Brief clinical and laboratory observationNeonatal germinal matrix hemorrhage: Evidence of a progressive lesion
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Cited by (18)
Peri/intraventricular haemorrhage: A cranial ultrasound study on 5286 neonates
1997, European Journal of Obstetrics and Gynecology and Reproductive BiologyObjective: We launched a prospective cranial ultrasound study at the Department of Obstetrics and Gynaecology of the University of Giessen. In this study we examined the incidence and severity of brain damage in neonates and related them to various obstetrical risk factors. Study design: More than 90% of all neonates born between 1984 and 1988 were included in the study (n=5286) and were screened by ultrasound for cerebral abnormalities on 5–8 days post-partum. The relation between the incidence of peri/intraventricular haemorrhages (PIVH) and obstetrical risk factors were analyzed by contingency tables. Results: The most frequent abnormality was PIVH (3.6%) of various degrees (grade I–III). Periventricular leucomalacia, porencephalia, subarachnoidal haemorrhages, and hydrocephali were rare (≤0.2%). The incidence of PIVH increased progressively with decreasing gestational age, e.g. from 1.6% at 38–43 weeks up to 50.0% at 24–30 weeks of gestation. A large percentage of babies with PIVH were clinically normal. In immature neonates there was a close inverse relationship between Apgar score at 1, 5 and 10 min and both incidence and severity of PIVH. This was in contrast to findings in mature neonates where a marked increase in the incidence of PIVH was found only with Apgar scores as low as 0–4 points. The relation between the incidence of PIVH and both cardiotocography and arterial cord blood pH was poor, independent of the gestational age. The incidence of PIVH was increased in growth retarded fetuses (pH≤7.29), premature rupture of membranes, fever sub partu and gestosis. It is interesting to note that in mature fetuses there was no difference in the incidence of PIVH between vaginally delivered (0.8%) and sectioned breech presentations (2.1%). In preterms at 35–37 weeks with prolonged labour and secondary cesarean section, the incidence of PIVH was very high (11.2%). Conclusion: From the present study we conclude that the incidence of PIVH especially in immature neonates is highly associated with low Apgar scores at birth. Since the Apgar score reflects the clinical condition and the degree of circulatory centralisation of neonates that is influenced by various ante- and intranatal risk factors, a protective obstetrical management is necessary to reduce the incidence of PIVH in neonates.
Clinical impact of neonatal thrombocytopenia
1987, The Journal of PediatricsIn a 1-year prospective study, the outcome in infants with a platelet count <100×109/L (n=97) was compared with the outcome in an age-, weight-, and disease-matched nonthrombocytopenic control group (n=80). The hemostatic impact of the thrombocytopenia was assessed by (1) modified template bleeding time, (2) hemorrhage score, and (3) determination of the presence and extent of intraventricular hemorrhage (IVH) in thrombocytopenic infants weighing <1500 at birth (n=39) compared with all nonthrombocytopenic infants <1500 g (n=122) admitted during the study period. The development outcome in infants <1500 g was compared at 12 months after dellvery. Neonatal thrombocytopenia had a major impact on hemostatic integrity: bleeding time was inversely related to platelet count (r=−0.56, P<0.001) and became prolonged when the platelet count fell to <100×109/L. In addition, many infants (40%) had evidence of platelet dysfunction with prolonged bleeding times despite only moderately reduced platelet counts (75 to 150×109/L). The hemorrhage score was greater in the thrombocytopenic infants compared with the sick control infants, and increased as the platelet count fell (r=−0.58, P <0.001). The incidence of IVH in thrombocytopenic infants <1500 g was 78%, compared with 48% in the nonthrombocytopenic infants (P<0.01). In addition, the more severe grades of IVH were more frequent in the thrombocytopenic infants. The serious neurologic morbidity for the surviving infants <1500 g was 41% in the thrombocytopenic infants and 7% in the nonthrombocytopenic infants. Thus, on the basis of three indices of abnormal bleeding, thrombocytopenic infants are at greater risk for bleeding than equally sick nonthrombocytopenic infants. The thrombocytopenia itself may have contributed to the high mortality and neurologic morbidity.
Perinatal events and intraventricular/subependymal hemorrhage in the very low-birth weight infant
1985, American Journal of Obstetrics and GynecologyOne hundred nineteen very low-birth weight infants were studied to see whether intrapartum fetal distress with or without acidosis correlated with the development of intraventricular and subependymal hemorrhage. Of 112 infants studied prospectively, 24% () had intraventricular/subependymal hemorrhage documented by real-time ultrasound studies shortly after birth; only 4.4% () had severe hemorrhage (grade ). Ominous fetal heart rate patterns occurred in 50% of monitored infants with severe intraventricular/subependymal hemorrhage compared to 8% of matched controls (p < 0.01). Reassuring fetal heart rate patterns were more predominant in infants without intraventricular/subependymal hemorrhage (p < 0.05). Neonatal depression and the need for assisted ventilation beyond the immediate delivery period were more frequent in infants who developed intraventricular/subependymal hemorrhage. Antepartum and intrapartum complications, fetal presentation, cesarean section, duration of labor, hyaline membrane disease, and volume expansion appeared to play no role in the incidence of intraventricular/subependymal hemorrhage. Preliminary data presented here suggest that intrapartum fetal distress and acidosis may be significant factors in predicting which very low-birth weight infant will develop intraventricular/subependymal hemorrhage. The condition of the infant at birth may be more significant with respect to the extent of intraventricular/subependymal hemorrhage than a variety of obstetric variables. Aggressive management of appropriately selected patients and judicious resuscitation of the very low-birth weight infant may keep the incidence of severe intraventricular/subependymal hemorrhage at a minimum, thereby optimizing neurological outcome for this high-risk group.
Neurosonographic identification of ventricular asymmetry in premature infants
1984, Clinical RadiologyRoutine head ultrasound scans have been performed on 185 consecutive infants weighing under 1500 g at birth. In 40 of these infants a significant difference in the size of the lateral ventricles was observed on one or more occasions. In 38 of these infants the left ventricle was larger than the right. The aetiology of this ventricular asymmetry is unknown. It is not believed to be due to germinal matrix or ventricular haemorrhage, hydrocephalus or the position of the infant at the time of scanning.
Intraventricular hemorrhage in the preterm neonate: Timing and cerebral blood flow changes
1984, The Journal of PediatricsSerial cranial ultrasound studies, 133xenon inhalation cerebral blood flow determinations, and risk factor analyses were performed in 31 preterm neonates. Contrast echocardiographic studies were additionally performed in 16 of these 31 infants. Sixty-one percent were found to have germinal matrix or intraventricular hemorrhage. Seventy-four percent of all hemorrhages were detected by the thirtieth postnatal hour. The patients were divided into three groups: early GMH/IVH by the sixth postnatal hour (eight infants) interval GMH/IVH from 6 hours through 5 days (10), and no GMH/IVH (12). Cerebral blood flow values at 6 postnatal hours were sigificantly lower for the early GHM/IVH group than for the no GMH/IVH group (P<0.01). Progression of GMH/IVH was observed only in those infants with early hemorrhage, and these infants had a significantly higher incidence of neonatal mortality. Ventriculomegaly as determined by ultrasound studies was noted equally in infants with and without GMH/IVH (50%) and was not found to correlate with low cerebral blood flow. The patients with early hemorrhage were distinguishable by their need for more vigorous resuscitation at the time of birth and significantly higher ventilator settings during the first 36 postnatal hours, during which time they also had higher values of Pco2. An equal incidence of patent ductus arteriosus was found across all of the groups. We propose that early GMH/IVH may be related to perinatal events and that the significant decrease in cerebral blood flow found in infants with early GMH/IVH is secondary to the presence of the hemorrhage itself. Progression of early GMH/IVH and new interval GMH/IVH may be related to later neonatal events known to alter cerebral blood flow.
Cerebral blood flow velocity in relation to intraventricular hemorrhage in the premature newborn infant
1982, The Journal of PediatricsThe relation of IVH to blood flow velocity in the anterior cerebral arteries has been studied in the premature newborn infant. The objectives of the study were to determine the effect of IVH on cerebral blood flow velocity, measured by a noninvasive Doppler technique, and to assess the reliability of this technique in the diagnosis of the hemorrhage. Thirty-two premature newborn infants with IVH were identified by real-time ultrasound scanning; IVH was present in the first 24 hours of life in approximately 50%, progressed postnatally in approximately, 20%, and was severe in approximately 50%. Cerebral blood flow velocity, determined daily in the first five days of life, was compared to the time of occurrence of IVH and to simultaneous measurements of systemic blood pressure and blood gases. No consistent relationship between timing or severity, of IVH and cerebral blood flow velocity could be discerned. We conclude that cerebral blood flow velocity in the anterior cerebral arteries is not likely to be affected by IVH and that the noninvasive Doppler technique for measurement of this velocity is not reliable for diagnosis of the lesion.