ASCITES--Clinical Aspects

ASCITES

INTRODUCTION:

Ascites is  abnormal collection of free fluid in the peritoneal cavity.

The term ascites is from greek origin ‘askos’ meaning bag or bladder.

Diagnostic features of Ascites:

1.Uniform distension of  abdomen

2.Flanks full (500ml)

Shifting dullness (1000ml)

Fluid thrill =massive ascites

Other associated  features:

Everted umbilicus,

umbilical hernia,

Divarication of recti,

Inguinal or epigastric hernia

Note:Absence of shifting dullness or fluid thrill or absence of both does not exclude the presence of ascites.

 Dullness in ascites

Moderate Ascites-   Flanks are dull

Large ascites (500ml)- Horse shoe shaped dullness

                                         Flanks and hypogastric regions are dull

Massive Ascites-   Whole of the abdomen is dull except for a small area over the umbilical region.

Puddles sign: to detect small volume of ascetic fluid 100ml.

Method to elicit: Patient is put in knee elbow position, keeping the diaphragm of stethoscope over the most dependent part of abdomen, flick on the flank repeatedly and lightly.

Diaphragm of stethoscope is moved gradually to the other flank.A change in the intensity and character of the note indicates fluid.

Shifting dullness: to be elicitable requires minimum of 1000 ml of free fluid

Fluid thrill _elicitable in massive ascites

Mechanism of shifting dullness:

The ascitic fluid will flow to the most dependent portion of the abdomen,

the air filled intestine will float on top of this liquid.

The technique of shifting dullness makes use of this relationship to detect the presence of ascitic fluid.

Symptoms of ascites

Increasing abdominal girth.

Shortness of breath because of elevation of diaphragm-dypnea /orthopnea

Reflux esophagitis causing heartburn

Secondary effects of ascites:

1.Pleural effusion Rt side:

 due to defect in diaphragm allowing ascetic fluid to pass into pleural space

2.IVC obstruction:

When massive ascites presses on IVC-can lead to pedal edema

3.Distended neck veins

Elevated Rt.atrial pressure following tense ascites raising the diaphragm

 

Common causes of Ascites

Hepatic cirrhosis

Malignant diseases (hepatic,peritoneal)

Cardiac failure

TB abdomen

 Learning  Points :

·         Ascites is a sign of ‘decompesated ‘liver

·         500ml  of fluid should be present before before flank dullness is detected.

·         Difficult to make out dulness in obese abdomen-diagnose by USG.

·         USG can detect as little as 100 ml of fluid in peritoneum

·         In ovarian masses characteristically flanks are resonant

·         Ascites developing in stable chronic cirrhosis,super imposed Hepatoma to be suspected.

·         Malignancy related ascites-painful

History in ascites

Chronic alcoholism

 Other Liver diseases risks-transfusion,parenteral therapy,tattoos,accupuncture

h/o alcoholic cardiomyopathy

h/o heart disease

H/o cancer- breast ,colon ,pancratic,gastric

H/o abdominal pain-malignancy related ascites,pancreatitis,infection

h/o fever ,abdominal pain-TB abdomen

h/oDM-nephrotic ascites

 h/o connective tissue disease-polyserositis

h/o hypothyroidism

Clinical examination

General examination: look for

Stigmata of liver disease-spider nevi,palmar erythema,jaundice,

Raised JVP,anemia,pedal edema

Virchow’s node-rt supraclavicular region

Firm umbilical nodule-Sister Mary Joseph’s nodule

Examination of abdomen

Inspection: •contour of abdomen, •movements of abdominal wall,

•Skin streched and shiny, odema of skin, •striae, •dilated veins, •position,

•shape of umbilicus(smiling umbilicus), •herniae(umbilical,epigastric)

•Transmitted pulsation in ca.stomach,,

Palpation

•Tenderness, •Rigidity,

•lump- intra abdominal/on abdominal wall •site,size,shape,surface edges

•Direction of blood flow in distended veins •viscera-liver,spleen,gall bladder,kidney

•Hernial orifices

Percussion: •Shifting dullness,fluid thrill,puddles sign

Auscul tation: •Hepatic rub, •bruit

Grading of Ascites

Gr1+: only on careful exam

Gr2: Easily detectable by small volume

Gr3: obvious ascites but not  tense

Gr4: Tense ascites

ASCITES dispropotionate to edema: coditions causing

1.cirrhosis of liver

2. constrictive pericarditis

3.restrictive cardiomyopathy

4.hepatic venous occlusion

5.Tuberculous peritonitis

6.Intra abdominal tumor

INVESTIGATIONS :

1.USG ABDOMEN-Confirms ascites

2.CT Abdomen

3.Peritoneoscopy

3.LAPROSCOPY and peritoneal biopsy if undiagnosed

4.Diagnostic PARACENTESIS

5.Other routine:

TC,DC,ESR,Xray chest,abdomen

6.Liver function tests

7.Liver biopsy-in cirrhosis/malignancy of liver

8.investigations for diagnosis of portal hypertension

Differences between transudate and exudate

Features	Transudate	Exudate
Appearance	Clear	Turbid,hemorrhagic,straw coloured
Specific gravity	Less than 1016	More than1016
Proteins	Less than30gms /L	More than 30gms/Litre
Serum ascetic fluid albumin gradient	>1.1/dl	<1.1/dl
Total cell count	low	high
Differential count	Mesothelial cells/lymphocytes	Polymorphs.lymphocytes/RBCs

ASCITIC FLUID ANALYSIS:
Points to note:

1.Gross appearance

2.Biochemical analysis

3.Microbiological with cytology

Gross appearance

transudate

exudate

cloudy –a. Infection-raised polymorphs>5000/mm3

b. purulent if >50000 cells/mm3

c. milky-chylus TGL->200mg /dl;clears on adding ether

d.Deep yellow colour-If bilirubin increased

bile stained also when there is bile duct perforation

Blood stained fluid-RBC more than10 thousand/mm³

Cell count

WBC >denotes inflammation/malignancy

Mainly polymorphs-Bacterial infection/SBP

In SBP->250cells/mm³ diagnostic

But in surgical peritonitis>10 thosand cells/mm³

Lymphocyte predominance in TB peritonitis

In malignancy cell type variable;in 20% RBC and also malignant cells seen.

Biochemical analysis

Proteins >3gms/dl in exudates

SAAB-Serum albumin minus ascetic fluid albumin

Less than1.1 in exudates

More than 1.1 in transudate

SAAB is is more useful (diuresis can affect total ascetic protein concentration)

Glucose- reduced or 0- in infected ascites

(Because it is consumed by bacteria and WBC)

Low glucose but normal cell count means intestinal contents aspiration

Enzymes-LDH normally less than 50% of serum value

In bacterial infection LDH more than serum value

It is produced by lysed WBCs.

Amylase-raised in pancreatic disease

Normal 250-1000 somayagi units per day

 Bacterial tests

Gram stain-in centrifuged specimens positive in severe infection only.

SBP-not positive because count is low

Culture if done specimen must be sent to the lab immeadiately.

AFB-often negative

Cytology for malignant cells

Positive  only if peritoneum is directly involved

Complications of Ascites

1. Spontaneous bacterial peritonitis:

Suspect In cirrhosis with ascites, going for fever, abdominal pain ,ileus ,hypotension, encephalopathy

Ascitic fluid PMN cell count->250/mm³

Culture positive-enterobacter, strept.pneumonia, S.viridans

Treament-Cefatoxime

2.Hepato renal syndrome

Progressive renal failure

Spontaneous or precipitated by diuresis, paracentesis, bleeding, or drugs.

?due to altered renal hemodynamics

Differential diagnosis for distension of abdomen

Fluid/Fat/flatus/foetus/Tumor in the abdominal cavity.

differential diagnosis of causes of ascites

1.Cirrhosis of liver:

.Signs of liver cell failure

 signs of portal hypertension         

Ascitic fluid-transudate

2.Tuberculous peritonitis

Doughy abdomen

Matted omentum and loops of intestine

Multiple palpable masses

Confirmation: peritoneal  biopsy shows tuberculous granuloma

 

3.Bacterial peritonitis

 Signs of septicemia with ascites

and a focus of infection like indwelling catheter.

4.Malignant Ascites:

Primary-stomach,colon,ovary,or other intra abdominal tumors,

Sister Joseph nodules in umbilicus

5.Pancreatic ascites

H/o acute abdominal pain radiating to the back

In chronic pancreatitis fluid leaks from the pseudo pancreatic cyst

Serum amylase raised

Ascitic amylase>1000Iu/L

Diagnosis:ERCP

6.Constrictive Pericarditis

Pulsus paradoxus;kussmauls sign

Hepatomegaly with ascites

Pericardial knock

Calcific pericardium

7.Portal vein thrombosis

Sudden rapid development of –ascites,splenomegaly,hemetemesis and melena

8.Hepatic vein thrombosis

Large tender liver

Absent hepatojugular reflux

9.Nephrotic syndrome

Initial puffiness of face

Massive protenuria

Hypercholestrolemia

Management

1.daily weight chart ,IO chart,

2.Fluid restriction -1500ml/day

3.Salt restriction2gms per day –most important initial step

4.Diuretics indicated in

Gross ascites,tense ascites,before biopsy,scan or venogram

Drugs used

Spiranolactone25mg qid,increase to maximum of 400mg/day.

Frusemide20-40mg in divided doses (may combine with spiranolactone)

Amiloride10mg/day ±frusemide/thiazide

5.Paracentesis in severe distension causing respiratory distress

6.Peritoneal shunt in intractable ascites

7. Salt free Albumin infusion

8. Treatment of the cause.

KEY TAKE HOME MESSAGE                             

1.Assessment of SAAG  helps to determine if diuretics  are likely to help.

SAAG of >1.1gm/dl  is associated with portal hypertension

2.About diuretic therapy

·         Avoid postural hypotension or fatgue from diuretic tmt  which

 is likely to produce falls ;that  is worse than having ascites

3. Abstinence from alcohol

 As a First step in treatment –convince patients to abstain from alcohol

Abstinence of few months greatly improves reversible component of ascites.

REFRACTORY ASCITES

Types:

I.                    Diuretic resistant ascites

II.                  Diuretic intractable ascites

Definition

I.                   Diuretic resistant ascites

Lack of response to high dose of diuretic i.e.

-400mg/day of spiranolactone and 160 mg/day of frusemide

-while remaining compliant with low sodium diet of 50-mmolsodium per day

- and lack of response with  weight loss of  less than200gm/day

This requires an  observation period of weeks to ensure diuretic resistance.

 Recent study shows single dose of 80 mg of IV frusemide and subsequent random

- urine sodium of less than 50mmol/l is indicates refractory ascites

II.                Diueretic-intractable ascites

Development of diuretic –induced complication like severe electrolyte disturbance,

Renal impairement,hepatic encephalopathy precluding the use of  an effective  diuretic dose.

(put in simple terms patient who cannot tolerate diuretics because of side effects)

Conditions contributing to refractory ascites

1.       Active inflammation

2.       Portal or hepatic vein thrombosis

3.       GI bleed

4.       Infection

5.       Spontaneous bacterial peritonitis

6.       Malnutrition

7.       Hepatoma

8.       Super imposed cardiac and renal disease.

9.       Hepato toxic and nephrotoxic drugs

Prognosis   poor

Treatment

I.                    Large volume paracentesis

Removal of 5 litre or more of  ascetic fluid

Total paracentesis –removal of all ascetic fluid also can be done (20L or more)

Complications of large volume paracentesis

Electrolyte imbalance ,raised serum creatinine

 Spplemental Albumin infusion  required

5gm albumin per each Litre above 5L tapped

Alternative to albumin – “Terlipressin”-avoids exposing patient to blood product

II.                    TIPS (trans jugular intrahepatic porto systemic stent shunt)

Effective in decreasing ascetic fluid reaccumulation

A flexible metal prosthesis is used to connect a branch of hepatic vein to portal vein thus reducing sinusoidal pressure

Demerit:

increased  risk of hepatic  encephalopathy.

Frequent TIPS occlusion demands careful follow up

III.                Peritonio venous shunt  (Nearly Abandoned therapy )

A surgically inserted tube connects  peritoneal cavity to superior vena cava

Tube courses subcutaneously

Allows only one way passage of ascetic fluid to SVC and so back into circulation

Demerits

Tecchnical problems like blockage of tube and others)

IV.              Recent research

 Aquaretics-Vasopressin receptor antagonist

Promote excretion of electrolyte free water

Useful in patients with ascites and hyponatremia

Not yet approved by FDA