Peritoneal cavity

• It is a potential space between the

parietal peritoneum and visceral
peritoneum, the two membranes
separate the organs in the abdominal
cavity from the abdominal wall.
• Derived from the coelomic cavity of the
embryo.
• Largest serosal sac in the body and
secretes approximately 50 ml of fluid per
day.
 Etiology of ascites
Most Common causes(90% of cases):
• Portal HTN secondary to chronic liver
diseases ( cirrhosis)
• Intra-abdominal malignancy
• Congestive Heart Failure
• Mycobacterium tuberculosis
 portal hypertension
• It is a high blood pressure in the portal
vein and its tributaries(portal venous
system).
• It is defined as a portal pressure gradient
(the difference in pressure between the
portal vein and the hepatic veins) of 5 mm
Hg or greater.
 Causes of portal hypertension

• Intrahepatic causes: liver cirrhosis and hepatic

fibrosis (e.g. due to Wilson's disease,
hemochromatosis, or congenital fibrosis).
• Prehepatic causes : portal vein thrombosis or
congenital atresia.
• Posthepatic obstruction occur at any level
between liver and right heart, including hepatic
vein thrombosis, IVC thrombosis, IVC congenital
malformation, and constrictive pericarditis.
 Cirrhosis
most common causes of cirrhosis:
• Alcoholic liver disease or alcoholic hepatitis
• viral hepatitis (B or C)
• fatty liver disease
 Other causes of ascites
Hypolalbuminemia
• Nephrotic syndrome
• Protein-losing enteropathy
• malnutrition
Other causes of ascites
• Bacterial, fungal or parasitic disease
• Vasculitis
• Whipple's Disease
• Familial Mediterranean fever
• Endometriosis
• Starch peritonitis
• Budd-Chiari Syndrome
• Myxedema
• Ovarian disease (e.g. Meigs' Syndrome)
• Pancreatic disease
• Chylous Ascites
 Pathophysiology
1- Increased hydrostatic pressure
• Cirrhosis
• Hepatic vein occlusion (Budd-Chiari
Syndrome)
• Inferior vena caval obstruction
• Constrictive Pericarditis
• Congestive heart failure
 Pathophysiology
2. Decreased colloid osmotic pressure
• End-stage liver disease with poor protein
synthesis
• Nephrotic syndrome
• Malnutrition
• Protein-losing enteropathy
3. Increase permeability of peritoneal
capillaries
• Tuberculous peritonitis
• Bacterial peritonitis
• Malignant disease of the peritoneum
 Pathophysiology
4. Leakage of fluid into the peritoneal
cavity
• Bile ascites
• Pancreatic ascites
• Chylous ascites
• Urine ascites
5. Miscellaneous causes
• Myxedema
• Ovarian disease (Meig’s syndrome)
• Chronic hemodialysis
 Morbidity and Mortality
• Ambulatory patients with an episode of
cirrhotic ascites have a 3-year mortality
rate of 50%. The development of
refractory ascites carries a poor prognosis,
with a 1-year survival rate of less than
50%.
 Diagnosis
1-history
Pts should be questioned about:
• Liver diseases
• Risk factors for Hepatitis C ( needle
sharing, tattoos, cocaine, heroin use and
emigration from Egypt or Southeast
Asia)
• Risk factors for Hepatitis B (needle
sharing, tattoos, acupuncture, and
emigration from China, Korea, Taiwan,
or Southeast Asia).
• Pts with obesity, diabetes,
hyperlipidemia and Nonalcoholic
steatohepatitis ( NASH ) should be ruled
out.
• Pts with ascites who lack risk factors for
cirrhosis should be questioned about
cancer, heart failure, TB, dialysis, and
pancreatitis.
• Operative injury to the ureter or bladder
can lead to leakage of urine into
peritoneal cavity.
• HIV pts may have infections lead to
ascites.
 diagnosis
2-Clinical Features
• A- Asymptomatic (fluid <100 - 400ml):
Mild ascites

• B- symptomatic (fluid >400ml):

Increased abdominal girth, presence of
abdominal pain or discomfort,
early satiety, pedal edema, weight gain
and respiratory distress depending on the
amount of fluid accumulated in the
abdomen.
Physical examination findings:
• Umbilicus Eversion (often with umbilical
herniation)
• Tympany at the top of the abdomen
• Fluid wave
• Peripheral edema
• Shifting dullness (> 500ml fluid)
• Bulging flanks (>500ml fluid)
Shifting Dullness
Bulging Flanks and Umbilical Hernia
 Diagnosis
3-paracentesis
• It is a diagnostic procedure to establish
the etiology of new-onset ascites or to
rule out spontaneous bacterial peritonitis
in patients with preexisting ascites. Large
volume paracentesis is performed in
hemodynamically stable patients with
tense or refractory ascites to alleviate
discomfort or respiratory compromise.
• For diagnostic purposes, a small amount
(20cc) may be enough for adequate
testing.
 Ascitic fluid analysis
Cell count:
• A white blood cell count is the most
important.
• A neutrophil > 250 cells/mm3 →
spontaneous bacterial peritonitis
• An elevated lymphocyte → tuberculosis or
peritoneal carcinomatosis
• Gram stain and culture:
for bacteria and acid fast bacilli
• Red cell count
> 50.000/microliter →hemorrhagic ascites,
which usually is due to malignancy,
tuberculosis or trauma.
Serum-Ascites Albumin Gradient
• Best single test for classifying ascites into
portal hypertensive and non-portal
hypertensive causes.
• Calculated by:
Serum albumin – Ascites albumin= SAAG
SAAG >1.1 g/dL= Portal HTN
SAAG < 1.1 g/dL= Non-Portal hypertensive
cause
 SAAG
SAAG >1.1 SAAG <1.1
1. Liver Disease 1. Peritoneal
carcinomatosis
2. Hepatic
Congestion 2. Peritoneal
Infection
3. CHF
(TB, Fungal, CMV)
4. Tricuspid
Insufficiency 3. Nephrotic
syndrome
5. Massive Hepatic
Metastasis 4. Pancreatic ascites
• Total protein:
Helpful in diagnosing spontaneous bacterial
peritonitis
Pts with a value<1 g/dl protein and glucose
of <50mg/dl
have high risk of SBP
• Cytology:
for malignant cells
• Amylase:
to exclude pancreatic ascites
 ascitic fluid
Appearance: The gross appearance of the ascitic fluid
can be helpful in the differential diagnosis.
Turbid or cloudy: infected fluid.
Milky: Triglyceride concentration of greater than 200mg/dl
(often greater than 1000mg/dl), malignancy is usually
MC cause, but cirrhosis may present with chylous fluid.
Pink or Bloody: Pink fluid usually traumatic tap. Frankly
bloody may occur in hepatocellular carcinoma, or other
malignancy related ascites.
Brown: Deeply jaundiced pts may present with brown
ascitic fluid, which may represent gallbladder rupture or
perforated duodenal ulcer.
 diagnosis
4-Imaging Studies

A- Chest and Plain Abdominal Films

• Elevation of the diaphram (usually with
>500 ml of fluid)
• Abdominal haziness
• Bulging Flanks
• Poor definition of intra abdominal organs

-
• Medial displacement of the cecum and
ascending colon.
• Hellmer's sign: the lateral liver angle is
displaced medially from the
thoracoabdominal wall in a patient with a
large extraperitoneal fluid collection
extending into the flank (Pathologic
processes in both the intra- and
extraperitoneal spaces).
bilateral pleural effusions
in a patient with ascites
loss of any
definition of
the edge of
the spleen or
liver and
displacement
of the bowel
loops out of
the pelvis and
bulging flanks
Pelvic Ascites
 Imaging Studies
B- CT scan
• Well visualized
• Fluid may be visualized in the:
• Right perihepatic space
• Posterior subhepatic space (Morison
pouch)
• Pouch of Douglas
 Large ascites
displacing bowel
posteriorly
Perihepatic ascites
[CT] Small amount of ascitic
fluid in the pouch of Douglas
and surrounding the adjacent
small bowel loops
Abdominal CT, showing Morison's
pouch as the dark margin surrounding
the right kidney (at lower left corner of
image).
 Imaging Studies

C- Ultrasound
• Easiest and most sensitive technique for
detection of ascitic fluid.
• Volume as small as 5-10ml can be seen.
.

Morison's
pouch with
abnormal fluid
collection (red
arrows)
between the
liver and right
kidney
 Management of Ascites
The goal is to prevent Na loading and increase
renal excretion of Na and H2O and produce a
net re-absorption of fluid from the ascites back
into the circulating volume.
• Dietary Na restriction
Diet of 2g sodium per day
• Fluid Restriction:
Only done when serum Na is <128mmol/L
• Check Labs
Ck serum electrolytes and creatinine every
other day.
Weigh the patient and measure urinary
output daily.
 Management of Ascites
Diuretic therapy:
• Spironolactone: diuretic of choice
(25-200mg PO daily or bid)
• Lasix: (20-80 mg/d PO/IV/IM)
• Zaroxolyn: (works on Edema of CHF)
(5-20 mg/dose PO q24hr)
• Mannitol: (0.5-2 g/kg IV over 30-60 min,
repeat q6-8hrs)
• Amilioride: 5-20 mg/d PO
 Management of Ascites
Large Volume Paracentesis
• To relieve symptomatic tense ascites and
peripheral edema.
• Up to 20L can be removed over 4-6hr.
• Removal of 5L or more of ascitic fluid
during a single session.
Paracentesis Contraindications:
• Acute abdomen (absolute)
• Severe bowel distention
• Previous abdominal surgery (if necessary perform
open procedure)
• Pregnancy (if necessary perform after first trimester
using an open technique above the umbilicus)
• Distended bladder that cannot be relieved by foley
catheder
• Infection at site of insertion (cellulitis or abscess)
• Thrombocytopenia (relative)
• Coagulopathy (relative)
Paracentesis Complications:
• Bladder perforation
• Small or large bowel perforation
• Stomach perforation
• Laceration of major vessels ( mesenteric, iliac,
aorta)
• Laceration of catheter or guide wire and loss in
peritoneal cavity (requires laparotomy)
• Abdominal wall hematoma
• Incisional hernia
• Wound infection
• Wound dehiscence
 Management of Ascites
Transjugular Intrahepatic
Portasystemic Shunt:
The TIPS procedure is an interventional
radiologic technique that reduces portal
pressure and may be the most effective
treatment for diuretic resistant ascites.

Risks:
• Hepatic Encephalopathy (30% of pts)
• Thrombosis and shunt stenosis.
 TIPS Procedure

• side to side portacaval shunt, usually placed

through the right internal jugular vein. A needle
is placed through the IJV into the hepatic vein.
Peritoneovenous shunt: •Developed to return
ascitic fluid from the
peritoneal cavity directly
:
to the systemic
circulation.
• Consists of an intra-
abdominal tube
connected through a
valve to silicone tube
that transverses the
subcutaneous tissue up
to the neck and enters
one of the jugular veins.
• This leads to diuresis and
mobilization of ascites.
Risks of Peritoneovenous shunt:
• DIC
• Infection
• Variceal bleeding
• Small bowel obstruction
• Shunt occlusion
• Death
Due to these risk this procedure is rarely
used.
Peritoneovenous shunts are therapeutic but
do not improve survival rates in patients
with cirrhosis and ascites.
 Management of Ascites
liver transplantation:
• Tx of choice
• Corrects portal hypertension
• Changes the natural course of progressive
liver failure due to cirrhosis
• Not all pts are candidates for transplant,
and those who are may wait for years for
a donor
• Many die from complications of ascites
while waiting for transplant donor
 Complications from Ascites

1. Refractory Ascites:
• Fluid overload that is unresponsive to
Na-restricted diet and high dose anti-
diuretic treatment.
• Usually in the setting of chronic or acute
liver diseases with associated portal
hypertension.
 Treatment of Refractory Ascites:
Liver transplantation is treatment of choice.
If unsuitable, treatment with:
• Serial paracentesis
• TIPS
• Peritoneovenous shunt
 Complications of Ascites
2. Hepatorenal syndrome:
Life-threatening medical condition that consists of
rapid deterioration in kidney function in individuals
with cirrhosis or fulminant liver failure. HRS is
usually fatal unless a liver transplant is performed,
although various treatments, such as dialysis, can
prevent advancement of the condition. It is a
common complication of cirrhosis, occurring in
18% of cirrhotics within one year of their
diagnosis, and in 39% of cirrhotics within five
years of their diagnosis.
Type 1 HRS:
• Doubling of initial serum creatinine level
to >2.5mg/dl or a 50% cause decreasing
in 24-hour creatinine clearance to
<20ml/min in < 2 weeks.
• Mortality is >90% without liver
transplantation.
Type 2 HRS:
• RF has a slower progressive course.
• Occur in the setting of chronic or acute liver
disease with portal hypertension.
• Low GFR (with creatinine >1.5mg/dl)
• No evidence of shock, bacterial infection, or
treatment with nephrotoxic agents + absence of
GI fluid losses or renal fluid losses.
• No improvement in renal function following
diuretic withdrawal.
• Proteinuria <500mg/dl and no US evidence of
renal disease or obstructive uropathy.
Treatment of hepatorenal syndrome:
• Supportive
• Liver transplantation: Tx of Choice.
• It corrects both liver and kidney disease.
• Is associated with up to 60% survival rate
in 3 years.
• Shortage of donor organs leads to a high
rate of death in these patients.
 Complications of Ascites
3- Spontaneous Bacterial Peritonits
• 20% of patients with cirrhotic ascites
• Diagnosed with neutrophil count of
>250/mm3
• Gram – neg organisms in 60% of cases
(E.coli and Klebsiella pneumoniae )
• Gram + organisms 25% of cases
(Strep species )
• Symptoms: Abdominal pain, fever,
development of hepatic encephalopathy,
diarrhea, hypothermia and shock.

• Ascitic Protein level<1 g/dl is a risk for

Spontaneous Bacterial Peritonits.

• Treatment: Cefotaxime sodium

Thank you