Ascites is the presence of excessive fluid within the peritoneal cavity. Individuals with ascites develop physical examination findings of increasing abdominal girth, a fluid wave, a ballotable liver, and shifting dullness. Ascites can develop in patients with conditions other than liver illness, including protein-calorie malnutrition (from hypoalbuminemia) and cancer (from lymphatic obstruction).
In patients with liver disease, ascites is due to portal hypertension. It’s helpful to recognize that liver disease with ascites formation occurs in a broad clinical spectrum. At a single end is fully compensated portal hypertension with no ascites present simply because the amount of ascites generated is much less than the around 800-1200 mL/d capability from the peritoneal lymphatic drainage.
In the other extreme is the typically fatal hepatorenal syndrome, in which patients with liver disease, generally with massive ascites, succumb to rapidly progressing acute renal failure. The hepatorenal syndrome appears to become precipitated by intense and unacceptable renal vasoconstriction and is characterized by severe salt retention standard of prerenal azotemia but within the absence of true volume depletion.
Nonetheless, the presence of clinically apparent ascites in a patient with liver disease is connected with poor long-term survival. Over the many years, various mechanisms have been proposed to explain ascites formation. No single hypothesis of pathogenesis easily explains all findings whatsoever points in time during the organic history of portal hypertension. Portal hypertension and unacceptable renal retention of salt are important elements of all theories.
The end result of ascites happens when excess peritoneal fluid exceeds the capacity of lymphatic drainage, primary to increased hydrostatic pressure. The fluid can then be observed to visibly weep from the lymphatics and pool within the abdominal cavity as ascites. The underfill/vasodilatation hypothesis proposes that the main event in ascites formation is vascular, with reduced efficient circulating amount leading towards the activation of the renin-angiotensin system and subsequent renal sodium retention.
The classic underfill hypothesis postulates that elevated hepatic sinusoidal pressure leads to sequestration of blood in the splanchnic venous bed. This outcomes in underfilling of the central vein with diversion of intravascular volume to the hepatic lymphatics, which, like the central vein, drain the space of Disse.
The peripheral arterial vasodilatation or splanchnic vasodilatation hypothesis adds the concept that, with portal-to-systemic shunting, vasodilatory items (eg, nitric oxide) that are normally cleared by the liver are instead delivered towards the systemic circulation, exactly where they trigger peripheral arteriolar vasodilation, particularly within the splanchnic arterial bed.
The resultant reduced arterial vascular resistance is associated with decreased central filling pressures, decreased renal arterial perfusion, reflex renal arterial vasoconstriction, and increased renal tubular sodium resorption. Retention of salt expands the intravascular amount, which exacerbates portal venous hypertension.
The imbalance between hydrostatic versus oncotic pressure in the portal vein results in ascites formation. Even though the splanchnic vasodilatation hypothesis accounts for many from the findings in ascites formation, the use of transhepatic intrajugular portal-to-systemic shunting (Ideas) as a signifies of decompressing the portal vein in patients with ascites provides a counterargument.
As a result of the procedure, peripheral arteriolar vasodilation seems to improve (perhaps consequently of shunting of vasodilators such as nitric oxide which are usually cleared by the liver), however ascites is usually dramatically improved. People who support the overflow hypothesis have proposed how the primary event within the improvement of ascites is inappropriate renal salt retention.
In this view, ascites may be the consequence of overflow of fluid from the intravascular volume-expanded portal system to the peritoneal cavity. But what triggers the inappropriate renal salt retention? A single possibility is that there might exist a hepatorenal reflex by which elevated sinusoidal stress triggers increased sympathetic tone or endothelin-1 secretion.
Either of these pathways could cause an unacceptable degree of renal vasoconstriction, a decrease in glomerular filtration rate, and, by tubuloglomerular feedback, salt retention. Note that endothelin-1 is both a renal vasoconstrictor along with a stimulant of epinephrine secretion, which in turn stimulates more endothelin-1 secretion.
Alternatively, it’s possible that an as yet unidentified product in the diseased liver interferes with atrial natriuretic peptide (ANP) action at the kidney or is in some other way responsible for an inappropriate increase in renal sodium retention. Supporters from the overflow hypothesis point to the fact that numerous cirrhotic individuals have sodium handling defects within the absence of ascites and do not have a measurable increase in renin-angiotensin activity.
However, studies have shown that the renal salt retention in these individuals could be reversed by the use of an angiotensin II receptor antagonist. Most most likely, multiple mechanisms contribute to the development of ascites and to its perpetuation, worsening, or improvement in diverse clinical situations.
Core 2 Duo E6600
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