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Premium member Presentation Transcript بسم الله الرحمن الرحيم: بسم الله الرحمن الرحيمJaundice: Jaundice By Dr/Waleed RadwanDefinition: Definition Jaundice , also known as icterus , is a yellowish discoloration of the Skin,Sclera and Mucus membranes caused by hyperbilirubinemia. Typically, the concentration of bilirubin in the plasma must exceed 1.5 mg/dl (> 40.0 mmol/L ) , three times the usual value of approximately 0.5 mg/dl ( 17 mmol/L .), for the coloration to be easily visible. Jaundice comes from the French word jaune , meaning yellowSource Of Bilirubin: Source Of Bilirubin 85% from old RBC , the rest from non haem proteins Hb is degraded to Haem and Globin Iron is extracted from Haem Rest is converted to bilirubin (porphorin metabolism) Bilirubin travels to liver bound to albuminJourney through the liver : Journey through the liver Bilirubin taken up Conjugated to form water soluble conjugate Conjugate secreted into bileIn The Gut: In The Gut Bilirubin diglucuronide may be Deconjugated by beta glucuronidase enzyme (eg. E.coli) then becomes insoluble and predisposed to pigment stones. Metabolised by bacteria to urobilinogen which is partially reabsorbed (remainder makes the stool brown)Enterohepatic circulation of Urobilinogen : Enterohepatic circulation of Urobilinogen Most is taken up by the liver and re excreted If it builds up in the blood then it may be filtered by the glomerulus and be detectable in urineUrobilinogen in the Urine : Urobilinogen in the Urine Conjugated bilirubin is reaching the gut (if Bile duct not blocked) The liver cell is not behaving well in that it is permitting urobilinogen to increase in the bloodBile salt metabolism : Bile salt metabolism Bile salts have nothing to do with bilirubin metabolism Bile salts are Bile acids 98% of bile is water , the rest 80% is bile salts 15% is phospholipid 5% is cholesterolBile salts metabolism : Bile salts metabolism 1. Source of bile salts 2. Bile salts in the small bowel 3. Bile salts in the large bowel Bile salts may be carcinogenic in the stomach and esophagusSource of bile salts : Source of bile salts Made in the liver from cholesterol Conjugated by liver to make soluble with; Glycine 75% Taurine 25% These are the primary bile acids/salts; Cholic acid (glycine or taurine conjugate) Chenodeoxycholic acid (glycine or taurine conjugate) The primary bile acids/salts are released into the intestine in bileBile salts in the small bowel : Bile salts in the small bowel The primary bile salts are reabsorbed in the terminal ileum, (enterohepatic circulation) In all there is about 3-5 g of bile salts in a person These are turned over 6 times a day In the presence of ileal disease, too much bile salt reaches the colon and causes diarrhoea A small amount of bile salt enters the colonBile salts in the large bowel : Bile salts in the large bowel Bacterial metabolism of the primary bile salts occurs in the colon; Cholic acid – Deoxycholic acid Chenodeoxycholic acid – Lithocolic acid Deoxycholic acid is reabsorbed and has an enterohepatic circulationPathophysiology Of Jaundice: Pathophysiology Of Jaundice Hyperbilirubinemia is due to: Excess bilirubin production Haemolytic Impaired uptake by hepatocyte Hep/cellular. Failure of Conjugation Hep/cellular. Impaired secretion of conj.bil. Hep/cellular. Impaired bile flow. Obst.JaundiceNormal Bilirubin Metabolism: Normal Bilirubin MetabolismGilbert Disease: Gilbert DiseaseCrigler-Najjar Disease: Crigler-Najjar DiseaseDubin-Johnson Disease: Dubin-Johnson DiseaseTypes of Jaundice: Types of JaundicePre-Hepatic: Pre-HepaticPre-Hepatic Jaundice : Pre-Hepatic Jaundice Clinical Features Jaundice not typically severe Increased unconjugated plasma bilirubin Increased urobilinogen in urine AP. ALT, AST - normalHepatic: HepaticPost-Hepatic: Post-HepaticExamples Of Jaundice In Practice: Examples Of Jaundice In PracticePowerPoint Presentation: Jaundice Haemolytic Hepatocellular Obstructive Extrahepatic IntrahepaticAetiology of Jaundice: Aetiology of Jaundice1-Gallstones: 1-Gallstones A/w Haemolytic anemia 1 ry Ductal StoneSymptoms of Cholelithiasis: Symptoms of Cholelithiasis Asymptomatic Gallstones can cause Chronic Cholecystitis Acute Biliary Colic Jaundice Cholangitis & Septicemia Acute pancreatitis Biliary fistula Mirrizi Syndrome + Gallstone ileus To D/B biliary colic & acute cholecystitis by U/S Oedema of Gallbladder wall2-Pancreatic & Biliary Malignancy: 2-Pancreatic & Biliary MalignancyRisk Factors: Risk FactorsPancreatic Cancer: Pancreatic Cancer Annual Deaths From Pancreatic cancer It is very important to distinguish between adenocarcinoma Head, Body , Tail & Periampullary Tumours because of different prognosis 8-12/100,000 Males 4-6/ 100,000 Females Periampullary 5 y survival 40 % Cancer Head <5 %Cancer Head of Pancreas: Cancer Head of PancreasBiliary Tract Cancer: Biliary Tract CancerBiliary Duct Tumors Incidence: Biliary Duct Tumors IncidencePeriampullary Cancer: Periampullary Cancer C/P Painless , Progressive Jaundice , Itching Rarely with Incresd S.Amylase Or Grey stool. Includes Cancer Of: The Ampulla Of Vater Distal CBD The duodenum. Prognosis: Stage dependant: T1,2 Very good 30-50% 5y.survival after surgery .Hepatic Metastasis: Hepatic Metastasis Incidence In Europe: 90% Of Hepatic Tumors are metastatic from 1ry in GIT, Lung and Breast The Commonest in 2ry hepatic deposit , is from colorectal cancerHepatic Tumors (Clinical): Hepatic Tumors (Clinical)Bile Duct Stricture: Bile Duct StrictureBile duct stricture: Bile duct stricture This lesion require expert remedial surgery, because of possible serious consequences as: Recurrent Cholangitis Hepatic fibrosis 2ry Biliary Cirrhosis Portal HTNExcessive traction during lap chole.: Excessive traction during lap chole.Bismuth-Corlette Classification of hilar tumors.: Bismuth-Corlette Classification of hilar tumors.Strasberg Classification of Biliary injury: Strasberg Classification of Biliary injuryHepatic Tumors (Morphology): Hepatic Tumors (Morphology) 1 ry Hepatic tumor. 2ry Hepatic Deposits Discretely Nodular Single,Multiple Uni or Bilobar. Miliary Widespread seedling deposit Diffusely Confluent Involving Multiple segments Or lobesHepatic tumors: Hepatic tumors Only Discretely Nodular is Potentially Curable. Overall , < 5% Of Patients w/Hepatic Metastasis are suitable for resection.Hepatic cancer: Hepatic cancerLiver Cirrhosis: Liver Cirrhosis It is the end result of hepatocyte death. Confluent necrosis of Zone I , III Of Hepatic lobules produces fibrotic Bridges , regeneration of Surviving hepatocyte With Nodule formation results in Further distortion of the hepatic architecture. Cirrhosis must be differentiated from Hepatic fibrosis , which can occur: Congenitally Chronic Bile Duct Obstruction. Around the Central Vein in Chronic Heart FailureCauses: CausesMorphological types: Morphological types Micronodular Cirrhosis Macronodular Cirrhosis Mixed Cirrh osisCauses of Each type: Causes of Each type Micronodular Mixed Macronodular Post –Hepatitic Alcoholic Cirrhosis Malnutrition Cryptogenic From Regeneration In Micronodular1 ry Biliary Cirrhosis: 1 ry Biliary Cirrhosis In this case Intra-hepatic ducts are progressively destroyed by an immunologic process. It affects females in Age of 40 y/o Diagnosed by: Antimitochondrial Abs . Symptoms : weight loss Jaundice Malaise S/C Fat deposits Itching2ry Biliary Cirrhosis: 2ry Biliary Cirrhosis Due to post Iatrogenic strictureSeverity Scores For Liver Cirrhosis: Severity Scores For Liver Cirrhosis 1-Child-Pough Classification A=5-7 B=8-10 C=11 Or more Parameter A B C Albumin g/dl > 3.5 3-3.5 < 3 Bilirubin mol/L <25 25-40 >40 P.T <4.0 4-6 >6 Prothrombin Level >64 40-65 <40 Ascites none Controlled Refractory Encephalopathy none Minimal AdvancedSeverity score: Severity score 2- Paul- Brousse Hospital Classification System. A =Non Criteria B =1-2 Criteria C = 3 Or More Parameter Number Of Criterion Albumin <3.0 g/ 100ml. 1 Hyperbilirubinemia >30 mmol/L 1 Encephalopathy 1 Clinical Ascites 1 Coagulation Factor II & V 40-60% 1 < 40% 2Hepatitis: HepatitisCauses: Causes Viral Hepatitis A, E Enteral B,C,D,G Through blood. Cytomegalo virus Yellow fever Epstein Barr Virus Ebola & Marburg VirusPowerPoint Presentation: Constitutes 40% of hospitalized patients, 20% of patients have fulminant Liver Failure.Drug Induced Liver Disease DILD: Drug Induced Liver Disease DILD Tetracycline Penicillin Paracetamol Salicylates Steroids Halothane Azathioprine Methotrexate PhynetoinLiver Cell Failure: Liver Cell Failure The Hallmark symptom: is encephalopathy , decreased level of consciousness and Coma. Occurs In: 1- Acute liver Failure. 2-Acute Fulminant Encephalopathy. 3-Subclinical chronic liver failure. 4-Shunt encephalopathy.Symptoms: SymptomsAcute Liver Failure: Acute Liver Failure (Fulminant) Sever Encephalopathy Occur within 6-8 weeks Of Onset. Acute Massive Hepatocellular necrosis, caused by Drugs (acetaminophen , halothane, viral infection).Chronic Liver Failure: Chronic Liver Failure As a Background Of Liver Cirrhosis Characterized by : Overt Chronic Encephalopathy Sever Mental Impairment Muscle Wasting Fluid & Salt Retention Bleeding tendency Episodes of Variceal HemorrhageObstructive Jaundice: Obstructive JaundiceMain causes of obstructive jaundice : Main causes of obstructive jaundice Bile duct In the lumen of the common bile duct (gallstones, parasites) In the wall of the duct (choledochal cyst, sclerosing Cholangitis, Cholangiocarcinoma) Pressing in/on the bile duct (Mirrizi, pancreatitis, pancreatic cancer, malignant nodes) Ampulla Periampullary carcinoma Tumor invading the ampullaConsequence of obstructive jaundice : Consequence of obstructive jaundice Malabsorbtion Fat (steatorrhoea) Fat soluble vitamins (DEKA) Jaundice – Bilirubin, No bilirubin metabolites in stool – Pale Itch – Bile salts Sepsis, cholangitis, Charcots triad ? Renal failure (Hepato-renal syndrome) Bleeding - High INRClinical features of cholangitis, Charcot’s triad: Clinical features of cholangitis, Charcot’s triad 1. Jaundice 2. Intermittent chills / fever or rigors 3. Abdominal pain Charcot’s triad indicats cholangitis, this causes severe sepsis and may result in liver abscess formationClinical Approach: Clinical ApproachDiagnostic Protocol: Diagnostic Protocol The Work-up is geared to Answer : Is the jaundice, Cholestatic Or Hepatocellular? Has the patient any evidence Of Parenchymal Liver Disease.? Is there any evidence of Malignancy On Clinical Examination? Is there dilatation Of the biliary tract on U/S Exam.?History : History Pale stools, Dark Urine Itch ? Pain or not Intermittent, or progressive Drugs, operations (anaesthetic gas) Blood transfusion, inoculations Occupation and hobbies, (rats and leptospirosis) Family History (Gilbert’s disease)History: History Important Aspects Of Patient History Any Abdominal Pain , Weight Changes And / Or Fever Injections Alcohol Abuse. Blood Transfusion Contact with Jaundiced patient. Travel to Endemic Area. Sexual Activity. Ingestion of Raw Shellfish, Mushroom.Physical Examination: Physical Examination General: Stigmata Of Liver Disease & Weight Loss. Neck: Enlarged L.Ns & Virchow L.N. Abdomen: Prominent ant.abd.wall veins. Enlarged Liver , Spleen Palpable Gallbladder (Courvoisier sign). Palpable Abdominal mass. Ascites Xanthomata : Of Biliary Cirrhosis 1-Spider Naevi 2-Palmar Erythema 3-Finger Clubbing 4-Leuchonychia 5-Gynecomastia 6-AscitesCourvoisier’s law: Courvoisier’s law If in the presence of jaundice the gallbladder is palpable, then a stone is not a likely causeInvestigations used for the biliary tract : Investigations used for the biliary tract Lab. Workup: Urinalysis CBC Liver blood tests: AST, ALT, GGT , ALKP, S.Albumin Fractionanted bilirubin.Radiological : Radiological Ultrasound (Abdominal ultrasound) X-ray ( Plain abdominal film) C.T C.T + PET PTC HIDA scan( with CCK) ERCP MRCPPowerPoint Presentation: History & Examination Bedside urine testing Bilirubin (Cholestatic) Urobilinogen (Hemolytic) Detailed Hematological Studies LFTs & Viral Screen Hepatocellular Cholestatic CT scan U/S Liver & Pancreas Dilated Biliary Not Dilated biliary Liver Biopsy ERCP +++ CT +/- MRCP Coagulation studies PTCCBD Stone in ERCP & MRCP: CBD Stone in ERCP & MRCPStent applied after complicated Lap chole. by bile Leakage: Stent applied after complicated Lap chole. by bile LeakageBiliary wall stent: Biliary wall stentBiliary wall stent: Biliary wall stentPlastic Biliary stents: Plastic Biliary stentsCholangiocarcinoma in ERCP: Cholangiocarcinoma in ERCPCancer Gallbladder: Cancer GallbladderCancer Head Of Pancreas: Cancer Head Of PancreasCancer tail of Pancreas: Cancer tail of PancreasTreatment Of Jaundice: Treatment Of Jaundice Preoperative Preparation : Parenteral Adminstration Of Vit.K , to normalize prothrombin time. I.V Hydration Urinary Catheter Forced Natruresis by mannitol or frusemide with induction of anaesthesia Antibiotic Prophylaxis against Gram –ve Bacteria (3 doses regimen) Frozen section booking for cancer resection. If the patient is not normalized after vit k injection consider hepatocellular failure.Gallstones Treatment: Gallstones Treatment 1-Cholecystectomy (Lap. Or Open) In the presence of Bile Duct Calculi Single stage Lap.Chole. And Ductal stone Clearance by ERCP. Currently, Most centers would submit the patient to ERCP Before Lap.Chole.Pancreatic & Biliary Malignancy Treatment: Pancreatic & Biliary Malignancy Treatment Surgical Resection if the patient is fit and disease is operable. Otherwise, Palliation by ERCP Or StentingTriple bypass: Triple bypassHepatic Metastasis: Hepatic Metastasis Surgical resection for selected cases Systemic chemotherapy Image guided ablation in-situ by alcoholinization of small lesions. Cryotherapy Radiofrequency thermal ablation. Interstitial laser hyperthermia.Bile Duct Stricture: Bile Duct Stricture Stent By ERCP. Roux En-Y Choledochojejunostomy. Choledochoduodenostomy. Lt. Hepatic Duct Anastmosis.Hepatecojejunostomy Roux-En-Y: Hepatecojejunostomy Roux-En-YRoux-En-Y choledochojejunostomy: Roux-En-Y choledochojejunostomy Less ComplicationOperative Injury Of Biliary Tree: Operative Injury Of Biliary TreePowerPoint Presentation: Operative injury Of Biliary Tree Excessive External bile drainage No External Drain RUQ Pain , Fever U/S Subhepatic Bile Collection Percutaneous Catheter Drainage subsided Persistent Excess Drainage ERCP CBD Transection Cystic Duct Leak No biliary Injury Or Leak Observe GB Leak Biliary Stenting +Cont’ Drainage Continue Ext Drainage PTC Sepsis Control Elective H/jejunostomy ObserveManagement of Bile Duct Injury: Management of Bile Duct Injury Discovered during Operation: Direct end to end suturing and T-tube Insertion . Discovered Post Op.: Biliary Stenting By ERCP . If Failed Choledochoduodenostomy Choledochojejunostomy Roux-En-YPowerPoint Presentation: Thank You You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.