Ascites Sadik 21-3-09

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CIRRHOTIC ASCITES DR SADIK MEMON FCPS (MEDICINE), FCPS (GASTROENTEROLOGY), AGA-M ISRA UNIVERSITY HYDERABAD.

NATURAL HISTORY OF CIRRHOSIS

Development of Complications in Compensated Cirrhosis 100 80

Ascites Jaundice Encephalopathy GI hemorrhage

Probability 60 of developing 40 event 20 0 0

20

40

60

80

100

Months Gines et. al., Hepatology 1987; 7:122

120

140

160

Case 1 Dr. Muhammad Sadik Memon Associate Professor / Gastroenterologist Head Section of Gastroenterology & Hepatology Department of Medicine Isra University Hospital

A 35 year old gentleman came to you, with progressive abdominal distension. Palmer erythna Wasting Anemia Shifting dullness positive Splenomegaly Pedal edema

What is your probable diagnosis?

How will treat? 1) RE-assurance 2) Salt- restriction, alternative to salt restriction 3) Water restriction 4) Diuretics.

HVPG > 12 mmHg IS NECESSARY FOR ASCITES TO DEVELOP AND IS ASSOCIATED WITH LOW SODIUM EXCRETION

HVPG > 12 mmHg is Necessary for Ascites to Develop and is Associated with Low Sodium Excretion 60

No ascites Ascites

50 40

Urinary sodium 30 (mEq/L) 20

10 0 0

5

Morali et al., J Hepatol 1992; 16:249

10 12

HVPG (mmHg )

15

20

25

URINARY SODIUM EXCRETION IS DECREASED IN CIRRHOTIC PATIENTS WITH ASCITES

Urinary Sodium Excretion is Decreased in Cirrhotic Patients with Ascites 140 120

Urinary sodium excretion (mmol/day )

100 80 60 40 20 4 0

No ascites

Moderate ascites

Eisenmenger et al, J Clin Invest 1950; 29:1491

Tense ascites

PATHOGENESIS OF ASCITES

Cirrhosis Hepatic venous outflow block

Arteriolar resistance

Sinusoidal pressure

Effective arterial blood volume

(vasodilation)

(HVPG ≥ 10-12 mmHg)

Ascites

Sodium and water retention

Activation of neurohumoral systems (renin, angiotensin, aldosterone)

ULTRASOUND IS THE MOST SENSITIVE METHOD TO DETECT ASCITES

Ultrasound is the Most Sensitive Method to Detect Ascites Ascites

Liver

MECHANISM OF ACTION OF THE DIFFERENT THERAPIES FOR ASCITES

Site of Action of Different Therapies for Ascites

Cirrhosis Arteriolar resistance

Intrahepatic resistance

Sinusoidal TIPS pressure

LVP

PVS

Ascites

(vasodilation)

Albumin Effective TIPS PVS arterial blood volume

Diuretics Sodium and water retention

Activation of neurohumora l systems

PREVENTION OF ASCITES

Treatment of Ascites Portal Hypertension No ascites Uncomplicated ascites Refractory ascites Hepatorenal syndrome

No specific therapy Consider salt restriction

TREATMENT OF UNCOMPLICATED ASCITES

Treatment of Ascites Portal Hypertension No ascites Uncomplicated ascites Refractory ascites Hepatorenal syndrome

MECHANISMS OF ACTION OF SODIUM RESTRICTION AND DIURETICS IN THE MANAGEMENT OF ASCITES

Cirrhosis Arteriolar resistance

Intrahepatic resistance

(vasodilation)

Sinusoidal pressure

Diuretics Na restrictiion

Ascites

Sodium Sodiumand and water water retention retention

Effective arterial blood volume Activation of neurohumora l systems

SPIRONOLACTONE IS MORE EFFECTIVE THAN FUROSEMIDE IN CIRRHOTIC PATIENTS WITH ASCITES

Spironolactone is More Effective Than Furosemide in Cirrhotic Patients with Ascites Response No response Total Furosemide

11

10

21

18

1

19

(80-160 mg/d)

Spironolactone (150-300 mg/d)

Perez-Ayuso et al. Gastroenterology 1983; 84:961

DIFFERENT DIURETIC REGIMENS IN PATIENTS WITH CIRRHOTIC ASCITES

Different Diuretic Regimens in Patients with Cirrhotic Ascites Progressive Schedule

Combination Schedule

(n=50)

(n=50)

Spironolactone (SP) 100 → 200 → 400 mg/d

SP 100mg/d + FUR 40mg/d

SP 400mg/d + Furosemide (FUR) 40 → 60 → 80 → 160 mg/d

SP 200mg/d + FUR 80mg/d

4days

4days

SP 400mg/d + FUR 160mg/d

Santos et al., J Hepatol 2003; 39:187

DIFFERENT DIURETIC REGIMENS IN PATIENTS WITH CIRRHOTIC ASCITES

Different Diuretic Regimens in Patients with Cirrhotic Ascites Progressive Schedule

Combination Schedule

(n=50)

(n=50)

Spironolactone (SP) 100 → 200 → 400 mg/d

SP 100mg/d + FUR 40mg/d

SP 400mg/d + Furosemide (FUR) 40 → 60 → 80 → 160 mg/d

SP 200mg/d + FUR 80mg/d

4days

4days

SP 400mg/d + FUR 160mg/d

Santos et al., J Hepatol 2003; 39:187

TREATMENT OF PATIENTS WITH UNCOMPLICATED ASCITES

Treatment of Ascites Portal Hypertension No ascites Uncomplicated ascites Refractory ascites Hepatorenal syndrome

1) Salt restriction + diuretics 2) Large volume paracentesis (LVP) in hospitalized patients with tense ascites

MANAGEMENT OF UNCOMPLICATED ASCITES

Management of Uncomplicated Ascites Definition: Ascites responsive to diuretics in the absence of infection and renal dysfunction Sodium restriction

• Effective in 10-20% of cases • Predictors of response: mild or moderate ascites, Urine Na excretion > 50 mEq/day

Diuretics • Should be spironolactone-based • A progressive schedule (spironolactone  furosemide) requires fewer dose adjustments than a combined therapy (spironolactone + furosemide)

MANAGEMENT OF UNCOMPLICATED ASCITES: SODIUM RESTRICTION

Management of Uncomplicated Ascites Sodium Restriction • 2 g (or 5.2 g of dietary salt) a day • Fluid restriction is not necessary unless there is hyponatremia (<125 mmol/L) • Goal: negative sodium balance • Side effect: unpalatability may compromise nutritional status

MANAGEMENT OF UNCOMPLICATED ASCITES: DIURETIC THERAPY

Management of Uncomplicated Ascites Diuretic Therapy Dosage • Spironolactone 100-400 mg/day • Furosemide (40-160 mg/d) for inadequate weight loss or if hyperkalemia develops • Increase diuretics if weight loss <1 kg in the first week and < 2 kg/week thereafter • Decrease diuretics if weight loss >0.5 kg/day in patients without edema and >1 kg/day in those with edema • Side effects • Renal dysfunction, hyponatremia, hyperkalemia, encephalopathy, gynecomastia

Case

A 45 years old gentleman came to you with altered sleep pattern. His son further added that he is not good at business (Accounting). He does not remember the prices of various goods since 4 days. He is known case of cirrhosis of liver and on diuretics (Furosemide40mg/day and spironolectone 100mg / day). He responded very well and his tummy size decreased very much.

Questions????

Q1. What is the new problems arises in this patient? Q2. Will you continue diuretics? Q3. What laboratory test you will perform?

TREATMENT OF REFRACTORY ASCITES

Treatment of Ascites Portal Hypertension No ascites Uncomplicated ascites Refractory ascites Hepatorenal syndrome

DEFINITION AND TYPES OF REFRACTORY ASCITES

Definition and Types of Refractory Ascites Occurs in ~10% of cirrhotic patients • Diuretic-intractable ascites 80% Therapeutic doses of diuretics cannot be achieved because of diuretic-induced complications

• Diuretic-resistant ascites 20% No response to maximal diuretic therapy (400 mg spironolactone + 160 mg furosemide/day)

Arroyo et al. Hepatology 1996; 23:164

PATIENTS WITH REFRACTORY ASCITES HAVE A WORSE SURVIVAL THAN PATIENTS WITH DIURETIC-RESPONSIVE ASCITES

Patients with Refractory Ascites Have A Worse Survival than Patients with DiureticResponsive Ascites 1.0 .8

Non refractory ascites Survival probability

.6 .4

p<0.001

.2

Refractory ascites 0

0

12

24

36

48

Months Salerno et al., Am J Gastroenterol 1993; 88:514

60

72

84

MECHANISMS OF ACTION OF LARGE VOLUME PARACENTESIS IN THE MANAGEMENT OF

Cirrhosis Arteriolar resistance

Intrahepatic resistance

(vasodilation)

LVP Sinusoidal pressure

Ascites Ascites

+ Albumin

Sodium and water retention

Effective arterial blood volume Activation of neurohumora l systems

MECHANISMS OF ACTION OF THE TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT IN THE MANAGEMENT OF ASCITES

Cirrhosis Arteriolar resistance

Intrahepatic resistance

Sinusoidal Sinusoidal pressure pressure

Ascites

(vasodilation)

TIPS

Sodium and water retention

Effective arterial blood volume Activation of neurohumora l systems

COMPARED TO LVP, TIPS IS ASSOCIATED WITH LESS ASCITES RECURRENCE BUT MORE ENCEPHALOPATHY

Compared to LVP, TIPS Reduces Ascites Recurrence But Increases Risk of Encephalopathy LVP p

TIPS

(n=35)

(n=35)

Recurrent ascites

11.7± 2.7* 0.003

3.6 ± 1.7

TIPS obstruction

-

40%

Grade 3-4 PSE

0.5 ± 0.02 0.02 Gines et al., Gastroenterology 2002; 123:1839

1.1 ± 0.02 * Episodes/patient

SURVIVAL IS NOT DIFFERENT BETWEEN PATIENTS TREATED WITH LARGE-VOLUME PARACENTESIS (LVP) OR TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS)

Survival is Not Different Between Patients Treated With LVP or TIPS 1

Paracentesis and albumin TIPS

0.8

p = 0.51 0.6

Probabilit y of survival

0.4

0.2

0 0

3

6

9

Gines et al., Gastroenterology 2002; 123:1839

12

Months

15

18

21

24

META-ANALYSIS OF TIPS VS. LVP+ALBUMIN FOR REFRACTORY ASCITES

Meta-Analysis of TIPS vs. LVP + Albumin for Refractory Ascites Ascites control (month 4) Ascites control (month 12) Survival (month 12) Encephalopathy More with LVP Deltenre et al., Liver International 2005; 25:349

0

More with TIPS

Risk Differenc e

PERITONEO-VENOUS SHUNT (PVS) IS USEFUL IN THE TREATMENT OF REFRACTORY ASCITES

Peritoneo-Venous Shunt (PVS) is Useful in the Treatment of Refractory Ascites Use of jugular vein will hinder TIPS placement

One-way valve

Intraabdominal adhesions may complicate liver transplant surgery

LARGE VOLUME PARACENTESIS (LVP) VS. PERITONEOVENOUS SHUNT (PVS) IN REFRACTORY ASCITES

Large Volume Paracentesis (LVP) vs Peritoneovenous Shunt (PVS) in Refractory Ascites

Episodes of recurrent ascites PVS obstruction Hospital stay Survival

Gines et al., N Engl J Med 1991; 325:829

LVP

PVS

p value

125

38

<0.001

-

40%

-

48 ± 8

44 ± 6

ns

57%

44%

ns

TREATMENT OF REFRACTORY ASCITES

Treatment of Ascites Portal Hypertension No Ascites Uncomplicat ed Ascites Refractory Ascites

1) LVP + albumin 2) TIPS 3) PVS (in non-TIPS, nontransplant candidates)

Hepatorenal Syndrome

LVP = large volume paracentesis TIPS = transjugular intrahepatic portosystemic shun

ASCITES II A 56 years old lady admitted to the hospital with increasing abdominal pain and fever for three days. She is K/C of HCV cirrhosis decompensated with ascites. On examination she has stigmata of chronic liver disease and tender abdomen. She is vitally stable and febrile.

1. What complication has this patient developed? What is the mechanism? 3. How will you diagnose this complication? 5. What is the treatment of this (immediate and long term)?

SPONTANEOUS BACTERIAL PERITONITIS (SBP) COMPLICATES ASCITES AND CAN LEAD TO RENAL DYSFUNCTION

Spontaneous Bacterial Peritonitis (SBP) Complicates Ascites and Can Lead to Renal Dysfunction

SBP

Portal Hypertension No Ascites

HVPG <10 mmHg Mild Vasodilation

Uncomplicate d Ascites

HVPG >10 mmHg Moderate Vasodilation

Refractory Ascites

Hepatorenal Syndrome

HVPG >10 mmHg Severe Vasodilation

HVPG >10 mmHg Extreme Vasodilation

BACTERIAL INFECTIONS ARE MORE FREQUENT IN SEVERE LIVER DISEASE

Bacterial Infections Are More Frequent in Severe Liver Disease Author Bleichner

n

Child A

Child B

Child C

149

3%

23%

48%

2589

1%

5%

17%

1140

3%

10%

27%

(1986) *

Kuo (1991)

Yoshida (1993)

* patients with GI hemorrhage

SPONTANEOUS BACTERIAL PERITONITIS (SBP) IS THE MOST COMMON INFECTION IN CIRRHOTIC PATIENTS

Spontaneous Bacterial Peritonitis (SBP) is the Most Common Infection in Cirrhotic Patients 150 125 100

# Hospitalize 75 d cirrhotic patients 50 25 0

SBP

UTI

Fernández et al., Hepatology 2002; 35:140

Pneumonia Procedure- Spontaneous related Bacteremia

TYPES OF BACTERIA ISOLATED FROM HOSPITALIZED CIRRHOTIC PATIENTS

Types of Bacteria Isolated from Hospitalized Cirrhotic Patients 100

Culture positive Gram (-) bacteria Gram (+) bacteria Both

80 60

%

40 20 0

SBP

UTI

Fernández et al., Hepatology 2002; 35:140

Pneumoni a

Overall

CLINICAL CHARACTERISTICS OF SPONTANEOUS BACTERIAL PERITONITIS (SBP)

Clinical Characteristics of Spontaneous Bacterial Peritonitis Fever Jaundice Abdominal pain Confusion Abdominal tenderness Hypotension No signs or symptoms 0

20

40

%

60

80

100

MORTALITY ASSOCIATED WITH SBP HAS BEEN DECREASING BY EARLY DIAGNOSIS AND TREATMENT

Mortality Associated with SBP has been Decreasing by Early Diagnosis and Treatment 100 80

% Mortality

60 40 20 0

1970’s

1980’s

Early 90’s Late 90’s

2000’s

EARLY DIAGNOSIS OF SPONTANEOUS BACTERIAL PERITONITIS (SBP)

Early Diagnosis of SBP • Diagnostic paracentesis: • If symptoms / signs of SBP occur • Unexplained encephalopathy and / or renal dysfunction • At any hospital admission • Diagnosis based on ascitic fluid PMN count >250/mm3 Rimola et al., J Hepatol 2000; 32:142

TREATMENT OF SPONTANEOUS BACTERIAL PERITONITIS (SBP)

Treatment of Spontaneous Bacterial Peritonitis

• Recommended antibiotics for initial empiric therapy • i.v. cefotaxime , ceftrioxone, amoxicillin-

clavulanic acid • oral ofloxacin (uncomplicated SBP) • avoid aminoglycosides

• Minimum duration: 5 days • Re-evaluation if ascitic fluid PMN count has not decreased by at least 25% after 2 days of treatment Rimola et al., J Hepatol 2000; 32:142

RENAL DYSFUNCTION IS A POOR PROGNOSTIC SIGN IN SPONTANEOUS BACTERIAL PERITONITIS (SBP)

Renal Dysfunction is a Poor Prognostic Sign in Spontaneous Bacterial Peritonitis Renal status Deaths No renal insufficiency

166

12 (7%)

Renal insufficiency

65

27 (42%)

Transient

21

1 (5%)

Stable

26

8 (31%)

Progressive

18

18 (100%)

Follo et al. Hepatology 1994; 20:1945

N

ALBUMIN DECREASES RENAL DYSFUNCTION AND SHORT-TERM MORTALITY IN SPONTANEOUS BACTERIAL PERITONITIS (SBP)

Albumin Decreases Renal Dysfunction and Shortterm Mortality in Spontaneous Bacterial Peritonitis Antibiotics

Antibiotics +

alone (n=63) p

albumin (n=63)

Resolution of SBP

93% ns

98%

Renal dysfunction

32% <0.001

10%

27% Sort et al., N Engl J Med 1999; 341:403 <0.001

10%

Hospital mortality

SPONTANEOUS BACTERIAL PERITONITIS (SBP): USE OF INTRAVENOUS ALBUMIN

Spontaneous Bacterial Peritonitis Use of Intravenous Albumin Albumin (plus antibiotics) is indicated if: • BUN > 30 mg/dL • creatinine > 1.0 mg/dL • bilirubin > 4 mg/dL

Albumin is not indicated in patients with a predicted 100% cure and survival: • • • •

community-acquired SBP no GI hemorrhage no encephalopathy normal renal function

SURVIVAL AFTER DEVELOPMENT OF SPONTANEOUS BACTERIAL PERITONITIS (SBP)

Survival After Development of Spontaneous Bacterial Peritonitis 1.0 .8 .6

Probability of survival .4 (%) .2 0 0

3

6

12

24

Months Tito et al., Hepatology 1988; 8:27

36

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