• View

  • Download

Embed Size (px)




  • 1. By - CHARAN TEJASVI Ml-608

2. ARTERIAL SUPPLY Mostly by anterior branch of abdominal aortaSuperiorInferior Celiac trunk - Mesenteric Mesenteric Foregut Artery - MidgutArtery - Hindgut left gastic inferior sigmoidarterypancreaticod arteries splenic arteryuodenal commonartery superior rectalhepatic artery jejunal andarteryileal arteries Left colic middle colic arteryartery right colicartery ileocolicartery 2/81 3. PORTAL VEINUnion of splenic vein and sup. Mesentric vein Tributaries ; -right and left gastric veins -cystic veins -para umbilical veins Portal vein drains to inferior vena cava (systemic system) through hepatic vein 3/81 4. INTRODUCTION Can be divided into 2clinical syndromes:-- upper GI bleed(pharynx toLIGAMENT OF ligament of Treitz) TREITZ- lower GI bleed(ligament of Treitzto rectum)4/81 5. EPIDEMIOLOGY Upper GI bleed remains a major medical problem. About 75% of patient presenting to the emergency room with GI bleeding have an upper source. In-hospital mortality of 5% can be expected. The most common cause are peptic ulcer, erosions, Mallory-Weiss tear & esophageal varices. 6/81 6. CLINICAL FEATURES Haematemesis : vomiting of blood (fresh and red or digested and black). Melaena : passage of loose, black tarry stools with a characteristic foul smell. Coffee ground vomiting : blood clot in the vomitus. Hematochezia : passage of bright red blood per rectum (if the haemorrhage is severe). 7/81 7. CLINICAL FEATURES Haematemesis without malaena is generally due to lesions proximal to the ligament of Treitz, since blood entering the GIT below the duodenum rarely enters the stomach. Malaena without haematemesis is usually due to lesions distal to the pylorus Approximately 60mL of blood is required to produced a single black8/81 8. AETIOLOGYLOCAL Stomach Oesophagus -Gastric ulcer GENERAL-Oesophageal varices-Erosive gastritis -Haemophilia-Oesophageal CA -Gastric CA-Leukemia-Reflux oesophagitis-gastric lymphoma-gastric leiomyoma -Thrombocytopenia-Mallory-Weiss syndrome -Dielafoys syndrome -Anti-coagulant therapy Duodenum-Duodenal ulcer-Duodenitis-Periampullary tumour-Aorto-duodenal fistula 9/81 9. 10/81 10. OESOPHAGEALVARICES Abnormal dilatation of subepithelial andsubmucosal veins due to increasedvenous pressure from portalhypertension (collateral exist betweenportal system and azygous vein vialower oesophageal venous plexus). Most commonly : lower esophagus. 11/81 11. Esophageal varices: a view of the evertedesophagus andgastroesophagealjunction, showing dilated submucosalveins (varices).12/81 12. OESOPHAGEALVARICES Management - blood transfusion - endoscopic variceal injection with sclerosant or banding. - Sengstaken Blakmore tube13/81 13. MALLORY-WEISSTEAR Longitudinal tears at theoesophagogastric junction. may occur after any event thatprovokes a sudden rise inintragastric pressure or gastricprolapse into the esophagus.Precipitating factors:-hiatus hernia-retching & vomiting-straining-hiccuping-coughing-blunt abdominal trauma-cardiopulmonaryresuscitation 14/81 14. MALLORY-WEISS TEAR:MANAGEMENT- Bleeding from MWTs stopsspontaneously in 80-90% ofpatients- A contact thermal modality, suchas multipolar electrocoagulation(MPEC) or heater probe.- Epinephrine injection -reducesor stops bleeding via a mechanismof vasoconstriction and tamponade- Endoscopic band ligation- Endoscopic hemoclipping 15/81 15. ESOPHAGEAL CANCER 8th most common cancer seen throughout the world. 40% occur in the middle 3rd of the oesophagus and are squamous carcinomas. adenoCA (45%) occur in the lower 3rd of the oesophagus and at the cardia. Tumours of the upper 3rd are rare (15%)16/81 16. PEPTIC ULCER:COMPLICATION Haemorrhage- posterior duodenal ulcer erode thegastroduodenal artery- lesser curve gastric ulcers erode theleft gastric artery Perforation- generalized peritonitis- signs of peritonitis Pyloric obstruction- profuse vomiting, LOW, dehydrated,weakness, constipation17/81 17. EROSIVE GASTRITIS Acute mucosalinflammatory process Accompanied byhemorrhage into themucosa and sloughingof the superficialepithelium (erosion).18/81 18. EROSIVE GASTRITIS:AETIOLOGY - NSAIDs - alcohol - smoking - chemotherapy - uraemia - stress - ischaemia and shock - suicide attempts - mechanical trauma - distal gastrectomy 19/81 19. EROSIVE GASTRITIS:CLINICAL FEATURES- asymptomatic- epigastric pain with nausea & vomiting- haematemesis and melaena- fatal blood loss It is one of the major causes ofhaemetemesis, particularly in alcoholic! 20/81 20. GASTRIC CANCERBENIGN GASTRIC NEOPLASM-adenomatous polyps-leiomyoma-neurogenic tumour-fibromata-lipoma GASTRIC CARCINOMA-gastric adenocarcinoma (90%)-lymphomas-smooth muscle tumour21/81 21. GASTRIC CANCER CLINICAL FEATURES TREATMENTEarly signs-Indigestion Radical total gastrectomy-Flatulence Palliative resection-Dyspepsia Palliative bypassLate signs- LOW-anemia-dysphagia-vomiting-epigastric/back pain- epigastric mass-sign of metastases (jaundice, ascites, diarrhoea, intestinal obstruction) 22/81 22. DIEULAFOYS DISEASE Rare erosion of mucosa overlying arteryin stomach causes necrosis arterial wall &resultant hemorrhage. Gastric arterial venous abnormality covered by normal mucosa profuse bleeding coming from an area ofapparently normal mucosa. 23/81 23. DUODENITISAETIOLOGY- aspirin,- NSAIDs- high acid secretionCLINICAL FEATURE- Symptoms are similar topeptic ulcer disease- stomach pain- bleeding from the intestine- nausea & vomiting- intestinal obstruction(rare) 24/81 24. DUODENITIS INVESTIGATIONMANAGEMENT- endoscopy, may be-stop all medications that cansome redness and make things worse (aspirin &nodules in the wallNSAIDS)of the smallintestine.- Sometimes, it can-H2 receptor blockersbe more severe and (ranitidine/cimetidine) orthere may be proton pump inhibitorsshallow, eroded(omeprazole) reduce the acidareas in the wall of secretion by the stomachthe intestine, alongwith some bleeding25/81 25. INVESTIGATIONS BASELINE INVESTIGATION-Complete blood count-Liver function test-Coagulation profile-Renal profile-EGDSIMAGING-Barium meal / Double-contrast barium meal-Ultrasound-CT scan26/81 26. Acute Upper Gastrointestinal BleedRoutine Blood TestResuscitation and Risk AssessmentEndoscopy (within 24 hrs)VaricesPeptic UlcerNo obvious causeManagementMajor SRHMinor SRH Minor MajorVaricesBleed BleedEradicate Endoscopic H.pylori & Other Treatment Riskcolonoscopy orReduction angiographyFailure OVERVIEW:Surgical MANAGEMENT OF UPPER GI BLEED27/81 27. RESUSCITATION airway and oxygen Correct clotting abnormalities Blood Transfusion Monitor Insert urinary catheter and monitorhourly urine output if shocked. Consider a CVP line to monitor CVP andguide fluid replacement. Organize a CXR, ECG, and check arterialblood gases in high-risk patient. Arrange an urgent endoscopy. Notify surgeon of all severe bleeds onadmission.28/81 28. DETECTION &ENDOSCOPIC Used to detect the site ofbleeding. May also be used in atherapeutic capacity (activebleeding from the ulcer, thepresence of a visiblevessel, adherent clot overlyingthe ulcer) Injection sclerotherapy is usedcommonly. Other methodinclude the use of heat probesand lasers. Angiography in whomendoscopy does not identifythe bleeding point. Limitation: 29/81 29. FORREST CLASSIFICATION FORBLEEDING PEPTIC ULCER Ia: Spurting Bleeding Ib: Non spurting activeMajor SRHbleeding IIa: visible vessel (no activebleeding) IIb: Non bleeding ulcer withoverlying clot (no visible vessel) IIc: Ulcer with hematin coveredMinor SRHbase III: Clean ulcer ground (noclot, no vessel) 30/81 30. MANAGEMENT MEDICAL H2 receptor antagonist - cimetidine, ranitidine Proton pump inhibitors omeprazole, lanzoprazole H. pylori irradication Triple regimen proton pump inhibitor + 2 antibiotics given for 1week (elimination rate > 90%)e.g. Omeprazol + metronidazole/amoxycillin + clarithromycin SURGICAL GU remove ulcer, gastrin secreting zone Billroth I gastrectomy DU Polya or Billroth II gastrectomy Vagotomy 31/81 31. UPPER GI BLEED:RISK FACTORS FOR DEATH1. Advanced AGE2. SHOCK on admission(pulse rate >100 beats/min; systolic blood pressure < 100mmHg)3. COMORBIDITY (particularly hepatic or renal failure and disseminated malignancy)4. Diagnosis (worst PROGNOSIS for advanced upper gastrointestinal malignancy)5. ENDOSCOPIC FINDINGS (active, spurting haemorrhage from peptic ulcer; non-bleeding visible vessel)6. RECURRENT BLEEDING (increases mortality 10 times)32/81 32. 33/81 33. LOWER GI BLEED:AETIOLOGY 1) Hemorrhoids 2) Diverticulosis 3) Arteriovenous malformations 4) Polyps 5) Inflammatory bowel disease 6) Infectious gastroenteritis 7) Meckel diverticulum34/81 34. INVESTIGATION LABORATORY 1.Full Blood Count (FBC) 2.BUSE 3.Coagulation profile 4.Cross-matched (Transfusion)IMAGING 1.Scintigraphy-Radioactive test using Technetium-99m (99mTc)- Labelled red cells-diagnose ongoing bleeding at a rate as low as 0.1 mL/min 2.Mesenteric angiography-Can detect bleeding at a rate of more than 0.5 mL/min.35/81 35. IMAGING 3. Helical CT scan 4.Colonoscopy 5.Proctosigmoidoscopy Exclude an anorectal source of bleeding 6.Esophagoduodenoscopy To exclude upper GI bleeding36/81 36. IMAGING 7. Double-contrast barium enema Elective evaluation of unexplained lower GIbleeding Do not use in the acute hemorrhage phase 8. Small bowel enema Often valuable in investigation of long-term, unexplained lower GI bleeding Example of barium enema study showing ulcerative colitis of the colon37/81 37. Colorectal polyps Adenomatous polyps andadenomas Has malignant potential Morphology: -polypoid and pedunculated-dome-shaped and sessile38/81 38. MANAGEMENT Subtotal colectomy & ileorectal anastomosis Panproctocolectomy & ileotomy / ileal pouch Follow-up colonoscopies - an adenomatous polyp is found / a colorectal cancer has been treated -intervals depend on number, size & pathology of polyps 39/81 39. ADENOCARCINOMA OF COLON &amp