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Surgery GI  bleeding
 

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 Surgery GI bleeding Presentation Transcript

  • GASTROINTESTINAL BLEEDING
    NUR JASHIMAH IDAYU JAMALUDIN
    TAN LAY TENG
    MOHD HANAFI RAMLEE
    1/81
  • CONTENTS
    Anatomy
    Definition
    Epidemiology
    Clinical features
    Aetiology
    History & Examination
    Investigation
    Management
    2/81
  • 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
  • ARTERIAL SUPPLY
    Mostly by anterior branch of abdominal aorta
    4/81
  • 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
  • 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
  • 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
  • UPPERGASTROINTESTINAL BLEEDING
    8/81
  • 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
  • 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
  • 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
  • AETIOLOGY
    Oesophagus
    -Oesophagealvarices
    -Oesophageal CA
    -Reflux oesophagitis
    -Mallory-Weiss syndrome
    LOCAL
    Stomach
    -Gastric ulcer
    • Erosive gastritis
    -Gastric CA
    -gastric lymphoma
    -gastric leiomyoma
    -Dielafoy’s syndrome
    -Haemophilia
    -Leukemia
    -Thrombocytopenia
    -Anti-coagulant therapy
    GENERAL
    Duodenum
    -Duodenal ulcer
    -Duodenitis
    -Periampullarytumour
    -Aorto-duodenal fistula
    12/81
  • 13/81
  • 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
  • Esophageal varices: a view of the everted esophagus and gastroesophageal junction, showing dilated submucosal veins (varices).
    15/81
  • OESOPHAGEAL VARICES: PORTAL HYPERTENSION
    16/81
  • 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
  • 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
  • OESOPHAGEAL VARICES
    Management
    - blood transfusion
    - endoscopic variceal injection with sclerosant or banding.
    - sengstaken tube
    19/81
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • PEPTIC ULCER
    gastric ulcer & duodenal ulcer
    Caused by imbalance between secretion of acid and pepsin, and mucosal defence mechanism.
    AETIOLOGY
    -Helicobacter pylori infection
    -Zollinger-ellison syndrome
    -NSAIDs
    -others: stress, smoking,alcohol, steroid
    SIGNS & SYMPTOMS
    • epigastric pain
    • haematemesis
    • Melaena
    • heartburn
    26/81
  • 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
  • PEPTIC ULCER
    28/81
  • 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
  • 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
  • EROSIVE GASTRITIS
    Acute mucosal inflammatory process
    Accompanied by hemorrhage into the mucosa and sloughing of the superficial epithelium (erosion).
    31/81
  • EROSIVE GASTRITIS: AETIOLOGY
    - NSAIDs
    - alcohol
    - smoking
    - chemotherapy
    - uraemia
    - stress
    - ischaemia and shock
    - suicide attempts
    - mechanical trauma
    - distal gastrectomy
    32/81
  • 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
  • GASTRIC CANCER
    BENIGN GASTRIC NEOPLASM
    - adenomatous polyps
    - leiomyoma
    - neurogenictumour
    - fibromata
    - lipoma
    - gastric adenocarcinoma (90%)
    - lymphomas
    - smooth muscle tumour
    GASTRIC CARCINOMA
    34/81
  • 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
  • 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
  • GASTRIC CANCER
    Early signs
    -Indigestion
    -Flatulence
    -Dyspepsia
    Late signs
    - LOW
    -anemia
    -dysphagia
    -vomiting
    -epigastric/back pain
    - epigastric mass
    -sign of metastases (jaundice, ascites, diarrhoea, intestinal obstruction)
    CLINICAL FEATURES
    TREATMENT
    • Radical total gastrectomy
    • Palliative resection
    • Palliative bypass
    37/81
  • 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.
    38/81
  • 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
  • DUODENITIS
    INVESTIGATION
    MANAGEMENT
    - 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
    • stop all medications that can make things worse (aspirin & NSAIDS)
    • H2 receptor blockers (ranitidine/cimetidine) or proton pump inhibitors (omeprazole) reduce the acid secretion by the stomach
    40/81
  • 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
  • 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
  • PHYSICAL EXAMINATION:UPPER GI BLEED
    RECTAL
    GENERAL INSPECTION
    • Perianal Skin Lesion
    • Masses
    • Melaena
    • SupraclavicularLN
    • Cervical LN
    • AxillaryLN
    • Inguinal LN
    • Confusion ( Shock, liver failure….)
    • Neurological Deficit
    • Anaemic
    • Bruishing/ Purpura
    • Cachexic
    • Dehydrated
    • Jaundice
    • Inspection - distension, scar, prominent vein.
    • Palpation - tenderness, mass/ organomegaly
    • Percussion - shifting dullness, fluid thrill.
    • Auscultation - hyperactive bowel sound.
    LYMPH NODES
    ABDOMEN
    CNS
    43/81
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • GASTROINTESTINAL BLEEDINGLOWER
    53/81
  • 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
  • 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
  • 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
  • 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
  • HISTORY TAKING
    PREVIOUS HISTORY
    Previous perianal disease
    Inflammatory bowel disease
    Peptic ulcer disease
    Liver disease
    Coagulopathy
    DRUGS HISTORY
    • Laxative agent
    • Anti-parkinson agent
    • Anti-coagulant therapy eg: warfarin
    • NSAID’s-risk factor of PUD
    • Low fiber diet
    • Smoking
    FAMILY HISTORY
    • History of malignancy
    • Familial AdenomatousPolyposis
    SOCIAL HISTORY
    58/81
  • PHYSICAL EXAMINATION:LOWER GI BLEED
    RECTAL
    GENERAL INSPECTION
    • Perianal Skin Lesion
    • Masses
    • Melaena
    • SupraclavicularLN
    • Cervical LN
    • AxillaryLN
    • Inguinal LN
    • Confusion ( Shock, liver failure….)
    • Neurological Deficit
    • Anaemic
    • Bruishing/ Purpura
    • Cachexic
    • Dehydrated
    • Jaundice
    • Inspection - distension, scar, prominent vein.
    • Palpation - tenderness, mass/ organomegaly
    • Percussion - shifting dullness, fluid thrill.
    • Auscultation - hyperactive bowel sound.
    LYMPH NODES
    SAME WITH UPPER GI BLEED
    ABDOMEN
    CNS
    59/81
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • SIGN AND SYMPTOM
    Rectal bleeding
    Iron deficiency anaemia
    Mucus
    Hypokalaemia
    Tenesmus
    Prolapse
    Obstructive symptoms
    67/81
  • FAMILIAL ADENOMATOUS POLYPOSIS
    • Autosomal dominant defect in APC gene
    • Mid teen years- hundred / more adenomatous polyps
    • Average age of 40- colorectal cancer
    • Symptoms:
    -rectal bleeding
    -diarrhoea
    • Gardner’s syndrome= +desmoidtumours + osteomas of mandible & skull
    68/81
  • 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
  • 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
  • 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
  • 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
    72/81
  • 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
  • 74/81
  • 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
  • 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
    76/81
  • 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
  • HAEMORRHOIDS: SIGNS & SYMPTOMS
    Rectal bleeding
    Perianal irritation & itching
    Mucus leakage
    Mild incontinence of flatus
    Prolapse
    Acute pain
    Skin tags at anal margin
    78/81
  • 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
  • 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 constipation & episodic diarrhoea)
    80/81
  • MANAGEMENT
    MEDICAL
    SURGICAL
    Vasoconstrictive agents:
    vasopressin
    2. Therapeutic embolization:
    -Embolic agents: Autologous clot, Gelfoam, polyvinyl alcohol, microcoils,
    ethanolamine, and oxidized cellulose
    -Selective angiography
    3. Endoscopic therapy:
    -Diathermy / laser coagulation
    -Short term control of bleeding during resuscitation
    • The bleeding point is localized, perform a limited segmental resection of the small or large bowel
    • 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
  • THANK YOU FOR YOUR aTTENTION
    LUNCH TIME !!!
    82/81