4. Causes of ascites:
A) Generalized Causes:
1) Hepatic e.g. liver cirrhosis/Chronic Liver Dz.
2) Cardiac e.g. congestive heart failure.
3) Renal e.g. nephrotic syndrome.
4) Nutritional e.g. severe malnutrition.
5. Causes of ascites:
B) Local causes:
1) Abdominal malignancy: mesothelioma or peritoneal
metatasis.
2) TB peritonitis.
3) Bacterial or fungal peritonitis.
6. Classification of ascites:
Ascites is better classified as:
1) Portal hypertensive ascites: serum ascites albumin
gradient (SAAG) more than 1.1 g/dl. e.g. hepatic and
cardiac.
2) Non-portal hypertensive ascites: SAAG <1.1 g/dl in renal,
malignant and inflammatory (TB) ascites.
7. Types of ascites:
Differential criteria between transudate and exudate
ascites:
Exudate
Transudate
Item
> 1017
< 1017
Specific gravity
> 2.5 g/dl
< 2.5 g/dl
Protein contents
> 0.5
< 0.5
Protein ascites/serum ratio
> 200 IU/L
< 200 IU/L
Lactic dehydrogenase
In association with
infections, malignancy, or
connective tissue diseases
Cases of generalized
anasarca due to hepatic,
renal and nutritional
causes
Causes
11. Clinical manifestations:
A) Symptoms:
• Insidious onset.
• Increased abdominal girth.
• Recent weight gain.
• Shortness of breath.
• Early satiety.
• Generalized abdominal pain.
12. Clinical manifestations:
B) Signs:
• Physical signs suggestive of cirrhosis and portal
hypertension (e.g., spider navei, palmar erythema,
splenomegaly, or flapping).
• The patient is sallow, muscle wasting is profound, and the
thin limbs with protuberant belly lead to the description
of the patient as a spider man.
13. Clinical manifestations:
B) Signs:
• The abdomen is enlarged (mainly in the flanks), the
umbilicus is everted, protrusion of hernias, visible or
distended abdominal wall veins (portal & IVC collaterals),
the latter disappeared when ascites is controlled.
Abdominal striae may develop.
• Ascites is mainly detected by percussion.
14. Clinical manifestations:
C) Associations:
• Pleural effusion: due to diaphragmatic defect allowing
ascites to pass into the pleural cavity, mainly right sided.
• Oedema usually follows ascites.
15. Investigations:
A) Ultrasonography:
• It detects minimal ascites, encysted ascites.
• It shows the size of the liver, spleen, portal vein diameter,
thus it can diagnose portal hypertension.
• It shows the echopattern and surface of the liver and thus
can diagnose liver cirrhosis and tumours.
16.
17. Investigations:
B) Diagnostic paracentesis:
• Parameters:
physical: color, aspect.
Chemical: proteins, albumin (for SAAG).
Cells: WBCs (PMNLs or lymphocytes), RBCs.
Bacteriological: culture and sensitivity.
18. Investigations:
Diagnostic paracentesis: Cirrhotic ascites
straw, clear
transudate (proteins <2.5 gm/dL)
SAAG is > 1.1 g/dL.
WBCs: usually less than 100/mm3 with a predominance
of mononuclear cells and a low number of PMNLs.
23. Investigations:
C) Plain X-ray abdomen:
• shows diffuse ground glass appearance.
D) Laparoscopy:
• It is highly diagnostic for TB lesions allowing biopsy,
histopathology and culture which settles the diagnosis
beyond doubt. Laparoscopy also show clearly the spleen,
liver and allow for aimed biopsy if needed.
26. Treatment of cirrhotic ascites:
1. Bed rest.
2. salt restriction.
3. Diuretics: spironolactone (100 up to 400 mg/day)
,frusemide (40 up to 160 mg/day).
4. Therapeutic paracentesis is generally a 2nd line treatment
except for patients with marked and refractory ascites.
27. Refractory ascites:
Definition: ascites that cannot be mobilized or prevented
from recurring by medical therapy. It is divided into:
• Diuretic-resistant: ascites is not mobilized despite
maximal diuretic dosage.
• Diuretic-intractable: development of diuretic-induced
complications that preclude the use of an effective
diuretic dosage.
28. Refractory ascites:
• Dietary history, use of NSAIDs, ACEIs or ARBs, and patient
compliance with the treatment regimen must be reviewed
before confirming the diagnosis.
29.
30. Treatment of refractory ascites:
1. Repeated large volume paracentesis (LVP) with or without
IV salt free albumin.
2. TIPS should be considered 2nd line treatment, and
reserved for patients who require frequent LVP.
3. Liver transplantation.
35. SBP – Antibiotic Therapy I
Initiate for PMN≥250/mm3
IV Cefotaxime 2g q8 hours or Ceftriaxone 2g
q24hours
Duration of therapy unclear
2 weeks suggested if Blood cultures(+)
If repeat paracentesis at 48 hours shows
PMN≤250/mm3, then 5-7 days of treatment may be
adequate
36. SBP – Antibiotic Therapy II
Prophylactic antibiotics should also be prescribed
indefinitely until ascites has eliminated
Options include:
-Bactrim DS 1 tab po 5 days/week
-Cipro 750mg po q week