Cause Of Ascites Research Articles

Etiology of ascites in adults living in the Hills of Himachal Pradesh, India: A hospital-based study

Aim: Ascites is one of the major complications of liver cirrhosis. In addition, ascites can develop because of peritoneal tuberculosis, malignancy, cardiac, and renal disorders. The purpose of this study was to evaluate epidemiological data on the etiological profile of ascites in adults in a tertiary care hospital in the Northern hilly state of the Western Himalayas. Materials and Methods: A 1-year hospital-based cross section observational study was conducted in the Department of Medicine and Gastroenterology in a tertiary care center of Himachal Pradesh, located in the Northern India. In all 168 patients who were diagnosed as ascites on the basis of history, physical examination, ultrasonography, and of age >18 years were included in the study. Detail history examination and investigation were carried in each case as per protocol. Results: Cirrhosis of liver was the leading cause of ascites in our study (60.7%), tuberculosis was the second most common cause of ascites (13%), malignancy and cardiac disorders were the third (7.7%) most common causes for ascites. Alcohol was the leading cause of cirrhosis in 75 patients (73.5%). Conclusion: The study identified cirrhosis of liver as the leading cause of ascites and alcoholism as the most common cause of cirrhosis. The measures on taking care of preventable risk factors are desired.

ESTIMATION OF SERUM ASCITIC ALBUMIN GRADIENT (SAAG) AND SERUM ASCITIC CHOLESTEROL GRADIENT (SACG) IN DIFFERENT CAUSES OF ASCITES

Background: The aim of present study was to differentiate the portal hypertension and non-portal hypertension as well as malignant causes of ascites by serum ascites albumin gradient (SAAG) and serum ascites cholesterol gradient(SACG). Material and method: a total of 130 patients having ascites were included in the study. Serum and Ascitic albumin and cholesterol was measured. SAAG and SACG were calculated by subtracting ascitic values from the respective serum values. Results: There was significant difference in SAAG in portal hypertension cases of ascites as compared to non-portal hypertension cases of ascites. In malignant cases the SACG was found significantly lower than non-malignant cases. The efficacy of SAAG in the present study to classify portal hypertension and non-portal hypertension etiology was 98.4%. SACG was able to accurately differentiate the malignant and non-malignant cases in 99.2% of cases at cut off value of 53mg/dl Conclusion: In view of the good diagnostic efficacy, easy availability and cost-effectiveness, serum ascitic albumin and cholesterol gradient is an excellent parameter for the diagnosis of portal hypertension and malignant ascites respectively.

Eozinofilik Gastroenteritin Nadir Bir Formu: Eozinofilik Asit

Eosinophilic gastrointestinal diseases are a group of inflammatory disorders characterized by signs and symptoms associated with eosinophil infiltration of the gastrointestinal tissues with the absence of any secondary cause of eosinophilia such as parasitic infection, vasculitis and malignancy. Eosinophilic gastrointestinal diseases are rare and eosinophilic ascite is probably the least common and least reported form. We reported a case of 24-year old women presented with eosinophilic ascites and we want to point out a rare cause of ascites that can be managed appropriately.

Ascites as a Manifestation of Constrictive Pericarditis

In the United States, ascites is most often due to portal hypertension related to liver cirrhosis. We describe a case of constrictive pericarditis presenting with abnormal liver function tests, anasarca, and ascites. A 50-year-old Caucasian man presented with anasarca. Two years prior to presentation, he experienced dyspnea, lower extremity swelling extending to the scrotum, and a 40 pound weight gain. One year later, he started developing ascites. On physical exam, he was found to have jugular venous distention, marked hepatomegaly, dullness in flanks, and anasarca. Laboratory tests revealed mildly elevated alkaline phosphatase, INR, and indirect bilirubin. Workup for chronic liver disease was unrevealing and ultrasound of the liver showed ascites and hepatosplenomegaly without evidence of cirrhosis, portal vein, or hepatic vein thrombosis. Paracentesis revealed an elevated serum-ascites albumin gradient (SAAG) and increased total protein in the ascites fluid. Computed tomography of the chest showed pericardial thickening and moderate ascites. A right heart catheterization showed a positive Kussmaul sign with markedly elevated and equal filling pressures in the heart consistent with constrictive pericarditis. The patient subsequently underwent a full pericardial resection with resolution of his symptoms and normalization of his liver tests. A cardiac cause of ascites can be easily mistaken for primary hepatic cirrhosis when a patient presents with ascites, elevated liver function tests, and peripheral edema. A SAAG of greater than or equal to 1.1 g/dL and an ascites fluid total protein level of greater than 2.5 g/dL suggest constrictive pericarditis. In cirrhosis, the SAAG is much greater than 1.1 g/dL while the ascites fluid total protein level is less than 2.5 g/dL. A right heart catheterization showing elevation and equalization of the right atrial pressure, pulmonary capillary wedge pressure, mean pulmonary arterial pressure, right ventricular diastolic pressure, and left ventricular diastolic pressure can support the diagnosis of constrictive pericarditis. In cases of constrictive pericarditis, diagnosis and treatment in a timely manner is important, as most patients have resolution of symptoms with pericardiectomy.Figure 1

Urinary Ascites

Introduction: Atraumatic bladder rupture is a rare occurrence and therefore not considered highly on the differential for a patient who presents with new onset ascites. We present this case to show the complexity of diagnosing and managing ascites secondary to bladder rupture. Case Report: A 43 year-old female with untreated multiple sclerosis (MS) presented with abdominal pain beginning immediately after voiding. Initial labs revealed mild leukocytosis with normal liver function, creatinine and lipase. Contrast tomography (CT) abdomen/pelvis showed large ascites with normal appearing liver. Pelvic ultrasound demonstrated a small left paraovarian cyst. General surgery and gynecology ruled out acute abdomen, thought the presentation was due to ruptured ovarian cyst and recommended conservative management. Paracentesis fluid was concerning for secondary bacterial peritonitis with labs showing serum albumin-ascites gradient of > 1.1, white blood cell count of 3610, polymorphonuclears of 88%, total protein of 1.3, glucose of 36, and creatinine of 8.27. Five days later, the patient started to have worsening abdominal pain, leukocytosis and renal function. Repeat CT of the abdomen/pelvis showed a marked increase in abdominal ascites as well as an abnormality of the bladder wall that likely represented a bladder diverticulum, but a bladder wall rupture or diverticular rupture could not be excluded. Cystogram confirmed bladder rupture which was thought to be from obstructive uropathy secondary to neurogenic bladder from her untreated MS. She failed conservative management with increased abdominal pain and ileus and subsequently underwent a cystoscopy, cystorrhaphy, and diverticulectomy with drain placement. Discussion: While traumatic rupture of the bladder is a more common occurrence, ascites secondary to a spontaneous bladder rupture is a rare occurrence, documented sparsely in case reports. Due to the delay in diagnosis, patients have poorer outcomes and a high mortality rate. A PubMed search found two other cases of bladder rupture in MS patients, but unlike our patient they presented with signs of acute abdomen. Conclusion: Perforated urinary bladder should be considered in the differential diagnoses in patients presenting with new onset ascites and acute kidney injury without any evidence of chronic liver or heart disease or any other common causes of ascites. Early diagnosis can greatly improve the patient's hospital course and overall outcome.

The diagnostic utility of serum ascites albumin gradient against ascitic fluid total protein for detection of liver disease in patients of ascites- A comparative study

Introduction: Various studies have demonstrated superiority of SAAG (serum ascites albumin gradient) in classifying ascites compared to transudate-exudate concept but with conflicting observations. Ascitic fluid total protein (AFTP) level in ascitic fluid is a much cheaper alternative to the serum ascites albumin gradient ratio. Hence in the study, we have compared the diagnostic accuracy of the old cheaper traditional method against the new method. Methods: Total 102 patients of Ascites were included in the study from J.A. group of hospital, G.R.Medical College (M.P.) in year 2013-15. All medical causes of ascites were included in our study and Non medical causes were excluded. The collected data was analyzed by using Pearson Chi-square statistical analysis to determine correlation between variables. Result: For prediction of liver disease it was found that SAAG was significantly (p value 0.0341) more predictive of Liver disease compared to AFTP. SAAG (p value<0.0009) and AFTP (p value 0.49) were both significant for differentiating cause of ascites when comparison was done between liver and non-liver disease. Conclusion: AFTP is a good surrogate marker for detection of liver disease in ascites. AFTP is an excellent diagnostic test for detection of certain extra hepatic diseases leading to ascites like tubercular peritonitis sub-acute bacterial peritonitis and anaemia-hypo-proteinemia.e

New-Onset Liver Failure: Pitfalls of an Unusual Diagnosis

Introduction: Heart failure is the second most common cause of ascites after cirrhosis. There are cardiac and noncardiac etiologies of ascites, and the multimodality imaging approach is a rich tool to redefine the final diagnosis. Case Presentation: We present a case-series where 3 patients were referred to our hospital for further hepatology assessment due to severe abdominal ascites and liver failure. Constrictive pericarditis was diagnosed in all of them. Nowadays, constrictive pericarditis is a wellknown disease, but sometimes its clinical presentation may delay the treatment and worsen the prognosis. Our 3 cases had similar clinical scenarios and hemodynamic patterns when undergoing right-heart catheterization, but they had different anatomical pericardiumcompromise, requiring different surgical strategies. Conclusions: Nowadays, multimodality imaging, especially cardiac magnetic resonance imaging and cardiac computed tomography, allows us to study a wide spectrum of the same disease in terms of anatomical compromise and cardiac physiology in order to stratify different prognosis and treatment options. We describe 3 unusual clinical cases where the initial differential diagnosis denoted noncardiac etiologies. The level of serum NT-proBNP proved pivotal to the redefinition of the clinical scenario and differentiation between the cardiac and noncardiac etiologies of new-onset ascites. A multidisciplinary approach in this setting between internists, hepatologists, and cardiologists was helpful to establish the final diagnosis in all the patients.

Causes, management and complications of ascites: a review

Ascites is the pathological state in which fluid accumulates in the peritoneal cavity. Fluid accumulation may be due to infection and malignancy or due to other diseases like liver disease, heart failure, and renal disease. The ascitic fluid can be graded into Transudative and Exudative fluid based on the serum ascites albumin gradient (SAAG). The prominent cause of ascites is found to be Liver Cirrhosis. The most common symptom of Ascites is recent weight gain, increased abdominal girth and dyspnea. The first line treatment of ascites includes education regarding dietary sodium restriction and oral diuretics. However, other mechanical methods can also be used if the patient is unresponsive to this approach. But, there are some limitations while using these mechanical methods. Ascites is also associated with certain complications like spontaneous bacterial perotinitis, hepatorenal syndrome and dilutional hyponatremia. Ascites itself is not fatal unless it becomes infected. So, early diagnosis and effective treatment should be ensured in order to avoid further complications. This review focuses on the grades, causes, symptoms, management and complications of Ascites.DOI: http://dx.doi.org/10.3329/icpj.v4i3.21936 International Current Pharmaceutical Journal, February 2015, 4(3): 370-377

Pharmacoepidemiology of ascites and associated complications in hospitalized patients: descriptive observational study

Ascites is the pathological accumulation of free fluid in peritoneal cavity. The aim of the present study was to observe the prevalence, clinical management and the assessment of complications associated with ascites in hospitalized patients. A Descriptive Observational Study was conducted at two tertiary care hospitals of Lahore. The data was collected on a data collection form containing questions regarding basic patient information, presenting symptoms, clinical management and associated complications. Verbal informed consent was taken and confidentiality was maintained. Pilot study was performed prior to performance of a full-scale research project. The results are expressed in the form of frequency and percentages. A total of fifty (50) ascitic patients were evaluated during two months. It was slightly more common in females (58%) as compared to males (42%). Common causes of Ascites were Liver Cirrhosis (80%), Chronic Renal Failure (10%), Peritoneal Malignancy and Peritoneal Tuberculosis (4%) each and Cardiac Failure (2%). The mainstay for the first line treatment in patients with cirrhosis includes education regarding dietary sodium restriction and oral diuretics. The major complications associated with Ascites were Protein malnutrition (87%), Mental Confusion (73%), Hepatorenal Syndrome (21%) and Spontaneous Bacterial Perotinitis (8%). In most patients ascites was being managed successfully by limiting the salt intake and provision of a diuretic regimen. As, ascites is a starting point for more serious complications; so, its early diagnosis should be ensured. Social media and NGOs should play their role in creating the awareness regarding this deadly disease.DOI: http://dx.doi.org/10.3329/icpj.v4i2.21482 International Current Pharmaceutical Journal, January 2015, 4(2): 343-346

Abstract A48: M2 macrophage inhibition reverses vascular leaks that cause malignant ascites in late-stage epithelial ovarian cancer

Abstract Introduction: Malignant ascites is a common symptom of epithelial ovarian cancer (EOC) that greatly reduces the quality of life for patients and has no good treatment options that target the source of the problem. Our study aims to find the cause of ascites in order for us to better know how to safely reverse this pathology. Experimental Procedures: Murine ID8 EOC tumor cells were implanted intraperitoneally or orthotopically into female C57BL/6 mice, and bioluminescent imaging was used to track the progress of the cancer. GW2580, a very selective colony stimulating factor 1 receptor (CSF1R) inhibitor, was given to mice for two weeks once ascites appeared. Flow cytometry, histology, and endothelial cell permeability assays were used to analyze the effects of blocking macrophages in the model. Flow cytometry and endothelial cell permeability assays were also used to analyze and characterize EOC patient ascites samples. Results: CSF1R inhibition blocked specifically M2 macrophages from the ascites and dramatically reduced ascites volume, leaving mice less anemic. When M2 macrophages numbers were reduced in the ascites, CD8 T cell numbers increased, causing the ascites microenvironment to be less immunosuppressive. Peritoneal vasculature that had grown disorganized and leaky became normalized with treatment. Ascites sera from GW2580-treated mice protected against endothelium permeability, while control mouse sera caused the endothelium to become leaky. This data agrees with our finding that patient ascites sera cause more endothelium permeability if more macrophages were present in the ascites. We also saw macrophage and myeloid cell depletion in the tumor and systemically with GW2580 treatment, along with a consistent reduction in tumor burden. Conclusions: M2 macrophages are key players that cause ascites through deregulating peritoneal vasculature. The leaky vessels are normalized once these macrophages are physically and functionally blocked from the ascites microenvironment. This finding suggests that macrophage inhibition could be a powerful tool for ascites management. VEGF inhibitors are currently in clinical trials for malignant ascites treatment with mixed, sometimes deadly, results. Targeting macrophages, the source of many vessel-deregulating proteins, might make it more difficult for resistance to build up than when just one protein, such as VEGF, is blocked, and CSF1R inhibitors have been shown to be safe and well-tolerated in the clinic. This novel approach toward ascites and EOC management should be further studied. Future work will focus on finding the specific factors that caused the vessel deregulation and normalization, looking at functional differences between macrophage from control and GW2580-treated ascites, seeing if endothelial cell-macrophage direct interaction may have any effects on the vasculature, and performing this study in genetic and human models of EOC. Citation Format: Diana Moughon, Huanhuan He, Shiruyeh Schokrpur, Ziyue Jiang, Madeeha Yaqoob, John David, Luisa Iruela-Arispe, Oliver Dorigo, Lily Wu. M2 macrophage inhibition reverses vascular leaks that cause malignant ascites in late-stage epithelial ovarian cancer. [abstract]. In: Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; 2014 Feb 26-Mar 1; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(1 Suppl):Abstract nr A48. doi:10.1158/1538-7445.CHTME14-A48

Large-Volume Paracentesis in Patients with Cirrhotic Ascites: Does It Increase the Risk of Serious Bleeding and the Need for Transfusion?

Background: Liver cirrhosis is the most common cause of ascites. For cirrhotic ascites that does not respond to diuretics and salt restriction, large-volume paracentesis is an alternative option. Methods: A retrospective cohort study of patients admitted to the Day care unit at King Abdulaziz University Hospital for therapeutic paracentesis of cirrhotic ascites was performed from March 2013-April 2014. The demographic data and results, including the platelet count, hemoglobin level, prothrombin time (PT), international normalized ratio (INR), serum creatinine, serum albumin, and bilirubin levels, were recorded. We recorded all of the bleeding episodes. Results: We recorded 118 admissions for 13 patients. Nine of them were male (69.2%), and the mean age was 58.6 ± 15.8 years. All patients had a Child-Pugh score of C. The platelet count was lower than normal for 78 admissions (66.1%), and the PT was prolonged for 99 admissions (84%). Three episodes of bleeding occurred in our cohort, all of which were mild and controlled by the local application of pressure. One patient required a platelet transfusion for severe thrombocytopenia, low platelets count was associated with elevated creatinine and low albumin levels (P = 0.014 and 0.003, respectively). Similarly, a prolonged PT was associated with low albumin, high bilirubin, low platelet, and high creatinine levels (P = 0.013, < 0.001, = 0.006, and < 0.001, respectively). Conclusions: Large-volume paracentesis is associated with only a small risk of bleeding in patients with cirrhotic ascites, and a transfusion of fresh frozen plasma (FFP) and platelets is not needed for the majority of patients.

Idiopathic chronic polyserositis with massive ascites responding to colchicine in an adult: A case report

Objective: While there are many different causes of ascites, most cases are due to cirrhosis. However, a serum/ascites albumin gradient <1.1 indicates that the ascites is not induced by portal hypertension and mandates a search for other etiologies, including causes of serositis. We describe a 70-year-old patient with persistent ascites and pleuropericarditis who underwent a successful outcome while on colchicine treatment. Methods: This study was delineated on a case-report basis. Besides supportive care measures, we performed a compre-hensive clinical and complementary assessment of the patient, which included laboratory tests, imaging techniques, endoscopic evaluation, full microbiological and pathological studies, diagnostic laparoscopy and thoracoscopy, and genetic testing for autoinflammatory diseases. Results: Diagnostic workup failed to demonstrate the presence of an underlying etiologic disorder. Large-volume paracentesis was performed once monthly during 13 consecutive months due to painless, massive accumulation of peritoneal fluid. Eventually, colchicine therapy induced a dramatic response with clinical and radiological disappearance of polyserositis within three months of starting on the drug. While on colchicine, the disease has not recurred throughout a thirty two months period of follow-up so far. To our knowledge, the occurrence of idiopathic, chronic refractory ascites and pleuropericarditis resolved under colchicine treatment in an adult not diagnosed with Familial Mediterranean Fever is an exceptional event. Conclusion: We suggest that in adult patients suffering from idiopathic chronic polyserositis including massive ascites the possible existence of an underlying autoinflammatory condition should be sought. In such a case, a colchicine trial might be regarded as an early suitable therapeutic option.

Pleural Effusion, Ascites, and Periportal Edema in the Absence of Fulminant Hepatic Failure Secondary to Nimesulide

Introduction: Nimesulide is a non-steroidal antinflammatory drug that has been associated with hepatoxicity leading to acute hepatitis, as well as fulminant hepatic failure. The mechanisms have been studied, but are still poorly understood. We hereby report the first case of nimesulide leading to ascites in the presence of bilateral pleural effusions in the absence of fulminate hepatic failure. Case Report: A 44-year-old Brazilian woman with no remarkable past medical history presented with sharp right upper quadrant epigastric pain following a recent 2-week trip to Brazil. She was visiting her family, who lived in a mountainous region and owned a farm that housed cows and pigs, but she did not have any direct contact with animals during her visit. However, she did drink local, unfiltered tap water. Prior to travel, she had sustained an ankle sprain and in Brazil; she was prescribed nimesulide 200 mg 3 tablets a day for 5 days. On presentation, she reported nausea with episodes of non-bloody emesis with body aches, chills, and weakness. On exam, she was afebrile with no scleral icterus. Abdomen was tender to palpation in the right upper quadrant, with positive Murphy’s sign. Her lungs exhibited absent to decreased breath sounds in the bilateral bases. Her white blood cell count was 7,600 per μL. Liver tests showed an AST 327 U/L and ALT 518 U/L. CT abdomen revealed large-volume ascites, periportal edema, and bilateral pleural effusions. Hepatitis A IgM antibody, hepatitis B core IgM antibody, hepatitis B surface antigen, hepatitis B surface antibody, hepatitis C, and hepatitis E antibodies were all negative. Anti-smooth muscle antibodies, antinuclear antibodies, antineutrophil cytoplasmic antibodies, and antimitochondrial antibodies were also negative. She subsequently underwent a transjugular liver biopsy, which was noted for acute lobular hepatitis with prominent zone 3 necrosis and a trans-sinusoidal gradient of 5 mm Hg. Additionally, a simultaneous diagnostic paracentesis was also obtained, which was significant for a SAAG gradient of 1.1. Further infectious work-up revealed a negative HIV, HSV, EBV, and CMV. Yellow fever, Strongyloides, Dengue fever, Leptospira, Schistosoma, and Brucella antibodies were also negative. Conclusion: There have been reports associating nimuselide with fulminant hepatic failure, but none involving nimuselide with pleural effusions and ascites without frank hepatic failure. Although the exact mechanism remains unclear, a clinician still needs to be aware of nimesulide as a possible cause of ascites and pleural effusion in spite of the absence of fulminant liver failure, as documented in our patient, and a thorough drug history is very pivotal.

Fitz-Hugh Curtis: A Rare Cause of Ascites

Clinical Presentation: A 16-year-old, previously healthy female presented to an outside hospital with right upper quadrant (RUQ) pain and hypotension requiring dopamine and norepinephrine. Exam was significant for RUQ tenderness without stigmata of chronic liver disease. Significant labs were: WBC 11 with 56% bands, lactate 8.6, creatinine of 1.7, AST 151, ALT 225, alk phos 113, t.bili 3.5. Subsequent tests were negative for hepatitis A, B, C, ANA, and ASMA. She was treated empirically with vancomycin, zosyn, and doxycycline, and was transferred to our ICU. Abdominal ultrasound was notable for moderate ascites and diffusely thickened edematous gallbladder wall with thickening measuring up to 1.5 cm without cholelithasisis, concerning for acute acalculous cholecystits. MRCP demonstrated gallbladder wall thickening without biliary dilation and moderate free peritoneal fluid. Gynecological examination revealed purulent cervical discharge and cervical motion tenderness. Gonorrhea and chlamydia PCR was negative. Sepsis was attributed to culture negative pelvic inflammatory disease (PID) with peri-hepatitis and gallbladder abnormalities due to Fitz-Hugh Curtis syndrome. Her liver enzymes normalized and abdominal pain improved over 5 days. She was discharged on a 14-day course of oral metronidazole and doxycycline, and on follow-up 3 weeks later, she had no complaints and had normal liver enzymes. Discussion: Fitz-Hugh-Curtis(FHC) is a syndrome of perihepatic inflammation that can occur in up to 14% of PID cases. It typically affects young, sexually active women who present with acute RUQ pain. Causative organisms are typically Chlamydia trachomatis or Neisseria gonorrhea, although in up to 25% of cases, etiology is unknown. Ultrasound is the usual initial test to evaluate the gallbladder and liver for other common cause of RUQ pain. Typically, hepatic capsular enhancement in the arterial phase on CT is helpful in making the diagnosis and avoiding laparoscopic evaluation. Broad spectrum antimicrobial treatment with anaerobic coverage is recommended if FHC is suspected. Most patients recover completely after appropriate treatment. FHC should be considered when a young woman presents with RUQ pain and pelvic examination is obligatory in this setting. Ascites is an extremely rare finding in patients with FHC, and other causes of ascites should be excluded prior to attributing it to FHC.

Significance of serum and ascitic fluid C-reactive protein in differential diagnosis of benign and malignant ascites.

The values of C-reactive protein (CRP) can prove useful in determining disease progress. Because of synthesis by the liver, production of CRP in response to inflammation may be attenuated in patients with liver dysfunction. This may result in differences interpreting CRP levels in patient with portal and non-portal hypertension ascites. The aim of the present study is to assess discriminant value of serum and ascitic fluid CRP, which is easily accessible and inexpensive laboratory marker of inflammation, concentrations for diagnosis of underlying cause of ascites. This prospective study was conducted at Dıskapı Yıldırım Beyazıt Educational and Research Hospital Department of Gastroenterology. Patients with ascites were further divided into two subgroups based on underlying cause of ascites: Group 1, patient with ascites due to portal hypertensive etiology (high-gradient ascites); Group 2, patient with ascites due to non-portal hypertensive etiology (low-gradient ascites). A total of 91 patients fulfilling the criteria for a diagnosis of ascites were enrolled in the study. Of these patients, 50 had proven (Group 1) ascites due to portal hypertensive etiology (high-gradient ascites) and 41 had clinical (Group 2) ascites due to non-portal hypertensive etiology (low-gradient ascites). Mean baseline serum and ascites levels of CRP were significantly higher in Group 2 compared to those in Group 1 (p=0.021, p=<0.0001, respectively). Increased levels of serum and ascitic fluid CRP were associated with malignant ascites.

Role of transgastric natural orifice transluminal endoscopic surgery in the diagnosis of ascites of unknown origin (with videos)

Natural orifice transluminal endoscopic surgery (NOTES) has been established in animal models and human studies. The aim of this study was to assess the feasibility and efficacy of applying transgastric NOTES to diagnose patients with ascites of unknown origin. Prospective study. Two university and teaching hospitals. Patients with ascites of unknown origin. Diagnostic transgastric NOTES. Characteristic of ascites cases, conditions of the abdominal cavity, diagnostic accuracy, adverse events, and follow-up time. Transgastric NOTES was performed successfully in 78 patients with ascites of unknown origin, and 72 cases (92.3%) were clearly diagnosed. They included malignant tumors (39 cases), tuberculous peritonitis (28 cases), chronic hepatic inflammation (3 cases), necrotizing lymphadenitis (1 case), and eosinophilic serositis of the small intestine (1 case). In addition, there were 6 nondiagnostic cases, and no severe adverse events were found. Nonrandomized control analysis. Transgastric NOTES in combination with biopsy can elucidate the causes of ascites of unknown origin in the majority of cases. Therefore, it is a feasible and effective approach to access the peritoneal cavity and also a valuable modality to detect the cause of diseases with ascites of unknown origin.

B-Type Natriuretic Peptide Levels in New-Onset Ascites

Cirrhosis and heart failure are common causes of ascites. The serum-ascites albumin gradient (SAAG) is usually ≥1.1 g/dL in both conditions, and the

An uncommon cause of ascites: spontaneous rupture of biliary cystadenoma

Biliary cystadenomas are cystic hepatic tumours of biliary origin. Cystadenomas are often slow-growing benign tumours, but always harbour the risk of malignant transformation. Cystadenomas are often asymptomatic, but may present with abdominal pain and distension. Though suspected with cross-sectional abdominal imaging, definitive diagnosis almost always requires histology. Spontaneous rupture of cystadenoma had been reported three times in the medical literature to date, all presenting with peritonitis. Here we report a case of spontaneous intraperitoneal rupture of biliary cystadenoma presenting as ascites without peritonitis.

Serum B-type natriuretic peptide in the initial workup of patients with new onset ascites: A diagnostic accuracy study

Heart failure (HF) is, after cirrhosis, the second-most common cause of ascites. Serum B-type natriuretic peptide (BNP) plays an important role in the diagnosis of HF. Therefore, we hypothesized that BNP would be useful in the differential diagnosis of ascites. Consecutive patients with new onset ascites were prospectively enrolled in this cross-sectional study. All patients had measurements of serum-ascites albumin gradient (SAAG), total protein concentration in ascitic fluid, serum, and ascites BNP. We enrolled 218 consecutive patients with ascites resulting from HF (n = 44), cirrhosis (n = 162), peritoneal disease (n = 10), and constrictive pericarditis (n = 2). Compared to SAAG and/or total protein concentration in ascites, the test that best discriminated HF-related ascites from other causes of ascites was serum BNP. A cutoff of >364 pg/mL (sensitivity 98%, specificity 99%, and diagnostic accuracy 99%) had the highest positive likelihood ratio (168.1); that is, it was the best to rule in HF-related ascites. Conversely, a cutoff ≤ 182 pg/mL had the lowest negative likelihood ratio (0.0) and was the best to rule out HF-related ascites. These findings were confirmed in a 60-patient validation cohort. Serum BNP is more accurate than ascites analyses in the diagnosis of HF-related ascites. The workup of patients with new onset ascites could be streamlined by obtaining serum BNP as an initial test and could forego the need for diagnostic paracentesis, particularly in cases where the cause of ascites is uncertain and/or could be the result of HF.

Clinical study of ascites with special reference to Serum-Ascitic Albumin Gradient

Background: The Serum – Ascites Albumin Gradient (SAAG) defined as serum albumin concentration minus ascitic fluid albumin concentration. SAAG has been proposed a physiologically based alternative criterion in the classification of ascites. Aims & Objective: The present study was designed to differentiate ascites based on serum/ascites albumin gradient and comparing transudate and exudate concept using biochemical parameters. The study also designed to know various aetiologies of ascites. Material and Methods: This cross sectional study was done among 60 patients with ascites in Kasturba Medical College Mangalore from September 2006 to September 2008. Ascitic fluid and blood samples were sent for various investigations depending on the presentation of the patient to hospital. Results: In our study Cirrhosis of liver was the most common cause of ascites (78%) followed by Tubercular peritonitis (8%) and alcohol was the commonest cause for cirrhosis of liver (85%) followed by Hepatitis B virus infection. Cirrhosis of liver showed high SAAG compared with tubercular peritonitis and malignant ascites which showed low SAAG. Among High SAAG patients 96% had portal hypertension. Transudative ascites observed in 72.5% of cirrhosis patients whereas tubercular peritonitis showed exudative type in60% of cases. Conclusion: Cirrhosis liver was the most common cause of Ascites and alcohol was the commonest cause for cirrhosis. SAAG is superior to transudate exudate concept in differentiating the causes of ascites. High SAAG indicates presence of portal hypertension and low SAAG indicates absence of portal hypertension.