Ascites Evaluation and Management Quiz

Management of Cirrhotic Ascites and its Complications

• Ascites is the most common complication of cirrhosis.
• 60% of compensated cirrhosis patients develop ascites within 10 years.
• Ascites development signifies a poor prognosis and impairs quality of life.
• Two types of ascites: uncomplicated and complicated.
• Complicated ascites are associated with poor prognosis.

Definition of Ascites

• Pathological accumulation of fluid within the peritoneal cavity.

Pathogenesis of Ascites in Cirrhosis

• Portal hypertension
• Vasodilator factors (NO, endocannabinoids, CO).
• Splanchnic arterial vasodilatation.
• Abnormal distribution of blood volume.
• Reduced effective arterial blood volume.
• Stimulation of antinatriuretic/vasoconstrictor systems.
• Increased tubular sodium reabsorption.
• Positive sodium balance.
• Sodium and fluid retention.

Grading of Ascites

• Grade I: Only detectable by ultrasound (USS).
• Grade II: Moderate symmetrical abdominal enlargement—shifting dullness.
• Grade III: Marked abdominal enlargement—transmitted thrill.

Initial Evaluation of Ascites

• Thorough history taking.
• Physical examination.
• Abdominal ultrasound (USS).
• Liver function tests (LFTS).
• Urea, creatinine, and serum electrolytes.
• Diagnostic paracentesis for Grade 2 or 3 ascites, and for worsening ascites or cirrhosis complications.

Paracentesis and Ascites Workup

• Routine tests: Ascitic fluid cell count, protein, and albumin levels.

• Serum ascites albumin gradient (SAAG): Serum albumin concentration minus ascitic fluid albumin concentration.

• SAAG > 1.1: Indicates portal hypertension-related ascites.

• Total protein < 2.5 g/dL: Suggests cirrhotic ascites.

• Total protein ≥ 2.5 g/dL: Suggests cardiac ascites (congestive heart failure, constrictive pericarditis), or Budd-Chiari syndrome

• SAAG < 1.1: Indicates non-portal hypertension-related ascites

• Total protein < 2.5 g/dL: Suggests nephrotic ascites.

• Total protein ≥ 2.5 g/dL: Suggests peritoneal carcinomatosis, tuberculous ascites, or other conditions.

• Polymorphonuclear (PMN) leukocyte count ≥ 250 cells/mm³ indicates infection, often spontaneous bacterial peritonitis (SBP).

Diagnostic Paracentesis

• Determining presence and progression of ascites associated with certain causes, such as cirrhosis.

Grade II Ascites Treatment

• Salt restriction: 80-120 mmol sodium/day.
• Diuretics (Spironolactone +/– Furosemide): Treatment of choice, focuses on negative sodium balance.
  • Starting dose: 100 mg/day spironolactone. Increasing dose (100 mg steps) until response.
  • Furosemide is added if the aldosterone antagonist is insufficient (40 mg/day increase, max 160 mg/day).
• Fluid Restriction: Only needed if serum sodium is abnormal.

Grade III Ascites Treatment

• Large volume paracentesis (LVP): 5 liters of ascitic fluid at one session (treatment of choice).
• Albumin administration: Prevents post-paracentesis circulatory dysfunction and prevents re-accumulation.

Refractory Ascites

• Ascites not responding to medical treatment.
• Median survival of patients with refractory ascites is approximately 6 months.
• Liver transplantation should be considered if medical management fails.
• Common causes: SBP, HRS, severe hyponatremia, portal vein thrombosis (PVT), hepatocellular carcinoma (HCC).
  • Diuretic-resistant ascites: poor response to sodium restriction and diuretic treatment
  • Diuretic-intractable ascites: response to treatment is further blocked by induced complications

Diagnostic Criteria for Refractory Ascites

• Intensive diuretic therapy (spironolactone 400 mg/day + furosemide 160 mg/day) with a low-sodium diet (<90 mmol/day) for at least 1 week.
• < 0.8 kg weight loss over 4 days.
• Reappearance of grade 2 or 3 ascites within 4 weeks of initial mobilization.
• Diuretic-induced encephalopathy absence of other precipitating factors.
• Renal impairment
• Hypo/hyperkalemia: despite appropriate measures
• Hyponatremia

Treatment Options for Refractory Ascites

• LVP plus albumin: Not effective or inducing complications in >90% of patients.
• TIPSS (Transjugular Intrahepatic Portosystemic Shunt): Considered with frequent or large-volume paracentesis.
• Liver Transplantation: Treatment of choice for refractory ascites

Spontaneous Bacterial Peritonitis (SBP)

• Diagnosis: Paracentesis is essential in all patients.
  • Critical assessment: of all high-risk patients with cirrhosis and ascites is encouraged
• Treatment: Third-generation cephalosporins (first-line treatment).
• Prophylaxis: High-risk groups (acute gastrointestinal hemorrhage, low total protein in ascites, prior history of SBP)

Hepatorenal Syndrome (HRS)

• Renal dysfunction in advanced liver disease without other causes.
• Diagnostic criteria crucial for early recognition and treatment
• Treatment of possible causes must be performed before HRS diagnosis
• Treatment: Albumin infusion, antibiotics for SBP
• Sepsis screen: Early identification of bacterial infection (blood, urine, and ascitic fluid cultures).
  • Maintain prophylactic antibiotics (if prescribed) in patients without signs of infection

HRS types and their criteria (Old and New Classification):

• There are new and old classifications for HRS types with different criteria and their definitions.

Hepatic Encephalopathy (HE)

• Brain dysfunction caused by liver and/or portal-systemic insufficiency.
• Pathogenesis: Ammonium accumulation.
  • Abnormal neurotransmission. Alterations in permeability of Blood brain barrier.
• Classification: Varies from minimal to coma.
• Grading: Grades 0-4 based on clinical abnormalities.
• Diagnosis: Exclusion of other causes of encephalopathy.
• Precipitating factors
  • Several factors may influence the severity
• Treatment:
  • Treat the precipitating factor alongside supportive measures
  • Lactulose, rifaximin, L-ornithine L-aspartate (LOOA), and other medications.

Acute Liver Failure (ALF)

• Severe liver injury, coagulopathy (INR >1.5), and encephalopathy within 26 weeks.
• Etiologies: Viral hepatitis, drug-induced injury, autoimmune hepatitis, vascular causes, and others.
• Clinical features: Often begins with malaise, nausea, jaundice, abdominal pain, and pruritus. Can demonstrate stigmata of chronic liver disease and physical findings
• Investigations (LAB): CBC, renal, hepatic panels, INR, arterial blood gases, serum lactate, viral serologies, autoimmune antibodies.
• Investigations (Imaging): Ultrasound, Doppler, MRI/CT, head CT.
• Treatment: ICU admission, supportive care (treat precipitating factors, manage fluid and electrolyte disturbances) and liver transplantation.
• Management considerations for pre-procedure treatments
• • Coagulopathy and thrombocytopenia: Treatment only when bleeding is present or prior to procedures.
• • GI bleeding: PPI for prophylaxis
• • Refractory hypotension: Vasopressors (norepinephrine)