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by
Dr Intekhab AlamProfessor of Medicine
Department of MedicinePostgraduate Medical Institute,
Lady Reading Hospital, Peshawar
MANAGEMENT OF ASCITES
Objectives
1. Understand the basic mechanisms of portal hypertension (PHT)
2. Study Ascites as a complication of PHT
3. Get an idea on the management of Ascites and its complications
What is Liver Cirrhosis?
Diffuse fibrosis of the liver with nodule formation
Abnormal response of the liver to any chronic injury
Causes of Cirrhosis
1. Chronic viral hepatitis2. Metabolic: hemochromatosis, Wilson dis,
alfa-1-antitrypsin, NASH3. Prolonged cholestasis (primary biliary
cirrhosis, primary sclerosing cholangitis)4. Autoimmune diseases (autoimmune
hepatitis)5. Drugs and toxins6. Alcohol
Anatomy of the portal venous system
The Effect of The Liver Nodule
Mechanism of Portal HTN
Cirrhosis
Resistance portal flow
MechanicalNodules
DynamicNitric oxide
Complications of Portal Hypertension in cirrhosis liver.
Development of Ascites.
Varices formation.
Hepatic encephalopathy.
Hepatorenal syndrome.
Ascites
Definition: presence of free fluid in the peritoneal cavity
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
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
Etiology
Cirrhosis (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
Pathophysiology of ascites in CLD:
Splanchnic HTN due to outflow obstruction Increased vasodilatation (NO) This sequesters volume in the abdomen Decreases systemic filling Decreases systemic BP Activates antinatriuretic factors Combination of increased splanchnic BP with
vasodilatation leads to capillary leak Lymph return can only keep up for sometime
then ascites develops.
Physical Examination
Bulging Flanks Flank Dullness Shifting Dullness Fluid Wave Puddle sign 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
Sensitivity-72-93% Pooled data 81%
Specificity-44-70% Pooled data 59%
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
Sensitivity-80-94% Most sensitive test Pooled data 84%
Specificity-29-69% 69% outlying value Pooled data 59%
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
Sensitivity-60-83% Pooled data 77%
Specificity-56-90% Pooled data 72%
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
Sensitivity-50-80% Pooled data 62%
Specificity-82-92% Most specific test Pooled data 90%
JAMA 1992; 267:2645-48
Puddle Sign
Have patient prone 3-5 minutes then rise to crawling
Place the diaphragm of the stethoscope over the most dependent area of the abdomen
Flick a finger until sound detected
No longer recommended Formerly used for high
sensitivity Sensitivity-43-55%
Pooled data 45% Specificity-51-83%
Pooled data 73%
JAMA 1992; 267:2645-48
International Ascites Club Grading
Grade 1 Mild, only detectable by U/S
Grade 2 Moderate, symmetrical distension
Grade 3 Gross or large with marked distension
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) Have to use caution as
small or even moderate ascites may be difficult to tap (even when marked)
Ensure mark is appropriate
Go with patient to U/S (ideal)
If not possible, in order specify location where you want to place your needle
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.
Complications: (1% of patients) Abdominal wall hematomas. Hemoperitoneum or bowel entry.
Contraindications:Clinically evident fibrinolysis or DIC.
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 Tuberculosis
The SAAG does not need to be repeated after the initial measurement.Note: Exceptions exist: may have mixed features
Adapted from www.gastro.org
Ascitic fluid analysis: If the PMN count is >250 cells/mm3, another specimen is injected into blood culture bottles at bedside.
Bacterial growth occurs in about 80% of specimens with count of >250 cells/mm3.
In a "bloody" sample that contains a high concentration of RBC, the PMN count must be corrected: One PMN is subtracted from the absolute PMN count for every 250 red cells/mm3 in the sample.
The results must be available within 1 hour, so that important diagnostic and therapeutic decisions can be made.
A Gram stain is of particular low yield unless free gut perforation, is suspected.
Based on clinical judgment, additional testing can be performed
a) Cytology ,smear & culture for mycobacteria.
b) Cytology : in peritoneal carcinomatosis (sensitivity increased by centrifuging large volume).
c) Elevated bilirubin level suggest biliary or gut perforation.
d) LDH >225mU/L, glucose <50mg/dL, total protein >1g/dL and multiple organisms on gram stain suggest secondary bacterial peritonitis.
e) High level of TG's confirms chylous ascites.
f) Elevated amylase level suggest pancreatitis or gut perforation.
Prognosis
Poor outcomes Refractory ascites SBP HRS MELD (Model for end-stage liver disease)
is not specifically validated for patients with ascites
NEJM 350:1646-54
Prognosis
Any person with ascites due to cirrhosis needs transplant evaluation If MELD is <15 can stop there Average US wait time 500d Average wait less in some other countries
120 days in UK180 days in Spain
If admitted for ascites 40% chance of dying within 2 years
Improves to 70-80% 5 year survival after transplant
Hepatology 2003; 38: 258-266
Dig Dis 2005; 23:30-38
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 studied bemetanide GFR lower standing as well
Sodium and water restriction Diuretics
Hepatology 2003; 38: 258-266
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
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
Sodium Restriction
No survival benefit related to ascites shown, does have benefit in GIB mortality
50mm restriction is equivalent to 120mm (approx. 2g/day) Tighter restriction had faster resolution Higher incidence of renal dysfunction and
hyponatremia
Hepatology 2003; 38: 258-266
Diuretics
Spironolactone start 100-200 per day Titrate to max of 400 per day in severe hyper-aldo
Can use potassium sparing diuretics Amiloride inferior to canrenoate (anti-
mineralocorticoid) No other comparison trials, but spironolactone
accepted as first line Use second line if spironolactone not possible 2/2
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 failureResponse rate in up to 90% patients
who do NOT have renal dysfunction
Hepatology 2003; 38: 258-266
Dig Dis 2005; 23:30-38
Paracentesis
Paracentesis
First 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
Total volume paracentesis is as effective and as safe as sequential 3L paracentesis
Hemodynamics RA pressure drops immediately PCWP takes 6h to decrease
Hepatology 2003; 38: 258-266
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
Hepatology 2003; 38: 258-266
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
TIPS
Ascites can only form when portal pressure is >12
Response rates 51-79% in RCT
Dig Dis 2005; 23:30-38
TIPS - Benefits
May improve nitrogen balanceWill decrease portal pressure reducing
GIB riskImproves hemodynamics
Increased CO, RA pressure, PCWP and decreased SVR with increased Na excretion
Improves response to diuresis
Hepatology 2003; 38: 258-266
NEJM 350:1646-54
TIPS - Risks
Encephalopathy 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
TIPS v. Paracentesis
Several studies (2 examples) Lebrec 1996
No ascites recurrence benefit in CP class C patients with worsened survival
CP class B showed decreased recurrenceSmall study (25 patients)
Salerno - 2004Shown to have survival improvement with multivariate
analysis (only trend to improved survival without this) Non-blinded 3 center studyHad to have 4 taps in the last monthDecreased ascites recurrence HR 0.37 (0.18-0.76)66 patients
Hepatology 2004;40:629-635
J Hepatol 1996;25:135-44
Cochrane Database
No difference in mortality Decreased re-accumulation at 3 and 12
months Increased PSE OR 2.11(1.22-3.66) Surprisingly no difference:
GIB, ARF, Infection or DIC Some issues in differences between the
studies, not all paracentesis had post-paracentesis albumin, differences in MELD/CP between studies
Hepatology 2003; 38: 258-266
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
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
Spontaneous Bacterial Peritonitis
H/O Chronic Liver Disease. Fever and abdominal pain (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
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 3rd generation Cephalosporins. Repeat PMN count after 48 hrs. 40% develop HRS during the course of illness. Human Albumin 1.5gm/Kg o day one and 1 gm/Kg on day three
has shown improvement in both morbidity and mortality.
Prophylaxis: 70% recur within one year.
Norfloxacin 400mg qd Ciprofloxacin 750mg q week Tri-Sulpha: Has never been tested in a trial with mortality.
Ultimate treatment:Liver transplant.
ReferencesMoore K, Wong F, Gines P, Bernardi M et al. The Management of Ascites in Cirrhosis: Report on the Consensus Conference of the International
Ascites Club. Hepatology 2003;38: 258-266Gines P, Cardenas A, Arroyo V, Rodes J. Management of Cirrhosis and Asictes. NEJM. 2004;350:1646-1654Haskal Z. Improved Patency of TIPS in Humans: Creation and Revision with PTFE Stent-Grafts. Radiology. 1999; 213: 759-766Cardenas A, Arroyo V. Refractory Ascites. Dig Dis. 2005; 23:30-38Russo M, Sood A, Jacobson I, Brown R. TIPS for Refractory Ascites: An Analysis of the Literature on Efficacy, Morbidity and Mortality. Am J
Gastroenterol. 2003; 98:2521-2527Heuman D, Abou-assi S, Habib A et al. Persistent Ascites and Low Serum Sodium Identify Patients with Cirrhosis and Low MELD Scores who are at
High Risk for Early Death. Hepatology. 2004; 40: 802-810Salerno F, Merli M, Riggio O, Cazzangia M, et al. Randomized Controlled Study of TIPS v. Paracentesis Plus Albumin in Cirrhosis with Severe
Ascites. Hepatology 2004;40: 629-635.Ring-Larsen H, Henriksen J, Wilken C, Clausen J, et al. Diuretic treatment in decompensated cirrhosis and congestive heart failure: effect of posture.
Br Med J 1986; 292: 1351-1353Lebrec D, Giuily N, Hadengue A, Vilgrain V, et al. TIPS: comparison with paracentesis in patients with cirrhosis and refractory ascites: a randomized
trial. French Group of Clinicians and a Group of Biologists.Saabs, Nieto JM, Ly D, Runyon BA. TIPS versus paracentesis for cirrhotic patients with refractory ascites. The Cochrane database of Systematic
Reviews 2004, Issue 3 Art. No.: CD004889Cattau EL, Stanley BB, Knuff TE, et al. The Accuracy of the Physical Examination in the Diagnosis of Suspected Ascites. JAMA. 1982; 247: 1164-
1166.Williams JW, Simel DL. Does This Patient Have Ascites?. JAMA. 1992; 267: 2645-2648.Mallory A, Schaefer JW. Complications of Diagnositc Paracentesis in Patients with Liver Disease. JAMA. 1978; 239: 628-630Runyon BA. Paracentesis of Ascitic Fluid a Safe Procedure. Arch Intern Med. 1986; 146: 2259-2261Simel DL, Halvorsen RA, Feussner JR. Quantitating bedside diagnosis: clinical evaluation of ascites. J Gen Intern Med. 1988; 3:423-428.www.uptodate.com
Images:www.lf2.cuni.cz/Projekty/interna/foto/001/www.scielo.br/img/revistas/rb/v38n1/www.krauth-medical.de/onlinekatalog/grafiken/bilder_mm/