Low Serum-ascites Albumin Gradient Research Articles

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.

S3495 What Do These Eosinophils Mean? Treatment Naive Systemic Lupus Erythematosus Presenting With Eosinophilic Ascites, Eosinophilic Pleural Fluid, and Enteritis of Unclear Etiology

Introduction: Eosinophilic ascites (EA), lupus enteritis (LE), and eosinophilic enteritis (EE) are rare systemic lupus erythematosus (SLE) complications. When they do occur, overlapping diagnostic criteria causes problems in distinguishing between a SLE-related etiology or EE. For example, intestinal eosinophil infiltration associated with EE is also consistently found in disseminated SLE autopsy case reports. Although both conditions are treated with steroids, therapies after treatment failure are different. We present a rare case of a SLE patient with this diagnostic dilemma with suboptimal response to SLE therapies, questioning whether an EE treatment algorithm may be more appropriate. Case Description/Methods: An afebrile 55 year old female with untreated SLE presented with constipation and a mildly tender distended abdomen. Imaging described moderate ascites, continuous small bowel thickening, ileus, and bilateral pulmonary infiltrates with pleural effusions. Significant results included a white blood cell count of 3.8 without eosinophils, erythrocyte sedimentation rate 5, C-reactive protein < 1, positive ANA (1:160), positive double stranded DNA, and low C3/C4 complement. Paracentesis yielded an exudative eosinophilic (71%) ascitic fluid with a low serum-ascites albumin gradient of 0.9 g/dL, high protein of 3.9 g/dL, and no evidence of malignancy or infection. She also had exudative eosinophilic pleural fluid. Endoscopy revealed mild cecal ischemia, mild gastritis, and a normal terminal ileum without eosinophils. Rheumatology diagnosed her with SLE serositis with peritoneal and pleural involvement complicated by LE, but they were unable to rule out EE. She responded to intravenous steroids but deteriorated when she was switched to oral prednisone. She then failed a regimen of hydroxychloroquine and oral prednisone. During her most recent hospitalization, the patient was transitioned to a regimen of hydroxychloroquine, mycophenolate mofetil, and oral prednisone. Discussion: It is unclear whether our patient’s sub-optimal therapy response is due to SLE or EE, with our case illustrating the difficulties in determining a diagnosis. Determining a diagnosis influences treatment and the patient's clinical course. In EE, treatment includes dietary therapy, antihistamines, leukotriene antagonists, and mast-cell stabilizers. However, our patient’s symptoms are attributed to serositis, leading to a focus on escalating her SLE immunosuppressive therapy rather than re-examine the diagnosis.

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.

Pseudomembranous colitis with negative Clostridium difficile PCR presenting with massive ascites: a case report and literature review

Pseudomembranous colitis (PMC) is characterized by the presence of an inflammatory pseudomembrane overlying the colonic mucosa, and is primarily caused by Clostridium difficile infection (CDI). PMC is often associated with the use of broad-spectrum antibiotics. Common symptoms include watery diarrhea, mucus in stool, abdominal cramps, and fever. We report a case of a 52-year-old female presenting with new abdominal distention, frequent bloody, mucoid, jelly-like diarrhea, and abdominal pain. Peritoneal fluid analysis showed neutrocytic ascites with low serum-ascites albumin gradient (SAAG). A diagnosis of pseudomembranous colitis was confirmed by flexible sigmoidoscopy. However, polymerase chain reaction (PCR) test for Clostridium difficile was negative. The patient was treated with metronidazole (500 mg IV q8h) and vancomycin (250 mg PO QID). Her symptoms resolved after several days of treatment with no ascites found by ultrasound. Neutrocytic ascites can be a complication of PMC. Physicians should also be aware that empirical treatment of Clostridium difficile may cause false negative diagnostic test result.

S2409 Histoplasmosis Presenting as New-Onset Ascites in a Crohn’s Disease Patient on Adalimumab

Introduction: Histoplasma capsulatum is the most frequently diagnosed endemic mycosis in the United States. The majority of cases are self-limiting but infections in immunocompromised patients may result in severe pulmonary or disseminated disease. We report a rare case of disseminated histoplasmosis presenting as new- onset ascites due to granulomatous hepatitis in a patient with perianal Crohn’s Disease on Adalimumab. Case description/methods: A 39-year-old white female with perianal but no intraluminal Crohn’s Disease currently on adalimumab and azathioprine presented with cyclical fevers and rapid onset ascites. In the preceding weeks she was noted to have uptrending alkaline phosphatase (600s) with isoenzymes consistent with liver etiology, GGT 162, mildly elevated AST (53) with normal ALT and total bilirubin. Further workup included positive anti-smooth muscle (1:160) and F-actin antibodies. Anti-nuclear and anti-mitochondrial antibodies both returned negative. MRCP demonstrated a circumferential 1.9 x 1.3cm peribiliary mass with segmental biliary duct dilation. Paracentesis with peritoneal fluid analysis demonstrated a low serum-ascites albumin gradient, lymphocytic predominance, and negative cytology, acid-fast stain, tuberculosis PCR, and adenosine deaminase. Transjugular liver biopsy revealed multiple non-necrotizing granulomas surrounded by chronic inflammation, consisting predominantly of lymphocytes and eosinophils. Grocott’s methenamine sliver stain was positive for narrow-based budding yeast, with morphology suggestive of Histoplasma species. Additionally, a quantitative serum Histoplasmosis antigen returned positive at 2.53 ng/ml. Following these findings, a course of IV Amphotericin B was started with eventual transition to PO Itraconazole for 1 year. Discussion: Histoplasmosis capsulatum is a dimorphic fungus that is endemic to the United States, specifically the Ohio and Mississippi River valleys. The majority of infections are subclinical, but when diagnosed are primarily in immunocompromised patients. A high degree of clinical suspicion is required to facilitate early treatment and prevent poor outcomes. Pulmonary histoplasmosis is by far the most common clinical presentation. Progressive disseminated disease is rare, but may involve the liver, skin, adrenals, gastrointestinal tract, central nervous system, and bone marrow. With the use of immunomodulating therapies on the rise, it is important to consider opportunistic infections in patients with atypical presentations.Figure 1.: A: H&E staining at 200x magnification of liver biopsy demonstrating non-caseating granulomas. B: Liver biopsy shows narrow-based budding yeast with positive silver stain suggestive of Histoplasma.

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.

2644 ACE Inhibitor-Induced Visceral Angioedema - A Rare Phenomenon

INTRODUCTION: Angiotensin Converting enzyme (ACE) inhibitors are widely used to treat hypertension and congestive heart failure. Common adverse reactions include cough, hypotension and dizziness. Angioedema is a rare reaction that occurs in less than 1% of patients. Most cases of angioedema are involving the lips, tongue, face and airway. More rarely, visceral angioedema can also occur with jejunal involvement. CASE DESCRIPTION/METHODS: A 24-year-old female with recently diagnosed hypertension treated with lisinopril presented for evaluation of abdominal pain, vomiting, and diarrhea. On examination, she had moderate epigastric tenderness with normal bowel sounds and no organomegaly. Labs revealed white blood cells 20 k/mm3, elevated C-reactive protein 34.2 mg/L and normal erythrocyte sedimentation rate 7 mm/hr. Complement levels including C1 esterase inhibitor, C1q and C4 were found to be normal. Stool culture also remained negative. Computed tomography (CT) of the abdomen revealed moderate ascites, marked mucosal thickening of jejunal and ileal loops with adjacent mesenteric edema (Figure 1). Magnetic Resonance Enterography did not reveal any pathological process. A paracentesis was performed with the ascetic fluid analysis revealing a low serum-ascites albumin gradient without infection. Endoscopy with small bowel enteroscopy revealed normal duodenum and jejunum (Figure 2). Jejunal biopsy returned negative for an infectious or inflammatory process. Due to negative diagnostic workup, a diagnosis of ACE inhibitor-induced visceral angioedema was suspected. Patients symptoms quickly improved 24 hours after cessation of lisinopril and she was discharged home. On follow up 4 weeks later, the patient remained symptom-free. DISCUSSION: Visceral angioedema is a rare side effect of ACE inhibitors most commonly affecting the small bowel. The jejunum is most often affected followed by ileum and duodenum. High levels of bradykinin can cause increased vascular permeability within the bowel mucous membrane causing edema. Symptoms commonly include abdominal pain, anorexia, vomiting and diarrhea. Symptoms typically begin 72 hours after starting the ACE inhibitor. Imaging studies show circumferential small bowel thickening with mesenteric edema and ascites. Endoscopic examination is usually normal. Diagnosis is made by exclusion of other etiologies and improvement of symptoms within 48 hours of drug cessation. Treatment includes discontinuation of the offending drug and supportive therapy until symptoms are resolved.

Ascites in acute pancreatitis: not a silent bystander

Background & aimAscites in patients with acute pancreatitis (AP) is understudied although recent literature hints at its evident role in the final outcome. This study was planned to study the characteristics of ascites in patients of AP and its effect on the disease course and outcome. MethodsConsecutive patients of AP were studied and patients with or without ascites were evaluated for the baseline parameters and severity assessment. Ascites was quantified and fluid analyzed for its characteristics. Intraabdominal pressure (IAP) was monitored. The various outcome parameters were compared between the two groups of patients with and without ascites. ResultsOf the cohort of 213 patients, 82 (38.5%) developed ascites. Ascites group had significantly higher rates of organ failure (p = 0.001), necrosis (p=<0.001) and higher severity assessment scores. The ascites group had significantly longer hospital and ICU stay and higher ventilator days compared to the non-ascites group. Mortality was also higher in the ascites group (34.1% vs 8.45; p = 0.001). Majority of patients with ascites had moderate to gross ascites (75.6%), low serum ascites albumin gradient (87.8%) with low amylase levels (71.9%). Sub-group analysis in ascites group showed that patients with fatal outcome had higher rates of moderate to gross ascites, higher baseline IAP and lower reduction in IAP after 48 h. Moderate to gross ascites and grades of intra-abdominal hypertension (IAH) were significant predictors of mortality (AUC – 0.76). ConclusionAP patients with ascites have a more severe disease with poorer outcome. Higher degrees of ascites and IAH grades are significant predictors of mortality.

Peritoneal Mesothelioma: A Rare Cause of Abdominal Ascites

Mesothelioma is a fatal malignancy typically located in the pleura of men in their 50's, many years after asbestos exposure. Peritoneal mesothelioma is rare and may be difficult to diagnose by cytologic analysis of ascetic fluid as it is often negative or inconclusive. Patients commonly present with nonspecific symptoms, however, the Gastroenterologist may be called to consider this in the work-up of ascites. A 23 year old female presented with increased abdominal girth, weight gain, and abdominal cramping. Pelvic ultrasound revealed moderate to large amount of simple-appearing nonspecific free fluid in the cul-de-sac and bilateral adnexal regions. Various examinations over the next few months revealed increased free fluid progressing to perihepatic ascites. Transvaginal paracentesis was performed with fluid sent for cytology revealing reactive mesothelial cells. The patient underwent exploratory laparoscopy and ascites analysis showed low serum ascites albumin gradient (SAAG) with high total protein. During the laparoscopy, several nodules attached to the peritoneum in the upper abdomen were biopsied. Histologic and immunohistochemical analysis of the biopsies demonstrated malignant mesothelioma, epithelioid type. The patient was subsequently referred to a tertiary cancer center for treatment with cytoreductive surgery and hyperthermic intraperitoneal chemotherapy.Figure 1Figure 2Figure 3This is a case of peritoneal mesothelioma, a rare fatal tumor, presenting with malignancy-related ascites in a young woman. Occupational and environmental exposure to asbestos remains the leading cause of mesothelioma with exposure preceding diagnosis by 15-60 years. 85% of cases of mesothelioma occur in men in their mid-50's who have identifiable asbestos exposure. This patient presents a rare case: a young female with peritoneal mesothelioma with no identifiable asbestos exposure. There are only 200-400 cases of peritoneal mesothelioma diagnosed in the United States each year which account for 10-15% of cases of mesothelioma overall. Symptoms are often non-specific and routine laboratory tests are not helpful in making this diagnosis. Although cytology of ascites fluid is usually helpful with peritoneal carcinomatosis, it is often inconclusive in instances of peritoneal mesothelioma, as demonstrated in this patient. Review of the literature indicates that this diagnosis was expected to peak in 2015 making increased awareness of this disease and its diagnostic challenges vital.

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.

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.

Coccidioidomycosis Masquerading as Eosinophilic Ascites.

Endemic to the southwestern parts of the United States, coccidioidomycosis, also known as “Valley Fever,” is a common fungal infection that primarily affects the lungs in both acute and chronic forms. Disseminated coccidioidomycosis is the most severe but very uncommon and usually occurs in immunocompromised individuals. It can affect the central nervous system, bones, joints, skin, and, very rarely, the abdomen. This is the first case report of a patient with coccidioidal dissemination to the peritoneum presenting as eosinophilic ascites (EA). A 27-year-old male presented with acute abdominal pain and distention from ascites. He had eosinophilia of 11.1% with negative testing for stool studies, HIV, and tuberculosis infection. Ascitic fluid exam was remarkable for low serum-ascites albumin gradient (SAAG), PMN count >250/mm3, and eosinophils of 62%. Abdominal imaging showed thickened small bowel and endoscopic testing negative for gastric and small bowel biopsies. He was treated empirically for spontaneous bacterial peritonitis, but no definitive diagnosis could be made until coccidioidal serology returned positive. We noted complete resolution of symptoms with oral fluconazole during outpatient follow-up. Disseminated coccidioidomycosis can present in an atypical fashion and may manifest as peritonitis with low SAAG EA. The finding of EA in an endemic area should raise the suspicion of coccidioidal dissemination.

Ovarian Cancer Despite Previous Oophorectomy in Liver Transplant Patient

Introduction: Paracentesis is the initial procedure to determine the etiology of ascites. Ascites is most commonly a result of increased portal pressure; however, other less common considerations include malignancies, which account for 7-10% of cases. We present an unusual case of ovarian cancer causing malignant ascites despite a previous oophorectomy. Case Report: A 70-year-old female with hepatitis C cirrhosis status post orthotopic liver transplantation 18 years prior to presentation and total abdominal hysterectomy with bilateral salpingooophorectomy (TAHBSO) 16 years prior, presented with new abdominal distention, shortness of breath, decreased appetite, and fatigue for 1 month. Physical examination was remarkable for abdominal distention and flank dullness. Right upper quadrant ultrasound was normal and showed no cirrhosis. A doppler ultrasound of the portal vessels showed no obvious clot. A paracentesis was performed with serum-ascites albumin gradient (SAAG) of 0.4, total protein of 3300 mg/dL, and cytology revealing adenocarcinoma. EGD and colonoscopy were negative for a primary source of cancer. An MRI of the abdomen/pelvis revealed a pelvic mass and omental thickening that was most consistent with a primary ovarian tumor despite the patient having a previous TAHBSO. She underwent resection of the pelvic mass, omentectomy, left ureterolysis, and radical dissection with suboptimal cytoreduction. Pathology showed clear cell carcinoma. Her post-operative course was complicated by a cardiac event. Despite aggressive care strategies, this led to respiratory failure and death. Discussion: Peritoneal fluid analysis is indispensable in diagnosing the etiology of ascites. In the setting of a low SAAG and elevated total protein, de novo and recurrent malignancies need to be included in the differential. This is amplified in the setting of previous transplant, as malignancy is a leading cause of death in liver transplant patients on immunosuppression. As our case typifies, this includes ovarian malignancies in all females, despite their previous gynecologic surgeries.Figure 1: Imaging shows multiloculated cystic mass with septations and solid components within the left pelvis.

84-Year-Old Man With Night Sweats, Weight Loss, and Diarrhea

An 84-year-old man with a history of coronary artery disease, hypertension, hyperlipidemia, ischemic stroke, and gastroesophageal reflux disease presented to the outpatient gastroenterology clinic with a 3-month history of night sweats, generalized weakness, nausea, vomiting, nonbloody postprandial diarrhea, and an 18-kg weight loss. He also reported a recent rash and daily morning stiffness in his fingers and knees lasting up to about 30 minutes. He denied alcohol or intravenous drug abuse. Previously, he had been taking several medications, but all had been recently discontinued because of the persistent diarrhea. On examination, the patient had normal vital signs. He appeared cachectic, with a distended abdomen with flank dullness but no pain on palpation. The joints of his fingers and knees were tender to palpation, and soft tissue swelling was evident. No other abnormalities were found on examination of the head, ears, eyes, nose and throat, skin, and lymphatic, cardiac, respiratory, and thyroid systems. A computed tomographic (CT) scan of the abdomen and pelvis obtained 1 month previously at another institution revealed abdominal and pelvic ascites and mildly prominent aortocaval and periportal lymph nodes. A positron emission tomographic/CT scan also obtained at another facility did not suggest malignancy.

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.

An Abnormal Presentation of Ascites

Purpose: A 73-year-old female patient with a history of hypertension, gastro-esophageal reflux disease, and hemorrhoids presented with abdominal distention, pain, and alternating constipation and diarrhea. On exam, she was hypotensive, and her abdomen was distended with a positive fluid wave. Computer tomography (CT) imaging of the abdomen showed minimal to moderate bilateral pleural effusions, and moderate abdominal pelvic ascites. Diagnostic paracentesis demonstrated a serum ascites-albumin gradient (SAAG) of greater than 1.1, with cytology revealing cells of malignant adenocarinoma, mullerian in origin. While the majority of patients who present with ascites have underlying liver disease, 20% demonstrate an extrahepatic etiology, half of which are malignancy-related ascites.1 Malignant ascites is a sign of peritoneal carcinomatosis,2 diagnosed when paracentesis demonstrates positive cytology, elevated protein concentrations, and a low SAAG.3 Accurate characterization of the malignancy is vital, as proper treatment can result in positive responses in a majority of patients, with a minority making complete recovery.4 Though surgical debulking with adjuvant chemotherapy is the preferred treatment,5 chemotherapy alone was initiated, as our patient was a poor surgical candidate. She responded to carboplatin and paclitaxel, with CA-125 decreasing from 15,000 to 600 over 5 months, but chemotherapy was stopped due to an illness, and her CA-125 increased to 7,000 over two months. A follow-up CT showed an increase in peritoneal carcinomatosis with upper abdominal lymphadenopathy and omental disease. She has since restarted chemotherapy. Common presentations of rare diseases are difficult to diagnose. This patient's rare cause of ascites, mullerian adenocarcinoma, is a prime example of this scenario. As ascites can signify a multitude of different diseases and pathologies, maintaining a broad differential when faced with ascites is important to decrease unnecessary treatment, reduce hospitalizations, and improve patient care.

A Case ofChlamydia trachomatisPeritonitis Mimicking Tuberculous Peritonitis

Lymphocytic ascites with low serum-ascites albumin gradient (SAAG) are observed mainly in tuberculous peritonitis, peritoneal carcinomatosis, and pancreatic disease. However, pelvic inflammatory disease (PID) induced generalized peritonitis causing diffuse ascites has been rarely described. We report a 26-year old female patient, who was diagnosed as generalized peritonitis with diffuse ascites due to Chlamydia trachomatis infection. Gynecologic examination did not show the clue of PID and in the analysis of ascites, low SAAG, predominant lymphocyte count and high level of adenosine deaminase were noted. Although the best impression was tuberculous peritonitis on the base of these findings, the laparoscopic finding was consistent with PID and the PCR for C. trachomatis infection in cervical swab was positive. This case suggests that C. trachomatis peritonitis should be considered as a rare cause of low SAAG and lymphocytic ascites in sexually active women and should be intensively evaluated including laparoscopic examination.

The Utility of Evaluating Low Serum Albumin Gradient Ascites in Patients With Cirrhosis

Serum-ascites albumin gradient (SAAG) has been used extensively in the diagnostic workup of patients with ascites. A SAAG level of <1.1 g/dl is usually thought of as a result of nonportal hypertension etiologies, including malignancies, tuberculous peritonitis, and nephrotic syndrome. However, the predictive value of a low SAAG in patients with existing cirrhosis in whom the pretest probability of portal hypertension is high is not clear. We identified all patients with a SAAG of <1.1 g/dl during a 5-year period at a single large veterans affairs medical center. Cirrhosis was defined by clinical, histological, and radiological features. Nonportal hypertension causes of low SAAG were identified, including bacterial peritonitis, peritoneal carcinomatosis, nephrogenous ascites, tuberculous peritonitis, chylous ascites, and pancreatic ascites. We identified 92 patients (76 with cirrhosis and 16 with no cirrhosis) with ascites and a SAAG of <1.1 g/dl. Of the 76 patients with cirrhosis, only 29 (38%) had an identifiable cause, most commonly primary bacterial peritonitis (11, 38%), followed by peritoneal carcinomatosis or malignant ascites (8, 28%) and nephrotic syndrome (5, 17%). There were 47 patients with cirrhosis and a low SAAG for whom no etiology was identified. Thirty-three patients underwent a repeat paracentesis, 24 (73%) of whom changed to a high SAAG. On the other hand, the 16 patients with no cirrhosis had significantly lower SAAG (0.66 vs. 0.81), and most (12, 75%) had an identifiable cause of ascites. Evaluation of a SAAG <1.1 g/dl in patients with known cirrhosis has low yield and is less likely to be helpful than that in patients without cirrhosis. A repeat paracentesis as part of the workup is recommended. Further studies of low SAAG cutoffs are needed.