A C TA Obstetricia et Gynecologica

MAIN RESEARCH ARTICLE

Acute pancreatitis in pregnancy

LIQUN SUN, WEIQIN LI, YANXIA GENG, BO SHEN & JIESHOU LI
Medical School of Nanjing University, Department of General Surgery, Jinling Hospital, Nanjing, China

Key words Biliary disease, hypertriglyceridemia, pancreatitis, pregnancy, complications Correspondence Weiqin Li, Department of General Surgery, Jinling Hospital, No. 305 East Zhongshan Road, Nanjing 210002, China. E-mail: njuslq@163.com Conict of interest The authors have stated explicitly that there are no conicts of interest in connection with this article. Received: 7 September 2010 Accepted: 22 December 2010 DOI: 10.1111/j.1600-0412.2011.01072.x

Abstract Objective. The highest maternalfetal risk from pancreatitis in pregnancy is likely to be posed by the most severe cases, which we have compared with mild cases. Design. Retrospective observational study. Setting. A general surgery department of a university referral hospital in Nanjing, China. Population. Eighteen pregnancies complicated with severe acute pancreatitis and 51 pregnancies complicated with mild acute pancreatitis. Methods. Medical records were reviewed for every pregnant woman with mild or severe acute pancreatitis during January 1999 to December 2009. Main Outcome Measures. Information on demographics, clinical and laboratory data, maternal and fetal outcomes. Results. Gestational age of onset was signicantly higher in the severe acute pancreatitis group than in the mild acute pancreatitis group. Severe hypertriglyceridemia was considered the main cause of severe acute pancreatitis (OR 20.7; 95% CI 4.692.4, p<0.001), while biliary disease contributed to the etiology of mild acute pancreatitis (OR 7.3; 95% CI 1.830.1, p<0.01). Abortions and preterm infants contributed to fetal loss in the mild group, while fetal death and stillbirth contributed in the severe group. Conclusions. Hyperlipidemic pancreatitis and biliary pancreatitis are the main causes of severe and mild disease, respectively. Severe acute pancreatitis in pregnancy usually occurs in the third trimester, and the affected severe patients are more liable to develop a critical condition that results in higher risk of intrauterine fetal death.
Abbreviations: AP, acute pancreatitis; APACHE, acute physiology and chronic health evaluation; MAP, mild acute pancreatitis; SAP, severe acute pancreatitis

Introduction
Acute pancreatitis (AP) is a rare complication in pregnancy, occurring in approximately three in 10 000 pregnancies (1,2). Biliary disease is the most common etiological factor of pancreatitis during pregnancy, and the majority of cases are connected to good maternal and perinatal outcomes. However, nonbiliary cases are related to elevated maternal and neonatal risks (13). The spectrum of AP ranges from mild to severe, as dened by the Atlanta Conference (4). Since the greatest danger to the mother and fetus from pancreatitis in pregnancy is likely to be posed by the most severe cases, understanding severe acute pancreatitis (SAP) during pregnancy is particularly important. To date, few reports pertain to severe pancreatitis in pregnancy. In this study, we reviewed all pregnant cases with the complication of SAP or mild acute pancreatitis (MAP) in order to distinguish the specic characteristics of SAP from MAP in pregnancy.

Material and Methods

This was a retrospective study over an 11 year period from January 1999 to December 2010 and was approved by the Institutional Review Board of Jinling Hospital, a university referral hospital in Nanjing. Medical records were reviewed for every pregnant woman consecutively admitted to the surgical department with SAP or MAP. Women in the puerperium or with chronic pancreatitis were not included. We collected information on maternal age, gestational age at onset and delivery, potential etiologic factors (biliary disease, high-fat diet, alcohol abuse), admission acute physiology and chronic health evaluation (APACHE) II score, diagnostic testing (biochemical parameters in a fasting state, transabdominal ultrasonography, arterial blood gas analysis), management, maternal outcomes (local complications or organ dysfunction induced by AP, hospital days and intensive care unit days) and fetal outcomes (term and preterm

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Table 1. Demographic data in the study populations. Demographic data Maternal age (years; median (range)) GAO (weeks; median (range)) GAD (weeks; median (range)) Nulliparous women (n (%)) Recurrent pancreatitis (n (%)) Trimester of onset (n (%)) First Second Third SAP (n=18) 29 (2138) 35.8 (28.039.7) 36.8 (28.140.0) 10 (55.6) 2 (22.2) 0 1 (5.6) 17 (94.4) MAP (n=51) 29 (1939) 25.0 (10.035.0) 38.0 (16.040.0) 42 (82.4) 3 (5.9) 5 (9.8) 28 (54.9) 18 (35.3) Total cases (n=69) 29 (1939) 28.9 (10.039.7) 38.0 (16.040.0) 52 (75.4) 5 (7.2) 5 (7.3) 29 (42.0) 35 (50.7) p-Value 0.518 <0.001 0.846 0.053 0.600 <0.001

Note: Comparisons were performed by t -test or Fishers exact test. Abbreviations: GAD, gestational age at delivery; GAO, gestational age at onset; MAP, mild acute pancreatitis; SAP, severe acute pancreatitis. Comparisons were between group of SAP and MAP.

infants, perinatal death). All the patients were followed up every month for a postpartum period of 618 months. The characteristics of patients are shown in Table 1. According to the Atlanta criteria (4), AP is dened as typical abdominal pain with serum lipase levels three times higher than the upper limit of normal and graded as mild or severe. Mild acute pancreatitis was associated with minimal organ dysfunction and an uneventful recovery. Patients with MAP responded to appropriate uid administration with prompt normalization of physical signs and laboratory values. Severe acute pancreatitis was dened as attacks of AP associated with organ failure or local complications, such as necrosis, abscess or pseudocyst. Organ failure was dened as shock (systolic blood pressure <90 mmHg), respiratory insufciency (arterial partial pressure of O2 60 mmHg), renal failure (creatinine level >177 mol/l after rehydration), gastrointestinal bleeding (>500 ml/24 h) or systemic complications, such as disseminated intravascular coagulation (platelets 100 000/mm3 , brinogen <1.0 g/l and brin split products >80 g/ml) or severe metabolic disturbances (calcium level 1.87 mmol/l). The further characterization was based on APACHE II score 8. Cause was ascertained based on the history and ultrasound and laboratory studies. Biliary pancreatitis was dened as the presence of gallstones or sludge in the biliary tree or the gallbladder (5). Hyperlipidemic pancreatitis was diagnosed when serum triglyceride level was >11.3 mmol/l (1 000 mg/dl) (6). The patients involving alcohol consumption were analyzed as alcoholic pancreatitis. Acute pancreatitis associated with drugs, postendoscopic retrograde cholangiopancreatography and abdominal surgery were gathered as other causes (7). Based on the weeks of gestational age of onset, trimester categorization was dened as rst (112 weeks), second (1328 weeks), and third (29 weeks) (5). Term pregnancy was dened as 37 completed weeks of gestation.

Statistical analysis
Results are presented as n (%) for categorical data, or median (range) for continuous variables. Comparison between groups was performed by a t -test or Fishers exact test. All tests were two-tailed, and p<0.05 was considered signicant. The statistical data analysis was performed using the SPSS 13.0 software package (SPSS, Chicago, IL, USA).

Results
Eighteen pregnant women with SAP and 51 with MAP were enrolled (Table 1). During the study period, 1 555 nonpregnant patients diagnosed with AP were admitted to the hospital. Thus, the percentage of pregnancy-associated AP was 4.25%. There were no signicant differences in maternal age, gestational age at delivery, nulliparous women or recurrent pancreatitis between SAP and MAP patients. The gestational age of onset was signicantly higher in the severe acute pancreatitis group than in the mild group (p<0.001). All women underwent abdominal ultrasonography, and abnormalities were found in 43 (62.3%) women. In the MAP group, 35 (68.6%) developed pancreatitis secondary to a biliary disease [odds ratio (OR) 7.3; 95% condence interval (CI) 1.830.1, p<0.01)], while in the SAP group only three women (16.7%) developed pancreatitis following biliary disease alone. In contrast, hyperlipidemic pancreatitis was identied in most SAP cases (77.8%), and the mean serum triglyceride level at onset was 27.9 mmol/l (13.247.5 mmol/l). Due to severe chylemia, the triglyceride level was not measured on admission in two patients, but was >30 mmol/l in both 12 hafter admission. Five patients with severe hypertriglyceridemia had simultaneous ultrasonographic gallstones or sludge. Excluding these ve women, hypertriglyceridemia alone was still the main independent etiologic factor in the SAP group (OR 20.7; 95% CI 4.692.4, p<0.001). In all patients with hypertriglyceridemia, the triglyceride level

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Table 2. Primary causes of acute pancreatitis in pregnancy (n (%)). Severe acute pancreatitis (n=18) 8 (44.4) 6 (33.3) 3 (16.7) 3 (16.7) 14 (77.8) 9 (50.0) 0 1 (5.6) Mild acute pancreatitis (n=51) 35 (68.6) 23 (45.1) 12 (23.5) 35 (68.6) 5 (9.8) 5 (9.8) 5 (9.8) 6 (11.8) Total cases (n=69) 43 (62.3) 29 (42.0) 15 (21.7) 38 (55.1) 19 (27.5) 14 (20.3) 5 (7.2) 7 (10.1)

Primary causes Biliary disease Gallstones Sludge Biliary disease alone Severe hypertriglyceridemia Hypertriglyceridemia alone Alcohol Other causes

Note: In one patient both gallstones and sludge were detected. Biliary disease contributed to the main etiology of mild acute pancreatitis (OR 7.3; 95% CI 1.830.1, p<0.01). Severe hypertriglyceridemia was the main cause of severe acute pancreatitis (OR 20.7; 95% CI 4.692.4, p<0.001).

One relapse case selected abortion during her recurrent episode in the second trimester, and four women had a spontaneous abortion at 9, 11, 12 and 14 gestational weeks, respectively. The term delivery rate of the MAP group was signicantly higher than the SAP group (p=0.01). There were 15 preterm deliveries related to the acute episode of pancreatitis; 11 infants survived and four infants died due to prematurity. All the fetal deaths and stillbirths were found in the SAP group (5 patients vs. 0, p=0.001). These ve patients included three diagnosed with multiple organ failure and two with both local and systemic complications. The difference between SAP and MAP groups was not signicant with respect to premature deliveries (p=0.05) and abortions (p=0.18). The overall fetal mortality rate was 23.2%, and there was no significant difference between the SAP and MAP groups (p=0.33; Table 3).

Discussion
declined rapidly (12 days bowel rest and hydration) after admission and remained normal during follow-up. Alcohol consumption was only identied in ve MAP patients (Table 2). The APACHE II score on admission, which indicates the severity of disease, was much higher in the SAP group (p<0.001). Likewise, intensive care unit admission, duration and hospital stay in the SAP group differed signicantly from the MAP group (Table 3). Of the SAP patients, 12 had local complications (acute uid collection and pseudocyst) and 10 had systemic complications. Four women had both local and systemic complications and three were diagnosed with multiple organ failure, with dysfunction of at least two organs. Respiratory insufciency was the most common systemic complication in this study (9 of 10 cases). Other rare systemic complications are shown in Table 3. All SAP patients were treated by bowel rest in the initial 13 days, followed by early enteral nutrition delivered directly into the proximal jejunum via feeding tube (8). Special managements performed included mechanical ventilation (n=7), continuous hemodialysis (n=5), percutaneous peripancreatic drainage (n=6), chest drainage (n=4) or open necrosectomy (n=8). In all the SAP patients, successful management was achieved and there was no maternal death. In the MAP group, 35 patients with biliary pancreatitis underwent laparoscopic cholecystectomy, percutaneous transhepatic gallbladder drainage (9) or endoscopic nasobiliary drainage upon admission. Sixteen women with nonbiliary pancreatitis recovered quickly through only temporary bowel rest followed by 12 weeks of enteral nutrition and intravenous hydration. No patient agreed to undergo diagnostic or therapeutic endoscopic retrograde cholangiography due to concern about the potential radiation risk to the fetus.
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To our knowledge, this is the rst observational study reporting specic characteristics that differ between SAP and MAP in pregnancy. Acute pancreatitis in pregnancy usually occurs in the second and third trimesters. More than 90% of the women developed pancreatitis in the last two trimesters, and almost all SAP cases were in the third trimester, consistent with case reports about SAP in pregnancy (10,11). Several etiologic factors may be suggested. The large uterus limits gallbladder motility and also produces pancreatic ischemic injury, which is increasingly recognized as an important mechanism in the pathogenesis of AP and multiple organ failure (12). Estrogen-related increases in serum triglyceride levels produce the hyperviscosity which is supposed to lead to ischemia and acidosis in pancreatic capillaries (13,14). Changes in bile composition secondary to high estrogen levels in the last trimester may induce the formation of gallstones and sludge (13), which are the main causes of AP. The etiology of pregnancy-associated pancreatitis is similar to that in nonpregnant patients. Biliary disease is considered to be the main cause of AP in pregnancy (1,2,14). In general, biliary pancreatitis is mild and prone to recur (5). Our data show that biliary pancreatitis is still the main cause of MAP, but the main cause of SAP is likely to be quite different; 77.8% of SAP patients had severe hypertriglyceridemia, with triglyceride levels higher than 13 mmol/l in the fasting state. Ewald et al. considered that pregnancy was one of the secondary causes of hypertriglyceridemia, and hypertriglyceridemia accounted for up to 50% of all pancreatitis cases in pregnancy (15). During pregnancy, an up to fourfold increase in plasma triglycerides and 50% increase in plasma cholesterol is regarded as normal and called physiologic hyperlipidemia of pregnancy (16). It is thought to represent a generalized increase in substrate mobilization, both for the placenta and for the growing fetus. Clinically signicant hyperlipidemia

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Table 3. Maternal clinical characteristics and pregnancy outcomes. Maternal clinical characteristics and pregnancy outcomes Maternal clinical characteristics APACHE II score on admission (median (range)) Complications (n (%)) Local complications Systemic complications Respiratory insufciency Renal failure Disseminated intravascular coagulation Shock Gastrointestinal bleeding Severe metabolic disturbances ICU admission (n (%)) ICU duration (days; median (range)) Hospital stay (days; median (range)) Death (n (%)) Pregnancy outcomes (n (%)) Term deliveries Premature deliveries Abortions Fetal death and stillbirths Perinatal deaths (mortality) Note: Comparisons were performed by t -test or Fishers exact test. SAP (n=18) 8.5 (422) 12 (66.7) 10 (55.6) 9 (50.0) 2 (11.1) 1 (5.6) 1 (5.6) 1 (5.6) 1 (5.6) 18 (100) 23 (3111) 35 (9195) 0 6 (21.4) 7 (38.9) 0 5 (17.9) 6 (33.3) MAP (n=51) 1.5 (07) 0 0 0 0 0 0 0 0 17 (33.3) 0 (011) 8 (428) 0 36 (70.6) 8 (15.7) 7 (13.7) 0 10 (19.6) p-Value

<0.001

<0.001 <0.001 <0.001 1.000 0.010 0.052 0.177 0.001 0.330

characteristically occurs in the third trimester when lipid clearance is outpaced by lipid synthesis and release (17). However, triglyceride levels higher than 11.3 mmol/l are considered as a risk factor to trigger AP in a pregnant woman (6). In agreement with previous reports (18,19), in the present study the pregnant women who developed hyperlipidemic pancreatitis had neither familial dyslipidemia nor nongestational hyperlipidemia. Moreover, the triglyceride level decreased rapidly after 12 days of bowel rest and hydration and remained normal after delivery as well as in the follow-up period. In addition, animal studies have shown that hyperlipidemia intensies the course of acute edematous and acute necrotising pancreatitis (20). A study of 129 patients with nonpregnant AP referred for severe hypertriglyceridemia showed that the severity of hyperlipidemic AP was higher than that of AP provoked by gallstones or alcohol (21). In pregnant populations, recent studies also suggested that the hyperlipidemic form was associated with particularly poor outcomes (1,22). The results of the current study were in line with these ndings. Although alcohol is considered as one of the main causes of pancreatitis, several studies suggested that alcohol abuse is uncommon in pregnancy (2,23). In China, the one-child family policy (24) and excessive concern for pregnant women may contribute to rare alcohol consumption during pregnancy. For AP in pregnancy, treatment should aim to minimize maternal and fetal mortality. Patients with MAP are usually clinically stable and have a favorable response to support-

ive therapy. Most achieve term pregnancy after appropriate management and, as in the current study, the gestational age at delivery was much higher than at the onset of pancreatitis in the MAP group. Biliary pancreatitis has to be treated promptly because it is prone to relapse (5,25). Bowel rest, intravenous hydration and slow progression to a nonfat diet are often adequate interventions for hyperlipidemia. Takaishi et al. (26) suggested that -3 fatty acids may prevent recurrent hypertriglyceridemia during pregnancy, but this needs further investigation. There are few data to guide treatment of SAP in pregnancy. Based on high mortality rates following the surgical management of severe pancreatitis in nonpregnant patients, some investigators attempted to minimize operative intervention in pregnant patients with severe pancreatitis. In line with this, we attempted percutaneous peripancreatic drainage in six patients with severe local complications. It has been demonstrated that computed tomography- or ultrasound-guided percutaneous peripancreatic drainage may decrease mortality in severe acute pancreatitis (27,28). Rapid progression to enteral nutrition delivered distal to the ligament of Treitz has proved to be both possible and benecial, because it helps to maintain the gut mucosal barrier and even limits the septic complications in SAP (29). All of our patients achieved enteral feeding, and there were no related complications. It should be emphasized that the formula of nutrition treatment for hyperlipidemic pancreatitis should be nonfat and low calorie.
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With improvements in neonatal intensive care, the high perinatal mortality is mainly due to fetal death. We observed no neonatal death. The fetal mortality was similar in both forms of the disease, but the component of fetal loss was different between MAP and SAP. Late abortion (70%) and preterm infants (30%) constituted the fetal loss in the women with MAP, while fetal death and stillbirth were the main fetal loss components (83.3%) in the SAP group. Since a severe maternal condition can result in a vicious circle of worsening maternal or fetal outcomes, termination of the pregnancy is recommended for these women when homeostatic conditions cannot be achieved rapidly. Moreover, as the severe maternal morbidity is an indicator of termination of pregnancy, timely termination may improve the maternal condition as well as the fetal outcome. Cesarean section will be the preferred mode for the prevention of other complications, such as aspiration. There are several limitations in the present study. Firstly, patients with acute pancreatitis were admitted to our hospital because our surgical department is a center for this condition, which resulted in a raised incidence of acute pancreatitis in pregnancy. We cannot calculate the accurate incidence of acute pancreatitis in this pregnant population. Secondly, the conclusions might not apply to other populations due to race and culture variations. We had few alcohol-related cases and more hyperlipidemic women in this sample. Finally, this is an observational study on clinical characteristics, and further studies are necessary to provide better understanding of the cause and types of hypertriglyceridemia. In conclusion, SAP in pregnancy usually occurs in the third trimester, whereas MAP commences mainly in the second trimester. Patients with the biliary-related MAP usually achieve term pregnancy, and the causes of fetal loss are abortion and preterm delivery, while women with SAP are more liable to critical conditions which result in a higher risk of intrauterine fetal death, with timely delivery being benecial. References
1. Eddy JJ, Gideonsen MD, Song JY, Grobman WA, OHalloran P. Pancreatitis in pregnancy. Obstet Gynecol. 2008;112:107581. 2. Ramin KD, Ramin SM, Richey SD, Cunningham FG. Acute pancreatitis in pregnancy. Am J Obstet Gynecol. 1995;173:18791. 3. Pitchumoni CS, Yegneswaran B. Acute pancreatitis in pregnancy. World J Gastroenterol. 2009;15:56416. 4. Bradley EL 3rd. A clinically based classication system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, GA, September 11 through 13, 1992. Arch Surg. 1993;128:58690. 5. Hernandez A, Petrov MS, Brooks DC, Banks PA, Ashley SW, Tavakkolizadeh A. Acute pancreatitis and pregnancy: a

6.

7. 8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

10-year single center experience. J Gastrointest Surg. 2007;11:16237. Tsuang W, Navaneethan U, Ruiz L, Palascak JB, Gelrud A. Hypertriglyceridemic pancreatitis: presentation and management. Am J Gastroenterol. 2009;104:98491. Sharp HT. The acute abdomen during pregnancy. Clin Obstet Gynecol. 2002;45:40513. Windsor AC, Kanwar S, Li AG, Barnes E, Guthrie JA, Spark JI, et al. Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improves disease severity in acute pancreatitis. Gut. 1998;42:4315. Yu W, Li W, Wang Z, Ye X, Li N, Li J. Early percutaneous transhepatic gallbladder drainage compared with endoscopic retrograde cholangiopancreatography and papillotomy treatment for severe gallstone associated acute pancreatitis. Postgrad Med J. 2007;83:18791. Ducarme G, Ch atel P, Alves A, Hammel P, Luton D. Management of necrotizing pancreatitis in the third trimester of pregnancy. Arch Gynecol Obstet. 2009;279:5613. Tang SJ, Rodriguez-Frias E, Singh S, Mayo MJ, Jazrawi SF, Sreenarasimhaiah J, et al. Acute pancreatitis during pregnancy. Clin Gastroenterol Hepatol. 2010;8:8590. Sakorafas GH, Tsiotou AG. Etiology and pathogenesis of acute pancreatitis: current concepts. J Clin Gastroenterol. 2000;30:34356. Maringhini A, Ciambra M, Baccelliere P, Raimondo M, Orlando A, Tine F, et al. Biliary sludge and gallstones in pregnancy: incidence, risk factors, and natural history. Ann Intern Med. 1993;119:11620. Swisher SG, Hunt KK, Schmit PJ, Hiyama DT, Bennion RS, Thompson JE. Management of pancreatitis complicating pregnancy. Am Surg. 1994;60:75962. Ewald N, Hardt PD, Kloer HU. Severe hypertriglyceridemia and pancreatitis: presentation and management. Curr Opin Lipidol. 2009;20:497504. Gosnell FE, ONeill BB, Harris HW. Necrotizing pancreatitis during pregnancy: a rare cause and review of the literature. J Gastrointest Surg. 2001;5:3716. Martin U, Davies C, Hayavi S, Hartland A, Dunne F. Is normal pregnancy atherogenic? Clin Sci (Lond). 1999;96:4215. Fujita N, Shirai Y, Tsukada K, Hatakeyama K. Gestational hyperlipidemic pancreatitis without non-gestational hyperlipidemia. Hepatogastroenterology. 1999;46:20189. Bildirici I, Esinler I, Deren O, Durukan T, Kabay B, Onderoglu L. Hyperlipidemic pancreatitis during pregnancy. Acta Obstet Gynecol Scand. 2002;81:46870. Hofbauer B, Friess H, Weber A, Baczako K, Kisling P, Schilling M, et al. Hyperlipaemia intensies the course of acute oedematous and acute necrotising pancreatitis in the rat. Gut. 1996;38:7538. Lloret LC, Pelletier AL, Czernichow S, Vergnaud AC, Bonnefont-Rousselot D, Levy P, et al. Acute pancreatitis in a

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2011 Nordic Federation of Societies of Obstetrics and Gynecology 90 (2011) 671676

675

Acute pancreatitis in pregnancy

L. Sun et al .

22.

23.

24. 25.

26.

cohort of 129 patients referred for severe hypertriglyceridemia. Pancreas. 2008;37:132. Abu MAA, Usta IM, Rechdan JB, Nassar AH. Recurrent hypertriglyceridemia-induced pancreatitis in pregnancy: a management dilemma. Pancreas. 2006;32:2278. Maringhini A, Lankisch MR, Zinsmeister AR, Melton LJ 3rd, DiMagno EP. Acute pancreatitis in the postpartum period: a population-based case-control study. Mayo Clin Proc. 2000;75:3614. Therese H, Li L, Zhu WX. The effect of Chinas one-child family policy after 25 years. N Engl J Med. 2005;353:11716. Swisher SG, Schmit PJ, Hunt KK, Hiyama DT, Bennion RS, Swisher EM, Thompson JE. Biliary disease during pregnancy. Am J Surg. 1994;168:5769; discussion 5801. Takaishi K, Miyoshi J, Matsumura T, Honda R, Ohba T,

Katabuchi H. Hypertriglyceridemic acute pancreatitis during pregnancy: prevention with diet therapy and -3 fatty acids in the following pregnancy. Nutrition. 2009;25:10947. 27. Ai X, Qian X, Pan W, Xu J, Hu W, Terai T, et al. Ultrasound-guided percutaneous drainage may decrease the mortality of severe acute pancreatitis. J Gastroenterol. 2010;45:7785. 28. Mortele KJ, Girshman J, Szejnfeld D, Ashley SW, Erturk SM, Banks PA, Silverman SG. CT-guided percutaneous catheter drainage of acute necrotizing pancreatitis: clinical experience and observations in patients with sterile and infected necrosis. AJR Am J Roentgenol. 2009;192:1106. 29. Meier R, Ockenga J, Pertkiewicz M, Pap A, Milinic N, Mace J, et al. ESPEN Guidelines on Enteral Nutrition: Pancreas. Clin Nutr. 2006;25:27584.

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