APPROACH TO ASCITESDR RUSHIKESH KUTE RUSHIKESH KUTE

NIRMAL HOSPITAL PVT LTD SURATNIRMAL HOSPITAL PVT LTD SURAT

Definition

-Ascites is of greek derivation(askos) which refers to bag or sack

-The word describes pathological fluid accumulation in peritoneal cavity

Background

• Peritoneum

• Portal HTN

• Impaired drainage in lymphatic system

• Hypoalbuminemia

Pathophysiology

• Under filling theory primarily there is inappropriate

sequestration of fluid within the splanchnic vascular bed as a consequence of portal hypertension (PHT) that produces decrease in effective circulating blood volume. This activates the plasma rennin, aldosterone, and sympathetic nervous system, resulting in renal sodium and water retention

Overflow theory

primary abnormality is inappropriate

renal retention of sodium and water in the absence of volume depletion. Basis of this theory is that patients with cirrhosis have intravascular hypervolemia rather than hypovolemia

Peripheral arterial vasodilatation

• The major factor of ascites formation is splanchnic vasodilation.

• Cirrhosis causes increased hepatic resistance to portal flow that results in PHT and shunting of blood to the syst emiccirculation.

• Local production of vasodilators, mainly nitric oxide due to PHT results in splnchnic and peripheral arterial vasodilatation. This leads to decrease in effective arterial blood volume (EABV)

Pathogenic mechanism• Increased hydrostatic pressure

• Decreased colloid osmotic pressure

• Increased permeability of peritoneal capillaries

• Leakage of fluid into peritoneal cavity

• Misc.

Etiology

• Neonatal ascites/congenital ascites1.Associated with hydrops > -cardiovascular rhythm dist. cardiac malformn. -hematological isoimmune hemolytic dis. homo alpha thal.

2. Isolated ascites

- chylous

congenital anomaly of lymphatic channels

-biliary

spontaneous perforn of biliary tree

- pancreatic duct anomaly

-chromosomal

turner synd

trisomy 13,18,21

-infections

TORCH

syphillis

-renal

nephrosis

PUV

-pulmonary diaphragmatic hernia-gastrointestinal atresia-maternal condn toxemia diabetes-placenta/cord cord compression chorangioma

-misc wilms tumour neuroblastoma-storage dis. mucopolysachharadosis 8-skeletal abn. osteogenesis imperfecta achondrogenesis

-cirrhosis

alpha antitrypsin def.

-liver failure

neonatal hemochromatosis

-unknown

2.Isolated asictes - chlylous congenital anomaly of lymphatics - biliary spontaneous perforation of biliary tree - pancraetic duct anomaly3. Peritonitis - chemical bile,meconium - bacterial

Etiology In Children1.Associated with portal hypertension -extrahepatic venous obstruction misc -intrahepatic biliary tract dis. hepatocellular dis. toxins misc -others

Etiology of acute ascites

-Venous obstruction

-Peritonitis

-Fulminant hepatic failure

Etiology in ref to normal /diseased peritoneum

Normal- portal HTN liver dis. hypoalbuminemia miscDiseased- infections malignancy others

Presentation

• Abdominal distension

• Increasing wt

• Respiratory embarras.

• Pedal oedema

Risk factors

• Chronic viral hepatitis

• Intravenous drug use

• Sexual promiscuity

• Transfusions

• Tattos

• Habitation or origination from endemic hepatitis

Examination• Flank dullness 90% sensitive

• Increased abdominal girth and wt loss

• Puddle sign

• Shifting dullness

• Fluid thrill

• Peritoneal tap

Monitoring

• Abdominal girth and weight

-jugular venous distension

-heart murmur/signs of CHF

-signs of pulmonary oedema

-skin changes

-asterixis/anasarca

-virchows node

• Grading

1.Mild

Puddle sign/usg

2.Moderate

Shifting dullness/no thrill

3.Tense

Fluid thrill/resp. difficulty

• Staging

1+ careful examin

2+ easily detectable

3+ obvious but no tense

4+ tense ascites

Confirm >cause >complications• Blood tests > Complete blood counts

Complete urine examination

LFT

Clotting screen

Imaging studies

• Chest and abdominal films

-elevation of diaphragm

-nonspecific signs

-hellmer sign

-obliteration of hepatic angle

-dogs ear/mickey mouse sign

-med displacement of cecum & ascending colon & lat displacement of properitoneal line

• USG

-site for paracentesis

-100ml fluid

-uncomplicated ascites

homogenous ,freely mobile, anechioc collection in peritoneal cavity,deep acoustic enhancement

-massive ascites

small bowel loops-polycyclic,lollypop like arcuate app.

-coarse internal echoes(blood)

-fine internal echoes(chyle)

-multiple septa(TB,pseudomyxoma peritonei)

-loculated /atypical fluid distribution

-matting or clumping bowel loops\

-thickening of interface betn fluid & adjacent structure

• Upper GI endoscopy

-oesophageal/fundal varices

CT/MRI

-rt perihepatic space,morrisons pouch,douglas pouch

-malignant ascites

prop fluid in lesser & greater sac

-benign ascites

fluid in greater sac

Abdominal paracentesis• Position• Site• Technique• Ascitic fluid analysis routine/optional tests total protein/gram stain albumin/AFB smear and culture cell count cytology amylase/LDH/glucoseComplications

• white cell count- <500 leukocytes/ml & <250 PMN L-NRed cell count- >50000/ml hemorrhagicGross- transluscent/yellow-N brown-hyperbili/GB perforatn cloudy/turbid-infection pink/blood tinged-mild trauma gross blood-malignanacy/trauma milky-cirrhosis/thor.duct injury/lymphoma

• Toatl protein

• Gram stain

• Cytology

• SAAG-sr albumin-ascitic fluid albumin portal/nonportal

• Culture

• LDH

• Triglycerides

• Amylase

• Bilirubin

Classification of ascitic fluid infection

Type PMN count

Cells/mm3

Bacterial culture

Spont bact

peritonitis

> 250 +

Culture negative

>250 _

monomicrobial <250 +

Polymicrobial <250 +

Sec.bact.peritonitis

>250 +

Types of ascitis acc to sr ascitis albumin gradient

High gradient >1.1g/dl Low gradient <1.1g/dl

Cirrhosis

Hepatitis

Fulminant hepatic failure

Cardiac ascitis

Portal vein thromb.

Veno-occlusive dis.

Myxedema

Massive liver metastasis

Tb peritonitis

Nephrotic syndrome

Pancreatic ascitis

Bowel obst/infarction

Biliary ascitis

Postop lymph leak

Serositis in CTD

Indication for admssion• For investigation• Not responsive• Diet limited to 88mmol of Na per day• Monitoring• Grade 3 ascitis • Susp bact peritonitis• Electrolyte imbalance• Hepatorenal syndrome• Hepatic encephalopathy• Refractory ascitis

Management 1.non drug –

bed rest

medical care

diet

fluid restriction

2.drugs

diuretics

b blockers

3.Diuretic resitance

therapeutic paracentesis

le veen or denver peritoneovenous shunt

liver transplantation

extracorporeal ultrafiltration with reinfusion

TIPSS

Surgical• TIPSS-

-hepatic vein and portal vein

-reduces pressure gradient betn portal and systemic

Peritoneovenous shunt

• A peritoneovenous shunt (also called Denver shunt) is a shunt which drains peritoneal fluid from the peritoneum into veins, usually the internal jugular vein or the superior vena cava

Portocaval shunt

• A portacaval shunt (or portal caval shunt) is a treatment for high blood pressure in the liver. A connection is made between the portal vein, which supplies 75% of the liver's blood, and the inferior vena cava, the vein that drains blood from the lower two-thirds of the body.

• Liver transplantation

• Follow up

• Spontaneous bacterial peritonitis

• Prevention

• Patient education

• Monitoring

• Prognosis

• Lows albumin gradient ascites

Refractory ascitis• Fluid load that is non responsive to

restriction of dietary sodium to 88mmol/day and maximal dose diuretic therapy in absence of ingestion of prostaglandin inhibitors(NSAID)

• Management

serial large volume paracentesis

100ml/kg at a time

iv albumin 6-8g/lit

Others

• ANP

• V2 receptor antagonist

• OPC-3126

• Niravoline

• FK352

• Chylous ascitis

• Pseudochylous ascitis

• Management

low fat,high protein,paracentesis

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