Cirrhosis is the late result of any disease that causes scarring of the liver.

Patients with cirrhosis are susceptible to a variety of complications that include ascites, hepatic encephalopathy, and portal hypertension. Quality of life and survival are often improved by the prevention and treatment of these complications. Ascites is defined as the accumulation of free fluid in the peritoneal cavity. It is a common clinical finding with a variety of both extraperitoneal and peritoneal etiologies. It is most often caused by liver cirrhosis which accounts for over 75% of patients while the remaining 25 % is due to malignancy (10%), heart failure (3%), pancreatitis (1%), TB (2%), or other rare causes.

Nonperitoneal Causes of Ascites Secondary to malignancy, trauma

Chylous Myxedema Ovarian tumors Pancreatic & Biliary ascites Miscellaneous disorders Nephrotic syndrome Protein-losing enteropathy Malnutrition

Hypoalbuminemia Hepatic vein obstruction (ie, Budd-Chiari syndrome) Congestive heart failure Extrahepatic portal hypertension Cirrhosis Fulminant hepatic failure Veno-occlusive disease Intrahepatic portal hypertension Examples

Non-peritoneal causes

Peritoneal Causes of Ascites

Eosinophilic gastroenteritis Whipple disease Endometriosis Miscellaneous disorders Systemic lupus erythematosus Henoch-Schnlein purpura Vasculitis Tuberculous peritonitis Fungal and parasitic infections Sarcoidosis Foreign bodies (cotton ,starch, barium) Granulomatous peritonitis Primary peritoneal mesothelioma Secondary peritoneal carcinomatosis

Malignant ascites Examples Peritoneal Causes

Prognosis The development of ascites is an indication of deterioration in clinical status and poor prognosis. Prognosis is worse for those with refractory ascites and SBP. Approximately 60% of patients with cirrhosis will develop ascites requiring therapy and/or liver transplantation in 10 years duration. Mortality in cirrhotic patients hospitalized with ascites is 40% at 2 years.

PATHOPHYSIOLOGY Ascites is derived from the vascular compartment subserving the hepatosplanchnic viscera.

Factors important in the formation of ascites: Increased total body sodium and water Increased sinusoidal portal pressure. In cirrhosis Hepatic dysfunction and sinusoidal portal pressure send a message to the kidney to retain excess sodium and fluid. PH serves to localize excess fluid to the peritoneal cavity rather than the periphery. The pathogenesis of ascites formation remains controversial. Underfill" theory Ascites occurs as a primary event. Sequestration of fluid into the peritoneal cavity as a result of changes in Starling's forces leads to reduction of the circulatory volume and stimulation of the sympathetic nervous & RAAS that promote renal sodium & water retention.

Overflow theory" Renal Na retention occurs as a primary event. It may be due to increased production of a sodium retaining factor or reduced synthesis of a natriuretic factor by the diseased liver. The circulatory volume is expanded & the retained fluid is preferentially localized to the peritoneal cavity as ascites.

The currently accepted theory of ascites formation which include features of both the underfill and overflow theories is the

Peripheral Arterial Vasodilation Hypothesis" : According to this theory, Portal pressure >12 mm Hg is required for the development of PH which will lead to formation of ascites.

As PH develops, vasodilators are released affecting the splanchnic arteries resulting in decrease in effective arterial blood flow and arterial pressures . The precise agent (or agents) responsible for vasodilation is a subject of wide debate; however, most recent literature has focused on the role of: Nitric Oxide :Chronic endotoxemia associated with cirrhosis may stimulate the synthesis and release of a potent endothelin-derived relaxing factor, Nitric oxide. NO is

the likely mediator in cirrhosis: (1) Increased activity of NO synthase . (2) High serum nitrite and nitrate levels (an index of NO synthesis). (3) Inhibition of NO leads to increased arterial pressures and systemic vascular resistance. Portal hypertension Vasodilatation, Decrease Splanchnic Systemic vascular resistance Reduction in arterial blood volume Activation of neurohumoral pressor systems Renal sodium & water retention When Na reabsorption cannot compensate for vasodilation, arterial underfilling leads to further activation of vasoconstrictor & antinatriuretic mechanisms which leads to increased Na retention & ultimately ascites is formed. In the late stages of cirrhosis, free water accumulation is more pronounced than the Na retention leading to dilutional hyponatremia. DIAGNOSIS I) History Approximately 85% of patients with ascites have cirrhosis. Patients who dont have cirrhosis should be questioned about lifetime body weight as NASH may be the cause. Past history of cancer, heart failure, or TB. II) Physical Examination Approximately 1.5 L must be present before flank dullness is detected. If no flank dullness is present, the patient has less than 10% chance of having ascites. Shifting dullness & fluid thrill mean that more fluid is present. Abdominal ultrasound to determine with certainty if fluid is present and in obese. Two grading systems for ascites have been used in the literature. An old system which grades ascites from 1+ to 4+, depending on the detectability of fluid on physical examination. More recently, the International Ascites Club has proposed a system of grading from 1 to 3.

The older system 1+ is minimal and barely detectable. 2+ is moderate. 3+ is massive but not tense. 4+ is massive and tense. The International Ascites Club grading (2003) Grade 1: mild ascites detectable only by US. Grade 2: moderate ascites manifested by moderate symmetrical abdominal distension. Grade 3: large or gross ascites with marked abdominal distension. III) Diagnostic Paracentesis Indications (1)Evaluation for a non-cirrhotic patient developing clinically apparent ascites of recent onset. (2)New development of ascites in a cirrhotic patient does not routinely require paracentesis only if : (a) General condition deteriorates. (b) In presence of unexplained fever, abdominal pain, encephalopathy. (c) Admission to hospital for any cause (SBP). (3)Laboratory investigations indicating infection: Leucocytosis Acidosis Worsening of renal functions Site Midline was usually chosen. Abdominal wall in the left lower quadrant, 2 finger breadths cephalic & 2 finger breadths medial to ASIS, has been shown to be thinner with larger pool of fluid than midline. Complications (1% of patients) Abdominal wall hematomas. Hemoperitoneum or bowel entry. Contraindications Clinically evident fibrinolysis or DIC.

Cirrhosis
Thoracic duct injury Lymphoma Milky ("chylous") Malignancy Abdominal trauma

Grossly bloody Mild Trauma Pink or blood tinged Infection Cloudy or turbid Hyperbilirubinemia GB or biliary perforation Brown Normal/sterile Translucent or yellow Appearance Color Gross Appearance of Ascitic Fluid

Ascitic Fluid Testing

TB smear and culture Cytology Bilirubin Triglycerides Amylase Gram stain Glucose Culture Lactate LDH Albumin

pH Total protein

Cell count & differential Rarely helpful Sometimes useful Routine

Ascitic fluid analysis (Routine) I) Cell count with differential Abnormal results are an indication for further non routine tests. If the PMN count is >250 cells/mm3, another specimen is injected into blood culture bottles at bedside. Bacterial growth occurs in about 80% of specimens with count of >250 cells/mm3. The PMN count is calculated by multiplying the white cells/mm3 by the percentage of neutrophils in the differential.

In a "bloody" sample that contains a high concentration of RBC, the PMN count must be corrected: one PMN is subtracted from the absolute PMN count for every 250 red cells/mm3 in the sample. The results must be available within 1 hour, so that important diagnostic and therapeutic decisions can be made. A Gram stain is of particular low yield unless free gut perforation, is suspected. )Total protein ,albumin & serum albumin . Serum-ascites albumin gradient (SAAG) = serum albumin - ascitic fluid albumin. If > 1.1 g/dL, the patient has PH-related ascites. If < 1.1 g/dL (about 97% accurate), the patient does not have PH-related ascites. The SAAG does not need to be repeated after the initial measurement. II)Based on clinical judgment, additional testing can be performed :

a) Cytology ,smear & culture for mycobacteria. b) Cytology : in peritoneal carcinomatosis (sensitivity increased by centrifuging large volume). c) Elevated bilirubin level suggest biliary or gut perforation. d) LDH >225mU/L, glucose <50mg/dL, total protein >1g/dL and multiple organisms on gram stain suggest secondary bacterial peritonitis. e) High level of TG's confirms chylous ascites. f) Elevated amylase level suggest pancreatitis or gut perforation. AASLD Recommendations 1.Paracentesis should be performed ,ascitic fluid should be obtained from inpatients & outpatients with clinically apparent new-onset ascites 2. Since bleeding is uncommon ,prophylactic use of FFP or platelets is not recommended. 3. Initial evaluation of ascitic fluid should include cell count ,differential, total protein & SAAG. 4. If infection is suspected, ascitic fluid should be cultured at the bedside in blood culture bottles. 5. Other studies can be ordered based on pretest probability of disease.
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Ascites Return to Encyclopedia Index A

Definition Ascites is an abnormal accumulation of fluid in the abdomen. Description Rapidly developing (acute) ascites can occur as a complication of trauma, perforated ulcer, appendicitis, or inflammation of the colon or other tubeshaped organ (diverticulitis). This condition can also develop when intestinal fluids, bile, pancreatic juices, or bacteria invade or inflame the smooth, transparent membrane that lines the inside of the abdomen (peritoneum). However, ascites is more often associated with liver disease and other long-

lasting (chronic) conditions. Types of ascites Cirrhosis, which is responsible for 80% of all instances of ascities in the United States, triggers a series of disease-producing changes that weaken the kidney's ability to excrete sodium in the urine. Pancreatic ascites develops when a cyst that has thick, fibrous walls (pseudocyst) bursts and permits pancreatic juices to enter the abdominal cavity. Chylous ascites has a milky appearance caused by lymph that has leaked into the abdominal cavity. Although chylous ascites is sometimes caused by trauma, abdominal surgery, tuberculosis, or another peritoneal infection, it is usually a symptom of lymphoma or some other cancer. Cancer causes 10% of all instances of ascites in the United States. It is most commonly a consequence of disease that originates in the peritoneum (peritoneal carcinomatosis) or of cancer that spreads (metastasizes) from another part of the body. Endocrine and renal ascites are rare disorders. Endocrine ascites, sometimes a symptom of an endocrine system disorder, also affects women who are taking fertility drugs. Renal ascites develops when blood levels of albumin dip below normal. Albumin is the major protein in blood plasma. It functions to keep fluid inside the blood vessels. Causes and symptoms Causes The two most important factors in the production of ascites due to chronic liver disease are:

Low levels of albumin in the blood that cause a change in the pressure necessary to prevent fluid exchange (osmotic pressure). This change in pressure allows fluid to seep out of the blood vessels. An increase in the pressure within the branches of the portal vein that run through liver (portal hypertension). Portal hypertension is caused by the scarring that occurs in cirrhosis. Blood that cannot flow through the liver because of the increased pressure leaks into the abdomen and causes ascites.

Other conditions that contribute to ascites development include:

hepatitis heart or kidney failure inflammation and fibrous hardening of the sac that contains the heart (constrictive pericarditis)

Persons who have systemic lupus erythematosus but do not have liver disease or portal hypertension occasionally develop ascites. Depressed thyroid activity sometimes causes pronounced ascites, but inflammation of the pancreas (pancreatitis) rarely causes significant accumulations of fluid. Symptoms Small amounts of fluid in the abdomen do not usually produce symptoms. Massive accumulations may cause:

rapid weight gain abdominal discomfort and distention shortness of breath swollen ankles

Diagnosis Skin stretches tightly across an abdomen that contains large amounts of fluid. The navel bulges or lies flat, and the fluid makes a dull sound when the doctor taps the abdomen. Ascitic fluid may cause the flanks to bulge. Physical examination generally enables doctors to distinguish ascities from pregnancy, intestinal gas, obesity, or ovarian tunors. Ultrasound or computed tomography scans (CT) can detect even small amounts of fluid. Laboratory analysis of fluid extracted by inserting a needle through the abdominal wall (diagnostic paracentesis) can help identify the cause of the accumulation. Treatment Reclining minimizes the amount of salt the kidneys absorb, so treatment generally starts with bed rest and a low-salt diet. Urine-producing drugs (diuretics) may be prescribed if initial treatment is ineffective. The weight and urinary output of patients using diuretics must be carefully monitored for signs of :

hypovolemia (massive loss of blood or fluid) azotemia (abnormally high blood levels of nitrogen-bearing materials) potassium imbalance high sodium concentration. If the patient consumes more salt than the kidneys excrete, increased doses of diuretics should be prescribed

Moderate-to-severe accumulations of fluid are treated by draining large amounts of fluid (large-volume paracentesis) from the patient's abdomen. This procedure is safer than diuretic therapy. It causes fewer complications and requires a shorter hospital stay. Large-volume paracentesis is also the preferred treatment for massive ascites. Diuretics are sometimes used to prevent new fluid accumulations, and the procedure may be repeated periodically. Alternative treatment Dietary alterations, focused on reducing salt intake, should be a part of the treatment. In less severe cases, herbal diuretics like dandelion (Taraxacum officinale) can help eliminate excess fluid and provide potassium. Potassiumrich foods like low-fat yogurt, mackerel, cantaloupe, and baked potatoes help balance excess sodium intake. Prognosis The prognosis depends upon the condition that is causing the ascites. Carcinomatous ascites has a very bad prognosis. However, salt restriction and diuretics can control ascites caused by liver disease in many cases. Therapy should also be directed towards the underlying disease that produces the ascites. Cirrhosis should be treated by abstinence from alcohol and appropriate diet. The new interferon agents maybe helpful in treating chronic hepatitis. Prevention Modifying or restricting use of salt can prevent most cases of recurrent ascites. Key Terms Computed tomography scan (CT) An imaging technique in which cross-sectional x rays of the body are compiled to create a three-dimensional image of the body's internal structures. Interferon A protein formed when cells are exposed to a virus. Interferon causes other noninfected cells to develop translation inhibitory protein (TIP). TIP blocks viruses from infecting new cells. Paracentesis A procedure in which fluid is drained from a body cavity by means of a catheter placed through an incision in the skin.

Systemic lupus erythematosus An inflammatory disease that affects many body systems, including the skin, blood vessels, kidneys, and nervous system. It is characterized, in part, by arthritis, skin rash, weakness, and fatigue. Ultrasonography A test using sound waves to measure blood flow. Gel is applied to a hand-held transducer that is pressed against the patient's body. Images are displayed on a monitor.