Development Of Ascites In Patients Research Articles

Pancreatic cancer associated ascites: Risk factors, outcomes, and management.

e16305 Background: Pancreatic ductal adenocarcinoma (PDAC) 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. Therefore, we performed a comprehensive analysis of PDAC patients with ascites, including clinical and biological data, to describe its incidence, associated clinical factors, and outcomes. Methods: Patients were prospectively consented and enrolled the Gastrointestinal Biobank (“GI-Bank”) at Cedars-Sinai Medical Center, which collected patient specimens, associated clinical data, and self-reported questionnaires. Data was consolidated using a standard software tool (Redcap). Statistical analysis was conducted using Excel and using Datatab.net software tools. Results: Of the 437 patients with PDAC, 182 (41.6%) developed ascites. Overall survival (OS) between ascites and non-ascites groups were significantly different by log-rank test (p = 0.001), and estimated median OS was 473 days (95% CI [407, 537]) in ascites patients versus 554 days [467, 678] in non-ascites patients. In Cox proportional hazards model analysis, ascites status, but not sex or race, was associated with decreased survival (HR 1.49, [1.18, 1.87]). Ascitic fluid data was obtained in 77 patients; 62 (80.5%) had SAAG > 1.1; 14(22.6%) of SAAG > 1.1 patients also had positive cytology. The estimated median OS from the diagnosis of ascites was 100 days [76, 128] and median time to puncture was 4 days. Estimated median time from first tap to death was 56 days [42, 95]. 90 (49.5%) were treated with diuretics and 41 (22.5%) were treated with PleurX catheter. Patients with ascites had a worse survival and were more likely to receive greater than one chemotherapy regimen. There was no relationship between ascites and receipt of surgery or radiation. Conclusions: The development of ascites in patients with pancreatic cancer is common and contributes to significant morbidity and mortality. The use of diuretics is lower than would be expected for patients with elevated SAAG. Prospective evaluation of management strategies is needed to improve this important clinical conundrum.

Urinary BA Indices as Prognostic Biomarkers for Complications Associated with Liver Diseases.

Hepatobiliary diseases and their complications cause the accumulation of toxic bile acids (BA) in the liver, blood, and other tissues, which may exacerbate the underlying condition and lead to unfavorable prognosis. To develop and validate prognostic biomarkers for the prediction of complications of cholestatic liver disease based on urinary BA indices, liquid chromatography-tandem mass spectrometry was used to analyze urine samples from 257 patients with cholestatic liver diseases during a 7-year follow-up period. The urinary BA profile and non-BA parameters were monitored, and logistic regression models were used to predict the prognosis of hepatobiliary disease-related complications. Urinary BA indices were applied to quantify the composition, metabolism, hydrophilicity, and toxicity of the BA profile. We have developed and validated the bile-acid liver disease complication (BALDC) model based on BA indices using logistic regression model, to predict the prognosis of cholestatic liver disease complications including ascites. The mixed BA and non-BA model was the most accurate and provided higher area under the receiver operating characteristic (ROC) and smaller akaike information criterion (AIC) values compared to both non-BA and MELD (models for end stage liver disease) models. Therefore, the mixed BA and non-BA model could be used to predict the development of ascites in patients diagnosed with liver disease at early stages of intervention. This will help physicians to make a better decision when treating hepatobiliary disease-related ascites.

Standardized Patient Education for Decompensated Cirrhotic Patients and Impact on Clinician Satisfaction.

The development of ascites in patients with cirrhosis can cause numerous complications including abdominal discomfort, pain, respiratory distress, decreased mobility, diminished quality of life, and contributes to an increased mortality. Symptom self-monitoring that incorporates evidence-based treatments has been effective when used by patients with noncirrhotic chronic diseases. Guided by the theory of Self-Care of Chronic Illness, a self-monitoring guide was adapted from an existing validated tool. In the context of a pilot quality initiative, staff nurses educated patients with ascites and their caregivers, with the adapted symptom self-monitoring guide using a standardized process. Clinicians were surveyed regarding their satisfaction with the patient education pre- and post-implementation. Results indicated improved clinician satisfaction with the education provided to patients and their caregivers during the clinic visit. Implementation of self-monitoring may improve clinician and patient satisfaction and clinic workflows. Additional evaluation of the self-monitoring guide and its effect on patient satisfaction, impact on hospital admissions, and outpatient paracentesis is warranted.

Hyponatremia in cirrhosis: pathophysiology and management.

Hyponatremia is frequently seen in patients with ascites secondary to advanced cirrhosis and portal hypertension. The development of ascites in patients with cirrhosis is multi-factorial. Portal hypertension and the associated systemic vasodilation lead to activation of the sodium-retaining neurohumoral mechanisms which include the renin-angiotensin-aldosterone system, sympathetic nervous system and antidiuretic hormone (ADH). The net effect is the avid retention of sodium and water to compensate for the low effective circulatory volume resulting in the development of ascites. Although not apparent in the early stages of cirrhosis, the progression of cirrhosis and ascites leads to impairment of the kidneys to eliminate solute- free water. This leads to additional compensatory mechanisms including non-osmotic secretion of ADH, also known as arginine vasopressin, further worsening excess water retention and thereby hyponatremia. Hyponatremia is associated with increased morbidity and mortality in patients with cirrhosis, and is an important prognostic marker both before and after liver transplant. The management of hyponatremia in this setting is a challenge as conventional therapy for hyponatremia including fluid restriction and loop diuretics are frequently inefficacious. In this review, we discuss the pathophysiology and various treatment modalities, including selective vasopressin receptor antagonists, for the management of hyponatremia in patients with cirrhosis.

P-0120 - Can Serum Tumor Markers Predict the Development of Ascites in Patients with Gastric and Pancreatic Cancer

P-0120 - Can Serum Tumor Markers Predict the Development of Ascites in Patients with Gastric and Pancreatic Cancer

How to improve care in outpatients with cirrhosis and ascites: A new model of care coordination by consultant hepatologists

The development of ascites in patients with cirrhosis is associated with a high rate of health care utilization. New models of specialized caregiving support are necessary to optimize its management. The aim of the study was to evaluate the efficacy and financial sustainability of the "Care management check-up" as a new model of specialized caregiving support based on a series of diagnostic facilities performed in real time and on the integrated activity of consultant hepatologists at the hospital unit for outpatients, dedicated nurses, physicians in training and primary physicians, compared to standard care in outpatients with cirrhosis and ascites. 100 cirrhotic patients admitted to our hospital were allocated, after discharge, to the "Care management check-up" group (group 1), or to the "Standard outpatient care" group (group 2), and followed prospectively as outpatients up to death or for at least 12 months. Patients of the two groups could also access to a "Day hospital" when an invasive procedure was required. In group 1, the "Care management check-up" and the "Day hospital" taken together defined the "Care management program". Twelve-month mortality was higher in group 2 than in group 1 (45.7% vs. 23.1%, p<0.025). The rate of 30-day readmission was also higher in group 2 (42.4% vs. 15.4%, p<0.01). The global cost attributable to the management per patient-month of life was lower (1479.19 ± 2184.43 €) in group 1 than (2816.13 ± 3893.03 €) in group 2 (p<0.05). The study suggests that this new model of specialized caregiving reduces 12-month mortality in patients with cirrhosis and ascites as well as the global health care costs for their management.

Moderate hyperkalemia in hospitalized patients with cirrhotic ascites indicates a poor prognosis

Objective. Development of ascites in patients with liver cirrhosis is an ominous sign with a poor outcome. A liver transplantation must be considered, and it then becomes important to know if there are any factors indicating a worsened prognosis. Material and methods. We used official registers for a follow-up study of at least 5 years considering the prognosis of 155 prospectively recruited in-patients with cirrhotic ascites from medical units at nine Swedish university hospitals. All patients had undergone at least one diagnostic ascites tap, and had initially been questioned about background factors and physically examined according to a standardized case record form, followed by sampling of blood, urine, and ascites. Results. Death occurred within 1 year after inclusion in 53% of the cases, and was primarily liver-related in 70%. In a multivariable analysis, the two ordinary variables that showed the strongest correlation with risk of death were serum potassium and abdominal tenderness. All 22 patients with a serum potassium concentration of at least 4.8 mmol/L (maximum 5.8 mmol/L) died within 1 year after inclusion. Potassium concentration was related to renal function and potassium-saving drugs. Conclusion.This follow-up study of a prospectively recruited cohort of in-patients with cirrhotic ascites confirms their poor prognosis. Awareness of an elevated serum potassium value, which would reflect a threatened renal function, seems essential, because it may offer a simple way to identify cases with the worst prognosis. An area for further research should be to explore the significance of including serum potassium in prognostic models.

Hepatic perfusion scintigraphy. Relationship of liver perfusion and ascites in patients with liver cirrhosis.

Radionuclide studies were performed on 38 patients with biopsy proven liver cirrhosis in an attempt to evaluate the interrelationship between liver perfusion and ascites in cirrhotic patients. Quantitative hepatic scintigraphy was used to evaluate the relative contribution of hepatic arterial and portal venous blood flow to the hepatic circulation. Using a gamma camera and on-line computer system, a bolus of 370 MBq Tc-99m pertechnetate was injected intravenously. Time activity curves of the abdominal aorta and right lobe of the liver were obtained using a region of interest analysis where arterial and portal components were calculated. Ascites was determined by clinical examination and by ultrasonography. Of 38 patients, 10 patients (26.3%) showed normal liver perfusion (group A), 22 patients (58%) showed reduced portal venous perfusion (group B), and 6 patients (15.7%) showed pure arterial hepatic perfusion (group C). The incidence, as well as the advancement, of ascites were significant (P < 0.05) and were most frequent in group C, frequent in group B, and less frequent in group A. The results of this study suggest that the development of ascites in patients with liver cirrhosis is closely correlated with the reduction in portal blood perfusion.

Mechanisms of ascites formation

Dr. Frederick K. Heath: The development of ascites in patients with cirrhosis of the liver has long been correlated with portal hypertension and hypoalbuminemia. The manner in which these and other factors may contribute to this process is considered in this clinic. In the otherwise normal animal obstruction to the hepatic outflow (hepatic veins or vena cava) produces ascites but occlusion of the portal system results in the development of collateral circulation and hypersplenism. Portal hypertension alone, then, may furnish a larger vascular bed for diffusion and because of stasis may also tend to render this area more permeable. While both conditions are favorable to ascites formation, they do not of themselves produce it. The role of the lymphatics has not been determined. On this background osmotic forces operate. The net hydrostatic pressure (capillary blood pressure minus ascitic hydrostatic pressure) tending toward the formation of ascites is opposed by the net colloid pressure (plasma colloid osmotic pressure minus ascitic colloid osmotic pressure). Dr. Mankin showed that in the presence of ascites, irrespective of whether it was increasing or decreasing, the difference between the capillary and ascitic colloid osmotic pressures remains fairly constant. This state of dynamic equilibrium between opposing forces need be only slightly altered to influence the direction of fluid flow before equilibrium is regained. Thus mercurial diuresis, presumably by hemoconcentration, tends to decrease ascites. In the same fashion intravenous albumin may or may not decrease ascites depending upon how rapidly it diffuses from plasma to the ascitic compartment. Of great interest is the finding that patients with ascites do not excrete sodium in the urine proportionally to their intake. The magnitude of this deficiency would appear to correlate with the degree of ascites and the deficiency in serum sodium levels. Ingested sodium is almost entirely diverted to the ascitic fluid which tends to increase when the daily intake of sodium chloride exceeds 1 gm. However, if salt be restricted to about 1 gm. daily, water excretion rises, serum protein values slowly increase, serum sodium concentration remains constant and no further ascitic fluid is formed. In this fashion progression of this phase of the disease may be interrupted. About one-half of Dr. Kunkel's patients maintained on low-sodium diets over a period of six months regained their ability to excrete sodium normally and concomitantly showed improvement in their ascites. Dangerous depletion of sodium has been observed on this regimen in the presence of renal damage or following the use of mercurial diuretics. Similar to the depression in the urinary excretion of sodium, Dr. Ralli described a marked reduction in water output in cirrhotic patients with ascites. She has proposed that the renal abnormality may be due to greater tubular reabsorption of water dependent upon an increase in the posterior pituitary antidiuretic hormone and has reported finding unusual amounts of antidiuretic substances in the urine of ascitic patients. According to this evidence, the disappearance of ascites without change in hypoalbuminemia becomes understandable. While the relative importance of these mechanisms undoubtedly varies from patient to patient and cannot be determined in advance so as to indicate a single line of therapy, they nevertheless suggest several special therapeutic approaches such as are indicated in the clinic.