 1A uteroplacental blood flow disorders; Group III — 20 children born from pregnancy without corticosteroids and antiplatelet and/or anticoagulant therapy. All newborns underwent clinical and neurological examination and neurosonography; data on somatic and obstetric anamnesis were obtained from accompanying medical records.Results. In children of Groups I and II a more severe condition of newborns with periventricular hemorrhage at birth was noted, a slower dynamics of restoration of muscle-postural tone and the pace of psychomotor development were observed compared to children in Group III. In Groups I and II a high incidence of epilepsy (5.7%) and cerebral palsy (6.4%) by 12 months of corrected age was revealed compared with the population.Conclusion. Gravidary anticoagulant and antiplatelet therapy might be considered as a risk factor for the development of intracranial hemorrhages and severe neurological disorders: epilepsy, cerebral palsy, mental and motor developmental delays.

Germinal Matrix-Intraventricular Hemorrhage: A Tale of Preterm Infants.

Germinal matrix-intraventricular hemorrhage (GM-IVH) is a common intracranial complication in preterm infants, especially those born before 32 weeks of gestation and very-low-birth-weight infants. Hemorrhage originates in the fragile capillary network of the subependymal germinal matrix of the developing brain and may disrupt the ependymal lining and progress into the lateral cerebral ventricle. GM-IVH is associated with increased mortality and abnormal neurodevelopmental outcomes such as posthemorrhagic hydrocephalus, cerebral palsy, epilepsy, severe cognitive impairment, and visual and hearing impairment. Most affected neonates are asymptomatic, and thus, diagnosis is usually made using real-time transfontanellar ultrasound. The present review provides a synopsis of the pathogenesis, grading, incidence, risk factors, and diagnosis of GM-IVH in preterm neonates. We explore brief literature related to outcomes, management interventions, and pharmacological and nonpharmacological prevention strategies for GM-IVH and posthemorrhagic hydrocephalus.

Reversal of blood flow in deep cerebral vein in preterm intraventricular hemorrhage: two case reports

BackgroundIntraventricular hemorrhage during the early stage is a major complication in very low birth weight infants. Elevation of venous pressure is one of the contributing factors. The internal cerebral vein receives most of the venous flow from the subependymal germinal matrix, the most common site of origin of intraventricular hemorrhage. Recently, it has been reported that pulsatile or partially interrupted internal cerebral vein waveforms might also be risk factors for intraventricular hemorrhage in extremely low birth weight infants. Here, we report two cases of partially reversed internal cerebral vein flow with intraventricular hemorrhage. There are no published reports documenting this unique flow pattern.Case presentationBetween 2013 and 2020, we had in our neonatal intensive care unit two cases of very low birth weight infants (27 and 25 weeks of gestational age) who showed a partially reversed internal cerebral vein waveform pattern, which was recognized as a new blood flow pattern. Their internal cerebral vein flow patterns were continuously flat early after birth. They showed an intraventricular hemorrhage on the unilateral side with partially interrupted internal cerebral vein flow at 31 and 41 hours after birth (27- and 25-week-old neonates, respectively). Consecutively, their internal cerebral vein flow changed to a partially reversed pattern with intraventricular hemorrhage on the contralateral side at 43 and 87 hours after birth (27- and 25-week-old neonates, respectively). Their flow patterns improved by day 7. These partially reversed patterns were equivalent to triphasic venous flow, and the reverse flow corresponded to A- and V-waves.ConclusionIn the two cases, the internal cerebral vein flow patterns were normal and flat before intraventricular hemorrhage and changed to a severe flow pattern (partially interrupted or reversed flow) at the same time as the detection of intraventricular hemorrhage. After the development of intraventricular hemorrhage, they improved. These cases indicate that a partially reversed or interrupted internal cerebral vein flow pattern may be derived from central venous pressure elevation and related to intraventricular hemorrhage in very low birth weight infants, however, it is difficult to determine when this flow pattern occurs in relation to intraventricular hemorrhage.

Astrogliosis inhibition attenuates hydrocephalus by increasing cerebrospinal fluid reabsorption through the glymphatic system after germinal matrix hemorrhage

Germinal matrix hemorrhage (GMH) results from the rupture of the immature thin-walled blood vessels and consequent bleeding into the subependymal germinal matrix and possible lateral ventricles. The purpose of this study is to investigate how astrogliosis impacts the glymphatic-meningeal lymphatic system in cerebrospinal fluid (CSF) reabsorption after GMH and how the anti-scarring agent olomoucine attenuates post-hemorrhagic hydrocephalus. GMH was induced by stereotaxic collagenase infusion into P7 Sprague-Dawley rats of both sexes. Western blot and immunofluorescence were used to assess astrogliosis and how astrogliosis affects glymphatic function by measuring Aquaporin-4 expression. Intracisternal injection of fluorescence tracer was used to measure CSF diffusion throughout the brain, its dispersion in the paravascular area and CSF drainage into the deep cervical lymph nodes at 28 days after GMH. Both short-term and long-term behavioral tests were used to assess the neurological outcomes. Nissl staining was used to assess the morphological changes at 28 days after hemorrhage. GMH elicited astrogliotic scarring and reduced the exchange between CSF and interstitial fluid, as well as CSF reabsorption through the meningeal lymphatic vessels. This might be associated with redistribution of Aquaporin-4. Olomoucine ameliorated scar tissue formation and attenuated post-hemorrhagic hydrocephalus. These findings of this study suggested that the glymphatic system might play a role in CSF reabsorption in neonates following GMH. Scar tissue formation impairs this CSF clearance route, and therefore astrogliosis inhibition might be a potential therapeutic strategy for neonatal post-hemorrhagic hydrocephalus.

Factores Asociados a Hemorragia Intraventricular En Neonatos Atendidos En Un Hospital de Segundo Nivel

Intraventricular hemorrhage (HIV) is a complication in neonates. It originates in the subependymal germinal matrix. This area is irrigated by a network of poorly differentiated vessels without a basement membrane. Also, it is fragile and vulnerable to the hemodynamic instability of cerebral blood flow. It is an important risk factor for periventricular leukomalacia, ventriculomegaly, and hydrocephalus. These neurological pathologies can generate sequelae in the pediatric population such as cerebral palsy (CP). Objective: To identify the factors associated with HIV in neonates treated in the early intervention program of the hospital of specialties of the child and the woman of the Secretary of Health of the State of Querétaro (HENMSESEQ). Material and Methods: Through the review of the clinical files, the factors associated with HIV present in the children attended to in the HENMSESEQ early intervention service were observed in 2015. Cases of HIV were corroborated by means of transfontanel ultrasound, statistical analysis with measures of central tendency, and comparison of the medians of children diagnosed with HIV and without diagnosis. Results: A group of 69 infants attended to in the early intervention program was studied. Out of them, 65.2% (45) were women and 34.3% (24) were men. They had a gestational age of 34.19 ± 4.22 weeks, birth weight of 2116.09 ± 859.36 g, and height of 44.06 ± 6.02 cm. Their stay in the Neonatal Intensive Care Unit (NICU) for the sample was 11.88 ± 16.84 days and they were 8.65 ± 12.20 days with invasive mechanical ventilation. There were 25 cases of HIV diagnosed by transfontanel ultrasound. Out of the 25 cases, 7 (10%) were HIV grade I, 14 (20%) II, 4 (5.7%) III, and no cases of grade IV were diagnosed. Using the Mann-Whitney U test, a difference was found between the groups of neonates diagnosed with HIV and without diagnosis in weeks of gestation, height, weight, APGAR, days of intubation, and days of stay in NICU.

Impaired Neurodevelopmental Outcome After Mild Germinal Matrix-Intraventricular Hemorrhage.

* Abbreviations: CI — : confidence interval GMH-IVH — : germinal matrix–intraventricular hemorrhage NDI — : neurodevelopmental impairment OPC — : oligodendroglial precursor cell Germinal matrix–intraventricular hemorrhage (GMH-IVH) is a common and characteristic form of intracranial hemorrhage occurring in the premature infant.1 The hemorrhage originates in small blood vessels in the subependymal germinal matrix (also termed the ganglionic eminence) and may disrupt the ependymal lining and extend into the lateral ventricle. Severe IVH consists of large amounts of intraventricular blood (usually termed grade 3 IVH) and may be complicated by hemorrhagic venous infarction in the periventricular white matter (often termed grade 4 IVH) or by post–hemorrhagic hydrocephalus or both. Many studies have documented increased short-term and long-term neurologic morbidity after severe IVH.1 In this issue of Pediatrics , Mukerji et al2 report the first meta-analysis of neurodevelopmental outcomes after GMH-IVH (termed periventricular/intraventricular hemorrhage in the report). Their review confirms previous data indicative of unfavorable outcomes after severe GMH-IVH but notably also reports impaired neurodevelopmental outcome after mild GMH-IVH. The findings raise 2 important questions: (1) the biological underpinning of the relationship between the severity of GMH-IVH and outcome, and (2) the extent to which the data should be used in counseling in the neonatal period. Severe GMH-IVH (when compared with no GMH-IVH) was associated with a distinctly increased risk of the … Address correspondence to Joseph J. Volpe, MD, Department of Pediatric Newborn Medicine, Harvard Institutes of Medicine, 4 Blackfan Circle, Suite 110A, Boston, MA 02115. E-mail: joseph.volpe{at}childrens.harvard.edu

Index of Suspicion in the Nursery

Twins are born at 37-5/7 weeks gestation to a 41-year-old G4P2 woman who had unremarkable serology results. The delivery is via cesarean section because of a nonreassuring fetal heart rate. Twin B appears to be acrocyanotic and initially requires positive-pressure ventilation for 30 seconds before being able to maintain her oxygen saturation on her own. Apgar scores are 7 and 8 at 1 and 5 minutes, respectively. She also appears to be “jittery,” and her screening glucose concentration is 24 mg/dL (1.3 mmol/L). She consumes 20 mL of infant formula and a 10% dextrose (D10) infusion is begun at a rate of 60 mL/kg per day. Three hours after birth, a follow-up glucose evaluation measures 30 mg/dL (1.7 mmol/L), prompting administration of a 4-mL/kg bolus of D10 over 20 minutes and increase of the maintenance infusion rate to 100 mL/kg per day. Six hours after birth, glucose measures 80 mg/dL (4.4 mmol/L), and the infusion rate is decreased to 60 mL/kg per day. She is transferred to a hospital that has a neonatal intensive care unit (NICU) for close monitoring. On transfer, the oxygen saturation dips into the upper 80s/lower 90s, and nasal cannula administration of oxygen is initiated. Furthermore, during transfer (8 to 9 hours after birth), the blood glucose value is 44 mg/dL (2.4 mmol/l), so the D10 infusion rate is increased back to 100 mL/kg per day. On arrival at the second hospital, her oxygen saturation is about 85% and glucose is 50 mg/dL (2.8 mmol/L). In the NICU, she receives noninvasive respiratory support as well as 15% dextrose (D15) at a rate of 70 mL/kg per day. Twin A remains stable and continues to receive routine newborn care in the newborn nursery of the first hospital. Two days after birth, twin B continues to have glucose …

Core Concepts: Intraventricular Hemorrhage

The very preterm infant is uniquely vulnerable to bleeding into the cerebral ventricles because of the numerous but unsupported blood vessels in the subependymal germinal matrix and unstable blood pressure and flow resulting from preterm delivery and respiratory distress. Approximately 25% of infants whose birthweights are 500 to 1,500 g have some intraventricular hemorrhage (IVH). Even a small IVH is associated with an increased risk of disability. A large IVH is sometimes complicated by hemorrhagic parenchymal infarction (also known as grade 4 IVH), which is believed to arise when venous occlusion from hematoma impairs perfusion in periventricular white matter. Large unilateral infarctions are usually associated with contralateral hemiparesis, but cognitive function may be less impaired. Prenatal glucocorticoid therapy reduces IVH by nearly 50% in randomized trials. Postnatal indomethacin reduces IVH, but reduced disability has not been consistently documented.

Hatch & Sumner’s Textbook of Paediatric Anaesthesia, 3rd Edition.

Hatch & Sumner’s Textbook of Paediatric Anaesthesia, 3rd Edition.

Does Platelet Dysfunction Mediate the Development of Intraventricular Hemorrhage in the Premature Neonate?.

The purpose of this investigation is to evaluate the potential of platelet dysfunction as a risk factor for the development of intraventricular hemorrhage (IVH) in the premature neonate. Intraventricular hemorrhage is relatively common, especially in infants weighing less than 1500 grs or less than 35 weeks of gestation. Neonates less than 32 weeks gestation are at significant risk for periventricular/intraventicular bleeding with mortality rates approaching 50% for those having a high grade (III-IV) IVH. The pathogenesis of IVH in the premature infant is thought to be related to loss of an ability to regulate cerebral blood flow (cerebral autoregulation) in the subependymal germinal matrix. This leads to abrupt changes in local blood pressure regulation and results in capillary bleeding. It is also apparent that birth weight and gestational age are not the only risk factors for IVH; relationships with lung development and ventilation, or lack thereof, also exist as risk factors.In a previous study of platelets obtained from umbilical cord blood, we have found that the neonate has a transient platelet dysfunction at the time of birth which appears to be related to a platelet (PL) dense granule (DG) storage pool deficiency (δ-SPD). We have found that platelets obtained from umbilical cord blood have an average of 0.79 ± 0.08 DG/PL (n=62), which is significantly decreased compared to the adult population (4–6 DG/PL) (Blood , 100(11):691a, 2002). Although the concentration of ADP and ATP were found to be decreased compared to normal adult platelets, the ATP/ADP ratio in neonatal platelets is 1.95 (n=61), consistent with established adult normal range ratio values (1.4–1.95). We have data establishing that a one-day-old full-term neonate has adenine nucleotide values consistent with adult levels. We postulate that a failure of platelet maturation related to gestational age of the preterm neonate, or an inherent δ-SPD, may extend the platelet dysfunction at birth and should therefore be considered a potential risk factor for development of IVH in the premature neonate.We have collected peripheral blood with informed consent from premature neonates, 26–33 weeks gestational age and their parents to assess the PL DG content and the adenine nucleotide content of each subject. Preliminary data (mean ± 2 SE) from the peripheral blood of premature infants (n=19) obtained 3–5 d after birth include: gestational age 30.18 ± 1.28 weeks and wt 1378.2 ± 27.8 gr. The DG number (1.00 ± 0.29/PL) is significantly decreased compared to normal adults, while the ATP (3.19 ± 0.36 M/1011 PL), ADP (2.63 ± 0.54 M/1011 PL) and ATP/ADP ratio (1.46 ± 0.13) are normal. The decreased DG number in premature PLs is essentially identical to the DG number in umbilical cord blood PLs. The parents studied to date have had a normal DG number and adenine nucleotide content. Our preliminary data suggests that at day 3–5 after birth, premature infants of gestational age 26–33 weeks have a δ-SPD similar to that observed in full-term umbilical cord blood PLs. Additional subjects are needed, especially premature neonates who have suffered a grade III or IV IVH to fully assess our hypothesis. A retrospective study of high-grade IVH survivors and their parents is currently being implemented to investigate an inherited δ-SPD mediator/risk factor for IVH in the premature neonate.

Fetal Germinal Matrix and Intraventricular Hemorrhage

Subependymal germinal matrix with intraventricular hemorrhage (GMIVH) is a common complication associated with delivery in preterm neonates but has rarely been observed in the fetus. Clinical and neuroradiological findings of 5 patients who were diagnosed as having fetal GMIVH with prenatal ultrasonographic examinations (US) and MRI, and postnatal MRI were reviewed retrospectively. During a seemingly uneventful pregnancy, fetal GMIVH occurred at approximately 30–33 weeks of gestation, with the absence of any known factor predisposing to fetal hemorrhage. Routine obstetric US revealed an intraventricular lesion in the enlarged ventricles. Prenatal MRI clearly demonstrated parenchymal change such as intracerebral hematoma adjacent to the subependymal and intraventricular hematoma, and periventricular leukomalacia as well as GMIVH. Although patients without parenchymal destruction (hemosiderin deposit alone) had a favorable neurodevelopmental outcome, encephalomalacia and periventricular leukomalacia contributed to long-term neurodevelopmental deficits. Evaluating parenchymal damage with prenatal MRI can therefore help to predict neurodevelopmental prognosis of the fetus with GMIVH.

1139: Brain ultrasound in intracranial hemorrhage and hypoxic-ischemic encephalopathy in high risk preterm patients

Germinal matrix hemorrhage (GMH) and intraventricular hemorrhage (IVH) are the most common and most important neurological injuries in preterm neonates. The neuropathology of GMH-IVH originates in the subependymal germinal matrix, a richly vascularized site of active cellular proliferation. The pathogenesis of GMH-IVH is multifactorial. Two major factors that contribute to the development of GMH-IVH are (1) loss of cerebral auto-regulation and (2) abrupt alterations in cerebral blood flow and pressure.

301 Intraventricular Haemorrhage on the Left Side of the Brain Induces Left-Handedness

Background: Prematurely born children are more often left-handed than their term born peers. It is unknown if this excess left-handedness, a marker for the extent of cerebral lateralisation, is caused by cerebral lesions.Methods: In a cohort of 221 preterm born infants (gestational age <= 32 weeks and/or birth weight <= 1500 grams), brains were serially examined in the neonatal period using cranial ultrasound (US) to detect intraventricular haemorrhage (IVH), periventricular leukomalacia (PVL) and other abnormalities. At age 7 to 10 years, magnetic resonance imaging (MRI) was done, and hand preference and current IQ were measured. MRI and US were classified as normal, mildly abnormal, or severely abnormal, blinded to handedness data.Results: Children with severely abnormal US (IVH grade III/IV, cystic PVL grade II/III, thalamic lesion, focal infarction or haemorrhage at the level of the convexity) had an increased chance to become left-handed: odds ratio (OR) severely abnormal US versus normal US 4.1, 95% CI 1.6 to 10.0, p=0.003. This was confirmed by MRI scans at school age: OR severely abnormal MRI versus normal MRI 4.0, 95% CI 1.5 to 10.7, p=0.005. Findings were attributable to IVH. Left-sided IVH showed a higher chance for left-handedness (OR left-sided IVH versus no IVH 4.4, 95% CI 1.7 to 11.3, p=0.002), whereas right-sided IVH did not. Neonates with left-sided mild IVH (grade I and II) still showed an increased chance for left-handedness: OR mild left-sided IVH versus no IVH 4.0, 95% CI 1.5 to 10.9, p=0.007. PVL was not related to left-handedness.Conclusion: Our findings strongly indicate that even a small intraventricular haemorrhage affecting the left side of the brain induces left-handedness. This is likely related to the role of the subependymal germinal matrix in the developing brain.

Biologic Limits of Viability

After completing this article, readers should be able to: 1. Define the gestational range for extremely preterm birth. 2. Explain the difference between possibility and probability in reference to survival following extremely preterm birth. 3. Describe the key lung development required for adequacy of gas exchange. 4. Describe the renal functional limitations for water, sodium, and creatinine homeostasis in the first postnatal week of the extremely preterm infant. 5. List at least one structural and/or functional limitation of at least five organ systems that increases mortality risks for the extremely preterm infant. With the advent of neonatal intensive care in the 1960s, preterm infants born at progressively lower gestational ages began to survive. The progression of the decrement did not follow a recognizable relationship; rather, it was erratic as the knowledge base of neonatal physiology and pathology expanded and new technical capabilities for life support were developed. The most dramatic increase in survival of extremely preterm birth (<26 completed weeks’ gestation) came with the introduction of surfactant replacement therapy in the late 1980s. The increased use of maternal antenatal corticosteroid therapy for induction of lung maturation with threatened preterm delivery following the National Institute of Child Health and Human Development Consensus Conference recommendations in 1994 also contributed to improved survival. Since that time, the survival of infants of gestational ages as low as 22 weeks’ has been reported. The purpose of this article is to review the current understanding of the biologic factors limiting survival potential, particularly as they inform clinical decision-making. Viability or survival potential, when used in reference to a fetus, frequently is used to indicate the possibility for a fetus to be live born and capable of living to a specified endpoint of either a designated time, reaching a certain age or a landmark event, admission to a neonatal intensive care unit, …

Fetal germinal matrix and intraventricular haemorrhage diagnosed by MRI.

Subependymal germinal matrix haemorrhage and intraventricular haemorrhage (GMIVH) is a common complication of delivery in preterm neonates but has rarely been observed in the fetus. We report two cases of GMIVH in fetuses of 36 weeks gestation, clearly demonstrated by antenatal MRI. In both cases progressive ventriculomegaly was observed, and ventriculoperitoneal shunts were placed at 19 and 6 months of age, respectively. Prenatal GMIVH may be a cause of congenital hydrocephalus, for which no aetiology has yet been found.

Hemorragia periventricular e intraventricular de recién nacidos prematuros

To review intracranial hemorrhage originated in the subependymal germinal matrix region. Incidence rates of germinal matrix-intraventricular hemorrhage (GMH) range from 20 to 40% of infants born before 32 weeks gestational age or with birth weight less than 1,500 g. Because the GMH is usually diagnosed during the first 72 postnatal hours, that is the optimal time to perform ultrasound scans. The pathogenesis of GMH is multifactorial and related to vascular, intravascular and extravascular factors. The grading system relies on the detection of blood in the germinal matrix region and into the ventricular system. Ultrasound scans are the diagnostic method of choice, once it is easy to perform and has low costs. In a prospective study of 146 preterm infants (< 2,200 g), the incidence of GMH in those weighing less than 1,501 g, was 36%. GMH occurred mainly in the first week of life (65%) and in 70% of cases was classified as grade I. Risk factors found to be related to the GMH were: general anesthesia for cesarean section, Apgar score below 4 in the first minute or below 8 in the fifth minute, low birth weight, the presence of respiratory distress, patent ductus arteriosus, anemia, repeated arterial functions and umbilical arterial catheterization. Mean gestational age, systolic and diastolic pressure in the first 24 hours of life and hematocrit were lower in patients with GMH. GMH is frequent in the preterm infant, and occurs mainly in the first week of life. Ultrasound scans are the method of choice for the diagnosis and follow-up. Risk factors associated were hypoxia and excessive handling.