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Obstructive jaundice

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Ankur Kajal

patho -physiology and workup of surgical jaundice

Health & Medicine
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OBSTRUCTIVE JAUNDICE PATHOPHYSIOLOGY AND WORKUP
DEFINITION Failure of normal amount of bile to reach intestine due to mechanical obstruction of the extra hepatic biliary tree or within the porta hepatis
JAUNDICE â–ȘJaundice (derived from French word ‘jaune’ for yellow) or icterus (Latin word for Jaundice) â–ȘYellowing of sclera at 3 mg% â–ȘBilirubin has got high affinity for elastin and sclera has high elastin content â–ȘYellowing of skin and mucous membrane at 6 mg% â–ȘD/D beta carotenemia,Quinacrine therapy malingering with picric acid â–ȘThey doesn’t stain mucous membrane and sclera â–ȘBilirubin level rise upto three weeks than stabilise
BILIRUBIN METABOLISM
PHYSIOLOGICAL FACTS â–ȘTotal bile flow-600ml/day(500-1000ml/day) â–ȘHepatocyte component is -450ml/day â–ȘCholangiocyte component-150ml/day â–ȘIt depends on secretin stimulation â–ȘTotal serum bilirubin is 0.3-1.2 mg/dl â–ȘWith conjugated bilirubin<15 %
PHYSIOLOGY OF OBSTRUCTION â–ȘNormal secretory pressure of bile is 15-25 cm of water â–ȘAt 35 cm of water there is suppression of bile flow â–ȘHigh pressure leads to cholangiovenous and cholangiolymphatic reflux of bile â–ȘDilatation of bile duct and intra hepatic biliary radicals(IHBR) â–ȘIHBR dilatation may be absent if there is secondary hepatic fibrosis or cirrhosis
PATHOPHYSIOLOGY â–ȘIncrease in biliary pressure leads to â–ȘDisruption of tight junctions between hepatocytes and bile duct cells with increased permeability â–ȘReflux of bile contents in liver sinusoids â–ȘNeutrophil infiltration,increased fibrinogenesis and deposition of reticulin fiberes in portal triad â–ȘReticulin fibers gets converted in to type 1 collagen â–ȘLaying down of collagen fibers leads to hepatic fibrosis obstruction of sinusoids and secondary biliary cirrhosis and portal hypertension â–ȘFibrosis can also lead to atrophy of obstructed liver
EFFECTS OF OBSTRUCTIVE JAUNDICE ON VARIOUS SYSTEMS
CHANGES IN LIVER BLOOD FLOW â–ȘAcute obstruction â–Ș increase in hepatic arterial blood flow â–ȘNo change in portal venous blood flow â–ȘChronic obstruction â–ȘDecrease in total liver blood flow , dilatation of sinusoids and elevation of portal pressure
CARDIOVASCULAR EFFECTS â–ȘDecreased cardiac contractability â–ȘReduced left ventricular pressure â–ȘImpaired response to beta agonist drugs â–ȘDecreased peripheral vascular resistance â–ȘBradycardia due to direct effect of bile salts on SA node. Net result â–ȘHypotensive patient â–ȘExaggerated hypotensive response to bleeding â–ȘMore prone to postoperative shock
RENAL FAILURE â–Ș10 % incidence with 70 % mortality â–ȘFactors responsible are â–ȘDecresed cardic function â–ȘIncreased levels of ANP resulting in hypovolemia â–ȘDecreased effect of bile salts on kidney mediated by increased prostaglandin E2 â–ȘEndotoxemia â–ȘResulting in â–ȘRenal vasoconstriction â–ȘShunting of blood from cortex â–ȘActivation of complement system peritubular and glomerular fibrin deposition leading to tubular and cortical necrosis
IMMUNE SYSTEM â–ȘDefects in cellular immunity â–ȘImpaired T cell proliferation â–ȘDecreased neutophil chemotaxis â–ȘDefective bacterial phagocytosis â–ȘDepressed function of RE system ie Kupffer cells
WOUND HEALING â–ȘDelayed wound healing â–ȘHigh incidence of wound dehiscence â–ȘDecresed activity of enzyme Propyl hydroxylase in the skin â–ȘThis helps in incorporation of proline in collagen â–ȘDefective synthesis of collagen
COAGULATION FACTOR DEFECTS â–ȘProlongation of Prothrombin time â–ȘLoss of calcium â–ȘEndotoxin induced damage to factor XI ,XII ,platelets â–ȘLow grade DIC with increased fibrin degradation products â–ȘThrombocytopenia from hyperspleenism â–ȘDecreased absroption of fat solube vitamins A,D,E,K
ITCHING â–ȘRetained bile salts â–ȘItching disappears in terminal liver failure but bile salt level still increased â–ȘOther theory â–ȘDue to endogenous opiate peptides â–ȘInducing opiod receptor mediated scratching activity of central origin
BIOCHEMICAL EFFECTS â–ȘBilirubin â–ȘRise by 25-43 micromol/litre/day â–ȘMechanism of hyperbilirubinemia â–ȘBiliary venous & biliary regurgitation of conjugated bilirubin due to disruption of tight intracellular junction â–ȘTrans hepatocytic regurgitation due to reversal of the secretory polarity of hepatocytes â–ȘRupture of dilated canaliculi in to sinusoids due to necrosis of hepatocytes
ALKALINE PHOSPHATSE â–ȘMost sensitive indicator â–ȘFactor responsible are â–ȘBiliary component regurgitation â–ȘIncrease in hepatic synthesis
Why Bilirubin levels plateau â–ȘIncreased excretion of bile pigments by kidney by products other than bilirubin not giving DIAZO reaction â–ȘA portion get covalently bounded to serum albumin â–ȘThis protein bound bilirubin-Delta bilirubin,is not measurable by routine technique
HISTORY AND CLINICAL EXAMINATION
HISTORY â–ȘPrevious dyspepsia, fat intolerance â–ȘJaundice- onset, course, itching â–ȘPain â–ȘPyrexia â–ȘWeight loss â–ȘDark urine and clay coloured stools â–ȘTravel to endemic area â–ȘContact with jaundice patient â–ȘHistory of upper abdominal operation â–ȘDrug intake ie ATT â–ȘHistory of injection in preceding six months
CLINICAL EXAMINATION â–ȘAge â–ȘAnaemia - hemolysis, cancer , cirrhosis â–ȘGross weight loss-malignancy â–ȘHunched up position-chronic pancreatitis or ca pancreas â–ȘFetor, flapping tremors,personality changes-impending hepatic coma â–ȘSkin changes-Bruising,purpuric spots,spider naevi,palmar erythema,white nails,loss of secondary sexual characters
ABDOMINAL EXAMINATION â–Ș Dilated peri umbalical veins- cirrhosis & portal collateral circulation â–ȘAscitis-Cirrhosis or malignant disease â–ȘNodular liver â–ȘCourvoisier’s Law-palpable non tender gall bladder in jaundice patient-malignant biliary obstruction â–ȘExceptions â–ȘDouble impaction of stones â–ȘImpaction of pancreatic calculus at ampulla of vater â–ȘMirizzi syndrome
BIOCHEMICAL INVESTIGATIONS â–ȘRoutine investigations-Hb,TLC,DLC, Blood sugar, RFT ,Serum electrolytes â–ȘUrinary bilirubin,Urobilinogen â–ȘSerum Bilirubin-Total and Direct â–ȘSGOT,SGPT,ALP.GGTP and 5- Nucleotidase â–ȘPT and Serum Albumin
ALKALINE PHOSPHATSE(ALP) â–ȘALP levels are elevated in nearly 100 % of patients with extra hepatic obstruction except in some cases of intermittent obstruction. â–ȘValues usually greater than 3 times the upper limit of reference range, and in most typical cases, they exceed 5 times the upper limit. â–Ș An elevation less than 3 times the upper limit is evidence against complete extra hepatic obstruction.
AST and ALT â–ȘSerum enzymes that provide evidence of hepato cellular damage.ALT found primarily in the liver, where as AST also found in heart ,kidney, skeletal muscle and brain â–ȘAST is less specific for liver function. The levels of AST and ALT should be done simultaneously since ALT can confirm the hepatic origin of the less specific but more sensitive AST. â–ȘIn extra hepatic obstruction usually AST levels are not elevated(< 10 times the upper reference limit)
GAMMA –GLUTAMYL TRANSPEPTIDASE(GGTP) â–ȘCorrelates with ALP level â–ȘMost sensitive indicator of biliary tract disease â–ȘBetter indicator of obstruction in children – levels are independent of age â–ȘHelpful in the diagnosis of acute biliary tract obstruction in contrast to ALP because ALP requires synthesis of fresh ALP and hence lags behind the onset of obstruction
5- NUCLEOTIDASE â–ȘThe principal value is to confirm the hepatic origin of an elevated ALP â–ȘThis is particularly helpful in children, pregnant women and patients who may have bone disease resulting in rise of ALP â–ȘIt is more useful than ALP/GGTP in detecting hepatic metastasis
OTHER LAB INVESTIGATIONS â–ȘProthrobin time â–ȘSerum albumin â–ȘStool for occult blood â–ȘPresence of occult blood in the stools of a patient with jaundice must raise the suspicion of malignancy.
Obstructive jaundice Medical jaundice Serum Bilirubun â–Ș conjugated â–Ș unconjugated +++ + + +++ Urobilinogen ↓ ↑ Urinary Bilirubin + 0 Urinary Bile salts + 0 Serum ALP ↑ No change Serum GGTP ↑ No change Serum 5-nucleotidase ↑ No change Transaminases Mildly raised Markedly raised
ETIOLOGY
TYPES OF BILIARY OBSTRUCTION â–ȘComplete obstruction â–ȘIntermittent obstruction â–ȘChronic incomplete obstruction â–ȘSegmental obstruction
INTERMITTENT OBSTRUCTION â–Ș Symptoms and typical biochemical changes â–ȘClinically jaundice may or may not be present â–ȘCauses â–ȘCBD stones â–ȘPeriampullary tumours â–ȘDuodenal diverticulum â–ȘCholedochal cyst â–ȘBiliary parasites â–Șhemobilia
CHRONIC INCOMPLETE OBSTRUCTION â–ȘWith or without classical symptoms or biochemical changes â–ȘPathological changes in bile ducts or liver â–ȘCauses â–ȘStrictures of CBD â–ȘStenosis of biliary-enteric anastamosis â–ȘChronic pancreatitis â–ȘCystic fibrosis â–ȘSphincter of oddi stenosis
SEGMENTAL OBSTRUCTION â–Ș one or more segment of intrahepatic biliary tract obstructed â–ȘCauses â–ȘTraumatic â–ȘIntrahepatic stones â–ȘSclerosing cholangitis â–ȘCholangiocarcinoma
BILIARY OBSTRUCTION INTRINSIC â–Ș Ductal calculi Primary - Develop de novo in bile ducts Secondary - Migrate from gall bladder â–Ș Acute Cholangitis â–Ș Biliary Strictures Idiopathic Iatrogenic â–Ș Sclerosing Cholangitis â–Ș Parasites â–Ș Haemobilia â–Ș Benign Biliary Tumours â–Ș Cholangiocarcinoma â–Ș Carcinoma of ampulla of vater and Periampullary tumours â–Ș Intraductal secondary tumour seeding
BILIARY OBSTRUCTION EXTRINSIC â–Ș Mirizzi syndrome â–Ș Pancreatitis- acute and chronic â–Ș Pancreatic pseudocyst â–Ș Carcinoma of gall bladder â–Ș Carcinoma of pancreas â–Ș Cystic tumours of pancreas â–Ș Metastatic carcinoma â–Ș Hepatocellular carcinoma
BILIARY OBSTRUCTION CONGENITAL AND GENETIC DISORDERS â–Ș Biliary atresia â–Ș Choledocal cyst â–Ș Caroli’s disease â–Ș Progressive familial intra hepatic cholestasis â–Ș Primary biliary cirrhosis â–Ș Alpha 1 antitrypsin defeciency â–Ș Tyrosinemia â–Ș Neonatal hepatitis â–Ș Wilson disease â–Ș Others - dyskinesia of sphincter of odi
IMAGING GOALS â–ȘTo confirm the presence of an extrahepatic obstruction â–ȘTo determine the level of the obstruction, to identify the specific cause of the obstruction â–ȘTo provide complementary information relating to the underlying diagnosis (eg., Staging information in cases of malignancy).
Ultrasonography Ultrasound of the abdomen is an extremely useful and accurate method for identifying gallstones and pathologic changes in the gallbladder consistent with acute cholecystitis. Abdominal ultrasound, if performed by an experienced operator, should be part of the routine evaluation of patients suspected of having gallstone disease, given the high specificity (>98%) and sensitivity (>95%) of this test for the diagnosis of cholelithiasis[1] ( Table 54-1 ). In addition to identifying gallstones, ultrasound can also detail signs of cholecystitis such as thickening of the gallbladder wall, pericholecystic fluid, and impacted stone in the neck of the gallbladder. It is often the initial screening test for patients with suspected extrahepatic biliary obstruction ( Fig. 54-7 ). Dilation of the extrahepatic (>10 mm) or intrahepatic (>4 mm) bile ducts suggests biliary obstruction. Intraoperative ultrasound is now used frequently to further evaluate intrahepatic lesions, assess resectability, and determine involvement of vascular structures
. MAGNETIC RESONANCE CHOLANGIOPANCREATOGRAPHY (MRCP) ‱Noninvasive test to visualize the hepato biliary tree ‱No contrast ‱Fluid found in the biliary tree is hyper intense on T2-weighted images. Surrounding structures do not enhance and can be suppressed during image analysis. ‱Sensitive in detecting biliary and pancreatic duct stones, strictures, or dilatations within the biliary system. ‱MRCP combined with conventional MR imaging of the abdomen can provide information about surrounding structures (eg, pseudocysts, masses). ‱ ERCP and MRCP similarly effective in detecting malignant hilar and perihilar obstruction ‱ MRCP is better able to determine the extent and type of tumor as compared to ERCP
Absolute contraindications â–Șcardiac pacemaker â–Șcerebral aneurysm clips â–Șocular or cochlear implants â–ȘFluid stasis in the adjacent duodenum or ascitic fluid may produce image artifacts on MRCP, making it difficult to clearly visualize the biliary tree.
ENDOSCOPIC ULTRASOUND (EUS) â–ȘCombines Endoscopy and US â–ȘHigher-frequency ultrasonic waves compared to traditional US (3.5 mhz vs 20 mhz) and allows diagnostic tissue sampling via EUS-guided fine-needle aspiration (EUS-FNA). â–ȘEUS has been reported to have up to a 98% diagnostic accuracy in patients with obstructive jaundice â–ȘThe sensitivity of EUS for the identification of focal mass lesions in pancreas has been reported to be superior to that of CT scanning, both traditional and spiral, particularly for tumors smaller than 3 cm in diameter. â–ȘCompared to MRCP for the diagnosis of biliary stricture, EUS has been reported to be more specific (100% vs 76%) and to have a much greater positive predictive value (100% vs 25%), although the two have equal sensitivity (67%). â–ȘThe positive yield of eus-fna for cytology in patients with malignant obstruction has been reported to be as high as 96%.
Investigations Metastasis poor Surgical risks No metastasis Good Surgical Risks Non operative procedures Operative Procedures Non resectable tumours Resectable tumours Biliary – enteric Bypass Surgically placed stents Percutanesly placed Stents Endoscopically placed stents Palliative resection Curative resection Malignant Obstructive jaundice
WORKUP AND MANAGEMENT OF POSTHEPATIC JAUNDICE three possible clinical scenarios:DUCTAL OBSTRUCTION SUSPECTED CHOLANGITIS SUSPECTED CHOLEDOCHOLITHIASIS WITHOUT CHOLANGITIS SUSPECTED LESION OTHER THAN CHOLEDOCHOLITHIASIS
SUSPECTED CHOLANGITIS â–ȘA clinical picture compatible with acute suppurative cholangitis (charcot's triad or raynaud's pentad) the most likely diagnosis is choledocholithiasis. â–ȘAppropriate resuscitation, correction of any coagulopathies if present, and administration of antibiotics â–ȘERCP is indicated for diagnosis and treatment â–ȘIf ERCP is unavailable or is not feasible (e.g., Because of previous roux-en-y reconstruction), transhepatic drainage or surgery may be necessary â–ȘMainstay of treatment of severe cholangitis is not just the administration of appropriate antibiotics but rather the establishment of adequate biliary drainage.
SUSPECTED CHOLEDOCHOLITHIASIS WITHOUT CHOLANGITIS â–ȘCholedocholithiasis is the most common cause of biliary obstruction. â–ȘStrongly suspected if the jaundice is episodic or painful or if usg has shown presence of gallstones or bile duct stones. â–ȘPatients with suspected cbd stones should be referred for lap cholecystectomy with either preoperative ERCP, intra operative cholangiography â–ȘPreoperative ERCP in this setting of jaundice is prefered â–ȘDiagnostic yield is high â–Ș Therapeutic-clearing the CBD of stones in 95% of cases. â–ȘMany authors, however favor fully laparoscopic approach, in which CBD stone is detected in the OR by means of intraoperative cholangiography and laparoscopic biliary clearance is performed when choledocholithiasis is confirmed. â–Ș The optimal approach in a particular setting should be dictated by local expertise.
SUSPECTED LESION OTHER THAN CHOLEDOCHOLITHIASIS â–ȘNo gallstones are seen â–ȘClinical presentation is less acute (e.g., constant abdominal or back pain) â–ȘAssociated constitutional symptoms (e.g., weight loss, fatigue, and long-standing anorexia) â–ȘPossible causes of may be classified into three categories depending on the location of the obstructing lesion â–Șthe upper third of the biliary tree â–Șthe middle third â–Ș the lower (distal) third
Upper-third obstruction â–Ș Polycystic liver disease â–Ș Caroli diseas â–Ș HCC â–Ș Oriental cholangiohepatitis â–Ș Hemobilia(e.g.,afterbiliarymani pulation) â–Ș Iatrogenic bile duct injury â–Ș Cholangiocarcinoma (Klatskin'stumor) â–Ș Sclerosing cholangitis â–Ș Papillomas of the bile duct Mid-third obstruction â–ȘCholangiocarcinoma â–ȘSclerosing cholangitis â–ȘPapillomas of the bile duct â–ȘGallbladder cancer â–ȘCholedochal cyst â–ȘIntrabiliary parasites â–ȘMirizzi syndrome â–ȘExtrinsic nodal compression (e.g., lymphoma) â–ȘIatrogenic bile duct injury â–ȘCystic fibrosis â–ȘBenign idiopathic bile duct stricture Lower-third obstruction â–ȘCholangiocarcinoma â–ȘSclerosing cholangitis â–ȘPapillomas of the bile duct â–ȘPancreatic tumors â–ȘAmpullary tumors â–ȘChronic pancreatitis â–ȘSphincter of Oddi dysfunction â–ȘPapillary stenosis â–ȘDuodenal diverticula â–ȘPenetrating duodenal ulcer â–ȘRetroduodenal adenopathy (e.g., lymphoma, carcinoid ETIOLOGY
DIAGNOSIS AND ASSESSMENT OF RESECTABILITY â–ȘInvolvement of the SUPERIOR MESENTERIC VEIN, THE PORTAL VEIN, THE SUPERIOR MESENTERIC ARTERY, and the PORTA HEPATIS and on whether there is evidence of significant LOCAL ADENOPATHY or EXTRAPANCREATIC EXTENSION OF TUMOR indicates UNRESECTABILITY â–ȘThe majority of lesions will be clearly unresectable, either because of tumor extension or because of the presence of hepatic or peritoneal metastases
NON OPERATIVE MANAGEMENT DRAINAGE PROCEDURES
â–ȘIn the majority of patients with malignant obstructions, treatment is palliative rather than curative. â–ȘCholangiography and decompression of obstructed biliary system â–ȘIn the absence of preexisting or concomitant hepatocellular dysfunction, drainage of one half of the liver is generally sufficient for resolution of jaundice
â–ȘRoutine preoperative drainage of an obstructed biliary system does not benefit patients who will soon undergo resection.1,2 â–ȘThere is evidence suggesting that in patients with either pancreatic 3,4 or hepatic malignancies, routine preoperative direct cholangiography with decompression is associated with a higher incidence of postoperative complications when tumor resection is ultimately carried out. 1. Pitt HA, Gomes AS, Lois JF: Does preoperative percutaneous biliary drainage reduce operative risk or increase hospital cost? Ann Surg 201:545, 1985 2. McPherson GA, Benjamin IS, Hodgson HJ, et al: Preoperative percutaneous transhepatic biliary drainage: results of a controlled trial. Br J Surg 71:371, 1984 3. Povoski SP, Karpeh MS Jr, Conlon KC, et al: Preoperative biliary drainage: impact on intraoperative bile cultures and infectious morbidity and mortality after pancreaticoduodenectomy. J Gastrointest Surg 3:496, 1999 4. Sohn TA, Yeo CJ, Cameron JL, et al: Do preoperative biliary stents increase postpancreaticoduodenectomy complications? J Gastrointest Surg 4:258, 2000
OPERATIVE MANAGEMENT AT SPECIFIC SITES BYPASS AND RESECTION
UPPER-THIRD OBSTRUCTION PALLIATION. â–ȘBecause the left hepatic duct has a long extrahepatic segment and is more accessible, the preferred bypass -is a left hepaticojejunostomy â–Ș Laparoscopic bypass techniques that make use of segment 3 have been developed, but their performance has yet to be formally assessed
RESECTION FOR CURE â–ȘThe hilar plate is taken down to lengthen the hepatic duct segment available for subsequent anastomosis. â–ȘA formal hepatectomy or segmentectomy is required to ensure an adequate proximal margin of resection â–Ș If the resection is carried out proximal to the hepatic duct bifurcation, several cholangiojejunostomies have to be done to anastomose individual hepatic biliary branches. â–ȘThe results of aggressive hilar tumor resections that included as much liver tissue as was necessary to obtain a negative margin appear to justify this approach. â–Ș In cases of left hepatic involvement, resection of the caudate lobe is indicated as well.
MIDDLE-THIRD OBSTRUCTION Palliation. â–ȘSurgical bypass of middle-third lesions is technically simpler â–Ș Hepaticojejunostomy is done distal to the hepatic duct bifurcation, â–Ș Exposure of the hilar plate or the intrahepatic ducts is unnecessary. Resection for cure. â–ȘTumors in this part usually quite amenable to resection along with the lymphatic chains in the porta hepatis. â–ȘMirizzi syndrome -extrinsic obstruction of the CBD, either by causing inflammation of the gallbladder wall or via direct impingement. â–ȘTreatment of this syndrome - Hepaticojejunostomy
Lower-third obstruction Palliation â–Ș The preferred bypass technique for lower-third lesions is a Roux-en-Y choledochojejunostomy. â–Ș Cholecystojejunostomy carries a higher risk of complications and subsequent development of jaundice Resection for cure. â–Ș Resection of a lower-third lesion usually involves a pancreaticoduodenectomy though transduodenal ampullary resection may be an acceptable alternative for a small adenoma of the ampulla â–ȘFor optimal results, pancreaticoduodenectomy is best performed in specialized centers. â–Șpostoperative adjuvant therapy may improve the prognosis after resection of a pancreatic adenocarcinoma
PALLIATION IN PATIENTS WITH ADVANCED MALIGNANT DISEASE â–ȘWhen a patient has advanced malignant disease, drainage of the biliary system for palliation is not routinely indicated, because the risk of complications related to the procedure may outweigh the potential benefit â–ȘThe best treatment for a patient with asymptomatic obstructive jaundice and liver metastases may be supportive care alone. â–ȘBiliary decompression is indicated if cholangitis or severe pruritus interferes with quality of life. â–ȘStent placed with ercp to be the palliative modality of choice for advanced disease, â–ȘUpper-third lesions may be managed most easily through the initial placement of an internal/external catheter at the time of ptc.
â–ȘMetal expandable stents remain patent longer than large conventional plastic stents â–ȘRCTs suggest that surgical biliary bypass should be reserved for patients who are expected to survive for 6 months or longer because bypass is associated with more prolonged palliation at the cost of greater initial morbidity. â–ȘThe role of prophylactic gastric drainage at the time of operative biliary drainage remains controversial,101,102 â–Ș RCTs demonstrated a reduced incidence of subsequent clinical gastric outlet obstruction when this measure was employed. â–Ș When a pancreatic malignancy is present, intraoperative celiac ganglion injection should be performed for either prophylactic or therapeutic pain
POSTOPERATIVE JAUNDICE â–ȘThe development of jaundice in the postoperative setting is approximately 1% of all surgical patients after operation.120 â–ȘWhen jaundice occurs after a hepatobiliary procedure, â–ȘAttributable to specific biliary causes, â–ȘRetained cbd stones, â–ȘPostoperative biliary leakage (through reabsorption of bile leaking into the peritoneum) â–Ș injury to the cbd â–ȘDevelopment of biliary strictures
JAUNDICE WITHIN 48 HOURS OF THE OPERATION â–ȘBreakdown of rbc –due to multiple blood transfusions , â–ȘThe resorption of a large hematoma, â–ȘTransfusion reaction. â–ȘKnown underlying hemolytic anemia and may be precipitated specific drugs (e.G., Sulfa drugs in a patient who has G6PD deficiency). â–ȘGilbert syndrome may first manifest itself early in the postoperative period. â–ȘIntraoperative hypotension or hypoxemia or the early development of heart failure can lead to hyperbilirubinemia within 5 to 10 days after operation. â–ȘThe hyperbilirubinemia may be associated with other end-organ damage (e.G., Acute tubular necrosis). â–ȘImpairment of renal function causes a decrease in bilirubin excretion and can be responsible for a mild hyperbilirubinemia.
Jaundice developing 7 to 10 days after operation â–Ș In association with a medication-induced hepatitis attributable to an anesthetic agent. â–ȘIncidence of 1/10,000 after an initial exposure. â–ȘAdministration of antibiotics or other medications used in the perioperative setting â–ȘJaundice associated with intrahepatic cholestasis is often a manifestation of a sepsis, particularly in patients with mods â–Ș Jaundice may occur in as many as 30% of patients receiving total parenteral nutrition (tpn). â–ȘIt may be due to steatosis, particularly with formulas containing large amounts of carbohydrates. â–ȘDecreased export of bilirubin from the hepatocytes may lead to cholestasis â–ȘAcalculous cholecystitis or even ductal obstruction may develop as a result of sludge in the gallbladder and the cbd.
â–ȘUnsuspected hepatic or post-hepatic causes (e.G., Occult cirrhosis, choledocholithiasis, or cholecystitis) â–ȘA rare cause of postoperative jaundice is the development of thyrotoxicosis. â–ȘA diagnosis of exclusion- is so-called benign postoperative cholestasis, a primarily cholestatic, self-limited process with no clearly demonstrable cause that typically arises within 2 to 10 days after operation. â–ȘMechanism-combination of an increased pigment load, impaired liver function, and decreased renal bilirubin excretion caused by varying degrees of tubular necrosis. â–Ș The predominantly conjugated hyperbilirubinemia may reach 40 mg/dl and remain elevated for as long as 3 weeks.
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Obstructive jaundice

  • 2. DEFINITION Failure of normal amount of bile to reach intestine due to mechanical obstruction of the extra hepatic biliary tree or within the porta hepatis
  • 3. JAUNDICE â–ȘJaundice (derived from French word ‘jaune’ for yellow) or icterus (Latin word for Jaundice) â–ȘYellowing of sclera at 3 mg% â–ȘBilirubin has got high affinity for elastin and sclera has high elastin content â–ȘYellowing of skin and mucous membrane at 6 mg% â–ȘD/D beta carotenemia,Quinacrine therapy malingering with picric acid â–ȘThey doesn’t stain mucous membrane and sclera â–ȘBilirubin level rise upto three weeks than stabilise
  • 5. PHYSIOLOGICAL FACTS â–ȘTotal bile flow-600ml/day(500-1000ml/day) â–ȘHepatocyte component is -450ml/day â–ȘCholangiocyte component-150ml/day â–ȘIt depends on secretin stimulation â–ȘTotal serum bilirubin is 0.3-1.2 mg/dl â–ȘWith conjugated bilirubin<15 %
  • 6. PHYSIOLOGY OF OBSTRUCTION â–ȘNormal secretory pressure of bile is 15-25 cm of water â–ȘAt 35 cm of water there is suppression of bile flow â–ȘHigh pressure leads to cholangiovenous and cholangiolymphatic reflux of bile â–ȘDilatation of bile duct and intra hepatic biliary radicals(IHBR) â–ȘIHBR dilatation may be absent if there is secondary hepatic fibrosis or cirrhosis
  • 7. PATHOPHYSIOLOGY â–ȘIncrease in biliary pressure leads to â–ȘDisruption of tight junctions between hepatocytes and bile duct cells with increased permeability â–ȘReflux of bile contents in liver sinusoids â–ȘNeutrophil infiltration,increased fibrinogenesis and deposition of reticulin fiberes in portal triad â–ȘReticulin fibers gets converted in to type 1 collagen â–ȘLaying down of collagen fibers leads to hepatic fibrosis obstruction of sinusoids and secondary biliary cirrhosis and portal hypertension â–ȘFibrosis can also lead to atrophy of obstructed liver
  • 8. EFFECTS OF OBSTRUCTIVE JAUNDICE ON VARIOUS SYSTEMS
  • 9. CHANGES IN LIVER BLOOD FLOW â–ȘAcute obstruction â–Ș increase in hepatic arterial blood flow â–ȘNo change in portal venous blood flow â–ȘChronic obstruction â–ȘDecrease in total liver blood flow , dilatation of sinusoids and elevation of portal pressure
  • 10. CARDIOVASCULAR EFFECTS â–ȘDecreased cardiac contractability â–ȘReduced left ventricular pressure â–ȘImpaired response to beta agonist drugs â–ȘDecreased peripheral vascular resistance â–ȘBradycardia due to direct effect of bile salts on SA node. Net result â–ȘHypotensive patient â–ȘExaggerated hypotensive response to bleeding â–ȘMore prone to postoperative shock
  • 11. RENAL FAILURE â–Ș10 % incidence with 70 % mortality â–ȘFactors responsible are â–ȘDecresed cardic function â–ȘIncreased levels of ANP resulting in hypovolemia â–ȘDecreased effect of bile salts on kidney mediated by increased prostaglandin E2 â–ȘEndotoxemia â–ȘResulting in â–ȘRenal vasoconstriction â–ȘShunting of blood from cortex â–ȘActivation of complement system peritubular and glomerular fibrin deposition leading to tubular and cortical necrosis
  • 12. IMMUNE SYSTEM â–ȘDefects in cellular immunity â–ȘImpaired T cell proliferation â–ȘDecreased neutophil chemotaxis â–ȘDefective bacterial phagocytosis â–ȘDepressed function of RE system ie Kupffer cells
  • 13. WOUND HEALING â–ȘDelayed wound healing â–ȘHigh incidence of wound dehiscence â–ȘDecresed activity of enzyme Propyl hydroxylase in the skin â–ȘThis helps in incorporation of proline in collagen â–ȘDefective synthesis of collagen
  • 14. COAGULATION FACTOR DEFECTS â–ȘProlongation of Prothrombin time â–ȘLoss of calcium â–ȘEndotoxin induced damage to factor XI ,XII ,platelets â–ȘLow grade DIC with increased fibrin degradation products â–ȘThrombocytopenia from hyperspleenism â–ȘDecreased absroption of fat solube vitamins A,D,E,K
  • 15. ITCHING â–ȘRetained bile salts â–ȘItching disappears in terminal liver failure but bile salt level still increased â–ȘOther theory â–ȘDue to endogenous opiate peptides â–ȘInducing opiod receptor mediated scratching activity of central origin
  • 16. BIOCHEMICAL EFFECTS â–ȘBilirubin â–ȘRise by 25-43 micromol/litre/day â–ȘMechanism of hyperbilirubinemia â–ȘBiliary venous & biliary regurgitation of conjugated bilirubin due to disruption of tight intracellular junction â–ȘTrans hepatocytic regurgitation due to reversal of the secretory polarity of hepatocytes â–ȘRupture of dilated canaliculi in to sinusoids due to necrosis of hepatocytes
  • 17. ALKALINE PHOSPHATSE â–ȘMost sensitive indicator â–ȘFactor responsible are â–ȘBiliary component regurgitation â–ȘIncrease in hepatic synthesis
  • 18. Why Bilirubin levels plateau â–ȘIncreased excretion of bile pigments by kidney by products other than bilirubin not giving DIAZO reaction â–ȘA portion get covalently bounded to serum albumin â–ȘThis protein bound bilirubin-Delta bilirubin,is not measurable by routine technique
  • 19.
  • 20. HISTORY AND CLINICAL EXAMINATION
  • 21. HISTORY â–ȘPrevious dyspepsia, fat intolerance â–ȘJaundice- onset, course, itching â–ȘPain â–ȘPyrexia â–ȘWeight loss â–ȘDark urine and clay coloured stools â–ȘTravel to endemic area â–ȘContact with jaundice patient â–ȘHistory of upper abdominal operation â–ȘDrug intake ie ATT â–ȘHistory of injection in preceding six months
  • 22. CLINICAL EXAMINATION â–ȘAge â–ȘAnaemia - hemolysis, cancer , cirrhosis â–ȘGross weight loss-malignancy â–ȘHunched up position-chronic pancreatitis or ca pancreas â–ȘFetor, flapping tremors,personality changes-impending hepatic coma â–ȘSkin changes-Bruising,purpuric spots,spider naevi,palmar erythema,white nails,loss of secondary sexual characters
  • 23. ABDOMINAL EXAMINATION â–Ș Dilated peri umbalical veins- cirrhosis & portal collateral circulation â–ȘAscitis-Cirrhosis or malignant disease â–ȘNodular liver â–ȘCourvoisier’s Law-palpable non tender gall bladder in jaundice patient-malignant biliary obstruction â–ȘExceptions â–ȘDouble impaction of stones â–ȘImpaction of pancreatic calculus at ampulla of vater â–ȘMirizzi syndrome
  • 24. BIOCHEMICAL INVESTIGATIONS â–ȘRoutine investigations-Hb,TLC,DLC, Blood sugar, RFT ,Serum electrolytes â–ȘUrinary bilirubin,Urobilinogen â–ȘSerum Bilirubin-Total and Direct â–ȘSGOT,SGPT,ALP.GGTP and 5- Nucleotidase â–ȘPT and Serum Albumin
  • 25. ALKALINE PHOSPHATSE(ALP) â–ȘALP levels are elevated in nearly 100 % of patients with extra hepatic obstruction except in some cases of intermittent obstruction. â–ȘValues usually greater than 3 times the upper limit of reference range, and in most typical cases, they exceed 5 times the upper limit. â–Ș An elevation less than 3 times the upper limit is evidence against complete extra hepatic obstruction.
  • 26. AST and ALT â–ȘSerum enzymes that provide evidence of hepato cellular damage.ALT found primarily in the liver, where as AST also found in heart ,kidney, skeletal muscle and brain â–ȘAST is less specific for liver function. The levels of AST and ALT should be done simultaneously since ALT can confirm the hepatic origin of the less specific but more sensitive AST. â–ȘIn extra hepatic obstruction usually AST levels are not elevated(< 10 times the upper reference limit)
  • 27. GAMMA –GLUTAMYL TRANSPEPTIDASE(GGTP) â–ȘCorrelates with ALP level â–ȘMost sensitive indicator of biliary tract disease â–ȘBetter indicator of obstruction in children – levels are independent of age â–ȘHelpful in the diagnosis of acute biliary tract obstruction in contrast to ALP because ALP requires synthesis of fresh ALP and hence lags behind the onset of obstruction
  • 28. 5- NUCLEOTIDASE â–ȘThe principal value is to confirm the hepatic origin of an elevated ALP â–ȘThis is particularly helpful in children, pregnant women and patients who may have bone disease resulting in rise of ALP â–ȘIt is more useful than ALP/GGTP in detecting hepatic metastasis
  • 29. OTHER LAB INVESTIGATIONS â–ȘProthrobin time â–ȘSerum albumin â–ȘStool for occult blood â–ȘPresence of occult blood in the stools of a patient with jaundice must raise the suspicion of malignancy.
  • 30. Obstructive jaundice Medical jaundice Serum Bilirubun â–Ș conjugated â–Ș unconjugated +++ + + +++ Urobilinogen ↓ ↑ Urinary Bilirubin + 0 Urinary Bile salts + 0 Serum ALP ↑ No change Serum GGTP ↑ No change Serum 5-nucleotidase ↑ No change Transaminases Mildly raised Markedly raised
  • 32. TYPES OF BILIARY OBSTRUCTION â–ȘComplete obstruction â–ȘIntermittent obstruction â–ȘChronic incomplete obstruction â–ȘSegmental obstruction
  • 33. INTERMITTENT OBSTRUCTION â–Ș Symptoms and typical biochemical changes â–ȘClinically jaundice may or may not be present â–ȘCauses â–ȘCBD stones â–ȘPeriampullary tumours â–ȘDuodenal diverticulum â–ȘCholedochal cyst â–ȘBiliary parasites â–Șhemobilia
  • 34. CHRONIC INCOMPLETE OBSTRUCTION â–ȘWith or without classical symptoms or biochemical changes â–ȘPathological changes in bile ducts or liver â–ȘCauses â–ȘStrictures of CBD â–ȘStenosis of biliary-enteric anastamosis â–ȘChronic pancreatitis â–ȘCystic fibrosis â–ȘSphincter of oddi stenosis
  • 35. SEGMENTAL OBSTRUCTION â–Ș one or more segment of intrahepatic biliary tract obstructed â–ȘCauses â–ȘTraumatic â–ȘIntrahepatic stones â–ȘSclerosing cholangitis â–ȘCholangiocarcinoma
  • 36. BILIARY OBSTRUCTION INTRINSIC â–Ș Ductal calculi Primary - Develop de novo in bile ducts Secondary - Migrate from gall bladder â–Ș Acute Cholangitis â–Ș Biliary Strictures Idiopathic Iatrogenic â–Ș Sclerosing Cholangitis â–Ș Parasites â–Ș Haemobilia â–Ș Benign Biliary Tumours â–Ș Cholangiocarcinoma â–Ș Carcinoma of ampulla of vater and Periampullary tumours â–Ș Intraductal secondary tumour seeding
  • 37. BILIARY OBSTRUCTION EXTRINSIC â–Ș Mirizzi syndrome â–Ș Pancreatitis- acute and chronic â–Ș Pancreatic pseudocyst â–Ș Carcinoma of gall bladder â–Ș Carcinoma of pancreas â–Ș Cystic tumours of pancreas â–Ș Metastatic carcinoma â–Ș Hepatocellular carcinoma
  • 38. BILIARY OBSTRUCTION CONGENITAL AND GENETIC DISORDERS â–Ș Biliary atresia â–Ș Choledocal cyst â–Ș Caroli’s disease â–Ș Progressive familial intra hepatic cholestasis â–Ș Primary biliary cirrhosis â–Ș Alpha 1 antitrypsin defeciency â–Ș Tyrosinemia â–Ș Neonatal hepatitis â–Ș Wilson disease â–Ș Others - dyskinesia of sphincter of odi
  • 39. IMAGING GOALS â–ȘTo confirm the presence of an extrahepatic obstruction â–ȘTo determine the level of the obstruction, to identify the specific cause of the obstruction â–ȘTo provide complementary information relating to the underlying diagnosis (eg., Staging information in cases of malignancy).
  • 40. Ultrasonography Ultrasound of the abdomen is an extremely useful and accurate method for identifying gallstones and pathologic changes in the gallbladder consistent with acute cholecystitis. Abdominal ultrasound, if performed by an experienced operator, should be part of the routine evaluation of patients suspected of having gallstone disease, given the high specificity (>98%) and sensitivity (>95%) of this test for the diagnosis of cholelithiasis[1] ( Table 54-1 ). In addition to identifying gallstones, ultrasound can also detail signs of cholecystitis such as thickening of the gallbladder wall, pericholecystic fluid, and impacted stone in the neck of the gallbladder. It is often the initial screening test for patients with suspected extrahepatic biliary obstruction ( Fig. 54-7 ). Dilation of the extrahepatic (>10 mm) or intrahepatic (>4 mm) bile ducts suggests biliary obstruction. Intraoperative ultrasound is now used frequently to further evaluate intrahepatic lesions, assess resectability, and determine involvement of vascular structures
  • 41.
  • 42.
  • 43. . MAGNETIC RESONANCE CHOLANGIOPANCREATOGRAPHY (MRCP) ‱Noninvasive test to visualize the hepato biliary tree ‱No contrast ‱Fluid found in the biliary tree is hyper intense on T2-weighted images. Surrounding structures do not enhance and can be suppressed during image analysis. ‱Sensitive in detecting biliary and pancreatic duct stones, strictures, or dilatations within the biliary system. ‱MRCP combined with conventional MR imaging of the abdomen can provide information about surrounding structures (eg, pseudocysts, masses). ‱ ERCP and MRCP similarly effective in detecting malignant hilar and perihilar obstruction ‱ MRCP is better able to determine the extent and type of tumor as compared to ERCP
  • 44. Absolute contraindications â–Șcardiac pacemaker â–Șcerebral aneurysm clips â–Șocular or cochlear implants â–ȘFluid stasis in the adjacent duodenum or ascitic fluid may produce image artifacts on MRCP, making it difficult to clearly visualize the biliary tree.
  • 45. ENDOSCOPIC ULTRASOUND (EUS) â–ȘCombines Endoscopy and US â–ȘHigher-frequency ultrasonic waves compared to traditional US (3.5 mhz vs 20 mhz) and allows diagnostic tissue sampling via EUS-guided fine-needle aspiration (EUS-FNA). â–ȘEUS has been reported to have up to a 98% diagnostic accuracy in patients with obstructive jaundice â–ȘThe sensitivity of EUS for the identification of focal mass lesions in pancreas has been reported to be superior to that of CT scanning, both traditional and spiral, particularly for tumors smaller than 3 cm in diameter. â–ȘCompared to MRCP for the diagnosis of biliary stricture, EUS has been reported to be more specific (100% vs 76%) and to have a much greater positive predictive value (100% vs 25%), although the two have equal sensitivity (67%). â–ȘThe positive yield of eus-fna for cytology in patients with malignant obstruction has been reported to be as high as 96%.
  • 46.
  • 47.
  • 48. Investigations Metastasis poor Surgical risks No metastasis Good Surgical Risks Non operative procedures Operative Procedures Non resectable tumours Resectable tumours Biliary – enteric Bypass Surgically placed stents Percutanesly placed Stents Endoscopically placed stents Palliative resection Curative resection Malignant Obstructive jaundice
  • 49. WORKUP AND MANAGEMENT OF POSTHEPATIC JAUNDICE three possible clinical scenarios:DUCTAL OBSTRUCTION SUSPECTED CHOLANGITIS SUSPECTED CHOLEDOCHOLITHIASIS WITHOUT CHOLANGITIS SUSPECTED LESION OTHER THAN CHOLEDOCHOLITHIASIS
  • 50. SUSPECTED CHOLANGITIS â–ȘA clinical picture compatible with acute suppurative cholangitis (charcot's triad or raynaud's pentad) the most likely diagnosis is choledocholithiasis. â–ȘAppropriate resuscitation, correction of any coagulopathies if present, and administration of antibiotics â–ȘERCP is indicated for diagnosis and treatment â–ȘIf ERCP is unavailable or is not feasible (e.g., Because of previous roux-en-y reconstruction), transhepatic drainage or surgery may be necessary â–ȘMainstay of treatment of severe cholangitis is not just the administration of appropriate antibiotics but rather the establishment of adequate biliary drainage.
  • 51. SUSPECTED CHOLEDOCHOLITHIASIS WITHOUT CHOLANGITIS â–ȘCholedocholithiasis is the most common cause of biliary obstruction. â–ȘStrongly suspected if the jaundice is episodic or painful or if usg has shown presence of gallstones or bile duct stones. â–ȘPatients with suspected cbd stones should be referred for lap cholecystectomy with either preoperative ERCP, intra operative cholangiography â–ȘPreoperative ERCP in this setting of jaundice is prefered â–ȘDiagnostic yield is high â–Ș Therapeutic-clearing the CBD of stones in 95% of cases. â–ȘMany authors, however favor fully laparoscopic approach, in which CBD stone is detected in the OR by means of intraoperative cholangiography and laparoscopic biliary clearance is performed when choledocholithiasis is confirmed. â–Ș The optimal approach in a particular setting should be dictated by local expertise.
  • 52. SUSPECTED LESION OTHER THAN CHOLEDOCHOLITHIASIS â–ȘNo gallstones are seen â–ȘClinical presentation is less acute (e.g., constant abdominal or back pain) â–ȘAssociated constitutional symptoms (e.g., weight loss, fatigue, and long-standing anorexia) â–ȘPossible causes of may be classified into three categories depending on the location of the obstructing lesion â–Șthe upper third of the biliary tree â–Șthe middle third â–Ș the lower (distal) third
  • 53. Upper-third obstruction â–Ș Polycystic liver disease â–Ș Caroli diseas â–Ș HCC â–Ș Oriental cholangiohepatitis â–Ș Hemobilia(e.g.,afterbiliarymani pulation) â–Ș Iatrogenic bile duct injury â–Ș Cholangiocarcinoma (Klatskin'stumor) â–Ș Sclerosing cholangitis â–Ș Papillomas of the bile duct Mid-third obstruction â–ȘCholangiocarcinoma â–ȘSclerosing cholangitis â–ȘPapillomas of the bile duct â–ȘGallbladder cancer â–ȘCholedochal cyst â–ȘIntrabiliary parasites â–ȘMirizzi syndrome â–ȘExtrinsic nodal compression (e.g., lymphoma) â–ȘIatrogenic bile duct injury â–ȘCystic fibrosis â–ȘBenign idiopathic bile duct stricture Lower-third obstruction â–ȘCholangiocarcinoma â–ȘSclerosing cholangitis â–ȘPapillomas of the bile duct â–ȘPancreatic tumors â–ȘAmpullary tumors â–ȘChronic pancreatitis â–ȘSphincter of Oddi dysfunction â–ȘPapillary stenosis â–ȘDuodenal diverticula â–ȘPenetrating duodenal ulcer â–ȘRetroduodenal adenopathy (e.g., lymphoma, carcinoid ETIOLOGY
  • 54. DIAGNOSIS AND ASSESSMENT OF RESECTABILITY â–ȘInvolvement of the SUPERIOR MESENTERIC VEIN, THE PORTAL VEIN, THE SUPERIOR MESENTERIC ARTERY, and the PORTA HEPATIS and on whether there is evidence of significant LOCAL ADENOPATHY or EXTRAPANCREATIC EXTENSION OF TUMOR indicates UNRESECTABILITY â–ȘThe majority of lesions will be clearly unresectable, either because of tumor extension or because of the presence of hepatic or peritoneal metastases
  • 56. â–ȘIn the majority of patients with malignant obstructions, treatment is palliative rather than curative. â–ȘCholangiography and decompression of obstructed biliary system â–ȘIn the absence of preexisting or concomitant hepatocellular dysfunction, drainage of one half of the liver is generally sufficient for resolution of jaundice
  • 57. â–ȘRoutine preoperative drainage of an obstructed biliary system does not benefit patients who will soon undergo resection.1,2 â–ȘThere is evidence suggesting that in patients with either pancreatic 3,4 or hepatic malignancies, routine preoperative direct cholangiography with decompression is associated with a higher incidence of postoperative complications when tumor resection is ultimately carried out. 1. Pitt HA, Gomes AS, Lois JF: Does preoperative percutaneous biliary drainage reduce operative risk or increase hospital cost? Ann Surg 201:545, 1985 2. McPherson GA, Benjamin IS, Hodgson HJ, et al: Preoperative percutaneous transhepatic biliary drainage: results of a controlled trial. Br J Surg 71:371, 1984 3. Povoski SP, Karpeh MS Jr, Conlon KC, et al: Preoperative biliary drainage: impact on intraoperative bile cultures and infectious morbidity and mortality after pancreaticoduodenectomy. J Gastrointest Surg 3:496, 1999 4. Sohn TA, Yeo CJ, Cameron JL, et al: Do preoperative biliary stents increase postpancreaticoduodenectomy complications? J Gastrointest Surg 4:258, 2000
  • 58. OPERATIVE MANAGEMENT AT SPECIFIC SITES BYPASS AND RESECTION
  • 59. UPPER-THIRD OBSTRUCTION PALLIATION. â–ȘBecause the left hepatic duct has a long extrahepatic segment and is more accessible, the preferred bypass -is a left hepaticojejunostomy â–Ș Laparoscopic bypass techniques that make use of segment 3 have been developed, but their performance has yet to be formally assessed
  • 60. RESECTION FOR CURE â–ȘThe hilar plate is taken down to lengthen the hepatic duct segment available for subsequent anastomosis. â–ȘA formal hepatectomy or segmentectomy is required to ensure an adequate proximal margin of resection â–Ș If the resection is carried out proximal to the hepatic duct bifurcation, several cholangiojejunostomies have to be done to anastomose individual hepatic biliary branches. â–ȘThe results of aggressive hilar tumor resections that included as much liver tissue as was necessary to obtain a negative margin appear to justify this approach. â–Ș In cases of left hepatic involvement, resection of the caudate lobe is indicated as well.
  • 61. MIDDLE-THIRD OBSTRUCTION Palliation. â–ȘSurgical bypass of middle-third lesions is technically simpler â–Ș Hepaticojejunostomy is done distal to the hepatic duct bifurcation, â–Ș Exposure of the hilar plate or the intrahepatic ducts is unnecessary. Resection for cure. â–ȘTumors in this part usually quite amenable to resection along with the lymphatic chains in the porta hepatis. â–ȘMirizzi syndrome -extrinsic obstruction of the CBD, either by causing inflammation of the gallbladder wall or via direct impingement. â–ȘTreatment of this syndrome - Hepaticojejunostomy
  • 62. Lower-third obstruction Palliation â–Ș The preferred bypass technique for lower-third lesions is a Roux-en-Y choledochojejunostomy. â–Ș Cholecystojejunostomy carries a higher risk of complications and subsequent development of jaundice Resection for cure. â–Ș Resection of a lower-third lesion usually involves a pancreaticoduodenectomy though transduodenal ampullary resection may be an acceptable alternative for a small adenoma of the ampulla â–ȘFor optimal results, pancreaticoduodenectomy is best performed in specialized centers. â–Șpostoperative adjuvant therapy may improve the prognosis after resection of a pancreatic adenocarcinoma
  • 63. PALLIATION IN PATIENTS WITH ADVANCED MALIGNANT DISEASE â–ȘWhen a patient has advanced malignant disease, drainage of the biliary system for palliation is not routinely indicated, because the risk of complications related to the procedure may outweigh the potential benefit â–ȘThe best treatment for a patient with asymptomatic obstructive jaundice and liver metastases may be supportive care alone. â–ȘBiliary decompression is indicated if cholangitis or severe pruritus interferes with quality of life. â–ȘStent placed with ercp to be the palliative modality of choice for advanced disease, â–ȘUpper-third lesions may be managed most easily through the initial placement of an internal/external catheter at the time of ptc.
  • 64. â–ȘMetal expandable stents remain patent longer than large conventional plastic stents â–ȘRCTs suggest that surgical biliary bypass should be reserved for patients who are expected to survive for 6 months or longer because bypass is associated with more prolonged palliation at the cost of greater initial morbidity. â–ȘThe role of prophylactic gastric drainage at the time of operative biliary drainage remains controversial,101,102 â–Ș RCTs demonstrated a reduced incidence of subsequent clinical gastric outlet obstruction when this measure was employed. â–Ș When a pancreatic malignancy is present, intraoperative celiac ganglion injection should be performed for either prophylactic or therapeutic pain
  • 65. POSTOPERATIVE JAUNDICE â–ȘThe development of jaundice in the postoperative setting is approximately 1% of all surgical patients after operation.120 â–ȘWhen jaundice occurs after a hepatobiliary procedure, â–ȘAttributable to specific biliary causes, â–ȘRetained cbd stones, â–ȘPostoperative biliary leakage (through reabsorption of bile leaking into the peritoneum) â–Ș injury to the cbd â–ȘDevelopment of biliary strictures
  • 66. JAUNDICE WITHIN 48 HOURS OF THE OPERATION â–ȘBreakdown of rbc –due to multiple blood transfusions , â–ȘThe resorption of a large hematoma, â–ȘTransfusion reaction. â–ȘKnown underlying hemolytic anemia and may be precipitated specific drugs (e.G., Sulfa drugs in a patient who has G6PD deficiency). â–ȘGilbert syndrome may first manifest itself early in the postoperative period. â–ȘIntraoperative hypotension or hypoxemia or the early development of heart failure can lead to hyperbilirubinemia within 5 to 10 days after operation. â–ȘThe hyperbilirubinemia may be associated with other end-organ damage (e.G., Acute tubular necrosis). â–ȘImpairment of renal function causes a decrease in bilirubin excretion and can be responsible for a mild hyperbilirubinemia.
  • 67. Jaundice developing 7 to 10 days after operation â–Ș In association with a medication-induced hepatitis attributable to an anesthetic agent. â–ȘIncidence of 1/10,000 after an initial exposure. â–ȘAdministration of antibiotics or other medications used in the perioperative setting â–ȘJaundice associated with intrahepatic cholestasis is often a manifestation of a sepsis, particularly in patients with mods â–Ș Jaundice may occur in as many as 30% of patients receiving total parenteral nutrition (tpn). â–ȘIt may be due to steatosis, particularly with formulas containing large amounts of carbohydrates. â–ȘDecreased export of bilirubin from the hepatocytes may lead to cholestasis â–ȘAcalculous cholecystitis or even ductal obstruction may develop as a result of sludge in the gallbladder and the cbd.
  • 68. â–ȘUnsuspected hepatic or post-hepatic causes (e.G., Occult cirrhosis, choledocholithiasis, or cholecystitis) â–ȘA rare cause of postoperative jaundice is the development of thyrotoxicosis. â–ȘA diagnosis of exclusion- is so-called benign postoperative cholestasis, a primarily cholestatic, self-limited process with no clearly demonstrable cause that typically arises within 2 to 10 days after operation. â–ȘMechanism-combination of an increased pigment load, impaired liver function, and decreased renal bilirubin excretion caused by varying degrees of tubular necrosis. â–Ș The predominantly conjugated hyperbilirubinemia may reach 40 mg/dl and remain elevated for as long as 3 weeks.