Cirrhosis Complications: Ascites and Spontaneous Bacterial Peritonitis

PATHOPHYSIOLOGY OF ASCITES
In a patient with cirrhosis, blood flow is reduced through the scarred liver and becomes retrograde to the normal flow pattern, causing portal hypertension. Portal hypertension causes vasodilators, such as nitric oxide, to be produced, leading to vasodilation of the splanchnic arterial system. Eventually, as vasodilation increases, the arterial receptors sense a decreased amount of blood flow in this part of the circulation. The body activates various systems (sympathetic nervous, antidiuretic hormone, and renin-angiotensin-aldosterone), resulting in increased water and sodium absorption and renal vasoconstriction. In turn, intestinal permeability and pressure in the capillaries respond, allowing fluid—ascites—to move into the peritoneal cavity.^4,5,7

SPONTANEOUS BACTERIAL PERITONITIS
Developing in approximately 25% of patients with cirrhosis and ascites,⁸ spontaneous bacterial peritonitis (SBP) is thought to occur by translocation of intestinal bacteria moving through the mesenteric lymph nodes into the bloodstream and other body fluids (eg, ascites).^4,7,9Escherichia coli, Klebsiella pneumoniae, and Streptococcus pneumonia are the bacteria most often responsible for SBP.²

If left untreated or treated too late, SBP can eventually lead to sepsis and septic shock.^4,7,9 About 30% of cirrhosis patients with SBP will die of it or related complications;⁸ the one-year survival rate is 30% to 50% and the two-year survival rate, 25% to 30%.⁹ Mortality is increased by up to 50% in hospitalized patients with SBP.^3,10,11

DIAGNOSIS
Ascites
In patients with cirrhosis, typical signs and symptoms of ascites include weight gain, increased abdominal girth and fullness, dullness to abdominal percussion, peripheral edema, and a positive fluid wave test.^2,4

In both inpatient and outpatient settings, ascites should be sampled by diagnostic abdominal paracentesis (see Figure), which requires 30 to 50 mL of fluid.¹² Laboratory analysis should include white blood cell count with differential, serum-ascites albumin gradient (SAAG), and total protein. If infection is suspected, samples should be sent for culture, using blood culture bottles, as well as for gram staining.^2,12

SAAG is calculated by measuring the albumin concentration in ascitic fluid and serum specimens taken on the same day and then subtracting the ascitic fluid value from the serum value. With 97% accuracy, a SAAG ≥ 1.1 g/dL indicates portal hypertension, meaning that the ascites is likely hepatic in origin.^2,12

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