Management of Ascites

1. Management
of Ascites
Dr. Gyaneshwar Yadav
DNB Resident,
General Medicine,
GIMS
Moderator : Dr. Enna
SR, General Medicine

2. Definition Of Ascites
According to the International Ascites club : Ascites is classified based on quantitative
parameters
• Grade 1 ascites : mild ascites that is detectable only by Ultrasonography.
• Grade 2 ascites : moderate ascites detectable by physical examination.
• Grade 3 ascites : large ascites with marked abdominal distention.
Recurrent ascites : Ascites that recurs at least 3 times within a one-year period, despite appropriate treatment.
Ascites is defined as the abnormal accumulation of fluid in the peritoneal cavity.
report on the consensus conference of the International Ascites Club. Hepatology 2003;38:258-66.

3. Causes Of Ascites
Ascites may be caused by other conditions such as : Heart failure, Malignancies,
Tuberculosis, or Pancreatic diseases.
most common cause of ascites : cirrhosis

4. Causes Of
Ascites
CMDT (2023) Diseases of the peritonium,
page no. 602

5. Pathophysiology

6. Pathophysiology of cirrhosis
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1472

7. Pathophysiology of Ascites in cirrhosis
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1472
Sodium retention
Portal
Hypertension
Systemic
circulatory
dysfunction
Systemic
inflammation

8. Sodium Retention and Extracellular Fluid
Volume Expansion
• Sodium is retained isosmotically with water, therefore, sodium retention is associated with
extracellular fluid volume expansion.
• Degree of sodium retention is highly variable from patient to patient.
• Patients with severe or difficult-to-control ascites have marked sodium retention (urinary sodium excretion <10
mEq/day).
• By contrast, patients with cirrhosis and mild-to-moderate ascites excrete more than 10 mEq/day (without diuretic
therapy).
In patients with cirrhosis without renal failure, sodium retention is caused by reabsorption of
sodium in both the proximal and distal tubules.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474

9. Portal Hypertension
• Hepatic venous pressure gradient (HVPG) - difference between wedged and free hepatic venous pressure,
measured by hepatic vein catheterization (Normal - 5 mmHg)
• Clinically significant portal hypertension - HVPG above 10 to 12 mm Hg
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1473
Development of cirrhosis causes marked disturbance in the intrahepatic circulation, which in
turn causes increased resistance to portal flow.
• Reduced NO production from endothelial nitric oxide synthase
• Activated HSCs have increased contractility, leading to increased vascular tone and
increased intrahepatic resistance.

10. Systemic Circulatory Dysfunction
At early stages, moderate splanchnic arterial vasodilation is counterbalanced by an increase
in cardiac output.
At advanced stages of cirrhosis, splanchnic arterial vasodilatation is intense that cannot be
compensated for by a further increase in cardiac outout.
• Vasoconstrictor systems [RAAS, SNS, vasopressin] get activated, and maintain effective arterial blood volume
and arterial pressure.
• It has important detrimental effects on kidney function, with sodium and solute free-water retention leading to
ascites and edema and to dilutional hypernatremia, respectively.
Initially Portal hypertension result in splanchnic arterial vasodilatation due to the release of
several vasodilating factors, such as NO, carbon monoxide, and endogenous endocannabinoids.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474

11. Sympathetic Nervous System
• It is increased in most cirrhotic patients with ascites, involved in sodium and water
retention.
• Activity of the SNS can be suppressed by increasing eftective arterial blood volume
[vasopressin analogs and albumin, or the insertion of a TIPS or peritoneovenous shunt]
• One study on patients with ascites showed that administration of diuretics together with clonidine to inhibit SNS
activity is more effective than diuretics alone in inducing diuresis.
• Plasma concentration of norepinephrine (NE) in the systemic circulation, is a marker of
the activation of the SNS.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474

12. Systemic Inflammation
• Injured liver due to local inflammation (DAMPs) - Also activate pattern recognition receptors.
• The systemic release of these inflammatory mediators contributes to further impairment of circulatory
dysfunction
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474
Decompensated cirrhosis is associated with increased serum levels of inflammatory
markers, such as C-reactive protein and the leukocyte count, proinflammatory cytokines
such as interleukin IL-6, IL-8, and TNF- alfa.
Bacterial translocation - Pathogen-associated molecular patterns (PAMPs) - activate pattern
recognition receptors present in circulating innate immune cells - activation of immune cells,
the release of proinflammatory mediators and reactive oxygen species - an inflammatory
response.

13. Pathophysiology of Ascites and renal
dysfunction
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1472

14. Cirrhosis : Functional renal abnormalities
Sodium
retention
Impaired
excretion of
solute-free water
Renal
vasoconstriction
(Decreased GFR)
Ascites and
edema
Dilutional
hyponatremia
Hepatorenal
syndrome (HRS)

15. Diagnosis

16. Evaluation of a patient of Ascites
Ruling out other causes of ascites, such as heart failure, malignancy, tuberculosis, or
pancreatic disease.
Careful clinical history, physical examination, laboratory tests to assess liver and kidney function, serum and urine
electrolyte concentrations, abdominal US, and an ascitic fluid analysis
Focus on confirming the diagnosis of chronic liver disease, as cirrhosis is the main cause of
ascites.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474

17. Laboratory Tests
Renal function - Serum creatinine level and serum and urine electrolyte concentrations, as
well as a 24-hour urine collection for sodium and protein.
Liver function - Liver biochemical and coagulation tests
These laboratory tests should be performed before diuretic treatment is initiated.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1475

18. Assessment of Renal Sodium Excretion
Measurement of baseline sodium excretion helps predict the response to diuretic treatment
and prognosis.
Urine collection -
• under controlled sodium intake (approximately 90 mEq/day during the previous 5 to 7 days)
• 24-hour assessment of sodium excretion is preferred over "spot" analysis of urinary sodium
• moderate sodium retention (urine sodium ≥10 mEq/day) - respond to lower doses of diuretic treatment than those
with marked sodium retention.
• Baseline urine sodium excretion <10 mEq/day - median survival time of only 1.5 years
• If urine sodium greater than or equal to 10 mEq/day - median survival time of 4.5years
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474

19. Renal Sodium Excretion : Prognosis
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1475
• Other prognostic factors - Arterial pressure,
serum sodium concentration, and serum
creatinine level.
• Patients with urine sodium concentration <10
mEq/L have a significantly lower probability of
survival than those with renal sodium
concentration greater than 10 mEq/L.

20. Abdominal Ultrasonography
• To all patients with the first presentation of ascites.
• In patients with known ascites who experience unexplained loss of response to treatment.
Evaluate the liver parenchyma and assess the patency of the portal vein and suprahepatic veins
and rule out a liver tumor.
• technique of choice
• simple
• cost effective
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474

21. Analysis of ascitic fluid
Diagnostic paracentesis - standard 1.5-inch (longer in obese persons), 22-gauge steel
needle
To detect ascitic fluid infection
If diagnosis is not clear, to exclude causes of ascites other than cirrhosis.
• To be performed in all patients who present with a first episode of grade 2 or 3 ascites,
• Those patients with ascites admitted to the hospital for any intercurrent complication.
• Ascitic absolute polymorphonuclear leukocyte (neutrophil) count and total protein and albumin concentrations
should always be assessed, along with an ascitic fluid culture.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474

22. Analysis of ascitic fluid
Ascitic fluid culture : innoculate at least 10 mL of ascitic fluid into blood culture bottles
immediately after paracentesis.
Ascitic neutrophil count higher than 250/mm is diagnostic of SBP
Ascitic fluid protein less than 1.5 g/dI is also associated with an increased risk of developing SBP.
• SBP - culture is expected to be monomicrobial.
• Secondary bacterial peritonitis - polymicrobial
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1474

23. Analysis of ascitic fluid
If the SAAG is 1.1 g/dL (11 g/L) or greater, the patient can be considered to have portal
hypertension with an accuracy of approximately 97%.
SAAG is an accurate index of portal hypertension.
Serum-ascites albumin gradient (SAAG) : by subtracting the ascitic fluid albumin from the serum
albumin.
A sensitive and specific measurement to determine whether ascites is related to portal
hypertension
• Secondary bacterial peritonitis -
A. Ascitic fluid glucose nearly zero (normally equal to serum glucose)
B. Ascitic fluid LDH markedly increased
C. Gram stain - polymicrobial
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1476

24. Analysis of ascitic fluid
Ascitic fluid cytology should be performed if malignancy is suspected,
Cytology is likely to be positive in patients with peritoneal tumor but not in those with tumor
limited to the liver.
Levels of pancreatic enzymes or mycobacterial culture : if pancreatic or tubercular cause
respectively, is suspected
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1476

25. Management

26. Management of ascites in cirrhosis
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
The absence of these complications defines ascites as uncomplicated.
Complicated ascites - if refractory ascites, SBP, or HRS.

27. Management of uncomplicated ascites
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
Aim - Negative sodium balance.
Uncomplicated ascites can be managed in an outpatient setting.
A. Reducing sodium intake
B. Increasing renal sodium excretion with diuretic treatment.

28. Management of Grade 1 ascites
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
Guidelines recommend no treatment for patients with grade 1 ascites.

29. Management of Grade 2 ascites
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
A negative sodium balance with loss of ascites can be easily obtained in most cases by
reducing dietary sodium intake and increasing renal sodium excretion with diuretics.
Grade 2 Ascites -
• Moderate renal sodium retention.
• Baseline urine sodium excretion greater than 20 mEq/L.
• Normal GFR without impairment of solute-free water excretion.
A. Bed rest is not recommended.
B. Fluid restriction is not necessary, unless patients have associated hyponatremia.

30. Sodium Restriction
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
Dietary sodium intake - moderately restricted to 80 to 120 mEq/day (approximately 4.6 to 6.9
g of salt per day)
Equivalent to a “no-added salt” diet with the avoidance of preprepared meals.
Cirrhotic patients -
• who has never developed ascites - No prophylactic dietary sodium restriction.
• first episode of grade 2 ascites - dietary salt restriction alone may lead to the resolution of
ascites
A. More severe restriction in sodium intake is not recommended
B. May lead to diuretic-induced hyponatremia.

31. Diuretics
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
If no response or hyperkalemia develops, add furosemide, 40 mg/day, increasing in a
stepwise manner to a maximum dose of 160 mg/day
Recurrent ascites:Combination diuretic treatment with spironolactone and furosemide (same
doses as above )
First episode of ascites:
Spironolactone, 100 mg/day; increase in a stepwise manner every 72 hr according to treatment
response to a maximum dose 400 mg/day

32. Monitoring
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
Once ascites has been mobilized, continue a low-sodium diet and the minimum diuretic dose
necessary to avoid reaccumulaton of ascites.
Daily body weight (recommended body weight loss is up to 0.5 kg/ day in patients without edema
and 0.5-1 kg/day in patients with ascites and edema

33. Management of Grade 3 ascites
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
Postparacentesis circulatory dysfunction (PPCD) syndrome - if done without plasma volume
expansion.
After LVP of more than 5 L, plasma volume expansion should be performed with the
administration of IV 20% albumin (8 g/L of ascites removed).
Treatment of choice - Large volume paracentesis
• Coagulopathy is not a contraindication.
• Contraindications - severe coagulopathy (e.g. DIC), abdominal skin infection at the puncture
site or severe bowel distention.
A. Administration of albumin after LVP is more cost eftective than use of other plasma expanders, because the
administration of albumin is associated with a reduction in the rate of complications of cirrhosis in the
subsequent month.

34. Management of Grade 3 ascites
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
Diuretic -
• Minimum doses of diuretics is recommended
• If the patient has not received diuretic treatment previously, start with spironolactone, 100
mg/day, and furosemide, 40 mg/day.
Diet -
• Low-sodium diet (80-120 mEq/day)
A. If the patient was receiving diuretic treatment, restart diuretics at a higher dose.
B. If there is no response to treatment, assess the patient's sodium intake for adherence to a low-sodium diet,
and increase the diuretic doses progressively to a maximum of spironolactone, 400 mg/day, and furosemide,
160 mg/day.

35. Complications of Diuretic Therapy
• Acute kidney injury - Circulatory dysfunction leading to renal hypoperfusion.
• Hepatic encephalopathy -
• Electrolyte imbalance -
Hyponatremia -
• Inhibition of Na-K-Cl cotransporter by loop diuretics.
• Hypovolumia leads to Argentine - vasopressin release (solute free water retention)
Hypokalemia - Loop diuretics can lead to potassium and magnesium depletion.
Hyperkalemia - Due to anti-mineralocorticoids.
• Painful gynecomastia - can reduce the dose of anti-mineralocorticoids, or change the anti-mineralocorticoids drug
like amiloride.
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1479

36. Complications of ascites
• Spontaneous bacterial peritonitis.
• Refractory ascites
• Hepato - renal syndrome
• Hepatic hydrothorax
• Abdominal wall hernias
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477

37. Prophylaxis SBP
Choice of
Antibiotics in SBP
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1480

38. Treatment
Refractory Ascites
Diagnostic Criteria of
Refractory Ascites
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1480
• LVPs
• Albumin
• TIPS
• Diuretics
• Salt restrictions
• Alfa pump system
• Midodrine
There is no evidence that vaptans such as
tolvaptan are ettective in the management of
ascites

39. Transjugular intrahepatic portosystemic shunt
(TIPS)
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1480
• Improves effective blood volume and
kidney hemodynamics
• increase in urinary sodium excretion
• Connects an intrahepatic portal
branch with the outflow of the
hepatic vein
• Frequency of hepatic encephalopathy
is less with the covered stents than
uncovered.
TIPS improves survival in the recurrent ascites
and better control of ascites in the refractory
ascites patients.

40. TIPS not recommended in
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1480
• A serum bilirubin level greater than 3 mg/dL
• Platelet count less than 75,000/mm3 (and especiall <20,000/mm3)
• TIPS can be detrimental in patients with advanced liver disease.
• More than grade 2 or chronic hepatic encephalopathy
• Multiple hepatic cysts, unrelieved biliary obstruction.
Progressive renal failure, severe systolic or diastolic cardiac dysfunction, or pulmonary hypertension or concomitant
active infection.

41. Alfa pump
system
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1480
• automated pump that moves ascites from the peritoneal
cavity to the urinary bladder,
• High number of device-related adverse events and
complications of cirrhosis, particularly AKI.
Only recommended in patients in whom TIPS is not indicated
• Unlike LVP, it is continuous elimination of ascites from the
peritoneal cavity to the bladder, daily amount can be
programmed through a wireless system.
• Albumin not recommended in these patients.

42. Hepatic Hydrothorax
Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 11th edition, page no. 1477
• Diagnostic thoracentesis - Low protein.
• Treatment - Diuretics, therapeutic thoracocentesis, TIPS, definitive treatment is Liver
transplant.
• Accumulation of fluid in the pleural space of patients with decompensated cirrhosis and
ascites, in the absence of pulmonary, cardiac, or pleural disease.
• Complications - Respiratory failure and spontaneous bacterial infection.
A. Pleurodesis - only recommended in patients who are not candidates for TIPS or LT.

43. Abdominal Tuberculosis
Training Module On Extrapulmonary Tuberculosis 2023, Central TB Division
Bacteriologically Confirmed Case:
• A patient who has a microbiological diagnosis of abdominal TB, based on positive
microscopy, culture or NAAT MTB/RIF.
Presumptive Abdominal TB:
• A patient with abdominal pain, distension, fever, unexplained weight loss, chronic diarrhea or
an abdominal mass.
A. Clinically Diagnosed Case: - A patient with negative microbiological tests but with strong clinical suspicion
and other evidence of abdominal TB, such as compatible imaging, histological findings, ancillary diagnostic
tests or response to anti - TB treatment.

44. Diagnostic Algorithm
Tuberculous Ascites
Training Module On Extrapulmonary Tuberculosis 2023, Central TB Division

45. Diagnostic Algorithm
Tuberculous Ascites
Training Module On Extrapulmonary Tuberculosis 2023, Central TB Division

46. Thank You