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Acute Care in Cirrhosis the First 24 Hours

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Acute Care in Cirrhosis the First 24 Hours Acute Care in Cirrhosis …the first 24 hours Royal College Physicians GIM Training Day, Sheffield March 2018 Rebecca Jones Consultant Hepatologist Chronic Liver Disease • Increasing prevalence of chronic liver disease – Rise in hospital admissions for complications • Decompensated cirrhosis • Acute on chronic liver failure – Large variation in in-hospital mortality rates across UK • E.g Dr Foster – 15% to 35% mortality for non-elective liver admissions – Rising mortality – 3rd commonest cause of premature mortality • Commonest causes are – Alcohol – Obesity – Viral hepatitis – “Liver screen” – remember co-factors exist Liver Disease Mortality Trends Atlas of Variation 2017 Decompensated Cirrhosis • An acute deterioration in liver function in a patient with cirrhosis that can manifest with the following: – jaundice – increasing ascites – hepatic encephalopathy – renal impairment/ hypovolaemia – gastrointestinal (GI) bleeding – signs of sepsis • Overall risk of death during admission with decompensated cirrhosis is 10-20% • If there is organ failure then “acute on chronic liver failure” (ACLF) carries a 30% mortality rate at 28 days. • If alcohol related cirrhosis is diagnosed in hospital, the 1 year mortality is 30% and the 5 year mortality is 60%. Complications of Cirrhosis HRS Ascites SBP Varices Cirrhosis HCC Encephalopathy Osteodystrophy Malnutrition Confused? Scared? What leads to an acute admission? And what causes people to die? Mortality • Patients with cirrhosis die from – Bleeding – Sepsis – Renal Failure • They are admitted with these complications • They develop them during their admission • Their care is often sub-optimal, with delays in appropriate diagnosis, prevention and management of complications of decompensation. 2013 NCEPOD Recommendation • NCEPOD 2013 Measuring the Units – Only 47% of patients who died of alcohol related liver disease received “good” care – Identified avoidable deaths – Recommended a toolkit for acute management of patients admitted with decompensated ARLD • Principles are the same for all causes of decompensated liver disease – Cirrhosis Care Bundle – Effective, evidence based care for first 24hrs How did patients arrive in hospital? 11 Age – wholeAge population 66% (1584/2418) of the ARLD deaths were male 12 Presenting features Complex patient group Risk of death increased if (any of): • Jaundice • Ascites • Encephalopathy • Renal failure • Acute alcoholic hepatitis At least one of these features present in 438/512 patients (85%) 13 Principles of Acute Care • Look for common precipitants and treat accordingly. • These include: – GI bleeding (variceal & non-variceal) – Sepsis (incl. look for SBP, chest, urine, cholangitis) – Alcoholic hepatitis – Portal vein thrombosis – Development of HCC – Drugs – opiates, NSAIDs, alcohol – Ischaemic liver injury (hypotension, any cause) – Dehydration – Constipation • Key words – Look – Treat – Prevent Varices Varices: endoscopy Varices Varices • Varices occur when HVPG is >10 mmHg – Present in ~50 % of cirrhotic patients – Bleeding rate 5-15% per year – Mortality associated with variceal bleed is 20% at 6 weeks • Will present acutely in a variety of ways – Shock – Not shocked – Haematemesis – Malaena – Anaemia • And in a variety of circumstances – Patient known to have varices – Patient known to have cirrhosis – Patient with decompensated liver disease – Patient not known to have cirrhosis/liver disease Varices Varices General management • Manage as for any GI bleed – ABC • Assess appropriate level of care – Transfuse as necessary • Support abnormal clotting or thrombocytopaenia – Request endoscopy • Assess urgency Varices Varices Specific medical management • If varices are known or strongly suspected – Care with transfusion • Aim Hb 8 • Caution in pushing up BP – aim for MAP of 65mmHg • Monitor urine output • Search for cause - AAH, PVT, Infection – Blood products • FFP (2) and platelets (50) – Actively seek out infection • Send blood cultures • CXR, urine, ascitic tap • Treat according to site – Actively prevent infection • Prophylactic antibiotics save lives – sepsis and rebleed risk • Broad spectrum IV – Use splanchnic vasoconstrictors • Terlipressin – 2mg qds • Caution in patients with history of ischaemic heart disease – They may be more shocked than you realise • Are they on beta-blockers? NICE Guideline on GI Bleeding (CG141; 2012) • Risk assessment – Use the following formal risk assessment scores for all patients with acute upper gastrointestinal bleeding: • the Blatchford score at first assessment, and • the full Rockall score after endoscopy. • Timing of endoscopy – Offer endoscopy to unstable patients with severe acute upper gastrointestinal bleeding immediately after resuscitation. – Offer endoscopy within 24 hours of admission to all other patients with upper gastrointestinal bleeding. • Management of variceal bleeding – Offer prophylactic antibiotic therapy at presentation to patients with suspected or confirmed variceal bleeding. – Offer terlipressin to patients with suspected variceal bleeding at presentation. – Stop treatment after definitive haemostasis has been achieved, or after 5 days, unless there is another indication for its use – Band ligation for oesophageal varices; Glue for gastric varices • Consider transjugular intrahepatic portosystemic shunts (TIPS) if bleeding from oesophageal varices is not controlled by band ligation. • Offer TIPS if bleeding from gastric varices is not controlled by endoscopic injection of N-butyl-2-cyanoacrylate. Case study 12 A 32 year old with cirrhosis due to ARLD was admitted midweek in normal working hours with a GI bleed. They were hypothermic, hypotensive, acidotic and in renal failure. They had ascites and encephalopthy. Hb was 6g/dl. They were transfused and actively warmed. No attempt was made to obtain gastroenterology review. They were referred to ICU but denied admission. They remained oliguric, had a further massive haematemesis and had a cardiac arrest and died The Advisors’ view was that more aggressive treatment of the bleed including endoscopy was indicated and that critical care admission was turned down inappropriately 20 Ascites Ascites • Most common complication of cirrhosis • Advancing cirrhosis • Development of portal vein thrombosis • Development of Hepatocellular Carcinoma (HCC) • Prognostic indicator: 50% mortality at 2 years • Spectrum of severity • Grade 1 (radiologically present, not clinically) • Grade 2 (modest, clinically evident) • Grade 3 (large, very distended abdomen) – Uncomplicated • Diuretic controlled • Not infected, no renal failure – Refractory • Diuretic intolerant • Diuretic resistant • Spontaneous Bacterial Peritonitis • Renal failure ?Hepatorenal syndrome Diagnostic paracentesis • Diagnosis of aetiology • Diagnosis of infective complications • Left lower quadrant may be preferable – Abdominal wall is thinner • Complications – Abdominal wall haematoma 1% – Haemoperitoneum/bowel entry Epigastric arteries <0.1% • Aseptic technique Anterior superior iliac crest • Over 70% will have “coagulopathy” 3cm above • Cirrhosis is a pro-coagulant condition 3cm medial – No evidence of increased bleeding rates – No evidence to support routine use of platelets/FFP • BSG guidelines recommend informed consent Runyon B. AASLD Guidelines 2009 Moore K, Aithal G. BSG Guidelines 2006 Interpreting ascitic cell counts • Spontaneous bacterial peritonitis is an important infection to diagnose • Ascitic neutrophil count – 250 cells/cm3 is diagnostic (0.25 x 109/L) – In absence of perforated viscus etc • Ascitic culture from universal containers is not as good as aseptic inoculation into blood culture bottles – 40% vs 80% organism identification – Organisms in SBP usually gram –ve and single • Multiple organisms – think secondary peritonitis • Gram +ve – seen after hospitalisation, instrumentation, antibiotic prophylaxis Interpreting ascitic albumin and protein levels Serum ascites-albumin Ascitic total protein gradient • Very useful to establish group of • Useful to determine risk of causes spontaneous bacterial • SA-AG ≥11g/L peritonitis – Cirrhosis – Ascitic protein is >25g/L in – Cardiac failure 25% patients with cirrhosis – Nephrotic syndrome – SBP uncommon with ascitic protein >15g/L • SA-AG <11g/L – Risk of SBP increased with – Malignancy ascitic protein levels ≤ 10g/L – Tuberculosis – Pancreatitis Ascites Ascites: investigation • Diagnostic tap – This is a mandatory urgent investigation for anyone admitted to hospital with ascites • For first presentations always send for – Cytology – Leucocyte count – Microbiology – Protein • In patients known to have cirrhosis, review previous results. It may not be necessary to repeat cytology if assessed recently but – Leucocyte count – Microbiology • Send ascitic fluid inoculated into blood culture bottles – Protein • Should always be done • And always looked up Ascites Management of ascites • Review medication – Stop NSAIDS • Fluid status – Commence daily weight chart – If no renal impairment, commence diuretics • Usually spironolactone • If lots of peripheral oedema can consider furosemide/bumetanide – If there is renal impairment • Avoid starting diuretics, stop any already prescribed • Infection – If SBP is present • Ensure a sample of ascites has been inoculated into blood culture bottles to get best chance of identifying organism. • Treat with appropriate antibiotics and adjust according to culture results • Treat for 5 days – if concerned about response then repeat tap Ascites Management of ascites • Paracentesis – Consider
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