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Dr Abinash Samal
 Gastrointestinal bleeding is typically categorized as either upper
or lower gastrointestinal bleeding depending on the anatomic
location of the bleeding site.
 Upper gastrointestinal bleeding occurs proximal to the ligament
of Treitz and may involve the esophagus, stomach, and
duodenum.
 Lower gastrointestinal bleeding occurs distal to
the ligament of Treitz and may involve the small
bowel, colon, and rectum.
Lower gastrointestinal bleeding is less common than upper
gastrointestinal bleeding and accounts for approximately 30% of
all gastrointestinal bleeding.
 Lower gastrointestinal bleeding tends to affect elderly patients
and is 200 times more likely to occur in an 80-year-old than in a
20-year-old
 Erosion or ulcer 55–74
 Variceal bleeding 5–14
 Mallory-Weiss tear 2–7
 Vascular lesions 2–3
 Neoplasms 2–5
 Diverticular disease 20–55
 Angiodysplasia 3–40
 Neoplasms 8–26
 Colitis 6–22
 Benign anorectal lesions 9–10
 The celiac axis and the superior mesenteric artery
(SMA) are the first two branches of the abdominal
aorta and provide a rich and well-collateralized
network of branch vessels that supply blood to the
upper gastrointestinal tract.
 Extensive collateralization between the celiac artery
and the SMA protects the upper gastrointestinal tract
from ischemic insult and permits surgical and
embolization procedures to be carried out with a
relatively low risk of ischemic injury.
 Similarly, branch vessels of both the SMA and the
inferior mesenteric artery (IMA) form a series of
interconnected arcades that provide a means of
collateral flow throughout the lower gastrointestinal
tract.
 Gastrointestinal bleeding can also have venous
sources. Venous bleeding within the upper
gastrointestinal tract is typically due to gastric or
esophageal varices arising from the coronary vein
or the short gastric veins in the setting of portal
hypertension.
 However, approximately 30% of patients
with portal hypertension and coexistent varices
who present with upper gastrointestinal bleeding
will have an arterial source of bleeding . Venous
bleeding within the lower gastrointestinal
tract is commonly due to hemorrhoids involving
either the internal or external rectal venous
plexus
 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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 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).
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 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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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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 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
gastroesophageal
junction, showing
dilated submucosal
veins (varices).
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Filling defects due to varices are characterized by change in
appearance during the examination related to breath holding
and thoracic pressure
CT images of a patient with large Uphill varices secondary to
cirrhosis with portal hypertension
With portal hypertension, elevated portal venous pressure
leads to reversed (hepatofugal) flow bypassing the liver through
the left gastric vein to dilated esophageal and periesophageal
veins that anastamose with the azygos and hemiazygos veins
which drain uphill into the superior vena cava.
Downhill varices in a patient with a superior vena cava obstruction due to
histoplasmosis.
On the barium study inconstant filling defects (arrows) represent downhill varices
in upper esophagus.
The angiogram demonstrates collateral vessels including a dilated left superior
intercostal vein (arrow).
Downhill Varices
With superior vena caval obstruction, upper body venous blood flows
caudally downhill through esophageal veins to the azygos vein which empties into
the superior vena cava caudal to the obstruction.
If the obstruction is at or below the azygos, the blood flow extends further caudally
to the portal system and then the hepatic veins to the inferior vena cava and the
right atrium.
PRE
HEPATIC
• Portal
vein
thrombosi
s
• Splenic
vein
thrombosi
s
INTRA
HEPATIC
• Cirrhosis
• Schistoso
miasis
• Sarcoidos
is
• Myeloprol
iferative
disorder
• Congenita
l hepatic
fibrosis
POST
HEPATIC
• Budd-
chiari
syndrome
• Right
heart
failure
• Constricti
ve
pericarditi
s
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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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- blood transfusion
- endoscopic variceal injection with sclerosant
or banding.
- sengstaken tube
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 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. Typical
longitudinal mucosal tear
with overlying fibrinous
exudate extending from the
distal esophagus to the
gastric cardia.
Courtesy of C.J. Gostout,
MD.
Mallory-Weiss tear with a pigmented
protuberance and active oozing
Spot films show barium (arrows) in linear mucosal tear near gastroesophageal
junction.
- 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 hemoclipping
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 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%)
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Leiomyomas are the most common benign esophageal neoplasm
and are often large yet nonobstructive.
On the chest film an abnormal opacity is seen behind the heart (arrow).
The barium study demonstrates a lobulated mass (arrow) that does not obstruct despite it
large size.
-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 GERD
- barrett’s
oesophagus
- tobacco smoking
ADENOCARCINOMA
SQUAMUS CELL
CARCINOMA
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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) Regurgitation
4) Aspiration pneumonitis
5) Weight loss
6) Anorexia
7) Anemia
8) Lassitude
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patient with an early esophageal carcinoma.
Lesion is not visible on single contrast esophagram.
Air-contrast esophagram shows surface irregularity
(arrows) indicating a mucosal lesion. This was both
a small lesion and a pathologically early squamous
carcinoma.
two cases of polypoid carcinoma.
PATTERN
Polypoid
Varicoid
Infiltrative
Ulcerative
Superficial spreading
Stricture
Pseudoachalasia
Esophageal carcinoma with ulcerations (arrows) and sharp right angle
junction with esophageal wall
Varicoid carcinoma
Unchanging appearance of filling defects
indicate tumor rather than varices.
Note sharp upper margin of lesion and
ulceration (arrows)
Long irregular distal stricture due to
carcinomaRIGHT: Distal narrowing is not
tapered and more proximal than achalasia.
Irregularity (arrow) at narrowed site is
subtle but persistent
An irregular, asymmetric stricture is
highly suggestive of carcinoma.
Smoothly tapered, symmetric strictures are
characteristic of a benign etiology
 Gastric ulcer & duodenal
ulcer
 Caused by imbalance
between secretion of acid and
pepsin, and mucosal defence
mechanism.
-Helicobacter pylori
infection
-Zollinger-ellison
syndrome
-NSAIDs
-others: stress,
smoking,alcohol,
steroid
- epigastric pain
- haematemesis
- Melaena
- heartburn
AETIOLOGY
SIGNS & SYMPTOMS
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 Ulcer projects within the anticipated wall of the stomach.
Ulcer is eccentrically located within the ulcer mound(a smooth, sharply delineated soft-
tissue mass surrounding a benign ulcer).
 Irregularly shaped ulcer crater
 Nodular ulcer mound
Abrupt transition between normal and abnormal mucosa several cms away from the ulcer
crater.
Rigidity, lack of distensibility and lack of changeability
Associated large mass
Carmen meniscus sign-a relatively shallow gastric ulcerating malignancy projecting as an
ulcer which is always convex inwards to the lumen and which does not project beyond
the wall=Kirklin meniscus complex

UGI series in a 70-year-old woman with a radiolucent halo (large
arrow) due to a Carman meniscus sign that surrounds a central
maliginant ulcer crater (small arrow).
Benign. lesser curvature gastric ulcer. Red arrows point to Hampton's Line, a thin,
straight line at neck of ulcer in profile view which represents the thin rim of undermined
gastric mucosa. The blue arrows point to the
ulcer mound, a smooth, sharply delineated soft-tissue mass surrounding a benign ulcer. Note
how the ulcer projects beyond the confines of the expected wall of the stomach.
Ulcer collar-smooth, thick, lucent band at neck of ulcer in profile view representing
thicker rim of edematous gastric wall
Ulcer mound-smooth, sharply delineated tissue mass surrounding a benign ulcer
Thickened folds radiating directly to the base of the ulcer en face
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
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 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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Bleeding gastric ulcer
Hemorrhage due to Duodenal Ulcer
 Acute mucosal
inflammatory process
 Accompanied by
hemorrhage into the
mucosa and sloughing of
the superficial
epithelium (erosion).
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- NSAIDs
- alcohol
- smoking
- chemotherapy
- uraemia
- stress
- ischaemia and shock
- suicide attempts
- mechanical trauma
- distal gastrectomy
42/81
Erosive gastritis obviously causing bleeding in the gastric
antrum, due to the use of NSAIDs
- adenomatous polyps
- leiomyoma
- neurogenic tumour
- fibromata
- lipoma
- gastric adenocarcinoma (90%)
- lymphomas
- smooth muscle tumour
BENIGN GASTRIC NEOPLASM
GASTRIC CARCINOMA
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 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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 Adenocarcinoma is by far the most common gastric malignancy,
representing over 95% of malignant tumours of the stomach. The
remaining malignant tumours include lymphoma, sarcoma
(e.g, malignant gastrointestinal stromal tumour), carcinoid tumour,
metastasis, and so on .
 Radiographic features
 Endoscopy is regarded as the most sensitive and specific diagnostic
method in patients suspected of harbouring gastric cancer.
 Fluoroscopy
 Early gastric cancer (elevated, superficial, shallow):
 type I: elevated lesion, protrudes >5 mm into lumen (polypoid)
 type II: superficial lesion (plaque-like, mucosal nodularity, ulceration)
 type III: shallow, irregular ulcer crater with adjacent nodular mucosa
and clubbing/fusion/amputation of radiation folds 4
 Advanced gastric cancer:
 polypoid cancer can be lobulated or fungating
 lesion on dependent or posterior wall; filling defect in barium pool
 lesion on nondependent or anterior wall; etched in white by a thin layer
of barium trapped between edge of mass & adjacent mucosa
 ulcerated carcinoma (penetrating cancer): 70% of all gastric cancers 4
 Ultrasound
 Not useful, unless a large epigastric mass is present or
on endoscopic ultrasound study.
 CT
 CT is currently the staging modality of choice because it
can help identify the primary tumour, assess for local
spread, and detect nodal involvement and distant
metastases 1.
 Demonstration of lesions facilitated by negative contrast
agents (water or gas):
 A polypoid mass with or without ulceration
 Focal wall thickening with mucosal irregularity or focal
infiltration of wall
 Ulceration: gas-filled ulcer crater within mass
 Infiltrating carcinoma: wall thickening and loss of
normal rugal fold pattern.
 Calcifications are rare but when present, they are usually
mucinous adenocarcinoma.
Endoscopic image of linitis plastica, entire
stomach is invaded, leading to a leather bottle-
like appearance
Prepyloric gastric cancer.
The tumor shows a rodent
pro- liferation in the shape
of a bowl in the prepyloric
antrum. Central hematin
hints at an oozing
hemorrhage prior to
endoscopy. The traces of
blood at the bottom are
caused by biopsy.
Peristaltic movements are
completly absent in this
part of the stomach
Pictures of an antral carcinoma, which developed a
huge tumorous cavity. Next to the ulcerations the
tumor also has exophytic parts bleeding easily. The
whole visible gastric section consists of tumor, there
is no normal, gastric tissue. In the background a
glimpse of the pylorus can be caught.
Double contrast barium meal demonstrates irregular narrowing
of the gastric fundus and body with antral sparing. There is only
mild loss of gastric distensibility.
A single contrast UGIS image
which demonstrates uniform
narrowing of the gastric body
and diffusely flattened mucosal
folds due to wall infiltration by
tumor (later proven to be
adenocarcinoma by endoscopic
biopsy). The wall was rigid and
thickened upon examination
with markedly abnormal
peristalsis
• 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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- 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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- 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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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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Crohn’s disease
Diverticula eg:
Meckel’s diverticulum,
Jejujanal diverticulosis
Benign neoplasm eg:
Peutz-Jegher’s syndrome
Leiomyoma.
Malignant neoplasm eg:
Lymphoma,
Angiodysplasia
Rectal carcinoma and
polyps
Rectal prolapse
Carcinoma of colon
Polyps eg:
Familial adenomatous
polyposis
Diverticular disease
Inflamation
Ischaemic colitis
Ulcerative colitis
Pseudomembranous
colitis
Angiodysplasia
Haemorrhoids
Fissure-in-ano
Anal carcinoma
Anal wart
SMALL
INTESTINE
RECTUM
COLON
ANUS
cDNA
PC
PACI
D
wCH
F
57/81
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
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ACR Appropriateness
Criteria
 The role of Tc-99m RBC scintigraphy in the evaluation of upper
gastrointestinal bleeding is limited due to the widespread use of
endoscopy as a first-line modality for such bleeding.
 locate the bleeding site and to determine who requires aggressive
treatment versus those who can be medically managed
 However, Tc-99m RBC scintigraphy can be useful when endoscopy is not
readily available or in patients in whom endoscopy is difficult or
impossible.
 Tc- 99m RBC scintigraphy plays a larger role in the evaluation of lower
gastrointestinal bleeding due to the limited sensitivity of endoscopy
within the lower gastrointestinal tract and has typically been used as a
screening examination to identify patients who require angiography or
surgery.
 Bleeding rate may be slow enough that right colon bleeding manifests
with melena or a combination of melena and dark red blood from the
rectum.
 Blood pressure and pulse measured to confirm
that they are not hypotensive.
 The in-vitro method for labeling red blood
cells is preferred due to its higher labeling
efficiency. The in-vivo/in-vitro method can be
used. The invivo method is not recommended.
 Continuous acquisition of images at a frame
rate of one image every 10–60 sec is important
in order to accurately localize the bleeding
site
 Patient position: Supine
 a.Abdominal Flow Study: Anterior abdominal flow images (1–5
secs/frame x 1 min) are recommended.
 b. Dynamic Abdominal Imaging
 i. Dynamic anterior abdominal images are acquired at a frame rate of 10–
60 sec per frame over a 60 to 90 min period. Acquiring these images in
multiple sets of 10–15 min each may facilitate review of these images by
the physician as the images are being acquired.
 ii. If computer acquisition is not possible: Sequential static images 1
million counts per image at least every 5 min for 60–90 min. Localization
might be aided by obtaining images at a shorter interval, every 2–3 min.
 C. Delayed Imaging :For Tc-99m RBCs, if no bleeding site is identified on
the initial 60–90 min dynamic images, delayed images may be acquired
These images are optional. Typically delayed images are done from 2–6
hr and/or at 18–24 hr after the injection of the radiopharmaceutical.
 Due to overlying bladder activity, activity in the
rectum can be difficult to appreciate. Lateral views
may be needed to see rectal bleeding. Anterior
oblique and posterior views are frequently helpful in
deciding if activity is located anteriorly versus
posteriorly.
 In cases where extravasated blood is seen but does not
move sufficiently to determine the location or where
the movement is unusual, the following may be useful:
review of prior barium studies; oral Tc-99m Sulphur
Colloid to outline the upper GI and small bowel
anatomy; or Tc-99m Sulphur Colloid enema to
outline the colon
 Extravasated radiolabeled RBCs within the
lumen of the bowel are identified as an area of
activity that increases in intensity with time,
and/or as a focus of activity that moves in a
pattern corresponding to the lumen of the large
or small bowel. Small bowel bleeding usually
can be distinguished from large bowel bleeding
by its rapid serpiginous movement
 Factors associated with a low bleeding rate
are visualization of blood after one hour and
activity less intense than the liver.
 Higher bleeding rates are associated with
early appearance of blood in the bowel and
intense activity equal to or greater than the
liver
Scintigraphic study demonstrated active bleeding in the right lower quadrant of the
abdomen (arrow on left image), most probably corresponding to the terminal ileum
Contrast angiography showed active contrast extravasation (shown by arrow) off a
small branch of the ileocolic artery.
This branch was successfully embolized with gelfoam. Another contrast
injection showed no signs of further extravasation
 Tc-99m RBC scintigraphy is 93% sensitive and 95%
specific for detecting a bleeding site with active arterial
or venous bleeding rates as low as 0.04 mL/min
 Limited resolution of scintigraphy does not allow
precise anatomic localization of gastrointestinal
bleeding.
 Angiography is an invasive examination that
can be used for accurate localization as well as
treatment of both upper and lower
gastrointestinal bleeding.
 Preffered in acutely unstable patient, after a
negative or failed endoscopic evaluation, or
as a first-line examination for lower
gastrointestinal hemorrhage.
 Bleeding rates as low as 0.5 mL/min can be detected
 sensitivity of 63%–90% for upper and 40%–86% for lower ,
specificity of up to 100% for both .
 The use of carbon dioxide (CO2) as the contrast agent and
provocative measures such as direct arterial infusion of
vasodilators, thrombolytics, or anticoagulants may
increase the sensitivity of selective catheter angiography.
 Extravasation of contrast material into the bowel lumen is
pathognomonic for active gastrointestinal hemorrhage.
 Indirect signs include detection of pseudoaneurysm,
arteriovenous fistula, hyperemia, neovascularity, and
extravasation of contrast material into a confined space.
 Diagnostic testing may be required following transcatheter
localization and treatment.
 Embolization of the bleeding vessel is the mainstay of transcatheter
treatment for non variceal gastrointestinal bleeding, and high technical
success rates (angiographic cessation of bleeding) of 91%–100% have been
reported.
 Clinical success rates (cessation of bleeding for 30 days) of 68%–82% for
upper GI and 81%–91% for lower gastrointestinal
 Microcoil embolization is typically preferred within the lower
gastrointestinal tract, whereas controversy exists regarding the optimal
agent within the upper gastrointestinal tract.
 In fact, combinations of different embolic agents may be more effective
than embolization with a single agent in the upper gastrointestinal tract.
 Common embolic agents include microcoils,polyvinyl alcohol particles,
gelfoam, n-butyl cyanoacrylate glue, and enbucrylate tissue adhesive.
 Direct intraarterial infusion of platelets and vasopressin has also been
used successfully in the transcatheter treatment of gastrointestinal
hemorrhage.
 This technique, the SMA or IMA is catheterized and vasopressin is
infused through the catheter
 Typical vasopressin therapy involves an initial 20-minute infusion at a
rate of 0.2 U/min followed by repeated arteriography to determine
whether bleeding has stopped and that the artery is not overconstricted.
 The infusion rate can be incrementally increased to 0.3 U/min and then to
0.4 U/min, if bleeding continues. Each change in infusion rate must be
followed by a waiting period (20 minutes) for the increased drug dose to
take effect and then another arteriogram to assess the effect. The infusion
is continued for another 12 to 24 hours
 The vasopressin infusion is then replaced with a saline solution infusion
for 6 to 12 hours
 The catheter is then removed if there are no clinical signs of bleeding but,
by this time, the average time the catheter is in situ is 1–2 days.
 the ability to stop bleeding relies on patient factors such as
atherosclerosis and coagulopathy.
 Prolonged presence of the catheter or catheter motion
can lead to thrombosis or dissection.
 Dislodgement of the catheter into another nontarget
artery, such as the renal artery can cause flank pain and
hematuria. Similarly, dislodgment of the catheter into
the phrenic artery can lead to chest pain and
arrhythmias. Other systemic complications due to
vasopressin infusion include arrhythmias (bradycardia
or ventricular tachycardia), hypotension, angina, and
cardiac arrest.
 mesenteric artery thrombosis, bowel infarction, and
spontaneous bacterial peritonitis. Minor complications
related to arterial access include hematoma,
pseudoaneurysm, arterial spasm, and infection.
 Embolization is defined as the deliberate occlusion of
vessels for a therapeutic purpose
 Embolization agents can be classified into
 Temporary embolics such as- Gelfoam
 Permanent embolics, which may be either solid or
liquid.
 Solid permanent embolic materials include polyvinyl
alcohol (PVA), tris-acryl gelatin
microspheres(Embospheres), detachable fiber coils,
platinum coils, and detachable balloons.
 Liquid embolic materials include absolute alcohol, N-
butyl cyanoacrylate (NBCA), and Onyx® (an ethylene
vinyl alcohol copolymer; Ev3 Endovascular, Inc.
Plymouth, MN).
 Microcoils (complex helical fibered platinum coils) range from 2 to 12
mm in diameter and are available in various lengths. These coils are
highly radiopaque and can be precisely deployed.
 Once deployed in a distal artery, they decrease the perfusion pressure
allowing thrombosis of the bleeding vessel
 Coils are easy to use and pose a lesser threat of ischemia than PVA
particles, which may disseminate to the smaller vessels.
 coils are usually preferred for embolization of pseudoaneurysms.
 N-butyl cyanoacrylate (NBCA) allows for rapid and permanent
embolization due to its fast polymerization when it comes in contact
with blood. A single injection may provide complete hemostasis through
simultaneous embolization of collateral vessels connected to the bleeding
focus. It is useful in patients with coagulopathy as the vessel occlusion is
independent of the coagulation process.
 Polyvinyl alcohol and Gelfoam® have certain disadvantages. Both
agents are more difficult to control than microcoils because neither can be
seen during fluoroscopy. An additional disadvantage of polyvinyl alcohol
particles is that the particles may reach intramural circulation beyond the
level of collateralization leading to bowel infarction or may reflux into
nontarget arteries.
 CT angiography has a crucial role in preprocedure evaluation of a patient with GI
bleeding.
 Oxygen saturation, blood pressure, and heart rate and rhythm are continuously
monitored.
 Intravenous glucagon (1 mg) or scopolamine butyl bromide is administered to decrease
bowel peristalsis.
 General anesthesia is highly useful during angiography to maintain haemodynamics
and decreasing motion artifact.
 Selective injections into the celiac axis, SMA, and IMA are routinely obtained. It is
important to cover the entire abdomen during injections into the SMA and the IMA.
 Once the bleeding source is localized angiographically,
 a 3-French microcatheter is advanced coaxially to the bleeding site through the
indwelling 4- or 5-French catheter. Attempts are made to position the catheter as close
to the bleeding site as possible. In the IMA distribution, the catheter is advanced to the
marginal artery or the terminal artery if possible. In the SMA, the catheter is advanced to
the vasa recta. If spasm occurs, intraarterial papaverine (25 mg) may be administered
 Embolization is performed only when the catheter can be
advanced to or distal to the mesenteric border of the colon.
Embolization is performed until no further arterial
extravasation is seen. Technical success is defined as
cessation of bleeding as seen on angiography.
 During the procedure, NBCA is mixed with iodized oil in
ratios varying from 1:1 to 1:334 and the microcatheter must
be flushed with 5% dextrose solution prior to injection to
prevent premature polymerization of NBCA within the
catheter.
 Injection is stopped when extravasation of the mixture
occurs from the bleeding site or when an underlying
pseudoaneurysm is completely opacified.
 Although catheterization may be possible, it may be difficult
to deliver the coils because of the tortuosity of the vessels. In
such instances, NBCA can be a good choice due to its low
viscosity.
 When a bleeding vessel is inaccessible for selective
catheterization, embolotherapy may be abandoned and
vasopressin infusion may be undertaken for control of GI
bleeding.
 Bowel infarction and gangrene.
 arterial dissections and nontarget embolization due to
migration of the embolic materials.
 Transcatheter embolization with NBCA has the potential
risk of embolization of the proximal segment without
adequate embolization at the bleeding site due to rapid
polymerization.
 Distal embolization of the nontargeted sites may occur due
to too rapid injection of the NBCA mixture or an excessively
prolonged polymerization time and reflux of NBCA into
another nontarget vessel due to overinjection.
 In general, embolization is safer than vasopressin infusion
as it has lower access site complications due to the shorter
catheter dwell times
Delayed image of proper hepatic arteriogram shows a large pseudoaneurysm arising
from the gastroduodenal artery. (B) The aneurysm was treated with coil embolization
of the aneurysm and feeding artery. Coil migration was noted during the procedure.
However, patient had an uneventful recovery
A 50-year-old man with pancreatitis presented with gastrointestinal (GI) bleeding. (A)
Superior mesenteric arteriogram reveals a pseudoaneurysm from a jejunal branch,
which was successfully treated with coils (B).
(C) Another pseudoaneurysm in a branch of the right hepatic artery is also treated with
coils (D)
In patients with endoscopy-proven nonvariceal gastric bleeding,
embolization of the left gastric artery is often practiced even no active
extravasation is found on angiography.
 Pseudoaneurysms secondary to pancreatitis may result in upper or lower
GI bleeding depending on the location of the aneurysm. These can be
successfully embolized with coils.
 Variceal bleeding is treated with transjugular intrahepatic
portosystemic shunt (TIPS) and retrograde embolization of the varices
 Both endoscopy and angiography have been used for the diagnosis of a
Dieulafoy lesion. Transcatheter arterial embolization has been reported
for gastric Dieulafoy lesions, with variable results.
 Partial splenic embolization is effective at reducing variceal bleeding
regardless of the underlying cause of the portal hypertension.
 Recent portal vein thrombosis may recanalize with systemic
anticoagulation in 80% of patients.
 Transsplenic recanalization of the portal vein has been described in
children. Splenic arterial embolization can be performed before the
transsplenic procedure to reduce splenic vein flow and prevent
bleeding.
 Similarly, isolated gastric varices secondary to splenic vein thrombosis
may be treated with splenic embolization or splenectomy.
 This technique has been shown to be effective in
adequately controlling a bleeding site by temporary
occlusion of the vessel due to vasospasm.
 The decrease in blood flow and pulse pressure caused
by vasospasm would allow normal physiologic
thrombosis of the bleeding site.
 In time, the spasm would resolve, thereby allowing
restoration of the blood flow and keeping the risk of
intestinal ischemia or infarction to a minimum.
 This technique may be employed as primary therapy in
patients who cannot tolerate vasopressin or when
embolotherapy is difficult or not feasible.
 EGD and colonoscopy are currently considered
the first-line diagnostic and therapeutic procedures
of choice for both upper and lower gastrointestinal
bleeding.
 Endoscopic evaluation allows relatively safe, direct
localization and characterization of bleeding lesions
within the majority of the upper gastrointestinal
tract as well as in the colon and distal ileum. The
distal duodenum and the majority of the small bowel
cannot be adequately assessed with conventional
endoscopy
 Visual characterization of a bleeding lesion can
provide important prognostic information
regarding the risk of recurrent bleeding and
may prompt tissue sampling if a neoplasm is
suspected.
 The reported sensitivity and specificity of EGD
for upper gastrointestinal bleeding are 92%–
98% and 30%–100%, respectively.
 Occasionally, rapid hemorrhage obscures
endoscopic visualization of the bleeding site
and precludes intervention.
 Bowel preparation is required prior to
colonoscopy, which can be completed in 3–4 hours,
typically by administering a polyethylene glycol–
based solution orally or via a nasogastric tube.
 Endoscopic interventions can be performed if
the bleeding lesion is adequately visualized.
 Endoscopic therapeutic treatments may be (a) by
injection (epinephrine, alcohol), (b) thermal
(heater probe, electrocoagulation, laser), or (c)
mechanical (clips, bands). Injection sclerotherapy
with epinephrine achieves primary hemostasis
rates of 96.7% for ulcers and 80%–90% for variceal
bleeding .
 Although all of the above mentioned therapeutic
modalities demonstrate similar efficacies in
randomized trials, they have shown increased
effectiveness when used in combination
 Approximately 15%–20% of patients with treated upper
gastrointestinal bleeding will develop recurrent bleeding after
endoscopic treatment, usually within 72 hours .
 Wireless Capsule Endocopy has proved beneficial in patients in
whom no source of bleeding has been identified despite
evaluation with esophagogastroduodenoscopy and colonoscopy.
 Patient preparation consists of a 10-hour fast, followed by
ingestion of the capsule with a glass of water. Data interpretation
occurs after 8 hours of transit time, after which 2–3 hours are
needed to download the data to a workstation.
 Capsule retention by intestinal stricture is the most serious
complication . Because of the prolonged imaging time and the
need for preprocedural fasting, there is presently no defined
role for Wireless Capsule Endocopy in the evaluation of acute
gastrointestinal bleeding.
 Helical CT has depicted active colonic
haemorrhage with bleeding rates as low as 0.3
mL/min, which is below the reported threshold
for selective catheter angiography
 Significant gastrointestinal bleeding that resulted
in either systemic hypotension (systolic blood
pressure
The CT angiographic diagnosis of active
gastrointestinal bleeding is made when
hyperattenuating extravasated contrast material is
seen within the bowel lumen. The extravasated
contrast material may demonstrate linear, jetlike,
swirled, ellipsoid, or pooled configurations or
may fill the entire bowel lumen, resulting in a
hyperattenuating loop
 Other studies see the HU contrast Threshold
 Most cases of acutely extravasated contrast
material into the bowel lumen will exceed the
90 HU threshold
 Although small amounts of bleeding or
thin contrast material “jets ” may not reach this
threshold due to volume averaging within
either the section itself or the user-defined
region of interest.
 In addition, comparison with unenhanced images
allows differentiation of active hemorrhage from
other high-attenuation material that may be
present within the gastrointestinal tract at
the time of CT angiographic evaluation, thereby
preventing false-positive interpretation.
 Therefore, high-attenuation material detected
within the bowel lumen at CT angiography that
was not present at unenhanced CT performed
immediately prior to the CT angiography
is diagnostic for acute gastrointestinal
hemorrhage.
.
 In addition to helping detect active gastrointestinal
hemorrhage,
CT angiography allows concurrent
evaluation of the gastrointestinal and proximal
femoral vasculature. Because significant anatomic
variation of the gastrointestinal vasculature
exists, preoperative knowledge of the active
gastrointestinal bleeding site and its vascular supply is
extremely useful for preinterventional planning this
preoperative knowledge will decreased number of
digital subtraction angiographic exposures, faster
catheterization of bleeding vessels, decreased
contrast material use during angiography, and shorter
procedure times. It has also reduced patient (and
operator) radiation exposure within the angiography
suite
 Evaluation of gastrointestinal bleeding with
CT angiography may also provide etiologic
information in many cases, especially with lower
gastrointestinal bleeding. CT angiography can
easily help diagnose colonic diverticuli, the most
common cause of lower gastrointestinal.
 CT angiography in the detection of colonic
angiodysplasia.
 Angiodysplasia may account for up
to 40% of cases of lower gastrointestinal bleeding
in patients over 60 years of age and is the second
most common cause of such bleeding
 Distinguishing diverticular from angiodysplastic
bleeding (when possible) is important because of
the prognostic differences between these two lesions.
 Although bleeding will cease spontaneously
in 80% or more of cases of angiodysplastic bleeding
and in 75% of cases of diverticular bleeding
recurrent bleeding will develop in up to
85% of cases of untreated angiodysplastic bleeding
as opposed to only 25% of cases of untreated
diverticular bleeding.
 CT angiography can also help accurately diagnose neoplasms
and colitis, the third and fourth most common
causes of lower gastrointestinal bleeding, respectively.
 Concurrent localization of active hemorrhage
and diagnosis of the underlying cause can also
have important treatment and management implications.
Hemorrhage from a Mallory-Weiss tear. Angiogram demonstrates hemorrhage caused
by a Mallory-Weiss tear appearing as a small focus of extravasated contrast material
(arrow).
(2) Stent-related upper gastrointestinal bleeding. Angiogram shows brisk hemorrhage
from the main trunk of the right hepatic artery due to erosion from an endoscopically
placed stent (Wallstent; Schneider, Minneapolis, Minn). Note the presence of
extravasated contrast material in the common duct and duodenum (arrows).
(A) Delayed phase contrast-enhanced computed tomography (CT) scan of the abdomen
shows active contrast material extravasation (arrow) into a jejunal loop consistent with
active gastrointestinal bleeding. (B) Superior mesenteric arteriogram shows active
extravasation (arrow) of contrast material from a branch supplying the jejunum. (C) The
bleeding vessel was selectively catheterized. (D) The bleeding vessel was embolized
with polyvinyl alcohol (PVA) 500–700 m particles. Postembolization angiogram shows
no more active contrast extravasation.
 Thank u

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Gi bleeding presentation

  • 2.  Gastrointestinal bleeding is typically categorized as either upper or lower gastrointestinal bleeding depending on the anatomic location of the bleeding site.  Upper gastrointestinal bleeding occurs proximal to the ligament of Treitz and may involve the esophagus, stomach, and duodenum.  Lower gastrointestinal bleeding occurs distal to the ligament of Treitz and may involve the small bowel, colon, and rectum. Lower gastrointestinal bleeding is less common than upper gastrointestinal bleeding and accounts for approximately 30% of all gastrointestinal bleeding.  Lower gastrointestinal bleeding tends to affect elderly patients and is 200 times more likely to occur in an 80-year-old than in a 20-year-old
  • 3.  Erosion or ulcer 55–74  Variceal bleeding 5–14  Mallory-Weiss tear 2–7  Vascular lesions 2–3  Neoplasms 2–5
  • 4.  Diverticular disease 20–55  Angiodysplasia 3–40  Neoplasms 8–26  Colitis 6–22  Benign anorectal lesions 9–10
  • 5.  The celiac axis and the superior mesenteric artery (SMA) are the first two branches of the abdominal aorta and provide a rich and well-collateralized network of branch vessels that supply blood to the upper gastrointestinal tract.  Extensive collateralization between the celiac artery and the SMA protects the upper gastrointestinal tract from ischemic insult and permits surgical and embolization procedures to be carried out with a relatively low risk of ischemic injury.  Similarly, branch vessels of both the SMA and the inferior mesenteric artery (IMA) form a series of interconnected arcades that provide a means of collateral flow throughout the lower gastrointestinal tract.
  • 6.  Gastrointestinal bleeding can also have venous sources. Venous bleeding within the upper gastrointestinal tract is typically due to gastric or esophageal varices arising from the coronary vein or the short gastric veins in the setting of portal hypertension.  However, approximately 30% of patients with portal hypertension and coexistent varices who present with upper gastrointestinal bleeding will have an arterial source of bleeding . Venous bleeding within the lower gastrointestinal tract is commonly due to hemorrhoids involving either the internal or external rectal venous plexus
  • 7.  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
  • 9.  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). 9/81
  • 10.  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. 10/81
  • 11. 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 11/81
  • 12. 12/81
  • 13.  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. 13/81
  • 14. Esophageal varices: a view of the everted esophagus and gastroesophageal junction, showing dilated submucosal veins (varices). 14/81
  • 15. Filling defects due to varices are characterized by change in appearance during the examination related to breath holding and thoracic pressure CT images of a patient with large Uphill varices secondary to cirrhosis with portal hypertension With portal hypertension, elevated portal venous pressure leads to reversed (hepatofugal) flow bypassing the liver through the left gastric vein to dilated esophageal and periesophageal veins that anastamose with the azygos and hemiazygos veins which drain uphill into the superior vena cava.
  • 16. Downhill varices in a patient with a superior vena cava obstruction due to histoplasmosis. On the barium study inconstant filling defects (arrows) represent downhill varices in upper esophagus. The angiogram demonstrates collateral vessels including a dilated left superior intercostal vein (arrow). Downhill Varices With superior vena caval obstruction, upper body venous blood flows caudally downhill through esophageal veins to the azygos vein which empties into the superior vena cava caudal to the obstruction. If the obstruction is at or below the azygos, the blood flow extends further caudally to the portal system and then the hepatic veins to the inferior vena cava and the right atrium.
  • 17. PRE HEPATIC • Portal vein thrombosi s • Splenic vein thrombosi s INTRA HEPATIC • Cirrhosis • Schistoso miasis • Sarcoidos is • Myeloprol iferative disorder • Congenita l hepatic fibrosis POST HEPATIC • Budd- chiari syndrome • Right heart failure • Constricti ve pericarditi s 17/81
  • 18. 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 18/81
  • 19.
  • 20. - blood transfusion - endoscopic variceal injection with sclerosant or banding. - sengstaken tube 20/81
  • 21.
  • 22.  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 22/81
  • 23. Mallory-Weiss tear. Typical longitudinal mucosal tear with overlying fibrinous exudate extending from the distal esophagus to the gastric cardia. Courtesy of C.J. Gostout, MD. Mallory-Weiss tear with a pigmented protuberance and active oozing
  • 24. Spot films show barium (arrows) in linear mucosal tear near gastroesophageal junction.
  • 25. - 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 hemoclipping 25/81
  • 26.  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%) 26/81
  • 27. Leiomyomas are the most common benign esophageal neoplasm and are often large yet nonobstructive. On the chest film an abnormal opacity is seen behind the heart (arrow). The barium study demonstrates a lobulated mass (arrow) that does not obstruct despite it large size.
  • 28. -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 GERD - barrett’s oesophagus - tobacco smoking ADENOCARCINOMA SQUAMUS CELL CARCINOMA 28/81
  • 29. 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) Regurgitation 4) Aspiration pneumonitis 5) Weight loss 6) Anorexia 7) Anemia 8) Lassitude 29/81
  • 30. patient with an early esophageal carcinoma. Lesion is not visible on single contrast esophagram. Air-contrast esophagram shows surface irregularity (arrows) indicating a mucosal lesion. This was both a small lesion and a pathologically early squamous carcinoma. two cases of polypoid carcinoma. PATTERN Polypoid Varicoid Infiltrative Ulcerative Superficial spreading Stricture Pseudoachalasia
  • 31. Esophageal carcinoma with ulcerations (arrows) and sharp right angle junction with esophageal wall
  • 32. Varicoid carcinoma Unchanging appearance of filling defects indicate tumor rather than varices. Note sharp upper margin of lesion and ulceration (arrows)
  • 33. Long irregular distal stricture due to carcinomaRIGHT: Distal narrowing is not tapered and more proximal than achalasia. Irregularity (arrow) at narrowed site is subtle but persistent An irregular, asymmetric stricture is highly suggestive of carcinoma. Smoothly tapered, symmetric strictures are characteristic of a benign etiology
  • 34.  Gastric ulcer & duodenal ulcer  Caused by imbalance between secretion of acid and pepsin, and mucosal defence mechanism. -Helicobacter pylori infection -Zollinger-ellison syndrome -NSAIDs -others: stress, smoking,alcohol, steroid - epigastric pain - haematemesis - Melaena - heartburn AETIOLOGY SIGNS & SYMPTOMS 34/81
  • 35.  Ulcer projects within the anticipated wall of the stomach. Ulcer is eccentrically located within the ulcer mound(a smooth, sharply delineated soft- tissue mass surrounding a benign ulcer).  Irregularly shaped ulcer crater  Nodular ulcer mound Abrupt transition between normal and abnormal mucosa several cms away from the ulcer crater. Rigidity, lack of distensibility and lack of changeability Associated large mass Carmen meniscus sign-a relatively shallow gastric ulcerating malignancy projecting as an ulcer which is always convex inwards to the lumen and which does not project beyond the wall=Kirklin meniscus complex 
  • 36. UGI series in a 70-year-old woman with a radiolucent halo (large arrow) due to a Carman meniscus sign that surrounds a central maliginant ulcer crater (small arrow).
  • 37. Benign. lesser curvature gastric ulcer. Red arrows point to Hampton's Line, a thin, straight line at neck of ulcer in profile view which represents the thin rim of undermined gastric mucosa. The blue arrows point to the ulcer mound, a smooth, sharply delineated soft-tissue mass surrounding a benign ulcer. Note how the ulcer projects beyond the confines of the expected wall of the stomach. Ulcer collar-smooth, thick, lucent band at neck of ulcer in profile view representing thicker rim of edematous gastric wall Ulcer mound-smooth, sharply delineated tissue mass surrounding a benign ulcer Thickened folds radiating directly to the base of the ulcer en face
  • 38. 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 38/81
  • 39.  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 39/81
  • 40. Bleeding gastric ulcer Hemorrhage due to Duodenal Ulcer
  • 41.  Acute mucosal inflammatory process  Accompanied by hemorrhage into the mucosa and sloughing of the superficial epithelium (erosion). 41/81
  • 42. - NSAIDs - alcohol - smoking - chemotherapy - uraemia - stress - ischaemia and shock - suicide attempts - mechanical trauma - distal gastrectomy 42/81
  • 43. Erosive gastritis obviously causing bleeding in the gastric antrum, due to the use of NSAIDs
  • 44. - adenomatous polyps - leiomyoma - neurogenic tumour - fibromata - lipoma - gastric adenocarcinoma (90%) - lymphomas - smooth muscle tumour BENIGN GASTRIC NEOPLASM GASTRIC CARCINOMA 44/81
  • 45.  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 45/81
  • 46.  Adenocarcinoma is by far the most common gastric malignancy, representing over 95% of malignant tumours of the stomach. The remaining malignant tumours include lymphoma, sarcoma (e.g, malignant gastrointestinal stromal tumour), carcinoid tumour, metastasis, and so on .  Radiographic features  Endoscopy is regarded as the most sensitive and specific diagnostic method in patients suspected of harbouring gastric cancer.  Fluoroscopy  Early gastric cancer (elevated, superficial, shallow):  type I: elevated lesion, protrudes >5 mm into lumen (polypoid)  type II: superficial lesion (plaque-like, mucosal nodularity, ulceration)  type III: shallow, irregular ulcer crater with adjacent nodular mucosa and clubbing/fusion/amputation of radiation folds 4  Advanced gastric cancer:  polypoid cancer can be lobulated or fungating  lesion on dependent or posterior wall; filling defect in barium pool  lesion on nondependent or anterior wall; etched in white by a thin layer of barium trapped between edge of mass & adjacent mucosa  ulcerated carcinoma (penetrating cancer): 70% of all gastric cancers 4
  • 47.  Ultrasound  Not useful, unless a large epigastric mass is present or on endoscopic ultrasound study.  CT  CT is currently the staging modality of choice because it can help identify the primary tumour, assess for local spread, and detect nodal involvement and distant metastases 1.  Demonstration of lesions facilitated by negative contrast agents (water or gas):  A polypoid mass with or without ulceration  Focal wall thickening with mucosal irregularity or focal infiltration of wall  Ulceration: gas-filled ulcer crater within mass  Infiltrating carcinoma: wall thickening and loss of normal rugal fold pattern.  Calcifications are rare but when present, they are usually mucinous adenocarcinoma.
  • 48. Endoscopic image of linitis plastica, entire stomach is invaded, leading to a leather bottle- like appearance
  • 49. Prepyloric gastric cancer. The tumor shows a rodent pro- liferation in the shape of a bowl in the prepyloric antrum. Central hematin hints at an oozing hemorrhage prior to endoscopy. The traces of blood at the bottom are caused by biopsy. Peristaltic movements are completly absent in this part of the stomach Pictures of an antral carcinoma, which developed a huge tumorous cavity. Next to the ulcerations the tumor also has exophytic parts bleeding easily. The whole visible gastric section consists of tumor, there is no normal, gastric tissue. In the background a glimpse of the pylorus can be caught.
  • 50. Double contrast barium meal demonstrates irregular narrowing of the gastric fundus and body with antral sparing. There is only mild loss of gastric distensibility.
  • 51. A single contrast UGIS image which demonstrates uniform narrowing of the gastric body and diffusely flattened mucosal folds due to wall infiltration by tumor (later proven to be adenocarcinoma by endoscopic biopsy). The wall was rigid and thickened upon examination with markedly abnormal peristalsis
  • 52. • 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. 52/81
  • 53. - 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 53/81
  • 54. - 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 54/81
  • 55. 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) 55/81
  • 56. 56/81
  • 57. Crohn’s disease Diverticula eg: Meckel’s diverticulum, Jejujanal diverticulosis Benign neoplasm eg: Peutz-Jegher’s syndrome Leiomyoma. Malignant neoplasm eg: Lymphoma, Angiodysplasia Rectal carcinoma and polyps Rectal prolapse Carcinoma of colon Polyps eg: Familial adenomatous polyposis Diverticular disease Inflamation Ischaemic colitis Ulcerative colitis Pseudomembranous colitis Angiodysplasia Haemorrhoids Fissure-in-ano Anal carcinoma Anal wart SMALL INTESTINE RECTUM COLON ANUS cDNA PC PACI D wCH F 57/81
  • 58. 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 58/81
  • 59. 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 59/81
  • 61.  The role of Tc-99m RBC scintigraphy in the evaluation of upper gastrointestinal bleeding is limited due to the widespread use of endoscopy as a first-line modality for such bleeding.  locate the bleeding site and to determine who requires aggressive treatment versus those who can be medically managed  However, Tc-99m RBC scintigraphy can be useful when endoscopy is not readily available or in patients in whom endoscopy is difficult or impossible.  Tc- 99m RBC scintigraphy plays a larger role in the evaluation of lower gastrointestinal bleeding due to the limited sensitivity of endoscopy within the lower gastrointestinal tract and has typically been used as a screening examination to identify patients who require angiography or surgery.  Bleeding rate may be slow enough that right colon bleeding manifests with melena or a combination of melena and dark red blood from the rectum.
  • 62.  Blood pressure and pulse measured to confirm that they are not hypotensive.  The in-vitro method for labeling red blood cells is preferred due to its higher labeling efficiency. The in-vivo/in-vitro method can be used. The invivo method is not recommended.  Continuous acquisition of images at a frame rate of one image every 10–60 sec is important in order to accurately localize the bleeding site  Patient position: Supine
  • 63.  a.Abdominal Flow Study: Anterior abdominal flow images (1–5 secs/frame x 1 min) are recommended.  b. Dynamic Abdominal Imaging  i. Dynamic anterior abdominal images are acquired at a frame rate of 10– 60 sec per frame over a 60 to 90 min period. Acquiring these images in multiple sets of 10–15 min each may facilitate review of these images by the physician as the images are being acquired.  ii. If computer acquisition is not possible: Sequential static images 1 million counts per image at least every 5 min for 60–90 min. Localization might be aided by obtaining images at a shorter interval, every 2–3 min.  C. Delayed Imaging :For Tc-99m RBCs, if no bleeding site is identified on the initial 60–90 min dynamic images, delayed images may be acquired These images are optional. Typically delayed images are done from 2–6 hr and/or at 18–24 hr after the injection of the radiopharmaceutical.
  • 64.  Due to overlying bladder activity, activity in the rectum can be difficult to appreciate. Lateral views may be needed to see rectal bleeding. Anterior oblique and posterior views are frequently helpful in deciding if activity is located anteriorly versus posteriorly.  In cases where extravasated blood is seen but does not move sufficiently to determine the location or where the movement is unusual, the following may be useful: review of prior barium studies; oral Tc-99m Sulphur Colloid to outline the upper GI and small bowel anatomy; or Tc-99m Sulphur Colloid enema to outline the colon
  • 65.  Extravasated radiolabeled RBCs within the lumen of the bowel are identified as an area of activity that increases in intensity with time, and/or as a focus of activity that moves in a pattern corresponding to the lumen of the large or small bowel. Small bowel bleeding usually can be distinguished from large bowel bleeding by its rapid serpiginous movement
  • 66.  Factors associated with a low bleeding rate are visualization of blood after one hour and activity less intense than the liver.  Higher bleeding rates are associated with early appearance of blood in the bowel and intense activity equal to or greater than the liver
  • 67. Scintigraphic study demonstrated active bleeding in the right lower quadrant of the abdomen (arrow on left image), most probably corresponding to the terminal ileum
  • 68. Contrast angiography showed active contrast extravasation (shown by arrow) off a small branch of the ileocolic artery. This branch was successfully embolized with gelfoam. Another contrast injection showed no signs of further extravasation
  • 69.  Tc-99m RBC scintigraphy is 93% sensitive and 95% specific for detecting a bleeding site with active arterial or venous bleeding rates as low as 0.04 mL/min  Limited resolution of scintigraphy does not allow precise anatomic localization of gastrointestinal bleeding.
  • 70.  Angiography is an invasive examination that can be used for accurate localization as well as treatment of both upper and lower gastrointestinal bleeding.  Preffered in acutely unstable patient, after a negative or failed endoscopic evaluation, or as a first-line examination for lower gastrointestinal hemorrhage.
  • 71.  Bleeding rates as low as 0.5 mL/min can be detected  sensitivity of 63%–90% for upper and 40%–86% for lower , specificity of up to 100% for both .  The use of carbon dioxide (CO2) as the contrast agent and provocative measures such as direct arterial infusion of vasodilators, thrombolytics, or anticoagulants may increase the sensitivity of selective catheter angiography.  Extravasation of contrast material into the bowel lumen is pathognomonic for active gastrointestinal hemorrhage.  Indirect signs include detection of pseudoaneurysm, arteriovenous fistula, hyperemia, neovascularity, and extravasation of contrast material into a confined space.  Diagnostic testing may be required following transcatheter localization and treatment.
  • 72.  Embolization of the bleeding vessel is the mainstay of transcatheter treatment for non variceal gastrointestinal bleeding, and high technical success rates (angiographic cessation of bleeding) of 91%–100% have been reported.  Clinical success rates (cessation of bleeding for 30 days) of 68%–82% for upper GI and 81%–91% for lower gastrointestinal  Microcoil embolization is typically preferred within the lower gastrointestinal tract, whereas controversy exists regarding the optimal agent within the upper gastrointestinal tract.  In fact, combinations of different embolic agents may be more effective than embolization with a single agent in the upper gastrointestinal tract.  Common embolic agents include microcoils,polyvinyl alcohol particles, gelfoam, n-butyl cyanoacrylate glue, and enbucrylate tissue adhesive.  Direct intraarterial infusion of platelets and vasopressin has also been used successfully in the transcatheter treatment of gastrointestinal hemorrhage.
  • 73.  This technique, the SMA or IMA is catheterized and vasopressin is infused through the catheter  Typical vasopressin therapy involves an initial 20-minute infusion at a rate of 0.2 U/min followed by repeated arteriography to determine whether bleeding has stopped and that the artery is not overconstricted.  The infusion rate can be incrementally increased to 0.3 U/min and then to 0.4 U/min, if bleeding continues. Each change in infusion rate must be followed by a waiting period (20 minutes) for the increased drug dose to take effect and then another arteriogram to assess the effect. The infusion is continued for another 12 to 24 hours  The vasopressin infusion is then replaced with a saline solution infusion for 6 to 12 hours  The catheter is then removed if there are no clinical signs of bleeding but, by this time, the average time the catheter is in situ is 1–2 days.  the ability to stop bleeding relies on patient factors such as atherosclerosis and coagulopathy.
  • 74.  Prolonged presence of the catheter or catheter motion can lead to thrombosis or dissection.  Dislodgement of the catheter into another nontarget artery, such as the renal artery can cause flank pain and hematuria. Similarly, dislodgment of the catheter into the phrenic artery can lead to chest pain and arrhythmias. Other systemic complications due to vasopressin infusion include arrhythmias (bradycardia or ventricular tachycardia), hypotension, angina, and cardiac arrest.  mesenteric artery thrombosis, bowel infarction, and spontaneous bacterial peritonitis. Minor complications related to arterial access include hematoma, pseudoaneurysm, arterial spasm, and infection.
  • 75.  Embolization is defined as the deliberate occlusion of vessels for a therapeutic purpose  Embolization agents can be classified into  Temporary embolics such as- Gelfoam  Permanent embolics, which may be either solid or liquid.  Solid permanent embolic materials include polyvinyl alcohol (PVA), tris-acryl gelatin microspheres(Embospheres), detachable fiber coils, platinum coils, and detachable balloons.  Liquid embolic materials include absolute alcohol, N- butyl cyanoacrylate (NBCA), and Onyx® (an ethylene vinyl alcohol copolymer; Ev3 Endovascular, Inc. Plymouth, MN).
  • 76.  Microcoils (complex helical fibered platinum coils) range from 2 to 12 mm in diameter and are available in various lengths. These coils are highly radiopaque and can be precisely deployed.  Once deployed in a distal artery, they decrease the perfusion pressure allowing thrombosis of the bleeding vessel  Coils are easy to use and pose a lesser threat of ischemia than PVA particles, which may disseminate to the smaller vessels.  coils are usually preferred for embolization of pseudoaneurysms.  N-butyl cyanoacrylate (NBCA) allows for rapid and permanent embolization due to its fast polymerization when it comes in contact with blood. A single injection may provide complete hemostasis through simultaneous embolization of collateral vessels connected to the bleeding focus. It is useful in patients with coagulopathy as the vessel occlusion is independent of the coagulation process.  Polyvinyl alcohol and Gelfoam® have certain disadvantages. Both agents are more difficult to control than microcoils because neither can be seen during fluoroscopy. An additional disadvantage of polyvinyl alcohol particles is that the particles may reach intramural circulation beyond the level of collateralization leading to bowel infarction or may reflux into nontarget arteries.
  • 77.  CT angiography has a crucial role in preprocedure evaluation of a patient with GI bleeding.  Oxygen saturation, blood pressure, and heart rate and rhythm are continuously monitored.  Intravenous glucagon (1 mg) or scopolamine butyl bromide is administered to decrease bowel peristalsis.  General anesthesia is highly useful during angiography to maintain haemodynamics and decreasing motion artifact.  Selective injections into the celiac axis, SMA, and IMA are routinely obtained. It is important to cover the entire abdomen during injections into the SMA and the IMA.  Once the bleeding source is localized angiographically,  a 3-French microcatheter is advanced coaxially to the bleeding site through the indwelling 4- or 5-French catheter. Attempts are made to position the catheter as close to the bleeding site as possible. In the IMA distribution, the catheter is advanced to the marginal artery or the terminal artery if possible. In the SMA, the catheter is advanced to the vasa recta. If spasm occurs, intraarterial papaverine (25 mg) may be administered
  • 78.  Embolization is performed only when the catheter can be advanced to or distal to the mesenteric border of the colon. Embolization is performed until no further arterial extravasation is seen. Technical success is defined as cessation of bleeding as seen on angiography.  During the procedure, NBCA is mixed with iodized oil in ratios varying from 1:1 to 1:334 and the microcatheter must be flushed with 5% dextrose solution prior to injection to prevent premature polymerization of NBCA within the catheter.  Injection is stopped when extravasation of the mixture occurs from the bleeding site or when an underlying pseudoaneurysm is completely opacified.  Although catheterization may be possible, it may be difficult to deliver the coils because of the tortuosity of the vessels. In such instances, NBCA can be a good choice due to its low viscosity.  When a bleeding vessel is inaccessible for selective catheterization, embolotherapy may be abandoned and vasopressin infusion may be undertaken for control of GI bleeding.
  • 79.  Bowel infarction and gangrene.  arterial dissections and nontarget embolization due to migration of the embolic materials.  Transcatheter embolization with NBCA has the potential risk of embolization of the proximal segment without adequate embolization at the bleeding site due to rapid polymerization.  Distal embolization of the nontargeted sites may occur due to too rapid injection of the NBCA mixture or an excessively prolonged polymerization time and reflux of NBCA into another nontarget vessel due to overinjection.  In general, embolization is safer than vasopressin infusion as it has lower access site complications due to the shorter catheter dwell times
  • 80. Delayed image of proper hepatic arteriogram shows a large pseudoaneurysm arising from the gastroduodenal artery. (B) The aneurysm was treated with coil embolization of the aneurysm and feeding artery. Coil migration was noted during the procedure. However, patient had an uneventful recovery
  • 81. A 50-year-old man with pancreatitis presented with gastrointestinal (GI) bleeding. (A) Superior mesenteric arteriogram reveals a pseudoaneurysm from a jejunal branch, which was successfully treated with coils (B). (C) Another pseudoaneurysm in a branch of the right hepatic artery is also treated with coils (D)
  • 82. In patients with endoscopy-proven nonvariceal gastric bleeding, embolization of the left gastric artery is often practiced even no active extravasation is found on angiography.  Pseudoaneurysms secondary to pancreatitis may result in upper or lower GI bleeding depending on the location of the aneurysm. These can be successfully embolized with coils.  Variceal bleeding is treated with transjugular intrahepatic portosystemic shunt (TIPS) and retrograde embolization of the varices  Both endoscopy and angiography have been used for the diagnosis of a Dieulafoy lesion. Transcatheter arterial embolization has been reported for gastric Dieulafoy lesions, with variable results.  Partial splenic embolization is effective at reducing variceal bleeding regardless of the underlying cause of the portal hypertension.  Recent portal vein thrombosis may recanalize with systemic anticoagulation in 80% of patients.  Transsplenic recanalization of the portal vein has been described in children. Splenic arterial embolization can be performed before the transsplenic procedure to reduce splenic vein flow and prevent bleeding.  Similarly, isolated gastric varices secondary to splenic vein thrombosis may be treated with splenic embolization or splenectomy.
  • 83.  This technique has been shown to be effective in adequately controlling a bleeding site by temporary occlusion of the vessel due to vasospasm.  The decrease in blood flow and pulse pressure caused by vasospasm would allow normal physiologic thrombosis of the bleeding site.  In time, the spasm would resolve, thereby allowing restoration of the blood flow and keeping the risk of intestinal ischemia or infarction to a minimum.  This technique may be employed as primary therapy in patients who cannot tolerate vasopressin or when embolotherapy is difficult or not feasible.
  • 84.  EGD and colonoscopy are currently considered the first-line diagnostic and therapeutic procedures of choice for both upper and lower gastrointestinal bleeding.  Endoscopic evaluation allows relatively safe, direct localization and characterization of bleeding lesions within the majority of the upper gastrointestinal tract as well as in the colon and distal ileum. The distal duodenum and the majority of the small bowel cannot be adequately assessed with conventional endoscopy
  • 85.  Visual characterization of a bleeding lesion can provide important prognostic information regarding the risk of recurrent bleeding and may prompt tissue sampling if a neoplasm is suspected.  The reported sensitivity and specificity of EGD for upper gastrointestinal bleeding are 92%– 98% and 30%–100%, respectively.  Occasionally, rapid hemorrhage obscures endoscopic visualization of the bleeding site and precludes intervention.
  • 86.  Bowel preparation is required prior to colonoscopy, which can be completed in 3–4 hours, typically by administering a polyethylene glycol– based solution orally or via a nasogastric tube.  Endoscopic interventions can be performed if the bleeding lesion is adequately visualized.  Endoscopic therapeutic treatments may be (a) by injection (epinephrine, alcohol), (b) thermal (heater probe, electrocoagulation, laser), or (c) mechanical (clips, bands). Injection sclerotherapy with epinephrine achieves primary hemostasis rates of 96.7% for ulcers and 80%–90% for variceal bleeding .  Although all of the above mentioned therapeutic modalities demonstrate similar efficacies in randomized trials, they have shown increased effectiveness when used in combination
  • 87.  Approximately 15%–20% of patients with treated upper gastrointestinal bleeding will develop recurrent bleeding after endoscopic treatment, usually within 72 hours .  Wireless Capsule Endocopy has proved beneficial in patients in whom no source of bleeding has been identified despite evaluation with esophagogastroduodenoscopy and colonoscopy.  Patient preparation consists of a 10-hour fast, followed by ingestion of the capsule with a glass of water. Data interpretation occurs after 8 hours of transit time, after which 2–3 hours are needed to download the data to a workstation.  Capsule retention by intestinal stricture is the most serious complication . Because of the prolonged imaging time and the need for preprocedural fasting, there is presently no defined role for Wireless Capsule Endocopy in the evaluation of acute gastrointestinal bleeding.
  • 88.  Helical CT has depicted active colonic haemorrhage with bleeding rates as low as 0.3 mL/min, which is below the reported threshold for selective catheter angiography  Significant gastrointestinal bleeding that resulted in either systemic hypotension (systolic blood pressure
  • 89. The CT angiographic diagnosis of active gastrointestinal bleeding is made when hyperattenuating extravasated contrast material is seen within the bowel lumen. The extravasated contrast material may demonstrate linear, jetlike, swirled, ellipsoid, or pooled configurations or may fill the entire bowel lumen, resulting in a hyperattenuating loop
  • 90.  Other studies see the HU contrast Threshold  Most cases of acutely extravasated contrast material into the bowel lumen will exceed the 90 HU threshold  Although small amounts of bleeding or thin contrast material “jets ” may not reach this threshold due to volume averaging within either the section itself or the user-defined region of interest.
  • 91.  In addition, comparison with unenhanced images allows differentiation of active hemorrhage from other high-attenuation material that may be present within the gastrointestinal tract at the time of CT angiographic evaluation, thereby preventing false-positive interpretation.  Therefore, high-attenuation material detected within the bowel lumen at CT angiography that was not present at unenhanced CT performed immediately prior to the CT angiography is diagnostic for acute gastrointestinal hemorrhage. .
  • 92.  In addition to helping detect active gastrointestinal hemorrhage, CT angiography allows concurrent evaluation of the gastrointestinal and proximal femoral vasculature. Because significant anatomic variation of the gastrointestinal vasculature exists, preoperative knowledge of the active gastrointestinal bleeding site and its vascular supply is extremely useful for preinterventional planning this preoperative knowledge will decreased number of digital subtraction angiographic exposures, faster catheterization of bleeding vessels, decreased contrast material use during angiography, and shorter procedure times. It has also reduced patient (and operator) radiation exposure within the angiography suite
  • 93.  Evaluation of gastrointestinal bleeding with CT angiography may also provide etiologic information in many cases, especially with lower gastrointestinal bleeding. CT angiography can easily help diagnose colonic diverticuli, the most common cause of lower gastrointestinal.  CT angiography in the detection of colonic angiodysplasia.  Angiodysplasia may account for up to 40% of cases of lower gastrointestinal bleeding in patients over 60 years of age and is the second most common cause of such bleeding
  • 94.  Distinguishing diverticular from angiodysplastic bleeding (when possible) is important because of the prognostic differences between these two lesions.  Although bleeding will cease spontaneously in 80% or more of cases of angiodysplastic bleeding and in 75% of cases of diverticular bleeding recurrent bleeding will develop in up to 85% of cases of untreated angiodysplastic bleeding as opposed to only 25% of cases of untreated diverticular bleeding.  CT angiography can also help accurately diagnose neoplasms and colitis, the third and fourth most common causes of lower gastrointestinal bleeding, respectively.  Concurrent localization of active hemorrhage and diagnosis of the underlying cause can also have important treatment and management implications.
  • 95. Hemorrhage from a Mallory-Weiss tear. Angiogram demonstrates hemorrhage caused by a Mallory-Weiss tear appearing as a small focus of extravasated contrast material (arrow). (2) Stent-related upper gastrointestinal bleeding. Angiogram shows brisk hemorrhage from the main trunk of the right hepatic artery due to erosion from an endoscopically placed stent (Wallstent; Schneider, Minneapolis, Minn). Note the presence of extravasated contrast material in the common duct and duodenum (arrows).
  • 96. (A) Delayed phase contrast-enhanced computed tomography (CT) scan of the abdomen shows active contrast material extravasation (arrow) into a jejunal loop consistent with active gastrointestinal bleeding. (B) Superior mesenteric arteriogram shows active extravasation (arrow) of contrast material from a branch supplying the jejunum. (C) The bleeding vessel was selectively catheterized. (D) The bleeding vessel was embolized with polyvinyl alcohol (PVA) 500–700 m particles. Postembolization angiogram shows no more active contrast extravasation.

Notas do Editor

  1. 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).
  2. - 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
  3. 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
  4. inflammation and irritation of the wall of the first part of the small intestine.
  5. 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