A 62-year-old man comes to the office for evaluation of abdominal swelling. Over the last few weeks his abdomen has become more distended with associated mild discomfort and decreased appetite. Past medical history includes multiple admissions for alcohol-induced pancreatitis. The patient currently drinks 1 pint of liquor daily and does not use tobacco or illicit drugs. Physical examination reveals mildly icteric sclera and multiple spider angiomas on the upper chest. The abdomen is distended and there is dullness to percussion that changes location when the patient lays on either side. Serum sodium is 130 mEq/dL and creatinine is 1.1 mg/dL. Which of the following would most likely be seen in this patient?

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11ec160b_3cc1_d5d5_9249_e75d59582fd1_MD0001_00 This patient with a history of heavy alcohol use, abdominal swelling with shifting dullness to percussion (indicative of intraabdominal fluid), and stigmata of chronic liver disease (eg, spider angiomas, jaundice) has ascites due to cirrhosis. Cirrhosis occurs from progressive hepatic fibrosis, resulting portal hypertension due to increased sinusoidal blood flow resistance. There is also increased formation of vasodilatory factors (eg, nitric oxide), possibly due to bacterial products (eg, endotoxins) that accumulate because of reduced host defenses and increased portosystemic shunting. This results in the following hemodynamic alterations: Reduced systemic vascular resistance along with blood pooling in the splanchnic vascular bed leads to reduced blood pressure. Heart rate and cardiac output increase to compensate (hyperdynamic circulation). Reduced renal perfusion leads to activation of the renin-angiotensin-aldosterone system (RAAS) and increased release of antidiuretic hormone (ADH) in an effort to restore circulating volume. The combined aldosterone and ADH effects lead to increased renal resorption of sodium (ie, lower urine sodium) and water. Although this restores renal perfusion, the resistance to splanchnic flow and hyperdynamic circulation promotes third-spacing of fluids into the abdominal cavity (ie, ascites) and interstitium (ie, edema). This is compounded by low serum oncotic pressure due to hypoalbuminemia from liver synthetic dysfunction. Therefore, despite increased total body volume, patients with cirrhosis remain intravascularly depleted and continue to release hypovolemic hormones. Eventually, the resultant elevated ADH secretion can lead to hypervolemic hyponatremia, which is common in patients with advanced cirrhosis. (Choices B, C, D, and E) Splanchnic vasodilation results in renal hypoperfusion, stimulating increased ADH secretion and activation of the RAAS. This leads to increased renal resorption of sodium, lowering the urinary sodium concentration. Third-spacing of fluid results in increased total body volume. Educational objective: Portal hypertension in cirrhosis leads to vasodilation and decreased systemic perfusion pressure, which causes antidiuretic hormone release and activation of the renin-angiotensin-aldosterone system, promoting sodium and water retention. However, due to resistance to splanchnic flow, low oncotic pressure, and hyperdynamic circulation, the fluid is third-spaced into the extravascular compartments (eg, ascites). Therefore, despite increased total body volume, patients with cirrhosis remain intravascularly volume depleted. __________ References: Hyponatremia in cirrhosis: pathophysiology and management. (http://www.ncbi.nlm.nih.gov/pubmed/25805925)

A 62-Year-Old Man Comes to the Office for Evaluation of Abdominal