GI BLEEDING WITH INTERVENSIONS

Dr Abinash Samal

INTRODUCTION 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

Common Causes of Upper GastrointestinalBleeding

Erosion or ulcer 55–74

Variceal bleeding 5–14

Mallory-Weiss tear 2–7

Vascular lesions 2–3

Neoplasms 2–5

Common Causes of Lower GastrointestinalBleeding

Diverticular disease 20–55

Angiodysplasia 3–40

Neoplasms 8–26

Colitis 6–22

Benign anorectal lesions 9–10

Vascular Considerations 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

INTRODUCTION Gastrointestinal bleeding

describe every form of haemorrhage in the GIT, from the pharynx to the rectum.

Can be divided into 2 clinical syndromes:-- upper GI bleed (pharynx to ligament of Treitz)- lower GI bleed (ligament of Treitz to rectum)

LIGAMENT OF TREITZ

7/81

UPPER GASTROINTESTINAL BLEEDING

8/81

CLINICAL FEATURES Haematemesis : Vomiting of blood

whether fresh and red or digested and black.

Melaena : Passage of loose, black tarry stools with a characteristic foul smell.

Coffee ground vomiting : Blood clot in the vomitus.

Hematochezia : Passage of bright red blood per rectum (if the haemorrhage is severe).

9/81

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.

10/81

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

11/81

12/81

OESOPHAGEAL VARICES Abnormal dilatation of subepithelial

and submucosal veins due to increased venous pressure from portal hypertension (collateral exist between portal system and azygous vein via lower oesophageal venous plexus).

Most commonly : lower esophagus.

13/81

Esophageal varices: a view of

the everted esophagus and

gastroesophageal junction, showing

dilated submucosal veins (varices).

14/81

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 VaricesWith 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.

OESOPHAGEAL VARICES: PORTAL HYPERTENSION

PRE HEPATIC• Portal

vein thrombosis

• Splenic vein thrombosis

INTRA HEPATIC

• Cirrhosis• Schistos

omiasis• Sarcoido

sis• Myelopro

liferative disorder

• Congenital hepatic fibrosis

POST HEPATIC

• Budd-chiari syndrome

• Right heart failure

• Constrictive pericarditis

• Veno-occlusive disease

17/81

OESOPHAGEAL VARICES: PATHOPHYSIOLOGY

Portal venous hypertension

Resistance to flow in portal venous system

Pressure

Portal systemic shunting(Abnormal venous communication between

portal system and systemic venous circulation)

Appearing of large submucosal veins at lower end of oesophagus and gastric fundus

Haemorrhage due to intravariceal pressure18/81

Management

- blood transfusion- endoscopic variceal injection with sclerosant or banding.- sengstaken tube

20/81

MALLORY-WEISS TEAR

Longitudinal tears at the oesophagogastric junction.

may occur after any event that provokes a sudden rise in intragastric pressure or gastric prolapse into the esophagus.

Clinical features:- An episode of haematemesis following retching or vomiting.- Melaena- Hematochezia- Syncope- Abdominal pain.

Precipitating factors:- Hiatus hernia- retching & vomiting- straining- hiccuping- coughing- blunt abdominal trauma - cardiopulmonary resuscitation 22/81

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.

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 hemoclipping

25/81

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%)

26/81

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 its large size.

ESOPHAGEAL CARCINOMA

-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

ADENOCARCINOMASQUAMUS CELL

CARCINOMA

28/81

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

29/81

 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.

PATTERNPolypoidVaricoidInfiltrativeUlcerativeSuperficial spreadingStricturePseudoachalasia

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

PEPTIC ULCER 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

Radiographic signs of malignant ulcers

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

PEPTIC ULCER

38/81

PEPTIC ULCER: COMPLICATION

Haemorrhage- posterior duodenal ulcer erode the gastroduodenal artery- lesser curve gastric ulcers erode the left gastric artery

Perforation- generalized peritonitis- signs of peritonitis

Pyloric obstruction- profuse vomiting, LOW, dehydrated, weakness, constipation

39/81

Bleeding gastric ulcer Hemorrhage due to Duodenal Ulcer

EROSIVE GASTRITIS

Acute mucosal inflammatory process

Accompanied by hemorrhage into the mucosa and sloughing of the superficial epithelium (erosion).

41/81

EROSIVE GASTRITIS: AETIOLOGY

- 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

GASTRIC CANCER

- adenomatous polyps- leiomyoma- neurogenic tumour- fibromata- lipoma

- gastric adenocarcinoma (90%)- lymphomas- smooth muscle tumour

BENIGN GASTRIC NEOPLASM

GASTRIC CARCINOMA

44/81

GASTRIC CANCER 60-80 years age group. Male:female , 2:1

- diet- H.pylori infection- gastric polyps- gastroenterostomy- chronic gastric ulcer disease- chronic atrophic gastritis- intestinal metaplasia- gastric dysplasia- host factors

AETIOLOGICAL FACTOR

45/81

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

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.

52/81

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

53/81

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

54/81

UPPER GI BLEED:RISK FACTORS FOR

DEATH1. Advanced AGE2. 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

GASTROINTESTINAL BLEEDING

LOWER

56/81

LOWER GI BLEED: AETIOLOGY

Crohn’s diseaseDiverticula eg:

Meckel’s diverticulum, Jejujanal diverticulosis

Benign neoplasm eg: Peutz-Jegher’s syndrome

Leiomyoma. Malignant neoplasm eg:

Lymphoma, Angiodysplasia

Rectal carcinoma and polypsRectal prolapse

Carcinoma of colonPolyps eg:

Familial adenomatous polyposis Diverticular diseaseInflamation

Ischaemic colitis

Ulcerative colitis

Pseudomembranous colitis Angiodysplasia

HaemorrhoidsFissure-in-anoAnal carcinomaAnal wart

SMALL INTESTINE

RECTUM

COLON

ANUScDNA

PC

PACID

wCHF

57/81

HISTORY TAKING:RECTAL BLEEDING

Blood on its own or streaking the stool:Rectum : polyps or carcinoma, prolapsedAnus : 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 colonBlood on the toilet paper: Fissure-in-ano, Heamorrhoids.Loose, black, tarry, foul smelling stool: from the proximal of DJ flexure

58/81

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

59/81

ACR Appropriateness Criteria

Radionuclide Imaging 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.

Procedure 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.

Additional views 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

Estimation of severity of the bleeding

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.

Catheter-directed Angiography 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.

Pharmacological control 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.

Complication-

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 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).

Agents used 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.

procedure 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.

Complication 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)

Arterial interventions 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.

Catheter induced vasospasm

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.

Endoscopy 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.

CT Angiography 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