Surgery GI 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
  • Clinical shock: restlessness, acute hypotension, tachycardia, thready peripheral pulse, pallor, cold clammy skin.Sign of liver disease & portal hypertension: spider naevi, bruising, palmarerythema, clubbing, jaundice, hepatomegaly, ascites.Sign of GI disease: lymphadenopathy, Virchow’s node, abdominal tenderness or masses.Sign of bleeding abnormalities: telangiectasis, purpura, ecchymoses, petichiae, bleeding gums, lymphadenopathy.Bloody / black stools on per rectal examination.
  • 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.
  • Surgery GI bleeding

    1. 1. GASTROINTESTINAL BLEEDING<br />NUR JASHIMAH IDAYU JAMALUDIN<br />TAN LAY TENG<br />MOHD HANAFI RAMLEE<br />1/81<br />
    2. 2. CONTENTS<br />Anatomy<br />Definition<br />Epidemiology<br />Clinical features<br />Aetiology<br />History & Examination<br />Investigation<br />Management<br />2/81<br />
    3. 3. Major duodenal papilla<br />JunctionB/w prox. 2/3 and distal 1/3 <br /> of tranverse colon. <br />Midway of anal canal <br />FOREGUTAbdominal esophagus<br />MIDGUT<br /> Major duodenal papilla<br />HINDGUT<br /> Junction B/w prox 2/3 and <br /> distal 1/3 of tranverse colon <br />ANATOMY OF GIT<br />3/81<br />
    4. 4. ARTERIAL SUPPLY<br />Mostly by anterior branch of abdominal aorta<br />4/81<br />
    5. 5. PORTAL VEIN<br />Union of splenic vein and sup. Mesentric vein<br />Tributaries ;<br /> -right and left gastric veins<br /> -cystic veins<br /> -para umbilical veins<br />Portal vein drains to inferior vena cava (systemic system) through hepatic vein<br />5/81<br />
    6. 6. PORTAL-SYSTEMIC ANASTOMOSES<br />Lower 3rd of esophagus<br /> Left gastric vein<br />Azygosvein<br />Anal canal<br /> Superior rectal vein<br /> Inferior rectal vein<br />Umbilicus <br />Paraumbilicalvein<br /> Superficial vein of anterior abdominal wall<br />Bare area of liver<br /> Vein in liver<br /> Diaphragmatic/phrenicvein<br />Retroperitoneal organs<br /> Colic vein<br /> Lumbar/renal vein <br />6/81<br />
    7. 7. INTRODUCTION<br />Gastrointestinal bleeding describe every form of haemorrhage in the GIT, from the pharynx to the rectum.<br />Can be divided into 2 clinical syndromes:-<br /> - upper GI bleed (pharynx to ligament of Treitz)<br /> - lower GI bleed (ligament of Treitz to rectum)<br />LIGAMENT OF TREITZ<br />7/81<br />
    8. 8. UPPERGASTROINTESTINAL BLEEDING<br />8/81<br />
    9. 9. EPIDEMIOLOGY<br />Upper GI bleed remains a major medical problem.<br />About 75% of patient presenting to the emergency room with GI bleeding have an upper source.<br />In-hospital mortality of 5% can be expected.<br />The most common cause are peptic ulcer, erosions, Mallory-Weiss tear & esophageal varices.<br />9/81<br />
    10. 10. CLINICAL FEATURES<br />Haematemesis : vomiting of blood whether fresh and red or digested and black.<br />Melaena : passage of loose, black tarry stools with a characteristic foul smell.<br />Coffee ground vomiting : blood clot in the vomitus.<br />Hematochezia: passage of bright red blood per rectum (if the haemorrhage is severe).<br />10/81<br />
    11. 11. CLINICAL FEATURES<br />Haematemesis without malaenais generally due to lesions proximal to the ligament of Treitz, since blood entering the GIT below the duodenum rarely enters the stomach.<br />Malaena without haematemesisis usually due to lesions distal to the pylorus<br />Approximately 60mL of blood is required to produced a single black stool.<br />11/81<br />
    12. 12. AETIOLOGY<br />Oesophagus<br /> -Oesophagealvarices<br /> -Oesophageal CA<br /> -Reflux oesophagitis<br /> -Mallory-Weiss syndrome<br />LOCAL<br /> Stomach<br />-Gastric ulcer<br /><ul><li>Erosive gastritis</li></ul>-Gastric CA<br />-gastric lymphoma<br />-gastric leiomyoma<br />-Dielafoy’s syndrome<br />-Haemophilia<br /> -Leukemia<br /> -Thrombocytopenia<br /> -Anti-coagulant therapy<br />GENERAL<br /> Duodenum<br />-Duodenal ulcer<br />-Duodenitis<br />-Periampullarytumour<br />-Aorto-duodenal fistula<br />12/81<br />
    13. 13. 13/81<br />
    14. 14. OESOPHAGEAL VARICES<br />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).<br />Most commonly : lower esophagus.<br />14/81<br />
    15. 15. Esophageal varices: a view of the everted esophagus and gastroesophageal junction, showing dilated submucosal veins (varices). <br />15/81<br />
    16. 16. OESOPHAGEAL VARICES: PORTAL HYPERTENSION<br />16/81<br />
    17. 17. OESOPHAGEAL VARICES: PATHOPHYSIOLOGY<br />Portal venous hypertension<br />Resistance to flow in portal venous system<br />Pressure<br />Portal systemic shunting<br />(Abnormal venous communication between portal system and systemic venous circulation)<br />Appearing of large submucosal veins at lower end of oesophagus and gastric fundus<br />Haemorrhage due to intravariceal pressure<br />17/81<br />
    18. 18. OESOPHAGEAL VARICES<br />Sudden onset<br />Painless<br />Large volume of blood<br />Dark red<br />History of (alcoholic) liver disease<br />Physical findings of portal hypertension – ascites, splenomegaly<br />18/81<br />
    19. 19. OESOPHAGEAL VARICES<br />Management<br /> - blood transfusion<br /> - endoscopic variceal injection with sclerosant or banding.<br /> - sengstaken tube<br />19/81<br />
    20. 20. MALLORY-WEISS TEAR<br />Longitudinal tears at the oesophagogastric junction.<br />may occur after any event that provokes a sudden rise in intragastric pressure or gastric prolapse into the esophagus. <br />Clinical features:<br /> - An episode of haematemesis<br /> following retching or vomiting.<br /> - melaena<br /> - hematochezia<br /> - syncope<br /> - abdominal pain.<br />Precipitating factors:<br /> - hiatus hernia <br /> - retching & vomiting <br /> - straining<br /> - hiccuping<br /> - coughing<br /> - blunt abdominal trauma <br /> - cardiopulmonary resuscitation<br />20/81<br />
    21. 21. MALLORY-WEISS TEAR: MANAGEMENT<br /> - Bleeding from MWTs stops spontaneously in 80-90% of patients <br /> - A contact thermal modality, such as multipolarelectrocoagulation (MPEC) or heater probe, with or without epinephrine injection, is typically used to treat an actively bleeding <br /> - Epinephrine injection -reduces or stops bleeding via a mechanism of vasoconstriction and tamponade<br /> - Endoscopic band ligation <br /> - Endoscopic hemoclipping<br />21/81<br />
    22. 22. ESOPHAGEAL CANCER<br />8th most common cancer seen throughout the world.<br />40% occur in the middle 3rd of the oesophagus and are squamous carcinomas.<br />adenoCA (45%) occur in the lower 3rd of the oesophagus and at the cardia.<br />Tumours of the upper 3rd are rare (15%)<br />22/81<br />
    23. 23. ESOPHAGEAL CANCER<br />SQUAMUS CELL CARCINOMA<br />ADENOCARCINOMA<br />-more common in men.<br />-risk factor:<br /> - tobacco smoking<br /> - heavy alcohol<br /> intake<br /> - plummer-vinson syndrome<br /> - achalasia<br /> - coeliac disease<br /> - tylosis<br /> - diet deficient in<br /> vitamins<br />high dietary carotenoids & vitamin C possibly decrease the risk.<br /> - arise in the columnar lined epithelium of the lower oesophagus.<br /> - risk factor:<br /> - long-standing GORD<br /> - barrett’soesophagus<br /> - tobacco smoking<br />23/81<br />
    24. 24. ESOPHAGEAL CANCER: CLINICAL FEATURES<br />Dysphagia<br /> - progressive & unrelenting<br /> - initially there is difficulty in swallowing solids, but eventually dysphagia for<br /> liquids also occur.<br />Odynophagia<br /> - retrosternal pain on swallowing.<br />Regurgitation<br />Aspiration pneumonitis<br />Weight loss<br />Anorexia<br />Anemia<br />Lassitude<br />24/81<br />
    25. 25. ESOPHAGEAL CANCER: TNM STAGING<br />T<br />Tumour confined to submucosa<br />Tumour extends into muscularispropria<br />Tumours extend outside muscle layer<br />Tumour invades adjacent structures<br />Lymph node metastases to paraoesophageal, cardia or left gastric regions.<br />No other metastatic spread<br />Lymph node metastases to all other areas. Metastases to liver, lung, brain, bone, etc.<br />N<br />M<br />25/81<br />
    26. 26. PEPTIC ULCER<br />gastric ulcer & duodenal ulcer<br />Caused by imbalance between secretion of acid and pepsin, and mucosal defence mechanism.<br />AETIOLOGY<br />-Helicobacter pylori infection<br />-Zollinger-ellison syndrome<br />-NSAIDs<br />-others: stress, smoking,alcohol, steroid<br />SIGNS & SYMPTOMS <br /><ul><li>epigastric pain
    27. 27. haematemesis
    28. 28. Melaena
    29. 29. heartburn</li></ul>26/81<br />
    30. 30. PEPTIC ULCER: PATHOGENESIS<br />Predisposing factors including H.pylori infection of mucosa<br />Acid-pepsin attack and/or breach of mucosal protection<br /> Acute inflammation resolution<br /> Destruction of mucosa<br /> Mucosal ulceration mucosal regeneration<br />Extension through submucosal & muscular layers causing deep ulceration<br />Perforation erosion of major granulation tissue<br /> blood vessel formed & attemps repair <br /> Peritonitis massive haemorrhage chronic & relapsing ulceration<br />27/81<br />
    31. 31. PEPTIC ULCER<br />28/81<br />
    32. 32. PEPTIC ULCER: COMPLICATION<br />Haemorrhage<br /> - posterior duodenal ulcer erode the gastroduodenal<br /> artery<br /> - lesser curve gastric ulcers erode the left gastric artery<br />Perforation<br /> - generalized peritonitis<br /> - signs of peritonitis<br />Pyloric obstruction<br /> - profuse vomiting, LOW, dehydrated, weakness, constipation<br />29/81<br />
    33. 33. PEPTIC ULCER: TREATMENT<br />Antacid – aluminium/Mg hydroxide, Mg Trisiclate<br />Mucosal protective agents – sucralfate<br />Prostaglandin analogues – misoprostol<br />H2 receptor antagonist – cimetidine & ranitidine<br />Proton pump inhibitor – omeprazole & lansoprazole<br />H.pylori eradication<br /> - triple therapy :metronidazole,amoxycilin,erythromycin<br />surgery should be done if <br /> -failed medical treatment<br /> -vagotomy, gastrectomy, pyloroplasty<br />30/81<br />
    34. 34. EROSIVE GASTRITIS<br />Acute mucosal inflammatory process<br />Accompanied by hemorrhage into the mucosa and sloughing of the superficial epithelium (erosion).<br />31/81<br />
    35. 35. EROSIVE GASTRITIS: AETIOLOGY<br /> - NSAIDs<br /> - alcohol<br /> - smoking<br /> - chemotherapy<br /> - uraemia<br /> - stress <br />- ischaemia and shock<br /> - suicide attempts <br /> - mechanical trauma<br /> - distal gastrectomy<br />32/81<br />
    36. 36. EROSIVE GASTRITIS: CLINICAL FEATURES<br /> - asymptomatic<br /> - epigastric pain with nausea & vomiting<br /> - haematemesis and melaena<br /> - fatal blood loss<br />It is one of the major causes of haemetemesis, particularly in alcoholic!<br />33/81<br />
    37. 37. GASTRIC CANCER<br />BENIGN GASTRIC NEOPLASM<br /> - adenomatous polyps<br /> - leiomyoma<br /> - neurogenictumour<br /> - fibromata<br /> - lipoma<br /> - gastric adenocarcinoma (90%)<br /> - lymphomas<br /> - smooth muscle tumour<br />GASTRIC CARCINOMA<br />34/81<br />
    38. 38. GASTRIC CANCER<br />60-80 years age group.<br />Male:female , 2:1<br /> - diet<br /> - H.pylori infection<br /> - gastric polyps<br /> - gastroenterostomy<br /> - chronic gastric ulcer disease<br /> - chronic atrophic gastritis<br /> - intestinal metaplasia<br /> - gastric dysplasia<br /> - host factors<br />AETIOLOGICAL FACTOR<br />35/81<br />
    39. 39. GASTRIC CANCER: TNM STAGING<br />T<br />T1 tumour extends to lamina propria or submucosa.<br />T2 tumour extend into muscle<br />T3 tumour extend into serosa<br />T4 tumour invades adjacent structures<br />N0 no lymph node involvement<br />N1 fewer than 7 lymph node involved by tumour<br />N2 7-15 lymph node involved by tumour<br />N3 more than 15 lymph node involved by tumour<br />M0 no metastases<br />M1 metastases present<br />N<br />M<br />36/81<br />
    40. 40. GASTRIC CANCER<br />Early signs<br /> -Indigestion<br /> -Flatulence<br /> -Dyspepsia<br />Late signs<br /> - LOW<br /> -anemia<br /> -dysphagia<br /> -vomiting<br /> -epigastric/back pain<br /> - epigastric mass<br /> -sign of metastases (jaundice, ascites, diarrhoea, intestinal obstruction)<br />CLINICAL FEATURES<br />TREATMENT<br /><ul><li>Radical total gastrectomy
    41. 41. Palliative resection
    42. 42. Palliative bypass</li></ul>37/81<br />
    43. 43. DIEULAFOY’S DISEASE<br /><ul><li>Rare – erosion of mucosa overlying artery in stomach causes necrosis arterial wall & resultant hemorrhage.
    44. 44. Gastric arterial venous abnormality
    45. 45. covered by normal mucosa
    46. 46. profuse bleeding coming from an area of apparently normal mucosa.</li></ul>38/81<br />
    47. 47. DUODENITIS<br />AETIOLOGY<br /> - aspirin, <br /> - NSAIDs<br /> - high acid secretion <br />CLINICAL FEATURE<br /> - Symptoms are similar to peptic ulcer disease<br /> - stomach pain<br /> -bleeding from the intestine<br /> - nausea & vomiting<br /> - LOA<br /> - intestinal obstruction(rare) <br />39/81<br />
    48. 48. DUODENITIS<br />INVESTIGATION<br />MANAGEMENT<br />- endoscopy, may be some redness and nodules in the wall of the small intestine. <br />- Sometimes, it can be more severe and there may be shallow, eroded areas in the wall of the intestine, along with some bleeding<br /><ul><li>stop all medications that can make things worse (aspirin & NSAIDS)
    49. 49. H2 receptor blockers (ranitidine/cimetidine) or proton pump inhibitors (omeprazole) reduce the acid secretion by the stomach</li></ul>40/81<br />
    50. 50. HISTORY TAKING<br /> - when?<br /> - have u vomited blood/passed black tarry stools?<br /> - had both haematemesis & malaena?<br /> - have u had, bleeding from the nose? Bloody expectoration? A dental extraction?<br />-what is the color, the appearance of the vomited blood?<br /> - red? Dark red? Brown? Black?<br /> - ‘coffee ground appearance?<br /> - bright red & frothy?<br /> - what is the color of the stool? Bright red? Black tarry?<br /> - have u vomited blood only once/several times?<br /> - has the bleeding been abrupt/massive?<br /> - have u had >1 black, tarry stool within a 24-h period?<br /> - for how long have the tarry stools persisted?<br />MODE OF ONSET<br />CHARACTER<br />EXTENT AND RATE<br />41/81<br />
    51. 51. HISTORY TAKING<br /> - retching & severe nonbloody vomiting?<br /> - lightheadedness? Nausea? Thirst? Sweating?<br /> - faintness when lying down/when standing/syncope?<br /> - following the haemorrhage did you have diarrhea?<br /> - aspirin? anticoagulant therapy? iron preparation?<br /> - age of the patient?<br /> - what is your smoke/alcohol intake?<br /> - have there been similar episode in the past? When? Diagnosis?<br /> - were u hospitalized on this occasion? Did u receive a transfusion?<br /> - are there any other members of your family who have intestinal disease/bleeding tendency/peptic ulcer/liver disease, History of Malignancy?<br />OTHER SYMPTOMS<br />IATROGENIC FACTORS<br />PREVIOUS EPISODES<br />FAMILY HISTORY<br />42/81<br />
    52. 52. PHYSICAL EXAMINATION:UPPER GI BLEED<br />RECTAL<br />GENERAL INSPECTION<br /><ul><li>Perianal Skin Lesion
    53. 53. Masses
    54. 54. Melaena
    55. 55. SupraclavicularLN
    56. 56. Cervical LN
    57. 57. AxillaryLN
    58. 58. Inguinal LN
    59. 59. Confusion ( Shock, liver failure….)
    60. 60. Neurological Deficit
    61. 61. Anaemic
    62. 62. Bruishing/ Purpura
    63. 63. Cachexic
    64. 64. Dehydrated
    65. 65. Jaundice
    66. 66. Inspection - distension, scar, prominent vein.
    67. 67. Palpation - tenderness, mass/ organomegaly
    68. 68. Percussion - shifting dullness, fluid thrill.
    69. 69. Auscultation - hyperactive bowel sound.</li></ul>LYMPH NODES<br />ABDOMEN<br />CNS<br />43/81<br />
    70. 70. PHYSICAL SIGN<br />Clinical shock<br />Systolic BP < 100mmHg<br />Pulse rate > 100 bpm<br />Postural sign: patient place in a upright position <br /> – pulse rate rises 25% or more<br /> - systolic BP alls 20mmHg or more<br />Sign of liver disease & portal hypertension<br />Sign of GI disease<br />Sign of bleeding abnormalities<br />Bloody / black stools on per rectal examination.<br />44/81<br />
    71. 71. INVESTIGATIONS<br /> - full blood count – Hb, WCC<br /> - liver function test – cirrhosis<br /> - coagulation profile<br /> - renal profile<br /> - RBC morphology<br /> - OGDS<br /> - Barium meal / Double-contrast barium meal<br /> - Ultrasound<br /> - CT scan<br />BASELINE INVESTIGATION<br />IMAGING<br />45/81<br />
    72. 72. Acute Upper Gastrointestinal Bleed<br />Routine Blood Test<br />Resuscitation and Risk Assessment<br />Endoscopy (within 24 hrs)<br />Varices<br />Peptic Ulcer<br />No obvious cause<br />Major SRH<br />Minor SRH<br />Minor Bleed<br />Major Bleed<br />Management Varices<br />Eradicate H.pylori & Risk Reduction<br />Endoscopic Treatment<br />Other colonoscopy or angiography<br />Failure<br />OVERVIEW:MANAGEMENT OF UPPER GI BLEED<br />Surgical<br />46/81<br />
    73. 73. RESUSCITATION<br />airway and oxygen<br />Insert 2 large-bore (14-16G) IV cannulate take blood<br />IV colloid - crossmatched. <br />In a dire emergency, give O Rh-ve blood.<br />haemodynamically stable.<br />Correct clotting abnormalities<br />Monitor<br />Insert urinary catheter and monitor hourly urine output if shocked.<br />Consider a CVP line to monitor CVP and guide fluid replacement.<br />Organize a CXR, ECG, and check arterial blood gases in high-risk patient.<br />Arrange an urgent endoscopy.<br />Notify surgeon of all severe bleeds on admision.<br />47/81<br />
    74. 74. BLOOD TRANFUSION<br />INDICATION OF BLOOD TRANSFUSION<br />BLOOD TEST<br />Haemoglobin - May be normal during the acute stages until haemodilution occurs<br />Urea and electrolytes - Elevated blood urea suggests severe bleeding<br />Cross match for transfusion - Two units of blood are sufficient unless bleeding is extreme.<br />If the transfusion is not needed urgently, group the blood and save the serum<br />LFT and coagulation profile<br />1.Systolic BP < 110 mmHg<br />2.Postural hypotension<br />3.Pulse > 110/min<br />4.Haemoglobin <8g/dl<br />5.Angina or cardiovascular disease with a Haemoglobin <10g/dl<br />48/81<br />
    75. 75. DETECTION & ENDOSCOPIC<br />Used to detect the site of bleeding.<br />May also be used in a therapeutic capacity (active bleeding from the ulcer, the presence of a visible vessel, adherent clot overlying the ulcer)<br />Injection sclerotherapyis used commonly. Other method include the use of heat probes and lasers.<br />Angiography in whom endoscopy does not identify the bleeding point. Limitation: can only detect active bleeding of greater than 1mL/min.<br />49/81<br />
    76. 76. FORREST CLASSIFICATION FOR BLEEDING PEPTIC ULCER<br />Ia: Spurting Bleeding<br />Ib: Non spurting active bleeding<br />IIa: visible vessel (no active bleeding)<br />IIb: Non bleeding ulcer with overlying clot (no visible vessel)<br />IIc: Ulcer with hematin covered base<br />III: Clean ulcer ground (no clot, no vessel)<br />Major SRH<br />Minor SRH<br />50/81<br />
    77. 77. MANAGEMENT<br />MEDICAL<br />H2 receptor antagonist - cimetidine, ranitidine<br />Proton pump inhibitors – omeprazole, lanzoprazole<br />H. pyloriirradication<br />Triple regimen – proton pump inhibitor + 2 antibiotics given for 1 week (elimination rate > 90%) <br /> e.g. Omeprazol + metronidazole/amoxycillin + clarithromycin<br />GU– remove ulcer, gastrin secreting zone <br /> – Billroth I gastrectomy<br />DU – Polya or Billroth II gastrectomy<br /> – Vagotomy<br />SURGICAL<br />51/81<br />
    78. 78. UPPER GI BLEED:RISK FACTORS FOR DEATH<br />1. Advanced AGE<br />2. SHOCKon admission(pulse rate >100 beats/min; systolic blood pressure < 100mmHg)<br />3. COMORBIDITY (particularly hepatic or renal failure and disseminated malignancy)<br />4. Diagnosis (worst PROGNOSISfor advanced upper gastrointestinal malignancy)<br />5. ENDOSCOPIC FINDINGS (active, spurting haemorrhage from peptic ulcer; non-bleeding visible vessel)<br />6. REBLEEDING(increases mortality 10 fold)<br />52/81<br />
    79. 79. GASTROINTESTINAL BLEEDINGLOWER<br />53/81<br />
    80. 80. LOWER GI BLEED: AETIOLOGY<br />COLON<br />SMALL INTESTINE<br /> Carcinoma of colon<br /> Polyps eg:<br /> Familial adenomatouspolyposis<br /> Diverticular disease<br /> Inflamation<br />Ischaemic colitis<br /> Ulcerative colitis<br />Pseudomembranous colitis<br /> Angiodysplasia<br /> Haemorrhoids<br /> Fissure-in-ano<br /> Anal carcinoma<br /> Anal wart<br />Crohn’s disease<br /> Diverticulaeg: <br />Meckel’sdiverticulum,<br />Jejujanaldiverticulosis<br /> Benign neoplasm eg:<br />Peutz-Jegher’s syndrome <br />Leiomyoma. <br /> Malignant neoplasm eg: <br /> Lymphoma, <br /> Angiodysplasia<br /> Rectal carcinoma and polyps<br /> Rectal prolapse<br />PACID<br />cDNA<br />ANUS<br />RECTUM<br />wCHF<br />PC<br />54/81<br />
    81. 81. HISTORY TAKING:RECTAL BLEEDING<br />Blood on its own or streaking the stool:<br /> Rectum : polyps or carcinoma, prolapsed<br /> Anus : Haemorrhoids, Fissure-in-ano, Anal carcinoma.<br />Stool mixed with blood:<br /> GIT above sigmoid colon. <br /> Sigmoid carcinoma or diverticular disease.<br />Blood separate from the stool:<br /> Follows defaecation : Anal condition eg: Haemorrhoids.<br /> Blood is passed by itself : Rapidly bleeding carcinoma, inflammatory bowel disease, diverticulitis, or passed down from high up in the gut. <br />Blood is on the surface of the stool: suggest a lesion such as polyp or carcinoma further proximally either in the rectum or descending colon<br />Blood on the toilet paper:Fissure-in-ano, Heamorrhoids.<br />Loose, black, tarry, foul smelling stool:from the proximal of DJ flexure<br />55/81<br />
    82. 82. HISTORY TAKING:COLOUR OF BLOOD/DISCHARGE<br />Bright red/ Fresh blood: Rectum and anus.<br />Dark blood:<br /> Upper GIT to above rectum.<br /> Drugs eg: iron tablets- appear as greenish black formed stool.<br />Discharge apart from blood:-<br /> -Mucus- irritable bowel syndrome<br /> -Copious mucus- villous adenoma, frank cancer of the rectum<br /> -Mucus and pus- IBD, diverticular disease<br />56/81<br />
    83. 83. HISTORY TAKING<br />ALTER BOWEL HABIT<br />ITCHINESS<br />Causes: Allergic, anal warts, anal leak of mucus in haemorrhoid, excessive used of liquid paraffin, generalized disorder. eg: jaundice, diabetes mellitus.<br />Normal bowel<br />Intermittent bouts of constipation interrupted by diarrhoea: Carcinoma or Diverticular disease.<br />Diarrhoea: Inflammatory bowel disease or rectal villous tumour.<br />Tenesmus: Irritable bowel syndrome or abnormal mass of rectum or anal canal (e.g. CA, polyps or thrombosedhaemorrhoid)<br />ANAL PAIN<br />During pregnancy/childbirth: Fissure-in-ano, haemorrhoids.<br /> Throbbing, severe pain occur during defaecation: Fissure-in-ano.<br />57/81<br />
    84. 84. HISTORY TAKING<br />PREVIOUS HISTORY<br />Previous perianal disease<br />Inflammatory bowel disease<br />Peptic ulcer disease<br />Liver disease<br />Coagulopathy<br />DRUGS HISTORY<br /><ul><li>Laxative agent
    85. 85. Anti-parkinson agent
    86. 86. Anti-coagulant therapy eg: warfarin
    87. 87. NSAID’s-risk factor of PUD
    88. 88. Low fiber diet
    89. 89. Smoking</li></ul>FAMILY HISTORY<br /><ul><li>History of malignancy
    90. 90. Familial AdenomatousPolyposis</li></ul>SOCIAL HISTORY<br />58/81<br />
    91. 91. PHYSICAL EXAMINATION:LOWER GI BLEED<br />RECTAL<br />GENERAL INSPECTION<br /><ul><li>Perianal Skin Lesion
    92. 92. Masses
    93. 93. Melaena
    94. 94. SupraclavicularLN
    95. 95. Cervical LN
    96. 96. AxillaryLN
    97. 97. Inguinal LN
    98. 98. Confusion ( Shock, liver failure….)
    99. 99. Neurological Deficit
    100. 100. Anaemic
    101. 101. Bruishing/ Purpura
    102. 102. Cachexic
    103. 103. Dehydrated
    104. 104. Jaundice
    105. 105. Inspection - distension, scar, prominent vein.
    106. 106. Palpation - tenderness, mass/ organomegaly
    107. 107. Percussion - shifting dullness, fluid thrill.
    108. 108. Auscultation - hyperactive bowel sound.</li></ul>LYMPH NODES<br />SAME WITH UPPER GI BLEED<br />ABDOMEN<br />CNS<br />59/81<br />
    109. 109. INVESTIGATION<br />LABORATORY<br />Full Blood Count (FBC)<br />2. BUSE<br />3. Coagulation profile<br />Cross-matched (Transfusion)<br />1. Scintigraphy<br /> -Radioactive test using Technetium-99m (99mTc)-<br />Labelled red cells<br /> -diagnose ongoing bleeding at a rate as low as 0.1 mL/min<br />2. Mesenteric angiography<br /> -Can detect bleeding at a rate of more than 0.5 mL/min.<br />IMAGING<br />60/81<br />
    110. 110. IMAGING<br />3. Helical CT scan<br />Abdomen and pelvis <br />Can also be used when routine workup fails to determine the cause of active GI bleeding <br />Multiple criteria are used to establish the bleeding sites:<br /> -vascular extravasation of the contrast medium <br /> -contrast enhancement of the bowel wall<br /> -thickening of the bowel wall<br /> -spontaneous hyperdensity of the peribowel fat<br /> -vascular dilatations with helical CT. <br />61/81<br />
    111. 111. IMAGING<br />4.Colonoscopy<br />• Bleeding slowly or who have already stopped bleeding.<br />Biopsy<br />5.Proctosigmoidoscopy<br />Exclude an anorectal source of bleeding <br />6.Oesophagoduodenoscopy (OGDS)<br />To exclude upper GI bleeding<br />62/81<br />
    112. 112. IMAGING<br />7. Double-contrast barium enema<br />Elective evaluation of unexplained lower GI bleeding <br />Do not use in the acute hemorrhage phase<br />Small bowel enema<br />Often valuable in investigation of long-term, unexplained lower GI bleeding<br />Example of barium enema study showing ulcerative colitis of the colon<br />63/81<br />
    113. 113. INTUSSUSCEPTION<br />Common in children within 1st year of life<br />Symptoms: abdominal pain, red-currant-jelly stool<br />Signs: palpable mass at right iliac fossa<br />Procedure: Barium enema, laparotomy<br />64/81<br />
    114. 114. Colorectal polyps<br />Adenomatous polyps and adenomas<br />Has malignant potential<br />Morphology:<br /> -polypoid and pedunculated<br /> -dome-shaped and sessile<br />Histology:<br /> -degree of epithelial dysplasia is<br /> highly variable<br /> -carcinoma in situ<br /> -early invasive cancer:-<br /> invasion of tumour cells through basement membrane->muscularismucosa->submucosa<br />65/81<br />
    115. 115. TYPES OF COLORECTAL POLYPS<br /> 1.Tubular adenomas<br /> - small pedunculated / sessile lesions<br /> -retain a tubular form similar to normal colonic <br /> mucosa<br /> -least potential for malignant transformation<br /> 2. Villous adenomas<br /> -sessile and frond like lesions<br /> -secrete mucus<br /> -more dysplastic<br /> -greater potential for malignant change<br /> 3. Tubulo-villous adenoma<br /> -intermediate between tubular and villous <br /> adenoma<br /> -pedunculated, stalk is covered with normal <br /> epithelium <br />66/81<br />
    116. 116. SIGN AND SYMPTOM<br />Rectal bleeding<br />Iron deficiency anaemia<br />Mucus<br />Hypokalaemia<br />Tenesmus<br />Prolapse<br />Obstructive symptoms <br />67/81<br />
    117. 117. FAMILIAL ADENOMATOUS POLYPOSIS<br /><ul><li>Autosomal dominant defect in APC gene
    118. 118. Mid teen years- hundred / more adenomatous polyps
    119. 119. Average age of 40- colorectal cancer
    120. 120. Symptoms:</li></ul> -rectal bleeding<br /> -diarrhoea<br /><ul><li>Gardner’s syndrome= +desmoidtumours + osteomas of mandible & skull </li></ul>68/81<br />
    121. 121. INVESTIGATION<br />Sigmoidoscopy<br />Colonoscopy<br /> -gold standard<br /> -visualize, biopsy, remove<br /> -disadvantage: full day’s bowel preparation<br /> sedation<br /> risk of haemorrhage & <br /> perforation<br />CT pneumocolon<br /> -elderly / infirm patient<br /> -< invasive & not require sedation.<br /> -bowel preparation<br />Double contrast barium enema<br />69/81<br />
    122. 122. MANAGEMENT<br />Subtotal colectomy & ileorectal anastomosis<br />Panproctocolectomy & ileotomy / ileal pouch<br />Follow-up colonoscopies<br /> - an adenomatous polyp is found / a colorectal <br /> cancer has been treated<br /> -intervals depend on number, size & <br /> pathology of polyps<br />70/81<br />
    123. 123. ADENOCARCINOMA OF COLON & RECTUM<br />Rare < 50 years old, Common > 60 years old<br />Common site- sigmoid colon, rectum<br />Clinical features: <br /> -altered bowel habit & large bowel obstruction<br /> -rectal bleeding<br /> -iron deficiency anaemia<br /> -tenesmus<br /> -perforation<br /> -anorexia & weight loss<br />71/81<br />
    124. 124. ANGIODYSPLASIA<br /><ul><li>1 or multiple small mucosal or submucosal vascular malformation.
    125. 125. > 60 years old
    126. 126. Common site : ascending colon and caecum
    127. 127. Malformations consist of dilated tortuous submucosal veins
    128. 128. In severe cases, the mucosa is replaced by massive dilated deformed vessels
    129. 129. Clinical features: </li></ul> -acute / chronic rectal bleeding<br /> -iron deficiency anaemia<br />72/81<br />
    130. 130. INVESTIGATION<br />Colonoscopy <br /> -bright red 0.5-1cm diameter submucosal <br /> lesion<br /> -small dilated vessels<br />Mesenteric angiography<br />Radioactive test using technetium-99m –labeled red cells<br />73/81<br />
    131. 131. 74/81<br />
    132. 132. MANAGEMENT<br />colonoscopic diathermy<br />if patient seriously ill-> catheter is placed in the appendix stump and the colon irrigated progradely with saline or water-> on-table colonoscopy carried out and site of bleeding can be confirmed<br />75/81<br />
    133. 133. ISCHAEMIC COLITIS<br /><ul><li>Elderly
    134. 134. Transient ischaemia of a segment of a large bowel, followed by sloughing of mucosa
    135. 135. Common site –splenic flexure
    136. 136. Clinical features:</li></ul> -abdominal pain<br /> -rectal bleeding ( dark red)<br /> -1-3x over 12 hours<br /><ul><li>Complication- fibrotic sticture</li></ul>76/81<br />
    137. 137. HAEMORRHOIDS<br />M > F<br />Female- late pregnancy, puerperium<br />Supine lithotomy position- 3 ,7, 11 o’clock positions<br />Classification:<br /> 1st degree : never prolapse<br /> 2nd degree: prolapse during <br />defaecation but<br /> return spontaneously<br /> 3rd degree : remain prolapse but <br /> can be reduced digitally <br /> 4th degree : long-standing <br />prolapse cannot be <br /> reduced<br />77/81<br />
    138. 138. HAEMORRHOIDS: SIGNS & SYMPTOMS<br />Rectal bleeding<br />Perianal irritation & itching<br />Mucus leakage<br />Mild incontinence of flatus <br />Prolapse<br />Acute pain<br />Skin tags at anal margin<br />78/81<br />
    139. 139. ANAL FISSURE<br />Longitudinal tear in mucosa & skin of anal canal<br />M > F<br />Common site: midline in posterior anal margin<br />Clinical features:<br /> - acute pain during defaecation<br /> - fresh bleeding at defaecation<br />79/81<br />
    140. 140. DIVERTICULAR DISEASE<br /><ul><li>Rare < 40 years old
    141. 141. F > M
    142. 142. Causes: </li></ul> -Chronic lack of dietary fibre<br /> -Genetic<br /><ul><li>Common site: sigmoid colon
    143. 143. Clinical features:</li></ul> -diverticulosis (asymptomatic)<br /> -chronic grumbling diverticular pain (chronic constipation & episodic diarrhoea)<br />80/81<br />
    144. 144. MANAGEMENT<br />MEDICAL<br />SURGICAL<br />Vasoconstrictive agents: <br /> vasopressin<br />2. Therapeutic embolization:<br /> -Embolic agents: Autologous clot, Gelfoam, polyvinyl alcohol, microcoils, <br /> ethanolamine, and oxidized cellulose<br /> -Selective angiography<br />3. Endoscopic therapy:<br /> -Diathermy / laser coagulation<br /> -Short term control of bleeding during resuscitation<br /><ul><li>The bleeding point is localized, perform a limited segmental resection of the small or large bowel
    145. 145. Poor prognostic features:</li></ul> -age over 60 years <br /> -chronic history<br /> -relapse on full medical treatment<br /> -serious coexisting medical conditions<br />-> 4 units of blood transfusion required during resuscitation<br />81/81<br />
    146. 146. THANK YOU FOR YOUR aTTENTION<br />LUNCH TIME !!!<br />82/81<br />

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