Ascites

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    Introduction

    • Most frequent complication of portal HTN.
    • 50% of pts with cirrhosis will get ascites in 10 years.
    • Diagnosis:
      • Physcal exam
      • Ultrasound for occult ascites
    • Diagnostic paracentesis is required:
      • Cell count, differential, albumin, total protein.
      • If infection suspected: culture! (AT BEDSIDE!!)
      • Calculate SAAG - Serum Ascites 

    Undifferentiated Ascites

    • If diagnosis is unclear, perform a diagnostic paracentesis:
    • AscitesApproach3b.png
    • Workup of Ascites

      Serum Ascites Albumin Gradient (SAAG) = Serum Albumin - Fluid Albumin

      • If SAAG ≥ 1.1 g/dL (≥ 11 g/L) => portal hypertension (90-95% of cases)
        • (Cirrhosis, Heart Failure, Budd-Chiari Syndrome, idiopathic portal fibrosis)
          • High ascitic protein level ≥ 2.5 g/dL  --> Cardiac etiology
            • (includes Budd-Chiari, constrictive pericarditis, R-heart failure).
          • Low Ascitic Protein Level < 2.5 g/dL  --> Portal Hypertension
             
      • If SAAG < 1.1 g/dL (< 11 g/L) => unlikely portal HTN
        • (TB, pancreatitis, nephrotic syndrome, serositis, peritoneal carcinomatosis)

       


       
    • Measuring hepatic venous pressure gradient
      • Only helpful if uncertain after extensive investigations (echo, etc..)
      • Measure hepatic vein pressure + wedge to get an estimate of portal vein pressure (seeing cross-liver gradient).
        • Helps understand if pre-hepatic, hepatic or post-hepatic cause of ascites.
    • Standard Workup of Ascitic Fluid:
      • CBC, Differential, Albumin, Protein, (Gram stain + culture if suspect SBP), (cytology if suspect malignancy).

     

    Treatment Principles

    • Sodium restriction < 2000 mg/day.
    • Oral diuretics
    • For moderate-to-severe ascites
      • Large volume paracetesis
      • Along with IV albumin 8g of Albumin per litre of fluid removed
        (5% albumin = 5g/100mL.  Multiply grams by 20 to get volume of 5% albumin, and by 4 for 25% albumin)
        (i.e. 4L removed--> requires 32g of Albumin --> (640cc of 5% albumin or 128cc of 25% albumin)

     

    Refractory Ascites

    • Definition of Refractory Ascites

      Refractory Ascites = Resistance to sodium restriction and high dose diuretics
                                          (Upwards of 400mg spironolactone + 160 furosemide /day).

      • Or if side effects prevent maximizing oral diuretics.
    • Treatment options:
      • Serial theraputic paracentesis
      • TIPS
      • Liver transplantation

    Spontaneous Bacterial Peritonitis

    • SBP - spotaneous infection of ascitic fluid w/o evidence of intraabdominal infection.
    • Pathobiology:
      • Translocation of bacteria from intestinal lumen to lymph nodes --> bacteremia --> ascitic fluid.
      • Most common organisms:
        • E.coli
        • Klebsiella pneumoniae
        • Pneumococcus
    • Prevalence remained stable, but mortality declined from 50% to 15%.
    • Diagnosis:
      • Spontaneous Bacterial Peritonitis Definition:
        • Ascitic fluid bacterial culture is POSITIVE
          AND
        • Absolute fluid PMN Count ≥ 250 cells/mL

         
    • Complications:
      • HRS (30%) --> high mortality!
      • Recurrence (70%)
    • Treatment:
      • 3rd generation cephalosporin(ceftriaxone, cefotaxime) until culture finalized.
      • Give IV albumin (Dose: 1.5 g/kg of body weight at diagnosis + 1 g/kg 48hrs later [some say day 3)
        • Salerno et al (2013) Meta Analysis: IV albumin improves mortality by 20%
          • Various regimens in RCTs include dose at dx and 48hrs, and at dx and on day 3.
        • Give only if significant kidney and/or liver dysfunction (survival benefit vs. abx alone).
      • Can repeat tap at 48hrs to document drop in PMNs (will rise if secondary peritonitis ie. bowel perf)
    • Secondary Prevention: (Post SBP episode)
      • Norfloxacin 400mg PO OD --> reduces recurrence in studies
        • Quinolone resident SBP emerging.
      • TMP-SMX is an alternative if allergic to quinolones or resistant (evidence is scarce)
        • (Double-Strength every other day or single strength daily, but VARIES!)
    • Primary Prevention:
      • Indications for primary prevention of SBP
        • ALL patients with low-protein ascitic fluid (<1 g/dL [10 g/L]) and severe liver dysfunction
          (especially when they are hospitalized)
      • Primary prophylaxis against SBP with norfloxacin is warranted in patients with low-protein ascitic fluid (<1 g/dL [10 g/L]) and severe liver dysfunction, especially when they are hospitalized.

    Cirrhosis and Ascites

    Pathophysiology

    • Chief factor: splanchnic vasodilatation.
    • Increased hepatic resistance --> portal HTN --> production of vasodilators (nitric oxide etc) --> splanchnic arterial vasodilatation --> decreased effective arterial blood volume --> increases in plasma volume and cardiac output (initially adequate to maintain arterial pressure).
      • If advanced --> worse splanchnic arterial vasodilatation --> activation of vasoconstrictor and antinatriuretic factors (to maintain BP) --> sodium + fluid retention.
        • Combination of: splanchnic arterial vasodilatation + portal HTN --> alters intestinal capillar pressure and permeability --> retained fluid in abdominal cavity.
          • In VERY advanced disease --> decrease in renal excretion of free H2O + renal vasoconstriction --> dilutional hyponatremia + hepatorenal syndrome (respectively).
          • Ascites Mechanism.png (click to enlarge)

    Management:

    • A. If sodium retention: Reduction of sodium intake (60-90mEq or 1.5-2g Na/day)
    • B. If dilutional hyponatremia: Fluid restriction to 1000mL/day) if Na < 130
    • if Moderate-Volume Ascites
      • Have positive sodium balance.  In most cases:
        • 1. Normal renal free water excretion (normal ADH and serum Na)
        • 2. Creatinine is normal.
      • Negative sodium balance and loss of ascitic fluid achieve with diuretics:
        • C. Spironolactone (50-200mg/day) or amiloride (5-10mg/day)
        • D. Can add furosemide (20-40mg/day)
          • LOW DOSE in initial stages to increase naturesis (esp if edema).  CAUTION: Can cause too much diuresis and worsening renal failure (pre-renal causes), window is small.
          • TWH internal medicine recommendation:
            spironolactone and furosemide (ratio: 100:40) to maintain normokalemia.
        • Target: loss 300-500g/day w/o peripheral edema and 800-1000 g/day with edema.
          • if no weight change, measure Urine Na.
            • Can tell you response to diuretics, and see if can increase diuretics dose.
    • If Large-Volume Ascites
      • Severe sodium retention (U sodium < 10mmol/L)
        • Therefore ascitic fluid rapidly accummulates even if salt restricted.
        • Most have normal free water excretion (some have less excretion --> dilutional hyponatremia).
      • Serum Creatinine (GFR) is often normal.
      • Two strategies:
        • 1. Large-volume paracentesis
        • 2. Massive doses of Diuretics until ascites is lost.
          • (maximal doses 400mg spironolactone/day and 160mg furosemide/day)
      • [Studies show: no difference in mortality between the two, but paracetesis is faster, more effective, associated with fewer adverse events]\
      • Regardless of strategy: diuretics need to be given to prevent recurrence.
    • ​Paracentesis:

      • Problem: derangement in circulatory function --> Decr BP --> activation of vasoconstrictor + antinatriuretic factors. --> complications; 20% develop:
        • Higher rate of recurrence 
        • Risk of hepatorenal syndrome.
        • Dilutional hyponatremia
        • To offset this: MUST use plasma expanders: albumin, dextran 70, polygeline.
          • [Study: Albumin is superior to other two (above) in preventing circulatory dysfunction after paracentesis (if >5L removed).  However, no difference in survival - prob b/c small sample sizes.]
          • Controversial: albumin is high cost, lack of survival benefit, but great circulatory protection!
        • Other complications:
          • Infection and GI perforation --> EXTERMELY rare - use appropriate technique and needle. 
          • Bleeding at site / hemoperitoneum extremely low (trials excluded pts with PTT > 21s, INR > 1.6, and platelets < 50,000).
    • Refractory Ascites

      • 5-10% incidence in those with ascites
      • Defined as:
        • Lack of response to high doses of diuretics (400mg spironolactone + 160 furosemide /day).
        • Patients w/ hepatic encephalopathy, hyponatremia, hyperkalemia, azotemia at lower doses.
      • Increased risk of recurrence of ascites + HRS.
      • Treatments:
        • Repeated large-volume paracentesis + plasma expanders (q2-4 weeks).
        • trans-jugular IHPS (intra-hepatic portosystemic shunt).

     

    • TIPS - Transjugular Intrahepatic Portosystemic Shunt

      • Stent placed btwn hepatic and portal veins by transjugular approach.
        • Advantages:
          • Effective to decrease recurrence in refractory ascites.
          • Decreases activity of Na-retaining mechanisms, increases response to diuretics.
        • Disadvantages:
          • Shunt stenosis (75% after 6-12mo).
            • --> Recurrent ascites
          • High cost  + lack of availability.
          • No survival benefit (initially showed survival benefit, but two recent randomized trials --> no survival benefit).
          • May make transplant difficult (but not a big problem)
        • Bottom line:
          • Only do if
            • Severe liver failure or encephalopathy
              AND
            • Loculated fluid cannot be accessed by paracentesis
            • Unwilling to undergo paracentesis.
    • CirrhosisAscitesComplciationManagement.png

     

    Hepatorenal Syndrome

    • Renal failure due to severe vasoconstriction of renal circulation (extreme arterial underfilling).
    • Incidence: 10% in cirrhosis/ascites:
    • Two patterns:
      • Type 1 HRS - Precipitating event triggers renal impairment (commonly SBP)
      • Type 2 HRS - Increase in creatinine is moderate and does not progress over time.
    • Must R/O non-functional causes (See table)
      • HRS Criteria.png
    • Poor prognosis (Esp Type 1 - less than a month w/o therapy)
    • Treatment Notes:
      • Dopamine and prostaglandins are ineffective.
      • Vasoconstrictor (vasopressins or a-adrenergic agents) + albumin effective in 2/3 of pts.
      • Octreotide is ineffective alone, but effective with midodrine.
      • Other notes:
        • Recurrence of HRS uncomming when discontinuing these.
        • Treatment of HRS improves survival to transplant and improve renal function before transplant.
        • TIPS: insufficient evidence (some evidence that helps HRS).
        • Hemodialysis: should not be used.  Only in select cases to bridge to transplant.
      • HRSVasoconstrictors.png
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