Ascites is the most common complication of cirrhosis, as approximately 50 % of cirrhotic patients develop ascites within a decade of being diagnosed with cirrhosis [3]. Ascites results from complex vascular consequences of sinusoidal portal hypertension, including endogenous vasoconstriction, renal vasoconstriction, and sodium and water retention. It has been shown to develop when the portal pressure is greater than 12 mmHg [4], and reducing the portal pressure below this threshold is the goal when treating refractory ascites with a transjugular intrahepatic portosystemic shunt (TIPS) . The development of ascites is associated with a 50 % mortality within 2 years [5], and ascites refractory to medical therapy is associated with a 50 % mortality within only 6 months [6]. The model for end-stage liver disease (MELD) score underestimates the mortality risk of about 25 % of patients with moderate ascites by roughly 4–5 MELD points [7].

Elevated portal pressure typically above 12 mmHg leads to the development of varices, formed by portosystemic collaterals commonly in the esophagus, stomach, and rectum. At such high portal pressures, varices are at risk for rupture and hemorrhage, which occurs in 25–40 % of patients with cirrhosis [14]. Each episode of variceal hemorrhage is associated with a 15–20 % mortality at 30 days [15].

Vasoconstriction of the renal circulation and portal hypertension-induced arterial vasodilatation in the splanchnic vascular bed can result in decreased renal perfusion. The consequence of these vascular changes is HRS, characterized by a rise in the serum creatinine in the absence of other causes of acute kidney injury. HRS is classified as type 1 (a twofold increase in creatinine to over 2.5 mg/dL over 2 weeks) or type 2 (renal insufficiency that progresses less rapidly than type 1). Additional features that are typical of HRS include a low rate of urine sodium excretion, a normal urine sediment with minimal proteinuria, and oliguria. The diagnosis of HRS requires deterioration in renal function after withdrawal of diuretics and administration of a weight-based volume expansion challenge with intravenous albumin [16, 17]. HRS is a common complication of advanced cirrhosis and is associated with a poor prognosis, especially for patients with type 1 HRS. HRS develops in as many as 18 % of patients with cirrhosis, and in 39 % of patients with ascites [18]. The prognosis for patients who develop type 1 HRS is grave and is associated with a median survival of less than 1 month without therapy. By 6 months, type 1 HRS is almost universally fatal [18].

Fluid can accumulate in cirrhotic patients’ thoracic cavity as it does in the peritoneal cavity. Hepatic hydrothorax develops in an estimated 5–10 % of cirrhotic patients in the absence of cardiopulmonary disease. Hepatic hydrothorax results from direct movement of ascitic fluid from the peritoneal cavity into the pleural space through small diaphragmatic defects. It involves the right hemithorax in approximately 85 % of cases [19].

Portopulmonary hypertension is present in up to 16 % of patients with severe liver disease [22]. It is defined as the presence of portal hypertension in addition to increased pulmonary arterial pressure or pulmonary vascular resistance, with no other identifiable cause for pulmonary hypertension. It typically presents with dyspnea on exertion [23] and can be diagnosed by echocardiography or right-heart catheterization [24]. The mechanisms for the development of portopulmonary hypertension remain incompletely understood, with genetic predisposition, a hyperdynamic circulation, and endogenous humoral substances and cytokines all potentially contributing [25–27]. Reports regarding prognosis vary widely, with 5 year survival rates ranging from 10 to 50 % [28].

In contrast to portopulmonary hypertension, hepatopulmonary syndrome (HPS) is a better defined cause of hypoxemia . It is the result of abnormal intrapulmonary vascular dilation combined with increased pulmonary blood flow, leading to anatomical shunting and a diffusion–perfusion abnormality that is correctable by oxygen supplementation [28]. The pulmonary vascular shunts seen in HPS are preferentially perfuse when the patient is upright, leading to the characteristic symptoms of platypnea and orthodeoxia [29]. Estimates of HPS prevalence vary widely, but the presence of HPS worsens prognosis among patients with cirrhosis [30]. Among cirrhotic patients, HPS is an independent risk factor for mortality, with median survival time of roughly 11 months compared to 41 months in cirrhotic patients without HPS [30], and more severe hypoxemia predicts higher posttransplant mortality [31].

Hepatic encephalopathy (HE) encompasses all the neuropsychiatric abnormalities that develop in the setting of portal hypertension. Overt HE develops in 30–45 % of patients with cirrhosis [32]. Subclinical HE is more subtle and characterized by psychomotor slowing, visuoconstructive disabilities, and attention deficits. It is present in up to 80 % of cirrhotics [33]. HE is precipitated by neurotoxins normally cleared by the liver, but that are shunted around the liver in the presence of portal hypertension-induced portosystemic collaterals, allowing them to influence the central nervous system. Patients hospitalized with HE experience mortality rates of 42 % at 1 year and 23 % at 3 years [34].