Obstructive jaundice.pptx

Surgical jaundice

1. OBSTRUCTIVE JAUNDICE By De Pope 7/16/2023 De Pope 1

2. OUTLINE INTRODUCTION AETIOLOGY PATHOPHYSIOLOGY CLINICAL FEATURES INVESTIGATIONS PRE-OPERATIVE TREATMENT TREATMENTS PROGNOSIS 7/16/2023 De Pope 2

3. INTRODUCTION Is the yellowish discoloration of the skin, mucus membranes and sclera due to hyperbilirubinea . Obstructive jaundice is caused by conditions that block the normal flow of bile from the liver into the intestines G allstones are the most common cause of biliary obstruction followed by cancer of the head of the pancreas Normal serum bilirubin level is 0.2 - 1 mg/dl of which no more than 0.2 mg/dl are directly reacting. 7/16/2023 De Pope 3

4. Continua………… 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. 7/16/2023 De Pope 4

5. AETIOLOGY Intraluminal causes: Choledocholithiasis Clonorchis sinensis Ascariasis & Schitosomiasis Mural causes: Malignant stricture cholangiocarcinoma Benign stricture Scelerosing cholangitis Extrinsic Causes: Ca Head of Pancreas Periampullary Carcinoma, Portal LN 7/16/2023 De Pope 5

6. BENJAMIN’S CLASSIFICATION Type 1 ( complete obstruction ) Primary or secondary liver tumors Iatrogenic ligation of CBD Pancreatic tumors, cholangiocarcinoma Type 2 ( intermittent obstruction ) Choledocholithiasis Periampullary tumor Choledochal cyst Bile duct papilloma Hemobilia , Duodenal diverticula Type 3 ( chronic complete obstruction) Bile duct stricture Biliary atresia Post radiotherapy Chronic pancreatitis Cystic fibrosis Type 4 ( segmental obstruction) Sclerosing cholangitis Traumatic Hepatolithisis 7/16/2023 De Pope 6

7. DIFFERENT CAUSES 7/16/2023 De Pope 7

8. PATHOPHYSIOLOGY 7/16/2023 De Pope 8

9. Continua…….... 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 . 12Hrs Biliary obstruction prevents carriage of bile to the small intestine 7/16/2023 De Pope 9

10. Continua……… 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 7/16/2023 De Pope 10

11. Continua…………. 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. 7/16/2023 De Pope 11

12. 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 7/16/2023 De Pope 12

13. Continua……… 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. 7/16/2023 De Pope 13

14. Continua………. 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 7/16/2023 De Pope 14

15. Continua……… 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 7/16/2023 De Pope 15

16. Continua……….. 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 7/16/2023 De Pope 16

17. Continua………. COAGULATION FACTOR DEFECTS Prolongation of Prothrombin time Decreased absorption of fat soluble vitamins A,D,E,K (vitamin K dependent clotting factors not formed- II, VII, IX and X ) Endotoxin induced damage to factor XI ,XII ,platelets Low grade DIC with increased fibrin degradation products ITCHING Retained bile salts stimulate nerve endings. Other theory: Due to endogenous opiate peptides Inducing opiod receptor mediated scratching activity of central origin 7/16/2023 De Pope 17

18. CLINICAL PRESENTATION 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. 7/16/2023 De Pope 18

19. 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, New onset type2 DM Progressive deepening jaundice associated with ca pancreas. Gall-bladder is palpably enlarged, Courvoisier’s Sign strongly suggests a malignant obstruction at the lower end of the common bile-duct, but its absence does not exclude this. 7/16/2023 De Pope 19

20. SUGGESTING AMPULLARY CA F luctuating obstructive jaundice (necrosis of the tumour with sloughing with temporary relief of jaundice). Silver coloured stools Weight loss and pain is a late feature 7/16/2023 De Pope 20

21. 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 7/16/2023 De Pope 21

22. 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 7/16/2023 De Pope 22

23. SUGGESTING HEPATOMA A large, hard, irregular liver A bruit is often present Ascites is common, and is often bloodstained. 7/16/2023 De Pope 23

24. 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 7/16/2023 De Pope 24

25. COMPLICATIONS ASCENDING CHOLANGITIS HEPATORENAL SYNDROME HYPOGYCEMIA ANAEMIA MALNUTRITION 7/16/2023 De Pope 25

26. 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). 7/16/2023 De Pope 26

27. 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 7/16/2023 De Pope 27

28. Sclera of the patient with obstructive jaundice is greenish yellow in colour . 7/16/2023 28 VIRCHOW`S NODE Or troisier’s sign BRUISING VIT.K DEF. De Pope

29. Urine in obstructive jaundice 7/16/2023 29 De Pope

30. INVESTIGATIONS LABORATORY IMAGING INVASIVE PROCEDURES 7/16/2023 De Pope 30

31. LABOROTORY URINALYSIS Presence of bilirubin in the urine Absent urobilinogen LIVER FUNCTION TEST Hepatic causes of jaundice (such as hepatocellular injury from hepatitis) are usually nonsurgical problems, whereas posthepatic causes (such as biliary obstruction from acute cholangitis) are typically surgical. Distinguishing between the two is not always straightforward. Both will have some degree of elevation in total bilirubin, AST, ALT, gammaglutamyl transpeptidase (GGT), and AP . 7/16/2023 De Pope 31

32. Continua………  AST and ALT are enzymes within the liver cells (though AST is also found in muscle and other cells). With hepatocellular injury, these enzymes are released. AP is present in the cells that line the bile ducts. A marked rise in ALP, out of proportion to the AST and ALT, is therefore indicative of posthepatic (biliary obstruction) pathology such as tumors or choledocholithiasis . 7/16/2023 De Pope 32

33. Continua………. 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 7/16/2023 De Pope 33

34. 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. 7/16/2023 De Pope 34

35. Continua……… ABDOMINAL CTSCAN: More accurate in determining the cause Visualizes structures more consistently than the USS Determine the involvement of the SMV, portal vein 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 7/16/2023 De Pope 35

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37. 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. 7/16/2023 De Pope 37

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39. Continua………….. 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. 7/16/2023 De Pope 39

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41. PREOPERATIVE CARE Coagulation : Vitamin K iv 10mg 0.d 5/7 until INR = 1.3, If > 1.3 give FFP 4units pre – op. Reduced glycogen stores: iv dextrose 10% IL 0.d Infection; Prophylactic antibiotics-Quinolones. 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 7/16/2023 De Pope 41

42. 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 7/16/2023 De Pope 42

43. 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 7/16/2023 De Pope 43

44. 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 7/16/2023 De Pope 44

45. W hipple’s operation in early ca head of the pancreas 7/16/2023 45 De Pope

46. STENT for ca head of the pancreas 7/16/2023 46 De Pope

47. Post op mgt Monitoring with prothrombin time, bilirubin, albumin, creatinine , electrolyte estimation. FFP or blood transfusion. Antibiotics. Observation for septicaemia , haemorrhage , pneumonia, pleural effusion, bile leak. Care of T-tube and drains. T-tube cholangiogram in 10-14 days. TPN, CVP line, nasogastric tube, urinary catheter. 7/16/2023 47 De Pope

48. Complications (secondary to causes above) Steatorrhea Bleeding tendencies Malabsorption Pancreatis due to the stone Cholangitis etc 7/16/2023 48 De Pope