Ascites SBP

Dr Manoj K Ghoda M.D., M.R.C.P.

Consultant GastroenterologistVisiting faculty, GCS Hospital

gujarat gastro group

Clinical history

A 42 year old male was referred for ascites. • He was unwell for some three months

– anorexia, – abdominal discomfort,– feverish feeling.

Treated locally

• A fortnight later he noticed abdominal distention for which a sonography was ordered which showed ..

• inhomogeneous echo texture of liver,• splenomegaly, • gross ascites. • No internal septation were seen

Personal history

• Alcohol for last 20 yrs.• There was no previous illness.

Clinical examination

– Conscious, co-operative and oriented. – Thin built, malnourished– Few spiders on his back and neck.

• P/A– Hepato-splenomegaly.– Moderate ascites.

• Positive fluid thrill• Horse shoe dullness

– No hernia

Investigations• S. Bilirubin 1.9 mg, • SGPT 94 IU, • Albumin 3.0 gm, globulin 3.9 gm. • Hb 10.4 with microcytic hypo-chromic picture.• Platelet count: 1.1 lacs • HBsAg and HCV were non-reactive• Upper g.i. endoscopy revealed grade - I esophageal

varices.

What would you do now??

There is a potential space between 2 layers of peritoneum. Collection of free fluid between these 2 spaces is called

ascites.

ASCITES

Ascites: Etiology

Pathology and Pathogenesis• Sinusoidal hypertension.• Na and water retention• Vasodilatation theory• Overflow theory

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

What are the features associated with ascites irrespective of its etiology?

Associated conditions

• Hernias. – Increased intra-abdominal pressure favors the

development of divarication of recti or hernias in umbilical, femoral or inguinal areas.

– Develop in about 20% of patients with cirrhosis and ascites whereas in only 3% with just cirrhosis.

• Hepatic hydrothorax; develops in 5-10%.right sided 85%.due to diaphragmatic seepage.

• Peripheral edema, due to hypoproteinemia. A functional inferior vana caval block due to pressure of abdominal fluid is an additional factor.

Diagnosing Ascites

• Ultrasound is the most sensitive test for ascites (5-10 mL 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

Approach to a case of ascites:

Clinical clues in differential diagnosis

Cirrhosis• Stigmata of cirrhosis

– spider angiomata– palmer erythema– muscle wasting– gynecomastia,– duputreyn’s contracture,– asterexis

• Jaundice • Signs of portal HT:

– splenomegaly and abdominal wall collaterals.

Tuberculosis

• Relatively short history of illness• History of contact• Evidence of immunosuppression• Anorexia, evening rise of fever, associated

cough with productive sputum or hemoptysis• No pedal edema

Cardiac ascites

• Past history• Precordial deformity• Raised JVP• Positive HJR• Pedal edema

Pancreatic ascites

• History of acute pain or past history of chronic pancreatitis.

• There may be blunt trauma to abdomen• Usually a pseudocyst is responsible.

Malignant Ascites

• Comes surreptitiously• Weight loss may be present• Commonly caused by cancers of:

– Breast, bronchus, ovary, stomach, pancreas, colon

Laboratory in Ascites:

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

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Types of ascites:

Serum to Ascites Albumin Gradient (SAAG)SAAG > 1.1 g/dL Portal HTN

SAAG < 1.1 g/dL Other causes • 97% accurate

The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Runyon BA; Montano AA; Akriviadis EA; Antillon MR; Irving MA; McHutchison Ann Intern Med 1992 Aug 1;117(3):215-20.

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 — – Chylous ascites - TG > 200 mg/dL, usually 1000

mg/dL; Ascitic fluid: S. Triglyceride raion >1.1• 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 metastasis, HCC, lymphoma are usually negative

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

Imaging in Ascites

Hepatic vein congestion in right sided heart failure

Omental cake in a case of malignant ascites

Pancreatic ascites

Role of diagnostic laparoscopy in ascites

Management principles:

Treatment of the cause:

• Cirrhosis: Diuretics, Albumin, paracentesis and TIPS

• Tuberculosis: AKT• Cardiac: Diuretics and removal of cardiac

cause if possible• Pancreatic: Somatostatin and Pancreatic

stenting• Malignant: Chemotherapy• Chylous: Medium chain triglycerides

Therapeutic intervention

Therapeutic intervention in ascites due to liver failure

• Sodium restriction• Diuretics• Therapeutic paracentesis• TIPS• Liver transplantation

Treatment

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

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Treatment

• Grade 2– Bed rest;increased renal perfusion and portal

venous flow during recumbancy.• Diuretics work better supine

– studied bemetanide– GFR lower standing as well

– 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

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 shunt

• PVS shown inferior to repeat paracentesis in NEJM study

Hepatology 2003; 38: 258-266

Diuretics• Spironolactone

– start with 50-100 per day– Titrate to max of 400 per day in increments of 100mg/day

if the response is insufficient after 3-4days(weight loss less than 300mg)

• Can use other 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; added if response with spironolactone inappropriate or hyperkalemia as a complication.– Frusemide: Initial dose 20-40 per day

• Can adjust up to 160mg per day

– Should be used only as an adjunct to spironolactone

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 failure• Response rate in up to 90% patients who do

NOT have renal dysfunction

Hepatology 2003; 38: 258-266

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

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TIPS

• Transjugular Intrahepatic Portosystemic Shunt

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

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

COMING BACK TO OUR CASE....

What do you think ascites is due to in this case?

• ALCOHOLIC CIRRHOSIS ?• TUBERCULOSIS ?• PANCREATITIS ASCITES ?• MALIGNANT ASCITES ?• CARDIAC ASCITES ?

However obvious is the cause..

Always do the diagnostic tap. (Sheila Sherlock)

Ascitic fluid

• Protein 6.4 gms, (Albumin 3.4 Vs S.Albumin 3.0)

• Sugar 67 mg, • Cells 900 mainly lymphocytes,• no malignant cells were seen.• Ascitic fluid amylase and lipase were normal• AFB culture was sent.• ADA 70

How will you proceed now?What are the options available with us?

Follow up in our case..

• Treated with 4 drug AKT• IV Albumin• Diuretics

Spontaneous Bacterial Peritonitis

• It is an acute bacterial infection of ascitic fluid.

• It occurs in both children and adults and is a well-known and ominous complication in patients with cirrhosis.

• Of patients with cirrhosis who have SBP, 70% are Child-Pugh class C. In these patients, the development of SBP is associated with a poor long-term prognosis.

• .

Epidemiology:

• Adults with SBP typically have ascites, but most children with SBP do not have ascites.

• Nearly one in six patients with ascites could develop SBP.

• Mortality could be low if the underlying etiology is nephrotic syndrome but in cirrhotics mortality could be as high as 40-70%.

• Any comorbid condition like renal failure could add to the mortality and morbidity.

• Early diagnosis and aggressive treatment may result in dramatic decrease in mortality and morbidity.

Pathophysiology:

• Intestinal bacterial overgrowth, impaired phagocytic function, low serum and ascites complement levels, and decreased activity of the reticuloendothelial system, are possible underlying factors

Microbiology:

• Enteric organisms  from GI tract are isolated from more than 90% of infected ascites fluid in SBP.

• There may be a hematogenous spread also.

• With wide spread use of fluoroquinolones for prophylaxis in cirrhotic patients, recently there is a higher predominance of gram-positive pathogens in ascitic fluid cultures.

Clinical presentation:

• Fever and chills followed by abdominal pain or discomfort is the most common presentation. Pain could be very severe and diffuse and may be confused with acute abdomen.

• Diffuse abdominal tenderness, which could be severe and sometimes with rebound tenderness and even guarding, is found in more than 50% of patients with SBP.

• In cirrhotics, there may be decompensation

• Diarrhea

• Completely asymptomatic cases are also seen in as many as 30% of patients.

Investigations and diagnosis:

Diagnostic ascitic tapping is the gold standard. Peritoneal fluid should be analyzed for protein, glucose, albumin, cell count, gram stain, and anerobic, aerobic and fungal culture.

Combination of an ascites fluid pH of <7.35 and polymorphonuclear neutrophil (PMN) count of >500 cells/µL is virtually diagnostic of SBP.

If PMN count is >250 cells, but less than 500 cells/µL, a positive bacterial culture is required for the diagnosis.

SBP could still exist if the culture is negative and the PMN count is between 250-500 cells. This is seen in monomicrobial SBP.

Sometimes blood culture is positive with cell count of less than250. This is taken as positive evidence for SBP.

Lactate level: An ascites lactate level of >25 mg/dL is suggestive of SBP.

Treatment:

• IV fluid is started to maintain peripheral perfusion.

• Pending culture, IV cefotaxime (or similar 3rd generation cephalosporins) is started at the dose of 2 gm IV every 8 hourly.

• Metronidazole is started at the dose of 400 mg. IV every 8 hourly.

• Aminoglycosides like gentamycin at the dose of 3 mg./Kg in divided doses is useful for Pseudomonas aeruginosa, E coli, Proteus, Klebsiella, and Staphylococcus species. Amikacin may also be used instead at the dose of 15mg./Kg as a single dose. These drugs are nephrotoxic and their levels must be monitored closely as well as renal functions.

• Sometimes Ampicillin 1-2 gms. every 6 hourly together with one of the aminoglycosides is also used effectively.

• IV albumin, especially when serum albumin is low is very useful in reducing ascites and increase phagocytosis by monophages.

Prophylaxis:

Outpatient prophylaxis, with norfloxacin 400 mg daily or ciprofloxacin 750 mg weekly is useful in patients with,

• Ascites and acute GI bleeding • Ascitic fluid protein levels of less than 1 g/dL • A history of SBP

Thank you..! Any questions??

Dr Manoj K Ghoda M.D., M.R.C.P.

Consultant GastroenterologistVisiting faculty, GCS Hospital

Gujarat gastro group