**2. Classification of ascites**

The purpose of this review is primarily focused on the various causes of ascites with emphasis on the hepatic origin. Based on this premise, ascites is classified broadly into hepatic, pre-hepatic and post-hepatic origin:


constrictive pericarditis, Budd-Chiari syndrome and stricture web formation in the inferior vena cava [8, 9].

iii.Hepatic origin emanates from various hepatic diseases including cirrhosis, portal hypertension and hepatitis. Approximately 85% of portal hypertension results in cirrhosis [8–10].

Earlier classification of ascites was centred on two broad categories, transudates and exudates, based on the total protein concentration of ascetic fluid. High total protein (>2.5 g/l) was described as exudates, while low total protein (<2.5 g/l) as transudate [11]. Both transudates and exudates were subcategorised into modified transudates and exudates based on the level of total protein concentration in the ascetic fluid. Transudates with <2.5 g/l of total protein usually occur with portal hypotension or hypoalbuminaemia [6]. Exudates with >2.5 g/l of total protein are associated with inflammatory disease conditions such as bacteria tuberculosis, neoplasm of unknown origin, pancreatitis, myxoedema, etc. Nevertheless, it has been observed that a total protein concentration of <2.5 g/l has an accuracy of only 56% [6] in detecting exudates from various conditions such as cardiac ascites and patients on diuretics and neoplasms [11]. The obvious challenge in the use of total protein concentration paved way to the discovery of serum ascites albumin gradient (SAAG) concentration as a more reliable tool in classification of ascites with efficacy ranging from 80 to 100% [11]. With the advent of SAAG, exudate ascites is replaced with (>1.1 g/l) high serum ascites albumin gradient and transudate with low (<1.1 g/l) serum ascites albumin gradient. The SAAG (>1.1 g/l) shows higher 94% sensitivity and 90% specificity in detecting portal hypertension than ascetic fluid total protein concentration of <2.5 g/ dl at percentage sensitivity and specificity of 78 and 50%, respectively [12]. The prognostic index value of SAAG was at 82–97% compared to total protein concentration at 38–85% [12]. Ascites from cardiac origin produces greater(>2.5g/dl) SAAG compared to cases of cirrhosis [13].

A more recent classification of ascites has endorsed the use of serum ascites albumin gradient (SAAG) in diagnosis of ascites [14]. The SAAG is derived by subtracting the ascetic fluid albumin level from the serum albumin level obtained on the same day [14]. Gradients greater than 1.1 g/dl indicate ascites of portal hypertension with an accuracy of 97–100% [14]. Gradients less than 1.1 g/dl are considered ascites of other sources other than portal hypertension such as neoplasm [15, 16] (**Table 1**).


#### **Table 1.**

*Classification of ascites based on SAAG.*
