Prepared by

ASCITES Darien Liew Daojuin

10 May 2017
DEFINITION
Ascites describes the condition of pathologic fluid collection within the
abdominal cavity.
Typically, it is described at exudative or transudative.
REFRACTORY ASCITES
Ascites is occasionally refractory despite salt restriction and the use of
diuretics.

The International Ascites Club Definition

Refractory ascites is defined as either:
1. diuretic-resistant ascitesascites that cannot be mobilized or the
early recurrence of which cannot be prevented because of a lack
of response to dietary sodium restriction and intensive diuretic
treatment; or
2. diuretic intractable ascitesascites that cannot be mobilized or
the early recurrence of which cannot be prevented because of the
development of diuretic-induced complications that preclude the
use of an effective diuretic dosage.
PATHOPHYSIOLOGY
Three theories of ascites formation have been proposed: underfilling,
overflow, and peripheral arterial vasodilation; in the presence of cirrhosis.

The underfilling theory suggests that the primary abnormality is

inappropriate sequestration of fluid within the splanchnic vascular bed
due to portal hypertension and a consequent decrease in effective
circulating blood volume.
This activates the plasma renin, aldosterone, and sympathetic nervous
system, resulting in renal sodium and water retention.
Portal hypertension leads to an increase in nitric oxide levels. Nitric oxide
mediates splanchnic and peripheral vasodilation. Hepatic artery nitric
oxide synthase activity is greater in patients with ascites than in those
without ascites.
PATHOPHYSIOLOGY

The overflow theory suggests that the

primary abnormality is inappropriate
renal retention of sodium and water in
the absence of volume depletion. This
theory was developed in accordance
with the observation that patients with
cirrhosis have intravascular
hypervolemia rather than
hypovolemia.
PATHOPHYSIOLOGY
The peripheral arterial vasodilation hypothesis, includes components
of both of the other theories. It suggests that portal hypertension leads
to vasodilation, which causes decreased effective arterial blood
volume. As the natural history of the disease progresses, neurohumoral
excitation increases, more renal sodium is retained, and plasma
volume expands. This leads to overflow of fluid into the peritoneal
cavity. The vasodilation theory proposes that underfilling is operative
early and overflow is operative late in the natural history of cirrhosis.
Portal hypertension apparently leads to an increase in nitric oxide
levels. Nitric oxide mediates splanchnic and peripheral vasodilation.
Hepatic artery nitric oxide synthase activity is greater in patients with
ascites than in those without ascites.
PATHOPHYSIOLOGY
Ascites in the absence of cirrhosis generally results from peritoneal
carcinomatosis, peritoneal infection, or pancreatic disease.
Peritoneal carcinomatosis can result from primary peritoneal
malignancies such as mesothelioma or sarcoma, abdominal
malignancies such as gastric or colonic adenocarcinoma, or metastatic
disease from breast or lung carcinoma or melanoma. The tumor cells
lining the peritoneum produce a protein-rich fluid that contributes to
the development of ascites. Fluid from the extracellular space is drawn
into the peritoneum, further contributing to the development of ascites.
Tuberculous peritonitis causes ascites via a similar mechanism;
tubercles deposited on the peritoneum exude a proteinaceous fluid.
Pancreatic ascites results from leakage of pancreatic enzymes into the
peritoneum.
AETIOLOGY
AETIOLOGY
INVESTIGATION
Ultrasonagraphy
Paracentesis to obtain ascitic
fluid for analysis.
Chest X-Ray may show pleural
effusion (10% of patients), on the
right side (hepatic hydrothorax).
Laparoscopy can be valuable in
detecting peritoneal disease.
Ascitic Fluid Culture
Cytological examination may
reveal malignant cells (one-third
of cirrhotic patients with a
bloody tap have a
hepatocellular carcinoma).
Polymorphonuclear leucocyte
counts >250 106/L strongly
suggest infection (SBP).
 Exudative Ascites
INVESTIGATION Ascites protein concentration > 25 g/L or a
SAAG < 11 g/L raises the possibility of
SAAG AND TOTAL PROTEIN infection (especially tuberculosis), malignancy,
hepatic venous obstruction, pancreatic ascites or,
rarely, hypothyroidism.
Serum-Ascites Albumin Gradient
(SAAG) to distinguish a Ascites amylase activity >1000 U/L
transudate from an exudate. identifies pancreatic ascites, and low
ascites glucose concentrations suggest
Transudative Ascites malignant disease or tuberculosis.
Cirrhotic patients typically develop a
transudate with a total protein
concentration (TPC) <25g/L.
However, in up to 30% of patients, TPC
>30g/L.
In these cases, it is useful to calculate the
SAAG by subtracting the concentration of
the ascites fluid albumin from the serum
albumin.
SAAG A gradient of >11 g/L is 96% predictive
that ascites is due to portal hypertension.
Venous outflow obstruction due to cardiac
failure or hepatic venous outflow
obstruction can also cause a transudative
ascites, as indicated by an albumin
gradient >11 g/L but, unlike in cirrhosis,
the TPC is usually >25 g/L.
INVESTIGATION
SAAG AND TOTAL PROTEIN

SAAG: The SAAG is the best single test for classifying ascites into portal
hypertensive (SAAG >1.1 g/dL) and nonportal hypertensive (SAAG <
1.1 g/dL) causes. Calculated by subtracting the ascitic fluid albumin value
from the serum albumin value, it correlates directly with portal pressure.
The specimens should be obtained relatively simultaneously. The accuracy
of the SAAG results is approximately 97% in classifying ascites. The terms
high-albumin gradient and low-albumin gradient should replace the terms
transudative and exudative in the description of ascites.
Total protein: In the past, ascitic fluid has been classified as an exudate if
the protein level is greater than or equal to 2.5 g/dL. However, the
accuracy is only approximately 56% for detecting exudative causes. The
total protein level may provide additional clues when used with the
SAAG. An elevated SAAG and a high protein level are observed in most
cases of ascites due to hepatic congestion. The combination of a low
SAAG and a high protein level is characteristic of malignant ascites (see
Causes).
INVESTIGATION
ASCITIC ANALYSIS
CHARACTERISTIC OF ASCITIC FLUID
INVESTIGATION
IMAGING CXR, AXR

Elevated diaphragm pleural Detection of intraperitoneal fluid on a plain

radiograph requires >500 mL to be present.
effusion (hepatic hydrothorax)
Some findings:
Diffusely increased density of the Specific signs
abdomen Hellmer sign - lateral liver edge is medially
poor definition of the the soft displaced from the thoracoabdominal wall
tissue shadows, such as the psoas Dog's ear" or "Mickey Mouse" appearance In
muscles, liver and spleen the pelvis, fluid accumulates in the rectovesical
pouch and then spills into the paravesical fossa,
medial displacement of bowel and
producing symmetric densities on both sides of the
solid viscera (away from bladder, which is termed a "
properitoneal fat stripe)
bulging of the flanks
increased separation of small
bowel loops
INVESTIGATION
IMAGING - ULRASONAGRAHY
May detect smaller volumes especially
if its adjacent diaphragm or the
anterior margin of the liver 3.
Assessment of fluid type:
simple ascites is anechoic
exudative, haemorrhagic or
neoplastic ascites contains floating
debris
septations suggest inflammatory or
neoplastic cause and may called
loculated ascites
Uncomplicated ascites appears as a
homogeneous, freely mobile, anechoic collection in
the peritoneal cavity that demonstrates deep
acoustic enhancement.
Free ascites does not displace organs but
typically situates itself between them, contouring
to organ margins and demonstrating acute angles
at the point at which the fluid borders the organ.
The smallest amounts of fluid tend to collect in the
Morison pouch (posterior subhepatic space) and
around the liver as a sonolucent band.
With massive ascites, the small bowel loops have
a characteristic polycyclic, "lollipop," or arcuate
appearance because they are arrayed on either
side of the vertically floating mesentery.
 INVESTIGATION
IMAGING CT

Ascites is demonstrated well on CT scan images. Small

amounts of ascitic fluid localize in the right
perihepatic space, the posterior subhepatic space,
and the Douglas pouch (rectouterine pouch).
A number of CT scan features suggest neoplasia.
Hepatic, adrenal, splenic, or lymph node lesions
associated with masses arising from the gut, ovary, or
pancreas are suggestive of malignant ascites.
Patients with malignant ascites tend to have
proportional fluid collections in the greater and lesser
sacs; whereas, in patients with benign ascites, the
fluid is observed primarily in the greater sac and not
in the lesser omental bursae.
STAGING
Ascites may be semi-quantified using the following system:
Stage 1+ is detectable only after careful examination.
Stage 2+ is easily detectable but of relatively small volume.
Stage 3+ is obvious, but not tense, ascites.
Stage 4+ is tense ascites.
MANAGEMENT
MEDICAL
Sodium and water restriction
Diuretics - it should be titred to remove no more than 1L of fluid daily so
the body weight should not fall by more than 1kg daily to avoid excess
fluid depletion
Spironolactone first line drug, powerful aldosterone antagonistl can cause painful
gynecomastia and hyperkalaemia
Furosemide (loop diuretic) - can cause fluid and electrolyte imbalance and renal
dysfunction.

Paracentesis First-line treatment of refractory ascites

Drugs containing relatively large amounts of sodium, and those promoting
sodium retention such as non-steroidal anti-inflammatory drugs (NSAIDs),
must be avoided.
 MANAGEMENT
SURGICAL
Peritoneo-venous shunting (PVS) a long tube
with a non-return valve running subcutaneously
from the peritoneum to the internal jugular vein.
This is a megalymphatic shunt that returns the
ascitic fluid to the central venous system.
Beneficial effects Increased cardiac output,
renal blood flow, glomerular filtration rate,
urinary volume, and sodium excretion and
decreased plasma renin activity and plasma
aldosterone concentration.
PVS has been shown to improve short-term
survival (compared with paracentesis) in cancer
patients with refractory malignant ascites.
COMPLICATIONS
SPONTANEOUS BACTERIAL PERITONITIS
Spontaneous bacterial peritonitis (SBP) is
infection of ascitic fluid without an
apparent source.
Manifestations may include fever,
malaise, and symptoms of ascites and
worsening hepatic failure.
PMN count of > 250 cells/L is
diagnostic of SBP. Blood cultures are also
indicated. Because SBP usually results
from a single organism, finding mixed
flora on culture suggests a perforated
abdominal viscus or contaminated
specimen.
Most organisms are enteric in origin and
E. coli is most frequently found.
Predisposing factor
1. Intestinal bacterial overgrowth found
in people with cirrhosis, mainly
attributed to delayed intestinal
transit time.
2. Impaired phagocytic function, low
serum and ascites complement levels
3. Decreased activity of the reticulo-
endothelial system, resulting in
increased number of microbes and
decreased capacity to clear them
from the bloodstream, resulting in
their migration into and eventual
proliferation within ascites fluid.
Interestingly, adults with spontaneous
bacterial peritonitis typically have ascites,
but most children with spontaneous
bacterial peritonitis do not have ascites.
COMPLICATIONS
SPONTANEOUS BACTERIAL
PERITONITIS

Harrisons Principles of Internal

Medicine, 19th Edition, pp. 288
COMPLICATONS
HEPATORENAL SYNDROME
This occurs in 10% of patients with advanced cirrhosis complicated by
ascites. There are two clinical types; both are mediated by renal
vasoconstriction due to underfilling of the arterial circulation.
Type 1 hepatorenal syndrome is characterised by progressive oliguria, a
rapid rise of the serum creatinine and a very poor prognosis (without
treatment, median survival is less than 1 month). There is usually no
proteinuria, a urine sodium excretion of less than 10 mmol/day and a
urine/ plasma osmolarity ratio of more than 1.5. Other non-functional
causes of renal failure must be excluded before the diagnosis is made.
Treatment consists of albumin infusions in combination with terlipressin and is
effective in about two-thirds of patients. Haemodialysis should not be used
routinely because it does not improve the outcome. Patients who survive
should be considered for liver transplantation.
Type 2 hepatorenal syndrome usually occurs in patients with refractory
ascites, is characterised by a moderate and stable increase in serum
creatinine, and has a better prognosis.
PROGNOSIS
Only 1020% of patients survive 5 years from the first appearance
of ascites due to cirrhosis. The outlook is not universally poor, however,
and is best in those with well-maintained liver function and a good
response to therapy. 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. The mortality at 1
year is 50% following the first episode of bacterial peritonitis.
REFERENCES
1. http://emedicine.medscape.com/article/789105-overview#a4
2. http://www.merckmanuals.com/professional/hepatic-and-biliary-
disorders/approach-to-the-patient-with-liver-
disease/spontaneous-bacterial-peritonitis-sbp
3. Davisons Principles and Practice of Medicine, 22nd Edition, pp.
939-941
4. Harrisons Principles of Internal Medicine, 19th Edition, pp. 288
ASCITES Last Reviewed
12 May 2017