WeiHou, MD, ArunJ. Sanyal, MBBS, MD*
Ascites is a common complication of cirrhosis. The development of ascites marks the
onset ofworsened prognosis and increased mortality inpatients with cirrhosis. Ascites
also causes considerable morbidity in the affected individual by producing abdominal
distension, respiratory distress, formation of hernias especially around the umbilicus,
worsening nutritional status, and increased susceptibility to infections. All of these
contribute to repeated hospitalizations in such patients and markedly impair their
quality of life. Appropriate management of ascites is thus an important pillar in the
care of a patient with cirrhosis. The current concepts about the pathophysiology, diag-
nosis, and management of ascites are reviewed in the following sections.
The main factor contributing to the development of ascites in a patient with cirrhosis is
the portal hypertension which results from increased intrahepatic resistance to blood
flow and is compounded by splanchnic vasodilatation as a result of local production of
vasodilators (Fig. 1).1–8Cirrhosis occurs as a consequence of chronic liver injury–
induced distortion of hepatic architecture and fibrosis. Increased resistance to portal
blood flow as a result of cirrhosis and vascular tone because of increased production
of vasoconstrictors, such as angiotensin, endothelin, cysteinyl-leukotrienes, and
thromboxane leads to gradual formation of portal hypertension, collateral vein circu-
lation, and shunting of blood to the systemic circulation. Splanchnic vasodilatation
develops as persistent portal hypertension results in local overproduction of vasodila-
tors such as nitric oxide (NO), calcitonin gene–related peptide, substance P, carbon
monoxide, and endogenous cannabinoids. Among these vasodilators, NO is a potent
This work is original and not under consideration elsewhere for publication. It was supported
in part by a grant from the NIH K24 DK 02755-09 to Dr. Sanyal.
Division of Gastroenterology, Hepatology and Nutrition, Department of Internal Medicine,
Virginia Commonwealth University School of Medicine, MCV Box 980341, Richmond, VA
* Corresponding author.
E-mail address: firstname.lastname@example.org (A.J. Sanyal).
? Cirrhosis ? Ascites ? Portal hypertension ? Refractory ascites
?Transjugular intrahepatic portosystemic shunts
? Spironolactone ? Furosemide
?Spontaneous bacterial peritonitis
Med Clin N Am 93 (2009) 801–817
0025-7125/09/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.
and predominant vasodilator. Endothelial stretching and bacterial translocation are
responsible for the local overproduction of vasodilators and other cytokines.9,10
Recent data suggest that bacteria translocate to mesenteric lymph nodes in cirrhosis,
and consequently stimulation of cytokine production plays an important role in the
process of arterial vasodilatation.11–13
Splanchnic arteriolar vasodilation and consequent pooling of blood in the
splanchnic circulation causes a decrease in effective arterial blood volume and arterial
pressure. In response to this change in effective arterial blood volume and arterial
pressure, baroreceptor-mediated activation of the sympathetic nervous system
(SNS), renin-angiotensin-aldosterone system (RAAS), and antidiuretic hormone
(ADH) cause avid renal water and sodium retention in order to restore homeostasis.
Cirrhosis is also associated with increased sinusoidal pressure and decreased plasma
oncotic pressure. These combine to increase hepatic lymph formation. When the
capacity of the hepatic lymphatics to return hepatic lymph to the circulation is
exceeded, the excess lymph (composed of an ultrafiltrate of plasma containing the
retained sodium and water) spills into the peritoneal cavity, producing ascites.
The cardiac output and plasma volume increase in the early stages of liver cirrhosis,
contributes to a further fall in effective arterial blood volume and arterial pressure. This
causes marked activation of systemic vasoconstrictive mechanisms that particularly
affect the kidneys and decrease glomerular filtration and renal plasma flow. In its most
severe form, this leads to progressive renal failure, that is, hepatorenal syndrome.
The goals of the diagnostic assessment of a patient with ascites are to establish the
presence of ascites, determine its severity, determine its cause, and detect the
Fig. 1. The pathophysiology of cirrhosis and ascites is shown. Cirrhosis is associated with
splanchnic arterial vasodilation. This leads to a decrease in effective circulating volume
and a hyperdynamic circulation. The decrease in effective circulating volume causes activa-
tion of renal sodium and water retentive pathways (eg, RAAS, renal SNS, and ADH). The
resulting sodium and water retention leads to ascites as a result of spillage of excess sodium
and water from hepatic lymph into the peritoneal cavity. As the disease progresses,
a progressive decrease in effective circulating volume develops, causing severe renal vaso-
constriction and a decrease in glomerular filtration rate. The onset of cirrhotic cardiomyop-
athy accentuates this problem and tips the patient into hepatorenal syndrome. The
accompanying circulatory disturbance leads to organ failure and death. Sepsis is frequently
associated with this process.
Hou & Sanyal
presence of complications of ascites, which include spontaneous bacterial peritonitis
and renal failure. A good clinical assessment provides invaluable information about
A correct diagnosis of the cause of ascites is the essential first step to its successful
treatment. Cirrhosis accounts for approximately 85% of ascites in the United States,
whereas nonhepatic diseases cause most of the remaining cases (Box 1).14A history
of risk factors for liver diseases such as viral hepatitis, alcohol abuse, metabolic
syndrome, familial liver diseases, autoimmune disease, and so on should be obtained.
Cancer is the second most common cause of ascites. A history of cancer should lead
to exploring the possibility that ascites could be caused by peritoneal carcinomatosis.
Heart failure is the third common cause of ascites and a history of heart failure could
hint at a cardiogenic etiology as a potential cause of ascites. A history of tuberculosis,
kidney disease on dialysis, pancreatic disease, and so on are also relevant, and ques-
tions about these less common diseases should also be asked.
The physical examination should focus on stigmata of cirrhosis and signs suggest-
ing the presence of ascites. Stigmata of cirrhosis such as spider angioma and palmar
erythema may coexist with ascites. A full and bulging abdomen should lead to the
evaluation of ascites. Flank dullness on percussion is usually characteristic of ascites.
A positive shifting dullness usually suggests the presence of more than 1500 mL of
1. Portal hypertension
Presinusoidal causes, eg, portal vein thrombosis (usually ascites is mild if present at all)
Sinusoidal causes, eg, cirrhosis, vitamin A toxicity
Postsinusoidal causes, eg, venoocclusive disease, Budd-Chiari syndrome, constrictive
pericarditis, congestive heart failure
2. Neoplastic causes
3. Inflammatory causes
Infectious causes, eg, tuberculosis, Whipple disease
Chemical causes, eg, talc peritonitis
Immunologic disorders, eg, systemic lupus erythematosus, vasculitis
Allergic causes, eg, eosinophilic gastroenteritis
4. Miscellaneous causes
Ovarian hyperstimulation syndrome
Thoracic duct obstruction
Ascites: Diagnosis and Management
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Ascites: Diagnosis and Management