Ascites, Spontaneous Bacterial Peritonitis, and Hepatorenal Syndrome

2015 ◽  
Author(s):  
Fredric D. Gordon

Ascites, a common occurrence in cirrhotic patients with portal hypertension, is the pathologic accumulation of fluid in the peritoneum. Associated conditions are spontaneous bacterial peritonitis (SBP) and hepatorenal syndrome (HRS). SBP occurs in 30% of patients with ascites and carries a 20% mortality, most often due to the severity of the underlying cirrhosis. HRS involves life-threatening sequela of refractory ascites with limited treatment options; a review that focuses exclusively on this disease can be found elsewhere in this section. The development of these diseases is a poor prognostic feature, and referral for liver transplantation should be a consideration. This review examines ascites, SBP, and HRS and their relation to each other. The primary focus is ascites, addressing its epidemiology, pathophysiology, diagnosis, differential diagnosis, and management. Figures show theories of ascites formation and pathophysiology of HPS. Tables list screening tests on ascitic fluid, serum ascites–albumin gradient, drugs and agents to avoid in patients with ascites, diagnostic criteria for HPS, and clinical features of type 1 HPS. Also included are two recommended, pertinent Web sites for those who wish to learn more about ascites, SBP, and HPS. This review contains 2 highly rendered figures, 5 tables, and 73 references.

2020 ◽  
Vol 3 (31) ◽  
pp. 53-61
Author(s):  
T. Bentsa ◽  

Introduction. Liver cirrhosis (LC) is an important medical and socio-economic problem not only in Ukraine, but throughout the world. The urgency of this disease is due to its significant spread, increase of the number of etiological factors, as well as the occurrence of severe complications, which often leads to death. The prognosis depends on several factors, such as etiology, the severity of liver damage, the presence of complications and concomitant diseases. The aim of the study. To review the scientific literature and summarize the published studies devoted to the study of the etiology, classification, clinical picture and diagnosis of liver cirrhosis. Materials and methods. The content analysis, the method of systemic and comparative analysis, the bibliosemantic method of studying the current scientific research on the etiology, classification, clinical picture and diagnosis of LC were used. The search for sources was carried out in scientometric databases: PubMed-NCBI, Medline, Research Gate, Cochrane Database of Systematic Reviews for the keywords: liver cirrhosis, diagnosis, treatment. 37 literary sources were selected and analyzed. Results. LC is currently ranked 11th among the most common causes of death. The common causes of LC are chronic alcohol intoxication and viral hepatitis B, C, and D. LC is represented by an increase in severity, which is characterized by the lesions of the liver parenchyma with necrosis, dystrophy of hepatocytes, their nodular regeneration, as well as its interstitium with diffuse proliferation of connective tissue, leading to liver failure and portal hypertension. Most patients with cirrhosis remain asymptomatic until they develop decompensated LC. Despite the existence of a number of LC classifications – by morphology, etiology, severity, course, hepatocellular insufficiency stage, the severity of the disease is usually assessed by evaluation of the hepatic functional reserve (according to the C. G. Child – R. N. Pugh classification). Patients with LC often have life-threatening conditions such as variceal hemorrhages, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome. Variceal bleeding is a major complication of portal hypertension, which is associated with significant mortality. Ascites represents the most common decompensating event in patients with LC. The appearance of ascites is strongly related to portal hypertension, which leads to splanchnic arterial vasodilation, reduction of the effective circulating volume, activation of endogenous vasoconstrictor systems, and avid sodium and water retention in the kidneys. Bacterial translocation further worsens hemodynamic alterations of patients with cirrhosis and ascites. Ascites is also associated with a high risk of developing the further complications of cirrhosis such as dilutional hyponatremia, spontaneous bacterial peritonitis and/or other bacterial infections and acute kidney injury. Pharmacotherapy for LC should be implemented in accordance with up-to-date guidelines and in conjunction with etiology management, nutritional optimization and patients’ education. The main treatment of uncomplicated ascites is diuretics such as spironolactone in combination with a loop one. Vasoconstrictors and albumin are recommended for the treatment of refractory ascites. In its turn antibiotics play a well-established role in the treatment and prevention of spontaneous bacterial peritonitis. The administration of vasopressor terlipressin and albumin is recommended for the treatment of hepatorenal syndrome. Pharmacological therapy of variceal bleeding aims to decrease the portal pressure by acting on its pathophysiological mechanisms such as increased hepatic vascular tone and splanchnic vasodilatation. Propranolol blocks the β-1 in the heart and the peripheral β-2 adrenergic receptors. β-1 blockade of cardiac receptors reduces heart rate, cardiac output and subsequently decreases flow into splanchnic circulation. β-2 blockade leads to unopposed α-1 adrenergic activity that causes splanchnic vasoconstriction and reduction of portal inflow. Both effects contribute to reduction in portal pressure. Carvedilol is more powerful in reducing hepatic venous pressure gradient than traditional nonselective β-blockers. Endoscopic treatment in many cases is used for the variceal bleeding (eg., ligation of the esophageal varices and tissue glue usage for the gastric varices). A shunt (transjugular intrahepatic portosystemic shunting – TIPS) is used to treat severe and often repeat variceal hemorrhage or refractory ascites. Non-selective β-blockers effectively reduce variceal re-bleeding risk in LC patients with moderate/large varices. Conclusions. Liver cirrhosis is one of the most dangerous multi-organ diseases of a human with multiple pathogenetic links, the causes of which invariably remain hepatitis viruses, alcohol, toxic substances, drugs, ultraviolet radiation, genetic factors, some chronic diseases of the internal organs. There are a number of classifications of liver cirrhosis – by morphology, etiology, severity, course, severity of hepatocellular insufficiency etc. Examination of this category of patients requires timeliness, scrupulousness, compliance with a comprehensive approach using modern clinical, laboratory and instrumental methods. During the objective examination of a patient a doctor traditionally draws attention to the presence of telangiectasia, palmar erythema, jaundice, “raspberry” tongue, scratching marks, gynecomastia in men, ascites and “caput medusae”, during the palpation the liver is enlarged, dense, with a sharp lower edge, spleen is enlarged. Among the laboratory methods, in addition to routine ones, the immunological tests are used, among the main instrumental examination – ultrasound, computed tomography, indirect elastometry of the liver or Fibroscan, esophagogastrofibroscopy, puncture biopsy of the liver, in particular modern ones – vibrational transient elastography and magnetic resonance elastography. Although liver cirrhosis is the final stage of liver disease, this diagnosis cannot be considered a verdict for a patient, because today there are quite effective treatments using the principles of differentiation – the impact on the etiological factor, liver state and comorbid lesions and their complications often allows if not to cure the patient, then to prevent the negative disease course. Among them, there are diet, the use of etiotropic drugs, intestinal sanitation, correction of clinical and laboratory syndromes, portal hypertension syndrome, endothelial and autonomic dysfunction as causes of comorbid lesions and their complications.


2021 ◽  
pp. 23-27
Author(s):  
T. M. Bentsa

This article provides information about the pharmacotherapy of liver cirrhosis (LC) and its complications, such as variceal hemorrhage, ascites, increased risk of bacterial infection, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome LC is a major healthcare problem and is associated with an increased mortality due to the development of complications. LC is currently the 11th most common cause of death globally. Prognosis of LC is highly variable and influenced by several variables, such as etiology, severity of liver disease, presence of complications and comorbidities. In advanced cirrhosis, survival decreases to one or two years. Pharmacotherapy for LC should be implemented in accordance with up-to-date guidelines and in conjunction with aetiology management, nutritional optimisation and patient education. The main treatment of uncomplicated ascites is diuretics such as spironolactone in combination with a loop diuretic. For treatment refractory ascites vasoconstrictors and albumin are recommended. Antibiotics play a well-established role in the treatment and prevention of spontaneous bacterial peritonitis. For hepatorenal syndrome, the administration of vasopressor terlipressin and albumin is recommended. Endoscopic treatment is used for variceal bleeding (for example, ligation for esophageal varices and tissue glue for gastric varices). A shunt (TIPS) is used to treat severe or repeat variceal hemorrhage or refractory ascites. Non-selective beta-blockers effectively reduce variceal re-bleeding risk in LC patients with moderate/large varices. Thus, the treatment of LC as one of the most formidable multiorgan pathologies involves a comprehensive approach aimed at the correction of the main pathology and the treatment and prevention of its complications.


2015 ◽  
Vol 33 (4) ◽  
pp. 582-585 ◽  
Author(s):  
Francesco Salerno ◽  
Vincenzo La Mura

Spontaneous bacterial peritonitis (SBP) is an infection of patients with cirrhosis and ascites. This peculiarity is due to the frequent intestinal translocation that allows bacteria to cross the intestinal barrier, colonizing the ascitic fluid. In cirrhosis, SBP is inferior only to urinary tract infections. It is prevalently sustained by Gram-negative bacteria such as Escherichia coli and Klebsiella. Risk factors for developing SBP are advanced age, refractory ascites, variceal bleeding, renal failure, low albumin levels (below 2.5 g/ml), bilirubin over 4 mg/dl, Child-Pugh class C and a previous diagnosis of SBP. Thus, this is an indication for a long-term antibiotic prophylaxis with norfloxacin. Renal failure - especially the hepatorenal syndrome - complicates SBP in about 20% of cases independently of the efficacy of the antibiotic therapy. The mortality of these patients is about 90%. Infusion of albumin significantly reduces the incidence of hepatorenal syndrome and consequently the risk of death. Long-term quinolonic prophylaxis as well as increased antibiotic therapies are causing the emergence of multidrug-resistant agents as frequent causes of SBP. In such cases, the antibiotic sensitivity to quinolones is low, and European recommendations suggest a second-line antibiotic therapy, including meropenem or piperacillin plus tazobactam. Collection of blood, urine and ascitic fluid for cultures is important for bacterial recognition, possibly before starting an empirical antibiotic therapy. Indeed, the probability of positive cultures rapidly vanishes when they are performed during already implemented antibiotic administration. It is important to know that a failure of the first-line therapy is associated with an increased probability of death.


Author(s):  
Mariangela Pampalone ◽  
Simona Corrao ◽  
Giandomenico Amico ◽  
Giampiero Vitale ◽  
Rossella Alduino ◽  
...  

AbstractCirrhosis is associated with dysregulated immune cell activation and immune dysfunction. These conditions modify gut flora, facilitate bacterial translocation, and increase susceptibility to bacterial peritonitis and consequent systemic infections by dramatically affecting long-term patient survival. Human amnion-derived mesenchymal stromal cells (hA-MSCs) exert immunomodulatory potential benefit, and have the ability to modulate their actions, especially in situations requiring immune activation through mechanisms not fully understood. In this study, we aimed to investigate, in vitro, the immunostimulant or immunosuppressive effects of hA-MSCs on cellular components of ascitic fluid obtained from cirrhotic patients with refractory ascites. We found that hA-MSCs viability is not affected by ascitic fluid and, interestingly, hA-MSCs diminished the pro-inflammatory cytokine production, and promoted anti-inflammatory M2 macrophage polarization. Moreover, we found that there was no simultaneous significant decrease in the M1-like component, allowing a continual phagocytosis activity of macrophages and NK cells to restore a physiological condition. These data highlight the plasticity of hA-MSCs’ immunomodulatory capacity, and pave the way to further understanding their role in conditions such as spontaneous bacterial peritonitis. Graphical abstract


2018 ◽  
Vol 17 (5) ◽  
pp. 0-10
Author(s):  
Tsung-Hsing Hung ◽  
Chih-Wei Tseng ◽  
Hsing-Feng Lee ◽  
Chih-Chun Tsai ◽  
Chen-Chi Tsai

Introduction and aim. Spontaneous bacterial peritonitis (SBP) is a life-threatening infection in patients with cirrhosis. However, it is unknown whether patients with SBP and cirrhosis who do not have active gastrointestinal bleeding have a poorer prognosis if treated with proton pump inhibitors (PPI). Material and methods. We used the Taiwan National Health Insurance Database to identify 858 patients with SBP and cirrhosis who were administered PPIs and hospitalized between January 1, 2010, and December 31, 2013. One-to-two propensity score matching was performed to select a comparison group based on age, gender, and comorbidities. All patients obtained follow-up for 1 year. Results: The overall 30-day, 90-day, and 1-year mortality was 27.9%, 49.0%, and 73.7%, respectively, in the PPI group and 25.6%, 43.8%, and 67.2%, respectively, in the non-PPI group. After adjusting the Cox regression model for age, gender, and comorbidities, the hazard ratios for PPIs regarding 30-day, 30- to 90-day, and 90-day to 1-year mortality were 1.074 (95% CI 0.917-1.257, P = 0.377), 1.390 (95% CI 1.154-1.673, P = 0.001), and 1.297 (95% CI 1.099-1.531, P = 0.002), respectively. Conclusions: PPIs did not increase the short-term mortality of patients with SBP and cirrosis who did not have active gastrointestinal bleeding, but PPIs increased the long-term mortality risk. For these patients, physicians should discontinue PPIs as early as possible.


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