Ascites

Definition and diagnosis

Whereas a normal peritoneal cavity contains only 25 mL of fluid, the peritoneum has the capacity to absorb 900 mL/day. Ascites is the pathologic accumulation of peritoneal fluid, occurring most commonly in decompensated liver cirrhosis (85%), with malignancy, tuberculosis, heart failure, and pancreatitis accounting for the remainder. ^, The International Club of Ascites classifies ascites severity, with fluid detectable only on imaging (<100 mL) as grade 1, moderate symmetric abdominal distention with up to 1 L of fluid as grade 2, and tense distention associated with a large volume of fluid as grade 3. Cirrhotic ascites can be uncomplicated or complicated, the latter involving concomitant development of spontaneous bacterial peritonitis (SBP), hepatorenal syndrome, or hepatic hydrothorax. Refractory ascites (5%–10% of cases) is persistent or rapidly recurring ascites despite maximal medical therapy.

Symptoms of ascites include weight gain, abdominal pain, fullness, early satiety, and shortness of breath. History and physical examination looking for signs of liver disease or other underlying cause form the foundation of diagnostic evaluation. Detecting ascites on examination can prove difficult if <1500 mL is present. If flank dullness on percussion is not appreciated, there is a 90% chance no ascites is present. Although computed tomography (CT) will identify ascites, ultrasound is the preferred imaging modality. It is a highly sensitive, low-cost, nonradiation-producing method that simultaneously allows evaluation of the liver and hepatic vasculature.

Patients with new-onset ascites should undergo diagnostic paracentesis, with removal of 20–30 mL for evaluation of fluid color, turbidity, and total protein and for calculation of the serum–ascites albumin gradient (SAAG). ^, A SAAG >1.1 g/dL is 97% accurate in identifying ascites resulting from portal hypertension ( Table 24.1 ). Infected ascites is a life-threatening complication, requiring timely assessment of the ascitic cell count and differential. A study of hospitalized patients with cirrhosis and SBP demonstrated a 3% increase in mortality for every hour that diagnostic paracentesis was delayed. Fluid can be sent for triglyceride levels if chylous ascites is suspected, amylase for pancreatitis, cytology for malignancy, or Mycobacterium culture for tuberculosis.

Pathophysiology

Portal hypertension from either increased hepatic resistance or increased portal blood flow is the key pathophysiologic event in the formation of ascites and is described in detail in Chapter 83 . Normal portal venous pressure is <5 mm Hg. Once it is over 10 mm Hg, fluid from hepatic sinusoids and splanchnic capillaries overwhelms the peritoneal lymph drainage. ^{, ,} However, increased pressure is only one aspect of the pathophysiology, as fluid dysregulation and development of ascites results from a complex interplay of hemodynamic and hormonal responses. ^, In liver cirrhosis, hepatic sinusoidal congestion with progressive fibrotic transformation leads to endothelial cell dysfunction, causing nitric oxide–mediated vasodilation of splanchnic and peripheral arterial vascular beds. Initially, a hyperdynamic circulatory response compensates for the vasodilation to maintain adequate perfusion pressure. As vasodilation worsens and effective circulating volume decreases, however, compensatory activation of the sympathetic nervous and renin – angiotensin – aldosterone systems results in renal sodium and water retention, leading to fluid overload and hyponatremia ( Fig. 24.1 ). This process is hastened when infection from bacterial translocation causes endotoxin release, compounding vasodilation. Ultimately, tissue perfusion is compromised, leading to life-threatening organ dysfunction, the most salient being hepatorenal syndrome with decreasing glomerular filtration rate and severe renal vasoconstriction, as detailed in Chapter 84 . In contrast to the mechanisms in cirrhosis, ascites in infection and malignancy is the result of inflammation and leakage of high-protein lymph.