Dr Pravakar Sethi

Diagnostic approach to ascites

ASCITES

Askites a Greek word which means ‘bag’ or ‘sac’.

definition

ASITES IS AN ACCUMULATION OF FREE FLUID WITHIN THE PERITONIAL CAVITY.

In CHILDREN,hepatic,renal,and cardiac disease are the most common causes.

CAUSES OF ASITES

HEPATICCirrhosisCong.hepatic fibrosisFulminant hepatic failureBudd-chiari syndromeLysomal storage ds.RENALNephrotic synd.Obst.uropathyPerforation of urinary tractPeritoneal cyst

CONT.

CARDIACHeart failureConstrictive pericarditisInferior venacaval web

INFECTION

TuberculosisAbscesschlamydiaschistosomiasis

CONT.GASTROINTESTINALInfected bowelPerforationNEOPLASMLymphomaNeuroblastomaGYNAECOLOGICOvarian tumorovarian torsion,rupture

PANCREATICPancreatitisrupture pancreatic duct.

CONT.

MISCELLANIOUSSLEVentriculo peritoneal shuntEosinophillic ascitesChyllous ascitisHypothyroidism

Pathophysiology of Ascites

From: Robbins Basic Pathology

pathogenesis

According to starling’s hypothesis the exchange of fluids between the blood and tissue spaces is controlled by the balance between two factors;

1. Capillary blood pressure 2. Osmotic pressure of plasma proteins

(plasma colloid osmotic pressure) capillary blood pressure / Plasma

colloid osmotic pressure Ascites

Mechanisms

Underfill theory

Overfill theory

Vasodilatation theory

UNDERFILL THEORY HYPOVOLAEMIA Kidney feels Body is under filled & require more

salt and water Stimulates JG cell to release RENIN

angiotensinogen anginsioten-I

in lungs by ACE

Angiotensin II Releases aldosterone from the zona glomerulosaIncrease the reabsorption of sodium and water &

excretion of potassium from the DCT ASCITES

Overfill theory

The combination of portal hypertension and circulating hypervolaemia results in ‘over flow’ from the congested portal system to the peritoneal cavity, to produce ascites

Decrease in vasodilatory prostaglandins like PGE2 & PGE1deteriorates the renal fuctionASCITES

NITRIC OXIDE THEORY(PERIPHERAL ARTERIAL VASODILATATION THEORY)

Most recent theory

When a portal pressure increases above a critical threshold, nitric oxide levels increase leading to vasodilatation

As the state of vasodilatation worsens plasma levels of vasoconstrictor, sodium retentive hormones increase and renal function deteriorates ASCITES

EVALUATION…

Evaluation of ascites patient history

Age child : Tuberculous ascites and nephrosis Middle age : cirrhosis of liver Old age : malignance

Sex Female : meigs synd., pelvic tumours and infection

and ovarian tumours Order of Development of Ascites

cardiac causes : Leg oedema precedes ascites . Kidney causes : Puffiness of face precedes ascites . Cirrhosis of liver : Ascites is the first feature .

Ascites is the part of generalised anasarca caused by nephrosis , anaemia , hypoproteinaemia etc.

General examinations

Enlarged lymph nodes : Suggestive of TB , leukaemia , malignancy , and lymphomas .

Associated jaundice : Cirrhosis of liver .Dyspnoea , PND , orthopnoea , and

oedema : congestive cardiac failure .Periorbital oedema , puffiness of face

and oedema associated with ascites : acute nephritis , nephrotic synd.

Severe anaemia : Ascites of haematologic origin .

Other signs of malnutrition with ascites : Kwashiorkor .

Systematic examination

Abdominal ExaminationInspectionAbdomen is distended .Umbilicus is everted and slit

transversely(laughing umbilicus) The distance between umbilicus and

xiphisternum is more than the distance between umbilicus and pubic symphysis .

Flanks are full. Nearly 1500 mL of fluid is required to make the flanks full .

Veins are dilated over the abdomen . Scrotal oedema indicates nephrotic synd.

Quantifications of ascites

1+ : Detectable only by careful examinations

2+ : Easily detectable but of relatively

small volume 3+ :obvious ascites but not tense 4+ :Tense ascites

Palpation of abdomen Features Significance

Tenderness and local rise of temperature

Peritonitis

Rebound tenderness or Blumberg sign

Peritonitis

Doughy or rubbery feel Tuberculous peritonitis

Presence of splenomegaly , ascites , and caput medusase

Cirrhosis of liver

Enlarged tender liver and ascites Congestive cardiac failure

Palpation of intra-abdominal masses TB

Palpation of lumps and enlarged glands

TB, malignancy , leukaemia , and Hodgkin’s lymphoma

Examination of veins over the abdomen

Vein obstructed Site of engorged veins

Direction of flow of blood

1. Portal vein obstruction

Veins around the umbilicus and upper abdominal wall

Veins above umbilicus : bellow upwards . Veins bellow umbilicus : from above down words . Veins around umbilicus is called caput medusae

2.Hepatic vein obstruction

Lower thorax and upper abdomen

From above downwards

3.Inferior vena cava obstruction

Lower third of abdominal wall and flanks

From bellow upwards

percussion

Shifting dullness is an important sign of free fluid in the peritoneal cavity . It requires nearly 500 mL of fluid to elicit this sign .

Fluid thrill is present in tense ascites . If the fluid is small in amount nearly 120

mL , it will be demonstrated by puddle sign (lawson’s sign ) .

Ausculation It is not of much use in ascites .

Onset of ascites

SUDDEN INSIDIOUS

Acute Budd- Chiari synd.

Acute right heart failure

Sudden decompensation of previously compensated cirrhosis

Pancreatic ascites

Decompensated cirrhosis

Chro.Budd-Chiari synd.

TB ascites Nephrotic synd. Hypothyroidism Constr. pericarditis

DEMONSTRATION OF ASCITESFIVE CLASSICAL PHYSICAL SIGN

1. Bulging flanks belly of a frog2. Flank dullness or horse-shoe dullness3. Shifting dullness high sensitivity

(85%) & low specificity (50%)4. Fluid wave / thrill 5. PUDDLE SIGN(Lawson’s sign)-

decreased auscultation of high freqency vibrations in the central abd.when flicking the side of the abd.with the patient of hands knees.

GRADING OF ASCITES

GRADE SEVERITY SIGNS

1 Mild Puddle signs +

USG abdomen+

2 Moderate Shifting dullness+

No fluid thrill

3 Severe Fluid thrill+Resp. embarrassment+

Minimum amount of fluid required Test Minimum fluid in ml.

Diagnostic tapPuddle signShifting dullnessFluid thrillUltrasound scanCT scan

10-20 120 500 1000-1500 100 100

After the diagnosis of ascites is made, its cause should be determined by laboratory analysis.

ascitic fluid study

(diagnostic paracentesis)

DIAGNOSTIC PARACENTESIS

10 to 20 mLThe bladder should be emptied prior to

the procedureMost common Site left lower quadrant Other site

1. In the midline between the pubic-symphysis & umbilicus,

2. Right iliac fossa, lateral to the inf. epigastric artery or a few cm above the inguinal lig.

Z-technique

DIAGNOSTIC PARACENTESIS

CONTRAINDICATIONS

Severe CoagulopathyAbdominal wall hematomaLocal infecctionRelative

Repeated surgeries

complications

1. Infection & peritonitis2. Bladder or bowel perforation3. Hypovolaemia & shock (>1 lit.

remove rapidly), especially if the patient does not have oedema

4. Blockage of needle

Tests on Ascitic FluidRoutine Optional Unusual

Cell count and differential

Glucose concentration Tuberculosis smear and culture, adenosine deaminase

Albumin concentration LDH concentration Cytology

Total protein concentration

Gram stain Triglyceride concentration

Culture in blood culture bottles

Amylase concentration Bilirubin concentration

Colour / appearance of ascitic fluid

Straw coloured / Transparent

Bloody fluid Opaque / milky

Dark -brown

Black / tea colour

normal

Cirrhosis

TB

Malignancies

Trauma

TB peritonitis

Pancreatitis

Perforated viscus

Traumatic tap

Chylous ascites

Billiary ascites

Deep jaundice

Pancreatic ascites (pigment ascites)

Malignant melanoma

CELLNORMAL UNCOMPLIC

ATED CIRRHOTIC ASCITES

SBP IN CIRRHOTIC ASCITES

TB ASCITES

WBC count

Cell

RBC

< 250 / cc

Lymphocytic

< 500 / cc

ANC < 250 cells

> 500 / cc

PMN > 250

High

Lymphocytic predominance

> 50,000 cellsAlso in trauma , malignancy

cytology

At least 50 ml of fluid50 – 80% accurate –diagnosis of

malignant ascitesDifferentiate malignant cells from

atypical mesothelial cells

GRAM STAINING/CULTURE

Gram stain – 10 % sensitive --approximately

10,000 bacteria / ml are required

Culture in blood culture bottle 92 % yield

TOTAL PROTEIN

Low sensitivity in differentiating exudate from transudate.

Elevated TP ( ≥2.5 g ) + high SAAG

hepatic congestion

Elevated TP + low SAAG malignancy

Differences bet. exudative & transudative ascites

Features Exudative ascites

Transudative ascites

Protein in g%Sp gravityLDHFibronectin

Cholesterol

Hyaluronic acid

ADA

>3 g%>1015High75 mg%--(malignant ascites)>48 mg%--(malignant ascites)>0.25 mg% (mesothelioma)High in TB ascites

<3 g%<1015LowLow

Low

Low

Normal

SERUM-ASCITES ALBUMIN GRADIENT (SAAG)

SAAG= serum albumin – ascitic fluid albumin The gradient correlates directly with portal

pressure. A gradient > 1.1 g/dL, ascitic is due to portal

hypertension (high gradient or transudative ascites or portal hyper tensive)

A gradient < 1.1g/dL (low gradient / exudative or non potal hyper tensive) suggests that the ascites is not due to portal hypertension .

The specificity & sensitivity of SAAG around 97% SAAG-Is far superior to the old exudate-

transudate concept . SAAG does not explain the pathogenesis of PTN

ERRORS IN SAAG

Timing of collection

Arterial hypotension

Chylous ascites

Serum hyperglobulinemia

Classification of ascites based on SAAG

SAAG

≥1.1gm/dl

Ascitic protein<3gm/dlCirrhosis

Late Budd-chiary synd.Massive liver metastasis

Ascitic protein ≥3gm/dlCHF/Constr. PericarditisEarly Budd-chiary synd.

IVC Obstr.Sinusoidal obstr. Synd.

≤1.1gm/dl

Biliary LeakNephrotic synd.

PancreatitisPeritonial carcinomatosis

TB

Classification of ascites based on SAAG

High-gradient ascites(SAAG>1.1 gm/dl)

Low gradient ascites(SAAG<1.1 gm/dl)

Cirrhosis Veno-occlusive

disease Budd-chiari syndrome Fulminant hepatic

failure Cardiac ascites Mixed ascites Massive liver

metastasis

Tuberculous ascites Nephrotic synd. Pancreatic ascites Chylous ascites Biliary ascites Serositis in collagen

disease Peritoneal carcinomatosis Postoperative lymphatic

leak Bowel obstr./infarction

imaging

X RAY

Non specificDirect signs

Elevation of diaphragm

Diffuse abdominal haziness

Bulging of flanks Indistinct psoas

margins Separation of small

bowel loops Centralization of

floating bowel

Hellmer’s sign ‘Dog’s ear’ or ‘Mickey

Mouse’ Medical displacement

of cecum and ascending colon

Lateral displacement of properitoneal fat line

USGExtreamly sensitive, can detect as little as

100 mL, “lollipop”/arcuate appearance of small bowel

loopsCoarse internal echoes bloodFine internal echoes chyleMultiple septa TB , pseudomyxoma peritoneiMatting or clumping of bowel loops, thickning of

fluid- wall interfaceTethering of bowel along post .abd. wall with

loculated fluid in between malignancyGall bladder thickening cirrhosis

CT

Can differentiate malignant from benignLymph nodesFocal liver , spleenic lesions Pancreatic and colonic massesMalignant ascites fills greater & lesser

sacMore useful than USG in detecting hepatic

lesions , primary or secondary Detect up to 100 ml of fluid

Complications of ascites

1. Spontaneous bacterial peritonitis ( SBP)

2. Hydrothorax3. Gastro-oesophageal reflux4. Respiratory distress and atelectasis

due to elevation of diaphragm5. Inguinal / umbilical / femoral hernia6. Scrotal oedema7. Collection of fluid in the pleural sac8. Mesenteric venous thrombosis9. Functional renal failure.

Spontaneous bacterial peritonitis

Characterized by the spontaneous infection of ascitic fluid in the absence of an intra-abdominal source of infection

Prevalence 10-30 %Sex M = FAge Before 6 year age – most commonMost cases occure in children with ascites nephrotic synd. cirrhosis infection.WBC >250 cells / mm3 (>50 % PMN)

Cont…Organisim- Pneumococci (most common) Gr. A strept. , Enterococci , Staph. Gr. –ve enterobiacteria E. coli, Klebsella pneu. Involves the translocation of bacteria from the

intestinal lumen to the lymph nodes, with subsequent bacteremia and infection of ascitic fluid .

Third – generation cephalosporins (cefotaxime) + Aminoglycoside . Duration 10-14 days

Amoxicicillin + clavulanic acid also effective Vancomycin resistant pneumococci

Sbp recurrence

70 % probability of recurrence at one year

Long – term antibiotic prophylaxis with quinolones reduces the rate of recurrence

Cotrimoxazole may be an alternative to quinolones.

Complication of sbp

The most severe is the hepato-renal syndrome, which occurs in up to 30 % of patients and carries a high mortality rate

Intravenous albumin (1.5 gm /kg at diagnosis and 1gm/kg 48 hours later ) helps to prevent the hepato-renal syndrome and improves the probability of survival

CHYLOUS ASCITES

Turbid, milky, or creamy peritoneal fluid due to the presence of thoracic or intestinal lymph.

Shows staining fat globules with sudan black Oil red

Opaque milky fluid usually has a triglyceride concentration of >1000 mg/dL.

Cont..

Is most often the result of lymphatic obstruction fromTrauma/ surgeriesTumorTuberculosisFilariasisCongenital abnormalitiesNephrotic syndrome

PSEUDOCHYLOUSA turbid fluid due to leukocytes or tumor

cells may be confused with chylous fluid.

TESTS

CHYLOUS ASCITES

PSEUDOCHYLOUS ASCITES

Fat globules by Sudan red stain

present absent

Ether test Top thick layer becomes clear, as fat dissolves in ether

Remains turbid

Alkali test No change in colour Becomes clear , as alkali dissolves cellular proteins

MUCINOUS ASCITIC FLUID

Pseudomyxoma peritonei

Colloid carcinoma of the stomach or colon with peritoneal implants.

Ascitic fluid study

CIRRHOSIS

TB PYOGENIC PERITONITIS

CCF NEPH.SYND.

PANCRE. ASCITES

NEOPLASMS

COLOR STRAW / BILE STAINED

Clear, turbid, hmgic or chylous

Turbid or purulent

Straw Straw / chylous

Turbid , hmgic or chylous

Straw, Hmgic,chylous,mucinous

PROTEIN

< 2.5 g/dl

>2.5 g/dl

< 2.5 g/dl

Variable <2.5 g/ dl

Variable / >2.5 g /dl

>2.5 g /dlVery high

SAAG >1.1 g/dl

<1.1 g/dl

< 1.1 g/dl

>1.1 g /dl

<1.1 g /dl

<1.1 g /dl

<1.1 g/ dl

RBC( / µl)

>10,000 - 1%

>10,000 - 7%

>10,000Unusual

>10,000

>10,000 unusual

>10,000Blood stain

>10,000- 20%

WBC( / µl)

< 250 >1000 lymph 70 %Definit Δ peritonial biopsy

Predom.Polymorphs

Gram stain +ve

<1000

Usually mesothelial mononuclear

< 250

mesothelial or mononuclear

Variable

Increase am ylase(>2000 u/ l )

>1000

TREATMENT

Management of ascites GOAL-To achieve ascites-free status -To maintain it thereafterINDICATION FOR HOSPITALIZATION1. If there is no response to outpatient

management for 4-6 weeks.2. Tense (grade III) ascites with respiratory

embarrassment3. Spontaneous bacterial peritonitis4. Diuretic – induced complications like ;

Hyponatraemia, Na < 125 mEq /L Hypokalaemia, K < 3 mEq /L Hyperkalaemia, K > 6 mEq /L Hepatorenal synd. Hepatic encephalopathy

5. Refractory ascites

TREATMENT OF HIGH SAAG ASCITES

Bed restSalt restriction Fluid restriction DiureticsTherapeutic paracentesis AlbuminPeritoneovenous shuntTIPStransplantation

1000 ml / day

Goalwt loss to prevent renal failure of prerenal origin is 300-500 g per day in patients without peripheral edema and 800 - 1000 g per day in those with peripheral edema

1 gm / D in smallar children,2 - 3 gm / D in adolescents.

TREATMENT OF LOW SAAG ASCITES

Peritoneal carcinomatosis therapeutic Paracentesis

Ovarian tumours surgery + chemo Tb ATT Pancreatic ascites endoscopic stenting, surgery,

or respond to somatostatin , octrotide therapy. Lymphatic leak after surgery peritoneovenous

shunting Chlamydia peritonitis tetracycline,doxycycline. Lupus steroid Dialysis related ascites aggressive dialysis Nephrotic syndrome steroid Malignant ascitesChemotherapy

diuretics Are the mainstay of treatment and should be

used liberally but carefully All diuretics are best given in a single dose in the

morning- maximizes the complianceA. Potassium-sparing diuretics

Aldosterone antagonists Spironolactone- DOC in cirrhotic ascites, 1- 6 mg/kg/D Carninone, Potassium canrenoate

Amiloride (10 mg /kg) or triamterene can be used if spironolactone is not effective

B. Loop diuretics (high-cilling diuretics) Furosemide, Torsemide, azosemide, tripamide,

bumetanide, piretanide, Muzolimine, Ethacrynic acid

C. Thiazides –hydroclorothiazide,dose 2- 3 mg / kg/D

Response to diuretic theraphyRelief of abdominal distension

Relief of respiratory distress Decrease in abdominal girth

Achieving a negative sodium balance (when sodium excretion is more than intake) indicates a good diuretic response

Monitoring during diuretic therapyPatient should be assessed 1 week after

starting therapy & than every 2 week Weight & abdominal girth should be

measured, Look for oedma, grade of ascites and subtle

sign of SBP

Therapeutic paracentesis Indications

Tense ascites that causes respiratory embarrassment

Intractable ascites not responding to the usual treatment

To release intra abdominal pressure in moderate to severe ascites

Large volume paracentesis, up to 200- 400 ml/ kg/D can be removed slowly over 4 – 6 hours if the patient has peripheral oedema

Large volume tap(>5 l) ,I.V. colloid replacement with albumin 6-8 gm /L

Dextran 70 is less effective than albumin

Criteria for discharge of the ascitic child

1. Adequate weight loss and natriuresis

2. Absence of of infection/peritonitis

3. Absence of diuretic- induced complications

REFRACTORY ASCITES

5 to 10 %

Defined as a lack of response to high doses of diuretics (400 mg of spironolactone per day + 160 mg of furosemide per day).

Patients in whom there are recurrent side effect

(e.g, hepatic encephalopathy , hyponatremia, hyperkalemia, or azotemia) when lower doses are given are also considered to have refractory ascites .

Theraputic options in refractory ascites

Chronic outpatient paracentesis

Ascites ultra filtration and re-infusion

Le Veen shunt

TIPS-(Transjugular Intrahepatic Peritonial Shunt )

Liver transplantation

TIPS(TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT)

TIPS consists of an intrahepatic stent inserted between one hepatic vein and the portal vein by a transjugular approach

Effective in preventing recurrence in patients with refractory ascites

Decreases the activity of sodium – retaining mechanisms and improves the renal response to diuretics.

Transjugular intrahepatic portosystemic shunt (TIPS)

disadvantage

High rate of shunt stenosis (up to 75 % after 6 to 12 months )

Lead to recurrence of ascites ;hepatic encephalopathy

High cost

Lack of availability in some centers .

Current therapeutic strategies include repeated large –volume paracentesis with the use of plasma expanders and transjugular intrahepatic portosystemic shunts

Peritoneovenous ShuntAscitic fluid is shunted from the high pressure peritoneal cavity to the low pressure superior vena cava by 1 . Le Veen shunt 2 .Denver shunt 3 . Minnesota shunt

Denver Shunt(Similar to LaVeen Shunt)

Contraindications•Protein > 4.5 g/l (occlusion)•Loculated ascites•Coagulopathy•Advanced renal/cardiac disease•GI malignancyComplications•Infection•DIC•Pulmonary edema•Pulmonary emboli•Shunt occlusion •Malfunction•Air embolism•Congestive cardiac failure•Variceal haemorrhage

Prognosis of ascites

Despite the recent advances in the treatment of ascites, the prognosis is always grave after ascites develops in a cirrhotic patient .

Only a change of 40 % being alive 2years later .

The presence of hepatocellular failure, evidenced by jaundice and encephalopathy is a very bad prognostic factor .

The prognosis may be better if ascites develops rapidly , especially if there is a well defined precipitating factor such as GI bleed .

Thank u. . .