Presentation regarding ascites

1. Ascites
By- Dr. Abhijeet & Dr. Ikram

2. • Ascites is defined as the pathologic fluid accumulation within the
peritoneal cavity.
• The word ‘ascites’ is derived from the Greek word “askos” which
means a sack or bag.
• Ascites occurs in the setting of portal hypertension as a result of
cirrhosis in nearly 85 % of cases.
• The pathogenesis of ascites can be classified as Cirrhotic and Non
Cirrhotic Ascites.
• There are many theories that explain the mechanism of development
of cirrhotic ascites like the underfill theory, overload theory and the
most recent theory “peripheral arterial vasodilation hypotheses”
which proposes that underfill and overload theories are both correct
but are operative at a different stage.
Introduction :

3. Pathogenesis of Ascites in Cirrhosis
• Following mechanisms are involved:
• Portal hypertension: increase in portal vein hydrostatic pressure
resulting in extravasation of fluid from plasma in the peritoneal cavity.
• Hypoalbuminemia: due to decreased synthetic function in a cirrhotic
liver, plasma oncotic pressure decreases and as a result extravasation
of fluid.
• Splanchnic vasodilatation: increase in NO synthesis causes pooling of
blood and decrease in effective circulating volume which is perceived
by the kidneys as hypovolemia and a compensatory vasoconstriction
via release of ADH hormone and renin – angiotensin aldosterone
system ensues leading to free water retention and renal sodium &
water retention respectively
• Percolation of Hepatic Lymph: hepatic lymphatic flow exceeds the
thoracic duct capacity thus causing excess lymph to ooze out freely
from surface of liver to peritoneal cavity.

5. Etiology of Ascites

6. Portosystemic Circulation

8. Pathogenesis in Absence of Cirrhosis
• Peritoneal Carcinomatosis - can result from
• Primary peritoneal malignancies(mesothelioma, sarcoma);
• Abdominal malignancies(Colonic or Gastric Adenocarcinoma);
• Metastatic disease(Ca Lung, Ca Breast, Melanoma)
• Peritoneal Infection (Tuberculous) –tubercles deposited on the
peritoneal lining secrete a proteinaceous fluid
• Pancreatic Disease –leakage of pancreatic enzymes into the
peritoneum

9. Mechanisms of fluid accumulation in non cirrhotic ascites
• Peritoneal carcinomatosis -production of proteinaceous fluid by
tumor cells
• Massive liver metastases - stenosis or occlusion of portal veins by
tumor nodules or tumor emboli.
•
• Hepatocellular carcinoma - cirrhosis-related portal hypertension,
tumor-induced portal vein thrombosis, or both.
•
• Chylous ascites in patients with malignant lymphoma - lymph node
obstruction by tumor and rupture of chyle-containing lymphatics.

10. • High-output or low-output heart failure or nephrotic syndrome -effective
arterial blood volume is decreased, and the vasopressin, renin-aldosterone,
and sympathetic nervous systems are activated- lead to renal vasoconstriction
and sodium and water retention
• TB, Chlamydia infection, and coccidioidomycosis - ascites through the
production of proteinaceous fluid
• Pancreatic or biliary ascites - leakage of pancreatic juice or bile into the
peritoneal cavity
•
• After abdominal surgery - lymphatics may be transected - lymphatic leak.

11. Causes of Ascites

12. Cause Frequency
• Parenchymal liver disease 78%
• Cirrhosis 77%
• Fulminant hepatic failure 1%
• Malignancy 12%
• Cardiovascular disease 5%
• Infection 2%
• Renal 1.5%
• Pancreatic 1%
• Bacterial peritonitis 0.5%
• Marked Hypothyroidism, Collagen Vascular disease, Familial Mediterranean fever,
Amyloidosis, Hereditary Angioneurotic oedema, Menetrier’s Disease and Protein losing
enteropathy, Starch Peritonitis, Trauma

14. Clinical Features
• Symptoms :
• Abdominal Distension often with peripheral oedema
• Dyspnea & orthopnea
• Gastroesophageal reflux
• Muscle wasting and excessive fatigue

15. Signs in Ascites:

16. • Signs :
• Distension of abdomen
• Fullness of flanks
• Umbilicus flat or everted
• Abdominal skin stretched & shiny
- Caput medusae
- Distended veins over the flanks
- Abdominal dullness

17. Flow of Veins (Harvey’s sign)

18. Associated findings which maybe found –
• Oedema of scrotum
• Pedal oedema
• Pleural effusion (commonly on the right side)
• Meralgia paresthetica
• Divarification of recti and hernia

19. • Ascites frequently develops during a patient’s first episode of
decompensation of alcoholic liver disease.
• Ascites can develop early in alcoholic liver disease in the precirrhotic
alcoholic hepatitis stage. At this stage, changes are reversible with
abstinence from alcohol.
• Many patients with cirrhosis and ascites will ultimately require liver
transplantation.
• Patients with ascites should be questioned about risk factors for liver
disease other than alcohol, such as injection drug use, blood
transfusions esp. prior to 1992, sex with a same gender partner,
acupuncture, tattoos, ear piercing, and country of origin.

20. • Another cause of “cryptogenic” cirrhosis and ascites is NASH from
long-standing obesity. Many patients who have been obese will
spontaneously lose 50 or even 100 pounds after their liver disease
decompensates.
• Patients with a long history of stable cirrhosis and the sudden
development of ascites should be suspected of harboring a
hepatocellular carcinoma that has precipitated the decompensation.
• Patients with ascites who have a history of cancer should be
suspected of having malignancy-related ascites.
• Malignancy-related ascites (e.g. breast, lung, colon, pancreatic
cancer) frequently is painful, whereas cirrhotic ascites usually is not,
unless bacterial peritonitis or alcoholic hepatitis is superimposed.

21. • A history of heart failure may raise the possibility of cardiac ascites.
•
• Tuberculous peritonitis usually manifests as fever and abdominal
pain.
•
• Ascites may occur in patients with acute pancreatitis with necrosis or
a ruptured pancreatic duct from chronic pancreatitis or trauma.
• Hemodialysis - may develop in a small percentage of patients
undergoing hemodialysis.
• Fitz Hugh–Curtis syndrome caused by chlamydia or gonorrhea may
cause inflammatory ascites in a sexually active woman.

22. • Patients in whom ascites and anasarca develop in the setting of
diabetes mellitus should be suspected of having nephrotic ascites.
• Ascites in a patient with symptoms and signs of myxedema should
prompt assessment of thyroid function.
• Serositis in a patient with a connective tissue disease may be
complicated by ascites.

23. • Physical Examination
• Flank Dullness –on percussion of the flanks dullness is greater than that
normally found on the lateral aspect of the abdomen with the patient supine),
the examiner should check for “shifting.”
• If flank dullness is absent, checking for shifting is unnecessary.
• Approximately 1500 mL of fluid must be present before dullness is detected.
• If flank dullness is not present, the chance that the patient has ascites is less
than 10%.
• Dd - Gaseous distention of the bowel, a thick panniculus, and an ovarian mass
can mimic ascites. Gaseous distention should be readily apparent on percussion.
• Ovarian masses usually cause tympanitic flanks with central dullness. The speed
of increase in abdominal girth also can be helpful: ascites develops in days to
weeks, whereas thickening of the omentum and panniculus takes months to
years.
•

24. Ultrasonography can detect as little as 100 mL of fluid in the
abdomen.
The presence of large veins on the patient’s back suggests inferior
vena cava blockage.
An immobile mass in the umbilicus, the Sister Mary Joseph
nodule, is suggestive of peritoneal carcinomatosis.
Alcoholic cardiomyopathy with cardiac ascites can mimic cirrhosis
with ascites; an elevated jugular venous pressure helps with this
aspect of the differential diagnosis.

25. • Constrictive pericarditis is one of the few curable causes of ascites.
Most patients with cardiac ascites have impressive jugular venous
distention. Some have no visible jugular venous distention but such
high central venous pressures that their bulging forehead veins rise to
the top of their skulls.
• When present, peripheral edema in patients with liver disease is
usually found in the lower extremities and occasionally may involve
the abdominal wall. Patients with nephrotic syndrome or cardiac
failure may have total body edema (anasarca)

26. Different methods of examination of Ascites

27. • Signs of Ascites –
• Horse Shoe dullness- both the flanks and the hypogastric area are dull on
percussion. Seen in moderate ascites
• Fullness (bulging) of flanks – Only the dullness note is found in the flanks.
Seen in mild ascites.
• Shifting Dullness – by altering the posture of the patient and
demonstrating a change in interface of air fluid interface. A minimum of
500 to 1000 ml of fluid is necessary for elicitation of shifting dullness.
• Fluid thrill – by appreciating the transmitted impulse on one side of
abdomen produced by flicking the abdomen with a finger on the other side
while firmly placing the ulnar border of patient’s hand over the midline.
Elicited in tense ascites with fluid more than 2000ml.
• Puddle Sign – with the patient in the prone position for atleast 5 mins
followed by knee elbow position and placing the stethoscope over the
most dependent portion of the abdomen and repeatedly flick one flank
lightly. On moving the stethoscope to the opposite flank a marked change
in intensity & character of sound indicates presence of fluid. Can detect
ascites as low as 120 ml

28. Investigations :
• Paracentesis-Passing a needle or a catheter transcutaneously
preferably across the left lower quadrant of abdomen
• Safe procedure even in pts with Coagulopathy with infrequent
complications(Abdominal wall hematomas, hypotension,
hepatorenal syndrome, infection)
• Fluid obtained should be examined for –
• Gross Appearance
• Albumin and total protein levels
• Differential counts
• Gram’s Stain & Culture
• Serum-Ascites Albumin Gradient(SAAG)
• Specific clinical circumstances- Ascitic Glucose, LDH, Amylase, ADA,
Cytology, Laparotomy, Laparoscopy for peritoneal biopsies,
Histology

29. Gross appearance of ascitic fluid
• Turbid (infection or tumor cells)
• Milky (Chylous with TGs level >200mg per dl
• Dark brown fluid-High bilirubin content
• Black fluid (Pancreatitis)
INVESTIGATIONS :

30. Serum-Ascites Albumin Gradient(SAAG)
• The ratio of Level of Albumin in Ascitic Fluid to that in serum is called
SAAG(serum Albumin is also sent simultaneously)
• Useful to differentiate Ascites caused due to Portal HTN from Non Portal
HTN
• It correlates with the hepatic veinous pressure gradient thus reflecting
pressure within the hepatic sinusoids
• Calculated by subtracting Ascitic albumin from Serum Albumin
• High SAAG >1.1 g/dL reflects high Portal HTN being reason for increased
pressure in sinusoids causing the Ascites
• Low SAAG <1.1 g/dL indicates Portal HTN not being the cause of Ascites
• High Ascitic Protein levels (>2.5g/dL) indicate sinusoids are normal allowing
passage of albumin into ascites eg. Cardiac ascites, Early Budd Chiari
syndrome

32. Ascitic protein <2.5g/dL indicates that the hepatic sinusoids have been
damaged & scarred and no longer allow passage of protein as in
Cirrhosis, Late Budd Chiari syndrome, Massive hepatic metastases
Also high BNP titres in serum indicate Heart Failure as cause of High
SAAG ascites
Secondary peritonitis due to suspected perforated hollow viscus in
contrast to Spontaneous Bacterial Peritonitis is suggested by an
elevated ascitic LDH than serum and with glucose < 50 mg/dL and
multiple pathogens on culture.

33. In pancreatic ascites the amylase level of ascitic fluid is > 1000 mg/dL.
Tuberculous peritonitis is difficult to diagnose as the AFB Smear has a
sensitivity of about 0 to 3% and culture increases sensitivity of
diagnoses to 35 to 50 %. In non cirrhotic pts the sensitivity of ADA is
more than 90%
In ascites of uncertain cause laparotomy or laproscopy with peritoneal
biopsies for histology and culture remains gold standard.

34. Ascitic fluid total protein and the serum-
ascites albumin gradient (SAAG)
• Ascitic total protein concentration has been used to determine
whether ascitic fluid was a transudate or exudate. Currently, it is
accepted that the accuracy of the relationship between ascitic protein
concentration and etiology of ascites was overestimated eg. cardiac
ascites was incorrectly considered to cause low protein concentration
or 24% of uncomplicated cirrhotic pts had greater than 25 g/L and
20% of malignant ascites cases had a low protein concentration. Now
considered outmoded and replaced with SAAG. SAAG is a more sensitive
and specific measure for the differentiation of ascites due to portal
hypertension from ascites due to other pathophysiological mechanisms
(e.g. peritoneal inflammation). Causal mechanism was identified in 97%
of cases with SAAG, whereas only 55% was identified using ascitic total
protein concentration.

35. Lactate Dehydrogenase LDH
• Combining LDH with total protein analysis for differentiation between
hepatic and non-hepatic ascites-
• LDH of 400 SU
• Fluid/serum LDH ratio of 0.6
• Fluid/serum total protein (TP) ratio of 0.5.
• Ascitic levels higher than cut-off (2 out of three parameters) indicate a non-
hepatic cause of the ascites
• Values below the cutoffs for all three parameters strongly suggest a hepatic
cause of ascites. LDH values are usually higher in patients with an SAAG of 1.1
g/dL or less than in those with an SAAG greater than 1.1.
• Mean ascitic fluid LDH level was much lower in patients with liver disease
than in those with malignant ascites
• High sensitivity but low specificity (malignant ascites)

36. ASCITIC FLUID GLUCOSE
• Under normal conditions, it is similar to that in the serum. Ascitic
glucose decreases due to consumption by bacteria, white blood cells or
cancer cells in the fluid in tuberculous peritonitis, spontaneous
bacterial peritonitis (SBP), and malignancy.
• Significantly lower than normal in tuberculous ascites compared to
cirrhosis
• Secondary peritonitis due to suspected perforated hollow viscus in contrast
to Spontaneous Bacterial Peritonitis is suggested by an elevated ascitic LDH
than serum with glucose < 50 mg/dL and multiple pathogens on culture
• considering the value of glucose in patients with SAAG greater or less
than 1.1 g/dL, there was no significant difference between them. Low
diagnostic sensitivity and specificity, the application of ascitic glucose
analysis is limited in routine practice

37. Ascitic Amylase
• Amylase-rich ascitic fluid commonly occurs in cases of pancreatic duct damage or
obstruction due to pancreatitis or pancreatic trauma.
• Elevation of amylase levels above the serum reference range in ascitic fluid was found in
up to 90% of patients with acute pancreatitis and pancreatic pseudocyst.
• When pancreatic ascites distinguished from ascites secondary to alcoholic cirrhosis, it
can be accomplished by detecting high amylase levels in the ascitic fluid.
• During the course of severe acute pancreatitis, the level of ascitic amylase can be 100
times higher than serum.
• However, increased amylase in ascites can also been found in patients with
malignancy, perforated peptic ulcer, upper abdominal surgery, mechanical intestinal
obstruction, mesenteric vascular disease, biliary obstruction, and acute cholecystitis.
Therefore, hyperamylasemia is not a specific marker for pancreatic damage.

38. Adenosine deaminase
• Ascitic fluid adenosine deaminase activity (ADA) has been reported to be
more sensitive and specific for the early diagnosis of tuberculous ascites than
for other types of ascites.
• High sensitivity (100%) and specificity (97%) on using cut-offs of ADA from
36 to 40 IU/L in the diagnosis of tuberculous ascites
• Valuable in differentiating between tubercular peritonitis and peritoneal
carcinomatosis
• ADA values of patients with TBP are notably higher than those with cirrhosis.

39. Non-biochemical tests
• Cell counts, bacterial culture, and polymerase chain reaction (PCR)
• SBP is defined by the presence of neutrophil cells greater than or equal to 250/μL or a
positive bacterial culture in the ascitic fluid without evidence of an abdominal source.
• Cultures are negative in as many as 60% of patients with increased ascites neutrophil
counts and clinical manifestations suggestive of SBP. So elevated ascitic neutrophil cell
counts and clinical signs and symptoms if present then antibiotic treatment must be
initiated without waiting for the culture result.
• Cell counts and bacterial culture should also be performed in patients with cirrhotic
ascites, especially those with symptoms, due to the high incidence of SBP.
•

40. Cell counts, bacterial culture, and polymerase
chain reaction (PCR)contd….
• The sensitivity of direct microscopic smear detection of acid-fast bacilli
in the ascitic fluid (0%–6%) and ascitic fluid mycobacterial culture
(20%–35%) is low, and mortality is high in patients with tuberculous
peritonitis and other various medical conditions, such as cirrhosis,
renal failure, diabetes mellitus, and malignancy.
• PCR can detect minimal amounts of bacterial DNA and improves the
rates and velocity of bacterial identification from four to six weeks for
microbiological cultures to 24 hours.
• PCR can be a rapid and reliable method for identification of infectious
ascites and accelerates the diagnostic decision making process relative
to microbiological cultures.

41. Viscosity
• Ascitic fluid viscosity is a newly proposed indicator in differentiating ascites.
• The mean ascitic fluid viscosities is less in SAAG >1.1 g/L and more in SAAG <
or =1.1g/L, respectively, indicating a close correlation between viscosity and
SAAG.
• Exhibited high sensitivity (98%), specificity (80%), and positive and negative
predictive values (79% and 94%, respectively) for the etiological
discrimination of ascites.
• The speed, simplicity, inexpensiveness, and necessity of only a small sample
volume make it a useful, and likely more popular, diagnostic tool for the
differential diagnosis of ascites in clinical research and practice.

42. Proton nuclear magnetic resonance (H NMR)
spectroscopy
• High-resolution H NMR spectroscopy of body fluids has emerged as an important tool for
differential diagnosis of diseases. In this technique, a few biochemical agents, such as β-
hydroxybutyrate (BHBT), lactate, acetone, and acetoacetate, are used.
• Can be used to differentiate benign cirrhotic ascites from malignant ascites.
• Ascitic concentrations of BHBT, lactate, acetone, and acetoacetate were significantly higher in
patients with malignant ascites than in those with cirrhotic ascites and the ascitic
concentrations of glutamine, citrate, glucose, tyrosine, and phenylalanine were significantly
lower in patients with malignant ascites than in those with cirrhotic ascites
• BHBT, lactate, citrate, and tyrosine were considered together as markers, 1H NMR
spectroscopy differentiated malignant ascites from cirrhotic ascites with 100% sensitivity
and 97.9% specificity

43. Vascular endothelial growth factor (VEGF)
• VEGF, initially known as vascular permeability factor, has a
recognized role in the accumulation of ascitic fluid.
• Several studies have confirmed, using enzyme immunoassay, the
presence of higher VEGF concentrations in malignant ascites than
in non-malignant (cirrhotic, tuberculous, inflammatory) ascites.
Although VEGF concentrations are significantly higher in
malignant ascites, the overlap in the concentrations of VEGF
between malignant and non-malignant ascites is rather large.

44. Tumor markers
• Ascitic levels of AFP, CEA, CA19-9, and CA125 are significantly higher in
patients with malignancies such as hepatocellular cancer, colorectal
cancer, pancreatic cancer, and ovarian cancer than in those with non-
malignant etiologies.
• However, other non-malignant conditions such as gastritis,
diverticulitis, cirrhosis, and other cholestatic, pancreatic, and hepatic
diseases are known to cause elevations in these tumor markers.
• Increased ascitic CEA and CA 19-9 can be present in cirrhosis, and high
levels of CA125 in ascitic fluid can occur in patients with tuberculous
peritonitis or with cirrhosis
• Gold standard for the diagnosis of malignant ascites is detection of
tumor cells in the ascitic fluid.

45. Treatment
• Initial step is to restrict Sodium to 2g/day.
• When this alone is inadequate oral diuretics are used typically the
combination of Furosemide and Spironolactone in a ratio of 40:100.
• Maximal daily dose of Furosemide is 160mg and Spironolactone is 400mg.
• Refractory cirrhotic ascites is when Na+ restriction and maximal or maximal
tolerated dose of diuretic used still there is persistence of ascites.
• Refractory Ascites can be managed by serial Large Volume Paracentesis
(LVP)
• Alternatively a Transjugular Intrahepatic Peritoneal Shunt (TIPS) to
decompress the hepatic sinusoids is done.
• TIPS better than LVP in reaccumulation of ascitic fluid but incidence of
Hepatic Encephalopathy is more

46. Treatment
• There is no difference in mortality rates between TIPS and LVP
• Pharmacologic therapy for refractory ascites includes the addition of
midodrine, an α1 -adrenergic agonist, or clonidine, an α2 -adrenergic
agonist, to diuretic therapy. These agents act as vasoconstrictors,
counteracting splanchnic vasodilation. Midodrine alone or in combination
with clonidine improves systemic hemodynamics and control of ascites
over that obtained with diuretics alone.
• β-adrenergic blocking agents (beta blockers) are often prescribed to
prevent variceal hemorrhage in patients with cirrhosis, the use of beta
blockers in patients with refractory ascites may be associated with
decreased survival rates. Intravenous (IV) infusion of albumin
accompanying LVP decreases the risk of “postparacentesis circulatory
dysfunction” and death. Patients undergoing LVP should receive IV albumin
infusions of 6–8 g/L of ascitic fluid removed.

47. Treatment
• The Alfapump system, which consists of an automated pump and tunneled
peritoneal catheter that transports ascites from the peritoneal cavity to the
urinary bladder, has shown promise in the management of refractory
ascites but is associated with a higher frequency of technical difficulties
and renal dysfunction.
• Malignant ascites does not respond to sodium restriction or diuretics.
Patients must undergo serial LVPs, transcutaneous drainage catheter
placement, or, rarely, creation of a peritoneovenous shunt (a shunt from
the abdominal cavity to the vena cava) or placement of the Alfapump
system, if available. Ascites caused by tuberculous peritonitis is treated
with standard antituberculosis therapy. Noncirrhotic ascites of other
causes is treated by correction of the precipitating condition.

48. THANK YOU