Ascites

ASCITES
 Accumulation of fluid within the peritoneal cavity.

 Most common cause of ascites is portal hypertension related to cirrhosis.

 However malignant or infectious causes of ascites can be present.

 In patients with cirrhosis, the development of ascites marks the transition from compensated
to decompensated cirrhosis

 Most frequent first decompensating event, occurring in 48%

Cirrhosis: The Most Common Cause of Ascites

Peritoneal malignancy

Cirrhosis Heart failure

85% Peritoneal tuberculosis

Others
·Pancreatic
·Budd-Chiari syndrome
·Nephrogenic ascites
Pathogenesis of ascites in the presence of cirrhosis

• It is the result of portal hypertension and renal salt and water retention. Similar mechanism contribute to
ascites formation in heart failure

• There is an increase in intrahepatic resistance, causing increased portal pressure, but there is also
vasodilation of the splanchnic arterial system, which, in turn, results in an increase in portal venous inflow.

• Both of these abnormalities result in increased production of splanchnic lymph. Vasodilating factors such as
nitric oxide are responsible for the vasodilatory effect.

• These hemodynamic changes result in sodium retention by causing activation of the renin-angiotensin-
aldosterone system with the development of hyperaldosteronism.

• The renal effects of increased aldosterone leading to sodium retention also contribute to the development of
ascites.
• Sodium retention causes fluid accumulation and expansion of the extracellular
fluid volume, which results in the formation of peripheral edema and ascites.

• Sodium retention is the consequence of a homeostatic response caused by under

filling of the arterial circulation secondary to arterial vasodilation in the
splanchnic vascular bed.

• Because the retained fluid is constantly leaking out of the intravascular

compartment into the peritoneal cavity, the sensation of vascular filling is not
achieved, and the process continues.

• Hypoalbuminemia and reduced plasma oncotic pressure also contribute to the

loss of fluid from the vascular compartment into the peritoneal cavity
Overfill hypothesis

• Reduced hepatic synthesis of a natriuretic

agent.
• Reduced hepatic clearance of a sodium -
retaining hormone, or
• Hepatorenal reflex of unknown aetiology.
Pathogenesis of ascites in the absence of cirrhosis
• Ascites in the absence of cirrhosis generally results from peritoneal carcinomatosis, peritoneal infection, or
pancreatic disease.

• Peritoneal carcinomatosis can result from primary peritoneal malignancies such as mesothelioma or sarcoma,
abdominal malignancies such as gastric or colonic adenocarcinoma, or metastatic disease from breast or lung
carcinoma or melanoma

• The tumor cells lining the peritoneum produce a protein-rich fluid that contributes to the development of ascites.

• Fluid from the extracellular space is drawn into the peritoneum, further contributing to the development of
ascites.

• Tuberculous peritonitis causes ascites via a similar mechanism; tubercles deposited on the peritoneum exude a
proteinaceous fluid.

• Pancreatic ascites results from leakage of pancreatic enzymes into the peritoneum.
 Clinical features
Presenting problems

• Abdominal distension
• Diffuse abdominal pain
• Bloating
• Dyspnea and orthopnea ( due to elevated diaphragm)
• Indigestion and heart burn (due to increased abdominal pressure)
Physical examination

• Abdominal distension
• Fullness of flanks
• Umbilicus flat and everted
• Distended abdominal veins
• Shifting dullness
• Fluid thrill
• Puddle sign
• Enlarged lymph nodes: TB, leukemia, malignancy and lymphomas
• Associated jaundice: cirrhosis of liver
• Dyspnea, orthopnea, PND and edema: congestive cardiac failure
• Periorbital edema, puffiness of face and edema: nephritic/nephrotic syndrome
• Sever anemia

Order of development of ascites

• Cardiac cause: leg edema precedes ascites
• Kidney causes: puffiness of face precedes ascites
• Cirrhosis of liver: ascites is the first feature
 Diagnosis
 Ultrasound is the gold standard
 Most cost -effective
 Grading of Ascites
 Grade 1 Ascites: Mild ascites only detectable by ultrasound

 Grade 2 Ascites: Moderate ascites evident by moderate symmetrical distension of

abdomen

 Grade 3 Ascites: Large or gross ascites with marked abdominal distension

Abdominal Paracentesis
Site

 left lower quadrant, 2 finger breadths (3 cm)

cephalad and 2 finger breadths medial to the
anterior superior iliac spine
 Ascitic fluid analysis
• Total protein – risk of SBP increased with low protein

• Glucose – PMN activity

(>50mg/dl in SBP, <50 in Sec.BP)

• Bilirubin – only for orange/brown fluid

> serum level (or) >6mg/dl viscus
perforation
• Ascites amylase activity of > 1000 U/L identifies pancreatic ascites
• Cytological examination may reveal malignant cells (one-third of cirrhotic patients with a bloody tap have a
hepatocellular carcinoma)
• The presence of triglyceride at a level > 1.1 g/L (110 mg/dL) is diagnostic of chylous ascites
Management
 Successful treatment relieves discomfort
 Does not prolong life
 Restricting sodium and water intake, promoting urine output with diuretics
 Removing ascites directly by paracentesis.
 Should be weighed regularly.
 Diuretics should be titrated to remove no more than 1 L of fluid daily
 If over-vigorous, produce serious disorders of fluid and electrolyte balance, and precipitate
hepatic encephalopathy
Sodium and water restriction

 Most average diets contain 6–8 g of sodium per day

 Ingest <2 g of sodium per day
 Restriction of water intake to 1.0–1.5 L/24 hrs is necessary only if plasma sodium falls
below 125 mmol/L.

 Small amounts of ascites managed with dietary sodium restriction alone.

 Simple recommendation is to eat fresh or frozen foods, avoiding canned or processed foods,
which are usually preserved with sodium.
 Drugs containing relatively large amounts of sodium, and those promoting sodium retention, such as non-
steroidal anti-inflammatory drugs (NSAIDs), must be avoided
Diuretics

 Addition to sodium restriction.

 Spironolactone (100–400 mg/day) is first-line drug powerful aldosterone antagonist inhibits sodium
resorption in the distal convoluted tubule of the kidney
 Cause painful gynaecomastia and hyperkalaemia, in which case Amiloride (5–40 mg/day) can be
substituted.
 Some patients also require loop diuretics, such as furosemide, 40–80 mg/d, particularly in patients who
have peripheral Edema
 Spironolactone can be increased to 400–600 mg/d and furosemide increased to 120–160 mg/d
 Diuresis may be improved if patients are rested in bed renal blood flow increases in the horizontal position.
 Oral route – Single morning dose
Progressive Schedule Combined Schedule

SP * SP 100 mg/d
100  200  300  400 mg/d + FUR 40 mg/d

Progressive increase every 3-5

days
SP 400 mg/d + FUR** SP 200  300  400 mg/d
40  80  120  160 mg/d + FUR 80  120  160 mg/d

*SP Spironolactone
**FUR Furosemide
 Follow-up of patients on diuretics
• Weight loss
o with edema  1.0 kg/day
o without edema  0.5 kg / day

• Weight loss less than desired

24-hour urine sodium
> 78 mmol/24h & no weight loss: patient not compliant
< 78 mmol/24h & no weight loss: increase diuretics
“spot” urine NA/K>1= 24-hour urine Na>78 mmol/24h
 Discontinuing Diuretics

 Severe hyponatremia (serum Na <120 mol/L)

 Progressive renal failure
 Worsening hepatic encephalopathy
 Furosemide:severe hypokalemia (<3 mmol/L)
 Aldosterone antagonists: Severe hyperkalemia (serum potassium>6 mmol/L):
gynaecomastia
 REFRACTORY ASCITES
 Patients who do not respond to doses of 400 mg spironolactone and 160 mg furosemide, or
who are unable to tolerate these doses due to hyponatraemia or renal impairment, who are
compliant with a low-sodium diet are considered to have refractory ascites.

 Diuretic-resistant ascites
 Ascites that cannot be mobilized or the early recurrence of which cannot be prevented because of a
lack of response to sodium restriction and diuretic treatment

 Diuretic-intractable ascites
 Ascites that cannot be mobilized or the early recurrence of which cannot be prevented because of the
development of diuretic induced complications that preclude the use of an effective diuretic dosage
 Requisites
1. Treatment duration:
 Patients must be on intensive diuretic therapy (spironolactone 400 mg/day and furosemide 160 mg/day)
for at least 1 week and on a salt-restricted diet of less than 90 mmol/day
2. Lack of response:
 Mean weight loss of <0.8 kg over 4 days and urinary sodium output less than the sodium intake
3. Early ascites recurrence:
 Reappearance of grade 2 or 3 ascites within 4 weeks of initial mobilization
4. Diuretic-induced complications
 Diuretic-induced hepatic encephalopathy in the absence of any other precipitating factor
 Diuretic-induced renal impairment is an increase of serum creatinine by >100% to a value >2 mg/dl
(177 lmol/L) in patients with ascites responding to treatment
 Management of Refractory Ascites

 Liver transplantation should be considered among the treatment options for

patients with cirrhosis and ascites—whether the fluid is diuretic-sensitive or
diuretic-refractory.
Paracentesis

 First-line treatment of refractory ascites is large-volume paracentesis.

 Paracentesis to dryness is safe, provided the circulation is supported with an intravenous colloid such
as human albumin
 (6–8 g per litre of ascites removed, usually as 100 mL of 20% or 25% human albumin solution)
 Paracentesis can be used as an initial therapy or when other treatments fail.
Pharmacologic therapy for refractory ascites includes

 Addition of midodrine, an α1-adrenergic agonist , to diuretic therapy.

 Act as vasoconstrictors, counteracting splanchnic vasodilation.

 Midodrine improves systemic hemodynamics and control of ascites over that obtained with diuretics
alone.

 Although β-adrenergic blocking agents (beta blockers) are often prescribed to prevent variceal
hemorrhage in patients with cirrhosis, the use of beta blockers in patients with refractory ascites may be
associated with decreased survival rates.
Transjugular intrahepatic portosystemic stent shunt (TIPSS )

 Can relieve resistant ascites but does not prolong life

 May be an option where the only alternative is frequent, large volume paracentesis.
 Can be used in patients awaiting liver transplantation or in those with reasonable liver function.
 Can aggravate encephalopathy in those with poor function

 Radiologically placed portosystemic shunt that decompresses the hepatic sinusoids.

 TIPS placement is superior to LVP in reducing the reaccumulation of ascites
Prognosis
 Only 10–20% of patients survive for 5 years from the first appearance of ascites due to cirrhosis.
 Best in those with well-maintained liver function and a good response to therapy
 Prognosis is also better when a treatable cause for the underlying cirrhosis is present
 The mortality at 1 year is 50% following the first episode of bacterial peritonitis.
 some studies have shown that <50% of patients survive 2 years after the onset of ascites.
 Thus, there should be consideration for liver transplantation in patients with the onset of ascites.
 SPONTANEOUS BACTERIAL PERITONITIS

Diagnosis of SBP is made when there is :

 Positive ascitic fluid culture and an elevated ascitic fluid absolute PMN count (i.e., at
least 250/mm3 [0.25 × 109/L])

 without evidence of an intra-abdominal surgically treatable source of infection (e.g., a

ruptured viscus).

 Many patients with SBP have a focus of infection (e.g., urinary tract infection or
pneumonia)
Monomicrobial non-neutrocytic bacterascites (MNB)

 Positive ascitic fluid culture for a single organism

 Ascitic fluid PMN count lower than 250/mm3 (0.25 × 109/L)
 No evidence of an intraabdominal surgically treatable source of infection.
Culture-negative neutrocytic ascites (CNNA)

 Ascitic fluid culture grows no bacteria

 Ascitic fluid PMN count is 250/mm3 (0.25 × 109/L) or greater
 No antibiotics have been given (not even a single dose)
 No other explanation for an elevated ascitic PMN count
(e.g., hemorrhage into ascites, peritoneal carcinomatosis, TB,or pancreatitis)

CNNA probably results from

(1) Previous antibiotic treatment (even 1 dose)
(2) Inadequate volume of fluid inoculated
(3) Spontaneously resolving SBP in which the paracentesis is performed after all bacteria have been killed by
host defenses but before the PMN count has normalized.
Secondary bacterial peritonitis

 Ascitic fluid culture is positive (usually for multiple organisms)

 PMN count is 250/mm3 or greater.
 Intra-abdominal surgically treatable primary source of infection
(e.g., perforated intestine, perinephric abscess) has been identified
Polymicrobial bacterascites

 Multiple organisms are seen on Gram stain or cultured

 PMN count is lower than 250/mm3 (0.25 × 109/L).

Diagnosis should be suspected when

 Paracentesis is traumatic
 Unusually difficult because of ileus or when stool or air is aspirated into the paracentesis
syringe.
 Polymicrobial bacterascites is essentially diagnostic of intestinal perforation by the
paracentesis needle.
 Escherichia coli, streptococci (mostly pneumococci), and Klebsiella caused most episodes of SBP and MNB in the past

 Now more Gram-positive and resistant Gram negative organisms are being isolated

 Anaerobic bacteria were present in approximately 6% of cases of SBP

 Detection of anaerobes probably reflected unrecognized cases of secondary bacterial peritonitis.

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