Omphalocele and 
Gastroschisis
Wendy Nguyen and Kumar Belani
In this chapter, the differences between the two
defects will be discussed. In addition, the pre-
operative management, anesthetic intraoperative
monitoring, anesthetic goals, and postopera-
tive outcomes will be outlined. Table  41.1 pro-
vides a summary of anesthesia considerations
in patients undergoing surgery for Omphalocele
and Gastroschisis.
Introduction
An omphalocele is a central defect of the umbili-
cal ring where the abdominal contents eviscerate
into the intact umbilical sac. They are frequently
accompanied with other anomalies and require
detailed further work-up.
Gastroschisis is a full thickness abdominal
wall defect with evisceration of bowel through
the defect. The bowel contents are exposed, with-
out a covering membrane. Gastroschises most
frequently present as the only anomaly.
W. Nguyen, M.D. (*)
Department of Anesthesiology, University of
Minnesota School of Medicine,
Minneapolis, MN, USA
University of Minnesota, Masonic Children’s
Hospital, Minneapolis, MN, USA
e-mail: nguye747@umn.edu
K. Belani, M.B.B.S., M.S., F.A.C.A., F.A.A.P
University of Minnesota, Masonic Children’s
Hospital, Minneapolis, MN, USA
© Springer International Publishing AG, part of Springer Nature 2018
B. G. Goudra et al. (eds.), Anesthesiology, https://doi.org/10.1007/978-3-319-74766-8_41
41
For the practicing anesthesiologist, ompha-
loceles and gastroschises are relatively com-
mon, but the size and complexity of the defect
can present unique challenges. Its accompany-
ing anomalies may be significant enough to
play a larger role in outcomes. As such, patients
with these abdominal wall defects may present
repeatedly for complications related to abdom-
inal wall defect closures and/or for other
procedures related to their other anomalies
­
(Fig. 41.1).
Omphalocele
Definition and Diagnosis
In omphaloceles, the umbilical cord inserts in the
protruding sac, containing the internal peritoneal
membrane, Wharton’s jelly, and an external
amniotic membrane. The sac frequently contains
the stomach, loops of the small and large intes-
tines, liver (up to 50% of the time), and some-
times gonads.
Omphaloceles occur due to a failure of bowel
loops to return to the abdominal cavity following
the physiological herniation of the umbilical cord
between the 6th and 11th week of development.
Small to medium omphaloceles are considered
2–4 cm in size. Although there is no consensus,
most surgeons define giant omphaloceles (GOC)
as 5 cm or larger [7]. In cases of GOC, the tho-
racic cavity may be abnormally shaped and
395
396 W. Nguyen and K. Belani

Table 41.1  Summary of anesthesia considerations in patients undergoing surgery for omphalocele and gastroschisis
Plan/preparation/adverse events Reasoning/management
Pre-procedural evaluation Management may change significantly if there are any other anomalies such
– Pre-operative work-up; related as cardiac conditions.
co-morbidities Securing of the airway may be necessary if there is significant respiratory
– Airway compromise from the defect and/or other anomalies.
– Size and complexity of the The size and the complexity of the defect guides the route of the delivery,
defect surgical and anesthetic management, and outcomes.
Access and monitoring Central access is necessary for TPN. It is also helpful for the measurement of
–  PICC, PIV ± arterial line CVP to monitor for increased abdominal pressures. A larger PIV is helpful
–  Orogastric or nasogastric tube for transfusing and administering drugs quickly. An arterial line may be
helpful for monitoring labs and blood pressure, but may not be necessary if
the patient is otherwise stable.
An orogastric or nasogastric tube is necessary for abdominal decompression.
Intraoperative management Maintaining normothermia can be challenging due to the amount of
–  Maintain normothermia insensible losses from the exposed abdominal organs.
– Maintenance fluid and Similarly, insensible losses must be aggressively replaced to maintain
replacement of insensible loss intravascular volume.
– Monitor for increased Intravesical line is helpful for monitoring for intraabdominal pressures during
abdominal pressures closure. In lieu of an intravesical pressure monitoring, end tidal CO2 and
– Consider extubation for small airway pressures can be tracked.
abdominal wall defects. Although not widely adapted, use of neuraxial anesthesia would be helpful
Neuraxial analgesia may help for post-operative pain control and facilitate extubation in the operating
facilitate this room.
Post-operative management and Abdominal compartment syndrome is an emergency requiring expedient
discharge considerations decompression to avoid ischemia and subsequent short gut syndrome.
– Monitor for signs of abdominal Some will require multiple procedures to mitigate complications, such as
compartment syndrome adhesions and volvulus, from the initial procedure.
– Monitor for surgically-related If there is significant pulmonary compromise prior to surgical closure,
complications prolonged intubation is likely.
– Extubate when surgically and Patients with small abdominal wall defects tend to be fair better than those
hemodynamically stable with large or complex defects.
–  Manage co-existing anomalies Co-existing anomalies, if significant, such as cardiac or pulmonary
–  May require prolonged TPN hypoplasia, may play a more significant role in outcomes than the abdominal
wall defect itself.

6.0

5.0
per 10,000 live births

4.0

Gastroschisis
3.0
Omphalocele
AWD
2.0
Fig. 41.1 The
incidences of both
omphalocele and 1.0
gastroschisis have been
increasing as outlined in 0.0
this study by Kong and
1992
1993
1994
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
2005
2006
2007
2008
2009

associates [6]
41  Omphalocele and Gastroschisis
reduced in size, which may lead to pulmonary
hypoplasia.
Prenatal diagnosis is made by ultrasound
screening during late first trimester to mid-­second
trimester. An elevated maternal alpha fetoprotein
level may be present, but is not diagnostic.
Antenatal echocardiography should be performed
as up to 50% of fetuses will have cardiac defects.
Most common cardiac lesions include muscular
ventricular septal defect, atrial septal defect, and
coarctation of the aorta [8].
A recent study using a large multi-center clini-
cal database in North America found the inci-
dence of at least one other anomaly with
omphaloceles was 35% [9]. Interestingly, another
recent large study examined births in Texas from
1999 to 2008 and found 80% of omphaloceles
had other anomalies [10]. This is more in line
with other studies that report multiple anomalies
occurred in 67–88% of omphaloceles [11].
Omphaloceles have been known to be associ-
ated with complex syndromes including cloacal
exstrophy, Donnai-Barrow syndrome, Beckwith-­
Wiedeman syndrome, and Pentalogy of Cantrell.
Chromosomal defects (Trisomy 13, 18 or 21) are
observed in up to 30–40% of babies with ompha-
locele [12–15].
Treatment
There is no benefit to delivering prior to 37 weeks
unless there are complicating features, such as
polyhydramnios [12]. However, the route of
delivery is controversial. Retrospective studies
reveal no differences in fetal outcome with a
C-section delivery [16]. However, these studies
did not stratify outcome by the severity of the
omphalocele. As such, when the defect includes
an extra-abdominal liver, C-section may be pru-
dent to avoid hepatic injury [17].
Repair is not urgent. Once delivered, goals
include stabilization, and characterization of abnor-
malities. All newborns with omphalocele must
undergo an evaluation for other defects because
even though an antenatal ultrasound and cardiac
echocardiogram suggests an isolated anomaly,
additional multiple defects are not uncommon
397
Fig. 41.2  An antenatal ultrasound examination at 14
weeks of pregnancy. Note the presence of an abdominal
wall defect as pointed by the arrow [22]
[18, 19]. Thus, soon after birth, additional stud-
ies include transthoracic echocardiography, renal
ultrasound, karyotyping, and additional genetic
evaluation as indicated (Fig. 41.2).
Preoperative care may require securing the
airway, use of oscillator ventilation, nitric oxide,
and even extracorporeal membrane oxygenation
(ECMO) because of significant ventilatory com-
promise related to pulmonary hypoplasia and
other defects [15]. More than gastroschisis,
babies with omphalocele carry a higher risk of
having pulmonary hypertension [9].
Bowel decompression minimizes aspiration
risk and worsening bowel distension. Antibiotics
are required to prevent infection. Intravenous iso-­
osmotic fluids three to four times the usual main-
tenance rate may be needed to provide adequate
hydration and to compensate for insensible losses
secondary to peritonitis, edema, ischemia, and
protein loss. Urine output goal should be approx-
imately 1–2  mL/kg/h, and acid base-status and
electrolytes should be frequently monitored.
A bowel bag over the sac has been useful to
mitigate heat loss [20]. Gauze may be used as
well. In the past, super moist gauze had been
advocated, but the moisture will cool and can
lead to hypothermia [15]. Great care needs to be
taken to not rupture the sac as that increases
infection risk. Central and arterial umbilical lines
are avoided. Early placement of a peripherally
398
inserted central catheter (PICC) is helpful, as
these babies will need total parental nutrition.
The primary goal of omphalocele repair is to
return of the viscera to the abdominal cavity. The
secondary goal is to close the fascia and skin.
Two to four centimeter omphalocele defects may
be undergo a primary closure with a good surgi-
cal outcome.
On the other hand, larger omphaloceles will
require a staged repair. This entails the use of a
silo chimney or prosthesis [21]. The sac is
removed and a silo mesh (usually Silastic™ or
Teflon™) is sutured to fascia of the defect.
Then, the extra-abdominal organs are gradually
returned to the peritoneal cavity in approxi-
mately 3–10 days. After the herniated bowel is
reduced, the prosthesis is removed, and the
defect closed under anesthesia in the operating
room. For complex omphaloceles, a conserva-
tive non-operative delayed closure is suggested.
This procedure involves placement of a topical
a b
c d
Fig. 41.3  Complex large omphaloceles may be treated
conservatively with escharotic treatment with the initial
application of silversulfadiazine (a). This allows epitheli-
W. Nguyen and K. Belani
solution, such as silver sulfadiazine, directly to
the sac to promote neoepithelialization and then
eventual closure of the remaining ventral hernia
(Fig. 41.3) [7, 22].
Anesthetic Considerations
A thorough preoperative analysis is essential to
define the extent of involvement and compromise
due to associated defects. These babies may
already be intubated at birth due to respiratory
compromise from the lesion and/or pulmonary
hypoplasia. Babies not intubated will require
decompression of the stomach with a nasogastric
or orogastric tube. Following this, a rapid-­
sequence induction of anesthesia is accomplished
in babies with a normal upper airway. Cardiac
status will dictate the choice of anesthetic agents.
However, nitrous oxide is avoided to reduce
bowel distension.
alization and eschar formation (b, c). The baby then is
taken to the operating room for repair of a ventral hernia
after reducing contents of the omphalocele [11]
41  Omphalocele and Gastroschisis
For intraoperative monitoring, an arterial line
is helpful, but not necessary for closure.
Placement of a central line is recommended to
allow not only measuring central venous pressure
but also for biochemical monitoring. Patients
with Beckwith-Wiedemann syndrome require
attentive management of glucose. Maintenance
and/or total parenteral nutrition (TPN) may be
infused through the central line. A peripheral
intravenous (PIV) line is placed for administering
drugs and fluids. It is important to keep up with
insensible losses during the case with an iso-
osmotic solution at a rate of 8–15  mL/kg/h.
Maintaining normothermia is important and can
be challenging with large abdominal defects.
Another challenge in babies with large ompha-
loceles is the increase in intraabdominal pressure
during closure. With tight closures, there will be
pressure on the inferior vena cava, aorta, and dia-
phragm. This can result in detrimental increases in
intrathoracic pressure, intracranial pressure, and
diminished perfusion of splanchnic organs. The
severity of the ensuing changes can be gauged at
the bedside by evaluating intragastric and intra-
vesical pressure via an orogastric tube and urinary
catheter [12], increase in end-tidal CO2 and peak
airway pressures, and reductions in SPO2 (pulse
oximetry) [11]. Intragastric pressure more than
20 mmHg and central venous pressure (CVP) less
than 4 mmHg may be associated with decreased
venous return and cardiac index requiring surgi-
cal decompression [11, 23]. Otherwise, abdominal
compartment syndrome (ACS) can ensue causing
diminished perfusion to abdominal organs and
congestion in the brain due to increased intracra-
nial pressure by way of increased intrathoracic
pressure [11, 24].
Following closure of small omphaloceles and
without other major significant anomalies, the
babies can be extubated after surgery. For neonates
undergoing a gradual reduction after an uncompli-
cated primary closure, mechanical ventilation is
usually required for 24–48 h or longer. Thereafter,
respiratory compliance usually improves dramati-
cally [25]. Adjuncts to general anesthesia include
a caudal catheter and chloroprocaine infusion to
help facilitate extubation [26].
399
Post-operative Care and Outcomes
Postoperatively, respiratory status, signs of infec-
tion, inferior vena cava compression (blue lower
limbs, or bowel ischemia), abdominal pressures
are monitored. TPN may need to be continued for
weeks due to ileus [12]. Babies with complex
omphaloceles or GOC may require unusual levels
of PEEP, months or “even years of positive pres-
sure support via a tracheostomy” [15].
Most patients with small omphaloceles
recover well and do not present any long-term
issues. However, only a small percentage have a
truly isolated lesion [18]. Isolated lesions confer
to a 95–97% survival [27, 28]. Larger lesions
including GOC and those with liver involvement
have worse outcomes [29, 30]. For GOC, nonop-
erative delayed closure may confer to reduced
mortality compared to staged closure (21.8% ver-
sus 23.4%) [7].
Morbidity and mortality may also be related to
the side effects of intravenous alimentation (e.g.,
liver failure or sepsis). Complications related to
the initial surgical care such as bowel perforation,
and presence of malrotation, adhesions, obstruc-
tion will require additional procedures. If malro-
tation is not treated in a timely manner, midgut
volvulus could lead to short bowel syndrome [11].
In cases of omphaloceles with other anoma-
lies, survival and morbidity is often dependent on
the associated defects such as cardiac malfunc-
tion and intestinal atresia [12]. Compared to gas-
troschises, babies with omphaloceles have a
higher mortality (18% compared to 4%) [9].
Gastroschisis
Definition and Diagnosis
Gastroschisis is usually 2–5 cm in diameter and
almost always to the right of the umbilical cord.
The eviscerated bowel is often small and large
bowel. The liver is rarely present. The bowel con-
tents are exposed, without a covering membrane.
Cryptorchidism coexists when the testes exit
along with the bowel.
400
Although some institutions recommend planned
late preterm delivery to avoid ongoing in utero
inflammation, the increased risks associated with
preterm delivery must be weighed against the risk
for intrauterine fetal demise [31]. No consensus has
been reached and no concrete evidence supports
induced early delivery [11]. Interestingly, spontane-
ous preterm delivery at approximately 36.5 weeks
gestational age is more common in mothers whose
babies have gastroschisises than the general popula-
tion (28% versus 6%) [32]. This may be secondary
to the inflammatory stimulus [12].
There are different theories regarding the
pathogenesis of gastroschisis. Exposure to acet-
aminophen, aspirin, and pseudoephedrine in
utero has been associated with an increased inci-
dence [33, 34]. Smoking has also been implicated
[12]. One theory suggests that gastroschisis is
associated with an earlier embryologic event
related to abnormal development to the right
omphalomesenteric artery or right umbilical
vein, causing ischemia to the right paraumbilical
area [11]. Another theory postulates that they are
caused by an imbalance between cell prolifera-
tion and planned cell death (apoptosis) during the
critical embryonic development period [13].
Stevens et  al., hypothesized that gastroschisis
may be the result of failure of the yolk sac and
vitelline structures to be included into the body
stalk [35].
Similar to omphalocele, the prenatal diagnosis
of gastroschisis is made towards the end of first
trimester (Fig. 41.2), after the physiological clo-
sure of the abdominal wall around 10 weeks of
gestation. The discerning factor is whether a
membrane is present [12]. An elevated maternal
alpha fetoprotein level may be seen and is more
common in gastroschisis than omphalocele.
Babies with gastroschisis do not usually have
any associated syndromes, nor do they have any
genetic defects. Thus, fetal karyotyping is not
routine [36]. Babies with complex gastroschisis
usually have intestinal atresia (around 10% of
cases), stenosis, necrosis or volvulus [37, 38].
However, cardiac, renal, musculoskeletal, and
central nervous system anomalies can occur [39].
A recent study found that gastroschises had asso-
W. Nguyen and K. Belani
ciated anomalies 32% of time compared to 80%
of omphaloceles [10].
Treatment
Swift protection of extruded bowel is mandatory
at birth by means of sterile moist sponges and
sterile covering, such as a plastic bag. Babies
should be cared for in the right flank decubitus
position to limit ischemic injury [12]. Similar to
the treatment of omphaloceles, normothermia,
antibiotics, bowel decompression, monitoring
acid-base status, and obtaining reliable access are
important. Since the protruding small and large
intestines are without a covering membrane,
patients with gastroschisis can require even more
aggressive fluid management. Urine output needs
to be closely monitored.
Definitive cover, either primary or staged,
should be undertaken within the next 4–7 h [40,
41]. If the herniated loops are without matting
and peel, it is possible to perform the reduction at
the bedside [42], under mild sedation [40].
However, surgeons need to know when it is no
longer safe to perform a bedside reduction and
convert to a reduction in the operative room under
general anesthesia. If the loops are edematous
and covered by an inflammatory peel, primary
reduction may still be feasible under general
anesthesia [12]. On the other hand, if the herni-
ated loops are very edematous, covered by a thick
peel and/or tightly matted together, then a stage
reduction is indicated. The process is similar to
that of an omphalocele staged reduction. An
extracorporeal bag is sutured around the enlarged
defect, or inserted within the abdomen when
using a preformed spring-loaded silo, and hung
from the roof of the crib. The intestine is gradu-
ally returned to the abdomen via gentle pressure.
It is not necessary to keep the infant intubated
and/or sedated while the bag is in place and dur-
ing manual reduction [12]. Similar to omphalo-
celes, it usually takes approximately 7–10 days
for the loops to return the abdomen. Then, the
patient is brought to the operating room to remove
the bag and close the abdominal wall.
41  Omphalocele and Gastroschisis
Anesthetic Considerations
The anesthetic considerations for the closure of
gastroschisis are similar to that of omphaloceles.
As part of routine evaluation, these babies should
also be evaluated for additional anomalies.
Gastroschisis babies will require more fluid sec-
ondary to insensible losses. Monitoring for
intraabdominal hypertension during closure via
peak pressures, end tidal CO2, CVP, SPO2 and/or
bladder catheter is important in preventing
abdominal compartment syndrome.
Vane et al., described using a spinal anesthetic
in selected patients with gastroschisis as an effec-
tive sole anesthetic [43]. Raghavan et  al.,
described using neuraxial anesthesia as an
adjunct technique with general anesthesia of 22
neonates and noted a decreased need for postop-
erative ventilation requirement (23% vs. 88%
with general anesthesia only) [44].
Post-operative Care and Outcome
The post-operative course depends on the sever-
ity of intestinal damage, co-existing stenosis,
atretic segments of small intestines, and the
occurrence of complications such as bowel perfo-
ration or volvulus [11, 27, 38]. With simple cases,
the more common scenario, primary reduction
occurs in 70% of cases with quicker start of gas-
tric feeding and achievement of full feeds, lower
complication rate, and shorter hospital stay.
Survival is greater than 95% if patients are treated
in pediatric centers [45]. In complex cases with
atresias, stenosis, perforations, and/or volvulus,
all parameters are worse, including mortality
[27]. They often require multiple operations and
prolonged parenteral nutrition [12]. In these situ-
ations, survival decreases to 70% [27, 46].
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