Abruptio Placentae Caused by Hypertriglyceridemia-Induced Acute Pancreatitis during Pregnancy: Case Report and Literature Review.
Acute pancreatitis (AP) is a rare complication in pregnancy, occurring in approximately three in 10000 pregnancies [1, 2]. Hypertriglyceridemia is recognized as the third most common cause of gestational acute pancreatitis after gallstones and alcohol and occurs in about 4% of all cases . An increase in plasma lipid level during pregnancy has been well documented. It is thought to represent a physiologic response to the hormonal changes; however, it is not sufficient to cause acute pancreatitis. Gestational pancreatitis due to hypertriglyceridemia usually occurs in pregnant women with preexisting abnormalities of the lipid metabolism. There are effective treatment choices during pregnancy such as dietary restriction of fat, intravenous heparin, and insulin and plasmapheresis. We report a case of abruptio placentae caused by hypertriglyceridemia-induced acute pancreatitis.
2. Case Report
A 22-year-old patient, Para 1, Gravida 2, presented to our Emergency Department of Gynecology and Obstetrics, at 35 weeks of gestation for acute onset of abdominal pain and uterine contraction. It was learned that the patient's history had no follow-up hypertriglyceridemia. On physical exam, her heart rate was at 100 pulses per minute, and her blood pressure was at 110/70 mm-Hg, respiratory rate 18 /min. Her abdomen was defensive. Her cervical os was dilated to 1-2 cm and minimal bleeding. The patient had mild epigastric tenderness. Decelerations were seen in pregnant cardiotocography follow-ups with abnormal abdominal pain and uterine contractions continued and simultaneous wide bleeding area (like abruptio placenta) was seen on the posterior part of placenta in ultrasound. Immediate cesarean section was performed under general anesthesia because of contraction of the tetanic type in the manual contraception. She gave birth to a healthy infant of 2980 g. Amylase, lipase, triglyceride, HDL, and LDL were studied in the patient's blood after emulsion of chylous fluid from abdomen during the cesarean section. Liver enzymes were high: ast: 241, sub. 147. It was observed that blood sample revealed a milky turbid serum. Laboratory finding included a triglyceride at 3297 mg/dl and amylase 827 U/L, lipase 1576 U/L. Abdominal ultrasound showed thickened pancreas without necrosis; acute pancreatitis compatible with diffuse edema was observed on pancreas. Biliary tract was naturally observed. Other causes of cholestasis of pregnancy, such as cholangitis, acute hepatitis, and hemophagocytic syndrome, were ruled out. Oral intake of the patient was stopped; intravenous fluid replacement therapy, antibiotherapy, proton pump inhibitor, insulin, and heparin therapy were started. She was discharged on the 10th day of treatment. Even though the patient did not have previous history of diabetes or gestational diabetes, the baby was born 4 to 3 weeks earlier. It was thought that this condition might be related to maternal hyperlipidemia for newborn's doctors.
Acute pancreatitis (AP) is a rare complication in pregnancy. Diagnosis becomes difficult because it can interfere with the physiological findings in pregnancy. Acute pancreatitis should be considered in pregnancies with nausea, vomiting, and epigastric pain. Gallstones, hypertriglyceridemia, and alcohol especially play a role in the etiology of acute pancreatitis.
Hypertriglyceridemia is the second most common cause of acute pancreatitis in pregnancy. Diagnosis is made when the serum triglyceride is > 1000 mg/dl. Hypertriglyceridemia in pregnant patients can occur with preexisting dyslipidemia, associated with others diseases (hypertension, diabetes mellitus, and alcoholism), or without any predisposing factor. Triglycerides concentration rises gradually, 2.5-fold over prepregnancy levels, reaching a peak during the third trimester to almost twice as high value of nonpregnant value. This is thought to be due to estrogen-induced increases in triglyceride synthesis and very low-density lipoprotein secretion . Therefore, AP is more common in the third trimester of pregnancy. Lipids decrease gradually postpartum to reach prepregnancy level in 6 weeks [30, 31]. Epigastric pain, spreading pain, nausea, vomiting, and distension can be seen at the beginning of the symptoms in acute pancreatitis cases. Findings of peritoneal irritation are not seen in general, especially when there is epigastric pain in mild cases as indicated by physical examination findings. In severe cases, epigastric tenderness and peritoneal irritation findings may be accompanied by ileus, fever, and tachycardia. The increase in serum amylase reaches peak values 6-12 hours after the onset of the event. The exact diagnosis of pancreatitis is based on the amylase/creatinine clearance rate. Serum lipase values also increase. Imaging methods can be used in the diagnosis of acute pancreatitis from ultrasonography, computed tomography, and magnetic resonance imaging. Ultrasound is the most appropriate method for pregnancy.
Acute pancreatitis treatment in pregnancy is similar to nonpregnant treatment of hyperlipidemia. Pregnancy pancreatitis treatment is primarily medicinal and approximately 90% of patients respond to medical treatment. Medical treatment of AP is mostly supportive. These treatments include low fat diet [32, 33], antihyperlipidemic therapy [32, 33], insulin [32, 34] (to increase lipoprotein lipase activity), heparin [33, 35] (to increase lipoprotein lipase activity), and even plasmapheresis [32, 35].
Our patient was admitted with acute onset of abdominal pain and uterine contraction to our clinics in the 35th week of gestation. She had lipid abnormality in her history, but her history had no follow-up hypertriglyceridemia. Pregnancy had induced aggravation of hypertriglyceridemia and associated pancreatitis. In addition, acute pancreatitis induced by the pregnancy was accompanied by abruptio placenta and delivery was performed with an emergency cesarean section. It was observed that blood sample revealed a milky turbid serum. We managed our patient conservatively in postoperative period. Oral intake of the patient was stopped; intravenous fluid replacement therapy, antibiotherapy, proton pump inhibitor, insulin, and heparin therapy were started. The patient's clinical condition subsequently improved.
Cases of acute pancreatitis induced by hypertrigliceridemia during pregnancy published in the literature are listed in Table 1. In the majority of published case, medical treatment was first tired. Oral intake was closed, supportive treatment started. However, pregnancy-induced pancreatitis has been mortal in some cases and has gone as far as maternal death.
Ihuang et al. performed a retrospective study on 21 pregnant women diagnosed with acute pancreatitis (AP). Patients were divided into acute biliary pancreatitis (A BP), hypertriglyceridemia-induced acute pancreatitis (HTG P), and idiopathic groups according to etiology. 95% of the patients were in the third trimester of gestation. The percentage of patients with HTGP was higher than that of ABP (48% versus 14%). The percentage of severe acute pancreatitis (SAP) in the HTGP group was higher than that in the ABP group (40.0% versus 0%). In the HTGP group, five patients given were plasma exchange therapy and five were not. According to the results of this study it was found that plasma exchange maybe safe and effectively administered for HTGP patients during pregnancy with SIRS or multiple organ dysfunction syndrome (MODS) .
In a study by Lingyu Luo et al., they retrospectively reviewed 121 acute pancreatitis in pregnancy (APIP) cases. The correlation between APIP types, severity, biochemical parameters, and mortality was analyzed. The most common causes of APIP were gallstone and hypertriglyceridemia. Lower level of serum calcium could be used as an indicator for the severity of the APIP. According to the result s of this study it was found that the severity of APIP was associated with higher risk for neonate asphyxia and maternal and fetal death .
In a prospective study performed by Athyros VG et al., 17 cases of acute pancreatitis induced by hypertriglyceridemia were included in the study. These patients were followed for 42 months. In the content of the study causative conditions of HTG-induced A P were familial HTG in eight patients, HTG caused by uncontrolled diabetes mellitus in five, HTG aggravated by drugs in two (one by tamoxifen and one by fluvastatin), familial hyperchylomicronemia (HCM) in one, and lipemia of pregnancy in one. During the acute phase of pancreatitis, patients underwent standard treatment. After that, HTG was efficiently controlled with high dosages of fibrates or a fibrate plus acipimox, except for the patient with H CM, who was on a specific diet (the only source of fat was a special oil consisting of medium chain triglyceride) and taking a high dosage of acipimox. One of the patients died during the acute phase of pancreatitis with acute respiratory distress syndrome. According to the results of the study it was found that appropriate diet and drug treatment, including dose titration, of severe HTG are very effective in preventing relapses of HTG-induced AP .
As a result, pancreatitis can be seen in pregnancy in cases with uncontrolled hypertriglyceridemia. Patients with known hypertriglyceridemia or family history should be followed up more closely. Acute pancreatitis should be considered in pregnant women who have sudden onset, severe, persistent epigastric pain and who have a risk factor for acute pancreatitis.
Conflicts of Interest
The authors declare that there are no conflicts of interest regarding the publication of this paper.
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Pinar Yalcin Bahat (iD), Gokce Turan (iD), and Berna Aslan Cetin
Department of Obstetrics and Gynecology, Kanuni Sultan Suleyman Training and Research Hospital, Istanbul Health Sciences University, Istanbul, Turkey
Correspondence should be addressed to Pinar Yalcin Bahat; firstname.lastname@example.org
Received 1 February 2018; Revised 16 August 2018; Accepted 27 August 2018; Published 5 September 2018
Academic Editor: Erich Cosmi
Table 1: Case literatures of acute pancreatitis induced by hypertriglyceridemia during pregnancy. First Author Year Age G/P Birth Medication Billion 1991 32 35 TPN JM  Achard 1991 Two JM  Lipaphereses Perrone 1996 37 35 Diet, G  Gemfibrozil Ibrahim 2002 26 G2P2 24 Insulin, Bildirici Plasmapheresis  Chee-Chuen 2002 37 G3P2 37 Ranitidine, Loo  Heparin, Insulin J.C. 2004 28 G2P1 37 Heparin Sleth  A.Abu 2006 39 G2P1 28 Plasmapheresis Musa  Shih-Chang 2006 28 G1P0 34 Antibiotics, Chuang  TPN Alptekin 2006 24 G1P0 37 Gursoy  V. 2007 31 33 Plasmapheresis, Exbrayat Heparin  Luminita S. 2008 27 G2P0 35 TPN, Crisan Analgesics, -1 Bowel Rest Luminita S. 2008 29 G3P1 30 TPN, Crisan Analgesics, -2 Bowel Rest Luminita S. 2008 34 G3P0 33 TPN, Crisan Analgesics, -3 Bowel Rest Luminita S. 2008 23 CIPO 35 TPN, Crisan Analgesics, -4 Bowel Rest L. Vanden- 2009 34 37 Heparin, A broucke  Low-Fat Diet Dilek Altun 2012 27 CIPO 5 Plasmapheresis, -1 Heparin Dilek Altun 2012 24 CIPO 34 Plasmapheresis, -2 A Low-Fat Diet Mindaugas 2012 31 G2P0 33 Heparin, Serpytis  Insulin, Plasmapheresis Kumar 2013 37 G3P0 14 Insulin, Thulasi-dass Metformin, -1 Fish Oil Therapy Kumar 2013 24 G1P0 8 Thulasi-dass -2 Rafet Basar 2013 32 G3P0 37 Heparin, -1 Fatty Acids, DF Rafet Basar 30 G2P1 36 Heparin, -2 Fatty Acids, DF, Plasmapheresis Ying 2013 31 G2P0 27 Hang  Bahiyah 2014 25 G4P3 8 Abdullah  Tejal 2014 40 G5P4 18 Insulin Amin  Natasha 2014 32 G5P4 38 Plasmapheresis Gupta  Fadi 2014 24 G9P8 35 Plasmapheresis Safi  Rachel 2015 27 G1P0 33 Insulin, Lim  Plasmapheresis Ying 2015 30 G1P0 32 Plasmapheresis Liu  Funda 2015 37 31 Insulin, DF Gok  Hae Rin 2016 28 G1P0 23 Jeon  Ioanna 2017 38 G2P1 30 Heparin, Poly-pathelli Fatty Acids,  Antibiotics Tamanna 2017 38 11 Chibber  First Author Other Mode BW Billion JM  Achard JM  Perrone G  Ibrahim C/S Bildirici  Chee-Chuen SVD Loo  J.C. C/S Sleth  A.Abu C/S Musa  Shih-Chang Pancreatic Chuang  Necrosectomy, Right Hemicolectomy Ileostomy, Cholecys-tostomy, Gastrostomy, Feeding Alptekin C/S Gursoy  (3230 g) V. C/S Exbrayat  Luminita S. ARDS C/S Crisan (2653 g) -1 Luminita S. Acute Forceps- Crisan Myocardial Assisted -2 Infarction Vaginal Delivery (1854 g) Luminita S. ARDS SVD Crisan (2147 g) -3 Luminita S. C/S Crisan (2498 g) -4 L. Vanden- C/S broucke  (3940 g) Dilek Altun -1 Dilek Altun C/S -2 (3100 g) Mindaugas Serpytis  Kumar Termination Thulasi-dass -1 Kumar ARDS Spontaneous Thulasi-dass Abortion -2 Rafet Basar C/S -1 Rafet Basar C/S -2 Ying Noninvasive C/S Hang  Positive (1180 g) Pressure Ventilation (NPPV), Drainage of Chylous Ascites, Peritoneal Lavage, ARDS Bahiyah Diagnostic Spontaneous Abdullah Laparoscopy, Abortion  Acute Hemorrhagic Pancreatitis Tejal IUMF Amin  Natasha Preeclampsia, C/S Gupta  Pleural Effusion, Chronic Pericarditis, Retinal Detachment Fadi C/S Safi  (1720 gr) Rachel Placental SVD Lim  Abruption Ying Compound C/S Fetal Liu  Heterozygosity Distress (Glu242Lys and Leu252VaL) Funda IUMF SVD Gok  Hae Rin IUMF, Jeon  Pancreatic Cells Necrotized, Diabetic Ketoacidosis, Metabolic Acidosis, Cardiac Arrest, EX Ioanna C/S Poly-pathelli  Tamanna Cardiac Chibber Arrest, EX  First Author Indication Laboratory * Billion JM  Achard JM  Perrone G  Ibrahim Fetal Serum Amylase: Bildirici Distress 487 Pane.  (750 g) Amylase: 184 Pane Lipase: 786 TG: 2316 Chee-Chuen Serum Amylase: Loo  956 TG: 2066 J.C. Unstable TG: 2316 Sleth  Condition Cholesterol: 1000 of the Mother Pane. Amylase: 574 Pane. Lipase: 1310 A.Abu A Repeat C/S TG: 3810 Pane. Musa  Delivery Amylase: 525 Pane. Lipase: 3524 Shih-Chang Unstable TG: 2184 Chuang  Condition Pane. Amylase: 1365 of the Pane. Lipase: 533 Mother Alptekin Fetal TG: 10092 Gursoy  Distress Cholesterol: 1159 Pane. Amylase: 367 Pane. Lipase: 797 V. Fetal TG: 11300 Exbrayat Distress Cholesterol: 2500  Pane Amylase: 334 Pane Lipase: 168 Luminita S. Fetal Crisan Distress -1 Luminita S. Crisan -2 Luminita S. Crisan -3 Luminita S. Low BPP Crisan -4 L. Vanden- Fetal TG: 8447 broucke  Distress Dilek Altun Termination TG: 2225 -1 Cholesterol: 470 Pane. Amylase: 959 Dilek Altun TG: 2699 -2 Cholesterol: 230 Pane. Amylase: 956 Pane. Lipase: 2580 Mindaugas TG: 1576 Serpytis  Kumar TG: 1421 Thulasi-dass Cholesterol: 481 -1 Serum Amylase: 1464 Kumar TG: 839 Thulasi-dass Cholesterol: 300 -2 Serum Amylase: 8962 Rafet Basar Elective TG: 1400 -1 Rafet Basar Elective TG: 12000 -2 Ying Fetal TG: 523 Hang  Distress Cholesterol:325 Pane. Amylase: 178 Bahiyah Serum Abdullah Amylase: 1273  Tejal TG: 836 Amin  Cholesterol: 300 Natasha Unstable TG: 12.570 Gupta  Condition Cholesterol: 1067 of the Pane. Amylase: 1617 Mother Pane. Lipase: 1330 Fadi Unresponsiveness TG: 2661 Safi  to Treatment Cholesterol: 683 Serum Amylase: 802 Rachel TG: 720 TG: 41 Lim  Cholesterol: 90 Pane. Lipase: 504 Ying TG: 2160 TG: 420 Liu  Cholesterol: 670 Pane. Amylase: 132 Funda TG: 9742 TG: 556 Pane. Gok  Cholesterol: 705 Amylase: 107 Pane. Amylase: 570 Pane. Lipase: 77 Pane. Lipase: 319 Hae Rin TG: 10392 Jeon  Cholesterol: 1006 Pane. Amylase: 1833 Pane. Lipase: 1863 Ioanna Resistant TG: 14440 Poly-pathelli Exaggerated Cholesterol: 1600  Thrombocytosis Serum Amylase: 540 Tamanna TG: >1254 Chibber Cholesterol: 648  Pane. Lipase: 1079 First After Author Treatment ** Billion JM  Achard JM  Perrone G  Ibrahim Bildirici  Chee-Chuen Serum Amylase: Loo  39 TG: 492 J.C. TG: 100 Sleth  A.Abu TG: 591 Musa  Pane. Amylase: 79 Pane. Lipase: 396 Shih-Chang TG: 319 Chuang  Alptekin TG: 143 Gursoy  Cholesterol: 274 Pane Amylase: 23 Pane Lipase: 41 V. TG: 1000 Exbrayat  Luminita S. Crisan -1 Luminita S. Crisan -2 Luminita S. Crisan -3 Luminita S. Crisan -4 L. Vanden- TG: 240 broucke  Dilek Altun TG: 278 -1 Cholesterol: 181 Dilek Altun TG: 570 -2 Cholesterol: 2500 Pane. Amylase: 208 Pane. Lipase: 208 Mindaugas TG:183 Serpytis  Kumar TG: 111 Thulasi-dass Cholesterol: 93 -1 Kumar TG: 57 Thulasi-dass Cholesterol:77 -2 Rafet Basar TG: 380 -1 Rafet Basar TG: 758 -2 Ying TG: Normal Hang  Cholesterol: Normal Bahiyah Serum Abdullah Amylase: 147  Tejal TG: 90 Amin  Natasha TG: 295 Gupta  Cholesterol: 179 Fadi TG: 425 Safi  Rachel Lim  Ying Liu  Funda Gok  Hae Rin Jeon  Ioanna TG: 521 Poly-pathelli  Tamanna Chibber  BW: birth weight, G: gravida, P: parity, SVD: spontaneous vaginal delivery, BPP: biophysical profile, TPN: total parenteral nutrition, DF: double filtration apheresis, C/S: cesarean section, TG: triglyceride, ARDS: Adult Respiratory Distress Syndrome, and IUMF: Intra-Uterine Mort Fetus. Triglyceride and total cholesterol units are calculated in mg/dL. Other units are converted to mg/dL. Serum Amylase: normal range is between 30 and 110 (U/L) . Pancreatic Amylase: normal range is between 17 and 115 (U/L) . Pancreatic Lipase: normal range is between 13 and 60 U/L (U/L) . TG: normal range is between 50 and 160 mg/dL (mg/dL) . Cholesterol: normal range is between 130 and 230 (mg/dL) . * Highest values. ** Lowest values.
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|Title Annotation:||Case Report|
|Author:||Bahat, Pinar Yalcin; Turan, Gokce; Cetin, Berna Aslan|
|Publication:||Case Reports in Obstetrics and Gynecology|
|Date:||Jan 1, 2018|
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