Ascites for undergraduates

1. Ascites
PROF. DR. MOHAMED-NAGUIB WIFI
PROFESSOR OF MEDICINE AND
HAPATOGASTROENTEROLOGY
CAIRO UNIVERSITY

2. Introduction
The word ascites is of Greek origin “askos” and
means bag or sac.
 Ascites is the condition of pathologic fluid
accumulation within the abdominal cavity.
Healthy men have little or no intraperitoneal fluid,
but women may normally have as much as 20 mL
depending on the phase of the menstrual cycle.

3. Causes Of Ascites
I- Increased
hydrostatic
pressure:
II- Diminished
colloid osmotic
pressure:
III- Increased
permeability of
peritoneal
capillaries:
1. Cirrhosis
2. Hepatic vein
occlusion (Budd-Chiari
syndrome)
3. IVC obstruction
4. Constrictive
pericarditis
5. Congestive heart
failure
1. End-stage liver ,disease
with poor protein synthesis
2. Nephrotic syndrome
with protein loss
3. Malnutrition
4. Protein-losing
enteropathy
1. T.B. peritonitis
2. Bacterial peritonitis
3. Malignant disease of
the peritoneum

4. Causes Of Ascites
IV- Leakage of
fluid into the
peritoneal cavity:
1. Bile ascites
2. Pancreatic ascites( secondary
to a leaking pseudocyst)
3. Chylous ascites
4. Urine ascites
V- Miscellaneous
causes:
1. Myxedema
2. Ovarian disease(Meigs'
syndrome)
3. Chronic hemodialysis

5. Pathophysiology
• This is probably due to renal retention of sodium and water, so many factors
are involved.
• The most important are:
1- Sodium & water retention as a result of splanchnic arterial vasodilatation with
consequent reduction in the effective blood volume leading to activation of both
sympathetic nervous and the renin- angiotensin (RAAS) system. This is what is
known as the Arterial Vasodilatation Theory.
2- Portal hypertension increases local hydrostatic pressure leading to increased
hepatic and splanchnic production of lymph and transudation of fluid into the
peritoneal cavity (Weeping Liver).
3- Low serum albumin (which is a result of poor hepatic synthesis), leads to
reduction in plasma oncotic pressure.
4- Lymphatic obstruction localizes the fluid accumulation in the peritoneal cavity.

6. Symptoms
1. Small amount of ascites: Asymptomatic
2. Large amount of ascites:
- Abdominal distention and discomfort
- Anorexia & Nausea
- Early satiety
- Heartburn (Gastroesophageal Reflux)
- Flank pain
- Respiratory distress

7. Signs
1. Wide subcostal angle, divarication of recti, Umbilicus is
shifted downwards and everted.
2. Bulging flanks when the patient is supine.
3. Tympany at the top of the abdominal curve and dullness in
the flanks
4. Shifting Dullness Test.
5. Transmitted thrill.

8. Laboratory Investigations
1- Ascitic fluid analysis: Serum Albumin minus ascites
albumin gradient (SAAG):
Peritonitis

10. Ascitic fluid cell count with
differential:
1- Ascites Red Blood Cells (RBC) elevated
- Neoplasm (Malignant ascites)
- Tuberculous peritonitis (variably elevated)
- Pancreatitis (variably elevated)
2- Ascites White Blood Cells (WBC) elevated> 1000 per mm3
- Neoplasm (>50% Lymphocytes)
- Bacterial peritonitis (WBC > 10,000 per mm3)
- Spontaneous Bacterial Peritonitis (PMN > 250 per mm3)
- Tuberculous peritonitis (>70% Lymphocytes)

11. Other laboratory tests in ascetic
fluid:
Lactate dehydrogenase
Amylase is elevated in pancreatitis and gut perforation
Lipids, triglycerides more than 200 mg% is present in
chylous ascites
Culture and sensitivity
Cytology for malignant cells

12. Abdominal Ultrasound
Abdominal ultrasound or CT abdomen are very
sensitive procedures.
Ultrasonography can detect ascites even in very
small amount
Can also diagnose the cause of ascites as in Budd
chiari syndrome.

13. Ascites

14. Treatment
Bed rest to improve renal blood flow
A diet limited to 2 grams of sodium per day
Fluid restricted to 1 liter a day if serum sodium
less than 125 mg per dl.
Hospitalization to monitor the daily weight and
salt balance

15. Treatment
Diuretics
- Common diuretics include spironolactone, amiloride,
and triamterene.
- If these are not effective, stronger diuretics may be used
i.e. loop diuretics ; these include frusemide, thiazide, and
ethacrynic acid.
- About 10% to 15% are resistant to even maximal doses
of diuretics or develop side effects of these drugs.

16. Refractory Ascites
Is that which cannot be mobilized or the
early recurrence after therapeutic
paracentesis.
It cannot be satisfactorily prevented by
medical therapy.

17. Refractory Ascites
Two different subtypes of refractory ascites:
(i) Diuretic-resistant ascites: Is that which cannot be
mobilized because of a lack of response to dietary
sodium restriction and intensive diuretic treatment.
(ii) Diuretic-intractable ascites: Is that which cannot be
mobilized because of the development of diuretic-
induced complications that preclude the use of an
effective diuretic dosage.

18. Side effects of diuretics include
the following:
Dehydration
Alteration of electrolyes levels in the blood
Renal impairment

19. Treatment options for
refractory ascites include:
Large volume (therapeutic) paracentesis (may be repeated every 2-4
weeks) with 8 gm albumin infusion per every liter of ascites removed.
Transjugular intrahepatic portosystemic stent shunt (TIPS)
Liver transplantation
Le Veen (peritoneovenous) shunt only in patients who are not
candidate to paracentesis, TIPS or transplantation.
Midodrine (vasoconstrictor material) was found to improve the
outcome and survival in refractory ascites .

20. Side effects of Removal of large volumes of
fluid using paracentesis:
Impaired renal function
Hypotension
Shock

21. Side effects that shunting procedures
can cause:
Abnormal blood clotting that may result in bleeding
Change in mental functions or level of
consciousness
Clotting of the shunt
Infection

22. Complications
Spontaneous Bacterial Peritonitis
Hepatorenal Syndrome

23. Spontaneous Bacterial
Peritonitis (SBP)
Spontaneous bacterial peritonitis (SBP) is defined as an
ascitic fluid infection without an evident intra-abdominal
surgically-treatable source
It primarily occurs in patients with advanced cirrhosis.
Usual organisms are G-ve bacteria (E.coli, Klebsiella and
enterococci).

24. Pathogenesis
•Offending organisms
reach the peritoneum
from the blood stream as
a result of bacterial
translocation from the
gut due to defective gut
barrier in cirrhotics.

25. Diagnosis
Is established by an elevated ascitic fluid absolute
polymorphonuclear leukocyte (PMN) count (≥ 250
cells/mm3) and empiric therapy can be started.
Any patient with new onset ascites, fever, abdominal
pain and tenderness, worsening ascites, or ascites that
became diuretic resistant should have a diagnostic
paracentesis with bedside blood culture inoculation and
cell count.

26. Treatment
Empiric therapy is usually started before results of
blood culture with cefotaxime (2gm/8hr-IV) or
ciprofloxacin (200 mg/8hr-IV) for 5-10 days.
Albumin infusion 1.5 gm per kg in day 1 and day 1
gm per kg in day 3 improve the survival and renal
function.

27. Prophylaxis
Primary prophylaxis if:
• Ascitic fluid protein is less than 1 gm per dl
• Ascitic fluid protein is less than 1.5 gm per dl plus renal
impairment or child classification.
• Upper GI bleeding.
Secondary prophylaxis in all patients with SBP:
Norfloxacin 400 mg daily or ciprofloxacin 250 mg daily.

28. Hepatorenal Syndrome (HRS)
This is a functional renal failure
occurring in patients with liver cirrhosis,
portal hypertension and ascites.

29. Pathogenesis
• The hallmark of HRS is renal
vasoconstriction, although the
pathogenesis is not fully
understood.
• The 2 main theories are the
arterial vasodilatation theory
and the hepatorenal reflex
theory.
• Evidence points to the
vasodilatation theory as a more
tangible explanation for the
development of HRS.

30. Pathogenesis
■ The arterial vasodilatation theory:
• Portal hypertension  splanchnic VD  underfilling of
the arterial circulation  arterial baroreceptor mediated
activation of the vasoconstrictor mechanisms (RAAS) 
VC in the renal only but also in the systemic circulation.
■ The Hepatorenal reflex theory:
• Renal vasoconstriction in HRS is unrelated to systemic
hemodynamics but is due to either:
• Deficiency in the synthesis of a vasodilatory factor
• Hepatorenal reflex that leads to renal vasoconstriction.

31. Precipitating factors:
• Large volume paracentesis without volume
replacement
• Extensive diuretic therapy
• Diminished intravascular volume due to e.g.
severe diarrhea
• Sepsis.

32. Types:
• Type 1 HRS: Rapidly progressive type with high mortality
rate. Defined by a doubling of the initial serum creatinine
level to greater than 2.5 mg/dL in less than 2 weeks.
The development of this form often is associated with a
mortality rate of over 90% without liver transplantation.
• Type 2 HRS: Slower progressive course and usually
present with diuretic resistant ascites.
It has a better outcome.

33. Criteria of Diagnosis
Chronic or acute liver disease with advanced hepatic failure and
portal hypertension.
Low glomerular filtration rate as indicated by serum creatinine
greater than 1.5 mg/dl.
Absence of shock, ongoing bacterial infection, current or recent
treatment with nephrotoxic drugs and absence of GI fluid losses.
No sustained improvement after withdrawal of diuretics and
expansion of plasma volume.
No ultrasonographic evidence of obstructive uropathy or
parenchymal renal disease.

35. Prevention
Care should be taken with diuretic therapy to
prevent volume depletion and underfilling of the
circulation.
Bacterial infections should be diagnosed and
treated to avoid sepsis and precipitation of
hepatorenal syndrome.

36. Treatment
Plasma expansion by albumin infusion, plus:
Vasoconstrictive drugs; assuming that splanchnic
vasodilatation is the original mechanism initiating the
syndrome, somatostatin analogues (octereotide), vasopressin
analogues (terlipressin), and sympathetic vasoconstrictors
have been used.
TIPS (transjugular Intrahepatic portosystemic shunt)

37. Treatment
Hemodialysis is not routinely recommended unless there is
severe hyperkalemia or metabolic acidosis and usually used as
a bridge to liver transplantation.
Liver transplantation.