Dr.

Hassan Shalby
A 63 year old woman has a 3-month history
of abdominal distention a 10lb weight gain
despite maintaining her normal diet. She
denies abdominal discomfort or change in
bowel habits. The patient has chronic
hepatitis C contracted from a blood
transfusion received 25 yrs ago.
 Abdominal x ray shows a moderate amount
of ascites, morphologic features of cirrhosis
without focal hepatic lesions, and
splenomegaly. Paracentesis is done, the
ascitic fluid PMN is 50/uL and the albumin
is 1.2 g/dL.
 Which of the following is the most
appropriate treatment at this time?
A. Ciprofloxacin
B. Spironolactone
C. Peritoneovenous shunt
D. TIPS
E. Large-volume paracentesis
A 55 year old man has a 3-day history of
sharp diffuse abdominal pain and fever.
The patient has alcoholic cirrhosis that
was documented by liver bx 2 yrs ago.
Current meds are spironolactone
200mg, Lasix 80mg, and nadolol 20mg.
On PE: T=102.0 The abdomen is
distended, tender to palpation, and there
is a reducable umbilical hernia.
Abdominal US shows a large amount of
ascites, cirrhosis without focal hepatic
lesions, varices and enlarged spleen.
Paracentesis is done, the ascitic fluid
PMN count is 650/uL and the albumin is
less than 1.0 g/dL
Which of the following is the most appropriate
treatment at this time?
A. Large-volume paracentesis

B. Increase in diuretic dosage

C. Intravenous cefotaxime

D. TIPS
E. Surgical reduction of hernia
 Derived from the Greek word “askos”, meaning
bag or sac
 A Condition of pathologic fluid accumulation
within the abdominal cavity which is a common
complication in liver cirrhosis
 Healthy men: have little or no intraperitoneal
fluid
 Healthy women: may have as much as 20ml of
intraperitoneal fluid, depending on phase of
menstrual cycle
 MC cause: Portal HTN secondary to chronic
liver disease (80%)
 Infections (TB peritonitis)
 Intra-abdominal malignancy
 Inflammatory disorders of the peritoneum
 Ductal disruptions (chylous, pancreatic, and
biliary)
1. Increased hydrostatic pressure
- Cirrhosis
-Hepatic vein occlusion (Budd-Chiari syndrome
-IVC obstruction
-Constrictive Pericarditis
-Congestive heart failure
2. Decreased colloid osmotic pressure
-End-stage liver disease with poor protein synthesis
-Nephrotic syndrome with protein loss
-Malnutrition
-Protein-losing enteropathy
3. Increase permeability of peritoneal capillaries
-Tuberculous peritonitis
-Bacterial peritonitis
-Malignant disease of the peritoneum
4. Leakage of fluid into the peritoneal cavity
-Bile ascites
-Pancreatic ascites
-Chylous ascites
-Urine ascites
5. Miscellaneous causes
-Myxedema
-Ovarian dz (Meig’s syndrome)
-Chronic hemodialysis
 Normal Peritoneum
Portal hypertension (SAAG > 1.1g/dL)
1. Hepatic Congestion
Congestive Heart Failure
Constrictive Pericarditis
Tricuspid Insufficiency
Budd-Chiari Syndrome
Veno-occlusive disease
2. Liver Disease
Cirrhosis
Alcoholic Hepatitis
NonAlcoholic Steato-Hepatitis
Fulminant Hepatic failure
Massive Hepatic metastases
Hepatic Fibrosis
Acute fatty liver of pregnancy
3. Portal vein occlusion
Hypolalbuminemia (SAAG < 1.1 g/dL)
Nephrotic syndrome
Protein-losing enteropathy
Severe malnutrition with anasarca
Miscellaneous conditions (SAAG <1.1g/dL)
Chylous ascites
Pancreatic ascites
Bile ascites
Nephrogenic ascites
Urine ascites
Ovarian disease
 Diseased Peritoneum (SAAG <1.1 g/dL)
Infections
Bacterial peritonitis
Tuberculous peritonitis
Fungal peritonitis
HIV-associated peritonitis
Malignant Conditions
Peritoneal carcinomatosis
Primary mesothelioma
Pseudomyxoma peritonei
Massive hepatic metastases
Hepatocellular carcinoma
Other conditions
Familial Mediterranean Fever
Vasculitis
Granulomatous peritonitis
Eosinophilic peritonitis
 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%
1. Pts should be questioned regarding risk factors for
liver disease since cirrhosis is the most common
cause of ascites in Egypt.
2. Risk factors for Hepatitis C should be ruled out.
Such as needle sharing, tattoos, cocaine and heroin use and emigration
from Egypt or Southeast Asia.
3. Risk factors for Hepatitis B should be rule out. Such
as needle sharing, tattoos, acupuncture, and emigration from China,
Korea, Taiwan, or Southeast Asia.
4. In pts with obesity, diabetes, and
hyperlipidemia, NASH should be ruled out.
5. Pts with ascites who lack risk factors for
cirrhosis should be questioned about cancer,
heart failure, TB, dialysis, and pancreatitis
6. Operative injury to the ureter or bladder can lead
to leakage of urine into peritoneal cavity.
Absorption of urine into the system circulation
mimics renal failure, but GFR is normal.

7. Patients who are HIV + may have unusual

infections that lead to ascites formation.
Symptoms may vary from an asymptomatic patients to
patients complaining of increased abdominal girth,
early satiety, and respiratory distress depending on
the amount of fluid accumulated in the abdomen
History:
 Increased abdominal girth
 Presence of abdominal pain or discomfort
 Pedal edema
 Weight gain
 H/O CHF
 H/O Hepatitis
PE 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)
Lab Studies
 A diagnostic aspiration of 10-20mL of fluid should be
obtained and the following should be performed:
Cell count:
- a white blood cell count is the most important
- a neutrophil count above 250 cells/mm3 is indicative of
and underlying spontaneous bacterial peritonitis
- an elevated lymphocyte count arouses suspicion of
tuberculosis or peritoneal carcinomatosis
Gram stain and culture:
for bacteria and acid fast bacilli
Serum-Ascites Albumin Gradient
 Best single test for classifying ascites into portal hypertensive and
non-portal hypertensive causes
 Calculated by:
 Subtracting the ascitic fluid albumin from the serum albumin

SAAG >1.1 g/dL= Portal HTN

SAAG < 1.1 g/dL= Non-Portal hypertensive cause
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 SBP
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
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.
 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
-Hellmer Sign- when the lateral liver angle is displaced
medially from the thoracoabdominal wall
-Medial displacement of the cecum and ascending
colon
-Dog’s ear sign- when the fluid accumulates in
the recto-vesical pouch and then spills into the
paravesical fossa, the fluid will produce
symmetrical densities on both sides of the
bladder
 CT scan
-Well visualized
-Fluid may be visualized in the:
Right perihepatic space
Posterior subhepatic space (Morison pouch)
Pouch of Douglas
 Ultrasound
-Easiest and most sensitive technique for detection of
ascitic fluid
-Volume as small as 5-10ml can be seen
-Fluid tends to collect in the Morison pouch around the
liver
Stage 1+: detectable only with careful
examination
Stage 2+ easily detectable but of relatively small
volume
Stage 3+ obvious ascites but not tense ascites
Stage 4+ tense ascites
 The goal is to prevent Na loading and
increase renal excretion of Na and H20 and
by doing so produce a net re-absorption of
fluid from the ascites back into the
circulating volume.
 Dietary Na restriction
-Diet of 2g sodium per day
2.
2. Fluid Restriction:
-Only done when serum Na is <128mmol/L
3. Check Labs
-ck serum electrolytes and creatinine every
other day
-weigh the patient and measure urinary
output daily
 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
 Large Volume Paracentesis
Used to relieve symptomatic tense ascites
Allows rapid therapy in patients with 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.
-CO increases immediately after removal of 4-5L of fluid
-Plasma Expander Addition (Albumin)
6-12 hours after paracentesis there is a decrease in CVP, PCWP, and
CO, these effects cause increase in plasma renin activity and
aldosterone concentration because of sensation of a decrease in
effective circulating volume.
-Albumin is usually use as the expander of choice
-6-8 g of albumin is added to every liter of fluid removed
Albumin is usually only use when removing 5L of fluid or greater
 Contraindications:
1. Acute abdomen (absolute)
2. Severe bowel distention
3. Previous abdominal surgery (if necessary perform open procedure)
4. Pregnancy (if necessary perform after first trimester using an open
technique above the umbilicus)
5. Distended bladder that cannot be relieved by foley catheder
6. Infection at site of insertion (cellulitis or abscess)
7. Thrombocytopenia (relative)
8. Coagulopathy (relative)
 Complications:
1. Bladder perforation
2. Small or large bowel perforation
3. Stomach perforation
4. Laceration of major vessels ( mesenteric, iliac, aorta)
5. Laceration of catheter or guide wire and loss in peritoneal cavity
(requires laparotomy)
6. Abdominal wall hematoma
7. Incisional hernia
8. Wound infection
9. Wound dehiscence
 Transjugular Intrahepatic Portasystemic Shunt:
-The TIPS procedure is an interventional radiologic technique
that reduces portal pressure and may be the most efficacious for
treatment of diuretic resistant ascites
-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. A self-expanding
metallic stent, is then deployed across the tract and dilated to
the desired diameter by using an angioplastic balloon.
Risks:
 Hepatic Encephalopathy (30% of pts)
 Thrombosis and shunt stenosis
 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:
 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
 Orthotopic 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
 Diagnostic workup including paracentesis
 2g Na diet
 Spironolactone
 If no change, add loop diuretic
 Therapeutic paracentesis for tense ascites with associated
symptoms
 OLT
 Consider Serial paracentesis, TIPS, or Peritoneovenous shunt
for patients who don’t respond to diuretics, and who are
unsuitable for transplantation
1. Refractory Ascites:
-Fluid overload that is unresponsive to Na-restricted
diet and high dose anti-diuretic tx
-Usually in the setting of chronic or acute liver dz with
associated portal htn
-Ominous- associated with about 50% mortality rate
with in 6 mons
 Orthotopic liver transplantation is tx of choice
 If unsuitable tx with:
 Serial paracentesis
 TIPS
 Peritoneovenous shunt
2. Hepatorenal syndrome:
-Development of renal insufficiency in pts with liver
failure and ascites
Type 1 HRS:
-Doubling of initial serum creatinine level to >205mg/dl or a
50% decrease in 24-hour creatinine clearance to <20ml/min in <
2 wks
-Mortality is >90% without OLT
Type 2 HRS:
-RF has a slower progressive course
-Occurs in the setting of chronic or acute liver dz with portal htn
-Low GFR (with creatinine >1.5mg/dl)
-no evidance 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
 Supportive
 OLT: Tx of Choice
It corrects both liver and kidney disease
Is associated with up to 60% survival rate in 3 yrs
Shortage of donor organs leads to a high rate of death in these pts
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 MC
-Gram + organisms 25% of cases
Strep species MC
SSX: Abdominal pain, fever, development of hepatic encephalopathy, diarrhea, ileus,
hypothermia and shock

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

Tx: Cefotaxime sodium

 Accumulation of plasma in the peritoneal cavity
 Caused by increased pressure forcing fluid out of intravascular
space into cavity
 Plasma contains albumin so circulating proteins decreased
  serum osmotic pressure
 Intravascular fluid depletion stimulates kidney to conserve
sodium and water =  hydrostatic pressure and creates more
ascites
 Also known as hepatic
coma
 Seen in end stage
hepatic failure
 Can be insidious or
rapid onset depending
on the severity of liver
disease
 Caused by impaired
ammonia metabolism
 Usually protein breaks down into ammonia in
GI tract, then ammonia into urea --- excreted
by the kidneys
 Liver cannot convert ammonia into urea
 Results in  serum ammonia levels
 Toxic to the central nervous system
 Other factors that add
to PSE:
High protein diet
Infection
Hypovolemia
Constipation
GI bleeding
Medications
 #1 - Prodomal – very
subtle changes
 Personality/behavior
changes
 Impaired
thinking/concentration
 Emotional highs and
lows
 Fatigue, drowsiness
 Slurred or slow speech
 Sleep pattern
disturbance
 #2 – Impending
 Continued mental

deterioration
 Confusion

 Disoriented

 Asterixis
 #3 – Stuporuous
 Marked mental

confusion
 Drowsy but

arousable
 Abnormal EEG

 Muscle twitching

 Hyperreflexia

 Continued asterixis
 #4 – Comatose (85%
mortality rate)
 Unresponsive
 Responds to painful
stimuli only
 No asterixis
 Positive Babinski’s sign
 Muscle rigidity
 Fetor hepaticus
 Seizures
 A primary cause of death with hepatic
failure/cirrhosis
 Kidneys cannot excrete ammonia and bilirubin
 Results in acute tubular necrosis
 Signs/symptoms
Sudden  urinary output
 BUN, Cr, urine osmolarity  Urine Na
B- Spironolactone
 C