This document discusses ascites, which is an accumulation of fluid in the peritoneal cavity. It was first coined by Aulus Cornelius Celsus, a Roman physician from 25 BC to 50 AD. The document covers the definition, pathogenesis, theories of ascites formation, differential diagnosis, management, and laboratory findings of ascites. It discusses how ascites can be caused by portal hypertension, liver damage, infection, or malignancy. Diagnosis involves analyzing ascitic fluid for characteristics like SAAG, cell count, protein level, and LDH to determine the underlying etiology. Management depends on the cause and may include salt restriction, diuretics, beta blockers, paracentesis, or antibiotics.

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