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OB > Fetal Thorax/Abdomen > Flashcards

Fetal Thorax/Abdomen Flashcards

1
Q

What is the shape of a normal thoracic cavity?

A

symmetrically bell shaped

ribs form lateral margins, clavicles form upper margins and diaphragm forms lower margin

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2
Q

What is the best determinate for predicting pulmonary hypoplasia?

A

chest area minus heart area times 100 divided by chest area

fetus with significantly narrow diameter of chest may have asphyxiating thoracic dystrophy

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3
Q

What is the normal sonographic appearance of inutero lungs?

A

appear homogeneous with moderate echogenicity
early in gestation, lungs similar to or slightly less echogenic than liver
as gestation progresses, trend is toward increased pulmonary echogenicity realative to liver

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4
Q

How much time does a mature fetus spend breathing?

A

almost 1/3 of its time breathing

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5
Q

What is pulmonary hypoplasia?

A

caused by decrease in number of lung cells, airways, and alveoli, with resulting decrease in organ size and weight
reduction in lung volume results in small, inadequately developed lungs

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6
Q

How is pulmonary hypoplasia diagnosed?

A

decreased ratio of lung weight to body weight is consistent method of diagnosing

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7
Q

What is the cause of pulmonary hypoplasia?

A

most commonly occurs from prolonged oligohydramnios or secondary to small thoracic cavity as result of structural or chromosomal abnormality

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8
Q

What kidney abnormalities result in lethal pulmonary hypoplasia?

A

bilateral renal agenesis, bilateral multicystic kidney disease, severe renal obstruction, unilateral renal agenesis with contralateral multicystic kidney development, severe obstruction, infantile polycystic kidney disease
(because these result in oligohydramios)

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9
Q

When may pulmonary hypoplasia occur?

A

in fetuses with IUGR and early rupture of membranes
masses within the thoracic cavity may lead to pulmonary hypoplasia (diaphragmatic hurnia)
may also be seen with cardiac defects, some skeletal dysplasia, CNS disorders, and chromosomal trisomies

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10
Q

What is the prognosis of pulmonary hypoplasia?

A

grave

severity depends on when pulmonary hypoplasia occurred during pregnancy and its severity and duration

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11
Q

What different ways can be used to detect pulomary hypoplasia?

A

thoracic measurements, various lung measurements, estimation of lung volume, doppler studies of pulmonary artieries, assessment of fetal breathing activity

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12
Q

Describe cystic lung masses.

A

echo free masses that replace normal lung parenchyma; variable in size; may cause notable shifts of intrathoracic structures

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13
Q

What is the most common cystic lung mass?

A

brochogenic cyst

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14
Q

Where does a bronchogenic cyst usually lay?

A

within mediastinum of lung

it lacks any communication with trachea or bronchial tree

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15
Q

Sonographically, what do bronchogenic cysts look like?

A

small, circumscribed masses without evidence of mediastinal shift or heart failure

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16
Q

What effect does a bronchogenic cyst have on the amniotic fluid?

A

no effect

amniotic fluid volume within normal range

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17
Q

What is pleural effusion?

A

hydrothorax

accumulation of fluid within pleural cavity that may appear as isolated lesion or secondary to multiple fetal anomalies

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18
Q

What is the most common reason for hydrothorax?

A

chylothorax
occuring as right-sided unilateral collection of fluid secondary to malformed thoracic duct
(polyhydramnios often accompanies chylothorax)

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19
Q

What is the sonographic appearance of pleural effusion?

A

echo-free peripheral masses on one or both sides of fetal heart; conform to thoracic cavity and often compress lung tissue; lung appears to float in fluid

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20
Q

With the presence of pleural effusion, what may it cause?

A

shift of mediastinal structures; compression of heart; inversion of diaphragm

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21
Q

Does pleural effusion change the shape of the lung?

A

no

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22
Q

Once hydrothorax is discovered, what else should be looked for?

A

lung, cardiac, and diaphragmatic lesions

sign of hydrops

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23
Q

What is the prognosis for pleural effusion?

A

mortality rate at 50%

when PE is large, lung development impaired, which may result in pulmonary hypoxia

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24
Q

What are the most common solid lung masses?

A

pulmonary sequestration and certain types of cystic adenomatoid malformations (CAMs)

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25
Q

What is pulmonary sequestration?

A

2nd most common lung lesion

a supernumerary lobe of lung, seperated from normal tracheobronchial tree

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26
Q

Describe the two types of pulmonary sequestration.

A

intralobar: extrapulmonary tissue present within pleural lung sac; has arterial supply; 2/3 occur in the left lung; most common of the two; not associated with other anomalies
extralobar: extrapulmonary tissue connected to inferior border of lung within its own pleural sac; male predomninance; associated with other anomalies in half of cases; 95% occure in left lung

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27
Q

What is the sonographic appearance of pulmonary sequestration?

A

echogenic solid mass resembling lung tissue; rarely occurs below diaphragm; normal intra-abdominal anatomy
doppler demonstrates arterial supply and multiple feeding vessels are common

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28
Q

What is congenital cystic adenomatoid malformation?

A

CCAM
a multicystic mass within the lung
consists of primitive lung tissue and abnormal bronchial and bronchiolar-like structures
may communicate with bronchial tree
result of abnormal development of bronchial tree at level of the trachea, bronchiloes, and alveoli

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29
Q

What is the most common congenital lung lesion?

A

congenital pulmonary airway malformation

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30
Q

What is the sonographic appearance of CCAM or CPAM?

A

cysts within the mass may be large or small; texture varies; most lesions are unilateral; most lesions are benign; no internal flow

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31
Q

How do you calculate the CPAM volume and CPAM volume ratio?

A

CPAM volume: LxHxWx0.52

CVR: CPAM volume / HC

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32
Q

What amount of CVR is associated with significant risk for hydrops?

A

CVR > 1.6

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33
Q

How does CPAM progress?

A

progress rapidly up to 20-26 weeks gestation and after that, they regress completely (90%)
type 4 usually does not regress

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34
Q

Why is diagnosis of CPAM important?

A

so a team can be ready at birth to provide respiratory support due to fetal respiratory distress

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35
Q

What is the prognosis of CCAM?

A

depends largely on presence of hydrops, polyhydramnios, and pulmonary hypoplasia

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36
Q

What is the chain of events involving a diaphragmatic hernia?

A

first, a failure of the diphragm to completely close during development; then herniation of abdominal contents into the chest; pulmonary hypoplasia results because lungs will not be able to develop normally

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37
Q

What is a congential diaphragmatic hernia?

A

herniation of abdominal viscera into chest that results from congenital defect in fetal diaphragm
is sporatic - occurs in 1: 2000-5000 births

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38
Q

CDH is the most common type of diaphragmatic defect that occurs where?

A

posteriorly and laterally in diaphragm (herniation through foramen of Bochdalek)
left sided organ enter chest through opening (stomach, spleen, portions of liver); abnormally positioned abdominal organs shift heart and mediastinal structures to right side of chest

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39
Q

Where do the majority of Bochdalek hernias occur?

A

on the left side

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40
Q

Where else may a CDH be seen (other than through foramen of Bochdalek)?

A

may occur anteriorly and medially in diaphragm, through foramen of Morgagni, and may communicate with pericardial sac
the heart may be normally positioned but surrounded by plerual fluid, while fetal stomach may be located in its normal postition in abdomen

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41
Q

What are the sonographic features of LEFT CDH?

A

intrathoracic stomach; displaced cardiac apex; cardiomediastinal shift, intrathoracic liver (look for portal venous flow), small right lung, small LV of heart

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42
Q

What is critical to make a diagnosis for left CDH?

A

cardiomediastinal shift

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43
Q

What are the sonographic features of RIGHT CDH?

A

cardiomediastinal shift to the left, intrathoracic liver, stomach may be inferior to diaphragm and the the right, herniated GB, small amount of ascitic fluid adjacent to the liver

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44
Q

What will be seen with CDH regarding measurements?

A

small AC

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45
Q

What measurements can be used to identify CDH?

A

lung to head ratio (lung area/HC) - lung area=L1xL2

AC

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46
Q

What is a hybrid lung lesion?

A

combination of bronchopulmonary sequestration and CPAM

cystic lesion supplied by systemic circulation

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47
Q

What is congenital lobar emphysema (CLE)?

A

over inflated, fluid filled lobe or lung
rare
diagnosed postnatally

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48
Q

What is the incidence of CLE?

A

male predominance

more common in left lung

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49
Q

How may an infant develop infantile respiratory distress with CLE?

A

overdistension and airtrapping in the affected lobe of lung

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50
Q

How will CLE appear on US?

A

echogenic lung

51
Q

How many types of CPAM are there?

A

5 types

52
Q

What is the most common type of CPAM?

A

type 1

53
Q

What does type 1 of CPAM look like sonographically?

A

lesions consist of multiple echolucent cysts (3-10cm) or single large cyst (up to 10cm)in lower lungs

54
Q

What does type 2 of CPAM look like sonographically?

A

lesions consist of multiple echolucent cysts (0.5-2cm), spongelike appearance

55
Q

What does type 3 of CPAM look like sonographically?

A

echogenic mass in lower lung

56
Q

What does type 4 of CPAM look like sonographically?

A

echolucent cysts up to 10cm

57
Q

Which type of CPAM has the highest association with chormosomal abnormalities and which typically does not resolve on its own?

A

type 2

type 4

58
Q

What are the differences between the fetal and adult abdomen?

A

patent ductus venosus, proportions of fetal body different from adult (fetal abdomen larger relative to body length and liver occupies larger volume of fetal abdomen), smaller fetal pelvic cavity (bladder, uterus, ovaries), apron of greater omentum smaller (contains little fat, remains unfused in fetus, therefore, fetal ascites may separate omental leaves)

59
Q

When does midgut herniation of the bowel return to the abdomen? What happens after?

A

by 10th or 11th week

intestines enlarge, lengthen, and assume final positions

60
Q

When may abdominal wall defects omphalocele and gastroschisis occur?

A

when midgut fails to return to abdominal cavity from umbilical cord during 10th week

61
Q

What is an omphalocele?

A

coils of intestine (and commonly liver) protrude from umbilicus and are covered by transparent sac of amnion
the umbilical cord pierces central part of omphalocele

62
Q

What is the prognosis of omphalocele?

A

depends on degree of pulmonary hypoplasia (due to large omphalocele) and severity of other abnormalities (2/3s of cases have)

63
Q

What is gastroschisis?

A

condition in which bowel and/or organs free floating from midline defect (usually just bowel)
usually located to right of umbilical cord

64
Q

How does an umbilical hernia form?

A

when intestines return normally to abdominal cavity; herniate either prenatally or postnatally through inadequately closed umbilicus

65
Q

How does a hernia differ from omphalocele?

A

protruding mass (omentum or loop of bowel) covered by subcutaneous tissue and skin

66
Q

What is a Meckel’s diverticulum?

A

remnant of proximal part of yolk stalk that fails to degenerate and diappear during early fetal period

67
Q

What is the sonographic appearance of meckel’s diverticulum?

A

small fingerlike sac, 3-6cm long, projects from border of ileum
not connected to GB or stomach; runs from pelvis to RUQ; is long and anechoic

68
Q

What may meckel’s diverticulum cause?

A

acute appendicitis symptoms

also possible to torse

69
Q

What is the fingerlike sac of the meckel’s diverticulum?

A 
vitelline duct (conects to anterior abdominal wall)
if the duct remains open = persistent vitelline duct
70
Q

When does the esophagus reach its final length?

A

by 7th week

short in beginning and rapidly lengthens as body grows

71
Q

If esophageal stenosis occurs, where does it usually happen?

A

distal third portion (where esophagus joins stomach)

72
Q

When should a fetus have fluid in their stomach?

A

most fetuses older than 14-16 weeks

73
Q

If no fluid is seen in stomach, what should be done?

A

reevaluate in 20-30 minutes to rule out posibility of CNS problem, obstruction, oligohydramnios, and atresia

74
Q

What is the sonographic appearance of the fetal stomach?

A

anechoic with linear rugae
echogenic debris may sometimes be seen along dependent wall of stomach representing vernix, protein, or intra-amniotic hemorrhage (result of placental abruption)

75
Q

Why must cord insertion be imaged?

A

to rule out omphalocele, gastroschisis, hernia, and mass formation

76
Q

When does meconium begin to accumulate in distal part of small intestine?
When can the large and small intestine be distinguished?

A

after 15th to 16th week

after 20 weeks

77
Q

What is meconium? What does it look like sonographically?

A

combination of desquamated cells, bile pigments, mucoproteins
hypoechoic relative to fetal liver and in comparison with bowel wall

78
Q

How does the small bowel appear sonographically?

A

small bowel is slightly hyperechoic, compared with liver and may appear ‘mass like’

79
Q

When will peristalsis be seen?

A

after 27 weeks

80
Q

What is the measurement of normal small bowel? Large bowel?

A

diameter of small bowel lumen less than or equal to 5mm with length of 15 cm near term

colon diameter range from 3-5 mm at 20 weeks to 23mm or larger at term

81
Q

How does the large bowel appear sonographically?

A

haustral folds appear as thin linear echoes within lumen of colon in early gestation
later, colon diameter increases and folds become longer and thicker

82
Q

Which lobe of liver is bigger?

A

left lobe is bigger inutero secondary to greater supply of oxygenated blood

83
Q

When does hemopoiesis start?

A

during 6th week

84
Q

When can the gallbladder be visualized?

A

after 20 weeks

85
Q

Why can the pancreas not be routinely visualized?

A

lack of fatty tissue within the gland

86
Q

How does the spleen appear sonographically?

A

homogeneous, similiar in echogenicity as kidney - slightly less echogenic than liver, increases in size during gestation
larger in fetus because more active in hematopoisis

87
Q

When does the liver enlarge in a fetus?

A

with Rh-immune disease in response to increased hematopoiesis

88
Q

What are possible liver tumors than may be seen?

A

hamartoma, hepatoblastoma, heptic teratoma, adenoma, metastases from neuroblastoma, hemangioendothelioma

89
Q

How do most liver tumors appear sonographically?

A

hypoechoic solid masses; cystic components have also been reported as mixed with solid masses
5% may be calcified (usually benign finding)
if multiple calcifications seen within liver, other organs may be affected

90
Q

What is the difference between situs solitus, situs ambigus, and situs inversus?

A

situs solitus: normal situs
situs ambigus: partial situs
situs inversus: may present as total reversal of thoracic and abdominal organs or as partial reversal

91
Q

Describe partial situs inversus.

A

is a more severe disorder, may develop in two different combinations of organ reversals, thoracic viscera may or may not be reversed
prognosis depends on functionality of organs and their vascular connection

92
Q

Partial situs can be divided into ___ and ___.

A

asplenia and polysplenia

93
Q

What is asplenia?

A

absence of spleen
abnormally positioned stomach and gallbladder, more centrally positioned liver, abnormal positioning of aorta and IVC on same side

94
Q

What is polysplenia?

A

represented as transposition of liver, spleen, stomach, and absence of gallbladder
interruption of IVC and azygoes vein directly posterior to heart in front of spine
at least two spleens
heart block is common

95
Q

In which type of partial situs is cardiac malformations more common? What cardiac defects may be seen?

A

is asplenia
and are seen less frequently in polysplenia syndrome
endocardial cushion defects, hypoplastic left heart, transposition of great vessels

96
Q

About 20% of situs inversus babies have what?

A

kartagener’s syndrome

immotile cilia, bronchiectasis

97
Q

What is the mortality rate of situs inversus?

A

total: usually normal outcome
partial: death occurs in 90-95% with asplenia and 80% with polysplenia syndrome
with severe cardiac defects

98
Q

What is the prognosis of gallstones inutero?

A

resolve spontaneously in utero or childhood period

99
Q

With choledochal cysts, what is important to remember about the sonographic appearance?

A

shows no connection with stomach or duodenum

100
Q

What is the sonographic criteria for choledochal cysts?

A

cose proximity of cyst to neck of gallbladder, ovoid right upper quadrant cyst with entering bile duct, cyst and gallbladder that enlarge as gestation progresses, absence of peristaltic activity in cyst

101
Q

What percentage of patients have an absent gallbladder with biliary atresia?

A

20%

102
Q

With GI atresias, what will be evident on ultrasound?

A

polyhydramnios

103
Q

What is esophageal atresia?

A

a congenital blockage of the esophagus resulting from faulty seperation of foregut into its respiratory and digestive components

104
Q

What is the most common form of esophageal atresia?

A

occurs in conjunction with a fistula, communicating between trachea and esophagus (tracheoesophageal fistula) allows passage of amniotic fluid into stomach

105
Q

What is the classic sonographic appearance of esophageal atresia?

A

polyhydramnios and no visualized stomach (unless fistula is present, then small secretions in stomach)
upper neck pouch sign has been observed as additional finding (posterior to trachea and anechoic tubular structure) in mediastinum

106
Q

Coexisting anomalies are common in a majority of fetuses with esophageal atresia. What is the most common anomaly?

A

anorectal atresia and VACTERL

107
Q

What is VACTERL?

A 
vertebral anomalies
anal atresia
cardiac defects
tracheoesophageal fistula and/or
esophageal atresia
renal and radial anomalies
limb defects
108
Q

What is duodenal atresia?

A

blockage of duodenal lumen by membrane that prohibits passage of swallowed amniotic fluid
amniotic fluid fails to move beyond obstruction and backs up in duodenum and stomach

109
Q

What is the sonographic appearance of duodenal atresia?

A

two echo-free communicating structures (stomach and duodenum) found in upper fetal abdomen, double bubble sign, polyhydramnios seen later in pregnancy

most cases found distal to ampulla and often coexist with annular pancreas

110
Q

What is slightly more common than duodenal atresia?

A

atresia or stenosis of jejunum or ileum, or both, and small bowel atresia

111
Q

What is associated with bowel instinal obstruction?

A

verious fetal malformations may occur with maternal drug use

thought to be secondary to vascular accident, volvulus or gastroschisis or be sporadic

112
Q

What happens to the ileum or jejunum if obstruction occurs?

A

ileum: can rupture and lead to peritonitis
jejunum: grows large
appears as multiple cystic structures proximal to sire of atresia within fetal abdomen

113
Q

What is the general rule with bowel instestinal obstructions?

A

the more distal the obstruction, the less severe the hydramnios and the later it will develop

114
Q

What are causes of fetal small-bowel obstruction?

A

malrotation, atresias, volvulus, peritoneal bands, cystic fibrosis

115
Q

What is an abnormal bowel loop diameter?

A

greater than 7mm

116
Q

What is meconium ileus?

A

small-bowel disorder marked by presence of thick meconium in distal ileum

117
Q

What are the top three most common forms of neonatal bowel obstruction?

A

atresia, malrotation, and meconium ileus

118
Q

Who do most cases of meconium ileus occur in?

A

newborns with cystic fibrosis

119
Q

When does meconium begin to accumulate in the bowel?

A

2nd tri

can be seen as tiny echogenic reflections within the peristaltic small bowel; meconium remains suspended in the rectum

120
Q

Will the fetus release meconium?

A

no, unless the fetus is stressed or traumatized
may happen during delivery - it may indicate hypoxia and damaged CNS
very serious condition

121
Q

What is a characteristic of cystic fibrosis?

A

increased production of mucus by GI organs and electrolyte imbalance explains overproduction of meconium

122
Q

What is meconium peritonitis?

A

condition that may arise when fetus has sterile chemical peritonitis secondary to in untero bowel perforation

123
Q

What may be a complicatino of meconium peritontits?

A

complication may result in formation of meconium pseudocyst, as inflammatory reaction seals perforation

124
Q

What is the sonographic appearance of meconium peritonitis?

A

calcifications seen on peritoneal surfaces or in scrotum via processus vaginalis; ascitic fluid may be echogenic; polyhydramnios
unusual to see calcification in meconium ileus in fetus with cystic fibrosis

OB (10 decks)

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