A 65-year-old man is evaluated for a 3-month history of malaise and abdominal distension with increasing abdominal girth. He has also had progressive shortness of breath and generalized weakness. Past medical problems include hypertension, hypercholesterolemia, type 2 diabetes mellitus, heart failure, and hepatitis C. The patient also has a history of prostate cancer, which was treated with radical prostatectomy and radiation therapy a year ago. He drinks 1 or 2 cans of beer a day and has smoked a pack of cigarettes daily for 20 years. He admits to using injection drugs in the past.
Vital signs are within normal limits. Chest examination reveals basilar crackles in the lungs and a grade 2 systolic murmur along the left sternal border. The abdomen is nontender and distended with ascites. There is no rebound tenderness or rigidity. The liver edge is palpable 2 cm below the right costal margin and mild splenomegaly is present. There is 2+ bilateral lower extremity pitting edema.
Laboratory results are as follows:
Which of the following is the most likely cause of this patient's ascites?

Question

A 65-year-old man is evaluated for a 3-month history of malaise and abdominal distension with increasing abdominal girth.  He has also had progressive shortness of breath and generalized weakness.  Past medical problems include hypertension, hypercholesterolemia, type 2 diabetes mellitus, heart failure, and hepatitis C.  The patient also has a history of prostate cancer, which was treated with radical prostatectomy and radiation therapy a year ago.  He drinks 1 or 2 cans of beer a day and has smoked a pack of cigarettes daily for 20 years.  He admits to using injection drugs in the past.
Vital signs are within normal limits.  Chest examination reveals basilar crackles in the lungs and a grade 2 systolic murmur along the left sternal border.  The abdomen is nontender and distended with ascites.  There is no rebound tenderness or rigidity.  The liver edge is palpable 2 cm below the right costal margin and mild splenomegaly is present.  There is 2+ bilateral lower extremity pitting edema.
Laboratory results are as follows:
 Which of the following is the most likely cause of this patient's ascites?

Quizplus · Accepted Answer

11ec193a_97f2_9e8a_853d_653bf3e94630_MD0002_00 Evaluation of the etiology of ascitic fluid should proceed in a stepwise fashion. In this patient: etiology Ascitic fluid leukocytes <500/mm³ and neutrophils <250/mm³ argue against infection (eg, bacterial peritonitis) or a significant inflammatory process (eg, malignancy, pancreatitis).Serum-to-ascites albumin gradient (SAAG) ≥1.1 g/dL (1.7 g/dL in this patient) is indicative of portal hypertension, occurring in conditions including cirrhosis, heart failure, and Budd-Chiari syndrome (hepatic vein thrombosis).Ascitic fluid total protein ≥2.5 g/dL makes an underlying low-protein state such as cirrhosis (decreased protein production) or nephrotic syndrome (increased urinary protein excretion) less likely. Ascitic fluid leukocytes <500/mm³ and neutrophils <250/mm³ argue against infection (eg, bacterial peritonitis) or a significant inflammatory process (eg, malignancy, pancreatitis). Ascitic fluid leukocytes <500/mm³ and neutrophils <250/mm³ argue against infection (eg, bacterial peritonitis) or a significant inflammatory process (eg, malignancy, pancreatitis). ³ ³ Serum-to-ascites albumin gradient (SAAG) ≥1.1 g/dL (1.7 g/dL in this patient) is indicative of portal hypertension, occurring in conditions including cirrhosis, heart failure, and Budd-Chiari syndrome (hepatic vein thrombosis). Serum-to-ascites albumin gradient (SAAG) ≥1.1 g/dL (1.7 g/dL in this patient) is indicative of portal hypertension, occurring in conditions including cirrhosis, heart failure, and Budd-Chiari syndrome (hepatic vein thrombosis). Ascitic fluid total protein ≥2.5 g/dL makes an underlying low-protein state such as cirrhosis (decreased protein production) or nephrotic syndrome (increased urinary protein excretion) less likely. Ascitic fluid total protein ≥2.5 g/dL makes an underlying low-protein state such as cirrhosis (decreased protein production) or nephrotic syndrome (increased urinary protein excretion) less likely. This patient with SAAG ≥1.1 g/dL and ascitic fluid total protein ≥2.5 g/dL has known heart failure and no evidence to suggest acute Budd-Chiari syndrome (eg, right upper quadrant pain, history of thrombophilia); therefore, decompensated heart failure is the most likely cause of ascites. (Choice A) Although cirrhosis (eg, due to hepatitis C virus) is the most common cause of ascites, it is a low-protein state; the SAAG is usually elevated due to portal hypertension, but the ascites total protein is usually low (<2.5 g/dL). (Choice C) Nephrotic syndrome is a low-protein state that does not cause portal hypertension. Therefore, ascites due to nephrotic syndrome typically has low total protein and low SAAG (<1.1 g/dL). This patient's proteinuria is most likely due to hypertensive or diabetic nephropathy in the absence of nephrotic syndrome. (Choices D and E) Peritoneal carcinomatosis and tuberculous peritonitis typically cause a high-protein ascites similar to heart failure. The SAAG is typically low, unlike in this patient. Portal hypertension can sometimes develop, resulting in a high SAAG. However, ascites due to heart failure is more likely in this patient with known history and evidence of current decompensation (eg, lower extremity edema, congestive hepatopathy). Educational objective: The etiology of ascites can often be determined by evaluation of the ascitic fluid cell count, serum-to-ascites albumin gradient (SAAG), and fluid total protein. Low levels of inflammatory cells and elevations in the SAAG (1.1 g/dL) and fluid total protein (2.5 g/dL) are consistent with ascites due to heart failure. __________ References: Evaluation of new-onset ascites. (http://www.ncbi.nlm.nih.gov/pubmed/27434446)

A 65-Year-Old Man Is Evaluated for a 3-Month History of Malaise