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Cirrhosis and Its Complications
- 1. Cirrhosis and Its Complications Prof. Dr.Osman Cavit Özdoğan Chief of the Gastroenterology & Hepatology Marmara University School of Medicine
- 2. Goals of This lecture • Part I: – What is cirrhosis? – Etiology of cirrhosis – Clinical presentation of cirrhosis – Pyhsıcal examination findings – Laboratory tests and liver biopsy – Prognosis of different etiologies
- 3. Part II: Complications • What is portal hypertension – Etiologies of portal hypertension – Results of portal hypertension • Occurence of varices – Acuta variceal bleeding • Hepatic encephalopathy • Spontaneous bacterial peritonitis • Hepatorenal Syndrome
- 4. Part II • Hepatopulmonary syndrome • Hepatocellular carcinoma and screening procedure • Liver transplantation • Discussion Part I-II will last 1.5 hours: I am sorry for you
- 5. 46 yrs old, man presented with ascites and jaundice , started 3 months ago, has been diagnosed HBS Ag carrier 20 years ago but had no follow up
- 6. What is liver disease? • Chronic injury • Chronic İnflammation • Fibrosis nodulation…..Cirrhosis
- 7. Cirrhosis • Nodule formation of the liver parenchyma by the extension of fibrosis
- 8. Acute onset or chronic injury of the liver by different etiologic factors • Acute • Acute viral hepatitis • Toxic Hepatitis – Drugs, herbal, chemicals • Acute Vasculer Liver disesases – Acute Budd-Chiari syndrome • Autoimmune Hepatitis • Acute presentations of metabolic liver diseases • Pregnancy related acute liver disases – Acute faty liver – Benign intrahepatic cholestasis of pregnancy • Ischemic Hepatitis
- 9. Chronic Liver Diseases • Chronic Viral Hepatitis – HBV/HDV – HCV • Alcoholic liver diseases – Alcoholic hepatitis – Hepatosteatosis and fibrosis – Alcoholic cirrhosis • Autoimmune Liver Diseases – Autoimmune Hepatitis – Primary Biliary Cirrhosis – Primary Sclerosing Cholangitis
- 10. Metabolic liver diseases Hemachromatosis Wilson disease Alfa-1 antitripsin deficiency Tyrosinemia Non-alcoholic steatosis and steatohepatitis Granulomatous hepatitis sarcoidosis Cholestatic liver diseases ◦ Primary Biliary Cirrhosis Primary Sclerosing Cholangitis ◦ Secondary biliary cirrhosis ◦ Vanishing Bileduct syndrome ◦ Drugs, toxins etc. Chronic Vascular liver diseases Cryptogenic liver diseases
- 11. ınjury Acute Fulminant Liver Failure Complete Cure Resolution Death Transplantation ınjury Chronic Hepatitis Compansated Cirrhosis Decompansation Complications Death TX
- 12. So what happens when cirrhosis occurs? • Synthesis function – Hypoalbuminemia – Decrease of coagulation factors • Conjugation function – High bilirubin • Detoksification function – Drug metabolism – Estrogen metabolism etc.
- 13. At early stages of cirrhosis there are no spesific symptoms or mostly no symptoms • Chronic fatique • Decrease in functional capacity • History of jaundice • Pruritis • Bleeding after teeth brush or shaving etc. • Positive tests for viral hepatitis • History of elevated liver enymes
- 14. Decrase in Coagulation factors • Easy bleeding – Nose – Gum – Ecchymosis, petechias and purpuras – Easy brusing – Bleeding after the minor surgeries
- 15. Bilirubin • Its the product of hem metabolism • Conjugates at the hepatic cells • Excreted by the biliary paths • Increases and causes icterus/jaundice
- 18. Ascites and peripheral edema
- 20. Examination of Abdomen • Percussion – liver – Spleen • Palpation – Liver – Spleen • Examination of ascites
- 21. Laboratory Findings • Hypersplenism – Anemia – Trombocytopenia – Leukopenia • Hypoalbuminemia • Increased Liver Enyzmes – AST/ALT > 1 • Increased Bilirubin • Increased protrombine time
- 22. Radiological findings • Abdominal ultasonography – Irregular and nodular surface of the liver – Splenomegaly – Ascites • Abdominal MRI and CT – Sometimes better than USG
- 23. How about liver biopsy • Its highly invasive • %1-2 severe bleeding and sometimes mortality • Hematologic problems at cirrhosis • So when biopsy? – if clinically, radiologically and laboratuary findings do not clearly indicate cirrhosis – If we do not clarify the etiologic factor and suspect of treatable condition
- 25. Staging of Cirrhosis Interpretation: Class A: 5-6 Class B: 7-9 Class C: 10-15
- 26. Prognosis of Cirrhosis Points Class One year survival Two year survival 5-6 A 100% 85% 7-9 B 81% 57% 10-15 C 45% 35%
- 27. Model of End Stage Liver Disease Score (MELD)
- 28. Treatment At Early Stage • Early treatment may affect prognosis – Stop alcohol drinking – Eradication of viruses – Treatment of the cause – Autoimmune – Wilson – Hemachromatosis – Sclerozing Cholangitis – Very good followup – Prevention of complications • Low Na Diet
- 29. Have a nice break Then Complications of Cirrhosis
- 30. Pathophysiology of Portal Hypertension: Hemodynamic Factors ∆∆ Portal Pressure = Resistance x Blood FlowPortal Pressure = Resistance x Blood Flow Increased Portal PressureIncreased Portal Pressure Increased Blood Flow (splanchnic / vasodilation) Increased Resistance (dynamic / mechanic) Architectural Disturbances Vascular distorsion due to fibrosis, scarring, regenerative nodules. Thrombosis Mechanical Component (“fixed”) Functional Alterations Active contraction of several cell types: HSC ,HMF, VSMC Dynamic Component (modifiable by drugs)∼70 %70 % ∼30 %30 % Increased production of vasodilators (NO, CO, PGI2, peptides, VEGF, endocann,…) Hyposensitivity to vasoconstrictors - - NitricOxide Others ? Vasodilators Carbon Monoxide Endothelin Angiotensin Norepinephrine Leucotrienes Prostanoids Other? Vasoconstrictors Courtesy of J Bosch
- 32. PORTAL HYPERTENSION> 5 mHg CIRRHOTIC PORTAL HYPERTENSION NON- CIRRHOTIC PORTAL HYPERTENSION COMPLICATIONS •Variceal Bleeding •Ascites •H.encephalopathy •SBP •HRS LIVER FAILURE Varıceal bleedıng Hyperseplenism GOOD LIVER FUNCTION
- 33. Asit >10 mmHg > 5 mmHgPortal Basınç GFR SBP Survi % 50 5 yıl HRS % 50 2 yıl Haftalar 10 yıl 2 yıl Haftalar Anti viral tedavi Cirrhosis path by the years
- 34. Pathogenesis Cirrhosis Portal Hypertension Splanchnic vasodilation Efektive Blood volume Na/water retantion RAAS Activation Renal Vasoconstriction HRS Presipitant factor Ascites Arterial underfillingCardiac dysfunction
- 35. Ascites: usually first complication !! • Sometimes no symptom • Abdominal distension • Feeling abdominal tenderness • Treatment – Na restriction – Dıuretics – Terapeutic parasentesis
- 36. •Serum alb – ascites alb >1.1 •LDH, protein, glucose •Cell count •Cytology •Culture
- 37. untreated treated Natural History of Varices Increased Portal PressureIncreased Portal Pressure (HVPG > 10 mmHg)(HVPG > 10 mmHg) Dilatation of VaricesDilatation of Varices Rupture of VaricesRupture of Varices (HVPG > 12 mmHg)(HVPG > 12 mmHg) Formation of VaricesFormation of Varices Courtesy of J Bosch
- 38. Portal System Normal portal basınç 5 mmHg
- 39. Anatomic Sites of Varices • Squamocolumnar junction of GİS • Esophageal • Anorectal • Umblical vein • Retroperitoneum • Sites of previous abdominal surgery or intra- abdomianl trauma • Other sites – Anal varices
- 40. We perform upper GI endoscopy for every patient whom has diagnosed cirrhosis • Small • Large • Color and bleeding stigmata
- 42. So what happens to the esophageal varices ?
- 43. Clinical Findings • Hematemesis • Melena • Senkop • Hypotension • Shock • History of cirrhosis or chronic hepatitis • Physical findings of cirrhosis • Mortality % 30-50
- 44. Treatment of Variceal Bleeding • Supportive treatment – ICU – Blood Tx – Vit K • Vasoactive drugs – Somatostatin – Terlipresin • Endoscopic treatment – Banding – Sclerotherapy • Baloon tamponade
- 45. untreated treated Natural History of Varices Increased Portal PressureIncreased Portal Pressure (HVPG > 10 mmHg)(HVPG > 10 mmHg) Dilatation of VaricesDilatation of Varices Rupture of VaricesRupture of Varices (HVPG > 12 mmHg)(HVPG > 12 mmHg) Formation of VaricesFormation of Varices Courtesy of J Bosch
- 46. Hepatic Encephalopathy History Hipocrates (460-370 BC): A patient with hepatitis who barked like a dog, could not be held and said things which could not be comprehended. Özdoğan: Hepatic encephalopathy (HE) is a complex,Hepatic encephalopathy (HE) is a complex, potentially reversible neuropsychiatric condition thatpotentially reversible neuropsychiatric condition that occurs as a consequence of acute or chronic liveroccurs as a consequence of acute or chronic liver disease.disease.
- 47. Hepatic Encephalopathy • Acute liver failure • Hyper acute: In a week • Acute: ın 4 weeks • Subacute: İn 4-12 weeks • Chronic Liver Failure • Acute on chronic • Chronic
- 48. PATOGENESİS • Failure of GUT derived substances • Hepatocellular failure • Portocystemic shunting • Altered amino acid metabolism • Reduced branched-chain amıno acids • Increased aromatic amino acids----false neurotransmission • Increased neuroactive toxins---false neurotransmission • Reduced cerebral OXYGEN consumption and astrocyte swelling
- 49. Increase in NH3 •Cerebral edema •Slow down at neuron transmission GLUTAMİN as false neurotransmitters Serotonin Benzodiazepine reseptor activation Manganez
- 50. What happens to the patient? • Changes in • Consciousness • Personality • Intellect • Speech • Personality Changes • Agitation • Childishness • Irritability • Loss of concern to family
- 51. Clinical picture • Grade 0 - Minimal hepatic encephalopathy . Lack of detectable changes in personality or behavior. Minimal changes in memory, concentration, intellectual function, and coordination. Asterixis is absent. • Grade 1 - Shortened attention span. Impaired addition or subtraction. Hypersomnia, insomnia, or inversion of sleep pattern. Euphoria, depression, or irritability. Mild confusion. Slowing of ability to perform mental tasks. Asterixis can be detected. • Grade 2 - Lethargy or apathy. Disorientation. Inappropriate behavior. Slurred speech. Obvious asterixis. Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior. • Grade 3 - Somnolent but can be aroused, unable to perform mental tasks, disorientation about time and place, marked confusion, amnesia, present but incomprehensible speech • Grade 4 - Coma with or without response to painful stimuli
- 53. Physical examination • Abnormality in orientation • Place • Time • Client • Writing, signature, number connection test • Fetor hepaticus • Flapping tremor: asterixis • Coma
- 54. 39 Minimal HE ve 18 kontrol Kale, Hepatology 2006
- 56. Treatment of HE • No clear data showing benefit to strict protein restriction – 40-60 mg/d mostly vegetable based proteins • Lactulose • Non-Absorbable Antibiotics – Prebiotics and probiotics • L-Ornithine-L-Aspartate (LOLA) – Infusion – Oral granul form • BCAA solutions • Liver Tx
- 58. Definition & Classification of HRS Devastating complication of end stage liver disease characterized by functional renal failure due to severe vasoconstriction in the absence of underlying kidney pathology. International Ascites Club; Hepatology, 1996
- 59. HRS Type 1 •Rapidly progressive •Serum creatinine>2.5 mg/dl or creatinine clearance<20 ml/min HRS Type 2 •Slowly progressive •Serum creatinine>1.5mg/dl or •Creatinine clearance<40ml/min Hepatology 1996;23:164-76
- 60. Presipitant Factors • Spontaneous bacterial peritonitis • Other infections • Dehidretation • Variceal bleeding • Diuretics
- 61. Gerçek Hipovolemi ATN % 40 Sepsis HRS Tip I ve II % 30 Radiokontrast ajanlar İlaçlar Renal parenkim Hastalıkları Renal Dysfunction at Cirrhosis
- 62. Transplantation Cirrhosis & Ascites Portal HipertensionTIPS Splanchnic VasodilationAlbumin & Vasoconstrictors Renal VasoconstrictionHRS Toxic Substances MARS
- 63. Spontaneous bacterial peritonitis • Spontaneous infection of ascites • Any cirrhotic patient with • Fever • Abdominal pain • Abdominal tenderness • Detoriation of clinical situation • Parasentesis • Neutrophil count>250/ml • Ascites culture: mostly E.coli • Treatment – i.v antibiotics: 3th generation cephalosporins (cefotaxim) first choise, – quinalons or penicilins
- 64. Spontaneus Bacterial Peritonitis: Mechanism Intesine Abdominal Cavity Ascitic Fluid Portal Vein LIVER Systemic Circulation IntestinalPermeability BacterialOvergrowth •Loss of opsanization •Decreased complemant amount Kupfher Cell Loss DecreasedRESFunction Collaterally pass
- 65. Causative microorganisms of spontaneous bacterial peritonitis, bacterascites and secondary peritonitis Microorganisms SBP Bacterascites Secondary peritonitis Monomicrobial Escherichia coli 37 27 20 Klebsiella pneumoniae 17 11 7 Pneumococcus 12 9 0 Streptococcus viridans 9 2 0 Staphylococcus aureus 0 7 11 Miscellaneous Gram- negative 10 14 7 Miscellaneous Gram- positive 14 10 0 Polymicrobial 1 0 53
- 66. • Hepatopulmonary syndrome: Hypoxia due to shants • Hepatocellular carcinoma and screening procedure • Liver transplantation • Discussion
- 67. Liver Transplantation • Each patient who has the complications must be listed for transplantation • Child Score > 9 • MELD Score > 10 • Urgent Tx – Acute fulminant liver failure – Acute on chronic liver failure
- 69. • Cadaveric Tx • Living donor Tx • 600-700 Tx each year in Turkey • Mostly living donor • Survival % 80 in 2 years, % 70 in 5 yrs • Immunsupressive treatment after Tx
- 70. You are free now !!!