Periventricular edema of newborns

Among neurological pathologies in newbornsa significant place is occupied by disorders of cerebral hemodynamics in the form of hemorrhagic and ischemic changes, which in frequency and localization depend on the severity of the morphofunctional immaturity of the central nervous system and the imperfection of the mechanisms of autoregulation of cerebral blood flow. Hemorrhagic and ischemic lesions of the brain can be observed in different combinations.

Of all hemorrhagic-ischemic lesionsof the brain, the most common vascular lesions, reliably determined by neurosonography, are peri-intrraventricular hemorrhages, periventricular and subcortical leukomalacia. They represent a serious problem in neonatology, as they are one of the main causes of deaths and neuropsychiatric disturbances in newborns, especially premature infants. Although the brain of premature newborns is more resistant to the effects of hypoxia, cerebrovascular damage is much more frequent due to the greater vulnerability of the vascular system, which has anatomical and physiological characteristics at different gestational age.

Disorders of cerebral circulation in newborn children.

  • Peri-intraventricular
    hemorrhage
  • Subarachnoid hemorrhage:
  • subdural hemorrhage
  • intracerebral (focal)
    hemorrhage
  • haemorrhage
  • hemorrhage in the vascular
    plexus of the lateral ventricle
  • cerebellar hemorrhage
  • periventricular leukomalacia
  • subcortical leukomalacia
  • parasagittal necrosis
  • defeat of visual tubercles and basal ganglia
  • cerebral infarcts
  • focal ischemic lesions of the trunk and cerebellum

It is known that cortical and subcorticalthe brain sections from 24 to 36-37 weeks of fetal development are well supplied with the leptomeningeal embryonic vasculature, which protects these structures from injuries in prematurely born children. The periventricular zone (white substance of the brain lying above the lateral ventricles by 4-5 cm), consisting of descending cortical tracts, suffers the greatest shortage of blood supply. Deep layers of periventricular white matter are a zone of adjacent blood supply between the middle, middle and posterior cerebral arteries. Vascular anastomoses during these terms of gestation are poorly developed, and therefore the violation of blood flow through deep arteries in low-birth babies causes a decrease in the perfusion of the brain tissue - periventricular ischemia and the development of periventricular leukomalacia.

The main source of periventricularhemorrhage (PVK) is a germinal matrix (GM), functioning in the brain from an embryonic period. The maximum structure is represented in the fetuses in 12-16 weeks of gestation. Strongly developing until the 6th month of intrauterine life, it later undergoes involution and by the 32nd week of gestation it practically ceases to exist. The germinal matrix is ​​located lower and lateral to the ependyma, lining the bottom of the lateral ventricle, and is directly above the head and body of the caudate nucleus. The germinal matrix is ​​the most important structure of the brain, supplying the neuronal and glial building material for the cortex and subcortical ganglia during early ontogeny. This structure is mainly from the anterior cerebral artery, but its immature vessels with wide lumens do not have a basal membrane and muscle fibers. In this zone, little supporting stroma, increased fibrilolytic activity. These factors contribute to increased vulnerability of the vessels of the germinal matrix, especially in children with extremely low body weight. At the heart of periventricular hemorrhages lies the disruption of autoregulatory possibilities of cerebral blood flow, i.e., the ability to maintain the constancy of blood filling of the brain regardless of fluctuations in systemic arterial pressure. Periventricular hemorrhages may be isolated (subependymal), spread to the ventricles (intraventricular) with the involvement of periventricular parenchyma (periventricular) of the brain due to the development of a secondary hemorrhagic infarction in the periventricular region.

The classification is based on the degreethe prevalence of hemorrhage and the response (expansion) of the ventricular system. In our work we use the classification of L. Papille et al, which implies four degrees of hemorrhage:

  • I degree - isolated subependimal hemorrhage (subependimal hematoma),
  • II degree - the spread of subependimal hemorrhage into the cavity of the lateral ventricle, without its expansion in the acute period,
  • III degree - massive intraventricular hemorrhage with expansion of the lateral ventricles,
  • IV degree - a combination of intraventricular hemorrhage and hemorrhagic periventricular infarction.

In our opinion, it most accurately reflectslocalization and extent of hemorrhage, takes into account the change in ventricular size, is the most simple and convenient for practical use.

With dynamic ultrasound monitoring fornewborns at high risk noted that the vast majority of periventricular hemorrhages occur and develops in the first week of life, mostly between the ages of 24 and 72 hours after birth. In small children in 15% of cases, hemorrhages occur later, after the second week of life. If periventricular hemorrhage occurs later, it almost always has a benign course and the possibility of complications is small. There are cases of intrauterine diagnosis of periventricular hemorrhages.

Echographic characteristics of periventricular hemorrhages

IHC of I degree (subependimal hemorrhage). Subependymal hematoma is visualized as a hyperechogenic rounded formation with distinct contours in the head region of the caudate nucleus, caudo-thalamic incision or interventricular orifice. Increases in the size of the lateral ventricle with this hemorrhage are not noted. Change in the shape of the lateral ventricle on the side of hemorrhage is possible with a large hematoma.

IVK II degree. Along with hyperechoic areas in the head of the caudate nucleus or interventricular orifice, additional cavities of the unexpanded lateral ventricle, often on both sides, are determined by additional hyperechogenic structures that are associated with the vascular plexuses and deform them. At the same time, the disappearance of the caudo-thalamic cutoff due to additional echoes from the blood clot is noted.

The presence of extended, asymmetric, with uneven contours of the lumbar vascular plexuses, allows to diagnose II degree II.

III degree PVC. Hyperechoic structures (blood clots) are observed in the enlarged lateral ventricles, in 85% of cases they can be on both sides. In the most severe cases, clots are formed that repeat the shape of the ventricles of the brain (tamponade). In III and IV ventricles, clots are detected much less frequently.

IVK IV degree. A thrombus formed in the lateral ventricle with grade III PVK may cause a violation of venous outflow through the branches of the terminal vein located periventricularly. This leads to venous infarction, which is the main factor in the development of periventricular lesions. This hemorrhage is characterized by the presence of an intraventricular blood clot, expansion of the ventricles and hemorrhagic venous infarction in the periventricular zone, represented by a hyperechoic region with distinct outlines. The latter may be located above the anterior horn, the body or near the posterior horn of the lateral ventricle. IVC IV degrees in 96-98% of cases are unilateral. In 15-23% of observations, the increase in hemorrhage from subendymal to parenchymal during the first week of life is noted.

With dynamic scanning (daily atthe first week of life, then 1 time per week after the 7th day of life). The IHC of the first degree remains until two to three months of life, changing in structure and echogenicity and decreasing in size. In 52% of the hematoma disappears without a trace, or in its place, in 48% of cases, within 2-4 weeks, subependimal pseudocyst (CK) is formed, the feature of which is the absence of subendymal lining. As a rule, the subependymal pseudocyst is reduced to 6-9 months of life.

Depression of intraventricular blood clotsafter IVC II and especially III degree occurs gradually, more often within 5-6 weeks. In the area of ​​parenchymal hemorrhage with IVC IV degree in 75-82% of cases on 24-36 days of life, a pancreatic pseudocyst is formed, associated with the cavity of the lateral ventricle. The most characteristic complication of IVC III-IV degree is the widening of the lateral ventricles, the severity and frequency of which is determined by the severity of the transferred pathological process. Subcompensated dilation occurs within 1-3 weeks and occurs in 48% of children with grade III IV. Usually, by the time the child is discharged from the hospital, it can be said whether the ventricular expansion was transient, persistent or progressive with the development of internal hydrocephalus. Full or partial occlusion is judged by the expansion of the overlying sections of the cerebrospinal fluid system.

Periventricular leukomalacia (PVL) -ischemic infarction of white matter of the brain around the outer corners of the lateral ventricles. Until recently, the diagnosis of PVL was the conclusion of only pathomorphologists, since there is no clinical symptomatology indicating a periventricular lesion in young children. Pathomorphologically, in PVL, small parts of the softened brain material are detected anterior to the anterior horns, near the lateral corners of the lateral ventricles and lateral to the hindbones. In some cases, several weeks after ischemic stroke, calcification and gliosis occur, leaving a periventricular scar; in others, single or multiple cavities (pseudocysts) are formed, which in time can subside and lead to a secondary expansion of the ventricles and subarachnoid space. In 25% of cases PVL is combined with focal hemorrhages. In 25% of cases secondary hemorrhages occur in the area of ​​necrotic tissue with the formation of hemorrhagic infarcts, and sometimes also PVK.

On the echogram in the coronary and parasagittalThe acute (initial) phase of PVL is characterized by a significant increase in the echogenicity of the periventricular zones on both sides, more pronounced in the region of the bodies and hindbusts of the lateral ventricles. Less marked increase in echogenicity of the anterior horns. Often the affected area is isoechoic with the vascular plexus and is separated from the lateral ventricle only by a strip of liquor. PVL is symmetrical, that is, it is always two-sided. Ultrasound diagnosis at this stage is complicated, as the increase in echogenicity can be due to the peculiarities of vascularization and incomplete myelination of periventricular zones in premature newborns. The most likely development of PVL, if repeated study after 10-14 days, retained pronounced echogenicity in periventricular areas. Differential diagnostics of the acute phase of PVL and a normal halo of increased echogenicity is assisted by spectral Doppler.

The late echographic stage of PVL isCystic degeneration, developing on the site of high echogenicity. Cysts do not have epithelial lining, it is possible to merge them and form larger cavities. In this case, a minimal and / or moderate expansion of the ventricular system, mainly of the lateral ventricles due to the anterior horns and bodies, is often observed. Further, within 6-8 weeks, the cysts subside, replaced with scar tissue and cause a secondary atrophy of the brain substance. With atrophy, the lateral ventricles do not lose their usual shape, but become more rounded in the region of the anterior horns and bodies. At the same time, there are no echographic signs of occlusion of the cerebrospinal fluid.

Subcortical leukomalacia (MLR) occursdue to the violation of the blood supply of subcortical structures by leptomeningeal vessels in the last trimester of pregnancy. Echograms in the initial stages observe swelling of the brain substance, which is characterized by a diffuse increase in the echogenicity of the brain tissues and a decrease in the absence of pulsation of cerebral vessels. In the future, as a rule, within two weeks, on the background of the edema foci of increased echogenicity develop without clear contours. By the end of the month, multiple, small, parenchymal cysts are formed in the brain substance. At the same time, the ventricular system and, in some cases, the subarachnoid space, slightly widens.

It is easy enough to identify ventricular dilation andasymmetry in ultrasound. If there is any doubt, it is necessary to conduct a re-examination after a certain period of time. One of the most common causes of dilation is the congenital stenosis of the Sylvian aqueduct.

Aging of the corpus callosum is another frequentcongenital anomaly of development, at which hydrocephalus develops. This causes a significant displacement of the lateral ventricles and anterior displacement of the third ventricle.

  1. Subependymal hemorrhage is visualized inthe appearance of one or several hyperechoic regions immediately below the lateral ventricles and is better identified in transverse sections, in the region of the anterior horns. Confirm the diagnosis with sagittal scanning: a hemorrhage can be bilateral. This is the first degree of hemorrhage.
  2. Intraventricular hemorrhage in unexposedventricles. There are additional echostructures against the background of anechogenic ventricles (as well as from hyperechoic vascular plexuses) corresponding to blood clots in the ventricles. If there is no evidence of ventricular dilatation, then this is the second degree of hemorrhage.
  3. Intraventricular hemorrhage into the enlarged ventricles. When there is intraventricular hemorrhage in the enlarged ventricles, this is the third degree of hemorrhage.
  4. Intraventricular bleeding, accompanied byhemorrhage into the brain substance is visualized as areas of increased echogenicity in the brain structure. This is the IV degree of hemorrhage, the most pronounced.
  5. Complications of hemorrhages. At I and II degrees, blood is usually reabsorbed during the first week of life, but more severe hemorrhages (grade III and IV) can cause posthemorrhagic hydrocephalus, as well as give resorption of the tissue with the formation of cysts in the cerebral hemispheres. In this case, there may be a delay in development with neurologic symptoms.
  • Necrosis of brain tissue, defined as a hypoechoic, with a fuzzy contour of the zone located lateral to the lateral ventricles (periventricular leukomalacia).
  • Edema of the brain can lead to obliteration of the ventricles and fissures of the brain. The brain is more echogenic than normal.
  • Brain infections can give a change in echogenicity, including the presence of point hyperechoic structures due to calcification.