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How toManage Common Pediatric
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Surgical Conditions: Infant
Emergencies, Hernias, Congenital
Malformations inLowandMiddle-Income Countries
RieSeu andVincentDuron
It is easier to build strong children than to repair broken men.
– Frederick Douglass
42
Abbreviations
AFP Alpha-fetoprotein
ARM Anorectal malformation
BA Biliary atresia
BWS Beckwith-Wiedemann syndrome
CDH Congenial diaphragmatic hernia
EA Esophageal atresia
GER Gastroesophageal reux
HD Hirschsprung’s disease
HIC High-income country
LHR Lung-to-head ratio
LMIC Low- and middle-income country
NICU Neonatal intensive care unit
PN Parenteral nutrition
PPV Patent processus vaginalis
PS Pyloric stenosis
TEF Tracheoesophageal stula
TFLV Fetal lung volume measurement
R. Seu (*)
Albert Einstein College of Medicine,
Bronx, NY, USA
e-mail: rie.seu@einsteinmed.edu
V. Duron
Columbia University Vagelos College of Physician &
Surgeons, NYP-Morgan Stanley Children’s Hospital,
New York, NY, USA
e-mail: vd2312@cumc.columbia.edu
TPN Total parenteral nutrition
WHO World Health Organization
Introduction: Pediatric Surgical
Problems inGlobal Context
This text is not meant to be an exhaustive review
of pediatric surgery or even pediatric surgery in
developing countries. Rather, this chapter highlights several pediatric surgical conditions that
the health practitioner caring for infants and children in a developing country should be able to
recognize and diagnose. The chapter offers guidance to determine, depending on the skills and
resources available, which conditions may be
treated at the receiving facility and which need to
be transferred to a higher level of care.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. A. Hardy, B. R. Hochman (eds.), Global Surgery,
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R. Seu and V. Duron
Stomach andSmall Intestine
Pyloric Stenosis
Epidemiology
The prevalence of pyloric stenosis (PS) is 2 to 4
per 1000 live births [1]. The prevalence varies
depending on the region, in which those of
Caucasian descent have a higher prevalence of
PS than Asian and Black populations [1]. The
male-to-female ratio is 4:1 [2]. A study has also
shown that PS is more common in less urban
areas [2].
Etiology andPathophysiology
The cause of the development of PS is unknown.
It is thought that it is a combination of both
genetic and environmental factors. With a hypertrophied pylorus, the gastric outlet is mechanically obstructed.
Due to excessive vomiting, there will be loss
of gastric contents, leading to dehydration. As a
result, the renin-angiotensin-aldosterone system
(RAAS) will be activated. Aldosterone will stimulate the excretion of potassium and absorption
of sodium. As potassium depletion worsens,
sodium is resorbed in exchange for hydrogen
ions, creating a paradoxical aciduria. This leads
to hypochloremic hypokalemic metabolic alkalo-
sis. Diagnostic delay can lead to hypoglycemia
and hypoalbuminemia [1].
2weeks and 3months (median is 6weeks) with
projectile, nonbilious emesis after feeds [5]. The
emesis resembles the feeds and should not be yellow/green, as the hypertrophied pylorus prevents
bile reux [4]. There may also be signs of dehydration and weight loss [4]. The infant may also
display signs of jaundice. Hyperbilirubinemia
occurs due to hepatic glucuronyl transferase
activity deciency from decreased PO intake [4].
Upon physical exam, one may be able to feel
an olive-shaped mass in the right upper quadrant
of the abdomen when the abdominal wall is completely relaxed [4]. If abdominal US is available,
repeat palpation to feel the olive should be
avoided, since it will only increase the irritation
of an infant who is already fussy.
Management
If PS is suspected, an upper abdominal ultrasound is the image modality of choice. In the longitudinal view, muscle thickness greater than
3mm and channel length greater than 15mm is
highly specic and sensitive for PS.In the transverse view, a target sign is seen [4] (Fig.42.1). If
US is not available, then transfer to higher level
of care is advisable. If that is not possible, and an
olive-shaped mass is palpated with the right clinical history, then surgical intervention should be
considered.
Risk Factors
Several risk factors have been associated with PS
development. Maternal alcohol use and cigarette
smoking are thought to be associated with PS [3].
Furthermore, prenatal and postnatal exposure to
medications such as erythromycin has been associated with increased incidence of PS [4]. Other
perinatal risk factors include being rstborn, prematurity, undergoing a cesarian delivery, young
maternal age (less than 20years old), and bottlefeeding [5]. Breastfeeding has been shown to be
a protective factor [1].
Clinical Manifestations
Infants with PS are usually term infants who are
otherwise healthy. They usually show up between
Fig. 42.1 Ultrasound images demonstrating pyloric stenosis. (https://med.emory.edu/departments/emergency-
medicine/_images/ultrasound/image- week/
channel- length.jpg)
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Serum electrolytes should be measured prior
to surgery, as electrolyte derangements are
common with prolonged vomiting. Intravascular
access should be promptly established.
Preoperatively, electrolyte derangements and
uid depletion should be addressed. If the electrolyte disturbance is mild, it can be corrected
with 0.45% normal saline (NS) with 5% dextrose (D5) solution. If there are severe disturbances, then 0.9% NS bolus of 10–20mL/kg,
followed with 0.9% NS with D5, should be
used. Electrolyte disturbances, specically
severe hypochloremia and metabolic alkalosis,
need to be corrected prior to surgery. For standard uid management, 120 mL/kg using
0.45% NS and D5 with 10 mmol potassium
chloride of 500 mL is advised only after the
patient has urine output. If dehydration is
severe, uids can be increased to 150 mL/kg
per 24h [1]. Feeds should also be stopped when
diagnosis is made. A nasogastric or orogastric
tube can be used to empty gastric contents if
there is persistent vomiting [4].
When the patient is stabilized and electrolyte
levels are corrected, the infant can undergo surgical correction. A pyloromyotomy can be performed open, through a right upper quadrant or
periumbilical incision, or laparascopically [4].
The steps elaborated here will be for the open
approach [1] (Fig.42.2):
1. A transverse incision is made in the right
upper quadrant over the rectus muscle, 1 ngerbreadth below the costal margin.
2. The peritoneum is entered, and the omentum
is brought into the wound to lift the transverse
colon and identify the antrum of the stomach.
The lower third of the stomach is elevated and
mobilized to deliver the pylorus to through the
incision.
3. At the mid-anterior surface of the pylorus, a
longitudinal incision is made through the
serosa and supercial muscularis. The incision is started 1–2mm from the pyloroduodenal junction, marked by the vein of Mayo
proximally to 0.5 cm into the lower antrum
muscle layer.
4. Using a clamp or pyloric spreader, blunt dissection is performed to divide the rm bers.
Relief of obstruction is demonstrated by an
upward protrusion of the gastric mucosa. Care
is taken not to deepen the incision and injure
the underlying mucosa.
Postoperatively, feeds can be started 3h after
returning from the recovery room. Maintenance
uids can also be continued postoperatively until
the patient tolerates a diet [4].
Possible immediate surgical complications are
mucosal perforation most frequently at the duodenal end. In this case, bilious uid would be
seen. This can be repaired using interrupted ne
absorbable sutures. Other complications include
bleeding, infection, and wound dehiscence [1].
Incomplete pyloromyotomy may occur if it is not
of adequate length, most often because of a failure to extend the cut onto the stomach.
Fig. 42.2 Pyloromyotomy for hypertrophic pyloric stenosis. The thickened pyloric musculature has been cut and
then spread apart to reveal the underlying mucosa. Source:
Sabiston Textbook of Surgery, 17th Ed. Warren BW Chap.
70 p.2108, Fig70–8 (Elsevier)
Neonatal Bowel Obstruction
Epidemiology
Neonatal intestinal obstructions arise from a variety of congenital anomalies of the gastrointestinal (GI) tract. More than 1 in 4000 births are
affected by an obstruction of the duodenum, jejunum, ileum, and colon. Congenital atresia or stenosis of the duodenum is the most common
intestinal atresia, which occurs in 1 in 5000–
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Proximal
duodenum
Distal atretic
bowel
Proximal
duodenum
Distal atretic
bowel
Proximal
duodenum
R. Seu and V. Duron
Atresia
Distal atretic
bowel
Fig. 42.3 Schematic of different types of duodenal atresia. Type 1, membrane or web causing duodenal obstruction; type 2, complete obliteration of duodenal segment
with proximal and distal segments attached by brous
10,000 live births [6]. Intestinal malrotation
occurs in 1in 6000 live births, although the true
incidence is expected to be as high as 1% of the
population [7].
Pathophysiology
Duodenal atresia is thought to occur because of
failure of recanalization normally occurring by
vacuolization of the duodenal lumen (Fig.42.3)
[8]. This mechanism differs from that which is
thought to cause other types of intestinal atresias,
which are thought to result from a vascular accident later on during gestation [9]. Intestinal rotation and xation occur from the fth to 12th
weeks of gestation. During this time, the midgut
naturally herniates through the umbilical ring as
there is rapid intestinal growth. Any disruption of
the steps of rotation and xation will lead to rotational abnormalities or malrotation [10].
Risk Factors
The incidence of duodenal atresia is similar in
males and females [11, 12]. Duodenal atresia is
associated with other congenital anomalies in
about half of patients, which include cardiac malformations, other intestinal atresias, biliary atresia, malrotation, gastroschisis, Hirschsprung’s
disease, anorectal malformations, renal defects,
vertebral defects, and polysplenia. Duodenal atresia is associated with chromosomal and genetic
cord; type 3, complete separation of proximal duodenum
from distal duodenal segment (Reprint with permission,
Artwork by Linda Li, MD, 2020)
syndromes. Approximately a third of patients
with duodenal atresia have trisomy 21 [13–16].
In terms of jejunoileal atresias, one third of
patients are premature. Maternal cigarette smoking and the use of vasoconstrictive medications in
the rst trimester of pregnancy have been shown
to increase the risk of small bowel atresia [17].
Other congenital anomalies are seen in less than
10% of patients with jejunoileal atresia. Most
common associations are gastroschisis, malrotation, and cystic brosis [18, 19].
Clinical Manifestations
In newborn infants, four signs raise the suspicion
for and guide diagnosis and management of
intestinal obstructions: [20].
1. Maternal polyhydramnios on prenatal ultra-
sound imaging.
2. Bilious vomiting, indicative of a proximal
obstruction.
3. Failure to pass meconium in the rst 48h of
life.
4. Abdominal distension, concerning for lower
tract obstruction.
The presence of bilious vomiting in a newborn
is a pathologic process and should raise the suspicion for malrotation with midgut volvulus until
proven otherwise. Bilious vomiting occurs in
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infants when the obstruction is distal to the
ampulla of Vater. A proximal obstruction will not
usually be accompanied by abdominal distension
(e.g., duodenal atresia, midgut volvulus). A more
distal obstruction (e.g., ileal atresia, anorectal
malformation) will usually be accompanied by
abdominal distension.
The rst step to diagnosis is a complete history and physical exam, including a prenatal history and any abnormal ultrasound ndings if
there was prenatal care. While 98% of women
receive prenatal care and 94% give birth under
the care of a skilled healthcare practitioner, the
WHO estimates that less than 65% of women in
LMICs do not receive adequate prenatal care [21,
22]. As such, there is a signicant chance that a
diagnosis of newborn intestinal obstruction will
be made after birth in developing countries.
Management of these patients is as follows: (1)
insertion of a nasogastric tube for decompression;
(2) intravenous access to replenish GI losses and to
hydrate for at least several days, most likely sev-
Fig. 42.4 Abdominal radiograph of neonate with double
bubble sign with paucity of distal air, consistent with duodenal atresia
eral weeks; and (3) parenteral nutrition, if available within 3days if the infant is not feeding, and
should include protein (many healthcare centers in
LMICs will not have access to peripheral nutrition
(PN), so crystalloid uid will be administered).
Chest and abdominal x-rays should be
obtained. If there is concern for malrotation, then
an upper gastrointestinal intestinal contrast study
should be obtained. In an infant with bilious
vomiting and signs of distress – tense, red, or
shiny abdomen, poor peripheral perfusion, lethargy, hemodynamic instability, electrolyte abnormalities– then an urgent exploratory laparotomy
needs to be performed. In centers without access
to radiologic studies or a pediatric surgeon, the
patient should be stabilized and transferred to a
higher level of care.
Infants with duodenal atresia will often also
present with bilious vomiting. An abdominal
x-ray will reveal a pathognomonic double bubble
completed. Until then, gastric decompression and
IV uid support are required.
Jejunal and ileal atresia may be suspected on
abdominal x-rays with dilated proximal loops of
bowel and no distal air. A retrograde contrast
enema will identify a microcolon which occurs
from lack of passage of amniotic uid during
fetal life. As with duodenal atresia, repair may be
planned after the patient has been rehydrated and
prepared for surgery.
Short bowel syndrome may result from intestinal atresia if a there is insufcient length or inappropriate function of the small intestine. This is a
chronic condition that may require long-term PN
and specialized care for electrolyte, uid, and
bowel management. This condition is very difcult to treat in LMICs if resources are not available. Early transfer to centers with PN availability
is necessary.
sign, delineating a dilated stomach and a dilated
duodenum, most often without distal gas
(Fig.42.4). Unlike the management required of
malrotation with midgut volvulus, duodenal atresia repair is not emergent and can be delayed
until workup for associated anomalies has been
Management
Surgical repair of duodenal atresia is most often
accomplished through a right upper quadrant
incision. An exploration of the abdomen to examine organs and rotation of the intestines is rst
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performed. The duodenum is mobilized using a
Kocher maneuver. The anastomosis is classically
performed with a diamond-shaped duodenoduodenostomy in which the proximal segment is
opened through a transverse incision and the distal end through a longitudinal incision to connect
the two ends in a diamond-shaped conguration.
This is thought to maximize the lumen of the
duodenum at the level of the anastomosis
(Fig. 42.5). When this technique is difcult
because of patient anatomy and in small or premature infants, a duodenojejunostomy is a good
option. Prior to performing the anastomosis, a
small-caliber Foley catheter should be passed
proximally into the stomach and distally into the
jejunum and pulled back with the balloon inated,
to ensure that there is no windsock deformity or
additional web. A web may be resected or may be
bypassed.
The classic procedure for malrotation with
midgut volvulus is a Ladd procedure. The steps
of a Ladd procedure are reproducible and include:
1. Evisceration of the bowel.
2. Counterclockwise detorsion of bowel until no
longer torsed.
3. Division of Ladd’s bands.
4. Broadening of the small bowel mesentery.
5. Appendectomy.
6. Placement of small bowel along the right abdomen and large colon along the left abdomen.
During the Ladd’s procedure, particularly if
there is presence of midgut volvulus, temporary
abdominal closure may be necessary if the abdomen is not able to be safely closed or if there is
doubt about the viability of the remaining bowel.
A temporary mesh may be sewed or a silo placed.
A second look laparotomy within 24–48 h will
allow the bowel to reperfuse, thus minimizing the
length of resected bowel.
Biliary Atresia
Clinical Manifestations
The newborn will present to the healthcare facility
with jaundice, acholic stools, dark urine, and hepatomegaly. If the condition continues for a few
months, the infant may present with weight loss,
irritability, and worsened jaundice. If presenting
late, the infant will most likely have developed
splenomegaly due to portal hypertension, ascites,
and hemorrhage due to impaired vitamin K absorption. If biliary atresia (BA) is not treated, it will
lead to cirrhosis and death [23].
Fig. 42.5 Representation of diamond anastomosis technique (Reprint with permission, Artwork by Linda Li,
MD, 2020)
Management
If an infant presents with jaundice for 2weeks or
more, they should be evaluated for biliary atresia.
An evaluation can be done rst via serologic
tests, imaging, and biopsy. Liver function tests
will show conjugated hyperbilirubinemia as well
as elevated alkaline phosphatase and gammaglutamyl transpeptidase [1]. An ultrasound can
be done to differentiate different causes of infant
cholestasis. After an infant fasts for 12 h, an
infant with BA would show shrunken gallbladder, hyperechogenic liver hilum, or a cyst at the
liver hilum and no bile duct dilation. A cholangiogram can also be done to assess the patency of
the biliary tree. A percutaneous liver biopsy will
show bile plugs, ductular proliferation, portal
edema, and brosis [23].
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Once diagnosis is made, treatment of BA is a
Kasai hepatoportoenterostomy procedure. The
failure to obtain bile drainage or the development
of cirrhosis-related complications would be an
indication of liver transplantation. Prior to the
Kasai operation, the infant should be optimized
with normal preoperative care, vitamin K provision several days prior to surgery, and monitoring
of coagulation factors [1]. The Kasai procedure is
a technically challenging procedure that should
be performed by a surgeon who has experience
performing this surgery, in a hospital that has the
resources to care for this complex patient.
Transfer to this type of setting should be done
early during the diagnostic phase to optimize the
patient’s outcome.
Hernias
Inguinal Hernia
Epidemiology
The global incidence of inguinal hernias in children less than 18years old ranges from 0.8 to 4%
[24]. The most common type of inguinal hernia is
on the right side (60%), although left-sided (25%)
and bilateral hernias (15%) are found [25].
Indirect inguinal hernias make up more than 95%
of inguinal hernias [25]. In infants and young
children, incarceration of an unrepaired inguinal
hernia could be as high as 31%, which could pose
intestinal and testicular complications [26].
Pathophysiology
During fetal development, the testicle descends via
the inguinal canal into the scrotum via the processus
vaginalis, a sac-like protrusion of the peritoneum.
Most of the time, this obliterates into a brous cord.
If the processus vaginalis does not obliterate, it is
called a patent processus vaginalis (PPV). This creates a canal for uid or abdominal contents to pass.
If only uid passes, it is called a communicating
hydrocele. If intestine, omentum, ovaries (in
females), or other abdominal contents pass, it is an
indirect inguinal hernia. It can be conned to either
the inguinal region or in the scrotum. The cause of
this is not completely understood [27].
Direct inguinal and femoral hernias are
uncommon in young children. Direct inguinal
hernias form medial to the inferior epigastric vessels in Hasselbach’s triangle, due to weakness in
the oor of the inguinal canal or after surgical
repair of indirect inguinal hernias [1]. Femoral
hernias form medial to the femoral vessels and
are below the inguinal ligament [28].
Risk Factors
Inguinal hernias are more common in premature
infants: a third of premature infants weighing less
than 1000 g are predicted to develop a hernia
[29]. Boys are six times more likely than girls to
have inguinal hernias [27]. Other risk factors
include family history of inguinal hernias, hypospadias, epispadias, exstrophy of bladder, and
ambiguous genitalia [1].
Clinical Manifestations
Inguinal hernias can be apparent from the time of
birth. They usually appear as an intermittent,
painless bulge along the inguinal canal, in the
scrotum, or in the labia [1]. An inguinal hernia
may spontaneously reduce or be reduced manually. It may appear in situations of increased
abdominal pressure, such as when the child is
crying, coughing, or walking [ 1]. Upon physical
exam, the physician can palpate the processus
vaginalis over the pubic tubercle; a thick cord
structure (silk glove sign) can signal the presence
of a hernia sac [30].
Complicated inguinal hernias occur when
hernia contents are not reducible. Symptoms
can include tenderness and rmness of the
bulge, vomiting, and refusal of feeds [29]. The
hernia contents may be incarcerated, in which
the mass is not tender [1]. An incarcerated hernia needs to be reduced and, if unable to be
manually reduced, then needs to be surgically
reduced and repaired. Incarcerated hernias can
become strangulated or obstructed [1]. In the
case of strangulation, the blood supply to the
hernia contents is compromised, leading to
infarction if not repaired. The child may have
erythema at the site of the bulge, tachycardia,
hypotension, and peritonitis [31]. This is a surgical emergency.
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Management
Surgical herniotomy under general anesthesia
within 2weeks of diagnosis is advised for inguinal hernias, due to its possible complications
such as incarceration, strangulation, and obstruction [29].
There are various methods to approach a herniotomy. The high ligation technique is most
commonly performed in children. It is described
below: [32].
1. An incision is made at the groin just superior
and lateral to the pubis. The external oblique
aponeurosis and external ring are exposed and
incised in the direction of the muscle bers.
2. The indirect hernia sac is identied and dis-
sected; the cord structures are separated from
the hernia sac, paying close attention not to
injure the vas deferens, testicular artery, and
testicular vein. Usually, the hernia sac is
retracted anteromedially as this is its habitual
anatomic location.
3. The hernia sac is opened, and the abdominal
contents are reduced.
4. The sac is suture ligated at the preperitoneal
level and transected distal to ties.
5. Hemostasis is ensured, and the external
oblique aponeurosis is closed.
6. Scarpa’s layer and the skin are closed, and a
dressing is applied.
Complicated inguinal hernias are a surgical
emergency. In addition to obstruction and strangulation, it can lead to bowel gangrene and perforation, peritonitis, septicemia, and
intra-abdominal abscess formation [1].
Furthermore, there are concerns for not only the
incarcerated bowel but also testicular vessels that
are compressed in the hernia sac. If the child does
not have signs of strangulation and if 24h have
not elapsed since the onset of symptoms, a manual hernia reduction can be attempted. If available, sedation and analgesia can be given to
facilitate the reduction. While having the patient
in as much Trendelenburg position as tolerated,
the non-dominant hand should pull the hernia to
make elongate it and make it more narrow. The
dominant hand should gently compress the con-
tents of the hernia in the direction of the inguinal
canal to massage them into the abdominal cavity
[31]. If manual reduction is not possible, surgical
intervention is necessary.
Umbilical Hernia
Epidemiology andRisk Factors
The global incidence is 10–25%, although it
seems to be more common in African countries
for currently unknown reasons [33]. Umbilical
hernias are more common in low-birth-weight
and premature infants. There is also an increased
risk of an umbilical hernia in children with Down
and Beckwith-Wiedemann syndromes [1].
Pathophysiology
Umbilical hernias form due to the incomplete
closure of the umbilical ring, where the umbilical
vessels pass, during the rst few weeks of infancy
[30]. The full-thickness protrusion can include
peritoneal uid, preperitoneal fat, intestine, or
omentum [1]. Small defects that are less than
1cm are more likely to close, than larger defects
that are greater than 2cm [1].
Clinical Manifestations
Umbilical hernias manifest as a palpable protrusion at the umbilicus, which are reducible. They
can be asymptomatic or tender upon pressure and
palpation. Most umbilical hernias close by the
second or third year of life, especially when
small, although it can take until their teenage
years.
strangulation, and rupture of umbilical hernias,
although rare, about 1% [1]. The physical exam is
essential to detect cases of these complications.
Children will experience localized tenderness or
pain, erythema of the skin or increased sensitivity
at the umbilicus, and/or wound drainage [34].
Management
Non-operative management is advised during the
rst 4 years of life, especially if the defect is
small and asymptomatic. In contrast, surgical
repair is recommended for large hernias that
Complications of concern are incarceration,
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become larger, for those that do not close by
4years of age, and hernias with signicant proboscoid components [1].
Treatment is advised if the child experiences
signs or symptoms of incarceration or strangulation. If the defect is less than 0.5cm, strangulation is less likely. However, studies have shown
that both medium- and large-sized defects may
be associated with incarceration and strangulation, although, again, the risk of this is low [35].
An open hernia repair under general anesthesia
is advised, with an infraumbilical incision. The
surgeon should remove the hernia sac, sew together
the tissue along the muscle edge, and resecure the
umbilicus to the underlying fascia. For complicated umbilical hernias or large defects, a mesh
could be used to lessen the tension of the fascia
and prevent the development of abdominal compartment syndrome. Although rare, patients can
experience postoperative pain, seroma, hematoma,
infection, and recurrence [36].
It is uncertain when surgery should be advised
in LMICs. Earlier surgical treatment may also be
considered for large hernias, as they are more
likely to incarcerate and least likely to spontaneously close. Patients living more than 1h away
from surgical availability should also be considered for repair [1].
Abdominal Wall Defects
Gastroschisis
cases, in particular gastrointestinal anomalies
such as atresia [42].
Pathophysiology
The pathophysiology is not completely understood but is suspected to be due to a malformation during ventral wall closure in the embryonic
period, possibly from an ischemic event, which
leads to the herniation of bowel [42]. There may
also be a gene-environment interaction, in which
polymorphism and maternal smoking increase
the risk for gastroschisis development in the
fetus.
Clinical Manifestations
Gastroschisis is a ventral body wall defect, in
which the intestines are freely oating in the
amniotic uid, without an amnion covering [42].
The fascial defect is usually at the right of the
umbilicus. It is identied prenatally via ultrasound, most commonly during the second trimester [43] (Fig. 42.6). If laboratory tests are
available, gastroschisis would show elevated
maternal serum alpha fetoprotein when performed between 15 and 20weeks’ gestation [43].
Gastroschisis can be simple or complex.
Complex gastroschisis describes a gastroschisis
that is accompanied by intestinal complications,
such as bowel atresia, stenosis, volvulus, perforation, or ischemia. These compounding factors
can lead to greater morbidity and mortality of the
infant. This occurs in 11–28% of gastroschisis
cases [43].
Epidemiology
The prevalence of gastroschisis ranges from 2.9
to 6.5 per 1000 infants [37]. It is more prevalent
in the fetuses of younger mothers, particularly
those less than 20years old [37]. In HICs, survival rate exceeds 90%, due to improvements in
neonatal care and nutrition [38, 39]. Nevertheless,
in LMICs, mortality varies depending on the
availability of NICU facilities and total parenteral nutrition (TPN) [40]. Some areas, such as in
Zimbabwe and Uganda, report a mortality rate of
more than 80% [41]. Gastroschisis is usually an
isolated defect, although it has been associated
with defects of other organ systems in 16–35% of
Fig. 42.6 Prenatal ultrasound image of gastroschisis
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R. Seu and V. Duron
Management
If gastroschisis is diagnosed during prenatal care,
it is recommended that the mother receives serial
growth ultrasounds, due to the risk of intrauterine
growth restriction, as well as twice-weekly antepartum fetal heart rate testing starting at
32–34 weeks [43]. It is important that delivery
occurs in a tertiary pediatric surgery center, for
surgical management post-delivery. Recent studies are attempting to determine the optimal time
for delivery. A cost-effective analytical study
showed that 38weeks may balance the risks of
respiratory distress syndrome and stillbirth [44].
It is recommended for the mother to undergo a
vaginal delivery, unless indicated otherwise [43].
When the baby is born, uid resuscitation and
minimization of insensible losses are the priority.
The patient must have large-bore IVs placed and
be started on crystalloid uid. The intestines
must be placed in a bowel bag to prevent uid
loss from the exposed GI tract. A plastic bag may
be placed over the lower half of the newborn. An
NG tube will be placed. Surgical closure or silo
placement may then be performed.
Surgical Management is Necessary The two
most common methods are primary closure under
general anesthesia or silo placement for several
days followed by closure with or without a general anesthetic [1].
• Primary closure: the defect is slightly
enlarged, and the abdomen is rst explored
to exclude other gastrointestinal anomalies.
The bowel is then reduced into the abdomen.
The fascial and skin layers are closed
separately.
• Silo closure: A silo is used to encase the
exposed bowel contents. If a silo is not
available, IV solution bags or blood bags
can be fashioned into silos. The infant
should be in an incubator in supine posi-
tion, with the silo hanging from the roof of
the incubator. The bowel is gradually
reduced into the abdominal cavity over sev-
eral days, preferentially less in less than
7 days. The wound can be closed using a
sutureless technique in which the preserved
umbilical cord is used to cover the defect
and covered by non-adherent dressing
(Fig.42.7). The advantage of this technique
is that it may be performed at the bedside
without anesthesia. Surgical closure may
also be performed.
a
def
Fig. 42.7 Silo placement and sutureless closure of gastroschisis: (https://media.springernature.com/full/springer-
static/image/art%3A10.1038%2Fs41372- 019- 0321- 1/MediaObjects/41372_2019_321_Fig1_HTML.jpg)
b c
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