Defect is adjacent to, and
almost always to the right of the normal umbilical cord insertion. Left
sided gastroschis has been reported but is rare.
The defect is small
(usually <2 cm) and involves the full thickness of the abdominal wall.
Freely floating bowel
loops outside the fetal abdomen (no limiting membranes).
Bowel wall may be
thickened (probably from exposure to fetal urine) (2) Meconium may be
present in small amounts, in normal amniotic fluid, and this may further
irritate exposed bowel (3,4). Langer et.al. (17) found that bowel wall
thickening of >3 mm to be present in 42% of their gastroschisis
fetuses, and was associated with an increase in time to initiate oral
feeding, but the difference was not statistically significant.
Dilated intra or
extraperitoneal bowel (a single cutoff value for bowel or subjective
assessment of fetal bowel dilatation is impractical) (13). Workers have
generally used >17 mm as bowel dilatation, however bowel dilatation of
> 17 mm without postnatal complications are well reported (16).
Small bowel extrusion
occurs consistently (large bowel rarely extrudes)
<3-5 cm defect, usually on the right
side of the cord insertion.
Normal insertion of the
umbilical cord on the fetal abdomen.
A small amount of skin is
present between the defect and the umbilicus.
Polyhydramnios may
be present. A study by Japaraj et.al. (16) suggests that polyhydramnios is
the only significant sonographic finding that was strongly predictive of
severe bowel complications in the neonatal period. It is thought that the
polyhydramnios may be a sign of severe bowel damage, and may be related to
bowel atresia and / or decreased or absent bowel motility.
No fetal ascites.
Abuhamad et.al. (18) found Doppler
velocimetry of the superior mesenteric artery and its branches to be
minimally useful in predicting the postnatal prognosis when compared to
bowel dilatation.
Structurally normal fetal
urinary tract may become functionally obstructed as increasing amounts of
abdominal contents herniated through the defect. The fetal bladder may
herniated through the defect (15) and appear as a large, fluid-filled cyst
in the amniotic cavity. Hydronephrosis can also develop both in the
presence and absence of bladder herniation. In either situation, the upper
tract dilatation appears to resolve postnatally following repair of the
abdominal wall defect.
Disappearing abdominal wall
defects have been described (5-7).
Pitfall –
gastroschisis that is obvious at mid-trimester scanning may be difficult
to perceive in the third trimester. Although the bowel loops are larger,
they are located at a distance from the defect in the anterior abdominal
wall. If the fetal back is facing anteriorly or if there is
oligohydramnios, the omphalocele may be invisible.
Closed gastroschisis –
this occurs when there is a significant progressive narrowing of the
abdominal wall defect around the prolaped bowel. This is very serious and
may lead to midgut infarction and vansihing bowel ending in short bowel
syndrome. It may be difficult to discriminate between relatively harmless
bowel obstruction and obstruction caused by a closure with possible fatal
consequences.. This may be suspected when there is persistent
intra-abdominal dilatation in the third trimester, especially if the
dilatation is newly developed.
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