This document presents a case of a 65-year-old male with ascites likely due to alcoholic liver disease. He presented with abdominal distension, fatigue, leg swelling, breathlessness, and jaundice. Examination found abdominal distension, shifting dullness, fluid thrill and other signs of ascites. Lab tests and fluid analysis supported alcoholic cirrhosis as the cause. Treatment included dietary changes, diuretics, and therapeutic paracentesis for fluid removal and management of complications from ascites.

1. Ascites Clinical Review
with Case
Presenter: Dr Ranjit Kumar Shah
BPKIHS,Dhran (JR-2 GP & EM)

2. 65 years old male active alcohol consumer, and smoker
presented with
CHIEF COMPLAINTS :
• Distention of abdomen since 6 months
• Fatigue since 4 months
• Swelling of both legs since 15 days
• Breathlessness since 15 days
• Yellowish discolouration of both eye and dark colour urine since 1
weeks

3. HISTORY OF PRESENT ILLNESS:
• Patient was apparently healthy 6 moths ago. Then when
noticed distention of abdomen which was insidious in onset
and gradually progressive.
• Swelling of both legs below knee since 15 days. It started at
ankles and gradually progressed up to knee. Not associated
with pain.
• Fatigue since 4 months which is gradually worsening and for
last 3 months he is not attending his duties.
• Breathlessness without wheeze since 15 days.

4. • Yellowish discoloration of both eye and dark colour urine since 1 weeks.
Decreased frequency of urination since 1 weeks is 2-3 times per days. There
is no history of generalized itching 0r pale stools
No history of fever
No history of abdominal pain.
No history of passage of black tarry stool.
No history of facial puffiness, hematuria and passage of frothy urine.
No history of chest pain, palpitation
No history of alter sensorium, unconscious , slurring of speech.

5. PAST HISTORY:
• K/C/O Chronic Liver Disease (Ethanol induced)
• H/O UGI bleed.
• H/O blood transfusion
• No H/O Type 2 DM, HTN and TB.
Drugs History :
For last 5 months he taking diuretics
• No known allergic history of any drugs

6. PERSONAL HISTORY:
• Decreased appetite.
• Irregular bowel & bladder habits.
Habits : 18 Unit (180 grams) per days 15 years
( 1-1.5 liter of jaad per day).
• Disturb sleep.

7. Generally considered safe.
14 units/week in women
21 units/week in men
The threshold for developing alcoholic liver disease :
Men (>14 drinks per week)
While women >7 drinks per week

8. Amount of alcohol in an average drink
Alcohols type % Alcohol
Beer / Tanaba 4 – 8 %
Wine / Jaad 8 – 12 %
Vodka / Rum / Gin /
Whisky /Raksi
1 drink = 14 g
30 – 45 %
1 Unit = 10 g

9. Quantity and duration
Most important risk factors involved in the
development of alcoholic liver disease.
Women :>20 g/d (increased susceptibility alcoholic
liver disease.
men : 80 g/d for 3-5 years Alcoholic hepatitis
160 g/d for 10–20 years causes hepatitis or cirrhosis.

10. PHYSICAL EXAMINATION:
Vitals
•BP= 90/60 mmHg
•Pulse = 115 bpm
•RR = 18 cycles/ min
Jaundice : (+)
Pallor : (+)

11.  Spider naevi (+) over chest 5
 Abdomen grossly distended.
Umbilicus hernia (+)
Umbilicus centrally everted.
Enlarged veins in the abdominal wall.
Bulging flanks.
No scar marks.
Edema : (+) b/l lower limb

12. ABDOMINAL EXAMINATION
Inspection :
Generalized distention abdomen, flanks appear full.
Umbilicus hernia (+)
Umbilicus centrally everted.
Enlarged veins in the abdominal wall
No scar marks.
Palpation :
• Superficial: No guarding and rebound tenderness.
• Deep: spleen is palpable 2 cm below left costal margin, no tenderness

13. Percussion
• Liver dullness –upper border of liver in 5th -11st intercostal space in
midclavicular line, lover border could not be appreciated.
• Splenic dullness - beyond the 11th intercostal space , spleen edge
palpated >2 cm below the costal margin
• Shifting dullness (+)
• Fluid Thrill = (+)

14. • Percussion
Shifting dullness (+)
With the patient lying flat, percuss in a straight line from the umbilicus towards the left
flank, until a dull percussion note is detected.
Keeping a finger in the same spot, ask the patient to roll towards you.
Wait for 10 seconds and percuss again in that spot.
If the note is now resonant, the fluid has shifted, indicating the presence of ascites
• Fluid Thrill = (+) Taps the flank with one hand, while the other hand feels for an impulse
on the opposite flank.

15. • Auscultation
• Normal bowel sound (5- 8/min)
• No venous hump ,friction rub and bruit sound heard.

16. SYSTEMIC EXAMINATION
• SYSTEMIC EXAMINATION
Resp : B/L basal crept.
Decreased air entry of right side lung.
CVS : S1S2Mo
• CNS : Patient oriented to time, place and person.
GCS : E4/V5/M6 15/15

17. Rectal examination
• On Digital Rectal Examination : (DRE)
Brown color stool no bloody.
Based on history :
Based on examination:
I consider him to be having Asciteswith Jaundice & Anemia
most likely due to Ethanol induced decompensated
Chronic liver Disease.

18. Ascites
Ascites is pathological accumulation of fluid within the peritoneal cavity
resulting in abdominal distention.
• Most common is portal hypertension
related to cirrhosis.
 What r the causes of abdominal
distention ?????

19. Causes of Ascites
Ascites can be classified based on the underlying pathophysiology:
1. Portal hypertension
– Cirrhosis
– Alcoholic hepatitis
– Acute liver
– Hepatic veno occlusive disease (e.g., Budd-Chiari synd.)
– Heart failure
– Constrictive pericarditis
– Hemodialysis-associated ascites (nephrogenic ascites

20. 2. Hypoalbuminemia
– Nephrotic syndrome
– Protein-losing enteropathy
– Severe malnutrition
3. Peritoneal disease
– Malignant ascites (e.g., ovarian cancer, mesothelioma)
– Infectious peritonitis (e.g., tuberculosis or fungal infection)
– Eosinophilic gastroenteritis
– Starch granulomatous peritonitis
– Peritoneal dialysis

21. Pathophysiologic
• Increased hydrostatic pressure .
• Increased capillary permeability.
• Decreased protein/albumin.

22. Hypoalbuminemia

23. History
About 85% of patients with ascites have cirrhosis, Past history of
cancer, heart failure, or TB.
Symptoms:
Abdominal distension:
• Painless or with abdominal discomfort
• Course of days (e.g. bloody ascites due to trauma) or months (e.g.
malignant ascites)

24. Clinical Presentation
Weight gain, shortness of breath, early satiety, and
dyspnea due to fluid accumulation and increased
abdominal pressure.
Spontaneous bacterial peritonitis
fever, abdominal tenderness, and altered
mental status.

25. Diagnosis of ascites
Physical examination
Shifting Dullness
Fluid Thrill
Puddle’s sign
Imaging
Ultrasound abdomen

27. International Ascites Club Grading system
Grade 1 – Mild ascites detectable only by ultrasound examination,
Grade 2 – Moderate ascites manifested by moderate symmetrical
distension of the abdomen.
Grade 3 Large or gross ascites with marked abdominal distension
with respiratory distress.

28. Older system grades
1+ is minimal and barely detectable,
2+ is moderate.
3+ is massive but not tense.
4+ is massive and tense.
Refractory ascites :
Ascites that cannot be mobilized or recurrence of
ascites not prevented by medical therapy
Diuretic resistant

29. Investigation
• Ascites fluid analysis
• CBC ,Blood grouping
• RBS
• Urea, Creat, Na/k
• LFT ,PT/INR ,BT & CT
• USG abdomen
• Serology
• Chest X ray

30. Ascites fluid Analysis
• Diagnostic paracentesis
• Gross Appearance of fluid
• SAAG
• Ascites fluid R/M/E
• Ascites fluid LDH & ADA
• Ascites Grams stain, C/S
• Ascites Cytology & Amylase

31. Diagnostic paracentesis

32. Contraindication
• Mild hematologic abnormalities , if risk of bleeding may be
increased.
Prothrombin time > 21 seconds
INR > 1.6
Platelet count < 50,000 per cubic millimeter
• Absolute contraindication : acute abdomen require surgery.
• Relative contraindication :
Pregnancy
Distended urinary bladder
Distended bowel

34. Serum-to-ascites albumin gradient (SAAG)
Accurately identifies the presence of portal hypertension and
More useful than the protein-based exudate/transudate
concept.
• SAAG ≥1.1 g/dL (≥11 g/L) predicts portal hypertension with 97
percent accuracy .
• SAAG <1.1 g/dL (<11 g/L) indicates that patient does not have portal
hypertension .

35. Serum-to-ascites albumin gradient (SAAG)
Ascites total protein
Serum Albumin - ascites albumin
Low S. Albumin High A. Albumin

36. Ascites fluid R/M/E
TLC and DLC single most helpful test performed on
ascitic fluid to evaluate for infection.
Polymorphonuclear count ≥ 250/mm3
TLC ≥ 500/mm3
– spontaneous bacterial peritonitis.

37. Culture
Bacterial cultures of ascitic fluid should be sent from patients with
New onset ascites
Admitted with ascites Who deteriorate with
– Fever
– Abdominal pain
– Azotemia,
– Acidosis
– confusion
Gram stain
 When SBP is suspected. Both Gram +ve &-ve staining in
peritonitis due to perforated viscus)

39. Protein, Glucose, LDH
Patients with a Protein value less than 1 g/dL have a high risk
of SBP.
Distinguishing SBP from bowel perforation.
If neutrophil ≥250 cells/mm3 and meets two out of the
following three criteria are unlikely to have SBP and
immediate evaluate to bowel perforation .
1. Total protein >1 g/dL
2. Glucose <50 mg/dL (2.8 mmol/L)
3. LDH greater than the upper limit of normal for serum

40. bowel perforation
100 IU/L

41. Triglyceride concentration
Triglyceride > 200 mg/dL and usually greater than
1000 mg/dL (11.3 mmol/L) .
Abdominal malignancy , Lymphatic abnormalities
Also cirrhosis

42. Tests for tuberculous peritonitis
• Direct smear : Only 0 to 2 % sensitivity for detecting mycobacteria
• Culture : When one liter of fluid is cultured, sensitivity for
Mycobacteria reportedly reaches 62 to 83 percent .
• Peritonea scopey : with culture of a biopsy specimen has a
sensitivity for detecting tuberculous peritonitis that approaches
100 % . Fluid and tissue can be sent for PCR for tuberculosis .

43. Cell count :
• Tuberculous peritonitis can mimic the culture-negative variant of SBP, but
mononuclear cells usually predominate in tuberculosis.
Adenosine deaminase :
• Non-culture method of detecting tuberculous peritonitis, however,
patients with tuberculous peritonitis who also have cirrhosis usually
have falsely low values . This test is useful in countries such as India,
but it is very limited in United States because most patients in the
United States with tuberculous peritonitis also have cirrhosis .

44. Cytology
Almost 100 % positive cytology. In peritoneal carcinomatosis.
The remaining patients have massive liver metastases,
chylous ascites due to lymphoma, or hepatocellular
carcinoma; these patients usually have negative cytology .
Sensitivity of cytology is 58 to 75 % .

45. Serum pro-brain natriuretic peptide concentration :
• Significantly higher in heart failure compared with cirrhosis,
with very little overlap BNP 166 pg./mL
• Patients with both heart failure and cirrhosis
BNP values in the heart failure range.

46. Ascites : Treatment
Goals:
Minimize ascitic volume and peripheral edema
Avoid intravascular volume depletion
Benefits:
◦ Patient comfort
◦ Reduced risk of hernia formation
◦ Possible reduction in SBP
◦ Improve nutrition

47. Management of uncomplicated ascites
Patients with cirrhosis and ascites are at high risk for other
complications of liver disease, including:
1. Refractory ascites,
2. SBP
3. Hepatorenal syndrome .
The absence of these ascites-related complications qualifies
ascites as uncomplicated.

48. 1-Medical
A. Abstinence of alcohol.
B. Diet.
C. Diuretics.
D. Therapeutic paracentesis
2-Surgical
A. TIPS
B. Liver transplantation
C. Peritoneovenous shunting

49. A. Abstinence from alcohol.
Tab. Baclofen 5 mg 3 times per day for 3 days.
10 mg 3 times per day.
Dose can be increased further as needed
until the craving.
Up to 95 mg daily in five divided doses.

50. Grade 1 – Mild ascites
A mainstay of treatment ascites restrict dietary sodium intake to 88
mEq (2g) per day (including all foods, liquids, and medications)
Grade 2 – Moderate ascites
1.) Spironolactone 100–200 mg/day
(Starting at 100 mg/day and increasing stepwise every 7 days (in 100 mg steps) to a
maximum of 400 mg/day if there is no response )
PLUS
2.) furosemide 40–80 mg/d, particularly in patients who have
peripheral edema.
(In patients who do not respond to aldosterone antagonists, as defined by a reduction of body
weight less than 2 kg/ week, or in patients who develop hyperkalemia, furosemide should be
added at an increasing stepwise dose from 40 mg/day to a maximum of 160 mg/day (in 40 mg
steps)

51. All diuretics should be discontinued if there is
1. Severe hyponatremia (serum sodium concentration <120 mmol/L)
2. Progressive renal failure
3. Worsening hepatic encephalopathy,
4. Incapacitating muscle cramps
Furosemide should be stopped if severe hypokalemia (<3
mmol/L).
Aldosterone antagonists should be stopped if patients
develop severe hyperkalemia (serum potassium >6 mmol/L)

52. Diuretics are generally contraindicated in patients with overt hepatic
encephalopathy .
Gynecomastia is common side effect of aldosterone antagonists, but it
does not usually require discontinuation of treatment.
• Patients who experience spironolactone side effects (e.g., Hyperuricemia
Hyperkalemia & painful gynecomastia),
Oral Amiloride may be given at 10 mg per day.

53. Grade 3 Large or gross ascites
A. Therapeutic paracentesis :
Removal of 4 - 5 liters, less than 5 liters of fluid albumin does not
necessary . (to reduce intra-abdominal pressure and relieve the associated dyspnea,
abdominal pain, and early satiety.
With 15-16G)
B. Large-volume paracentesis (LVP) : is the first-line therapy in
patients with large ascites (grade 3 ascites) .
Removal of >5 liters of ascitic fluid need for colloid replacement after
a therapeutic paracentesis remains controversial
Albumin (6 to 8 g/L of fluid removed)

54. Prevention of post- paracentesis circulatory
dysfunction:
Terlipressin (1 mg every 4 hours for 48 hours).
Initial studies suggest that terlipressin is as effective as albumin
for this purpose.
Use of plasma expanders other than albumin is not recommended
because they are less effective in the prevention of post-
paracentesis circulatory dysfunction
After LVP, patients should receive the minimum dose of diuretics
necessary to prevent the re-accumulation of ascites.

55. • There are no data to support the use of fresh frozen plasma or
pooled platelets before LVP, yet in many centers these products are
given if there is severe coagulopathy (prothrombin activity less than
40%) and/or thrombocytopenia (less than 40,000).

56. Refractory ascites :
Ascites that cannot be mobilized or
the early recurrence of which
(i.e. After LVP) cannot be prevented
by medical therapy.

57. • Recent studies have shown that : while managing the ascites , with
TIPS. does not improve survival in these patients. Unfortunately, TIPS
is associated with an increased frequency of hepatic encephalopathy.
• Prognosis for patients with cirrhosis and ascites is poor, and some
studies have shown that <50% of patients survive 2 years after the
onset of ascites.
• There should be consideration for liver transplantation in patients
with the onset of ascites.

58. COMLICATION OF ASCITES
1. SPONTANEOUS BACTERIAL PERITONITIS
2. HEPATORENAL SYNDROME
3. Hepatic Hydrothorax

59. SPONTANEOUS BACTERIAL PERITONITIS
Common and severe complication of ascites due to spontaneous
transmigration gut bacteria (single pathogen) into peritoneal cavity.
C/F:
fever, altered mental status,
Abdominal pain or discomfort.
Inv. Ascites Fluid:
Neutrophil ≥250 cells/mm3
Total protein >1 g/dL
Culture : M.C Escherichia coli

60. Patients with cirrhosis and ascites severe enough for hospitalization.
SBP can occur in up to 30% of individuals.
 Hospitalization patient mortality rate 25%.
Treatment : (Empiric antibiotic therapy)
Third-generation cephalosporin :
 IV Cefotaxime 2 g every eight hours for 7 days .OR
 Oral Norfloxacin 400 mg BD for 7 days (in inpatients without prior exposure to
quinolones, vomiting, shock, grade II (or higher) hepatic encephalopathy, or serum creatinine >3
mg/dL.)

61. PMN counts ≥250 cells/mm3 and clinical suspicion of SBP,
Serum creatinine >1 mg/dL,
Blood urea nitrogen >30 mg/dL, or
Total bilirubin >4 mg/dL
Give IV albumin 1.5 g /kg within 6 hours of detection.
F/b 1.0 g/kg on day three.

62. Prophylaxis for recurrent SBP
Patients who have survived an episode of SBP should receive:
Long-term prophylaxis with
Oral norfloxacin 400mg OD.
Oral Ciprofloxacin 750 mg/wkly

64. HEPATORENAL SYNDROME
Form of functional renal failure without renal pathology that occurs in
about 10% of patients with advanced cirrhosis or acute liver failure.
Marked disturbances in the arterial renal circulation.
Renal vasoconstriction is most due to under-filling of
the arterial circulation.
• Diagnosis is made usually in the presence of a large amount of
ascites in patients who have a stepwise progressive increase in
creatinine.

66. Type 1 hepatorenal syndrome
Progressive impairment in renal function and a significant reduction in
creatinine clearance within 1–2 weeks of presentation .
Rapid rise of the serum creatinine > 2.5 mg/dl.
At the time of diagnosis, some patients with type 1 hepatorenal
syndrome have a urine output less than 400 to 500 mL per day .
Very poor prognosis (without treatment survival is less than 1
month) .
There is usually no proteinuria
Urine sodium excretion of < 10 mmol/24 hrs.
Urine/plasma osmolarity ratio of > 1.5 .

67. TREATMENT
Difficult to treat” in the past,
Dopamine or Prostaglandin analogues were used.
(Studies have failed to show clear-cut benefit from these therapeutic approaches.)
1. Currently treated with:
Midodrine, an α-agonist, along with
Octreotide and intravenous albumin
(effective in about two-thirds of patients.)
2. TIPSS is an effective treatment in appropriate patients.
3. Liver transplantation.

68. Hepatic hydrothorax
Presence of a pleural effusion (usually >500 mL) in a patient with
cirrhosis who does not have other reasons to have a pleural effusion
(e.g., cardiac, pulmonary, or pleural disease).
Chest tube insertion is contraindicated.
First-line therapy dietary sodium restriction and diuretics
• TIPS Second-line treatment for hepatic hydrothorax once it becomes
refractory to sodium restriction and diuretics.

69. Take home message
• Ascites is the most common decompensating event in cirrhosis
• Its pathophysiology is mostly explained by splanchnic and peripheral
vasodilatation that lead to a decrease in effective blood volume.
• Most patients respond to diuretics.
• Patients who no longer respond with diuretic should be treated with
repeated large volume paracenteses. Trans jugular intrahepatic
portosystemic shunt (TIPS) should be considered in those requiring
frequent paracenteses.

70. Reference
• Harrison internal medicine 20 ed.
• Upto Date
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