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GIT BLEEDING

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  • Is an acute mucosal inflammatory process usually of a transient nature.May be accompanied by hemorrhage into the mucosa and in more severe circumstances, by sloughing of the superficial epithelium (erosion).
  • - heavy use of NSAIDs - excessive alcohol consumption - heavy smoking - treatment with cancer chemotherapy drugs - uraemia - severe stress (e.g. trauma, burns, surgery) - ischaemia and shock - suicide attempts with acid and alkali - mechanical trauma - after distal gastrectomy with reflux of bilious material
  • Rare – erosion of mucosa overlying artery in stomach causes necrosis arterial wall & resultant hemorrhage.Gastric arterial venous abnormality that has a characteristically histological apperance.The lesion itself is covered by normal mucosa and, when not bleeding, it may be invisible.If it can be seen while bleeding, all that may be visible is profuse bleeding coming from an area of apparently normal mucosa
  • inflammation and irritation of the wall of the first part of the small intestine.
  • endoscopy, may be some redness and nodules in the wall of the small intestine. - Sometimes, it can be more severe and there may be shallow, eroded areas in the wall of the intestine, along with some bleeding
  • coagulation profile – primary or secondary clotting defectsRBC morphology – hypochomic, microcytic anemia, chronic blood loss
  • Protect airway and give high-flow oxygenInsert 2 large-bore (14-16G) IV cannulate take blood for FBC, U&E, LFT, clotting, cross-match 4-6 units (1 unit per g/dL < 14g/dL)Give IV colloid while waiting for blood to be crossmatched. In a dire emergency, give group O Rh-ve blood.Transfuse until haemodynamically stable.Correct clotting abnormalities (vit K, FFP, platelet)Monitor pulse, BP, and CVP at least hourly until stable.Insert urinary catheter and monitor hourly urine output if shocked.Consider a CVP line to monitor CVP and guide fluid replacement.Organize a CXR, ECG, and check arterial blood gases in high-risk patient.Arrange an urgent endoscopy.Notify surgeon of all severe bleeds on admision.
  • Transcript

    • 1. By - CHARAN TEJASVI Ml-608
    • 2. ARTERIAL SUPPLY • Mostly by anterior branch of abdominal aorta Superior Inferior Celiac trunk - Mesenteric Mesenteric Foregut Artery - Midgut Artery - Hindgut• left gastic • inferior • sigmoid artery pancreaticod arteries• splenic artery uodenal• common artery • superior rectal hepatic artery • jejunal and artery ileal arteries • Left colic • middle colic artery artery • right colic artery • ileocolic artery 2/81
    • 3. PORTAL VEIN Union 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 2 clinical syndromes:- - upper GI bleed (pharynx to LIGAMENT OF ligament of Treitz) TREITZ - lower GI bleed (ligament of Treitz to 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 black 8/81
    • 8. AETIOLOGY LOCAL 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 -Dielafoy’s syndrome -Anti-coagulant therapy Duodenum -Duodenal ulcer -Duodenitis -Periampullary tumour -Aorto-duodenal fistula 9/81
    • 9. 10/81
    • 10. OESOPHAGEALVARICES• Abnormal dilatation of subepithelial and submucosal veins due to increased venous pressure from portal hypertension (collateral exist between portal system and azygous vein via lower oesophageal venous plexus).• Most commonly : lower esophagus. 11/81
    • 11. Esophageal varices: a view of the everted esophagus and gastroesophageal junction, showing dilated submucosal veins (varices). 12/81
    • 12. OESOPHAGEALVARICES • Management - blood transfusion - endoscopic variceal injection with sclerosant or banding. - Sengstaken Blakmore tube 13/81
    • 13. MALLORY-WEISSTEAR• Longitudinal tears at the oesophagogastric junction.• may occur after any event that provokes a sudden rise in intragastric pressure or gastric prolapse into the esophagus.Precipitating factors: - hiatus hernia - retching & vomiting - straining - hiccuping - coughing - blunt abdominal trauma - cardiopulmonary resuscitation 14/81
    • 14. MALLORY-WEISS TEAR: MANAGEMENT- Bleeding from MWTs stops spontaneously 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 the gastroduodenal artery - lesser curve gastric ulcers erode the left gastric artery• Perforation - generalized peritonitis - signs of peritonitis• Pyloric obstruction - profuse vomiting, LOW, dehydrated, weakness, constipation 17/81
    • 17. EROSIVE GASTRITIS• Acute mucosal inflammatory process• Accompanied by hemorrhage into the mucosa and sloughing of the superficial epithelium (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 of haemetemesis, particularly in alcoholic! 20/81
    • 20. GASTRIC CANCER BENIGN GASTRIC NEOPLASM- adenomatous polyps- leiomyoma- neurogenic tumour- fibromata- lipoma GASTRIC CARCINOMA- gastric adenocarcinoma (90%)- lymphomas- smooth muscle tumour 21/81
    • 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. DIEULAFOY’S DISEASE• Rare – erosion of mucosa overlying artery in stomach causes necrosis arterial wall & resultant hemorrhage.• Gastric arterial venous abnormality• covered by normal mucosa• profuse bleeding coming from an area of apparently normal mucosa. 23/81
    • 23. DUODENITIS AETIOLOGY - aspirin, - NSAIDs - high acid secretionCLINICAL FEATURE- Symptoms are similar to peptic ulcer disease- stomach pain- bleeding from the intestine- nausea & vomiting- intestinal obstruction(rare) 24/81
    • 24. DUODENITIS INVESTIGATION MANAGEMENT- endoscopy, may be -stop all medications that can some redness and make things worse (aspirin & nodules in the wall NSAIDS) of the small intestine.- Sometimes, it can -H2 receptor blockers be more severe and (ranitidine/cimetidine) or there may be proton pump inhibitors shallow, eroded (omeprazole) reduce the acid areas in the wall of secretion by the stomach the intestine, along with some bleeding 25/81
    • 25. INVESTIGATIONS BASELINE INVESTIGATION - Complete blood count - Liver function test - Coagulation profile - Renal profile - EGDS IMAGING - Barium meal / Double-contrast barium meal - Ultrasound - CT scan 26/81
    • 26. Acute Upper Gastrointestinal Bleed Routine Blood Test Resuscitation and Risk Assessment Endoscopy (within 24 hrs) Varices Peptic Ulcer No obvious causeManagement Major SRH Minor SRH Minor Major Varices Bleed Bleed Eradicate Endoscopic H.pylori & Other Treatment Risk colonoscopy or Reduction angiography Failure OVERVIEW: Surgical MANAGEMENT OF UPPER GI BLEED 27/81
    • 27. RESUSCITATION• airway and oxygen• Correct clotting abnormalities• Blood Transfusion• Monitor• Insert urinary catheter and monitor hourly urine output if shocked.• Consider a CVP line to monitor CVP and guide fluid replacement.• Organize a CXR, ECG, and check arterial blood gases in high-risk patient.• Arrange an urgent endoscopy.• Notify surgeon of all severe bleeds on admission. 28/81
    • 28. DETECTION &ENDOSCOPIC• Used to detect the site of bleeding.• May also be used in a therapeutic capacity (active bleeding from the ulcer, the presence of a visible vessel, adherent clot overlying the ulcer)• Injection sclerotherapy is used commonly. Other method include the use of heat probes and lasers.• Angiography in whom endoscopy does not identify the bleeding point. Limitation: 29/81
    • 29. FORREST CLASSIFICATION FOR BLEEDING PEPTIC ULCER – Ia: Spurting Bleeding – Ib: Non spurting activeMajor SRH bleeding – IIa: visible vessel (no active bleeding) – IIb: Non bleeding ulcer with overlying clot (no visible vessel) – IIc: Ulcer with hematin coveredMinor SRH base – III: Clean ulcer ground (no clot, 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 1 week (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 diverticulum 34/81
    • 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 bleeding 36/81
    • 36. IMAGING 7. Double-contrast barium enema • Elective evaluation of unexplained lower GI bleeding • 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 colon 37/81
    • 37. Colorectal polyps• Adenomatous polyps and adenomas• Has malignant potential• Morphology: -polypoid and pedunculated -dome-shaped and sessile 38/81
    • 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 & RECTUM• Common > 60 years old• Common site- sigmoid colon, rectum• Clinical features: -altered bowel habit & large bowel obstruction -rectal bleeding -iron deficiency anaemia -tenesmus -perforation -anorexia & weight loss 40/81
    • 40. ANGIODYSPLASIA • 1 or multiple small mucosal or submucosal vascular malformation. • > 60 years old • Common site : ascending colon and caecum • Malformations consist of dilated tortuous submucosal veins • In severe cases, the mucosa is replaced by massive dilated deformed vessels • Clinical features: -acute / chronic rectal bleeding -iron deficiency anaemia 41/81
    • 41. 42/81
    • 42. ISCHAEMIC COLITIS• Elderly• Transient ischaemia of a segment of a large bowel, followed by sloughing of mucosa• Common site –splenic flexure• Clinical features: -abdominal pain -rectal bleeding ( dark red) -1-3x over 12 hours• Complication- fibrotic sticture 43/81
    • 43. HAEMORRHOIDS• M>F• Female- late pregnancy, puerperium• Supine lithotomy position- 3 ,7, 11 o’clock positions• Classification: 1st degree : never prolapse 2nd degree: prolapse during defaecation but return spontaneously 3rd degree : remain prolapse but can be reduced digitally 4th degree : long-standing prolapse cannot be reduced 44/81
    • 44. ANAL FISSURE • Longitudinal tear in mucosa & skin of anal canal • M>F • Common site: midline in posterior anal margin • Clinical features: - acute pain during defaecation - fresh bleeding at defaecation 45/81
    • 45. DIVERTICULAR DISEASE• Rare < 40 years old• F>M• Causes: -Chronic lack of dietary fibre -Genetic• Common site: sigmoid colon• Clinical features: -diverticulosis (asymptomatic) -chronic grumbling diverticular pain (chronic 46/81
    • 46. 47/81
    • 47. MANAGEMENT MEDICAL SURGICAL1. Vasoconstrictive agents: • The bleeding point is vasopressin localized, perform a limited segmental2. Therapeutic embolization: resection of the small or -Embolic agents: Autologous large bowel clot, Gelfoam, polyvinyl alcohol, microcoils, • Poor prognostic features: ethanolamine, and oxidized -age over 60 years cellulose -chronic history -Selective angiography -relapse on full medical3. Endoscopic therapy: treatment -Diathermy / laser coagulation -serious coexisting -Short term control of medical conditions bleeding during resuscitation -> 4 units of blood transfusion required 48/81

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