The Role of Cranial Ultrasonography in Detecting Neurological Abnormalities in Preterm Neonates


Doctoral Thesis / Dissertation, 2022

84 Pages


Free online reading

INTRODUCTION

Neurological evaluation of premature neonates has become increasingly important as the incidence of premature deliveries has increased. The survival rate of very low birth weight babies has also increased due to the advent of newer NICU technologies. The survivors are at a greater risk for developing neurological impairments.1

About 10% of new borns that are born prematurely will acquire neurological injuries that may lead to significant learning disabilities, motor developmental disabilities, cerebral palsy, seizures and mental retardation.2 Some the brain injuries may be result of secondary hemodynamic alterations like white matter injury, germinal matrix hemorrhage, intra ventricular hemorrhage, periventricular leucomalacia, and cerebellar hemorrhage and atrophy.

It is essential for the timely identification of the intracranial abnormalities so that adequate management can be provided to the neonates and will help in the life outcome thereby reducing mortality and morbidity.3

Neonatal sonography of the brain has become a crucial part of new born screening and management, especially in the care of high-risk premature neonates due to its non-invasive nature. Ultrasound technology now enables rapid and bedside evaluation of neonates in intensive care. 4

Other imaging modalities for neonatal evaluation are CT brain and MRI brain. Due to risk of radiation exposure CT is not a preferred modality and also due to ineffective grey / white matter differentiation caused by higher water content in the brain of new borns.

The wide acceptance of ultrasonography over computed tomography (CT) / magnetic resonance imaging (MRI) for brain screening is due to its portability, cost effectiveness, no ionizing radiation exposure, speedy and no sedation).4

AIM AND OBJECTIVES

This study was done with following Aim and objective

- To study the role of neurosonogram in preterm neonates in detection of various intracranial abnormalities like, intracranial haemorrhage, periventricular leukomalacia, ventriculomegaly and other evolutionary changes.

REVIEW OF LITERATURE

Sonography of head was first performed in 1955 and involved the use of Amode to detect midiine structure and obtain a crude estimation of ventricular size.5 In 1963, two-dimensional bidirectional echoencephalogram appeared and was significant technical advance since it provided better information about ventricular size ,as well as intracranial spatial relationships.6

With the advent of the Octoson and of sector-format real-time ultrasonic instruments, two-dimensional imaging of infant head became a reality. Resolution and image display is equal to that obtained with computerized tomography and in some cases appears to be superior.7

In 1980, sonography was recommended as the primary technique for detecting intracranial hemorrhage in preterm neonates . This technique is both sensitive and specific for subependymal germinal matrix hemorrhage, intraventricular hemorrhage, and ventniculomegaly . Satisfactory studies can be performed at the bedside with little risk to the infant.8

A prospective study of 25 consecutive premature infants under 1,500 g was undertaken to evaluate the frequency and sonographic appearance of subependymal germinal matrix hemorrhage. In all 12 sonographically positive cases, the hemorrhage was initially imaged in the area immediately anterior to the caudothalamic groove. Special attention to this area permits early detection of germinal matrix hemorrhage, and neurosonography of neonates should be considered incomplete unless this area has been thoroughly imaged.95

In a study done over a 14-month period, 112 consecutively born neonates with a birth weight between 1,501 and 2,000 g were screened by cranial ultrasonography. Nineteen patients (17%) had abnormal scans. Of these abnormalities, 14 (13%) were germinal matrix hemorrhage and/or intraventricular hemorrhage. More than half of the hemorrhages identified were severe, ie, grades III and IV.10

Neurosonogram was performed on 96 infants weighing 1500 g or less over a 9-month period. Intracranial subependymal / intraventricular hemorrhage occurred in 22 (23%) of the infants. Of these 13 (59%) developed ventricular enlargement, the ventricular enlargement developed within 2 weeks of the hemorrhage in 77% of cases." ln a prospective study of 49 neonates delivered less than or equal to 32 weeks gestation, the initial hemorrhage typically occurred in the first three days of life, with 36% occurring on day 1, 32% on day 2, and 18% on day 3.By the sixth day, 91% of all intracranial hemorrhage had occurred.12

In a study of 75 infants weighing less than 2,000 g at birth the findings demonstrate that with extensive IPE there is little or no Chance for survival with normal neurologic and cognitive outcome, but with localized IPE, although major motor deficits are common, an appreciable proportion of infants have cognitive function in the normal ränge. 13

In a retrospective study of 742 premature neonates evaluated over a 3-year period. Study concluded that intracranial hemorrhage occurred in 44% of patients with 20% being Grade 1, 10% Grade 2, 7% Grade 3, and 7% Grade 4. All hemorrhages occurred during the first week of life.146

In prospective study of 75 preterm infants of 34 weeks gestation or more and birth weight above 1500 g (ränge 1500 g to 2500 g). All neonates were screened by cranial ultra-sonography for evidence of peri-intraventricular hemorrhage (PIVH). Sonographie abnormalities were detected in 16 (21.3%) of patients. Intracranial hemorrhage was frequently associated with a low Apgar score, need of resuscitation and/or assisted Ventilation immediately after birth.15

In a prospective study of 124 neonates of less than 1250 g birth weight. by cranial sonography. IPE occurred both early, at 36 hours or before, and later, ie, between 48 and 96 hours. Study concluded that in GM-IVH and IPE were noted simultaneously in neonate with the earlier onset IPE (diagnosed within 36 hours); GM-IVH preceded the IPE by 6 to 48 hours when the lesion was of a later onset.16

In a prospective study done on 499 preterm infants. Demographie features of infants screened in the Ist vs. 2nd week of life were similar, more patients screened in the Ist week had questionable PVL diagnosed. Study concluded that routine screening may be delayed until the 2nd week without compromising patient care. Widespread use of a similar screening protocol would result in significantly fewer studies being performed reducing the cost.17

An understanding of brain development and anatomy is vital for Interpretation of neuroradiological studies.

BRAIN DEVELOPMENT

The central nervous System appears in the beginning of the 3rd week of gestation inform of a slipper-shaped plate of thickened ectoderm, the neural plate. This plate is located in the middorsal region in front of the primitive gut. Its lateral edges elevate soon after to form the neural folds. These neural folds become even more elevated, and progress to develop and approach one another in the midiine, and they finally fuse, leading to the formation of neural tube. By the fourth week of gestation, there is development of three vesicular dilations at the rostral portion of the neural tube, resulting in definition of forebrain (prosencephalon), midbrain (mesencephalon), and hindbrain (rhombencephalon)'23

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Fig.1 : Diagrammatic Sketches of the brain Vesicles showing the adult derivatives of its walls.

By the fifth week of gestation, the developing forebrain has divided into a cranial part telencephalon and a caudal part diencephalon.

Similarly, the developing hindbrain is subdivided into a cephalic part metencephalon and a caudal part myelencephalon.

The metencephalon then progresses to become pons and cerebellum while the myelencephalon forms the medulla oblongata 24 Bilateral outpouchings from the telencephalon of the neural tube result in formation of the cerebral hemispheres. These hemispheres undergo extensive expansion and folding leading to formation of permanent primitive fissures by the end of fourth month.

Early in development the cerebral hemispheres are lissencephalic ie smooth- surfaced, and a germinal matrix of primitive cells surrounds each lateral ventricle. From these germinal matrix cells proliferate, migrate outward to the cortex in an 'inside out' sequence, and mature as neural and glial cells.

The germinal matrix is formed at about 7 weeks of gestational age and involutes at about 28 to 30 weeks; however, it persists in form of clusters of cells up to weeks 36 through 39.25 Düring the sixth and seventh months, the cerebral surfaces convolute to form primitive gyri and sulci. Therefore the adult pattem of brain can be recognized toward the end of gestation. Simultaneously there is formation of fibre tracts, including the commissural fibres. The new born brain constitutes approximately 15% of the total foetal body weight, while the adult brain weighing about 1400g only upto 2% of the total body weight.

The brain is enclosed in the cranial cavity and is continuous with the spinal cord through the foramen magnum.

It is covered by three layers of meninges, namely dura matter, arachnoid and pia matter from outside to inside. The brain is divided into three major divisions consisting of forebrain, midbrain, hindbrain and the spinal cord. The forebrain consists of the diencephalon, which is the central part and the cerebrum.26 The hind brain is subdivided into the medulla oblongata, the pons, and the cerebellum.

CEREBRUM

It is the largest part of brain and consists of two cerebral hemispheres.26

The two cerebral hemispheres are connected to each other at the midiine by corpus callosum. The cerebral cortex consists of folds, or gyri, separated by fissures, or sulci. A number of the large sulci have been used to subdivide the surface of each hemisphere into various lobes. These lobes are named after the cranial bones underwhich they lie.

FOUR LOBES: The superolateral surface of cerebral hemisphere is divided into four lobes.

1. Frontal lobe
2. Parietal lobe
3. Occipital lobe and
4. Temporal lobe

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Figure 3: Cerebral hemisphere depicting the different lobes.

CORPUS CALLOSUM

They are the largest commissural fibres of the brain that connect the two cerebral hemispheres.

Parts:

1. Genu, which is the anterior end.
2. Rostrum is directed downwards and backwards from the genu and ends at the lamina terminals in front of the anterior commissure.
3. Trunk is the middle part between genu and splenium. It provides attachment to septum pellucidum and fornix and forms roof of the central part of lateral ventricle.
4. Splenium is the posterior most part and forms the thickest part of corpus callosum. Inferior surface of which is related to tela choroidea of third ventricle, pulvinar, pineal body and tectum of mid brain.

Septum pellucidum: It is a thin portion consisting of two laminae separated throughout a greater or lesser part of their extent by a narrow interval termed the cavum septum pellucidum which does not communicate with the ventricles of the brain.

THALAMUS

t is the dorsal part of the diencephalon lying obliquely with its long axis directed backwards and laterally. Each thalamus has two ends, and four surfaces. Narrow anterior end forms the tubercle of thalamus which forms the posterior boundary of the intraventricular foramen. Posterior end is expanded and is known as pulvinar.

Superior surface is divided into lateral ventricular part that forms the floor of lateral ventricle (central portion) and medial extra ventricular part that is covered by tela choroidea of third ventricle.

Inferior surface lies on subthalamus and hypothalamus. Medial surface forms the postero superior boundry of lateral wall of 3rd ventricle. Lateral surface forms medial boundary of the posterior limb of internal capsule.

INTERNAL CAPSULE:

They are large band of fibers situated in the inferiomedial part of the each cerebral hemisphere. Parts of internal capsular are:

a. Anterior limb lies between the head of the caudate nucleus and the lentiform nucleus.
b. Posterior limb lies between the thalamus and the lentiform nucleus.
c. Genu is the band between anterior and posterior limbs.
d. Retrolentiform part lies behind the lentiform nucleus.
e. Sublentiform part lies below the lentiform nucleus.

CAUDATE NUCLEUS:

lt is a C-shape nucleus which is surrounded by the lateral ventricle. The concavity of C encloses thalamus and internal capsule.

METENCEPHALON:

CERBELLUM

It is located in the posterior cranial fossa and forms the largest part of the hindbrain.

It consists of three parts, two cerebellar hemispheres joined by the median vermis.

The cerebellum is connected to the midbrain by superior cerebellar peduncles, to the pons by the middle cerebellar peduncles, and to the medulla by the inferior cerebellar peduncles. Each cerebellar surface hemisphere is called cortex and is composed of gray matter. The cortex consists of folds or folia, which are separated by closely set transverse fissures. Certain masses of gray matter are embedded in white matter; the largest of these is known as the dentate nucleus.

MEDULLA OBLONGATA

It is conical shaped structure that connects superiorly to and inferiorly to the spinal cord. It contains many nuclei and serves as a conduit for ascending and descending nerve fibers.

PONS

It is located anterior to the cerebellum, inferior to the midbrain and superior to the medulla oblongata. It also contains many nuclei and ascending and descending nerve fibers.

VENTRICULAR SYSTEM

Ventricles are nothing but cavities within the brain that enclose the cerebrospinal fluid (CSF) and choroid plexus.

There are two lateral, one third and one fourth ventricles.

The lateral ventricles are present in cerebral hemispheres and communicate through the formen of Monro with the third ventricle.

The third ventricle is a slit like cleft present between the two thalami and via the cerebral aqueduct of Sylvius communicates with the fourth ventricle.

The fourth ventricle is located anterior to cerebellum and posterior to the pons and medulla. It communicates with the subarachnoid space through the three foramina in its roof and continues distally with the central canal of spinal cord.

CSF is secreted by a specialised structure called Choroid plexus. CSF Supports the nervous System by flowing through the ventricles and subarachnoid space and is primarily absorbed through the arachnoid villi into the superior sagittal sinus.

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Figure 4: Diagrammatic representation of the ventricular System.

BLOOD VESSELS OF BRAIN

Arterial supply of brain is by a pair of internal carotid and a pair of vertebral arteries.26

At the lower border of pons the two vertebral arteries join together to form the basilar artery.

The interconnection of the main arteries at the base of the brain forms the arterial circle called circle of Willis or circulus arteriosus. It is a direct arterial anastomosis helping in managing the arterial pressure of the two sides.

BRANCHES OF THE MAIN ARTERIES:

Cerebral part of the internal carotid artery gives off:

1. Ophthalmie artery
2. Anterior cerebral artery
3. Middle cerebral artery
4. Posterior communicating artery
5. Anterior choroidal artery-it may arise from middle cerebral artery.

Fourth part of vertebral artery gives off:

1. Meningeal artery
2. Posterior spinal artery
3. Anterior spinal artery
4. Posterior inferior cerebellar artery
5. Medullary artery

Basilar artery gives off:

1. Pontine arteries 2
2. Labyrinthine artery
3. Anterior inferior cerebellar artery
4. Superior cerebellar artery
5. Posterior cerebral artery

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Figure 5: Arterial blood supply of brain.

HISTORY OF ULTRASOUND

The Piezoelectric effect which is the basis of ultrasound dates back to 1880. This effect was first demonstrated by the Curie brothers, Pierre and Jacques Curie in 1880.

The technology of producing ultrasound was known for many years before its first major attempt in practical use was made in the search for the sunken Titanic in the North Atlantic which was unsuccessful. Paul Langevin then became the first one to use pulse echo technique for the detection of Submarines.

SONAR (Sound Navigation And Ranging) turned to be the first successful application.

The first medical application of ultrasound was made by Karl Kursik in 1942, who attempted to locate brain tumours using two opposing ultrasound transducers.

NORMAL ULTRASONIC APPEARANCE OF NEONATAL BRAIN

Thorough knowledge of normal ultrasonic anatomy of neonatal brain is essential in order to utilize ultrasound to diagnose and evaluate the various conditions that affect the brain. In premature infants, the surface of the brain is smooth because the gyri and sulci are underdeveloped. 27

Lateral ventricles Asymmetry of the lateral ventricles is a common variant. More often, the left ventricle is larger than the right, the occipital horns are larger than the frontal horns. The ventricles of the premature infant are usually larger than those of term infant, they appear as fluid filled comma-shaped structures.28

Cavi septi pellucidi and vergae The cavum septum pellucidum is seen in the midiine between the anterior horns of lateral ventricles. The posterior part of the cavum septum pellucidi is termed cavum vergae. The cavum vergae is interposed between the bodies of the lateral ventricles. The foramen of Monro marks the dividing line between these two parts of the cavum.

Choroid plexus

The choroids plexus is responsible for producing CSF in the ventricles. It lines the body as well as the occipital and temporal horns of each lateral ventricle. The largest part of the choroids plexus, which is known as glomus, is in the trigones of the lateral ventricles. At the level of the glomus, the choroids plexus tapers as it courses anteriorly to the roof of the third ventricle and posteriorly into the temporal horns of each lateral ventricle. Choroid plexus ends at the caudothalamic groove and it never extends into the frontal or occipital horns of the lateral ventricles.28

Germinal matrix

The germinal matrix develops deep to the ependyma and consists of loosely organized, proliferating cells that give rise to the neurons and glia of the cerebral cortex and basal ganglia. Its vascular bed is the most richly perfused region of the developing brain. Vessels in this region form an immature vascular rete of fine capillaries, extremely thin-wall veins and larger irregulär vessels. Although germinal matrix is not visualized on sonography, it is important as the typical anatomic site that lies above the caudo-thalamic groove and beneath the ependymal lining of ventricles where haemorrhage occurs in preterm infants 4 Periventricular white matter echogenicity An echogenic bound paralleling the posterior part of the lateral ventricles is a normal finding seen in virtually all neonates. This band of echogenicity is referred to as periventricular halo. The degree of echogenicity should be less than or equal to that of normal choroids plexus. The halo should have a homogenous brush like appearance. The differential of periventricular echogenicity includes cerebral haemorrhage and periventricular leukomalacia. Either of these conditions should be suspected if the periventricular halo is Symmetrie or more echogenic than choroids plexus.28

CROSS-SECTIONAL SONOGRAPHIC ANATOMY42728

The echo free ventricular System, echogenic sulci, nuclei and septa and the pulsatile intracranial major arterial branches serve as landmarks for identifying the normal structures within the brain in coronal, sagittal and parasagittal views.

Coronal view

The anatomy in the coronal plane will be described in six sections, as seen when the ultrasonic transducer is swept from the frontal to the occipital regions.

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Fig. 7: Coronal sections for NSG

Coronal plane 1

The most anterior image is acquired just anterior to the frontal horns of the lateral ventricles. Visualisation of the anterior cranial fossa is obtained, including the frontal lobes of the cerebral cortex with the orbits deep to the floor of the skull base. In this case the transducer is angled forward.

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Figure 8: Coronal plane 1 section of neurosonogram Coronal plane 2

As the transducer is angled backwards from Coronal plane 1 the frontal horns of the lateral ventricles appear as symmetrical, anechoic, comma shaped structures with the hypoechoic caudate heads within the concave lateral border. Structures visualized from superior to inferior in the midiine include interhemispheric fissure, Cingulate sulcus, genu and anterior body of corpus callosum and septum pellucidum between the ventricles. Moving laterally from the midiine, the caudate nucleus is separated from the putamen by internal capsule. Lateral to the putamen, the sylvian fissure is echogenic because it contains middle cerebral artery.

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Figure 9: Coronal plane 2 section of neurosonogram

Progressing farther posteriorly to the level above the midbrain, the body of the lateral ventricles is seen on either side of the cavum septi pellucidi. Below this, the thalami lie on either side of the third ventricle.

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Fig. 10: Coronal plane 3 section of neurosonogram Coronal plane 4

A slightly more posterior transducer angulation results in a plane that includes the cerebellum. The body of the lateral ventricles becomes more rounded. At this level in the midiine, the body of the corpus collosum is deep to the cingulate sulcus, and the third ventricle is located between the anterior portions of the thalami. Echogenic material visualized in the floor of the lateral ventricles is the choroids plexus. Echogenic choroids plexus is also seen in the roof of the third ventricle, resulting in three echogenic foci of choroids. Below this, in the posterior fossa, vermis is the echogenic structure in the midiine surrounded by more hypoechoic cerebellar hemispheres.

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Figure 11: Coronal plane 4

Coronal plane 5

Further posteriorly, the trigone or atrium of the lateral ventricles and occipital horns are visualized. The extensive echogenic glomus of the choroids plexus nearly 20 obscures the lumen of CSF filled ventricle at the trigone. Inferiorly the cerebellum is separated from the occipital cortex by the tentorium cerebelli.

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Fig. 12: Coronal plane 5 section

The most posterior section visualizes predominantly occipital lobe cortex and the most posterior aspect of the occipital horns of the lateral ventricles that do not contain choroids plexus. This section is angled posterior to the cerebellum.

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Fig. 13: Coronal Plane 6

Saqittal imaginq: The sagittal images are obtained by placing the transducer longitudinally across the anterior fontanelle and angling it to each side.

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Midiine sagittal plane

The midiine is first identified through the interhemispheric fissure by recognition of the curving line of the corpus collosum above the cystic cavum septi pellucidi and cavum vergae, the third and fourth ventricles and the highly echogenic cerebellar vermis. The cingulate sulcus lies parallel to and above the corpus collosum. Standard sagittal planes above the lateral ventricle is the cerebral cortex, and below it is the cerebellar hemisphere. The caudate nucleus and the thalamus are within the arms of the ventricle. The caudothalamic groove at the junction of these two structures is an important area as it is the most common site for germinal matrix hemorrhage in the subependymal region of the ventricle

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Fig. 14: Standard sagittal planes

Parasagittal plane s (through lateral ventricles and insulae.)

More pronounced lateral angultion will demonstrate the peripheral aspect of the ventricles and the more lateral cerebral hemisphere, including the temporal lobes. Where middle cerebral artery branch extend toward the ventricle parasagittal view almost always demonstrates a normal hyperechoic peritrigonal blush just posterior and superior to ventricular trigones.

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Figure 15: Midsagittal plane through the third and fourth ventricles.

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Figure 16: Parasagittal plane through the insula S3.

BRAIN INJURIES IN PRETERM BABIES

Preterm infant is an infant born at less than 37 completed weeks or 259 days of gestation. Preterm birth is a major determinant of neonatal mortality and morbidity and has long term adverse consequences for health. Children who are born prematurely have higher rates of cerebral palsy, sensory deficits, learning disabilities and respiratory illnesses compared with children born at term. The morbidity associated with preterm birth often extends to later life. The neurologic manifestations of brain injury in the premature infant ränge from the less severe morbidity and cognitive deficits to major spastic motor deficits, including spastic diplegia and spastic quadriplegia with more profound intellectual deficits. Of all the neonatal deaths (i.e., deaths within first 7 days of life) that are not related to congenital malformations, 28% are due to preterm birth.30

Incidence and aetiology:

World-wide the preterm birth rate is estimated at 9.6% representing about 12.9 million babies. Incidence of preterm birth in India is approximately 21%. Although the incidence of germinal matrix hemorrhage was as high as 55% previously and incidence of PVL was 25-40% in babies born less than 32 weeks gestational age and in very low birth weight infants. Recent reports of GMH ränge from 10-25% and incidence of PVL has decreased to 7% due to increased usage of antenatal steroids and improved neonatal respiratory care such as Surfactant therapy31

Multiple factors have been studied as cause for GMH. Common associations include prematurity with complications such as hypoxia, hypertension, hypercapnia, hypernatremia, rapid volume increase and pneumothorax. PVL is anticipated to follow maternal chorioamnionitis and severe hemodynamic insult like cardiorespiratory compromise resulting in hypotension and severe hypoxia and ischaemia.31

PATHOPHYSIOLOGY3

Brain damage in preterm infants may result from a series of events rather than one specific insult. Maturational characteristics with a failing adaptation capacity may predispose the brain to harmful events during both intrauterine and extrauterine life. Structural and functional immaturity of the organs responsible for Ventilation and circulation in a preterm infant is the basic reason leading to lack of an acceptable cerebral blood flow and arterial oxygen delivery in the brain under unfavourable clinical conditions. Immature vascular structures, certain developmental characteristics in the cerebral circulation, intrinsic cell vulnerability and various toxic mechanisms overlap and contribute to predisposition to cerebral damage.

ARTERIAL WATERSHED DETERMINES REGIONAL PATTERN OF BRAIN DAMAGE IN PRETERM INFANTS 32

The immature new born brain has very characteristic angioarchitecture at this age. Normally there is a watershed zone between the ventriculopetal and ventriculofugal arteries. Below 34 weeks of gestation this water shed zone is located in the periventricular area. With increasing maturity the sulci deepen and the course of subcortical and long straight medullary arteries changes from a gentle bend to more 28 acute bend. The watershed area thus moves from preventricular zone to subcortical location. Since the watershed area in preterm is in immediate periventricular region, the germinal matrix hemorrhage and periventricular leucomalacia are common pathological findings.

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Figure 17: The premature neonatal brain (left) has a ventriculopetal vascular pattern. In the term infant (right), a ventriculofugal vascular pattern develops as the brain matures, and the border zone during hypoperfusion is more peripheral.43

1. GERMINAL MATRIX HEMORRHAGE

The germinal matrix is a fine network of blood vessels and primitive neural tissue that lines the ventricular System in the sub ependymal layer during fetal life. As the fetus matures germinal matrix regresses towards the foramen of munro, so that by full term only small amount of germinal matrix is present in the caudothalamic groove.

Sonography is the most effective method for detecting this hemorrhage in the newborn period and for follow up in the subsequent weeks. Most hemorrhage (90%) occurs in the first 7 days of life, but only one third of these occur in the first 24 hours.34

The brain of the premature infant lacks the ability to auto-regulate cerebral blood pressure, thus fluctuations in cerebral blood pressure and flow can rupture this fine network of blood vessels which is highly susceptible to pressure and metabolic changes.4

The germinal matrix is rarely a site of hemorrhage after 32 weeks of gestation because it has almost disappeared.

Germinal matrix hemorrhage may occur in subependymal, intraventricular or intraparenchymal regions. However, GMH originates predominantly as hemorrhage in the germinal matrix below the subependymal layer and may be contained by the ependyma or may rupture into the ventricular System or less often into the adjacent parenchyma.33

The optimal cost-effective timing to screen premature infants is at 1 to 2 weeks of age to identify patients with significant hemorrhage as well as those developing hydrocephalus.35 Small subependymal hemorrhages might be missed when screening is done late because they resolve quickly, but these have not proven clinically important.34

The Classification of GMH most widely used was proposed by Burstein et al.33

GRADES OF GERMINAL MATRIX HEMORRHAGE

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Grade I SUBEPENDYMAL HEMORRHAGE4

Neurosonogram show subependymal hemorrhage as a region of increased echogenicity. Images acquired in the coronal plane show a well defined area of increased echogenicity adjacent to the ventricular wall. The most common location is at the caudothalamic notch, inferior to floor of frontal horn. Sagittal plane is often very useful in differentiating germinal matrix hemorrhage from the echogenic choroids plexus because choroid plexus does not extend anterior to foramen of munro, whereas caudate head and adjacent ganglionic eminence hemorrhage lie immediately anterior to the foramen.

This subependymal hemorrhage is typically noted in first weeks of life. As the hematoma ages, the clot becomes less echogenic with its centre becoming sonolucent.

The clot retracts and necrosis occurs with complete resolution of hemorrhage or occasionally development of a subependymal cyst. It may persist as linear echo adjacent to the ependyma.

GRADE II : INTRAVENTRICUALR HEMORRHAGE.28

Grade II hemorrhage results when subependymal blood ruptures through the ventricular wall entering the lumen. It appears as echogenic material within part or all of a non-dilated ventricular System. Most often, the blood accumulates in the dependent part of ventricle (the occipital horns). In some neonates, it can be difficult to identify small amounts of hemorrhage in a non dilated ventricle, particularly if choroid plexus is large.

Doppler imaging is useful to distinguish normal vascularised choroids plexus from non-vascularised clot. Use of posterior fontanellae views helps the detection of small IVH in third and fourth ventricle or CSF blood fluid levels in the occipital horns.4

Over the first few weeks after the acute event, the intra ventricular clot organizes and become well defined and less echogenic. At this stage, it appears as a relatively sonolucent mass within the lateral ventricle usually in the body or the atrium. At this time the clot is less echogenic than the choroids plexus which is situated adjacent to the thalamus. As the grade II hemorrhage resolves the ventricular wall often becomes echogenic.29

Early onset IVH, in the first 6 hours of life is uncommon and has been associated with higher risk of both cognitive and motor impairment including cerebral palsy.

GRADE III - INTRAVENTRICULAR HEMORRHAGE WITH HYDROCEPHALUS.4

Grade III hemorrhage fills and also enlarges one or both lateral ventricles. Because of hydrocephalus, the clot and choroids plexus are better defined.

The echogenic clotmay be adherent to the ventricular walls or may become dependent within the ventricular wall.

In the acute phase after the intra ventricular hemorrhage, ventricular dilatation results from blockage of the CSF pathways by hemorrhagic particulate matter. This acute hydrocephalus often resolves and is of no prognostic value.

When hemorrhage is severe it can cause obiiterative arachnoiditis that usually occurs in the basilar cisterns, the arachonoidal adhesions block the normal flow of CSF and necessitate permanent ventriculoperitoneal CSF diversion.29

As the intraventricular clot retracts, echogenic debris or floating clot fragments may be seen in the ventricles.

Patients with post hemorrhagic ventricular dilation have an increased incidence of periventricular white matter injury and olivocerebellar injury.28

GRADE IV: INTRA PARENCHYMAL HEMORRHAGE

Intra parenchymal hemorrhage is usually in the cerebral cortex and located in frontal or parietal lobes, because it often extends from the subependymal layer over the caudo-thalamic groove.

Studies suggest that intra parenchymal hemorrhage is caused by emorrhagic venous infarction secondary to obstruction of the terminal veins by large subependymal hemorrhage or intraventricular hemorrhage. Periventricular hemorrhagic infarctions are ischaemic parenchymal injuries associated with hemorrhage that typically occur in deep white matter adjacent to lateral ventricle.4

On sonography they appear as globular, crescentic, or fan shaped areas of mixed hyper and hypo-echogenicity. As the clot retracts the edges form an echogenic rim around the centre, which becomes sonolucent. The clot may move to a dependent position and by 2-3 months after the injury an area of porencephaly or encephalomalacia develops.29

2. PERIVENTRICULAR LEUCOMALACIA

Periventricular leucomalacia, the principle ischaemic lesion of the premature infant, is infarction and necrosis of the periventricular white matter.

The pathogenesis of PVL has been found to relate to 3 main factors.

i) Immature vasculature in the periventricular watershed area.
ii) The absence of vascular autoregulation in premature infants.

IM) Maturation dependent vulnerability of the oligodendroglial precursor cell damage in PVC. These cells are extremely vulnerable to attack by free radicals generated in the ischemia - reperfusion sequence. Pathologically, the periventricular white matter undergoes coagulation necrosis, followed by phagocytosis of the necrotic tissue.3

In PVL, the white matter most affected is in the arterial border zones at the level of the optic radiations adjacent to the trigones of the lateral ventricle and the frontal cerebral white matter near the foramen of munro33

The initial sonographic examination in PVL may be normal within 2 weeks of the initial insult, the periventricular white matter increases in echogenecity until it is greater than the adjacent choroids plexus. This increased echogenicity is usually caused by edema from infarction and may also result from hemorrhage (heterogenous flares). 2-4 weeks after the insult, cystic changes may develop in the area of abnormal echogenic parenchyma. The cyst can be single or multiple and are parallel to the ventricular border in the deep white matter. These cysts measure from 5mm to 1-2 cm in diameter. Cystic changes are usually bilateral and symmetrical 36

Tissue loss secondary to cavitatory white matter injury results in ventricular enlargement that usually appears towards the end of 2nd week. A late screening for periventricular leucomalacia should be performed to search for cystic changes of PVL and ventricular enlargement which may be missed if the late screening is not done.

Classification of periventricular leucomalacia according to de vries.

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Late neurologic problems from PVL include developmental delay and symmetrical spastic diplegia involving both legs, often notic eable by 6 months of age.

Spastic diplegia occurs because of the pyramidal tracts from the motor cortex that innervate the legs pass through the internal capsule and travel close to the lateral ventricular wall. Severe cases of PVL will also affect the arms, resulting in spastic quadriplegia and cause Vision and intellectual deficits.

2. Porencephalic Cystic changes

Porencephalic (Greek for „holes in the brain") are hemispheric cavitary lesions, in the neonates porencephalic most frequently follow grade 4 haemorrhage. Heschl originally described Porencephaly in 1859. Drew and Grant, 1948 substituted the term „benign cyst of brain" thus avoiding the controversy.44

It is now feit that cavities may be in communication with the ventricles or subarachnoid spaces or they may be totally isolated, Freeman et al., 1964.45

Contu and Lemay (1967) described the evolution of cerebral hematoma to porencephalic cyst documented by pneumocephalography in 6 adult patients.

Courvillie, 1957 and Furlow, 1941, also addressed the development of such post hemorrhagic porencephalic cyst.46

1. CEREBELLAR HEMORRHAGE4:

Cerebellar haemorrhage can occur in premature infants because there is germinal matrix in the fourth ventricle. Mastoid fontanelle imaging is now routinely used to visualize the cerebellum in the Optimum focal zone to allow cerebellar haemorrhage to be seen and the posterior fossa fully evaluated.

On sonogram, cerebellar haemorrhage produces either ill defined, asymmetric cerebellar echogenicity or focal mass. It can resolve completely or produce an area of encephalomalacia.

Resolution of cerebellar haemorrhage into a cyst in the posterior fossa may allow easier diagnosis, the normal echogenic cerebellum may obscure haemorrhage when acute.

On follow up they develop cognitive deficits and developmental delay without signs of motor abnormalities.

METHODOLOGY

Type of studv

An prospective observational study conducted in the Department of Radio diagnosis, Krishna institute of medical Sciences and Hospital, Karad, Maharashtra comprising of 100 preterm neonates.

All the preterm neonates including those suspected of brain injuries were referred to Department of Radio diagnosis for neuro ultrasonography for their neurological screening and further evaluation.

Selection Criteria

Inclusion criteria:

- All Preterm neonates (less than 37 weeks).

Exclusion criteria:

- Inability to perform the sonography (excessive cry , surgical bandage etc)
- Morbid neonates

Patient preparation:

- All neonates coming to the department for ultrasonography were transported by comfortably wrapping them in warm clothes in order to maintain normal body temperature.
- lt was made sure that the baby was well fed before examination.
- The baby was ideally accompanied by the mother or any one relative.
- No sedation used.
- Baby was positioned in supine position.
- Before performing the examination hands were sanitised and the transducer probes were cleaned.

Equipment:

All the babies included in this study were examined with a curvilinear transducer and linear assay high frequency transducer of Siemens Accuson Juniper ultrasound machine.

Technique:

After appropriate preparations the neonates were transported to ultrasound rooms. Adequate feeding prior to examination was mandatory. Babies were wrapped in warm clothing to prevent hypothermia.

The baby is laid supine.

The ultrasound transducer and media gel (profuse coupling agent) were placed on the anterior fontanelle of neonatal head and images are obtained in coronal and sagittal planes.

At first the examination began in coronal plane along the coronal suture, with probe angled towards the frontal region. By sweeping the transducer from anterior to posterior, the brain was examined in various coronal planes.

After completing the coronal plane evaluation, sagittal and parasagittal images were obtained. This was done by placing the transducer on the anterior fontanelle, just perpendicular to coronal plane and then sweeping from midiine thorough the lateral ventricles towards the cerebral parenchyma on each side. Absolute symmetry while performing the scans was maintained, as dense and echogenic choroid plexus on each side may give a false image of Subependymal haemorrhage.

Average time taken for the examination ranged from 10-15minutes.

Cranial ultrasonogram done in first week of birth. The evaluation was done giving special attention to the echogenicity of cerebral parenchyma, size of the ventricles, symmetry of the ventricles, hemorrhage , any focal echodense or cystic changes and PVE.

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Figure 18: Siemens Accuson juniper ultrasound machine.

RESULTS

METHOD:

Data is analyzed using Statistical Software R Version 4.1.1 and Microsoft Excel. Continuous variables were represented by mean± sd/median (ränge) and categorical variables represented by frequency. To check the association between categorical variables Chi-square test is used. To compare mean over groups one-way Analysis of Variance (ANOVA) is used. To compare distributions over groups Kruskal-Wallis test will be used. P-value less than or equal to 0.05 indicates Statistical significance.

SUMMARY:

The study comprises of 100 babies. There were 52 males and 48 females in the study. Below table gives the distribution gender of children in the study.

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Table 1: Distribution ofgender.

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Figure 19: Distribution ofsubjects by gender.

Below table gives the distribution of subjects according to gestational age. Table 2: Distribution of subjects according to gestational age.

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Figure 20: Distribution of subjects by gestational age.

Below table gives the distribution of birth weight of babies. Table 3: Distribution ofsubjects according to birth weight.

In the study minimum birth weight and maximum birth weight observed was 1Kg and 2.5 kg respectively. Mean birth weight observed is 2.15±0.21 Kg. Below plot gives the distribution of birth weight in the study.

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Figure 21: Distribution ofsubjects by birth weights.

Below table gives the distribution of type of delivery and clinical features observed in the study.

Table 4: Distribution oftype of delivery and clinical features.

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There were 44 LSCS delivery and 36 vaginal deliveries were observed in the study. In the overall study, there were 27% of the subjects don’t had any complaints in clinical features and 28% had lethargy. Below plot visualizes the same.

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Figure 22: Distribution of subjects by type of delivery.

Below table gives the distribution of subjects according to the presenting complaints.

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Figure 23: Distribution of subjects by clinical features.

Below table gives the distribution of lesions in the first scan.

Table 5: Distribution offindings in first neurosonograms

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Figure 24: Distribution of subjects by lesions at first scan.

Below table gives the distribution of grading of GMH lesions and PVL lesions at first scan.

Table 6: Distribution of grade of GMH lesions

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There were 80.8% with grade 1 of GMH and 15.4% and 3.8% of the subjects with grade 3 GMH and grade 4 GMH respectively. Below plot visualizes the same.

Figure 25: Distribution of subjects by grade of GMH lesions.

Table 7: Distribution of grade of PVL lesions in first scan

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There were 78.9% with grade 1 of PVL and 15.8% and 5.3% of the subjects with grade 2 PVL and grade 2 PVL respectively. Below plot visualizes the same.

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Figure 26: Distribution of subjects by grade of PVL lesions.

Below table gives the relationship of mortality with GMH.

Table 8: Relationship between grade ofGMH and survival outcome.

Abbreviations: MC: Monte-Carlo’s Simulation usedin Chi-square test.

By Chi-square test, there is significant association present between grade of GMH and survival outcomes. Below plot gives the visualization of the above table.

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Figure 27: Relationship between grades of GMH and survival outcomes.

Below table gives the relationship between different Parameters and result of first scan.

Table 9: Relationship between different Parameters and first scan outcome.

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By Chi-square test, there is no significant association present between gender and type of delivery with outcome of first month scan.

BY Chi-square test, there is significant association present between gestational age and birth weight with outcome of first month scan.

By Kruskal-Wallis test, there is significant difference in the distribution of gestational age over outcome of first month scan. Dunn’s test is used for post- hoc analysis and it’s observed that, there is significant difference in the distribution of gestational age between no abnormality subjects and GMH patients (p-value: <0.0001), no abnormality subjects and PVL patients (p- value: <0.0001). However, there is no significant difference observed between GMH patients and PVL patients (p-value: 0.8836).

By One-way Analysis of Variance (ANOVA), it is observed that, mean of birth weight is significantly different over outcome of first scan. Tukey’s HSD is used for post-hoc analysis and it’s observed that, mean of birth weight is significantly different between no abnormality subjects and GMH patients (p- value: <0.0001), no abnormality subjects and PVL patients (p-value: <0.0001). However, there is no significant difference observed between GMH patients and PVL patients (p-value: 0.9838).

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Figure 29: Relationship between first scan outcomes and gestational age.

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Figure 30: Relationship between first scan outcomes and birth weight.

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Figure 31: Relationship between first scan outcomes and type of delivery.

At the end of first month scan, 10 subjects had grade 1 GMH. Below plot visualizes the above table.

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Figure 32: Distribution of subjects by grades of GMH at follow up scan.

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Table 11: Distribution of PVL grades at follow up scan.

Out of 6 subjects, 3 each had grade 1 and grade 2 PVL.

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Figure 33: Distribution of subjects by grades of PVL at follow up scan.

Below table gives the comparison between grades of PVL with outcome. Table 12: Comparison of PVL grades with outcome.

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Figure 34: Distribution ofsubjects by PVL grade and survival outcome

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In the study, initially 21 subjects diagnosed with Grade 1 GMH, out of these 21, one subject lost to follow up, two subjects developed grade 2 GMH, 9 subjects had same grade of lesions and for remaining 9 subject’s problem was resolved. Similarly we can inferfrom the above table.

OBSERVATION - CASES

Case 1: Coronal neurosonogram showing bilateral germinal matrix hemorrhage.

BO JAYSHREE THORAWADE

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Case 2: Coronal neurosonogram showing bilateral germinal matrix hemorrhage extending to the lateral ventricles without causing their dilatation.

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Case 3: Coronal neurosonogram showing bilateral germinal matrix hemorrhage extending to the lateral ventricles causing their dilatation.

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Case 4: Coronal neurosonogram showing Grade IV GMH.

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Case 5: Coronal neurosonogram showing periventricular increased echogenecity.

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Case 6: Coronal neurosonogram showing Grade 2 PVL with development of small sized periventricular cysts.

Case 6: Coronal neurosonogram showing Grade 3 PVL with development of extensive periventricular cysts.

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Case 7: Sagittal neurosonogram showing Grade 3 PVL with development of extensive periventricular cysts.

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DISCUSSION

This is a prospective observational study of 100 neonates. The study group consists of 52 males and 48 female neonates.

The included babies were from a gestational ränge of 28 to 36 weeks. Among these cases, 10 (10%) were in the gestational age of 28-30 weeks. 30 babies (30%) were between 30-32 weeks, 35 babies (35%) were between 32-34 weeks and 23 babies (25%) were in 34-36 weeks.

Most of the abnormal sonograms were from the gestational ränge of 28-30 weeks. 100% of this gestational age scans were abnormal consisting of 6 babies with (60%) GMH and(4) 40% PVL.

The babies included in the study had birth weight ranging between 1.5 to 2.5 kg (low birth weight). Minimum observed birth weight and maximum birth weight was 1Kg and 2.5 kg respectively. Mean birth weight observed is 2.15±0.21 Kg. out of all the subjects 15% (15) babies had birth weight ranging from 1.5 - 2kg and 85 (85%) from 2 - 2.5 kg.

Maximum abnormal scans were seen in the babies between 1.5-2kg birth weight ränge. While maximum normal neurosonograms were seen in babies ranging between 2-2.5 kg birth weight.

The commonest clinical manifestation in neonates with suspected brain injuries in our study was lethargy (28%) followed by delayed cry (13%). Other clinical complaints included hypotonia (7%), low Saturation (8%), poor suckling (5%) and seizures (1%).

The modes of delivery of the included babies is also taken into consideration. Most of the babies were delivered by LSCS (44%) followed by vaginal (36%) and then forceps assisted deliveries (20%).

Initial sonogram was performed within 7 days of birth followed by a repeat scan at the end of one month.

First neurosonogram study performed within 7 days of birth showed abnormal neurosonogram findings in 45 babies and rest of the 55 babies had normal study.

The most common abnormality depicted in the first study was Germinal matrix haemorrhage (26%). The grading was done based on Papile Classification - including Grade I, Grade II , Grade III and Grade IV. This was seen in correlation with the study done by Paneth N et al on preterm neonates.38

Our study showed that 24 (80%) babies had Grade I GMH, 4 (15%) had Grade 2 GMH and 1 (3%) had grade 3 GMH. Majority of the findings were grade I and grade II. This was seen in correlation with study of Kadri et al in 2006.41

Second most abnormality on neurosonogram was PVL (19%). There were 15 (78.9%) with grade 1 of PVL and 3 (15.8%) and 1 (5.3%) of the subjects with grade 2 PVL and grade 3 PVL respectively. This was corelated with the study of Skullred et al. 42

On follow-up at the end of one month death had occurred in 4 babies with GMH and 1 baby with PVL.

In the follow up study the 55 neonates having no abnormality in the first scan (55%), follow up was lost in 2 babies while neurosonograms of rest of them were unchanged and unremarkable.

In the first scan 21 subjects diagnosed with Grade 1 GMH. In the follow up scan out of these 21, one subject lost to follow up, two subjects developed grade 2 GMH, 9 subjects had same grade of lesions and for remaining 9 subject’s neurosonogram was unremarkable. Four babies were diagnosed with Grade 3 GMH. One baby was diagnosed with Grade 4 GMH which expired before the follow up scan.

In the first scan 19 babies were diagnosed with perventricular leukomalacia 15were diagnosed with Grade I , 3 babies with grade 3 and 1 baby with grade 4. In the scan at the end of the month, follow up was lost in 3 patients of Grade I. Findings of grade I PVL were resolved in 7 patients, findings persisted in 4 patients. In 3 patients with Grade 2 PVL, the findings persisted at the month end scan. While 1 patient with grade 3 PVL expired.

In our study the neonates of the gestational age ranging between 28 weeks to 32 weeks, were found to have most frequent abnormal scans. While the incidence of abnormalities in gestational age ranging between 32 to 36 weeks were comparatively lower. This helps us to establish the relationship between lower the gestational age more probability of abnormal neurosonogram findings. This correlates to numerous studies done previously including Koksal et al.40

Similarly in our study the birth weight of the neonates were ranging between 1.5 to 2.5 kg. The most abnormal neurosonograms were seen in the neonates ranging between 1.5 to 2.0 kg weight. This helps in establishing the relationship of lower the birth weight, seen associated with lower gestational age, more the probability of abnormal neurosonograms. This correlates with numerous studies.

SUMMARY

- Preterm neonates are at highest risk of developing intracranial abnormalities of which most common being the germinal matrix hemorrhage.
- Early evaluation of the preterm neonates within first week of life, aids in identification of underlying intracranial abnormality. Most common lesion noted in preterm neonates are the various grades of intracranial hemorrhage and PVL which can be detected as early as within first 24 hours of birth.
- The highest grade of mortability is seen with the Grade IV GMH and grade 3 PVL and more so seen in neonates with low birth weight.

CONCLUSION

- Real time Neurosonography is a most essential primary screening modality for initial investigation of the various intracranial abnormalities in the neonates. Easy accessibility, cost effectiveness and time sensitivity being few of its merit factors.
- The non-invasive and effective aspects of neurosonography are mostly useful in the initial evaluation of the specifically high-risk preterm infants, who are suspected of having germinal matrix hemorrhage, intraventricular hemorrhage and then follow up scans.
- Due to extensive availability of advanced and latest NICU Services and technologies, there is early Intervention done in patients with suspected brain injuries. Therefore the occurrence of adverse outcomes have great reduction.
- Neurosonography has only a few limitation which includes difficulty in distinguishing focal parenchymal echo dense lesion from hemorrhagic and non-hemorrhagic etiology, in which case CT scan is more superior to neurosonogram. CT is more accurate and sensitive in determining lesions as hemorrhagic or non hemorrhagic, but transport, sedation, IV contrast administration, temperature maintenance and the risk of ionizing radiation lim its use of CT in routine assessment of fragile neonates. Therefore Neurosonogram is the non-invasive primary method of choice in assessing neonatal brain.
- Finally the technique is relatively economical, helps in early detection and aids proper management of preterm neonates, helps in preventing neonatal morbidity, mortality and further maldevelopment.

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3. Volpe JJ. Neurological evaluation; hypoxic-ischemic encephalopathy; and intracranial hemorrhage. In : Neurology of the newborn. Third edition. Philadelphia, Pennsylvania, W.B. Saunders Company,.1995. p. 95-463.

4. Rumack CM, Drose JA. Neonatal and infant brain imaging. In: Diagnostic ultrasound. 4th edn. Philadelphia, Elsevier, Mosby; 2011.p.1558-163

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10. McGuinness GA, Smith WL. Head ultrasound screening in premature neonates weighing more than 1,500 g at birth. Am J Dis Child. 1984 Sep;138(9):817-20. 65

11. SIabaugh RD, Smith JA, Lemons J, Schreiner R, Macdonald N, Cohen MD. Neonatal intracranial hemorrhage and complicating hydrocephalus. J Clin Ultrasound 1984; 12(5):261-266. 12.

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13. Guzzetta F, Shackelford GD, Volpe S, Perlman JM, Volpe JJ. Periventricular Intraparenchymal Echodensities in the Premature Newborn: Critical Determinant of Neurologie Outcome .Pediatrics 1986 dec;78(6):995-1006

14. Kirks D, Rand Bowie JD. Cranial ultrasonography of neonatal periventricular /intraventricular hemorrhage: who, how, why and when? Pediatric Radiology 1986.Volume 16, Number2, p114-119. 15.

15. Amato M, Howald H, von Muralt G.lncidence of peri-intraventricular hemorrhage in premature neonates weighing more than 1500 g. J Perinat Med. 1987;15(1):91-94.

16. Perlman JM, Rollins N, Burns D, Risser R. Relationship between periventricular intraparenchymal echodensities and germinal matrix- intraventricular hemorrhage in the very low birth weight neonate. Pediatrics. 1993 Feb;91(2):474-80.

17. Boal DK, Watterberg KL, Miles S, Gifford KL.Optimal cost-effective timing of cranial ultrasound screening in low-birth-weight infants. Pediatr Radiol. 1995;25(6):425-8.

18. Ment LR, Schneider KC, Ainley MA, Allan WC .Adaptive mechanisms of developing brain. The neuroradiologic assessment of the preterm infant. Clinics in Perinatology 2000, 27(2):303-23 66

19. Antoniuk S and da Silva RV. Periventricular and intraventricular hemorrhage in the premature infants. Rev Neurol 2000;31(3):238-43.

20. Rezaie, P and Dean, A . MPeriventricular leukomalacia, inflammation and white matter lesions within the developing nervous systemM. Neuropathology : official journal of the Japanese Society of Neuropathology. 2006 sep; 22 (3): 106-132.

21. Linder N, Haskin 0, Levit 0, Klinger G, Prince T, Naor N, et al. Risk factors for intraventricular hemorrhage in very low birth weight premature infants: a retrospective case control study. Pediatrics 2003;111:590-595.

22. Perry RN, Bowman ED, Murton LJ, Royl RN, Crespigny DE. Cranial ultrasound screening of preterm and term neonates. Journal of Paediatrics and Child Health 2008 march: 23 (1); 31 - 33.

23. SadlerTW. Langman’s Medical Embryology. 7 th edn, USA : Williams and Wilkins 1995:374.

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27. Cremin BJ, Childton SJ, Peacock WJ. Anatomical landmarks in anterior fontanelle ultrasonogrpahy; The BrJ Radiol 1988;56:517-526.

28. Sanders RC, Winter T. Clinical sonography. A practical guide. 4th edn, USA : Lippincott Williams& Wilkins. 2007;347-348. 29.

29. Barkovich AJ (ed). Brain and spine injuries in infancy and childhood. pediatric neuroimaging. 4 th edn. Philadelphia, Lippincots Williams and Wilkins, 2005:207- 225. 67

30. Beck S, Wojdyla D, Say L, Betran AP, Merialdi M, Requejo JH et al. The world wide incidence of preterm birth. Bulletin of the World Health Organization. 2010;88:31-38

31. Singh U, Singh N and Shikha S. A prospective analysis of etiology and outcome of preterm labour. The journal of Obstetrics and Gynaecology of India. 2007;57(1):48.

32. DeReuck JL. Cerebral angioarchitecture and perinatal brain lesions in premature and full term infants. Acta Neurol Scand 1984;70:391-395.

33. Burstein J, Papile LA, Burstein R. Intraventricular hemorrhage and hydrocephalus in premature newborns : a prospective study with CT. Am J Roentgenol 1979;132:631-635.

34. Rumack CM, Manco-Johnson ML, Manco-Johnson MJ. Timing and course of neonatal intracranial hemorrhage using real-time ultrasound. Radiology 1985;154:101-105.

35. Boal DK, Watterberg KL, Miles S, Gifford KL. Optimal cost-effective timing of cranial ultrasound screening in low-birth weight infants. Pediatr Radiology 1995;25:425-428.

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37. DeVries LS, Eken P, Dubowitz LMS. The spectrum of leucomalacia using cranial ultrasound. Behav Brain Res 1992;49:1-6.

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ANNEXURES

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Name of Institute: Krishna Institute Of Medical Sciences Name of Principal Investigator: Dr. Apurva Jagtap Name of co-Investigator (at least 1)

Title of study: Role of cranial ultrasonography in detecting neurological abnormalities in preterm neonates.

You are invited to take part in the above mentioned research study. You are invited because you fulfill the eligibility (inclusion) criteria- i)—( < 37 weeks of gestational age)

Cranial ultrasonography will be performed on the neonate within 7 days of birt. The neonate will then be followed up after 1 month.

The purpose of study- To study the role of neurosonography in detecting neurological abnormalities in preterm neonates.

The study procedure- The preterm neonate will be brought to the department of Radiodiagnosis. Cranial ultrasonography will be performed within one week of birth. The neonate will be followed up after 1 month.

Possible benefits to participants- The study will benefit in early detection of the neurological abnormality. Early detection will facilitate early intervention and also adequate care of the baby. The neonate will then be followed up after 1 month to see increase , decrease or occurrence of any new lesion.

Possible benefits to society-The results of this research may provide benefit to the society in terms of advancement of medical knowledge and therapeutic benefit to future patients

Confidentiality of information obtained- You have the right to confidentiality regarding the privacy of medical information (your personal details results of physical examination, investigations and medical history). Your identity will not be disclosed to unrelated persons.

By signing the informed consent document you will be allowing the research team investigators, institutional ethics committee, sponsors and any higher authority like drug controller General of India, to view your data if required.

The results of this research may be published in scientific journal or presented at scientific meetings without disclosing your identity.

Effect of your decision-Your decision not to participate in this research will not affect your medical care or you relationship with the investigator or the institute in future.

The participation in this study is purely voluntary and you have the right to withdraw from this study at any point of time with or without giving any reason through not mandatory it will be advisable to consult your investigator before you withdraw. Contact persons-For further information/questions you can contact any of the following Principal Investigator: Dr. Apurva Jagtap Dept. of Radiodiagnosis Name of Institution-Krishna Institute of medical sciences , Karad.

Phone: 9373331111

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Title of study:

‘ROLE OF CRANIAL ULTRASONOGRAPHY IN DETECTING NEUROLOGICAL ABNORMALITIES IN PRETERM NEONATES’

Name of Participant:

Name of Principal Investigator: Dr. Apurva Jagtap Name of Department: Radiodiagnosis I, have read the Information orthe Information has been read to me. The nature of study possible risk and benefits to me precautions to be taken by me my rights and responsibilities related to this study are explained to me by the investigator to my satisfaction. I have understood that the information/data obtained from this study may be used for scientific purpose (Publication/presentation) by the investigators, without revealing my identity. I have no objection or this.

I have understood that I can withdraw from this study at any point of time without giving any reason and this will not affect my future treatment in this hospital. I have understood whom to contact in case of any adverse effect/doubt.

I am also aware that the investigator can terminate my participation in this study at any time due to any reason, without taking my consent.

I hereby give my consent to participate in the study titled ‘ROLE OF CRANIAL ULTRASONOGRAPHY IN DETECTING NEUROLOGICAL ABNORMALITIES IN PRETERM NEONATES’

1. Signature/Ieft thumb impression of participant
2. Signature & Name of impartial witness (In case of participant/legal guardian is illiterate person)
3. Address & contact No
4. Name & signature of Investigator/Co-investigator

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Details

Title
The Role of Cranial Ultrasonography in Detecting Neurological Abnormalities in Preterm Neonates
Author
Year
2022
Pages
84
Catalog Number
V1162356
ISBN (Book)
9783346596789
Language
English
Tags
role, cranial, ultrasonography, detecting, neurological, abnormalities, preterm, neonates
Quote paper
Apurva Jagtap (Author), 2022, The Role of Cranial Ultrasonography in Detecting Neurological Abnormalities in Preterm Neonates, Munich, GRIN Verlag, https://www.grin.com/document/1162356

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