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Chapter7: Bowel Obstruction 37
https://t.me/med1917
Glucose replacement
Blood glucose levels should be monitored during resuscitation and glucose solution (10% dextrose) should be
given as well as Hartmann’s solution. Lack of glucose
exacerbates acidosis and may cause fitting.
Correction of acidosis
Acid-base measurement is an important part of neonatal
resuscitation. Correction of hypothermia, fluid and
glucose replacement will help to correct any acidosis.
Sodium bicarbonate given intravenously may some-
times be necessary.
Hypothermia
Hypothermia is a major risk to sick neonates. An
overhead heater with monitoring of the neonate’s temperature is used during all procedures. X-ray imaging is
another time of risk for hypothermia. Much of the
expertise involved in neonatal transport services is
directed towards preventing hypothermia during
transfer to the neonatal surgical centre.
Sepsis
There is a risk of sepsis with neonatal bowel obstruction
and intravenous antibiotics are commenced after cultures are taken.
Hirschsprung disease
In 1887, Hirschsprung described two infants who died
with gross abdominal distension due to a severely
dilated colon containing masses of faeces. Hirschsprung
assumed that the disease was caused by the megacolon.
However, the disease was later shown to be in the
narrow distal bowel where there is a lack of ganglion
cells (the intrinsic nerves of the gut) in the submucosal
and myenteric plexes. In addition, thickened abnormal
(extrinsic) cholinergic nerve fibres are found in the
affected segment. The affected gut is in a constant state
of spasm and will not relax, causing functional obstruction (and secondary ‘megacolon’ is not treated).
Hirschsprung disease occurs in 1:5000 births, and
there are different sub-types:
1 A larger group (≈80%), in which males are affected
five times as often as females, with a relatively short
aganglionic segment, usually involving the sigmoid
colon and rectum.
2 A smaller group with a long aganglionic segment,
equally common in boys and girls, with a higher
degree of ‘penetrance’ and more likely to affect
subsequent siblings.
3 Specific genetic abnormalities (e.g. GDNF-ret oncogene;
endothelin B receptor system) are being described in
Hirschsprung disease and it is likely these genetic
markers will become increasingly important in the
understanding of the basis of this disease.
The affected segment begins above the anal canal and
extends proximally for a variable distance – in most
cases as far as the sigmoid colon but sometimes as high
as the ascending colon. In a few cases, the affected
segment extends into the small bowel, and in rare
instances, the entire alimentary canal is devoid of ganglia, excluding hope of survival.
The most common presentation is with complete
bowel obstruction in the early neonatal period. In some
cases, the infant may present at a few months of age
with a history of chronic constipation and failure to
thrive. Paradoxically, some of these late-presenting
cases have long-segment disease.
The three classic signs are (1) delayed passage of
meconium (i.e. beyond 24 h after birth), (2) bile-stained
vomitus and (3) abdominal distension.
Clinical features
Abdominal examination will reveal marked gaseous
distension. Rectal stimulation with a probe may cause
explosive decompression of meconium and faeces through
the tight anal sphincters. A nasogastric tube will drain
bile-stained fluid.
Investigation
A plain abdominal x-ray usually shows marked gaseous
distension of the gut, often with air-fluid levels. A contrast enema will show constriction of the segment of
bowel affected by Hirschsprung disease, expanding
through a transition zone to a distended megacolon
above the functional blockage of the affected segment.
The diagnosis is made by suction rectal biopsy. The
biopsy is processed to examine for the absence of ganglion cells by standard microscopy, and histochemical
preparations are made for acetylcholinesterase staining of
the overgrown extrinsic cholinergic submucosal nerve
fibres. The diagnosis of Hirschsprung disease requires
sophisticated paediatric pathological services.
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Figure 7.1 Hirschsprung disease transition zone between dilated
proximal colon and narrow distal bowel as seen on contrast enema.
mechanical obstruction of the bowel called meconium
ileus. In Western countries, cystic fibrosis is the usual
underlying cause, and this may be confirmed by genetic
tests or by finding high sodium chloride levels in a sweat
specimen. Occasionally, meconium ileus occurs as an
isolated event and there is no underlying disease.
The sticky meconium impacts as a putty-like substance in the terminal ileum, leading to a small, disused
colon distal to the obstruction (known as ‘microcolon’).
The bowel proximal to the obstructed ileum is distended
with sticky meconium.
Clinical findings
The baby presents with abdominal distension, bilestained vomiting and failure to pass meconium. There
may be a family history of cystic fibrosis. The loops of
distended gut may be palpable as they are already filled
with meconium, rather than the gaseous distension
seen in other forms of bowel obstruction. Rectal examination reveals no normal meconium, but pale, mucoid
pellets may be passed.
Treatment
The bowel is decompressed daily with saline enemas.
Although an initial colostomy or ileostomy is sometimes
required in more complex cases.
A pull-through operation is performed at a later date
when the baby is thriving. The operation delivers the
aganglionic rectum and colon out through the anus.
The aganglionic segment is excised and normal gut is
anastomosed to the anal canal. Laparoscopy for intraoperative biopsy is useful [Fig.7.1].
Prognosis
The operation for Hirschsprung disease is life-saving, but
there may be prolonged morbidity in some cases.
Hirschsprung-associated enterocolitis, either before or
after the operation, may be life-threatening, with the
outpouring of fluid stools causing rapid, severe electrolyte
problems along with sepsis. Bowel dysfunction, with
diarrhoea and soiling, may be a long-term problem.
Meconium Ileus
Cystic fibrosis causes a change in the physical properties
of the meconium that fills the fetal gut. The meconium
becomes excessively sticky and tenacious, leading to a
Imaging studies
Plain abdominal x-rays show distended loops of gut
filled with a foamy substance. On the erect film (which
is done rarely in a neonate) there may be no air-fluid
levels as the meconium is too viscous to layer out with
gravity. A lower gastrointestinal contrast study will
show a microcolon with pellets in the terminal ileum
[Fig.7.2]. Contrast may then pass into the dilated small
bowel proximal to the obstructed ileum.
Treatment
Treatment is based on the assumption that the neonate
has cystic fibrosis. Antibiotics are commenced at once,
and dehydration, which would make secretions even
more tenacious, must be prevented.
Sometimes the obstructing meconium may be
encouraged to evacuate following a water-soluble contrast enema under fluoroscopy. If this non-invasive
method fails, laparotomy is performed and a temporary
ileostomy is often performed to allow subsequent bowel
washouts to clear the meconium. The prognosis for
meconium ileus depends on the underlying cystic
fibrosis. Occasionally there is recurrent bowel obstruction due to faecal impaction in the terminal ileum in
older children and adolescents. This is known as ‘distal
intestinal obstruction syndrome’.
Chapter7: Bowel Obstruction 39
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abdomen is soft and non-distended. The diagnosis should
be suspected at this stage and confirmed with an urgent
upper gastrointestinal contrast study. Abdominal distension with tenderness and passage of blood per rectum are
late features and indicate major gut ischaemia.
Investigations
An upper gastrointestinal contrast study will demonstrate
the abnormal position of the duodeno-jejunal junction
and the contrast may spiral through the twisted gut
[Fig.7.3]. Investigation is urgent but must not be allowed
to delay the definitive surgical treatment.
Treatment
Laparotomy is urgently required, as ischaemia may lead
to gangrene of the midgut (duodenum to the right
colon). The volvulus is untwisted, often requiring
two or three full rotations to release the caecum. The
malrotation of the gut is then corrected by Ladd’s
operation. The narrow base of the mesentery is broadened by dissection that separates the caecum from the
Figure 7.2 ‘Microcolon’. The unexpanded but otherwise normal
bowel distal to any complete intestinal obstruction in utero.
Volvulus neonatorum
The normal mesentery of the small bowel has a wide
base between the duodeno-jejunal flexure just to the
left of the midline in the epigastrium and the ileo-caecal
junction in the right iliac fossa. In the case of malrotation of the midgut, the duodeno-jejunal junction and
the ileo-caecal junction lie side by side. There is a very
narrow base to the small bowel mesentery, allowing
the gut to twist around the superior mesenteric vessels
(i.e. malrotation with volvulus).
A 360° twist may cause venous and lymphatic engor
gement with bile-stained vomiting. An emergency laparotomy at this stage should have a good outcome. A 720°
twist will cause arterial ischaemia of the gut from the
duodenum to the mid transverse colon, with the potential
for a significant increase in morbidity and mortality.
Clinical features
The typical case is a healthy full-term baby who is well for
the first few days of life but then develops feeding difficulties with bile-stained vomiting. At this early stage, the
-
Figure 7.3 Volvulus neonatorum. Upper gastrointestinal
contrast study shows a spiral twist of the bowel below the
mid-duodenum.
40 Part II: Neonatal Emergencies
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duodenum by dividing abnormal peritoneal adhesions.
The small bowel is placed on the right side of the
abdomen and the colon is placed on the left side. This
leaves the appendix up in the left upper quadrant for
which reason appendicectomy may be performed to
prevent future confusion. Sometimes the early diagnostic features of volvulus are missed and extensive gut
ischaemia occurs. When this happens the surgeon finds
nearly all the gut is gangrenous. This situation poses a
major problem for future management. The gut is
untwisted and a ‘second look’ laparotomy is performed
24–48 h later to see if any viable gut may be saved.
Duodenal obstruction
Duodenal obstruction is caused by duodenal atresia or by
stenosis due to a membrane. Less commonly, an annular
pancreas may be wrapped around the duodenum, but
usually this is accompanied by severe stenosis or atresia
of the duodenum at the site of the envelopment.
Duodenal atresia occurs most commonly in the second part and is associated with Down syndrome in
about 30% of cases. An antenatal diagnosis may be suggested by features of polyhydramnios, Down syndrome
and/or a double bubble on ultrasonography.
The obstruction develops acutely in the early neonatal period, but signs may be delayed for a day or so
while the secretions accumulate in the enlarged stomach
and proximal duodenum. In the majority of neonates
with duodenal atresia, the obstruction is just distal to
the ampulla of Vater (80%), resulting in bile-stained
vomiting.
Abdominal x-rays demonstrate a ‘double bubble’
pattern: two large air bubbles (one in the stomach and
the other in the dilated proximal duodenum) each with
a fluid level and no gas in the more distal bowel [Fig.7.4].
A duodenal septum with a hole in the centre may
form an incomplete obstruction with episodic vomiting
that may be bile-stained. These babies may present in
the neonatal period or at a later age if the obstruction
isnot so severe. The diagnosis is confirmed by a upper
gastrointestinal contrast study.
Treatment
In duodenal atresia, with or without an annular pancreas,
the obstruction is repaired by duodeno- duodenostomy.
The operative treatment for duodenal septum is
Figure 7.4 Duodenal atresia. Abdominal x-ray shows a ‘double
bubble’, one in the stomach and the other in the dilated
proximal duodenum.
duodenoplasty, but the bile ducts may pose a special
problem as they typically open very close to, or actually
into the edge of, the septum.
Small bowel atresia
Atresia of the bowel beyond the duodenum may occur
at any point [Fig. 7.5], most frequently in the distal
ileum [Fig.7.6], and rarely in the colon. There is often
only one atresia, although there may be several close
together or widely scattered.
Chapter7: Bowel Obstruction 41
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Figure 7.5 Intestinal atresia. Abdominal x-ray shows an
obstruction of the jejunum. The neonate also has situs inversus.
The cause may be interruption of the mesenteric
arcades by a vascular accident in utero, a theory supported
by experimental surgery on fetal animals.
The form of the atresia may be a membranous atresia
or web with an intact mesentery (type 1), two blindending loops with an intact mesentery (type 2), two
blind-ending loops with a mesenteric defect (type 3) or
bowel affected by multiple atresias (type 4). The adjacent vascular arcades are distorted and their terminal
branches may be very small or absent. All the bowel
distal to the atresia is collapsed. A lower gastrointestinal
contrast study will typically demonstrate a microcolon.
Duplications of the alimentary tract
These are rare developmental anomalies in which a
length of bowel is duplicated in such a way that the two
segments share the same blood supply and a common
wall, while the mucosal linings are separate. They may
arise at any point from the mouth to the anus and
Figure 7.6 Ileal atresia.
involve any length from 1 to 2 cm to the entire length of
the large bowel. A duplication may or may not communicate with the main alimentary channel.
There are two basic types:
1 Short, closed cystic duplication. The duplicated seg-
ment forms a cyst which bulges into the lumen or
compresses and angulates the adjoining small bowel,
causing obstruction. A small intraluminal cyst may
cause obstruction in the neonatal period, but larger
ones less intimately connected with the common wall
usually cause progressive obstruction later in infancy
or in early childhood. Occasionally a large tense cyst
is palpable as a very mobile mass in a child without
obstructive symptoms.
2 Long, tubular communicating duplication. These
cysts are much less common and more likely to be
lined by heterotopic (gastric) mucosa, which may
cause a peptic ulcer (Chapter23). If the diagnosis of a
duplication containing heterotopic gastric mucosa is
42 Part II: Neonatal Emergencies
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99m
suspected, it may be demonstrable by a
Technetium
scan. The resection of a long duplication involves the
removal of an equivalent length of bowel, but when
this is unacceptable because of the inadequate length
of bowel remaining, a practical alternative is to
remove the lining alone.
Neonatal necrotising enterocolitis
Necrotising enterocolitis is a disease with combined
ischaemia and infection of the bowel wall. Although not
strictly a ‘cause’ of intestinal obstruction, it typically
presents with abdominal distension and bile-stained
vomiting, resembling obstruction. The passage of blood
per rectum and a characteristic appearance on abdominal x-ray help to distinguish necrotising enterocolitis
from neonatal bowel obstruction. A greater awareness
of the entity may have contributed to the increased incidence in recent years, but there has been an absolute
increase in the number of cases reported in developed
countries.
Predisposing factors
Sick premature neonates may develop necrotising
enterocolitis as a further complication of the predisposing factors listed in Table7.1.
Aetiology
The mechanism has not been elucidated fully. The most
widely held theory to explain the intestinal ischaemia is
that in a stressed, hypoxic state, blood is preferentially
Table 7.1 Predisposing factors and observed associations in
neonatal necrotising enterocolitis
Prematurity
Respiratory distress:
Atelectasis
Hyaline membrane disease
Birth asphyxia
Foetal distress during labour
Prolonged antepartum rupture of membranes
Twins
Caesarean section
Congenital heart disease
Jaundice
Catheterisation of the umbilical vessels
Hyperosmolar feeds
Sepsis
distributed to the heart and brain, at the expense of the
splanchnic circulation, skin and muscle.
Local vascular changes have been implicated: for
example, a catheter in the umbilical vein, if badly positioned, alters the portal haemodynamics; a catheter in
the umbilical artery may have a similar effect on the
arterial supply if advanced too far up the aorta and also
has the potential to produce emboli.
Certain bacteria appear to be important; Klebsiella
species resistant to the commonly used antibiotics are
found in a significant number of neonates who develop
necrotising enterocolitis. Other enteropathogens (e.g.
Escherichia coli, Clostridium difficile, Streptococcus faecalis
and Pseudomonas species) have also been isolated.
The type of enteral feed and when it is commenced
may be relevant: for example, the disease appears to
occur more frequently in neonates who were fed early
with formula. Breast milk may afford some protection
against the disease in the ‘at risk’ neonate.
Pathology
Necrotising enterocolitis may be generalised and involve
most of the small and large intestine, or may be localised
in distribution. The ileum and colon are the two most
commonly affected sites. There is histological evidence
of impaired perfusion, resulting in tissue anoxia and
necrosis. The mucosa is affected most, because of a
shunting mechanism, but the process may involve the
entire thickness of the bowel wall.
When the mucosa is damaged, production of mucus is
impaired and the bacteria normally present in the lumen
may invade the intestinal wall (further damaging the
bowel) and enter the bloodstream to produce bacteraemia
or septicaemia. The damaged mucosa bleeds into the
lumen with resultant rectal bleeding, and gas collects in
the bowel wall (pneumatosis intestinalis) either due to the
activity of gas-forming organisms or by diffusion of intraluminal gas through breaches in the damaged mucosa.
The consequent pathological course is variable:
1 Perforation with generalised peritonitis
2 Perforation with local abscess formation
3 Healing with return of normal function
4 Healing with stricture formation
Clinical picture
A neonate with complications of prematurity is most at
risk of necrotising enteterocolitis. The onset of symptoms is between 2 and 14 days after birth. The neonate
Chapter7: Bowel Obstruction 43
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becomes ill, lethargic, febrile and not interested in feeds.
Abdominal distension and bile-stained vomiting occur,
and there may be passage of loose stools containing a
variable amount of blood.
When complicated by peritonitis, the anterior abdominal wall becomes oedematous and red, with dilated
veins, and palpation causes pain. A mass may be palpable if a localised intraperitoneal abscess has formed or
if there is a persistently dilated loop of bowel.
Investigations
The radiological findings are typical. Plain abdominal
x-rays demonstrate dilated loops of bowel in which
there are intramural bubbles of gas (pneumastosis intestinalis) [Fig.7.7]. Gas within the portal vein and/or its
radicles may be visible. Free gas in the peritoneal cavity,
best seen under the diaphragm, is present if the intestine
has perforated. Separation of adjacent loops of bowel
suggests appreciable amounts of intraperitoneal exudate, an indication of peritonitis, with or without a
perforation.
Bacteriological specimens (e.g. blood culture, nose,
throat, umbilicus and rectal swabs) should be taken
before antibiotics are commenced or altered.
Biochemistry, haematology, electrolytes, acid–base
and bilirubin are monitored. The haemoglobin level
may fall progressively as a result of sepsis and haemorrhage, and serial measurements are required. The
platelet and white cell counts are depressed in severe
disease, and the neonates are frequently acidotic.
Management
Initially this consists of commencing intravenous antibiotics, placing a nasogastric tube to aid intestinal
decompression, stopping enteral feeds and ensuring
parenteral nutrition.
Intensive measures listed in the section on the preand post-operative care of the neonate and adequate
respiratory management also may be required.
Frequent clinical and radiological reassessments are
essential, for they may show the need for operative
intervention.
The indications for operation are as follows:
1 Clinical deterioration despite maximal intensive
resuscitation
2 Evidence of bowel necrosis and perforation
Features which are useful in determining the need for
operation include free gas on abdominal x-ray, progressive signs of peritonitis (distended, red and tender
abdomen), persistent acidosis despite attempted
correction and a sudden and profound fall in the platelet
count.
Operation is confined to resection of perforated or
necrotic bowel, evacuation of intraperitoneal soiling
and placement of diverting stomas. The mortality rate
until recently was high, but with earlier diagnosis and
more effective treatment, the outlook has improved.
Figure 7.7 Necrotising enterocolitis. Intramural gas.
KEY POINTS
• Bile-stained vomiting in the neonate is always serious.
• Abdominal distension, bile-stained vomitus and failure to
pass meconium indicate bowel obstruction.
• Bile-stained vomiting in a normal baby suggests possible
malrotation with volvulus and is an emergency.
• Neonates with bowel obstruction need special transport to
the surgical centre.
44 Part II: Neonatal Emergencies
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Further reading
Applebaum H, Sydorak R (2012) Duodenal atresia and stenosis –
Annular pancreas. In: Coran AG, Adzick NS, Krummel TM,
Laberge J-M, Shamberger RC, Caldamone AA (eds) Pediatric
Surgery, 7th Edn. Elsevier Saunders, Philadelphia, pp. 1051–1058.
Frisker JS, Azizkhan RG (2012) Jejunoileal atreaia and stenosis.
In: Coran AG, Adzick NS, Krummel TM, Laberge J-M,
Shamberger RC, Caldamone AA (eds) Pediatric Surgery, 7th
Edn. Elsevier Saunders, Philadelphia, pp. 1059–1072.
Hajivassiliou CA (2003) Intestinal obstruction in neonatal/pedi-
atric surgery. Sem Ped Surg 12(4): 241–253.
Langer JS (2012) Hirschsprung’s disease. In: Coran AG, Adzick
NS, Krummel TM, Laberge J-M, Shamberger RC, Caldamone
AA (eds) Pediatric Surgery, 7th Edn. Elsevier Saunders,
Philadelphia, pp. 1265–1278.
CHAPTER8
https://t.me/med1917
Abdominal Wall Defects
CASE 1
Ultrasonography at 18 weeks’ gestation showed that the fetus
had bowel loops within an expanded umbilical cord. Careful
scanning of the remainder of the fetus showed no other
abnormality, although the mother was warned of the possibility.
Amniocentesis and karyotyping failed to show trisomy 13 or
18 and it was elected to continue the pregnancy. A paediatric
surgeon was consulted for advice about management at birth.
Q 1.1
What is the abnormality?
Why did it occur?
Q 1.2
What ‘rst aid’ treatment is needed before transfer to the
Q 1.3
surgical centre?
Q 1.4
What is the management and prognosis?
CASE 2
A teenage girl did not want her parents to know she was
pregnant. She presented in labour with no prior antenatal visits.
Exomphalos and gastroschisis
These two developmental abnormalities in the region of
the umbilicus are either diagnosed on antenatal ultrasonography or present at birth as neonatal emergencies,
and they require urgent treatment.
Currently, the prevalence of exomphalos (omphalocele) and gastroschisis is relatively similar, although
the incidence of gastroschisis is increasing in most
regions for reasons that are unclear. The relatively high
risk of coexisting and signficant abnormalities in a
fetus with exomphalos (35%) may be a reason for
termination, particularly if amniocentesis identifies a
major chromosomal abnormality [Fig.8.1].
Avigorous neonate was delivered, but the midwife noted that
most of the small bowel was protruding through a small hole in
the abdominal wall, just to the right of the umbilicus.
Q 2.1 Will the baby live?
Q 2.2
Why is the baby’s life at risk?
Is the baby likely to have multiple congenital anomalies?
Q 2.3
CASE 3
Frank was born without trouble at term. Antenatally the
ultrasonographer was concerned about no urine being visible in
the bladder. At birth the attachment of the umbilical cord was low
and lay adjacent to an unusual defect with wet, pouting mucosa.
The penis was found to be bid and one testis was undescended.
What is the embryological defect?
Q 3.1
Q 3.2
How may this abnormality be treated?
Why is the penis split into two halves and what is the likely
Q 3.3
outcome for sexual function and urinary control?
First aid at birth
A baby with an anterior abdominal wall defect is at
great risk of heat and water loss from evaporation
because of the moist exposed viscera. For this reason,
the baby should be placed in a humidicrib, with the
entire torso wrapped, including the exposed viscera, in
fresh plastic kitchen wrap or aluminium foil. Care must
be taken to ensure that the exposed bowel is not twisted
at the opening in the abdominal wall [Fig.8.1]. Do not
use hot wet packs as these cool too quickly with evaporative heat loss and chill the neonate. The main objective
is to prevent excessive fluid and heat loss during transfer
to the receiving neonatal surgical unit.
Jones’ Clinical Paediatric Surgery, Seventh Edition. Edited by John M. Hutson, Michael O’Brien, Spencer W. Beasley,
Warwick J. Teague and Sebastian K. King.
© 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd.
45
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Figure 8.1 First-aid management of gastroschisis. The torso is wrapped in plastic kitchen wrap to reduce heat loss from evaporation.
A nasogastric tube keeps the bowel decompressed which facilitates operative reduction of the eviscerated bowel. An intravenous
line has been inserted.
Insert a nasogastric tube to decompress the stomach
and herniating bowel and do not feed the baby: minimising the gut volume facilitates operative reduction of
the herniated bowel.
Commence an intravenous fluid infusion of 10% dextrose to prevent hypogylcaemia during transport, particularly if the baby might have Beckwith–Wiedemann
syndrome (organomegaly, exomphalos and hypoglycaemia secondary to dysregulation of insulin-like growth
factor 2 expression with hyperinsulinaemia).
Transport
The neonate with an abdominal wall defect should be
referred to a fully equipped paediatric surgical centre
without delay. Transport should be arranged via a
specialised neonatal transport service, if available. If the
diagnosis has been made on antenatal ultrasonography,
delivery should be undertaken in a tertiary obstetric
centre with paediatric surgeons standing by [Box 8.1].
Exomphalos
This congenital hernia into the base of the umbilical
cord is caused by incomplete folding of the embryonic
disc and failure of the umbilical ring to form normally.
The hernia is covered by fused amniotic membrane and
peritoneum.
Box 8.1 Immediate ‘first aid’ for abdominal wall defect
• Wrap the exposed viscera in fresh kitchen wrap
(ensuring prolapsed bowel is not twisted)
• Careful examination for other anomalies
• Place infant in Humidicrib
• Nil orally
• IV line with 10% dextrose
• IV Nasogastric tube with aspiration to keep bowel
deflated
• If born outside a tertiary paediatric surgical centre:
c Call Neonatal Emergency Transport Service (NETS)
c Call Surgical Registrar at tertiary hospital
• Explain management plan to parents
• Get consent for surgery
Very occasionally, the membrane ruptures before
birth and the eviscerated bowel becomes matted and
indurated with dense adhesions, so that the bowel
appears to be shorter than normal. The inflammation is
believed to be caused by chemical irritation from meconium and urine in the amniotic fluid. On the uncommon
occasion rupture occurs during delivery, the exposed
bowel may appear normal.
The size of the defect in the abdominal wall and the
volume of the sac are variable: exomphalos major has
defect greater than 5 cm in diameter and contains gut,
liver and/or spleen, whereas exomphalos minor has
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