Large Ascites Research Articles

Sex differences in patient-reported outcomes and perception of ascites burden amongst outpatients with decompensated cirrhosis and ascites.: Sex Differences in Ascites Burden Perception.

Perception of the ascites burden and its effects on quality of life may be different between sexes. This study assessed sex differences in perception of ascites burden and its impact on health related QoL (HRQoL) in patients with recurrent or refractory ascites. The North American Consortium for the Study of End-stage Liver Disease prospectively enrolled outpatients with cirrhosis and large ascites requiring repeat large volume paracenteses. Demographics, laboratory results, co-morbidities, medications, frailty measurements, self-reported questionnaires related to functional status, physical activities, and HRQoL (generic = SF36 & ascites specific = ascites Q) were compared between sexes. 392 men (59.6±10.7yrs) and 184 women (59.5±11.1yrs) with predominantly alcohol related liver disease 51% and 43% respectively), median MELD-Na: 13, were enrolled. Both groups had similar co-morbidities and cirrhosis complications, ascites duration and severity, and frailty scores (p=0.94). Women had more symptoms related to their ascites (Ascites Q score =66±21 vs. 60±21 in men, p=0.001) (higher value = feeling worse). 35% of women felt depressed versus 22% of men (p=0.0009), with lower mental but not physical functioning components of SF36 (p=0.019). Women continued to conduct their daily activities as adequately as men as indicated by Duke Status Activity index (p=0.27) and Godin Leisure Activity Index (p=0.47). Women with cirrhosis and ascites experienced worse emotional HRQoL than men without difference in daily function. Our analyses underscore the differences in the lived experience of women versus men with cirrhosis and highlight the need for patient-reported metrics to provide patient-centered care.

Intra-abdominal nocardiosis and scedosporiosis in a dog: case report and literature review.

A 2-y-old, intact female, mixed-breed dog was presented to the veterinary hospital with abdominal distension, anemia, and lethargy following a chronic history of nonspecific gastrointestinal signs. CBC and serum biochemistry revealed moderate nonregenerative anemia with neutrophilia, hypoalbuminemia, hyperglobulinemia, hypoglycemia, decreased urea and creatinine, and hypercholesterolemia. Abdominal radiographs and ultrasound revealed a large heterogeneous mesenteric mass and ascites. Abdominocentesis confirmed septic peritonitis with filamentous bacteria. Fine-needle aspiration of the mass yielded pyogranulomatous inflammation and hyphae. An exploratory laparotomy revealed a large cranial abdominal mass with granulomas present throughout the abdominal cavity. Due to the poor prognosis and disseminated disease, the owner elected euthanasia. Postmortem and histologic examinations detected intralesional mycetomas and bacterial colonies within the mesenteric masses. 16S ribosomal RNA gene PCR and sequencing using formalin-fixed, paraffin-embedded sections identified Nocardia yamanashiensis, Nocardioides cavernae, and Nocardioides zeicaulis. Fungal culture, PCR, and sequencing confirmed Scedosporium apiospermum. Our report highlights the importance of molecular methods in conjunction with culture and histologic findings for diagnosing coinfections caused by infrequent etiologic agents. Additionally, we provide a comprehensive literature review of Scedosporium apiospermum infections in dogs.

Meigs syndrome after treatment for catamenial pneumothorax

In the field of thoracic surgery, catamenial pneumothorax (CP) is known as a disease peculiar to women, but it is rare among female pneumothoraces and is rarely encountered in clinical practice. Meigs syndrome (MS) is another female-specific disease, defined as a benign ovarian tumor with pleural and ascites effusions, but it is rare and the details of the pathogenesis of MS have not yet been elucidated.A 40-year-old Japanese woman came in with dyspnea. Chest radiography revealed a collapsed right lung. She underwent video-assisted thoracoscopic surgery, which revealed multiple diaphragmatic foramens. She was therefore diagnosed with CP. Later, when she was 50-year-old, returned with chest pain. Computed tomography of the chest and abdomen showed right massive pleural effusion and a large tumor and ascites in the pelvis. This condition was suggestive of MS. The patient underwent bilateral oophorectomy, and the right pleural effusion and ascites resolved promptly after surgery.In conclusion, both menstrual-associated CP and MS are very rare conditions, and to the best of our knowledge, there are no reported cases of the combination of the two. However, it is possible that some MS patients may have MS without CP, and the present case is considered to be valuable because a small diaphragmatic foramen was identified via thoracoscopy, which has been a minority opinion among the mechanisms of pleural effusion in MS.

SAT477 Consumptive Hypothyroidism In A Patient With Plasma Cell Neoplasm

Abstract Disclosure: G. Sidhu: None. I. Madahar: None. A. Haider: None. J. Giordano: None. Introduction: Thyroxine (T4) is converted into metabolically active form triiodothyronine (T3) by deiodinase enzyme 1 & 2 (D1 & D2). Deiodinase 3 converts T4 and T3 into metabolically inactive form reverse T3 (rT3)& di-iodothyronine (T2) . Consumptive hypothyroidism syndrome (CHS) is a very rare form of hypothyroidism seen in patients with neoplasms, which express high levels of D3 enzyme. Case: 68-year-old female withhistory of Multiple Myeloma (MM), POEMS, hyperlipidemia and hypothyroidism was admitted with acute kidney injury, cirrhosis of unclear etiology, large volume ascites and anasarca. She weighed 92 kg on admission. She was complaint with her 50 mcg of levothyroxine and on admission her TSH was 7.14 (N: 0.43-3.55 uIU/ml), Free T4 (FT4): <0.42 (N: 0.7-1.25 ng/dl), total T4 (TT4): 2.6 (N: 4.8-11.7 ug/dl), total T3 (TT3): <20 (N: 80-200 ng/dl). Oral LT4 was switched to IV form due to underlying concerns of malabsorption from anasarca. rT3 was noted to be 40 (N: 8-25 ng/dl). Despite escalated intravenous levothyroxine doses for seven days her FT4, FT3 continued to remain undetectable So her LT4 dose was increased to 75 mcg IV daily initially and eventually to 100 mcg IV daily and 125 mcg daily. On 10th day of hospitalization, after her IV LT4 dose was increased to 200 mcg daily, (almost 2.5 mcg/kg/day) her FT4 levels became detectable, 0.50, rT3: 68 and TT3: <20 and TT4: 3.1. Since her rT3 levels were noted to rise after increasing the dose of LT4, liothyronine (LT3) 5 mcg BID was added to her regimen. PET scan showed small sclerotic bone lesions suspicious for active malignancy. Chromogranin A was elevated 313 (N: <311 ng/ml). IR guided biopsy of scapular sclerotic lesion was done and specimen was sent University of Chicago to measure DI-3 activity in the specimen Pathology results were suggestive of plasma cell neoplasm but unfortunately deiodinase activity could not be quantified. Patient developed hepato-renal syndrome during hospitalization and her family decided to pursue hospice care. Discussion: Critical care illness thyroid disease is also associated with increased DI-3 activity and increases rT3, however T4 and TSH are also low in the setting of critical care illness, and most patient do not require supraphysiologic T4 replacements. The presence of D3 in normal tissues such as the brain & placenta has been hypothesized to protect tissues from the effects of excessive thyroid hormone. However, aberrant expression of the enzyme can lead to severe hypothyroidism from inactivation of both endogenously produced and exogenously administered thyroid hormone. Previously this rare syndrome was described in association with massive hemangiomas in children and in a single case of a hemangioendothelioma in an adult. However case reports in adults have been described in nonvascular tumors who required supraphysiologic doses of levothyroxine prior to the resection of a large malignant solitary fibrous tumor. Presentation Date: Saturday, June 17, 2023

An unusual cause of portal hypertension.

A 66-year-old male with a medical history of coronary artery disease presented with nonspecific symptoms of anorexia, lethargy and an increase in abdominal girth. He was diagnosed 3 months ago with chronic liver disease of undetermined aetiology. He did not smoke and was a social drinker till 4 months ago. He was taking tests showed progressive cholestatic liver enzymes (total bilirubin 1,09 mg/dL, AST 130 U/L, ALT 129 U/L, GGT 517 U/L and ALP 641 U/L) and a severe hypoalbuminemia. Laboratory workup made a metabolic, autoimmune, and viral aetiology of the suspected cirrhosis less probable. Urinalysis showed a rapidly progressive proteinuria in the nephrotic range accompanied by the presence of serum spike of monoclonal lambda light Furosemide, Aldactone, Pantoprazole, Acetylcysteine and Atorvastatin. He had no personal or familial history of liver diseases. Physical examination revealed a tender but distended abdomen and large ascites was present. The laboratory chain protein on electrophoresis with immunofixation. Doppler echocardiography revealed a hypertrophic cardiomyopathy based on diffuse left and right ventricular hypertrophy with relative apical sparing. A diagnostic paracentesis was undertaken and the results were consistent with portal hypertension (SAAG 1,6 g/ dL). Considering the concomitant presence of hypertrophic cardiomyopathy, nephrotic syndrome and a presentation of portal hypertension of undetermined aetiology in presence of a monoclonal IgG lambda light chain spike, a transjugular liver biopsy (figure 1 and 2) was performed with HVPG measurement consistent with significant portal hypertension (15 mmHg).

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.

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.

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).

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.

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.

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.

S3566 Birthing a Baby or Surfacing a Hidden Tumor?

Introduction: Malignancy is a rare finding during pregnancy and if present, often carries poor prognosis. We present to you a case of Krukenberg tumor- a metastatic malignancy of the ovary- in a 29 year old female. Case Description/Methods: A 29-year-old female with no past medical history, presented to the hospital with preterm labor at 30 weeks gestation which lead to low transverse caesarian delivery secondary to recurrent prolonged decelerations and preterm contractions. Patient had an uneventful pregnancy course until this hospitalization. Intraoperatively, a large right sided ovarian mass was discovered. Tissue pathology revealed metastatic poorly differentiated adenocarcinoma. CT scan of the abdomen pelvis was suggestive of right adnexal mass measuring 10 × 14 × 13 cm with increased vascularity, large degree of abdominal pelvic ascites, with few lymph nodes in the upper mesenteric arcade, along with moderate thickening of the gastric wall. Esophagogastroduodenoscopy (EGD) revealed a gastric mass at cardia (Figure a), and tissue pathology was consistent with adenocarcinoma with presence of signet ring cells (Figure b). Additional work up was positive for elevated CA 125 and AFP tumor marker measuring 355 U/ml and 10.8 U/ml, respectively. Subsequent follow up with CT abdomen revealed bilateral ovarian metastasis with large volume ascites. Diagnostic paracentesis was negative for malignant ascites. Clinical course was complicated by recurrent ascites and progressive clinical deterioration. Due to poor performance status, the patient did not undergo any surgical intervention. Patient is currently being managed with palliative chemotherapy and paracentesis for symptomatic relief. Discussion: Krukenberg tumor is a metastatic malignancy of the ovary which is characterized by mucin-rich signet-ring adenocarcinoma that arises primarily from a gastrointestinal site. It accounts for almost 1%–2% of all ovarian tumors. The incidence of gastric cancer in the women of reproductive age group is 0.4%–0.5%, making these tumors extremely rare during pregnancy. Pregnancy symptoms masks the presence of the disease leading to diagnosis at a later stage. Unfortunately, no optimal treatment strategy for these tumors have been identified so far. Chemotherapy as well as radiation therapy does not seem to have any significant role in the prognosis of these patients. Due to metastatic nature and lower rate of resectability, surgery is deferred as it does not offer any increased survival time. The overall prognosis remains poor.Figure 1.: (a) EGD revealing gastric mass at cardia (b) Tissue pathology showing adenocarcinoma with presence of signet ring cells.

S2943 Budd-Chiari Syndrome Diagnosis Achieved With High Clinical Suspicion Raised by EUS-Guided Portal Pressures and Liver Biopsy

Introduction: Budd Chiari syndrome (BCS) is a rare syndrome due to hepatic venous obstruction in the absence of cardiac cause, mostly secondary to thrombosis. As high as 80%of patients present with ascites. The diagnosis should be suspected in patient with acute or chronic liver disease without identified cause. Venous obstruction can be seen on Doppler ultrasound, CT, or MRI of the hepatic veins and inferior vena cava. In some cases, hepatic venogram is needed for its diagnostic and therapeutic advantages. We report a 50-year-old woman with BCS who underwent successful wire recanalization, angioplasty and thrombolysis of the right hepatic vein. Case Description/Methods: 50-year-old woman with no significant past medical history presented with abdominal distension and bilateral lower extremity swelling of two weeks duration. On exam, abdomen was distended with positive signs of fluid collection with +3 bilateral lower extremity edema. Labs revealed total bilirubin 3.3 direct bilirubin 1.4, ALP 477, ALT 38, AST 96, PT 14.4, INR 1.35. Ultrasound showed Heterogeneous appearance of liver and large volume ascites. Doppler study showed normal hepatic and portal venous flow. Abdominal MRI showed hepatic steatosis and caudate lobe hypertrophy. Large volume paracentesis was done with analysis showing SAAG of 3.1, WBC 364, Neutrophils 8. EGD revealed large esophageal varices. Viral hepatitis panel, ceruloplasmin, alpha-1antitripsin, ASMA, AMA antibodies were negative. EUS guided liver biopsy and portal pressure measurement was done showing venous pressure gradient of 13 consistent with portal hypertension. Liver biopsy showed grade 2 fibrosis and zone 3 congestion. Hepatic venogram showed chronically occluded right hepatic vein on which successful wire recanalization was done. Pt was worked up for hypercoagulable state and was found to have JAK 2 mutation and Protein C deficiency. Apixaban, Beta blocker and diuretics were started. Patient showed significant improvement with ascites and MELD score. Discussion: First line investigation for diagnosis of BCS is doppler ultrasound. Doppler US and MRI venography didn’t reveal the hepatic venous thrombosis in our patient. However, high index of suspicion, finding of elevated IVC pressure on EUS, and caudate lobe hypertrophy found on imaging as well as congestion liver biopsy findings led us to further investigate with hepatic venogram which confirmed the diagnosis and provided therapeutic advantages. Table 1. - Prothrombotic risk factors for BCS ACG Clinical Guideline A. Acquired thrombophilia B. Inherited thrombophilia C. Systemic factors D. Hormonal factors Myeloproliferative disorderPolycythemia veraEssential thrombocytosisIdiopathic myelofibrosisJAK 2 mutationPNH Hyperhomocysteinemia Factor V LeidenProthrombin gene G20210A mutationMTHFR C677T mutationThalassemiaPC deficiencyProtein C deficiencyAntithrombin deficiency SarcoidosisVasculitisBehcet’s diseaseConnective tissue diseaseInflammatory bowel diseases OCP usePregnancy Disorders of the Hepatic and Mesenteric Circulation Simonetto, Douglas A.; Singal, Ashwani K.; Garcia-Tsao, Guadalupe; Caldwell, Stephen H.; Ahn, Joseph; Kamath, Patrick S. Official journal of the American College of Gastroenterology | ACG115(1):18-40, January 2020. doi: 10.14309/ajg.0000000000000486

S2686 A Rare but Potentially Fatal Cause of Abdominal Pain: Segmental Arterial Mediolysis

Introduction: Segmental arterial mediolysis (SAM) is a rare disease, defined as a nonatherosclerotic, noninflammatory disruption of the arterial medial layer of a medium- to large-sized artery. We describe a case of a healthy woman with acute onset abdominal pain subsequently found to have spontaneous peritoneal hemorrhage from SAM. Case Description/Methods: A 52-year-old former professional female athlete developed abrupt onset lower abdominal pain with nausea and vomiting. Pain was 10/10 in severity with a sharp and crampy quality. She denied fevers, diarrhea, melena, bloody stool, ill contacts, recent travel, or prior episodes. Past medical history was significant for endometrial polyp, menopause, and iron deficiency. She had no prior surgeries. Family history included colon cancer in her father and ovarian cancer in her mother. Her abdomen was soft with tenderness in the lower quadrants with the remainder of the exam unremarkable. Labs including CBC, BMP, LFT, lipase, beta hCG, troponin, ESR, CRP, serum acetone, urinalysis, and lactic acid were reassuring. CT abdomen and pelvis with and without contrast demonstrated hyperenhancing hepatic lesions suggestive of hemangiomas. Ultrasound of the pelvis with duplex was normal with arterial and venous duplex waveforms to both ovaries. On the second day of hospitalization, she had another episode of abdominal pain with labs demonstrating a hemoglobin drop from 13.7 g/dL to 10.2 g/dL. Repeat CT abdomen pelvis with contrast demonstrated large volume hemorrhagic ascites up to 16 cm in size with concerns for active hemorrhage in the left upper quadrant. Diagnostic angiography was performed by Interventional radiology which did not show active arterial hemorrhage although demonstrated fusiform dilatation of the distal middle colic artery and short segment focal fusiform dilatation of the left colic artery at the splenic flexure suggestive of SAM. She subsequently underwent diagnostic laparoscopy and evacuation of hemoperitoneum with over 1L of unclotted blood evacuated with a mesenteric hematoma noted in the distal transverse and proximal descending mesocolon. The spontaneous peritoneal hemorrhage was thought to be secondary to underlying arterial abnormalities triggered by minor trauma. (Figure) Discussion: Vascular causes of abdominal pain such as segmental arterial mediolysis are uncommon. Awareness of noninflammatory and nonatherosclerotic artery diseases such as SAM need to be recognized since they can be fatal if not treated promptly.Figure 1.: Fig 1 demonstrates a bleeding artery as seen on CT abdomen and pelvis with intravenous contrast. Fig 2 demonstrates the large hemoperitoneum in the left upper quadrant seen on CT abdomen and pelvis.

Living Donor Liver Transplantation for Budd-Chiari Syndrome: A Propensity Score-Matched Analysis.

There are unique technical and management challenges associated with living donor liver transplantation (LDLT) for Budd-Chiari Syndrome (BCS). The outcomes of LDLT for BCS in comparison to other indications remain unclear and warrant elucidation. Data of 24 BCS patients who underwent LDLT between January 2012 and June 2019 were analyzed. There were 20 adults and 4 children. The early and long-term outcomes of adult LDLT BCS patients were compared to a control group of LDLT patients for other indications and matched using propensity scoring methodology. Primary BCS was observed in 18 (90%) patients. Caval replacement was performed in 7 (35%) patients. Early and late hepatic venous outflow tract (HVOT) complications were seen in 1 (5%) and 3 (15%) patients. Preoperative acute kidney injury was identified as a risk factor for mortality in the BCS cohort (p = 0.013). On comparison, BCS recipients were younger with fewer comorbidities, more large volume ascites and higher rates of PVT. They also had longer cold ischemia time, increased blood loss and transfusion requirements, increased hospital stay, and higher late outflow complications. The 1-year and 3-year survivals were similar to non-BCS cohort (84.2% vs. 94% and 71.3% vs. 91.9%, respectively, log rank test p = 0.09). LDLT is a good option for symptomatic BCS who have failed non-transplant interventions. The clinical and risk factor profile of BCS recipients is distinct from non-BCS recipients. By following an algorithmic management protocol, we show on propensity-score matched analysis that outcomes of LDLT for BCS are similar to non-BCS indications.

Ascitic Senescent T Cells Are Linked to Chemoresistance in Patients With Advanced High-Grade Serous Ovarian Cancer.

Senescent T cells are reported to be increased in patients with cancer and are poor prognostic indicators. However, the distribution of senescent T cells and their correlation with clinical features in high-grade serous ovarian cancer (HGSOC) is unknown. We detected the percentage of senescent T cells in the peripheral blood and ascites of patients with advanced HGSOC (n = 86) at diagnosis by flow cytometry. Compared with healthy donors, patients with HGSOC exhibited an accumulation of CD28−CD57+ (Tsen) CD8+ T cells in the peripheral blood and ascites. The frequency of Tsen CD8+ T cells in the peripheral blood was positively correlated with age and pretreatment serum CA125 and increased in patients with large volume ascites, whereas the frequency of Tsen CD8+ T cells in ascites was elevated in patients with lymph node metastasis. Patients with Tsen-high in ascites (>19.92%), but not in the peripheral blood, were more likely to be resistant to chemotherapy and had shorter progression-free survival. Tsen CD8+ T cells exhibited common senescence features including increased SA-β-gal activity, declines in proliferation, loss of CD27 and gain of KLRG-1, and the production of cytokines. In ascites, the percentage of Tsen CD8+ T cells was positively correlated with levels of interleukin-10 and granzyme B. This study suggests the potential of ascitic Tsen CD8+ T cells at diagnosis as a prognostic biomarker in HGSOC.

Clinical, Laboratory and Bacterial Profile of Spontaneous Bacterial Peritonitis in Vietnamese Patients with Liver Cirrhosis.

AimTo determine several clinical and laboratory features as well as the bacterial profile of spontaneous bacterial peritonitis (SBP) in 58 Vietnamese patients admitted to a single center due to liver cirrhosis.MethodsWe retrospectively analyzed bacteriological, clinical and laboratory characteristics of patients with SBP admitted to the Gastroenterology and Hepatology Center from July 2019 to July 2020.ResultsOut of a total 58 SBP patients, 41 (70.9%) had culture-negative neutrocytic ascites. The majority of patients experienced abdominal pain (93,1%) and large ascites (65,5%). Gram-negative bacteria formed the main pathogens (14/17). Escherichia coli (9/17) was the predominant cause followed by Burkholderia cepacia (2/17). Antibiotic sensitivity rate of E. coli for third generation cephalosporin was low but high for aminoglycoside and carbapenem antibiotics. The resistance of E. coli was significant against fluoroquinolones (100%). All 3 cases of gram-positive bacteria were sensitive to vancomycin.ConclusionOur study reported the bacteriological and clinical characteristics of patients with SBP and compared these findings between two groups: positive ascitic fluid culture and negative fluid culture. Ascitic fluid culture can guide for the right antibiotic choice since resistance to commonly prescribed antibiotics is common in SBP patients.

A Rare Case of Secondary Streptococcus pyogenes Peritonitis in a Patient With Cirrhosis

CASE REPORT A 42-year-old woman with autoimmune hepatitis with decompensated cirrhosis and ascites presented with 8 days of worsening abdominal pain. She was afebrile with diffuse abdominal tenderness without rebound or guarding and a large umbilical hernia with overlying skin breakdown. Diagnostic paracentesis produced a protein 5.2 g/dL, glucose < 5 mg/dL, lactate dehydrogenase 14,252 U/L, and a white blood cell count of 59,200/μL with 83% polymorphonuclear cells. Cultures grew Streptococcus pyogenes. Imaging showed large ascites communicating with a loculated fluid collection in the umbilical hernia (Figure 1). The loculated collection drained purulent fluid positive for moderate Gram-positive cocci in chains and clusters. Despite 2 weeks of ceftriaxone (2 g) and metronidazole (500 mg), clinical peritonitis with fevers persisted. Repeat paracentesis showed an increase in white blood cells to 82,760/μL. Laparoscopy with peritoneal washout was performed with removal of 6 L of purulent fluid and lysis of dense adhesions and fibrinous exudate (Figure 2). Pathology demonstrated acute fibrinous inflammatory exudate with dense fibrous tissue. Antibiotics were broadened to piperacillin-tazobactam (3.375 g) with improvement, and she was discharged on cefpodoxime (200 mg).Figure 1.: Abdominal and pelvic computed tomography with large volume ascites and loculated fluid collection in the umbilical hernia.Figure 2.: Dense adhesions and fibrinous exudate is seen throughout the peritoneum on laparoscopy.Secondary peritonitis in patients with cirrhosis is uncommon and has a high mortality (53.8%) with appropriate surgical management, so rapid differentiation from primary spontaneous bacterial peritonitis is paramount.1 Runyon's criteria can be used and require 2 of 3 criteria: ascitic fluid protein >1 g/dL, glucose <50 mg/dL, and lactate dehydrogenase greater than normal serum's upper limit. Ascitic fluid growing multiple organisms and clinical failure to respond to appropriate antibiotics are other clues in establishing the diagnosis.2 S. pyogenes peritonitis is rare, limited to case series and reports of individuals without previous underlying liver disease, peritoneal dialysis, or pelvic inflammatory disease. A case series of available evidence until March 2018 identified 30 published cases of S. pyogenes peritonitis in previously healthy individuals. Given female predominance (75%), a hypothesized portal of entry was translocation from the vaginal tract.3 There are 240 cases of culture-positive peritonitis in patients with cirrhosis contained only 2 cases of S. pyogenes, although without case details.4 One case report documented S. pyogenes peritonitis in a patient with cirrhosis with umbilical hernia rupture.5 Given the similarity in the examination, this was considered the likely portal of entry in our patient. This case highlights the challenges in managing secondary peritonitis in patients with cirrhosis, including the importance of early differentiation between primary and secondary peritonitis and successful stepwise management. DISCLOSURES Author contributions: A. Philippou and C. Bowman-Zamora wrote the manuscript. G. Ezaz edited the manuscript and is the article guarantor. Financial disclosure: None to report. Previous presentation: This case was presented at the New York ACP poster presentation; April 8, 2021; Virtual. Informed consent was obtained for this case report.

Therapeutic endoscopic ultrasound.

Endoscopic ultrasound (EUS) has been continuously evolving for the past three decades and has become widely used for both diagnostic and therapeutic purposes. The efficacy of therapeutic EUS (TEUS) has proven to be superior and better tolerated than conventional percutaneous or surgical techniques. TEUS has allowed the performance of multiple procedures including gallbladder, pancreatic duct and biliary drainage as well as gastrointestinal anastomoses. TEUS procedures generally require the following critical steps: needle access, guidewire placement, fistula creation and stent deployment. The indications and contraindication for TEUS procedures vary with different procedures but common contraindications include hemodynamic instability, severe coagulopathy unable to be reversed, large volume ascites or the inability to obtain access to the target site. Proficiency and high volume in endoscopic retrograde cholangiopancreatography (ERCP) and diagnostic EUS procedures are required for training in TEUS. The complexity of the cases performed can be seen as a pyramid with drainage of pancreatic fluid collections at the base, pancreaticobiliary decompression in the middle, and creation of digestive anastomosis at the top. The mastery of each level is crucial prior to reaching the next level of complexity. TEUS has been incorporated in our arsenal and is impacting on a daily basis the way we offer minimally invasive therapy.