Management of Cirrhotic Ascites and its Complications PDF

Management of Cirrhotic ascites and it´s complications Ahmed Othman Abodooh, MD ‫الموضوع قديم‬ ‫ابوقراط قال ايه‬  Father of Medicine observed in one of his aphorisms (VII:55), When the liver is filled with water “ and bursts into the epiplöon, i.e., the omentum – the belly is filled...

Management of Cirrhotic ascites and it´s complications Ahmed Othman Abodooh, MD ‫الموضوع قديم‬ ‫ابوقراط قال ايه‬  Father of Medicine observed in one of his aphorisms (VII:55), When the liver is filled with water “ and bursts into the epiplöon, i.e., the omentum – the belly is filled with water and the patient dies.” Definition Pathological accumulation of fluids in peritoneal cavity  Introduction  Ascites is the most common complication of cirrhosis, and 60% of patients with compensated cirrhosis develop ascites within 10 years during the course of their disease.  The development of ascites is associated with a poor prognosis and impaired quality of life in patients with cirrhosis  Prognosis  Generally there are two types of ascites: Uncomplicated ascites Complicated ascites The development of ascites in cirrhosis indicates a poor prognosis. Pathogenesis  Grading of ascites Definition Grade I Only detectable by USS Grade II Moderate symmetrical enlargement of abdomen – shifting dullness Grade III Marked abdominal enlargement – transmitted thrill  Initial evaluation Any case of newly discovered ascites should undergo :  thorough history taking,  physical examination,  abdominal USS,  LFTs, Urea, Creatinine and serum electrolytes.  A diagnostic paracentesis should be performed in all patients with new onset grade 2 or 3 ascites, and in all patients hospitalized for worsening of ascites or any complication of cirrhosis. Paracentesis and ascites workup  Routine tests include ascetic fluid cell count, protein, and albumin levels.  Calculate the serum ascites albumin gradient (SAAG). (Albumin concentration of serum minus Albumin concentration of ascitic fluid)  SAAG > 1.1 indicates portal hypertension related ascites. Total protein of < 2.5 g/dL: cirrhotic ascites. Total protein of ≥ 2.5 g/dL: cardiac ascites (congestive heart failure, constrictive pericarditis) or Budd-Chiari syndrome. Paracentesis and ascites workup  SAAG < 1.1 indicates non-portal hypertension related ascites. Total protein of < 2.5 g/dL: nephrotic ascites. Total protein of ≥ 2.5 g/dL: peritoneal carcinomatosis, tuberculous ascites.  Polymorphonuclear (PMN) leukocyte count of ≥ 250 cells/mm3 is indicative of infection, which is most commonly secondary to spontaneous bacterial peritonitis (SBP). Grading of ascites Definition Treatment Grade I Only detectable by USS Salt restriction Grade II Moderate symmetrical Salt restriction + diuretics enlargement of abdomen – shifting dullness Grade III Marked abdominal Large volume paracentesis enlargement – transmitted + salt restriction + thrill diuretics Management of Grade II Ascites ► Patients with moderate ascites can be treated as outpatients and do not require hospitalization unless they have other complications of cirrhosis. ► Treatment is aimed at counteracting renal sodium retention and achieving a negative sodium balance. This is done by reducing the sodium intake and enhancing the renal sodium excretion by administration of diuretics.  Management of Grade II Ascites ► Salt restriction: Moderate restriction of salt intake is an important component of the management of ascites (intake of sodium of 80–120 mmol/day, This is generally equivalent to a no added salt diet with avoidance of pre-prepared meals. There are no data to support the prophylactic use of salt restriction in patients who have never had ascites.  Management of Grade II Ascites ► Fluid restriction: There are no data to support the use of fluid restriction in patients with ascites with normal serum sodium concentration. Fluid restriction is only indicated in hypervolemic patients with serum Na less than 125 mmol.  Management of Grade II Ascites ► Diuretics ( Spironolactone+/-Furosemide): Evidence demonstrates that renal sodium retention in patients with cirrhosis and ascites is mainly due to increased proximal as well as distal tubular sodium reabsorption rather than to a decrease of filtered sodium load. Aldosterone antagonists are more effective than loop diuretics in the management of ascites and are the diuretics of choice.  Management of Grade II Ascites ► Diuretics: Patients with the first episode of grade 2 (moderate) ascites should receive an aldosterone antagonist such as spironolactone alone, starting at 100 mg/day and increasing stepwise every 3 days (in 100 mg steps) to a maximum of 400 mg/day if there is no response  Management of Grade II Ascites ► Diuretics: In patients who do not respond to aldosterone antagonists, as defined by a reduction of body weight of less than 2 kg/ week, or in patients who develop hyperkalemia, furosemide should be added at an increasing stepwise dose from 40 mg/day to a maximum of 160 mg/day (in 40 mg steps).  Management of Grade II Ascites ► Diuretics: The maximum recommended weight loss during diuretic therapy should be 0.5 kg/day in patients without edema and 1 kg/day in patients with edema. All diuretics should be discontinued if there is severe hyponatremia (serum sodium concentration 1.5) and encephalopathy in a patient without preexisting cirrhosis and a disease duration of less than 26 weeks  Etiologies of acute liver failure (ALF)  Drugs: acetaminophen and other drug induced liver injuries.  Viral hepatitis: hepatitis A, B and HSV.  Autoimmune hepatitis.  Vascular: ischemic hepatitis, Budd-Chiari syndrome.  Acute fatty liver of pregnancy and HELLP syndrome.  Mushroom poisoning (Amanita phalloides) Phallotoxins lead to enterocyte injury and gastroenteritis. Clinical features   Symptoms: malaise, nausea, jaundice, abdominal pain, pruritus.   Physical: fever, hepatomegaly, jaundice, rash. Examine for stigmata of chronic liver disease.   Assess the mental status and the need for intubation. Encephalopathy develops due to cerebral edema and increased intracranial pressure, rather than porto-systemic shunting. Investigations (LAB)  Obtain a CBC, renal and hepatic panels, INR, Arterial blood gas, serum lactate.  Viral serologies: HAV-IgM Ab, HBsAg, HBc-IgM Ab, HBsAb, HCV Ab, HSV-IgM Ab, CMV IgM Ab, HSV  PCR, CMV PCR, EBV serology, RPR, HIV antibody, ceruloplasmin, alpha-1 antitrypsin level.  Autoimmune antibodies (ASMA, ANA). Investigations (LAB)  Consider Wilson's disease if age