Ascitic fluid- pathogenesis

Intro…..
• Def : pathological acuumulation of fluid in ascetic fluid in
peritoneal cavity
• More than 25ml in adults
• Incidence –
• Cirrohosis - 44%
• Presinusoidal PHT – 10-12%
• Postsinusoidal PHT – 80%
• ALF – 50%
• AVH – 10%
Etiology
• Hepatic –
• CLD
• Portal hypertention
• Postsinusoidal – Budd-Chiari syndrome, IVC obstruction, HVOTO
• Sinusoidal – HBV,HCV,WILSONS,AUTOIMMUNE, BILIARY OBSTRUCTION
• Presinusoidal – Intrahepatic: CHF,NCPF, Extrahepatic : EHPVO
• TRAUMATIC – Liver injury sec to accidents, liver biopsy
• Biliary – perforation of bile duct
• Pancreas – Anterior disruption of pancreatic duct, rupture
of pseudocyst
Etiology (cont…)
• GIT – Perforation , Appendicitis
• Peritoneal – TB, pseudo ascities- omental cyst, RP lymphngioma
• Renal – Nephrotic syn, PD
• Haematological – hemolysis , tumors
• Lymphatic – primary intestinal lymphangectasia
• Cardiac – CCF, arrhythmia
• Vasculitis – HSP , SLE
• Infections – dengue fever , typhoid , leptospirosis, scrub typhus
Etiopathogenesis
• Broadly classified into

• Non cirrhotic ascities

• Cirrhotic ascities
Non cirrhotic ascities
• Hepatic causes –
• A . Acute Viral hepatitis –
1. Transient PHT due to sinusoidal collapse
2. SBP
3. Hypoalbuminemia
• B . Postsinusoidal PHT
• When the hydrostatic and osmatic pressures with in hepatic capiullaries produces
shift of fluid from blood to lymphatics at rare which exceed its drainage capacity
• C. presinusoidal PHT
• Rare
• May occur following haemorrhage or depressed hepatocellular function
Non cirrhotic ascities
• Pancreatic ascities
• Leakage from duct or rupture of pseudocyst
• Sec to chemical burn
• Biliary
• Leakage
• Tuberculous ascites / Malignancy
• Peritonial tubercles secrete proteinaceous material which cause
osmatic drag presented as diffuse or loculated ascities
• Chylous ascities
Non cirrhotic ascities
• Eosinophilic ascities
• In eosinophilic GE
• Eosionophilic infiltration
• Infections
• Third space loss
• Serosities
Cirrhotic ascities
Approach to a child with ascities
• clinical signs
• 1. puddle or Lawson sign- 150ml
• 2. shifting dullness – 500ml
• 3. fluid thrill – 1000ml

• Imaging – usg with doppler, MRI/CT

PARACENTESIS
• Color – transparent , straw colored , bloody , biliary , milky
• Cell count – TLC , PMN
• Staining n culture n sensitivity
• SAAG-
• HIGH (>1.1) – PHT (Diagnostic accuracy 97%), ALF, HYPOTHYRO
• LOW(<1.1) – TB peritonitis, pancreatic ascities, biliary, nephrotic,
serositis
• Special investigations – amylase (AF/serum >0.4) , urea n
creatinine, bilirubin >6mg/dl
Specific investigations
• infection workup
• UGI scopy
Management
• Non cirrhotic ascities – underlying cause
• Cirrhotic ascities –
• Restriction of sodium and fluids
• Na – 1-2meq/kg/day
• Diuretics – spironolactone 2-3mg/kg/day (max 4-6mg/kg)
Furosemide 1mg/kg/day
• Paracentesis – 50ml/kg under albumin cover
Management
• Refractory ascities
• Unresponsive to 1 week of max. dosage of dual therapy
• Shunts
• TIPSS
• PERITONIOVENOUS SHUNTING
• LIVER TRANSPLANT
• NEWER-
• ANP, TERLIPRESSIN, V2 RECEPTOR ANTAGONIST,
ADENOSINE-1 RECEPTOR ANTAGONIST
• PREVENTION OF SBP- NORFLOXACIN 5-7.5MG/KG/DAY
Management
THANK YOU….