Pregnancy is a special time in a woman’s life, when waiting for a new life is accompanied by fear for its proper development. A noticeable, but also confirmed by researchers, trend is the increasingly late age of women when they decide to procreate. This has ramifications for both the mother and baby. Pancreatic diseases, observed incidentally during pregnancy until recently, have occurred much more frequently in the last 2–3 decades. This is related to many other changes observed in the modern world, including inappropriate eating habits leading to obesity. These changes generate a greater risk of developing various diseases, including pancreatic diseases and especially acute pancreatitis (AP). The management of AP requires the consideration of physiological and anatomical changes during pregnancy in conjunction with the local and systemic effects of AP. More problems arise when endoscopic or surgical intervention is urgently needed, as both have a potentially serious risk to the mother and the fetus.

2. Epidemiology of Acute Pancreatitis in Pregnancy

Acute pancreatitis in pregnant women occurs with a frequency of 1/1000 to 1/5000 pregnancies ^[1][2][1,2]. Due to significant progress in the prevention, diagnosis, and proper treatment, the death rate of pregnant women due to AP, once very high (37%), has dropped to 3.3%, and fetal mortality from almost 60% to 11.6–18.7%, according to various reports ^[1][3][1,3]. The mean age of onset of AP in pregnancy was 28.5 years. AP was most common in the third trimester of pregnancy. About one-third of the women with AP develop severe pancreatitis. Mortality in pregnant women with acute pancreatitis in pregnancy is comparable to the rate in the general population, but the cumulative maternal death rate was the highest in the first trimester at 12.7%, compared with 7.9 and 6.4% in the second and third trimesters, respectively. The same data were obtained for fetal deaths: the highest death rate was recorded in the first trimester (20.9%). Intrauterine fetal death was the most common in the third trimester (8.8%), while stillbirths were highest in the second trimester (6.2%) [3].

3. Etiological Factors of AP in Pregnancy

There are many risk factors for the development of acute pancreatitis in pregnancy that should be identified before or during the first weeks of pregnancy. These include gallstone disease; hyperlipidemia, especially hypertriglyceridemia; subsequent pregnancies; obesity; a high-fat diet [4]. In contrast to the general population, where gallstone disease and alcohol abuse are the two most common etiological factors, cholelithiasis comes to the fore in pregnant women. Worryingly, despite the widespread knowledge of alcohol’s detrimental effects on fetal development, alcohol is still a common etiological factor [5]. Hypertriglyceridemia has recently been a common cause of AP [6]. Less frequently observed etiological factors are hyperparathyroidism, infectious agents, medications, or injuries. In some cases, it is not possible to determine the cause of AP [7]. Idiopathic pancreatitis is diagnosed on the basis of clinical and laboratory tests confirming AP after excluding all the above-mentioned causes.

4. Gallstone Disease and AP in Pregnancy

Particular attention should be paid to the risk of acute pancreatitis in women diagnosed with cholelithiasis before pregnancy. The possibility for the complications of gallstone disease, including AP, is greater in pregnancy than that in the general population. Pregnancy is also a period that increases the risk of gallstone formation [8]. There is a tendency to change the composition of bile, leading to the bile ducts malfunctioning. The tendency to vomit observed in the first trimester also has an undoubted influence on the formation of bile deposits; in some women, it takes the form of incontinence or vomiting, which promotes dehydration and the thickening of bile [5]. During pregnancy, as a result of the action of hormonal factors, the composition of bile changes, which consists of elevated cholesterol content, the inhibition of the conversion of cholesterol into bile acids, and quantitative changes in the proportion of bile acids. Metabolic disorders such as insulin resistance and elevated leptin levels are also involved in the formation of gallstones [9]. As a result of the action of progesterone, water absorption by the gallbladder mucosa decreases already in the first trimester of pregnancy, which increases its volume and impairs contractility. All these phenomena contribute to the possibility of gallstone formation at the end of the first trimester, and the risk increases significantly in the second and third trimesters of pregnancy [10]. Therefore, to assess the gallbladder and bile ducts, it is recommended to perform an ultrasound of the abdominal cavity at the end of the first trimester of pregnancy; the next ones should be performed at the end of the second trimester of pregnancy [5].

5. Alcohol and AP during Pregnancy

Although alcohol’s detrimental effects on fetal development are well-known, there are reports of acute pancreatitis of this etiology. In caring for a pregnant woman, special attention is paid to emphasizing the need to give up drinking alcohol during pregnancy and breastfeeding. Unfortunately, many people still underestimate this limitation, leading to many complications for both the mother and the fetus. In practice, documenting alcohol as a cause is quite difficult; therefore, the diagnosis is most often performed after excluding other causes, family and environmental history, and high levels of gamma-glutamyltranspeptidase (GGTP) in the blood serum ^[10][11][10,11].

6. Hypertriglyceridemia and AP during Pregnancy

Hypertriglyceridemia (serum triglycerides > 150 mg/dL) is a known etiology of acute pancreatitis. During physiological pregnancy, changes in the carbohydrate and lipid metabolism are observed to ensure the greatest possible availability to the fetus: increased glucose production, progesterone synthesis, lipogenesis, and impaired lipolysis. In women with impaired lipoprotein metabolism, these adaptive changes can lead to severe hypertriglyceridemia. In physiological pregnancy, triglyceride levels increase by 2–4 times in the third trimester, but rarely exceed 300 mg/dL. The increased risk of AP is above 500 mg/dL, but it is most common at triglyceride levels above 1000 mg/dL. The risk of AP increases with the progression of pregnancy: 19% in the first trimester, 26% in the second trimester, and 53% in the third [10]. It is recommended to measure the lipid profile of women in early pregnancy if a family member has a history of hyperlipidemia. If a patient is diagnosed with high lipid values, AP prophylaxis is initiated by following a diet with a fat content of less than 20% and enriched with omega-3 acids, especially docosahexaenoic acid (DHA). The use of insulin enhances the action of lipoprotein lipase and leads to the degradation of chylomicrons, which in turn reduces the level of triglycerides. On the other hand, the use of heparin stimulates the release of lipoprotein lipase. Statins must not be used during pregnancy because they have a proven teratogenic effect on the fetus, and other drugs such as fibrates, cholestyramine, and niacin should not be administered to pregnant women due to a lack of safety studies [12]. There are reports in the literature about the beneficial effect of the use of plasmapheresis in the case of high triglycerides in the prevention of AP in pregnant women [6]. Zeng et al. suggested the use of mean platelet volume (MPV) levels as a predictor of severe AP in pregnant women with hypertriglyceridemia, but such results require additional large-scale prospective research [13]. In women diagnosed with hypertriglyceridemia before pregnancy, it is recommended to change the lifestyle (low-fat diet, omega-3 acids, physical activity, alcohol abstinence), to control other adverse factors (diabetes), and to avoid drugs that may cause acute pancreatitis (glucocorticoids, estrogens). Significant weight gain [14] should be avoided during pregnancy. Gupta et al. suggested that high-risk women check their triglyceride levels once each trimester. Fasting triglycerides > 250 mg/dL should prompt monthly triglyceride levels, screening for gestational diabetes, implementing a strict low-carbohydrate, low-fat diet, and exercising. Fasting triglycerides > 500 mg/dL, despite stringent dietary and lifestyle modifications, should prompt treatment with omega-3 fatty acids and continuing a low-fat diet (<20 g fat/day or <15% calories) under the guidance of a registered dietitian. Plasmapheresis should be considered early in asymptomatic pregnant women with fasting triglycerides > 1000 mg/dL or in pregnant women with clinical symptoms of pancreatitis and triglycerides > 500 mg/dL despite maximal lifestyle changes and pharmacological treatment ^[15][16][15,16].