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Jaundice and LFT interpretation
This document provides guidance on evaluating a patient presenting with jaundice. It outlines a systematic approach including focused history, examination, differential diagnosis, and appropriate lab tests and imaging. Liver function tests can indicate hepatitic or cholestatic patterns. Case examples demonstrate applying this approach, such as using imaging and endoscopy to diagnose an ampullary tumor, managing a variceal bleed in cirrhosis, and identifying acute hepatitis B. Key considerations include complications of liver disease and importance of screening high-risk populations.
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Jaundice and LFT interpretation
- 1. JAUNDICE & LFTINTERPRETATION Dr. Sharma,Academic F1 Aintree University Hospital
- 2. LEARNING OBJECTIVES • Todevelop a systematic approach to the patient who presents with jaundice. • To identify key serological and imaging tests to request. • To be able to confidently interpret liver function tests. • To be able to confidently interpret hepatitis serology results.
- 3. FOCUSSED HISTORY (1) •Presence of abdominal pain • Painful, colicky → Gallstones? Cholangitis? • Absence → Cholangiocarcinoma/pancreatic malignancy? • Obstructive symptoms • Pale stools • Dark urine • Pruritis • Systemic symptoms • Fever, chills and rigors → Cholangitis? Biliary sepsis? Hepatitis?
- 4. FOCUSSED HISTORY (2) •Risk factors for hepatitis • Travel history • Sexual history • Intravenous drug use • Risk factors for acute/chronic liver injury • Alcohol • Paracetamol • Other drugs e.g. amoxicillin, flucloxacillin
- 5. FOCUSSED HISTORY (3) •Other symptoms of ‘decompensated’ chronic liver disease (N.B. < 7 days: hyperacute liver failure; 5–12 weeks: subacute liver failure) • Abdominal swelling (= ascites) • Episodes of confusion (= encephalopathy) • Easy/abnormal bruising (= coagulopathy) • Haematemesis/malaena (= bleeding varices 2° to portal hypertension) • Past medical history • Known chronic liver disease? Known cirrhosis?
- 6. EXAMINATION (1) • Apartfrom the jaundice itself… • Abdominal tenderness (RUQ pain) • Organomegaly (hepatomegaly, splenomegaly) • Signs of acute liver failure • Bruising (coagulopathy) • Encephalopathy (asterixis +/- lethargy/confusion) • Risk factors • Injection marks • Tattoos
- 7. EXAMINATION (2) • Stigmataof chronic liver disease
- 8. DIF F ER E NT IA L DIA G NO S IS ?
- 10. ENTEROHEPATIC CIRCULATION OFBILE SALTS
- 11. PREHEPATIC (OR ‘HAEMOLYTIC’) JAUNDICE •Causes • Haemolytic anaemia (hereditary spherocytosis/elliptocytosis, sickle cell anaemia, G6PD deficiency, etc.) • Gilbert’s Syndrome (↑ unconjugated bilirubin) • Mechanism • Excessive haemolysis of red blood cells → ↑ unconjugated bilirubin • ↑ Conjugation of bilirubin in liver {saturation of enzymes} • ↑ Urobilinogen {forms in SI} → resorbed into circulation → ↑ dark urine • ↑ Stercobilinogen {converted from urobilinogen} → ↑ dark stools
- 12. HEPATIC JAUNDICE • Causes •Viral hepatitis (A-E) • Alcoholic hepatitis • Ischemic hepatitis • Drug-induced hepatitis (esp. paracetamol) • Autoimmune hepatitis • Malignancy (primary or secondary) • Decompens ated chronic liver disease {which may have developed as a result of above – also consider haemochromatosis,Wilson’s disease}
- 13. POST-HEPATIC JAUNDICE • Causes •Any cause of ‘cholestatic’ or obstructive jaundice: • Gallstones • Cholangiocarcinoma • Pancreatic carcinoma • Primary biliary cholangitis (autoimmune) • Primary sclerosing cholangitis (associated with ulcerative colitis) • Parasites • CONJUGATED BILIRUBIN & LIPASE FROM GALLBLADDER → BLOCKED ENTEROHEPATIC CIRCULATION → PALE, FATTY STOOLS + DARK URINE
- 15. INVESTIGATIONS (1) • Routinebloods 💉 • LFTs, yGT (=deranged) • Glucose (↓ due to ↓gluconeogenesis) • Clotting screen (PT, aPTT ↑ due to ↓ synthetic function) • If suspect haemolytic anaemia → ↑ LDH, ↑ haptoglobin • ABG • pH is used as part of King’s College transplant criteria for ALF (hepatic dysfunction is a cause of lactic acidosis) • Non-invasive liver screen
- 16. ALBUMIN • Marker ofsynthetic function of liver • But also, a… • Marker of nutritional status • Marker of inflammation/disease severity • Negative acute phase protein • ↓ production by liver so more amino acids available for production of positive acute phase proteins • ↑ proteolysis (catabolism) • ↑ transcapillary escape rate
- 17. N.B. ALT isliver-specific,AST is not. yGT may be helpful in confirming that source of raised ALP is the liver. A ‘cholestatic’ liver function test profile can be caused by intrahepatic causes of jaundice.
- 18. ‘PATTERNS’ OF LIVERFUNCTION TESTS ‘Hepatitic’ • Hepatocellular damage → hepatocyte release of enzymes • Transaminitis ↑ ALT ↑ AST ‘Cholestatic’ • Obstructed outflow • ↑ ALP ↑ yGT A ‘mixed’ picture is also possible e.g. hepatitic liver damage can lead to obstruction
- 19. ALT ↑ ↑↑ ↑ (THOUSANDS) • Toxin/drugs ☠️ e.g. paracetamol • Acute viral hepatitis • Ischemic hepatitis • Autoimmune hepatitis (not really for alcoholic hepatitis, NAFLD, hepatocellular carcinoma, Wilson’s disease, chronic viral hepatitis, cirrhosis…)
- 21. ANTIBODIES • ↑ anti-mitochondrial antibodies(AMA) → Primary biliary cholangitis (PBC) • ↑ anti-smooth muscle antibodies (A- SMA)/antinuclear antibodies (ANA) → Autoimmune hepatitis • ↑ anti-neutrophil cytoplasmic antibodies (ANCA) → Primary sclerosing cholangitis (PSC) associated with ulcerative colitis
- 22. SEROLOGY Constant region ofantibody varies by heavy chains IgM: 1st class produced during antibody response; binds and agglutinates microorganisms early in response; production of large immune complexes Production downregulated with generation of IgG IgG: binds to C1w and receptors on phagocytic cells; gain access to extravasci;ar spaces
- 26. N.B. HbeAg (theenvelope antigen) and anti-HbeAg play an important role in indicating disease activity in patients with chronic hepatitis.
- 28.
- 29. INVESTIGATIONS (2) • Imaging •Abdominal ultrasound • Liver echotexture (cirrhotic? Helps differentiate acute vs. chronic damage) • Focal lesions (mets?) • Biliary obstruction (CBD/extrahepatic/intra-hepatic duct dilatation) • Gallstones • Portal vein patency (thrombosis?) • CT • MRCP
- 30. INVESTIGATIONS (3) • Fibroscan(transient elastography) – measures liver stiffness and allows gradation of fibrosisWITHOUT need for liver biopsy! • Intervention • Endoscopic Retrograde Cholangio-pancreatography (ERCP) (balloon trawling, stenting, sphincterotomy) • PercutaneousTranshepatic Cholangiogram (PTC)
- 32. ASCITIC TAP • EVERYPATIENT PRESENTING TO HOSPITAL WITH ASCITES SHOULD HAVE AN ASCITIC TAP. • This is to rule out SPONTANEOUS BACTERIAL PERITONITIS, which can be asymptomatic.
- 33. ANALYSIS OF ASCITICFLUID
- 34. CASE 1 • A75-year old lady presents with a 4-week history of jaundice, 3 kg weight loss, pale stools, and dark urine. She has not experienced any abdominal pain. She has no past medical history. • On examination, she is jaundiced but apyrexial.The remainder of her observations are normal. Her liver edge is palpable at 2-cm below the costal margin. She has no signs of chronic liver disease.
- 35. BLOOD TESTS • FBC •Hb 135 g/L • WCC 4.5 x 109/L • Platelets 124 x 109/L (↓) • U&Es • Normal • LFTs • Bilirubin 240 uM ↑ • ALT 120 IU/L (↑) • ALP 1506 IU/L (↑ ↑) • Albumin 36 g/L • Clotting • INR 1.3
- 36. QUESTIONS (1) • Whatpattern of LFTs is demonstrated here? • Obstructive • Differential diagnosis? • Pancreatic head tumour • Ampullary tumour • Cholangiocarcinoma • Gallstones • Benign biliary stricture
- 37. QUESTIONS • Next steps? •Imaging • CT abdomen, pelvis and thorax → dilated CBD @ 12 mm, with mildly dilated intrahepatic ducts • Dilated pancreatic duct • No gallbladder stones • No visible lesion in head of pancreas, no evidence of lymphadenopathy or metastasis “Double duct” sign: simultaneous dilatation of pancreatic and bile ducts, suggestive of pancreatic or ampullary tumour
- 38. QUESTIONS • Next steps? •ERCP • Double duct sign observed again • Appearances suggestive of ampullary carcinoma → biopsies obtained • Biliary stent inserted • Prophylactic antibiotics commenced post-ERCP (↑ risk of cholangitis) • Management • Local resection orWhipple’s procedure (pancreatoduodenectomy)
- 39. CASE 2 • A52-year old retired army major, with a background of alcoholic liver cirrhosis andType II diabetes mellitus, is brought in by his wife. He presents with worsening jaundice, recurrent haematemesis and malaena over the past 3 days. He has no previous hospital admissions. • On examination, he appears unwell. Heart rate is110 bpm, BP 95/55 mmHg, oxygen saturation 95% on room air, and temperature 35.8C. • There are multiple signs of chronic liver disease. He is alert and mildly confused, with asterixis and mild ascites present. • His drug history includes metformin and spironolactone.
- 40. BLOOD TESTS • FBC •Hb 72 g/L (↓) • WCC 7.1 x 109/L • Platelets 83 x 109/L (↓) • U&Es • Na+ 136 mM • K+ 4.6 mM • Urea 9.1 mM (↑) • Creatinine 110 uM (baseline 83) • LFTs • Bilirubin 212 uM ↑ • ALT 300 IU/L (↑) • ALP 100 IU/L ↑ • yGT 320 IU/l ↑ • Albumin 32 g/L (mildly ↓) • Clotting • INR 1.8
- 41. QUESTIONS (1) • Differentialdiagnosis? • Decompensated alcoholic liver disease • UGI bleed • Variceal bleed (must exclude as has signs of portal hypertension - ascites!) • Peptic ulcer • CHILD-PUGH Score? • 11 (Class C – severe, decompensated disease) • Glasgow-Blatchford Score? • 15
- 42. QUESTIONS (2) • Initialmanagement? • IV access and fluid resuscitation • X-match 2 units RBC (aim 70-90 g/L) • IV Terlipressin 2 mg STAT, then QDS • IVVitamin K 10 mg STAT • Prophylactic antibiotics for variceal bleeds (tazocin @ Aintree) • Urgent gastroscopy
- 43. CASE (CONT.) • Gastroscopyshowed four oesophageal varices protruding halfway across the lumen. • Seven variceal bands were applied, with a good result.
- 44. QUESTIONS (3) • Subsequentmanagement? • Treatment of hepatic encephalopathy: • Lactulose 10-20 mL TDS (aim BO 3 x / day) • Rifaximin 550 mg TDS • Prophylaxis for variceal bleeding (non-selective beta-blocker once BP stable): • Carvedilol 6.25 mg OD or propanolol 40 mg BD • Treatment of ascites (N.B. should’ve been tapped on admission!): • Spironolactone 50 mg BD • Paracentesis, if required
- 45. CASE 3 • A36-year old businessman, with a history of intravenous drug use, presents with a 2 day history of jaundice, fever, chills and general malaise. He does not complain of abdominal pain. • He has a past history of sexual intercourse with other men, and has previously been diagnosed with HIV (on antiretroviral therapy). • On examination, he appears jaundiced, and a liver edge is palpable. He is mildly tender in the right upper quadrant. Observations are otherwise normal.
- 46. BLOOD TESTS (1) •FBC • Hb 145 g/L • WCC 5.4 x 109/L • Platelets 220 x 109/L • U&Es • Na+ 140 mM • K+ 3.9 mM • Urea 5.2 mM • Creatinine 75 uM (baseline 80) • LFTs • Bilirubin 110 uM ↑ • ALT 1430IU/L (↑) • ALP 150 IU/L ↑ • yGT 800 IU/l ↑ • Albumin 37g/L • Clotting • INR 1.2
- 47. QUESTIONS (1) • Whatpattern do the LFTs show? • Hepatitic • What is your differential diagnosis? • Viral hepatitis (Hepatitis A-E, CMV, EBV) • Ischemic hepatitis • Autoimmune hepatitis • Drug-induced liver injury • Acute alcoholic hepatitis • Biliary obstruction • Primary or secondary hepatocellular carcinoma • Other congenital causes: Wilson’s disease, haemochromatosis, etc.
- 48. QUESTIONS (2) • Whatfurther tests would you like to perform? • US abdomen (?cirrhosis) • Full liver screen, including viral serology
- 49. RESULTS (2) Marker Result HbsAg+ Anti-HBs (total) - Anti-HBc IgM ++ Anti-HBc Ig (total) + In keeping with acute hepatitis B Next investigations worth ordering would be HbeAg, HBV PCR to determine viral load, and HBV genotyping.
- 50. CASE 3 (CONT.) •This man was referred to a liver specialist for consideration of antiviral therapy and liver transplantation. • Treatment for Hepatitis C is otherwise conservative. Patients commenced on antiretroviral therapy are high risk (e.g. pregnant), have high viral loads and/or a marked transaminitis.
- 51. IMPORTANT CONSIDERATIONS • Recurrentepisodes of acute-on-chronic hepatitis B can lead to cirrhosis. • Note that the majority of patients will be asymptomatic, and that a recent multi-centred RCT trial (HepFREE) demonstrates significant cost-effectiveness to primary-care level screening of hepatitis B and C in high-risk migrant populations.