Overview of Ascites

1. DR. SAI LAKSHMIKANTH BHARATHI
De Medicina

2. Aulus Cornelius Celsus
Roman
25 B.C to 50 A.D
Coined “ASCITES” ; askites – baglike
(Greek)

3. Definition
Pathogenesis & theories of ascites
formation
Approach
Differential Diagnosis
Management

4. Accumulation of fluid in the peritoneal
cavity
Hydroperitoneum
Hydraskos or abdominal dropsy

6. Similar to edema formation
I. Increased hydrostatic pressure
II. Reduction in colloid osmotic pressure
III. Disturbance of capillary permeability
IV. Insufficiency of lymphatic drainage

7. Portal hypertension
IVC obstruction
Anatomic disruption of Hepatic veins

9.  Minimum albumin concentration – 2.5 to
3g/100ml
 Decreased albumin production
 Increased excretion of albumin
Hypoalbuminenia + Portal HTN- a pre-requisite for
ascites

10. Trauma
Inflammation
Immune mediated

11. Mesentric lymph adenopathy
Parasitic lymphatic obstruction

12. Underfill theory
Overflow theory
Lymph imbalance theory
Vasodilation theory

13. Primary
• Imbalance of Starling’s forces
• Reduced effective plasma volume
• Stimulation of Volume receptors,RAAS &
sympathetic system
• Increased circulating ADH levels
• Increased Sodium reabsorbtion and
reduced GFR
• Ascites formation
Lymphatic insufficiency
secondary to portal HTN
Opening of
Portosystemic shunts
Decreasing PVR
Formation or
breakdown of
vasodilatory substances

14. Primary
• Liver damage
• Portal hypertension sends salt retaining signal
• Retention of Sodium
• Volume expansion
• Overflow from Intravascular volume
• Ascites formation

15. Do not explain in each case
Both theories not mutually exclusive
Doesn’t effectively explain the initial event

16. Contradicts “classical” theories
Extravasation from intravascular
space
(Lymph Production)
Reflux into vascular system
(Lymphatic Drainage)

17. Obliteration of diaphragmatic lymphatics
Dilated lymphatic vessels – reduced flow
Limited lymph kinetics at the communion
of lymphatics and venous systems

18. • Portal Hypertension
• Peripheral vasodilation
• Plasma volume reduction
• Volume retention
• Salt retention
• Plasma volume expansion
• Ascites formation

19. Clinical features
Laboratory findings

20. Is the distension due to Ascites??
Acute or Chronic??
Possible etiological factors??
Grade of Ascites??

21. Manifest ascites – 1.5 to 2 liters
Puddle sign 100-150 ml
Shifting dullness 1-1.5 liters
Fluid thrill >2 liters

23. Colour
Cell count & Differential
Protein
Sugar(Glucose < 50g/dL – Bacterial infection)
LDH
Bacteriology-Culture & Gram Stain, TB
ADA

24. Clear and straw coloured
Turbid
Hemorrhagic
Chylous

25. Exudate ->1000/cu.mm; Transudate <
250cu.mm
PMN > 250/cu.mm – Bacterial
Lymphocytes >20% of Total Counts – TB
(also Ascitic:Blood Glucose <0.7)

26. SAAG – Serum albumin: Ascitic Albumin
>1.1 – Ascites secondary to Portal
Hypertension
<1.1 – Malignancy or Inflammation
Transudate Exudate
Protein <2.5g/L Protein >2.5g/L
Specific Gravity <1,015 Specific gravity >1,016

27. Gram stain
Culture – Aerobic and anaerobic
AFB staining
PCR for Tuberculosis

28. Ascites:serum <1.4 – portal hypertension
Absolute value >400 IU/L

29. Ferritin
Fibronectin
Cholesterol
α1- antitrypsin

30. Parameters Portal hypertension Infectious etiology malignancy
Clinical
features
Splenomegaly, spider
naevi, jaundice,
Dupytren’s
contracture
Fever, tenderness,
guarding..
Sister Mary Joseph
nodules,
Troisier’s sign
Loss of weight
SAAG
Protein
>1.1
<2.5g/dL
<1.1
>3g/dL
<1.1
>3g/dL
Cell count <250cells/cu.mm >1000cells/cu.mm >>1000cells/ cu.mm
Ascites:
Serum LDH
<1.4 >1.4 >>1.4
Color Clear Clear to turbid Clear, turbid,
hemorrhagic or
chylous

31. Portal hypertension
Infective etiology
Malignancy

32. Salt restriction
Diuretics
Beta blockers
Aldosterone antogonist
Paracentesis

33. Based on culture & sensitivity
Empirically, cefotaxime 2g IV q12h for min.
5 days
Alternatively, Oral ofloxacin 400mg q12h
ESBL antibiotics and aminoglycosides-
avoided

34. Norfloxacin daily;
At risk -ascitic fluid protein <1g/dL, UGI
bleed, previous SBP