JAUNDICE. Zdeněk Fryšák 3rd Clinic of Internal Medicine Nephrology-Rheumatology-Endocrinology Faculty Hospital Olomouc

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1 JAUNDICE Zdeněk Fryšák 3rd Clinic of Internal Medicine Nephrology-Rheumatology-Endocrinology Faculty Hospital Olomouc

2 Definition of Jaundice Icterus A yellowish staining of the skin, sclerae and deeper tissues with bile pigments which are increased in plasma Can be seen on examination at serum bilirubin levels μmol/l (1.5 2 mg/dl)

3 Types of Jaundice Cholestatic-obstructive Hepatocellular Haemolytic

4 Some detailes of origine Pre-hepatic, hepatic and post-hepatic Can usually determine type from history, exam, simple investigations- urine and blood tests. Pitfalls: some patients don t fit just one type and have a combined picture In the production of jaundice more than one mechanism may be involved Increased use of pharmaceuticals which can cause any type of jaundice account for up to 10% of pts presenting to hospital with jaundice

5 Bilirubin metabolism Bilirubin comes from breakdown of haem by the RES (splenic, hepatic and marrow macrophages) 80% from RBC breakdown and 20% from other haem containing proteins. Within macrophages is oxidised to biliverdin and then reduced to uncongulated bilirubin which is released into plasma (water insoluble), transported bound to plasma proteins (albumin).

6 Bilirubin metabolism This is then actively transported into hepatocytes, where it is conjugated mostly to glucoronic acid (by glucuronyl transferase congenital failure of which is Gilbert s disease). Then it becomes water-soluble conjugated bilirubin which is concentrated and actively excreted into the bile canaliculi (failure of this is Dubin Johnson type hyperbilirubinaemia).

7 Bilirubin metabolism Bilirubin is then secreted along with bile salts and sodium into the intestine (bile), where it is broken down to urobilinogen of which 90% is broken down in the gut to urobilin and stercobilin (excreted in stools), other 10% is re-absorbed. The reabsorbed urobilinogen either recirculate into bile by liver or is excreted in urine. Only conjugated bilirubin can be excreted in urine because of water-solubility. Therefore haemolytic jaundice is acholuric. Van den Bergh reaction detects conjugated (direct) or unconjugated (indirect) bilirubin.

8 Bilirubin metabolism Therefore examination of the stools and testing urine for urobilinogen can help differentiate types of jaundice. In obstructive jaundice the pale stools are due to decreased bile pigments, whereas stools may be darker than usual in haemolytic jaundice due to excess stercobilinogen production. If liver function is impaired there will be decreased ability to re-excrete urobilinogen and stercobilinogen and more will appear in urine.

9 Bilirubin metabolism Complete obstruction of biliary tree will lead to absence of urobilinogen from urine prolonged absence indicates pancreatic head malignancy rather than stones because they will let some bile through Bilirubin functions as an anti-oxidant Cholecystographic media compete with conjugated bilirubin for concentration and therefore will not be concentrated in the setting of excess bilirubin

10 Bilirubin Metabolism

11 Causes of Jaundice Pre-hepatic unconjugated hyperbilirubinaemia Haemolysis, eg. spherocytosis, pernicious anaemia, incompatible blood transfusion Congenital defects: Gilbert s syndrome (uptake/conjugation defect) Crigler-Najar (conjugation defect)

12 Causes of Jaundice Acute Viral hepatitis A, B, C.. Other viruses: EBV, CMV Drugs Dose-dependant e.g. paracetamol Idiosyncratic Toxins Autoimmune hepatitis Alcoholic hepatitis Tumours Hepatocellular Chronic Viral hepatitis B, C Chronic AI hepatitis End-stage liver disease (of any cause) Alcoholic Hepatitis B, C Autoimmune Haemochromatosis Wilson s disease

13 Causes of Jaundice Cholestatic Extra-hepatic Intra-hepatic Gallstones Drugs Carcinoma of head of pancreas Benign stricture Congenital Traumatic iatrogenic Carcinoma of ampulla of Vater or bile ducts Sclerosing Cholangitis Primary biliary cirrhosis Cholestatic phase of viral hepatitis Alcoholic hepatitis Primary or secondary cancer Lymphoma Pregnancy pancreatitis

14 History pain Colour of stools and urine Drugs Recent blood transfusion Alcohol intake Contact with hepatitis infection Occupation FHx anaemia, splenectomy, gallstones

15 Examination Pale yellow vs. deep yellow Signs of cirrhosis Liver tender, enlarged, firm, shrunken, irregular Gallbladder tender (Murphy s sign), palpable Splenomegaly

16 Laboratory testing Urine Pre-hepatic Hepatic Post-hepatic No Bilirubin Urobilinogen? Bilirubin Urobilinogen Faeces Dark Pale Pale Blood FBC - Reticulocyte count Coombs test Bilirubin (up to 100μmol/L) unconjugated ALP Normal PT Normal Bilirubin mixed conjugated & unconjugated ALP, γgt AST, ALT PT not correctable with Vit K Bilirubin Urobilinogen Bilirubin (up to 1000μmol/L) conjugated ALP, γgt PT correctable with Vit K

17 Imaging Ultrasound Gallstones Bile duct dilatation Intra-hepatic lesions CT Liver lesions Pancreatic lesions CT-IVC MRI Liver lesions MRCP X-ray Gallstones only 10% radioopaque PTC, ERCP can also be means of therapy Isotope scan HIDA

18 Management Symptom relief Pain, itch Fluid resuscitation Correction of coagulopathy Treat secondary complications Sepsis, bleeding, anaemia Treat underlying cause Medical or surgical

19 Surgical Management Post-Hepatic Jaundice Initial therapy Analgesia IV fluids Vit K Nothing by mouth (NBM) Consider Antibiotics

20 Surgical Management Relieve obstruction Definitive or temporising, curative or palliative ERCP / PTC Remove stones Stent or dilate stricture Surgery Cholecystectomy with bile duct exploration Resection of obstructing tumour Whipple s procedure Bypass of irresectable lesion

21 Transcystic Exploration of Common Bile Duct

22 Transcystic Exploration of Common Bile Duct

23 Transcystic Exploration of Common Bile Duct

24 Benign distal CBD stricture

25 PTC and balloon dilatation of post-cholecystectomy stricture

26 ERCP and stent insertion for obstructing cholangiocarcinoma

27 Děkuji za pozornost V případě potřeby se se svými odbornými problémy můžete obrátit na Endokrinologickou ambulanci III. interní kliniky FN a LF Olomouc tel frysakz@fnol.cz david.karasek@fnol.cz milan.halenka@fnol.cz