Ascites

ASCITES
Definition
• Ascites is the pathological accumulation of fluid in the peritoneal

cavity.
Etiology
• The etiology can be determined using the serum-ascites albumin
gradient (SAAG) based on Starling's law.
• Calculation: SAAG = (albumin levels in serum) - (albumin levels in
ascitic fluid)
SAAG Interpretation
• A high gradient (SAAG >1.1 g/dL) indicates portal hypertension and

suggests a nonperitoneal cause of ascites. Such conditions may include the
following:
1) Presinusoidal; -Splenic/portal vein thrombosis.
-Schistosomiasis.
2)Sinusoidal: -Liver Cirrhosis.
-Intrahepatic malignancies.
3)Postsinusoidal: -Cardiac; -Right sided heart failure.
-Constrictive pericarditis.
-Budd-Chiari Syndome.
SAAG Interpretation
• A low gradient (SAAG < 1.1 g/dL) indicates nonportal hypertension and
suggests a peritoneal cause of ascites. Such conditions may include the
following:[1]
• Primary peritoneal mesothelioma
• Secondary peritoneal carcinomatosis
• Tuberculous peritonitis
• Fungal and parasitic infections (eg, Candida, Histoplasma,
Cryptococcus,Strongyloides, Entamoeba histolytica)
• Sarcoidosis
• Foreign bodies (ie, talc, cotton and wood fibers, starch, barium)
• Systemic lupus erythematosus
• Nephrotic syndrome.
Pathophysiology
• Three theories of ascites formation have been proposed: underfilling,
overflow, and peripheral arterial vasodilation.
• The underfilling theory suggests that the primary abnormality is
inappropriate sequestration of fluid within the splanchnic vascular
bed due to portal hypertension and a consequent decrease in
effective circulating blood volume.
• This activates the plasma renin, aldosterone, and sympathetic
nervous system, resulting in renal sodium and water retention.
Pathophysiology cont…
• The overflow theory suggests that the primary abnormality is inappropriate
renal retention of sodium and water in the absence of volume depletion.
• This theory was developed in accordance with the observation that patients
with cirrhosis have intravascular hypervolemia rather than hypovolemia.
• Although the sequence of events that occurs between the development of
portal hypertension and renal sodium retention is not entirely clear, portal
hypertension apparently leads to an increase in nitric oxide levels. Nitric
oxide mediates splanchnic and peripheral vasodilation. Hepatic artery nitric
oxide synthase activity is greater in patients with ascites than in those
without ascites.
Pathophysiology cont..
• The third theory which is the most recent one is the arterial
vasodilation theory.
• This theory suggests that portal hypertension causes arterial
vasodilation which in turn causes a fall in the systemic vascular
resistance and mean arterial pressure.
• This activates the plasma renin, aldosterone, and sympathetic
nervous system, resulting in renal sodium and water retention.
• Regardless of the initiating event, a number of factors contribute to
the accumulation of fluid in the abdominal cavity.
• Elevated levels of epinephrine and norepinephrine are well-
documented factors.
• Hypoalbuminemia and reduced plasma oncotic pressure favour the
extravasation of fluid from the plasma to the peritoneal fluid, and,
thus, ascites is infrequent in patients with cirrhosis unless both portal
hypertension and hypoalbuminemia are present.
In the absence of cirrhosis
• Peritoneal carcinomatosis ,peritoneal infection , pancreatic disease
1. In infections eg Tb tubercles exude a protenecous material
2. Pancreatic ascites results from rupture of the pancreatic duct or leakage of the
pancreatic secretions from a pseudocyst. Irritation of the peritoneum by the
pancreatic secretions can cause accumulation of protein rich exudate in the peritoneal
cavity.
3. Chylous ascites can occur after transection of lymphatics, such as after abdominal
surgery
4. Malignancies; Obstruction of lymphatics by tumor
• Prevents absorption of fluid and protein
• Decreased circulating blood volume
• Activates RAAS leading to Na retention
HISTORY
 RELATED TO ASCITES
-Increase in abdominal girth abdominal heaviness
-Peripheral edema
-shortness of breath
-Weight gain
-Diarrhoea
 RELATED TO RISK FACTORS OF LIVER DISEASE
-history alcohol consumption,
-drug abuse,
-blood transfusions or
-hepatitis in the past(Infection and immunization)
 MEDICAL HISTORY
-History of malignancy ,
-Nephrotic syndrome,
-heart disease.
Physical Examination.
• Features of liver disease
-Jaundice ,
-spider naevi,
-palmar erythema
• Features of ascites
-puddle sign(120cc),
-shifting dullness & Fluid thrill(>500cc)
• Sister mary joseph nodule
-peritoneal carcinomatosis(originating from Ca stomach, pancreas,liver)
• Virchows node
-upper abdominal malignancy
Physical Examination
• Anasarca
-CCF,
-Nephrotic syndrome
• Presence of splenomegaly and large collateral veins may suggest portal
hypertension.
• Patients with cardiac causes of ascites may show engorged jugular veins.
• Collaterals in the back may indicate an obstruction of the inferior vena
cava.
• Presence of enlarged lymph nodes may suggest tuberculosis or
lymphoma.
Investigations
Abdominal paracentesis and analysis of ascitic fluid
1. Gross Apperance
• Ascites due to portal hypertension or hypoalbuminaemia, the fluid is
clear and straw coloured
• Turbid ascites may indicate infection.
• Chylous ascites typically has a milky appearance
• Blood stained fluid
-due to malignancy but may occur with tuberculosis,
pancreatitis,hepatic vein thrombosis, recent abdominal punctures or
due to a traumatic tap.
2. Cell count and differential
-Provides immediate information about the possible bacterial
infection.
-absolute neutrophil count of > 250 /mm indicates an infection.
Tests Done on Ascitic Fluid
Routine Optional Unusual
Cell count and differential Glucose concentration Tuberculosis smear and culture,
adenosine deaminase
Albumin concentration LDH concentration Cytology
Total protein concentration Gram stain Triglyceride concentration
Culture in blood culture bottles Amylase concentration Bilirubin concentration

Glucose and LDH
• Glucose:
-Consistent with infection or malignancy?
-Infection and cancer consume glucose -low
• LDH is a larger molecule than glucose, enters ascitic fluid with

difficulty.
• Ascitis/Serum LDH ratio
• ~ 0.4 in cirrhotic ascites
• Approaches 1.0 in SBP
• >1.0, usually infection or tumor
Other Tests.
• Amylase
– Uncomplicated cirrhotic ascites
-The AF/S ratio is about 0.4
– Pancreatic ascites
-The AF/S ratio is about 6
• Triglycerides — run on milky fluid.
– Chylous ascites - TG > 200 mg/dL.
• Bilirubin — run on brown ascites.
– Biliary perforation – AF Bili > serum Bili
TB TESTS
• Smear – extremely insensitive
• Culture – 62-83% when large volumes cultured
• Cell count – mononuclear cell predominance
• Adenosine deaminase –
• Enzyme involved in lymphoid maturation
• Falsely low in pts with both cirrhosis and TB
CYTOLOGY
• Malignant ascites from massive hepatic metastasis, HCC, lymphoma
are usually negative.
• Overall sensitivity for detection of malignancy-related ascites is 58 to
75 %
Imaging
• Abdominal sonography may detect as little as 100 ml of
intraperitoneal fluid
• Ct scan
• Plain radiographs
Complications
• Umbilical hernia
• Hydrothorax
• Bowel perforation
• Spontaneous bacterial peritonitis (SBP)
Spontaneous Bacterial Peritonitis(SBP)
• is defined as the spontaneous bacterial infection of the ascitic fluid without
any apparent intraabdominal source
• A count of 250 cells/mm3 or more is considered diagnostic
• Etiology and risk factors
• Often seen in patients with progressed liver cirrhosis or patients
receiving peritoneal dialysis.
• Bacterial species: E. coli most common in ascites.
• Klebsiella spp. and streptococci are frequently involved in nosocomial cases
of SBP.
SBP Cont…
• Clinical features
• Often asymptomatic
• Abdominal pain,
• Tense abdominal wall(Guarding),
• Fever is possible.
SBP Cont…
• Diagnosis
• Gold standard: diagnostic paracentesis BEFORE application of antibiotics.
• > 250 polymorphonuclear leukocytes/μL ascites: SBP per definition
• Determination of pathogens is rarely successful
• Treatment:
• First-line: 3rd generation cephalosporin IV broad spectrum therapy
• Follow-up after 48 h via repeated paracentesis
• If granulocytes decrease to < 250 /μL, treatment can be terminated after five additional
days
• If granulocytes do not decrease by ≥ 25%: modify treatment according to resistogram
• Prognosis: high recurrence and mortality rate.
MANAGEMENT; ASCITES
General measures
• Treatment of the underlying disease (e.g., using anticoagulation in case of
a thrombosis or Anti-TBs in case of a tubercular peritonitis)
• Sodium restriction
• Salt restriction-allows diuresis since the patient has more fluid that salt.
• Sodium intake needs to be restricted to about 800-1000 mg (2g NaCl) in order to induce a
negative sodium balance and permit diuresis
• Water restriction or avoiding over hydration.
• Bed Rest.
-The upright posture in patients with cirrhosis and ascites is associated with marked activation
of renin angiotensin-aldosterone and sympathetic nervous system, reduction of glomerular
filtration rate (GFR) and sodium excretion and a decreased response to loop diuretics
Diuretic therapy
• Indications
• Portal hypertensive ascites(transudate): usually responsive.
• Non-portal hypertensive ascites (exudate):
usually not effective; therefore it is essential to focus on treating the underlying
disease!
• Approach
• Spironolactone
• Additionally, or in the case of massive ascites,
-also those with peripheral edema: loop diuretics(Furosemide)
• Regular control of potassium and creatinine during diuretic therapy
• Diuretics should be used with precaution in cases of severe hyponatremia, hepatic
encephalopathy, or deterioration of renal function.
Monitoring Diuresis
• Monitor patients weight daily.
• Aim at weight loss of <1kg/day in patients with both edema & ascites.
• Weight loss of <0.5kg/day in those with ascites alone
• Once ascites has disappeared, diuretic treatment should be adjusted
to maintain the patient free of ascites.
Large Volume Paracentesis
• Used if severe (tense ) ascites is present.
• Complements medical therapy.
• Up to 11 liters may be removed.
• May deplete albumin in blood (administer iv albumin in proportion of fluid
removed.
• If drainage >5l,give iv albumin (25% albumin-8gm/l) to prevent hypotension.
• Contraindicated if;
• PT>21sec.
• INR>1.6
• Platelet count <50,000/ml
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ASCITES

• Ascites is the pathological accumulation of fluid in the peritoneal

• A high gradient (SAAG >1.1 g/dL) indicates portal hypertension and

Albumin concentration LDH concentration Cytology

Total protein concentration Gram stain Triglyceride concentration

Culture in blood culture bottles Amylase concentration Bilirubin concentration

• LDH is a larger molecule than glucose, enters ascitic fluid with

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