Cirrhosis is the most common cause of ascites. The pathogenesis involves splanchnic vasodilatation and portal hypertension leading to increased hydrostatic pressure and exudation of fluid and proteins from the liver into the peritoneal cavity. Diagnosis is confirmed by ultrasound detection of ascites and diagnostic paracentesis. The serum-ascites albumin gradient (SAAG) helps differentiate between cirrhotic and non-cirrhotic causes. Treatment involves salt and fluid restriction along with diuretics. Large volume paracentesis is used for tense ascites.

1. ASCITES
1
MOST PATIENTS
HAVE CIRRHOSIS
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2. Hepatocellular carcinoma
2
 When to suspect?
Sudden
development of
ascites in a stable cirrhotic
patient
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3. Constrictive pericarditis
3
Tuberculosis
One
of the few curable
causes of ascites
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4. Tuberculous peritonitis
4
Very important cause
Curable
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5. Peritoneal carcinomatosis
5
 Protein rich fluid by tumor cells lining
the peritoneum

ECF enters the peritoneal cavity to maintain oncotic
balance
 Tuberculosis

Also causes production of protein rich fluid
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6. Sister Mary Joseph's nodule
6
Hard periumbilical nodule
Metastatic
Pelvic
disease
or gastrointestinal
primary tumor
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10. Virchow's node
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Supraclavicular
adenopathy
GI malignancy
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14. IVC blockage
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Large veins
Back
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15. Portal hypertension
15
 First pathogenetic abnormality in
ascites formation in cirrhosis
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16. Obstruction of hepatic lymphatics
16
Cause exudation of
hepatic lymph from the
surface
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17. Increased hepatic lymph
17
 Normal physiology
 Lymph
 To
produced in the hepatic sinusoids
systemic circulation by the thoracic duct
 When sinusoidal pressures rise
 Lymph
spills over from the surface of the
liver to the peritoneal cavity
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18. PATHOGENESIS OF ASCITES
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 Splanchnic vasodilatation

Chief factor contributing to ascites
 Increased hydrostatic pressure within the
splanchnic capillary bed
 Exudation of lymph from the surface of the
cirrhotic liver
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19. Kidneys
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 Increased sodium and water reabsorption
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20. Hypoalbuminemia
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 Reduced plasma oncotic pressure
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22. PRECIPITATING FACTORS
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1. Excessive salt intake
2. Failure to take drugs
3. Peritoneal infection
4. Worsening of liver disease
5. Hepatocellular carcinoma
6. Portal vein thrombosis
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23. USS
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 Best test to detect even small amount
of ascites
 Can detect as little as 100 mL of fluid
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26. Morrison’s pouch
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
Earliest fluid collection

Hepato-renal pouch
 POD
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28. More than 500 to 1000 mL
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Shifting
dullness
 Fluid thrill
Not very useful
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29. No flank dullness
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Ascites
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unlikely

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33. Paracentesis
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 Final confirmation of ascites
 Best method for diagnosing the
cause
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34. Routine tests on ascitic fluid
34
1. Cell count
2. Albumin
3. Total protein
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35. Optional
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4. Culture
5. Glucose
6. Gram’s stain
7. Amylase
8. Cytology
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36. Cell count
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Single most helpful
ascitic fluid test
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37. WBC count
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 Uncomplicated cirrhotic ascites
 < 500 WBCs/mm3 in
 Absolute neutrophil count
 < 250/mm3 in uncomplicated cirrhotic ascitic fluid
 Empiric antibiotic treatment
 Based on absolute neutrophil count rather than the
culture
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38. Spontaneous bacterial peritonitis
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 Most common cause of an elevated
ascitic WBC count

PMN > 70% of the total WBC count
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39. Elevated ascitic WBC count – other causes
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Tuberculous peritonitis
2. Peritoneal carcinomatosis
Predominance of lymphocytes
1.
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40. SAAG
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 Serum ascites albumin gradient

Serum albumin in g/dL minus ascites albumin in g/dL
 To differentiate cirrhotic ascites from
other causes of ascites

Better than total protein content in the ascitic fluid
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41. High SAAG (> 1.1 g/dL)
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 Uncomplicated cirrhotic ascites
 Serum albumin concentration
At
least 1 g/dL higher than that of the
ascitic fluid albumin concentration.
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42. SAAG - indirect but accurate index of portal
pressure
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 1.1 g/dL or more
 Portal hypertension
Accuracy
97%
 < 1.1 g/dL
 No portal hypertension
Accuracy
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97%

43. Accuracy > 97%
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 Even with
 Ascitic
fluid infection
 Diuresis
 Paracentesis
 IV albumin
 Varying causes of liver disease
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44. High SAAG
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 Does not confirm cirrhosis
Indicates
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portal hypertension

45. Typical of cirrhosis
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4.
SAAG >1.1 g/dL
WBC count < 500 cells/mm3
Predominant lymphocytes
Specific gravity less than 1016
5.
Urine Na low
1.
2.
3.
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46. High gradient (transudative) ascites
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 Right heart failure
Another
common cause
 Nephrotic syndrome
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47. HIGH GRADIENT ≥1.1 g/DL
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 Cardiac


TR
Constrictive pericarditis
 Alcoholic hepatitis
 Massive liver metastases
 Fulminant hepatic failure
 Budd-Chiari syndrome
 Portal vein thrombosis
 Myxedema
 Meigs' syndrome
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48. LOW GRADIENT <1.1 g/DL
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 Peritonitis

TB, Bacterial
 Peritoneal carcinomatosis
 Pancreatic ascites
 Bowel obstruction or infarction
 Biliary ascites
 Postoperative lymphatic leak
 Serositis in connective tissue diseases
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49. Blood-stained ascitic fluid
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 Traumatic tap
 Frequently
clots
 Tuberculous peritonitis
 Hepatoma
 Peritoneal secondaries
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50. Peritonitis
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 Bacterial
 Polymorphonuclear cells predominate
 Gram's stain may be positive
 TB
 Predominant lymphocytes
 Diagnosis
 Granulomas on peritoneal biopsy
 AFB
 Difficult to recover from ascitic fluid
 May take 4 to 6 weeks
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51. CHYLOUS ASCITES
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 Lymphatic obstruction
 Trauma
 Tumor
 TB
 Filariasis
 Cirrhosis
 Nephrotic syndrome
 Congenital abnormalities
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52. Salt restriction
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 Most important treatment of
cirrhotic ascites
 Normal diet contains

5 to 15 grams of sodium chloride
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53. Spironolactone plus furosemide produce a diuresis
in most patients
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 If sodium restriction alone does not
cause diuresis and weight loss
 Spironolactone

Drug of choice
 Furosemide
 Risk
of excessive diuresis
 Hypokalemia
Precipitate
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encephalopathy

54. Fluid intake
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 Restricted only if there is
dilutional hyponatremia
 High
levels of antidiuretic hormone
Diagnosis
Serum
sodium < 130 mEq/L in the
presence of ascites
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55. Large-volume paracentesis
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Treatment of choice for
large-volume ascites
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56. LARGE VOLUME PARACENTESIS
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 Tense ascites
 Respiratory distress
 Poor response to medical
therapy
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59. Hepatorenal syndrome
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 Renal failure
 Profound vasoconstriction in the
renal circulation
Due
to excessive activity of endogenous
vasoactive substances
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60. Hemodynamic hallmark
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 Systemic vasodilation
 Renal vasoconstriction
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61. Clinical hallmarks
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Worsening azotemia
Hyponatremia
Progressive oliguria
Hypotension
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62. Treatment
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 Vasoconstrictor drugs
 Norepinephrine, midodrine,
terlipressin or alpha-adrenergic
agents
 In combination with albumin
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63. Liver transplantation
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Most effective treatment for
hepatorenal syndrome
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64. SBP
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 No obvious primary source of
infection
 Contrast-enhanced CT
To
exclude an intra-abdominal
source for infection
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65. Cefotaxime and an aminoglycoside
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90 %
Monomicrobial
Enteric GNB
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66. What is the diagnosis
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 A 30-year-old male is admitted with mild
abdominal swelling, fever, and loss of weight.
Ascitic fluid shows the following changes.
Macroscopic appearance - hemorrhagic.
Proteins = 3 grams/dl. SAAG = < 1.1 g/dl.
Cells = WBCs in plenty. 70% of cells are
lymphocytes. Few mesothelial cells are also
present. He occasionally takes alcohol. What
is the most probable diagnosis?
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67. Answer
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 TB
 Predominant
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lymphocytes