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Obstructive jaundice

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obstructive jaundice, cholestasis, cholangitis, pancreatic head tumour, periampullary tumour, cholangiocarcinoma,

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Obstructive jaundice

  3. 3. INTRODUCTION • In obstructive jaundice, there is the failure of normal amount of bile to reach the intestine due to the impediment of bile flow along the hepato-biliary tree. • Surgical jaundice is any jaundice amenable to surgical treatment. Majority are due to extra-hepatic biliary obstruction. • Not all surgical jaundice is due to obstruction e.g. congenital spherocytosis, here surgical treatment can be offered as splenectomy.
  4. 4. AETIOLOGY INTRAHEPATIC: Cirrhosis, Hepatitis EXTRAHEPATIC a. Intraductal causes • stone disease (Choledocholithiasis- CBD stones ), • Neoplasms (cholangiocarcinoma-CBD Ca), • Traumatic bile duct stricture, • parasites (Ascaris), • primary sclerosing cholangitis (PSC), • AIDS-related cholangiopathy and biliary tuberculosis. b. Extraductal obstruction • Neoplasms Primary; ca head of pancreas, Carcinoma ampulla of Vater, Primary duodenal cancer Secondary; Tumour in the porta hepatis, usually from a primary in the stomach • Chronic pancreatitis, • Cystic duct stones with subsequent gallbladder distension (Mirizzi syndrome)
  6. 6. • Bile is produced continuously by hepatocytes. It contains cholesterol and waste products, such as bilirubin and bile salts, which aid in the digestion of fats. • Half the bile produced runs directly from the liver into the duodenum via a system of ducts, ultimately draining into the common bile duct (CBD). The remaining 50% is stored in the gallbladder. • Biliary obstruction prevents carriage of bile to the small intestine
  7. 7. • Normal secretory pressure of bile is 15-25 cm of water • At 35 cm of water there is suppression of bile flow • High pressure leads to cholangiovenous and cholangiolymphatic reflux of bile • Dilatation of bile duct and intra hepatic biliary radicals(IHBR) • IHBR dilatation may be absent if there is secondary hepatic fibrosis or cirrhosis
  8. 8. • Increase in biliary pressure leads to disruption of tight junctions between hepatocytes and bile duct cells with increased permeability • Reflux of bile contents in liver sinusoids • Neutrophil infiltration,increased fibrinogenesis and deposition of reticulin fiberes in portal triad • Reticulin fibers gets converted in to type 1 collagen • Laying down of collagen fibers leads to hepatic fibrosis, obstruction of sinusoids and secondary biliary cirrhosis and portal hypertension • Fibrosis can also lead to atrophy of obstructed liver.
  9. 9. SYSTEMIC EFFECTS CHANGES IN LIVER BLOOD FLOW • In Acute obstruction • increase in hepatic arterial blood flow • No change in portal venous blood flow • Chronic obstruction • Decrease in total liver blood flow , dilatation of sinusoids and elevation of portal pressure
  10. 10. CARDIOVASCULAR SYSTEM • Decreased cardiac contractability • Reduced left ventricular pressure • Impaired response to beta agonist drugs • Decreased peripheral vascular resistance • Bradycardia due to direct effect of bile salts on SA node. • Net result : Hypotensive patient, Exaggerated hypotensive response to bleeding, More prone to postoperative shock.
  11. 11. RENAL FAILURE 10 % incidence with 70 % mortality Factors responsible are • Decreased cardiac function • Increased levels of ANP resulting in hypovolemia • Decreased effect of bile salts on kidney mediated by increased prostaglandin E2 • Endotoxemia • Bile salt deposition • Result: in renal vasoconstriction, shunting of blood from cortex, Activation of complement system, peri-tubular and glomerular fibrin deposition leading to tubular and cortical necrosis
  12. 12. IMMUNE SYSTEM • Defects in cellular immunity • Impaired T cell proliferation • Decreased neutophil chemotaxis • Defective bacterial phagocytosis • Depressed function of RE system i.e Kupffer cells
  13. 13. WOUND HEALING • Delayed wound healing • High incidence of wound dehiscence • Decreased activity of enzyme Propyl hydroxylase in the skin -This helps in incorporation of proline in collagen • Defective synthesis of collagen
  14. 14. COAGULATION FACTOR DEFECTS Prolongation of Prothrombin time; • Decreased absorption of fat soluble vitamins A,D,E,K (vitamin K dependent clotting factors nor formed- II, VII, IX and X) • Endotoxin induced damage to factor XI ,XII ,platelets • Low grade DIC with increased fibrin degradation products
  15. 15. ITCHING • Retained bile salts stimulate nerve endings. • Other theory • Due to endogenous opiate peptides • Inducing opiod receptor mediated scratching activity of central origin
  16. 16. CLINICAL FEATURES The features that suggest obstructive jaundice are as follows • Jaundice • Generalized pruritus • Pale, bulky and oily stool • Dark urine • However their mode presentation depends on the aetiology of the jaundice.
  17. 17. SUGGESTING CA HEAD OF PANCREAS OBSTRUCTING CBD • An older patient • Vague Epigastric pain • Usually painless obstructive jaundice. (presents with jaundice then later pain. Pain is due to; involvement of the retropancreatic nerve, obstruction of pancreatic duct, or disruption of the nerve sheeth by tumour ) • Weight loss • Progressive deepening jaundice associated with ca pancreas. • Gall-bladder is palpably enlarged, strongly suggests a malignant obstruction at the lower end of the common bile-duct, but its absence does not exclude this.
  18. 18. SUGGESTING AMPULLARY CA • fluctuating obstructive jaundice (necrosis of the tumour with sloughing with temporary relief of jaundice). • Silver coloured stools • Weight loss and pain is a late feature
  19. 19. SUGGESTING GALLSTONES • Severe intermittent colicky pain (painful jaundice- develop pain before jaundice). • A long history of intermittent varying jaundice (fluctuating jaundice) • Fever, chills, and rigors (suggesting cholangitis, often complicate the jaundice of gallstones) • Little or no weight loss, • flatulent dyspepsia • A non-palpable gall-bladder. • A raised white count suggests cholecystitis
  20. 20. SUGGESTING A CARCINOMA OF STOMACH WITH SECONDARIES TO PORTA HEPATIS • Pain • Anorexia, • Vomiting, • An upper abdominal mass, and • Visible peristalsis of pyloric stenosis. • Anaemia is common
  21. 21. SUGGESTING HEPATOMA • A large, hard, irregular liver • A bruit is often present, • Ascites is common, and is often bloodstained.
  22. 22. SUGGESTING CARCINOMA OF THE GALL-BLADDER • The patient is a woman with an enlarged liver and a hard, irregular mass in her right hypochondrium. • Cirrhosis – Alcohol intake • Hepatitis – injections and transfusions • Hereditary spherocytosis – Family Hx of anaemia, splenectomy and gallstones
  23. 23. • PANCREATIC CANCER RELATED DIABETES MELITUS • Longstanding diabetes is an aetiologic factor for pancreatic cancer • New-onset diabetes (<24months) is also a manifestation pancreatic cancer • The pancreatic cancer cells produce soluble factors that can impair glucose metabolism and causes hyperglycemia. • Resent onset diabetes tends to improve following resection. • It is unlikely due to destruction of the gland by tumour; high prevalence in tumours < 2cm and early stage tumour or radiological undetectable
  25. 25. ASCENDING CHOLANGITIS • Acute cholangitis results from bacterial superimposed infection on biliary obstruction. The infection ascends into the hepatic duct causing serious infection. The classical triad – Charcot triad- RUQ pain, fever, and jaundice. A pentad – Raynold’s pentad- in which alter sensorium and hypotension is added to the triad. • Most common organisms; E coli, Klebsiella, Enterococcus, Streptococcus, Enterobacter, Pseudomonas aeruginosa • Treatment involve iv fluids, antibiotics, analgesics then non-surgical decompression (ERCP or PTC).
  26. 26. HEPATORENAL SYNDROME • Renal failure occurring in the setting of a Hepatic disease. It is an acute, progressive, oliguric renal failure occurring in the absence of any other apparent clinical cause. • Cause of Hepatorenal Syndrome in Obstructive Jaundice • Extracellular water depletion • Gram negative endotoxaemia • Myocardial dysfunction • Increased plasma level of atrial natriuretic peptide (ANP) • Bile deposit in the renal tubules
  28. 28. LABORATORY • URINALYSIS • Presence of bilirubin in the urine • Absent urobilinogen
  29. 29. • LIVER FUNCTION TEST • Alkaline phosphatase(ALP); markedly elevated (heat stable type) The value is not specific to cholestasis, however, to determine if the value is hepatic in origin, measure GGT or 5’ nucleotedase. These values parallel that of ALP in liver disease. • The values are usually morethan 3X the upper limit of the reference range, and most typically > 5X the upper limits. • Values < 3X the upper limits indicate partial obstruction or intrahepatic obstruction
  30. 30. • AST and ALT • Are not elevated unless secondary parenchymal damage • Mild to moderate elevation (<10X the upper limit of the reference range) • Occassionally markedly elevated in cholangitis • A ≥ 3X increase in ALT strongly suggest pancreatitis • ALT predominates in the liver and more specific than AST • GGT • Levels parallel the level of ALP and 5’-nucleotidase • More sensitive • The levels would distinguish hepatobiliary disease as a cause of isolated ALP elevation.
  31. 31. • CLOTTING PROFILE • PT is prolonged • NB; parenteral administration of Vitamin K improves PT, unlike in hepatocellular failure. • Other laboratory tests • Hepatitis serology • Antimicrobial antibody level • FBC • U/ECR • FBS • GXM
  32. 32. IMAGING STUDIES • ULTRASONOGRAPHY • Accuracy is close to 95% • Dilated CBD > 10mm • Dilated intrahepatic duct > 4mm • Distended gall bladder. • Pancreatic mass. • Has limited ability in detecting specific causes • Poorly visualize the CBD and cystic duct due to intervening bowel.
  33. 33. • ABDOMINAL CTSCAN • More accurate in determining the cause • Visualizes structures more consistently than the USS • Determine the involvement of the SMV, portal vein
  34. 34. ABD CTSCAN Demonstrate a resectable pancreatic adenocarcinoma of the head of pancreas with SMV abutment of less than 180⁰ and a clear fat plane between the tumour and the SMA NCCC definition of a resectable tumour; any tumour with ≤ 180⁰ contact of the superior mesenteric –portal vein but without any vein contour irregularity
  35. 35. Outline of the pancreas with a tumour of the head
  36. 36. Locally advanced disease with obliteration of the SMV Locally advance is defined as tumour > 180⁰ contact with the SMA, CA or 1st jejunal branch of the SMA No technical option for reconstruction
  37. 37. A borderline resectable pancreatic adenocarcinoma with SMV abutment of approximately 180⁰ and subtle haziness posterior to the SMA. Borderline are group of patient at high risk for margin positive and for whom neoadjuvant therapy should be considered Definitions; • ≤ 180⁰ contact with the SMA • >180⁰ contact with the SMV-PV • ≤180⁰ contact with the SMV-PV with irregularity or thrombus amenable to resection and reconstruction
  38. 38. • MRCP • Non invasive and sensitive method of visualizing pathologies of the hepatobiliary system • Better able to determine the type and extent of tumour than ERCP • Does not require contrast • Unlike ERCP has only diagnostic potential rather than therapeutic
  39. 39. MRCP
  40. 40. MRCP
  41. 41. INVASIVE PROCEDUES • ERCP (Endoscopic retrograde cholangiopancreatography) • It is especially useful in lesions distal to bifurcation of the hepatic duct • Has diagnostic and therapeutic application • Obstruction can be relieved by removal of stones, sphincterotomy, placement of stent and drains • Allows for brush cytology • Has limited capacity to image site proximal to the site of obstruction • Cannot be performed in altered anatomy that prevent access to the ampulla e.g Roux loop Complications; pancreatitis, perforation, biliary peritonitis, sepsis, hemorrhage, stricture
  42. 42. ERCP
  43. 43. • PTC (Percutaneous transhepatic cholangiogram) • Especially useful in lesions proximal to the common hepatic duct • Has both diagnostic and therapeutic application • Can be used to decompress the biliary system • The liver is punctured to enter the peripheral intrahepatic bile system. • Iodine based contrast medium is injected into the biliary system. • Performed under fluoroscopic guidance • ERCP still preferred, it is reserved for failed ERCP or altered anatomy preclude assess to the ampulla. • Complications; reaction to contrast, peritonitis, hemorrhage, sepsis, cholangitis, subphrenic abscess, lung collapse.
  44. 44. PTC
  45. 45. PREOPERATIVE CARE 1. Coagulation: • Vitamin K iv 10mg 0.d 5/7 until INR = 1.3 • If > 1.3 give FFP 4units pre – op. 2. Reduced glycogen stores: iv dextrose 10% IL 0.d 3. Infection; • Prophylactic antibiotics. • Quinolones. 4. Endotoxemia • Lactulose • Oral Bile acid. • Metronidazole 5. Hepatorenal syndrome • Iv fluids • Mannitol • Achieve a urine output > 60ml/hour. 6. Nutritional problems. • Avitaminosis – give pabrinex 1 and 2 • Calories – give Iv dextrose 10% • Serum protein – High pro diet Iv nutrition. 7. Pruritus – cholestyramine/Antihistamine
  46. 46. TREATMENT • Treatment depends on the cause; • Stone in the biliary tract • Cholecytectomy + common bile duct exploration • ERCP • Biliary stricture • Roux-en Y hepatico-jejunostomy • Stenting for short stricture
  47. 47. • Periampullary and pancreatic head tumours • Early – whipple procedure • Late • Endoscopic biliary stenting • Percutaneous transhepatic endobiliary radiofrequency ablation + stent • Photodynamic therapy (PDT) + stent • Bypass procedure; triple bypass, double bypass. • Cholecysto-jejunostomy/choledoco-jejunostomy • Gastro-jejunostomy • Jejuno-jejunostomy • Liver transplant; ESLD, PSC, HCC, Secondary biliary cirrhosis and portal hypertension, congenital biliary atresia
  48. 48. PROGNOSIS • Better with benign causes of obstruction • Poor prognosis for malignant causes • Upto 90% die within the first year of diagnosis (especially proximal tumours) • Prognosis is better with distal tumours
  49. 49. REFERENCES • 1. Long W, Wei-Feng Y. Obstructive and perioperative management. Acta Anaesthesiology Taiwanica 2014;52: 22-29. • 2. Jennifer LB. (2019, October 16). Biliary obstruction. Retrieve from https://www.emedicine.Medscape.com • 3. NCCN Guidelines. Pancreatic cancer, 2019. • 4. Rahul P et al. New-onset diabetes: A potential clue to the early diagnosis of pancreatic cancer. Lancet Oncol. 2009; 10(1);88-95