ASCITES

Ascites is the derived from Greek word ‘ASKITES’

It means ‘Bag’ or ‘Sac’
DEFINITION
“Ascites is the abnormal accumulation of the excess fluid within the peritoneal
cavity. It is the most encountered in patients with cirrhosis & other forms of
severe liver diseases.”
CAUSES
Common causes of ascites to either transudative or exudative ascites.
1.) Transudative (Protein <25g/l)
Cirrhosis
Budd Chiari Syndrome
Congestive Heart Failure
Constrictive Pericarditis
Nephrotic Syndrome
End Stage of Renal Disease
Protein losing Enteropathy
Low Plasma Protein Concentration
Hypothyroidism
2.) Exudative (Protein >25g/l)
Tuberculosis Peritonitis
Peritoneal Carcinoma
Secondary Bacterial Peritonitis
Pancreatic ascites
Chylous Ascites
Poly Serositis(Connective Tissue Disorder)
Capillary Leak Syndrome
Primary Mesothelioma
Distension of abdomen due to fat, flatus, feces, fluid, fetus (5F)
 PATHOPHYSIOLOGY
The accumulation of ascetic fluid represent a state of total body sodium &
water excess, but the event that initiates the unbalance is unclear.

It is mostly occur as a result of portal Hypertension.

Three theories of ascites formation have been proposed

1. Under filling
2. Overflow
3. Peripheral Arterial Vasodilatation
1. Underling Theory
→It suggest that the primary abnormality is inappropriate sequestration of fluid
within the splanchnic vascular bed due to portal Hypertension & a consequent
decrease in effective circulating blood volume.
→This activates the plasma renin, aldosterone& sympathetic nervous system,
resulting in renal sodium & water retention.

Portal HTN
↓
Splanchnic Vasodilation
↓
Sys. Arterial under filling
↓
Activation of ADH & rennin
↓
Renal Na & water retention
(Hypovolemia)
↓
ASCITES
 2. Overflow Theory
→It suggest that the primary abnormality is inappropriate renal retention of
sodium & water in absence of volume depletion.
→This theory was developed in accordance with the observation that patients
with cirrhosis have intravascular hypervolemia rather than hypovolemia.
3. Peripheral Arterial Vasodilation
→It includes components of both of other theories.
→It suggest that portal Hypertension lads to vasodilation which causes decrease
effective arterial blood volume.
→As the natural history of disease progresses, neurohumoral excitation increases,
more renal sodium is retained & plasma volume expands.
→This leads to overflow of fluid into the peritoneal cavity.
→The vasodilation theory proposes that under filling is operative early &
overflow is operative late in the natural history of cirrhosis.
→Although the sequence of events that occurs between the development of portal
hypertension & renal sodium retention is not entirely clear portal HTN apparently
leads to an increase in nitric oxide levels.
→Nitric oxide mediates splanchnic & peripheral vasodilation.
→Hepatic artery oxide synthase activity is greater in patients with ascites than in
those without ascites.
→Regardless of the initiating event, a number of factors contribute to the
accumulation of fluid in the abdominal cavity.
→Elevated levels of epinephrine & norepinephrine are well documented factors.
Hypoalbuminemia & reduced plasma oncotic pressure favor the extravasation of
fluid & thus, ascites is infrequent in patient with cirrhosis unless both portal
hypertension & hypoalbuminemia are present.
Clinical Features
›Symptoms:
- Weight gain
- Increase in girth of the abdomen
- Abdominal discomfort
- Dyspnoea on exertion
- Oedema of lower extremities
›Signs:
1. General appearance
- ‘Spider man’ thin limbs with protuberant abdomen.
2. Free fluid in peritoneal cavity
- Generalized abdominal distension
- Bulging in flanks
- Umbilicus becomes everted
- Central tympany & shifting dullness
- Fluid thrill
3. Increase Intra abdominal Pressure
- Hernias (Umbilical/ Inguinal)
- Increased IVC Pressure leads to lower limb oedema
-Abdominal wall venous collaterals
4. Causative condition
- Portal HTN
- Chronic liver disease
- Evidence of Tb
5. Rectal examination for hemorrhoids, malignant lesion in pelvis or fluid in
pouch of Douglas.
Appearance to patient with ascites
• History
It is most important steps in the evaluation of a patient with ascites.
Foremost step in this is to rule out other causes of abdominal distension.
5F – Fat, Flatus, Feces, Fluid & Fetus
Once one in sure that case deals with fluid accumulation i.e. Ascites
→Looks for its etiology
- Ask about risk factors;
- Liver diseases,
- Alcohol overuse,
- IV drug abuse,
- BT;
- Cirrhosis,
- Hyperlipidemia,
- Diabetes mellitus
Sudden development of ascites in previously compensated Patient of cirrhosis
should raise the suspicion of hepatocellular carcinoma.
• Personal History
- Dietary habits
- Alcohol intake
• Past history
Tb, jaundice, hematemesis, piles, congestive heart failure; results in venous
pressure in Vena cava & consequent obstruction to venous out flow from
liver . This increases pressure can be seen as engorgement of veins of neck
(striking sign).
Early morning puffiness of face ,anasarca & decrease urine output suggests
renal involvement.
• Inspection
- Abdominal distension
- Umbilicus everted
- Distance between umbilicus & xiphisternum is more than the distance
between umbilicus & pubic symphysis
- Discoloration present or not
- Veins are dilated over abdomen
•Palpation & percussion
*Shifting Dullness
*fluid thrill
- Palpate with warm hand
*Shifting dullness
› Lie patient supine, percuss laterally from midline out to the flanks.
›There are 2 methods
I) Keep finger on the site of dullness in flank & ask the patient to turn on
to the opposite side. Pause for at least 10 second to allow any ascites to
gravitate ,then percuss again & if that area is now resonant ,Demonstrated
shifting dullness as the ascitic fluid became dependent
II) Mark the point which the percussion note changes from resonant to dull
with a pen on a line parallel to flank.
Ask the patient to turn to the same side & repeat the manoeuvre : if line
has moved up the abdomen towards the midline . It demonstrate shifting
dullness.
Always wait a few moments after the patient turns before repeating
percussion ,to allow time for the fluid to shift & settle.
*Fluid thrill
›If abdomen is tense, assess for a fluid thrill.
›Place the palm of left hand flat against the left side of abdomen, flick a finger of
right hand against the right side of abdomen.
›If the feeling of ripple against left hand ask the patient to place the edge of a
hand on midline of the abdomen.
›This prevents the transmission of impulse via skin.
›If still feeling of ripple against left hand that suggests the fluid thrill positive.
›It suggests the ascites is obvious.
* Pen filled method
› Patient is advised to sit up on bed.
› Keep one hand in anterior abdomen wall and with the other hand directly percuss
over one of the quadrant muscle.
› Feel the succession wave of fluid at the other hand kept at anterior abdominal
wall if fluid is present.
* Puddle's sign
› Patient is in prone position with knee elbow position for 5 minute.
›Asked to change the position & simultaneously percussion is done.
›Gradually move stethoscope to opposite flank. Change in percussion are noted
as we move towards the opposite flanks.
*Horse shoe dullness (shape)
›Patient is in knee chest position.
›Percuss from umbilicus to flank.
›note the changes from tympanic to dull sound & mark that point with a marker,
dullness extends from flank to pubic & hypo gastric region, due to gravitation of
fluid to most dependent part.
›A small area near the umbilicus will remain tympanic because of the floating up
of intestine.
INVESTIGATION
* CBC
* X ray
* CT
* USG
* Ascitic fluid analysis
→Signs of ascitic correlated to fluid quantity
› CT scan – 80 ml
› Ultrasound – 100 ml
› Pen filled method – 120 ml
› Puddle sign – 150 ml
› Shifting dullness – 1-1.5 ltr
› Horse shoe shaped dullness – 2-3 ltr
› Fluid thrill - >3 ltr
→Ascitic fluid analysis
ᴓ Macroscopic appearance
- Clear : Congestive heart failure
Cirrhosis
- Turbid : Bacterial infection (Tb, peritonitis)
- Blood stained : Trauma
Malignancy
Perforation
- Milky : Chylous ascites
Lymphatic obstruction
ᴓ Cytology
- Red cells – hemorrhagic
- White cells – infection, inflammation, tumor
- Malignant cells – carcinomatosis
ᴓ Biochemistry
1. SAAG (serum ascites albumin gradient)
SAAG = serum albumin - ascitic fluid albumin
Value >1.1 g/dl – ascites due to portal hypertension
Value < 1.1 g/dl – ascites due to the infection or other malignant condition
2. Protein content
>1.5 g/dl – infection, hepatic venous obstruction malignancy
<1.0 g/dl – Spontaneous Bacterial peritonitis
3. Glucose
4. Amylase
Increased in pancreatic ascites
5. Triglycerides
Increased in chylous ascites
*Additional Tests
› Liver Biopsy – malignancy of liver
› Liver function test – confirm Cirrhosis
› Liver scan – Space Occupying lesions of liver
› USG- detect as well as 100 ml of abdominal fluid cause of disease
› Laparoscopy – Paracenthesis
Direct visualization of abdominal viscera
Biopsy of liver
› Selective arteriography (hepatic & splenic artery) - visualize portal vein may be
helpful in ascites of obscure cause.
› Needle biopsy of peritoneum – Tb & malignant peritonitis
Complications
→ Further infection – Spontaneous Bacterial peritonitis
→ Hepatic hydrothorax- fluid in lungs (rt side mainly)
→ Renal failure
Differential diagnosis
› Abdominal distension causes
- Pregnancy
- Excessive fat
- Tumors
- Gaseous distension
- Distended bladder
› Other causes
- Cirrhosis of liver
- Tb. Peritonitis
- Malignant ascites
- Portal Hypertension
- Constrictive pericarditis
- Budd – chiari syndrome
- Spontaneous bacterial peritonitis
- Chylous ascites
- Pancreatic ascites
› According to ascitic fluid characteristics
Clear : Congestive heart failure, Cirrhosis
Turbid : bacterial infection (tb, peritonitis)
Blood stained : Trauma ,Malignancy, Perforation
Milky : chylous ascites, Lymphatic obstruction
Mucinous : colloid carcinoma of stomach
Pseudochylous : tumor cells
 MANAGEMENT
→ Bed rest improves renal profusion.
→ Diet: low sodium diet if fluid is non inflammatory.
Restrictions fluid to 1 ltr/day.
→ Diuretics
Spironolactone 100 mg, if no response add frusemide 40 mg.
Increase doses step wise to spironolactone 400 mg & frusemide 160 mg.
→Aim is to achieve weight loss of 300-500 g/day in ascitic patients with
peripheral oedema.
ᴓ Therapeutic paracenthesis
› It is also used for diagnosis purpose.
›Ensure that the patient’s bladder is empty, if there is any doubt a catheter should
be passed before paracenthesis attempted.
› The patient should lying flat or prepped up at slight angle.
› Aspiration usually performed in the right iliac fossa sterilize the skin with
antiseptic skin & drape it.
› Chosen point should be infiltrated with local anesthetics then injected down to
the parietal peritoneum (5 ml syringe & 25 gauze Needle use)
› If the puncture made simply for diagnostic purpose, 10 ml syringe & suitable
Needle can be used.
› If it is intended to drain the peritoneum, a trocar & flanged cannula should be
employed.
› A tiny incision should be made in anaesthetized area of skin and then trocar &
cannula inserted.
› Resistance is full as the trocar perforates the parietal peritoneum.
›Trocar is then withdrawn from the cannula & the fluid drained into a bottle.
›The binder is then secured over the abdomen, which helps to promote drainage.
›The rate of flow, which should not be too fast, can be controlled by means
of a clip on the tubing.
›When aspiration is complete, the cannula should be withdrawn. The puncture
wound is sealed with a plastic dressing & a dry dressing applied.
*Contraindications of paracenthesis
- An acute abdomen
- Pregnancy
- Intra-abdominal wall adhesions
- Bowel distension
- Bleeding disorders
- Severe Jaundice
In that cases if possible as diuretics are preferable.
*Indications of paracenthesis
- To diagnose nature of fluid
- Tb
- Therapeutic
- Bacterial peritonitis
- Malignancy
- Ascites
*Complications of paracenthesis
- Hepatic coma
- Intra-abdominal hemorrhage
- Peritonitis
- Bladder infection
- Fainting
• Treatment according to cause
›Digitalis – cardiac failure
›Anti-tuberculosis drugs – tub Peritonitis
›Pericardiolysis – constrictive Pericarditis
›Vit B1-Beriberi
›Acute venous obstruction – Thrombolytic therapy
Angioplasty
ᴓ Trans jugular intrahepatic Porto systemic shunts (TIPS)
› This has helped to improve variceal hemorrhage which didn’t respond to
either drug treatment or endoscopic therapy, this technique seems to be the
best.
› Under local anesthesia & analgesia with sedation , the shunts are introduced
under fluoroscopic & ultrasono graphic guidance.
› A guide wire is inserted into the hepatic vein & ultimately into a branch of
portal vein through internal jugular vein & superior Vena cava.
› The track of guide wire is dilated with a balloon catheter.
›By this time a drop in portal venous pressure with reasonable control of
variceal hemorrhage can be detected.
›Now a metallic shunt introduced through the expanded channel.
*Complication of TIPS
- Perforation of liver capsule
- Fatal intra peritoneal bleeding
- Post shunt encephalopathy
- Stenosis leads to further variceal hemorrhage.
*Contraindications of TIPS
- Portal vein occlusion
*Treatment of Complication
1. Shock: sedation with barbiturates
Fresh BT
2. Clotting problems: vit K administration
Fresh BT
3. Encephalopathy: continuous gastric lavage (prevents absorption of blood
protein)
Neomycin 500 mg in first & every 2 hrs.
Mg sulphate
4. Liver failure : plenty of carbohydrates should be given by mouth
Fat reduce in diet
5.Ascites :low sodium diet
Diuretics
ᴓ Peritoneovenous shunt
›A peritoneovenous shunt is a shunt which drains peritoneal fluid from the
peritoneum into veins, usually the internal jugular vein or the superior vena cava.
It is sometimes used in patients with refractory ascites.

› It is a long tube with a non-return valve running subcutaneously from the

peritoneum to the internal jugular vein in the neck, which allows ascitic fluid to
pass directly into the systemic circulation.

* Complications of peritovenous shunt

1. Infection
2. Superior vena caval thrombosis
3. Pulmonary edema
4. Bleeding from varices

ᴓ Surgery

›Ascites that is refractory to medical therapy is considered an indication for

liver transplantation.