Ascites Volume Research Articles

Struma ovarii with synchronous ascites and elevated CA125 level: a retrospective cohort study

Background Benign struma ovarii (SO) with synchronous ascites and elevated CA125 level is extremely rare that the incidence, clinical characteristics, and risk factors remain unclear. Methods We conducted a retrospective study of patients with SO treated in our hospital between 1980 and 2022. Logistic regression was used to identify potential risk factors for SO patients presenting with ascites and elevated CA125 levels. The receiver operating characteristic (ROC) curve was used to evaluate the predictive performance of the identified risk factors. Results A total of 21 patients with synchronous ascites and elevated CA125 levels were identified in 229 patients with SO, the crude incidence rate was 9.17%, and four patients (1.75%) had pseudo-Meigs’ syndrome. Ascites were completely involuted within 1 month postoperatively and the serum CA125 level decreased to normal between 3 d and 6 weeks after surgery. Multivariate logistic regression showed that age ≥49 years (OR 3.71, 95% CI 1.29 − 10.64, p = 0.015), tumor size ≥10.0 cm (OR 8.79, 95% CI 3.05 − 25.35, p < 0.001), and proliferative SO (OR 11.16, 95% CI 3.01 − 41.47, p < 0.001) were the independent risk factors for patients presenting ascites and elevated CA 125 level. The ROC curve revealed that the predictive performance for age and tumor size was unsatisfactory with an area under the curve (AUC) was 0.646 and 0.682, respectively. Linear regression demonstrated that the serum CA125 level has a moderate positive correlation with the volume of ascites (log2 CA125 = 0.6272*log2 ascites + 2.099, p = 0.0001, R 2 = 0.5576). Conclusions Less than one-tenth of patients with SO would present ascites and elevated CA125 levels, while age ≥49 years, tumor sizes ≥10 cm, and the presence of proliferative SO were the risk factors.

Establishment of a Bayesian network model to predict the survival of malignant peritoneal mesothelioma patients after cytoreductive surgery plus hyperthermic intraperitoneal chemotherapy

Objectives To establish a Bayesian network (BN) model to predict the survival of patients with malignant peritoneal mesothelioma (MPM) treated with cytoreductive surgery (CRS) plus hyperthermic intraperitoneal chemotherapy (HIPEC). Methods The clinicopathological data of 154 MPM patients treated with CRS + HIPEC at our hospital from April 2015 to November 2022 were retrospectively analyzed. They were randomly divided into two groups in a 7:3 ratio. Survival analysis was conducted on the training set and a BN model was established. The accuracy of the model was validated using a confusion matrix of the testing set. The receiver operating characteristic (ROC) curve and area under the curve were used to evaluate the overall performance of the BN model. Results Survival analysis of 107 patients (69.5%) in the training set found ten factors affecting patient prognosis: age, Karnofsky performance score, surgical history, ascites volume, peritoneal cancer index, organ resections, red blood cell transfusion, pathological types, lymphatic metastasis, and Ki-67 index (all p < 0.05). The BN model was successfully established after the above factors were included, and the BN model structure was adjusted according to previous research and clinical experience. The results of confusion matrix obtained by internal validation of 47 cases in the testing set showed that the accuracy of BN model was 72.7%, and the area under ROC was 0.74. Conclusions The BN model was established successfully with good overall performance and can be used as a clinical decision reference.

The role of cytology in patients undergoing pressurized intraperitoneal aerosol chemotherapy (PIPAC) treatment for peritoneal carcinomatosis.

Cytology of ascites or peritoneal washing is a routine part of staging of peritoneal metastases (PM). We aim to determine value of cytology in patients undergoing pressurized intraperitoneal aerosol chemotherapy (PIPAC). Single-center retrospective cohort study included consecutive patients having PIPAC for PM of different primary between January 2015 and January 2020. A total of 75 patients (median 63 years (IQR 51-70), 67 % female) underwent a total of 144 PIPAC. At PIPAC 1 59 % patients had positive and 41 % patients had negative cytology. Patients with negative and positive cytology only differed in terms of symptoms of ascites (16% vs. 39 % respectively, p=0.04), median ascites volume (100 vs. 0 mL, p=0.01) and median PCI (9 vs. 19, p<0.01). Among 20 patients who completed 3 PIPACs (per protocol), cytology changed in one from positive to negative, and in two from negative to positive. Median overall survival was 30.9months in the per protocol group and 12.9months in patients having <3 PIPACs (=0.519). Positive cytology under PIPAC treatment is more frequently encountered in patients with higher PCI and symptomatic ascites. Cytoversion was rarely observed and cytology status had no impact on treatment decisions in this cohort.

Hemodynamic Variability During Drainage of Large Volumes of Malignant Ascites in Patients With Cancer.

This study compared the variability in mean arterial pressure (MAP) during drainage of ascites in patients with cancer who underwent drainage of a large (5-10 L) or small (<5 L) volume of ascites. We prospectively enrolled 50 patients scheduled for cell-free and concentrated ascites reinfusion therapy. Equivalence was considered to be established if the 95% confidence interval (95% CI) for the highest variability rate of MAP was within ±20%. The median volume of ascites removed was 3.30 L (95% CI [2.84, 4.40]) in the small-drainage-volume group (n = 15) and 6.75 L (95% CI [6.40, 7.30]) in the large-drainage-volume group (n = 34). The 95% CIs for the highest variability rates in MAP ranged from -19.60 to -6.23 and from -19.16 to -12.95 (p = .594), respectively, indicating equivalence. These findings indicate that variability in MAP during drainage of ascites is not dependent on drainage volume.

Engineered Apoptosis-Bioinspired Nanoparticles Initiate Immune Cascade for Cancer Immunotherapy of Malignant Ascites.

Malignant ascites (MA) is a common symptom of peritoneal metastasis in liver cancer. Cancer immunotherapy can modulate immune cells to induce antitumor immune efficiency. Reprogramming tumor immune microenvironment (TIME) is a momentous strategy to overcome immunosuppression and achieve immune functional normalization. Inspired by the inherent apoptotic bodies and vesicles, we proposed and systematically studied engineered apoptosis-bioinspired nanoparticles (EBN) for cancer immunotherapy of MA. Using both in vitro and in vivo experimental validations, we elucidated that EBN could be efficiently engulfed by the tumor-associated macrophages (TAMs) and manipulate their polarization. Moreover, a boosted immune cascade response as a result of heightening cytotoxic T-lymphocytes (CTLs) activity was investigated. Based on these results, EBN was confirmed to have strong immune cascade activation capability. Remarkably, the injection of EBN further reduced ascites volume and reformed immune cell subtypes, compared to the injection of either PBS or free TMP195 alone. In short, this novel nanodrug delivery system (NDDS) represents a prospective immunotherapeutic approach for clinical therapeutics of hepatoma ascites and other malignant effusion.

A multicenter retrospective cohort study evaluating the clinical significance of CA125 in later line of patients with metastatic colorectal cancer.

253 Background: The peritoneal dissemination is one of the metastatic forms of gastrointestinal cancer and has a poor prognosis. It has been reported that the presence of CA125 in mesothelial cells lining the peritoneum is involved in the elevation of CA125 due to peritoneal dissemination and inflammation of cancerous ascites, and CA125 may be a useful predictor of peritoneal dissemination in gastrointestinal cancer. It has also been reported that CA125 correlates with ascites volume and prognosis. However, there are no reports evaluating the clinical significance of CA125 in the later line of metastatic colorectal cancer (mCRC). Therefore, we conducted a multicenter retrospective study. Methods: We retrospectively analyzed the clinical data of 121 patients who received trifluridine/tipiracil (FTD/TPI) or Regorafenib from January 2012 to May 2018 in 10 centers and had the result of serum CA125 just before the treatment. Patients who had received either FTD/TPI or Regorafenib were excluded. In this study, the levels of ascites were classified as follows: "none" as undetectable by computed tomography scanning, "mild" as confined to the pelvic cavity or upper abdomen, "severe" as continuous from the pelvic cavity to the upper abdomen, and "moderate" as between "mild" and "severe". RECIST ver.1.1 was used for analysis of tumor response. Survival analyses were performed with Kaplan-Meier method, log-rank test and Cox proportional hazards model. Results: There were 75 patients in the baseline CA125 normal group (group N) and 46 patients in the high group (group H). ECOG PS tended to be worse in group H than in group N (ECOG PS (0/1/2) 26/43/6 and 9/28/9 in N and H groups, p=0.076). There were significantly more patients with ascites in group H than in group N (Yes/No 7/68 and 26/20 in N and H groups, p&lt;0.001). Furthermore, ALP, CRP, CA19-9 and NLR were significantly higher, and Alb was significantly lower in group H than in group N. Baseline CA125 correlated with baseline ascites volume (p&lt;0.001). PFS and OS were significantly shorter in group H compared to group N (PFS; 1.9 vs. 3.0 months; HR 1.576 [95%CI 1.081-2.299]; p=0.016, OS; 4.1 vs. 11.0 months; HR 2.418 [95%CI 1.634-3.576]; p&lt;0.001). The rate of change for CA125 was significantly higher in patients with progressive disease on first evaluation CT compared to patients with disease control (p=0.002), and PFS and OS were significantly shorter in the increased CA125 group measured first after treatment than in the non-increased CA125 group (PFS; 1.9 vs. 4.6 months; HR 3.104 [95%CI, 2.004-4.809]; p&lt;0.001, OS; 5.9 vs. 13.0 months; HR 2.199 [95%CI, 1.474-3.282]; p&lt;0.001). Conclusions: In this retrospective analysis, baseline CA125 correlated with ascites volume in later line treatment of patients with mCRC, suggesting that increased CA125 may be a predictive and prognostic factor. Clinical trial information: UMIN000040059 .

A case of mysterious ascites

A 69-year-old woman presented to our major trauma hospital after being involved in a motor vehicle accident. She had past medical history of renal transplant, insulin dependent diabetes mellitus and ischaemic heart disease. She was admitted to our trauma ICU for multi-system trauma including subarachnoid haemorrhage, spinal fractures, flail chest, liver lacerations and haemoperitoneum. She had multiple operations for her injuries including exploratory laparoscopy. Her condition deteriorated from day 35 of admission, and she was noted to have a large volume ascites which drained six litres of fluid.

Predicting dry weight in patients with cirrhotic ascites undergoing large-volume paracentesis

Ascites impairs the correct diagnosis and nutritional management in patients with cirrhosis, because the body weight, which is needed for nutritional assessment and calculation of nutritional needs, is overestimated. To adjust the weight in patients with ascites, dietetic guidances indicate substracting 2.2-14kg or 5-15% of the measured body weight according to the degree of ascites, however, there is a lack of evidence to substantiate these values. The aim of this study was to develop new prediction equations to estimate the dry weight, comparing them with the currently used weight adjustments in patients with refractory cirrhotic ascites. Cross-sectional study, that included patients with decompensated cirrhosis undergoing large-volume paracentesis. Patients were submitted to nutritional risk screening, nutritional assessment, and anthropometric measurements that included body weight, abdominal circumference (both measured before and after paracentesis) height, and upper mid-arm circumference. The volume of ascitic fluid drained was also registered. For the predictions of dry weight, linear regression models were performed using as predictor variables: height, pre-paracentesis weight, pre-paracentesis abdominal circumference, or mid-upper arm circumference, and as response variable: post-paracentesis weight. The capacity of these models to predict the post-paracentesis weight was evaluated by comparing it with the currently used predictions through the intraclass correlation coefficient (ICC) and the mean squared error (MSE). Nineteen patients were included, 15 male, and 18 with high nutritional risk and malnutrition. The difference between post-paracentesis weight and pre-paracentesis weight was-5.0 (-3.6 to-9.9) kg, similar to ascitic fluid volume drained. Two equations were developed to predict post-paracentesis weight. ICC values showed that both prediction equations were strongly correlated (r>0.94) with post-paracentesis weight. Our models also showed lower MSEs (<17.97), compared with the current predictions (MSEs <64.19, when the pre-paracentesis weight is adjusted from absolute values and MSEs <33.24 when adjusted from percentage values), indicating a more accurate prediction. The predictive equations from this study may be better options for dry weight estimation in patients with refractory cirrhotic ascites since they showed higher reliability compared to the currently used weight adjustment. External validation in a larger sample is still needed to confirm the clinical applicability of these equations.

8880 Recurrent Endometriosis-Associated Massive Hemorrhagic Ascites: A Case Report and Literature Review

<h3>Study Objective</h3> To discuss the presentation, pathophysiology, and management of large-volume endometriosis-related ascites. <h3>Design</h3> Case report and literature review. <h3>Setting</h3> University-based teaching hospital. <h3>Patients or Participants</h3> A 31-year-old with cyclic pelvic pain presented with new-onset hemorrhagic ascites up to 6L in volume requiring recurrent paracentesis. <h3>Interventions</h3> Initial ultrasound imaging (Figure 1) revealed large volume ascites, normal uterus, and normal ovaries. Computed tomography scan revealed a large amount of ascites with a normal-appearing liver. Paracentesis revealed hemosiderin laden macrophages and no evidence of malignancy or bacterial growth. The patient's medical and hepatologic workup was unremarkable. After undergoing two additional paracentesis procedures, she underwent diagnostic laparoscopy and peritoneal biopsies. Findings included stage 4 endometriosis with posterior cul-de-sac disease, right adnexal and large bowel disease, and diaphragmatic disease (Figure 2). <h3>Measurements and Main Results</h3> The patient was started on high-dose oral progestins postoperatively. Thereafter, she noted symptom improvement and less frequent paracentesis, but stopped therapy due to side effects. She was started on Elagolix and add-back therapy with no recurrence of ascites over one month of follow-up. Large-volume endometriosis-associated ascites is rare, usually recurrent, and thought to be due to massive ovarian transudate plus altered lymphatic drainage¹. Symptoms may mimic those of an ovarian malignancy. Associated CA-125 levels vary and do not correlate with the presence of ascites^2,3. Additionally, 38% of patients present with pleural effusion². Suppressive therapy with gonadotropin-releasing hormone (GnRH) agonists temporarily prevents ascites recurrence, but medical management regimens and outcomes vary^1,3,4. Surgical management of endometriosis without bilateral salpingo-oophorectomy (BSO) is associated with a recurrence rate of over 50%, while BSO is curative¹. <h3>Conclusion</h3> Clinicians should consider endometriosis in the workup for patients presenting with pelvic pain and recurrent large-volume hemorrhagic ascites after ruling out ovarian malignancy. Suppressive therapy with high-dose progestins or GnRH agonists/antagonists may improve symptoms and reduce the risk of recurrent ascites, but rigorous studies are lacking.

Mechanisms of the ascites volume differences between patients receiving a left or right hemi-liver graft liver transplantation: From biofluidic analysis

Background and objectivePost-transplant refractory ascites (RA) is common in patients receiving living donor liver transplantation (LDLT) using a left hemi-liver graft than in those using a right hemi-liver graft. However, there is currently no clear mechanism explaining the effect of grafts on ascites drainage. The purpose of this study is to analyze the values of blood flow parameters in the portal vein under different grafts using computational fluid dynamics (CFD) to interpret the relationship between portal pressure values with ascites drainage. MethodsIn this work, ascites drainage was counted in 30 patients who underwent left-sided liver transplantation and 26 patients who underwent right-sided liver transplantation. The portal vein flow models of the transplanted liver under different flow rates were established based on computed tomography (CT) images and finite element theory. Ascites drainage and blood flow parameters were qualitatively compared. ResultsThe results show that the ascites drained from patients who received LDLT with a left hemi-liver is three times as that with a right hemi-liver. The simulation results show that the coefficient of the pressure-velocity curve of the left-liver is 1.7 times of the right-liver under the same hydrodynamic conditions, which qualitatively agrees with the clinical data. Moreover, the streamline of the transplanted left liver shows more vortexes compared with the right liver, which is a major reason for the left liver's higher pressure value. ConclusionThis clinical phenomenon is reproduced and comprehensively explained by the hemodynamic parameters of the portal vein. This work establishes the relationship between portal pressure values and floating water drainage, and offers a new way for physicians to predict postoperative risks intuitively.

METTL3-mediated N6-methyladenosine modification and HDAC5/YY1 promote IFFO1 downregulation in tumor development and chemo-resistance

Ovarian cancer (OC) is a malignant tumor that seriously threatens women's health. Due to the difficulty of early diagnosis, most patients exhibit advanced disease or peritoneal metastasis at diagnosis. We discovered that IFFO1 is a novel tumor suppressor, but its role in tumorigenesis, development and chemoresistance is unknown. In this study, IFFO1 levels were downregulated across cancers, leading to the acceleration of tumor development, metastasis and/or cisplatin resistance. Overexpression of IFFO1 inhibited the translocation of β-catenin to the nucleus and decreased tumor metastasis and cisplatin resistance. Furthermore, we demonstrated that IFFO1 was regulated at both the transcriptional and posttranscriptional levels. At the transcriptional level, the recruitment of HDAC5 inhibited IFFO1 expression, which is mediated by the transcription factor YY1, and the METTL3/YTHDF2 axis regulated the mRNA stability of IFFO1 in an m6A-dependent manner. Mice injected with IFFO1-overexpressing cells had lower ascites volumes and tumor weights throughout the peritoneal cavity than those injected with parental cells expressing the vector control. In conclusion, we demonstrated that IFFO1 is a novel tumor suppressor that inhibits tumor metastasis and reverses drug resistance in ovarian cancer. IFFO1 was downregulated at both the transcriptional level and posttranscriptional level by histone deacetylase and RNA methylation, respectively, and the IFFO1 signaling pathway was identified as a potential therapeutic target for cancer.

Efficacy and safety of splenic artery embolization for intractable ascites using Amplatzer vascular plug versus coil after living donor liver transplantation.

PURPOSE Intractable ascites (IA) is an uncommon but challenging complication after liver transplantation. Splenic artery embolization (SAE) modulates the splenic artery and regulates portal flow. This study aimed to evaluate the efficacy and safety of SAE using the Amplatzer vascular plug (AVP) versus coil embolization for post-living-donor liver transplantation (LDLT) IA. METHODS This retrospective study evaluated consecutive patients from 1 center who received LDLT (n=1410) between March 2006 and August 2019. The inclusion criteria for SAE were splenomegaly with IA after LDLT. RESULTS Totally 15 patients underwent SAE for post-LDLT IA. Eleven patients who received AVP embolization (age, 51.2 ± 15.1 years; range, 8-63 years; 5 men and 6 women) were compared with 4 patients receiving coil embolization (age, 30.8 ± 30.8 years; range, 1.5-63 years; 2 men and 2 women). AVP and coil embolization both significantly reduced portal vein hyperflow (plug/ coil; P <.001/.006) and decreased ascites volume (plug/coil; P <.003/.042). The benefits of AVP embolization included shorter procedure time (P =.029), significantly reduced splenic volume (P =.012), increased liver volume (P =.012), decreased spleen/liver ratio (P =.012), and improvement of pancytopenia (P =.008) due to secondary hypersplenism. No significant differences were found between the two groups in the length of hospital stay or complications such as splenic infarction, pancreatitis, or sepsis. CONCLUSION SAE using AVP and coil embolization provide effective and safe methods for managing patients with IA after LDLT. AVP embolization may be more efficient than coil embolization, providing more effective reduction of ascites volume and the advantages of shortened procedure time and improvement of hypersplenism.

S3278 A Rare Case of Gabapentin-Induced Hepatotoxicity

Introduction: Gabapentin is an anti-convulsant that is also used off-label to treat neuropathic pain. It is not metabolized by the liver, and there have been few reports of hepatotoxity associated with it. We present a rare case of gabapentin-induced hepatotoxicity occurring in a young male. Case Description/Methods: A 41-year-old male with an extensive past medical history including type 1 diabetes, end stage renal disease on hemodialysis, TIA, hypertension, and hyperlipidemia was admitted for severe hyperkalemia with K 8.2 and peaked T waves on EKG, and hyperglycemia with glucose 561. He was admitted to the intensive care unit for urgent dialysis. Lab work revealed abnormal liver function tests, with ALP 1,232 IU/L, AST 291 IU/L, and ALT 188 IU/L, and normal total bilirubin of .8 mg/dL. Prior records revealed completely normal liver function tests 6 months prior to presentation. Ultrasound of the RUQ revealed small volume of ascites but was otherwise unremarkable with no abnormality of hepatic parenchyma or biliary ducts noted. Patient reported having a below-knee amputation 3 months prior to presentation, after which he started taking gabapentin 300 mg three times per day. He denied any other medication changes. He reported taking acetaminophen occasionally, and acetaminophen level was < 10 mcg/mL. A full hepatitis panel was negative. An autoimmune workup was planned including Anti-LKM, ASMA, AMA but patient insisted on leaving prior to those labs being drawn. Gabapentin was held and patient’s liver function tests improved, with ALP 1058 IU/L, AST 158 IU/L, and ALT 149 IU/L, and remained stable. Patient discontinued gabapentin and was advised to follow up outpatient, unfortunately he was lost to follow-up. Discussion: Although the exact mechanism of gabapentin is unknown, it is structurally related to GABA and high-affinity binding sites for gabapentin which modulate the release of excitatory neurotransmitters which participate in epileptogenesis have been found throughout the brain. Gabapentin is not hepatically metabolized, and therefore was not studied in patients with hepatic impairment during the FDA approval process. There have been very few cases of gabapentin induced liver injury. In our patient there was a clear temporal association of liver injury occurring after our patient began gabapentin therapy, and slight improvement after a few days of discontinuation. Although further studies on this topic are needed, gabapentin should be considered as a cause of drug induced liver injury.

S2927 Persistent Spontaneous Bacterial Peritonitis in a Patient With Cardiogenic Ascites

Introduction: Ascites is defined as a collection of more than 25mL of fluid in the peritoneal cavity, most commonly caused by liver cirrhosis. Cardiogenic ascites from heart failure contributes to 5% of cases. Spontaneous bacterial peritonitis (SBP) is a common complication of ascites, defined as an infection of ascitic fluid in the absence of a surgically treatable source. This is more commonly associated with hepatic cirrhosis. Here we present a case of SBP in a patient with cardiogenic ascites. Case Description/Methods: Patient is a 37-year-old male with right sided heart failure secondary to bronchopulmonary dysplasia with no history of liver disease. The patient was found to have dyspnea and anasarca, so he was admitted for heart failure exacerbation. CT of the abdomen showed large volume ascites and hepatomegaly. While being diuresed, 5L of ascitic fluid was removed via paracentesis. Analysis revealed a serum albumin-ascites gradient (SAAG) of 0.7, protein 4.5, absolute neutrophil count (ANC) 948, and negative culture. The patient was then started on ceftriaxone for SBP. An additional 4.5L was removed via paracentesis 3 days later due to worsening ascites. Analysis at that time showed SAAG 0.6, protein 4.2, and ANC 4,808. No cultures were reported. Antibiotics were escalated to piperacillin-tazobactam due to worsening ANC. A third paracentesis was performed 3 days later after reaccumulation of ascites (3.2L) and to assess therapeutic response. Peritoneal fluid analysis revealed SAAG 0.8, protein 3.7, ANC 2,931, and negative culture. At this point, the infectious disease team was consulted, recommending discontinuation of antibiotics and close monitoring. Patient was discharged 6 days later as he was afebrile and without leukocytosis. Discussion: The pathophysiology of SBP is thought to be related to bacterial translocation and impaired immunity, specifically deficiencies in complement protein neutrophil function. This is reflected by low ascites protein. However, SBP is exceedingly rare in cardiogenic ascites with only 8 cases reported. This is likely secondary to the high protein and opsonic character in this type of ascites, developing from elevated intrahepatic pressures and congestive hepatopathy. This composition of ascites fluid yields antimicrobial activity similar to normal peritoneal fluid. Perhaps this was the reason for the patient’s elevated ANC despite negative cultures. Future studies could focus on the role of antibiotics and prophylaxis in these patients.

S2217 A Rare Case of Synchronous Double Volvulus of the Sigmoid Colon and Cecum

Introduction: Colonic volvulus is one of the leading causes of large bowel obstruction. Synchronous cecal and sigmoid volvulus is a rare presentation. Cecal volvulus and sigmoid volvulus have traditionally been thought of as separate clinical presentations with distinct clinical features, radiological findings, and treatment modalities. We focus on the classical radiological findings, uncharacteristic presentations, and definitive treatment to prevent recurrence, morbidity, and mortality. Case Description/Methods: A 67-year-old female with a past medical history of severe chronic constipation secondary to stercoral colitis presents to the emergency department complaining of abdominal pain for 5 days. Pain is diffuse, and associated with nausea and vomiting. The last colonoscopy performed 4 years ago, was normal. The patient was in immense pain and was not able to provide further information. On presentation, the patient was afebrile, BP 127/52, HR 73, RR 16 breaths/min. The abdomen was distended, and peritoneal sounds were auscultated in all quadrants but were worse in lower quadrants bilaterally. X-ray of the abdomen showed pneumoperitoneum and dilated bowel related to stercoral colitis. Subsequent CT abdomen showed small volume ascites, hollow perforated viscus, markedly distended cecum with peri-cecal inflammatory changes, and significant wall thickening with inflammation in the sigmoid colon secondary to concurrent cecal and sigmoid volvulus. The patient immediately underwent exploratory laparotomy, ileocecectomy with primary anastomosis, sigmoidectomy with primary anastomosis, and abdominal washout (Figure). Discussion: When evaluating acute abdomen, we propose consideration of synchronous large bowel volvulus is a rare and easily missed etiology of large bowel obstruction due to challenging radiological presentation. Even with detailed cross-sectional imaging like CT scan, it is possible to miss coexisting cecal volvulus due to massively enlarged sigmoid volvulus causing mass effect. The preferred treatment is total or subtotal colectomy with or without anastomosis on a case-to-case basis. This approach provides the advantage of avoiding the risk of recurrence and histopathological analysis to rule out underlying malignancy. Commonly, only one type of large bowel volvulus is found radiologically, it is advisable to pay attention to the possibility of coexisting cecal volvulus and a definitive diagnosis being made intraoperatively.Figure 1.: A. Chest X-ray showing gas under diaphragm; B. Volvulous with dilated caecum and Sigmoid colon on Abdominal X-ray; C. Scout film of the CT scan abdomen; D. Twisted Caecum with dilated sigmoid colon on axial film.

S2186 A Case of Abdominal Cocooning From Appendiceal Carcinomatosis

Introduction: Abdominal cocooning is a rare radiologic finding where thickened peritoneal membrane surrounds the intestines causing bowel to become trapped and adhered to each other. This is usually a result of chronic inflammation and can be associated with infections like tuberculosis (TB) or chronic processes like sarcoidosis, peritoneal dialysis, VP shunts, or carcinomatosis. Patients typically present with intractable nausea, vomiting, abdominal pain and distension. Here, we present a case of abdominal cocooning with recurrent ascites secondary to appendiceal carcinomatosis. Case Description/Methods: 41-year-old male with history of remote polysubstance use (IV and alcohol) and incarceration who presented to the ED with progressively worsening abdominal distension and intractable nonbloody, nonbilious emesis. This patient had been hospitalized for a similar presentation weeks prior. At that time, he was found to have large volume ascites (SAAG 1.1, 774 nucleated cells, 3% segs) and was diagnosed with alcoholic cirrhosis though RUQ ultrasound with liver doppler and lab work were normal. CT abdomen and pelvis showed “peritoneal thickening concerning for peritonitis” (Figure) and the patient was treated for presumed spontaneous bacterial peritonitis. He presented to our facility weeks later with recurrent ascites (SAAG 1.2, 795 nucleated cells, 1% segs). Triphasic liver CT showed findings that were “highly suspicious for encapsulating peritoneal sclerosis/abdominal cocoon”. Ultimately, a peritoneal biopsy was performed given concerns for carcinomatosis vs. TB infection. Final pathology showed goblet cell adenocarcinoma with presumed appendiceal origin. Colonoscopy was unsuccessful due to cementing of the peritoneum. Patient was not a candidate for chemotherapy due to having severe malnutrition requiring the initiation of total parenteral nutrition. He was discharged with outpatient GI oncology follow up. Discussion: Although cirrhotic ascites is commonly diagnosed and treated by physicians, it is vital that clinicians are also aware of the diagnostic findings of noncirrhotic ascites. In this case, the degree of WBC count elevation with low segmented cells likely indicated TB or carcinomatosis at the initial presentation. Familiarity with imaging findings of abdominal cocooning may have also contributed to an expedited diagnosis. This case reiterates the importance of questioning and further exploring symptom etiologies when routine workup is not consistent with common causes of an everyday complaint.Figure 1.: Peritoneal thickening consistent with abdominal cocooning with large-volume ascites.

S3281 A Rare Case of Drug-Induced Liver Injury (DILI) Due to Valproate Hepatocellular Injury

Introduction: Valproate is a widely-used antiepileptic drug which works by increasing gamma-aminobutyric acid (GABA) levels in the brain. We present a unique form of drug-induced liver injury (DILI) in a patient prescribed valproate for trigeminal neuralgia pain. Case Description/Methods: A 45-year old African American female with a history of hypertension and trigeminal neuralgia was prescribed divalproex for trigeminal neuralgia pain after trials of duloxetine, gabapentin, baclofen, oxcarbazepine, carbamazepine, topiramate, amitriptyline, and tizanidine failed to provide relief. Six weeks later she presented with a two week history of worsening nausea, diarrhea, fever, facial rash, production of dark phlegm, and grade 1 encephalopathy. Lab results showed acute liver failure (ALF) with total bilirubin 15.6 mg/dL, ALP 180 U/L, AST 937 U/L, ALT 943 U/L, and INR 2.8. Exam findings included scleral icterus, hepatomegaly, small volume ascites, and some small liver cysts. A diagnosis of DILI was made, with likely drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome. Divalproex was discontinued and the patient was admitted for two weeks of stabilizing treatment including N-acetylcysteine, lactulose, rifaximin, Vitamin K, and L-carnitine transfusion (Figure 1). The patient was evaluated for liver transplant, but it was ultimately not indicated given her subsequent improvement in liver function. An acute kidney injury developed but was resolved before patient discharge. Two weeks later the patient presented with signs of acute kidney injury. Upon readmission, complications including hepatic encephalopathy, macrocytic anemia, spontaneous bacterial peritonitis, and acute respiratory failure developed over the course of several weeks. All stabilizing treatment efforts were made but the patient ultimately developed septic shock and died. Discussion: DILI is the most common cause of ALF in the United States. Valproate-induced hepatotoxicity as a result of mitochondrial injury from impaired beta-oxidation and decreased tissue carnitine levels is one rare effect of use. Such hepatocellular injury typically shows very elevated AST and ALT levels with a smaller elevation in ALP. Early diagnosis of DILI is crucial to promptly discontinue use of the causative agent and begin optimal treatment. In the case of valproate, it is recommended that patients receive intravenous (IV) carnitine until symptoms improve. Liver transplant evaluation is crucial for ALF patients given the high morality risk.Figure 1.: 1A. Patient’s AST and ALT values over the course of her hospital admission. Figure 1B. Patient’s INR values over the course of her hospital admission.

S1790 Portal Biliopathy in a Patient Who Underwent a Whipple Procedure With Portal Vein Reconstruction

Introduction: Portal biliopathy is a condition that is defined as abnormalities in the biliary tract due to portal hypertension. Some patients may present with abdominal pain, fever, jaundice, or pruritis. Rarely, portal hypertension secondary to portal vein abnormalities cause peri-biliary varices. We report a case of a patient with a peri-biliary variceal bleed due to portal hypertension from acquired portal vein stenosis. Case Description/Methods: A 59-year-old female with a past medical history of pancreatic ductal adenocarcinoma presented to the hospital with 5 days of Black tarry stools. Two years prior, she was diagnosed with pancreatic head adenocarcinoma and underwent a pancreaticoduodenectomy with portal vein reconstruction. Subsequent CT scans demonstrated post surgical portal vein stenosis. On admission, she denied fevers, abdominal pain, or hematemesis. Labs were notable for a hemoglobin of 5.7 g/dl, INR of 1.6, and bilirubin of 1.0 mg/dl. Physical exam demonstrated an abdominal fluid wave and melena on digital rectal exam. CT abdomen showed post Whipple anatomy, severe portal vein stenosis, large volume ascites, and extensive upper abdominal collaterals including peri-portal and peri-biliary varices. Upper endoscopy revealed blood in the afferent jejunal limb. Bleeding was found to be originating from the choledochojejunostomy. Multiple large visible vessels with stigmata of recent bleeding were visualized within the common bile duct. A single hemostatic clip was placed on one of the vessels, resulting in increased bleeding. Hemostasis was achieved with cyanoacrylate injection. The patient was transferred to the interventional radiology suite, where she underwent portal venography confirming severe stenosis of the porto-mesenteric confluence. Interventional radiology performed portal vein balloon dilation and stent placement. The patient had no further bleeding following the procedure (Figure). Discussion: Bleeding from peri-biliary varices is a rare cause of upper GI bleeding. In this case, non cirrhotic portal hypertension from acquired portal vein stenosis after pancreaticoduodenectomy led to clinically significant gastrointestinal bleeding. Portal biliopathy is an uncommon and late presentation in patients with extrahepatic portal vein obstruction. In many cases, patients present with signs and symptoms of biliary obstruction. Treatment of PB should involve a multidisciplinary discussion among various subspecialties including gastroenterology, interventional radiology, and hepatobiliary surgery.Figure 1.: A. Choledochojejunostomy with visible varices. B. Hemostatic clip placement with subsequent bleeding. C. Injection of cyanoacrylate glue with hemostasis. D. Portal venography demonstrating portal vein stenosis at the porto-mesenteric confluence.

S1834 Spontaneous Bacterial Peritonitis in a Postpartum Female Secondary to Necrotizing Pancreatitis

Introduction: SBP is an infection of the fluid that accumulates in the abdomen caused by translocation of bacteria without an obvious source, such as bowel perforation. Typically, this translocation represents a failure in defensive factors to contain pathogens to the bowel and can lead to seeding other extra-intestinal sites. Our patient is unique in that her SBP was characterized in the setting of a recent pregnancy. Her course was complicated by pre-eclampsia resulting in emergent c-section, further complicated by hypertriglyceridemia-induced pancreatitis. After significant intervention, necrotizing pancreatitis leading to retroperitoneal fat saponification and abscess formation was the likely etiology for SBP. Case Description/Methods: A 27-year-old female presented with diffuse abdominal pain, nausea, vomiting, and diarrhea. Past medical history is significant for recent emergency c-section due to pre-eclampsia complicated by hypertriglyceridemia-induced pancreatitis. On admission, she was hypotensive, tachycardic, tachypneic and febrile, with significant bilious emesis. CT revealed large volume ascites, peri-pancreatic fluid, small volume fluid and gas within the endometrial cavity. Peritoneal fluid analysis presented an SBP picture. Abdominal drains were placed to mitigate peritoneal fluid collection, which settled in the retro-peritoneal space. Cultures resulted in pan-sensitive E.coli growth and the patient was started on appropriate therapy. However, the patient continued to have persistent fevers and severe abdominal pain while on medical management. At this point, exploratory abdominal surgery was indicated revealing significant amounts of retroperitoneal saponified fat secondary to necrotizing pancreatitis, and extensive communicating abscesses which were subsequently drained. Discussion: SBP is an infection of fluid that accumulates within the abdomen, typically seen in patient's with chronic liver disease and can be managed with medical therapy. In our patient's case, there was no know history of liver disease. Our patient presented febrile, with diffuse abdominal pain. Imaging revealed significant ascites and cultures resulted in pan-sensitive E.coli. Multiple differentials were assessed including recurrent pancreatitis, C.difficile infection leading to bowel perforation and/or protein-losing enteropathy, endometritis given recent c-section amongst others. After surgical assessment, our likely diagnosis was necrotizing pancreatitis seeding pancreatic enzymes into the retroperitoneal cavity.

S1828 Recurrent Pancreatitis Secondary to Adderall Use With Pancreatic Ascites: A Sight Typically Unseen

Introduction: Pancreatic ascites is a rare disease with a prevalence of 3.5% resulting from pancreatic duct injury. While small ascites resolves spontaneously, large volume, persistent ascites can cause significant morbidity and mortality. We present a case of pancreatic ascites in a patient with recurrent pancreatitis from Adderall use. Case Description/Methods: 38-year-old female with attention deficit hyperactive disorder (ADHD), remote alcohol use, and recurrent pancreatitis complicated by pseudocyst and ascites presented with acute on chronic epigastric pain. Her last reported alcohol use was 2 years ago. Home medications included Adderall (amphetamine and dextroamphetamine) and benzodiazepines. Physical examination revealed normal vital signs, severe cachexia and peripheral edema. Abdomen was distended with epigastric tenderness. Pertinent labs included hemoglobin of 10.8g/dl, calcium 7.6mg/dl, albumin 1.7g/dl and a lipase of 462U/l. Bilirubin, transaminases, alkaline phosphatase and INR were normal. Quantitative immunoglobulins, IgG4, triglycerides and thyroid stimulating hormone were within normal limits. Blood alcohol and phosphatidylethanol (PETH) levels were negative. Previous CT scan demonstrated pancreatic head cyst (4.6cm), stable pseudocysts in the head and body, peripancreatic inflammation and large abdominal ascites. MRCP this admission revealed pancreatic head fluid collection decreased in size (2.3cm), consistent with walled off necrosis (Figure). Diagnostic paracentesis was significant for: WBC 93 cells/mm3, PMN 25%, RBC 2050 cells/mm3, protein 1.9g/dl, lactate dehydrogenase 102U/L, amylase 1496U/L and a serum ascites-albumin gradient (SAAG) < 1.1. An endoscopic retrograde cholangiopancreatography (ERCP) was pursued due to suspicion for pancreatic ascites which showed abrupt cut off of the pancreatic duct in the head, without filling of the pancreatic duct in the body or tail likely due to stricture. A pancreatic stent was placed into the ventral pancreatic duct to maintain patency with plan for endoscopic ultrasound examination (EUS) to exclude obstructive pathology. Discussion: Pancreatic ascites is often seen with recurrent pancreatitis commonly of alcoholic etiology. Our patient had recurrent pancreatitis and ascites due to chronic adderall use. While pancreatitis from adderall use is rare, presentation with ascites can pose a diagnostic challenge. Hence, clinicians should familiarize themselves with early diagnosis and endoscopic management which improves prognosis in this rare disease.Figure 1.: MRCP images revealing large volume ascites (red arrow), walled off necrosis in the pancreatic head (yellow arrow) and peripancreatic inflammation (blue arrow).