Learning materials

1. Anatomy and pathophysiology

2. Indications and contraindications

3. Techniques for treatment

4. Post procedural management and follow-up

5. Outcome

6. Take-home message

Site: CIRSE Academy

Course: Management of acute arterial gastro-intestinal haemorrhage
Book: Learning materials
Printed by: David Ryan
Date: Thursday, 9 April 2020, 11:16 PM
Table of contents
1. Anatomy and pathophysiology

2. Indications and contraindications

3. Techniques for treatment

4. Post procedural management and follow-up

5. Outcome

6. Take-home message

7. Finish the course

1. Anatomy and pathophysiology

Knowledge of normal arterial anatomy and awareness of possible anatomic variations of blood supply to the GI tract is essential in the int
management of acute GI haemorrhage.

Normal Anatomy
The coeliac axis and SMA usually arise from the anterior abdominal aorta at the level of T12 and L1-2 vertebral bodies, respectively. The IM
at the level of L3, approximately 3–4 cm above the level of the aortic bifurcation.

The coeliac axis is the arterial supply to the embryonic foregut supplying the gut from distal oesophagus to the second part of the duode
supplying the liver, gallbladder, spleen and pancreas (Figure 1).

Figure 1: Coeliac axis angiogram (coeliac axis CA; splenic artery SA; left gastric artery LGA; left hepatic artery LHA; right hepatic artery RHA
gastroduodenal artery GDA; right gastroepiploic artery RGEA).

The SMA is the main supply to the embryonic foregut, which extends from the second part of the duodenum to the distal third of the tran
2).

Figure 2: SMA angiogram.

The SMA also supplies the pancreas. The IMA supplies the embryonic hindgut, which extends from the distal third of the transverse colon
GI bleeding is more common than lower GI bleeding and the upper GI tract arterial anatomy is subject to greater variation so will be desc

The coeliac axis divides in to three major branches: the left gastric, splenic and common hepatic arteries. The first branch of the coeliac ax
artery. The coeliac further divides after 1-2 cm into the splenic and common hepatic arteries. The dorsal pancreatic artery or inferior phren
arise from the coeliac trunk.

The common hepatic artery becomes the proper hepatic artery after the origin of the gastro-duodenal artery (GDA). The characteristic cy
of the right hepatic artery. The right gastric artery, which supplies the pylorus and lesser curve of the stomach, arises from the common, p
artery but is often difficult to identify on angiography.

The left gastric artery runs cranially, supplying the distal oesophagus and fundus of the stomach. It communicates with the right gastric a
the gastroepiploic arteries, the short gastric branches of the splenic artery, and often the inferior phrenic artery.

The splenic artery runs along the superior surface of the pancreas. This accounts for it being the most common site of pancreatitic pseudo
supplies the spleen, stomach and pancreas. It provides the dorsal pancreatic artery, pancreatica magna and short gastric arteries. Its term
splenic hilar superior and inferior divisions, with the left gastroepiploic artery arising from the latter and supplying the greater curve of th

The first branch of the GDA is the posterior superior pancreaticoduodenal artery, which supplies the duodenum to the right and the panc
terminal divisions of the GDA are the anterior superior pancreaticoduodenal and the right gastroepiploic arteries. The latter anastomoses
gastroepiploic artery, which is a branch of the splenic artery. The superior pancreaticoduodenal arteries form a rich arterial network in the
neck, with numerous anastomoses with the inferior pancreaticoduodenal branch of the SMA. The inferior pancreaticoduodenal artery aris
the proximal SMA or the first jejunal arteries.

Variant anatomy
Variant anatomy is common, particularly in the upper GI tract, where variation is seen in approximately 30% of patients. Common variants

A replaced or accessory left hepatic artery arising from the left gastric artery;
A replaced proper, replaced right or accessory right hepatic artery from the SMA;
Either the left gastric, hepatic or splenic arteries, or all three, arising separately from the aorta;
A common coeliac-mesenteric trunk;
The dorsal pancreatic or inferior phrenic arteries arising from the coeliac trunk;
The GDA arising from the right or left hepatic artery;
The arc of Buehler, which is a persistent embryonic connection between the coeliac trunk and proximal SMA;
Rarely, the middle colic branch to the transverse colon arises from the dorsal pancreatic branch of the coeliac axis. If not identif
procedure imaging for lower GI bleeding, this variation is suspected if there is a gap in the vascular distribution of the SMA and
the transverse colon.

Occlusion of the coeliac axis, SMA or IMA origin is not uncommon, particularly in patients with arterial disease, and in such cases it is impo
collaterals to access the target vessel beyond the occluded origin. The pancreatico-duodenal arcade is an important communication betw
coeliac artery. The arc of Buhler, an embryonic communication between the main trunks of the coeliac and SMA is rarely present but can b
and IMA usually communicate via the marginal artery of Drummond and can also have a communication via the arc of Riolan if this is pres
haemorrhoidal branches from the internal iliac arteries can also be a source of supply to the IMA territory.

Pathophysiology
Upper GI bleeding is defined as bleeding in to the gut proximal to the ligament of Treitz, which is a double fold of peritoneum suspending
flexure. Upper GI (U-GI) bleeding is far more common than lower GI (L-GI) bleeding, with the incidence of U-GI bleeding being approximat
100,000 adults per year and L-GI bleeding being 25 cases per 100,000 adults per year by comparison [1]. Whilst L-GI bleeds are less comm
commonly encountered by the interventional radiologist due to the relatively good availability and use of U-GI endoscopy as a diagnostic
modality.

The underlying cause of GI bleeding is often unclear at presentation although a history of gastro-oesophageal reflux, excessive alcohol co
non-steroidal anti-inflammatory drugs (NSAIDs), pancreatitis, known GI tract tumour, recent surgery or percutaneous intervention may of
possible cause. Usually either endoscopy or CT is most likely to reveal the probable cause of bleeding. The common causes of U-GI bleedin
Table 1 below. It should also be noted that in up to 20% of cases there will be multiple causes of U-GI bleeding [2].
 Cause of U-GI bleeding %

Erosion/Ulcer 55-74

Variceal 5-14

Mallory-Weiss 2-7

Vascular lesions (Dieulafoy’s lesions and telangiectasis) 2-3

Neoplasm 2-5

Table 1: Causes of U-GI bleeding in percent.

L-GI bleeding has a different range of common causes which are summarised in Table 2 below.

Causes of L-GI bleeding %

Diverticular disease 20-55

Angiodysplasia 3-40

Neoplasm 8-26

Colitis 6-22

Benign anorectal lesions 9-10

Table 2: Causes of L-GI bleeding in percent.

2. Indications and contraindications

Indications
The indication for acute treatment is any active GI bleeding causing haemodynamic instability or requiring hospitalisation.

GI bleeding is notoriously intermittent, often stopping and starting, even in patients presenting with acute massive bleeding. Identifying
usually requires the patient to be actively bleeding, and if CT or angiography is performed during a period of temporary haemostasis then
the source of bleeding. A useful indicator of active bleeding is the degree of haemodynamic compromise (systolic blood pressure < 100 m
100 beats/min or clinical shock). [3] In addition, as bleeding can be intermittent, any signs of GI bleeding in conjunction with a transfusion
least 4 units of blood products during a 24 hour period in hospital should prompt the need for further investigation and imaging such as
endoscopy, CT-angiography or investigation with radio-nuclide imaging.

It should also be noted that as a consequence of GI bleeding being intermittent, there should be a consideration for empiric or prophylac
territory which has been shown to be responsible for the cause of bleeding on prior endoscopy. Typical practice is when upper GI endosc
active bleeding either in the duodenum or stomach with endoscopic clips positioned in the area of concern, if the patient continues to bl
angiography fails to reveal active bleeding at these sites then empiric embolisation of the appropriate territory should be performed (GDA
left gastric artery for stomach; if these vessels supply the area marked by the endoscopic clips). Empiric embolisation of the GDA and left g
angiographically negative upper GI bleeding has been found to be safe and effective at reducing the risk of re-bleeding. [6][7][8][9]

Contraindications
In the setting of acute bleeding where embolisation could be a life-saving procedure, contraindications should be considered relative in t

Severe iodinated contrast allergy – alternative contrast agents such as carbon dioxide and Gadolinium contrast media can be considered.

Severe bleeding disorders – efforts should be made to correct clotting disturbances which can usually be corrected over time, and arteria
be left in-situ appropriately monitored, or vascular closure devices can be used to achieve access site haemostasis. Successful embolisatio
in coagulopathic patients, but is still preferable to open surgery.

Renal insufficiency – the possible risk of acute kidney injury must be balanced against the risk of uncontrolled bleeding if embolisation is
Appropriate IV hydration should be started to reduce the risk of contrast induced acute kidney injury.
3. Techniques for treatment

Video 1: Techniques for treatment

Cited literature in Video 1

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gastrointestinal bleeding uncontrolled by endoscopy. Eur J Gastroenterol Hepatol 2012;24:929-938.

Anthony S, Milburn S, Uberoi R. Multi-detector CT: review of its use in acute GI haemorrhage. Clin Radiol. 2007 Oct;62(10):938-49.

Appleyard M, Glukhovsky A, Swain P. Wireless-capsule diagnostic endoscopy for recurrent small-bowel bleeding. N Engl J Med. 2001;

Bandi R, Shetty PC, Sharma RP, Burke TH, Burke MW, Kastan D. Superselective arterial embolization for the treatment of lower gastroi
hemorrhage. J Vasc Interv Radiol 2001;12:1399-1405.

Chaudhry V, Hyser MJ, Gracias VH, Gau FC. Colonoscopy: the initial test for acute lower gastrointestinal bleeding. Am Surg. 1998 Aug;

Cummings CL. Value of early capsular endoscopy for severe gastrointestinal bleeding. J Natl Med Assoc. 2004;96(12):1653-6.

Eriksson LG, Ljungdahl M, Sundbom M, Nyman R. Transcatheter arterial embolization versus surgery in the treatment of upper gastr
after therapeutic endoscopy failure. J Vasc Interv Radiol 2008;19:1413-1418.

Eriksson LG, Sundbom M, Gustavsson S, Nyman R. Endoscopic marking with a metallic clip facilitates transcatheter arterial emboliza
ulcer bleeding. J Vasc Interv Radiol. 2006 Jun;17(6):959-64.

Ernst O, Bulois P, Saint-Drenant S, Leroy C, Paris JC, Sergent G. Helical CT in acute lower gastrointestinal bleeding. Eur Radiol. 2003;13(1

Funaki B, Kostelic JK, Lorenz J, Ha TV, Yip DL, Rosenblum JD, et al. Superselective microcoil embolization of colonic hemorrhage. AJR A
2001;177:829-836 7.

Gordon RL, Ahl KL, Kerlan RK, Wilson MW, LaBerge JM, Sandhu JS, Ring EJ, Welton ML. Selective arterial embolization for the control of
gastrointestinal bleeding. Am J Surg. 1997;174(1):24-8.

Imbembo AL, Diverticular disease of the colon. In: Sabiston D, Editor. Textbook of Surgery (14th edn). Philadelphia, PA:WB Saunders, 1992:
Koh DC, Luchtefeld MA, Kim DG, Knox MF, Fedeson BC, Vanerp JS, et al. Efficacy of transarterial embolization as definitive treatment in
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Laing CJ, Tobias T, Rosenblum DI, Banker WL, Tseng L, Tamarkin SW. Acute gastrointestinal bleeding: emerging role of multidetector C
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1992;182(3):703-7.

Lee EW, Laberge JM. Differential diagnosis of gastrointestinal bleeding. Tech Vasc Interv Radiol 2004; 7: 112-22

Lefkovitz Z, Cappell MS, Lookstein R, Mitty HA, Gerard PS. Radiologic diagnosis and treatment of gastrointestinal hemorrhage and isc
North Am. 2002 Nov;86(6):1357-99.

Leitman IM, Paull DE, Shires GT 3rd. Evaluation and management of massive lower gastrointestinal hemorrhage. Ann Surg 1989;209:1

Lim JK, Ahmed A. Endoscopic approach to the treatment of gastrointestinal bleeding. Tech Vasc Interv Radiol. 2004 Sep;7(3):123-9.

Lipof T, Sardella WV, Bartus CM, Johnson KH, Vignati PV, Cohen JL. The efficacy and durability of super-selective embolization in the tr
gastrointestinal bleeding. Dis Colon Rectum 2008;51:301-305

Loffroy R, Guiu B, Cercueil JP, Lepage C, Latournerie M, Hillon P, Rat P, Ricolfi F, Krausé D. Refractory bleeding from gastroduodenal ulcer
embolization in high-operative-risk patients. J Clin Gastroenterol. 2008 Apr;42(4):361-7.

Loffroy R, Guiu B, D'Athis P, Mezzetta L, Gagnaire A, Jouve JL, Ortega-Deballon P, Cheynel N, Cercueil JP, Krausé D. Arterial embolotherapy
unmanageable acute gastroduodenal hemorrhage: predictors of early rebleeding. Clin Gastroenterol Hepatol. 2009 May;7(5):515-23

Loffroy R, Rao P, Ota S, De Lin M, Kwak BK, Geschwind JF. Embolization of acute nonvariceal upper gastrointestinal hemorrhage resist
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Mar 16.

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Gastroenterol. 1997;92(3):419-24.

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4. Post procedural management and follow-up
Active follow-up and management is required to ensure the success of embolisation following GI bleeding. In the early post-procedure pe
should be monitored for any signs of re-bleeding as well as being evaluated for any complications such as bowel ischaemia. Haemodynam
and blood pressure) as well as monitoring of haematocrit +/- blood gas analysis with lactate should continue along with appropriate IV flu
products. Supplemental oxygen therapy is also vital to minimise the impact on the oxygen-carrying capacity of blood due to loss of red b
haemodilution from IV fluids.

In the medium to longer term, once the bleeding has stopped and the patient stabilised, plans for definitive longer-term therapy should b
aetiology of bleeding was not clear then endoscopy or cross-sectional imaging should be considered to define the underlying pathology.
5. Outcome
In a large systematic review, technical success rates for embolisation of U-GI bleeding were reportedly between 84% and 93% with clinica
reported between 64% and 89% [4]. Clinical outcomes were adversely affected by multiorgan failure, shock, corticosteroids, transfusion a
bleeding within 30-days in U-GI bleeding has been reported to be between 0% and 55%.

For L-GI bleeding, the range of technical success for embolisation is reported between 73% to 100%. Clinical success in L-GI bleeding emb
between 69% to 100%. Rebleeding is reported to occur in 10% to 53% of patients. Predictors of re-bleeding are coagulopathy, longer time
massive transfusion, previous surgery, trauma, cancer bleeding, use of coils as the sole embolic agent and multiorgan failure. [5][6]
6. Take-home message
The safety and efficacy of embolisation in life-threatening GI bleeding is well established.

Embolisation has largely replaced surgery in the treatment of endoscopy-refractory GI bleeding.

Most GI bleeding is intermittent. Diagnostic and therapeautic success is dependent on the best achievable image quality and a thorough
and variant anatomy.

CT angiography is a reliable and accurate imaging technique to identify bleeding and plan transcatheter therapy in patients who are clini
bleeding, particularly in cases where endoscopy is negative or incomplete.
7. Finish the course
Complete the Final quiz with a passing grade of 70% and submit your Feedback to receive your CME Certificate.