Liver Cirrhosis Complications PDF

liver cirrhosis/complication DR SAEED OMAR BAAOUM CONSULTANT GASTROENTEROLOGY C2/PMAH  Cirrhosis is abnormal response of the liver to any chronic injury characterized by diffuse hepatic fibrosis and nodule formation. Any condition leading to persistent or recurrent hepatocyte...

liver cirrhosis/complication DR SAEED OMAR BAAOUM CONSULTANT GASTROENTEROLOGY C2/PMAH  Cirrhosis is abnormal response of the liver to any chronic injury characterized by diffuse hepatic fibrosis and nodule formation. Any condition leading to persistent or recurrent hepatocyte injury may lead to cirrhosis.  As in chronic viral hepatitis, prolonged excessive alcohol consumption and NAFLD. 9 E  Cirrhosis may also occur in prolonged biliary injury, as is found in primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) and post-surgical biliary strictures.  Persistent impairment of venous return from the liver, such as is found in sinusoidal.  obstruction syndrome (SOS;VOD), Budd–Chiari syndrome and cardiac hepatopathy can also result in cirrhosis. Yradiate 0 I CLINICAL FEATURES: non-specific and include weakness, fatigue, muscle cramps, weight loss, anorexia, nausea and upper abdominal discomfort Hepatomegaly (although liver may also be small) Jaundice Ascites  Circulatory changes: spider telangiectasia, palmar erythema Endocrine changes: loss of libido, hair loss 00 Men: gynaecomastia, testicular atrophy, impotence Women: breast atrophy, irregular menses, amenorrhoea  Hemorrhagic tendency: bruises, purpura, epistaxis Portal hypertension: splenomegaly, collateral vessels, variceal bleeding Hepatic encephalopathy Other features: pigmentation (haemochromatosis), Dupuytren’s contracture estrogens INVESTIGATIONS: CBC (Low Hb , low platelet) Kidney Function test (normal or high Urea ,High creatinine) Liver function tests (PT ↑ , Alb ↓, Bili↑ ) g Liver damage tests (AST>ALT, Alk.Ph) Liver ultrasound ,CT( coarse echotexture , nodularity, decrease in size) Surveillance tests (AFP, sonography, endoscopy, paracenteses,) Etiological diagnostic tests. Management 1.treatment of the underlying cause. 2. maintenance of nutrition. 3.treatment of complications. Nutrition in cirrhosis Malnutrition affecting up to 50% of patients with decompensated cirrhosis. Loss of muscle mass (sarcopenia) is associated with a higher rate of complications Although BMI is the most widely used measure of nutritional status, sarcopenia can coexist with obesity, Daily calorie intake 35 kcal/kg body weight with a daily protein intake of 1.2–1.5 g/kg Prognosis: Cirrhosis can be categorized into two prognostic groups:  Decompensated: cirrhosis is defined by the presence of complications, including ascites, variceal bleeding, jaundice and encephalopathy, which are the main determinants of patient survival.  Compensated patients have a relatively good prognosis with median survival >12 years. In decompensated cirrhosis median survival is around 2 years. Raised bilirubin, low albumin and prolonged PT ,renal dysfunction and hyponatremia, these are all bad prognostic features Child–Pugh SCORE One-year survival rate depending on MELD score Screening for complications: endoscopy -------------to screen for esophageal varices. US abdomen and alph fetoprotein -----hepatocellular carcinoma bone mineral density---- osteoporosis Complications 1. Ascites 2. Spontaneous Bacterial Peritonitis 3. Variceal hemorrhage 4. Hepatic Encephalopathy 5. Hepatocellular carcinoma 6. Hydrothoracic. ASCITES: Ascites is accumulation of free fluid in the peritoneal cavity. Small amounts of ascites are asymptomatic. Larger accumulations of fluid (> 1 L) there is abdominal distension, fullness in the flanks, shifting dullness on percussion. When the ascites is marked, a fluid thrill/fluid wave is detected. Other features include eversion of the umbilicus, hernia, abdominal striae, divarication of the recti and scrotal oedema. Dilated superficial abdominal veins may be seen if the ascites is due to portal hypertension.  Investigations US Abdomen. Paracentesis: Us Abdomen diagnostic aspiration of 10–20 mL of fluid should be obtained for:  Cell count  Gram stain and culture  Protein/albumin measurement  Cytology  Amylase Triglyceride  ASCITIS: calculate SAAG gradient of > 11 g/L (1.1 g/dL) is96% predictive that ascites is due to portal hypertension Management t Sodium restriction Restriction of dietary sodium intake is essential to achieve negative sodium balance. Restriction of sodium intake to 100 mmol/24 hrs (‘no added salt diet’) is usually adequate. __ Drugs containing relatively large amounts of sodium, and those promoting sodium retention As(NSAIDs), must be avoided. Restriction of water intake to 1.0–1.5 L/24 hrs is rarely needed unless the plasma sodium falls below 125 mmol/L..  Diuretics Most patients require diuretics in addition to sodium restriction. Spironolactone (100–400 mg/day) is the first-line drug because it is a powerful aldosterone antagonist. loop diuretic, such as furosemide (40–160 mg/day)then added. monitor electrolyte imbalance and renal dysfunction. Monitor complaint.  s not Paracentesis First-line treatment of refractory ascites is large-volume paracentesis. The circulation is supported with an intravenous colloid such as human albumin (6–8 g per litre of ascites removed). a um a man um Transjugular intrahepatic portosystemic stent shunt  TIPSS This technique uses a stent placed between the portal vein f and the hepatic vein within the liver to provide a portosystemic shunt.  Hepatic encephalopathy occurs in up to a third of patients following TIPSS liver transplant  Hepatic encephalopathy: Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease that occurs in 30%–40% of patients with cirrhosis. It causes a spectrum of symptoms ranging from mild fluctuating cognitive impairment to coma. Examination usually shows a flapping tremor (asterixis), inability to perform simple mental arithmetic tasks. Management: The principles are to treat or remove precipitating causes. To suppress the production of neurotoxins by bacteria in the bowel. Lactulose and increased gradually until the bowels are moving 2-3 daily. 550 twice daily Rifaximin (550 mg twice daily). F Tg  Spontaneous bacterial peritonitis Spontaneous bacterial peritonitis (SBP) is the most common bacterial infection in patients with cirrhosis. results from translocation of bacteria from the intestine into ascites. Clinical features:  Abdominal pain.  fever.  hepatic encephalopathy.  non-specific deterioration of liver function.  Examination: ascites and tenderness on abdominal examination Diagnosis:  paracentesis may show cloudy fluid,.  ascites neutrophil count of > 250 × 106/L so  Most organisms isolated are of enteric origin and Escherichia coli is the commonest.  Ascitic culture in blood culture bottles gives the highest yield of organisms.  SBP needs to be differentiated from other intra-abdominal emergencies, and the finding of multiple organisms on culture should arouse suspicion of a perforated viscus. Treatment : Broad-spectrum antibiotics, such as cefotaxime or piperacillin/tazobactam). Intravenous albumin (1.5 g/kg on day 1 and 1.0 g/kg on day 3)- Patients with jaundice or renal impairment. Prophylactic antibiotics such as norfloxacin (400 mg/day), ciprofloxacin (750 mg/week) or cotrimoxazole (960 mg/day).  Primary antibiotic prophylaxis also reduces the incidence of SBP in patients with low ascitic protein < 15 g/L.  Splanchnic dilation Hepatorenal syndrome: renal constriction I HRS is renal dysfunction in advanced liver disease that occurs due to reduced renal perfusion, resulting from both hemodynamic alterations in the arterial circulation (splanchnic vasodilatation/renal vasoconstriction) and a overactivity of endogenous vasoactive systems. Types: Acutekidneyinjury Type-1 HRS (now termed HRS-AKI) involves a rapid reduction in renal function (AKI) that is usually precipitated by an acute event, including bacterial infection, GI haemorrhage, alcoholic hepatitis or acute liver failure, which disturbs the abnormal renal haemodynamics and has a poor prognosis. Type II HRS (now termed HRS non-acute kidney injury or HRS-NAKI) is a stable or slowly progressive form of renal dysfunction developing over weeks to months, in the absence of an obvious precipitant.  Diagnostic criteria for HRS-AKI Diagnosis of cirrhosis, acute liver failure, acute on chronic liver failure  increase in serum creatinine ≥ 26.5 μmol/L (≥ 0.3 mg/dl) within 48 hours or≥ 50% from baseline according to IAC-AKI criteria and/or Urinary output ≤ 0.5 ml/kg per hr for ≥ 6 hrs No response after 2 consecutive days of diuretic withdrawal and volume atexpansion with albumin.  Absence of shock No current or recent treatment with nephrotoxic drugs Absence of parenchymal kidney disease, as defined as s 1 Absence of proteinuria (> 500 mg/day) 2 Absence of microhematuria (> 50 RBC per high power eld) 3 Normal findings on renal ultrasound Management : Identifying and treating precipitating factors. Diuretics and beta-blockers should be discontinued. Nephrotoxic drugs including vasodilators and NSAID should be stopped. Infections should be sought and treated. Volume replacement. Intravenous albumin infusions in combination with terlipressin (1–2 mg every v8 4–6 hours)or midodrine Haemodialysis.  Hepatocellular carcinoma:  Hepatocellular carcinoma (HCC) is the most common primary liver tumour, and the sixth most frequent cause of cancer worldwide.  Cirrhosis is present in 75%–90% of individuals with HCC  Chronic hepatitis B infection increases the risk of HCC 100-fold and is the major risk factor worldwide.  The risk of HCC is 0.4% per year in the absence of cirrhosis and 2%–6% in cirrhosis.  Other risk factors cirrhosis due to haemochromatosis, alcohol, NAFLD and alpha-1-antitrypsin deficiency.  Macroscopically, the tumour usually appears as a single mass in the 0 absence of cirrhosis.  a single nodule or multiple nodules in the presence of cirrhosis.  It takes its blood supply from the hepatic artery and tends to spread by invasion into the portal vein and its radicals Clinical features: Asymptomatic through screening of high-risk patients. Deterioration of cirrhosis, with worsening ascites, jaundice or variceal haemorrhage. weight loss, anorexia and abdominal pain. Tumour vascularity can lead to an abdominal bruit, and hepatic rupture with intra-abdominal bleeding. Examination may reveal hepatomegaly or a right hypochondrial mass. Investigations: Serum markers:  Alpha-fetoprotein (AFP) is produced by 60% of HCCs.  Levels increase with the size of the tumour  In the absence of active liver inflammation, a significantly elevated or progressively rising AFP is suggestive.  In HCC patients serial measurements can be a useful biomarker of disease progression or response to treatment. Imaging Ultrasound will detect focal liver lesions as small as 1 cm. Ultrasound may also show evidence of portal vein involvement and features of coexistent cirrhosis. The diagnosis is usually confirmed on either multi-phase contrast- enhanced CT or MRI, which demonstrate the typical hallmarks of HCC: arterial enhancement with washout on the portal venous phase Management Treatment options depend on e s tumour size and number-severity of liver disease (Child–Pugh score) -performance status.  HEPATIC HYDROTHORACIC Pleural effusion in a patient with cirrhosis and no evidence of underlying cardiopulmonary disease Movement of ascitic fluid into the pleural space through defects in the diaphragm, and is usually right-sided Diagnosis -pleural fluid analysis : reveals a transudative fluid serum to fluid albumin gradient greater than 1.1  Treatment : diuretic therapy periodic thoracentesis TIPS liver trasplantation