新生儿脑室内出血英文.docx

1、新生儿脑室内出血英文Clinical manifestations and diagnosis of intraventricular hemorrhage in the newbornAuthorLisa M Adcock, MDSection EditorsJoseph A Garcia-Prats, MDDouglas R Nordli, Jr, MDDeputy EditorMelanie S Kim, MDDisclosures:Lisa M Adcock, MDNothing to disclose.Joseph A Garcia-Prats, MDNothing to discl

2、ose.Douglas R Nordli, Jr, MDNothing to disclose.Melanie S Kim, MDNothing to disclose.Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be p

3、rovided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.Conflict of interest policyAll topics are updated as new evidence becomes available and ourpeer review processis complete.Literature review current through:F

4、eb 2015.|This topic last updated:May 22, 2014.INTRODUCTIONIntraventricular hemorrhage (IVH; also known as subependymal or germinal matrix hemorrhage) is an important cause of brain injury in premature infants. Although the incidence has declined since the 1980s, IVH remains a significant problem, as

5、 improved survival of extremely premature infants has resulted in a greater number of survivors with this condition 1,2.The epidemiology, pathogenesis, clinical presentation, and diagnosis of IVH are discussed in this topic review. The management, complications, and outcome of IVH in the newborn are

6、 discussed separately. (SeeManagement and complications of intraventricular hemorrhage in the newborn.)PATHOLOGYPreterm infantsIn preterm infants, the site of origin of bleeding is generally the subependymal germinal matrix, which is located between the caudate nucleus and the thalamus at the level

7、of the foramen of Monro 3. Neuropathologic studies suggest that the hemorrhage is primarily within the capillary network, which freely communicates with the venous system, although bleeding can also occur from the arterial circulation 4. Vessels in this region occupy border zones between cerebral ar

8、teries and the collecting zone of the deep cerebral veins, and have increased permeability when subjected to hypoxiaand/orincreased venous pressure 5. (SeeGerminal matrix fragilitybelow.)Severity and grading of IVHSeverity of hemorrhage is based on whether the bleeding is confined to the germinal ma

9、trix region or if it extends into the adjacent ventricular system or white matter (intraparenchymal). The following grading system is used to define the extent of bleeding (table 1) 3:Grade I Bleeding is confined to the germinal matrix (image 1andimage 2)Grade II Intraventricular hemorrhage (IVH) oc

10、cupies 50 percent or less of the lateral ventricle volumeGrade III IVH occupies more than 50 percent of the lateral ventricle volume (image 3)Grade IV Hemorrhagic infarction in periventricular white matter ipsilateral to large IVH (image 4)Grade I corresponds to mild, grade II moderate, and grades I

11、II and IV severe IVH. Each grade of IVH may be unilateral, or bilateral with either symmetric or asymmetric grades of IVH.Term infantsIn contrast, the initial site of bleeding in term infants is variable based on limited data, as illustrated by the following:In one neuropathologic study of 32 term i

12、nfants, the majority of IVH arose from the choroid plexus 6.In another study of term infants, ultrasonographic imaging showed subependymal germinal matrix and choroid plexus hemorrhages occurred at similar rates 7.Thalamic hemorrhage may also contribute to IVH in term infants, as described in a seri

13、es of 19 cases, of which two-thirds had associated thalamic hemorrhage detected by computed tomography 8. This is likely a venous hemorrhagic infarction caused by thrombosis in the internal cerebral vein(s), or more extensive venous thrombosis, rather than a primary hemorrhage.These findings suggest

14、 that the origin of intracranial bleeding in term infants differs from that seen in preterm infants with subependymal IVH.EPIDEMIOLOGYIntraventricular hemorrhage (IVH) generally occurs in preterm infants, and the incidence increases with decreasing gestational age and birth weight.Premature infantsI

15、VH occurs most frequently in infants born before 32 weeks gestation or less than 1500 g birth weight. Since the late 1990s, the reported rate of IVH in the United States is about 20 percent in very low birth weight (VLBW) infants (birth weight 1500 g) and 45 percent in extremely low birth weight (EL

16、BW) infants (birth weight 1000 g) 9-12.A population-based study of 2896 premature infants (32 weeks gestation) exemplifies the relationship between gestational age and IVH, showing that IVH rates decreased 3.5 percent with each added week of gestation 13.The risk of severe IVH also increases with de

17、creasing gestational age and birth weight as noted by the following studies (seeSeverity and grading of IVHabove):In a study from the National Institute of Child Health and Human Development (NICHHD) neonatal research network of 9575 infants with gestational age between 22 and 28 weeks and birth wei

18、ght 401 to 1500 g, the overall incidence of IVH was 36 percent for all grades of IVH, which increased with decreasing gestational age 12. The prevalence of severe IVH (defined as grades III and IV) also increased with decreasing gestation with rates of 38, 36, 26, 21, 14, 11, and 7 percent of surviv

19、ors for infants with gestational ages 22, 23, 24, 25, 26, 27, and 28 weeks, respectively 12.In a population-based prospective study of all preterm infants with gestational age below 27 weeks born in Sweden from 2004 to 2007, the incidence of IVH increased from 5.2 percent of survivors born at 26 wee

20、ks gestation to 19 and 20 percent for those born at 22 and 23 weeks gestation, respectively 14.Although older literature has suggested that VLBW infants who were small for gestational age (SGA) were less likely to have IVH 15, subsequent data have shown no difference in the incidence of IVH between

21、SGA and appropriate size for gestational age premature infants 16,17.In a prospective study from the Gene targets of Intraventricular Hemorrhage Study, which includes premature infants with birth weights between 500 and 1250 g, infants born to mothers of African ancestry appeared to be at increased

22、risk for grade II to IV IVH compared with those born to mothers who were white, after controlling for confounding variables 18. However, the risk was reduced by maternal attendance at a single prenatal visit, suggesting that race may still be a marker for healthcare disparities, which increases the

23、risk of IVH, rather than a truly independent factor.Term infantsSevere IVH occurs infrequently in term infants, although minor hemorrhages are not uncommon. In a study of 505 healthy asymptomatic term infants who underwent head ultrasonography within 72 hours of life, the incidence of IVH was 4 perc

24、ent 19. In the term infant, IVH may be associated with trauma (eg, abdominal compression), alloimmune thrombocytopenia, rupture of a vascular malformation, sinovenous thrombosis (particularly in infants with thalamic involvement), and a diagnosis of hemophilia and other coagulation abnormalities 20-

25、22. In some cases, it is unclear whether the coagulation abnormality is causal or is a result of IVH 22.PATHOGENESISThe pathogenesis of intraventricular hemorrhage (IVH) inprematureinfants is due to 23:Germinal matrix fragility from a lack of structural support due to immaturity.Disturbances of cere

26、bral blood flow (CBF), particularly related to hypoxia-ischemia and reperfusion, elevated arterial flow, or elevated venous pressure.Germinal matrix fragilityIn preterm infants, IVH generally originates within the germinal matrix, the highly cellular and richly vascularized layer in the subependymal

27、, subventricular zone that gives rise to neurons and glia during fetal development 24. As the fetus matures, the germinal matrix begins to involute starting at 28 weeks as its cellularity and vascularity decrease, and by term it is generally absent 25.In the germinal matrix, the capillary network co

28、nsists of numerous thin-walled, large blood vessels that lack structural support, which contributes to the increased risk of hemorrhage in this area of the brain compared with other regions 3,23,26-28. The microvasculature of the germinal matrix is particularly fragile because of the abundance of an

29、giogenic blood vessels that have a paucity of pericytes, have immature basal lamina, and have deficiency of tight junctions and glial fibrillary acidic protein (GFAP) in the astrocyte endfeet (which are components of a competent blood-brain barrier) 23. Glial fibers normally develop with increasing

30、maturation, as demonstrated in a study showing minimal immunocytochemical staining of GFAP at 27 weeks gestation, which became more prominent with increasing gestational age, especially after 31 weeks gestation 29. The deficient structural support makes the germinal matrix vulnerable to injury prima

31、rily due to hemodynamic instability in preterm infants, related to altered CBF caused by a variety ofperinatal/neonatalevents or disorders (eg, hypoxia-ischemia).This fragile capillary network drains into a well-developed deep venous system that forms the terminal vein, which changes direction in a

32、U-turn fashion as it empties into the internal cerebral vein. It is postulated that the venous system is prone to congestion and stasis, resulting in increased cerebral venous pressure, which contributes to germinal matrix IVH 22.Cerebral blood flow instabilityFluctuations of CBF in preterm infants are associated with IVH 30-33. Preterm infants are particularly vulnerable to alterations in CBF because they have impaired autoregulation of CBF compared with term infants. T