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S. Sprayregen
ivalon or with coils is the treatment of choice and is
usually effective.
58
See Chapter 31 for details regarding
diagnosis and treatment of hemobilia.
Aortoenteric fistula
Aortoenteric fistula is an infrequent (0.4–2.4%) but lifethreatening late complication of aortic vascular grafting
and must be considered in any patient with UGI bleeding
who has had previous aortic surgery; a fistula may occur
even more rarely with a mycotic or noninfected aortic
aneurysm without previous surgery, erosion of a tumor,
or a pancreatic pseudocyst into the aorta or as a sequela
of radiation therapy. Aortoduodenal fistulas account for
80% of all aortoenteric fistulas. The postsurgical mechanisms include direct fistulous communication between
the graft lumen (due to disruption of the suture line) and
bowel (duodenum), pseudoaneurysm at the suture line
with erosion into the bowel lumen, and erosion of the
graft body into the bowel lumen remote from a vascular
suture line.
59
GI bleeding occurs in nearly all patients
with these conditions. Characteristically, the initial bleed,
whether hematemesis, melena, hematochezia, or a combination of these, is brief and self-limited and followed
from several hours to days by massive GI bleeding; rarely,
there is massive initial GI bleeding without a sentinel
bleed. Lesser degrees of chronic bleeding occur when the
graft erodes into the duodenum; these patients may also
present with septicemia. The third and fourth portions of
the duodenum most commonly are involved, with the
small bowel or colon involved in 10 to 20% of cases.
Endoscopy is the diagnostic procedure of choice, but
because the fistulas are usually in the third or fourth
portion of the duodenum, they may not be seen endoscopically. Any bleeding or erosion distal to the second
portion of the duodenum should arouse the suspicion of
an aortoduodenal fistula. CT may show an aneurysm, and
the diagnosis is confirmed if extraluminal gas is detected
at the site of previous surgery. Angiography may show
extravasation, an aneurysm, or pseudoaneurysm, but it
also may be normal. All diagnostic studies may be normal; when the possibility of an aortoenteric fistula is
considered, surgery must be performed because up to
one third of patients die within 6 to 12 hours of the
sentinel bleeding.
Vascular lesions
Two infrequent vascular lesions that cause UGI bleeding,
usually in patients aged 60 to 80 years, are gastric antral
vascular ectasia (watermelon stomach) and gastroduodenal
arteriovenous malformations (AVMs).
stomach is much more common in women than men;
there is no sex predilection in AVMs. Both can present
with occult bleeding or melena. Diagnosis usually is made
37
Watermelon
by characteristic endoscopic findings, and patients can be
treated by endoscopic techniques. Angiography may show
a feeding artery, nidus, and early drainingvein in AVMs.
■ Endoscopic Therapy
59
Many lesions causing UGI bleeding, including 85% of
bleeding ulcers, can be treated effectively by endoscopy.
20,61
Therapeutic modalities currently used in
conjunction with endoscopy are the heat probe, electrocoagulation, injection (with ethanol, epinephrine, or hypertonic saline), combinations of these modalities, and
laser therapy. There is no conclusive evidence that one
modality is more effective or safer than the others. Lesions that have been treated successfully by endoscopy
include gastric and duodenal ulcers, Mallory-Weiss tears,
angiodysplasias, and Dieulafoy’s lesions. Erosive gastritis
is usually not amenable to endoscopic treatment because
of the diffuse nature of the lesion. Gastric ulcers high on
the lesser curvature and ulcers in the posteroinferior
aspect of the duodenal bulb are at high risk for bleeding
during endoscopic therapy (as well as for catastrophic
rebleeding) as a result of their close relationship to the
left gastric artery and the gastroduodenal artery, respectively; therefore, most endoscopists do not treat these
lesions endoscopically.
20
Complications of endoscopic
hemostatic therapy include ulceration, bleeding, and
perforation.
20,61
In only 1 to 2% of cases is induced bleeding not controlled with further therapy. Ulceration is
self-limited and does not appear to prolong ulcer healing
rates. The rate of perforations is usually 1% or less but
may be as high as 3%.
■ Diagnostic Arteriography
Diagnostic arteriography for acute UGI bleeding is indicated when continued bleeding and unsuccessful or indeterminate endoscopy occur. The arteriogram should
be directed toward the suspected site of bleeding as determined clinically and endoscopically. The angiographic sign of bleeding is contrast extravasation (Figs.
30-2A, 30-3, and 30-4), which may be tubular and simulate a vein (Fig. 30-3), but differentiation from a vein is
possible because contrast does not drain into more central veins and remains in its original position. This
angiographic sign of bleeding (which also applies to
bleeding in other areas) was first described in the upper
GI tract and is referred to as the pseudovein sign.
been shown experimentally that a bleeding rate as low as
0.5 mL/min can be demonstrated angiographically.
On the other hand, even massive bleeding may not be
demonstrated if the angiogram is not performed at the
exact instant that bleeding is occurring, because bleed-
62
60
It has
63
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A
B
FIGURE 30-2. Bleeding duodenal ulcer: angiographic demon-
stration and embolization. A: Gastroduodenal artery injection
arrow
shows extravasation (
gastroduodenal artery, obstructing it. B: Superior mesenteric
arteriogram shows no extravasation in the duodenum. Note the
coils (
arrows
) in gastroduodenal artery.
). Coils then were placed in the
ing is frequently intermittent.64For a reasonable chance
at demonstrating extravasation, blood loss should be in
the order of at least two to three units per day.
travasation on angiography with UGI bleeding is more
frequent than with lower GI bleeding.
has been demonstrated in up to 97% of patients
66–68
Extravasation
67
UGI bleeding; the highest reported rate with lower GI
bleeding is 72%.
68
Arteriography can show only arterial
and capillary bleeding but will not show venous bleeding
(as in bleeding esophageal varices).
The arteriogram usually is performed from the femoral
artery and far less frequently from the left axillary or brachial artery. Aortography is not performed unless an aortoduodenal fistula is suspected. Aortography may show a
nipple at the site of the fistula,
65
or it may show no evidence of the fistula. One report emphasizes the value of a
prone lateral view to visualize an aortoenteric fistula.
Although many different catheters can be used for se-
lective studies, we favor the 5 F Sos Omni catheter (Angio-
65
with
69
FIGURE 30-3. Bleeding marginal ulcer with pseudovein sign.
Extravasation in the left upper quadrant (
jejunal artery. The patient had a Billroth II operation.
arrows
Dynamics, Queensbury, NY) because it can be used for
superior mesenteric, celiac, and left gastric catheterizations. If the Sos Omni catheter is not successful in
catheterizing the left gastric artery, a Rosch left gastric
catheter (Cook Incorporated, Bloomington, IN) or the
Waltman loop technique may be used with a cobra catheter; this latter technique is said to be successful incatheter-
Ex-
izing 90% of left gastric arteries.
70
Using cut-film or nonsubtracted digital acquisition, celiac and superior
mesenteric arteries are injected with 50 mL of contrast
(approximately half the amount of contrast is used with
digital subtraction technique) and filmed at a rate of 1
film/sec for 10 sec followed by 1 film/every other second
for 20 sec. For left gastric arteriography, approximately 15
mL at 3 mL/sec isinjected with filming at 1/sec for 15 sec.
The angiographer should be aware that a normal adrenal
stain (Fig. 30-5), hyperemic or compressed mucosa, or
staining caused by injection with the catheter wedged all
may produce stains that can be mistaken for contrast extravasation.
71
Aortography is rarely indicated, except, as mentioned,
when there is clinical suspicion of an aortoenteric fistula
or occasionally for a distal esophageal lesion, which may
) fed by a
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FIGURE 30-4. Erosive gastritis. Late capillary/venous phase
of left gastric arteriogram shows extravasation of contrast (
) and hyperemic gastric fundus (
row
filling of left inferior phrenic artery branches.
FIGURE 30-5. Normal adrenal stain. Capillary phase of celiac
arteriogram shows bilateral adrenal stains. (Courtesy of Jonathan Trambert, M.D.)
arrowheads
). Also noted is
ar-
be fed directly bysmall aortic branches. If endoscopydemonstrates bleeding from the distal esophagus or stomach,
the first injection should be into the left gastric artery. For
duodenal bleeding,a common hepatic or gastroduodenal
arteriogram should be obtained first. If no abnormality is
seen, the superior mesenteric artery should be studied; it
is even more desirable with duodenal bleeding toperform
a selectiveinferior pancreaticoduodenal arteriogram (the
inferior pancreaticoduodenal artery arises from the first
jejunal artery in 50% of cases). If endoscopy cannot be
performed or does not reveal a bleeding site, celiac and
superior mesenteric arteriograms should be obtained; all
the arterial branches that could supply a UGI bleeding
lesion must be well visualized.
In a large series of patients with angiographically dem-
onstrated gastric bleeding,
72
extravasation was from a
branch of the left gastric artery in 85% of cases, the right
gastric and the short gastric arteries each in 5%, the
gastroepiploic artery in 3%, and the gastroduodenal and
the left inferior phrenic artery each in 1%. Bleeding was
at the gastroesophageal junction in 11%, in the fundus
and proximal two thirds of the body in 81%, and in the
distal third of the body and antrum in 8%. Most cases
were stress mucosal bleeding, which in 95% of these cases
was in the proximal stomach. The authors pointed out
that there was a 33% correlation between endoscopy and
angiography in localizing bleeding sites, but they also
showed that despite endoscopic findings of diffuse oozing or bleeding from multiple sites, angiography revealed
more than one bleeding site in only two of the 103 patients with extravasation. Figure 30-4 demonstrates extravasation from the left gastric artery resulting from
erosive gastritis. Other authors have reported that often
gastric stress bleeding does not demonstrate extravasation but rather demonstrates diffuse hypervascularity,
mucosal hyperemia, and prominent draining veins (Fig.
73
30-6).
It is usually difficult to state with certainty based on the
angiographic extravasation whether the bleeding is from
a stress erosion, Dieulafoy’s lesion, or Mallory-Weiss tear
because all these bleeding sites are in the proximal stomach; gastric ulcers also may occur in the proximal stomach. Not infrequently, a left adrenal blush is produced
from injection of the left inferior phrenic artery, which
can originate from or near the left gastric artery and
should not be mistaken for a gastric bleed.
Clinically significant bleeding occurs in up to 5% of
patients following endoscopic sphincterotomy
74
and usually is identified endoscopically immediately after sphincterotomy. Angiography identified the bleeding site in
four of five patients in one report,
75
and the usual source
is a branch of the gastroduodenal artery. Hemobilia due
to PBD can be diagnosed and managed via the angiographic catheter as discussed in Chapter 31.
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367
A
FIGURE 30-6. Erosive gastritis: angiographic diagnosis and embolization. A: Left gastric arteriogram shows hyperemic stomach
but no extravasation. B: Occlusion of left gastric artery post-embolization with Gelfoam pledgets.
■ Angiographic Treatment of UGI Bleeding
toma, abscess at puncture site and in the spleen) or to the
pharmacological effects of vasopressin (cardiac arrhyth-
Therapy primarily depends on the location of the bleeding and the ability to place the angiographic catheter in
the artery feeding the area. Historically, vasopressin infusion of the left gastric artery preceded embolization as a
means of treating UGI bleeding.
76–78
An infusion of 0.1
to 0.2 units per minute of vasopressin into the left gastric
artery reduces gastric blood flow by 95%, whereas the
same dose infused into the celiac arter y reduces gastric
blood flow by only 60%.
catheterized in 75% of patients,
79
The left gastric artery can be
78
and left gastric artery
infusion of vasopressin will stop bleeding in 75 to 85% of
patients with acute gastric hemorrhage,
mately 18% of patients will have rebleeding.
67,78
but approxi-
67
Major com-
plications occurred in 6.5% and minor complications in
17.5% of patients with left gastric artery vasopressin infu-
67
sion.
All complications were related to the catheter
(femoral artery thrombosis, leg ischemia, groin hema-
mia and ischemia, peripheral vasoconstriction, reduced
urinary output, and fluid retention). Because of the success and complication rates, the authors cautiously suggest that the primary treatment of gastric bleeding might
be switched from vasopressin to embolization. In 1986,
80
Gomes et al.
compared vasopressin infusion and embolization with a variety of agents including Gelfoam
(Upjohn, Kalamazoo, Ml), Ivalon particles (Unipoint Industries, Inc., Highpoint, NC), coils, and detachable balloons for treating GI bleeding; for gastric bleeding, the
control rates were similar, but the authors recommended
embolization because it produces more rapid control of
bleeding, has a lesser incidence of rebleeding, and avoids
the cardiovascular effects of vasopressin and the problems associated with long-term catheter placement. Selective infusion of vasopressin into the superior mesenteric
artery also has been reported to control bleeding in pa-
B
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tients with marginal ulcers after partial gastrectomy and
gastrojejunostomy. Rosenbaum et al.
81
demonstrated extravasation in five patients with bleeding marginal ulcers;
of the four patients treated with vasopressin infusion,
permanent and temporary control of bleeding was
achieved in two cases.
The stomach is quite resistant to ischemia because of its
rich submucosal plexus, and preservation of a single major branch is usually sufficient to maintain viability.
82
In
keeping with this finding, ischemic injury from left gastric
artery embolization or vasopressin infusion is exceedingly
rare; when it does occur after catheter-directed ther-
83,84
apy,
additive factors usually account for the ischemia
(i.e., previous surgery, combination of particulate and vasopressin therapy, shock, and perhaps severe diffuse
atherosclerosis) to account for the ischemic injury. Embolotherapy of the left gastric artery should be with Gelfoam pledgets or polyvinyl alcohol particles. Gelfoam
powder should not be used because it obstructs peripheral arteries and can lead to ischemic necrosis.
85
Gelfoam
powder should be considered only in the presence of a
major coagulopathy.
As described in Chapter 2, the blood supply to the
distal esophagus arises from the left gastric and left inferior phrenic arteries. Other than Mallory-Weiss tears, few
reports of catheter treatment of lesions of the distal
esophagus by embolization of these arteries
39
have appeared. A single case was reported in which bleeding
from a distal esophageal ulcer was controlled by injecting
an artery arising directly from the lower thoracic aorta
with a combination of Gelfoam and vasopressin.
86
In summary, acute arterial or capillary bleeding from
the distal esophagus or stomach (with the exception of
the antrum) due to esophagitis, Mallory-Weiss tear, hemorrhagic gastritis, gastric ulcer, and Dieulafoy’s lesion currently is treated by embolization of the left gastric artery
with Gelfoam pledgets or polyvinyl alcohol particles in
most centers. If the angiographer is unable to catheterize
the left gastric artery, the algorithm shown in Figure 30-7
for vasopressin infusion of the celiac artery, described by
Eckstein et al.,
67
can be tried. If rebleeding occurs, repeat
left gastric arteriography should be performed, and an
angiographic search should be undertaken to visualize
FIGURE 30-7. Algorithm for vasopressin infusion of the celiac
artery for gastric bleeding.
additional feeding arteries, such as the left inferior
phrenic, short gastrics, right gastric, and other branches
of the celiac artery.
The presence of a coagulopathy negatively influences
the success rate of embolotherapy. In a series of 29 GI
bleeding patients, most of whom presented with UGI
bleeding, embolotherapy was unsuccessful in 8 of 14 patients with a coagulopathy and in only 3 of 15 patients
without a coagulopathy.
87
Pyloroduodenal bleeding is much more difficult to
control by catheter-directed techniques than gastric
bleeding primarily because of the dual blood supply
(from the celiac and superior mesenteric arteries). Vasopressin infusion of arteries supplying pyloroduodenal
bleeding controlled the bleeding in only 15 of 46 patients, five of whom had rebleeding.
88
Other possible
contributing causes for the poor results postulated by the
authors, in addition to the dual blood supply, were involvement of large arteries that do not respond to vasopressin and the transmural inflammation that inhibits
both the vascular and bowel wall constriction actions of
vasopressin. Of five bleeding duodenal ulcer patients
treated by Gomes et al.
80
with intraarterial vasopressin,
bleeding was initially successful in stopping bleeding in
two patients, both of whom had rebleeding; in this same
series, the authors successfully embolized five of six
bleeding duodenal ulcers and successfully treated six of
eight gastric bleeds with vasopressin. In 1977 Ring et al.
identified pitfalls in the angiographic management of
hemorrhage, particularly related to vasopressin infusion,
which include the following: (a) pressure injection into
one limb of a vascular arcade (possibly intensified by
partial obstruction of the catheter) may alter the
hemodynamics so that an injected artery that appears to
feed a bleeding site is not the feeder; (b) catheter-induced vasospasm may reduce or stop antegrade flow in
the infused artery so that another part of the arcade
(which is not being infused) feeds the bleeding site; (c)
whereas vasopressin typically begins its constricting effect
distally,
90
infusion of vasopressin into one limb of an
arcade may produce proximal constriction such that flow
is reversed in the infused artery; the same principle applies when embolic occlusion is produced proximal to a
bleeding site.
The first embolization for pyloroduodenal bleeding
was performed by Rosch et al.
91
in 1972, who used autogenous clot injected into the right gastroepiploic artery
for a gastric antral bleed with the cessation of bleeding.
Subsequently, authors have used coils, balloons, Gelfoam,
polyvinyl alcohol, and cyanoacrylate for embolic occlusion of the gastroduodenal and pancreaticoduodenal arteries. Figure 30-2 shows treatment of a bleeding duodenal ulcer by placement of a coil in the gastroduodenal
artery. The advantages of embolotherapy over vaso-
89
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TABLE 30-1.
Artery embolized patients bleeding bleeding obstruction
Pancreaticoduodenal 28 27 15 5
Gastroduodenal 29 25 8 2
From Lang EK. Transcatheter embolization in management of hemorrhage from duodenal ulcer: long-term results and complications.
Radiology
Results of Embolotherapy for Pyloroduodenal Bleeding
No. of Initial control of control of stenosis with
1992;1882:703–707.
pressin infusion mentioned previously in regard to gastric bleeding also pertain to pyloroduodenal bleeding.
The largest series on embolotherapy for pyloroduodenal
bleeding was reported by Lang,
92
who described the results of embolotherapy for bleeding duodenal ulcer in 57
patients. The results are shown in Table 30-1. In summary, selective embolization of a pancreaticoduodenal
artery supplying the bleeding site offers better initial and
long-term control of bleeding than gastroduodenal occlusion. The main complication of embolotherapy, duodenal stenosis with obstruction, occurs more than twice
as frequently with pancreaticoduodenal than gastroduodenal embolization.
It is perhaps somewhat surprising that only a few cases
of infarction after embolotherapy or vasopressin infusions have been reported. Duodenal infarction requiring
surgery has been reported in only two cases of somewhat
more than 100 cases of pyloroduodenal bleeding in the
literature treated by catheter-directed techniques;
93,94
in
one additional case of embolization of both the gastroduodenal and pancreaticoduodenal arteries, postmortem
examination revealed pancreatitis.
95
Thus, in all three
cases, further ischemic insult in addition to embolization
(gastroduodenal surgery and vasopressin infusion) was
found.
Should the angiographer embolize when endoscopy
shows a bleeding site but the angiogram does not demonstrate extravasation? Reports in the literature have
conflicting conclusions. Lang et al.
96
reported that
approximately 20% of patients with endoscopically confirmed UGI bleeding had normal findings at angiography; additionally, two thirds of the lesions that were not
treated during angiography had massive rebleeding, and
lesions supplied by the left gastric artery that were prophylactically embolized did not rebleed. On the other
hand, Dempsey et al.
97
retrospectively studied patients
with nonvariceal massive UGI bleeding. Embolization,
mostly of the left gastric artery, was performed based on
clinical, endoscopic, and angiographic findings in patients who did not show extravasation. Subsequent surgery to control bleeding was necessary in approximately
30% of both embolized and nonembolized patients. It is
Long-term Duodenal
our policy to embolize the appropriate artery when a
bleeding site is demonstrated endoscopically but not
angiographically. We are less certain regarding embolization if a nonbleeding lesion (such as an ulcer) is endoscopically demonstrated; in view of the low morbidity
of embolization, we lean toward embolotherapy in these
cases.
Duodenal bleeding following endoscopic sphincterotomy often cannot be controlled endoscopically. As
stated, bleeding is usually from a branch of the gastroduodenal artery. Bleeding usually can be successfully treated
by embolization; in the four cases (of the five studied)
with extravasation, Saeed et al.
75
successfully treated three
patients by Gelfoam pledget embolization of the bleeding
branch (in the fourth, celiac stenosis precluded selective
catheterization). The author’s treatment plan for catheter-directed therapy of endoscopically demonstrated pyloroduodenal bleeding is shown in Figure 30-8.
In the largest series dealing with embolotherapy of
pancreatic pseudoaneurysms,
98
the authors successfully
occluded 15 of 19 (79%) peripancreatic aneurysms and
pseudoaneurysms (13 were due to pancreatitis). The article did not specify precisely what embolic materials
were used, but in the single case described, the splenic
artery was occluded with coils and Gelfoam. Two patients
died of sepsis, and four additional patients required ancillary surgery, including “drainage of pseudocyst and
intraabdominal sepsis.” Most other articles also describe
coils as the most appropriate agent for arterial occlusion,
although Gelfoam often has been used for small arteries
leading to pseudoaneurysms. Two principles of embolotherapy of pseudoaneurysms to ensure optimal treatment and to prevent recurrence must be emphasized:
(a) if possible, the artery distal and proximal to the pseudoaneurysm should be occluded (also, coils should be
deposited directly into the pseudoaneurysm), and (b)
angiography of potential collaterals should be performed, because it is not unusual for these pseudoaneurysms to be fed by more than one artery. Success and
follow-up can be monitored by duplex sonography.
99
Figure 30-9 shows a pseudoaneurysm of a pancreaticoduodenal arter y before and after coil embolization.
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FIGURE 30-8. Algorithm for catheter-directed therapy of endoscopically demonstrated polyroduodenal bleeding. If it is not possible to catheterize the gastroduodenal artery (GDA) vasopressen can be infused into the celiac artery, following the algorithm in Figure 30-7.2Following
pancreaticoduodenal artery (PDA) embolization, GDA angiography should be performed to make
certain that there is no additional bleeding from PDA or GDA;
(SMA) angiography and follow flow chart for SMA angiography. Danger of infarction from
embolization is heightened with pre-embolization or gastroduodenal surgery (see text).
†
then do superior mesenteric artery
‡
A B
FIGURE 30-9. Pseudoaneurysm of pancreaticoduodenal artery. A: Before treatment (
Coils in aneurysm, with aneurysm no longer opacified (
arrowheads
arrowheads
). B: After coil embolization.
).
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371
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