Gastric perforation in an extremely low birth weight infant recovered with percutaneous peritoneal drainage.
ABSTRACT Neonatal gastric perforation is an uncommon but life-threatening condition, which is mainly encountered in premature infants. Primary surgical repair is the principal mode of the treatment. Gastric perforation in neonates improving with percutaneous peritoneal drainage alone has not been described previously. Therefore, an extremely low birth weight infant is presented herein in order to emphasize that gastric perforation may improve with percutaneous peritoneal drainage alone. Isolated gastric perforations in newborn infants may be improved with percutaneous peritoneal drainage alone without need for primary surgical repair.
- [Show abstract] [Hide abstract]
ABSTRACT: Premature infants continue to have a high mortality after gastrointestinal perforation. This report describes 179 patients with gastrointestinal perforation and peritonitis and compares etiologic factors, mortality, and causes of death in premature infants and older children in an attempt to predict outcome. The 113 boys (63.1%) and 66 girls (36.9%) had an age range of newborn (n = 139, 77.6%) to 17 years. Site of perforation was gastric in 16, duodenal in 9, small bowel in 105, colon in 37, and undesignated in 12. Eighteen had multiple perforations. Etiologic factors in newborns (younger than 2 months) included necrotizing enterocolitis (NEC) (75, 41.9%), isolated ileal perforations (30, 21.5%), malrotation/volvulus (8), iatrogenic causes (5), and others (6). Gestational age was 29.6 +/- 4.3 weeks for NEC versus 31.4 +/- 5.4 weeks for non-NEC. Birth weight for patients with NEC was 1.45 +/- 0.8 gm and 1.81 +/- 1.0 gm for non-NEC babies. Etiologic factors in 33 older children (older than 2 months to 17 years) were trauma (10), Meckel's diverticulum (4), intussusception (2), pseudomembranous colitis (2), adhesions (2), stomal leak (2), others (4), and nondesignated (7). Gastric perforations (n = 16) were iatrogenic in 7, idiopathic in 5, and caused by an ulcer in 4. Mortality for NEC was 36 of 75 (48%), 15 of 55 (27.2%) for non-NEC infants (p < 0.05 versus NEC), 15.1% (5 of 33) for older children (p < 0.05 versus NEC), and 4 of 16 (25%) for gastric perforation. Infant deaths were related to overwhelming sepsis, immaturity of systems, and multiorgan failure. Deaths for older children were a result of sepsis, multiorgan failure, and immunodeficiency. Gastrointestinal perforation is more common in premature infants with the highest mortality (48%) noted in NEC. Despite surgical intervention and advances in neonatal intensive care unit care, premature low birth weight infants (especially NEC) continue to have a high mortality.Surgery 11/1996; 120(4):650-5; discussion 655-6. · 3.37 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: This report describes a newborn infant girl who presented with abdominal distension and pneumoperitoneum. At operation, near total necrosis of the stomach was observed. The esophagus was ligated, the stomach resected. The baby was fed by an transpyloric feeding tube. At 8 weeks, an esophagojejunal anastomosis was performed with a Hunt-Lawrence Pouch. A good outcome was achieved.Journal of Pediatric Surgery 05/1999; 34(4):649-51. · 1.38 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: The etiology of idiopathic gastric perforation (IGP) in neonates is unclear. Interstitial cells of Cajal (ICC) express tyrosine kinase receptor C-kit, and act as gastrointestinal pacemaker cells. Stem cell factor (SCF) is a C-kit ligand and plays an important role in immune system homeostasis in the gastrointestinal tract. The authors hypothesized that abnormal distribution of ICC or SCF in the gastric wall (ie, abnormal motility or impaired immunity) could predispose the stomach to IGP. Stomachs obtained at postmortem from neonates who died of IGP (n = 7) and other causes (control group; n = 10) were used. Biopsy sections were taken at random from various sites in the stomach, including macroscopically intact areas, and labeled immunohistochemically using antibodies to C-kit(a marker for ICC) and SCF. In all control specimens, ICC were present between the muscle layers and around the myenteric plexuses of the stomach wall. In contrast, ICC were absent in all biopsy sections from 3 of the 7 IGP stomachs. In the remaining 4 IGP stomachs, there were fewer ICC in the muscle layers compared with controls, and ICC were absent around the myenteric plexuses. The distribution of SCF immunoreactivity in IGP and control specimens was similar. The findings suggest that a lack of ICC (ie, gastric hypomotility) may be implicated in the etiology of IGP in neonates.Journal of Pediatric Surgery 06/2000; 35(5):673-6. · 1.38 Impact Factor
Gastric perforation in an extremely low birth weight infant
recovered with percutaneous peritoneal drainage
Mustafa Aydın1, Ayşegül Zenciroğlu1, Nilay Hakan1, Derya Erdoğan2, Nurullah Okumuş1,
Mehmet Şah İpek1
Departments of 1Neonatology and 2Pediatric Surgery, Dr. Sami Ulus Maternity and Children’s Hospital, Ankara,
SUMMARY: Aydın M, Zenciroğlu A, Hakan N, Erdoğan D, Okumuş N,
İpek MŞ. Gastric perforation in an extremely low birth weight infant recovered
with percutaneous peritoneal drainage. Turk J Pediatr 2011; 53: 467-470.
Neonatal gastric perforation is an uncommon but life-threatening condition,
which is mainly encountered in premature infants. Primary surgical repair is
the principal mode of the treatment. Gastric perforation in neonates improving
with percutaneous peritoneal drainage alone has not been described previously.
Therefore, an extremely low birth weight infant is presented herein in
order to emphasize that gastric perforation may improve with percutaneous
peritoneal drainage alone. Isolated gastric perforations in newborn infants
may be improved with percutaneous peritoneal drainage alone without need
for primary surgical repair.
Key words: conservative management, extremely low birth weight infant, gastric
Gastric perforation is an uncommon clinical
condition in newborns, and is mainly seen
in premature infants and threatens life when
diagnosed and treated late1. Its incidence
is reported to be 1 in 5,000 live births2.
Gastric perforations constitute 7% of all
gastrointestinal perforations3. In most cases,
the underlying cause could not be precisely
determined. Prematurity is a facilitating factor4.
Some mechanical factors are also considered
as risk factors (i.e. the mechanical pressure by
nasogastric or orogastric catheters, excessive
gastric distension due to positive pressure
ventilation)4,5. Despite early diagnosis and
treatment, the mortality rate is still high
due to accompanying problems. Success can
be achieved with early recognition of the
clinical signs in the patients at risk and rapid
interventions for treatment6.
Although primary surgical repair is the principal
mode of treatment, there is an exceptional
case report in which perforation improved
spontaneously with conservative treatment7.
Nevertheless, to the best of our knowledge,
it has not been described previously that
gastric perforation in neonates improved
with percutaneous peritoneal drainage alone.
Therefore, an extremely low birth weight
(ELBW) infant is presented herein in order to
emphasize that gastric perforation may improve
with percutaneous peritoneal drainage alone.
A male baby was born at 28 weeks’ gestation
by emergent cesarean section, due to
oligohydramnios and fetal distress, to a 21-
year-old gravida 1, para 1 mother. His birth
weight was 1000 g. On prenatal history,
although there was a history of early rupture
of the membranes lasting about 48 hours, there
was no history of preterm labor, abruption
of placenta, maternal chorioamnionitis, fever,
antibiotic use, or steroid receipt. After delivery,
because of insufficient spontaneous respiration,
cardiopulmonary resuscitation was attempted
at once including endotracheal tube-positive
pressure ventilation and chest compression
lasting about 30 seconds. The patient responded
well to resuscitation by turning pink in color
and with an increase in heart rate (>100 beats/
min). The Apgar scores were 3 and 7 at one
and five minutes, respectively. No esophageal
intubation or placement of a nasogastric tube
was undertaken in the delivery room. He
The Turkish Journal of Pediatrics 2011; 53: 467-470Case Report
also did not receive surfactant or any drug
in the delivery room. Following resuscitation,
the patient was transferred to our neonatal
intensive care unit (NICU). On admission
to NICU, blood gas analysis revealed mild
hypoxemia with an oxygen partial pressure
of 43 mmHg and oxygen saturation of 73%.
He was put on mechanical ventilation and
then given surfactant because of the severe
respiratory distress syndrome. Subsequently,
because of the persistence of low oxygen
saturation levels and insufficient aeration of
the lungs on auscultation and follow-up X-
rays, he was given two additional doses of
surfactant within the first 24 hours of life.
The patient’s poor clinical condition did not
allow us to perform an echocardiographic
study for evaluation of cardiac status until
the 10th postnatal day, when echocardiography
revealed a hemodynamically insignificant small
ductal shunt. Because he was hypotensive,
probably due to a hemodynamically significant
ductal shunt, inotrope support was given with
dopamine. Over the clinical course, the patient
needed resuscitation several times. He did not
receive postnatal steroid therapy for hypotension
resistant to dopamine or any nonsteroidal
anti-inflammatory drugs (i.e. indomethacin or
ibuprofen) for treatment of a hemodynamically
significant ductal shunt. At the 30th hour of the
life, his general condition deteriorated suddenly
with a distended abdomen and increased
respiratory distress. Drainage of the free air,
saliva and gastric content was observed from
the placed nasogastric tube. To that point,
he had not received any feeds. At that time,
complete blood count, biochemical analyses
and C-reactive protein levels were found within
normal limits. Abdominal X-ray demonstrated
excessive amount of free air in the peritoneal
cavity (massive pneumoperitoneum) with a
small stomach shadow (Fig. 1A). However,
there was no preceding bowel dilatation or
pneumatosis on previous X-rays. These clinical
and radiological findings led us to the clinical
suspicion of gastric perforation.
When the baby’s clinical status worsened,
insertion of a Penrose drain was done
under local anesthesia without performing a
preceding percutaneous peritoneal paracentesis.
Radiocontrast imaging of the stomach prior
to the laparotomy was not considered. An
excessive amount of free air and some amount
of gastric content, but no intestinal content
or bile, were drained from the abdominal
cavity when the Penrose drain was first placed
(Fig. 1B). Afterward, surgical repair was
planned when the patient’s general status
would permit it. On the 10th day of the
hospitalization, with recovery in the general
status of the patient, follow-up abdominal X-ray
demonstrated complete resolution of the free
air with presence of gastric gas shadow (Fig.
1C). While the drain was in place, drainage of
gastric contents and saliva was noted, but there
was no drainage of intestinal content. Overall,
the patient was mechanically ventilated for 15
days. Feeding with mother’s milk was started
on the 24th postnatal day via a nasogastric
tube. Without requirement for primary surgical
repair, percutaneous drainage was terminated
on the 27th postnatal day. After tolerating oral
feeding and showing an increase in weight, the
patient was discharged from the hospital on
the 72nd postnatal day. He remains well after
eight months of follow-up.
Although the most common cause of
gastrointestinal perforation in premature infants
is necrotizing enterocolitis, perforation in the
present case was thought to be gastric in origin
based on his clinical and radiological findings.
The etiopathogenesis of gastric perforation in
newborns is still not completely understood.
It is encountered mainly in premature infants
and male babies. The first opinion on the
pathogenesis is that it develops spontaneously
due to congenital gastric muscular agenesis, with
no accompanying gastrointestinal problem8. It
is also suggested that gastric acidity reaches
its highest level on the second day of life
and the perforations are likely related to the
high level9. It has been reported that ischemic
necrosis due to hypoxia, perinatal stress and
shock10 and extensive resuscitation performed
postnatally5 could also cause gastric perforation.
Furthermore, some pathologies like duodenal
obstruction and tracheoesophageal fistula may
increase the risk of gastric perforation by
causing excessive gastric distension11. It is also
known that dexamethasone and indomethacin
may cause gastric perforation in newborns11,
but these were not administered to our patient.
There are some cases (20%) not related to any
known underlying factors that are accepted
468 Aydın M, et al The Turkish Journal of Pediatrics • July-August 2011
as spontaneous/idiopathic. Recent studies
suggested that spontaneous gastric perforation
may be caused by the lack of intestinal Cajal
cells12. In present case, it is considered that,
on the basis of prematurity, perinatal stress
and hypoxia together with gastric distension
due to positive pressure ventilation might
have played a role in the etiopathogenesis of
As in this case, abdominal distension with
sudden onset and rapid progress and tachypnea
with respiratory distress are the most common
clinical findings. Other clinical findings include
feeding intolerance, temperature instability,
acidosis, and shock1,10. Gastric perforation is
the most common cause of pneumoperitoneum
in the first week of life. On the abdominal
X-ray, as with our patient’s radiological
findings, an oval gas shadow was reported
in which the lower and upper margins were
constituted by the pelvic floor structures and
the diaphragm with an opacity related to the
falciform ligament laying on the medial axis
at the midline of this shadow13. As seen in
the present case, free air under the diaphragm
and the absence of gastric air together with
the displacement of intraabdominal organs are
the other important radiological findings that
support the diagnosis14.
Idiopathic spontaneous intestinal perforation
is a currently described novel condition, which
does not show clinical or diagnostic features
of necrotizing enterocolitis. Neonatal stress
consequent to preterm birth is a determining
factor in the etiopathogenesis. Infants under 28
weeks of gestational age and with LBW show
a particular predisposition to this entity15. In
the present case, massive pneumoperitoneum
with a small stomach shadow on the abdominal
X-ray, drainage of an excessive amount of
free air and some gastric contents but of no
intestinal content or bile when the drain was
first placed, and drainage of gastric contents
and saliva but of no intestinal content while the
drain remained in place excluded the diagnosis
of intestinal perforation.
Due to the fact that gastric perforation is a
rapidly progressing pathological condition, early
diagnosis and treatment are very important.
Urgent primary surgical repair together with
medical approaches including reconstitution
of liquid-electrolyte balance, correction of
Figure 1: Abdominal radiographs of the patient.
A) note the excessive amount of free air in the
peritoneal cavity (massive pneumoperitoneum) with
a small stomach shadow; B) note the lower tip of
the orogastric/nasogastric catheter and absence of
gas shadows in the abdomen following insertion of
the drain; C) complete resolution of the free air with
presence of gastric gas shadow on follow-up abdominal
Volume 53 • Number 4 Gastric Perforation in an ELBW Infant & Peritoneal Drainage 469
acidosis and use of wide spectrum antibiotics
are the appropriate treatment modalities.
These patients usually need intubation and
mechanical ventilation support because of
respiratory distress, which is caused by the
excessive amount of free air in the peritoneal
cavity that leads to diaphragmatic pressure.
With percutaneous peritoneal paracentesis in
the preoperative period, respiratory distress and
abdominal compartment syndrome developing
secondary to abdominal distension caused by
free air can be reduced7,8.
Primary surgical repair is the principal mode
of treatment, and partial gastric resection may
sometimes be required. However, there is an
exceptional case report in which perforation
improved spontaneously with conservative
treatment7. In the present case, however,
gastric perforation improved with percutaneous
peritoneal drainage alone. This approach can
be considered especially in patients in whom
their clinical condition does not permit surgical
repair. However, if persistence of free air,
ongoing acidosis and presence of peritonitis
findings exist, surgical exploration should be
The mortality rates vary between 27% and
83%5,6. Despite the decrease in mortality
rates in recent years with early diagnosis and
appropriate surgical intervention, mortality is
still high due to accompanying pathologies
that cause multi-organ failure. The degree
of prematurity, the duration of peritoneal
contamination and asphyxia are the most
important factors increasing the mortality
rate1,5,6. Problems like sepsis and respiratory
distress are frequently accompanying clinical
conditions in premature infants, which
increase the mortality. With early diagnosis
and appropriate treatment, the prognosis of
idiopathic perforations is reported to be better
than with gastric perforations secondary to an
In conclusion, the gastric perforation in our
patient was thought to have developed due
to gastric distension as a result of positive
pressure ventilation on the basis of prematurity
and perinatal stress. It has been observed
that isolated gastric perforations in newborn
infants may be improved with percutaneous
peritoneal drainage alone without need for
primary surgical repair.
1. Lin CM, Lee HC, Kao HA, et al. Neonatal gastric
perforation: report of 15 cases and review of the
literature. Pediatr Neonatol 2008; 49: 65-70.
2. Jawad AJ, Al-Rabie A, Hadi A, et al. Spontaneous
neonatal gastric perforation. Pediatr Surg Int 2002;
3. Attridge JT, Clark R, Walker MW, Gordon PV. New
insights into spontaneous intestinal perforation using
a national data set: (2) two populations of patients
with perforations. J Perinatol 2006; 26: 185-188.
4. Duran R, Inan M, Vatansever U, Aladag N, Acunas
B. Etiology of neonatal gastric perforations: review of
10 years’ experience. Pediatr Int 2007; 49: 626-630.
5. Rosser SB, Clark CH, Elechi EN. Spontaneous neonatal
gastric perforation. J Pediatr Surg 1982; 17: 390-
6. Leone RJ Jr, Krasna IH. ‘Spontaneous’ neonatal gastric
perforation: is it really spontaneous? J Pediatr Surg
2000; 35: 1066-1069.
7. Guha DK, Rashmi A, Khanduja PC, Kochar M. Neonatal
gastric perforation. Report of 3 cases with one survival.
Indian J Pediatr 1969; 36: 404-406.
8. Herbut PA. Congenital defect in the musculature of
the stomach with rupture in the newborn infant. Arch
Pathol 1943; 36: 191-194.
9. Miller FA. Neonatal gastrointestinal tract perforations.
Lancet 1957; 77: 439-442.
10. Kuremu RT, Hadley GP , Wiersma R. Neonatal gastric
perforation. East Afr Med J 2004; 81: 56-58.
11. Grosfeld JL, Molinari F, Chaet M, et al. Gastrointestinal
perforation and peritonitis in infants and children:
experience with 179 cases over ten years. Surgery
1996; 120: 650-656.
12. Ohshiro K, Yamataka A, Kobayashi H, et al. Idiopathic
gastric perforation in neonates and abnormal
distribution of intestinal pacemaker cells. J Pediatr
Surg 2000; 35: 675-676.
13. Rampton JW. The football sign. Radiology 2004; 231:
14. Durham MM, Ricketts RR. Neonatal gastric perforation
and necrosis with Hunt-Lawrence pouch reconstruction.
J Pediatr Surg 1999; 34: 649-651.
15. Messina M, Molinaro F, Ferrara F, Messina G, Di Maggio
G. Idiopathic spontaneous intestinal perforation: a
distinct pathological entity in the preterm infant.
Minerva Pediatr 2009; 61: 355-360.
16. Dillon PW, Cilley RE. Lesions of the stomach. In:
Ashcraft KW, Murphy PJ, Sharp RJ, Sigalet DL, Snyder
CL (eds). Pediatric Surgery (3rd ed). Philadelphia: WB
Saunders; 2000: 391-402.
470 Aydın M, et al The Turkish Journal of Pediatrics • July-August 2011