Managing Ascites in Liver Disease
Added on 2020-03-02
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Aetiology and Pathophysiology of AscitesAscites is identified by the peritoneal fluid accumulation in a patient affected with the pattern of decompensated liver cirrhosis (1). The multifactorial causes of ascites include the portal hypertension, dysregulation of hormones (i.e. cytokine imbalance) as well as volume dysregulation. The development of negative intrathoracic and hemostatic pressures as well as diaphragmatic defects increases the predisposition of the patient towards acquiring ascites and associated clinical complications (1). The development of hepato-hydrothorax facilitates the drainage of ascites fluid through the peritoneal cavity. Cirrhotic patients experience the symptoms of cough and shortness of breath and the abnormal accumulation of fluid predisposes them towards acquiring the pattern of empyema, pneumonia, atelectasis and hypoxemia (1). Ascites develop gradually in the cirrhotic patients. This condition might appear painless and followed by abdominal discomfort emanating from the mechanical distension. Other causes of ascites include the pancreatic disorders, nephrosis, congestive heart failure, pyogenic peritonitis, tuberculous peritonitis and neoplasm (2). Ascites might also develop under the influence of pancreatic, gastric, colonic, breast, endometrial and ovarian carcinomas. This condition could also manifest from the pattern of constructive pericarditis that remains undiagnosed for a longer duration (2). The pattern of chronic ascites develops due to sustained impairment in the pattern of sodium excretion that leads to the abnormal accumulation of sodium ions thereby facilitating elevation in the volume of the extracellular fluid. The pathogenesis of ascites is based on the factors attributing to neurohumoral activation, peripheral arterial vasodilation and portal hypertension (3). The pattern of portal hypertension assists in elevating the hydrostatic pressure inside the hepatic sinusoids that results in the accumulation of transudates inside the peritoneal cavity. Therefore, the measurement of hydrostatic pressure indicates the quantity of ascites fluid in the affected patient. Portal hypertension develops in response to the structural alterations in
the liver cells that occur in its cirrhotic state. The intensity of portal hypertension is based on the vascular resistance of the hepatic cells as well as inflow inside the portal veins. This pattern of dynamic alterations in liver cells, nodular development and hepatic fibrosis is indicative of the development of hepatic vascular resistance. The abnormal contraction of myofibroblasts and hepatic stellate cells impairs the hepatic portal pressure that is measured by the defected sinusoidal tone. Hepatic vascular resistance in the ascites patient might aggravate further under the influence of elevated concentrations of the vasoconstrictors like leukotrienes, catecholamines, angiotensin II and endothelin I (3). Cirrhotic ascites manifests with the development of hyponatremia that emanates because of arterial underfilling and systemic vasodilation (4). The reduction in mean arterial pressure and systemic vascular resistance and an elevated cardiac output lead to the development of hyperdynamic circulation in patients affected with cirrhotic ascites. The splanchnic vasodilation in ascites occurs due to an abnormal elevation in the circulating vasodilators attributing to prostacyclins, prostaglandins, platelet activating factor, substance-P, intestinal peptide, glucagon and nitric oxide (4). The multifactorial induction of nitric oxide synthase inside the endothelial cells assists in the development of portal hypertension as well as advanced cirrhosis. This induction occurs because of mechanical activation from several factors attributing to bacterial DNA, endotoxins, tumour necrosis factor – α, growth factor as well as shear stress (4). The pattern of steatohepatitis proves to be the exogenous attribute that elevates the predisposition of the affected patient in terms of developing cirrhotic ascites (5). Furthermore, the genetic risk of acquiring cirrhotic ascites exists in patients with a family history of the disease. The pattern of abnormal hepatocellular regeneration, collagen deposition, necrosis as well as inflammation leads to the transformation of the liver in terms of an elevated resistance system manifested with smooth muscle abnormality and fibrotic spectrum (5). Elevated portal pressure when exceeds above 8mmHg, leads to the formation of
ascites in the cirrhotic patient. Cirrhotic patients experience an elevated risk of developing variceal haemorrhage that might lead to the establishment of hepatorenal syndrome, hepato-hydrothorax, bacterial peritonitis and hepatic encephalopathy (5). The splanchnic hypoperfusion leads to the activation of RAAS (renin-angiotensin-aldosterone system) that results in the retention of peritoneal fluid. The abnormal induction of the SNS (sympathetic nervous system), alteration in the concentration of serum sodium and vascular pressure leads to the abnormal secretion of renin near proximal nephrons that facilitates the formation of angiotensin II (from angiotensin I) in liver under the influence of ACE (angiotensin converting enzyme) (5). Angiotensin II induces the release of vasopressin and aldosterone that concomitantly increases the thirst drive as well as abnormal retention of fluid in the liver cells. The elevated volume of fluid (i.e. blood) passes through the mesenteries as well as the surface of the liver under the influence of elevated hydrostatics, hypoalbuminemia, permeability of the vascular wall as well as reduced osmotic fluid. This leads to the sustained increase in the process of fluid reabsorption through the lymphatic channels as well as the peritoneal surface. The peritoneal cavity that assimilates 25-50 ml serous fluid experiences 5-10mmHg pressure in the state of decompression (5). Retention of peritoneal fluid decreases the pattern of resistance and friction between the bowel parts that evidentially leads to serosalsurface hydration. In conclusion, the sustained defects in the peritoneal surface and lymphaticsystem properties (under the influence of fibrotic defects and infectious as well as inflammatory manifestations) profoundly disrupt the reabsorption mechanisms in human body that evidentially leads to the development of cirrhotic ascites and associated co-morbidities (5). Diagnostic ToolsLaboratory analysis of the ascites fluid is necessarily required for the systematic configuration of differential diagnoses (6). The total protein analysis is required with the
objective of measuring the generation of exudate or transudate across hepatocytes as well as the peritoneal cavity. The diagnostic modality attributing to serum-ascites albumin gradient warrants administration with the objective determining the occurrence of portal hypertension (6). Tumour markers including VEGF (vascular endothelial growth factor) and LDH (lactate dehydrogenase) assist in identifying development of benign as well as malignant co-morbid conditions (6). The development of tuberculosis manifestation along with cirrhotic hepatitis requires tracking with the utilization of diagnostic modalities including adenosine deaminase and blood glucose levels (6). However, the precision of the diagnosis is based on the appropriateness of clinical correlation between the laboratory findings and patient’s symptomatology. The most significant measure warranted in evaluating the pattern of ascites attributes to abdominal paracentesis (7). This diagnostic tool is considered as a safest modality with less than 1% complication rate. Evidence-based clinical literature reveals the minimum risk of haemorrhagic manifestations in relation to the administration of paracentesis modality (7). Therefore, this intervention does not require the evaluation of platelet count and fresh frozen plasma sampling of the selected patients. The ascitic fluid assessment is based on the laboratory analysis of neutrophil count as well as the total serum protein. The ascitic fluid requires inoculation in the blood culture containers with the objective of evaluating the presence of bacterial infection of the fluid of interest (7). The protein content of the ascites fluid requires assessment for calculating the predisposition of the affected patient in terms of developing SBP (spontaneous bacterial peritonitis). The protein quantity of less than 1.5 g/dL elevates the risk of acquiring SBP and associated clinical complications (7). Patients with elevated ascitic neutrophil count (i.e. > 0.25 g/L) are diagnosed with SBP (7). Large volume abdominal paracentesis allows the withdrawal of 5 litres of peritoneal fluid in the absence of PPCI (postparacentesis colloid infusion) (8). However, the extraction and retrieval of more than five litres of ascitic fluids requires the
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