nur jashimah idayu jamaludin tan lay teng mohd …miasis •sarcoidos is •myeloprol iferative...
TRANSCRIPT
NUR JASHIMAH IDAYU JAMALUDIN
TAN LAY TENG
MOHD HANAFI RAMLEE
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CONTENTS
• Anatomy
• Definition
• Epidemiology
• Clinical features
• Aetiology
• History & Examination
• Investigation
• Management
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• FOREGUT
Abdominal esophagus
• MIDGUT
Major duodenal papilla
• HINDGUT
Junction B/w prox 2/3 and
distal 1/3 of tranverse colon
Major duodenal papilla
Junction B/w prox. 2/3
and distal 1/3
of tranverse colon.
Midway of anal canal
ANATOMY OF GIT
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ARTERIAL SUPPLY
• Mostly by anterior branch of abdominal aorta
Celiac trunk -Foregut
• left gastic artery
• splenic artery• common
hepatic artery
Superior Mesenteric
Artery - Midgut
• inferior pancreaticoduodenalartery
• jejunal and ileal arteries
• middle colic artery
• right colic artery
• ileocolic artery
Inferior Mesenteric
Artery - Hindgut
• sigmoid arteries
• superior rectal artery
• Left colic artery
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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 vein5/81
PORTAL-SYSTEMIC
ANASTOMOSES
• Lower 3rd of esophagus
Left gastric vein
Azygos vein
• Anal canal
Superior rectal vein
Inferior rectal vein
• Umbilicus
Paraumbilical vein
Superficial vein of anterior
abdominal wall
• Bare area of liver
Vein in liver
Diaphragmatic/phrenic vein
• 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
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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.
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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 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 stool.
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AETIOLOGY
Oesophagus
-Oesophageal varices
-Oesophageal CA
-Reflux oesophagitis
-Mallory-Weiss syndrome
-Haemophilia
-Leukemia
-Thrombocytopenia
-Anti-coagulant therapy
Stomach-Gastric ulcer-Erosive gastritis-Gastric CA-gastric lymphoma-gastric leiomyoma-Dielafoy’s syndrome
Duodenum-Duodenal ulcer-Duodenitis-Periampullary tumour-Aorto-duodenal fistula
LOCAL
GENERAL
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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.
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Esophageal varices: a view of the everted
esophagus and gastroesophagealjunction, showing
dilated submucosalveins (varices).
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OESOPHAGEAL VARICES:
PORTAL HYPERTENSION
PRE HEPATIC
• Portal vein thrombosis
• Splenicvein thrombosis
INTRA HEPATIC
• Cirrhosis• Schistoso
miasis• Sarcoidos
is• Myeloprol
iferativedisorder
• Congenital hepatic fibrosis
POST HEPATIC
• Budd-chiarisyndrome
• Right heart failure
• Constrictive pericarditis
• Veno-occlusive
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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
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OESOPHAGEAL
VARICES
• Sudden onset
• Painless
• Large volume of blood
• Dark red
• History of (alcoholic) liver disease
• Physical findings of portal
hypertension –
ascites, splenomegaly
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OESOPHAGEAL
VARICES
• Management
- blood transfusion
- endoscopic variceal injection with
sclerosant or banding.
- sengstaken tube
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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
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MALLORY-WEISS TEAR:
MANAGEMENT
- Bleeding from MWTs stops spontaneously in 80-90% of
patients
- A contact thermal modality, such as multipolar electrocoagulation(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 hemoclipping21/81
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
-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
ADENOCARCINOMASQUAMUS CELL CARCINOMA
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ESOPHAGEAL CANCER:
CLINICAL FEATURES
1) Dysphagia- progressive & unrelenting- initially there is difficulty in swallowing solids, but eventually dysphagia for
liquids also occur.2) Odynophagia
- retrosternal pain on swallowing.3) Regurgitation4) Aspiration pneumonitis5) Weight loss6) Anorexia7) Anemia8) Lassitude
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ESOPHAGEAL CANCER:
TNM STAGING
1. Tumour confined to submucosa
2. Tumour extends into muscularis propria
3. Tumours extend outside muscle layer
4. Tumour invades adjacent structures
1. Lymph node metastases to paraoesophageal, cardia or left gastric regions.
o. No other metastatic spread
1. Lymph node metastases to all other areas. Metastases to liver, lung, brain, bone, etc.
T
N
M
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PEPTIC ULCER
• gastric ulcer & duodenal ulcer
• Caused by imbalance between secretion of acid and pepsin, and mucosal defence mechanism.
-Helicobacter pylori infection-Zollinger-ellisonsyndrome-NSAIDs-others: stress, smoking,alcohol, steroid
- epigastric pain
- haematemesis
- Melaena
- heartburn
AETIOLOGY
SIGNS & SYMPTOMS
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PEPTIC ULCER:
PATHOGENESISPredisposing 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 tissueblood vessel formed & attemps repair
Peritonitis massive haemorrhage chronic & relapsing ulceration 27/81
Feature Gastric ulcer Duodenal ulcer
Onset Soon after eating 2-3 hours after eating
Relieving factor vomiting Eating
Precipitating factor
eating Missing a meal, anxiety, stress
Duration of attack
A few weeks A month or two
PEPTIC ULCER
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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
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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).
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EROSIVE GASTRITIS:
AETIOLOGY
- NSAIDs
- alcohol
- smoking
- chemotherapy
- uraemia
- stress
- ischaemia and shock
- suicide attempts
- mechanical trauma
- distal gastrectomy
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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!
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GASTRIC CANCER
- adenomatous polyps- leiomyoma- neurogenic tumour- fibromata- lipoma
- gastric adenocarcinoma (90%)- lymphomas- smooth muscle tumour
BENIGN GASTRIC NEOPLASM
GASTRIC CARCINOMA
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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
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GASTRIC CANCER:
TNM STAGING
T1 tumour extends to lamina propria or submucosa.T2 tumour extend into muscleT3 tumour extend into serosaT4 tumour invades adjacent structures
N0 no lymph node involvementN1 fewer than 7 lymph node involved by
tumourN2 7-15 lymph node involved by tumourN3 more than 15 lymph node involved by
tumour
M0 no metastasesM1 metastases present
T
N
M
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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)
• Radical total gastrectomy• Palliative resection• Palliative bypass
CLINICAL FEATURESTREATMENT
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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.
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DUODENITIS
- aspirin,
- NSAIDs
- high acid secretion
- Symptoms are similar to peptic ulcer disease
- stomach pain- bleeding from the intestine- nausea & vomiting- LOA- intestinal obstruction(rare)
AETIOLOGY
CLINICAL FEATURE
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DUODENITIS
- 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
INVESTIGATION MANAGEMENT
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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
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- 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
OTHER SYMPTOMS
IATROGENIC FACTORS
PREVIOUS EPISODES
FAMILY HISTORY
HISTORY TAKING
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PHYSICAL EXAMINATION:
UPPER GI BLEED
Anaemic Bruishing/ Purpura Cachexic Dehydrated Jaundice
Inspection -distension, scar, prominent vein.
Palpation - tenderness, mass/ organomegaly
Percussion - shifting dullness, fluid thrill.
Auscultation - hyperactive bowel sound.
Perianal Skin Lesion Masses Melaena
Supraclavicular LN Cervical LN Axillary LN Inguinal LN
Confusion ( Shock, liver failure….)
Neurological Deficit
GENERAL INSPECTION
ABDOMEN
RECTAL
LYMPH NODES
CNS
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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.
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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
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Acute Upper Gastrointestinal Bleed
Resuscitation and Risk Assessment
Routine Blood Test
Endoscopy (within 24 hrs)
Varices Peptic Ulcer No obvious cause
Management Varices
Major SRH Minor SRH Minor Bleed
Major Bleed
Eradicate H.pylori &
Risk Reduction
Endoscopic Treatment
Failure
Surgical
Other colonoscopy or
angiography
OVERVIEW:
MANAGEMENT OF UPPER
GI BLEED 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
– 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
BLOOD TEST INDICATION OF BLOOD TRANSFUSION
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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: can only detect active bleeding
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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)
Min
or
SRH
Maj
or
SRH
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MANAGEMENT
• 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
• GU – remove ulcer, gastrin secreting zone – Billroth I gastrectomy
• DU – Polya or Billroth II gastrectomy– Vagotomy
MEDICAL
SURGICAL
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UPPER GI BLEED:RISK FACTORS FOR DEATH
1. Advanced AGE
2. 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. REBLEEDING (increases mortality 10 fold)
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LOWER GI BLEED:
AETIOLOGY
Crohn’s disease
Diverticula eg:
Meckel’s diverticulum,
Jejujanal diverticulosis
Benign neoplasm eg:
Peutz-Jegher’ssyndrome
Leiomyoma.
Malignant neoplasm eg:
Lymphoma,
Angiodysplasia
Rectal carcinoma and polyps
Rectal prolapse
Carcinoma of colon
Polyps eg:
Familial adenomatouspolyposis
Diverticular disease
Inflamation
Ischaemic colitis
Ulcerative colitis
Pseudomembranouscolitis
Angiodysplasia
Haemorrhoids
Fissure-in-ano
Anal carcinoma
Anal wart
SMALL INTESTINE
RECTUM
COLON
ANUS
cDNA
PC
PACID
wCHF
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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
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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
HISTORY TAKING:
COLOUR OF
BLOOD/DISCHARGE
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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 thrombosed haemorrhoid)
HISTORY TAKING
ALTER BOWEL HABIT
ANAL PAIN
ITCHINESS
Causes: Allergic, anal warts, anal leak of mucus in haemorrhoid, excessive used of liquid paraffin, generalized disorder. eg: jaundice, diabetes mellitus.
During pregnancy/childbirth: Fissure-in-ano, haemorrhoids.
Throbbing, severe pain occur during defaecation: Fissure-in-ano.
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•Previous perianal disease
•Inflammatory bowel
disease
•Peptic ulcer disease
•Liver disease
•Coagulopathy
HISTORY TAKING
• Laxative agent
• Anti-parkinson agent
• Anti-coagulant therapy eg:
warfarin
• NSAID’s-risk factor of PUD
• Low fiber diet
• Smoking
PREVIOUS HISTORY
•History of malignancy
•Familial Adenomatous
Polyposis
FAMILY HISTORY
DRUGS HISTORY
SOCIAL HISTORY
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PHYSICAL EXAMINATION:
LOWER GI BLEED
Anaemic Bruishing/ Purpura Cachexic Dehydrated Jaundice
Inspection -distension, scar, prominent vein.
Palpation - tenderness, mass/ organomegaly
Percussion - shifting dullness, fluid thrill.
Auscultation - hyperactive bowel sound.
Perianal Skin Lesion Masses Melaena
Supraclavicular LN Cervical LN Axillary LN Inguinal LN
Confusion ( Shock, liver failure….)
Neurological Deficit
GENERAL INSPECTION
ABDOMEN
RECTAL
LYMPH NODES
CNS
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INVESTIGATION
1. Full Blood Count (FBC)2. BUSE3. Coagulation profile4. 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.
LABORATORY
IMAGING
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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 peribowelfat
-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
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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 bleedingExample of barium enema study showing ulcerative colitis of the colon
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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
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Colorectal polyps
• Adenomatous polyps and adenomas
• Has malignant potential• Morphology:
-polypoid and pedunculated-dome-shaped and sessile
• Histology:-degree of epithelial dysplasia ishighly variable-carcinoma in situ-early invasive cancer:-invasion of tumour cells through basement membrane→muscularismucosa→submucosa
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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
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SIGN AND SYMPTOM
• Rectal bleeding
• Iron deficiency anaemia
• Mucus
• Hypokalaemia
• Tenesmus
• Prolapse
• Obstructive symptoms
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FAMILIAL ADENOMATOUS
POLYPOSIS
• Autosomal dominant defect in APC gene
• Mid teen years- hundred / more adenomatouspolyps
• Average age of 40-colorectal cancer
• Symptoms:
-rectal bleeding
-diarrhoea
• Gardner’s syndrome= +desmoid tumours + osteomas of mandible & skull
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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 enema69/81
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
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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 anaemia72/81
INVESTIGATION
• Colonoscopy
-bright red 0.5-1cm diameter submucosal
lesion
-small dilated vessels
• Mesenteric angiography
• Radioactive test using technetium-99m –labeled red cells
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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
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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
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HAEMORRHOIDS
• M > F
• Female- late pregnancy, puerperium
• Supine lithotomy position- 3 ,7, 11 o’clock positions
• Classification:1st degree : never prolapse2nd degree: prolapse during
defaecation butreturn 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
80/81
MANAGEMENT
1. Vasoconstrictive agents:
vasopressin
2. Therapeutic embolization:
-Embolic agents: Autologousclot, 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
MEDICAL SURGICAL
81/81
THANK YOU FOR YOUR
aTTENTIONLUNCH TIME !!!
82/81