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“The only thing necessary for these diseases to the triumph is for good people and governments to do nothing.”
      

Ascites

http://www.vh.org/adult/provider/familymedicine/FPHandbook/Chapter05/18-5.html

 

University of Iowa Family Practice Handbook, Fourth Edition, Chapter 5

Gastroenterology And Hepatology: Ascites and Spontaneous Bacterial Peritonitis

Jatinder P. S. Ahluwalia, MD, Mark A. Graber, MD, and William B. Silverman, MD
Division of Gastroenterlogy and Hepatology and Departments of Internal Medicine, Family Medicine, and Emergency Medicine
University of Iowa Hospitals and Clinics and College of Medicine
Peer Review Status: Externally Peer Reviewed by Mosby

    
  1. Ascites. General Information
    1. Ascites is a pathologic accumulation of serous fluid within the abdomen. It may be caused by decompensated liver disease (alcohol- and virus-related cirrhosis), heart failure, abdominal carcinomatosis, tuberculosis, fulminant liver failure, pancreatic disease, pelvic inflammatory disease, connective tissue diseases and hypoproteinemia.
    2. Cirrhosis is the underlying cause in ~80% of the patients with ascites.
      1. Unlike nonalcohol-related causes of liver disease, ascites may be reversible in alcoholic liver disease with abstinence and salt restriction.
      2. An abrupt development of ascites after many years in a patient with stable cirrhosis should suggest the possibility of hepatocellular carcinoma.
  2. Physical Examination and Radiologic Assessment
    1. Percussion of the flanks helps differentiate ascites from other causes of increased abdominal distention. The dullness should shift upon rotating the patient in the right or left lateral positions. Shifting dullness indicates the presence of at least 1.5 liters of ascites.
    2. Plain abdominal X-ray may show the ground glass appearance with centrally located bowel loops, but is not necessary or recommended in the assessment or treatment of ascites.
    3. Ultrasonography may be necessary to determine the presence or absence of ascites. Doppler studies of the portal system are helpful in cases in which Budd-Chiari syndrome or a vena caval web are suspected.
    4. A chest X-ray and an echocardiogram are helpful in assessing patients suspected to have ascites of cardiac origin.
  3. Paracentesis and Ascitic Fluid Analysis
    1. Diagnostic paracentesis should be performed routinely in all patients with new onset ascites and in all patients admitted to the hospital with ascites. A 22-gauge needle can be inserted in a Z-tract fashion, to minimize leakage of fluid after the paracentesis, in midline between the umbilicus and the pubis symphysis in order to avoid collateral vessels. In the presence of a midline scar, a position ~1.5 inches above and medial to the anterior superior iliac spine can be used safely.
    2. Ascitic fluid is mostly straw colored or yellow tinged. Cloudiness or opacified appearance is due to the presence of neutrophils. Milky appearing ascites is due to the presence of triglycerides and is also known as chylous ascites. Non-traumatic bloody ascites should raise the suspicion for tuberculosis and malignancy. A tea-colored fluid is occasionally seen in pancreatic ascites.
    3. The initial ascitic fluid analysis should include the following studies: cell count with WBC differential (mandatory test in all cases), albumin, total protein and culture (in blood culture bottles to increase the yield). Glucose, amylase, and Gram stain are of little or no value except in cases of suspected gut perforation.
      1. Patients with >250 polymorphonuclear leukocyte count (PMN) per milliliter are assumed to be infected and need to be treated. In cases of bloody taps, only 1 PMN per 250 red cells can be attributed to contamination of the ascitic fluid with blood.
      2. In ascites due to tuberculous peritonitis and peritoneal carcinomatosis, lymphocytes predominate.
      3. The serum-ascites albumin gradient (SAAG) is equal to [albu-min]serum - [albumin]ascites. A gradient of >1.1 g/dl is indicative of portal hypertension with greater than 90% reliability.
  4. Other causes of Ascites
    1. High SAAG
      1. Cardiac ascites is due to congestion of hepatic sinusoids and has high total protein.
      2. Nephrogenous ascites occurs in patients on hemodialysis with volume overload and tends to have high total protein as well.
      3. Massive liver metastases can result in portal venous inflow obstruction and tumor emboli in portal vein radicals cause- portal hypertension. The ascites total protein is <2.5 mg/dl in two-thirds of the cases. Consider also Budd-Chiari syndrome, etc.
      4. In myxedema, ascites forms due to congestive heart failure and also has high protein (>2.5 mg/dl).
    2. Low SAAG
      1. Tuberculous peritonitis is most often diagnosed in Asians and immigrants from Central America.
      2. Peritoneal carcinomatosis accounts for ~50% of all cases of ascites due to a malignancy. Cytology is positive in 97% to 100% of the cases.
      3. Pancreatic ascites accounts for <1% of ascites. Patients often have underlying liver disease due to alcohol abuse. The fluid has high amylase and the total protein of the ascites is usually high.
      4. Biliary ascites is due to leakage of bile into the peritoneum, is dark brown, has bilirubin value $6 mg/dl and an ascitic fluid/serum bilirubin ratio of >1.
      5. Ascites with low SAAG may be seen in patients with connective tissue diseases due to serositis in the absence of portal hypertension.
      6. Nephrotic syndrome is a cause of ascites with low protein.
      7. Ascites in a febrile, sexually active young woman should raise a suspicion for chlamydia peritonitis. This ascites has high protein and has elevated WBC.
  5. Treatment of Ascites.
    1. Discontinue any prostaglandin inhibitors or other drugs which reduce GFR (e.g., NSAIDS).
    2. Sodium restriction is the key to successful treatment of ascites. Patient should be instructed to follow a 2 g/day sodium diet. Fluid restriction is not necessary unless hyponatremia is present.
    3. Avoidance of salt substitutes that contain KCl and potassium-enriched foods should be emphasized especially if the patient is also on a potassium-sparing diuretic.
    4. If salt restriction alone is not effective, oral diuretics can be initiated. A combination of spironolactone and furosemide is usually successful in causing natriuresis without precipitating hyper- or hypokalemia. The usual beginning doses are spironolactone 100 mg QD and furosemide 40 mg QD.
    5. Random urinary sodium and urinary potassium can be checked and the diuretics’ doses adjusted to effect Na/K ratio >1. (Increase in furosemide dose causes increased urinary sodium and potassium loss and increase in spironolactone dose causes increased potassium retention.)
    6. The doses of spironolactone and furosemide can be titrated to a maximum of 400 mg qd and 160 mg QD, respectively, using the 100 mg:40 mg ratio to maintain normokalemia. The goal of diuretic therapy should be to effect a 1-2 lb weight loss daily.
    7. Body weight, serum electrolytes, urea and creatinine are important pa-rameters to follow.
    8. Diuretic therapy should be stopped in the event that encephalopathy, hyponatremia (Na <120 mmol/L despite fluid restriction), or renal insufficiency (creatinine >2 mg/dl) develop. Overaggressive diuresis can also lead to hepatorenal syndrome, a non-reversible condition resulting in progressive renal failure due to renal hypoperfusion in patients with advanced liver disease. Avoid diuresis of greater than 1 liter per day.
    9. Large volume paracentesis can be performed in patients with tense ascites affecting satiety and respiration. Approximately 4-6 L can be removed resulting in improvement of symptoms. No albumin replacement is recommended for removal of up to 5 liters of ascitic fluid. Intravenous albumin (8 g/liter of ascitic fluid removed) can be given for larger volume paracentesis.
    10. Refractory or diuretic-resistant ascites, defined as minimal to no weight loss despite diuretics or development of complications of diuretic therapy, occurs in <10% of cirrhotic patients with ascites. It can be managed by repeated therapeutic paracenteses, peritoneovenous shunt or TIPS placement. TIPS is superior to repeated large volume paracentesis in resolving ascites and there is a trend towards better survival. However, patients with TIPS must be monitored for shunt malfunction and hepatic encephalopathy which may be more frequent than in those undergoing paracentesis (data is contradictory). While orthotopic liver transplantation should be considered initially after the onset of ascites, eligible patients who are diuretic-resistant need to be prioritized for transplantation as 50% die in 6 months.
    11. Spontaneous Bacterial Peritonitis. Patients with ascitic fluid total protein concentration <1.0 g/dl and gastrointestinal hemorrhage are at high risk for spontaneous bacterial peritonitis. There is good evidence that Bactrim (1 DS tablet daily 5 days a week) is effective in preventing spontaneous bacterial peritonitis and decreasing mortality. Norfloxacin 400 mg qd has been used but there is rapid development of resistant organisms. Weekly use of ciprofloxacin 750 mg, as well as levofloxacin 250 mg qd are being used increasingly. Also see treatment for SBP below.

Hepatic Hydrothorax

  1. Defined as the presence of a large pleural effusion that is seen as a complication of ascites in 5% to 9% of the cirrhotic patients with ascites, is often right-sided and can occasionally be found in the absence of ascites. It is most likely due to defect(s) in the tendinous portion of the right hemi-diaphragm. The pleural fluid tends to recur and, like ascites, is usually transudative in nature.
  2. The diagnosis can be confirmed by obtaining a nuclear study that establishes the presence of a peritoneo-pleural communication. The study involves the instillation of 99mTc-sulfur colloid into the peri- toneum and documenting the presence of the radiotracer in the pleural space.
  3. Hepatic hydrothorax is a relative contraindication to chest tube placement due to the potential for life-threatening fluid and electrolyte depletion. Rather, it is treated like ascites. In cases not responding to usual therapy, pleurodesis with tetracycline or thoracotomy to repair the diaphragmatic defect can be performed.
    

Spontaneous Bacterial Peritonitis (SBP)

  1. General Information
    1. SBP is a common complication in patients with cirrhosis and ascites, and occurs mostly in the setting of low ascitic fluid total protein level (<1 g/dl).
    2. Pathogenesis involves bacterial translocation from the gut to the systemic circulation and then to ascitic fluid.
    3. E. coli, Klebseilla pneumoniae, and pneumococcus are the three most common isolates.
    4. Renal failure occurs in approximately one-third of the patients despite treatment of the infection.
  2. Presentation and Diagnosis
    1. Abdominal pain and fever are the most characteristic symptoms, but hepatic encephalopathy, gastrointestinal bleeding, vomiting, diarrhea, shock, or hypothermia may be the presenting symptom(s) in a large number of patients.
    2. It can also be totally asymptomatic. Therefore one must have a low threshold for performing a paracentesis to obtain ascitic fluid for analysis.
    3. SBP is diagnosed when there is a positive ascitic fluid culture or when the ascitic fluid PMN count is >250 cells/mm3 in the absence of an identifiable intraabdominal source of infection.
    4. Ascitic fluid culture must be placed directly into blood culture preferably at bedside to increase the sensitivity of culture.
    5. Secondary peritonitis due to perforated viscus usually results in PMN count in the thousands, multiple organisms on gram stain and culture, and at least 2 of the following: total protein >1 g/dl, LDH > the upper limit of normal for serum, and glucose <50 mg/dl.
  3. Treatment.
    1. Empiric antibiotic treatment should be begun before the culture results become available to prevent demise of the patient.
    2. A broad-spectrum therapy is recommended in suspected ascitic fluid infection until culture results and susceptibility are available. Cefotamine 2 g IV Q8h or a comparable third-generation cephalosporin is the treatment of choice. Five days of treatment is appropriate. A repeat paracentesis can be performed after completion of 5 days of therapy with IV antibiotics to ensure efficacy of the treatment especially in patients with atypical presentation or response.
    3. Intravenous albumin at a dose of 1.5 g per kilogram body weight on day 1 and 1 g per kilogram on day 3 has been shown to reduce significantly the incidence of renal impairment and death in comparison with treatment with antibiotics alone.
    4. Subsequently, these patients should be placed on SBP prophylaxis therapy (norfloxacin 400 mg QD or levofloxacin 250 mg QD) for the remaining part of their hospital stay.