TOC   |  GI   

ASCITES

CAUSES:

• Cirrhosis 81% (alcohol 65%, viral hepatitis 10%, others 6%)
• Cancer 10%
• Congestive Heart Failure 3%
• Tuberculosis 2%
• Dialysis 1%
• Pancreatic disease 1%
• Misc. 2%

(REF: Textbook of Gastroenterology 1991 - Runyon, Reynolds TB - Lippincott)

Ascitic Fluid Analysis:

• Cell count: Leukocyte>500/cc or absolute neutrophil >250/cc suggests infection.
• Protein < 1g/dL in spontaneous peritonitis; >1 g/dL in secondary peritonitis.
• Glucose <50 mg/dL or increased LDH in secondary peritonitis.
• Albumin serum-ascites gradient = serum albumin - ascitic albumin
  - Gradient of > 1.1 g/dL suggests portal hypertension; seen in cirrhosis, alcoholic hepatitis, CHF, massive liver metastasis, fulminant liver failure, portal-veiin thrombosis, Budd-Chiari synd, veno-occlusive disease, fatty liver of pregnancy, myxedema.
  - Gradient of < 1.1 g/dL seen in peritoneal carcinomatosis, TB, pancreatic ascites, biliary ascites, nephrotic synd, bowel obstruction or infarction, serositis.
• Gram stain & C/S
• Amylase in pancreatic or perforation.
• Cytology or TB smear & culture prn.

A. Transudative ascites (Serum Albumin - Ascites Albumin >1.1 gm/dl)

1. Liver cirrhosis
2. Congestive heart failure
3. Hepativ vein obstruction (Budd Chiari syndrome) a. Assoc. with tumors (hepatoma, hypernephroma, pancreatic Ca) b. Assoc. with hematologic disorders (myeloproliferative disease, polycythemia vera, myeloid metaplasia c. Due to infections
4. Nephrotic syndrome
5. Meig's ovarian tumor syndrome
6. Constrictive pericarditis
7. Inferior vena cava obstruction
8. Viral hepatitis with submassive or massive hepatic necrosis

B. Exudative ascites (Serum Albumin - Ascites Albumin <1.1 gm/dl)

1. Neoplastic diseases involving the peritoneum: Peritoneal carcinomatosis, Lymphomatous disorders
2. Tuberculous peritonitis
3. Pancreatitis
4. Post surgery talc or starch powder peritonitis
5. Transected lymphatics following portal caval shunt surgery
6. Myxedema
7. Sarcoidosis
8. Lymphatic obstruction: a. Intestinal lymphangiectasia, b. Lymphoma
9. Pseudomyxoma peritonei
10. Struma oovarii
11. Amyloidosis
12. Prior abdominal trauma with ruptured lymphatics
13. Hemodialysis CRF related ascites

C. Disorders simulating ascites

1. Pancreatic pseudocyst
2. Hydronephrosis
3. Ovarian cyst
4. Mesenteric cyst
5. Obesity

RX of ascites depending on underlying cause.

1. Paracentesis to remove large amount of ascitic fluid 4-6 L/day.
   Several large randomized, controlled trials have shown that repeated large-volume paracentesis (4 L-6 L) is safer and more effective for the treatment of tense ascites compared with larger-than-usual doses of diuretics.
2. Bed rest
3. Low salt diet <2 g NaCL/d and fluid restriction <1500 mL/day.
4. Aldactone 25-50 mg qid PO (if urine Na 5-25 meq)
5. Furosemide 40-80 mg/day (if urine Na < 5 meq)
6. LeVeen or Denver peritoneaovenous shunt
7. TIPS (Transjugular Intrahepatic Portosystemic Stent Shunt)
8. Extracorporeal ultrafiltration of ascitic fluid.
9. Liver transplantation

(REF: NEJM 2/3/94; 330:337 Runyon BA)

Ascites - Differential Diagnosis  

A.  Normal Peritoneum

• Portal Hypertension: Cirrhosis, IVC Obstruction, Budd Chiari Syndrome
• Cardiac Dysfunction: Congestive Heart Failure, Tricuspid Insufficiency, Cardiomyopathy, Constrictive Pericarditis
• Portal Vein Occlusion: Thrombosis, Compression
• Hepatocellular Carcinoma - screen with Alpha-Fetoprotein (AFP) level
• Hepatic Fibrosis: Hemochromatosis, Wilson's, Polycystic Disease, Syphilis, Sarcoidosis
• Hypoalbuminemia (Severe): Nephrotic Syndrome, Malabsorption, Malnutrition, Liver Failure
• Miscellaneous: Pancreatic Ascites, Ovarian Disease (Meig's Syndrome, Struma ovarii)

B.  Diseased Peritoneum (usually exudative)

• Infections: Bacterial, Tuberculous, Fungal, Parasitic Peritonitis
• Subacute Bacterial Peritonitis
• Neutrophilic Peritonitis
• Chronic Inflammatory Peritonitis
• Neoplasia: Metastatic Disease, Primary mesothelioma
• Granulomatous Peritonitis: Infections, Cancer, Barium
• Vasculitis
• Miscellaneous: Eosinophilic Peritonitis, Whipple's Disease, Gynecologic Disease

C. Transudative (Serum Albumin - Ascites Albumin >1.1gm/dl)

• Heart Failure Group
• Alcoholic Liver Disease (Micronodular Cirrhosis, Alcoholic Hepatitis)
• Hepatic Necrosis
• Hepatic Vein Thrombosis (Budd-Chiari Syndrome) or IVC Obstruction
• Portal Vein Occlusion
• Meig's Syndrome
• Hemochromatosis, Wilson's Disease

D. Exudative (Serum Albumin - Ascites Albumin <1.1)

• Peritoneal Carcinomatosis
• Pancreatic Ascites (amylase level)
• Nephrogenous (Dialysis) Ascites
• Peritoneal Infections
• Chylous Ascites
• Myxedema (Hypothyroidism)

E. Budd-Chiari Syndrome

• Neoplasm, Local
• Coagulopathy
• Neoplastic association
• Collagen Vascular Disease - eg. Systemic Lupus (SLE), Vasculitis, Antiphospholipids
• Factor Deficiency (eg. Factor S, C, anti-thrombin III)
• Birth Control Pills (Estrogens)      

Ref: Outlines in Clinical Medicine on Physicians' Online 2000

The Management of Cirrhotic Ascites  Elaine Yeung, MD; Florence S. Wong, MD, FRCP(C)
Medscape General Medicine 10/22/2002

Spontaneous Bacterial Peritonitis (SBP)  

It is defined as an ascitic fluid infection associated with

• a positive bacterial culture and
• an ascitic fluid polymorphonuclear cell count of > 250/mm3,
• in the absence of a surgically treatable abdominal source of infection.   

In hospitalized patients with cirrhosis, 10% to 25% will have an episode of SBP with a mortality rate of 17% to 50%, with outcome dependent on the association with a recent gastrointestinal bleed, the severity of infection, and degree of renal and liver failure.

Pathogenesis

• Bacteremia is most often from intestinal bacterial overgrowth, but may also result from bacteriuria or intravascular catheters.  

Types of SBP

• Culture-positive neutrocytic ascites (SBP)  (the most common form of SBP) with a positive bacterial culture and a polymorphonuclear (PMN) cell count of >/= 250/mm3. About two thirds of ascitic fluid infections belong to this subgroup and are almost invariably monomicrobial.  Other variants of SBP include
• Culture-negative neutrocytic ascites (CNNA) characterized by PMN cell count of >/= 250/mm3 with negative ascitic fluid cultures
  The differential diagnosis of CNNA includes peritoneal carcinomatosis, pancreatitis, and tuberculous peritonitis. CNNA has the same prognosis as SBP and should therefore be treated similarly.
• Monomicrobial nonneutrocytic bacterascites (MNB), characterized by isolation of bacteria in cultures but with a PMN cell count of </= 250 mm3.
  Asymptomatic MNB usually signifies colonization and does not require antibiotic therapy unless there are clinical signs and symptoms suggestive of infection.
• Polymicrobial bacterascites occurs when ascitic fluid contains multiple organisms and the PMN cell count is < 250/mm3. The latter usually results from inadvertent puncture of the intestines during attempted paracentesis and occurs in about 1/1000 paracenteses.  Risk factors include ileus, presence of multiple surgical scars, and operator inexperience. If the ascitic fluid contains > 1 g/dL of protein and the opsonic activity of fluid is adequate, colonization usually resolves spontaneously. Secondary bacterial peritonitis is also polymicrobial but has a PMN cell count of > 250/mm3. The latter can be distinguished from SBP by a total protein > 1 g/dL, glucose concentration < 50 mg/dL, and a lactate dehydrogenase level > 225 U/mL. Prompt diagnosis through imaging is necessary because without surgical correction, death is the usual outcome.

Clinical Signs and Symptoms

• Fever - 69%; Abdominal pain - 59%; Hepatic encephalopathy - 54%; Abdominal tenderness - 49%; Diarrhea - 32%; Ileus - 30%
• Shock - 21%; Hypothermia - 17%
• Asymptomatic - 10%

A rigid abdomen is not necessary for diagnosis, especially in patients with large-volume ascites, which prevents the contact of visceral and parietal peritoneal surfaces to elicit the spinal reflex that causes rigidity.

Treatment of SBP

Treatment should be started empirically if SBP is suspected clinically, regardless of the availability of laboratory results.

In community-acquired SBP and in patients not on SBP prophylaxis, Escherichia coli and Klebsiella pneumoniae are seen in up to 60% of isolates. About 25% are Gram-positive cocci, mostly streptococcal species. Anaerobes are rarely seen.

• Intravenous cefotaxime 2 gm q12h for a minimum of 5 days is the empiric antibiotic of choice and has been shown to cure SBP episodes in 85% of patients compared with in 56% of those receiving ampicillin and tobramycin.  
• Intravenous amoxicillin-clavulanic acid followed by oral therapy has been shown to be as effective as cefotaxime, but may not be widely available.
• Intravenous ciprofloxacin followed by oral treatment has also been shown to be effective.[87]
• Trials of oral ofloxacin vs intravenous cefotaxime in patients without septic shock, encephalopathy, azotemia, gastrointestinal bleed, or ileus showed an SBP resolution rate of 84% in the ofloxacin group vs 85% in the cefotaxime group.