Fetal Pathologies

Question 1

Choanal atresia

Answer 1

Occlusion of the passage way between the nose and pharynx

Question 2

Pulmonary hypoplasia

Answer 2

Underdevelopment of the lung

Question 3

Congenital diaphragmatic hernia

Answer 3

Birth defect where the diaphragm fails to fully develop, allowing abdominal organs to enter the chest cavity.

Question 4

Why is Congenital Diaphragmatic Hernias a problem?

Answer 4

Displaces the heart and compresses the lungs, leading to lung underdevelopment (pulmonary hypoplasia).

Question 5

What are the consequences of pulmonary hypoplasia?

Answer 5

Reduces alveolar surface area for gas exchange and risk of hypertension (abnormal blood vessels + Persistent fetal circulation)

• air leaks are also very common

Question 6

Polyhydramnios

Answer 6

Excessive amount of amniotic fluid when fetus does not swallow and absorb the usual amount of amniotic fluid

Question 7

Oligohydramnios

Answer 7

Deficient amount of amniotic fluid

Question 8

Why does polyhydramnios occur?

Answer 8

• Impaired swallowing dysfunction
• maternal diabetes
• Premature rupture of amniotic membranes which could lead to premature birth

Question 9

Why does Oligohydramnios occur?

Answer 9

Fetal urine production issue, placental insufficiency, or premature membrane rupture

Question 10

what anatomical/physiological affects does polyhydramnios have?

Answer 10

Excessive fluid can overstretch the uterus, leading to preterm labor or uterine atony after delivery.

• Increases risk of umbilical cord prolapse
• Mispositioning to breech position
• Respiratory complications for mom

Question 11

what anatomical/physiological affects does oligohydramnios have?

Answer 11

Limited amniotic fluid restricts fetal movement, potentially leading to pulmonary hypoplasia and skeletal deformities, such as clubfoot or contractures, due to constrained fetal positioning.

• amniotic fluid is crucial for development and cushioning; so growth may be affected

Question 12

What is a PDA?

Answer 12

Failure of ductus arteriosus to close

• blood shunts from aorta -> pulmonary artery (L->R shunt)
• Causes prematurity and hypoxia

Question 13

Signs of a PDA?

Answer 13

Bounding pulse or widened pulse pressure

Question 14

Treatment for PDA?

Answer 14

Indomethacin (nsaids), NSAIDs, or surgery

Question 15

What is a ASD?

Answer 15

Foramen ovale fails to close

• L->R shunt = increased pulmonary blood flow
• May be asymptomatic or cause fatigue, poor growth

Question 16

Ventricular Septal Defect (VSD)

Answer 16

Hole between ventricles (L->R shunt)

• can lead to pulmonary congestion or CHF
• Lout systolic murmur

Question 17

What 4 defects are associated with tetralogy of allot (TOF)

Answer 17

“PROVe” mnemonic:

• Pulmonary stenosis
• Right ventricular hypertrophy
• Overriding aorta
• Ventricular septal defect

Question 18

Why is a PDA or ASD necessary for Transposition of the Great Arteries (TGA)?

Answer 18

Aorta arises from RV, pulmonary artery from LV → parallel circulation

• Needs PDA or ASD to survive (mixing of blood)
• Treatment: Prostaglandin E1 to keep PDA open, surgery

Question 19

Persistent Pulmonary Hypertension of the Newborn (PPHN)

Answer 19

Fetal circulation fails to adapt → PVR stays high

• R→L shunting via PDA and foramen ovale
• Causes: Meconium aspiration, MAS, RDS
• Treatment: O₂, iNO, ventilation, sedation, ECMO

Question 20

How can you identify RDS from TTN?

• key differences

Answer 20

1. Onset of RDS is within mins of birth while TTN is typically 1-2hrs of birth
2. Ground glass appearance on CxR = RDS
3. RDS occurs in preterm infants (<34 weeks) while term or late infants can get TTN