Gastric rupture during pregnancy is very rare and the few identified case reports
in the literature are primarily associated with either bariatric surgery or undiagnosed
diaphragmatic hernias.[1]
[2]
[3]
[4] Early identification of the condition is essential because diagnostic delay increases
maternal and perinatal morbidity and mortality.[5]
We performed a PubMed literature search of English language articles from 1900 to
2015 using key words: “gastric rupture,” “stomach rupture,” and “pregnancy.” The same
search terms were entered in Google Scholar. We also examined the cited references
for any additional cases. Nine case reports described gastric ruptures during pregnancy.
The few cases of spontaneous gastric rupture reported in the literature are typically
complicated by previously undiagnosed congenital anomalies, gastric carcinoma, or
ascariasis.
We present three cases of gastric rupture during pregnancy and managed at the University
Teaching Hospital of Kigali (CHUK). CHUK is the largest public hospital in Rwanda
and serves as one of the primary teaching and tertiary care referral centers for the
country. CHUK receives referrals from 29 district hospitals.
Case Presentations
Case 1
An 18-year-old primiparous patient was transferred to CHUK from the district hospital
due to progressive abdominal distension 4 days following an uncomplicated cesarean
delivery. The patient had a medical history of epigastric pain, unresponsive to medical
treatment with cimetidine. Postoperatively, she experienced fever, abdominal pain,
and distension. Endometritis and ileus were suspected. She was treated with ampicillin,
gentamycin, and metronidazole, and a nasogastric tube was placed. The patient was
transferred to the tertiary care hospital CHUK for further management.
On arrival at CHUK, her Glasgow coma score was 15/15. Her blood pressure was 100/70 mm
Hg, pulse 165 beats/min, and temperature was 37.5°C. Her abdomen was noted to be distended
and diffusely tender. No rebound or guarding was noted.
Abdominal ultrasound demonstrated a moderate amount of free fluid in the abdomen.
The initial impression was hemoperitoneum, possible peritonitis. The patient was aggressively
resuscitated with intravenous fluids. The antibiotic regimen was changed to ceftriaxone
and metronidazole on admission. The nasogastric tube was maintained. The white blood
count was 3.2 × 103/mm3; hemoglobin 16 g/dL, and platelet count 218 × 103/mm3. After review of the laboratory values and confirming that the patient was hemodynamically
stable, hemoperitoneum was ruled out.
On hospital day 1, she was clinically improved with reduced abdominal pain and tenderness
on examination; however, she was febrile with a temperature of 38.5°C. She reported
no flatus or stool.
Abdominal X-ray demonstrated distended bowels without air fluid levels.
She improved clinically on hospital day 2 and tolerated an advance to regular diet.
She was afebrile and noted to have flatus and passage of stool.
She acutely decompensated 48 hours after admission. She became febrile, tachycardic,
dyspneic, hypoxic, and abdominal distension markedly increased. Bedside ultrasound
confirmed increased free fluid. Providers suspected sepsis due to worsening peritonitis.
Emergent laparotomy was performed. Intraoperatively, five ascaris worms measuring
approximately 20 cm each were found in the peritoneal cavity. A mass of intestinal
worms was palpable in the intestines. Feculent peritoneal fluid was aspirated.
A 3 × 3 cm perforation in the lesser curvature of the stomach was diagnosed and repaired.
Despite resuscitation efforts, the patient died of septic shock 4 hours following
surgery.
Case 2
A 35-year-old gravida6, para4024 patient was transferred from a district hospital
19 days following a normal vaginal delivery. She reported feeling well until about
3 days prior to admission when she developed progressive abdominal pain and distension.
Peritonitis was suspected and the patient was transferred to CHUK for further management.
On admission, she was febrile with temperature of 39.4°C, tachycardic (150 beats/min),
hypotensive (nonmeasurable blood pressure), and pale. The abdomen was distended and
tender on palpation, but no rebound or guarding was noted. The remainder of the physical
examination was unremarkable. Available laboratories demonstrated hemoglobin of 8.8
g/dL and platelet count of 154 × 103/mm3. Ultrasound revealed elevated free fluid in the abdominal cavity. Resuscitation was
initiated with blood, intravenous fluids, and broad-spectrum antibiotics (cefotaxime
and metronidazole). The working diagnosis was sepsis in the setting of generalized
peritonitis. Emergent laparotomy was performed after maternal stabilization. Intraoperatively,
3 L of foul-smelling pus was aspirated. Further exploration revealed a posterior gastric
perforation measuring 1 to 2 was diagnosed and repaired. There was no obvious underlying
cause for the perforation. In addition, the patient had no documented history of peptic
ulcer disease (PUD), but clinically ulcer disease was suspected as the possible cause
of perforation.
The postoperative course was uneventful and the patient was discharged home in stable
condition.
Case 3
A 34-year-old primiparous patient transferred to CHUK from a district hospital due
to suspected pulmonary edema 1 day following cesarean delivery for non-reassuring
fetal status in the setting of preeclampsia. The neonate died on the day of delivery.
The patient reported a history of epigastric pain prior to her cesarean delivery.
She denied nausea or vomiting. She received 80 mg of Lasix at the district hospital
prior to transfer. At CHUK, the patient was dyspneic, tachypneic with an oxygen saturation
of 88% on room air. Her blood pressure was 138/89 mm Hg, pulse 117 beats/min, and
respiratory rate 30 breaths/min. The physical examination was significant for marked
facial and lower extremity edema, but the lungs were described as “clear” by the admitting
physician. The cardiac examination was significant for tachycardia. The abdomen was
markedly distended and diffusely tender. No rebound or guarding was noted. Abdominal
ultrasound demonstrated a large amount of free fluid in the abdominal cavity. The
working diagnosis was pulmonary edema and abdominal ascites in the setting of severe
preeclampsia. The differential diagnoses also included pulmonary embolus and hemoperitoneum.
The patient was given 5 L of oxygen per minute and placed on therapeutic enoxaparin.
On admission the white blood (cell) count (WBC) was 6.2 × 103/mm3, hemoglobin 9.1 g/dL, and platelet count 59 × 103/ mm3. A chemistry panel was requested but not available at the time of admission. Antibiotics
were not initiated at the time of admission. Hospital day 2, the patient was noted
to have minimal clinical improvement. She remained afebrile and a repeat WBC was 3.7 × 103/mm3. Ceftriaxone and metronidazole were initiated; however, the site of infection was
not clear. She did not show signs of acute abdomen. Lovenox was discontinued. The
abdominal free fluid progressively increased and peritoneocentesis was performed.
The peritoneocentesis demonstrated blood tinged ascitic fluid. Additional studies
included Gram stain/culture and cytology; however, these results were not immediately
available to providers.
Fig. 1 Intraoperative image (case 3) demonstrating gastric rupture site in postpartum patient.
The patient's clinical status improved slightly. She was eating, ambulating without
difficulty and did not have nausea/vomiting. Her WBC, however, progressively increased
despite antibiotic therapy. The results of the initial paracentesis demonstrated WBC
100 mm3, red blood (cell) count (RBC) 2,000 mm3, and polymorphonuclear (PMN) 100%.
On hospital day 11, the patient was noted to be hypothermic with a temperature of
35°C, pulse 122 beats/min, respiratory rate 40 breaths/min, and blood pressure of
128/68 mm Hg. The paracentesis was repeated and frank pus was aspirated. Emergent
laparotomy was performed due to suspected peritonitis.
Intraoperatively, undigested food particles were noted. Three liters of inflammatory,
foul-smelling ascitic fluid was aspirated. A 1.5 × 1 cm anterior gastric perforation
was noted ([Fig. 1]). The perforation was repaired in two layers.
Antibiotics were continued and nasogastric tube placed. The patient improved clinically
on postoperative day 1. However, on postoperative day 2, she developed respiratory
distress and an acute abdomen. She was taken back to the operating room for exploratory
laparotomy due to suspected leakage of the gastric repair site.
At the time of the second laparotomy, the gastric repair was intact and 1.5 L of inflammatory
fluid was aspirated. No other pathologic findings were noted.
Postoperatively she remained intubated, on antibiotics, and with a nasogastric tube
in place. Because of to lack of intensive care unit (ICU) beds, she was transferred
to another tertiary care center ICU. She died from sepsis 1 day later.
Discussion
In the general population, gastric perforation is primarily associated with advanced
PUD. Additional risk factors may also increase the life-long risk of PUD. Helicobacter pylori infection, smoking, alcohol, and nonsteroidal anti-inflammatory drugs (NSAIDS) are
exposures known to increase the risk for PUD and perforation.[6]
[7]
[8]
[9] Bariatric surgery is increasingly common in wealthy nations and, therefore, more
frequently encountered in pregnancy.[10] Bariatric surgery increases the risk for gastric perforation. Maternal congenital
diaphragmatic hernias also increase the risk for gastric perforation. In the setting
of maternal gastrointestinal symptoms and known congenital diaphragmatic hernia or
bariatric surgery, gastric rupture should be considered in the differential diagnosis.
Gastric perforation should be suspected in the patient with preexisting PUD who manifests
sudden-onset, severe, diffuse abdominal pain. Early diagnosis is essential to improve
outcomes because the prognosis is favorable when diagnosis and treatment occur within
the first 6 hours, but life-threatening when the diagnosis is delayed more than 12
hours.[6]
Understanding of the phases of ulcer perforation may decrease diagnostic delays.
In the first phase (within 2 hours following perforation), abdominal pain is usually
sudden and may produce syncope or cardiovascular collapse. Pain is typically localized
to the epigastric region but quickly becomes generalized. The initial phase reflects
exposure of the peritoneal cavity to acidic fluid triggering release of vasoactive
mediators. Tachycardia, weak pulse, cool extremities, and hypothermia may characterize
this phase. The first-phase duration may range from minutes up to 2 hours. The severity
of symptoms depends on the amount of peritoneal fluid released in the abdomen.
In the second phase, (2–12 hours after onset), abdominal pain may lessen and the inexperienced
observer may be led to believe that the patient is clinically improving. Pain is usually
generalized and often worsens with movement. The abdomen typically demonstrates board-like
rigidity. Liver dullness to percussion may disappear secondary to peritoneal air.
On rectal examination, the pelvic peritoneum may reveal tenderness due to irritation
from inflammatory fluid. Right lower quadrant tenderness may develop due to fluid
in the pelvic gutter.
In the third phase (> 12 hours after onset), increasing abdominal distention is noted,
but abdominal pain, tenderness, and rigidity may be less prominent. Fever and hypovolemia
may result from third spacing. Acute cardiovascular collapse may occur as a result
of advanced peritonitis.
Treatment delay greater than 12 hours increases the risk of severe morbidity and mortality.
Delayed diagnosis may occur during pregnancy and the puerperium due to anatomic changes
of pregnancy that may result in diminished peritoneal signs and nonclassic disease
localization.[2]
[11]
In two of our cases, the cause of gastric perforation was unclear. The patients had
no clear history of PUD. Spontaneous gastric rupture is rare for several reasons:
the stomach is protected by the liver and ribs; has mobile, distensible walls; and
the gastroesophageal and pyloric valves decrease intragastric pressure.[1]
Our literature search identified nine cases of gastric perforation associated with
pregnancy ([Table 1]).[1]
[2]
[3]
[4]
[5]
[12]
[13]
[14]
[15] Two of these cases occurred in the setting of bariatric surgery.[3]
[4]
Table 1
Summary of pregnancy associated gastric rupture case reports
|
Author, year, country
|
Case summary
|
Timing of rupture and risk factor (antepartum/postpartum)
|
Maternal/neonatal outcome
|
|
Miller (1933)[15]
USA
|
A 29-year-old primipara presented in labor at term. Her prenatal course was complicated
by emesis during the last month of pregnancy. During the second stage of labor, she
developed hypovolemic shock and initially responded to fluid resuscitation. A healthy
infant was delivered with forceps. However, 20 h after delivery, she went into a coma
and died. At autopsy, a 3-cm perforation of the greater curvature of the stomach was
found. The etiology of the rupture was unknown.
|
Antepartum
Spontaneous
|
Maternal death/neonatal survival
|
|
Christoph and Pinkham (1961)[19]
USA
|
A 17 year-old at 39 weeks s/p surgery for acute appendicitis. She developed circulatory
collapse secondary to gastric perforation postpartum.
|
Postpartum
Spontaneous
|
Maternal and neonatal survival
|
|
Fiester and Zinn (1975)[14]
USA
|
A 30-year-old woman in her sixth month of pregnancy presented with nausea, vomiting,
and headache. She died soon after admission. Autopsy findings included a 4–5-cm perforation
on the greater curvature of the stomach, fetal death.
|
Antepartum
Spontaneous
|
Maternal death/in utero fetal death
|
|
Seon Cha et al (2002)[1]
USA
|
A young, primigravida delivered a 34-week stillborn infant. Shortly after delivery,
she developed signs of hypovolemic shock. Ultrasound examination showed a large amount
of free intra-abdominal fluid. At laparotomy, gastric rupture was encountered and
repaired. Congenital eventration of the left hemidiaphragm was also noted. After a
complicated postoperative course, the patient recovered and did well.
|
Postpartum
Maternal congenital diaphragmatic hernia
|
Maternal survival/in utero fetal death
|
|
Erez et al (2004)[3]
Israel
|
A 27-year-old primigravida at 35 weeks' gestation and history of gastric banding presented
to labor and delivery with protracted nausea and vomiting. She was initially diagnosed
and treated for a small bowel obstruction but hours later developed an acute abdomen
and non-reassuring fetal testing. Exploratory laparotomy and cesarean delivery were
performed. Gastric secretions and blood were found in the abdomen. A perforated gastric
ulcer was diagnosed and repaired. Neonate and mother were discharged home.
|
Antepartum
Maternal bariatric surgery (gastric banding)
|
Maternal and neonatal survival
|
|
Luu et al (2006)[2]
USA
|
A healthy 34-year-old primigravida woman presented to the emergency department at
33 weeks' gestation, with history of nausea, vomiting, and back pain. She was diagnosed
with pneumonia and discharged home on azithromycin.
The patient returned 8 d later with a new onset of shortness of breath and severe
left-sided chest and back pain.
Chest X-ray showed a left pleural effusion.
The patient went into preterm labor and vaginal delivered of a healthy 34-week neonate.
A computed tomography (CT) scan the following day showed extravasation of oral contrast
into the left pleural space.
Urgent thoracotomy demonstrated a herniated portion of necrotic stomach protruding
through a 2-cm diaphragmatic defect. A 2-cm perforation of the stomach was identified
and repaired.
|
Postpartum
Maternal congenital diaphragmatic hernia
|
Maternal and neonatal survival
|
|
Strezelczyk and Peczak (2008)[11] Poland
|
A 23-year-old at 36 weeks' gestation presented with mild pain of entire abdomen for
several hours prior to admission preceded by severe vomiting after a heavy meal the
day prior to admission. Taken for cesarean delivery for tense abdomen and recurrent
fetal decelerations. Intraoperatively, gas and gastric contents were noted in peritoneal
cavity with perforation of the anterior wall and fundus of stomach and repaired. Both
neonate and mother were discharged to home.
|
Antepartum
Spontaneous
|
Maternal and neonatal survival
|
|
Morcillio-Lopez et al (2010)[5]
Spain
|
A 35-year-old primigravida at 15 weeks' gestation presented to the emergency department
with intense, sudden onset of dyspnea. She had a known congenital diaphragmatic hernia.
CT scan demonstrated herniation of abdominal contents through the diaphragmatic defect.
Thoracotomy demonstrated diaphragmatic and gastric rupture. Both defects were repaired
and she underwent cesarean delivery at 38 weeks' gestation.
|
Antepartum
Maternal congenital diaphragmatic hernia
|
Maternal and neonatal survival
|
|
Policiano et al (2013)[4]
Portugal
|
A 37-year-old primigravida at 33 weeks' gestation with a history of gastric band who
developed abdominal pain, vomiting, and non-reassuring fetal testing. Emergency cesarean
delivery demonstrated hemoperitoneum, and gastric rupture was identified and repaired.
Both neonate and mother were eventually discharged home.
|
Antepartum
Maternal bariatric surgery (gastric banding)
|
Maternal and neonatal survival
|
Isolated gastric ruptures are very rare during pregnancy and reported cases are often
associated with congenital diaphragmatic hernias.[1] Ideally, pregnant women with diaphragmatic disorders should be identified antenatally
or during the first weeks of pregnancy. Correction of the defects and avoidance of
situations that may lead to increased intra-abdominal pressure are essential to reduce
the risk for diaphragmatic hernia-associated gastric perforation.[1]
All of our cases occurred unexpectedly in the postpartum period. No clear medical
histories of gastric ulcers were identified. Patients reported epigastric pain, but
PUD was not considered in the differential diagnosis. Peritonitis, following cesarean
delivery, is a very common clinical finding at CHUK and is the leading cause of severe
maternal morbidity and mortality.[16] As a result, the cases described here were managed as cases of peritonitis.[16]
Our first case occurred only 2 days after a caesarean section in the setting of ascariasis.
In addition to intestinal obstruction, case reports also link ascaris lumbricoides
with gastric perforation.[12]
[17] In 2004, a case from Nigeria described a 65-year-old woman with an acute abdomen.
Exploratory laparotomy 6 hours later demonstrated 3 L of feculent peritoneal fluid,
fibrinoid adhesions, and a 25-cm-long live worm in the peritoneal cavity. The patient
was noted to have a gastric perforation. Investigators theorize that the worm converted
a near perforation into frank perforation or the perforation occurred initially, followed
by egress of the worm into the peritoneum.[18] In 2012, Gupta et al describe the case of a 48-year-old man from India who presented
with an acute abdomen. At the time of laparotomy, 1.2 L of bilious fluid was drained
and a 1 cm × 1 cm stomach perforation was noted. Two live ascaris worms were seen
protruding through the perforation site. No scarring or induration around the perforation
site was noted. These findings were more consistent with an ascariasis-related perforation
rather than long-standing PUD.[12]
Our cases demonstrate the high maternal mortality and morbidity associated with gastric
rupture. Part of the diagnostic delay was associated with the rare nature of this
condition. In all cases reported in the literature, gastric rupture was not considered
in the differential diagnosis at the time of presentation. One patient survived the
event in our case series. Her circulatory collapse prompted immediate laparotomy for
suspected sepsis. The unexpected gastric rupture was diagnosed and repaired. Although
she survived the event, gastric rupture caused a severe, life-threatening, maternal
morbidity.
In the first case, the presentation began 2 days following the cesarean delivery.
The initial diagnosis did not include gastric perforation. The patient probably arrived
in the second or the third phase of gastric perforation where signs in favor of acute
abdomen (perforation) may be less evident and may lead to a false impression of clinical
improvement. The pain of labor and the puerperium may have interfered with the clinical
interpretation. All of these reasons led to poor outcome that ended with maternal
death despite all resuscitative and operative interventions.
Conclusion
The diagnosis of gastric perforation relies on extensive medical history and a thorough
physical examination; however, the pregnant or postpartum state may interfere with
interpretation of the clinical features and complicate the ability to make the diagnosis.
Pregnant women may experience diagnostic delays if providers are reluctant to expose
the fetus to X-ray or computerized tomography
Given the importance of early and accurate management of gastric perforation, obstetricians
and surgeons should be aware of this condition and consider it as part of the differential
diagnosis in the pregnant and postpartum patient with acute-onset gastrointestinal
symptoms. The diagnosis should be highly considered in pregnant patients with history
of bariatric surgery or PUD. Clinical investigations including abdominal ultrasound
and chest X-ray add to the history and clinical picture and enable providers to narrow
the differential diagnosis. Both modalities are available in our low-resource clinical
setting. These cases highlight the importance of early diagnosis and treatment to
improve maternal outcome.
