High Serum-ascites Albumin Gradient Research Articles

Ascites Is a Poor Prognostic Factor in Advanced Pancreatic Adenocarcinoma and May Be Undertreated: A Prospective Cohort Study.

Pancreatic ductal adenocarcinoma is associated with significant morbidity and mortality as most patients present with advanced disease. The development of ascites has been associated with poor outcomes and further characterization and contemporary management strategies are needed. A total of 437 patients enrolled in the Gastrointestinal Biobank at Cedars-Sinai Medical Center who had epithelial pancreatic malignancy were included in the prospective cohort group. Overall, 41.7% of patients included in this study developed ascites. Most patients with ascites (>80%) had high serum-ascites albumin gradient ascites. In both univariate and multivariate analysis, a history of ≥1 form of chemotherapy was significantly associated with ascites. Estimated median overall survival in patients with ascites was significantly lower than in patients without ascites, 473 days vs 573 days, and ascites had a hazard ratio of 1.37. Patients with ascites who received diuretics and indwelling peritoneal catheter had an estimated median survival of 133 days from diagnosis of ascites, and those who received only the indwelling peritoneal catheter without diuretics had an estimated median survival of only 54 days. The estimated median survival from the diagnosis of ascites was 92 days, and the median time to puncture was 7 days. The median time from first tap to death was 45 days. The use of diuretics is lower than would be expected for patients with pancreatic ductal adenocarcinoma with elevated serum-ascites albumin gradient. Other therapies such as beta blockers should be investigated in this subset of patients. The etiology of ascites in these patients is poorly understood, and further research is needed to establish treatment guidelines and improve outcomes.

Severe Mitral Stenosis Presenting as Chronic Liver Disease: A Rare Case Report

High Serum Ascites Albumin Gradient (SAAG) ascites in severe rheumatic mitral stenosis is very uncommon. Hereby, the authors present a similar case with this rare combination. The present case report describes a 42-year-old male with no history of hypertension or diabetes, but occasional alcohol consumption, who presented to department with complaints of recurrent anasarca over the past five years. The electrocardiogram showed an irregular R-R interval with no P waves, indicating atrial fibrillation. Ascitic fluid analysis revealed a high serum ascites albumin gradient with low ascitic protein levels. The patient responded well to treatment and was discharged with appropriate medications. He was referred to a higher centre with cardiothoracic surgical facilities for mitral valve replacement and tricuspid annuloplasty. The present case report highlights the uniqueness of the combination of severe rheumatic mitral stenosis and ascites.

CLINICAL PROFILE OF ASCTES BASED ON PRESENTATION AND LABORATORY FINDINGS:AN INSTITUTIONAL EXPERIENCE FROM MAHARASHTRA,INDIA

Introduction: Ascites is the fluid collection in the potential space of the peritoneal cavity. Alcoholic liver disease and intra-abdominal malignancy are two major etiologies behind it. Also, diagnosis of tuberculous ascites should be thought of due to endemicity. Cirrhotic patients at any time during the course of disease, invariably present with ascites which is one of the marker of decompensation. In our context, etiology behind ascites and its correlation with symptoms and clinical findings not yet studied, so present study is conceptualised. Aim: To study clinical profile of ascites based on presentation and laboratory findings Methods: This is a cross-sectional retrospective descriptive hospital based record review of patients presented with ascites in a tertiary center of Maharashtra . One hundred fourteen patients with ascites under regular follow up of SMBT Hospital were reviewed. Data regarding presenting complaints, examination findings, relevant investigations during first visit and final diagnosis were retrieved from our own record keeping and recorded information were then evaluated. Results: Patients having ascites have myriad of symptoms and signs, commonest clinical feature being icterus (74, 64.9%). Most of them were anemic at presentation. Forty-two (36.8%) had high blood urea and 36 (31.5%) with high creatinine suggesting approximately 30-40% cases presented with deranged renal function test. Ninety-three (81.5%) had raised total serum bilirubin. Similarly, PT/INR derangements were in 74 (64.9%) and 57 (50%) suggesting deranged liver function. Serum albumin was less than 3.5 gram/decilitre in 83(72.8%) cases. Among the patients studied, 80 (70.1%) had high Serum-Ascites Albumin Gradient (SAAG) suggesting transudative type of ascites and rest 34 had low SAAG suggesting exudative type of ascites. Overall assessment revealed, majority of patients (71.05%) had Chronic liver disease (CLD) as the cause of ascites. Conclusions: Ascites due to chronic liver disease was the main finding with etiology supported by laboratory findings. Significant numbers of the patients had deranged renal function on top of liver function derangement, so these parameters need to be properly taken care of.

S3028 Identifying and Screening At-Risk Patients for Hepatitis Delta Virus

Introduction: Hepatitis delta virus (HDV) is associated with the most severe forms of viral hepatitis with rapid progression to cirrhosis and hepatocellular carcinoma. The prevalence of HDV may be significantly higher than formerly acknowledged in the United States, making it doubly important to identify at-risk individuals. Case Description/Methods: A recently emigrated 29-year-old Afghani male with chronic hepatitis B virus (HBV) infection presented with abdominal pain, nausea and vomiting to an outside facility. He underwent a laparoscopic cholecystectomy for symptomatic cholelithiasis. He developed postoperative abdominal distension with imaging initially concerning for a large bile leak however ERCP and a diagnostic laparoscopy were unrevealing. Four liters of fluid were drained, and a surgical drain was placed which continued to drain up to two liters of fluid daily. Upon transfer to our hospital, diagnostic workup showed AST 583 U/L, ALT 452 U/L, alkaline phosphatase 88 U/L, total bilirubin 1.8 mg/dL, and albumin 2.8 g/dL. HBV DNA PCR was < 10 IU/mL. HBV core antibodies, HBV e antibody, and HBV surface antigen were reactive. HBV e antigen and HBV surface antibody were non-reactive. Ascites fluid studies showed a high serum ascites albumin gradient and low protein, prompting a liver biopsy that showed cirrhosis (image 1). The patient was ultimately found to be positive for HDV antibody, confirming a diagnosis of cirrhosis due to HDV superinfection. The patient had his drains removed and was discharged on oral diuretics and entecavir for treatment of HBV infection. Diuretic uptitration is ongoing with plans to enroll in a trial in the future pending clinical status. Discussion: In patients with chronic HBV who acquire HDV as a superinfection, 70-80% develop cirrhosis or hepatocellular carcinoma within 5-10 years. Superinfection is the likely cause of cirrhosis in our patient, as cirrhosis in a 29-year-old would not be expected with HBV infection alone. Early recognition of at-risk individuals can aid in faster diagnosis and earlier treatment. Screening should be considered in all individuals with a reactive HBV surface antigen, and especially in migrants from endemic areas, hemodialysis patients, healthcare employees, and IV drug users. Total HDV antibodies should be obtained for screening, with diagnosis confirmation by serum RT-PCR. Currently, therapeutic options are only available for compensated patients, with pegylated interferon alpha approved in the United States and buleviritide in Europe.Figure 1.: (A) Trichrome stain showing markedly active chronic hepatitis consistent with cirrhosis. (B) Immunohistochemical stains demonstrate patchy staining with HBV surface antigen but (C) negative for HBV core antigen.

CLINICAL AND ETIOLOGICAL PROFILE OF MALIGNANT ASCITES WITH SPECIAL REFERENCE TO SAAG CRITERIA AND BIOLOGICAL MARKERS

Objective: The aim and objective of the study are to the analysis of the various patterns of malignant ascites (MA) in our setup. Methods: This prospective observational study was conducted from November 2008 to August 2010 in the Postgraduate Department of General Medicine, S.C.B. Medical College, Cuttack. Diagnosed patients with ascites due to malignancy (intra-abdominal or extra-abdominal) were enrolled into the study. A thorough history and clinical examination were recorded. Patients underwent abdominal paracentesis in the first 24 h after the admission. Ascitic fluid was obtained from the left lower abdominal quadrant and samples were sent for biochemical, cytological, and microbiological analysis. Results: Among 62 patients, male predominance was 71% and mean age of presentation was 55±20.5 years. Histopathological study revealed malignant cells in 32 cases in their ascitic fluid and was classified as MA or peritoneal carcinomatosis. In 30 patients, the ascitic fluid was negative for malignant cells and was classified as malignant-related ascites (MRA). The most common cancers causing MA were gastric (62.5%) followed by ovarian (25%). The most frequently associated cancers in MRA were hepatobiliary (53.3%) and ovarian (13.3%) cancers. Biomarkers were positive in total 32 cases. All 32 patients with carcinomatous peritonitis demonstrated a low (&lt;1.1 mg/dL) serum ascites-albumin gradient (SAAG) and all 30 patients with MRA had high SAAG (&gt;1.1 mg/dL). Conclusion: The incidence of MA was 51.61% and MRA was 48.39%, and highest incidence was seen in the elderly males. SAAG was diagnostic in differentiating MA from MRA with an accuracy of 100%.

Effect of intra-peritoneal induction of ascites fluid on the rate of postoperative intraabdominal adhesion in a rat model

IntroductionIntra-abdominal adhesions (IAAs) are secondary to peritoneal injuries such as previous surgery or intra-abdominal infections (IAIs). Accordingly, it is crucial to employ fitting techniques to minimize the likelihood of adhesions in any surgery. Due to a paucity of similar data available, this study sought to explore the effects of induced high serum ascites albumin gradient (SAAG) and low serum ascites albumin gradient (SAAG) on the rate of post-operative microscopic and macroscopic adhesion in a mouse model. Material and methodsSixty mice were compared in six groups of ten each. Control groups (1 &4) received normal saline, groups 2&5 received high SAAG ascites fluid, and groups 3&6 received low SAAG ascites fluid intraperitoneally. These groups underwent exploratory laparotomy on day zero, followed by the same procedure on the 10th (groups 1,2,3) and the 30th (Groups 4,5,6) day of surgery. Then, microscopic and macroscopic IAAs were evaluated. Data were analyzed in SPSS software and compared with a p-value less than 0.05. ResultsBy comparison, the least microscopic and macroscopic IAAs after 10 and 30 days were found in the low SAAG ascites group. Revealing a statistically significant difference compared to the other two groups (P = 0.01). After 10 days of surgery, macroscopic IAA in the high SAAG group was significantly lower compared to the control and Low SAAG ascites groups. ConclusionIntraabdominal low SAAG ascites fluid can significantly decrease the probability of postoperative fibrosis and adhesion band formation. Protocol numberIR. BUMS.REC.1399.503.

Hepatic Histoplasmosis Masquerading as Cirrhosis and Portal Hypertension: A Case Report

AbstractHistoplasmosis is an uncommon cause of pyrexia of unknown origin in India. We present a case of hepatic histoplasmosis presenting as pyrexia of unknown origin. The patient had splenomegaly, thrombocytopenia, high serum-ascites albumin gradient, and imaging suggestive of cirrhosis. The patient had received 2 months of antitubercular treatment and came to us because of a lack of improvement. A liver biopsy was done because of cholestatic liver function tests and normal biliary system on imaging, thus raising the possibility of infiltrative liver disease. A transjugular liver biopsy revealed histoplasmosis. The patients improved after treatment. It is a common practice to start antitubercular treatment in patients with pyrexia of unknown origin, which should not be practiced in the current era. Every effort should be made for a correct diagnosis. The case highlights the importance of liver biopsy in cases with no definite diagnosis and also that hepatic histoplasmosis could mimic cirrhosis.

The Correlation between Serum Ascites Albumin Gradient and Oesophageal Varices in Chronic Liver Disease

Background: Oesophageal varices are abnormally enlarged veins in the tube that connect the throat and esophagus. Such condition occurs most often in people with serious liver diseases. On the other hand, chronic liver disease denotes the disease of the liver which lasts over a period of months or more. The serum ascites albumin gradient (SAAG) is a formula that is used to assist in determining the etiology of ascites. We don’t have any research-based information regarding the correlation between serum ascites albumin gradient and Oesophageal varices in chronic liver disease. Aim of the study: The aim of this study was to assess the correlation between serum ascites albumin gradient and Oesophageal varices in chronic liver disease. Methods: This prospective observational study was conducted in the Department of Hepatology, BSMMU, Dhaka, Bangladesh during the period from January 2005 to December 2005. In total 50 patients with cirrhosis with ascites with high SAAG values (&gt;1.1 gm/dl) were included as the study people. The age of the patients was 15 to 70 years. Both males and females were included in the study. All data were entered into a personal computer, thoroughly checked for any possible error, and then processed and analyzed by the SPSS program. The significance of the test was tested by the chi-square test. P-value of &lt;0.05 was taken as statistically significant. Correlation analysis was done by the Pearson correlation test. Results: In this study, in the SAAG group 1.10-1.49 gm/dl, there were 15 patients, 8 patients (53.28%) of them had small varices, 4 patients (26.64%) had medium-sized varices and 2 patients (13.32%) had large-sized varices. In the SAAG group 1,50-1.99 gm/dl, there were 9 patients, 1 patient (11.11%) of them had small sized varices, 6 patients (66.66%) had medium sized varices and 2 patients (22.22%) had large-sized varices. In SAAG group &gt;2 gm/dl, there were 26 patients. Nine (9) patients (34.2%) of them had small-sized varices, ..........

S2412 Not All Ascites Is Created Equal: A Rare Case of Urinary Ascites Masquerading as a High Serum-Ascites Albumin Gradient (SAAG), Low Protein Fluid

S2412 Not All Ascites Is Created Equal: A Rare Case of Urinary Ascites Masquerading as a High Serum-Ascites Albumin Gradient (SAAG), Low Protein Fluid

Placing a lumen-apposing metal stent despite ascites: feasibility and safety.

Background and AimsPlacing a lumen-apposing metal stent (LAMS) through ascites carries serious risks, including death from leakage around the LAMS and failure to create a mature fistula between the 2 lumens. However, sometimes no options exist or are equally dangerous. We present 5 patients who underwent LAMS placement despite ascites in 2 different locations.MethodsThis is a retrospective review of 5 patients who underwent LAMS placement despite ascites in 2 different locations from 2016 to 2018.ResultsThree patients with cholecystitis and 2 patients with afferent limb syndrome and severe ascites were treated with a combination of preprocedural and intraprocedural paracentesis. Serum ascites albumin gradient was measured. Weight was recorded daily. Patients were encouraged to sleep at an incline, and periodic paracentesis (every 3-7 days) was performed when ascites reaccumulated over 4 weeks. Median volume of ascites aspirated was 2 L preprocedurally and 300 mL intraprocedurally. Only 1 patient had ascites with a high serum ascites albumin gradient and was treated with diuretics. Technical and clinical success was achieved in all 5 patients without any adverse events over a median follow-up of 28 weeks.ConclusionsIn situations in which no better options remain, LAMS placement appears to be safe after adequate and aggressive treatment of the underlying ascites pre-, intra-, and postprocedurally. Larger studies are needed to establish the safety of this approach.

Sterile cerebrospinal fluid ascites presenting as high SAAG ascites: a case report

BackgroundCerebrospinal fluid ascites is a rare complication of ventriculoperitoneal shunting and is the result of infection and subsequent peritonitis in the majority of cases. Sterile cerebrospinal fluid ascites in which no known infectious etiology is identified, is even more unusual.Case PresentationA 26-year-old female with Loeys-Dietz syndrome and congenital hydrocephalus treated with a ventriculoperitoneal shunt, was evaluated after developing new-onset ascites of unclear etiology after abdominal surgery for repair of an aortic aneurysm requiring multiple therapeutic paracenteses. Her serum ascites albumin gradient (SAAG) was greater than 1.1, suggestive of a portal hypertensive etiology. Gram stain as well as multiple cultures of her ascites fluid were both negative. Extensive investigation including hepatic venous portal gradient measurement and liver biopsy revealed no evidence of hepatic disease or portal hypertension. She was ultimately found to have sterile cerebrospinal fluid ascites which was treated successfully with a peritoneovenous shunt.ConclusionSterile cerebrospinal fluid ascites is a rare clinical entity that has only been reported approximately 50 times in the medical literature. In this report, we also highlight it as a rare cause of high SAAG ascites. Moreover, we describe the use of a peritoneovenous shunt as a novel therapeutic option in the management of this condition.

2956 The Utility of Repeating Paracentesis in Patients With Cirrhosis and Low SAAG Ascites

INTRODUCTION: The use of serum-ascites albumin gradient (SAAG) is widely stablish and a key part for the workup of ascites. It can differentiate portal hypertension (cirrhosis) from non-portal hypertension causes (malignancy, tuberculosis, nephrotic syndrome, pancreatic ascites), however literature on the interpretation and value of a low SAAG ascites in patients with cirrhosis is very limited and its clinical significance is unclear. Our aim was to investigate patients with cirrhosis who had low SAAG ascites, the presence of a causative factor not related to portal hypertension and the value of repeating paracentesis for SAAG re-assessment. METHODS: We conducted a retrospective designed study in which we obtained a cohort of patients with low SAAG ascites defined as &lt;1.1 g/dl, between the years of 2008 to 2017 in a single large tertiary community Hospital in Chicago, IL. Cirrhosis was defined by clinical, histopathological and radiological findings. Non-portal hypertension causes were reviewed including bacterial peritonitis, peritoneal carcinomatosis, nephrogenous ascites, tuberculous peritonitis, chylous ascites and pancreatic ascites. Receiver operating curve and multivariable logistic regression models using SAS software version 9.4 were performed. RESULTS: A total of 77 patients were evaluated, of whom 53 (69%) were patients with cirrhosis and 24 (31%) without cirrhosis. Patients with cirrhosis were more likely to be males, smokers, alcoholics (Table 1). 47 (89%) patients had a repeat paracentesis that allowed re-calculation of the SAAG. 13 (28%) patients had persistent low SAAG ascites: 3 cardiac, 2 tuberculosis, 1 pancreatic, 1 malignancy and 6 idiopathic. 7 (53%) out of the 13 had identifiable secondary etiology that explained the low SAAG and in 1 (7.7%) case, malignant ascites was diagnosed. Importantly, in 34 (72%) patients the SAAG changed to high SAAG. Of note, the repeat SAAG in those with low SAAG was not difference from the initial one (mean 0.71 vs. 0.84, P = NS). CONCLUSION: High SAAG &gt;1.1 g/dl is specific for cirrhosis as shown in previous studies. However, in patients with known cirrhosis and a low SAAG &lt;1.1 g/dl further evaluation with a repeat paracentesis is recommended; in patients with a persistent low SAAG value up to 53% a secondary etiology of the ascites was identified, including malignancy, in these cases we recommend further investigation to clarify the cause of the ascites.

2332 Large Hepatic Arteriovenous Fistula Leading to Non-Cirrhotic Portal Hypertension and Associated Complications

INTRODUCTION: Portal hypertension (and its complications including bleeding, ascites, encephalopathy) often occur in patients with liver cirrhosis as a result of intrahepatic resistance to portal blood flow and increased portal collateral blood flow. Non-cirrhotic portal hypertension (NCPH) is less common, but can also lead to similar complications. Arteriovenous fistulas are an uncommon presinusoidal intrahepatic cause of NCPH. We present a rare case of a patient with a remote history of a liver biopsy who presented with new onset ascites and found on imaging to have a large hepatic arteriovenous fistula which was subsequently treated with embolization. CASE DESCRIPTION/METHODS: A 61 year old male with no significant past medical history presented to clinic for evaluation of progressively worsening abdominal and lower extremity swelling. Laboratory findings on presentation were remarkable for hemoglobin 7.4 g/dL, platelets 59,000/microliter, INR 1.6, Na 137mmol/L, Cr 1.56 mg/dL T bilirubin 2.4 mg/dL. Paracentesis fluid studies showed high serum-ascites albumin gradient (SAAG) and high protein without evidence of heart failure on echocardiogram. Magnetic resonance imaging of the abdomen showed a 6.3 × 4 centimeters hepatic arteriovenous fistula within segment VIII of the liver; the portal vein was noted to be patent. Liver biopsy showed focal perivenular and subsinusoidal fibrosis without bridging (fibrosis stage 1/6) and nodular regenerative hyperplasia changes with bands of hepatocyte atrophy without any evidence of cirrhosis. Right hepatic arteriogram demonstrated a dilated and tortuous vessel with early filling of the portal venous system and a large aneurysm at the communication point between the arterial and venous fistula. Successful embolization of the anterior segmental branch of the right hepatic artery was achieved. The patient’s hospital course was also complicated by upper gastrointestinal bleeding secondary to esophageal varices which required banding x5. DISCUSSION: The presence of portal hypertensive changes with minimal hepatic fibrosis on liver biopsy is best categorized as non-cirrhotic portal hypertension (NCPH). This patient manifested complications of portal hypertension including variceal bleeding and recurrent ascites secondary to a large hepatic arteriovenous fistula which likely formed following his liver biopsy. Closure of large arteriovenous fistulas can be beneficial in preventing worsening portal hypertension and associated potentially fatal complications.

A Case of Arterioportal Fistula Leading to Non-cirrhotic Portal Hypertension

Introduction: Arterioportal fistula (APF) is a rare cause of non-cirrhotic portal hypertension. This is a case of a hepatic artery-portal vein fistula presenting with recurrent variceal hemorrhage and ascites in a patient with no known liver disease. Case: A 61-year-old woman with aplastic anemia on cyclosporine, remote colon cancer status post sigmoid resection and workup notable for a percutaneous liver biopsy to evaluate a benign liver lesion as a possible metastasis 10 years prior to current presentation, initially presented with hematemesis following 2-3 weeks of increased abdominal girth and new lower extremity edema. EGD showed bleeding esophageal varices that were successfully band ligated. Over the next 6 weeks, the patient required multiple EGDs with banding for recurrent variceal bleeding, and she was then referred to our center for tranjugular intrahepatic portosystemic shunt (TIPS) evaluation. As part of the TIPS evaluation, an MRI identified a right hepatic lobe arteriovenous malformation between the right hepatic artery and portal vein with evidence of portal hypertension. Diagnostic paracentesis demonstrated a high serum ascites albumin gradient (SAAG) of 3.1. Transjugular liver biopsy with pressures was notable for a mean hepatic venous pressure gradient (HVPG) of 7.5 mmHg. The biopsy showed perisinusoidal fibrosis in zone three without cirrhosis, and intimal hyperplasia of the portal vein (arteriolization) consistent with arterioportal fistula (Figure 1). Rather than pursuing TIPS, we elected to perform coil embolization of the two right hepatic arteries supplying the fistula (Figure 2). Despite technical success, a small fistula persisted and repeat embolizations were required. Following these interventions, rebleeding has not occurred during the 1 year follow-up.Figure 1Figure 2Discussion: APFs are a rare cause of pre-hepatic non-cirrhotic portal hypertension, and can be either acquired or congenital. Acquired etiologies include penetrating hepatic trauma, splanchnic artery aneurysms, surgical complications, or they may occur spontaneously in the setting of cirrhosis or liver tumors. Small APFs can occur following percutaneous liver biopsies, but large APFs complicating a remote percutaneous biopsy, as in our case, are rare. APF should be considered in patients with non-cirrhotic portal hypertension and, when identified, treatment is embolization or surgery, not TIPS.Figure 3

Ascites in Patients on Maintenance Hemodialysis: Causes, Characteristics and Predicting Factors.

To describe the causes, characteristics and factors associated with ascites in patients on maintenance hemodialysis. Observational study. Department of Hepatogastroenterology, Sindh Institute of Urology and Transplantation, Karachi, from November 2007 to November 2014. All patients on maintenance hemodialysis and age > 16 years with ascites were included. Frequencies and percentages were computed for different categorical variables. Chi-square or Fischer exact test were used to identify factors associated with ascites like frequency of hemodialysis, serum albumin and cardiac ejection fraction (EF). Odds ratios were calculated for associated factors. Ninety patients were included in this study; 55.5% were males. Median age was 33 years. Cause of ascites was nephrogenic in 77.8%, cardiac failure in 16.7%, hypothyroidism in 6.67%, liver cirrhosis in 4.4%, abdominal tuberculosis in 2.2%, and peritoneal carcinomatosis in 1.1% patients. The ascites was severe in 53.3% patients and severity was associated with serum albumin < 2.8 gm/dL(p=0.007) and cardiac EF < 40% (p=0.028). The ascites was low serum ascites albumin gradient (SAAG), high protein type (LSHP) in 60% patients and associated with hemorrhage (p=0.040). High SAAG, high protein (HSHP) ascites, found in 33.3%, was associated with cardiac EF < 40% (p=0.005) and portal hypertension (p=0.048). High SAAG, low protein (HSLP) ascites, seen in 6.7%, was associated with portal hypertension (p=0.006). The commonest cause of ascites in hemodialysis dependent patients is nephrogenic followed by cardiac failure. Low serum albumin and low cardiac EF predispose to severe forms of ascites.

Unexplained ascites.

Unexplained ascites.

Delay in Diagnosis of Extra-Pulmonary Tuberculosis by Its Rare Manifestations: A Case Report

Introduction: Tuberculosis is now more frequently observed in older individuals, often with underlying illnesses or conditions that may confuse diagnosis. Rapid diagnosis is mandatory. However, treatment should be initiated immediately based on strong clinical suspicion, because mortality from tuberculosis is most often due to delays in treatment. Case presentation: A 68-year-old male was admitted to our hospital with fever. He had splenomegaly, ascites and right-sided psoas abscess. Chest X-ray was normal. Although the vertebral column was intact, he had asymptomatic sacroiliitis. Bony changes of the right sacroiliac joint seemed to be chronic on computerized tomography (CT) scan. Lack of associated clinical symptoms strengthened this assumption. However, signal alterations of respective areas on magnetic resonance imaging (MRI) suggested active inflammation. Analysis of aspirated pus was positive for acid-fast bacilli and the culture depicted mycobacterial growth. The patient was not cirrhotic yet he had high serum-ascites albumin gradient ascites. He had two hypodense lesions in his liver with a cholestatic pattern in the liver test. He had pancytopenia. Biopsy from his liver and bone marrow showed multiple granulomas. Treatment was started with an anti-tuberculosis regimen of four drugs. He responded well to our therapeutic protocol. Conclusions: Tuberculosis is still a diagnostic challenge, especially when the presentation is atypical and extra-pulmonary.

Identifying high and low serum-ascites albumin gradient in ascitic fluid by the point of care dipstick test

Objective: To evaluate the capability of ascitic fluid dipstick results for pH, glucose, and protein in order to predict a low serum-ascites albumin gradient (SAAG) at the bedside of the patient in the emergency department (ED). Methods: This prospective cross-sectional study was conducted during one year in the ED of Afzalipour hospital in Kerman, Iran. All patients with diagnostic or therapeutic paracentesis of ascitic fluid were considered as eligible patients. Exclusion criteria included clinical suspicion for spontaneous bacterial peritonitis (SBP), any contraindications to paracentesis, and patients’ refusal to participate in the study. Dipstick values were obtained at the bedside, and SAAG was calculated after the determination of serum and ascitic fluid albumin by laboratory. A low SAAG ascitic fluid was defined as the study outcome. We also used our study population as a test group to evaluate an equation proposed in one previous study: K = 0.012 Protein−0.012 Glucose−3.329 pH+23.498 Results: A total of 50 patients were enrolled in the study. Based on multivariate regression analysis, dipstick values for protein and glucose were independently predictive of a low SAAG ascitic fluid (P = 0.23, OR = 1.04; and P = 0.001, OR = 0.81, respectively). The formula proposed in one of the previous studies was tested by our data set, with sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) at 84%, 83%, 84%, and 80%, respectively. Conclusion: Dipstick test of ascitic fluid for pH, glucose, and protein has an acceptable sensitivity and specificity as a point of care test, but it cannot be recommended as a substitute for SAAG determination based on the current findings.

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.

Diagnostic Value of Serum Ascites Lipid Gradients in Patients with Ascites

Introduction: Differential diagnosis of ascites is a common clinical problem. Aim of the work: To study the value of Serum Ascites Lipid Gradients (SALG) of total cholesterol, triglyceride, HDL cholesterol, and LDL cholesterol in the diagnosis of ascites. Materials and methods: The study was conducted on patients with ascites admitted to Tropical Medicine and Gastroenterology Department, Assiut University. The study included 115 patients with ascites of different etiologies (liver cirrhosis, tuberculosis, and malignant ascites). Clinical evaluation, abdominal ultrasonography, and laboratory investigations were conducted as follows: Serum Ascites Albumin Gradient (SAAG), serum lipid profile, and SALG of total cholesterol, triglyceride, HDL cholesterol, and LDL cholesterol. Results: SAAG values were 1.87 ± 0.537 (>1.1), 0.58 ± 0.112 (<1.1), and 0.69 ± 0.201 (<1.1) gm/dL respectively for patients with liver cirrhosis, tuberculosis, and malignancy. The SALG levels for differentiating high SAAG (cirrhosis) from low SAAG (tuberculosis and malignancy) were 97.9 ± 28.6 versus 52.7 ± 32.35 and 49.4 ± 28.64 for SALG- total cholesterol, 74.7 ± 28.2 versus 56.9 ± 48.0 and 48.3 ± 29.23 for SALG- triglyceride, 28.67 ± 9.11 versus 18.53 ± 15.7 and 14.7 ± 14.8 for SALG- HDL cholesterol, 55.7 ± 26.1 versus 17.93 ± 38.5 and 28.5 ± 13.65 for SALGLDL cholesterol respectively. These values are significantly higher in cirrhosis than tuberculosis or malignancy. The cut-off SALG values being 67 mg%, 66 mg%, 26 and 49 mg% in cholesterol, triglyceride, HDL cholesterol, LDL cholesterol respectively in differentiating cirrhotic ascites from tuberculosis or malignant ascites A close relationship between the levels of SALG and severity of cirrhosis is found but it is not significant. Conclusion: SALG has important value in differentiation cirrhotic ascites from tuberculosis or malignant ascites but cannot differentiate tuberculosis ascites from malignant ascites.