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