Bowel obstruction is a common surgical emergency for newborns.

Early
diagnosis and appropriate treatment usually results in positive outcomes.
Delay in carrying out surgery may result in the loss of large amounts of
bowel.
Not all infants with bowel obstruction require transfer by PIPER neonatal.
Infants diagnosed early and without fluid or electrolyte problems may be
safely transferred with local ambulance services. However, it is advisable to
discuss such infants with the receiving hospital or PIPER.

Signs of bowel obstruction

Signs of bowel obstruction can include:
Vomiting with or without bile stained material. Never ignore bilestained vomiting in the newborn
Increased gastric residuals before feedings

 Failure to pass meconium in the first 24 hours of life

Abdominal distension (particularly with low level obstruction)
Absent or decreased bowel sounds

Differential diagnosis
Intestinal obstruction without bilious vomiting

This may occur in:

duodenal atresia (if obstruction proximal to Ampulla of Vater 20% of
cases)
duodenal stenosis
annular pancreas
pyloric stenosis (usually presents at 4-6 weeks of life but may present
as early as the first week)
Intestinal obstruction with bilious vomiting

This may occur in:

malrotation and volvulus
duodenal atresia (if obstruction distal to Ampulla of Vater 80% of
cases)
jejunoileal atresia
meconium ileus
meconium plug syndrome (18%)
Hirschsprungs disease (8%)
Intestinal obstruction with marked abdominal distension

This may occur in:

ileal atresia
Hirschsprung's disease
meconium ileus
meconium plug syndrome
imperforate anus

Duodenal atresia
Duodenal atresia may take the form of either a membranous or interruptedtype lesion at the level of the papilla of Vater.
In 80% of cases the papilla of Vater opens into the proximal duodenum
causing the vomiting to be bilious.
Facts about duodenal atresia:
obstruction is due to failure of recanalisation of the 2nd part of the
duodenum during fetal development
occurs in 1:5,000-10,000 live births
more common in males
associated with Down syndrome in 25% of cases
polyhydramnios is seen antenatally
x-ray usually shows a characteristic 'double-bubble' appearance

Figure 1. X-ray showing characteristic double bubble appearance in

duodenal atresia

Midgut malrotation and volvulus

Malrotation is a result of abnormal rotation of the gut as it returns to the
abdominal cavity during embryogenisis. It occurs in 1:6000 live births and is
often associated with other conditions including duodenal atresia or
stenosis, congenital diaphragmatic hernia, abdominal wall defects,
heterotaxy or choanal atresia.
Most patients with midgut malrotation develop volvulus within the first week
of life. Features include:
Bilious vomiting is the initial symptom and abdominal distention is
minimal until a much later stage.
Bowel can become strangulated at any time and age. Once midgut
ischaemia occurs, unstable haemodynamics, intractable metabolic
acidosis and necrosis with perforation develop.
Abdominal X-ray may be normal.
Malposition of the superior mesenteric vessels demonstrated by
ultrasound examination is diagnostic.

 Upper gastrointestinal contrast study is the investigation of choice but

should be performed by experienced practitioners only. The key
feature with malrotation is:
o abnormal position of the duodeno-jejunal (DJ) junction. The DJ
junction fails to cross to the left of the vertebral bodies and lies
inferior to the first part of the duodenum
o spiral configuration of the jejunum or a duodenojejunum that
occupies the right hemi-abdomen is seen with volvulus
Symptomatic infants require immediate surgery

Jejunoileal atresia
Jejunoileal atresia is caused by a mesenteric vascular accident during fetal
life. Features include:
Abdominal distention with bilious vomiting is observed within the first
24 hours after birth. The more proximal the lesion, the earlier the bilestained vomiting.
X-ray shows air-fluid levels proximal to the lesion.
Calcification due to meconium peritonitis may be present.

Meconium ileus
Thick tenacious meconium in the bowel (ileum, jejunum or colon) causes
obstruction. 50% of infants may have associated:
volvulus
jejunoileal atresia
bowel perforation and/or meconium peritonitis
Meconium ileus occurs in 15% of newborns with cystic fibrosis and at least
90% of patients with meconium ileus have cystic fibrosis.

Presentation of meconium ileus

Presentation includes:
early marked bowel distension
bilious vomiting
remarkable abdominal distention, tenderness and/or erythema of the
abdominal skin may indicate perforation
on rectal examination mucus plugs may be evacuated after
withdrawal of the examination finger (fifth finger)
X ray investigation of meconium ileus

X-ray shows:
distended loops of intestine with thickened bowel walls
a large amount of meconium mixed with swallowed air produces the
so-called 'ground-glass' sign typical of meconium ileus, a
characteristic feature but often absent
calcification, free air or very large air-fluid levels suggest bowel
perforation
Treatment of meconium ileus

Patients with uncomplicated meconium ileus may be successfully treated

with hypertonic enemas performed while adequate intravenous fluid is
maintained.
Immediate surgery is indicated for infants with complicated meconium ileus
or where conservative treatment fails.

Meconium Plug Syndrome

Most common form of functional distal intestinal obstruction in the
neonate

 Caused by inspissated meconium within the distal colon or rectum

Occurs in 1:500-1:1000 live births, with uncertain etiology
Generally present with marked abdominal distension and failure to
pass meconium
Generalised intestinal dilatation is seen on x-ray
Contrast enema is diagnostic showing outlines of the meconium
plugs
Contrast enema or digital exam is often curative with the plugs being
extruded
Stooling pattern should be normal afterwards
If any concern about stooling pattern a rectal suction biopsy should
be performed to rule out Hirschsprungs disease

Hirschsprung's disease
Hirschsprung's disease is the cause of 15-20% of newborn intestinal
obstructions occurring in 1:4000 live births. It is characterised by abnormal
innervation of the colon. It can affect the anal sphincter or extend
throughout the entire colon into the small bowel.
Features include:
80% of cases present in the first 6 weeks of life.
4:1 male:female ratio.
8% of patients also have Down syndrome
Presents with failure to pass meconium in the first 24 hours plus
gradual onset of abdominal distension and vomiting.
Distal short segment disease can present later in life with persistent
and progressive constipation.

 The most serious complication is enterocolitis. This occurs as a result

of progressive colonic dilation with decreased ileal and colonic fluid
resorption, stasis with bacterial overgrowth and mucosal ischaemia
which may lead to massive acute fluid loss into the bowel with
diarrhoea, shock and dehydration.
Enemas should be avoided during episodes of enterocolitis
because of the possibility of perforating the colon.
Diagnosis of Hirschsprung's disease

A definitive diagnosis is made by a suction rectal biopsy with

acetylcholinesterase staining showing prominent nerve fibres and absence
of ganglion cells in the submucosa. There is absence of ganglion cells in
the myenteric plexus of the colon on histological examination.

Investigation of bowel obstruction

When you investigate bowel obstruction you should:
Conduct a thorough physical examination and an assessment of the
circulation with documentation of findings.
Look for any associated abnormalities because bowel obstruction
may be a part of multiple anomalies for example: vertebral, anal,
cardiac, tracheo-esopageal atresia, renal, limb (VACTERL) sequence
with imperforate anus, trisomy 21 with duodenal atresia.
Get plain abdominal X-rays.
Note that digital rectal examination, contrast studies and ultrasound
examinations are best undertaken in centres with paediatric surgical
services.

Management of bowel obstruction

To manage bowel obstruction you should:
Place the infant in an incubator for close observation and temperature
control.

 Nurse supine with the head elevated.

Place an orogastric tube (8 - 10FG) on low pressure suction (or
aspirate with a syringe every 60 minutes and leave on free drainage).
The amount and type (eg bile-stained, faeculent) of fluid aspirated
should be recorded.
Place nil by mouth.
Commence IV fluids. If signs of shock may need fluid resuscitation
with normal saline in 10-20 ml/kg aliquots. Give maintenance fluids
plus ml for ml replacement of NG aspirate with normal saline and
10mmol KCL/500ml.
Obtain abdominal x-rays (include supine and lateral decubitus view).
Note that a relatively gasless abdomen is compatible with midgut volvulus.
Consult with a paediatric surgeon or PIPER neonatal to arrange
transfer to an appropriate surgical centre.
It may be appropriate to commence antibiotics preferably after blood
culture taken (discuss with the receiving unit or PIPER).
Obtain blood for FBE, electrolytes, blood gas and lactate (and blood
cultures if commencing antibiotics).
Be aware that these infants frequently have associated problems
of acidosis and shock.

References
Hutson, J. et al (eds) Jones Clinical Paediatric Surgery Diagnosis and
Management, 6th ed., 2008, Blackwell Publishing