Portal Hypertension-related Ascites Research Articles

S2917 Acute Alcoholic Hepatitis With Portal Hypertension Complicated by Tuberculous Peritonitis and Ascites

Introduction: Peritonitis related to tuberculosis (TB) infection is rare in the US and normally associated with immunocompromised states. We present a patient found to have TB peritonitis during evaluation of alcoholic hepatitis without evident lung disease. Case Description/Methods: The patient is a 39 yo male born in Mexico with no medical history who presented with three days of abdominal distention, jaundice, and fevers in the setting of alcohol use disorder. He had no other historic risk factors for TB or cough. Exam was remarkable for a distended abdomen. Laboratory results showed leukocytosis, total bilirubin 3.5 (mg/dL), alkaline phosphatase 295 (U/L), AST 147 (U/L), ALT 62 (U/L), and positive quantiferon gold. Chest x-ray had no pulmonary lesions. Ascites fluid studies were significant for high white count (2214 k/uL) with lymphocytic predominance (91%). The serum ascites albumin gradient was consistent with portal hypertension, and ascites total protein was elevated (3.6 g/dL). Fluid ADA was positive. Cross sectional imaging of the abdomen showed omental caking, peritoneal lining nodularity, and hepatosplenomegaly. Fine needle aspiration of the peritoneum showed necrotizing and non-necrotizing granulomas. Sputum gram stain was negative for acid fast bacilli although sputum and ascites cultures ultimately grew TB (Figure). The patient was started on rifampin, isoniazid, pyrazinamide and ethambutol for TB and abstained from further alcohol use. Three months after discharge, jaundice and ascites had resolved and his liver tests had significantly improved. Discussion: TB peritonitis makes up 4-10% of extrapulmonary TB infections. Though rare in the US, it has a high mortality rate (50-60%). Diagnosis can be complicated by difficulty isolating the organism and culture results can take weeks. TB peritonitis can be supported by ascites fluid studies with elevated lymphocyte count, total protein, and positive ADA; although for more definitive diagnosis peritoneal biopsy should be considered. This patient represents a unique confluence of portal hypertension related ascites, induced by acute alcoholic hepatitis, along with TB peritonitis. It is possible that transient immunosuppression from alcoholic hepatitis served as a risk factor in reactivation and dissemination of latent TB. An index of suspicion for TB infection, based on his foreign birth, along with his abnormal ascites fluid studies, led to the peritoneal biopsy and ultimate culture diagnosis of his infection that might otherwise have been overlooked.Figure 1.: Nodularity of the peritoneal lining.

The challenges of ascites management: An Indian perspective.

Content available: Author Interview and Audio Recording.

Splenic vein stenting for recurrent chylous ascites in sinistral portal hypertension: a case report

BackgroundSinistral portal hypertension results from obstruction or stenosis of the splenic vein and is characterized by normal portal vein pressures and liver function tests. Gastrointestinal bleeding is the most common presentation and indication for treatment. Although sinistral portal hypertension-related chylous ascites is rare, several cases have described successful treatment with portal venous, rather than splenic venous, recanalization. Splenectomy is effective in the treatment of sinistral portal hypertension-related bleeding, although recent studies have evaluated splenic vein stenting and splenic arterial embolization as minimally-invasive treatment alternatives. Splenic vein stenting may be a viable option for other presentations of sinistral portal hypertension.Case presentationA 59-year-old gentleman with a history of necrotizing gallstone pancreatitis was referred to interventional radiology for management of recurrent chylous ascites. Analysis of ascites demonstrated a triglyceride level of 1294 mg/dL. Computed tomography revealed splenic and superior mesenteric venous stricture. The patient elected to undergo minimally invasive transhepatic portal venography, which confirmed the presence of splenic vein and superior mesenteric vein stenosis. Venography of the splenic vein showed reversal of portal venous flow, multiple collaterals, and a pressure gradient of 14 mmHg. Two 10 mm × 40 mm Cordis stents were placed, which decreased the pressure gradient to 7 mmHg and resolved the portosystemic collaterals. At 6 months follow-up, the patient had no recurrent episodes of ascites.ConclusionThe current case highlights the successful treatment of sinistral portal hypertension-related intractable chylous ascites treated with transhepatic splenic vein stenting. Splenic venous stent patency rates of 92.9% at 12 months have been reported. Rebleeding rates of 7.1% for splenic vein stenting, 16% for splenectomy, and 47.8% for splenic arterial embolization have been reported in the treatment of sinistral portal hypertension-related gastrointestinal bleeding. The literature regarding splenic vein stenting for sinistral portal hypertension-related ascites is less robust. Technical and clinical success in the current case suggests that splenic vein recanalization may be a safe and viable option in other sinistral portal hypertension-related symptomatology.Level of Evidence: Level 4, Case Report.

Paracentesis Model for Junior Doctors.

Paracentesis Model for Junior Doctors.

A Comparative Study of Serum-Ascitic Fluid Albumin Gradient (SAAG) and Ascitic Fluid Total Protein (AFTP) as a Diagnostic Parameter in Patients Having Ascites

Ascites is a manifestation of various number of diseases and the aetiopathogenesis of ascites is varied. The differential diagnosis of ascites remains a clinical problem. Although cirrhosis is the cause of ascites in most patients (80%), approximately 20% have a cause other than liver disease. Approximately 5% of patient with ascites have more than one cause (i.e. ‘mixed’ ascites). The present study was conducted on 75 consecutive patients admitted to indoor wards, Department of Medicine, Mayo Institute of Medical Science, Barabanki (UP), between June 2015 to May 2016 of age group 18–70 years having clinical symptoms and signs of ascites. Samples of blood and ascitic fluid were obtained simultaneously. The aim of present study was to evaluate various parameters especially serum ascitic fluid albumin gradient in case of ascites in an Indian setting and to compare the SAAG with the AFTP levels in terms of usefulness in establishing a cause of ascites. In the present study value of SAAG was 1.56 ± 0.37 gm/dl (mean ± standard deviation) for patients with portal hypertension related ascites whereas for non-portal hypertension related ascites excluding cardiac ascites SAAG was 0.95 ±0.14 gm%. Corresponding values for cirrhosis and cardiac ascites were 1.6 ± 0.39 gm/dl and 1.44 ± 0.21 gm/dl respectively. It was observed that SAAG in cardiac ascites group (even though placed in non portal hypertension related ascites group based on absence of portal hypertension) resembled the SAAG of portal hypertension related ascites group. It was concluded from our present study that serum ascitic fluid albumin gradient(SAAG) is a better diagnostic parameter than ascitic fluid total protein (AFTP) in the patients having ascites. During the study we observed that SAAG has greater sensitivity and specificity values in comparision to AFTP for detection of portal hypertension related ascites.

Clinical profile and comparison of SAAG with ascites fluid total protein (AFTP) in cases of ascites at a tertiary referral hospital in Maharashtra

Aims: This observational prospective study was carried out with aims of 1) study various presentations and clinical features in ascites cases, 2) assess different etiological factors, 3) compare serum ascitic albumin gradient (SAAG) and ascitic fluid total protein (AFTP) in differentiating portal hypertension related causes of ascites from others, 4) study in hospital outcome in cases of ascites . Material and Methods : 100 consecutive ascites cases admitted in wards with clinical diagnosis and sonographic confirmation were recruited in the study. After history and detailed clinical examination cases were subjected to ultrasonography and portal vein Doppler to diagnose portal hypertension which was followed by paracentesis. Serum Albumin & total protein, ascitic fluid albumin and total protein, AFTP and SAAG was determined. Results : Mean age of diagnosis of ascites was 42.41 ±7.72 years and maximum cases in 30-49 years age group. 68% of cases of ascites had cirrhosis of liver, 16% peritoneal (abdominal) tuberculosis, 10% chronic heart failure (CHF), 4% nephrotic syndrome and 2% had ovarian malignancy. Mean AFTP and Mean SAAG was 1.77±0.73gm% and 2.05±0.52 gm% in 78 cases of portal hypertension related ascites respectively. In normal portal pressure cases (n=22) of ascites it was 3.01±0.37 gm% and 0.72±0.19 gm% respectively. Sensitivity of AFTP and SAAG in differentiating portal hypertension related etiology from other causes was 70.51% and 92.31% respectively .Though sensitivity was less, specificity was equal ( 95.45%). Eight cases had variceal bleeding, 9 had hepatorenal syndrome and 15 had hepatic encephalopathy. Total 16 cases of liver cirrhosis with ascites died in hospital commonest cause was hepatic encephalopathy and hepatorenal syndrome.

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.

An Evidence-Based Manual for Abdominal Paracentesis

The purpose of this study was to provide evidence-based approaches to detect ascites, perform paracentesis, order tests, and interpret the results. A Medline search was performed to identify relevant articles. Of 731 identified articles, 50 articles were used. The most sensitive findings for ascites detection are ankle edema (93%), increased abdominal girth (87%), flank dullness (84%), and bulging flanks (81%). Paracentesis is safe, with bleeding rates and leakage of <1%. An ascitic fluid polymorphonuclear cell count >or=250 cells/mm(3) is the most sensitive test (86%-100%) to diagnose spontaneous bacterial peritonitis. The serum-ascites albumin gradient is the most useful test in identifying portal hypertension-related ascites. Large-volume paracentesis is effective in the treatment of refractory ascites. We conclude that paracentesis is a safe and vital procedure in patients with new-onset ascites. Once detected, an algorithmic approach to ordering tests and their interpretation is useful to determine etiology and direct further management.

Portal decompression by transjugular intrahepatic portosystemic shunt and changes in serum-ascites albumin gradient.

The serum ascites albumin gradient (SAAG) is widely used to help determine the cause of ascites formation. A serum ascites albumin gradient of > or = 1.1 g/dL reliably distinguishes portal hypertension-related ascites from other causes. To date, there are no published data on the impact of portal decompression on this gradient. The recent development of transjugular intrahepatic portosystemic shunt (TIPS) allows for nonsurgical decompression of portal hypertension by radiologically creating a portosystemic shunt. This study examines the short-term impact of portal decompression on the serum ascites albumin gradient (SAAG) in patients with portal hypertension-related ascites undergoing transjugular intrahepatic portosystemic shunt. Portal pressure measurements were obtained before and after TIPS placement. Serum ascites albumin gradient was determined before and at 6 and 24 hours post-TIPS placement. Fifteen patients were enrolled in the study. The mean portosystemic gradient (PSG) before TIPS was 21.0 +/- 9.2 mmHg, whereas the post-TIPS mean PSG was reduced to 11.0 +/- 6.3 mmHg, consistent with portal decompression (p = 0.005). The mean pre-TIPS serum ascites albumin gradient was 1.9 +/- 0.5 g/dL and was reduced to 1.7 +/- 0.5 g/dL at 6 hours (p = 0.003) and 1.4 +/- 0.4 g/dL at 24 hours (p = 0.002) after TIPS placement. These findings further solidify the association between the SAAG and portal hypertension.

Refractory Ascites

The first step in the approach to the ascites patient, after the history and physical examination, is to perform a diagnostic abdominal paracentesis for SAAG to determine whether portal hypertension is present (SAAG 1.1 g/dl or higher) or not (SAAG less than 1.1 gm/dl) (Table 1). Patients without portal hypertension probably do not have liver disease as the cause of their ascites formation and probably should not be treated with dietary sodium restriction and diuretics. Patients with portal hypertension-related ascites usually have chronic parenchymal liver disease and usually require hospitalization for diet education, diuretic treatment, and evaluation of the underlying liver disease. Approximately 90% of patients with ascites due to chronic parenchymal liver disease respond to dietary sodium restriction and diuretics. Because of the poor prognosis associated with ascites, patients who are good candidates for transplantation should be considered for listing when they develop this complication of their underlying liver disease. The 10% of patients with cirrhosis whose ascites is refractory to routine medical treatment must be offered alternative therapy. Transplant candidates should be listed, in my opinion, once they are documented to have diuretic-resistant ascites. Fortunately, alcoholics (who are usually not good candidates for transplantation) who abstain from alcohol may revert from diuretic-resistant to diuretic-sensitive ascites over a period of months. Chronic outpatient therapeutic paracentesis is the most popular short-term treatment for patients with diuretic-resistant ascites. Paracentesis can be used as a "bridge" to alternative therapies or can be continued indefinitely.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Pharmacokinetics of Newer Antibacterial Agents in Liver Disease

Liver disease may produce significant, albeit highly variable, effects on the pharmacokinetic behaviour of antibiotics in serum. Drug disposition may be altered through several pathophysiological mechanisms including reduced hepatobiliary clearance, and modifications in the volume of distribution induced by albumin synthesis deficiency or portal hypertension-related ascites. Antibacterial agents are not affected by potential alteration in hepatic first-pass effects. Only liver cirrhosis-induced effects on serum pharmacokinetics of antibiotics have been extensively studied, unlike those possibly produced by other forms of liver disease. In liver cirrhosis, pharmacokinetic alterations of nearly all beta-lactam or quinolone agents appear not to be marked enough to require dosage adjustment, provided that renal function stays normal. Adaptation in therapeutic schedule, however, is warranted for those drugs that are substantially cleared by the hepatobiliary system, namely mezlocillin, clindamycin, erythromycin, pefloxacin, enoxacin, antituberculous agents or nitroimidazole derivatives. Special caution should also be exercised when using aminoglycosides or vancomycin because of the wide interpatient variability of their pharmacokinetic disposition and their toxic potential. When renal function is impaired and there is an increased volume of distribution due to ascites, as frequently observed in severe liver insufficiency, the elimination half-life of most antibiotics is markedly prolonged, resulting in potential side effects due to drug accumulation. Accordingly, dosage adjustment applies to all drugs. In this regard, it should be remembered that delineating the dosage guidelines for a given antibiotic on the basis of reported pharmacokinetic parameters in patients with liver cirrhosis is awkward and probably of limited value. This pattern is ascribed to large interpatient variability in the active hepatic cell mass, the degree of portal hypertension and the alteration of serum binding capacity. Furthermore, there is no way of predicting accurately the extent of liver insufficiency in an individual patient. Dosage reduction is thus done empirically in most cases. Whenever possible, direct measurements of serum antibiotic concentrations should be the reasonable approach to manage antibiotic therapy in this kind of clinical condition.

Mobilization of malignant ascites with diuretics is dependent on ascitic fluid characteristics

Serial ascites and plasma volumes were measured during diuresis in nine patients with ascites caused by peritoneal carcinomatosis, four patients with chylous malignant ascites, and three patients with portal hypertension-related ascites caused by massive hepatic metastases. Oral diuretics were given to achieve an adequate natriuresis on a sodium-restricted diet. During the study period (7.8 ± 3.2 days), patients with peritoneal carcinomatosis and chylous ascites lost 0.49 ± 0.31 and 0.51 ± 0.42 kg/ day in weight, respectively, with negligible change in ascites volumes (−0.03 ± 0.11 and 0.02 ± 0.09 L/day). Patients with ascites caused by massive hepatic metastasis lost 1.06 ± 0.15 kg/day in weight (P = 0.01 for massive hepatic metastasis vs. peritoneal carcinomatosis) and 0.23 ± 0.13 L/day of ascites (P < 0.05 vs. other groups). Plasma volume changes were not significantly different among the three groups. Patients with edema (9/16) had a greater natriuresis and daily weight loss. Three patients with peritoneal carcinomatosis and one with chylous ascites developed renal dysfunction or symptomatic hypotension. No patient with massive hepatic metastasis developed these complications. In patients with ascites caused by peritoneal carcinomatosis or chylous malignant ascites there is no mobilization of ascites, whereas in patients with massive hepatic metastasis, ascites may be mobilized with diuretics.

The Opacity of Portal Hypertension-Related Ascites Correlates with the Fluid's Triglyceride Concentration

To determine if an elevated triglyceride concentration can explain the opacity of some cirrhotic ascites specimens, the authors measured triglyceride concentration by Coulter DACOS (Hialeah, FL) on 133 paired serum and ascitic fluid specimens. The specimens were categorized as clear or cloudy by coded visual inspection. In addition, the ascitic fluid specimens were inspected for a lipid supernatant after 48 hours of refrigeration at 4 degrees C. The ascitic fluid triglyceride concentration of the 87 clear specimens was 1.9 +/- 1.0 mmol/L compared with 7.0 +/- 4.6 mmol/L for the opalescent specimens (P less than 0.001). Only 17% of the clear specimens demonstrated any lipid layer after refrigeration, compared with 94% of opalescent specimens (P less than 0.001). The triglyceride concentrations were not significantly different between the serum samples obtained from patients with clear compared with opalescent ascites. The opacity of portal hypertension-related ascites appears to be related to the triglyceride concentration of the fluid.

Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis.

To assess the risk of development of spontaneous bacterial peritonitis in relation to ascitic fluid opsonic activity, routine admission abdominal paracentesis was performed on 119 patients during 141 hospitalizations. Paracentesis was repeated if evidence of peritonitis developed during the hospitalization. The ascitic fluid opsonic activity (0.2 +/- 0.5 log kill) of 24 spontaneously infected specimens was significantly (p less than 0.001) lower than that of the group with sterile portal hypertension-related ascites (0.8 +/- 1.1 log kill), and significantly lower than the group with ascites of miscellaneous type (2.4 +/- 1.0 log kill, p less than 0.001). The C3 and C4 concentrations of the spontaneous peritonitis specimens were also significantly lower than in the specimens from the other groups. Of the 55 patients whose initial sterile ascitic fluid opsonic activity was less than 0.2 log kill, 8 (14.5%) developed spontaneous bacterial peritonitis during the hospitalization; whereas none of the 70 patients with sterile ascitic fluid opsonic activity greater than or equal to 0.2 log kill developed spontaneous peritonitis. This difference in the risk of development of peritonitis was significant (p less than 0.01). Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis.

Large-volume paracentesis in nonedematous patients with tense ascites: its effect on intravascular volume.

In patients with portal hypertension and tense ascites, large-volume paracentesis improves patient comfort and may improve systemic hemodynamics. However, it has been avoided in nonedematous patients because of concern for complications, including intravascular volume depletion. In this study, 12 nonedematous patients with chronic liver disease, portal hypertension and tense ascites underwent 14 large-volume (5-liter) paracenteses for the relief of discomfort and/or respiratory distress. Plasma volume was measured directly by a dilution method with 125I-labeled human serum albumin prior to and at 24 or 48 hr after 13 of the paracenteses. All patients felt better postparacentesis. No dizziness, hypotension, tachycardia, encephalopathy or change in mean serum sodium, creatinine or blood urea nitrogen occurred. Two patients experienced a decrease in hematocrit, which was not explained by blood loss or increase in plasma volume. Mean plasma volume was 3,713 +/- 129 ml (55.1 +/- 1.5 ml per kg ideal body weight) preparacentesis and 3,684 +/- 136 ml postparacentesis, the difference being -0.78% (p = 0.48, NS). Our results suggest that 5-liter paracentesis in nonedematous patients with tense portal hypertension-related ascites improves patient comfort and is not associated with a decrease in measured plasma volume.

Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis

To assess the risk of development of spontaneous bacterial peritonitis in relation to the ascitic fluid total protein concentration, routine admission abdominal paracentesis was performed on a group of 107 patients during 125 hospitalizations. The paracentesis was repeated if evidence of peritonitis developed during hospitalization. Twenty-one episodes of spontaneous peritonitis (or its culture-negative variant) were documented in 17 patients. The ascitic fluid protein concentration in the spontaneous peritonitis group (0.72 ± 0.53 g/dl) was significantly lower (p < 0.001) than that in the group of patients with sterile portal hypertension-related ascites (1.36 ± 0.89 g/dl) and was significantly lower than that of patients with ascites due to miscellaneous causes. Of the patients whose initial sterile ascitic fluid protein concentration was ≤1.0 g/dl, 7 of 47 (15%) developed spontaneous peritonitis during their hospitalization; whereas only 1 of 65 (1.5%) patients who had an initial sterile ascitic fluid protein concentration >1.0 g/dl developed spontaneous peritonitis. This difference in risk of development of peritonitis in relation to initial ascitic fluid protein concentration was also significant (p < 0.01). Low-protein-concentration ascitic fluid predisposes to spontaneous bacterial peritonitis.

Diuresis of cirrhotic ascites increases its opsonic activity and may help prevent spontaneous bacterial peritonitis.

Serial ascitic fluid samples were obtained during diuresis in seven patients with portal hypertension-related ascites. The samples were tested for concentrations of total protein, CH100, C3 and C4 as well as for in vitro opsonic activity. These parameters were all found to increase to a statistically significant degree when the initial specimen was compared to the final specimen: total protein = 1.5 vs. 2.7 gm per dl; CH100 = 9.3 vs. 20.2 units per ml; C3 = 13.4 vs. 23.8 mg per dl; C4 = 1.9 vs. 3.6 mg per dl, and opsonic activity = 0.8 vs. 1.9 log kill. This increased opsonic activity resulted in a greater than 10-fold increase in bacterial killing. This study demonstrates that diuresis of patients with cirrhotic ascites increases the concentrations of ascitic fluid complement components and increases the opsonic activity of ascitic fluid and may help protect patients from bacterial infection of their ascites.

Elevated ascitic fluid fibronectin concentration: A non-specific finding

Ascitic fluid fibronectin concentration was measured in 111 specimens by laser nephelometry. Sterile, portal hypertension-related fluid fibronectin concentration (24 +/- 14 micrograms/ml) was significantly lower than the concentration in infected, portal hypertension-related ascites (49 +/- 44 micrograms/ml, P less than 0.001), peritoneal carcinomatosis (123 +/- 45 micrograms/ml, P less than 0.001), massive liver metastases-related ascites (55 +/- 21 micrograms/ml, P less than 0.001), as well as in ascites of other types (94 +/- 42 micrograms/ml, P less than 0.001). The percentage of samples with fibronectin concentration, greater than 75 micrograms/ml, was 0% for sterile, portal hypertension-related ascites, 28% for infected, portal hypertension-related ascites, 89% for peritoneal carcinomatosis, 20% for massive liver metastases-related ascites, and 72% for ascites of other types. Ascitic fluid fibronectin concentration correlated in a linear fashion with ascitic fluid total protein (r = 0.81, P less than 0.001). Fibronectin concentration in ascites appears to be elevated under a variety of conditions and does not appear to be a specific marker for cancer.