The biliary acute pancreatitis in pregnancy requires surgical treatment only when there is: 1) acute cholecys- titis which does not resolve with conventional treatment, 2) peritonitis, 3) obstructive jaundice and severe symp- toms which will resolve after the operational interven- tions . However, in necrotizing biliary acute pancrea- titis cholecystectomy has to wait until active inflamma- tion subsides and fluid collections resolve or stabilize in order to avoid infection of the necrotic tissue no matter the severity of the disease . As for the preferred ap- proach, although laparoscopic and open cholecystectomy show no significant difference in maternal or fetal out- come, there are still the benefits of laparoscopic opera- tions such as less postoperative pain, less postoperative ileus, significantly reduced hospitalization, decreased narcotic use, quick return to regular diet, faster recovery, less manipulation of the uterus and less chances of post- operative deep vein thrombosis [11,13]. As for the timing of laparoscopic operation, recent guidelines of the Soci- ety of American Gastrointestinal and Endoscopic Sur- geons (SAGES) suggest that cholecystectomy is safe in all trimesters of pregnancy . However, there are con- siderations about the effect of sedation during the or- ganogenesis of the first trimester and the increased sur- gical capacity required as the uterus augments in size during the third trimester. Therefore, the best timing might be the second trimester, although there is no indi- cation to delay the operation if it is necessary, no matter the trimester of pregnancy. Finally, there are few precau- tions that should be followed during laparoscopic opera- tion of pregnant woman, such as the use of an open tech- nique in order to insert the umbilical trocar, special cau- tion at the intraperitoneal pressures, left lateral position to diminish aortocaval compression and avoiding the use of electrocautery near uterus .
Pancreatitis in pregnancy is reported around 3-4 % worldwide [1-3]. Hyperglyceridemia induced pancreatitis accounts for 4 % of all cases of acute pancreatitis in pregnancy . The triglyceride level may increase two to four times the normal level during pregnancy and may cause injury of the endothelium. This may lead to preeclampsia or pancreatitis. Though rare, hypertriglyceridemia induced pancreatitis may lead to fatal maternal and fetal complications, even maternal death [4-6]. Acute complications of electrolyte imbalance, acute respiratory distress syndrome, disseminated intravascular coagulation and preterm labour may worsen the clinical situation. Patients are also reported to have several other complications including preeclampsia, gestational diabetes retinal detachment, ascites, pleural effusion, and pericarditis [4,5]. Its management during pregnancy remains a challenge for physicians. As Feno ibrate is not safe in pregnancy, insulin infusion remains the treatment of choice in most of the cases [7,8]. However in patients with need of prolonged Insulin infusion, its effects on fetus are unpredictable and the psycho-socio-economic impact of prolonged hospitalization on both the patient and her family and the hospital. In refractory cases timing of delivery remains a challenge for physicians. Here we report a patient presenting with hyperlipidemia induced pancreatitis and the challenges faced in her management.
Our series includes 37 cases of acute pancreatitis and pregnancy collected over a 7-year period from January 2010 to January 2016. In terms of epidemiology the average age was 29 years with an incidence of 1/2450. Acute pancreatitis occurred more frequently in multiparous multiparous women (68%) in the third trimester (59.5%). The clinical picture was dominated by abdominal pain (100%) and vomiting (100%). The occurrence of organ failure was rare. The positive diagnosis is based on lipaseemia which was on average 20 times normal. The severity assessment was based on clinico-biological scores (Ranson score and SRIS score). Biliary origin was the main etiology in our study (54%). Management is based on hospitalization and symptomatic treatment including pain management, stopping feeding, gastric protection, rehydration and management of organ failure. Maternal complications were dominated by superinfection of necrosis (10.75%). Maternal mortality was 2.7%. Fetal complications included abortion, premature labor, and acute fetal distress.
Background: Acute pancreatitis is rare in pregnancy, but it is associated with increased incidence of maternal and fetal mortality. It should be one of the differential diagnosis of upper abdominal pain with or without nausea or vomiting. S. amylase, lipase and ultrasound abdomen were the diagnostic methods. Conservative management is the main stay in mild cases. Severe cases have multiorgan involvement and needs multidisciplinary approach. The objectives of this study were to study the maternal and fetal outcome in pregnant women diagnosed with acute pancreatitis and to identify the risk factors for acute pancreatitis in pregnancy.
As the mortality of patients with IAH is higher than those without IAH, surveillance and early management of IAH is increasingly implemented in these IAH-prone patients. Pregnancy have physiologic progressive IAP elevation usually close to the diagnostic threshold of IAH in the third trimester . Acute intra-abdominal inflammation due to acute pancreatitis developing in the third trimester definitely has an effect on IAP. In this study, IAH was observed in all the third trimester preg- nancy diagnosed with MSAP or SAP. The incidence of IAH in pregnancy was 82.4 %, which was higher than our previous study in the non-pregnancy pancreatitis group (around 65 %, 39/60)  but there was no sig- nificant difference (p = 0.24, χ 2 test). The likely reason was the abdominal wall which was already strained by the enlarged uterus had less ability to tolerant any rapid increase of IAP. The difference need to be observed with more samples in each group in the future.
Acute pancreatitis (AP) is a rare cause of abdominal pain in pregnancy with a cited incidence of 1/1000–10,000 depend- ing on the diagnostic criteria used and provided accurate diagnosis is not always achieved [1–3]. The majority of cases occur in the third trimester or early postpartum and carry an increased maternal and fetal morbidity and mortal- ity potential . Maternal death rate due to pancreatitis was reportedly 37% and fetal death rate 60%, in decline re- cently as a result of more advanced diagnostic and thera- peutic possibilities [5–7]. Pregnancy associated pancreatitis may occur on the background of gallstone disease, alcohol abuse and hypertriglyceridemia (HTG) [8–10]. It appears that HTG aggravates the severity score and prognosis of disease [7, 11, 12].
Abstract: Aim: Acute pancreatitis (AP), in particular, severe acute pancreatitis (SAP), is a rare but challenging com- plication during pregnancy in terms of diagnosis and management. The objective of this paper is to investigate the causes and therapeutic strategies of AP in patients during the third trimester of pregnancy. Methods: We performed a retrospective analysis of the clinical features, laboratory data, and outcomes in 16 patients with acute pancreatitis during the third trimester of pregnancy. Results: Information was collected on admission, management, and out- come. A total 16 patients were diagnosed with acute pancreatitis during pregnancy. In 7 of 9 patients with mild AP, pregnancy was terminated by cesarean section and all 9 cases were cured. In 4 out of 7 patients with SAP, pregnan- cy was terminated by cesarean section in conjunction with peritoneal irrigation and drainage, and the mothers and infants survived. In the remaining 3 patients with SAP, there was one case of intrauterine death in which Induced labor was performed and 2 patients died of multiple organ failure. Conclusion: A high-fat diet and cholelithiasis are the triggers of AP in pregnancy. Conservative treatment is the preferred therapeutic method; in particular, for mild AP. Endoscopic surgery and peritoneal drainage are effective for acute biliary pancreatitis. Patients with hyperlipid- emic pancreatitis should undergo lipid-lowering therapy, and hemofiltration should be done as soon as it becomes necessary. For patients with SAP, termination of pregnancy should be carried out as early as possible.
hormone and causes hypercalcaemia . It is an uncom- mon clinical entity in women of childbearing age. The prevalence of PHPT during pregnancy is unknown and may occur in less than 1% of cases . In fact, many authors believe that the true prevalence in pregnancy is underestimated because of physiological pregnancy changes and mild non-specific symptoms [8, 9]. Early diag- nosis and appropriate intervention for the mother and foetus are crucial to prevent problems, such as nephro- lithiasis, bone disease, preeclampsia, spontaneous abortion, intrauterine demise, and lethal pancreatitis or severe hyper- calcaemia . Potentially life-threatening acute pancreatitis is also rare during pregnancy, especially acute pancreatitis due to PHPT . Clinical knowledge about pancreatitis due to PHPT is limited to isolated case reports, such as the case report presented here [11 – 17].
epigastrium with cholelithiasis on ultrasound with or without stones in common bile duct (CBD). Findings of pancreatic edema on ultrasound or CT scan, raised pancreatic enzymes (serum amylase) above three times than normal, raised alanine aminotransferase (ALT) by three times or more. Alcohol induced acute pancreatitis was excluded by history. When patient revealed alcohol consumption of >40 grams daily and biliary stone disease was excluded by ultrasound, pancreatitis was assumed to be due to alcohol. Other causes of acute pancreatitis like drugs, hyperlipidemia, ERCP (endoscopic retrograde cholangiopancreatography), postoperative and idiopathic were labeled accordingly and excluded from study. Severity of the disease was graded for selection purpose according to ranson’s criteria. 9 Mild acute biliary pancreatitis (ABP) was categorized by patients with ranson’s score <3, while patients with score >3 were considered as severe disease. These patients with severe disease were excluded from study and treated conservatively.
It is important to note that the generation of these hal- ogenated fatty acids requires a combination of processes that are triggered during the development of pancreatitis, particularly when the enhanced inflammatory response acquires such characteristics that herald the progres- sion to severe AP. This inflammatory response involves the recruitment of macrophages and neutrophils to the damaged pancreas and to the surrounding adipose tis- sue. These cells release active MPO in the areas where large amounts of pancreatic lipase catalyze the hydroly- sis of triacylglycerols from adipocytes . Therefore, fatty acid chlorohydrins (and in particular OAC) genera- tion is fostered by the combined action of two enzymatic systems (myeloperoxidase and lipase) that are overactive in severe AP. Furthermore, OAC can be released to the bloodstream and its blood levels quantitated.
Drug-induced acute pancreatitis remains rare but should not be disregarded when medical practitioners are faced with a patient presenting with acute pancrea- titis with no obvious cause. Being familiar with reports of drugs causing acute pancreatitis can be helpful in identifying the causality and association with a certain drug. Despite the fact that DIP can have a benign course with good prognosis, fatal outcomes still occur and thus DIP should not be overlooked. This case describes a pa- tient with DIP after the intake of amoxicillin/clavulanic acid and when all other common causes of acute pan- creatitis were excluded. We again stress on the import- ance of identifying and reporting cases of DIP to raise awareness among physicians and clinicians. We also stress on the importance of encouraging scientists and researchers to better understand the mechanism of developing drug-induced acute pancreatitis.
Trypsin self-digestion theory in twentieth Century was put forward in the 20th century. The doctrine deems that abnormal activation of pancreatic enzymes from proteolytic cleavage of trypsinogen in acinar cells leads to pancreatic auto- digestion, which happens in the early stage of acute pancreatitis, and eventually results in severe acute pancreatitis . Bile reflux, duodenal reflux, obstruction of the pancreatic duct and the alcohol effect on pancreatic acinar and Audi sphincter causes ectopic activation of trypsinogen in the pancreas, the activation of trypsin, in turn, can activate other protease, leading to pancreatic chain diges- tive. The activation of trypsin in addition to destroying the pancreas itself re- sulting in destruction of pancreatic pancreatic hemorrhage and tissue necrosis, but also causes damage to surrounding tissue and distant organs through the circulatory system with damaged vascular endothelial and venous reflux  .
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background and objectives The global incidence of hospitalisation due to acute pancreatitis (AP) has been rising in the recent decades. In the USA alone, there was a 13.2% increase between 2009 and 2012 compared with 2002–2005. There remains a lack of approved treatments to prevent disease progression, leaving many liable to developing complications that include multisystem organ failure (OF) and death. This therapeutic deficit raises questions about the scale of the current burden of illness (BOI) associated with severe forms of AP. The aim of the systematic literature review (SLR) was to assess clinical, humanistic, and economic outcomes associated with moderately severe AP (MSAP) and severe AP (SAP) in the USA and the European Union-5 (EU-5).
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to find the prevalence of pancreatitis in OP poisoning. Four of the total 47 patients with acute OP poisoning had obviously elevated Amylase and Lipase levels (Amylase> 300 U/L ; Lipase >60 U/L). Only two of the patients with Amylase levels between 100 and 300 U/L had elevated levels of Lipase. None of the patients with normal Amylase levels had elevated levels of Lipase. A total of 12.76% were diagnosed as acute Pancreatitis. It was concluded that acute pancreatitis is not a rarecomplication of organophosphorus poisoning. In order to improve the outcome of OP poisoning early diagnosis of acute pancreatitis is important and serum Amylase and Lipase levels should be routinely considered carefully.W C Lee et alcarried out a retrospective study of medical records of 121 patients with the diagnosis of OP poisoning over three years in Veterans General Hospital, National Yang- Ming University in 1998. Serum amylase, pancreatic amylase, salivary amylase, lipase and cholinesterase levels and the clinical manifestations were analyzed. It was observed that 44 patients (36%) had hyperamylasemia (Amylase>360 U/L). Lipase was measured in 28 patients with hyperamylasemia; nine of 28 had hyperlipasemia (Lipase > 380 U/L). The finding of hyperamylasemia was closely related to clinical severity and presence of shock. It was concluded that hyperamylasemia is frequent in severe OP poisoning. However, hyperamylasemiais not synonymous with acute pancreatitis and pancreatic amylase is not reliable parameter in the diagnosis of organophosphate induced pancreatitis due to its low sensitivity and specificity. Lipase assay is indicated in patients with hyperamylasemia for early diagnosis of pancreatitis. NMatsumiya et alperformed a retrospective study of OP poison in intensive care unit to analyze the incidence of respiratory failure in Department of Anesthesiology & Critical care medicine, Kyodo General Hospital , Ibaraki, Japan in 1996. Of the 32 OP poisoning patients, 16 developed respiratory failure and received ventilator support. An increase in plasma amylase above the normal range was found in patients who developed respiratory failure. Thus in OP poisoning, the elevation of amylase levels was predictive of subsequent respiratory failure. Chaturvedi et al in their 2013 one year study, 30 of 96 patients(31.25%) were found to have hyperamylasemia. 16 patients(16.67%) had more than threefold elevated amylase levels. Among
An international symposium was conducted in Sep 11 through 13, 1982, and a unanimous consensus on a series of definition and a clinically based classification system for acute pancreatitis was achieved by a diverse group of 40 international authorities from six medical disciplines and 15 countries. The proposed classification system is of value to practicing clinicians in the care of individual patient and to academicians seeking to compare inter institutional data. The Atlanta symposium defined terms like acute pancreatitis (severe and mild), acute fluid collection, necrosis, pseudocyst and abscess. The symposium also discarded term like phelgmon, infected pseudocyst and hemorrhagic pancreatitis.
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Alcoholism is responsible for about one-third of cases of acute pancreatitis 9 . The pathophysiology may be multifactorial. . Proposed mechanisms in- clude sphincter of Oddi spasm, precipitation of in- soluble protein plugs, gall stone or tumour that ob- struct the pancreatic ductules, activation of pan- creatic proteases, and overstimulation of pancreat- ic secretion by cholecystokinin 7 . Alcoholic pancre- atitis generally requires drinking more than eight alcoholic drinks per day for more than 5 years 7 . Acute alcoholic pancreatitis most likely results in the development of chronic pancreatitis.
In this condition the second part of the duodenum is encircled by a band of normal pancreatic tissue which is partial or complete and extends into the pancreatic head. It is also having small duct which communicates with the main pancreatic duct. The etiology of annular pancreas is not clear. It may due to absence of ventral pancreatic bud in clockwise rotation during development or extension of pancreatic tissue in duodenal wall. It causes duodenal obstruction either partially or completely. This condition is usually associated with other system congenital malformations. Pancreatitis can be developed from the abnormal segment of pancreas. It is treated by diversion rather than segment resection by duodenojejunostomy.
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Although research on the pathogenesis and mechanisms of severe acute pancreatitis has progressed in recent years, the primary cause of the high mortality remains unknown. In early stages of pancreatitis, macrophages, neutrophils, endothelial cells are activated. Preinflammatory cytokines are released and inflammation factors re elevated during acute pancreatitis and have been implicated in progression of pancreatitis associated microvascular disturbance and hemorrhagic necrosis. Ischemia, reperfusion injury and tiny thrombosis are closely associated with pancreatic microcirculation disturbance 1
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the concentration of IL-10. With the experimental pro- gress of Chinese herbs, we found that it is essential to study DCQD on the molecular level . As discussed above, rhein and naringenin were relatively higher and might be potentially effective components of DCQD for SAP-induced AKI. Rhein, one major component of Dahuang, bore comparison to the accredited painkiller ibuprofen with its anti-inflammatory effects in adjuvant- induced inflammation by ameliorating oxidative stress significantly . Rhein induces a necrosis-apoptosis switch of damaged pancreatic acinar cells to ameliorate AP in a dose-dependent manner  and to prevent an endotoxin-induced AKI by inhibiting NF-κB activities . The naringenin might be another effective compo- nent and was reported to alleviate acute inflammation by adjusting the degradation by intracellular cytokines  and to reduce kidney damage in diabetic nephropathy through Let-7a/transforming growth factor-β1 receptor (TGFBR1) signalling . Li et al. concluded that emodin had an effect on the lipopolysaccharide-induced AKI by inhibiting the toll-like receptor 2 (TLR2) signalling path- way . Future studies should focus on the relationship between the quantified molecules of DCQD and their pharmacological effects considering their target tissues in SAP.
Therefore, we investigated the value of PLR in predicting AP outcomes and compared differences between NLR and PLR patterns in two distinct forms of AP. We ex- cluded pancreatitis caused by factors other than gallstone or alcohol. When all AP cases were combined, NLR and PLR were not significant independent predictive factors of POF. However, after subgrouping AP by etiology, both NLR and PLR were independent predictive factors of POF in gallstone AP. In alcoholic AP, NLR was a significant predictor, but PLR was not. This can be explained by the different mechanism of alcohol AP. Alcoholic AP is usu- ally associated with chronic liver disease. In our results, the number of liver cirrhosis patients was larger and the platelet count was lower in alcoholic AP compared to gall- stone AP. Thrombocytopenia is related to chronic liver disease due to impaired platelet production and decreased hepatic synthesis of thrombopoietin . Therefore, PLR can vary according to liver function as well as systemic inflammation. Interestingly, CRP, a marker traditionally used to assess the severity of inflammation [21–23], failed to predict POF in gallstone AP and alcoholic AP. This suggests the superiority of NLR and PLR to CRP in predicting the course of gallstone AP.