Pedia 👶 Flashcards by mkb drs

Gyral pattern is established at what week?

38 weeks

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Pattern of Myelination: True or False
Back to Front
Caudad to Cephalad
Central to Peripheral

True

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Sequence of DEVELOPMENT of the corpus callosum:
Genu>body>isthmus>Splenium

True

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Sequence if MYELINATION of the Corpus Callosum:
Genu> body> isthmus

FALSE

Splenium> genu
(Posterior to Anterior)

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Pattern of vascularity in Preterm neonatal brain wherein the penetrating arteries supply the periventricular regions by extending INWARD from the surface of the brain

VentriculoPETAL

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Pattern of vascularity where in the blood flow goes AWAY from the ventricles extending into the brain from the lateral ventricles; the intervascular border is moved peripherally to parasagittal region, hence affecting the subcortical white matter and parasagittal region in hypoxic injury

VentriFUGAL

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Type of asphyxia with INTACT autoregulation, hence, there is redistribution of blodd flow to the hypermetabolically deep gray matter structures resulting to INJURY predominantly in the WATERSHED zones of the cerebrum

Mild to Moderate asphyxia

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Type of asphyxia characterized by loss of autoregulation resulting to injury of the vulnerable regions such as the deep gray matter and early or active myelinating fibers.

Profound Asphyxia

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Effects of hypoxic ischemic injury in premature infants (< 36 weeks)

Geminal matrix hemorrhage
Intraventricular hge
Periventricular White Matter Injury

Cranial US - preferred modality for evaluation

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Germinal matrix hemorrhage extending into and distending the ventricles.

Grade III

Grade I - Mild; confined to the GM notch

Grade II - Intraventricular extension with no associated distention of the ventricle.

Grade IV- Hemorrhagic venous infarct in the periventricular white matter.

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This hypoxic brain injury is due to the selective vulnerability of the periventricular white matter secondary to the ventriculoPETAL pattern of vascularity in the pretem infant.

Periventricular Leukomalacia

US: Echogenic lesion in the white matter adjacent to the atria of the lateral ventricles.

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Destructive lesions PRIOR to 28-30 weeks results in cavitation (PORENCEPHALY) True or False?

True

*capacity to develop gliosis does not occur until 28-30 weeks.

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PVL Grading characterized by INCREASE periventricular echogenicityin deep WM into SUBCORTICAL cysts.

Grade IV

Grade I : Increase periventricular echogenicity WITHOUT cystic formation persistent for > 7 days.

Grade II: SMALL periventricular cyst.

Grade III: EXTENSIVE periventricular cyst in occipital and frontoparietal regions.

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Perinatal Arterial Ischemic Stroke occurs between 20 wks AOG to 28 postnatal days, commonly affecting the MCA and is usually seen in TERM neonates. True or False?

True

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Most common cause of small amounts of Subarachnoid, subdural and intraventricular hemorrhages in the TERM New Born

Normal Delivery

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MC congenital heart disease?

Bicuspid aortic valve

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Edema which may be accompanied by hemorrhage within the SUBCUTANEOUS tissues typically seen after vaginal delivery. It is NOT LIMITED by sutures and resolves within a few days without complication.

Caput Succedaneum

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SUBPERIOSTEAL HEMORRHAGE CONFINED BY SUTURES which may ba ssociated with skull fractures and epidural hematomas. Increases in size after birth and may calcify.

Cephalhematoma

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Most common cause of neonatal brain abscess

Citrobacter
Serratia
Proteus

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Most common form of pediatric CNS infection

Bacterial Meningitis

Neonate: GBS, E. coli
>1 yo: HiB, S. pneumonia, E. coli and N. meningitides

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Typical imaging findings of CNS VIRAL INFECTION

US: Echogenic
CT: HYPOdense
MR: T2/FLAIR HYPERintense

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Earliest sign og VIRAL encephalitis on MRI

Restricted diffusion in DWI

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Often caused by REACTIVATION of previous OROFACIAL INFECTION with the following imaging findings:

MR: unilateral/bilateral T2/FLAIR HYPERintense signals in the MIDDLE TEMPORAL lobe

CT: HYPOdensities in the TEMPORAL lobe and INSULAR CORTEX

Herpes Simplex Virus 1 encephalitis

-leptomeningeal and cortical enhancement and focal calcification and hemorrhage may also be present

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ATROPHY and resultant ventricular and SAS prominence associated with SUBCORTICAL and BASAL GANGLIA CALCIFICATIONS

HIV encephalitis

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Focal or multifocal PERIVASCULAR INFLAMMATORY and DEMYELINATING disorder presenting as T2 HYPERintense signals with corresponding T1 HYPO- to ISOintense signal abnormalities with variable pattern of enhancement (solid, ring-like, or none), affecting both gray and white matter. History of RECENT VIRAL illness or VACCINATION is key in diagnosis

Acute Demyelinating EncephaloMyelitis (ADEM)

Caused by REACTIVATION of MEASLES virus years after infection presenting as T2/FLAIR HYPERintense signals in the cortex and basal ganglia

Subacute Sclerosing Panencephalitis

Cause of intractable epilepsy in children, presenting @ 1-15 yo. Imaging shows 1. HEMISPHERIC atrophy 2. T2/FLAIR hyperintense signals in the FRONTAL and TEMPORAL lobes (predominantly WM regions) and in the BASAL GANGLIA

RASMUSSEN'S encephalitis

Bacterial and Viral infections are most commonly transmitted intrapartum and post-natally. True or False

False. Bacterial and FUNGAL

Infections most commonly transmitted in utero

1. Syphilis 2. Rubella 3. CMV 4. Toxoplasma

Infections acquired during the 1st trimester cause severe congenital malformations, while that acquired during the 3rd trimester cause destructive lesions. Tue or False

True

Most common serious viral infection in the New Born associated with polyMICROGYRA, especially in the Sylvian Fissure

Cytomegalovirus (CMV)

Congenital viral infection characterized by the following imaging findings: 1. Periventricular/subependymal calci or hge. 2. Ventricular or Sulcal prominence 3. Periventricular and subcortical white matter changes

Cytomegalovirus (CMV)

Splenium should be as thick as the genu at what age?

1 yo

The lateral ventricles have parallel orientation, with posterior dilation (Colpocephaly), upturned anterior horns, and interhemispheric sulci extending up to the 3rd ventriclular margin with associated underrotation of the hippocampi

Complete Agenesis of Corpus Callosum

Seen as truncation of the anterior-posterior dimension of the corpus callosum

Partial Agenesis/ hypogenesis of the Corpus Callosum

*Texas Longhorn* appearance of the lateral ventricle is seen in this condition

Complete Agenesis of the Corpus Callosum

Partial agenesis of the Corpus Callosum is frequently associated with these interhemispheric lesions

Interhemispheric Cyst or Lipoma

Optic Nerve dysplasia is most reliably diagnosed on

Ophthalmologic Examination

Malformation caused by abnormalities in differentiation and midline cleavage of the prosencephalon on 5th week AOG. Hallmark: abnormal communication of the gray and/or white matter across the midline. There is facial dysmorphism (80%) (hypotelorism, cyclopia, cleft lip/palate)

HOLOPROSENCEPHALY

Gene mutation involving ciliary proteins characterized by vermian hypoplasia, thickening and elongation of the superior cerebellar peduncle (MOLAR sign) clinically manifesting as "panting" or "laughing" respiration with occulomotor apraxia in infancy

Joubert Syndrome

Characteristic enlargement of the ventricular atria

Colpocephaly

Complete absence of cleavage with anterior displacement of the cerebral tissue into "PANCAKE" configuration, large MONOVENTRICLE expanding posteriorly into a dorsal cyst.

Alobar Holoprosencephaly

Lack of separation of the posterior frontal and parietal regions with separation of the anterior frontal and the occipital lobes

SYNtelencephaly

Triad of enlarged posterior fossa, cystic dilation of 4th ventricle and vermian hypoplasia/agenesis.

Dandy-Walker Malformation

Majority of the Neuronal MIGRATION MALFORMATION occurs at what gestational week?

Between 12-24 weeks

A severe in utero brain injury which is attributed to bilateral internal carotid artery occlusion that often result to fetal demise?

Hydranencephaly

Absence of all brain parenchyma supplied by carotid arteries, with preservation of the posterior fossa structures and medial temporal lobes. Treatment: CSF DIVERSION WITH VENTRICULAR SHUNT

Hydranencephaly

Distinct pattern of WHITE MATTER INJURY in utero (bet 24-34 weeks GA) caused by damage of OLIGODENDROCYTE PRECURSOR CELLS due to HYPOXIA

Periventricular Leukomalacia

This PATTERN WHITE MATTER INJURY shows a symmetric loss of periventricular white matter surrounding the TRIGONES of the lateral ventricles and shows a characteristic ANGULAR morphology of adjacent lateral VENTRICLES

Periventricular Leukomalacia

Also known as WHITE MATTER INJURY OF PREMATURITY US: hyperechoic in the WM bordering the bodies of the lateral ventricles MR: Punctate foci of abnormal hyperintensity on T1WI

Periventricular Leukomalacia

Characterized by Hemicerebral ATROPHY, IPSILATERAL compensatory osseous HYPERtrophy, and Enlargement of the FRONTAL SINUS

Dyke-Davidoff-Masson Syndrome

Characterized by Hemicerebral ENLARGEMENT, Ipsilateral osseous hypertrophy and paradoxical ENLARGEMENT of the LATERAL VENTRICLE, and thickened and ill-defined cortical ribbon? A. Rassmussen Encephalitis B. Dyke-Davidoff-Masson Sundrome C. Hemimegalencephaly D. HIV encephalitis

HEMIMEGALENCEHALY

Characterized by HEMICEREBRAL ATROPHY, T2/FLAIR HYPERintense signals in he FRONTAL and TEMPORAL lobes, as well as in the BASAL GANGLIA? A. Rassmussen Encephalitis B. Dyke-Davidoff-Masson Sundrome C. Hemimegalencephaly D. HIV encephalitis

RASMUSSEN Encephalitis

complete failure of division of the promesencephalic vesicle. A monoventricle is identified with “kissing choroid” by ultrasound. The thalami and basal ganglia are fused. The falx, corpus callosum, and interhemispheric fissure are absent

Alobar Holoprosencephaly

Fetal vermis is not completely developed until how many weeks gestation?

18 weeks AOG

It is characterized by fluid collection posterior inferior to the vermis and COMMUNICATES with the 4th ventricle. The vermis is typically intact. The tentorium is ELEVATED. No connection with the subarachnoid space is noted. a. Dandy-walker b. mega cisterna magna c. Chiari Malformation d. Arachnoid Cyst

Blake's Pouch Cyst

Retrocerebellar cyst that COMMUNICATES with the 4th ventricle. The POSTERIOR FOSSA is ENLARGED, with an elevated tentorium. The *vermis* is INCOMPLETE, elevated, and rotated (>180 deg): a. Dandy-walker b. mega cisterna magna c. Chiari Malformation d. Arachnoid Cyst

Dandy-Walker Malformation

Cystic lesion taht amy develop in the posterior fossa, causing mass effect in the otherwise NORMAL VERMIS. It does NOT COMMUNICATE with the 4th ventricle and the tentorium MAY BE elevated. a. Dandy-walker b. mega cisterna magna c. Chiari Malformation d. Arachnoid Cyst

Arachnoid Cyst *MC locaion: MIDDLE cranial fossa (50-60%) other common location: Retrocerebellar

Galassi classification of middle cranial fossa arachnoid cysts characterized by small, spindle-shaped, limited to the anterior portion of the middle cranial fossa, below the sphenoid ridge, and FREELY COMMUNICATING with the subarachnoid space. This type of represents the most common type of arachnoid cyst. A. Type I B. Type II C. Type III D. Type IV

Type I Type II: extends to the Sylvian Cistern, displaces the temporal lobe with slow communication to subarachnoid space Type III: LARGE, fills the whole middle cranial fossa, w/ midline shift, little communication with subarachnoid space

Results from arrest of migration of neuroblasts with abnormal cortical lamination and failure of sulcation

Agyra/ Pachygyra

This results from excessive folding of the cerebral cortical cells layers w/ fusiosn of the gyral surface. It is common after CMV infection in the 2nd trimester. It appears as mulitple SMALL, IRREGLAR SULCI.

Polymicrogyra

This is the leading infectious cause of sensorineural hearing loss. It is cahracterized by periventricular and subependymal calcifications. Ct may demonstrate Mondini malformation.

CMV infection *Mondini Malformation - absent interscalar septum - large vestibule - enlarged vestibular aqueduct

Maternal infection with toxoplasmosis after 20 weeks AOG has LESSER rate of transmission to fetus with less severe sequela such as blindness, epilepsy, and mental retardation.

FALSE; much HIGHER rate of transmission

The following are imaging findings of congenital TOXOLASMOSIS except: a. Non-shadowing cerebral and hepatic calcifications b. intracranial calcifications mau be periventricular or random distribution. c. Subependymal cysts d. "Candle stick" sign e. None of the above.

None of the Above

Findings of pituitary hypoplasia, absent septum pellucidum, and optic dysplasia: A. Syntelencephaly B. Septo-optic Dysplasia C. Semilobar Holoprosencephaly D. Lobar Holoprosencephaly

Septo-Optic Dysplasia P-A-O P ituitary hypoplasia A bsent septum pellucidum O ptic dysplasia

Refers to the dilation of the ventricular trigone and occipital lobes due to agenesis of the corpus callosum

Colpocephaly

Texas longhorn, Viking Helmet, Race Car appearance

Corpus Callosal Agenesis

Most severe form of malformation due to generalized ABNORMAL transmantle MIGRATION. The brain is smooth with *hour glass* shape due to mild infolding of the Sylvian fissure

Lissencephaly

It results from the DISRUPTION of the normal TERMINAL neuronal MIGRATION resulting in an increased in small gyri; associated thickened dysplatic overlaying of leptomeninges

Polymicrogyra (PMG) * often BILATERAL

Most common location of Polymicrogyra

PeriSylvian Cortex

Abnormal Gray matter-lined cleft extending from the ventricular ependymal surface to the pial cortical surface. The cleft is lined by polymicrogyra, extending full length of the cleft.

SCHIZENCEPHALY Open Lip - communicates w/ ventricle Close Lip - cleft walls closely appose

Unilateral schizencephaly is often associated with contralateral periSylvian polymicrogyra (PMG). True or False

TRUE *Porencephaly vs Schizencephaly Porencephaly = lined by white matter Schizencephaly = lined by PMG

Trapped nest of gray matter within the brain, which appear as variable sized nodules that are isointense to gray matter in all sequences.

Heterotopias Does NOT enhance or CALCIFY

Results from early ARREST of MIGRATION. *Double Cortex* syndrome. Symmetric band of gray matter is separated from the overlying cortex by a thin band of white matter producing a *three-layer cake* appearance.

Band Heterotopia *Lissen = smooth agyric, thick cortex *Band heterotopia= thin cortex, multiple gyri, shallow sulci

Results from abnormal PROLIFERATION and DIFFERENTIATION of neurological precursors: a. Band heterotopia b. Focal cortical dysplasia c. Schizencephaly d. Lissencephaly/Pachygyra

Focal Cortical Dysplasia (FCD) *Histo Hallmark: Lack of normal cortical lamination * Subcortical HYPERINTENSE T2 w/ adjacent subtly thickened cortex

FCD types Type I = Alteration in cortical layering Type II = Cortical dyslamination/ Dysmorphic neurons Type III = Encephaloclastic lesion

True *FCD present as intractable epilepsy

Radial extension of the balloon cells and ectopic neurons into the deep white matter seen in type I FCD

Transmantle Sign

Differential diagnosis for posterior fossa cyst

D andy walker Complex A arachnoid cyst M ega Cisterna Magna B lake's pouch cyst

Angle formed by 2 lines along the anterior surface of the vermis and the dorsal surface of the brainstem; Normal is <18 deg

Tegmento-Vermian Angle

Line drawn horizontally from the fastigium (dorsal point of the 4th ventricle) and most dorsal point of the vermis taken in sagittal view

Fastigium-Declive line

posterior fossa = enlarged vermis = hypoplastic T-V angle = >18

Classic Dandy-Walker Malformation

Posterior fossa = Normal Vermis = hypoplastic T-V angle = >18

Vermian Hypoplasia

Posterior fossa = Normal Vermis = Normal T-V angle = >18 deg

Blake Pouch Remnant *Due to non-perforation o fthe foramen of Magendie

Posterior fossa = Normal Vermis = Normal T-V angle = Normal

Mega Cisterna Magna *Normal size Cisterna Magna 2-10 mm

Largest of the subarachnoid cisterns

Cisterna Magna a.k.a *cerebellomedullary* cistern

Midline fusion o fthe cerebellar hemispheres & absence of vermis; best seen in coronal view as cerebellar folia that is contiguous across the midline

Rhombencephalosynapsis

Failure of decussation of the superior cerebellar peduncles; superior cerebellar peduncles appear thickened *Molar Tooth* appearance

Joubert Syndrome

Increased/prominent inner table convolutions, sellar erosions, and enlargement.

Copper Beaten Skull * seen in: Craniosynostosis Hydrocephalus Hypophosphatamia

Closing of fontanelles: Posterior Fontanelle Anterior Fontanelle Metopic Suture

2- 3 months - post fontanelle 18 months - ant fontanelle 1 yo - metopic suture

Closed suture: Sagittal Head shape: Long, narrow

Scaphocephaly/ Dolicocephaly

Closed suture: Bilateral Coronal &/or Lambdoid Head shape: Short, wide, Associated Syndromes: Apert Carpenter's Cornelia Down's

Brachycephaly/ Bradycephaly

Closed suture: Metopic Head shape: Frontal wedging, KEEL

TrigOnocephaly * Omega sign TriM (TrigonoMetopic)

Closed suture: All Head shape: Tower-like skull Associated with: * 8th cranial nerve lesion * optic nerve compression * mental deficiency * syndactyly

Turricephaly * most severe form

Closed suture: Sagittaal, coronal, Lambdoid Head Shape: Cloverleaf skull/

Cloverleaf skull/ Kleeblattschadel

Most common primary craniosynostosis

Scaphocephaly/ Dolicocephaly *bitemporal pinching

2nd most common craniosynostosis

Brachycephaly *premature closure of bilateral coronal and lambdoid sutures

Sphenoid is drwan upward toward the closed suture; seen in PLAGIOCEPHALY

Harlequin's Eye

Most common anomaly associated with craniosynostosis:

Limb Defects *syndactyly *polydactyly

Bicoronal synostosis associated with symmetric syndactyly of the 2nd to 4th digits resulting to *Mitten* or *Paddle* hand

Apert Syndrome (Apir 🙏; Apert, paddle hand)

Brachycephaly, facial dystosis with hooked *PARROT NOSE* and small maxilla, bilateral exopthalmos, and genetic transmission

Crouzon Syndrome

Not associated with increased ICP; appear as *soap bubble* rarefractions of the upper calvarium; fade after birth; Disappears after 4-5 months of age

Lacunar skull a.k.a Lückenschädel skull

Soft, fluctuant, red-to-blue scalp mass over the sagittal or transverse sinuses;

Cranial venous anomaly in which there is an abnormal communication between intracranial dural sinuses and extracranial venous structures, usually via an emissary transosseous vein

Sinus Pericranii

Most common phakomatosis

Neurofibromatosis Type 1 - a.k.a *Peripheral Neurofibromatosis* C A F E S P O T C afe au lait spots A axillary or inguinal ferckling F ibromas (2 or more) or plexiform (1) S keletal abnormalities (leg bowing) P ositive family hx OT optic tumor (optic gliomas) Lisch nodules

Characteristic/pathognomonic lesion of NF1; presenting as "bag of worms"

Plexiform Neurofibromas

Central neurofibromatosis with characteristic *"bilateral acoustic Schwannoma"* and dorsal nerve roots in *dumbbell* configuration.

Neurofibromatosis Type 2 *M I S M E M ultiple I nherited S chwannomas M eningiomas & E pendymomas

Characterized by hamartomas within multiple organ system with epilepsy as the MC neurologic symptom. dermal manifestation includes *ADENOMA SEBACEUM*.

Tuberous Sclerosis *Vogt Triad 1. Seizure 2. Adenoma sebaceum 3. Mental retardation

MC lesion seen in TS

Subependymal Hamartomas *DDx: Gray matter heterotopia (does not calcify)

Autosomal dominant. Consist of retinal ANGIOMAS, and cerebellar and spinal HEMANGIOBLASTOMA

Von Hippel Lindau Syndrome * associated with Renal/ Heaptic Cysts RCC, Pheochromocytoma Hemagioblastoma (cyst w/ murallll nodule in the cerebellum)

Encephalotrigeminal angiomatosis; angiomatous lesions of the skin and meninges; Facial *port-wine stain*; Pathology in the brain: PIAL ANGIOMATOSIS and ipsilateral CHOROID PLEXUS Hypertrophy

Sturge-Weber Syndrome

Cutaneous lesion of NF1 except: a. cutaneous neurofibromas b. portwine stain c. Lisch nodules d. cafe au lait spot

Port-wine stain - Sturge Wr Syndrome

Cutaneous lesion of Sturge-Weber: a. cutaneous neurofibromas b. portwine stain c. Lisch nodules d. cafe au lait spot

Port-Wine stain (facial)

Cutaneous lesion of tuberous sclerosis: a. cutaneous neurofibromas b. adenoma sebaceum c. Lisch nodules d. cafe au lait spot

Adenoma sebaceum

True of supratentorial embryonal tumor except: a. well-defined lesion & may be solid homogeneous or heterogenous w/ cyst formation b. calcifies c. w/ necrosis and hge d. leptomeningeal dissemination and drop mets are frequent e. none of the above

None of the above

Lesion that is ALMOST ALWAYS INTRAventricular; commonly seen in adults; DOES NOT usually ENHANCE; WITHOUT perilesional edema

Subependymoma

MC location of Subependymoma

Frontal horn of lateral ventricle (near foramen of Monro followed by: fourth ventricle septum pellucidum

MC seen in children under 3 YO; intraventricular in location w/ transependymal extension; WITH perilesional edema; EXTRUDES into the foramens of LUSCHKA and MAGENDIE.

EPENDYMOMA

MC location of ependymoma

Posterior Fossa (4th ventricle)

MC choroid plexus tumor

Choroid plexus Papilloma MC location children: trigone lat vent MC location adult: 4th ventricle

Slow-growing, benign, non-glial tumors that arise from the etoderal remnant of the Rathke's Pouch in the sellar/suprasellar region. WHO Grade I

Craniopharyngioma *Chidren: Adamantinomatous; encases vessels;calcifies *Adult: Squamous papillary variant

MC posterior fossa tumor in childhod

Medulloblastoma *Classic - MC; cental post fossa (fills the 4th ventricle) *Large cell-anapastic - most maliganant

Vascular structure engulfed by Diffusse Intrinsic Pontine Glioma

Basilar artery

MC tumor in children; CYST W/ enhancing MURAL NODULE

Pilocytic Astrocytoma *COMMONLY arises in the CEREBELLUM

MC pineal gland tumor

Pineal Germinoma

Pineal tumor that is hyperdense on CT with homogeneous enhancement; central calcification *ENGULFED PATTERN*

Pineal Germinoma *compresses the tectal plate resulting in PARINAUD SYNDROME; "upward gaze" palsy

Malignant, unencapsulated tumor of the pineal gland, CALCIFIES less than pineocytoma that is PERIPHERAL in location *EXPLODED PATTERN* w/ lateral displacement of the pineal gland

Pineoblastoma

MC benign lesion in the pineal region

Pineal Cyst

MC cause of lobar pneumonia

S. pneumoniae

MCC of NEONATAL pneumonia

Group B hemolytic Streptoccoccus Pneumonia (Lobar pneumonia)

Multiple bilateral patchy alveolar opacities is suggestive of

Bacterial infection

MCC of interstitial pattern (hazy, reticular, or reticulonodular) in the lung of a child

Viral or Mycoplasma infection

The following pulmonary conditions predominate in the lower lungs except: a. Tuberous Sclerosis b. Langerhans cell histiocytosis c. Connective tissue disease d. Primary interstitial pneumonia

Langerhans cell histiocytosis

Pulmonary underdevelopment presenting as ABSENT bronchus, pulmonary parenchyma, and pulmonary arteries

Pulmonary AGENESIS

Pulmonary underdevelopment presenting as RUDIMENTARY bronchus with ABSENT pulmonary parenchyma and pulmonary arteries.

Pulmonary APLASIA

Pulmonary underdevelopment presenting with hypoplastic bronchus and pulmonary arteries with VARIABLE amounts of pulmonary parenchyma

Pulmonary HYPOPLASIA

Result from proximal arrest of the bronchial branching; Characterized by peripheral bronchioles (near the pleura) containing cartilage in their walls; hypoplasia or absence of the ipsilateral pulmonary artery

Congenital Pulmonary Hypoplasia

Hypoplastic lung DRAINED by an ANOMALOUS RIGHT PULMONARY VEIN seen as a curvilinear vertical vein extending along the right heart border emptying into the IVC.

Hypogenetic lung or SCIMITAR Syndrome *right lung is the hypoplastic lung Anomalous PV usually drains into the IVC

Curvilinear vertical vein extending along the right heart border emptying USUALLY into the IVC. Classic vertically oriented curvilinear density projecting over the right hemithorax

Scimitar Sign *Scimitar vein may also drain in: hepatic vein portal vein azygous vein coronary sinus right atrium

MCC of pulmonary hypoplasia due to INTRATHORACIC compression

Congenital Diaphragmatic hernia *Pumonary insufficiency -Most significant cause of morbidity and mortality

MCC of pulmonary hypoplasia secondary to EXTRATHORACIC compression

OLIGOHYDRAMNIOS WITH RENAL DISEASE *Potter syndrome -failure of kidney to develop *Bilateral cystic kidney *Obstructive uropathy

ACQUIRED pulmonary hypoplasia secondary to OBLITERATIVE bronchiolitis resulting to *AIR TRAPPING*; Unilateral HYPERlucent lung

Swyer James Syndrome *lung size DOES NOT change with respiration *congenital pulmonary hypoplasia changes lung size during respiration

Consist of a large posterior right-sided aortic arch and small anterior left-sided aortic arch encasing the trachea and esophagus

Double aortic arch *Lateral Radiograph 1. increased retrotracheal density 2. Anterior bowing of trachea 3. Tracheal narrowing

Components of vascular ring

1. Right ascending aorta 2. Aberrant left subclavian artery 3. Ligamentum arteriosum or persistent Ductus Arteriosus stretching from the LSA to the PA anterior to the trachea

LEFT PA ARISES from the RIGHT PA and courses lateraly to the left side in b/w the trachea and esophagus compressing the trachea posteriorly

Pulmonary SLING anomaly *Types: Type 1- normal located carina Type 2- inferior located carina; MC

Thin-walled lung cavities that commonly occur with pulmonary infection in children

Pneumatocoele

Results from early maldevelopment of the airway; there is abnormal bronchial communication or bronchial atresia; stomach is normal in location.

Congenital Pulmonary Airway Malformation (CPAM) a.k.a Congenital cystic adenomatoid malformation *Type 1 = Uniform air cyst, >2cm; MC Type 2 = Variable size <2cm Type 3 = MICROcyst

MC location of congenital diaphragmatic hernia

Foramen of Bochdalek *posterolateral, left side *solid viscera MC herniates through the right side

The ff are true of surfactant deficiency dse except: a. MC of death in preterm infants b. occurs in fullterm infants of DM mothers c. both structural and functional immaturity d. None of the above

None of the above

Complication of positive airway pressure treatment usually for SDD. Results from increased capillary permeability due to oxygen toxicity resulting to leakage of lfuid into the pulmonary interstitium.

Leaky Lung Syndrome

Abnormal development of the pulmonary lymphatic system resulting in dilation and obstruction of the lyphatic channels; patiet present with *REFRACTORY PLEURAL EFFUSION*

Pulmonary Lymphangiectasia

Bilateral pleural effusion is most commonly seen in

Renal disease (e.g. AGN, nephrotic syndrome)

MCC of massive pleural effusion in neonates; usually UNILATERAL

Chylothorax *caused by traumatic tear or congenital defect of the thoracic duct

MCC of PULMONARY MASS in CHILDREN

PSEUDOTUMOR - from round pneumonia others: pulmonary abscess

MC TRUE lung mass in children

Post-inflammatory granuloma due to TB or fungal infection

Reactive lesion developing from healing pneumonia; solitary; well-defined; peripheral; predilection to the lower lobes

Inflammatory myofibroblastic tumor

MC foregut duplication cyst

Bronchogenic Cyst Subcarinal = MC location *does NOT communicate w/ airway *Cyst in the RIGHT paratracheal or subcarinal region

Mass of lung tissue W/O connection to the bronchial tree and is supplied by SYSTEMIC ARTERY

Pulmonary Sequestration *MC in the left side *INTRAlobar - MC type; child/teens *EXTRAlobar - newborns; w/ own pleura; unaerated; drains via azygos/hemiazygos

Triad of bronchial atresia

1. Bronchocoele 2. Hyperlucent distal lung 3. Hypoperfusion of the distal lung segment

MC MALIGNANT neoplasm of childhood

Metastasis

MC childhood tumors to metastasize to the lungs

W ilm's tumor O steosarcoma R habdomyosarcoma E wing Sarcoma *Neuroblastoma metastasize to the LIVER

MCC of apparent anterior mediastinal mass

Thymus

Faulty development of the 3rd and 4th pharyngeal pouches resulting to: Thymic aplasia, absent parathyroid, CV abnormalities

DiGeorge syndrome

Anterior mediastinal masses except: a. teratoma b. neuroenteric cyst c. dermoid d. cystic hygroma

neuroenteric cyst

MC MIDDLE mediastinal mass

Lymphadenopathy *massive adenopathy = lymphoma/leukemia *unilateral adenopathy = TB

Primary subpleural lesion in the mid to lower lobes commonly seen in PTB

Ghon Focus

Calcified subpleural lesion (Ghon focus) with associated ipsilateral lympadenopathy

Ghon Complex

Calcified Ghon Focus and hilar lymph nodes

Ranke Complex

MC origin of POSTERIOR mediastinal mass

Neurogenic *Clues: Pedicle erosion Interpedicular/ rib space widening Bone erosion

Terrible 'T's of anterior mediastinum

Thymoma Terrible lymphoma Thyroid tumor Teratoma

MC malignancies to involve the chest wall in children

1. Ewing sarcoma 2. PNET (Primitive NeuroEctodermal Tumor; Askin tumor) *Large extrapleural soft tissue mass w/ rib destruction and pleural effusion

Metastatic RIB lesion common in infants and children are lesions from

Neuroblastoma

Useful in assessing location, size, and flow pattern of aortic and ductal arches; Can evaluate arch sidedness

Three Vessel Tracheal View

Indication most predictive of cardiac disease

Abnormal *Four-chamber* view on routine obstetric ultrasound

Asymmetric Pulmonary Vascularity is seen in

* TOF = Diminished flow to the left lung * TA = Diminished flow to 1 or both lungs * Valvular PS = Preferential FLOW to left

Causes of enlarged PA

1. Increased pulmonary blood flow 2. Post stenotic dilation 3. Pulmonary valve insufficiency (regurgitation)

Causes of small or absent PA

1. Pulmonary outflow tract obstruction 2. Abnormal position of PA (PTA, TOGA)

MC abnormality in the contour of the heart

Coarctation Of the Aorta *figure of 3 sign*

Most often an isolated anomaly; if accompanied by CHD, seen with PTA and TOF. * "Reverse S" * configuration in barium esophagogram.

Right-sided Aortic Arch *may be a clue in the presence of a vascular ring

ACYANOTIC heart disease with INCREASED pulmonary blood flow

VSD ASD Aortic Pulmonary Window PDA

MC congenital heart abnormality AFTER bicuspid aortic valve

VSD

MC type of VSD

Perimembranous *near junction o fthe membranous and muscular portions

MC type of VSD associated with TOF, PTA and AVSD

High in membranous septum

Characteristic findings of: Elarged PA, Left-sided cardiomegaly, and Increased pulmonary vascularity

VSD

MC type of ASD

Ostium SECUNDUM *defect @ the center of fossa ovalis

Results form abnormal development of the endocardial cushion forming the interatrial and interventricular septum. Usually large defect seen anterior to the fossa ovalis @ the base of the atrial septum.

Ostium Primum ASD *commonly seen in Trisomy 21

Increased pulmonary vascular resistance from conversion of a long-standing acyanotic left-to-right shunt into cyanotic right-to-left shunt.

Eisenmenger Syndrome

There is Right-sided cardiomegaly with RV volume overload, small aorta, diastolic bowing of the septum to the left, with NON-enlarged LA

ASD *non enlarged LA, distinguishing feature of ASD from other left-to-right shunt

Results from failure of complete division of the prmitive truncus arteriorsus which leaves a c ommunication b/w the aorta and PA JUST ABOVE the valves

Aortopulmonary Window

Characterized by: * Dilated PA * Enlarged LA, LV (Left-sided cardiomegaly) * Increased pulmonary vasculature * Enlarged proximal aorta

Patent Ductus Arteriosus *normally closes after birth *persist as complication of hypoxia in premature infants

CYANOTIC heart dse with INCREASED pulmonary vascularity

TOGV ( D and L transposition) TAPVR PTA DORV SV (kulang sya sa oxygen kaya TTPiDS sya)

MC form of CYANOTIC heart disease with INCREASED pulmonary blood flow

Complete Transpostion Of Great Vessel (TOGV D- transposition) *position of aorta and PA are reversed *needs an ASD, VSD, or PDA to survive

MC CYANOTIC heart disease

Tetralogy of Fallot (TOF)

Cardiomegaly with an ovoid appearance; *EGG on a STRING* appearance; anteriorly placed aorta results in increased RETROSTERNAL opacity.

Transposition Of Great Vessels - Complete (D transposition)

Dx is suggested by prominence along the left upper cardiac border representing the right ventricular outflow tract with a left-sided aorta.

Transposition of the Great Vessels - Corrected (L transposition)

Cyanotic heart disease with increased pulmonary blood flow wherein the AORTA is anterior and lateral to PA and ARISES from the RV.

Double Outlet Right Ventricle (DORV) Type I = Subaortic VSD; MC; covers Ao Type II = subpulmonic VSD; covers PA TYpe III = doubly committed; covers both Ao and PA Type IV = not committed; inferior to the IV septum

MC type of TAPVR

SUPRACARDIAC - Type I *empties into a large SUPRACARDIAC VEIN (perisistent left SVC, left brachiocephalic vein, Right SVC, azygos vein)

Venous drainage of Type II TAPVR (Cardiac)

Right Atrium Coronary sinus

Venous drainage of Type III TAPVR - Infracardiac

Portal Vein *common vein travels into the esophageal hiatus and drains into PV, or less commonly an abdominal vein

Classic *SNOWMAN* appearance on radiograph due to prominent superior mediastinum from large inverted U-shaped vessel emptying to the SVC

Total Anomalous Pulmonary Venous Return (TAPVR) *types 1 & 2 overload the right side of the heart

Failure of the truncus arteriosus to divide into PA and Aorta with both vessel being fed by a singel vessel that overrides a high VSD; seen as CONCAVITY in the usual site of PA

Persistent Truncus Arteriosus Type I = MC; Ao and PA arise from same trunk

MC PTA where both Aorta and PA arise FROM a COMMON trunk.

Type I PTA

PA arises separately from the posterior aspect of the trunk just above the truncal valve

Type II PTA *type III - least common; arise independently from either side of the trunk Type IV - Neither arise from the common trunk

Group of anomalies in w/c one ventricle is rudimentary and the other is large and the only functional

Single Ventricle *MC underdeveloped RV

MC chd to cause DIMINISHED pulmonary vascularity; MC cause of CYANOTIC heart disease

Tetralogy of Fallot *TOGV - MC cyanotic heart disease WITH increased pulmonary vascularity.

Classic finding of *BOOT-shaped* heart sec to RVH; decreased pulmonary vascularity; combination of right-sided aorta and decreased pulmonary vascularity is highly suggestive

Tetralogy of Fallot

Egg on a string a. DORV b. TGV c. TAPVR d. TOF

TGV

Snowman Configuration a. DORV b. TGV c. TAPVR d. TOF

TAPVR

BOOT-shaped heart a. DORV b. TGV c. TAPVR d. TOF

TOF

Cyanotic CHD with decreased pulmonary vascularity consisting of: *Tricuspid valve atresia *Pulmonary atresia/stenosis *Underdeveloped RV The PA shadow appears flat with enlarged RA

Hypoplastic RIGHT heart syndrome

Cyanotic chd with decresaed pulmonary vascularity consisting of: *TRicuspid valve atresia *Pulmonary valve atresia/stenosis *Hypoplastic RV The PA is flat with enlarged RA

Hypoplastic RIght Heart Syndrome

Type of PA w/ ABSENT PA and is supplied by major AORTOpulmonary collaterals

Type C *Type A- supplied by pdA *Type B - supplied by Both native PA and major Aortopulmonary window collaterals

Consist of malformed tricuspid valve that is displaced downward, resulting in *ATRIALIZATION* of the RV.

Ebstein Anomaly *classic "BOX-shaped" heart

Classic "BOX-shaped* heart a. DORV b. Ebstein Anomaly c. TAPVR d. TOF

Ebstein Anomaly

Focal and complex ABSENCE of the RV myocardium; the RV wall appears THIN

UHL anomaly

MC affected valves in congenital cardiac valves STENOSIS

SEMILUNAR VALVES *Aortic *Pulmonic

Cardiac valve stenosis associated with *POST-STENOTIC* dilation of PA with prominence of LEFT PA and INCREASED pulmonary blood FLOW to the LEFT lung.

VALVULAR Pulmonic Stenosis *ONLY VALVULAR forms of aortic and pulmonic stenosis are associated with post-stenotic dilation

MC type of aortic stenosis

SUBvalvular Aortic Stenosis

Tyoe of aortic stenosis associated with WILLIAMS Syndrome

SUPRAvalvular Aortic Stenosis

MC form of SUBvalvular Pulmonic stenosis associated with TOF

INFUNDIBULAR

Form of COA presenting w/ PRE and POST STENOTIC dilations resulting in *figure of 3* sign; Stenosis is seen @ or just distal to the level of DA

Juxtaductal COA *collaterals: 1. intercostal arteries (T4-T8) rib notching 2. Internal mammary arteries 3. Arteries around the scapula

Aortic arch appears tortuous, dilated and kinked, WITHOUT evidnece of pressure gradient across the kinking

Pseudocoarctation of the Aorta

Condition wherein the pulmonary veins drain into a common vein that is abnormally incorporated into the SUPERIOR POSTERIOR aspect of the LA creating an EXTRA CHAMBER; an unnecessary fibromuscular membraneous subdivision through the atrial chamber.

Cor TriaTriatum (Classic/Sinister); MC *CXR: heart is normal sized with changes of chronic interstitial oedema.

MC type of cardiac malposition

Mirror-Image Dextrocardia *cardiac chambers are completely inverted, and cardiac apex points to the right

Bilateral right-sidedness; severe form; Absent splee, bilateral trilobed lungs; bilateral SVC

Asplenia (IVEMARK Syndrome)

Bilteral left-sidedness; Multiple spleen; bilateral bilobed lungs; interrupted IVC with azygos continuation; biliary atresia;

Polysplenia *Liver is @ midline and intestinal malrotation occurs