Pediatric Ultrasound Midterm 1

From birth to 18 and sometimes to 21

bones grow from the epiphyseal plates which tend to be radiolucent (on x-ray - can’t see it on image)

kidneys look very unique when dealing with a newborn or baby - up to age 10 you can see significant changes.

10-15%

Many microorganisms, patients weakenedimmune system, transmission train through thestaff, the equipment, therapeutic aids and foodservices can cause urinary tract infections, pneumonia, diarrhea, or a surgical wound infection.

Matching tissue for transplant is not asessen6al in young infants or neonates basedon immature immune systems- but supressedchildren are highly susceptible to pathogens(gown, mask, glove and clean machine)

Maternal antibodies can cross the placenta and therefore children tend to have more resistance to things that mom has been immunized for - protects the baby for a while

90 % Preterm infants weighing less than1500gms; 10% term infants

Exact cause unknown but risk factors:asphyxia, UA catheterization, patent ductusarteriosus, polycythemia, enteral feeding,indomethacin (NSAID), vitamin e andxanthines (mild s6mulant and bronchodilator)

Reduced perfusion of the intestinal wallleading to ischemia, hypoxia, necrosis andgangrene- mucosa or submucosa ->superficialinvolvement or through wall causingperforation can lead to peritonitis.

Ileum most affected, then ascending colon,cecum, transverse colon and recto sigmoid

Abdominal distention, gastric aspirates,bilious stools, lethargy, apnea and poorperfusion- infant appears septic

Pneumatosis intestinalis-intramural air, gasless abdomen can indicateperitonitis, free air with a perforation,potentially hyperechogenic pericholecystic area,air in liver

• Intussusception

• Appendicitis

• Inflamed bowel

• Bowel obstruction

• Ovarian/testicular torsion

• Septic hip

• Obstructive hydronephrosis

• Acute bleed

• thrombus

• Pyloric Stenosis

Special smaller transducers with high resolution, isolettes, cribs, strollers, or wheelchairs

Drop in hematocrit, WBC increase, bilirubin increase, creatinine increase, increased or low BUN.

The germinal matrix - involved in brain development (and gives rise to the choroid plexus) in the lateral ventricles - it is really vascular and extensive in early gestation (if any pressure in the area will cause a bleed)If this area bleeds the blood can be found in the ventricle or in the caudothalamic groove (area between caudate nucleus and thalamus)

The occipital and parietal bones

The anterior, middle, and posterior cranial fossa

Made up of 8 bones: 2 temporal, 2 parietal, one frontal, one occipital, one sphenoid and one ethmoid.

Petrous process is part of the temporal bone.

The left and right temporal bones are on the sides of the cranium. Each of them consists of several parts. The squamous portion of the bone extends upward to make up part of the cranial wall surrounding the brain. Projecting medially from the base of the temporal bone is the petrous portion. When writing out the name of the temporal bones, you should always include the side (right or left) as part of the name.

The anterior fontanelle (posterior is used when there is flare - bright white matter tracks)

Anterior fontanelle remains open through the first yr of life. RWC 4th ch 48 49. after the closure 3 windows can be used. Trans temporal, orbital, foramen magnum.

Anterior (12-14 mths good scanning window), posterior, posterolateral (mastoid), and anterolateral (sphenoid/temporal).

Metopic (frontal), lamboidal, coronal, sagittal, and squamosal.

Craniosynostosis

Dura mater (outer - tough mother), arachnoid, and pia mater.

A double layer: periosteal and meningeal, that encases the veins (venous sinuses), which creates the falx cerebri, cerebelli, and tentorium. This is the strongest layer, and located between its two layers are meningeal arteries and dural sinus-venous drainage of the brain. Folds of dura provide cushioning for the brain and separate structures (cerebri and tentorium).

This is spiderlike and creates the subarachnoid space, and contains the cisterns (CSF pools), and the arachnoid villi. This is a delicate, transparent membrane that is separated from the dura by a potential space (subdural space). The arachnoid follows the contour of the dura - vessels fill this space.

A highly vascular and delicate structure that touches the surfaces of the brain and adheres to its contour. The name means tender mother and it is separated from the arachnoid membrane by the subarachnoid space which is where the CSF circulates around the brain and the spinal cord - protection.

- Falx cerebri (separates cerebral hemispheres)

- Tentorium cerebelli

- Falx cerebelli

- Diaphragma sellae

Diaphragma sellae- lines sella turcica of the sphenoid bone. Dura attaches to the sella and ensheaths the pitutary gland.

A fold of dura mater which projects between the cerebral hemispheres in the longitudinal fissure. It attaches to the crista galli inferiorly and the internal occipital crest and tentorium cerebelli posteriorly. Both the inferior sagittal sinus and superior sagittal sinus travel in this dural fold - largest fissure in the brain.

Part of the ethmoid bone

The cribriform plate is received into the ethmoidal notch of the frontal bone and roofs in the nasal cavities. Projecting upward from the middle line of this plate is a thick, smooth, triangular process, the crista galli, so called from its resemblance to a cock’s comb

Separates and protects the cerebellar hemispheres from those of the cerebrum. It extends across the cranium at right angles to the falx cerebri, and the transverse sinus lies within the tentorium cerebelli.

The straight sinus (sinus rectus; tentorial sinus) is situated at the line of junction of the falx cerebri with the tentorium cerebelli. It is triangular in section, increases in size as it proceeds backward, and runs downward and backward from the end of the inferior sagittal sinus to the transverse sinus of the opposite side to that into which the superior sagittal sinus is prolonged. Its terminal part communicates by a cross branch with the confluence of the sinuses. Besides the inferior sagittal sinus, it receives the great cerebral vein (great vein of Galen) and the superior cerebellar veins. A few transverse bands cross its interior.

The longitudinal fissure (falx and SupSagSin), and the lateral (sylvian) fissure

A deep furrow that separates thetemporal and the parietal lobes ofthe cerebrum. MCA located herealong with many other vessels

Throw colour Doppler on- with a subarachnoid hemorrhage you willsee the small intricate vessels with, where a subdural hemorrhagewill compress the subarachnoid vessels

Folds on the brain. Gyri are the areas that project out and sulci are the grooves. These develop as a brain matures and as brain tissue becomes more expansive.

The cerebrum - original forebrain in development (right and left hemispheres)

5: frontal, parietal, temporal, occipital, insula.

the sylvian fissure

A straight line in the midline sagittal images seen at 20 weeks.

24/25 weeks

by 28 weeks seen over the corpus callosum

by 28 weeks over the corpus callosum superior and lateral

30 weeks, by 33-40 weeks we can see multiple bends and folds.

central, callosal, cingulate, calcarine, and parieto-occipital

The cingulum is a collection of white matter fibers projecting from the cingulate gyrus to the entorhinal cortex in the brain, allowing for communication between components of the limbic system.

• Cerebrum- forebrain

• Midbrain- mid brain

• Cerebellum, pons, and medulla - hindbrain

The thalamus, hypothalamus, and epithalamus

Part of the insula - The insular cortex is a complex structure which contains areas that subserve visceral sensory, motor, vestibular, and somatosensory functions. The role of the insular cortex in auditory processing was poorly understood until recently.

The second part of the insula - covers the insula

The frontal lobe

The parietal lobe (posterior to the central sulcus)

The temporal lobe

A hypoxic event causing edema (brain draws fluid in) - the bright then hypoechoic appearance is not normal.

White matter is brain tissue that glistens due to fat in the myelinated axons in a lipid and protein sheath.

neuron cell bodies and unmyelinated axons, neuroglia, etc.

Commisures: from side to side (corpus callosum, ant/post commisures)

Associations: longitudinal front to back (links cortical area within the hemispheres)

Projections: Up and down (corticospinal tract, spinothalamic tract, internal capsule, and corona radiata - centrum semiovale)

A c-shaped pathway for the limbic system and connects to the hippocampus. The fornix is white matter that lines the lateral walls of the CSP.

A great projection tract that pierces the basal nuclei to for the corpus striatum. They are white matter tracts that run between the nuclei of the basal ganglia.

The septum pellucidum and the fornix

It stops at the corpus callosum and this is important because it is the largest neural commisure.

Cavum is the space, the midline anechoic area which closes back to front, also includes the cavum vergae and the cavum veli interpositi.

Cavum Velum Interpositi: a small potential space that may be seen above the choroid plexus of the 3rd ventricle, below the columns of the fornices - it may look like an inverted helmet inferior to the splenium

The cortex, and the basal nuclei

Caudate, lentiform (putamen and globus pallidus), amygdala, and claustrum - they are relays.

The term for grey matter deep in the cerebrum, also called basal ganglia. These support our motor control

memory, emotional associations, fear, pleasure

The globus pallidus (medial) and putamen - lens shaped.

• Lateral to lentiform at insula

• Thin layer of gray substance that is just belowthe insula

• External capsule (white matter tracts) separates claustrum from the more medial lentiform

The connection between the thalami and goes through the third ventricle - when third ventricle has fluid in it then we can see this really well indicating that we are in the middle of the third ventricle

This is in-between brain buried grey matter

1. Thalamus(2 lobes, connected by massa intermedia)-relays sensory messages**

2. Hypothalamus- floor of the 3V, temp. Regulation **

3. Epithalamus - roof of 3V. Membranous portion hastela choroidea (fold of pia mater). Pineal gland (body cycles, circadian rhythms)

- Cerebral peduncles - "little feet" (paired white matter tracts, internal capsule above, pons below, the interpeduncular cistern lies btw toes)

- Quadrigeminal bodies (colliculi - superior and inferior - sensory nuclei)

- Cerebral aqueduct (3rd to 4th ventricle - narrowest part of the ventricular system - common for clot)

Circle of Willis and the interpeduncular cistern

The quadrigeminal cistern

(1)Pons (belly, pontine cistern anterior, 4th ventricle posterior)

(2)Medulla Oblongata (decussation of projection tracts - continuous with spinal cord below)

The little brain - white matter with grey cortex at the surface - two hemispheres divided by a falx cerebelli, covered by tentorium. Centrally there is an arbor vitae (tree of life), and a vermis. There are 2 tonsils (Chiari II malf), 3 pairs of cerebral peduncles, and the 4th ventricle within (*dandy walker malf) - foramen of lushka, and magendie to pontine cistern. Pons are for balance and coordinated movement.

3 pairs: superior (midbrain/thalamus), middle (pons, largest), and inferior (medulla oblongata). They function for posture and balance, plus skilled movements like scanning!

Midbrain, pons, and medulla oblongata.

Vessels that contain CSF

1. Lateral ventricles (2) – right/left – inter-ventricular foramen [of Monro] to

2. Third Ventricle – Aqueduct [of Sylvius] narrowest point (cerebral aqueduct)

3. 4th Ventricle – 3 Foramina [of LUSCHKA(2 lateral) &MAGENDIE(medial)] to cisterns & centralcanal of spinal cord – Foramina are Lateral and Median

anterior, temporal, and occipital horns. The trigone connects the 3 horns

Contains the glomus of the choroid plexus - the most CSF is produced here - widest point of the ventricular system.

Anteriorly at the caudothalamic grooves within the temporal horns.

In the occipital horn (if seen here then it is a bleed)

Medial: septum pellucidum

Lateral: head of caudate nucleus

Superior: corpus callosum

Frontal horn cysts, coarctation of the frontal horns, connatal cysts, or septations caused by the frontal horn folding in on itself

A continuous cystic midline structure in the fetal life, which closes from back to front (back portion is called the cavum septum vergae).

This is above the roof of the 3rd ventricle and below the fornix. It is anechoic and helmet like inferior and posterior to the splenium.

only 2mm - thin, but long and deep.

Only in ventriculomegaly (hydrocephaly or brain atrophy)

The cerebral aqueduct or aqueduct of sylvius

It is diamond-shaped and fits into the vermis of the cerebellum (echogenic choroids blend in and can't be seen). The 4th ventricle drains into the foramina of Luschka and Magendie, which allows CSF to flow into cisterns and sub-arachnoid spaces around the brain and cord. This is continuous with the spinal canal below.

you mastoids are located right behind your ears (lump) - acts as a window in youth to look at the 4th ventricle and cerebellum, but you can sweep up and look at the occipital horns

The lateral and third, but not the fourth since it blends in.

A single layer of ependymal cells

The blood brain barrier - membrane permiability, prevents bacteria from crossing into the brain.

A dual blood supply: anterior and posterior choroidal arteries

Vein of Galen, sinuses, and jugular vein

The foramen of Munroe

The "end" of the choroid, where choroid bends in - a thin delicate layer of pia mater on the roof of the third ventricle

Consists of loosely arranged proliferating cells that give rise to neurons and glia of the cerebral cortex and basal ganglia. It develops below the ependymal lining of the ventricles. This is found near the foramen of Munroe and caudate nucleus (CT groove)

At 24-30 weeks, and the GM gradually recedes and there is lower risk >32 weeks.

They form echogenic landmarks, except the cisterna magna, which appears anechoic.

Quadrigeminal cistern (superior) - vein of galen, Ambient and interpeduncular cistern, supracellar cistern (at sela turcica - COW), pontine cistern (ant to pons), lateral cisterns in sylvian fissure, and the lumbar cistern.

Extra-cellular fluid but with higher Na, lower glucose, and K

500-600 ml in adults, and there may be only 100 ml in an infant at any given time.

130mm water/ 10mm Hg

Through arachnoid granulations to return to venous flow in superior sagittal sinus.

Cushions and protects cortical surface, maintains stable ionic concentrations (synapses), and moves waste into the venous system.

(1) Hydrocephaly - under pressure from CSF from blocked aqueduct or arachnoid granulation

(2) Colpocephaly - malformations cause enlarged lateral ventricles (occipital) - Chiari II, ACC, DW

(3) Atrophy of the brain - passive expansion of the ventricles as the brain shrinks

The absence of the 4th ventricle while the 3rd ventricle is well seen.

Vertebral arteries (post supply), basilar arteries, and internal carotids (ant supply).

The vert arteries come from the subclavian arteries through the transverse processes of the vertebral bodies and enters the cranium through the foramen magnum. Notable branches include the spinal arteries and the cerebellar artery.

Created by the right and left vertebral arteries. Notable branches include 2 more cerebellar arteries and the posterior cerebral arteries.

The ICA is a branch off the CCA, and enters the cranium through the carotid foramen in the temporal bone. Notable branches include: ant cerebral arteries (lt and rt), and the MCA (largest branch that feeds the lateral lenticulostriate branches)

Pericallosal, callosomarginal, and medial lenIculostriate arteries.

Frontal lobes, and medial surfaces

The basal nuclei, lateral surface ofcerebrum, insula white matter tracts, cortex oftemporal & parietal lobes+ anterior choroidal artery

The occipital lobe, visual areacerebral peduncles and+ posterior choroidal artery

This is an incredibly important anastomosis that ensures that the brain is always receiving blood and allows collateral circulation between the hemispheres.

Mainly in the suprasellar cistern

(1) Cortex to the venous sinuses (superior or inferior sagittal sinus)

(2) Deep - MCA territory to straight sinus via:

- thalamostriate v. and choroid v.

- Internal cerebral veins

- Great cerebral vein (of Galen)

- straight > transverse > sigmoid > internal jugular vein through the jugular foramen.

– basilar art – internal caroId ICA– anterior cerebral – internal cerebral v’s– Vein of Galen– superior sag sinus– straight sinus

• ICA & branches• MCA• Lenticulostriate art’s• ACA branch intopericallosal art’s• Supra-sellar cistern

Sphenoid (ant-lat) fontanelle (MCA and COW), and the mastoid fontanelle (transverse sinus)

Increased PI due to decreased perfusion

It is hard to get true arterial waveforms based on the fact that the pressure changes are being caused my mechanical ventilation , and not from its own body. Impeded venous return causes flow reversal.

This occurs in term infants with acute respiratory failure - cannulation and ligation of the CCA and jugular vein = non-pulsatile partial cardio-pulmonary bypass

Hemorrhagic Infarction - unsuitable for premature infants - heparin + germinal matrix = high risk.

The neural plate - derivative of the ectoderm

early in the 4th week (~22-23 days)

Neurulation-formation of neural plate and neural tube.

In cranial and caudal directions until only small openings remain at both ends (cranial opening = rostral, caudal = caudal).

The establishment of a blood circulation for the neural tube (cranial neuropore closes at the 25th day, and caudal closes at the 27th day).

(1) Establish gestational age

(2) Go over diagnostic checklist: ventricles, parenchyma, pulsation, and extra-axial spaces.

The brain cortex is very echogenic

Yes, they develop more as the child ages.

The sela tursica (the cow surrounds it)

A- 25 wks gestation. No sulci. CC lies above completely cystic csp and cavum vergae. Arrow pointing to occipito-parietalfissure.

B- 27 wks. Cingulate just developed

C- 30 wks cingulate sulcus has few branches. Cavum velum interpositum long arrow. Cavum velum int=potential space above the roof of 3V and below the columns of fornices -anechoic space inferior and post to splenium in the pineal region

D- 40 wks cingulate sulcus has many branches CSP no longer cystic

Because of anisotropy. Peritrigonal blush- echogenic whiter matter tracts coursing from the deep white matter towards the cortex and also could be due to the blood vessels.

Bulky Choroids

a projection on the medial wall of the posterior horn of the lateral ventricle of the brain. It is associated with the lateral extension of the calcarine fissure.

It hides the insula - Opercula means= a lid formed by growth and elongation of the cerebral lobes forming a lid or flap which covers the insula. Lack of opercularization associated with lissencepahly.

In premature infants, before the growth and proliferation of sulci and gyri, insula may be viualized. However, it term infants-it is not visualized.

Minimum 6-8 using the anterior fontanelle window - for symmetry

A portion of the white matter tracts deep to the grey matter.

Bulky choroids, lobulated choroids, or a clot indicating intraventricular hemorrhage.

21% - uncommon by 2 years

The calcar avis

In 1890 Chiari identified malformations I - IV

Abnormal neural tube closure may result in a spinal defect such as a myelomeningocele* - decompresses ventricles and a small posterior fossa developes.

II

Chiar-1-downward displacement of tonsil without the displacement of 4 V or medulla.

Chiari 3- associated with a high cervical encephalocele in which medulla, 4th ventricle and entire cerebellum reside.

- 4th ventricle is not visible: compressed

- 3rd ventricle is very visible but the massa intermedia is enlarged

- lateral ventricles have a classic shape: colpocephaly-occipital horns, batwings-frontal horns

- Hydrocephaly especially after meningomyelocele repair (98% have progressive communicating hydro that gets worse after closure of the spinal defect - may be fenestrated)

- Parenchyma: herniated cerebellar tonsils, meningomyelocele

- Inferior displacement of brainstem & vermis ofcerebellum (dysplastic/displaced cerebellum - banana sign, and tentorium)

- Hypoplastic corpus callosum (wide longitudinal fissure, esp after shunting)

8-18 (20) weeks

It can be either

Because 80% of patients will have other anomalies such as Chiari II, DW, lipoma, holopros, hydro, arachnoid cysts, etc.

8, 13, and 18 (also teratogens are associated)

The genu and anterior body, the rostrum and the splenium develop late - so if ACC is partial these two will be missing

The Ventricles - widely spaced (parallel choroids),narrow anterior horns, abs septi pellucidi – colpocephaly - large occipital horns (teardrops)– dilated 3rd ventricle may rise between lat vent’s

The Parenchyma - “sunburst” radial sulci– absent cingulate gyrus– CFD may help Diagnosis - Ant Cerebral Art is missing!

• Probst bundles - callosal fibres remain inlongitudinal “bundles”, no migration across midline

• Lipoma - echogenic mass replaces CC

30-50% - may have associated calcification

The interhemispheric fissure

Abnormal neural tube closures, with 4th ventricle malformation

70%

20-50% are also trisomy 13, 18, 21

- Dilated 4th ventricle that communicates with the cisterna magna (cystic post. fossa) [cause: atresia of the foramina of M & L]

- Cyst compresses aqueduct, causing hydro: above and below 4th ventricle (or may develop later in 80% of cases)

Shunts may need to be placed separately (in lateral ventriclesand cyst) to ensure effective drainage

• hypoplastic cerebellar hemispheres, displaced laterally

• absent vermis (normal vermis seen @ 17-18 wks)

• elevated tentorium (straight and trans sinuses elevated)

- Large (mega) cisterna magna

- Arachnoid cyst (but cysts are usually symmetrical)

(1) Enlarged 4th ventricle connecting to the cisterna magna

(2) Large Posterior Fossa

(3) Hypoplastic Vermis

(4) Hypoplastic cerebellar lobes displaced laterally

(5) Hydro (80%) above and below the 4th ventricle

(6) Absent Corpus Callosum (70%)

(1) Joubert's Syndrome: absent vermis, like ACC of the cerebellum, white matter is unable to migrate rt to lt.

(2) Meckel-like syndrome: DW, polycystic kidneys, hepatic fibrosis, hand, and genital anomalies.

Alobar

MRI

• Alobar - single ventricle

• Semi-lobar - single ventricle, but occipital horns

• Lobar-near normal occ & temp horns, 3rd Ventricle, fused anterior horns with no septi pellucidi

• Alobar - minimal brain tissue

• Semi-lobar-more occipital tissue w/falx & longitudinal fissure, single thalamus, part ACC

• Lobar-quite normal!! Shallow anterior falx/fissure, abssepti pellucidi, fused frontal lobes (and horns), partialACC (genu and rostrum only)

Looks like lobar

Septo-optic dysplasia - absent CSP, optic tract hypoplasia (MRI to confirm since not seen on US).

Semi-lobar specimen with occipital lobes, fused thalamus and choroids (U-shaped). There is a partial corpus callosum, a partially separated thalamus with mid-facial anomalies such as hypotelorism or cleft lip.

Single midline crescent shaped ventricle with a thin layer of cerebral cortex. No interhemispheric fissure, no falx, no corpus callosum. Fused thalami, choroid plexus, and basal ganglia. No 3rd ventricle and a large dorsal cyst.

A destructive process, in utero, clefts, ventricle to lateral fissure, lined with dysplastic grey matter, unlike porencephaly. Can be uni or bi lateral and is associated with an absent CSP and/or optic-nerve hypoplasia.

pre-migration - in the second trimester

Smooth brain, without sulci (may be caused by infection in utero - 3-4 months along). There is also absent opercularization in the lateral fissures.

Complete destruction of normal brain tissue.

Occlusion of the ICA after 14 weeks gestation

The posterior cerebral artery suppliesthalamus, choroids, brain stem &cerebellum – these structures are OK!

Hydranencephaly, it is not holoprosencephaly because the falx and the thalamus are present

Destruction of normal brain parenchyma - the cysts always connects with the ventricles but not to cortex.

hemorrhage, infection (TORCH), or trauma

Gliotic White Matter

Focal brain damage (softening) - glial tissue may form septa, and neurons are destroyed.

with cystic encephalomalacia the cysts are not connected to the ventricles

• LARGE cysts - from diffuse causes - infection, birth asphyxia

• focal cystic areas - secondary to thrombus

It can obstruct blood flow, destroy brain cells, and cause herniation.

hemorrhage, infection, etc.

5-25% per 10,000 births

Blood (10%), Tissue (80%), and CSF (10%)

Venous Circulation

To the lumbar cistern

(1) Obstruction

(2) Decreased absorption

(3) Over production

A shunt can decrease the risk of infection and hemorrhage and also decrease the need for endoscopic surgery.

Increased head circumference and bulging fontanelles.

A lumbar puncture (manometer) - can also drain CSF

• Developmental delay – Edema may cause delayed myelination – Ischemia: compression of vessels

• Rapid Increases in ICP can compress brain stem, vital functions– may cause herniation of brain (through the foramen of munroe) ... death

Infection, hemorrhage, or rapid decompression (leads to slit like ventricles)

ETV - hole put into the third ventricle to drain into the subarachnoid space (when cerebral aqueduct is obstructed)

CPC = done when the choroid is overproducing CSF

- Dilated 3rd ventricle or open wide 4th ventricle

- Rounded frontal horns

- lateral ventricles that rise above the corpus callosum

- dilated temporal horns and 4th ventricle

- Intraventricular Obstruction (non-communicating)

- Extraventricular Obstruction (communicating) - subarachnoid space or cisterns

- Choroid plexus Papiloma

- Venous obstruction

- Vascular malformation (AVM)

- Non-obstructive, as a result of brain atrophy

Brain atrophy

Infection, hemorrhage, or congenital abnormalities such as aqueductal stenosis, DW, fibrosis of the foramen of monro, tumour, cyst, AVM, or Chiari II.

Hemorrhage, infection, fibrosis of cisterns/arachnoid villi.

Look at what parts of the system are dilated

A term used to describedispropor=onate prominenceof the occipital horns of thelateral ventricles (eg. ACC)

• Hypoxic-ischemic injuries

– Severe cases result in brain atrophy

– 2-4 weeks arer global ischemia

– Passive expansion, not due to pressure

• “Glutaric aciduria type 1”- unusual cause

– Macrocephaly at birth – atrophy later

- Bilateral widening of the Sylvian fissures

Infants of moms with:

- Chronic cardiac or lung diseases

- Cardio-respiratory arrest during delivery

- Placental insufficiency

- Shock

- Placental Abruption (assoc. with cocaine and alcohol abuse)

Also, infants who are on mechanical ventilation or suction (causing venous obstruction), tension pneunothorax, exchange transfusions, immature hypothalamus that distorts BP.

(1) Hypothalamus: will not function until term

(2) Germinal Matrix: risk of hemorrhage

(3) Arterial Watersheds: deep white matter (lacks proper perfusion)

The dense layer below the ependyma of the lateral ventricle, whose job it is to create brain tissue.

There is no autoregulation and it is very fragile.

Focal hemorrhage in the germinal matrix

Focal or diffuse infarct to the watershed areas.

A portion of the ventricular system that is filled with clot

The age of the patient determines where the watershed area is:

Premature Infants > Periventricular/subcortical regions (white matter)

Term Infants > Para sagittal cortical/subcortical regions (grey/white border)

- Metabolically Active areas are more susceptible to HIEs like white matter tracks, oligodendrocytes, or babies in the 2nd trimester

- Length of time: focal infarct=partial obstruction with short time, and global/profound infarct (lengthly hypoxic event)

Edema of the cerebrum and development of cystic structures.

In premature infants – born at 24 to 30 weeks:

• GMH - germinal matrix hemorrhage, also called subependymal hemorrhage – SEH

• PVL - periventricular leukomalacia (infarc&on and necrosis of the periventricular white matter)

In term infants:

• Parasagittal infarction, edema

• Thalamus, basal ganglia (rare)

At 3 months:

• Thalamus, basal ganglia, & cortex

At 1 yr:

• just like adults - cortex

Most will with no complications, but the most common complication will be subependymal cysts

About 7 days

Only 1/3 of GMHs occur in the first 24 hours and 90% occur by day 7

Between day 10-14 with follow-up at 1 month for all babies less than 32 weeks, and 1500 grams.

They were once as common as 55%, but this has decreased because of prenatal steroids and respiratory therapies like surfactant being used.

10-14 day: GMH or Post-hemorrhagic hydro

1 month: PVL or ventricular enlargement

I - GMH, small hemorrhage at caudate area

II - Intraventricular, hemorrhage spills into ventricles, but they are not dilated

III - Larger hemorrhage with dilated ventricles (hydro)

IV - Intraparenchymal hemorrhage due to hemorrhage or infarct

Where is it? subependymal, intraventricular, intraparenchymal, sub-arachnoid, intracisternal, etc.

Homogenous, echogenic, seen at caudothalamic groove under the ependyma, swelling at the head of the caudate, and possible involvement of the ventricles - grade II (inflammed ventricle walls).

Echogenic, especially in the dependent lateral horns, possibly a ventricular cast or bulky choroids, or CSF with echoes, or a change in the CSF-blood fluid levels.

Blood is an irritant and can cause chemical ventriculitis - thick, echogenic ventricular walls.

Hemorrhagic venous infarction - when there is a germinal matrix bleed there can be obstruction of the terminal veins causing congestion in the tissue and this leads to infarction.

Usually unilateral and echogenic in the frontal, parietal, and/or occipital lobes. Causes a mass effect.

1-7 days: echogenic

2-5 weeks: echogenic rind, liquefy, retraction (porencephalic cysts created)

>4 weeks: porencephaly with ventriculomegally and atrophy with widened sulci.

It will leave porencephaly

80-100% of children will have motor defects - permanent spastic hemiparesis on the contralateral side.

From echogenic, to centrally echolucent, to shrinking and dissolving over several weeks.

The posterior fossa and the subarachnoid/dural space.

- Diffuse Cerebral edema (profound infarct)

- Focal infarction (watershed regions - partial infarct)

- Cerebellar infarction

- Basal ganglia vasculopathy

No, it is rare except for PVL

Infants of the MOMS with:

– chronic cardiac or lung diseases

– cardio-respiratory arrest

– placental insufficiency

– shock

– abruption – rare assoc w. cocaine, alcohol abuse

• Babies with meconium aspiration, birth asphyxia– Affects their ability to auto-regulate blood pressure

The integrity of the blood brain barrier is disrupted allowing fluid to escape into the extra-cellular fluid surrounding the brain cells. This is due to prolonged ischemia, hemorrhage and infection. AFFECTS THE WHITE MATTER

Swelling of the cells due to hypernatremia caused by severe ischemia. If severe this can lead to infarction and necrosis. GREY MATTER AFFECTED.

Both Vasogenic and cytotoxic (grey and white matter affected)

Slit-like ventricles from compression of edema, echogenic parenchyma abscures landmarks such as the sulci (silhouetting).

Atrophy of the brain tissue and ventriculomegaly. The head circumference will be normal and progressively get smaller.

The MCA circulation (often a single area impacted) so structures supplied by the MCA are affected.

Echogenic parenchyma with sharp borders

Focal cystic encephalomalacia (softened brain tissue) and later atrophy and ventriculomegaly.

– severe birth asphyxia

– prematurity

– congenital heart (irregular beats cause clots)

– meningitis

– emboli

– polycythemia

– trauma

Asymmptomatic, seizures, lethargy, or coma

An increase in the number of vessels and the size of existing vessels in response to a focal infarct often occurring hours after the insult.

This is a very uncommon pathology, and also the vermis is very echogenic so it is hard to pick up a small infarct or hemorrhage here.

A basal ganglia vasculopathy characterized by echogenic linear echoes around the vessels of the thalamus and basal ganglia - can sometimes be demonstrated under colour Doppler

Viral infections, trisomy 13/21, and twin-twin transfusions

A stoke caused by the vessels being walled of in some way. 90% of children become handicapped from this.

Those with sickle cell anemia.

- Traumatic Birth

- ECMO

- Coagulopathy

- Germinal matrix within the 4th ventricle (premies)

Echogenic when it is acute, and as it becomes chronic, cysts will form.

subarachnoid hemorrhage

Birth asphyxia, trauma, DIC, or premies with intraventricular hemorrhage.

Enlarged sylvian and IH fissure with thickened and echogenic sulci. You can see the cisterns in the posterior fossa view.

Vessels will be seen crossing into the subarachnoid space.

Term infants with birth trauma like SBS (massive in children with bleeding disorders)

We will see the vessels compressed into the brain surface

increased head circumference after 2 weeks of age (since it is so superficial)

Meningitis (check S&S) or non-accidental trauma (SBS - if subdural fluid is seen after neonatal period)

The infarction and necrosis of the perventricular white matter (including the corpus callosum)

Hx of cardio-respiratory compromise>hypotension>ischemia

GM hemorrhage and 80% are associated with IVH. Chorioamnionitis is also associated.

Antenatal steroids

Often bilateral, supero-lateral to the trigones, edema and hemorrhage causes increased echogenicity of the white matter tracts that appears patchy and brighter than the choroid. Infarct leads to coagulation necrosis (cysts).

Deep white matter is a watershed zone

(1) hypothalamus-will not function till term

(2) Immature vasculature (watershed)

(3) Immature oligodendroglial cells (vulnerable to hypoxic episodes)

Normal periventricular blush so it is important to screen for PVL (cystic stage is obvious after 2-3 weeks)

Subtle atrophy and ventriculomegaly - gliosis eventually fills the cysts and sonographically appears normal

Day 1-3: patchy echogenicity

Week 1-2: Decreasing echoes

Week 2-3: Cystic (bilateral and symmetric)

Month 1-3: Return to "normal" but with atrophy and ventriculomegaly

No - unlike porencephalic cysts caused by IPH

84% which caused absent and delayed myelination.

MRI is better than CT to diagnose glial scarring.

Decreased myelination causing spastic diplegia of the legs or quadriplegia if severe. This is a feature of cerebral palsy

Large ventricles with echogenic debris, developed in patients with meningitis (60-95%) - shaggy bright ependyma with fibrous septations. Abscess is rarely seen, but if it is present it will have a mass effect, echogenic walls, with an anechoic cavity.