Objectives

1. Study different etiologies of Ascites including PHT

2. Get an idea on the management of Ascites and its complications

Peritoneal Causes of Ascites

Peritoneal Causes Examples

Malignant ascites Primary peritoneal mesotheliomaSecondary peritoneal carcinomatosis

Granulomatous peritonitis Tuberculous peritonitisFungal and parasitic infections SarcoidosisForeign bodies (cotton ,starch, barium)

Vasculitis Systemic lupus erythematosusHenoch-Schönlein purpura

Miscellaneous disorders Eosinophilic gastroenteritisWhipple diseaseEndometriosis

Nonperitoneal Causes of AscitesNon-peritoneal causes Examples Intrahepatic portal hypertension Cirrhosis

Fulminant hepatic failureVeno-occlusive disease

Extrahepatic portal hypertension

Hepatic vein obstruction (ie, Budd-Chiari syndrome)Congestive heart failure

Hypoalbuminemia Nephrotic syndromeProtein-losing enteropathy Malnutrition

Miscellaneous disorders MyxedemaOvarian tumorsPancreatic & Biliary ascites

Chylous Secondary to malignancy, trauma

Complications of Portal Hypertension in cirrhosis liver.

Development of Ascites.

Varices formation.

Hepatic encephalopathy.

Hepatorenal syndrome.

Ascites•Derived from the Greek word “askos”,

meaning bag or sac.• Defined as the accumulation of fluid in

the peritoneal cavity. • It is a common clinical finding, with many

extraperitoneal and peritoneal causes , but most common from liver cirrhosis .

Ascites

Definition: presence of >25ml free fluid in the peritoneal cavity

EtiologyCirrhosis (75%)

Most common cause of ascites Most common complication of cirrhosis Other causes occur more frequently in cirrhotics

Malignancy (10%) Cardiac (3%) TB (2%) Pancreatic Ascites(1%) Various others

Hepatology 38:258-66

Physical Examination

Bulging Flanks Flank Dullness Shifting Dullness Fluid Wave Approximately 1.5 L

must be present before flank dullness is detected. If no flank dullness is present, the patient has less than 10% chance of having ascites.

JAMA 1992; 267:2645-48

Bulging Flanks

Occur when weight of ascites is sufficient to push the flanks outwards

Difficult to distinguish from obesity

JAMA 1992; 267:2645-48

Flank Dullness

Similar to bulging flanks, although uses percussion

Typically bowel will float to the top and ascitic fluid sinks to the bottom

JAMA 1992; 267:2645-48

Shifting Dullness Find the point where

flank dullness occurs

Mark it Roll the patient

away from the examiner

Repeat percussion and ensure that the point moves to the dependent side

JAMA 1992; 267:2645-48

Fluid Wave (fluid thrill)

Medial edges of both hands down midline

Tap flank firmly and feel for an impulse on the other side

JAMA 1992; 267:2645-48

International Ascites Club Grading

Grade 1 Mild, only detectable by U/S

Grade 2 Moderate, symmetrical distension,not tense

Grade 3 Gross or large with marked distension,tense

Large typically means painful/uncomfortable Refractory Ascites (5-10%)

Can not be mobilized or early recurrence refractory to medical management

NEJM 350:1646-54

Hepatology 2003; 38: 258-266

Diagnosing Ascites

Ultrasound is the most sensitive test for ascites (100mL detection)

Image from www.gastro.org

Paracentesis: General Tips

Do NOT do paracentesis to see if ascites present, should know before

If unclear need U/S

Ensure patient has voided

FFP/Platelet transfusion if indicated

Ensure landmarks

Get Quick-Tap kit, plastic catheter does not work as well as the metal one.

Picture from www.kchealthcare.com

Paracentesis:

Site: 5cm cephalic & 5 cm medial to ASIS in the left lower quadrant of the abdomen has been shown to be the ideal site with larger pool of fluid.to avoid injury to inf.epigastric artery.

Complications: (1% of patients) Abdominal wall hematomas. Hemoperitoneum or bowel entry.

Contraindications:Clinically evident fibrinolysis or DIC.

Indications for diagnostic paracentesis• Patients with new-onset ascites

• Cirrhotic patients with ascites at admission

• Cirrhotic patients with ascites & symptoms or signsof infection: fever, leukocytosis, abdominal pain

• Cirrhotic patients with ascites & clinical conditiondeteriorating during hospitalization: renal functionimpairment, hepatic encephalopathy, GI bleeding

Color Appearance

Translucent or yellow Normal / sterile

Brown HyperbilirubinemiaGB or biliary perforation

Cloudy or turbid Infection

Pink or blood tinged Mild Trauma

Grossly bloody MalignancyAbdominal trauma

Milky ("chylous") CirrhosisThoracic duct injuryLymphoma

Gross Appearance of Ascitic Fluid

Diagnostic Studies

Recommended Studies

Albumin Protein Cell count

Looking for PMNs Cultures

If clinically appropriate

Glucose LDH Amylase RBC count TB smear/culture Cytology Triglycerides

www.gastro.org

Diagnostic StudiesSAAG > 1.1 SAAG < 1.1

Ascites Protein <2.5 Ascites Protein >2.5

1. Check serumand fluid albumin

Ascites Protein >2.52. Check AscitesProtein

Hepatic Sinusoid source Peritoneum source

Capillarized sinusoid Normal sinusoidPeritoneal lymph

CirrhosisLate Budd-Chiari

3. DifferentialDiagnosis

Cardiac ascitesEarly Budd-ChiariVeno-occlusive disease

Malignancy Tuberculosispacreatic asciteshypothyroidismThe SAAG does not need to be repeated after the

initial measurement.Note: Exceptions exist: may have mixed features

Adapted from www.gastro.org

Cell Count, differential and cultureIs ascites infected?

Greater than 250 PMN = SBP If ascites is bloody ( > 50,000 RBC/mm3), correct by subtracting 1

PMN / 250 RBC one neutrophil should be subtracted from the absolute neutrophil

count for every 250 red cells to yield the "corrected neutrophil count"Is ascitesbloody?

5% of pts w/ cirrhosis - spontaneous or s/p traumatic tap. Non-traumatic associated with malignancy

20% of malignant ascites10% of peritoneal carcinomatosis

Total Protein

• Exudate ( > 2.5 g/dL) or Transudate?– Supplanted by SAAG

• Is there gut perforation? (vs SBP)– Total protein >1 g/dL – Glucose <50 mg/dL (2.8 mmol/L) – LDH greater than serum ULN

SBP VS SBP SPONTANEOUS BACTERIAL PEROTINITIS SINGLE ORGANISM IN CULTURE,TP<1GM/DL,GLUCOSE >50GM/DL,LDH <225IU/L

SECONDARY BACTERIAL PEROTINITS POLY ORGANISMS IN CULTURE,TP>1GM/DL,GLUCOSE <50MG/DL,LDH >225IU/L

FROM UPTODATE

Glucose and LDH

• Consistent with infection or malignancy?– Infection and cancer consume glucoselow

• LDH is a larger molecule than glucose, enters ascitic fluid with difficulty.– Ascitis/Serum LDH ratio

• ~ 0.4 in cirrhotic ascites• Approaches 1.0 in SBP• >1.0, usually infection or tumor

Other tests• Amylase

– Uncomplicated cirrhotic ascites • About 40 IU/L. The AF/S ratio is about 0.4

– Pancreatic ascites• About 2000 IU/L. The AF/S ratio is about 6

• Triglycerides — run on milky fluid. – Chylous ascites - TG > 200 mg/dL, usually 1000

mg/dL

• Bilirubin — run on brown ascites. – Biliary perforation – AF Bili > serum Bili

Tests for TB

• Smear – extremely insensitive• Culture – 62-83% when large volumes

cultured• Cell count – mononuclear cell predominance• Adenosine deaminase –

– Enzyme involved in lymphoid maturation– Falsely low in pts with both cirrhosis and TB

Cytology

• “almost 100%” with peritoneal carcinomatosis have positive cytology

• Malignant ascites from massive hepatic mets, HCC, lymphoma are usually negative

• Overall sensitivity for detection of malignancy-related ascites is 58 to 75 %

Treatment

Grade 1 No treatment necessary Modify risk factors Start low sodium diet

Hepatology 2003; 38: 258-266

Treatment

Grade 2 Bed rest

Diuretics work better supine SPIRONOLACTONE 100MG TO 400MG FUROSEMIDE 40MG TO 160MG

Sodium and water restriction Diuretics

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Br Med J. 1986;292:1351-3

Treatment

Grade 3 Paracentesis is the treatment of choice

Shown to have fewer complications than diuresis

Faster response After this would do Grade 2 treatment

options

Hepatology 2003; 38: 258-266

Refractory ascites (10 %)

• Diuretic resistant ascitesUnresponsive to LSD (< 88 mmol/day)

& High-dose diuretics SP 400 mg & FUR 160 mg/d

• Diuretic intractable ascitesDiuretic induced complications Encephalopathy

Creatinine > 2.0 g/dLNa < 125 mmol/LK > 6 or < 3 mmol/L

International ascites clubArroyo V et al. Hepatology 1996 ; 23 : 164 – 76.

for at least 1 week

Treatment

Refractory ascites Paracentesis with colloid infusion TIPS

Choice between these is controversial If repeated paracentesis is

contraindicated,TIPS not an option then consider porto-venous shuntPVS shown inferior to repeat paracentesis in

NEJM study

Hepatology 2003; 38: 258-266

Refractory Ascites

LT evaluationLVP + Albumin

Na restricted diet (90 mEq/d)Fluid restriction if Na < 130 mEq/L

Repeated LVP + albumin

Preserved liver function?Loculated ascites?

Paracentesis more frequent than 2-3 /month?

Continue LVP + Albumin Consider TIPS

1st Step

MaintenanceTreatment

YesNo

Clin Gastroenterol Hepatol 2005 ; 3 : 1187 – 1191.

DiureticsSpironolactone

start 100-200 per day Titrate to max of 400 per day in severe

hyper-aldoCan use potassium sparing diuretics

No other comparison trials, but spironolactone accepted as first line

Use second line if spironolactone not possible due to complications (ie gynecomastia)

Hepatology 2003; 38: 258-266

Diuretics

Loop diuretics Lasix

Initial dose 20-40 per dayCan adjust up to 160mg per day

Should be used only as an adjunct to spironolactone

Risks of K depletion, hyperchloremic alkalosis, hyponatremia and hypovolemia with subsequent renal dysfunction

Hepatology 2003; 38: 258-266

Dig Dis 2005; 23:30-38

Assessing Diuretic Response

Weight loss Lose 0.5kg a day when no edema Lose 1kg a day when edema is present

Avoid renal failureCheck urea,creat,SEResponse rate in up to 90% patients

who do NOT have renal dysfunction

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Dig Dis 2005; 23:30-38

Follow-up of patients on diuretics – 2

• Body weight

• Blood pressure

• Pulse

• Electrolytes

• Urea

• Creatinine

Every 2 – 4 weeks

Every few months thereafter

Side effects of diuretics

• SpironolactoneMen libido, impotence, gynecomastiaWomen Menstrual irregularity

• Hydro-electrolytes disturbancesHypovolemia: hypotension – renal insufficiency HyponatremiaHypo or hyperkalemia Hepatic encephalopathy

Paracentesis

ParacentesisFirst used by the Ancient Greeks Decreased in the 1950s when diuretics

were discoveredResurgence in 1980s after 1987 article

found paracentesis with lower complications than diuretics

More effective than diuresis Shorter hospital stay

Dig Dis 2005; 23:30-38

Paracentesis

Post paracentesis volume expansion Side effects and albumin

without 30%with 16%

Albumin prevents increased renin/aldo better than synthetic agents

HRS decreases Less Hyponatremia

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NEJM 350:1646-54

Paracentesis-Complications Bleeding - can be fatal Ascitic fluid leak

Purse string suture Lie with puncture site

up Bowel perforation Renal impairment Hypotension/

Cardiovascular collapse

TIPS

Transjugular Intrahepatic Portosystemic Shunt

Creates a conduit from the high pressure portal system to the lower pressure systemic circulation

Reasons for TIPS over Paracentesis

TIPS better if Loculated ascites Patient unwilling to have repeat taps Frequent recurrences

Am J Gastro 2003;98:2521-27

TIPS

Ascites can only form when portal pressure is >12

Response rates 51-79% in RCT

Dig Dis 2005; 23:30-38

TIPS - RisksEncephalopathy

30% those treated Typically can improve with shunt revision

or medical management Increased risk if

Age >60History of Encephalopathy

100% mortality if refractory to TIPS occlusion

CHF - this is due to increased preload

Am J Gastro 2003;98:2521-27

NEJM 350:1646-54

TIPS - Complications

Capsule perforationStenosis

75% in 6-12 months Decreased risk with stents coated in

polytetrafluoroethylene (PTFE)Increased cost relative to paracentesis

Radiology 1999;231:759-766

NEJM 350:1646-54

Peritoneovenous Shunts

Peritoneovenous Shunts

Creates a communication between the peritoneal cavity and the systemic circulation by a vein

Used in only in limited cases currently Used for palliation if TIPS and paracentesis

are not available or contraindicated

Hepatology 2003; 38: 258-266

Peritoneovenous Shunt

Denver Shunt(Similar to LaVeen Shunt)

Contraindications•Protein > 4.5 g/l (occlusion)•Loculated ascites•Coagulopathy•Advanced renal/cardiac disease•GI malignancy

Complications•Infection•Hematogenous spread of mets•DIC•Pulmonary edema•Pulmonary emboli

Spontaneous Bacterial Peritonitis H/O Chronic Liver Disease. Fever and abdominal pain,absent bowl

sounds,rebound tenderness (66%) Signs of peritonitis uncommon (<50%) Neutrocytic ascites on diagnostic paracentesis. 20-30% of pts with CLD develop SBP. Almost always monomicrobial. Anaerobes are not associated with SBP 20% are asymptomatic. Typically due to translocation

This is why E. Coli is the most common

DEFINE SBP VS BACTERASCITES SBP is infectious complication of portal htn related

acites charcterised by Neutrophil>250[great sensitivity} OR Neutrophil>500{great specificity }

Bacterascites is culture +ve ascities in the presence of normal ascitic neutrophil count,<250

Risk factors for SBP

AF protein <1gm/dlacute GI bleedingprior episode of SBP

In about 1/3 of patients abdominal signs of SBP are mild or absent ,In these 1/3 of patients

HE and Fever are main features.

SBP: Diagnosis.

Diagnosed with >250 polys or > 50-70% of the total cell count.

Ascitic protein >1gm/dl against SBP.10-30% are ascitic fluid culture negative.3% have secondary Bacterial Peritonitis.Ascitic fluid Glucose, LDH and total

proteins may be helpful in DDx.Erect Abd X-ray in suspicious cases.

Hepatology 2003; 38: 258-266

NEJM 350:1646-54

SBP: Treatment and Prophylaxis

Treat with iv cefotaxime,ceftriaxone or piperacilline/tazobactum.

Repeat PMN count after 48 hrs. 40% develop HRS during the course of illness. Human Albumin 1.5gm/Kg on day one and 1 gm/Kg

on day three has shown improvement in both morbidity and mortality.

Ultimate treatment:Liver transplant.

Prophylaxis

Prophylaxis: 70% recur within one year.FIRST LINE 1= Patient with acute GI bleed should receive iv

ceftriaxone1gm daily for 7 days

2 =Patient with severe CLD with AF protein <1gm should receive longterm norfloxacin 400mg daily

SECOND LINE Norfloxacin 400mg dailyis the Rx of choice for

recurrent SBP

Prognosis only 10% to 20% of patient

survive 5 years from the first appearance of ascites.

However prognosis is better in those with

good liver function good respose to theraphy when treatable cause for

underlying cirrhosis is present precipitataing cause such NA

excess intake is found. MORTALITY at 1 year

is 50% after Ist episode of SBP.

• Ascites 50 % survival at 2 years

• Refractory ascites 50% survival at 6 months25% survival at 1 year

• SBP 30 - 50% survival at 1 year• HRS-2 40% survival at 6 months

• HRS-1 < 5% survival at 6 months

Prognosis of ascites in cirrhotic patients

Referral to liver transplantation unit

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