Complications of End-Stage Liver Diseases PDF

Complications of end-stage liver disease  End-stage liver disease (Cirrhosis) Definition: “It is a chronic, irreversible degeneration of liver cells followed by scarring and infiltration of the tissues with dense fibrotic strands and regeneration nodules”. This leads to a progre...

Complications of end-stage liver disease  End-stage liver disease (Cirrhosis) Definition: “It is a chronic, irreversible degeneration of liver cells followed by scarring and infiltration of the tissues with dense fibrotic strands and regeneration nodules”. This leads to a progressive loss of liver function and circulatory obstruction, the latter causing portal hypertension. The associated complications of portal hypertension (gastroesophageal varices, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, and hepatorenal syndrome) Etiology (risk factors): Mainly alcoholic liver disease and viral hepatitis. To lesser extent: Biliary diseases, metabolic disorders or drug reaction.  End-stage liver disease (Cirrhosis) MICRONODULES Pathogenesis: After inflammation and necrosis of hepatocytes, the normal architecture is replaced by interconnecting fibrous scar. Regenerative nodules ranging from micronodules (less than 3 mm) to macronodules (greater than 3mm), are created by the regeneration of hepatocytes. The manifestations: MACRONODULES 1. Asymptomatic. 2. Early symptoms: weight loss (sometimes masked by ascites), weakness, anorexia, hepatomegaly, jaundice and abdominal pain.  End-stage liver disease (Cirrhosis) 3- The late manifestations are: CAPUT MEDUSA SPIDER NEVII Portal hypertension and liver failure. Splenomegaly. Ascites. Portosystemic shunts (i.e., esophageal varices, anorectal PALMER ERYTHEMA varices, and caput medusae) result from portal hypertension. Bleeding caused by decreased clotting factors. Thrombocytopenia caused by splenomegaly. Gynecomastia, a feminizing pattern of hair distribution, because of altered testosterone and estrogen metabolism. Spider angiomas and palmar erythema. Hepatic encephalopathy. ASCITIS  End-stage liver disease (Cirrhosis) Portal hypertension Portal hypertension is characterized by “Increased resistance to flow in the portal venous system and sustained portal vein pressure above 10 mm Hg (normal, 5–10 mm Hg)”. Portal hypertension results from both: 1. An increase in resistance to portal flow (due to formation of fibrotic scares, regeneration nodules and intrahepatic nitric oxide (NO) ) and 2. An increase in portal venous inflow (due to splanchnic vasodilatation from NO production in the extrahepatic circulation).  Complications of portal hypertension (pathogenesis): Increased intrahepatic venous pressure and dilatation of the venous channels behind the obstruction. Collateral channels opened that connect the portal circulation with the systemic circulation leading to development of complications (Hypersplenism)  End-stage liver disease (Cirrhosis): classification Cirrhosis classified into two main categories: compensated and decompensated. 1. Compensated: is cirrhosis with a portal pressure 10 mm Hg with complications of cirrhosis. The aim is to treat the complications and prevent sequela (secondary prevention).  End-stage liver disease (Cirrhosis) LABORATORY FINDINGS : 1. Conventional liver “function” tests: (see lecture 1), but these Laboratory evaluations in cirrhosis may not reflect the extent of the parenchymal necrosis, regeneration, and fibrotic nodular scarring. Therefore we use other scoring systems. 2. Child–Turcotte–Pugh classification of liver disease severity: it is scoring system helps clinicians grade disease severity, and predicts the long-term risk of mortality and quality of life. class A: compensated. classes B and C: decompensated.  End-stage liver disease (Cirrhosis) LABORATORY FINDINGS : 3. Model for End-Stage Liver Disease (MELD) score: An alternate method for assessing survival in patients with liver disease which predicts a 90-day mortality. End-stage liver disease (Cirrhosis): Complications 1- Ascites Definition: Free fluid in the abdominal cavity owing to increased resistance within the liver (forces fluid accumulation in the abdominal cavity) and reduced osmotic pressure within the bloodstream (hypoalbuminemia). The systemic compensation to the generalized vasodilation in cirrhosis is increased cardiac output as well as sodium and water retention through activation of the renin–angiotensin– aldosterone system (RAAS). End-stage liver disease (Cirrhosis): Complications 1- Ascites Clinical features: shifting dullness, fluid wave, bulging flanks, abdominal pain. Diagnosis: A. Medical History B. Clinical features C. Abdominal ultrasonography D. Diagnostic Paracentesis (all patients with new-onset ascites), use to determine serum-ascites albumin gradient (SAAG), calculated by subtracting the ascites albumin concentration from the serum albumin concentration; a value greater than 1.1g/dL indicates ascites caused by portal hypertension. E. Ascitic fluid test should include also ascitic fluid neutrophil (PMNL) count, ascetic fluid total protein.  Classification of Ascites No treatment is recommended for grade 1 ascites, as there is no evidence that it improves patient outcomes.  End-stage liver disease (Cirrhosis): Complications 1- Ascites Treatment 1. Alcohol cessation if alcohol induced 2. Dietary sodium restriction (48 hr of admission) contact with H. care facilities >90 ds) in the absence of and/or in the presence of recent Β-lactam recent Β-lactam antibiotic exposure antibiotic exposure Should receive empiric antibiotic therapy, e.g., an intravenous third-generation cephalosporin, preferably Should receive antibiotic therapy based on local cefotaxime 2 g every 8 hours or ceftriaxone (2 g/day) for susceptibility testing of bacteria in patients with 5 days. cirrhosis. Health care associated (within 48 hr/contact with H. care facilities 1 mg/dL, BUN > 30 be considered a substitute for mg/dL) and/or jaundice (total bilirubin > 4 mg/dL) at intravenous cefotaxime in inpatients time of diagnosis of SBP. without: ▪ Rationale: The hemodynamics of patients with cirrhosis prior exposure to quinolones, vomiting, reflect a state of intravascular hypovolemia and organ shock, grade II (or higher) hepatic hypoperfusion; SBP is thought to exacerbate this effect, encephalopathy, or serum creatinine resulting in progressive renal hypoperfusion and greater than 3 mg/dL. precipitation of renal failure or hepatorenal syndrome.  End-stage liver disease (Cirrhosis): Complications 4- Spontaneous bacterial peritonitis (SBP) Treatment of acute SBP…cont’d Patients with ascitic fluid polymorphonuclear leukocyte counts ≥ 250 cells/mm3 Response to empirical antibiotic therapy may be assessed by repeating diagnostic paracentesis 2 days after initiation. A decrease in fluid PMN< 25% from baseline indicates lack of response and should lead to broadening of antibiotic coverage and further evaluation to rule out secondary bacterial peritonitis.  End-stage liver disease (Cirrhosis): Complications 4- Spontaneous bacterial peritonitis (SBP) Treatment of acute SBP Patients with ascitic fluid PMN counts < 250 cells/mm3 and signs or symptoms of infection (high temperature or abdominal pain or tenderness) should also receive empiric antibiotic therapy, e.g., intravenous cefotaxime 2 g every 8 hours, while awaiting results of cultures. To reduce the chance of bacterial translocation from GIT Primary prevention of SBP: During acute upper GI bleeding, give 7-day course of ceftriaxone during hospitalization.: In patients with cirrhosis and ascites (without bleeding), indefinite use of norfloxacin 400 mg/d (or trimethoprim/ sulfamethasoxazole) if: the ascitic fluid protein