Ascites

DR. SAI LAKSHMIKANTH BHARATHI

De Medicina

Aulus Cornelius Celsus

Roman

25 B.C to 50 A.D

Coined “ASCITES” ; askites – baglike

(Greek)

Definition

Pathogenesis & theories of ascites

formation

Approach

Differential Diagnosis

Management

Accumulation of fluid in the peritoneal

cavity

Hydroperitoneum

Hydraskos or abdominal dropsy

Similar to edema formation

I. Increased hydrostatic pressure

II. Reduction in colloid osmotic pressure

III. Disturbance of capillary permeability

IV. Insufficiency of lymphatic drainage

Portal hypertension

IVC obstruction

Anatomic disruption of Hepatic veins

Minimum albumin concentration – 2.5 to

3g/100ml

Decreased albumin production

Increased excretion of albumin

Hypoalbuminenia + Portal HTN- a pre-requisite for

ascites

Trauma

Inflammation

Immune mediated

Mesentric lymph adenopathy

Parasitic lymphatic obstruction

Underfill theory

Overflow theory

Lymph imbalance theory

Vasodilation theory

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

Primary

• Liver damage

• Portal hypertension sends salt retaining signal

• Retention of Sodium

• Volume expansion

• Overflow from Intravascular volume


Do not explain in each case

Both theories not mutually exclusive

Doesn’t effectively explain the initial event

Contradicts “classical” theories

Extravasation from intravascular space

(Lymph Production)

Reflux into vascular system

(Lymphatic Drainage)

Obliteration of diaphragmatic lymphatics

Dilated lymphatic vessels – reduced flow

Limited lymph kinetics at the communion

of lymphatics and venous systems

• Portal Hypertension

• Peripheral vasodilation

• Plasma volume reduction

• Volume retention

• Salt retention

• Plasma volume expansion


Clinical features

Laboratory findings

Is the distension due to Ascites??

Acute or Chronic??

Possible etiological factors??

Grade of Ascites??

Manifest ascites – 1.5 to 2 liters

Puddle sign 100-150 ml

Shifting dullness 1-1.5 liters

Fluid thrill >2 liters

Colour

Cell count & Differential

Protein

Sugar(Glucose < 50g/dL – Bacterial infection)

LDH

Bacteriology-Culture & Gram Stain, TB

ADA

Clear and straw coloured

Turbid

Hemorrhagic

Chylous

Exudate ->1000/cu.mm; Transudate <

250cu.mm

PMN > 250/cu.mm – Bacterial

Lymphocytes >20% of Total Counts – TB

(also Ascitic:Blood Glucose <0.7)

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

Gram stain

Culture – Aerobic and anaerobic

AFB staining

PCR for Tuberculosis

Ascites:serum <1.4 – portal hypertension

Absolute value >400 IU/L

Ferritin

Fibronectin

Cholesterol

α1- antitrypsin

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

Portal hypertension

Infective etiology

Malignancy

Salt restriction

Diuretics

Beta blockers

Aldosterone antogonist

Paracentesis

Based on culture & sensitivity

Empirically, cefotaxime 2g IV q12h for min.

5 days

Alternatively, Oral ofloxacin 400mg q12h

ESBL antibiotics and aminoglycosides-

avoided

Norfloxacin daily;

At risk -ascitic fluid protein <1g/dL, UGI

bleed, previous SBP

Health & Medicine

Ascites