This document provides information on gastrointestinal bleeding, including its anatomy, definition, epidemiology, clinical features, etiology, history and examination, investigation, and management. It discusses the major sites of upper and lower GI bleeding. For upper GI bleeding it covers topics such as esophageal varices, Mallory-Weiss tears, esophageal cancer, peptic ulcer disease, erosive gastritis, gastric cancer, and Dieulafoy's disease. For lower GI bleeding it briefly mentions duodenitis. It provides details on the pathogenesis, clinical presentation, investigations and treatment of many of these conditions.

1. GASTROINTESTINAL BLEEDING NUR JASHIMAH IDAYU JAMALUDIN TAN LAY TENG MOHD HANAFI RAMLEE 1/81

2. CONTENTS Anatomy Definition Epidemiology Clinical features Aetiology History & Examination Investigation Management 2/81

3. Major duodenal papilla JunctionB/w prox. 2/3 and distal 1/3 of tranverse colon. Midway of anal canal FOREGUTAbdominal esophagus MIDGUT Major duodenal papilla HINDGUT Junction B/w prox 2/3 and distal 1/3 of tranverse colon ANATOMY OF GIT 3/81

4. ARTERIAL SUPPLY Mostly by anterior branch of abdominal aorta 4/81

5. 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 5/81

6. PORTAL-SYSTEMIC ANASTOMOSES Lower 3rd of esophagus Left gastric vein Azygosvein Anal canal Superior rectal vein Inferior rectal vein Umbilicus Paraumbilicalvein Superficial vein of anterior abdominal wall Bare area of liver Vein in liver Diaphragmatic/phrenicvein Retroperitoneal organs Colic vein Lumbar/renal vein 6/81

7. INTRODUCTION Gastrointestinal bleeding describe every form of haemorrhage in the GIT, from the pharynx to the rectum. Can be divided into 2 clinical syndromes:- - upper GI bleed (pharynx to ligament of Treitz) - lower GI bleed (ligament of Treitz to rectum) LIGAMENT OF TREITZ 7/81

8. UPPERGASTROINTESTINAL BLEEDING 8/81

9. 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. 9/81

10. CLINICAL FEATURES Haematemesis : vomiting of blood whether 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). 10/81

11. CLINICAL FEATURES 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. Malaena without haematemesisis usually due to lesions distal to the pylorus Approximately 60mL of blood is required to produced a single black stool. 11/81

13. 13/81

14. OESOPHAGEAL VARICES 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. 14/81

15. Esophageal varices: a view of the everted esophagus and gastroesophageal junction, showing dilated submucosal veins (varices). 15/81

16. OESOPHAGEAL VARICES: PORTAL HYPERTENSION 16/81

17. OESOPHAGEAL VARICES: PATHOPHYSIOLOGY Portal venous hypertension Resistance to flow in portal venous system Pressure Portal systemic shunting (Abnormal venous communication between portal system and systemic venous circulation) Appearing of large submucosal veins at lower end of oesophagus and gastric fundus Haemorrhage due to intravariceal pressure 17/81

18. OESOPHAGEAL VARICES Sudden onset Painless Large volume of blood Dark red History of (alcoholic) liver disease Physical findings of portal hypertension – ascites, splenomegaly 18/81

19. OESOPHAGEAL VARICES Management - blood transfusion - endoscopic variceal injection with sclerosant or banding. - sengstaken tube 19/81

20. MALLORY-WEISS TEAR 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. Clinical features: - An episode of haematemesis following retching or vomiting. - melaena - hematochezia - syncope - abdominal pain. Precipitating factors: - hiatus hernia - retching & vomiting - straining - hiccuping - coughing - blunt abdominal trauma - cardiopulmonary resuscitation 20/81

21. MALLORY-WEISS TEAR: MANAGEMENT - Bleeding from MWTs stops spontaneously in 80-90% of patients - A contact thermal modality, such as multipolarelectrocoagulation (MPEC) or heater probe, with or without epinephrine injection, is typically used to treat an actively bleeding - Epinephrine injection -reduces or stops bleeding via a mechanism of vasoconstriction and tamponade - Endoscopic band ligation - Endoscopic hemoclipping 21/81

22. 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%) 22/81

23. ESOPHAGEAL CANCER SQUAMUS CELL CARCINOMA ADENOCARCINOMA -more common in men. -risk factor: - tobacco smoking - heavy alcohol intake - plummer-vinson syndrome - achalasia - coeliac disease - tylosis - diet deficient in vitamins high dietary carotenoids & vitamin C possibly decrease the risk. - arise in the columnar lined epithelium of the lower oesophagus. - risk factor: - long-standing GORD - barrett’soesophagus - tobacco smoking 23/81

24. ESOPHAGEAL CANCER: CLINICAL FEATURES Dysphagia - progressive & unrelenting - initially there is difficulty in swallowing solids, but eventually dysphagia for liquids also occur. Odynophagia - retrosternal pain on swallowing. Regurgitation Aspiration pneumonitis Weight loss Anorexia Anemia Lassitude 24/81

25. ESOPHAGEAL CANCER: TNM STAGING T Tumour confined to submucosa Tumour extends into muscularispropria Tumours extend outside muscle layer Tumour invades adjacent structures Lymph node metastases to paraoesophageal, cardia or left gastric regions. No other metastatic spread Lymph node metastases to all other areas. Metastases to liver, lung, brain, bone, etc. N M 25/81

27. haematemesis

28. Melaena

29. heartburn26/81

30. PEPTIC ULCER: PATHOGENESIS Predisposing factors including H.pylori infection of mucosa Acid-pepsin attack and/or breach of mucosal protection Acute inflammation resolution Destruction of mucosa Mucosal ulceration mucosal regeneration Extension through submucosal & muscular layers causing deep ulceration Perforation erosion of major granulation tissue blood vessel formed & attemps repair Peritonitis massive haemorrhage chronic & relapsing ulceration 27/81

31. PEPTIC ULCER 28/81

32. 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 29/81

33. PEPTIC ULCER: TREATMENT Antacid – aluminium/Mg hydroxide, Mg Trisiclate Mucosal protective agents – sucralfate Prostaglandin analogues – misoprostol H2 receptor antagonist – cimetidine & ranitidine Proton pump inhibitor – omeprazole & lansoprazole H.pylori eradication - triple therapy :metronidazole,amoxycilin,erythromycin surgery should be done if -failed medical treatment -vagotomy, gastrectomy, pyloroplasty 30/81

34. EROSIVE GASTRITIS Acute mucosal inflammatory process Accompanied by hemorrhage into the mucosa and sloughing of the superficial epithelium (erosion). 31/81

35. EROSIVE GASTRITIS: AETIOLOGY - NSAIDs - alcohol - smoking - chemotherapy - uraemia - stress - ischaemia and shock - suicide attempts - mechanical trauma - distal gastrectomy 32/81

36. 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! 33/81

37. GASTRIC CANCER BENIGN GASTRIC NEOPLASM - adenomatous polyps - leiomyoma - neurogenictumour - fibromata - lipoma - gastric adenocarcinoma (90%) - lymphomas - smooth muscle tumour GASTRIC CARCINOMA 34/81

38. GASTRIC CANCER 60-80 years age group. Male:female , 2:1 - diet - H.pylori infection - gastric polyps - gastroenterostomy - chronic gastric ulcer disease - chronic atrophic gastritis - intestinal metaplasia - gastric dysplasia - host factors AETIOLOGICAL FACTOR 35/81

39. GASTRIC CANCER: TNM STAGING T T1 tumour extends to lamina propria or submucosa. T2 tumour extend into muscle T3 tumour extend into serosa T4 tumour invades adjacent structures N0 no lymph node involvement N1 fewer than 7 lymph node involved by tumour N2 7-15 lymph node involved by tumour N3 more than 15 lymph node involved by tumour M0 no metastases M1 metastases present N M 36/81

41. Palliative resection

42. Palliative bypass37/81

44. Gastric arterial venous abnormality

45. covered by normal mucosa

46. profuse bleeding coming from an area of apparently normal mucosa.38/81

47. DUODENITIS AETIOLOGY - aspirin, - NSAIDs - high acid secretion CLINICAL FEATURE - Symptoms are similar to peptic ulcer disease - stomach pain -bleeding from the intestine - nausea & vomiting - LOA - intestinal obstruction(rare) 39/81

49. H2 receptor blockers (ranitidine/cimetidine) or proton pump inhibitors (omeprazole) reduce the acid secretion by the stomach40/81

50. HISTORY TAKING - when? - have u vomited blood/passed black tarry stools? - had both haematemesis & malaena? - have u had, bleeding from the nose? Bloody expectoration? A dental extraction? -what is the color, the appearance of the vomited blood? - red? Dark red? Brown? Black? - ‘coffee ground appearance? - bright red & frothy? - what is the color of the stool? Bright red? Black tarry? - have u vomited blood only once/several times? - has the bleeding been abrupt/massive? - have u had >1 black, tarry stool within a 24-h period? - for how long have the tarry stools persisted? MODE OF ONSET CHARACTER EXTENT AND RATE 41/81

51. HISTORY TAKING - retching & severe nonbloody vomiting? - lightheadedness? Nausea? Thirst? Sweating? - faintness when lying down/when standing/syncope? - following the haemorrhage did you have diarrhea? - aspirin? anticoagulant therapy? iron preparation? - age of the patient? - what is your smoke/alcohol intake? - have there been similar episode in the past? When? Diagnosis? - were u hospitalized on this occasion? Did u receive a transfusion? - are there any other members of your family who have intestinal disease/bleeding tendency/peptic ulcer/liver disease, History of Malignancy? OTHER SYMPTOMS IATROGENIC FACTORS PREVIOUS EPISODES FAMILY HISTORY 42/81

53. Masses

54. Melaena

55. SupraclavicularLN

56. Cervical LN

57. AxillaryLN

58. Inguinal LN

59. Confusion ( Shock, liver failure….)

60. Neurological Deficit

61. Anaemic

62. Bruishing/ Purpura

63. Cachexic

64. Dehydrated

65. Jaundice

66. Inspection - distension, scar, prominent vein.

67. Palpation - tenderness, mass/ organomegaly

68. Percussion - shifting dullness, fluid thrill.

69. Auscultation - hyperactive bowel sound.LYMPH NODES ABDOMEN CNS 43/81

70. PHYSICAL SIGN Clinical shock Systolic BP < 100mmHg Pulse rate > 100 bpm Postural sign: patient place in a upright position – pulse rate rises 25% or more - systolic BP alls 20mmHg or more Sign of liver disease & portal hypertension Sign of GI disease Sign of bleeding abnormalities Bloody / black stools on per rectal examination. 44/81

71. INVESTIGATIONS - full blood count – Hb, WCC - liver function test – cirrhosis - coagulation profile - renal profile - RBC morphology - OGDS - Barium meal / Double-contrast barium meal - Ultrasound - CT scan BASELINE INVESTIGATION IMAGING 45/81

72. Acute Upper Gastrointestinal Bleed Routine Blood Test Resuscitation and Risk Assessment Endoscopy (within 24 hrs) Varices Peptic Ulcer No obvious cause Major SRH Minor SRH Minor Bleed Major Bleed Management Varices Eradicate H.pylori & Risk Reduction Endoscopic Treatment Other colonoscopy or angiography Failure OVERVIEW:MANAGEMENT OF UPPER GI BLEED Surgical 46/81

73. RESUSCITATION airway and oxygen Insert 2 large-bore (14-16G) IV cannulate take blood IV colloid - crossmatched. In a dire emergency, give O Rh-ve blood. haemodynamically stable. Correct clotting abnormalities 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 admision. 47/81

74. BLOOD TRANFUSION INDICATION OF BLOOD TRANSFUSION BLOOD TEST Haemoglobin - May be normal during the acute stages until haemodilution occurs Urea and electrolytes - Elevated blood urea suggests severe bleeding Cross match for transfusion - Two units of blood are sufficient unless bleeding is extreme. If the transfusion is not needed urgently, group the blood and save the serum LFT and coagulation profile 1.Systolic BP < 110 mmHg 2.Postural hypotension 3.Pulse > 110/min 4.Haemoglobin <8g/dl 5.Angina or cardiovascular disease with a Haemoglobin <10g/dl 48/81

75. 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 sclerotherapyis used commonly. Other method include the use of heat probes and lasers. Angiography in whom endoscopy does not identify the bleeding point. Limitation: can only detect active bleeding of greater than 1mL/min. 49/81

76. FORREST CLASSIFICATION FOR BLEEDING PEPTIC ULCER Ia: Spurting Bleeding Ib: Non spurting active bleeding IIa: visible vessel (no active bleeding) IIb: Non bleeding ulcer with overlying clot (no visible vessel) IIc: Ulcer with hematin covered base III: Clean ulcer ground (no clot, no vessel) Major SRH Minor SRH 50/81

77. MANAGEMENT MEDICAL H2 receptor antagonist - cimetidine, ranitidine Proton pump inhibitors – omeprazole, lanzoprazole H. pyloriirradication Triple regimen – proton pump inhibitor + 2 antibiotics given for 1 week (elimination rate > 90%) e.g. Omeprazol + metronidazole/amoxycillin + clarithromycin GU– remove ulcer, gastrin secreting zone – Billroth I gastrectomy DU – Polya or Billroth II gastrectomy – Vagotomy SURGICAL 51/81

78. UPPER GI BLEED:RISK FACTORS FOR DEATH 1. Advanced AGE 2. SHOCKon admission(pulse rate >100 beats/min; systolic blood pressure < 100mmHg) 3. COMORBIDITY (particularly hepatic or renal failure and disseminated malignancy) 4. Diagnosis (worst PROGNOSISfor advanced upper gastrointestinal malignancy) 5. ENDOSCOPIC FINDINGS (active, spurting haemorrhage from peptic ulcer; non-bleeding visible vessel) 6. REBLEEDING(increases mortality 10 fold) 52/81

79. GASTROINTESTINAL BLEEDINGLOWER 53/81

80. LOWER GI BLEED: AETIOLOGY COLON SMALL INTESTINE Carcinoma of colon Polyps eg: Familial adenomatouspolyposis Diverticular disease Inflamation Ischaemic colitis Ulcerative colitis Pseudomembranous colitis Angiodysplasia Haemorrhoids Fissure-in-ano Anal carcinoma Anal wart Crohn’s disease Diverticulaeg: Meckel’sdiverticulum, Jejujanaldiverticulosis Benign neoplasm eg: Peutz-Jegher’s syndrome Leiomyoma. Malignant neoplasm eg: Lymphoma, Angiodysplasia Rectal carcinoma and polyps Rectal prolapse PACID cDNA ANUS RECTUM wCHF PC 54/81

81. HISTORY TAKING:RECTAL BLEEDING Blood on its own or streaking the stool: Rectum : polyps or carcinoma, prolapsed Anus : Haemorrhoids, Fissure-in-ano, Anal carcinoma. Stool mixed with blood: GIT above sigmoid colon. Sigmoid carcinoma or diverticular disease. Blood separate from the stool: Follows defaecation : Anal condition eg: Haemorrhoids. Blood is passed by itself : Rapidly bleeding carcinoma, inflammatory bowel disease, diverticulitis, or passed down from high up in the gut. 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 Blood on the toilet paper:Fissure-in-ano, Heamorrhoids. Loose, black, tarry, foul smelling stool:from the proximal of DJ flexure 55/81

82. HISTORY TAKING:COLOUR OF BLOOD/DISCHARGE Bright red/ Fresh blood: Rectum and anus. Dark blood: Upper GIT to above rectum. Drugs eg: iron tablets- appear as greenish black formed stool. Discharge apart from blood:- -Mucus- irritable bowel syndrome -Copious mucus- villous adenoma, frank cancer of the rectum -Mucus and pus- IBD, diverticular disease 56/81

83. HISTORY TAKING ALTER BOWEL HABIT ITCHINESS Causes: Allergic, anal warts, anal leak of mucus in haemorrhoid, excessive used of liquid paraffin, generalized disorder. eg: jaundice, diabetes mellitus. Normal bowel Intermittent bouts of constipation interrupted by diarrhoea: Carcinoma or Diverticular disease. Diarrhoea: Inflammatory bowel disease or rectal villous tumour. Tenesmus: Irritable bowel syndrome or abnormal mass of rectum or anal canal (e.g. CA, polyps or thrombosedhaemorrhoid) ANAL PAIN During pregnancy/childbirth: Fissure-in-ano, haemorrhoids. Throbbing, severe pain occur during defaecation: Fissure-in-ano. 57/81

85. Anti-parkinson agent

86. Anti-coagulant therapy eg: warfarin

87. NSAID’s-risk factor of PUD

88. Low fiber diet

90. Familial AdenomatousPolyposisSOCIAL HISTORY 58/81

92. Masses

93. Melaena

94. SupraclavicularLN

95. Cervical LN

96. AxillaryLN

97. Inguinal LN

98. Confusion ( Shock, liver failure….)

99. Neurological Deficit

100. Anaemic

101. Bruishing/ Purpura

102. Cachexic

103. Dehydrated

104. Jaundice

105. Inspection - distension, scar, prominent vein.

106. Palpation - tenderness, mass/ organomegaly

107. Percussion - shifting dullness, fluid thrill.

108. Auscultation - hyperactive bowel sound.LYMPH NODES SAME WITH UPPER GI BLEED ABDOMEN CNS 59/81

109. INVESTIGATION LABORATORY Full Blood Count (FBC) 2. BUSE 3. Coagulation profile Cross-matched (Transfusion) 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. IMAGING 60/81

110. IMAGING 3. Helical CT scan Abdomen and pelvis Can also be used when routine workup fails to determine the cause of active GI bleeding Multiple criteria are used to establish the bleeding sites: -vascular extravasation of the contrast medium -contrast enhancement of the bowel wall -thickening of the bowel wall -spontaneous hyperdensity of the peribowel fat -vascular dilatations with helical CT. 61/81

111. IMAGING 4.Colonoscopy • Bleeding slowly or who have already stopped bleeding. Biopsy 5.Proctosigmoidoscopy Exclude an anorectal source of bleeding 6.Oesophagoduodenoscopy (OGDS) To exclude upper GI bleeding 62/81

112. IMAGING 7. Double-contrast barium enema Elective evaluation of unexplained lower GI bleeding Do not use in the acute hemorrhage phase 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 63/81

113. INTUSSUSCEPTION Common in children within 1st year of life Symptoms: abdominal pain, red-currant-jelly stool Signs: palpable mass at right iliac fossa Procedure: Barium enema, laparotomy 64/81

114. Colorectal polyps Adenomatous polyps and adenomas Has malignant potential Morphology: -polypoid and pedunculated -dome-shaped and sessile Histology: -degree of epithelial dysplasia is highly variable -carcinoma in situ -early invasive cancer:- invasion of tumour cells through basement membrane->muscularismucosa->submucosa 65/81

115. TYPES OF COLORECTAL POLYPS 1.Tubular adenomas - small pedunculated / sessile lesions -retain a tubular form similar to normal colonic mucosa -least potential for malignant transformation 2. Villous adenomas -sessile and frond like lesions -secrete mucus -more dysplastic -greater potential for malignant change 3. Tubulo-villous adenoma -intermediate between tubular and villous adenoma -pedunculated, stalk is covered with normal epithelium 66/81

116. SIGN AND SYMPTOM Rectal bleeding Iron deficiency anaemia Mucus Hypokalaemia Tenesmus Prolapse Obstructive symptoms 67/81

118. Mid teen years- hundred / more adenomatous polyps

119. Average age of 40- colorectal cancer

121. INVESTIGATION Sigmoidoscopy Colonoscopy -gold standard -visualize, biopsy, remove -disadvantage: full day’s bowel preparation sedation risk of haemorrhage & perforation CT pneumocolon -elderly / infirm patient -< invasive & not require sedation. -bowel preparation Double contrast barium enema 69/81

122. 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 70/81

123. ADENOCARCINOMA OF COLON & RECTUM Rare < 50 years old, 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 71/81

125. > 60 years old

126. Common site : ascending colon and caecum

127. Malformations consist of dilated tortuous submucosal veins

128. In severe cases, the mucosa is replaced by massive dilated deformed vessels

129. Clinical features: -acute / chronic rectal bleeding -iron deficiency anaemia 72/81

130. INVESTIGATION Colonoscopy -bright red 0.5-1cm diameter submucosal lesion -small dilated vessels Mesenteric angiography Radioactive test using technetium-99m –labeled red cells 73/81

131. 74/81

132. MANAGEMENT colonoscopic diathermy 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 75/81

134. Transient ischaemia of a segment of a large bowel, followed by sloughing of mucosa

135. Common site –splenic flexure

137. 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 77/81

138. HAEMORRHOIDS: SIGNS & SYMPTOMS Rectal bleeding Perianal irritation & itching Mucus leakage Mild incontinence of flatus Prolapse Acute pain Skin tags at anal margin 78/81

139. 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 79/81

141. F > M

143. Clinical features: -diverticulosis (asymptomatic) -chronic grumbling diverticular pain (chronic constipation & episodic diarrhoea) 80/81

145. Poor prognostic features: -age over 60 years -chronic history -relapse on full medical treatment -serious coexisting medical conditions -> 4 units of blood transfusion required during resuscitation 81/81

146. THANK YOU FOR YOUR aTTENTION LUNCH TIME !!! 82/81