CAUSES OF ASCITES AND ITS DIFFERENT TYPES

Definition :

  Ascites refers to the accumulation of free fluid in the peritoneal cavity .

•          CAUSES OF ASCITES
Common causes

•          Malignant disease

–        Hepatic

–        Peritoneal

•          Cardiac failure

•          Hepatic cirrhosis

•          Hypoproteinaemia

–        Nephrotic syndrome

–        Protein-losing enteropathy

–        Malnutrition

•          Hepatic venous occlusion

–        Budd-Chiari syndrome

–        Veno-occlusive disease

•          Pancreatitis

•          Lymphatic obstruction

•          Infection

–        Tuberculosis

–        Spontaneous bacterial peritonitis

•          Rare

–        Meigs' syndrome

–        Vasculitis

–        Hypothyroidism

   _ Renal dialysis

1. According to the appearance of ascitic fluid
   Straw – coloured

                      Malignancy

Exudate         T . B

                       S B P

Transudate              L ¢

                                CHF

                                Const  pericandites

                                Megic synrome

                                Nephrotic syndrome

ii  Chylous

Iii Haemorrhagic

–        Malignancy

–        Rupture ectopic pregnancy

–        Acute Pancreatitis

–        Clinical features

–        Ascites causes abdominal distension with fullness in the flanks, shifting dullness on percussion and when the ascites is marked, a fluid thrill .

–        These signs do not appear until the ascites volume exceeds 1 litre, even in thin patients, and much larger volumes can be hard to detect in the obese.

1. Associated features of ascites include
   distortion or eversion of the umbilicus,
2. herniae,
3. abdominal striae,
4. divercation of the recti
5. scrotal oedema.
6. Pleural effusions are found in about 10% of patients, usually on the right side (hepatic hydrothorax); most are small and only identified on chest X-ray .-
   
7. Pathogenesis of ascites in cirrhosis
   
   
8. Sodium and water retention.

      Peripheral arterial vasodilatation (by NO and prostaglandin) with reduction in the effective blood volume,activate rennin-angiotensin system→ salt and water retention.

2.   Portal hypertension :

      P H leads to↑ hydrostatic pressure, increased hepatic and splanchnic production of lymph and transudation of fluid into the peritoneal cavity

3.  Low serum albumin

     Leading to decreased albumin plasma oncotic pressure.

Theories of Ascites secondary to L ¢

Under filling theory :

Ascites lead to decrease intravascular volume,

Release of renin , aldosterone and ADH,

Na and water retention →       increase     ascites formation.

Over filling theory:

Systemic VD           excessive renal reabsorption of Na and water          hypervolemia →        overflow of fluid into peritoneum .

Investigations

1- Cause :

          Liver function tests

          Kidney function tests

          Abdominal ultrasonographly

          Echo cardiography

2- Laparoscopy :

          Peritoneal tumours

          T . B

3- Tapping and ascitic fluid examination :

          Bacteriology , culture and sensitivity

          Protein content

•          Cirrhotic patients typically develop a transudate with a total protein concentration below 2,5 g/l and relatively few cells.

•             However, in up to 30% of patients, the total protein concentration is more than 30 g/l. In these cases it is useful to calculate the serum-ascites albumin gradient by subtracting the concentration of the ascites fluid albumin from the serum albumin.( SAAG )

•          SAAG = serum albumin – Ascitic fluid albumin

•                                                                                                                                                                                                                                                                                          ≥      1.1 gm / dl = portal   hypertensive 

•                           ascites

•                   ≤      1.1 gm / dl = non portal

•                           hypertensive ascites 

•             A gradient of more than 1,1 g/l is strongly suggestive of portal hypertension and cirrhosis.

•          Exudative ascites 

•            (ascites protein concentration above 25 g/l or a serum-ascites albumin gradient of less than 11 g/l) raises the possibility of infection (especially tuberculosis), malignancy, hepatic venous obstruction, pancreatic ascites or, rarely, hypothyroidism   Ascites amylase activity above 1000 U/l identifies pancreatic ascites, and low ascites glucose concentrations suggest malignant disease or tuberculosis.

•            Cytological examination may reveal malignant cells (one-third of cirrhotic patients with a bloody tap have a hepatoma).

•          .

•             Polymorphonuclear leucocyte counts above

•            250 × 106/l strongly suggest infection (spontaneous bacterial peritonitis.

•             Laparoscopy

•             can be valuable in  

•             detecting peritoneal  

•             disease.

•             Ultrasonography

•             is the best means of confirming ascites, particularly in the obese and those with small volumes of fluid. Paracentesis (if necessary under ultrasonic guidance) can also be used to confirm the presence of ascites but is most useful for obtaining ascitic fluid for analysis .

Management

   Successful treatment of ascites relieves discomfort but does not prolong life, and if over-vigorous, can produce serious disorders of fluid and electrolyte balance and precipitate hepatic encephalopathy .

    1- Rest in bed

        This improves renal blood flow and   

        lead to diuresis

2- Sodium and water restriction

     Restriction of dietary sodium intake is essential to achieving negative sodium balance in patients with ascites. Restriction to 100 mmol/day ('no added salt diet') may be adequate, but restriction to 40 mmol/day (which requires close dietetic supervision) is necessary in more severe ascites.

   Drugs containing relatively large amounts of sodium and those promoting sodium retention, such as non-steroidal analgesic agents, must be avoided .

   Restriction of water intake to 0.5-1.0 litre/day is necessary only if the plasma sodium falls below 125 mmol/l..

   SOME DRUGS CONTAINING RELATIVELY LARGE AMOUNTS OF SODIUM OR CAUSING SODIUM RETENTION

Avoid these medication

High sodium content

•          Antacids

•          Alginates

•          Antibiotics

•          Phenytoin

•          Sodium valproate

•          Effervescent preparations, e.g. aspirin, calcium, paracetamol

Sodium retention

•          Carbenoxolone

•          Corticosteroids

•          Diazoxide

•          Metoclopramide

•          NSAIDs

•          Oestrogens

SOME ANTIBIOTICS WITH
A HIGH SODIUM CONTENT

Ampicillin	Amoxicillin
Cefotaxime	Benzylpenicillin
Cefradine	Cefoxitin
Cefuroxime	Ceftazidime
Flucloxacillin	Chloramphenicol
Ticarcillin	Piperacillin

3 - Diuretic drugs
The aim is to achieve wight loss 500 gm / d .

If these is no peripheral  oedema ,1000 gm / d

If  peripheral oedema is present .

•          Monotherapy :

   Aldosterone antagonist ( spironolactone ) 100 – 400 mg / d .

•          Combination theray :

    Furosemide ( lasix ) + spironlactone

       40 – 160 mg /d + 100 – 400 mg /d

                       Ratio 2 : 5

•          Patients who do not respond to doses of 400 mg spironolactone and 160 mg furosemide are considered to have refractory or diuretic-resistant ascites and should be treated by other therapeutic measures.

•          Refractory ascites 

   ( diuretic resistant ascites )

    i-e Ascites not responding to salt. fluid restriction and frusemide 160 mg + spironolactone 400 mg for at least 2 weeks .

•           Intractable ascites

    ( diuretic intractable ascites)

   i.e Ascites can not be treated by duiretic because of complications e.g encephalopathy

4 - Salt poor albumin
I . V to increase plasma oncotic pressure

•          -5- Therapeutic abdominal paracentesis
The first-line treatment of refractory ascites is large-volume paracentesis with intravenous albumin.

•          Paracentesis to dryness or the removal of 3-5 litres daily is safe, provided the circulation is supported by giving intravenous colloid such as human albumin (6-8 g per litre of ascites removed) or another plasma expander.

•          Total paracentesis can therefore be used as an initial therapy or when other treatments fail.

1. Complications of paracentesis :
   Hypovolemia
2. Encephalopathy
3. Hepatorenal syndrome

1. To avoid complications:
    ( selection criteria )
   Tense ascites
2.  Lower limb oedema
3. Child grade B
4. Prothrombin  ≥ 40 %
5. Serum bilirubin ≤ 10 mg / dl .
6. Platelet ≥ 40.000 mm3 .
7. S.creatinine ≤ 3 mg / dl .
8. Urinary sodium ≥ 10 mmol / 24 hrs .

      If ascites is resistant or refractory to the previous treatment, the following causes must be considered and treated:

1. Salt retention            good regimen
2. Marked hypoalbuminemia             salt free      albumin I.V
3. Hyponatremia             fluid restriction and stop diuretic for few days then resume.
4. T. B peritonitis
5. Malignancy
6. Decreased kidney function
7. Weak diuretics
8. Peritoneo-venous (LeVeen) shunt
9. The peritoneo-venous shunt 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.
10. It is effective in ascites resistant to conventional treatment but complications, including infection, superior vena caval thrombosis, pulmonary oedema, bleeding from oesophageal varices and disseminated intravascular coagulopathy, limit its use and insertion of these stents is now rare.

Ultra filtration & reinfusion
Mechanism of  Action :

•          Passage of ascitic fhuid out side the body through a machine that can extract the excem water and reintroduce the concentrated fluid through I.V set .

•          Side effects :

            -Peritonitis

-            Volume overload

Transjugular intrahepatic portosystemic stent shunt (TIPSS)

( TIPSS )

     TIPSS can relieve resistant ascites but does not prolong life. It can be used where liver function is reasonable or in patients awaiting liver transplantation, but should not be used in the terminally ill.

•          Prognosis Ascites is a serious development in cirrhosis, as only 10-20% of patients survive 5 years from its appearance. The outlook is not universally poor, however, and is best in those with well-maintained liver function and where the response to therapy is good. The prognosis is also better when a treatable cause for the underlying cirrhosis is present or when a precipitating cause for ascites, such as excess salt intake, is found.

Complications

•          Ascites may be complicated by renal failure and also by infections which are spontaneous or, more commonly, precipitated by invasive investigations or treatment, such as upper gastrointestinal endoscopy and injection sclerotherapy.

•          Spontaneous Bacterial peritonitis
It is a precipitating factor of hepatic encephalopathy  

•          Consider it if a patient with liver cirrhosis and ascites deteriorate progressively without obvious precipitating cause .

•          The organism gain acceSS to the peritoneum by hematogenous spread.

C P :

1. Fever  , abdominal pain , rebound tenderness
2. Marked deterioration in patient with l¢ , ascites .
3. It may be silent .

Investigation :

Ascetic fluid ≥ 250 PNL / m3

Culture         E . Coli klebsiella

Treatment :

Third generation cephalosporin 4 gm / d .