The Yellow Patient. Dr Chiradeep Raychaudhuri, Consultant Hepatologist, Hull University Teaching Hospitals NHS Trust

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1 The Yellow Patient Dr Chiradeep Raychaudhuri, Consultant Hepatologist, Hull University Teaching Hospitals NHS Trust

2 there s a yellow patient in bed 40. It s one of yours.

3 Liver Cirrhosis Why.When.What.etc. Compensated and Decompensated. Clinical states Acute on Chronic Liver Failure. Management of Common Complications.

4 Definition Liver cirrhosis is anatomically defined as a diffuse process with fibrosis and nodule formation. It is the end result of the fibrogenesis that occurs with chronic liver injury Although causes are many, the end result of fibrogenesis is the same Can be compensated or decompensated Cirrhosis and End-stage liver disease ARE NOT THE SAME THING!!

5 Causes Alcohol Non-alcoholic fatty liver disease Viral Hepatitis: B/C/D Haemochromatosis Autoimmune: AIH, PBC, PSC Drugs: Methotrexate, Amiodarone Alpha 1 Antitrypsin deficiency

6 Scores Child-Pugh MELD and MELD-Na UKELD CLIF-OF and CLIF-ACLF

7 Cirrhosis is typically classified as compensated or decompensated, based on the absence or presence (or previous history) of Variceal bleeding Ascites Jaundice Hepatic encephalopathy Compensated patients have Significantly longer survivals Usually asymptomatic Much better quality of life The transition from compensated asymptomatic cirrhosis to decompensated cirrhosis occurs at a rate of about 5-7% per year Once decompensation occurs, cirrhosis becomes a systemic disease Decompensation represents a prognostic watershed wherein median survival drops from 12 years to about 2 years

8 Where and how does things go wrong Cirrhosis Portal Hypertension Bacterial translocation Peripheral arterial vasodilatation End-organ damage Hyperdynamic circulation Splanchnic vasodilatation Cardiovascular dysfunction Release of proinflammatory molecules

9 Clinically significant portal hypertension (CSPH) This is defined by a Hepatic venous pressure gradient (HVPG) 10mmHg Development of gastro-oesophageal varices and decompensation usually doesn t happen below CSPH Histological stages of cirrhosis run parallel to the progression of portal hypertension and clinical states of disease

10 Clinical states of Cirrhosis Stage 0: Compensated cirrhosis without CSPH Stage 1: Compensated cirrhosis with CSPH but without varices Stage 2: Compensated cirrhosis with varices Stage 3: Variceal bleed (only) Stage 4: First non-bleed decompensation Stage 5: Further decompensation Stage 6: Late advanced decompensation (End Stage Liver Disease) refractory ascites, infections, persistent encephalopathy, jaundice, renal/circulatory/respiratory dysfunction

11 Stage of Cirrhosis 0/1 Low 5 year Risks 2 Death before decompensation 10% Variceal bleeding 8% Single non-bleed decompensation 20% 3 Death before other complications 18-20% Re-bleed before other decompensation 19% Further decompensation 45-54% 4 Death before further decompensation 25% 5 5 year mortality up to 88% 6 1 Year Mortality 60-80%

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13 Acute on Chronic Liver Failure (ACLF) ACLF is characterised by acute decompensation, organ failure(s) and high short term mortality It may occur in previously compensated or decompensated cirrhosis Major cause of death in patients with cirrhosis (50% mortality rate) Precipitating events vary between populations and may include: Bacterial infections (30 57% of cases) Active alcohol intake or alcohol binge Reactivation of HBV Superimposed HAV and HEV infection

14 Chronic liver failure organ failure score system 1 Organ/system 1 point 2 points 3 points Liver (bilirubin, mg/dl) <6 6 < Kidney (creatinine, mg/dl) < < or renal replacement Brain/HE (West Haven Criteria) Grade 0 Grades 1 2 Grades 3 4 Coagulation (INR, PLT count) < < Circulation (MAP, mmhg and vasopressors) 70 <70 Use of vasopressors Lungs PaO 2 /FiO 2, or > > SpO 2 /FiO 2 >357 > Grades of ACLF NO ACLF ACLF 1a ACLF 1b ACLF II ACLF III Clinical characteristics No organ failure, or single non-kidney organ failure, creatinine <1.5 mg/dl, no HE Single renal failure Single non-kidney organ failure, creatinine mg/dl and/or HE grade 1 2 Two organ failures Three or more organ failures

15 App Hull Audit: 30-day mortality was significantly greater in those with ACLF than without (71% vs 12% :p <0.001)

16 Management of ACLF Management of precipitants where possible Organ support and management of complications ITU involvement Involve Gastroenterology/Hepatology early

17 Common Complications

18 Ascites Most common complication Impacts quality of life, both work and social Frequently leads to hospitalisation Development of ascites in patients with cirrhosis is associated with a poor prognosis 1-year mortality: 40% 2-year mortality: 50% Ascites is uncomplicated when not infected, refractory or associated with impairment of renal function Can lead to other complications such as SBP and renal failure There are other causes of ascites.

19 Grading of Ascites Grade 1 Mild ascites: only detectable by ultrasound examination Grade 2 Moderate ascites: manifest by moderate symmetrical distension of abdomen Grade 3 Large or gross ascites: provokes marked abdominal distension

20 Management of ascites Diagnostic tap (deranged clotting/low platelets not a contra-indication) Moderate sodium restriction (no added salts/avoid prepared meals) Grade 1 value of pharmacotherapy unknown Grade 2 Hospitalisation not required First episode of uncomplicated Grade 2 ascites, start spironolactone 100mg OD aiming for weight loss of 0.5kg per day (no oedema) to 1kg/day (oedema+) Monitor U&Es post diuretic Review in 72 hours Grade 3 - LVP

21 Variceal Bleed 2 nd most common decompensating event Resuscitate A B C Do not over-transfuse Hb 7-8 Terlipressin + Antibiotics Early scope

22 Spontaneous Bacterial Peritonitis Fluid neutrophil >250 May or may not have clinical signs and symptoms Early diagnosis and treatment has reduced mortality form 90% when first described to 20% now Antibiotics as per local protocol, if high clinical suspicion then don t wait for results (particularly out of hours) Albumin significantly decreases the incidence of type-1 hepatorenal syndrome and reduces mortality The administration of albumin recommended in patients with SBP 1.5 g/kg at diagnosis and 1 g/kg on Day 3

23 Renal Failure

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25 ICA diagnostic criteria for HRS-AKI Cirrhosis and ascites Diagnosis of AKI according to ICA-AKI criteria No response after 2 consecutive days of diuretic withdrawal and plasma volume expansion with albumin 1 g per kg of body weight Absence of shock No current or recent use of nephrotoxic drugs (NSAIDs, aminoglycosides, iodinated contrast media, etc.) No macroscopic signs of structural kidney injury,* defined as: Absence of proteinuria (>500 mg/day) Absence of microhaematuria (>50 RBCs per high power field) Normal findings on renal ultrasonography

26 Management of Type 1 HRS Terlipressin 1mg iv QDS, to be reviewed after 48 hours and can be increased to 2mg QDS Albumin 20-40g per day Monitor renal function daily

27 Hyponatraemia Sodium <130 Associated with increased mortality and morbidity Review drugs Volume status assessment and management Hepatic encephalopathy Look for precipitating factors Review drugs Avoid/stop opiates/benzodiazepines Lactulose first line 20-30mls TDS aiming for 3 soft/loose stools per day (NG if too drowsy for oral intake) Phosphate enema Rifaximin

28 Take home messages Proper assessment Don t miss ACLF Look for infection Correct volume status Review drugs Urgent USS Check AFP, particularly in patients who suddenly decompensate for no apparent reason NUTRITION

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