Ultrasound signs of vascular abnormalities

Among neurological pathologies in newborns, a 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 brain lesions, the most common vascular lesions reliably determined by neurosonography are periventricular hemorrhages, periventricular and subcortical leukomalacia. They represent a serious problem in neonatology, since they are one of the main causes of death and psychoneurological disorders in newborns, especially premature babies. Although the brain of premature babies is more resistant to hypoxia, cerebrovascular damage occurs much more often due to the greater vulnerability of the vascular system, which has anatomical and physiological features at different stages of gestational age.

Cerebral circulatory disorders in newborns.

Hemorrhagic	Ischemic
Peri-intraventricular hemorrhages Subarachnoid hemorrhage: subdural hemorrhage intracerebral (focal) hemorrhage thalamic hemorrhage hemorrhage into the choroid plexus of the lateral ventricle cerebellar hemorrhage	periventricular leukomalacia subcortical leukomalacia parasagittal necrosis defeat of the optic thalamus and basal ganglia cerebral infarctions focal ischemic lesions of the brainstem and cerebellum

It is known that the cortical and subcortical parts of the brain from 24 to 36-37 weeks of intrauterine development are well supplied with blood by the leptomeningeal embryonic vascular network, which protects these structures from damage in premature babies. The periventricular zone (white matter of the brain located 4-5 cm above the lateral ventricles), consisting of descending cortical tracts, experiences the greatest deficiency of blood supply. The deep layers of the periventricular white matter are a zone of adjacent blood supply between the anterior, middle and posterior cerebral arteries. Vascular anastomoses are poorly developed at these gestation periods, and therefore the disruption of blood flow through the deep arteries in low-weight newborns causes a decrease in brain tissue perfusion - periventricular ischemia and the development of periventricular leukomalacia.

The main source of periventricular hemorrhages (PVH) is the germinal matrix (GM), which functions in the brain from the embryonic period. This structure is maximally represented in fetuses at 12-16 weeks of gestation. Developing intensively until the 6th month of intrauterine life, it subsequently undergoes involution and by the 32nd week of gestation practically ceases to exist. The germinal matrix is located below and lateral to the ependyma lining the bottom of the lateral ventricle and is located directly above the head and body of the caudate nucleus. The germinal matrix is the most important structure of the brain, supplying neuronal and glial building material for the cortex and subcortical ganglia during early ontogenesis. This structure is supplied with blood mainly from the anterior cerebral artery basin, but its immature vessels with wide lumens do not have a basement membrane and muscle fibers. In this zone there is little supporting stroma, and fibrilolytic activity is increased. These factors contribute to increased vulnerability of the vessels of the germinal matrix, especially in children with extremely low body weight. Periventricular hemorrhages are based on the failure of the autoregulatory capabilities of cerebral blood flow, i.e. the ability to maintain a constant blood supply to the brain regardless of fluctuations in systemic arterial pressure. Periventricular hemorrhages can be isolated (subependymal), spread to the ventricles (intraventricular) with the involvement of the periventricular parenchyma (periventricular) of the brain due to the development of secondary hemorrhagic infarction in the periventricular region.

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

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

In our opinion, it most accurately reflects the localization and extent of hemorrhage, takes into account changes in the size of the ventricles, and is the simplest and most convenient for practical use.

Dynamic ultrasound monitoring of high-risk newborns has shown that the vast majority of periventricular hemorrhages occur and develop in the first week of life, primarily between 24 and 72 hours after birth. In low-birth-weight infants, hemorrhages occur in 15% of cases at a later date, after the second week of life. If periventricular hemorrhage occurs later, it is almost always benign and the risk of complications is low. Cases of intrauterine diagnosis of periventricular hemorrhages have been reported.

Echographic characteristics of periventricular hemorrhages

Grade I PVH (subependymal hemorrhage). Subependymal hematoma is visualized as a hyperechoic rounded formation with clear contours in the area of the head of the caudate nucleus, caudothalamic notch, or interventricular opening. No increase in the size of the lateral ventricle is observed with this hemorrhage. A change in the shape of the lateral ventricle on the side of the hemorrhage is possible with a large hematoma.

Grade II PVK. Along with hyperechoic areas in the region of the head of the caudate nucleus or interventricular opening, in the cavity of the still unexpanded lateral ventricle, often on both sides, additional hyperechoic structures are determined that are associated with the vascular plexuses and deform them. In this case, the disappearance of the caudo-thalamic notch is noted due to additional echo signals from the blood clot.

The presence of dilated, asymmetrical, lumpy vascular plexuses with uneven contours allows for the diagnosis of grade II PVS.

Stage III PVK. Hyperechoic structures (blood clots) are observed in the dilated 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 cerebral ventricles (tamponade). In the III and IV ventricles, clots are detected much less frequently.

Grade IV PVH. A thrombus formed in the lateral ventricle in grade III PVH may cause impaired 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, ventricular dilation, and hemorrhagic venous infarction in the periventricular zone, represented by a hyperechoic area with clear contours. The latter may be located above the anterior horn, body, or near the posterior horn of the lateral ventricle. Grade IV PVH is unilateral in 96-98% of cases. In 15-23% of cases, hemorrhage increases from subependymal to parenchymatous during the first week of life.

With dynamic scanning (daily during the first week of life, then once a week after the 7th day of life), grade I PVK persists for up to two to three months of life, changing in structure and echogenicity and decreasing in size. In 52% of cases, the hematoma disappears without a trace, or in its place, in 48% of cases, within 2-4 weeks, a subependymal pseudocyst (SC) is formed, the peculiarity of which is the absence of a subependymal lining. As a rule, the subependymal pseudocyst is reduced by 6-9 months of life.

Resorption of intraventricular blood clots after grade II and especially grade III PVS occurs gradually, usually within 5-6 weeks. In the area of parenchymal hemorrhage in grade IV PVS, a porencephalic pseudocyst associated with the cavity of the lateral ventricle is formed in 75-82% of cases on the 24-36th day of life. The most typical complication of grade III-IV PVS is dilation of the lateral ventricles, the severity and frequency of which are determined by the severity of the pathological process. Subcompensated dilation develops within 1-3 weeks and is observed in 48% of children with grade III PVS. Usually, by the time the child is discharged from the hospital, it is possible to say whether the dilation of the ventricles was transient, persistent, or progressive with the development of internal hydrocephalus. Complete or partial occlusion is judged by the dilation of the overlying sections of the cerebrospinal fluid system.

Periventricular leukomalacia (PVL) is an ischemic infarction of the white matter of the brain around the outer angles of the lateral ventricles. Until recently, the diagnosis of PVL was a conclusion made only by pathologists, since there are no clinical symptoms indicating damage to the periventricular region in young children. Pathologically, PVL reveals small areas of softened brain matter anterior to the anterior horns, near the lateral angles of the lateral ventricles and lateral to the posterior horns. In some cases, calcification and gliosis occur several weeks after the ischemic stroke, leaving a "periventricular scar", in others, single or multiple cavities (pseudocysts) are formed, which can collapse over time and lead to secondary dilation 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 infarctions, and sometimes PVS.

On the echogram in the coronary and parasagittal planes, the 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 area of the bodies and posterior horns of the lateral ventricles. Less often, an increase in echogenicity is noted above 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 cerebrospinal fluid. PVL is symmetrical, i.e. always bilateral. Ultrasound diagnosis at this stage is difficult, since the increase in echogenicity can be due to the peculiarities of vascularization and incomplete myelination of the periventricular zones in premature infants. PVL is most likely to develop if, upon repeated examination after 10-14 days, pronounced echogenicity in the periventricular areas remains. Spectral Dopplerography helps in the differential diagnosis of the acute phase of PVL and the normal halo of increased echogenicity.

The late echographic stage of PVL is cystic degeneration, developing at the site of high echogenicity. Cysts do not have an epithelial lining, and may merge to form larger cavities. In this case, minimal and/or moderate expansion of the ventricular system is often observed, mainly the lateral ventricles due to the anterior horns and bodies. Then, within 6-8 weeks, the cysts collapse, are replaced by scar tissue and cause secondary atrophy of the brain matter. With atrophy, the lateral ventricles do not lose their normal outlines, but become more rounded in the area of the anterior horns and bodies. In this case, no echographic signs of cerebrospinal fluid occlusion are observed.

Subcortical leukomalacia (SCL) occurs due to impaired blood supply to the subcortical structures by leptomeningeal vessels in the last trimester of pregnancy. In the initial stages, echograms show edema of the brain tissue, which is characterized by a diffuse increase in the echogenicity of brain tissue and a decrease (absence) of pulsation of the brain vessels. Later, as a rule, within two weeks, foci of increased echogenicity without clear contours develop against the background of edema. By the end of the month, multiple, small, parenchymatous cysts are formed in the brain tissue. At the same time, the ventricular system and often the subarachnoid space slightly expand.

Ventricular dilation

It is quite easy to detect ventricular dilation and asymmetry during ultrasound examination. If there is any doubt, a repeat examination should be performed after some time. One of the most common causes of dilation is congenital stenosis of the aqueduct of Sylvius.

Agenesis of the corpus callosum is another common congenital malformation that results in hydrocephalus. It causes significant displacement of the lateral ventricles and anterior displacement of the third ventricle.

Intracranial hematoma

1. Subependymal hemorrhage is visualized as one or more hyperechoic areas just below the lateral ventricles and is best seen in cross-sections, in the area of the anterior horns. Confirm the diagnosis with a sagittal scan: the hemorrhage may be bilateral. This is a first-degree hemorrhage.
2. Intraventricular hemorrhage into non-dilated ventricles. Additional echostructures appear against the background of anechoic ventricles (as well as from hyperechoic vascular plexuses), corresponding to blood clots in the ventricles. If there are no signs of ventricular dilation, then this is the second degree of hemorrhage.
3. Intraventricular hemorrhage into dilated ventricles. When there is intraventricular hemorrhage into dilated ventricles, this is grade III hemorrhage.
4. Intraventricular hemorrhage, accompanied by hemorrhage into the brain substance, is visualized as areas of increased echogenicity in the brain structure. This is grade IV hemorrhage, the most pronounced.
5. Complications of hemorrhages. In grades I and II, blood is usually reabsorbed during the first week of life, but more severe hemorrhages (grades III and IV) can cause posthemorrhagic hydrocephalus and also result in tissue resorption with the formation of cysts in the cerebral hemispheres. This may result in developmental delay with neurological symptoms.

Pathology of the brain of newborns

• Necrosis of brain tissue, defined as a hypoechoic zone with an unclear outline, located lateral to the lateral ventricles (periventricular leukomalacia).
• Cerebral edema may lead to obliteration of the ventricles and sulci of the brain. The brain is more echogenic than normal.
• Brain infections can cause changes in echogenicity, including the presence of punctate hyperechoic structures due to calcification.