A 42-year-old man comes to the office due to leg swelling. He has also had yellowing of the eyes and progressive abdominal distension for the past 3 weeks, as well as an associated 7-kg (15.4-lb) weight gain. The patient drinks at least 8 beers a day and in the past has been admitted to the hospital for intoxication and seizures. He denies smoking or intravenous drug use. Vital signs are within normal limits. Scleral icterus, spider angiomas, and palmar erythema are present. There is no jugular venous distension, and cardiac auscultation reveals a normal rate and rhythm. Breath sounds are normal. The abdomen is diffusely enlarged, and a fluid wave is easily elicited. Pitting edema is present in the bilateral lower extremities. Which of the following pathophysiologic changes is most likely present in this patient?

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11ec160b_3cc0_2821_9249_11ea0f023892_MD0001_00 This patient has ascites, characterized by the accumulation of fluid within the peritoneal cavity. Ascites may occur in a variety of diseases (eg, peritoneal metastasis, congestive heart failure); however, in this patient with a history of heavy alcohol use and stigmata of chronic liver disease (eg, jaundice, spider angiomas, palmar erythema), it likely occurred from cirrhosis. Cirrhosis is characterized by progressive liver fibrosis, which results in the formation of a high-resistance system (ie, portal hypertension). This results in the following alterations: Nitric oxide is released, possibly due to stimulation by bacterial products (eg, endotoxin), which can more easily translocate from the gastrointestinal tract due to reduced host defenses (eg, impaired reticuloendothelial function) and portosystemic shunt formation (eg, decreased toxin clearance). Splanchnic vasodilation occurs as a result, which decreases the splanchnic vascular resistance and lowers the effective arterial blood volume (EABV) due to blood pooling in the splanchnic vascular bed. Low perfusion pressure results in activation of the renin-angiotensin-aldosterone system along with increased secretion of antidiuretic hormone, leading to retention of sodium and water. Additionally, cirrhosis results in impaired synthetic function, leading to hypoalbuminemia and low plasma oncotic pressure, which reduces fluid resorption from the interstitium. Paired with portal hypertension (ie, increased hydrostatic pressure), these changes result in a vicious cycle of hypervolemia and third spacing, promoting the formation of ascites and peripheral edema. The capillaries remain physiologically normal, so permeability is unchanged. (Choice B) Congestive heart failure causes low EABV (due to low cardiac output) with a consequent increase in sympathetic tone that results in increased splanchnic vascular resistance. Oncotic pressure and capillary permeability are unaffected. (Choice C) Nephrotic syndrome causes edema due to increased permeability of the glomerular capillary wall, leading to loss of albumin, which decreases capillary oncotic pressure. Most patients also have a defect in sodium excretion from the kidneys, resulting in sodium retention and increased EABV. Splanchnic vascular resistance is unaffected. (Choice D) Localized allergic reactions (eg, insect sting) can lead to increased capillary permeability, leading to dermal edema. Oncotic pressures, splanchnic vascular resistance, and EABV are unaffected. (Choice E) Increased capillary oncotic pressure tends to inhibit fluid accumulation in the interstitial spaces, thereby decreasing peripheral edema and ascites. Educational objective: Ascites in cirrhosis develops from hemodynamic changes related to portal hypertension. Splanchnic vasodilation decreases the splanchnic vascular resistance and lowers the effective arterial blood volume, which causes activation of the renin-angiotensin-aldosterone system and promotes sodium and water retention. Additionally, low oncotic pressure (ie, hypoalbuminemia due to impaired hepatic function) reduces fluid resorption from the interstitium. __________ References: Fluid retention in cirrhosis: pathophysiology and management. (http://www.ncbi.nlm.nih.gov/pubmed/18184668)

A 42-Year-Old Man Comes to the Office Due to Leg