ASCITES

ASCITES - Anne Walsh, PA-C, MMSc
BASICS
DESCRIPTION
Accumulation of fluid >25 mL in abdominal cavity. May occur in any condition that causes generalized edema.
GENERAL PREVENTION
Varies with etiology
EPIDEMIOLOGY
• Determined by etiology
• Children: Nephrotic syndrome and malignancy most common
• Adults: Cirrhosis, heart failure, nephrotic syndrome, peritonitis most common
RISK FACTORS
Those associated with possible causes
ETIOLOGY
• Peritoneal infection and inflammation
- Tuberculosis
- Fungal disease
- Bacterial infection (foreign body, fistula)
- Perforated viscus
- Granulomatous peritonitis (e.g. sarcoidosis)
- Parasitic infection
• Metabolic diseases
- Cirrhosis
- Prehepatic and posthepatic portal hypertension
- Myxedema
- Nephrogenous
- Dialysis-related
- Protein malnutrition (hypoalbuminemia 2 g/dL)
• Cardiac congestion
- Congestive heart failure
- Constrictive pericarditis
- Tricuspid stenosis or insufficiency
• Traumatic
- Pancreatic or biliary fistula
- Lymphatic tear (chylous ascites)
- Hemoperitoneum (trauma, ectopic pregnancy, tumor)
• Malignancy
- Peritoneal seeding: Ovarian, colon, pancreas, others
- Primary peritoneal carcinoma
- Leukemia, lymphoma
ASSOCIATED CONDITIONS
Listed in "Etiology"


DIAGNOSIS
SIGNS AND SYMPTOMS
• Abdominal pain
• Abdominal distention
• Shortness of breath
• Anorexia
• Nausea
• Early satiety
• Heartburn
• Flank pain/bulging
• Weight gain
• Dyspnea/orthopnea
• Abdominal fluid wave
• Shifting dullness or "puddle sign" (dull over dependent abdomen)
• Penile/scrotal edema
• Umbilical/inguinal herniae
• Pleural effusion
• Pedal edema
• Rales
• Tachycardia
• Flatulence
• Palmar erythema, spider angiomata in cirrhosis
History
(As pertinent to underlying cause)
Physical Exam
Include abdominal, pelvic, rectal, cardiac, lungs, lymph nodes, skin, mental status. Positive findings listed above.
TESTS
Lab
Ascitic fluid should be sampled in all new-onset or new-to-treat cases.
• Obtain in all
- Culture via blood culture bottles
- Total cell count
- Polymorphonuclear leukocytes: >250 mm3 suggests infection requiring antibiotics
- Albumin in both serum and ascites: Calculate SAAG (serum to-ascites albumin gradient)
 1.1 g indicates exudate, i.e., inflammatory, biliary/pancreatic, carcinomatosis
 >1.1 g indicates transudate/portal hypertension
- Protein: >2 g (some sources cite 2.5 g) indicates exudate
• Of use in specific circumstances
- Amylase, triglycerides, glucose
- Lactate dehydrogenase
- Acid-fast or fungal cultures/smears
- Cytology only if exudate
Blood tests
• BUN/creatinine
• Electrolytes
- Sodium levels in single sample
 10 mEq/L (10 mmol/L) diuretic response unlikely
 >10-70 mEq/L (>10-70 mmol/L) diuretic response likely
 >70 mEq/L (>70 mmol/L) diuretics unnecessary
• Other labs as indicated by underlying condition (liver enzymes, tumor markers, etc.)
• Drugs/disorders that may alter lab results
- Refer to laboratory test reference
Imaging
• Abdominal ultrasound highly sensitive
• CT scan to rule out intra-abdominal pathology
• MRI best for evaluation of liver disease
Diagnostic Procedures/Surgery
• Diagnostic paracentesis
• Diagnostic laparoscopy
Pathological Findings
• Peritoneal biopsy may reveal tuberculosis or malignancy; of no value in other types of fluid
• Culture may reveal organism(s) responsible for inflammatory disease (e.g., TB)
• Cytology may reveal malignant cells from metastatic disease
- Typically adenocarcinoma (ovary, breast, GI tract)
- Rarely primary peritoneal carcinoma
DIFFERENTIAL DIAGNOSIS
• Obesity
• Bowel obstruction (air and liquid in distended intestine)
• Pregnancy in reproductive-age female
• Fluid type, transudate: Likely causes include
- Congestive heart failure
- Constrictive pericarditis
- Cirrhosis
- Nephrotic syndrome
- Protein malnutrition/hypoalbuminemia
• Fluid type, exudate: Likely causes include
- Neoplasm
- Tuberculosis
- Pancreatitis
- Myxedema
- Biliary pathology
- Budd-Chiari syndrome
TREATMENT
GENERAL MEASURES
• Care may be outpatient or inpatient, depending on physical condition
• For all patients
- Sodium restriction required:
- 2 g daily until renal excretion improves, usually required 3-6 months. Consultation with dietician helpful to increase patient compliance
- Water restriction only necessary if serum sodium 130 mEq/L
- Persistent elevation of creatinine >2.5 mg/dL should lead to decreasing diuretic doses and therapeutic paracentesis.
- Daily record of weight to monitor gains and losses
• For ascites with edema
- Salt restriction and diuretics usually effective
- Maximum weight loss of 5 pounds per day
- Weekly electrolytes on serum during rapid weight loss
• For ascites without edema
- Dietary restrictions and diuretics as above
- Maximum weight loss of 2 pounds per day
- Refractory ascites
• Confirm patient compliance with adequate sodium restriction (most common cause)
• Diuretic-intractable ascities: (worse despite max doses spironolactone [300 mg/day] and furosemide [160-200 mg/day] and Na restriction OR progressive rise in creatinine to 2)
- Start paracentesis 5-10 L per session
 Complication: Hemodynamic collapse and renal failure
 Replace albumin IV for all removals >5 L at rate of 8 g albumin for each liter removed
- Continue diuretics at 1/2 previous dose
Diet
Consultation with dietician helpful
• Sodium restriction, 2 g/day monitor
• Adequate nutrition
• Protein restriction not likely beneficial but often recommended; avoid high-protein diet (can precipitate hepatic encephalopathy if cirrhosis)
• Fluid restriction (1-1.5 L/day) only if dilutional hyponatremia (Na 125 mmol/L).
Activity
Bed rest only if heart failure and/or prominent leg edema
Complementary and Alternative Medicine
Caution patients to avoid herbs and other supplements unless approved by physician (risk drug interactions, hepatotoxicity, coagulopathy)
MEDICATION (DRUGS)
First Line
• Diuretics needed in nearly all patients
- Spironolactone 100-300 mg/day PO in single dose best for cirrhotic ascites; typical initial dose is 100-200 mg given in AM
- Furosemide 20-120 mg/day PO best for all other etiologies; typical initial dose is 40 mg given in AM
- May use spironolactone and furosemide together
- Dose should be sufficient to obtain net sodium loss in urine
- Discontinue NSAIDs except 81 mg dose of aspirin. Follow body weight daily. If there is a 2-pound loss in the next 4 days, increase either spironolactone by 100 mg or furosemide by 40 mg. If the 2-pound weight loss continues in the next 4 days, continue with the same dose. Emphasize sodium restriction.
- Spot sodium in mEq/L  estimated urine output (1 L if no information) should equal estimated dietary sodium. Increase diuretics daily until this goal attained. Measure serum electrolytes before each dose change.
• Contraindications: Consult manufacturer
• Precautions
- In hospital, or when rapid diuresis, observe creatinine weekly. NSAIDs may worsen or initiate oliguria or azotemia. Potassium supplements usually required when diuresis exceeds 1 pound per day.
- Spironolactone or amiloride may increase potassium; monitoring necessary after 1st week of therapy and at least monthly thereafter.
- Observe patients closely for signs of volume depletion, encephalopathy, and renal insufficiency.
• Significant possible interactions: Avoid concomitant potassium supplements if spironolactone used alone
Second Line
• Only rarely do alternative diuretics lead to success if combinations of spironolactone and furosemide fail or result in increased BUN/creatinine
- Most commonly used in cases of GI intolerance or allergic reactions
- Alternatives to spironolactone: Amiloride up to 10 mg/day; triamterene up to 200 mg/day in divided doses
- Alternatives to furosemide: Torsemide up to 100 mg per day; ethacrynic acid 50 mg IV (may be effective when oral drugs cannot be used)
SURGERY
• TIPS (transjugular intrahepatic portosystemic shunt; radiological procedure); effective for intractable ascites
- At time of placement, measured portal pressure should drop 20 mm Hg or to 12 mm Hg, and ascites should be readily controlled with diuretics. Conduct yearly ultrasonographic study to confirm functional shunt.
- Dilation/replacement may be required after 2+ years. Encephalopathy is a possible complication of TIPS.
• Surgical portacaval shunt: An 8-10 mm mesenteric caval shunt often is effective.
- Significant operative mortality, morbidity, encephalopathy; most experts prefer TIPS instead.
• When recurrent pleural effusion present in patient with chronic ascites, fusing of pleural surfaces is sometimes used. Alternative is TIPS.
• Liver transplant referral should be considered in all patients with decompensated liver disease, regardless of whether ascites is present/controlled.
FOLLOW-UP
PROGNOSIS
• Varies depending on underlying cause
• Rarely life-threatening in itself but may be a symptom of life-threatening disease (e.g., cancer, end-stage liver disease)
- Conservative therapy usually successful if cause is reversible or treatable (e.g., infection)
COMPLICATIONS
• Overly aggressive diuresis may lead to hypokalemia, worsening encephalopathy, intravascular volume depletion, azotemia, renal failure, and death.
• Hepatorenal syndrome: Urine volume 500 mL/day, decreasing urine sodium, rising blood urea, and creatinine >1.5 mg/dL
- Stop all diuretics. IV fluid challenge of 1.5 L plasma expander after 1 day if no improvement.
- Vasopressors (e.g., terlipressin IV every q4-6h) may resolve renal failure in 50% of patients.
• Spontaneous bacterial peritonitis: Ascitic fluid cell count >250 polymorphonuclear leukocytes, fever, clinical deterioration. Treat with 3rd generation cephalosporin or comparable antibiotic; combined antibiotic treatment plus IV albumin results in improved survival in some patients.
• Hydrothorax: Always on right side; cell and lab properties same as ascites. Do not place chest tube. Treat ascites vigorously; if hydrothorax does not disappear, consider TIPS.
• Other complications may be associated with specific etiologies of ascites.
PATIENT MONITORING
• Daily body weight
• Weekly electrolytes when appreciable diuresis present (>1 pound weight loss/day) and 1 week post change in dose/type of diuretic
• Mental status to assess for encephalopathy
• Monitor underlying disease as indicated (comprehensive panel, CBC, etc.).
REFERENCES
1. Russo MW, Jacques PF, Mauro M, Odell P, Brown RS Jr. Predictors of mortality and stenosis after transjugular intrahepatic portosystemic shunt. Liver Transpl. 2002;8:271-277.
2. Runyon BA. Management of adult patients with ascites due to cirrhosis. Hepatology. 2004;39:841-856.
3. Gines P, Uriz J, Calahorra B, Garcia-Tsao G, et al. Transjugular intrahepatic portosystemic shunting versus paracentesis plus albumin for refractory ascites in cirrhosis. Gastroenterology. 2002;123:139-147.
4. Nietsch H. Management of portal hypertension. J Clin Gastroenterol. 2005:39:232-236.
5. Saadeh S, Davis GL. Management of ascites in patients with end-stage liver disease. Rev Gastroenterol Disord. 2004;4:175-185.
6. Talwalker J, Kamath P. Influence of recent advances in medical management on clinical outcomes of cirrhosis. Mayo Clin Proc. 2005;80:1501-1508.
MISCELLANEOUS
See also: Cirrhosis of the Liver; Congestive Heart Failure; Nephrotic Syndrome