Cirrhosis

Cirrhosis is a histological diagnosis characterised by the development of fibrous septa surrounding hepatocellular nodules, and results in synthetic deficiencies and portal hypertension.

Aetiology

• Chronic viral hepatitis
• Alcoholic liver disease
• Haemochromatosis
• Nonalcohol fatty liver disease
• Also:
  • Autoimmune hepatitis
  • Primary and secondary biliary cirrhosis
  • PSC
  • Medications
  • Wilson disease

Pathophysiology

• The end result of a healing process initiated by chronic liver injury
• Fibrous septa develop around regenerating hepatocellular nodules
  • Distortion of hepatic architecture
• May be reversible in early stages if cause is treated

Presentation

• Compensated
  • Anorexia
  • Weight loss
  • Weakness
  • Fatigues
• Decompensated
  • Jaundice
  • Pruritis
  • Upper GI bleeding
  • Ascites
  • Confusion
• Look for jaundice, spider angiomata, gynaecomastia, ascites, splenomegaly, palmar erythema, digital clubbing, asterixis

Diagnosis

• Cirrhosis is a histological diagnosis established on liver biopsy
• However presence can be suspected based on clinical signs of chronic liver disease and portal hypertension along with imaging signs
• Fibroscan
  • Assesses the stiffness of liver via transient elastography - a 'vibration wave'/'shear wave' is generated on the skin, and velocity of this wave is assessed by determining the time taken to travel to a particular depth inside the liver
  • Because fibrous tissue is harder/stiffer than normal liver, the higher the stiffness, the higher the likelihood of cirrhosis
  • Cutoff is >14kPa

Management

• No effective treatment
• Treat cause
• Palliative: treat portal hypertension and treat complications
• Definitive: liver transplant

Complications (decompensated - primarily CAVE - coagulopathy, ascites, variceal bleed, encephalopathy)

• Risk factors/triggering events for decompensation:
  • Bleeding
  • Infection
  • Alcohol intake
  • Medications
  • Dehydration
  • Constipation

• Variceal bleed
  • Large volume, melaena, shock
• Portal hypertensive gastropathy bleed
  • Often slower, IDA
• Ascites
  • Requires portal HTN
  • Occurs in 50% of previously compensated cirrhotic patients over a 10 year period, and marks a 2-year survival of 50%. Associated with a deterioration in QoL.
  • Consider concomitant viral hepatitis/vascular disease, along with cardiac/renal/malignant disease.
  • Exam
    • Shifting dullness = 2L of ascites
  • Generally treated with diuretics and sodium restriction, but pay require therapeutic paracentesis or TIPS
• SBP
  • Infected ascites collection
• Hepatic encephalopathy
• HCC
• Hepatorenal syndrome
  • Renal failure in a patient with advanced liver disease
• Hepatopulmonary syndrome
• Umbilical herniae often occur in this setting, which presents a management dilemma
  • Ruptured/incarcerated herniae are repaired immediately
  • Those with symptomatic herniae/skin changes should be referred for elective repair
  • Asymptomatic herniae are managed conservatively - involves aggressive management of ascites
  • Repair asymptomatic herniae at time of liver transplantation
• Coagulopathy
  • Rebalanced haemostasis with both procoagulant and anticoagulant effects
    • Impaired haemostasis - coagulation factor deficiencies, most notably I, II, V, VII, IX, X and CI; thrombocytopaenia/platelet dysfunction; altered fibrinolytic system
    • Prothrombotic changes: reduced protein S, C and antithrombin; increased VWF

Indications for albumin in cirrhosis

• Prevention of paracentesis-induced circulatory dysfunction
• Diagnosis and treatment of hepatorenal syndrome AKI
• Treatment of SBP

Prognosis

• Child-Pugh classification was originally developed to assess risk of non-shunt operations in patients with cirrhosis
  • 1-year mortality of 0%, 20% and 55% for A, B and C respectively
  • Mortality rate after abdominal surgery
    • A 10%
    • B 30%
    • C 70-80%
  • Scoring
    • Score of 5-15
    • 5-6 = CPA
    • 7-9 = CPB
    • 10-15 = CPC
  • Breakdown
    • 1, 2 or 3 points for each category
    • Ascites: Absent, slight, moderate
    • Bili: <35, 36-51, >51
    • Albumin: >35, 28-35, <28
    • INR: <1.7, 1.7-2.3, >2.3
    • Encephalopathy: None, Grade 1 or 2, grade 3 or 4
• MELD (Model for End-stage Liver Disease)
  • Determines prognosis and prioritises liver transplant allocation
  • Versions
    • Original MELD
    • MELD-Na (2016)
    • MELD 3.0 (2022) - swap out ascites and encephalopathy for sodium and creatinine levels
      • Creatinine level (receive max value if on dialysis)
      • Bilirubin level
      • INR
      • Sodium level
      • Albumin level

• Elective surgery well tolerated in CP-A or MELD <10
• Might be able to optimise a CP-B/MELD 10-15 to safety
• All surgery contraindicated in CP-C/MELD >15
  • Only if there is no other option, and should be clearly informed about their high mortality risk

Operating on patients with cirrhosis

• Risks
  • Surgical factors
    • Recanalised umbi veins
    • Stiff, nodular liver
  • Physiological
    • Coagulopathy - bleeding and clots
    • Decompensated liver
    • Renal failure
    • Infection
    • Leaking ascites and hernia recurrence
    • Mortality - see above
• Pre-op
  • Ensure seeing a gastroenterologist - optimise liver function, treat underlying cause
  • Consider timing and location
    • Should it be done by HPB surgeon?
    • Is a transplant happening soon, and it should be done at the same time?
    • Should be done in a centre with gastroenterologist, experienced anaesthetist and ICU
  • Minimise ascites
  • Correct malnutrition, including vitamin K
  • Optimise coagulopathy
    • Correcting the coagulopathy with FFP is difficult and frequently does not help; vitamin K is obligatory but frequently also doesn't help. There is an expert opinion in Schein's that an INR of 2.5 in a cirrhotic patient is not necessarily as prone to bleeding as an INR of 2.5 in a patient taking warfarin, and that he wouldn't give FFP to any liver patients pre-op. This is supported by modern studies - INR and PLT don't seem to predict bleeding risk, whereas abnormal TEG does.
    • Use ROTEM/TEG to guide clotting ability
    • Generally aim fibrinogen >1 and platelets >50
    • Avoid prothrombinex in severe chronic liver disease - very prothrombotic - risk of dead toes etc.
  • Identify abdominal wall varices - CT
  • Check for portal hypertension and avoid operating near portal system if present
  • Ensure group and hold done
• Intra-op
  • Obsessive haemostasis, haemostatic agents and energy devices available
  • Meticulous respect for peritoneal integrity
  • Avoid abdominal wall varices
  • Drains are controversial - risk of infection - may be better off performing periodic ascitic tap
  • Conservative intra-op fluids, and generally avoid saline due to higher risk of hyperchloraemic metabolic acidosis - give Hartmann's instead, or albumin
• Post-op
  • High-risk for infections, haematomas, ascites and renal failure. Restrictive fluid management, possibly with low-dose diuretics. Oliguria may mean volume overload.
  • Protein losses of prolonged post-op drainage are prohibitive.
  • Consider AWS/thiamine
  • Resume diet and lactulose early to reduce the risk of decompensation