Downloaded 101 times
![MODEL FOR END-STAGE LIVER DISEASE (MELD)
SCORE
MELD = 3.78×ln[serum bilirubin (mg/dL)] +
11.2×ln[INR] + 9.57×ln[serum creatinine
(mg/dL)] + 6.43×aetiology(0: cholestatic or
alcoholic, 1- otherwise)
In interpreting the MELD Score in hospitalized
patients, the 3 month mortality is:
1. 40 or more — 71.3% mortality
2. 30–39 — 52.6% mortality
3. 20–29 — 19.6% mortality
4. 10–19 — 6.0% mortality
5. <9 — 1.9% mortality](https://image.slidesharecdn.com/hepaticpancreatictumors-copy-150504033539-conversion-gate01/85/Hepatic-pancreatic-tumors-28-320.jpg)
More Related Content
Similar to Hepatic & pancreatic tumors
Hepatic & pancreatic tumors
- 1. HEPATIC & PANCREATIC TUMORS Dr. AbdulQadeer MBBS; FCPS; FICS Assistant Professor in Surgery King Faisal University College of Medicine
- 2. OBJECTIVES 1. Clinical anatomyof liver 2. Physiology of liver 3. Different types of benign hepatic tumors 4. Management of different types of benign hepatic tumors 5. Types of malignant hepatic tumors 6. Epidemiology of malignant hepatic tumors 7. Management of different malignant hepatic tumors
- 3. OBJECTIVES (CONTD…) 9. Clinicalanatomy of pancreas 10. Physiology of pancreas 11. Different types of pancreatic tumors 12. Management of different types of pancreatic tumors
- 4. 1. CLINICAL ANATOMYOF LIVER Largest organ in the body Situated in the RHC Weight = 1.5 kg in a 70 kg man Covered by a capsule & visceral peritoneum except ‘bare area’ on its posterior surface Two lobes, right & left; right lobe = 3/4th, left lobe = smaller
- 5.
- 6. LIGAMENTS & PERITONEALREFLECTIONS Left & right triangular ligaments Falciform ligament (remnant of umbilical vein) Lesser omentum between stomach & liver, contains the hilar structures Porta hepatis = hilum of the liver Hepatic artery, portal vein & bile duct are present within the free edge of the lesser omentum
- 7.
- 8. BLOOD SUPPLY OFLIVER Portal vein = 80% Hepatic artery = 20% Venous drainage = hepatic veins into IVC Liver regenerates fully after partial resection
- 9.
- 10. SEGMENTAL ANATOMY OFLIVER Eight segments (described by Couinaud) Each segment is a functional unit with a branch of hepatic artery, portal vein & bile duct
- 11.
- 12. 2. FUNCTIONS OFLIVER Maintains core body temperature pH balance & correction of lactic acidosis Synthesis of clotting factors Glucose metabolism, glycolysis & gluconeogenesis Urea formation from protein catabolism Bilirubin formation from Hb degradation Drug & hormone metabolism & excretion Removal of gut endotoxins & foreign antigens
- 13. 3. DIFFERENT BENIGNHEPATIC TUMORS Hemangioma Hepatic adenoma Focal nodular hyperplasia (FNH)
- 14. LIVER HEMANGIOMAS Havingabnormal plexus of veins Often multiple, may be giant Usually found incidentally (incidentaloma) Usually diagnosed by US CT scan shows characteristic slow contrast enhancement due to small vessel uptake Percutaneous biopsy should be avoided Rarely need surgery
- 15.
- 16. HEPATIC ADENOMA Mostlyoccur in women of child-bearing age Associated with sex hormones (OC pills) CT or MRI shows a well-circumscribed vascular solid tumor Difficult to differentiate from HCC Biopsy may be necessary May bleed and have malignant potential Resection is the treatment of choice
- 17.
- 18. FOCAL NODULAR HYPERPLASIA(FNH) It is a focal overgrowth of functioning liver tissue supported by fibrous stroma Usually middle-aged women US helps to diagnose but may not be able to discriminate Contrast CT/MRI may show central scarring & well-vascularized lesion FNH contains both hepatocytes & Kupffer cells A sulphur colloid liver scan may be useful, since Kupffer cells take up the colloid Does not have malignant potential If diagnosis is confirm, no treatment is required
- 19.
- 20. 4. MANAGEMENT OFBENIGN HEPATIC TUMORS Liver hemangiomas = Rarely require surgery Hepatic adenoma = Resection is the treatment of choice FNH = No treatment is required
- 21. 5. MALIGNANT HEPATICTUMORS 1. Primary tumors: Hepatocellular carcinoma Cholangiocarcinoma 2. Secondary tumors (Metastasis)
- 22. HEPATOCELLULAR CARCINOMA (HCC) Primary liver cancer Associated with chronic liver disease (CLD), due to HBV & HCV Many patients with CLD are now screened for HCC by serial USS of liver or serum α-FP Surgical treatment options include: 1. Resection of the tumor 2. Liver transplant
- 23.
- 24. Choice ofsurgical option from the above two depends upon: a. Stage of the underlying liver disease b. Site & size of the tumor c. Availability of organ transplantation d. Management of the immunosuppressed patient
- 25. STAGING & CLINICALASSESSMENT OF HCC General assessment of patient for fitness of surgery Severity of underlying liver disease (by CTP classification or MELD score) Size, number and site of the tumor
- 26. Points 1 point each 2points each 3 points each Bilirubin (µmol/L) <34 34-50 >50 Albumin (g/L) >35 22-35 <25 Ascites None Easily controlled Poorly controlled Encephalopath y None Grade I-II Grade III-IV INR <1.7 1.7-2.2 >2.2 CHILD-TURCOTTE-PUGH (CTP) CLASSIFICATION OF HEPATOCELLULAR FUNCTION IN CIRRHOSIS CTP A = 5-6 Points; CTP B = 7-9 Points; CTP C = 10-15 Points
- 27. MODEL FOR END-STAGELIVER DISEASE (MELD) SCORE It is a scoring system for assessing the severity of chronic liver disease It was initially developed to predict death within three months of surgery in patients who had undergone a transjugular intrahepatic portosystemic shunt (TIPS) procedure and was subsequently found to be useful in determining prognosis and prioritizing for receipt of a liver transplant This score is now used by the United Network for Organ Sharing (UNOS) and Eurotransplant for prioritizing allocation of liver transplants instead of the older CTP score
- 28. MODEL FOR END-STAGELIVER DISEASE (MELD) SCORE MELD = 3.78×ln[serum bilirubin (mg/dL)] + 11.2×ln[INR] + 9.57×ln[serum creatinine (mg/dL)] + 6.43×aetiology(0: cholestatic or alcoholic, 1- otherwise) In interpreting the MELD Score in hospitalized patients, the 3 month mortality is: 1. 40 or more — 71.3% mortality 2. 30–39 — 52.6% mortality 3. 20–29 — 19.6% mortality 4. 10–19 — 6.0% mortality 5. <9 — 1.9% mortality
- 29. USS CXR/CT Bone scan Contrast CT/MRI WHVP (Wedged hepatic venous pressure); suggests portal hypertension, poor outcome after liver resection in cirrhotic patients Indocyanine green (ICG) clearance test: for hepatic flow & function Patients with CTP class A and high ICG clearance are suitable for major liver resection
- 30. CHOLANGIOCARCINOMA Bile ductcancers typically present with painless obstructive jaundice PSC (Primary Sclerosing Cholangitis) is the cause Slow growing tumors Klastskin tumors: arise at the confluence of right & left hepatic ducts, eventually invading the liver parenchyma
- 31. INVESTIGATIONS FOR CHOLANGIOCARCINOMA LFTs: Obstructive jaundice Tumor marker: CA 19-9 may be elevated USS MDR-CT: Multidetector row computed tomography MRI/MRCP ERCP PTC PET
- 32. 6. EPIDEMIOLOGY OFMALIGNANT HEPATIC TUMORS Sixth most common cancer worldwide 5.7% incidence over all cancers Developing countries = 82%, third most common cancer in men after lung & stomach HBV & HCV infections account 75% cases of primary liver cancers http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3036307/
- 33. 7. MANAGEMENT OFMALIGNANT HEPATIC TUMORS For HCC: Surgical resection with 1 to 2-cm safety margin Liver transplantation Non-surgical therapy for advanced disease: a. Transarterial embolization (TAE) b. Transarterial chemoembolization (TACE) c. Percutaneous ethanol ablation (PEA) d. Radiofrequency ablation (RFA)
- 34. 8. CLINICAL ANATOMYOF PANCREAS Exocrine & endocrine pancreas Head, body, tail, uncinate process Main pancreatic duct (Wirsung) Accessory pancreatic duct (Santorini) Islets of Langerhans a) B-cells (65-80%) : Insulin b) A-cells (15-20%) : Glucagon c) D-cells (3-10) : Somatostatin d) PP-cells (1%) : Pancreatic polypeptide
- 35. 9. PHYSIOLOGY OFPANCREAS In response to meal, secretin from duodenal mucosa: stimulates pancreas to secrete digestive enzymes in an alkaline (pH 8.4) bicarbonate-rich fluid Cholecystokinin-panceozymin (CCK-PZ) Vagal stimulation: secretomotor
- 36. 10. DIFFERENT TYPESOF PANCREATIC TUMORS Chronic pancreatitis may be the main cause Carcinoma of pancreas: 85% are ductal adenocarcinomas Serous and mucinous cystadenomas including intraductal papillary mucinous neoplasms (IPMNs) Lymphangiomas, dermoid cysts
- 37. NEURO-ENDOCRINE TUMORS OFPANCREAS These include: Insulinoma, Gastrinoma, VIPoma, Glucagonoma, Somatostatinoma, Carcinoid, ACTHoma (causing Cushing’s syndrome), GRFoma (causing acromegaly)
- 38. 11. MANAGEMENT OFDIFFERENT TYPES OF PANCREATIC TUMORS 1/3rd of pancreatic tumors arise in its head Ampullary carcinoma Causing characteristic painless obstructive jaundice Pruritus, dark urine, pale stools, steatorrhea If no jaundice, symptoms are vague e.g. discomfort, anorexia, weight loss
- 39. INVESTIGATIONS CBC, UCE,FBS, RBS, LFTs USS Contrast CT/MRI ERCP ±Transduodenal or Transgastric FNA or Trucut biopsy performed under EUS guidance Percutaneous transperitoneal biopsy should be avoided
- 40. PREOPERATIVE PREPARATION Ina patient with obstructive jaundice: a. Well hydration to prevent hepatorenal shut down b. Vitamin K injections c. Prophylactic antibiotics
- 41. TREATMENT Curative surgeryif possible ± chemotherapy of 5-FU, radiotherapy is not effective 1. Pylorus-preserving panceatoduodenectomy (PPPD) 2. Whipple procedure 3. Total pancreatectomy if the disease is multifocal 4. Distal pancreatectomy with splenectomy + local lymphadenectomy: tumors of body/tail
- 42.
- 43. CONTRAINDICATIONS TO SURGICALRESECTION Presence of: 1. Hepatic or peritoneal metastases 2. Lymph node metastases distant from the pancreatic head 3. Encasement of the SMA, hepatic or coeliac artery
- 44. Palliation of pancreaticcancer A.Relieve jaundice & treat biliary sepsis Surgical biliary bypass Stent placed at ERCP or PTC B.Improve gastric emptying Surgical gastroenterostomy Duodenal stent C.Pain relief Stepwise escalation of analgesia Coeliac plexus block Transthoracic splanchnicectomy D.Symptom relief & quality of life Encourage normal activities Enzyme replacement for steatorrhea Treat diabetes E.Consider chemotherapy
- 45. References: Bailey& Love’s Short Practice of Surgery; 26th Edition; Chapters 52, 65, 68