A 68-year-old man comes to the hospital due to abdominal distension. His waist has progressively enlarged over the past few weeks, leading to a feeling of "heaviness." In addition, the patient has trouble walking more than two city blocks before becoming severely short of breath. He has a long history of heavy alcohol use. Scleral icterus is present on physical examination as well as 2+ pitting edema in the bilateral lower extremities. Multiple spider angioma are identified. The abdomen is grossly distended and mildly tender to palpation. Shifting dullness is elicited. Which of the following changes are most likely present in this patient?

Question

A 68-year-old man comes to the hospital due to abdominal distension.  His waist has progressively enlarged over the past few weeks, leading to a feeling of "heaviness."  In addition, the patient has trouble walking more than two city blocks before becoming severely short of breath.  He has a long history of heavy alcohol use.  Scleral icterus is present on physical examination as well as 2+ pitting edema in the bilateral lower extremities.  Multiple spider angioma are identified.  The abdomen is grossly distended and mildly tender to palpation.  Shifting dullness is elicited.  Which of the following changes are most likely present in this patient?

Quizplus · Accepted Answer

This patient with progressive abdominal distension and shifting dullness on examination has new-onset 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, spider angioma, scleral icterus) on examination, 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 and other vasodilatory factors are formed, possibly from bacterial products (eg, endotoxin) that accumulate due to the reduced host defenses (eg, impaired reticuloendothelial function) and increased portosystemic shunting (eg, decreased toxin clearance) seen with cirrhosis.Splanchnic vasodilation occurs as a result, leading to significantly decreased systemic vascular resistance (SVR) and a compensatory increase in heart rate and cardiac output (hyperdynamic circulation).The renin-angiotensin-aldosterone system (RAAS) is activated and antidiuretic hormone is released to maintain renal perfusion, leading to retention of sodium and water. Nitric oxide and other vasodilatory factors are formed, possibly from bacterial products (eg, endotoxin) that accumulate due to the reduced host defenses (eg, impaired reticuloendothelial function) and increased portosystemic shunting (eg, decreased toxin clearance) seen with cirrhosis. Nitric oxide and other vasodilatory factors are formed, possibly from bacterial products (eg, endotoxin) that accumulate due to the reduced host defenses (eg, impaired reticuloendothelial function) and increased portosystemic shunting (eg, decreased toxin clearance) seen with cirrhosis. Splanchnic vasodilation occurs as a result, leading to significantly decreased systemic vascular resistance (SVR) and a compensatory increase in heart rate and cardiac output (hyperdynamic circulation). Splanchnic vasodilation occurs as a result, leading to significantly decreased systemic vascular resistance (SVR) and a compensatory increase in heart rate and cardiac output (hyperdynamic circulation). The renin-angiotensin-aldosterone system (RAAS) is activated and antidiuretic hormone is released to maintain renal perfusion, leading to retention of sodium and water. The renin-angiotensin-aldosterone system (RAAS) is activated and antidiuretic hormone is released to maintain renal perfusion, leading to retention of sodium and water. renin-angiotensin-aldosterone system (RAAS) Hyperdynamic circulation and resistance to flow promote third spacing of fluids into the abdominal cavity while low oncotic pressure (ie, hypoalbuminemia due to impaired synthetic function) reduces fluid resorption from the interstitium. This results in a vicious cycle of hypervolemia and third spacing, promoting the formation of ascites. (Choices A, C, and D) Patients with ascites from cirrhosis have increased RAAS activity in response to the low SVR associated with splanchnic vasodilation. This results in increased circulating angiotensin levels (promoting renal vasoconstriction) and retention of urinary sodium (promoting volume retention). Although this compensatory mechanism is required to overcome the effects of splanchnic vasodilation, excessive renal vasoconstriction can cause renal hypoperfusion and kidney injury (eg, hepatorenal syndrome). (Choice B) Severe hypothyroidism can lead to accumulation of mucopolysaccharides in the interstitial space, which promotes development of nonpitting edema (eg, myxedema), and ascites may occur. However, other signs of hypothyroidism would be expected (eg, cold intolerance, constipation, periorbital edema), and spider angioma and sclera icterus would not occur. Educational objective: Ascites in cirrhosis develops from hemodynamic changes related to portal hypertension. Splanchnic vasodilation decreases the systemic vascular resistance, which causes activation of the renin-angiotensin-aldosterone system and promotes sodium and water retention. Hyperdynamic circulation and resistance to flow promote third spacing of fluids into the abdominal cavity while low oncotic pressure (ie, hypoalbuminemia due to impaired synthetic function) reduces fluid resorption from the interstitium. References: Renal and circulatory dysfunction in cirrhosis: current management and future perspectives. (http://www.ncbi.nlm.nih.gov/pubmed/20850887)

A 68-Year-Old Man Comes to the Hospital Due to Abdominal