Lecture 12 (Cirrhosis, Ascites, & H-R Syndrome) PDF

Cirrhosis  General data - final common histologic pathway for a wide variety of chronic liver diseases= end stage liver disease The term cirrhosis was first introduced by Laennec in 1826. It is derived from the Greek term scirrhus and refers to the orange or tawny surface of...

Cirrhosis  General data - final common histologic pathway for a wide variety of chronic liver diseases= end stage liver disease The term cirrhosis was first introduced by Laennec in 1826. It is derived from the Greek term scirrhus and refers to the orange or tawny surface of the liver seen at autopsy.  Definition Cirrhosis is defined histologically as a diffuse hepatic process characterized by: fibrosis conversion of the normal liver architecture into structurally abnormal nodules.  Classification There are 2 main stages in the natural history of cirrhosis: compensated decompensated defined by the absence or presence of : ascites esophageal /gastric varices encephalopathy jaundice.  Ascites, Spontaneous Bacterial Peritonitis,Hepatorenal Syndrome, and H.Encephalopathy  Mecanism of portal mechanical hypertension factors related increase in to the PORTAL resistance to distortion of HYPERTENSION portal venous liver outflow architecture vasodilation and hyperdynamic circulation and increased flow at the peripheral vasodilation. level of the splanchnic arterioles An increase in the hepatic venous pressure gradient—of at least 10 mm Hg is required for varices. Ascites  Definition Fluid accumulation within the peritoneal cavity. Clinicaly detected >1 L Main cause : Portal Hypertension+Hypoalbuminemia  General data the most common major complication occurs in about 50% of patients with compensated cirrhosis in 10 years. denotes the transition from compensated to decompensated cirrhosis. It causes : increased morbidity from abdominal distention increased mortality from complications : spontaneous bacterial peritonitis and renal dysfunction, with a median survival of 2 to 5 years.  Pathogenesis of Ascites A minimum portal pressure gradient of 10 to 12 mm Hg is necessary for ascites to develop.  Diagnostic paracentesis should be performed in : all patients who present with new-onset ascites, who are hospitalized with cirrhotic ascites, who have cirrhotic ascites and any deterioration in liver function, with fever, worsening encephalopathy, or renal failure. ascitic fluid analysis should include : a cell count bacterial culture Ascitic fluid protein albumin Evaluation of Patients With Ascites Evaluation of Patients With Ascites Other tests =>only if a specific diagnosis is suspected clinically. Lactate dehydrogenase and glucose =>if secondary peritonitis is suspected. amylase (>1,000 U/L ) => pancreatic ascites Mycobacterial culture =>tuberculosis Treatment of ascitis  Diuretics(1) General rule : a weight loss of 0.5 to 1.0 kg/day is optimal to avoid side effects After the ascites is mobilized by whatever method, diuretic therapy should be adjusted to keep the patient free of ascites.  Diuretics(2) Spironolactone (aldosterone antagonist ). initial dose of 100 mg/day, to 400 mg/day, according to the clinical response side effects : hyperkalemia. Furosemide : started at a dose of 40 mg/day in combination with spironolactone and increased to 160 mg/day until the desired effect is achieved or side effects occur. Complications : 1) deterioration in renal function, 2) excessive weight loss 3) orthostatic symptoms, 4) encephalopathy, 5) dilutional hyponatremia.  Therapeutic Paracentesis repeated large-volume paracentesis (with intravenous infusions of albumin) vs. diuretic therapy more effective in eliminating ascites; associated with a lower incidence of hyponatremia (5% vs 30%), renal impairment (3.4% vs 27%), hepatic encephalopathy (10.2% vs 29%) Intravenous infusion of albumin is an important measure in patients with cirrhosis and tense ascites who are treated with repeated largevolume or total paracentesis. 5 L can be removed safely without the infusion of albumin. > 5 L : 8 to 10 g of albumin is infused for every 1 L of ascites removed.  Refractory Ascites 10% to 20% of patients. is due to avid renal retention of sodiu. Clinically : patient has adequate sodium restriction and receives maximal tolerable doses of diuretics without desired weight loss 400 mg/day of spironolactone and 160 mg/day of furosemide Treatment Options of refractory ascitis The long-term prognosis after the development of refractory =>1-year mortality rate >70%. Liver transplantation is the only therapeutic modality capable of e both the quality of life and patient survival. Other therapeutic options repeated therapeutic (large-volume or total) paracentesis transjugular intrahepatic portosystemic shunt (TIPS).  SPONTANEOUS BACTERIAL PERITONITIS SBP is an infection of ascitic fluid without a known source of infection. It occurs in 10% to 30% of patients with cirrhotic ascites and is frequently recurrent (70% recurrence rate in 1 year). the infecting organisms : 70% -gram-negative bacilli (especially Escherichia coli and Klebsiella) 30% by gram-positive cocci (mainly Streptococcus and Enterococcus species), anaerobes very uncommon (empiric therapy : Cefotaxime, 1 to 2 g intravenously every 8 hours amoxicillin-clavulanic acid organism has been identified,=> antibiotic therapy  2. Albumin Infusions albumin infusion : day 1 (1.5 g of albumin per kilogram) day 3 (1 g/kg) prevented the renal complications Albumin infusions are now the recommended therapy for spontaneous bacterial peritonitis.  3.Repeat Paracentesis Indication : for patients who do not show clinical improvement If the PMN count is greater than baseline =>patient must be reexamined carefully for secondary sites of infection (repeated abdominal radiography for free air, computed tomography of the abdomen, and surgical consultation.)  Primary Prophylaxis A disadvantage of antibiotic prophylaxis = >drug-resistant bacteria. Oral or systemic antibiotics should be given for 7 days to all patients with cirrhosis. Hepato-renal syndrome  HRS - definition HRS is a potentially reversible functional renal failure in patients with cirrhosis, advanced liver failure and portal hypertension in the absence of shock or an intrinsic parenchymal kidney disease.  Major Diagnostic Criteria for Hepatorenal Syndrome presence of all the following criteria is necessary for the diagnosis of hepatorenal syndrome: advanced liver failure and portal hypertension serum creatinine level greater than 1.5 mg/dL or creatinine clearance less than 40 mL/minute Absence of shock, bacterial infection, nephrotoxic drugs, or significant fluid loss No sustained improvement in renal function following diuretic withdrawal or plasma volume expansion Proteinuria of less than 500 mg/dL and no ultrasonographic evidence of obstructive uropathy or parenchymal renal disease.  Diagnostic In most cases, the diagnosis is made on the basis of serum creatinine + low urine volume (