In the nongravid patient, gastroesophageal reflux disease (GERD) affects close to 40% of patients; during pregnancy, approximately 30–50% of patients are affected [1]. GERD symptoms , including heartburn and regurgitation, most frequently occur in the third trimester of pregnancy [2], but the most important risk factor is pre-existing GERD [1]. Interestingly, GERD symptoms can disappear after delivery, and can recur with subsequent pregnancies [3]. This is, perhaps, due to the effects of progesterone which mediates lower esophageal sphincter relaxation leading to a decrease in muscle tone by approximately 33–50% by 36 weeks’ gestation [4, 5]. Recent studies have shown the significant impact of GERD on quality of life , with more than 70% of gravid patients reporting heartburn and regurgitation which lead to significant reductions in social and emotional functioning [1].

Typical symptoms of GERD include heartburn and regurgitation, but it is also associated with nausea and vomiting. Extra-esophageal manifestations are oftentimes present, including asthma (3.5%), chest pain (6%), and cough (1.2%) [6]. Usually the diagnosis of GERD can be made clinically without the use of further imaging. If necessary for intractable cases, endoscopy is the procedure of choice for diagnosis [7]. However, manometry and pH studies can also be performed safely if necessary [5].

Lifestyle modifications are the primary modality employed to treat GERD during pregnancy. This includes changes in meal sizes and frequency as well as timing. Identification of foods which trigger symptoms is critical, and avoidance of those foods is encouraged. If nighttime GERD is problematic, those patients should elevate the head of the bed.

Medical management of GERD is used in conjunction with lifestyle modifications as first-line therapy and effective for most patients [8]. Mild-to-moderate cases of GERD should be treated with H₂ antagonists and antacids. All proton pump inhibitors are classified as safe for consumption during pregnancy with no adverse outcomes reported such as spontaneous abortion or congenital malformations [1].

Surgical management for GERD, such as laparoscopic fundoplication, has not been reported in the gravid population owing to the efficacy of medical management. In some instances, patients with underlying severe GERD have undergone surgery prior to pregnancy, with good results [9].

The incidence of peptic ulcer disease (PUD) in pregnancy is low, occurring in 78 of 60,994 women with a medically diagnosed ulcer [10]. Peptic ulcer disease, including ulceration of the stomach, duodenum or any combination thereof, often presents with nausea, emesis, and dyspepsia and rarely can be asymptomatic with gastrointestinal bleeding as the presenting symptom [1, 11]. Other conditions that can present similarly include GERD, nonulcer dyspepsia, and hyperemesis gravidarum [12].

There is some thought that PUD improves during pregnancy [1]. Possible explanations include increased prostaglandins and estrogens that offer protective effects to the gastric and duodenal mucosa, immunologic tolerance from pregnancy, healthier lifestyle including reduction in tobacco and alcohol use, diet alterations, and better medical care [1–3].

Diagnosis of PUD in pregnancy is limited, due in part to self-treatment and decreased reporting, hesitancy of physicians to recommend diagnostic workup during pregnancy, and misdiagnosis with similarly presenting conditions common in pregnancy [3]. While esophagogastroduodenoscopy (EGD) is an accepted and studied diagnostic tool in pregnancy, the use of other studies for nausea and emesis which may otherwise be used for diagnosis, such as the upper GI series, would be contraindicated due to the risk of radiation exposure [3]. The most frequent indications for EGD in pregnancy are refractory dyspepsia and GI hemorrhage [3]. A 2011 European study involving treatment for PUD found that only a small number of those diagnosed with PUD have had an endoscopic exam for diagnosis and the majority of those cases were self-diagnosed [1].

Diagnosis of a perforated peptic ulcer is typically clinical, with findings of peritonitis and acute abdomen. Performance of a plain film to document free intraperitoneal air is critical and not contraindicated in pregnancy [13]. EGD, however, is contraindicated when perforation is suspected.

Diagnosis of a bleeding ulcer is also clinical, with patients presenting with melena, hematemesis, hematochezia, and hypotension. Initial diagnostic maneuvers include performance of nasogastric lavage. Nasogastric decompression is also critical to prevent pulmonary aspiration during subsequent EGD [14].

Once diagnosed, recommended treatment for ulcer disease first includes lifestyle modifications. This means smaller, more frequent meals, separate liquid intake from meals, maintaining upright position postprandially, avoiding late night meals, and triggering foods such as caffeine, fatty foods, and if applicable, tobacco, and alcohol [3].

If PUD is refractory to lifestyle modifications, then drug therapies are commonly recommended [1]. Frequently utilized medications include antacids, gastric acid secretion inhibitors (H₂ blocker), proton pump inhibitors, and cytoprotective medications (carafate). Eradication of Helicobacter pylori , a treatment option in the nonpregnancy population, should be deferred to the postpartum period [3]). A 2011 European study failed to identify a higher occurrence of congenital abnormalities in women with PUD or those who received drug treatments during pregnancy [1]. Another European study of proton pump inhibitors similarly did not show an increased risk of congenital abnormalities in those exposed [15].

Perforation and bleeding are the two most frequent indications for surgical intervention, and treatment in the gravid patient is the same as in the nongravid patient. A perforated peptic ulcer necessitates emergent surgical intervention with concurrent resuscitation and broad-spectrum antibiotics. Medical management of perforated ulcers is associated with poor prognosis for both mother and fetus, with mortality ranging between 60% and 100% [5]. In the operating room, either Graham patch closure or partial gastrectomy is indicated depending on clinical findings.

Should gastrointestinal bleeding be the presenting symptom, the patient should be hospitalized, observed, and fluid resuscitated as indicated. The bleeding patient should be placed in the left lateral decubitus position to improve venous return through the vena cava and maintenance of uterine perfusion [16]. Endoscopic management with possible therapeutic intervention should be considered first to manage hemorrhage [3]. Indications for surgery for PUD bleeding include failure of endoscopic management, hemodynamic instability, or continued hemorrhage after transfusion of six or more units of red blood cells. As with perforated ulcers, surgical as opposed to medical management of bleeding ulcer disease is associated with improved maternal and fetal outcomes [5].

Hepatic rupture can occur spontaneously or after an inciting event, such as trauma . The liver is a protected organ owing to its location adjacent to the ribs and diaphragm. Nevertheless, the liver parenchyma itself or lesions within the liver, such as tumors or cysts, can rupture. In the gravid patient, there is an association between pre-eclampsia, eclampsia, and HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) with spontaneous hepatic rupture, with a case-to-delivery ratio of 1:45,000 [17, 18]. In fact, the vast majority (approximately 80%) of spontaneous ruptures are associated with pre-eclampsia [19].

Hepatic rupture usually occurs in the third trimester. In approximately 75% of patients, intraparenchymal hemorrhage occurs in the right lobe; 11% of rupture occurs within the left lobe; and in 14% of patients there is bilateral involvement [20]. Intraparenchymal hemorrhage progresses to contained subcapsular hemorrhage. After the capsule ruptures, the tamponade effect is released, and in patients who are thrombocytopenic, appropriate clotting will not contain progressive hemorrhage [21]. Maternal mortality remains high with this diagnosis, ranging from 25% to 75% [1].

Other rare causes of hepatic rupture include hepatic cysts , which are relatively common and occur in up to 5% of patients [22]. Intraperitoneal or extraperitoneal hemorrhagic cyst rupture is rare, occurring in only 1% of patients. The risk of rupture corresponds to the intracystic pressure and not to the intra-abdominal pressure, so the resultant effects of pregnancy are not necessarily a risk factor [23], and there have only been case reports of ruptured cysts in the gravid population [24].

Liver abscess is a serious condition which can result from a variety of intra-abdominal processes , such as perforated viscus due to appendicitis or diverticulitis with resultant hematogenous spread to the liver [27]. Not surprisingly, then, enteric bacteria including Bacteroides and Escherichia coli are the most prevalent causative organisms. In areas where endemic, amoebic liver abscesses (Entamoeba histolytica) should also be considered. However, liver abscesses can also occur from liver necrosis secondary to liver infarction resulting from pre-eclampsia.

Biliary disease is the second most common gastrointestinal disorder requiring surgery during pregnancy [31]. Perhaps, this is due to the changes in biliary physiology induced by the hormones of pregnancy. Increased serum estrogen and progesterone during pregnancy induce metabolic changes in the synthetic and excretory physiology of bile.

Bile, which is composed of bile salts derived from cholesterol, increases in viscosity and volume with elevated estrogen [32]. This risks increased cholesterol crystal aggregation and therefore gallstones. Increased progesterone has been shown to cause relaxation within the smooth muscle of the gallbladder which leads to bile stasis [33]. Studies have widely demonstrated that gravid patients are at increased risk for biliary tract disease, as more than 25% of postpartum patients were demonstrated to have biliary sludge as a result of hormonal changes induced by pregnancy [34].

Among the most frequent causes of acute abdomen in pregnancy is acute cholecystitis. Its incidence ranges from between 0.2 and 0.5 per 1000 pregnancies [35]. In the nongravid patient, this typically presents with right upper quadrant pain and fevers, and treatment of cholecystitis can vary, ranging from medical therapy, endoscopic therapy, percutaneous drainage, or surgery depending on the patient’s underlying medical conditions and presentation. In the gravid patient, however, the differential diagnosis for right upper pain is broad, and can include uterine contractions, fetal movement, adnexal torsion or rupture, liver hematoma, cholangitis, hepatitis, peptic ulcer, and pancreatitis. It is important then, to first accurately make the diagnosis and then offer the appropriate treatments in a timely fashion.

The biliary tract can be prone to complications from benign and malignant conditions which can cause an acute abdomen in the pregnant patient. The diagnosis and treatment of these conditions should ultimately be undertaken with the health and safety of the mother primarily, but modifications in workup and treatment stratagems can be considered to maximize the chance of successful pregnancy and minimize harm to the fetus.

Medical treatment with endoscopic therapy has become the standard of care to treat choledocholithiasis. With endoscopic retrograde cholangiography, it becomes possible to both diagnose obstructing lesions within the biliary tree and treat them using extraction and stenting techniques.

Endoscopic retrograde cholangiopancreatography (ERCP) does not come without increased risk, however. The ability to visualize the biliary tree requires the use of fluoroscopy, iodinated contrast, radiation, and sedation. In the first trimester, this combination of factors can result in increased complications. Tang and colleagues reported a lower rate of full-term pregnancy (73%), lower birth weight (21%), and higher rate of preterm delivery (20%) in 65 patients who underwent ERCP in the first trimester [30].

The radiation exposure risk from ERCP can be clinically significant. In the pregnant patient, the typical radiation doses using ERCP range from 3.4 mGy to 55.9 mGy [52]. Fortunately, the fetus lies outside the radiation beam during ERCP, but there is potential to exceed the safe clinical radiation thresholds of 50 mGy stipulated by ACOG guidelines [53]. Doses in excess of 100 mGy can result in significant fetal complications, such as growth restrictions, mental retardation, fetal malformations, and intrauterine death [54, 55]. Strategies to mitigate radiation exposure include minimizing fluoroscopic time and performance of ERCP by an experienced practitioner. Smith and colleagues demonstrated that when ERCP was performed by a specialty biliary endoscopist with more than 500 cases yearly, the estimated fetal radiation dose was less than 0.5 mGy [17].

Another strategy that can minimize radiation exposure is performance of endoscopic ultrasound (EUS) to visualize the biliary tree. Only after obstructing stones are located and identified can ERCP and fluoroscopy be performed. Lee and colleagues demonstrated that this approach led to fewer complications and allowed for proper selection of patients which would benefit from ERCP [37].

When a calculus within the common bile duct is unable to be retrieved endoscopically, a number of options exist. If the stone is partially obstructing, allowing the passage of a plastic stent, that may be a temporizing measure to ensure proper flow of bile. At some point, however, the patient will require removal of the offending obstruction. This will need to be performed surgically in the form of a common bile duct exploration, which can be performed laparoscopically or in an open fashion. Typically, laparoscopic exploration is successful in 80–90% of patients, but does require a skilled surgeon [56]. Laparoscopic exploration can be performed transcystically when the stone burden is low (<5 stones), small (<0.8 cm), not located in the common hepatic duct, and anatomy is favorable (i.e., cystic duct joins common bile duct laterally and not medially) [57]. In cases where the stone is larger and more impacted , a choledochotomy may be necessary to remove the stone [58]. Though the number of laparoscopic common bile duct explorations is limited in the pregnant population, the case reports of such a technique have yielded successful outcomes with no obstetric complications [43, 59].

The decision to operate after successful ERCP should be made on a case-by-case basis. If ERCP was successful in stone removal and sphincterotomy was performed, the necessity for emergent cholecystectomy to prevent future episodes may be minimized. It seems more advantageous to delay cholecystectomy in this situation until after delivery. On the other hand, if the patient seems to have continued symptoms or develops acute cholecystitis, more immediate surgery should be performed [23].

The incidence of pancreatitis in pregnancy varies between 1:882 and 1:4,449 pregnancies [60–64]. Despite the overall low number of cases in the literature, general trends do arise. The most common causes of pancreatitis in pregnancy were related to biliary etiology and hypertriglyceridemia . Acute pancreatitis related to a biliary etiology was estimated 57–73% of the cases studied [46–49, 65]. A variety of less common causes, including alcohol consumption, hypercalcemia, hyperparathyroidism, trauma, anatomic variables, cystic fibrosis, medications, and idiopathic causes, are also known to be causes [46, 49, 50]. There is a trend toward both mild and severe pancreatitis presenting later in gestation [50], with 43–95% of cases in the third, 5–33% in the second, and 0–24% in the first trimester [45, 46, 48, 50, 66, 67].

Several pregnancy-related risk factors have been identified which predispose one to biliary pancreatitis. Weight gain and hormonal changes associated with pregnancy lead to increased biliary sludge and gallstone production [49, 68]. Hormonal changes also lead to smooth muscle relaxation and bile stasis resulting in reduced gallbladder motility [52]. It is thought that cholesterol secretion increases in the second and third trimesters of pregnancy leading to saturated bile, and that while the fasting and postprandial gallbladder volumes are greater, the emptying rate and volume are reduced [53]. After delivery with normalization of hormones, gallbladder motility normalizes and the stones may disappear as biliary homeostasis is restored [53].

Estrogen is believed to be related to increases in triglycerides during pregnancy, with up to a fourfold increase in levels considered “physiological hyperlipidemia or pregnancy” [69, 70]. Despite this rise, levels generally do not reach above 300 mg/dL, and hypertriglyceridemia is more pronounced during the second and third trimesters [55, 71]. Many cases of hypertriglyceridemic pancreatitis did not have pre-gestational hyperlipidemia nor familial dyslipidemia [10]; however, an underlying genetic predisposition, obesity, excessive weight gain, diabetes, alcohol consumption, and some drugs may contribute to dyslipidemia [4, 6].

The overall majority of cases of acute pancreatitis were noted to be mild with generally favorable maternal and fetal outcomes [45]. However, in cases of severe acute pancreatitis more than 77% were caused by hypertriglyceridemia [51]. Nonbiliary pancreatitis was associated with more complications, worse outcomes such as preterm delivery when compared to biliary pancreatitis as well [51, 54]. Others have reported biliary and idiopathic causes had better overall outcomes with fewer incidences of organ failure and fetal mortality [50].

In patients with severe pancreatitis, despite the aggressive management required—including mechanical ventilation , hemodialysis, percutaneous drainage, chest drainage, and open necrosectomy—there are no maternal deaths reported [54]. The organ systems most vulnerable to failure are respiratory, renal, and hepatic, with renal and coagulation disorders denoting poor prognosis. Fetal death was more likely when two or more organ systems were affected [50].

The clinical presentation of acute pancreatitis often elicits complaints of epigastric, right, or left upper quadrant pain, with associated nausea or emesis. The pain is often constant with radiation to the back, chest, and flanks [72]. Despite the common complaints of nausea and emesis in pregnancy, any patient presenting with prolonged nausea and emesis should elicit a pancreatitis workup [17]. Initial workup begins with bloodwork including amylase, lipase, complete blood counts, metabolic panel including liver function testing and a triglyceride level. Serum amylase and lipase continue to be reliable markers during pregnancy, with lipase level unchanged and amylase remaining normal or mildly elevated [53]. Elevation of serum lipase and amylase to levels three times higher than normal has a good positive predictive value [52]. Elevation of alanine aminotransferase to levels greater than three times normal is a sensitive marker for a biliary etiology of pancreatitis [53]. Triglyceride levels rise gradually and reach a peak during the third trimester, to almost twice nonpregnant levels, then return to prepregnancy levels by 6 weeks postpartum [52]. Nonbiliary causes of pancreatitis have been found to produce worse outcomes and thus screening for these etiologies is of particular importance [50, 55]. The use of serum calcium and triglycerides, parathyroid levels, and discussions about alcohol consumption allow for comprehensive assessment of etiology [46, 50, 55].

Abdominal ultrasonography is a safe and reliable way to diagnose biliary pancreatitis and identifies cholelithiasis or sludge in up to 70% of patients [48]. It can be limited in detection of common bile duct stones; therefore, alternative imaging may be considered when ultrasound or lab findings suggest choledocholithiasis despite an inconclusive ultrasound [53]. Due to concerns of radiation exposure related to computed tomography (CT) imaging and endoscopic retrograde cholangiopancreatography (ERCP) , magnetic resonance cholangiopancreatography (MRCP), and endoscopic ultrasonography (EUS) should be considered for diagnosis [49, 52, 53]. Additionally, MRCP use can limit the use of ERCP to therapeutic procedures only [53, 55], given concerns about radiation exposure to the fetus.

Treatment of pancreatitis in pregnancy generally follows similar principles to that in the nonpregnant population. Hospitalization is indicated for diagnosis, pain management, aggressive rehydration, electrolyte replacement, nasogastric decompression, and, in limited cases, hyperalimentation [17]. Following the American College of Gastroenterology (ACG) guidelines, aggressive hydration is most beneficial and of vital importance in the first 12–24 h [56], with lactated ringers as the choice crystalloid replacement fluid. Frequent reassessment within the first 48 h and use of BUN, creatinine, and hematocrit as surrogate markers for successful rehydration are standard means to follow the clinical course of pancreatitis.

Bowel rest is indicated though nutrition is of obvious importance to the pregnant state. According to the ACG, bowel and pancreatic rest until complete resolution of pancreatitis is no longer indicated. Current guidelines indicate that complete bowel rest is associated with intestinal mucosal atrophy and increased infectious complications [56]. There is some suggestion that the frequency of maternal complications secondary to central venous catheters is higher in the pregnant population [53]. While studies are limited in addressing this factor specifically during pregnancy, general principles for the nonpregnant population recommend enteral feeding over parenteral feeding when possible [56]. Enteral nutrition has recognized benefits including maintenance of the gut flora and mucosal barriers, promoting of gut immunity, and reduction of bacterial translocation [48, 54]. For patients with mild pancreatitis, immediate refeeding with a soft, low-fat, low residual diet is safe and may lead to shorter hospitalization than advancing through from the clear liquid diet [56]. Early enteral nutrition (within 1–3 days) in severe pancreatitis was initiated in a 2010 study where 18 of 69 cases were deemed severe, there were no maternal deaths reported in the study nor feeding-related complications [54].

It is believed that early diagnosis, aggressive treatment and intervention, and improvements in intensive care for both mother and fetus have played a role in the decrease in morbidity and mortality associated with pancreatitis [55]. The main causes of perinatal mortality were preterm delivery, while additional risks include threatened preterm labor and in utero fetal death [52, 55]. Intensive fetal monitoring has been suggested when recurrence or prolonged disease is encountered. This may consist of nonstress testing and serial ultrasounds for fetal growth as well as biophysical profiles [17].